Small Animal

Neurological
Emergencies
SIMON R PLATT BVM&S, DipACVIM(NEUROLOGY), DipECVN, MRCVS
Professor Neurology Service
Department of Small Animal Medicine and Surgery
College of Veterinary Medicine
University of Georgia
Athens, Georgia, USA

LAURENT S GAROSI DVM, DipECVN, MRCVS

Director and Head of Neurology/Neurosurgery Service
Davies Veterinary Specialists
Higham Gobion
Hertfordshire, England, UK

MANSON PUBLISHING/THE VETERINARY PRESS

For my girls, Jade, Danielle and Georgina
Simon Platt

To my son, George
Laurent Garosi

Copyright © 2012 Manson Publishing Ltd

ISBN: 978-1-84076-152-8

All rights reserved. No part of this publication may be

reproduced, stored in a retrieval system or transmitted
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Commissioning editor: Jill Northcott

Project manager and book design: Ayala Kingsley
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Illustration: Cactus Design, Diacritech, Ayala Kingsley
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 CONTENTS

Contributors 5
Preface 7
Abbreviations 8
PART 1 Admission and neurodiagnostic tests 13
CHAPTER 1 Examining the neurological emergency Laurent Garosi 15
CHAPTER 2 Respiratory and cardiovascular support Anthea Raisis & Gabrielle Musk 35
CHAPTER 3 Metabolic evaluation of critically ill neurological patients Louise Clark 61
CHAPTER 4 Imaging of neurological emergencies Fraser McConnell 83
CHAPTER 5 Cerebrospinal fluid analysis Amy Wood, Laurent Garosi & Simon Platt 121

PART 2 Decision making 137

CHAPTER 6 Obtundation, stupor and coma Peter Dickinson 139
CHAPTER 7 Seizures Simon Platt 155
CHAPTER 8 Exercise-associated weakness and collapse Arianna Negrin & Simon Platt 173
CHAPTER 9 Ataxia Jonathan Levine 193
CHAPTER 10 Acute paresis and paralysis John McDonnell 205
CHAPTER 11 Spinal pain Ronaldo da Costa 219
CHAPTER 12 Acute blindness Peter Nghiem & Scott Schatzberg 229
CHAPTER 13 Acute tremors and involuntary movements Marc Kent 243
CHAPTER 14 Head tilt and nystagmus Laurent Garosi 253
CHAPTER 15 Acute disorders of the head and face Lara Matiasek & Alberta de Stefani 265
CHAPTER 16 Monoparesis and neurological causes of lameness 299
Toby Gemmill & Malcolm McKee
 CONTENTS

PART 3 Specific emergencies 317

CHAPTER 17 Cerebrovascular accidents Laurent Garosi 319
CHAPTER 18 Ischaemic myelopathy Luisa de Risio 333
CHAPTER 19 Infectious and inflammatory diseases of the CNS 341
Scott Schatzberg & Peter Nghiem

CHAPTER 20 Head trauma Courtenay Freeman & Simon Platt 363

CHAPTER 21 Spinal trauma Natasha Olby 383
CHAPTER 22 Acute disc disease Joan Coates 399
CHAPTER 23 Status epilepticus Allison Haley & Simon Platt 417
CHAPTER 24 Myasthenia gravis Kerry Smith Bailey 433
CHAPTER 25 Tetanus and botulism Jacques Penderis 447
CHAPTER 26 Intracranial neoplasia and secondary pathological effects 461
John Rossmeisl & Theresa Pancotto

CHAPTER 27 Metabolic encephalopathies Kate Chandler & Robert Goggs 479

CHAPTER 28 Neurological toxicities Jennifer Pittman, Benjamin Brainard & Katrin Swindells 499

PART 4 Specific management issues 533

CHAPTER 29 Emergency neuroanaesthesia Anthea Raisis & Gabrielle Musk 535
CHAPTER 30 Analgesia for patients with neurological disease 557
Gabrielle Musk & Anthea Raisis

CHAPTER 31 Fluid therapy Anthea Raisis & Katrin Swindells 571

CHAPTER 32 Postoperative supportive care and physical rehabilitation 591
Sebastien Behr & Rebecca Green

APPENDICES 1: Emergency drug use; 2: Units and reference ranges; 609

3: Blood transfusion monitoring sheet
Amy Wood, Simon Platt & Laurent Garosi

Further reading 623

Index 651
 CONTRIBUTORS
5

Kerry Smith Bailey Ronaldo C da Costa Robert A N Goggs

DVM, DipACVIM(Neurology) DVM, MSc, PhD, BVSc, DipACVECC, MRCVS
Oradell Animal Hospital DipACVIM(Neurology) Faculty of Medical and Veterinary
Paramus, New Jersey, USA Department of Veterinary Clinical Sciences
Sciences University of Bristol
Sebastien Behr College of Veterinary Medicine Bristol, UK
DVM, DipECVN, MRCVS The Ohio State University
Willows Veterinary Centre and Columbus, Ohio, USA Rebecca J Green
Referral Service BSc (Hons), ABW, RVN, CertCH
Shirley, Peter J Dickinson Davies Veterinary Specialists
Solihull, West Midlands, UK BVSc, PhD, Higham Gobion, Hertfordshire, UK
DipACVIM(Neurology)
Benjamin M Brainard Department of Surgical and Allison C Haley
VMD, DipACVA, DipACVECC Radiological Sciences BSc, DVM, MRCVS
Department of Small Animal School of Veterinary Medicine Faculty of Veterinary Medicine
Medicine and Surgery University of California-Davis University of Glasgow
College of Veterinary Medicine Davis, California, USA Bearsden Road
University of Georgia Glasgow, UK
Athens, Georgia, USA Courtenay Freeman
DVM Marc Kent
Kate E Chandler Department of Small Animal DVM, DipACVIM(Internal
BVetMed, PhD, DipECVN, Medicine and Surgery Medicine and Neurology)
FHEA, MRCVS College of Veterinary Medicine Department of Small Animal
Park Road University of Georgia Medicine and Surgery
Northaw, Athens, Georgia, USA College of Veterinary Medicine
Hertfordshire, UK University of Georgia
Laurent S Garosi Athens, Georgia, USA
Louise Clark DVM, DipECVN, MRCVS
BVMS, DipECVAA, CertVA, Davies Veterinary Specialists Jonathan M Levine
MRCVS Higham Gobion, Hertfordshire, UK DVM, DipACVIM(Neurology)
Davies Veterinary Specialists Department of Small Animal
Higham Gobion, Hertfordshire, UK Toby J Gemmill Clinical Sciences
BVSc, MVM, DSAS(Orth), College of Veterinary Medicine
Joan R Coates DipECVS, MRCVS Texas A&M University
DVM, MS, DipACVIM(Neurology) Willows Veterinary Centre and College Station, Texas, USA
Department of Veterinary Referral Service
Medicine and Surgery Shirley,
College of Veterinary Medicine Solihull, West Midlands, UK
University of Missouri
Columbia, Missouri, USA
 6 CONTRIBUTORS

Lara A Matiasek Natasha J Olby John H Rossmeisl Jr.

DrMedVet, DipECVN, MRCVS MA, VetMB, PhD, DVM, MS, DipACVCIM
Clinic of Small Animal Medicine DipACVIM(Neurology), MRCVS (Internal Medicine and Neurology)
at the Centre for Clinical Department of Clinical Sciences Virginia-Maryland Regional
Veterinary Medicine, College of Veterinary Medicine College of Veterinary Medicine
Veterinary Faculty, LMU Munich North Carolina State University Virginia Tech
Munich, Germany Raleigh, North Carolina, USA Blacksburg, Virginia, USA

J Fraser McConnell Theresa Pancotto Scott Schatzberg

BVM&S, DipECVDI, DVR, DVM, MS DVM, PhD,
CertSAM, MRCVS Virginia-Maryland Regional DiplACVIM(Neurology)
Small Animal Teaching Hospital College of Veterinary Medicine Veterinary Emergency & Specialty
Faculty of Veterinary Science Virginia Tech Centers LLC
University of Liverpool Blacksburg, Virginia, USA 2001 Vivigen Way
Leahurst Santa Fe, NM 87505, USA
Neston, Wirral, UK Jacques Penderis
BVSc, MVM, PhD, CertVR, Alberta de Stefani
John J McDonnell DipECVN, MRCVS DVM, PhD, DipECVN, MRCVS
DVM, MS, DipACVIM(Neurology) Faculty of Veterinary Medicine Centre for Small Animal Studies
Veterinary Neurology of the University of Glasgow Animal Health Trust
Chesapeake Bearsden Road Lanwades Park
Annapolis Glasgow, UK Newmarket, Suffolk, UK
Maryland, USA
Jennifer Pittman Katrin Swindells
W Malcolm McKee DVM, DipACVECC BVSc, MACVSc, DipACVECC
BVMS, MVS, DSAO, MACVSc, Georgia Veterinary Specialists Veterinary Clinical Sciences
MRCVS Atlanta, Georgia, USA School of Veterinary and
Willows Veterinary Centre and Biomedical Science
Referral Service Simon R Platt Murdoch University
Shirley, BVM&S, DipACVIM(Neurology), Perth, Western Australia, Australia
Solihull, West Midlands, UK DipECVN, MRCVS
Department of Small Animal Amy J Wood
Gabrielle C Musk Medicine and Surgery DVM
BSc, BVMS, CertVA, DipECVAA College of Veterinary Medicine Department of Small Animal
Veterinary Clinical Sciences University of Georgia Clinical Sciences
Division of Veterinary and Athens, Georgia, USA Veterinary Teaching Hospital
Biomedical Sciences University of Tennessee
Murdoch University Anthea L Raisis Knoxville, Tennessee, USA
Perth, Western Australia, Australia BVSc, PhD, DVA, MACVSc,
MRCVS, MVetClinSt
Arianna Negrin Veterinary Clinical Sciences
DVM, PhD Division of Veterinary and
Faculty of Veterinary Medicine Biomedical Sciences
University of Padova Murdoch University
Legnaro, Padova, Italy Perth, Western Australia, Australia

Peter P Nghiem Luisa de Risio

DVM DVM, PhD, DipECVN, MRCVS
Center for Genetic Medicine Centre for Small Animal Studies
Research Animal Health Trust
Children’s National Medical Center Lanwades Park
Washington DC, USA Newmarket, Suffolk, UK
 PREFACE
7

T HE field of clinical veterinary neurology has expanded

dramatically over the last couple of decades due in
part to the increased availability of advanced imaging
respectively, and should be informative to those with
imaging, critical care, anaesthesia, pathology and neurol-
ogy interests. With this multi-level goal in mind, we have
facilities, improved dispersion of knowledge through put together an outstanding array of experts in these
electronic media and greater consumer demand for fields, who have provided not only up-to-date informa-
therapy in the face of an unknown prognosis. A large part tion, but also invaluable opinion on how to deal with the
of this field is emergency based and many neurology vast range of neurological emergencies. What we hope
patients will require critical care. Rapid and practical we have also achieved with this group of authors is a more
decisions often need to be made based on uncertain global approach than is typical for such a focused text.
diagnoses and prognoses and frequently accompanied by Specialists from Australia, Europe and the USA have
restricted finances. Couple this with a justifiable fear of helped achieve this goal and we are deeply indebted to all
clinical neurology and we find ourselves faced with an of them for their contributions.
extremely challenging genre of cases. We are grateful to the students, residents and practi-
Such daily challenges prompted our interest in the tioners whom we have been fortunate enough to work
project that has become this book. Our aim was to with and who have helped us understand what is needed
develop a textbook that addressed small animal neuro- in a book such as this. We would also like to thank our
logical emergencies on multiple levels. The main focus mentors and colleagues, too numerous to mention, who
was always the need to be able to address cases quickly have inspired us to be who and what we are. However,
based on their presenting syndrome, whether this be Simon wishes to personally thank Dr Cheryl Chrisman
seizures, head tilt or paralysis. The chapters in Part 2 for her guidance, sincerity, knowledge, passion for
of this book have therefore been the fulcrum from neurology and friendship; and Laurent would like to
which everything else developed. In addition to the prac- thank Dr Laurent Cauzinille, Dr Alexander de Lahunta
tical aspect, it is essential to have an in-depth section and Professor Jacques Penderis. Final thanks should go
addressing the most common specific emergencies on a to Jill Northcott and all of those at Manson Publishing
pathophysiological, therapeutic and prognostic basis. who have believed in this project and supported us over
This is dealt with in Part 3 and hopefully will be benefi- the time it has taken to be completed.
cial to practitioners, students, residents and specialists We hope that you enjoy this text and that in some way
alike. More detailed diagnostic and emergency support- it helps you feel more comfortable with the next neuro-
ive therapies have been addressed in Parts 1 and 4, logical emergency.

Simon Platt and Laurent Garosi

 ABBREVIATIONS
8

AA atlantoaxial CA cytosine arabinoside

AAROM active assisted range of motion cAMP cyclic adenosine monophosphate
ACD-A acid citrate dextrose-A CaO2 arterial oxygen content
ACE angiotensin-converting enzyme CAT choline acetyltransferase
acetyl CoA acetyl coenzyme A CBC complete blood count
ACh acetylcholine CBF cerebral blood flow
AChE acetylcholinesterase CDI central diabetes insipidus
AChR acetylcholine receptor CDV canine distemper virus
ACT activated clotting time CHEM serum chemistry panel
ACTH adrenocorticotropic hormone CK creatine kinase
ADC apparent diffusion coefficient CMAP compound muscle action potential
ADH antidiuretic hormone CMC cerebellomedullary cistern
ADP adenosine diphosphate CMG congenital myasthenia gravis
AED antiepileptic drug CMOP craniomandibular osteopathy
AGID agar gel immunodiffusion CMR cerebral metabolic rate
AH abductor halluci CN cranial nerve
ALI acute lung injury CNS central nervous system
ALP alkaline phosphatase CO cardiac output
ALT alanine aminotransferase CO2 carbon dioxide
AMG acquired myasthenia gravis CoA coenzyme A
AMPA alpha-amino-3-hydroxy-5-methyl- COP colloid osmotic pressure
4-isoxazole propionic acid CPAP continuous positive airway pressure
ANNPE acute non-compressive nucleus pulposus CPCR cardio–pulmonary–cerebral
extrusion resuscitation
ANP atrial natriuretic peptide CPDA-1 citrate phosphate dextrose adenine-1
APPs acute phase proteins CPP cerebral perfusion pressure
aPTT activated partial thromboplastin time CRI constant rate infusion
ARAS ascending reticular activating system CRP C-reactive protein
ARDS acute respiratory distress syndrome CRT capillary refill time
AROM assisted range of motion CS chondroitin sulphate
AST aspartate aminotransferase CSF cerebrospinal fluid
AT antithrombin CSM cervical spondylomyelopathy
ATP adenosine triphosphate CT computed tomography
AV atrioventricular CVA cerebrovascular accident
CVP central venous pressure
BAER brainstem auditory evoked response CVR cerebral vascular resistance
BMBTs buccal mucosal bleeding times
BP blood pressure D5W 5% dextrose in water
bpm beats per minute DDS dialysis disequilibrium syndrome
BUN blood urea nitrogen DEA dog erythrocyte antigen
DEET diethyltoluamide
DI diabetes insipidus
 A B B R E V I AT I O N S 9

DIC disseminated intravascular coagulation GP general proprioceptive (ataxia/system)

DINAMAP device for indirect non-invasive, GRE gradient-echo (images)
automated, mean arterial pressure GTP guanosine triphosphate
DISH disseminated idiopathic skeletal
hyperostosis 5-HT 5-hydroxytryptamine
DNA deoxyribonucleic acid Hb haemoglobin
DO2 oxygen delivery HCO3- bicarbonate
DTPA diethylenetriamine penta-acetic acid HE hepatic encephalopathy
DV dorsoventral HME heat and moisture exchange
DWI diffusion-weighted imaging HR heart rate
HRPO horse-radish peroxidase
ECF extracellular fluid HTIG human tetanus immunoglobulin
ECG electrocardiogram
EDB extensor digitorum brevis IABP invasive arterial blood pressure
EDTA ethylenediamine tetra-acetic acid iCa2+ ionized calcium concentration
EEG electroencephalogram ICF intracellular fluid
ELISA enzyme-linked immunosorbent assay ICP intracranial pressure
EME eosinophilic meningoencephalomyelitis ICU intensive care unit
EMG electromyogram ID intradermal
EMLA eutectic mixture of local anaesthetics IFA immunofluorescent antibody
EMS electrical muscle stimulation Ig immunoglobulin
EPP end plate potential IGF-1 insulin-like growth factor-1
ERG electroretinogram IHC immunohistochemistry
ETT endotracheal tube IL-1 interleukin-1
IM intramuscular
FADH2 reduced form of flavin adenine dinucleotide IN intranasal
Fat Sat fat saturation (image) iNOS ionized nitric oxide synthetase
FCE fibrocartilaginous embolism IPPV intermittent positive pressure ventilation
FCEM fibrocartilaginous embolic myelopathy ITN idiopathic trigeminal neuropathy/neuritis
FDP fibrin (fibrinogen) degradation product IV intravenous
F’ECO2 fractional concentration of carbon dioxide IVDD intervertebral disc disease
in mixed expired air
FeLV feline leukaemia virus KBr potassium bromide
FFP fresh frozen plasma kPa kilopascal
FHS feline hyperaesthesia syndrome KS keratan sulphate
FiO2 fractional concentration of oxygen in
inspired air L lactate
FIP feline infectious peritonitis L:P lactate:pyruvate ratio
FLAIR fluid attenuated inversion recovery (image) L2-HGA L2-hydroxyglutaric aciduria
FSE fast spin echo (image) LD50 median lethal dose
fT4 free thyroxine LGN lateral geniculate nucleus/i
LMN lower motor neuron
GA general anaesthesia LS lumbosacral
GABA gamma-aminobutyric acid
GAG glycosaminoglycan MABP mean arterial blood pressure
GCMPS Glasgow Composite Measure Pain Scale MAC minimum alveolar concentration
GCS Glasgow coma scale MAP mean arterial pressure
GFAP glial fibrillary acid protein ME meningoencephalitis
GFR glomerular filtration rate MEM meningoencephalomyelitis
GI gastrointestinal MG myasthenia gravis
GME granulomatous meningoencephalitis MGCS Modified Glasgow Coma Scale
 10 A B B R E V I AT I O N S

MIR main immunogenic region PEEP positive end-expiratory pressure

MLAER middle latency auditory evoked response PEG polyethylene glycol
MMC mitochondrial membrane megachannel P’ETCO2 end-tidal carbon dioxide partial pressure
MMM masticatory muscle myositis PHPTH primary hyperparathyroidism
MNCV motor nerve conduction velocity PIP peak inspiratory pressure
MOF multiple organ failure PLR pupillary light reflex
MPSS methylprednisolone sodium succinate PMMA polymethyl methacrylate (cement)
MRA magnetic resonance angiography PMN polymorphonuclear (cells)
MRI magnetic resonance imaging PNS peripheral nervous system
MUA meningoencephalitis of unknown aetiology PR per rectum
MUP motor unit potential PROM passive range of motion
MW molecular weight PSS portosystemic shunt
PT prothrombin time
NaHCO3 sodium bicarbonate PTH parathyroid hormone
NADH nicotinamide adenine dinucleotide PTHrP parathyroid hormone-related protein
NASCIS National Acute Spinal Cord Injury Study PTN pretectal nucleus
(trials) PTT partial thromboplastin time
NIBP non-invasive arterial blood pressure PU/PD polyuria/polydipsia
NLE necrotizing leucoencephalitis PVE plasma volume expansion
NM neuromuscular
NMDA N-methyl-D-aspartate RAS reticular activating system
NME necrotizing meningoencephalitis RBC red blood cell
NMES neuromuscular electrical stimulation REM rapid eye movement
NO nitric oxide ROM range of motion
N2O nitrous oxide ROS reactive oxygen species
NSAID nonsteroidal anti-inflammatory drug RR respiratory rate
NSE neuron-specific enolase RTA road traffic accident

OCD osteochondrosis dissecans SAE sepsis-associated encephalopathy

OH obstructive hydrocephalus SAP systolic arterial blood pressure
OP organophosphate SARDS sudden acquired retinal degeneration
OPIDN organophosphate-induced delayed syndrome
neuropathy SBT [1] secondary brain tumour
SBT [2] systemic blood pressure
P pyruvate SC subcutaneous
PaCO2 arterial carbon dioxide partial pressure SE status epilepticus
PACO2 alveolar carbon dioxide partial pressure SF-EMG single-fibre electromyography
2-PAM pralidoxime (2-pyridine aldoxime methyl SG specific gravity
chloride) SIADH syndrome of inappropriate antidiuretic
PaO2 arterial oxygen partial pressure hormone secretion
PAO2 alveolar oxygen partial pressure SIRS systemic inflammatory response syndrome
PARP- poly[ADP-ribose] polymerase-1 SMFA sodium monofluoroacetate
PARR PCR for antigen receptor rearrangement SNAR soluble NSF attachment protein receptor
PBT primary brain tumour SPA staphylococcal protein A
PCO2 partial pressure of CO2 SpO2 saturation of haemoglobin with oxygen
PCP phencyclidine SRMA steroid responsive meningitis–arteritis
PCR polymerase chain reaction SSEPs somatosensory evoked potentials
PCV packed cell volume STIR short-tau inversion recovery (image)
PD proton density (image) SV stroke volume
PDH pituitary-dependent hyperadrenocorticism SVR systemic vascular resistance
PDS paroxysmal depolarizing shift
 A B B R E V I AT I O N S 11

T1/2 half-life UA urinalysis

T1W T1-weighted (image) UMN upper motor neuron
T2*GRE T2* gradient-echo (image) UOP urine output
T2W T2-weighted (image) URT upper respiratory tract
T3 triiodothyronine USG urine specific gravity
T4 thyroxine UTI urinary tract infection
TCA tricarboxylic acid
TCI target controlled infusion VC vasoconstriction
TENS transcutaneous electrical nerve stimulation VD [1] vasodilatation
TFPI tissue factor pathway inhibitor VD [2] ventrodorsal
TIA transient ischaemic attack VEGF vascular endothelial growth factor
TIVA total intravenous anaesthesia VILI ventilator-induced lung injury
TMJ temporomandibular joint VP ventriculoperitoneal
TMS trimethoprim–sulphonamide VT tidal volume
TNCC total nucleated cell count
TNF-α tumour necrosis factor-alpha WBC white blood cell
TOD target organ damage
TP total protein
TPR temperature, pulse, respiration
TS total solids
TSH thyroid-stimulating hormone
TSS approximate time to steady state
tT4 total thyroxine
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PART 1

ADMISSION AND 13

NEURODIAGNOSTIC TESTS

CHAPTER 1 Examining the neurological emergency

CHAPTER 2 Respiratory and cardiovascular support

CHAPTER 3 Metabolic evaluation of critically ill neurological patients

CHAPTER 4 Imaging of neurological emergencies

CHAPTER 5 Cerebrospinal fluid analysis

This page intentionally left blank
 ADMISSION AND NEURODIAGNOSTIC TESTS Chapter 1

EXAMINING THE
NEUROLOGICAL EMERGENCY 15

Laurent Garosi

INTRODUCTION Table 1 Initial assessment of the neurological

emergency patient
Neurological emergencies require rapid and accurate
Respiratory system
decision making and treatment. Inappropriate manage-
Respiratory rate, effort and rhythm, patency of upper airway,
ment in the early stages of the disease can have cata- auscultation of trachea and all areas of thorax
strophic consequences for the animal. The aims of this Cardiovascular system
chapter are to describe the step-by-step approach to the Mucous membrane colour, capillary refill time, pulse rate,
neurological emergency, including primary survey exam- quality and rhythm, auscultation of the heart
ination, rationale and principles of lesion localization Renal system
within the nervous system, and how to establish a Ability to urinate and palpation of urinary bladder
differential diagnosis list. Neurological system
Evaluation of mentation, ability to ambulate and pain
PRELIMINARY SURVEY EXAMINATION perception

It is all too tempting when presented with an emergency

patient that has severe neurological signs to rush
into evaluating its nervous system. However, initial phys-
ical assessment should focus on any imminent life- that a detailed anamnesis is obtained from the owner and
threatening abnormalities and evaluation of vital a comprehensive neurological examination performed.
functions (see Chapter 2), all of which can influence not Other body systems should also be evaluated, with a
only the interpretation of the neurological examination, complete physical examination to detect abnormalities
but also the prognosis for the patient. Preliminary survey that might affect the nervous system (e.g. animals pre-
examination assures identification and immediate treat- sented for epileptic seizures and abnormal mentation that
ment of conditions that are life threatening. have liver disease), that mimic a primary neurological dis-
On arrival, every animal should be evaluated to order (e.g. bilateral cruciate ligament rupture in an
determine whether it is stable, requires treatment of animal presented for a hindlimb gait abnormality) or that
immediate life-threatening conditions and/or requires could influence the prognosis (e.g. bladder rupture in an
appropriate monitoring so that potential problems can animal with a traumatic spinal fracture).
be anticipated and prevented. Four major organ systems
should be evaluated as part of the preliminary survey ANAMNESIS
examination: respiratory, cardiovascular, urinary and
neurological (Table 1). While the animal is being The onset, evolution and course of the illness are of
evaluated during the preliminary survey examination, paramount importance and may provide insight into
the owners must be encouraged to give a clear and specific differentials. Through careful questioning,
concise description of their concerns. the onset should be defined as peracute to acute (onset
After the preliminary survey examination and stabi- over minutes to hours), subacute (onset over days),
lization of immediate life-threatening conditions, the chronic (onset over several days, weeks or months) or
secondary evaluation is performed. It is during this time episodic (animal returns to normal in between episodes).
 16 ADMISSION AND NEURODIAGNOSTIC TESTS

The evolution of the signs should be recognized as simple observation and testing a number of reflexes and
progressive, static, improving or waxing and waning. responses (see Hands-off examination [p. 17] and Hands-
Factors that trigger or improve the signs and previous on examination [p. 22]), the clinician should be able to
therapy and its effect on disease course are also important determine if the animal is neurologically sound or not.
to identify. After determining the chief complaint, col- The neurological examination aims to test the
lecting the history should end with general information integrity of the various components of the nervous
regarding any previous medical or surgical conditions, system and, if present, detect any functional deficits.
current medications, family history, vaccination status, diet, Normal findings are as important as the abnormal ones
previous travel history, drug reactions and the animal’s in localizing the lesion. Neurological abnormalities
environment, including the potential for toxin exposure. detected on examination should be noted and added to
the list of abnormal findings collected from the history.
AIMS OF THE NEUROLOGICAL EXAMINATION Each of these abnormal findings should then be
correlated to a specific region or to specific pathways
Before rushing into the specifics of the neurological within the peripheral and/or central nervous system
examination, attention should be focused on what ques- (CNS). An attempt should then be made to explain all of
tions need to be answered: the abnormal findings by a single lesion within one of the
• Do the clinical signs observed refer to a nervous regions of the central and peripheral nervous systems, as
system lesion? illustrated in 1: (i.e. focal forebrain, brainstem, cere-
• What is the location of this lesion within the bellum, C1–C5 spinal cord segments, C6–T2 spinal cord
nervous system? segments, T3–L3 spinal cord segments, L4–S3 spinal
• What are the main types of disease process that can cord segments, peripheral nerve, neuromuscular junc-
explain the clinical signs? tion, muscle). Lesions within these regions result in pre-
• How severe is the disease? dictable and specific neurological signs. Note that in
localizing a lesion, it is not necessary for all the clinical
The first two questions are answered by performing a signs referable to one location or syndrome to be present.
general physical and neurological examination with a view If a single lesion cannot explain all the listed abnormal
to defining the neuroanatomical diagnosis (location and findings, the lesion localization is considered as multi-
distribution of the lesion within the nervous system). By focal or diffuse.

1 Overview of the central and C1–C5

peripheral nervous systems. C6–T2
T3–L3
L4–S3

Forebrain Peripheral nerve

Cerebellum Neuromuscular junction
Brainstem Muscle
 EXAMINING THE NEUROLOGICAL EMERGENCY 17

The third question is answered by compiling infor- SYSTEMATIC APPROACH TO LOCALIZING

mation on the patient signalment and history of the THE LESION
problem with the neuroanatomical diagnosis in order to
determine the differential diagnosis list. Disease severity The neurological examination can be divided into
helps to determine the prognosis of the differential diag- two main parts: hands-off examination and hands-on
noses. Diagnostic tests are then carried out to investigate examination.
the differential diagnoses. The choice and interpretation
of these tests must rely on a clear knowledge of the lesion Hands-off examination
localization within the nervous system and the expected State of consciousness, awareness and behaviour
disease processes. The first step in the neurological examination should
focus on evaluating the animal’s state of consciousness,
RATIONALE AND PRINCIPLES OF LESION awareness of its environment and response to being
LOCALIZATION handled.
Disturbances of level or quantity of consciousness are
The purpose of the neurological examination is to deter- classified in order of severity as obtundation, stupor
mine the neurologic abnormalities and, based on that, (semicoma) and coma. Stupor and coma both represent a
the location of the lesion or lesions responsible for state of unconsciousness. While a stuporous animal can
causing these abnormalities. The location is the anatom- be roused by a painful stimulus, a comatose animal will
ical diagnosis. Narrowing down which part(s) of the fail to respond to any environmental stimulus, including
nervous system may be affected can present a number of pain. As a rule, altered states of consciousness relate to
advantages: either a diffuse lesion or widespread multifocal lesions of
• From a diagnostic point of view, the differential both cerebral hemispheres or a focal lesion affecting the
diagnosis is very dependent on the anatomical ascending reticular activating system (ARAS) of the
diagnosis. brainstem. The latter functions to arouse the cerebral
• Aside from determining which part of the nervous cortex and maintains the state of wakefulness. Acute
system is affected, localizing the lesion also involves coma usually results from extensive brainstem lesions or
determining if the problem is focal, multifocal (i.e. diffuse forebrain lesions secondary to intoxications or a
affecting multiple parts of the nervous system) or metabolic disorder.
diffuse (i.e. affecting globally and symmetrically one Common changes in quality of awareness and
or more parts of the nervous system). Such behaviour include disorientation, aggression, vocalizing,
information can then be used to further narrow circling, compulsive walking or head pressing. Alter-
down the differential list (see How to establish a ations in the patient’s level of awareness and behaviour
differential diagnosis list, p. 33). reflect disturbances in the ARAS and limbic system com-
• A number of disease processes may only be ponents of the cerebrum or rostral brainstem.
diagnosed by exclusion of other causes mimicking a Circling can be caused by a lesion in the vestibular
similar clinical history and presentation. This system as well as by an asymmetrical or focal lesion in the
process of exclusion implies evaluating the correct forebrain. Tight circles are usually but not exclusively
part of the nervous system in order confidently to associated with a vestibular disorder, while wide circles
rule out these similar clinical diseases. Failure to are often associated with a forebrain lesion. With
localize the lesion, the interpretation of negative vestibular disease, circling is associated with other signs
diagnostic test results (as seen with some vascular or of vestibular dysfunction (head tilt, nystagmus, position-
degenerative diseases of the CNS) or findings al strabismus and/or falling) and is usually ipsilateral to
incompatible with the clinical history can end up the lesion (except with lesions affecting the caudal cere-
creating a significant challenge for the clinician. bellar peduncle, fastigial nucleus and flocculonodular
• Running a limited number of investigations aimed lobes of the cerebellum). Circling is usually towards the
at narrowing down the differential list will result in side of a focal or asymmetrical forebrain lesion.
less cost for the owners and less time spent reaching
a diagnosis for the clinician.
 18 ADMISSION AND NEURODIAGNOSTIC TESTS

Hemi-neglect syndrome, also known as hemi- • Schiff–Sherrington posture. This posture is

inattention syndrome, refers to an abnormal behaviour observed with an acute severe thoracic or cranial
in which an animal with structural forebrain disease lumbar spinal cord lesion. Such a lesion may
ignores sensory input from one half of its environment interfere with inhibitory ascending neurons
(e.g. eating from only one half of the food bowl, turning that project from the lateral grey matter of the
in the wrong direction in response to sound). This syn- cranial lumbar spinal cord segments cranially to
drome indicates a diencephalic lesion contralateral to inhibit the forelimb extensor muscles. This posture
the side ignored by the animal. consists of an extensor hypertonia of the forelimbs,
with retention of normal conscious proprioception,
Posture and body position at rest voluntary movements and a flaccid paralysis of the
The posture and body position at rest should be hindlimbs (despite the fact that the paralysis is
evaluated and determined as being normal or abnormal. caused by direct interference with the upper motor
With reference to lesion localization, a number of char- neuron). This posture is present only in severe
acteristic abnormal postures can be encountered in the and acute lesions, but it does not have prognostic
evaluation of the emergency neurology patient: significance.
• Head tilt. This abnormal head posture is • Wide-based stance. This posture is
characterized by a rotation of the median plane of characteristic of a balance disorder indicating
the head along the axis of the body, resulting in one diseases particularly affecting the cerebellum or
ear being held lower than the other one. A head vestibular apparatus.
tilt indicates a vestibular disorder (peripheral or
central) and occurs as a result of the loss of anti- Identification of abnormal involuntary movements
gravity muscle tone on one side of the neck (2). • Myoclonus. Myoclonus is the clinical sign of sudden
• Head turn. Compared with a head tilt, the median contraction followed immediately by relaxation of a
plane of the head remains perpendicular to the specific muscle group. It can be sporadic or
ground, but the nose is turned to one side (3). repetitive. Sporadic myoclonus can be benign and
A head turn is often associated with a body turn idiopathic or be a form of simple focal seizure due
(pleurothotonus) and circling. These signs (called to a forebrain disorder. Repetitive myoclonus can
adversive syndrome) are usually towards the side of be constant (often as a result of encephalitis or
a forebrain lesion. myelitis caused by distemper virus in dogs), action
• Decerebrate rigidity. This posture is observed as a related (congenital and most commonly caused by a
result of a rostral brainstem lesion (between the diffuse abnormality of CNS myelination or
colliculi of the midbrain). It is characterized by rigid acquired [e.g. idiopathic generalized tremor
extension of all limbs and opisthotonus (extension syndrome]), postural (head bobber) or episodic
of the head and neck) associated with a stuporous or (myokymia).
comatose mental status (4). • Tremor. With rapid and repeated cycles, repetitive
• Decerebellate rigidity. The rostral part of the cere- myoclonus demonstrates as a tremor. Tremors can
bellum is inhibitory to the stretch reflex mechanism affect all or part of the body and be classified as
of antigravity muscles (extensor muscle tone). resting tremors or action-related tremors (also
Lesions at this level can result in opisthotonus, with known as kinetic). A resting tremor is present only
the forelimbs extended (decerebellate posture). during rest. An action-related tremor occurs
Compared with decerebrate posture, the hips may following initiation of voluntary movement. It
be flexed by the increased tone in the iliopsoas worsens with increasing levels of activity and
muscle and mentation remains normal (5). This disappears with rest. An action-related tremor can
posture is often caused by an acute cerebellar lesion be classified in veterinary patients as postural or
and can sometimes be episodic. kinetic.
 EXAMINING THE NEUROLOGICAL EMERGENCY 19

 2 Left-sided head tilt and facial paralysis in a 6-year-old  3 Left-sided head and body turn (pleurothotonus) in a
Boxer with otitis media/interna. 4-year-old West Highland White Terrier with a left
forebrain lesion caused by granulomatous
meningoencephalitis.

 4 Decerebrate posture in a 7-month-old Weimaraner  5 Decerebellate posture in a 2-year-old Hungarian

with head trauma following a road traffic accident. Vizsla with a rostral cerebellar artery infarction.

• Myokymia. Myokymia is defined as undulating • Epileptic seizure. Epileptic seizures are the clinical
vermiform movements of the overlying skin due manifestation of excessive and/or hypersynchronous
to contraction of small bands of muscle fibres. electrical activity in the cerebral cortex. They can
• Myotonia. Myotonia is a sustained repetitive be focal or generalized. An epileptic seizure refers
contraction of a muscle or group of muscles without to a forebrain disorder. Its cause may originate from
relaxation following physiological stimulus. It outside (extracranial causes) or inside (intracranial
occurs in certain congenital and acquired muscle causes) the brain.
cell membrane disorders.
 20 ADMISSION AND NEURODIAGNOSTIC TESTS

• Movement disorder. A movement disorder is

Gait generation
defined as an episodic sudden involuntary
contraction of a group of skeletal muscles in a
Gait generation requires the interaction between two motor
conscious patient, with a normal sensorium during
systems: the upper motor neuron (UMN) system and the lower
the activity. Various terms have been used to motor neuron (LMN) system (6).
describe clinical observations in affected animals
(dyskinesia, dystonia, chorea, athetosis, ballism; see The UMN system is the motor system that is confined to the
CNS. It is responsible for the initiation and maintenance of
Chapter 13). normal movements and for the maintenance of tone in the
extensor muscles in order to support the body against gravity.
Evaluation of the gait Its cell body lies predominantly within the brainstem. It travels
Examination of the gait should be done in a place where through the brain and/or spinal cord white matter and
synapses indirectly (via an interneuron) with an LMN to
the patient can be allowed to move freely. This is best
modulate its activity (essentially via inhibition).
accomplished by having the owner walk the animal over
a non-slippery surface. If the animal is not making any The LMN system is the motor system connecting the CNS
attempt to walk, body support (e.g. a sling or harness) with the muscle to be innervated. Its cell body lies within the
ventral horn of the spinal cord grey matter or within the
should be provided as necessary so that any subtle cranial nerve nucleus of the brainstem. Its axon leaves the CNS
voluntary movement can be detected. A normal gait by the ventral nerve roots to join, successively, a spinal nerve
requires intact function of the brainstem, cerebellum, and a peripheral nerve before it synapses with an effector
spinal cord and sensory and motor peripheral nerves, muscle. The LMN is the last neuron in the chain of neurons that
produces the muscular contraction necessary to maintain
neuromuscular junctions and muscles. The cerebrum’s posture, support weight and provide the gait (i.e. it is the final
contribution to the gait is less important in dogs and cats common pathway to the effector).
when compared with primates.
The UMN pathways are responsible for stimulating the
Evaluation of the gait should be done with the aim of
appropriate LMN that induces the postural and protraction
determining if the animal is ataxic, paretic or lame (from phases of locomotion.
either peripheral nerve disease or an orthopaedic dis-
order) and which limb(s) is/are involved.

 6 Upper motor neuron (UMN) and lower

motor neuron (LMN) systems.

UMN UMN
C6–T2 L4–S3
LMN LMN
 EXAMINING THE NEUROLOGICAL EMERGENCY 21

Ataxia paresis/paralysis can be further defined as tetraparesis/

Ataxia is defined as an uncoordinated gait and can arise plegia (all four limbs affected, caused by a lesion located
from either a sensory peripheral nerve or a spinal cord cranial to T3 spinal cord segment or a generalized LMN
lesion (general proprioceptive ataxia), a vestibular lesion disorder), paraparesis/plegia (hindlimbs affected, caused
(vestibular ataxia) or a cerebellar lesion (cerebellar ataxia). by a lesion caudal to T2), monoparesis/plegia (only one
Ataxia can be further divided into hypometria (shorter limb affected, caused by a lesion of the LMN innervating
protraction phase of gait) or hypermetria (longer protrac- the affected limb) and hemiparesis/plegia (limbs on one
tion phase of gait). General proprioceptive (GP) ataxia side affected due to ipsilateral lesion located between T2
reflects the lack of information reaching the CNS respon- and the caudal midbrain or contralateral lesion located in
sible for the awareness of the movement and position of the rostral midbrain) (see Chapter 10).
the neck, trunk and limbs in space. As a consequence,
there may be a delay in the onset of protraction of the Based on whether a lesion affects the UMN or LMN
limb, which may cause a longer stride than normal. The system, two types of paresis can be distinguished: UMN
patient may walk on the dorsal part of its foot or may drag paresis and LMN paresis (Table 2):
its digits. These signs often overlap with those caused by • UMN paresis causes a delay in the onset of
UMN paresis (see below). Vestibular or cerebellar ataxias protraction (swing phase of the gait), with the
are accompanied by other signs of dysfunction of the resultant stride being longer than normal and with
vestibular apparatus or cerebellum, respectively (see a stiff quality of movement. Lesions of the UMN
Chapter 9). system typically result in release of the inhibitory
effect that the UMN system has on LMNs located
Paresis caudal to the level of the injury
Paresis is defined as a loss of ability to support weight (dysinhibition). This dysinhibition effect is usually
(LMN disease) or inability to generate a gait (UMN more apparent on the extensor muscles, which
disease) (see Table 2). The term paresis implies that results clinically in a spastic paresis/paralysis.
some voluntary movement is still present as compared Lesions at many different levels of the CNS can
with paralysis, which refers to a more severe paresis produce the same set of UMN clinical signs. Due
(plegia) with complete loss of voluntary movement. to their close anatomical relationship within the
Depending on which limbs are affected, the terms brainstem and spinal cord, most gait abnormalities

Table 2 Lower motor neuron paresis/upper motor neuron paresis differentiation criteria

CRITERION LOWER MOTOR NEURON PARESIS UPPER MOTOR NEURON PARESIS

Posture Difficulty supporting weight. Crouched stance Often normal (unless the animal is paralysed).
as a result of overflexion of the joints Abnormal limb position (knuckling, abducted,
adducted or crossed over)

Gait Short strides. Tendency to collapse Stiff and ataxic strides. Delayed protraction

Motor function Flaccid paresis/paralysis Spastic paresis/paralysis

Segmental reflexes Decreased to absent Normal to increased

Resting muscle tone Decreased resistance Slight resistance

Passive limb flexion/extension Decreased resistance Slight resistance

Muscle atrophy Early and severe neurogenic atrophy Late and mild disuse atrophy
 22 ADMISSION AND NEURODIAGNOSTIC TESTS

involving the UMN pathways necessary for gait The postural reactions commonly tested are:
generation are also associated with some degree of • The paw replacement reaction, which is evaluated
GP ataxia. From a lesion localization point of view, by placing the paw in an abnormal position (turned
UMN paresis and GP ataxia visible in the gait can over so that the dorsal surface is in contact with the
occur as a consequence of lesions affecting the ground) and determining how quickly the animal
brainstem or spinal cord. Apart from lesions caused corrects the paw position (7). The majority of the
by peracute disease processes (i.e. infarct, animal’s weight should be supported when under-
haemorrhage and head trauma), lesions affecting taking this test in order to improve test sensitivity
the forebrain cause such a mild contralateral paresis and reduce the interference introduced by ortho-
that it is usually not apparent in the gait. paedic disease. Paw replacement reaction can be
• LMN paresis reflects the degree of difficulty in very difficult to assess in cats that resent having their
supporting weight and varies from a short stride, feet handled. Other postural reaction tests, such as
choppy gait to a complete inability to support the hopping response, wheel-barrowing and tactile
weight, causing collapse of the limb whenever placing, are preferred in this species and should be
weight is placed on it. When standing, affected considered in animals in which the paw replacement
limbs may exhibit a tremor in the muscles. LMN reaction is equivocal or difficult to interpret.
paresis affects the gait with lesions in the peripheral • Hopping response, which is tested by holding the
nerves, neuromuscular junction and muscles. Motor patient so that the majority of its weight is placed
deficits observed are ipsilateral to the lesion. on one limb while the animal is moved laterally (8).
Compared with UMN paresis, dysfunction of the Normal animals hop on the tested limb in order to
LMN does not cause ataxia. accommodate a new body position as their centre of
gravity is displaced laterally.
Lameness • Wheel-barrowing, where the animal’s hindlimbs
Lameness usually presents with a short stride on the are lifted off the ground by supporting the animal
affected limb and a long stride on the contralateral under the abdomen and forcing it to walk
limb. Lameness is usually associated with pain from forwards (9). Abnormal animals may scuff their
orthopaedic disease. Additionally, it can be associated digits, drag their paws or cross their limbs.
with nervous system dysfunction referred to as nerve
root signature (referred pain down a limb causing lame-
ness or elevation of the limb, resulting from entrapment
of the spinal nerve, usually due to a lateralized disc extru-
sion or nerve root tumour).

Hands-on examination
Postural reaction testing
The primary aim of postural reaction testing is to detect
subtle deficits that were not obvious on gait evaluation.
In a patient that is recumbent with tetraplegia or paraple-
gia, evaluation of the postural reactions in the affected
limbs is redundant. However, evaluation of the forelimb
postural reactions in a paraplegic patient is important in
order to detect an abnormality that could suggest a focal
cranial thoracic lesion or a multifocal disorder. The pos-  7 The paw replacement reaction is elicited by gently
tural reactions test the animal’s awareness of the precise placing the dorsal part of the foot on the floor. A normal
position and movements of parts of its body, especially animal should immediately replace its foot in a normal
the limbs, as well as the animal’s ability to generate move- position. This cortically-mediated response tests the
ment in the part tested. conscious awareness of limb position (proprioception).
 EXAMINING THE NEUROLOGICAL EMERGENCY 23

• Tactile placing response, where the animal is All the components of the peripheral nervous system and
lifted and the distal part of the forelimb is brought CNS that affect the limb tested are needed in order for
into contact with the edge of a table. When the the animal to perform postural reactions (10). These
dorsal surface of the paw makes contact with the responses are complex in their pathways, but generally
edge of the surface, the animal should immediately involve an afferent arm and an efferent arm. The afferent
place its foot on the surface. arm consists of a joint proprioceptor, peripheral sensory

 8 The normal dog responds to hopping by quickly

replacing the limb under the body as it moves laterally.
The hopping movement should be smooth and fairly rapid
and not irregular or excessive. One forelimb should be
carefully compared with the other.

 9 Wheel-barrowing is performed with the neck

extended and the hindlimbs elevated.

Sensory perception of Spinothalamic pathway

proprioception in contra-
lateral cerebral cortex

Decussation in caudal
brainstem

Proprioceptive receptors
in joints detect abnormal
position of paw
 10 Proprioceptive (paw)
positioning response in the hindlimb.
 24 ADMISSION AND NEURODIAGNOSTIC TESTS

nerve, spinal cord and brainstem ascending pathways, An exception to this rule exists in the context of the
and contralateral forebrain, and the efferent arm involves emergency patient. Animals with a severe peracute trans-
the contralateral forebrain, descending motor pathways verse thoracolumbar spinal cord lesion usually show
within the brainstem and spinal cord, peripheral motor severe hindlimb hypotonia and depressed spinal reflexes
nerve and skeletal muscle. A lesion affecting any of for a few days after the onset. Although there is a similar
these components could potentially result in an abnor- condition in man (‘spinal shock’), the reasons for a UMN
mal postural reaction. Although these reactions are a sen- pathway interruption to cause LMN-like hindlimb signs
sitive test for detecting neurological dysfunction, they do are poorly understood. Despite many spinal reflexes
not provide specific information for lesion localization. being described, the most reliable are the withdrawal
Their importance in localizing the lesion is dependent on reflex in the forelimbs and the patellar and withdrawal
the results of the rest of the neurological examination. In reflexes in the hindlimbs. Other spinal reflexes are more
general, postural reactions remain normal in neuro- difficult to perform and to interpret.
muscular junction and muscle diseases as long as the
animal has the strength to support its weight. Withdrawal (flexor) reflex
A noxious stimulus is applied to the tested limb by pinch-
Spinal nerve reflexes, muscle mass and tone ing the nail bed or digit with fingers or a haemostat. This
assessment stimulus causes reflex contraction of the flexor muscles
Spinal reflexes evaluation should be considered as a con- and withdrawal of the tested limb (11). If this withdrawal
tinuation of gait evaluation and postural reaction testing reflex is absent, individual toes can be tested to detect if
and not as a sole entity. Functionally, the spinal cord can specific nerve deficits are present. In the forelimb, com-
be divided into four regions: cranial–cervical (C1–C5); pression of the digits stimulates nociceptors in the radial
cervicothoracic (C6–T2); thoracolumbar (T3–L3); and nerve dorsally (ulnar nerve in digit five) and in the
lumbosacral (L4–S3). LMN cell bodies are located median or ulnar nerve on the palmar surface. In the
within the grey matter of the cervicothoracic intumes- hindlimb, compression of digits three to five stimulates
cence (segments C6–T2) for the forelimbs and lumbo- nociceptors of the sciatic nerve (peroneal branch dorsal-
sacral intumescence (segments L4–S3) for the hindlimbs. ly and tibial branch on the plantar surface).
Following gait and postural reaction testing, the clinician
should be able to narrow down the lesion localization as
being cranial to T3 spinal cord segments, caudal to T3
spinal cord segments or within the peripheral nervous
system (peripheral nerve, neuromuscular junction or
muscles) (see Table 3, page 26). Spinal reflexes evaluation
helps to narrow down further the lesion localization by
testing the integrity of the C6–T2 and L4–S3 intumes-
cences, as well as the respective segmental sensory and
motor nerves (LMN) that form the peripheral nerves and
the muscles innervated. Spinal reflexes are segmental.
They only evaluate the spinal segment(s) within the intu-
mescences corresponding to the stimulated nerve. They
do not require normal consciousness. Lesions at the level
of these intumescences or affecting the peripheral
nervous system result in loss of segmental spinal reflexes
as well as reduced muscle tone and mass. Lesions cranial  11 A normal withdrawal reflex in the hindlimb implies
to the intumescence (UMN dysfunction) will result in flexion of the hock, stifle and hip. This should normally be
normal to exaggerated segmental spinal reflexes (due to performed with the animal in lateral recumbency;
release of the inhibitory modulatory effect of the UMN however, in some animals it is possible to perform this test
on the LMN). only when they are standing and minimally restrained.
 EXAMINING THE NEUROLOGICAL EMERGENCY 25

Agonist muscle Contralateral

Noxious stimulus extensor inhibition

Interneuron
Flexor contraction
Extensor inhibition

 12 Withdrawal (flexor) reflex. When a noxious

stimulus is applied to a digit, the limb should be
withdrawn towards the body. Sensory input enters the
spinal cord through the dorsal root to activate ipsilateral
flexor motor neurons via interneurons and simultaneously
inhibit the antagonist extensor muscles.

 13 The patellar reflex is elicited by hitting the patellar

tendon with a reflex hammer and observing a reflex
extension of the stifle joint.

The withdrawal reflex is a segmental spinal cord Patellar reflex

reflex that only depends on the function of the local The patellar reflex is elicited by hitting the patellar
spinal cord segments (12). In the forelimb it evaluates the tendon and observing a reflex contraction of the quadri-
integrity of the spinal cord segments C6–T2 (and associ- ceps muscle and extension of the stifle joint (13). It is per-
ated nerve roots), the brachial plexus, the peripheral formed when the dog is in lateral recumbency, with the
nerves (radial, axillary, musculocutaneous, median stifle slightly flexed and the tested limb supported by
and ulnar nerves) and the muscles innervated. placing one hand under the thigh. It is best performed in
In the hindlimbs it evaluates the integrity of the spinal cats with the cat in dorsal recumbency between the thighs
cord segments L4–S1 (and associated nerve roots), the of the examiner. This position allows the stifle to be
femoral and sciatic nerves and the muscles innervated. slightly flexed and a comparison to be made between the
It should be stressed that the withdrawal reflex in the two sides.
fore- or hindlimbs does not depend on the animal’s noci- The patellar reflex evaluates the integrity of spinal
ception (perception of a noxious stimulus). cord segments L4–L6 (and associated nerve roots) as well
as the femoral nerve. A weak or absent reflex indicates a
 26 ADMISSION AND NEURODIAGNOSTIC TESTS

Table 3 Determination of an anatomical diagnosis based on gait, postural reactions

and segmental spinal reflex evaluation

LIMB(S) PRESENTING WITH SEGMENTAL SPINAL REFLEXES LIKELY ANATOMICAL DIAGNOSIS

ABNORMAL GAIT AND/OR IN AFFECTED LIMB
ABNORMAL POSTURAL REACTIONS

All four limbs Normal to increased all four limbs Brainstem or (C1–C5) spinal cord segments

Decreased to absent all four limbs Generalized polyneuropathy/

junctionopathy/myopathy

Decreased to absent forelimbs (C6–T2) spinal cord segments

and normal to increased hindlimbs

Bilateral hindlimbs Normal to increased (T3–L3) spinal cord segments

Decreased to absent (L4–S3) spinal cord segments, peripheral

nerve roots/nerve of the hindlimbs

Fore- and hindlimbs on the same Normal to increased fore- Ipsilateral brainstem or (C1–C5) spinal
side of the body and hindlimbs cord segments

Decreased to absent forelimbs Ipsilateral (C6–T2) spinal cord

and normal to increased hindlimbs segments

Unilateral forelimb Normal to increased Ipsilateral brainstem or (C1–C5) spinal

cord segments

Decreased to absent Ipsilateral (C6–T2) spinal cord segments or

in that limb affecting either the nerve roots,
brachial plexus or peripheral nerves

Unilateral hindlimb Normal to increased Ipsilateral (T3–L3) spinal cord segments

Decreased to absent Ipsilateral (L4–S3) spinal cord segments

or in that limb affecting either the nerve
roots or peripheral nerves

lesion of the L4–L6 spinal cord segments or the femoral reflexic with a sciatic nerve or L6–S2 spinal cord segment
nerve. A similarly weak or absent reflex can on occasion lesion. This pseudohyperreflexia is a result of decreased
be seen with stifle disease. A lesion cranial to the L4 tone in the muscles that flex the stifle and normally
spinal cord segment can cause a normal or exaggerated counteract stifle extension during the patellar reflex.
patellar reflex. In the absence of other neurological
deficits, an exaggerated patellar reflex means little and Perineal reflex
can be observed in an excited or nervous animal. Evalua- The perineal reflex is elicited by stimulation of the
tion of the extensor tone of the hindlimb can be used as a perineum with a haemostat, resulting in contraction of
control in animals with an ambiguous patellar reflex, as it the anal sphincter and flexion of the tail.
involves the same neuroanatomical components (L4–L6 This reflex tests the integrity of caudal nerves of the
spinal cord segments, femoral nerve and quadriceps tail, the pudendal nerve, spinal cord segments S1 to Cd5
muscle). Finally, the patellar reflex can appear hyper- and associated nerve roots.
 EXAMINING THE NEUROLOGICAL EMERGENCY 27

Cutaneous trunci (panniculus) reflex transverse myelopathy. Pinching the skin cranial to the
This reflex is elicited by pinching the dorsal skin of the lesion results in a normal reflex, while stimulation of the
trunk on either side of the dorsal spinous processes skin caudal to the lesion does not elicit any reflex. Such
between the vertebral level T2 and L4 to L5 and findings help to further localize lesions between T3 and
observing a contraction of the cutaneous trunci muscle L3. This reflex can also be lost ipsilaterally (with normal
bilaterally producing a twitch of the overlying skin. This reflex on the other side) with conditions affecting the
reflex is present in the thoracolumbar region and is brachial plexus, regardless of the level that the skin is
absent in the neck and sacral regions. Testing is started at stimulated. In the absence of other neurological deficits,
the level of the ilial wings. If the reflex is present at this the absence of the cutaneous trunci reflex means little.
level, the entire pathway is intact and further testing is
not necessary. Nociceptive testing
From the dermatome tested, the sensory nerve from Although it only defines the degree of dysfunction and
the skin enters the spinal cord at the level of the segment not the degree of structural damage, nociceptive testing
corresponding to that dermatome (approximately two has significant prognostic value in cases of spinal cord or
vertebrae cranial to the level tested) (14). Afferent peripheral nerve lesions. The purpose of this test is to
sensory information ascends the spinal cord and synapses detect and map out any areas of sensory loss. This may
bilaterally at the C8–T1 spinal cord segments with the help in identification of specific peripheral nerves, nerve
motor neurons of the lateral thoracic nerve, which roots and spinal cord segments involved in the disease
courses through the brachial plexus and innervates the process. Assessment of pain sensation requires a noxious
cutaneous trunci muscle. The panniculus reflex can be stimulus and evaluation of the animal’s response. If an
decreased or lost with a lesion anywhere in this pathway area of diminished or absent nociception is encountered,
(dorsal nerve roots, spinal cord, lateral thoracic nerve). its boundaries should be demarcated to see whether it has
With spinal cord lesions, this reflex is lost caudal to the a segmental or peripheral nerve distribution and whether
spinal cord segment affected, indicating the presence of a it is absent below a certain level of the trunk.

 14 Schematic representation of the neurological

pathways responsible for the cutaneous trunci reflex.

Spinal lesion Stimulation more than two

vertebral segments caudal to
lesion will not elicit a reflex

Stimulation cranial to a lesion Sensory afferent

up to C8–T1 dermatomes will
elicit a reflex

Lateral thoracic nerve from

C8–T1 spinal cord segments

Cutaneous trunci muscle

 28 ADMISSION AND NEURODIAGNOSTIC TESTS

Nociception is commonly tested by pinching the Vision, pupil size and response
digits with the fingers or with haemostats. If no response Menace response
is elicited when using fingers, the test should be repeated The menace response is elicited by making a threatening
with haemostats to confirm that the response is absent. gesture at the eye tested (16). The expected response is
Other areas of cutaneous sensory testing include the tail, closure of the eyelids. The contralateral eye must be
perineum and perianal region, as well as cutaneous blindfolded with the other hand in order to assess each
sensory distribution of the fore- and hindlimb nerves (see eye separately. Care must be taken not to touch the eye-
Chapter 16). lashes or to create air currents that might stimulate sen-
Only a behavioural response to noxious stimulus sation of the face (CN V; trigeminal nerve), which could
(turning of the head, attempt to bite) indicates conscious elicit a palpebral or corneal reflex (see below).
pain perception (15). Withdrawal of the limb is only the This reaction is a learned response that may not be
flexor reflex and should not be taken as evidence of noci- developed until 10–12 weeks of age in puppies and kittens.
ception. The afferent arc of this response involves three neurons:
• The first neuron in this arc is the bipolar cell of the
Cranial nerve examination retina. This receives impulses from the neuro-
Cranial nerve (CN) examination can be performed indi- epithelial cells of the retina (rods and cones).
vidually and sequentially from CN I to CN XII, or by • The second afferent neuron is the ganglion cell of
more of a regional approach (Table 4). The latter method the retina. Its axons lie in the optic nerve (CN II)
is more appropriate to the evaluation of the emergency and continue through the optic chiasm and
neurology patient. Testing of these nerves should be proximal part of the optic tract on the opposite side
done in conjunction with the assessment of mentation, to the eye being menaced.
gait, postural reaction and segmental spinal reflexes to • This second neuron synapses with neuron three in
determine whether there is brainstem disease versus the lateral geniculate nucleus. The axons then
peripheral CN disease. project to the visual cortex (mostly occipital cortex)
in a band of fibres called the optic radiation.

 15 Nociception is tested by pinching the digits with  16 The menace response is elicited by making a
the fingers or with haemostats and observing a threatening gesture at the eye. The expected response is
behavioural response to the noxious stimulus (turning of closure of the eyelids. The contralateral eye should be
the head, as in this picture, vocalization and/or an attempt blindfolded with the other hand to assess each eye
to bite). separately.
 EXAMINING THE NEUROLOGICAL EMERGENCY 29

Table 4 Cranial nerve examination

CRANIAL NERVE AFFERENT BRAIN EFFERENT PRINCIPAL EFFECT

TEST CRANIAL NERVE REGION CRANIAL NERVE NOTED

Menace response CN II – optic Forebrain, CN VII – facial Blink elicited by a

cerebellum, menacing gesture
brainstem

Visual placing CN II – optic Forebrain None Reach out for support on

approaching the table

Pupillary light CN II – optic Brainstem CN III – oculomotor Pupillary constriction

reflex elicited by shining a
light in the eye

Dark adaptation CN II – optic Hypothalamus, Sympathetic supply Pupillary dilation in

test brainstem to the eye darkness

Palpebral reflex CN V – trigeminal Brainstem CN VII – facial Blink elicited by touching

(ophthalmic or of the medial or lateral
maxillary) canthus of the eye

Corneal reflex CN V – trigeminal Brainstem CN VII – facial; Blink and globe retraction
(ophthalmic) CN VI – abducens elicited by touching the cornea

Response to nasal CN V – trigeminal Forebrain, None Withdrawal of the head

stimulation (maxillary and ophthalmic) brainstem elicited by touching the
nostril

Oculovestibular CN VIII – vestibular Brainstem CN III – oculomotor; Nystagmus induced by moving

reflex CN IV – trochlear; the head
CN VI – abducens

Gag reflex CN IX – glossopharyngeal; Brainstem CN IX – glossopharyngeal; Contraction of the pharynx

CN X – vagus CN X – vagus elicited by palpating
the pharynx

The efferent arc of this response is not well understood. Visual placing response
The information generated in the occipital cortex (con- This placing reaction is tested by carrying a small dog or
tralateral to the eye stimulated) is forwarded to the motor a cat under its chest towards a table edge, but without
cortex via association fibres. The corticobulbar pathways letting the forelimbs touch the table. On approaching
to the facial nerve nucleus (CN VII) then transmit the the surface the animal will reach out to support itself
motor information. This response requires intact facial on the table. Each eye can be tested separately by cover-
nerve function. This function should be separately ing the eye contralateral to the one being tested.
evaluated with the palpebral reflex (see below). There is This response requires intact visual pathways, menta-
some experimental and clinical evidence for cerebellar tion and postural control of the forelimbs. It can be used
involvement in the menace response efferent pathways. to assess visual function in an animal where the menace
Unilateral cerebellar lesions can lead to an ipsilateral response is ambiguous.
menace response loss with retention of normal vision.
The neuronal pathways through the cerebellum are,
however, not known.
 30 ADMISSION AND NEURODIAGNOSTIC TESTS

Evaluation of pupil size The PLR involves an afferent arm and an efferent
Immediately after menace response testing, the pupil’s arm. The afferent arm of this reflex shares some common
size and response to light and darkness should be evalu- pathways (ipsilateral retina, optic nerve, optic chiasm and
ated. Pupillary abnormalities are common following contralateral optic tract) with part of the afferent arm of
intracranial trauma or vascular compromise. The size of the menace response and visual placing. These tests use
the pupils represents a balance of the parasympathetic different integration centres within the brain and differ-
system (responsive to the amount of light entering the ent efferent pathways. The PLR does not test the
eye) and the sympathetic system (responsive to the emo- animal’s vision and the cerebrum is not involved in the
tional state of the animal). The pupil regulates the PLR pathway. The efferent arm of the PLR reflex is
amount of light reaching the retina through the parasym- mediated by the parasympathetic portion of CN III.
pathetic nerve pathways that innervate the iris. The para- While axons involved in vision reach the conscious level
sympathetic component of the oculomotor nerve (CN after synapse with the lateral geniculate nucleus, the
III) is involved in the control of pupillary constriction, axons involved in the PLR synapse with a third neuron in
while the somatic efferent component of the oculomotor the pretectal nucleus. Most of the axons arising from this
nerve controls the motor innervation of the levator nucleus decussate again and synapse on the parasympa-
palpebrae superioris (elevation of the upper eyelid) ipsi- thetic component of the oculomotor nucleus (ipsilateral
lateral dorsal, ventral and medial recti extraocular to the stimulated eye) in the mesencephalon. There are
muscles, as well as the ventral oblique muscle (movement also neurons that do not decussate and which project to
of the eyeball). The tone of the iris dilator muscle is the oculomotor nucleus on the contralateral side of the
maintained by the sympathetic system, which keeps the stimulated eye. The proportion of axons that decussate is
pupil partially dilated under normal conditions and higher than that of the ones that do not decussate,
dilates it more notably during periods of stress, fear and explaining why the direct response (constriction in the
painful stimuli. The ocular sympathetic nervous system eye receiving the light stimulus) is greater than the con-
also innervates and provides tone to the smooth muscle sensual response (constriction in the eye not receiving
of the periorbita and eyelids. This tone keeps the eyeball the light stimulus). Combining the results of the menace
protruded, the palpebral fissure widened and the third response, visual placing and PLR tests helps to localize
eyelid retracted. the lesion as being within the common pathways or not
Assessment of pupillary size and equality should be (see Chapter 12).
determined in ambient light as well as in darkness. Nor- In the dark adaptation test the eyes are dark adapted
mally, the pupils should be symmetrically shaped and in complete darkness for a couple of minutes in order to
equal to each other in size. Animals with pupils of unequal allow complete relaxation of the pupillary sphincter
size (anisocoria) or shape (dyscoria) must be found free of muscle.
primary or secondary anatomical or mechanical ocular
abnormalities (iris atrophy, uveitis or glaucoma) before Trigeminal and facial nerve functions
consideration is given to a neurological dysfunction. The trigeminal nerve (CN V) provides sensory innerva-
Determining which pupil is abnormal is achieved by tion of the face (cutaneous elements of the face as well as
checking the pupillary light reflex (PLR) and determining the cornea, mucosa of the nasal septum and mucosa of
if the asymmetry in pupil size increases in bright light or the oral cavity) and motor innervation to the masticatory
in complete darkness (dark adaptation test). muscles (temporalis, masseter, medial and lateral ptery-
goid and rostral part of the digastric muscles). The motor
Pupillary light reflex function of CN V is assessed by evaluating the size and
The PLR is tested by shining a bright light into the pupil symmetry of the masticatory muscles and testing the
and assessing for pupillary constriction (direct reflex). resistance of the jaws when opening the mouth.
The opposite pupil should constrict at the same time The sensory function (sensation of the face) can be
(consensual or indirect reflex). A slight dilation usually individually tested by the corneal reflex (ophthalmic
follows the initial pupillary constriction (pupillary escape) branch) and the palpebral reflex (ophthalmic or maxillary
as a consequence of light adaptation of photoreceptors. branch when touching the medial or lateral canthus of
 EXAMINING THE NEUROLOGICAL EMERGENCY 31

the eye, respectively) (17), by pinching the skin of the face • Palpebral reflex (CNs V and VII ).
with haemostat forceps and observing an ipsilateral blink • Corneal reflex (CNs V and VII ).
or facial twitch, and by the response to nasal stimulation. • Menace response (CNs II and VII ).
As for the menace response, the response to nasal stimu- • Pinching of the face (CNs V and VII ).
lation requires an intact contralateral forebrain. One of
the two nostrils is stimulated using a pair of forceps or a The Schirmer tear test helps to evaluate the parasym-
pen, while the animal’s eyes are masked to prevent any pathetic supply of the lacrimal gland associated with
visual input. The afferent arc involves the sensory com- CN VII. Examining the mouth for a moist mucosa can
ponent of the trigeminal nerve (ophthalmic and maxil- subjectively assess salivation.
lary branch of CN V ), which conducts the information
to the brainstem where it is continued to the contralater- Eye movement and position
al forebrain. The expected response is a withdrawal Observation of the animal’s body and head posture at rest
movement of the head and neck (18). As with the menace and evaluation of its gait can provide a lot of information
response, this response might be abnormal in the pres- about the vestibular function of CN VIII (see
ence of a structural contralateral forebrain lesion. Chapter 14). This function can also be more specifically
The facial nerve (CN VII ) is motor to the muscles of assessed by testing the oculovestibular reflex and looking
facial expression and sensory (providing the sense of for pathological nystagmus. Nystagmus is an involuntary
taste) to the rostral two-thirds of the tongue and palate. rhythmic movement of the eyeballs. Physiological (or
Its parasympathetic component innervates the lacrimal vestibular) nystagmus is a nystagmus that occurs in
glands and the mandibular and sublingual salivary normal animals, while pathological nystagmus reflects an
glands. The motor function of CN VII is primarily underlying vestibular disorder. In both instances the nys-
assessed by observation of the face for movement of the tagmus has a slow and fast phase (i.e. jerk nystagmus).
ears, eyelids, lips and nostrils and for symmetry of the A physiological nystagmus can be induced in normal
lips. The facial nerve is also the motor efferent part of the individuals by rotation of the head from side to side
following tests: (oculovestibular reflex). The test is best performed on a

 17 The palpebral reflex is elicited by touching the  18 The response to stimulation of the nasal mucosa is
medial or lateral canthus of the eye and observing a reflex a cortically mediated withdrawal of the head. The afferent
closure of the eyelids. The afferent arm of this reflex is arm is mediated by the trigeminal nerve (CN V sensory).
mediated by the trigeminal nerve (CN V sensory), while The integration of this response occurs in the
the efferent arm is mediated by the facial nerve (CN VII). contralateral forebrain.
 32 ADMISSION AND NEURODIAGNOSTIC TESTS

cat or a small dog by holding the animal at arm’s length Laryngeal, pharyngeal and tongue function
and rotating it from side to side; nystagmus may only be Because of their proximity in the brainstem, the glos-
seen at the end of the movement. Physiological nystag- sopharyngeal (CN IX) and vagus (CN X) nerves share
mus stabilizes images on the retina during head move- sensory (nucleus solitarius) and motor (nucleus ambigu-
ment. It is always observed in the plane of rotation of the us) nuclei. CN IX innervates the musculature of the
head and consists of a slow phase in the direction oppo- pharynx and palatine structures. It provides sensory
site to that of the head rotation and a fast phase in the innervation to the caudal third of the tongue and
same direction as the head rotation. In the absence of any pharyngeal mucosa (taste). Its parasympathetic compo-
head movement, nystagmus should never be present in a nent innervates the parotid and zygomatic salivary
normal animal. glands. CN X controls motor function of the larynx
Two types of pathological nystagmus can be observed (recurrent laryngeal branch), pharynx and oesophagus
with vestibular dysfunction. It can be spontaneous (cervical oesophagus innervated by the pharyngeal and
(observed when the head is in a normal position at rest) recurrent laryngeal branches; thoracic oesophagus
and/or positional, which occurs when the head is held in innervated by the vagal branches). It provides sensory
different positions (for example to either side, dorsally or function to the larynx, the pharynx and the thoracic and
by placing the animal upside down on its back). Nystag- abdominal viscera. Its parasympathetic component pro-
mus is usually classified on the basis of its direction (the vides innervations to all the thoracic and abdominal
fast movement) and may be horizontal, vertical or rota- viscera, except those of the pelvic region.
tory. With disorders of the peripheral components of the The pharyngeal reflex can assess CN IX and X
vestibular system in the inner ear, the direction of the function. This reflex is also known as the swallowing or
nystagmus is always opposite to the side of the lesion and gag reflex. It is evaluated by applying external pressure
is usually horizontal or rotatory. Lesions of the central to the hyoid bones to stimulate swallowing or by stim-
components of the vestibular system can cause patholog- ulating the pharynx with a finger to elicit a gag reflex. It
ical nystagmus in any direction and occasionally it can also be evaluated by watching the animal eat and/or
changes direction with different head positions. A verti- drink and by opening the mouth wide: the animal will
cal nystagmus is more commonly due to a central lesion. usually close its mouth, swallow and lick its nose,
Strabismus refers to an abnormal position of the allowing simultaneous evaluation of the tongue. The
eyeball within the orbit. While examining the eyes, the parasympathetic innervation of CN X can be evaluated
eyeballs should be assessed as to whether they are by testing the oculocardiac reflex. This is achieved by
normally positioned in the orbits. Normal position of the applying digital pressure to both eyeballs and observ-
eyeball is dependent on the innervation of the extraocu- ing simultaneously a reflex bradycardia (mediated as
lar muscles by the oculomotor (CN III ), trochlear well by CN V).
(CN IV ) and abducens (CN VI ) nerves. The function of CN IX dysfunction results in dysphagia, an absent
these CNs can be tested during the oculovestibular gag reflex and reduced pharyngeal tone. Animals
reflex, evaluating the degree of abduction (CN VI ) and frequently cough after drinking and swallow repeatedly
adduction (CN III ). Strabismus can be seen with vestibu- because of an accumulation of saliva in their pharynx.
lar dysfunction when the head is placed in an abnormal CN X dysfunction abnormalities include dysphagia,
position (extended dorsally or the animal placed upside inspiratory dyspnoea (due to laryngeal paralysis), voice
down on its back). Vestibular dysfunction often causes a changes and regurgitation (due to megaoesophagus if
ventral or ventrolateral positional strabismus in the eye there is a bilateral vagal disorder). The pharyngeal and
on the same side as the vestibular lesion. oculocardiac reflexes are absent.
 EXAMINING THE NEUROLOGICAL EMERGENCY 33

CN XII provides motor innervation to the muscles of HOW TO ESTABLISH A DIFFERENTIAL

the tongue. The nucleus is in the caudal medulla and can DIAGNOSIS LIST
therefore be affected by high cervical lesions. The nerve
exits the skull via the hypoglossal foramen. CN XII func- The differential diagnosis list is dependent on the
tion can be evaluated by inspecting the tongue for anatomical diagnosis. Compiling a differential diagnosis
atrophy, asymmetry or deviation to one side. Manually list is essential in choosing and interpreting any diagnos-
stretching the tongue and observing a voluntary retrac- tic test however sophisticated it may be. The aim of per-
tion helps assess the tongue’s tone. Applying food ‘paste’ forming such diagnostic tests should be only to confirm
to the nose and observing the animal licking can assess its or exclude the differentials in the list and not replace the
movement. Lesions affecting CN XII can result in prob- clinical evaluation. The differential diagnosis list should
lems with prehension, mastication and deglutition. With be developed taking into account:
unilateral and recent lesions, the tongue tends to deviate • Signalment.
towards the contralateral side. With unilateral and • Historical data. Questioning of the owner should
chronic lesions, the tongue protrudes towards the side of be aimed at defining the mode of onset (acute,
the lesion and atrophy is observed ipsilaterally. Muscle subacute, chronic or episodic) and evolution of the
fasciculations may be obvious on the affected side in the condition. Furthermore, historical data can give
denervated tongue. clues as to how widespread or focal the disease
process is in the nervous system, whether there was
Palpation evidence of asymmetry, and how severe the signs
Palpation and manipulation to detect painful areas have been.
and/or restricted movement are usually performed last in • Neurological findings. The aim of the neurological
order to avoid losing the cooperation of the patient. evaluation is to define the lesion localization
(forebrain, brainstem, cerebellum, spinal cord
Head segment, peripheral nerve, neuromuscular junction
The head must be palpated to detect any asymmetry, and muscle) and distribution of the disease (focal,
focus of pain or persistence of the fontanelles. multifocal, diffuse) within the nervous system.

Spine Disease processes that can affect the nervous system can
Palpation of the spine starts by applying gentle down- be classified according to the mnemonic ‘VITAMIN D’
ward pressure on the spinous process and then along the (Vascular–Inflammatory / Infectious–Traumatic / Toxic–
transverse processes. The degree of pressure applied Anomalous–Metabolic–Idiopathic–Neoplastic–Nutri-
should be progressively increased. The presence of spinal tional–Degenerative). Each of these disease processes
hyperaesthesia or deformity should be noted. has a typical signalment, onset and progression, as well
as distribution within the nervous system (see Table 5,
Limbs next page). In the context of the neurology emergency
Palpation of the limbs is indicated to evaluate the animal patient, the mnemonic can be abbreviated to ‘VITIMN’
for musculoskeletal conditions that can mimic a neuro- (Vascular–Inflammatory/Infectious–Traumatic / Toxic–
logical disorder. The joints should be carefully palpated Idiopathic–Metabolic–Neoplastic), as it is unlikely
for evidence of swelling, pain or instability. Palpation of (although not impossible) that the other disease
the muscular system can help to detect focal muscle processes (Anomalous, Nutritional, Degenerative) will
atrophy. Such findings could indicate disease in the spinal have an acute presentation.
cord segment, nerve root or peripheral nerve that inner-
vates a specific muscle (LMN dysfunction), or they could
be related to disuse atrophy associated with an ortho-
paedic condition.
 34 ADMISSION AND NEURODIAGNOSTIC TESTS

Table 5 Disease processes classified according to the mnemonic ‘VITAMIN D’

PATHOLOGICAL PROCESS MODE OF ONSET EVOLUTION DISTRIBUTION

Vascular Peracute or acute Non-progressive or regressive Focal and often asymmetrical

(haemorrhage may cause (haemorrhage may cause
subacute onset) progression over a very
short period)

Inflammatory/infectious Acute, subacute or insidious Progressive Focal or multifocal.

(wax and wane in some Asymmetrical or symmetrical
cases early after onset)

Traumatic Peracute or acute Static or improve over time Often focal.

Asymmetrical or symmetrical

Toxic Acute Variable Diffuse and bilaterally

symmetrical

Anomalous Chronic (occasionally acute) Non-progressive or slowly Variable

progressive, usually early in life

Metabolic Variable (often acute) Wax and wane or progressive Diffuse and bilaterally
symmetrical

Idiopathic Acute Non-progressive or regressive Specific to each syndrome

Neoplastic Chronic (occasionally acute) Progressive Often focal. Asymmetrical or

symmetrical

Nutritional Variable (acute or insidious) Progressive Diffuse and bilaterally

symmetrical

Degenerative Chronic Progressive Often diffuse and symmetrical

WHAT DO DO NEXT?

With a clear knowledge of the region of the nervous

system involved and the differential list reduced to no
more than three or four disease processes, consideration
should only be given to diagnostic tests that help to
further narrow down the list and can be afforded by the
client. The least invasive tests should be performed first.
 ADMISSION AND NEURODIAGNOSTIC TESTS Chapter 2

RESPIRATORY
AND CARDIOVASCULAR SUPPORT 35

Anthea Raisis
& Gabrielle Musk

INTRODUCTION Treatment methods for acquiring and maintaining

a patent airway
Maintenance of normal oxygenation, ventilation and Oral endotracheal intubation
perfusion (the ABC of resuscitation) is essential in the Specific indications
neurological patient to prevent secondary neurological • Emergency management of upper airway
injury or exacerbation of the underlying condition. In obstruction (e.g. laryngeal spasm, laryngeal
addition, correction of hypoxaemia, hypercapnia and paralysis).
poor perfusion are the most important strategies for • Protection of airway in an obtunded/unconscious
reducing intracranial pressure (ICP). The type and animal.
extent of supportive care required will depend on the • Animals that need mechanical ventilatory support.
cause of respiratory and/or cardiovascular impairment
and the severity of disruption to normal oxygenation, Precautions
ventilation and perfusion. Techniques for maintaining Oral endotracheal intubation in most animals will
normal respiratory and cardiovascular function and, require sedation or anaesthesia. Details of how to
therefore, adequate oxygen delivery to the tissues are sedate/anaesthetize a neurological patient safely are
outlined in this chapter. descibed in Chapter 29.
Selection of an appropriately sized endotracheal
PROVIDING AN ARTIFICIAL AIRWAY tube (ETT) is essential (19). Resistance to breathing
is markedly increased as the diameter of the ETT
The indications for providing an artificial airway are decreases. If the diameter of the tube is halved, resistance
listed below: increases 16-fold. To minimize resistance to breathing,
• Laryngeal paresis or paralysis, which can be caused the largest diameter tube that can be easily and safely
by cranial nerve deficits associated with disorders of passed should be used. If the ETT is too long, resistance
the brainstem or generalized neuromuscular to expiration will also increase (doubling the length will
disease. double the resistance to flow) and the risk of excessive
• Laryngeal spasm (e.g. tetanus).
• An inability to protect the airway adequately
(e.g. severe depression/recumbency associated with
intracranial disease).
• Mechanical ventilation. 9.0 mm

 19 Selection of an appropriate endotracheal tube for 8.5 mm

each animal is required to ensure that resistance to
breathing is not excessive. When preparing for intubation,
8.0 mm
select the most appropriate endotracheal tube size in
addition to tubes 0.5–1.0 mm above and below that size as
shown here.
 36 ADMISSION AND NEURODIAGNOSTIC TESTS

equipment dead space or inadvertent endobronchial 25 mmHg. Careful inflation of the cuff is required to
intubation increases (20). minimize damage to the mucosa. During prolonged
The increased work of breathing associated with intubation, occasional repositioning of the endotracheal
increased resistance can be overcome by mechanical tube may help reduce mucosal ischaemia; however,
ventilation. The potential for this increased work to repositioning the ETT increases the risk of aspiration of
reduce the adequacy of ventilation and cause hypercapnia secretions that have accumulated above the cuff. If the
will be greatest in any animal expected to breathe sponta- tube is repositioned, the pharynx and oesophagus should
neously or when attempting to wean an animal off the be suctioned prior to cuff deflation to reduce the risk of
ventilator. An excessively long ETT will also increase the secretions entering the airway.
apparatus dead space, leading to rebreathing of expired
carbon dioxide (CO2). This also increases the risk of Tracheostomy
hypercapnia and increased ICP in the neurological Specific indications
patient. • Chronic management of airway dysfunction in
As oral intubation bypasses the nasal cavity, which conscious patients (e.g. animals with tetanus,
normally humidifies inspired air, the airways are predis- laryngeal paresis).
posed to desiccation. Humidification of gases is essential • To reduce the amount of sedation/anaesthesia
to minimize drying of lower airways and should always required to immobilize animals requiring
be used in patients that are ventilated for anything mechanical ventilation.
other than a short period of time. • Severe laryngeal trauma.
Inflation of the ETT cuff is required to prevent aspi-
ration of saliva or gastric contents. The cuff should be Precautions
inflated just enough to create a seal. If excessive or pro- The tracheostomy tube must be secured adequately in
longed inflation pressure is created, the risk of pressure place to prevent accidental removal and loss of the
necrosis of the tracheal mucosa increases. The pressure airway. It is essential that the tube can still be removed
of the small arterioles in the tracheal mucosa is very low, rapidly should obstruction occur. Tying the tube in place
so the pressure within the cuff should not exceed is preferred over suturing (21).

 20 Endotracheal tubes and other apparatus (such as  21 A tracheostomy tube is used to provide a patent
the capnograph sampling connector; arrow) extending airway in animals with severe compromise of the upper
beyond the level of the animal’s incisors may increase respiratory tract. The tube should be tied in place (arrow)
apparatus dead space, resistance to expiration and the to allow rapid removal should obstruction of the tube
work of breathing. Always pre-measure the endotracheal occur.
tube before placement.
 R E S P I R AT O RY AND C A R D I O VA S C U L A R S U P P O RT 37

The accumulation of secretions may occlude the Precautions

tube. When mechanical ventilation is not required and This method of oxygenation is for short-term use only
the risk of aspiration is considered minimal, it is rec- (<5 minutes) and must be used with conservative oxygen
ommended that an uncuffed tube is used (22). It is also flow rates. When the airway is completely obstructed,
recommended that the diameter of the tube is one half oxygen insufflated into the lung via a narrow needle or
the diameter of the trachea, so the animal can breathe catheter cannot be expired, therefore there is a risk of
around the tube for short periods should the tube rupturing the lung, resulting in a pneumothorax. To
become occluded. determine suitable flow rates, the volume of the animal’s
Care of the tracheostomy site is labour intensive. lungs must be considered. For example: a 20 kg dog
Animals need constant monitoring, as occlusion of the would have an approximate tidal volume of 200 ml (based
tube can result in death within minutes. Regular suction- on 10 ml/kg). Therefore, an oxygen flow of 1 litre
ing is required to prevent accumulation of secretions. minute-1 would fill the tidal volume of the lungs in 12
The tube should be replaced 1–2 times a day. seconds, while an oxygen flow rate of 200 ml/minute
would take 1 minute.
Intratracheal catheter This method does not allow for mechanical venti-
If the upper airway is completely obstructed, an intratra- lation of the animal, and hypercapnia will occur. Intu-
cheal catheter or needle (large dog: 16 g; small to bation should be performed promptly and mechanical
medium dog: 18 g) can be placed (23). Oxygen can be ventilation instigated as soon as a patent airway is
insufflated via these catheters/needles for <5 minutes. available.

Specific indications
• Obstructed airway and impending respiratory
arrest.
• Short-term oxygenation while oral intubation or
tracheostomy is performed.

 22 A cuffed tracheostomy tube (a) is required when  23 An intratracheal catheter, as shown here, can be
mechanical ventilation is being performed. However, used to provide short-term (<5 minutes) oxygen supple-
when the animal is conscious and spontaneously mentation in animals that are completely obstructed.
breathing, an uncuffed tracheostomy tube (b) is preferred.
 38 ADMISSION AND NEURODIAGNOSTIC TESTS

BREATHING Common causes of hypoxaemia in animals with

neurological disease
Adequate oxygenation (arterial oxygen partial pressure • Aspiration pneumonia. Animals with CN deficits
[PaO2] ≥80 mmHg [10.7 kPa]; saturation of haemo- associated with brainstem or neuromuscular
globin with oxygen [SpO2] ≥95%) and ventilation (arte- disease are predisposed to regurgitation and
rial carbon dioxide partial pressure [PaCO2] 35–40 aspiration due to impairment of upper respiratory
mmHg [4.7–5.3 kPa]; end-tidal carbon dioxide partial tract (URT) function. Recumbency and
pressure [P’ETCO2] 30–35 mmHg [4–4.7 kPa]) are severe depression also predispose the animal to
required to maintain cerebral oxygen delivery and aspiration.
prevent increases in ICP. • Atelectasis (25). Recumbency, immobility and a
high inspired oxygen concentration all predispose
Oxygen supplementation to alveolar collapse. This creates a mismatch in
Indications ventilation and perfusion and results in shunting of
Oxygen supplementation is indicated if there is a critical blood through the lungs. The shunt prevents
decrease in oxygen delivery to the brain. Oxygen delivery oxygenation of the blood as it bypasses ventilated
(DO2 ) is a product of cardiac output (CO) and oxygen alveoli.
carrying capacity (CaO2) measured as the oxygen • Acute lung injury (ALI). Lung injury secondary to
content of arterial blood: systemic inflammation, prolonged exposure to high
inspired oxygen concentrations and trauma due to
DO2 = CO × CaO2 high ventilation pressures all contribute to the
incidence and severity of ALI. These processes
The oxygen content of arterial blood is a combination of cause the release of inflammatory mediators within
oxygen bound to haemoglobin (haemoglobin × SpO2 × the lung, which stimulate a vicious cycle of patho-
1.34) and that dissolved in the plasma (0.003 × PaO2). As logical changes within the alveoli and surrounding
the majority of oxygen is carried in the blood bound to lung tissues. The net result is interference with
haemoglobin, decreases in oxyhaemoglobin saturation pulmonary gas exchange. ALI is tentatively
and haemoglobin concentration have the greatest influ- diagnosed when the ratio of arterial oxygen tension
ence on oxygen delivery to tissues, including the brain.
Decreases in oxygen saturation of haemoglobin may
occur due to decreased inspired oxygen percentage,
decreased ventilation or decreased transfer of oxygen
across the alveoli, or ventilation/perfusion mismatch or Oxygen tension (mmHg)
right-to-left shunting of pulmonary blood flow. A 20 40 60 80 100
100
decrease in haemoglobin concentration (anaemia) will Arterial (90%)
occur due to blood loss or red cell destruction.
Oxygen saturation (%)

80 Mixed venous (75%)

Hypoxaemia 60
Definition
Although only a small amount of oxygen is carried 40
dissolved in blood, assessment of oxygenation is
frequently performed by measurement of PaO2. Severe 20
hypoxaemia is defined as a PaO2 of <60 mmHg (8 kPa).
5.3 13.3
This is equivalent to an SpO2 of 90% (24). SpO2 is meas- 0
ured using pulse oximetry (see below). For animals with 2 4 6 8 10 12
Oxygen tension (kPa)
intracranial disease, it is recommended that the PaO2 is
maintained at >80 mmHg (10.7 kPa) to prevent increas-
es in ICP.  24 Oxygen–haemoglobin dissociation curve.
 R E S P I R AT O RY AND C A R D I O VA S C U L A R S U P P O RT 39

 25 Recumbency and immobility are very common

causes of atelectasis and hypoxaemia in the neurological
patient.

 26 Pneumothorax secondary to chest trauma, as shown

in this lateral radiograph, can contribute to hypoxaemia in
animals with concurrent head trauma. (Photo courtesy
Shannon Holmes)

to fractional inspired oxygen concentration inspiration damage the alveolar membrane, causing
(PaO2:FiO2) is <300. Supportive care of ALI is fluid to flood the alveoli.
based on supplemental oxygenation via mask, nasal • Hypoventilation. In an animal breathing room air,
catheters or oxygen cage. hypoventilation causes increased alveolar CO2,
• Acute respiratory distress syndrome (ARDS). which dilutes alveolar oxygen and results in less
ARDS occurs as the pathological changes in ALI oxygen being available to diffuse into the arterial
progress and cause greater interference with gas blood. Restoring normal CO2 values by the use of
exchange. ARDS is defined as a PaO2:FiO2 ratio of ventilation should also correct the hypoxaemia. If
<200. These patients require ventilatory support. the hypoxaemia is not corrected with ventilation
• Pulmonary contusions or pneumothorax (26) in and the return of CO2 to normal, then other causes
animals with concurrent chest trauma. of hypoxaemia need to be investigated.
• Neurogenic or non-cardiogenic pulmonary oedema
occurs in response to increased sympathetic nervous Management
system stimulation and blood pressure (BP) Hypoxaemia is managed by treating the underlying cause
secondary to brainstem ischaemia or compression. when possible and providing supplemental oxygen
URT obstruction may also cause pulmonary (see below) until the cause of the hypoxaemia has been
oedema if the negative pressures generated during corrected.
 40 ADMISSION AND NEURODIAGNOSTIC TESTS

Anaemia • Oxygen cage. Cages are useful for initial stabiliza-

The clinical significance of anaemia varies according to tion of small dogs and cats in respiratory distress
whether the anaemia is acute or chronic: while minimizing the stress of handling (27). The
• Acute anaemia (e.g. haemorrhage): clinical signs advantage of using an oxygen cage is that an FiO2
will usually occur if the PCV (packed cell volume) is of >50% can be achieved when the cage remains
<0.30 l/l (30%) in dogs and <0.25 l/l (25%) in cats. closed. The disadvantages include limited access to
• Chronic anaemia (e.g. haemolytic anaemia): clinical the patient if continuous oxygen support is
signs will generally be apparent when the PCV is required. In addition, patients are also at risk of
<0.20 l/l (20%) in dogs and <0.15 l/l (15%) in cats. hyperthermia and should be monitored carefully.
• Head collar. Head collars can be used for larger
Causes of anaemia in neurological disease animals where size prevents the use of oxygen
The most common cause is haemorrhage secondary to cages. The use of head collars covered with plastic
trauma or surgical blood loss. film can provide a personalized oxygen cage.
Oxygen is delivered via tubing attached on the
Management inside of the head collar (28). Head collars have the
The definitive treatment for reduced tissue oxygenation advantage of providing a high FiO2 while still
due to anaemia is whole blood or red blood cell (RBC) allowing access to the rest of the animal. The
transfusion. For further information on blood transfu- disadvantages include:
sion see Chapter 31. • The risk of jugular occlusion and increased ICP
If there is a delay in administering blood or RBCs, if the collar is too tight.
oxygen supplementation can be useful. While oxygen • Hypercapnia can occur if the collar is tight, the
supplementation in these cases may only provide oxygen flow is too low or the supply tubing
extremely small amounts of dissolved oxygen in the becomes disconnected, allowing CO2 to build up
blood, this can be life saving in the short term. within the enclosed head collar. Hypoxaemia will
also develop if the oxygen tubing detaches. Flow
Treatment methods for supplementing oxygen rates equivalent to those used in non-
Increasing the FiO2 rebreathing anaesthetic systems (200–300
The aim of techniques that increase the inspired per- ml/kg/minute) are probably adequate.
centage of oxygen is to use the lowest FiO2 that will • Hyperthermia can also occur with this technique
maintain the PaO2 at between 80 and 100 mmHg (10.7– as the animal is rebreathing expired warm and
13.3 kPa). As haemoglobin is fully saturated when the humidified air.
PaO2 is approximately 100 mmHg (13.3 kPa), further
increases in arterial oxygen tension produce very little
increase in the amount of oxygen carried by the blood. In
addition, there is an increased risk of lung damage as
exposure to higher than normal levels of alveolar oxygen
triggers pathological changes within the pulmonary
tissues (oxygen toxicity). The higher the alveolar oxygen
tension and the longer the duration of treatment, the
greater the risk of irreversible alveolar damage.
Increased inspired oxygen can be delivered by a
number of methods, including oxygen cage, head collar,
mask or nasal catheter.

 27 An oxygen cage can be used to provide oxygen

supplementation in small- to medium-sized animals.
 R E S P I R AT O RY AND C A R D I O VA S C U L A R S U P P O RT 41

 28 A head collar covered in plastic film can be used to  29 Face masks can be used to provide oxygen during
provide oxygen supplementation to larger animals when initial stabilization or prior to induction of anaesthesia.
other methods are not feasible. Care should be taken to
avoid jugular vein compression and overheating.

 30 ‘Flow-by’ oxygen therapy can be used to provide  31 Nasal catheters can be used to provide continuous
short-term oxygen supplementation to animals that will oxygen supplementation and also allow continuous access.
not tolerate a face mask. They should be avoided in animals with increased
intracranial pressure, coagulopathy and nasal fractures.

• Face mask. Face masks are generally used for initial oxygenation can be used (30). A tight-fitting mask
stabilization only, particularly in animals not can also exacerbate hyperthermia, as rebreathing of
amenable to oxygen cages due to their size (29). The expired humidified gases occurs. An open mask or
advantage of using face masks for oxygen flow-by technique provides limited increase in FiO2.
supplementation is that they are easily accessible and • Nasal catheter. An intranasal catheter is inserted
allow for prompt administration of oxygen in an into the ventral nasal meatus, directing the catheter
emergency setting. One of the disadvantages is that ventromedially (31). The tip can be positioned just
animals in respiratory distress may not tolerate a inside the nostril or in the nasopharynx.
mask held over their face. In these cases ‘flow-by’
 42 ADMISSION AND NEURODIAGNOSTIC TESTS

To position the catheter tip in the nasopharynx, the

catheter should be pre-measured to the level of the
medial canthus to ensure correct positioning. If the
tip is inserted too far, it risks being introduced into
the oesophagus, causing aerophagia and gastric
dilation. Most animals will tolerate an oxygen flow
of 100 ml/kg/minute/nostril. Higher flows may
cause increased irritation, sneezing or removal of
the catheter by the patient. If flows >100 ml/kg/
minute are required to achieve adequate oxygena-
tion, a catheter can be placed in each nostril,
allowing a total oxygen flow of up to 200 ml/kg/
minute to be delivered comfortably. Nasal catheters  32 Endotracheal intubation and delivery of high
have the advantage of allowing long-term supple- inspired oxygen concentration may be needed in animals
mentation of oxygen in animals with respiratory that do not improve with other methods of oxygen
disease and continuous access to the patient. supplementation.
Furthermore, there is no risk of hyperthermia or
hypercapnia. The disadvantages include sneezing
associated with placement of nasal catheters, which
can be detrimental if there is: (1) increased ICP, as
sneezing will cause further increases, which may
result in fatal herniation of the brainstem, or (2)
coagulopathy, as sneezing may cause bleeding from
the nostril or haemorrhage into the eye or brain.
This procedure should also be avoided in the head-
trauma patient, when fractures within the nasal
cavity can lead to misplacement of the catheter
within neural tissue. Finally, there is a limited
increase in FiO2 of 0.3–0.4 (30–40% inspired
oxygen concentration) observed with this method.
 33 Mechanical ventilation is commonly used to
Endotracheal intubation ‘breathe’ for patients that have inadequate spontaneous
Endotracheal intubation and connection to a breathing ventilation or are unresponsive to other methods of
system may be necessary when other methods of oxygen supplementation.
increasing FiO2 fail to achieve adequate arterial oxygen
tension or if the animal becomes increasingly depressed
(32). Intubation must be performed before the animal
becomes unconscious. This will require careful admin-
istration of intravenous anaesthetic agents. If intubation
is delayed until the animal becomes unconscious requires some degree of sedation or anaesthesia and
because of the pathological process, cardiopulmonary (2) the depressant effects of sedative and anaesthetic
arrest is highly likely. agents will also necessitate some form of positive pres-
Endotracheal intubation has the advantage of allow- sure ventilation, particularly in animals with intracranial
ing connection to a breathing system and the delivery of disease where maintenance of normal PaCO2 is essential.
100% oxygen. The clinician can therefore be more con- Assisted ventilation is indicated when increasing FiO2
fident of the delivered FiO2. Disadvantages include: fails to correct hypoxaemia (33). Details of ventilation
(1) maintenance of oral endotracheal tubes generally techniques are described in the next section.
 R E S P I R AT O RY AND C A R D I O VA S C U L A R S U P P O RT 43

VENTILATION tidal volume and/or respiratory frequency), or

(2) inadequate respiratory compensation for
The aim of mechanical ventilation is to recruit and metabolic acidosis. In animals with intracranial
stabilize alveoli and deliver oxygen to and remove disease, any increase in CO2 may have detrimental
carbon dioxide from them without causing lung injury. effects on ICP. Mechanical ventilation is required
Careful monitoring of ventilation to ensure normo- in any animal with intracranial disease if the
capnia and satisfactory oxygenation is essential to guide PaCO2 is >40 mmHg (5.3 kPa). The causes of
management strategies. Furthermore, the haemodyn- ventilatory failure in animals with neurological
amic consequences of mechanical ventilation should be disease include:
continuously monitored. During spontaneous ventila- • Neuromuscular weakness: tetrodotoxin, snake
tion, a negative pressure is created within the thoracic envenomation, tick paralysis, botulism,
cavity to draw air into the lungs. During mechanical polyradiculoneuritis, myasthenia gravis (MG).
ventilation, a positive pressure is generated to push gas • Cervical spinal cord injury.
into the lungs. This positive pressure compresses blood • Intracranial disease with involvement of
vessels within the chest, especially in the low-pressure respiratory centres (i.e. caudal fossa pathology).
venous circulation and right side of the heart. The net • Drug-induced CNS depression: anaesthesia,
effect is a decrease in cardiac output. Ideally, cardiac opioid overdose.
output should be monitored in ventilated animals, but • Hypoxaemic respiratory failure (inadequate
arterial BP measurement is a common surrogate measure oxygen exchange): generally defined as arterial
in a clinical setting. oxygen tension <60 mmHg (8 kPa) when the FiO2
Mechanical ventilation is indicated in animals with is >0.5.
respiratory failure. Respiratory failure can be divided
into two types: Treatment methods for providing ventilation
• Hypercapnic ventilatory failure (inadequate The most common type of ventilation used routinely in
alveolar ventilation = hypoventilation): generally animals is intermittent positive pressure ventilation
considered to be present when the PaCO2 is (IPPV). The factor determining the termination of inspi-
>50 mmHg (6.7 kPa). Ventilatory failure should ration and the onset of expiration is most often volume,
also be considered in animals with normal PaCO2 pressure or time. Positive end-expiratory pressure
if there is: (1) clinical evidence of increased (PEEP) and continuous positive airway pressure (CPAP)
respiratory work and impending fatigue (high are also used, particularly in animals with pulmonary
respiratory rate; change in respiratory pattern; pathology. Table 6 gives a summary of the modes of ven-
increased inspiratory effort; erratic changes in tilation that can be used in neurological patients.

Table 6 Modes of mechanical ventilation

MODE MECHANISM USES/ADVANTAGES DISADVANTAGES/CAUTIONS

Volume-cycled IPPV Inspiration terminated when Preferred use in normal lungs Increases risk of lung injury
pre-set volume delivered. in animals with altered lung
Delivers desired VT regardless compliance
of lung compliance

Pressure-cycled IPPV Inspiration is terminated when a Preferred method for animals Poor airway, lung or chest wall
pre-set pressure is delivered. VT with altered lung compliance compliance will require high
will therefore be determined by or very small patients inflation pressures to achieve an
lung and chest wall compliance adequate minute volume
(Continued)
 44 ADMISSION AND NEURODIAGNOSTIC TESTS

Table 6 Modes of mechanical ventilation (continued)

MODE MECHANISM USES/ADVANTAGES DISADVANTAGES/CAUTIONS

Time-cycled IPPV Inspiration is terminated when Infrequently used in current PIP is determined by lung and
a set inspiration time has passed. clinical practice chest wall compliance. Decreases
VT is determined by lung and in compliance will cause
chest wall compliance increases in PIP and increase
risk of injury

OTHER DEFINITIONS
PEEP Maintains positive pressure Minimizes atelectasis and High PEEP may compromise
at the end of expiration during associated ventilation/perfusion venous return and cardiac
controlled ventilation, preventing mismatch in normal lungs. output. Decreased venous
complete alveolar collapse at Minimizes volutrauma in lung return can lead to increased
the part of the respiratory cycle pathology cerebral blood volume and
when airway pressure is usually increased ICP
0 cmH2O

CPAP Technique used in spontaneously Can help stabilize open alveoli Animals may not tolerate nasal
breathing animals to prevent and prevent alveolar collapse. catheters or prongs. Higher
alveolar collapse at the end of May improve oxygenation in than normal pressure at the
expiration and increase spontaneously breathing end of expiration may
functional residual capacity animals and negate need compromise venous return and
for IPPV cardiac output

VT = tidal volume; PEEP = positive end-expiratory pressure; CPAP = continuous positive airway pressure; ICP = intracranial pressure;
PIP = peak inspiratory pressure; IPPV = intermittent positive pressure ventilation.

A wide range of other ventilation strategies are used Adverse effects of ventilation
to promote ventilation and oxygenation, minimize lung Mechanical ventilation may have numerous adverse
injury and prevent haemodynamic compromise. Tech- effects on a variety of body systems, including the
niques including high-frequency ventilation, inverse cardiovascular, respiratory, neurological, renal and
ratio ventilation, biphasic airway pressure and extra- gastrointestinal systems. A summary of these effects and
corporeal membrane oxygenation have been used to how to minimize them is given in Table 7. Before ventila-
reduce airway pressures in human patients with severe tion of any animal is undertaken it is essential to under-
pulmonary disease. These techniques are limited to stand the potential adverse effects and how to avoid
specialist centres with specialist equipment, a thorough them.
understanding of which is essential before embarking on
either short- or long-term management. A detailed Guidelines for use of mechanical ventilation
description of the equipment and techniques is beyond The aim of ventilation is to optimize oxygenation and
the scope of this book. For more information, the reader ventilation, while minimizing adverse effects on cardio-
is referred to the Further reading list, p. 623. vascular, pulmonary and neurological functions.
Different ventilatory strategies are used to manage
different types of respiratory failure. The ventilation
strategy may need to be further altered if the animal has
concurrent intracranial disease. Guidelines for use of
ventilation in these situations are described below (see
also Table 8, page 46).
 R E S P I R AT O RY AND C A R D I O VA S C U L A R S U P P O RT 45

Table 7 Adverse effects of mechanical ventilation

SYSTEM EFFECT METHODS OF MINIMIZING ADVERSE EFFECTS

Cardiovascular Positive airway pressure during IPPV interferes • To minimize the detrimental effects on cardio-
with venous return and CO during inspiration. vascular performance it is important to ensure
CPAP and PEEP interfere with venous return adequate blood volume and minimize PIP, the
and CO during expiration. PEEP in combination amount of time spent in inspiration (inspiratory
with IPPV interferes with venous return time) and PEEP.
throughout the respiratory cycle. Decreased • Monitor blood pressure and CVP during
CO leads to decreased oxygen delivery to the ventilation.
tissues and may offset improvement in oxygen • Monitor ICP in animals with intracranial
content disease.

Pulmonary Barotrauma: excessive airway pressure causes • Use the minimum VT and PIP necessary to
physical disruption of lung tissue and extra- achieve adequate oxygenation and ventilation.
alveolar air (e.g. pneumothorax). Volutrauma: • Lung disease: lower VT, higher RR and PEEP.
overdistension of alveoli causes increased perme- Slight hypoventilation and permissive hyper-
ability, oedema and inflammation. Repetitive capnia (PaCO2 45–60 mmHg).
stretching and recoil of alveoli induces inflamma- Note: Permissive hypercapnia must be avoided
tory and structural changes, leading to increased in patients with intracranial disease.
permeability of alveoli and oedema formation.
Inflammation associated with ventilator-induced
lung injury may be an important inciting factor for
development of SIRS and MOF

Renal function Decreased urine output due to release of ADH and • Use the minimum VT and PIP necessary to
decreasing ANP production causing fluid retention. achieve adequate oxygenation and ventilation.
Decreased GFR and intrarenal blood flow redistrib-
ution may interfere with the renal elimination of
drugs

Gastrointestinal system Increased incidence of gastric ulceration and liver • Use the minimum VT and PIP necessary to
dysfunction. Decreased portal blood flow may also achieve adequate oxygenation and ventilation.
reduce the elimination of drugs that undergo
hepatic metabolism

Central nervous system Interference with venous return can lead to • Use the minimum VT and PIP necessary to
increased cerebral venous blood volume and ICP achieve adequate oxygenation and ventilation.
• Neuromuscular relaxation in anaesthetized
animals can help reduce the PIP required to
ventilate to normocapnia.
• Use PEEP very carefully in animals with intra-
cranial disease.
• Monitor CVP and ICP in animals with intra-
cranial disease.

VT = tidal volume; RR = respiratory rate; PIP = peak inspiratory pressure; PEEP = positive end-expiratory pressure;
CPAP = continuous positive airway pressure; ICP = intracranial pressure; CVP = central venous pressure; CO = cardiac output;
GFR = glomerular filtration rate; SIRS = systemic inflammatory response syndrome; MOF = multiple organ failure;
ADH = antidiuretic hormone; ANP = atrial natriuretic peptide; IPPV = intermittent positive pressure ventilation.
 46 ADMISSION AND NEURODIAGNOSTIC TESTS

Table 8 Guidelines for mechanical ventilation

NORMAL LUNGS ABNORMAL LUNGS INTRACRANIAL DISEASE

Preferred Pressure or volume cycled Pressure cycled Pressure cycled

ventilator type

Settings

VT 10–20 ml/kg <6 ml/kg Settings are a compromise between

pre-existing lung condition and
RR Comparable to resting respiratory Adequate to maintain appropriate need to maintain normocapnia and
rate F’EtCO2 prevent increased ICP
I:E ratio 1:3 1:3

PIP 10–20 cmH2O will adequately Higher PIP required due to reduced Use the minimal PIP required to
ventilate most animals with compliance (see Further reading) achieve normoxia and normocapnia,
normal lungs; cats will sometimes but limit adverse effects on venous
require <10 cmH2O due to higher drainage and ICP
chest compliance

PEEP 0–5 cmH2O Start at 3 cmH2O and increase Avoid/use carefully in animals with
up to 10 cmH2O as required intracranial hypertension
to achieve adequate oxygenation
without decreasing oxygen delivery

VT = tidal volume; RR = respiratory rate; I:E ratio = inspiratory:expiratory time ratio; PIP = peak inspiratory pressure;
PEEP = positive end-expiratory pressure; ICP = intracranial pressure; F’ECO2. = Fractional concentration of carbon dioxide in mixed expired air

Mechanical ventilation in cases of ventilatory failure the inspiratory phase follows the pathway of least
In animals with ventilatory failure, peak inspiratory resistance and distributes to areas of lung that are more
pressure (PIP) is adjusted until the minimum pressure compliant (i.e. normal lung tissue is preferentially
that maintains adequate ventilation and oxygenation is ventilated compared with less compliant diseased tissue).
obtained. For normal chests, a PIP of 8–10 cmH2O in Overdistension of normal lung contributes to ventilator-
dogs and slightly less in cats will adequately ventilate induced lung injury (VILI) and triggers a cascade of
most animals in normal body condition. Higher pres- worsening pulmonary function and the development
sures may be required in obese animals and animals of multiple organ failure. Unfortunately, this type of
with barrel chests. ventilation strategy is unable to maintain normal CO2.
The majority of these animals will have normal lungs However, in animals with normal intracranial compli-
at least initially, so only conservative PEEP may be ance the increases in PaO2 are generally tolerated.
required (up to 3 cmH2O). This will help prevent the PEEP is particularly useful in animals with reduced
development and progression of atelectasis, especially if lung compliance, as there is a tendency for lungs to
a high FiO2 is used. PEEP must be used with extreme collapse during expiration. In these conditions, PEEP
care in animals with increased ICP. prevents alveolar collapse and atelectasis. By preventing
alveolar collapse, PEEP prevents the cyclic collapse and
Mechanical ventilation of animals with lung re-opening of alveoli that contribute to VILI. By mini-
pathology in the absence of intracranial disease mizing atelectasis, PEEP also reduces physiological dead
Smaller tidal volumes (5–6 ml/kg) and higher respiratory space and improves pulmonary gas exchange.
rates are recommended in animals with diseased lungs to Adverse effects of PEEP includes interference with
prevent overdistension of normal lung tissue. Over- normal venous return during the expiratory phase of ven-
distension of normal lungs occurs as gas delivered during tilation. To minimize this effect, the amount of PEEP
 R E S P I R AT O RY AND C A R D I O VA S C U L A R S U P P O RT 47

applied is adjusted to optimize arterial oxygenation while to return to the heart. PEEP should be avoided or used
maintaining normal cardiac output (and oxygen deliv- extremely carefully in animals with intracranial disease.
ery). Clinically, where measurement of cardiac output is (For details of neuromuscular blockers see Chapter 29.)
not available, the effect of IPPV on arterial BP and Increases in ICP negate any improvement in
central venous pressure (CVP) can be used to assess the oxygenation by reducing cerebral perfusion pressure
impact on cardiovascular function. (CPP). Furthermore, increased ICP increases the risk
of herniation and death. The use of ICP monitoring
Mechanical ventilation of animals with lung may be worthwhile in animals with concurrent intra-
pathology in the presence of intracranial disease cranial disease and lung disease warranting mechanical
Ventilation of animals with both lung and intracranial ventilation to ensure ventilation strategies do not exacer-
disease presents a unique challenge, as many of the bate intracranial hypertension. (For more details on
ventilator strategies designed to minimize VILI have a ventilation in ARDS see Further reading.)
detrimental effect on ICP. Ventilation of animals with pulmonary disease and
The low tidal volume ventilation strategies recom- concurrent CNS disease requires intensive monitoring
mended in animals with lung pathology cause permissive of pulmonary, cardiovascular and neurological functions.
hypercapnia and are harmful in animals with intracranial This is limited to referral hospitals.
disease, as a marked increase in ICP accompanies
increasing PaCO2. Increasing mean airway pressure also CARE OF THE VENTILATED ANIMAL
has the potential to increase ICP due to detrimental
effects on venous return increasing cerebral blood Appropriate monitoring and supportive care of the
volume. The level of PIP required to ventilate these ventilated patient are required to minimize adverse effects
animals adequately may be reduced by use of non-depo- of chronic intubation, ventilation and recumbency. This
larizing neuromuscular blockers, which increase compli- section discusses some important aspects of this care.
ance of the chest wall. Venous return is optimized by Table 9 gives a summary of the general nursing require-
increasing expiratory time and, thus, the time for blood ments of these animals.

Table 9 General nursing of the ventilated patient

PROCEDURE RATIONALE

Lubricate eyes Paralysed animals are unable to close eyelids and are predisposed to corneal
ulcers if eyes are allowed to dry out

Moisten and reposition tongue every 1–2 hours Prevents desiccation, circulatory stasis and swelling. Wrapping the tongue in a
swab soaked with water can be useful for preventing desiccation

Reposition endotracheal tube every 2 hours Prevents local tracheal necrosis at site of inflated cuff. Do not inflate the cuff of
the ETT excessively. The cuff should be inflated until there is no audible leak
during inspiration. High-volume low-pressure cuffs are preferred. Ties used to
secure the ETT in place should also be repositioned every 2–4 hours to prevent
circulatory stasis of muzzle

Swab pharynx and suction stomach/ Helps minimize regurgitation and aspiration. Even when the cuff of the ETT is
oesophagus every 2 hours inflated, fluid can accumulate proximal to the cuff and enter the airway when
the cuff is deflated. It is important that animals with intracranial disease are
adequately sedated or anaesthetized during this procedure, as coughing will
cause a marked increased in ICP

(Continued)
 48 ADMISSION AND NEURODIAGNOSTIC TESTS

Table 9 General nursing of the ventilated patient (continued)

PROCEDURE RATIONALE

Positioning Maintain in sternal recumbency if possible, as this optimizes pulmonary and

cardiovascular functions. If positioned in lateral recumbency, turning every 2
hours may help prevent atelectasis and compression of dependent muscle groups

Head elevation In animals with intracranial disease the head should be supported so that it is
level with or slightly above the heart in order to encourage venous drainage.
Excessive elevation of the head will impair perfusion. Care must be taken to avoid
jugular venous occlusion

Environmental temperature control Monitor body temperature and warm as needed using circulating warm air,
blankets, heating pads or hot water bottles. Care must be taken to avoid
discomfort or burns from the heat source

Clean and dry Incontinence pads can be used, but must be changed regularly; alternatively,
place an indwelling urinary catheter

Sedation/analgesia Cardiovascular function

Most animals with respiratory disease will require anaes- To ensure adequate circulating blood volume and BP and
thesia to allow endotracheal intubation and ventilation. to minimize the detrimental effects of ventilation on car-
Some degree of sedation or anaesthesia will also be diovascular function, measurement of arterial BP and
required in animals with neuromuscular disease, particu- CVP should be performed in ventilated animals. These
larly during recovery when animals will attempt to move, techniques are described in detail in Monitoring the
but are still too weak to maintain their own spontaneous cardiovascular system, p. 56.
ventilation or protect their upper airway. If anaesthesia is
not required to maintain immobility (e.g. animal paral- Pulmonary function
ysed by snake envenomation), it is important to remem- Adequacy of ventilation
ber that these animals are conscious and aware of Assessment of the adequacy of ventilation can be made by
environmental stimuli, including noise and touch. Some measurement of airway pressure, capnography (see p. 50)
form of analgesia/sedation is recommended to minimize and measurement of arterial CO2.
the stress associated with handling. Agents used to Measurement of airway pressure is essential whenever
sedate/anaesthetize animals requiring ventilation are mechanical ventilation is performed, as sudden changes
discussed in Chapter 29. in pressure can have dramatic consequences. Failure to
achieve a predetermined airway pressure indicates inad-
Monitoring equate delivery of volume to the patient and may be due
As mechanical ventilation may have detrimental effects to insufficient gas supply, leaks in the breathing system or
on a variety of organ systems, close monitoring of venti- disconnection. Abrupt increases in airway pressure
lated animals is essential. suggest sudden changes in compliance or resistance and
can be caused by obstruction or kinking of tubing, acute
bronchoconstriction or development of pneumothorax.
Gradual increases in airway pressure suggest deteriora-
tion in pulmonary function, with associated decreases in
compliance and increases in resistance.
 R E S P I R AT O RY AND C A R D I O VA S C U L A R S U P P O RT 49

Neurological function
Neurological function is influenced by the adequacy of
oxygenation, ventilation and perfusion, and a reduction
in these variables can lead to neurological deterioration.
Deterioration of neurological status will be observed
clinically by progressive mental depression in conscious
animals, dilation of pupils with absence of a PLR and
development of cardiorespiratory abnormalities (e.g.
cardiac arrhythmias, Cushing reflex [reflex bradycardia],
abnormal breathing patterns). ICP monitoring may
also be useful in animals with concurrent intracranial
and pulmonary disease, particularly in those requiring
ventilation.
 34 Multivariable monitoring recording haemoglobin
saturation and plethysmograph using pulse oximetry. Renal function
The level of CO2 expired over time is measured using Measurement of urine output (see p. 60) and urine
capnography (blue wave form). Arrow = end-tidal CO2. specific gravity (SG) should be performed regularly in
chronically ventilated animals to monitor the effects of
ventilation on renal function and to assess fluid balance.
Ideally, this should be performed via a sterile indwelling
Adequacy of oxygenation urinary catheter and closed collection system (35).
The amount of oxygen within the blood can be assessed Measurement of blood urea, creatinine and electrolytes
by measuring oxyhaemoglobin saturation (SpO2) with a should also be performed daily to monitor for changes in
pulse oximeter (34) and measuring the partial pressure of renal function.
oxygen in arterial blood (PaO2). Calculation of oxygen
delivery to the tissues requires measurement of both Fluid therapy (for more details see Chapter 31)
arterial oxygen content and cardiac output. Measure- Once volume deficits have been corrected, crystalloid
ment of mixed venous oxygen can provide an indirect fluids are required to maintain adequate hydration.
measure of adequacy of oxygen supply to the tissues. As large amounts of water can be lost through evapora-
Details of these techniques are described below. tion from the airways of ventilated animals, particularly
when non-rebreathing systems are used, it is generally
recommended that fluid administration is supplied at
1.5–2 × maintenance to prevent dehydration and
maintain adequate hydration of the airway mucosa.
Humidification of ventilator gases will offset this effect.
In ventilated animals with intracranial disease, fluid
therapy should ideally be monitored using CVP to
prevent excessive fluid administration and increases in
hydrostatic pressure.

 35 A closed urinary collection system allows continuous

monitoring of urine output in critical patients.
 50 ADMISSION AND NEURODIAGNOSTIC TESTS

Humidification of the airway Monitoring oxygenation and ventilation

Ventilation with dry gases causes drying of airway Pulse oximetry
secretions, decreased mucociliary clearance and asso- The factors that interfere with a reliable pulse oximeter
ciated increased risk of secondary infection. Water lost reading include local vasoconstriction, interference from
from the airway will increase fluid requirements. extraneous lighting, movement, haemoglobin abnormal-
Adequate intravenous fluid therapy is essential for ities and pigment. Pulse oximetry can be used to provide
maintaining airway hydration, but heat and moisture a guide to oxygenation. It provides a non-invasive beat-
exchange (HME) devices (see Chapter 29) placed by-beat assessment of the amount of oxygen carried by
between the animal and the breathing circuit can reduce haemoglobin within the arterial blood. However, to
water loss by up to 80%. These devices need to be ensure accuracy, the pulse quality must be good and
replaced every 6 hours to ensure optimal efficiency. reflected in the generation of a continuous plethysmo-
Ideally, humidified gases should be used if ventilation gram.
is expected to be prolonged. Even a couple of hours of Pulse oximetry measures the percentage of haemo-
ventilation with dry gases can cause significant damage to globin (Hb) molecules that are saturated with oxygen and
the upper airways and lungs. Humidifiers can be fitted to the pulse rate. Due to the shape of the oxyhaemoglobin
most ventilators and are placed in the inspiratory limb of dissociation curve (see 24), a saturation of >95% is
the ventilator breathing system. Sterile saline can be required to ensure a PaO2 of >80 mmHg (10.7 kPa).
instilled into the airway at the level of the tracheal bifur- There are many physiological and technical factors that
cation and then removed via suctioning every 1–2 hours. can interfere with the pulse oximeter, so the readings
As this increases the risk of nosocomial infection, suc- should be interpreted with a thorough understanding of
tioning is only recommended when secretions are exces- the limitations of the equipment. (Note: Pulse oximetry
sive. Suctioning generally requires the patient to be does not assess the adequacy of ventiliation and severe
disconnected from the ventilator (open suctioning). This hypercapnia can develop despite adequate oxygen satura-
predisposes to alveolar collapse. The performance of an tion, especially if the patient is inspiring gases with a high
alveolar recruitment manoeuvre may be necessary to FiO2. Pulse oximetry can only be relied on to measure
re-recruit collapsed alveoli. Alveolar recruitment is oxyhaemoglobin saturation and pulse rate.)
achieved by manually inflating the lung with a larger than
normal tidal volume or PIP than that being used for Capnography
ventilation, holding for a prolonged inspiratory time. Capnography provides a breath-by-breath assessment of
the adequacy of ventilation, assuming normal cardiovas-
Cardiovascular support in the ventilated patient cular function. This technique measures CO2 in the
Vasoactive agents may be indicated in animals with expired patient gases (P’ETCO2) (see 34), which approx-
hypotension unresponsive to normalization of blood imates the CO2 tension in the alveoli (PACO2). As alve-
volume and techniques used to reduce mean airway olar gases should be in equilibrium with arterial blood,
pressure during ventilation. Conservative approaches P’ETCO2 can be used to approximate PaCO2.
to the correction of hypotension should be performed Intermittent analysis of arterial blood gas samples
first (fluid therapy and minimizing the delivery of vaso- should also be performed to ensure capnography is
dilating agents such as anaesthetics) and preparations providing a reliable indication of ventilation, as dis-
made for the administration of vasoactive drugs if indi- crepancies between arterial and end-tidal CO2 can occur.
cated. Close monitoring must be performed before, Differences between PaCO2 and P’ETCO2 are caused
during and after pharmacological management of BP by reduced pulmonary blood flow (and increased
abnormalities. Pharmacological manipulation of BP is physiological dead space) due to pulmonary thrombo-
described in the sections on hypotension (p. 52) and embolism, air embolism and reduced cardiac output
hypertension (p. 55). (heart failure, hypovolaemia). In small animal patients
 R E S P I R AT O RY AND C A R D I O VA S C U L A R S U P P O RT 51

Arterial blood gases

Measurement of PaO2 is the gold standard for determin-
ing the amount of oxygen within arterial blood and
should be performed whenever the accuracy of pulse
oximetry is in doubt. Measurement of mixed venous
oxygen tension (blood collected from the right atrium via
a central venous catheter) can provide an indication of
the relationship between oxygen supply and demand.
An increase in the difference between arterial and mixed
venous oxygen tension suggests either decreased tissue
perfusion or increased tissue consumption.

Calculation of oxygen delivery

Oxygen delivery to tissues is a product of cardiac output
and arterial oxygen content (DO2 = CO × CaO2). A cal-
 36 A humidifying and moisture exchange (HME) culation of DO2 is the ultimate measure of adequacy
device, placed between the patient and the anaesthetic of tissue oxygenation, but is not always practical. CaO2
circuit, prevents excessive heat and fluid loss during is easily calculated, as it is the sum of oxygen bound
anaesthesia. A capnograph attached to the HME provides to haemoglobin and oxygen dissolved in the plasma
breath-by-breath assessment of adequacy of ventilation. (CaO2 = [SpO2 × Hb × 1.34] + [0.003 × PaO2]). Because
of the requirement for specialist equipment, assessment
of cardiac output is usually limited to referral institutions.
As a result, cardiac output is usually extrapolated from
the measurement of BP (mean arterial pressure [MAP] =
cardiac output × systemic vascular resistance [SVR]). An
inability to obtain direct measurement of cardiac output
prevents the calculation of DO2 in a clinical setting.

CIRCULATION: CARDIOVASCULAR SUPPORT OF

THE NEUROLOGICAL PATIENT

Abnormalities of cardiovascular function can cause sec-

ondary neurological damage in animals with intracranial
with cardiovascular compromise, PaCO2 may differ from disease. Hypotension leads to reduced CPP, particularly
P’ETCO2 by 10–20 mmHg or more due to development in the presence of increased ICP (CPP = MAP − ICP).
of physiological dead space. Discrepancies will also occur Hypertension has the potential to increase ICP in the
due to increased dead-space ventilation, as less of the presence of intracranial disease. This occurs when
inspired tidal volume actually reaches the alveoli. An increases in MAP are in excess of normal autoregulation
example of this is panting in a spontaneously breathing or when autoregulation is impaired. When autoregula-
animal. tion is impaired, any increase in MAP can cause linear
As capnography provides breath-by-breath informa- increases in cerebral blood volume and ICP. Therefore,
tion and is a non-invasive monitor, it is an important tool cardiovascular function needs to be monitored closely in
for assessing pulmonary and circulatory emergencies in neurological patients and hypotension and hypertension
the ventilated patient (36). managed as required.
 52 ADMISSION AND NEURODIAGNOSTIC TESTS

Circulatory shock/hypotension
Definition
Circulatory shock causes a significant reduction in organ
perfusion. During the compensatory phase, BP is main-
tained by the responses to reduced tissue perfusion,
including increases in heart rate (37, 38), peripheral vaso-
constriction, shifts in fluid from the interstitial space to
the intravascular space and reduced urine production.
Once the fluid deficit exceeds the ability of the body to
compensate (decompensatory shock), decreases in BP
occur (39).
In humans with head trauma, hypotension is defined
as systolic arterial blood pressure (SAP) ≤90 mmHg.
Similar limits of MAP in the trauma patient have not
been established in small animals, although maintenance  37 Recording from a patient taken before blood loss.
of CPP (MAP − ICP) at between 60 and 70 mmHg and Heart rate (seen here to be 106 beats per minute) and
MAP >70 mmHg is associated with a better outcome in blood pressure (wave marked with arrow), measured using
head-trauma cases. In the absence of ICP monitoring it is an arterial catheter, are within normal ranges.
recommended that the MAP should be 70–80 mmHg
and the SAP should be 100 mmHg to maintain CPP in
the presence of increased ICP. Further increases in CPP
above 70 mmHg are not recommended, as the use of
aggressive fluid therapy and vasopressors to maintain
CPP above 70 mmHg is associated with systemic com-
plications such as ARDS.

Clinical signs of circulatory shock

Instigation of appropriate therapy is dependent on early
recognition of shock. This requires a good understand-
ing of the clinical signs of circulatory shock. The clinical
signs of shock will vary depending on the severity, the
degree of compensation and the cause.
Reduction in cardiac output causes sympathetic
nervous stimulation, leading to tachycardia and peri-
pheral vasoconstriction (pale mucosal membranes, cold  38 When loss of blood volume is severe or prolonged,
extremities, reduced rectal temperature). If these changes compensatory mechanisms fail and hypotension occurs, as
can compensate for the reduction in cardiac output, BP can be seen in this recording.
will be normal. Once these compensatory responses are
overwhelmed, BP will decrease. It is essential that therapy
is started before decompensation and decreases in BP
occur in order to minimize organ damage.

 39 Electrocardiogram showing tachyarrhythmia,

here associated with poor cardiac output and hypotension.
In this case urgent management is required, including
rapid correction of the cause of the arrhythmia.
 R E S P I R AT O RY AND C A R D I O VA S C U L A R S U P P O RT 53

Management of circulatory shock hypotension will also occur in any animal that develops
Appropriate treatment depends on the cause. Arterial BP concurrent systemic inflammatory response syndrome
is influenced by cardiac output and total peripheral (SIRS). SIRS may develop in the presence of any factor
resistance. A decrease in either cardiac oputput or total that can stimulate a widespread inflammatory response
peripheral resistance will decrease BP. Cardiac output is (e.g. multiple organ trauma, hypoxaemia and ventilator-
the product of heart rate and stroke volume. Stroke induced lung injury).
volume is determined by preload (blood volume), In most cases, management requires treatment of the
myocardial contractility and afterload. underlying cause. Symptomatic treatment includes fluid
therapy and administration of vasoconstrictive agents.
Hypovolaemic shock Drugs used to increase BP in human patients with head
A reduction in circulating blood volume results in a trauma include noradrenalin (norepinephrine) infusion,
decreased amount of blood returning to the heart dopamine and phenylephrine. Vasopressin has also been
(preload), with a resultant decrease in stroke volume and used to increase BP in critically ill animals with SIRS.
cardiac output and, therefore, BP. The most common The dose rates of those agents that have been used in
cause of hypovolaemic shock in the neurological patient small animals are: noradrenalin (norepinephrine) (0.05–2
is haemorrhage associated with trauma or surgical losses. μg/kg/minute); dopamine (5–10 μg/kg/minute); vaso-
Trauma may also cause hypovolaemia due to loss of pressin (0.5–2 IU/kg/minute) and phenylephrine (1–3
protein-rich fluid into damaged tissues such as muscle μg/kg/minute) (see Further reading).
bruises and large wounds. In immobile animals unable to When sedative and anaesthetic agents are responsible
access water, dehydration may lead to hypovolaemia for the hypotension, the dose of the administered agent
once the fluid deficit exceeds 10% of body weight. should be reduced and fluid therapy given to animals that
Fluid therapy forms the cornerstone of the manage- do not respond to the reduction in anaesthesia.
ment of hypovolaemia. (For details on fluid therapy see
Chapter 31.) Cardiogenic shock
Cardiogenic shock may occur due to marked changes in
Vasodilatory/distributive shock heart rate and rhythm, and reduced myocardial contrac-
Vasodilatory shock is caused by marked peripheral tility. Abnormalities in cardiac rhythm include those
vasodilation, which results in relative hypovolaemia as associated with fast heart rates (tachyarrhythmias) and
the vascular volume increases relative to the volume slow heart rates (bradyarrhythmias). Hypotension occurs
of blood within the circulation. A primary cause of secondary to fast heart rates, as there is decreased time
peripheral vasodilation and hypotension in animals with for the heart to fill during diastole, resulting in reduced
neurological disease is spinal disease that interferes with stroke volume and cardiac output. In addition, the high
the sympathetic innervation of the splanchnic vascula- heart rate increases myocardial oxygen demand when
ture. A secondary cause is the use of anaesthetic agents oxygen delivery may be compromised. This predisposes
that cause peripheral vasodilation (e.g. propofol, iso- to myocardial ischaemia, which may further exacerbate
flurane, sevoflurane). Vasodilation associated with the arrhythmia. Slow heart rates cause hypotension, as
administration of these agents is dependent on the dose cardiac output is dependent on heart rate (CO = SV ×
and rate of administration. The higher the dose or the HR). Poor myocardial contractility decreases the
faster the rate of administration, the greater the amount amount of blood able to be pumped by the heart and,
of vasodilation and the lower the BP. Vasodilation and therefore, cardiac output.
 54 ADMISSION AND NEURODIAGNOSTIC TESTS

Abnormalities in cardiac rhythm also increases; however, the marked hypertension ulti-
Tachyarrhythmias mately causes a reflex decrease in heart rate due to
Causes of tachyarrhythmias associated with neurological baroreceptor stimulation. Bradycardia may also occur
disease include brainstem disease/compression. Myo- secondary to drug overdose (e.g. opioid administration).
cardial degeneration and necrosis are also reported to Severe hypothermia and electrolyte abnormalities
occur following cranial and spinal trauma in dogs. Causes (hyperkalaemia and hypokalaemia) may also contribute
associated with other systemic abnormalities include to bradycardia in any critically ill patient.
myocardial contusions secondary to thoracic trauma and Brainstem compression requires specific treatment to
myocardial ischaemia secondary to hypovolaemia reduce ICP (diuretics, hyperventilation). (For details on
(e.g. haemorrhage from trauma or surgery). Fluid, specific management of increased ICP see Chapter 20.)
electrolyte and acid–base abnormalities may also occur Bradycardia secondary to opioid overdose requires a
secondary to inappetence, an inability to eat and drink or reduced dose of opioids +/- administration of reversal
losses from the gastrointestinal tract or kidneys. (For agents such as naloxone. Specific treatment of bradycar-
more details on fluid and electrolyte abnormalities that dia requires administration of anticholinergics such as
occur commonly in neurological disease see Chapters 3 atropine. As these agents can mask the signs of brainstem
and 31.) Persistent tachycardia can also lead to myo- herniation (e.g. pupil and heart rate changes), use of these
cardial ischaemia and arrhythmias, as the increase in agents in animals with intracranial disease needs to be
heart rate causes both an increase in myocardial oxygen performed carefully and increased ICP as a cause of the
consumption and a reduction in oxygen delivery due to bradycardia needs to be ruled out before these agents are
decreased time for the heart muscle to be perfused. administered.
Management of arrhythmias involves the correction
of all possible underlying causes. Brainstem compression Poor myocardial contractility
and/or herniation requires specific treatment for Decreased cardiac muscle contraction most commonly
increased ICP (see Chapter 20). Brainstem ischaemia can occurs in neurological patients secondary to the use of
occur due to either increased ICP or decreased BP. Any anaesthetic and sedative drugs. Development of SIRS
concurrent electrolyte and acid–base abnormalities also secondary to prolonged hypotension, hypoxaemia, ven-
need to be corrected. Any cause of persistent tachycardia, tilator-induced injury or multiple organ trauma may be
including pain, hypovolaemia or hypotension, needs to another cause of reduced myocardial contractility in the
be corrected to minimize the risk of exacerbating or con- neurological patient.
tributing to the development of tachyarrhythmias. Improving myocardial contractility requires the
Specific anti-arrhythmic medication is indicated if the identification and treatment of underlying causes. For
arrhythmia persists despite treatment of all possible drug-induced decreases in contractility, delivery of the
causes and/or if tissue perfusion is compromised. Specif- agent needs to be decreased or stopped if possible. Use of
ic anti-arrhythmics for ventricular tachyarrhythmias multimodal anaesthesia with opioid-based protocols will
include lidocaine (sodium channel blocker) and beta reduce the requirement for the more cardiovascular and
blockers (e.g. esmolol). Supraventricular tachyarrhyth- respiratory depressant anaesthetic drugs. The undesir-
mias can be treated using beta blockers. (For dose rates able effects of anaesthesia can also be minimized by using
commonly used in clinical cases see Further reading.) short-acting agents that can be titrated to effect. (For
more details of methods of reducing anaesthetic-related
Bradyarrhythmias cardiovascular depression see Chapter 29.)
The main cause of bradycardia and bradyarrhythmias in Inotropes are indicated when management of the
animals with neurological disease is brainstem compres- underlying cause does not improve myocardial contrac-
sion (Cushing reflex). Brainstem compression causes tility or when urgent improvement in perfusion is
sympathetic stimulation, which results in a marked required. Inotropes that can be used include dopamine
increase in peripheral arterial BP. Initially, the heart rate (2–5 μg/kg/min) or dobutamine (2–5 μg/kg/min).
 R E S P I R AT O RY AND C A R D I O VA S C U L A R S U P P O RT 55

Obstructive shock Causes of hypertension

Obstructive shock occurs due to physical interference As described above, MAP = CO × SVR. Cardiac output is
with venous return to the heart resulting in decreased dependent on heart rate and stroke volume, which in
preload and, therefore, stroke volume and cardiac turn are dependent on preload, contractility and after-
output. In animals with trauma, obstruction to venous load. Therefore, an increase in any of these factors may
return may occur in association with pneumothorax. In increase BP. The extent of the increase will depend on
these cases, prompt removal of the air by thoracocentesis the degree of compensation.
or a chest drain will result in resolution of the shock. Causes of hypertension in neurological patients
include peripheral vasoconstriction, tachycardia and
Hypertension hypervolaemia (increased preload). Peripheral vasocon-
Definition striction can occur due to increased ICP and brainstem
In non-neurological patients, hypertension is defined as compression (Cushing reflex) in animals with intracranial
an MAP of >100 mmHg and a SAP of >150 mmHg. In disease. Peripheral vasoconstriction, tachycardia and
neurological patients, increases in mean BP and, there- associated hypertension may also occur secondary to
fore, CPP outside the normal autoregulatory range of sympathetic stimulation caused by pain and anxiety.
the brain cause linear increases in blood volume and ICP
(40). In addition, abnormal brain tissue loses the ability to Management
autoregulate. In these regions, any increase in mean BP is Specific management of increased ICP is detailed in
associated with an increase in cerebral blood volume and, Chapter 20. To minimize other causes of hypertension,
potentially, an increase in ICP. Maintenance of a stable adequate pain management and careful administration of
normal BP is therefore important in these animals to fluids are important. Where hypertension persists
prevent increases in ICP. despite correction of underlying causes, specific pharma-
cological treatment may be required to prevent detri-
 40 Relationship between cerebral blood flow and mental effects on ICP and neurological function.
intracranial pressure in response to changes in cerebral Persistent hypertension, despite adequate analgesia,
perfusion pressure, arterial carbon dioxide and oxygen can be treated by the administration of beta receptor
tension. Normal pressure autoregulation of blood flow antagonists or calcium channel blockers. Agents that
(dotted red line) maintains appropriate cerebral blood have been used in human patients with head trauma
flow despite fluctuation in the mean arterial pressure. include esmolol (β blocker), labetalol (mixed α and β
Increased PaCO2 (green line) causes a global increase in blocker) and nicardipine (calcium channel blocker). Use
cerebral blood flow that exceeds demand. Cerebral blood of these agents in small animal neurological patients has
flow is unchanged until PaO2 levels fall below approxi- not been reported. Esmolol is commonly used to treat
mately 60 mmHg, when it rises sharply. tachyarrhythmias in small animals and labetolol has been
described for use in a hypertensive crisis. Nicardipine is
not used clinically in small animals at present; however,
100
amlodipine, a calcium channel blocker used in small
PaO2 PaCO2 animals with cardiovascular disease, may be a suitable
80 CPP
alternative. The dose rates of these agents can be found
CBF (ml/100 gm/min)

in critical care texts (see Further reading).

60
Sodium nitroprusside is also used in small animal
patients with cardiac disease to control hypertension;
40
ICP
however, this agent is best avoided in patients with
neurological injury due to its risk of causing increases
20
in ICP.
00 50 100 150 200
MAP (mmHg)
 56 ADMISSION AND NEURODIAGNOSTIC TESTS

The use of any agent that decreases BP should be  42 Arterial blood pressure is commonly measured
associated with close monitoring of BP to ensure exces- directly via a catheter placed in the dorsal pedal artery.
sive reduction and hypotension do not occur. (a) Prior to placement, the hair over the medial surface of
the dorsal tarsus is clipped and the site disinfected.
Monitoring the cardiovascular system (b) A small amount of lidocaine (2%) can be injected sub-
Arterial blood pressure cutaneously over the artery at the intended site of catheter
Arterial BP can be measured non-invasively using oscil- insertion. This is particularly useful in conscious animals
lometric or Doppler techniques (41). Oscillometric tech- to prevent discomfort and movement during insertion.
niques (e.g. device for indirect non-invasive, automated, It can also be useful in anaesthetized animals as the vaso-
mean arterial pressure [DINAMAP]) provide automatic dilation associated with the lidocaine administration can
intermittent measurement of mean, systolic and diastolic aid catheter placement. (c) Prior to catheter placement, a
pressure and pulse rate. The minimum amount of time small stab incision can be made in the skin. This allows
between repeated measurements is 2 minutes. Many of the catheter to be inserted with greater control as there is
the commercial systems available are unreliable in very no longer any skin resistance. The artery is then gently
small animals, such as cats, and in hypotensive or palpated at the site of insertion and the catheter inserted
bradycardic patients. However, the accuracy in these sit- gently but firmly in the direction of palpation. If the artery
uations is improving with newer equipment that is continues to be palpable as the catheter is inserted, then it
becoming more readily available. The Doppler tech- is likely that the catheter is too far lateral or medial to the
nique is performed manually and is limited to measure- artery. If the artery cannot be palpated, the catheter may
ment of SAP. However, this technique is more reliable in be between the artery and skin. A flash of blood will enter
small animals and in shocked patients. the hub of the stylet once the arterial wall has been
In unstable animals or chronically ventilated animals, penetrated by the bevel of the stylet. It is essential that the
invasive BP monitoring via an arterial catheter (42) is catheter is not separated from the stylet until at least
preferred over non-invasive methods. Invasive tech- 5 mm have been inserted to ensure that both stylet and
niques allow continuous monitoring of BP. Catheters are catheter have penetrated the wall of the artery. If this has
most commonly inserted in the dorsal pedal artery in not occurred, the catheter will not be able to be inserted.
small animals. In addition, arterial blood gases can be (d) Taping and/or superglue can be used to secure the
obtained via the arterial catheter, allowing accurate catheter in place. (e) The catheter can then be connected
assessment of pulmonary function and oxygen delivery. to the fluid line to allow blood-pressure monitoring.

 41 The Doppler technique can be very useful for

measuring blood pressure, particularly in small animals.
 R E S P I R AT O RY AND C A R D I O VA S C U L A R S U P P O RT 57

a b

c d

e
58 ADMISSION AND NEURODIAGNOSTIC TESTS

a b

c d

e f

g h
 R E S P I R AT O RY AND C A R D I O VA S C U L A R S U P P O RT 59

 43 Insertion of a catheter into the jugular vein. Central venous pressure

Prior to placement, the dead space of the catheter is CVP is measured using a fluid-filled catheter inserted
filled with saline or heparinized saline and an area into the cranial vena cava via the jugular vein (43).
over the selected jugular vein is clipped. The site is then Placement of the catheter in the jugular vein may
disinfected. A roll of bandage or gauze placed under the increase the risk of disturbance to venous return and
neck can be useful for increasing visibility of the vein, increased ICP. An alternative is to place a percutaneous
but care should be taken not to occlude the dependent central catheter, which is passed into the caudal vena cava
jugular vein in animals with intracranial disease. via a catheter in the medial saphenous vein (44). Where
(a) A small stab incision can be made (carefully) in the this is not possible, a jugular venous catheter can be
skin over the jugular vein, as shown by tenting the skin placed, taking care not to occlude the jugular during
between two fingers; this assists placement of the placement (surgical exposure may be required) and
catheter. (b) With an assistant compressing the vein utilizing a catheter with as small a diameter as possible to
proximally, the introducer (a needle or catheter) is minimize interference with venous return. The use of
inserted through the stab incision into the jugular vein. neck bandages over these catheters is discouraged in
(c) Once the guide wire has been placed, the needle animals with intracranial disease.
introducer is removed, leaving the wire in place. CVP in spontaneously breathing animals is normally
(d) The dilator is then passed over the wire and between 0 and 10 cm H2O. CVP is determined by the
threaded into the vein. (e) A gentle but firm twisting amount of blood returning to the heart and the ability of
action will help insert the dilator through the skin and the heart to pump this blood. Therefore, measurement
vessel wall. The dilator is them removed, again leaving of CVP will help differentiate cardiac and hypovolaemic
the wire in place. At this stage some haemorrhage will causes of hypotension and determine appropriate treat-
occur at the entry site as the hole in the vessel wall is ment. A low BP accompanied by a high CVP suggests
larger than the wire. Gentle pressure at the entry site that the heart is unable effectively to pump blood
using a sterile swab will reduce the amount of returning to the heart, while low BP and CVP supports a
haemorrhage until the catheter is placed. (f) The reduction in the volume of blood returning to the heart
catheter is then passed over the guide wire. During (i.e. hypovolaemia). In contrast, a high CVP and high
insertion of the catheter it is essential to maintain a hold MAP would suggest hypervolaemia.
on the guide wire at all times. The wire is inserted into Measurement of CVP is helpful to determine the
the proximal end of the catheter and gradually passed up extent of adverse effects of ventilation. A high CVP can
the catheter. (g) When the hub of the catheter is be caused by high mean intrathoracic pressure used for
reached, the injection port is removed and the wire ventilation. In such a case, the PIP and/or PEEP requires
passed through the end of the catheter. Once the wire adjustment.
passes through the hub, the operator can hold the wire
and pass the catheter over the wire into the vein.
The wire is then removed and the injection port
replaced. The catheter is flushed with saline. (h) The
catheter is sutured in place. A sterile dressing is placed
over the entry wound. Neck bandages should not be
used in animals with intracranial disease, but can be
used in other patients to help secure the catheter in
place.

 44 Central venous pressure can be measured via a

catheter placed in the caudal vena cava via the medial
saphenous vein.
 60 ADMISSION AND NEURODIAGNOSTIC TESTS

Urine output (For more details on interpretation of changes in urine

Urine output provides an indirect indication of renal output see Chapter 31.)
perfusion and therefore circulating blood volume and Monitoring of urine output is easy, cheap and inform-
hydration status. It is an extremely valuable tool for ative. An indwelling urinary catheter is inserted and a
assessing the adequacy of cardiovascular function in closed collection system set up. It is an extremely useful
neurological patients. way of assessing fluid balance in unstable neurological
Urine output is normally 1–2 ml/kg/hour in patients, particularly those receiving diuretics, where
normovolaemic patients on normal maintenance fluid fluid losses in the urine are higher than normal. In
rates. Higher rates should be expected in normally addition, animals with traumatic brain injury may have
hydrated animals receiving more than maintenance rates alterations in the reabsorption of renal sodium and water
of fluid. Higher than normal output is also expected in (e.g. central diabetes insipidus [DI] resulting in abnormal
animals that have received diuretics or glucocorticoids. urine production and urine SG).
 ADMISSION AND NEURODIAGNOSTIC TESTS Chapter 3

METABOLIC EVALUATION OF
CRITICALLY ILL NEUROLOGICAL PATIENTS 61

Louise Clark

INTRODUCTION coagulation status and blood typing may also be appro-

priate. Further diagnostic testing and imaging may be
When presented with a severely ill animal with primary indicated where there is polytrauma or where serious co-
neurological dysfunction it is important to consider any existing disease is suspected.
deleterious metabolic consequences that this disease may The relevant tests in critically ill neurological patients
cause. The animal should be considered as a whole and should include:
thought given as to how the pathophysiology of the pre- • Minimum database:
senting disease may affect the systemic metabolic • Complete blood count (CBC) (haematology)
function. and examination of blood smears.
In addition to a careful serial neurological evaluation, • Serum biochemical (including electrolytes)
it is important that the whole animal is thoroughly analysis.
assessed. The neurological presentation may be only • Urinalysis (including cytology).
part of the global presentation and underlying patho- • Bedside tests (where equipment is available):
logy. Consideration should be given to the presence of • Serum osmolality.
any co-morbidities (i.e. any other potentially unrelated • Acid–base status (lactate).
pathology that may influence assessment, management • Tests of haemostasis.
and prognosis of the primary presenting neurological • Blood typing.
disease). This chapter will focus on how to utilize the • Other biochemical assays including ammonia.
information provided by bedside testing modalities, and
the tests that might be more appropriate with Many cases of neurological dysfunction with a metabolic
specific neurological presentations. aetiology have significant and sometimes specific
minimum database abnormalities (see Chapter 27).
GENERAL APPROACH Many animals with disease restricted to the CNS do not
present with specific minimum database findings;
The history and clinical and neurological examinations however, this information can be useful in detecting
will provide information to direct the clinician as to concurrent and potentially unrelated systemic disease
which tests are most appropriate for any particular case. and may direct further investigation. Infectious and
Blanket testing is inappropriate, expensive and will not sterile inflammatory disease processes demonstrate non-
necessarily yield clinically relevant information. In any specific haematological changes and some biochemical
critically ill patient it is always appropriate to obtain a abnormalities (see Chapter 19). Neoplastic and toxic
minimum database. The most useful information will be disease processes may also manifest as haematological,
obtained from an assessment of packed cell volume/total biochemical and urinalysis changes. In the emergency
protein (PCV/TP), a basic biochemical evaluation, patient with primary neurological disease, data from
including glucose plus electrolytes and acid–base bedside tests can reveal abnormalities that require
analysis, and urinalysis. An evaluation of haematology, prompt treatment.
 62 ADMISSION AND NEURODIAGNOSTIC TESTS

Packed cell volume and total protein

Fundamentals
Tissue oxygen delivery is reliant on an adequate circu-
lating Hb concentration, cardiac output and tissue perfu-
sion. Circulating Hb concentration can be directly
measured at the bedside with a ‘HemoCue’ (45); however,
in most clinical situations in veterinary medicine, PCV is
determined by centrifugation of whole blood. Dividing
the PCV (%) obtained by three gives an approximation of
the circulating Hb (g/dl) concentration.
Assessment of PCV or Hb is mandatory. If the animal
is presented immediately after trauma and significant
haemorrhage, the PCV/Hb will not be reflective of
actual oxygen-carrying capacity until the animal is ade-
quately volume resuscitated. Splenic contraction may
further complicate interpretation. Therefore, serial
blood sampling may be appropriate.  45 HemoCue® for bedside analysis of haemoglobin
An appropriate intervention threshold for transfusion concentration.
might be higher than in most routine anaemia cases,
which is generally a PCV of <0.2 l/l (20%). Mild more quickly than PCV in the presence of acute haemor-
haemodilution (PCV ~0.25 l/l [25%]) improves cerebral rhage. Wherever haemorrhage is suspected or con-
oxygen delivery by decreasing blood viscosity, but when firmed, serial PCV/TP evaluation is useful to evaluate
PCV falls further, cerebral oxygen delivery may be com- the effects of fluid therapy and detect ongoing haemor-
promised. Thus, in critically ill neurological patients the rhage. Appropriate cardiovascular monitoring should
PCV should ideally be maintained above 0.2 l/l (20%). also be established (see Chapter 2). TP may also be
Where there has been significant haemorrhage, blood decreased in animals with severe hepatopathies, protein-
typing should be undertaken (see Chapter 31), and where losing nephropathies and protein-losing enteropathies.
there is any clinical suspicion of coagulopathy, a manual The presence of a low TP on bedside tests should direct
platelet count (blood smear) and coagulation evaluation further investigation. Conversely, the presence of
are prudent. Where the PCV is low, a CBC, including dehydration may result in an artificially elevated PCV
blood smear, should always be performed in order to and TP and these findings should direct the clinician to
further characterize the anaemia. re-evaluate the patient. (Note: TP elevation may also be
Concomitant assessment of TP may be advanta- identified when hyperglobulinaemia is present due to an
geous (46); there is some evidence that TP may fall infectious, immune-mediated or neoplastic aetiology.)

 46 Refractometer for measurement of total solids

(often considered equivalent to total protein) and urine
specific gravity.
 M E TA B O L I C E VA L U AT I O N OF C R I T I C A L LY I L L N E U R O L O G I C A L P AT I E N T S 63

Clinical relevance Glucose

The brain relies entirely on aerobic metabolism, and so it Fundamentals
is very susceptible to hypoxic damage. It is therefore Normoglycaemia is maintained by a balance between the
essential to maintain an adequate circulating Hb con- glucose-lowering hormone insulin and the glucose-
centration in order to ensure adequate tissue oxygen elevating hormones glucagon, cortisol, epinephrine
delivery. The brain is especially vulnerable in cases of (adrenalin) and growth hormone.
head trauma and raised ICP (due to any cause). Early
correction of a low circulating Hb concentration will Clinical relevance
optimize oxygen delivery to the brain. The brain is an obligate consumer of glucose. Inadequate
Plasma proteins play an important role in the mainte- glucose supply to the brain (neuroglycopaenia) can
nance of colloid osmotic pressure (COP) and, therefore, lead directly to CNS signs. These include altered menta-
vascular volume, in addition to their other homeostatic tion, weakness and recumbency, ataxia, alterations in
functions. Hypoproteinaemic animals may be at risk vision and seizures. Pacing, restlessness and vocalization
from oedema formation and therefore fluid therapy must may be evident prior to neurological signs; however,
be tailored to their needs (see Chapter 31). these are not consistent signs. There is some evidence
that chronic hypoglycaemia, such as experienced in
Testing insulinoma cases, may result in upregulation of cerebral
PCV and TP measurements are easily performed. glucose uptake and a lack of neurological signs associated
Samples must be taken into the correct volume of anti- with hypoglycaemia. Hyperglycaemia may result in
coagulant and be spun for the appropriate duration, neurological signs and severe hyperglycaemia may
always ensuring that the refractometer is calibrated cor- manifest as hyperglycaemia–hyperosmolar syndrome, a
rectly. When there are concerns that a patient has raised complication of diabetes mellitus (see Chapter 27). Mild
ICP and blood tests are required, consideration should hyperglycaemia is common in cats presented as neuro-
be given to sampling from a large intravenous catheter at logical emergencies; this is a manifestation of the stress
the time of placement or from other peripheral veins. response. Hyperglycaemia may also be documented in
Jugular occlusion must be avoided when blood sampling. dogs, secondary to catecholamine release. In people,
This applies to all the tests discussed below. hyperglycaemia immediately after hypoxic–ischaemic
injury causes damage to brain cells, and in acute
Normal ranges cerebrovascular accidents, hyperglycaemia is associated
Normal ranges will vary slightly according to the specific with larger infarct volumes and a poorer prognosis.
analyser and laboratory, but the following are guidelines: Hyperglycaemia has been documented in veterinary
• Canine: PCV, 0.37– 0.55 l/l (37–55%); TP, 54 –71 g/l species following head trauma and the degree of
(5.4 –7.1 g/dl). hyperglycaemia is associated with the severity of
• Feline: PCV, 0.25– 0.45 l/l (25– 45%); TP, 60–86 g/l the trauma. The significance of this finding is yet to be
(6.0 – 8.6 g/dl). determined. However, because hyperglycaemia may
potentiate neurological injury, it is prudent to avoid
Monitoring iatrogenic hyperglycaemia in patients with head trauma.
Daily assessment of PCV and TP is appropriate in Although there is a growing consensus amongst intensive
critically ill patients. Serial blood samples may be required care unit (ICU) clinicians working with human patients
for an assessment of the response to volume resuscitation that maintaining normoglycaemia improves outcome,
or where ongoing haemorrhage is suspected. this topic remains controversial, especially as to the
degree of glycaemic control required. Currently, no
Treatment guidelines exist in veterinary practice. The use of soluble
Fluid therapy and transfusion medicine are addressed in insulin to achieve normoglycaemia comes with a signifi-
Chapter 31. cant risk of inducing iatrogenic hypoglycaemia.
 64 ADMISSION AND NEURODIAGNOSTIC TESTS

Testing
Hand-held portable glucometers are available with
species-specific (canine and feline) software (47).

Normal ranges
The normal ranges for blood glucose will vary slightly
between laboratories:
• Canine: 3.6–6.2 mmol/l (65–112 mg/dl).
• Feline: 3.7–9.3 mmol/l (67–167 mg/dl).

Neurological signs may be seen when blood glucose is

<2.5 mmol/l (45 mg/dl) or >33.3 mmol/ (600 mg/dl)
and associated with hyperosmolar syndrome. Some
reports suggest that plasma glucose of 55.5 mmol/l (>1,000
mg/dl) may be associated with overt neurological signs.  47 Glucometer validated for use in cats and dogs.

Monitoring
The frequency of blood glucose monitoring will be
determined by the underlying disease process. More
details are given in Chapter 27.

Treatment Electrolytes
Hypoglycaemia should be treated as an emergency. Fundamentals
Initial treatment is usually symptomatic (1 ml/kg of The primary electrolytes that are considered relevant
50% [0.5 g/kg] dextrose/glucose diluted to a 5–10% in disease processes in the neurological patient are
solution and administered slowly IV). (Note: This solu- sodium (Na+), potassium (K+), calcium (Ca2+), magne-
tion is hypertonic and can cause thrombophlebitis.) sium (Mg2+) and chloride (Cl-). Bicarbonate (HCO3-) is
The response to treatment should be carefully moni- addressed later in this chapter (p. 70). There is a subtle
tored by serial glucose evaluation and, more impor- and complex electrolyte balance between the intracellu-
tantly, by clinical signs. A constant rate infusion (CRI) lar and extracellular compartments. Electrolytes may
of 2.5–5% dextrose/glucose, preferably in an isotonic enter or leave the cell membrane through various ion
crystalloid such as 0.9% NaCl, can then be adminis- channels. The maintenance of osmotic gradients of elec-
tered. Where solutions of concentration >5% are nec- trolytes is important. Such gradients affect and regulate
essary, they should be given through a central line to the hydration of the body and blood pH, and are critical
reduce the incidence of thrombophlebitis. Five percent for nerve and muscle function. Various mechanisms exist
glucose/dextrose in water should not be used for bolus in living species that keep the concentrations of different
administration; it may cause acute decreases in osmo- electrolytes under tight control. The major extracellular
lality and cerebral oedema. (Note: The ongoing glucose ions are Na+ and Cl-. The major intracellular ions are
supplementation can result in a tendency toward hypo- K+ and Mg2+.
kalaemia.) If appropriate, oral glucose administration
should be considered. Glucagon CRIs may be appro-
priate for animals with confirmed insulin or insulin- Clinical relevance
like peptide-secreting tumours. It is not clear whether Metabolic causes of neurological disease are considered
a ‘lone’ elevated glucose level should be treated. (Note: in Chapter 27. There are several primary neurological
This situation does not apply to hyperglycaemic diseases that may manifest with electrolyte abnormalities
hyperosmolar syndrome or to diabetic ketoacidois, and the aetiology, clinical significance and management
which should be treated as an emergency.) are briefly discussed below.
 M E TA B O L I C E VA L U AT I O N OF C R I T I C A L LY I L L N E U R O L O G I C A L P AT I E N T S 65

Hyperkalaemia There are several ways of reducing extracellular

In the context of neurological emergencies, hyper- potassium concentrations, either by driving K+ into cells
kalaemia is most likely to occur in an animal that has suf- or increasing K+ excretion. Multiple strategies may be
fered polytrauma and urinary tract rupture. Uroabdomen required in the severely hyperkalaemic patient:
may result in profound dehydration and hypovolaemia, • Volume expansion with crystalloids (usually NaCl
life-threatening hyperkalaemia, severe azotaemia, chem- 0.9% because this contains no K+) aims to resolve
ical peritonitis and metabolic acidosis. Hyperkalaemia is any underlying acidosis (acidosis potentiates
immediately life threatening because it affects the depo- hyperkalaemia), dilute the K+ and also promote K+
larization of cardiac myocytes. Clinical signs include excretion by diuresis.
inappropriate bradycardia. In particular, cats may not be • Dextrose/glucose saline infusion causes endogenous
truly bradycardic, but their heart rate is inappropriately insulin release, and insulin drives K+ into cells.
low for their stressed situation. An immediate electro- NaCl 0.9% with 5% dextrose will also promote
cardiogram (ECG) is required (48). Classical ECG volume expansion. Hypotonic glucose-containing
changes seen with hyperkalaemia include T-wave fluids (e.g. NaCl 0.18% with 4% glucose) do not
changes, bradycardia and atrial standstill progressing to contribute to volume resuscitation. In practice this
asystole. Wide complex (ventricular) tachycardias are approach may result in insufficient insulin release to
also possible. (Note: Some animals can be severely hyper- reduce serum K+.
kalaemic without obvious ECG changes.) • Regular (soluble) insulin (0.2–0.5 IU/kg IV),
In any case where the K+ concentration is >7 mmol/l followed by 2 g dextrose (4 ml of 50% dextrose) per
(mEq/l), and particularly if this is accompanied by ECG unit of insulin administered and then a 2.5–5%
changes, calcium administration is indicated. In the first dextrose infusion. Concentrations of dextrose or
instance, 10% calcium gluconate can be administered glucose in excess of 5% can cause thrombophlebitis
(0.5–1.0 ml/kg over about 10 minutes). This will restore and it should be administered via a central catheter.
the ‘normal’ gap between the resting membrane poten- It is prudent to evaluate glucose and K+ concentra-
tial and threshold potential of cardiac cells and reduce the tions every 15–20 minutes for the first hour to
risk of cardiac arrhythmias. However, it will not alter ensure efficacy of treatment and to avoid iatrogenic
extracellular potassium concentrations and is only effec- hyperglycaemia or hypoglycaemia.
tive for up to 1 hour.

 48 ECG demonstrating
I aVR V1 V4 hyperkalaemia in a dog.
ECG findings may include
the following: a reduction in
P-wave amplitude and pro-
II aVL V2 V5 longation of PR interval to
complete absence of P waves
(a); increase in QRS
duration; increase in QT
duration (b); slowing of the
III aVP V3 V6
heart rate; T waves become
tall and spiked; decreased
R-wave amplitude.

a b

RHYTHM STRIP, 11 50 mm/sec: 1 cm/mg

 66 ADMISSION AND NEURODIAGNOSTIC TESTS

• Bicarbonate (1–2 mEq/kg IV slowly over 15 Hyponatraemia

minutes). Bicarbonate is hyperosmolar and should Hyponatraemia is relatively uncommon in critically ill
be diluted according to the manufacturer’s dogs and cats, but neurological patients with head trauma
instructions. This approach relies on the patient or intracranial masses, particularly pituitary lesions, may
being able to remove (by ventilation) the additional be predisposed. Dogs and cats with hyponatraemia
CO2 produced. It should not be used in patients almost always have free-water retention rather than an
with respiratory compromise or a pre-existing absolute sodium deficit. When serum sodium falls below
metabolic alkalosis. 120 mmol/l (mEq/l) or falls rapidly, clinical signs may be
• Administration of all K+-containing fluids or evident. These include obtundation, seizures, head
nutrition and any drugs that promote hyperkalaemia pressing, coma and death.
(e.g. spironolactone, angiotensin-converting enzyme Hyponatraemia by itself produces brain oedema
[ACE] inhibitors) should be stopped. because it causes free-water to move into the relatively
hyperosmolar cell. This may result in increased ICP, with
Hypernatraemia potential neuropathological sequelae. When serum
Normal animals deprived of water for considerable sodium decreases, the brain prevents further cellular
periods of time can become severely hypernatraemic. swelling by extruding intracellular electrolytes and
Loss of low-sodium fluid through vomiting, diarrhoea organic osmolytes, a process that is almost fully achieved
or polyuria may also cause hypernatraemia. In the after 48 hours. Conversely, during the subsequent
primary neurological patient the most common cause of increase in serum sodium, re-establishment of intra-
hypernatraemia is probably central diabetes insipidus, cerebral osmolytes occurs, but their reuptake is more
which may occur secondary to traumatic brain injury or delayed (+/- 5 days). Rapid or excessive correction of this
pituitary masses and has been reported in granulo- hyponatraemia can be followed by development of brain
matous meningoencephalitis, hydrocephalus and CNS demyelinating lesions (central pontine myelinolysis, also
lymphoma. known as osmotic demyelination syndrome). This is a
Iatrogenic hypernatraemia can result from excess result of neuronal shrinking as water moves out of the
NaCl administration, either orally or via IV fluids cell during correction of hyponatraemia (i.e. as extra-
(e.g. hypertonic saline or sodium bicarbonate). Serum cellular osmolality increases, water is drawn into the
sodium levels in excess of 180 mmol/l (mEq/l) may be extracellular space). Guidelines suggest that sodium
associated with neurological signs such as head pressing should not be corrected at a rate greater than 0.5
and stupor and progressing to coma, seizures and death. mmol/l/hour (mEq/l/hour). Further details on the treat-
Hypernatraemia causes free water to move out of the ment of hyponatraemia can be found in Chapter 27.
cell into the relatively hyperosmolar extracellular space,
leading to a decreased cell volume. This results in the Testing
formation of intracellular osmolytes in order to replen- There are both wet and dry chemistry analysers available
ish cell volume; complete compensation can take 24 that can determine electrolytes. EDTA contamination
hours. These osmolytes must be considered during the and red cell haemolysis must be avoided to prevent
management of hypernatraemia. apparent hyperkalaemia. Excess heparin may result in
Patients with hypernatraemia have a free water deficit apparent hypocalcaemia. Animals receiving potassium
and should be managed as such, aiming to reduce serum bromide may demonstrate an apparent hyperchloraemia
sodium by no more than 0.5 mmol/l/hour (mEq/l/hour). dependent on the type of analyser used.
Rapid drops in plasma sodium concentration (and there-
fore osmolality) cause a rapid movement of free water Normal ranges
back into the intracellular space. Overly rapid correction See Table 10.
will result in cellular swelling (i.e. neuronal oedema)
because the osmolytes are broken down relatively slowly.
Further details on the management of hypernatraemia
can be found in Chapter 27.
 M E TA B O L I C E VA L U AT I O N OF C R I T I C A L LY I L L N E U R O L O G I C A L P AT I E N T S 67

Table 10 Typical electrolyte composition of Urine is normally clear. Semen, mucus and lipid may
extracellular and intracellular fluids cause turbidity in normal urine. Increased numbers of
cells, crystals, casts or organisms can increase the
Electrolyte Extracellular fluid Intracellular fluid
(mmol/l)* (mmol/l)*
turbidity of urine in disease conditions. An unpleasant
odour may indicate sepsis. Animals with ketosis/ketoaci-
Na+ 140–150 10 dosis may have urine with an acetone odour.
K+ 3.5–5.0 141
Clinical relevance
Ca2+ 1.5 <1 Urinalysis in conjunction with USG is a useful indicator
Mg2+ 3 50 of renal perfusion and volume status in an animal with
previously normal renal and endocrine functions. An ele-
Cl- 106–120 4
vated USG and a low urine output suggest hypovolaemia
HCO3- 19–25 10 (see Chapter 31). USG may also provide additional
information to support a diagnosis of endocrine disease.
Other ions not included
Dogs with Cushing’s syndrome and central or nephro-
* mmol/l = mEq/l for univalent ions genic DI are often hyposthenuric (can be isosthenuric).
Central DI may occur with pituitary neoplasia or after
head trauma or craniectomy. Secondary nephrogenic DI
Monitoring is very common and is caused by a failure of the kidney to
During the correction of hyponatraemia, serum sodium respond to vasopressin (Table 11). Other differential
should be monitored every 1–2 hours and during the cor- diagnoses that must be considered when USG is inap-
rection of hypernatraemia at least every 4 hours. Where propriately low include chronic renal failure and ethyl-
animals are hyperkalaemic, monitoring may be required ene glycol toxicity, which also results in the formation of
every 30 minutes initially in order to establish that there calcium oxalate monohydrate crystals. (Note: Many
is an appropriate response to treatment and that the drugs, including steroids, diuretics, phenobarbital and
serum potassium level is falling below that considered to alpha 2 agonists, can have effects on USG.)
be life threatening. Differentials for myoglobinuria include seizures,
crush injuries and severe muscle disease (e.g. necrotizing
Treatment myopathy).
See Chapter 27 for the treatment of metabolic diseases
and Chapter 31 for the treatment of hyponatraemia.

Urinalysis
Fundamentals
Bedside urinalysis tests include urine SG (USG) and a
Table 11 Common causes of secondary
dipstick. Cytology, culture and further tests, including nephrogenic diabetes insipidus
urine protein:creatinine ratio, may be indicated in the
diagnosis and management of specific diseases. Urine Disease process
volume depends on hydration status and renal concen- • Gram-negative sepsis including pyometra
trating ability and is inversely related to the USG. Urine
• Hypercalcaemia
concentration will affect the depth of the colour. Cloudy
• Hypokalaemia
red urine that clears after centrifugation is seen when
• Pyelonephritis
RBCs (haematuria) are present. Dark red to brown
• Portosystemic shunts and liver failure
colour may be due to haemoglobinuria or myo-
• Hypoadrenocorticism (dogs)
globinuria. Yellow-brown, greenish-yellow or dark
• Hyperthyroidism (cats)
brown urine may be due to bilirubinuria. Other urine
colours may result from certain drug therapies.
 68 ADMISSION AND NEURODIAGNOSTIC TESTS

Testing Glucose
Urine samples obtained by catheterization may have red Glucose in urine, an abnormal finding, occurs when
cell, epithelial cell, lubricant and bacterial contamination. blood glucose levels exceed the renal threshold for
Free catch samples are also non-sterile. Cystocentesis reabsorption. Glucosuria with hyperglycaemia occurs in
samples may contain red cells, but are indicated where diabetes mellitus, following dextrose administration
urinary culture is required. Urine is unstable and must be or secondary to catecholamines or glucocorticoids.
analysed promptly. It should be collected in clean or Glucosuria without hyperglycaemia may occur when
sterile containers and, if not analysed within a short hyperglycaemia is transient or in selective renal proximal
period of time, it should be refrigerated. Cold urine tubule dysfunction. Urine containing glucose is an
should be allowed to return to room temperature prior excellent culture medium for bacteria.
to analysis to avoid a false increase in SG. Precipitates
may form in urine as it cools, and cold may interfere Ketones
with some chemical tests. Refractometers must be Ketonuria occurs when ketone production exceeds the
calibrated prior to use. renal tubular absorption capacity. Dipsticks are semi-
quantitative only. The urine ketone test detects aceto-
Dipstick analysis acetate, but not beta hydroxybutyrate. False-positive test
Dipsticks are labile. They must be kept dry, in well- results may occur if urine is highly pigmented. False-
capped jars and used prior to the expiration date for negative results are uncommon in fresh urine, but may
accurate results. Prolonged exposure to air may cause occur when urine has been standing due to the volatility
false-positive tests for glucose and false-negative tests of ketones. Ketonuria may occur in diabetic ketoacidosis,
for occult blood. pregnancy, ketosis, insulinoma, glycogen storage disease
or starvation.
Urine pH
Acidic urine is caused by increased acid excretion or pro- Haemoprotein (occult blood)
duction (increased protein catabolism, metabolic or res- Haemoproteinuria may result from increased RBCs
piratory acidosis, paradoxical aciduria with alkalosis). (haematuria, especially dilute urine with lysed RBCs),
Alkaline urine is caused by increased alkali excretion or haemoglobinuria or myoglobinuria. Sediment evalua-
production (decreased protein catabolism, cystitis due to tion may differentiate haematuria from haemoglobinuria
urea-splitting bacteria, prolonged storage at room tem- and myoglobinuria. Typically, red urine supernatant
perature, metabolic or respiratory alkalosis). Urine pH is indicates haemoglobin or myoglobin. Haemoglobinuria
not an accurate indicator of systemic acid–base balance. is often accompanied by haemoglobinaemia.

Protein Bilirubin
Urine protein results must always be interpreted in con- Dogs with concentrated urine may have trace to 1+
junction with SG. A small amount of protein is normally bilirubinuria; they have a lower renal threshold for biliru-
present in urine and may be detected in concentrated bin than do other species, and canine renal epithelium
urine. Many false-positive protein tests occur, especially can also conjugate and excrete bilirubin (especially in
with alkaline urine. The protein test mainly detects male dogs).
albumin on the dipstick. Physiological pre-renal protein-
uria may result from excessive muscular exertion, Urobilinogen
convulsions or excess protein ingestion. Pathological Testing for urobilinogen in the urine should not be relied
proteinuria may be pre-renal (haemoglobinuria, myo- on in dogs and cats.
globinuria), renal (glomerular or tubular) or post-renal
(urogenital haemorrhage or inflammation).
 M E TA B O L I C E VA L U AT I O N OF C R I T I C A L LY I L L N E U R O L O G I C A L P AT I E N T S 69

Normal ranges • Osmolality. Osmotic concentration of a solution

USG is one of the most important tests in a urinalysis expressed as osmoles of solute per kg (i.e. mass) of
and should be done using refractometry. (Note: Do not solution.
use dipstick tests for SG.) Turbidity of the urine can • Oncotic pressure. A small portion of the total
affect the SG (usually increases it). Ideally, urine should osmotic pressure that is due to the presence of large
first be centrifuged and the supernatant used for protein molecules.
determination of SG. Normal SG values vary widely • Hyperosmolarity. Increase in the osmolarity of a
(usually between 1.015 and 1.045, up to 1.065+ in cats) solution to above the normal plasma concentration.
depending on hydration status and water intake. • Hypertonicity. Ability of a hyperosmolar solution
Cat urine contains different solutes from dog urine, to redistribute fluid from the intra- to the extracel-
therefore some refractometers have separate scales for lular compartment. Urea, for example, may be
cat urine to adjust for this. SG must be evaluated in light hyperosmotic, but because it equilibrates rapidly
of the blood urea nitrogen (BUN)/creatinine values and across membranes, it is not hypertonic.
hydration status. Abnormal substances, such as glucose
and proteins, may falsely increase the SG. Clinical relevance
Serum osmolality is a useful preliminary investigation for
Monitoring identifying the cause of hyponatraemia and may be useful
A single sample may be adequate in some disease process- in the assessment of fluid therapy (see Chapter 27).
es. In contrast, urine output and USG may be measured Assessment of the osmolar gap may be useful in identify-
every 1–4 hours in an animal that is severely hypo- ing toxicity caused by hyperosmolar compounds such as
volaemic and receiving fluid therapy. In an animal that has ethylene glycol. Urine osmolality is an important test to
had a craniectomy and is receiving multiple drugs, includ- evaluate the concentrating ability of the kidney.
ing steroids, serial electrolyte and USG evaluation should
be performed in the period following surgery. Testing
Clinical measurement of osmolality requires a cryo-
Treatment scopic (freezing point) osmometer (49). This is a rela-
Urinalysis findings always reflect the underlying disease tively expensive instrument, but convenient, rapid and
process. It is important not to treat the urinalysis find- easy to use.
ings themselves, but to establish what the underlying
disease process is. Extensive guidance on fluid therapy
can be found in Chapter 31. Thermistor
read-out circuit
Serum osmolality Thermistor
Fundamentals Stirrer/vibrator wire
Serum osmolality is the determinant of osmotic pressure, Insulation
which determines movement of water in and out of cells, Freezing bath
therefore clinically it is an indicator of electrolyte abnor- Sample
malities, renal function, etc. In the majority of cases,
sodium disorders in cats and dogs result from abnormal-
ities in water handling rather than a change in the
number of sodium ions. Plasma sodium concentration is
the major determinant of plasma osmolality. An osmole
is one mole of any fully dissociated substance dissolved in
water.
• Osmolarity. Osmotic concentration of a solution  49 The cryoscopic osmometer uses the principle of
expressed as osmoles of solute per litre (i.e. volume) freezing point depression to assess the number of osmoles
of solution. present in a serum sample.
 70 ADMISSION AND NEURODIAGNOSTIC TESTS

If it is not possible to measure osmolality, the following Acid–base status and blood gas analysis
equation can be used to estimate osmolarity: Fundamentals
Normal electrolyte concentrations and acid–base equi-
Plasma osmolarity = (2 × serum Na [mmol/l]) librium are important for normal neuronal function.
(mOsm/l) + urea (mmol/l) Evaluating these parameters is useful for assessing the
+ glucose (mmol/l) metabolic and respiratory status of a patient. While
arterial samples are required for accurate assessment of
or respiratory function, venous samples are sufficient for
assessment of metabolic disorders. Samples must always
Plasma osmolarity = (2 × serum Na [mEq/l]) be anaerobically collected, heparinized and analysed
+ (BUN [mg/dl]/2.8) immediately (or stored on ice).
+ (glucose [mg/dl]/18)
Clinical relevance
The doubling of sodium accounts for the negative ions Blood gas evaluation is the ‘gold standard’ for assessing
associated with sodium and the exclusion of potassium respiratory function and arterial blood gas analysis is the
allows approximately for the incomplete dissociation of only available method of assessing PaO2. Mild to moder-
sodium chloride. The difference between the measured ate hypoxaemia is often encountered in animals with
osmolality and calculated plasma osmolarity is known thoracic trauma or other lung pathology. It is essential to
as the osmolar gap; this is normally between 0 and maintain arterial oxygen content in order to maintain
10 mOsm/kg (osmolar gap = osmolality – osmolarity). tissue oxygen delivery. Hypoventilation may occur in
An elevated osmolar gap suggests the presence of animals with neuromuscular disease and in those with
osmotically active agents in the plasma (e.g. mannitol or head trauma or high cervical injury.
ethylene glycol). Any disease process that causes hypoperfusion
The following should be noted: (e.g. shock) may result in lactate accumulation and a
• There are several equations available in the metabolic acidosis. Early recognition of these metabolic
literature to calculate osmolarity. abnormalities allows early and appropriate treatment.
• The terms osmolarity and osmolality are used
interchangeably in much of the medical literature. Testing
• The units of osmolality (mOsm/kg) and osmolarity Systematic approach to blood gas analysis
(mOsm/l) are different, so strictly they cannot be • Acidosis: an abnormal process or condition, which
subtracted from one another. The value of the would lower arterial pH if there were no secondary
difference is clinically useful, so this problem is changes in response to the primary aetiological
ignored. factor.
• Alkalosis: an abnormal process or condition, which
Normal ranges would raise arterial pH if there were no secondary
The normal range of plasma osmolarity is 285–295 changes in response to the primary aetiological
mOsm/l. factor.
• Simple (acid–base) disorders are those in which
Monitoring there is a single primary aetiological acid–base
Where hyperosmolar therapy is used, some authors disorder.
quote an outcome goal for osmolarity: 300 mOsm/l or an • Mixed (acid–base) disorders are those in which two
Na+ of 145–155 mmol/l (mEq/l). Increasing plasma or more primary aetiological disorders are present
osmolarity to >320 mOsm/l with hypertonic fluids (e.g. simultaneously.
mannitol) should be avoided, as this has been associated • Acidaemia: arterial pH <7.36.
with acute renal failure. When correcting acute, severe • Alkalaemia: arterial pH >7.44.
hyponatraemia, serial osmolality measurements may also
be useful.
 M E TA B O L I C E VA L U AT I O N OF C R I T I C A L LY I L L N E U R O L O G I C A L P AT I E N T S 71

A step-by-step overview on how to interpret blood gas Step 3: Check for evidence of specific disease in the
samples is described below. other biochemistry results, especially electrolytes
Certain disorders are associated with predictable changes
Step 1: Check arterial pH in other biochemistry results (see above). For example,
Any increase in H+ ions will decrease pH. The net devia- an animal with head trauma and severe volume depletion
tion in pH will indicate whether an acidosis or an alka- from haemorrhage is likely to have a primary metabolic
losis is present (but will not indicate mixed disorders). acidosis with (or without) respiratory compensation.
pH changes can be produced by metabolic or respiratory Routine haematological and biochemical evaluation is
changes. Changes produced by one component will be likely to demonstrate a pre-renal azotaemia and possibly
opposed by the other. For example, to compensate for a fall in PCV and a decreased TP. USG is likely to be very
respiratory acidosis (secondary to hypoventilation) the high and little urine will be produced.
organism will attempt to increase the HCO3- in the
blood. Step 4: One problem or many?
If an acidaemia is present, an acidosis must be present. The appropriateness of the compensatory response
If an alkalaemia is present, an alkalosis must be present. should be assessed. A full discussion of compensatory
If pH is normal, either no acid–base disorder or a com- responses is beyond the scope of this chapter, but can
pensating disorder (i.e. a mixed disorder with an acidosis easily be obtained from other sources. Essentially, each
and an alkalosis) is present. abnormality (e.g. acute respiratory acidosis) will result
in an expected compensation. In this case, HCO3-
Step 2: What is happening with ventilation and meta- increases by 0.1 mmol/l (0.1 mEq/l) for every 1 mmHg
bolic indices? Look for a suggestive pattern in pCO2 change in pCO2.
and HCO3- If the expected (having worked out the compensation)
Each of the simple disorders produces predictable and actual values match, this implies no evidence of a
changes in pCO2 and HCO3-. mixed disorder. If the expected (having worked out the
If both HCO3- and pCO2 are low, this suggests the compensation) and actual values differ, this implies a
presence of either a metabolic acidosis or a respiratory mixed disorder is present.
alkalosis (a mixed disorder cannot be excluded). If both
HCO3- and pCO2 are high, this suggests the presence of Step 5: What is happening with oxygenation?
either a metabolic alkalosis or a respiratory acidosis PaO2 is a very useful parameter, but it is dependent
(a mixed disorder cannot be excluded). If HCO3- and on the PAO2. Adequate oxygenation requires a PaO2
pCO2 move in opposite directions, a mixed disorder of >80 mmHg. Generally, PaO2 should be within
must be present. Which disorder is present is dependent 10 mmHg of PAO2 in a conscious animal breathing
on which change is primary and which is compensatory, room air. Oxygenation is considered in more detail in
and this requires an assessment based on the history, Chapter 2.
examination and other results. Primary metabolic acido-
sis due to hypoperfusion or seizures (with respiratory Step 6: Formulate the acid–base diagnosis
compensation) and respiratory acidosis due to hypoven- It is imperative that blood gas samples are collected
tilation (with minimal compensation) are the most likely anaerobically into the correct amount of anti-coagulant
acid–base derangements in neurological emergency and analysed immediately or stored on ice (for 2 hours).
patients. Even with maximum compensation, the pH Sampling errors are a common cause of misdiagnosis of
usually moves in the same direction as the primary blood gas abnormalities (see Table 12). (Note: A clinical
problem (i.e. the body does not usually overcompensate assessment is vital to ensure that the assessment of blood
for an acid–base disturbance). gas analysis ‘makes sense’ and fits with the clinical
diagnosis.)
72 ADMISSION AND NEURODIAGNOSTIC TESTS

Table 12 Common acid–base abnormalities in Normal ranges

neurological patients See Table 13.
Respiratory acidosis
Monitoring
• Central respiratory depression (e.g. raised ICP/
Blood gas equilibrium is a dynamic equilibrium and
head trauma)
reassessment may be appropriate to gauge response to
• Neuromuscular disease (e.g. myasthenia gravis, botulism,
polyradiculoneuritis, tick paralysis) therapy. The frequency of measurement will be deter-
• Pleural space disease/chest wall disruption – secondary to mined by the severity of disease. A venous blood gas
trauma, diaphragmatic hernia sample taken on admission and shown to be normal may
• High cervical spinal coral injury be adequate in some patients. In comparison, an animal
with tetanus on a ventilator should have arterial blood
Respiratory alkalosis
gases checked approximately every half hour in the initial
• Excessive mechanical ventilation stabilization period. Pulse oximetry and capnography
• Pulmonary thromboembolism may then be used for monitoring, with blood gases being
• Pulmonary oedema performed every 4–6 hours.
• Pneumonia
• Pneumothorax/haemothorax Treatment
• Heat stroke Treatment of acid–base abnormalities should always be
• Corticosteroid therapy directed at the underlying cause; the aetiology of the
• Pain and anxiety disease process will guide the clinician appropriately.
• Pyrexia Treatment of respiratory acidosis is also considered in
• Compensation for metabolic acidosis (e.g. in hypovolaemic Chapter 2.
shock or sepsis)

Metabolic acidosis Lactate

• Lactic acidosis (see Table 14)
Fundamentals
Lactate is a by-product of anaerobic glycolysis. Glucose
• Hyperchloraemic – excess 0.9% NaCl administration
is broken down into pyruvate by the glycolytic pathway
• Ketoacidosis (diabetes)
and, in the presence of sufficient oxygen, is able to enter
Metabolic alkalosis the Kreb’s cycle and electron transfer chain situated in the
• Hypoalbuminaemia – sepsis/systemic inflammatory mitochondria (50). In the absence of oxygen, pyruvate
response syndrome does not enter the Kreb’s cycle; to maintain glycolysis and
• Diuretic use limited adenosine triphosphate (ATP) production, it is
• Gastric vomiting metabolized in the cytoplasm to lactate. The liver then
clears more than 50% of blood lactate, while the kidneys
and muscles metabolize the remainder. Thiamine is a
necessary cofactor of pyruvate dehydrogenase, which
Table 13 Normal ranges for blood gas
analyses turns pyruvate into acetyl coenzyme A before it enters the
Kreb’s cycle. Thiamine deficiency can therefore potenti-
PARAMETER DOG CAT ate problems with lactate metabolism.
pH 7.39 ± 0.03 7.39 ± 0.08
Clinical relevance
PaCO2 (mmHg) 37 ± 3 31 ± 6 Lactic acidosis is essentially a form of metabolic acidosis,
PaO2 (mmHg) 102 ± 7 107 ± 12 caused by an excess of lactic acid in the cells and
circulation. There are major adverse consequences of
HCO3- (mmol/l) 21 ± 2 18 ± 4
severe acidaemia, which affect all body systems, and there
Base excess (mmol/l) 2±2 2±2 is an associated increased mortality in critically ill
human patients with a raised lactate concentration.
 M E TA B O L I C E VA L U AT I O N OF C R I T I C A L LY I L L N E U R O L O G I C A L P AT I E N T S 73

 50 Overview of selected metabolic pathways: glycolysis

Glucose converts glucose into pyruvate, which enters the mito-
ADP chondria and then oxidizes to give acetyl CoA, the starting
point of the Kreb’s cycle. In the absence of oxygen,
Glucose-6-phosphate pyruvate is instead metabolized to lactate in the cell
Glycolysis cytoplasm. NADH and FADH2 generated in the Kreb’s
cycle are oxidized in the electron transport chain,
Glucose-3-phosphate providing energy to power ATP synthetase.

ATP

Pyruvate Lactate Acetylcholine

CYTOPLASM MITOCHONDRIAL MEMBRANE

Pyruvate Acetyl CoA

Citrate

Oxaloacetate

Kreb’s cycle MITOCHONDRIAL

MATRIX

NADH, α-Ketoglutarate
FADH2
Succinate

ADP
ATP
I II III
IV
V V
Electron transport chain

Lactate concentrations and the response to treatment Testing

have been shown to have a prognostic value in dogs. Many blood gas machines have lactate cartridges avail-
Sepsis and shock are common causes of lactic acidosis in able. Lactate can be evaluated from hand-held machines
the ICU. Considerations in a neurological patient designed for sportsmen and women.
presenting acutely with lactic acidosis include seizures,
diabetic ketoacidosis, thiamine deficiency, hypoxia, rhab- Normal ranges
domyolysis, hepatorenal failure and poisoning. When Lactic acidosis is defined as a pH of <7.35 and a lactate
lactate levels are profoundly elevated, it is likely that value of >5 mmol/l (45 mg/dl) in human practice. Hyper-
type A and type B acidosis (Table 14, next page) are both lactataemia is defined as a lactate value of >2.5 mmol/l
present. Generalized seizures induce profound muscle (22.5 mg/dl) in dogs and >1.5 mmol/l (13.5 mg/dl) in
activity. In this scenario, oxygen demand may significant- cats. (Note: Severe hyperlactataemia [>20 mmol/l; 180
ly outstrip supply, with resultant widespread muscle mg/dl] can resolve with appropriate therapy. Sustained
hypoxia. hyperlactataemia, demonstrating a lack of response to
treatment, has been associated with a poorer prognosis.)
 74 ADMISSION AND NEURODIAGNOSTIC TESTS

Monitoring
The frequency of monitoring will be determined by the
severity of the clinical disease. During aggressive volume
resuscitation, serial lactate measurements may be taken
at intervals of 30 minutes or less to evaluate response to
therapy.

Treatment
Treatment of lactic acidosis involves identification and
treatment of the underlying cause. Oxygen delivery can
be optimized through fluid resuscitation and manipula-
tion of cardiac output and arterial oxygen content (see  51 Petechiae on a dog with severe thrombocytopenia.
Chapters 2 and 31). The routine use of hyperventilation,
sodium bicarbonate or buffers for the treatment of meta-
bolic acidosis is not universally recommended. Reversal
of the metabolic acidosis is generally an indication of suc-
cessful therapy. An increasing base deficit suggests that
the therapeutic measures instigated are either inadequate
or inappropriate. It is likely that the profound acidosis
that is often seen after a generalized seizure does not
cause significant physiological compromise per se and
only requires supportive therapy.

 52 Epistaxis due to coagulopathy.

Table 14 Classification and causes of acquired
lactic acidosis
Tests of haemostasis
TYPE A TYPE B
Due to tissue hypoxia Not due to tissue hypoxia* Fundamentals
Animals with defects in haemostasis may present with
• Tissue hypoperfusion • Sepsis
neurological signs secondary to haemorrhage (e.g. spinal
• Abnormal vascular tone • Hepatic failure
or permeability cord or brain parenchymal bleeding secondary to Angio-
• Renal failure
• Left ventricular failure strongylus infection or anticoagulant toxicity). There is
• Hypoglycaemia
• Decreased cardiac output
also some evidence that traumatic brain injury may itself
• Diabetes mellitus
• Strenuous muscular
result in coagulopathy, at least in humans. Defects in
• Neoplasia, especially
exercise platelet numbers or function may be related to the pre-
haematological
• Seizures senting clinical signs (e.g. thrombocytopenia in dissemi-
• Cyanide
• Reduced arterial oxygen nated intravasular coagulation [DIC]) or may be due to
• Ethanol
content an unrelated disease process (e.g. thrombocytopathia in
• Ethylene glycol
• Asphyxia von Willebrand’s disease).
• Drugs
• Hypoxaemia Animals with primary haemostatic disorders may
• Mitochondrial myopathies
• Carbon monoxide present with petechiae (51) or ecchymoses and sponta-
• Thiamine deficiency
poisoning neous haemorrhage from mucosal surfaces (52). This
• Life-threatening anaemia may include hyphaema, haematuria, epistaxis and
* Non-hypoxic processes affecting the production and melaena. However, they commonly present in a similar
elimination of lactate.) manner to animals with defects of secondary haemosta-
sis, which are characterized by multiple haematomas,
 M E TA B O L I C E VA L U AT I O N OF C R I T I C A L LY I L L N E U R O L O G I C A L P AT I E N T S 75

bruises and haemorrhage into joints and body cavities. Thrombocytopathia may also be present and may be
Acquired disorders (e.g. DIC) do not fit this description inherited (e.g. as with von Willebrand’s disease) or
because of the multiple abnormalities often present. acquired, either as a result of drug administration or
The assessment of haemostasis should be systematic, secondary to other disease processes, such as neoplasia.
based on the clinical and neurological examinations. Coagulopathies result from defects in the coagulation
cascade (53). They may be either acquired (e.g. DIC,
Clinical relevance hepatopathies, pharmacologic administration of anticoag-
Thrombocytopenia is a common finding in critically ill ulants and vitamin K or rodenticide toxicity) or they may
patients and results from either lack of platelet production, be inherited. The extrinsic (tissue factor) and common
sequestration, consumption or destruction. It is important pathways of the coagulation cascade can be assessed by
to determine the underlying cause of the thrombocytope- determining prothrombin time (PT), and the intrinsic
nia, to determine whether the platelet count is low enough (contact activation) and common pathways by determin-
to warrant therapy, and then to act accordingly. ing the activated partial thromboplastin time (PTT).

Contact activation Tissue factor

(intrinsic) pathway Vascular (extrinsic) pathway
Damaged trauma
surface
X Clotting factors

Xa Activated clotting factors

TFPI
XII
XII XIIIa
a Regulators

XI
XI XIa VIIIa
a VII
VII
VIIIIIaa VIII
V
VIIII

IX
X IX
Xa Tissue factor

Antithrombin

X Xa Xa X

Prothrombin (II) Thrombin (IIa) Common pathway

V Va

Active protein C Fibrinogen (I) Fibrin (Ia)

XIIIIIIa XIII
XIII
Protein C
+ thrombomodulin
Cross-linked
fibrin (clot)
 53 Schematic representation of the coagulation cascade.
 76 ADMISSION AND NEURODIAGNOSTIC TESTS

Testing and normal ranges placed in a 37°C (98.6ºF) heating bath and inverted
Platelets should always be counted manually on a smear. every 10 seconds. ACT is the time to first clot forma-
Sampling (e.g. clumping) and laboratory artefacts can tion. ACT is relatively insensitive; it is not abnormal
give erroneous results. Greyhounds tend to have lower until one factor is less than 10% of normal concentra-
numbers of platelets and Cavalier King Charles Spaniels tions or multiple factor deficits are present.
may have macroplatelets. In cats there is an overlap in Portable machines are available for the assessment of
size between platelets and RBCs, potentially leading to PT and activated PTT. It is important that the correct
incorrect platelet counts with automated cell counters. methodology is followed to prevent erroneous results.
Normal platelet counts range from 200,000–800,000 Normal values are supplied by the manufacturer. It is an
cells/μl, which equates to 8–15 platelets per ×100 excellent screening test, but false positives do occur
high-power field. Platelet counts below 20,000–50,000 in both the PT and the activated PTT tests and some
cells/μl may lead to clinical bleeding. defects of the extrinsic pathway will not be detected. It is
Buccal mucosal bleeding times (BMBTs) should be prudent to validate all abnormal results by conventional
performed in any animal where a primary haemostatic methodology.
defect is suspected (54). The normal BMBT in the dog D-dimers are fibrin split products that indicate the
is <4.3 minutes and in the cat it is <2.5 minutes. A pro- activation of thrombin and plasmin. Several bedside tests
longed BMBT time in a patient with a normal platelet have been developed involving various technologies.
count confirms a thrombocytopathia. They are reasonably sensitive, but not specific for DIC.
Activated clotting time (ACT) is a screening test for
the intrinsic and common pathways of the coagulation Monitoring and treatment
cascade. Blood (2 ml) is drawn into a pre-warmed Treatment of coagulopathies is based on the appropriate
commercial tube that contains diatomaceous earth after administration of canine or feline blood products includ-
discarding the first few drops of blood. The sample is ing fresh frozen plasma, cryoprecipitate and platelet-rich
plasma (not available globally). Further details of fluid
therapy can be found in Chapter 31.

Ammonia
Ammonia is elevated in animals with significant liver
disease or portosystemic shunts. While less sensitive
than bile acids for the detection of hepatic dysfunction,
the presence of an elevated circulating ammonia con-
centration warrants immediate treatment. Hyper-
ammonaemia may contribute to the clinical signs of
hepatic encephalopathy, and therefore appropriate
treatment can produce a marked clinical improvement.
(See Chapter 27 for further details on management of
hepatic encephalopathy.)

 54 Buccal mucosal bleeding time testing on a dog with

a suspected primary haemostatic defect. The upper lip of
the dog is folded back and held in place with a gauze
bandage. This causes moderate engorgement of the
mucosal surface. A bleeding device creates a small incision
in the buccal mucosa. A timer is started and at 15 seconds
a filter paper is placed 1–3 mm below the incision, without
dislodging the clot, to stop the blood flow. The timer is
stopped when bleeding ceases.
 M E TA B O L I C E VA L U AT I O N OF C R I T I C A L LY I L L N E U R O L O G I C A L P AT I E N T S 77

Temperature regulation Testing

Fundamentals Oesophageal temperature is often considered to
Thermoregulation is controlled mainly by the hypo- approximate core temperature. However, this cannot
thalamus. Such homeostatic control is separate from the be obtained in conscious or sedated patients, therefore
conscious sensation of temperature. The overall inte- rectal temperature is most commonly used as a surro-
grated responses that maintain normothermia despite gate. (Note: The introduction of a thermometer into
changes in external environment and physical workload the rectum can cause straining and a rise in ICP.)
are complex and are integrated by the hypothalamus. Oesophageal probes inserted into inadequately anaes-
When body temperature increases, neurons in the hypo- thetized patients can cause gagging and coughing, with
thalamus turn on mechanisms for heat dissipation that a similar outcome.
include sweating and dilation of blood vessels in the skin.
When body temperature decreases, neurons in the hypo- Normal ranges
thalamus are responsible for heat production through There is some diurnal variation in body temperature.
shivering, vasoconstriction in the skin and piloerection. The normal ranges for daytime body temperatures
Therefore, lesions in the hypothalamus can result in are: dog, 37.5–39.2ºC (99.5–102.5ºF); cat, 37.8–39.5ºC
hyperthermia or hypothermia when the environmental (100–103.1ºF).
temperature is low. The hypothalamus also contains the
‘biological clock’, which regulates certain body functions Monitoring
that vary at different times of the day (e.g. body tempera- Hypothermic animals should have their rectal tempera-
ture, hormone secretion, hunger) or those that vary over ture (if conscious) or core temperature (if intubated)
a period of many days. measured at least every 30 minutes to ensure that they
are responding appropriately to treatment. Where an
Clinical relevance animal is normothermic but considered to be at risk from
Severe traumatic brain injury can result in hyperthermia becoming pyrexic (e.g. through sepsis), it is prudent to
secondary to hypothalamic damage. (Note: This damage measure rectal temperature every 4–6 hours.
may have other effects, such as blocking the production
of ADH, resulting in DI.) Other lesions that affect the Treatment
hypothalamus may potentially affect thermoregulation. Hyperthermia increases cerebral metabolic oxygen
Hyperthermia can also result when the underlying cause demand, may cause cerebrovasodilation and should gen-
for the neurological presentation is heatstroke. This is a erally be avoided. Severe hyperthermia can manifest as
life-threatening situation and must be managed appro- neurological abnormalities. Active cooling must be
priately and aggressively (see Chapter 27). undertaken if the temperature is significantly >39.5ºC
More commonly, obtunded and immobile animals (103.1ºF). This can be achieved by dousing the fur with
present with a decreased rectal (and core) body tempera- tepid water and blowing air across the patient. Addition-
ture. Clinicians should be aware that moderate to severe al measures, such as cool water enemas or peritoneal
hypothermia can influence the findings of the neurolog- lavage (10–20 ml/kg room temperature sterile saline),
ical examination. There is some evidence that patients may be required, although experimental studies suggest
that present with hypothermia secondary to disease, that evaporative cooling may be as effective as peritoneal
trauma, surgery or drug-induced alterations in heat pro- lavage.
duction and thermoregulation have more severe clinical Aggressive cooling will be required where animals
signs when less severely hypothermic than those that are present with neurological signs secondary to heat stroke.
accidentally hypothermic through exposure to low envi- Cooling may also be required in patients with seizure-
ronmental temperature alone. induced hyperthermia. Care must be taken to avoid
rebound hypothermia in such patients. Some guidelines
suggest that cooling should be stopped when the body
temperature reaches 39.5ºC (103.1ºF).
 78 ADMISSION AND NEURODIAGNOSTIC TESTS

Animals that present with hypothermia should be hypothermia during prolonged CPCR in dogs preserves
actively warmed, ideally with circulating warm air the viability of extracerebral organs and improves
blankets or in an incubator. Warm fluids may also be outcome. Therefore, there are currently no indications
administered. Heat pads, ‘hot hands’ or hot water bottles for permissive hypothermia in critically ill veterinary
and warmed bedding may also be utilized (55). Extreme neurology patients. Most patients present with mild
care should be taken to avoid contact burns from direct hypothermia and require active warming.
heat sources. (Note: Examination and nursing proce-
dures will predispose to further decreases in body COMMON METABOLIC ABERRATIONS IN
temperature and care should be taken to minimize SPECIFIC NEUROLOGICAL PRESENTATIONS
further heat loss.) It is prudent to avoid sedation or anaes-
thesia until the body temperature is within normal limits. While every case must be approached on an individual
Induced hypothermia for the treatment of refractory basis, particular metabolic aberrations are seen in certain
intracranial hypertension remains a controversial topic neurological presentations and may only be diagnosed
in human neurointensive care. The only potential following appropriate testing. They do not occur in all
indication in veterinary intensive care appears to be in patients with a specific presentation, but should be con-
prolonged cardio–pulmonary–cerebral resuscitation sidered during clinical evaluation. Equally, other findings
(CPCR). There is some evidence that mild or moderate may also be present that are not listed in Table 15.

 55 Forced warm air heating being used to maintain

normothermia in a critically ill patient.
 M E TA B O L I C E VA L U AT I O N OF C R I T I C A L LY I L L N E U R O L O G I C A L P AT I E N T S 79

Table 15 Common metabolic aberrations in specific neurological presentations

PRESENTATION EVALUATION METHOD FINDINGS/AETIOLOGY

Traumatic brain injury CBC evaluation • Anaemia – haemorrhage

• Haemoconcentration – hypovolaemia

Biochemical evaluation • Pre-renal azotaemia – hypovolaemia

• Hyperglycaemia – catecholamine release
• Hyponatraemia – SIADH
• Increased TP – haemoconcentration
• Decreased TP – haemorrhage

Urinalysis • Often increased USG and decreased urine output –

hypovolaemia
• SIADH leads to urine sodium >20 mmol/l and osmolality
>150 mmol/l

Osmolality • SIADH leads to serum osmolality <280 mmol/l

Blood gas analysis • Evidence of hypoperfusion: metabolic acidosis

• Decreased pH
• Decreased HCO3-
• Increased base deficit
• Increased lactate
• Changes in PaCO2, especially if brainstem involved
• Changes in PaO2 – pneumothorax, pulmonary contusions,
atelectasis and aspiration pneumonia

Coagulation evaluation • Purported increased PT/aPTT

Endocrine analysis • Acute adrenal failure (hypoadrenocorticism), central hypo-

thyroidism, SIADH, diabetes insipidus. (Note: Do not present
acutely at time of injury)

Temperature • Abnormalities possible

Cerebrovascular accident Biochemical evaluation • Evidence of underlying systemic disease (e.g. Cushing’s
syndrome, hypothyroidism)
• Hyperglycaemia, hyponatraemia – SIADH

Urinalysis • SIADH leads to urine sodium >20 mmol/l and serum osmolality
<280 mmol/l

Coagulation evaluation • Increased PT/aPTT

Endocrine analysis • Based on minimum database

Temperature • Abnormalities possible

Seizure Biochemical evaluation • Elevated CK, AST, ALP and ALT

• Hypoglycaemia (uncommon)
• Hyperglycaemia
• Hyperkalaemia
(Continued)
80 ADMISSION AND NEURODIAGNOSTIC TESTS

Table 15 Common metabolic aberrations in specific neurological presentations (continued)

PRESENTATION EVALUATION METHOD FINDINGS/AETIOLOGY

Seizure Urinalysis • Myoglobinuria reported to lead to renal failure

Blood gas analysis • Lactic acidosis – muscular contractions

• Increased PaCO2 – increased CO2 production and hypoventila-
tion. (Note: May be exacerbated by drug administration)
• Iatrogenic alkalaemia may reduce the seizure threshold
• Changes in PaO2 – atelectasis and aspiration pneumonia

Coagulation evaluation • Increased PT/aPTT promoted by hyperthermia

• DIC – extremely rare

Temperature • Hyperthermia secondary to seizure activity

Intracranial mass/lesions CBC evaluation • Anaemia of chronic disease (inconsistent)

• Haemoconcentration – hypovolaemia

Biochemical evaluation • Evidence of co-existing disease or systemic disease

• Pre-renal azotaemia – hypovolaemia
• Increased TP – haemoconcentration
• Decreased TP – haemorrhage
• Multiple electrolyte abnormalities possible depending on
anatomical location

Urinalysis • Often increased USG and decreased urine output –

hypovolaemia

Osmolality • Consider electrolyte changes in interpretation

Blood gas analysis • Evidence of hypoperfusion: metabolic acidosis

• Decreased pH
• Decreased HCO3-
• Increased base deficit
• Increased lactate
• Changes in PaCO2, especially if brainstem involved
• Changes in PaO2 – atelectasis and aspiration pneumonia

Pituitary tumour CBC evaluation • May be consistent with endocrinopathy

Biochemical evaluation • Look for evidence of endocrinopathy (e.g. hyponatraemia –

SIADH, hypoadrenocorticism; hyperkalaemia – hypoadreno-
corticism; hypochloridaemia – secondary to SIADH)
• Hypernatraemia, hyperchloridaemia and hypokalaemia
reported
• Increased urea – precludes SIADH, present in hypoadreno-
corticism
• (Note: Multiple electrolyte abnormalities reported)

(Continued)
 M E TA B O L I C E VA L U AT I O N OF C R I T I C A L LY I L L N E U R O L O G I C A L P AT I E N T S 81

Table 15 Common metabolic aberrations in specific neurological presentations (continued)

PRESENTATION EVALUATION METHOD FINDINGS/AETIOLOGY

Urinalysis • Increased USG and decreased urine

output – hypovolaemia
• Decreased USG – diabetes insipidus/ Cushing’s
syndrome/hypoadrenocorticism
• SIADH leads to urine sodium >20 mmol/l and osmolality
>150 mmol/l

Osmolality • SIADH leads to serum osmolality <280 mmol/l

Endocrine analysis • Cushing’s syndrome, central hypothyroidism, SIADH, diabetes

insipidus, hypoadrenocorticism

Temperature • Abnormality possible

Neuromuscular diseases CBC evaluation • Evidence of primary systemic disease

Biochemical evaluation • Elevated serum cardiac troponin-I

• Elevated CK and AST
• Evidence of endocrine or electrolyte abnormalities in aetiology
• Hypokalaemia due to lack of oral intake

Urinalysis • Myoglobinuria

Blood gas analysis • Increased PaCO2 – hypoventilation

• Changes in PaO2 – atelectasis and aspiration pneumonia

Tetanus CBC examination • Neutrophilic leukocytosis

Biochemical evaluation • Elevated CK and AST

• Hypokalaemia due to lack of oral intake

Urinalysis • Watch for urinary retention

Blood gas analysis • Increased PaCO2 – hypoventilation exacerbated by sedatives

• Changes in PaO2 – atelectasis and aspiration pneumonia,
nurse on an incline

Exogenous acute CBC evaluation • Anaemia – haemorrhage

spinal cord injury
Evaluation method • Haemoconcentration – hypovolaemia

Biochemical evaluation • Evidence of co-existing disease

• Pre-renal azotaemia – hypovolaemia
• Increased TP – haemoconcentration
• Decreased TP – haemorrhage
• Electrolyte abnormalities – urinary tract rupture

Urinalysis • Often increased USG and decreased urine output –

hypovolaemia

(Continued)
82 ADMISSION AND NEURODIAGNOSTIC TESTS

Table 15 Common metabolic aberrations in specific neurological presentations (continued)

PRESENTATION EVALUATION METHOD FINDINGS/AETIOLOGY

Blood gas analysis • Evidence of hypoperfusion: metabolic acidosis

• Decreased pH
• Decreased HCO3-
• Increased base deficit
• Increased lactate
• Changes in PaCO2, especially if high cervical lesion
• Changes in PaO2 – pneumothorax, pulmonary contusions,
atelectasis and aspiration pneumonia

SIADH = syndrome of inappriate antidiuretic hormone secretion; USG = urine specific gravity; PT = prothrombin time; aPTT = activated
partial thromboplastin time; CK = creatine kinase; AST = aspartate aminotransferase; ALP = alkaline phosphatase; ALT = alanine aminotrans-
ferase; DIC = disseminated intravascular coagulation; TP= total protein.
 ADMISSION AND NEURODIAGNOSTIC TESTS Chapter 4

IMAGING OF
NEUROLOGICAL EMERGENCIES 83

Fraser McConnell

INTRODUCTION Patient handling

The majority of imaging studies will require sedation or
Diagnostic imaging is important in the characterization general anaesthesia (GA), which may exacerbate neuro-
and identification of gross structural abnormalities logical disease; the risk/benefits of anaesthesia and
affecting the nervous system. All imaging studies in the imaging need to be considered in light of the clinical and
neurological patient should be preceded by clinical neurological examination. (Further information on
assessment aimed at ruling out non-neurological causes anaesthesia for these procedures can be found in
of signs (e.g. bilateral cruciate ligament rupture or sys- Chapter 29.) With neurological disease caused by high-
temic disease), determining the lesion localization within impact trauma or spinal instability, care needs to be taken
the nervous system and identifying possible concurrent when moving and positioning the animal for imaging
injuries. The role of imaging is not to determine if the studies. Manipulating animals with unstable spinal
clinical signs are neurological in origin. As with anatom- lesions for any imaging modality may exacerbate spinal
ical imaging elsewhere in the body, functional disorders cord injuries. In cases where spinal trauma is suspected it
and diseases that do not result in a gross structural change is essential that the animal is handled without torsion/
in an organ may not be visible on images. Such imaging rotation or excessive flexion/extension of the spine.
is only useful if interpreted along with the patient’s High-quality radiographs are required to diagnose many
signalment and history and with the information spinal conditions and this requires the use of GA or seda-
provided by a comprehensive neurological examination. tion. Sedation/GA, however, results in muscle relaxation
and can reduce the protective ‘splinting action’ of the
Which imaging modality to use? paraspinal muscles, thus potentially exacerbating spinal
The choice of imaging modality depends on the neuro- fractures/luxations. In cases of known or suspected spinal
localization and what is available (56, page 85). Advanced fractures or high-impact trauma, survey radiographs
neuroimaging is expensive and interpretation is depend- should be taken with the animal conscious, and these may
ent on correlation of the neurological examination with be adequate to reveal gross fractures or luxations. If
the imaging findings. Magnetic resonance imaging survey radiographs fail to identify lesions, better quality
(MRI) or computed tomography (CT) should not be radiographs can be taken once the animal is anaes-
used as substitutes for a thorough neurological evalua- thetized. (Note: In cases of spinal trauma, assume that
tion. MRI requires general anaesthesia and imaging may there is an unstable fracture until proven otherwise.)
need to be delayed until the animal’s condition is stable.
If the neurological examination indicates a central lesion,
advanced imaging will be required to rule in/out a gross
structural lesion. Other than in cases of known or
suspected trauma, MRI is preferred to CT due to its
excellent soft-tissue contrast. In the majority of cases of
intracranial disease, radiography is of limited or no value.
The advantages and disadvantages of the different
imaging modalities are shown in Table 16, next page.
 84 ADMISSION AND NEURODIAGNOSTIC TESTS

Table 16 Comparison of imaging modalities

MODALITY ADVANTAGES DISADVANTAGES

Radiography Cheap and readily available. Useful for diagnosis Technique critical for subtle lesions. May be time
of spinal fractures/luxation, bony congenital consuming. No information on brain or spinal cord
malformations, discospondylitis and neoplasia if without use of contrast medium. Very limited
involving bone. Dynamic studies possible. Chest utility for brain disease. Limited information about
and abdominal imaging useful in investigating paraspinal soft tissues. Most cases need
systemic causes of neurological disease GA/sedation unless suspect fracture/instability

Myelography Readily available. Good for overview of spine as Invasive and requires use of ionizing radiation.
can image entire spinal cord relatively quickly. GA required. May be difficult to perform in obese
Accurate and sensitive for identifying sites of dogs. Technique critical to obtain fully diagnostic
spinal cord compression. Dynamic studies possible study. Does not provide information on brain or
peripheral nerves. Provides limited information
compared with MRI/CT for intramedullary or
intradural lesions

Computed tomography Quick to perform (especially multislice CT units). Requires GA/sedation. Expensive and limited
Excellent bone imaging and easy to perform 3-D availability. Evaluation of spinal cord often
reconstructions. Useful for evaluation of complex requires CT myelogram. Older machines may give
bony malformations and fractures. Modality of poor reconstructions in oblique planes. Artefacts
choice for assessing bony lesions. Acute disc may prevent evaluation of brainstem/caudal fossa
extrusions can be identified without the need for lesions. Poor soft-tissue contrast compared with
contrast. Much better soft-tissue contrast than MRI
radiography and cross-sectional imaging means
lack of superimposition. Can be performed
following insertion of surgical implants and where
metallic fragments are present within the body.
Dynamic studies possible

Magnetic resonance Excellent soft-tissue contrast and ability to obtain Expensive and time consuming. Image quality
imaging images in any plane. Does not use ionizing variable (user and equipment dependent). May be
radiation. Modality of choice for investigation of difficult adequately to image very large dogs or
brain, soft tissues, spinal cord and peripheral small cats/dogs. Cannot be used if mobile metal
nerve lesions. Capable of detecting haemorrhage fragments within body or surgical implants in area
of interest. Limited dynamic studies

Ultrasound Widely available, cheap and does not require In most animals limited use due to inability of
GA/sedation. Allows guided biopsy/aspiration. ultrasound to penetrate thick bones of the skull
May be used to identify peripheral nerve and spinal column
masses/lesions. Allows aspiration of disc material
in cases of discospondylitis. If open fontanelle is
present, may be used to diagnose hydrocephalus

Animals with spinal trauma can be restrained on a Small dogs and cats can be positioned in a radiographic
rigid board (e.g. plywood or non-metallic stretcher [57]) positioning trough, which will support the spine. For
for radiography. Radiographs obtained through a board larger dogs, sufficient personnel should be present to
will have reduced image quality, but should show large ensure that all parts of the spine and head are supported
displaced fractures/luxations. Similar care should be when rotating the patient.
taken when positioning patients for advanced imaging.
 IMAGING OF NEUROLOGICAL EMERGENCIES 85

 56 Imaging decision-making in
Gait abnormality with
spinal injury as an example of how the spinal neurolocalization?
neurological examination assists with
the diagnostic planning process.
Spinal imaging not
YES NO* indicated

*i.e. decreased reflexes in

all four limbs/orthopaedic
disease
• Traumatic injury?
• Spinal pain?
• Is lesion localization focal
peripheral C6–T2 or cauda
equina?
YES NO • Do main differentials include
inflammatory/infectious or
vascular disease?

Survey radiography NORMAL YES

NO

• Discospondylitis
• Fracture/luxation
• Tumour lysis
Myelography CT + myelography

Is further information
required for prognosis
or treatment YES
planning?

Discuss treatment
NO MRI
options

 57 Animals with potential spinal injuries should

be handled carefully when being moved for imaging.
The use of a stretcher, as in this case, allows the animal
to be moved with reduced risk of exacerbating any
potential injury. It is possible to radiograph animals
through non-metallic stretchers.
 86 ADMISSION AND NEURODIAGNOSTIC TESTS

SURVEY RADIOGRAPHY Survey radiography of the spine and cranium provides

information largely limited to the osseous component of
Survey radiographs of the thorax are indicated in all the skeleton; however, without the use of contrast (myel-
animals that have been involved in a road traffic accident ography) it provides minimal information on the spinal
(RTA) or suffered other high-impact trauma. There is a cord (60, 61). Nonetheless, plain radiographs are quick to
high incidence of concurrent thoracic injury associated obtain and relatively cheap, but in many cases of neuro-
with long bone and spinal fractures (21% in one logical emergency have a low diagnostic yield. There is
study) (58). Such injuries may preclude GA for advanced often a poor correlation between radiographic abnor-
imaging or other investigations until the animal has been malities and neurological status, and fractures are often
stabilized. If there are clinical signs of respiratory disease, missed.
thoracic radiographs should be obtained. Thoracic radi- Radiography has a very low diagnostic yield for the
ographs may identify thoracic pathology secondary to diagnosis of intracranial pathology and survey radi-
intracranial disease or neuromuscular/peripheral nerve ographs are not usually indicated unless there is external
diseases. For example: swelling or a known history of severe head trauma. Even
• Megaoesophagus. in cases of skull fractures, radiography will not provide
• Aspiration pneumonia. information on the severity of the brain injury and many
• Non-cardiogenic pulmonary oedema
(uncommon) (59).
• Lung metastases from a primary brain
tumour (rare).

 58 Lateral thoracic radiograph of an 18-month-old  59 CT image of a Flat-coated Retriever with non-

Whippet with acute-onset paraplegia following a cardiogenic pulmonary oedema (in this case secondary to
presumed traumatic incident. The radiograph shows the upper airway obstruction). Similar changes may occur
presence of pleural fluid. There is a high incidence of secondary to intracranial disease (seizures, increased
thoracic injuries associated with pelvic and spinal intracranial pressure). Neurogenic non-cardiogenic
fractures. Non-neurological injuries should be assessed pulmonary oedema is thought to occur secondary to
and identified prior to general anaesthesia for imaging. massive release of catecholamines resulting in peripheral
vasoconstriction and myocardial ischaemia.
 IMAGING OF NEUROLOGICAL EMERGENCIES 87

 60 Lateral radiograph (a) and sagittal T2-weighted a

MR image (b) of the lumbar spine of a 2-year-old male
Staffordshire Bull Terrier following trauma (hit by car).
The radiograph is within normal limits, but the MR image
shows severe swelling and diffuse increased signal within
the spinal cord consistent with contusion/oedema. Radio-
graphs give information about the osseous components of
the spine and limited or no information on the soft tissues.
The severity and extent of the spinal cord changes have
some correlation with prognosis, with more extensive
cord changes having a poorer prognosis. In this case the
dog recovered some hindlimb function, but was unable to
urinate. b

 61 Lateral radiograph (a) and sagittal T2-weighted a

MR image (b) of the thoracic spine of an 18-month-old
Whippet with a traumatic intervertebral disc extrusion
(same dog as 58). The radiograph shows subtle narrowing
of the disc space at T9/10 (arrow) and ventral subluxation
of T10. The severity of the spinal cord injury cannot be
determined from the radiograph. The MR image shows
extensive spinal cord changes including swelling and
increased signal consistent with contusion/concussive
injury. b
88 ADMISSION AND NEURODIAGNOSTIC TESTS

a b

c d

e f
 IMAGING OF NEUROLOGICAL EMERGENCIES 89

 62 Lateral oblique radiograph (a), CT image with a a

bone window and algorithm (b), CT image with a soft-
tissue window and algorithm (c), ultrasonographic
image (d) and CT 3-D reconstruction (e) of a Yorkshire
Terrier with a skull fracture secondary to a dog bite injury.
The skull radiograph shows the large fragment that lies
superficial to the skull defect, but the depressed fragment
that compresses the brain is not seen. The CT study
allowed accurate assessment of the fracture and localiza-
tion of the fracture and the presence of hypoattenuating
fluid/tissue adjacent to the depressed fragment, which
probably represents oedema/contusion. The 3-D recon-
struction adds no further information in this case, but can
aid interpretation and surgical planning of complex
b
fractures or malformation. The ultrasound image shows
the presence of echogenic fluid (arrows) adjacent to the
fractures, consistent with haemorrhage or seroma.
(f ) Transverse T2-weighted MR image of a different dog
with a penetrating injury of the brain due to a dog bite.
Compared with (b) and (c) the MR image gives much
more information on the extent and nature of the brain
injury and still allows accurate assessment of the fractures.

 63 Rostrocaudal open mouth radiograph (a) and

transverse T1-weighted MR image post contrast at the
level of the tympanic bullae (b) of a cat with otitis media.
The radiograph shows the typical appearance of chronic
otitis media, with increased opacity within the bullae and
thickening of the bullae walls (arrows). The MR image, in
addition to the bulla pathology (yellow arrows), shows
extension of the infection into the caudal fossa, with a
large abscess/fluid accumulation around the brainstem
(red arrow). The brainstem is displaced dorsally and
compressed by the abscess.

skull fractures may be missed (62). Depressed fractures or mouth oblique or lateral obliques and a dorsoventral
swellings will only be visible if the x-ray beam is tangen- (DV) view. The sensitivity of radiography for the diag-
tial to the lesion. A specific lesion-orientated oblique nosis of otitis media compared with CT was only 85% in
view may be required. This is obtained by angling the one study, with a specificity of 68%. Bullae radiographs
x-ray beam so that it skylines the swelling or depression. may be difficult to interpret in large dogs due to large
Skull radiographs can be used in the investigation of amounts of overlying soft tissue, and radiographs provide
peripheral vestibular syndromes and facial nerve paresis no information about the intracranial extension of otitis
due to otitis media/interna, but have limited value in the media (63). Soft-tissue/fluid opacity within the bullae
investigation of most CN or peripheral nerve lesions. may also be non-significant, as primary secretory otitis is
Survey radiography to assess the bullae in cases of a common, apparently incidental, finding in brachy-
peripheral vestibular disease involves a rostrocaudal open cephalic dogs.
 90 ADMISSION AND NEURODIAGNOSTIC TESTS

Radiographic technique In cases of suspected spinal fracture, a horizontal

Spinal radiography requires high-quality radiographs, as beam can be used to obtain a VD or DV projection and
many lesions are subtle and may be missed if the radio- this is preferable to trying to rotate the animal. The
graphs are suboptimal. For small dogs and cats, a table- animal is kept in lateral recumbency and the x-ray tube
top technique with a high-resolution film–screen head is rotated through 90° with the x-ray cassette
combination and small focal spot should be used to max- placed dorsal to the spine (65). With some digital radiog-
imize image detail. For larger dogs (>10 cm thickness) raphy systems, the x-ray detector is built into the x-ray
and obese animals, a grid and bucky should be used. table, in which case horizontal beam radiography
Orthogonal views (lateral and ventrodorsal [VD]/ may not be possible. If the animal needs to be moved,
DV) should be obtained in all cases (64) and specific there should be enough assistants to stabilize the spine
oblique projections may be required to visualize the dens and head to prevent axial rotation while the animal is
and intervertebral foramina of the cervical spine. rotated.

 64 Lateral (a) and ventrodorsal (b) radiographs of the a

lumbar spine of a cat with a fracture-luxation at L4/5.
The degree of overriding is underestimated on the lateral
radiograph, although the fracture is clearly visible with
shortening of the vertebral body of L4 and a step in the
ventral surface of the vertebral body. The ventrodorsal
projection shows an obvious displacement of the
L4 vertebra to the right and the vertebral fracture is more
clearly seen. Orthogonal projections are required to assess b
accurately the alignment of the vertebral canal. Note the
difference in appearance of the spinous processes cranial
and caudal to the fracture. This is due to torsion of the
caudal part of the spine relative to the cranial segment.
The vertebral canal is reduced in width by approximately
30% on the radiographs, but the degree of spinal cord
compression and severity of spinal cord pathology cannot
be determined without advanced imaging or myelography.
 IMAGING OF NEUROLOGICAL EMERGENCIES 91

b
 65 The use of a horizontal x-ray beam allows a
ventrodorsal radiograph to be taken with the animal lying
in lateral recumbency. An orthogonal view can be obtained
without moving the animal. Care needs to be taken with
radiation safety when using a horizontal beam.

 66 Lateral (a) and left 30° ventral-right dorsal oblique

(lateral oblique) (b) radiographs of C1/C2. On the
standard lateral projection the dens is overlying and
obscured by the wings of C1. The lateral oblique
projection allows clear visualization of the dens (arrow)
without the need to flex the neck.

Assessment of the dens of C2 is important in cases Assessment of spinal radiographs

of cervical trauma and suspected atlantoaxial (AA) insta- A systematic approach to the assessment of spinal radio-
bility. The rostrocaudal oblique view to assess the dens is graphs is important and the following should be critical-
contraindicated in cases where AA instability is suspect- ly evaluated:
ed, as the extreme flexion required for this view will cause • The vertebral canal as a whole:
spinal cord compression. A lateral oblique view of the • Check for alterations in alignment on both
cervical spine allows assessment of the dens without projections (64).
requiring neck flexion (66). The animal is positioned as • Look for presence of any steps, which indicates
for a lateral cervical spinal radiograph and rotated luxation. This is most easily performed by criti-
dorsally by 20–30° (by placing small foam wedges under cal evaluation of the alignment of the dorsal part
the mandible and sternum). (Note: Stressed views may of the vertebral bodies and the dorsal laminae on
demonstrate an instability not visible on radiographs the lateral projections.
taken with the spine in a neutral position, but they may • Look at alignment of the spinous processes,
exacerbate spinal cord injury.) pedicles and lateral margins of the vertebral
Lateral oblique views of the cervical spine allow bodies on the VD projection.
assessment of the intervertebral foramina, which are
not visible on a lateral projection. Positioning is as for a
VD projection of the cervical spine, with the animal then
tilted laterally by 45°.
 92 ADMISSION AND NEURODIAGNOSTIC TESTS

• The width of the vertebral canal: • The width and opacity of disc spaces (71).
• Look for bone extending into the vertebral canal • The size and opacity of the intervertebral
(67, 68). foramina (71).
• Note: there is normally widening of the • The opacity and margination of the
vertebral canal at both the cervical and lumbar endplates (72).
intumescences. • Paraspinal soft tissues for: swelling, loss of normal
• The conformation of each vertebra (check for fascial planes and presence of gas/foreign
alterations in opacity, shape and margination) material (70).
(69, 70).

a b

a  67 Lateral radiograph (a) and transverse T2* GRE MR

image (b) of the cervical spine of a dog with a comminuted
fracture of C2 following external trauma (hit by car).
In addition to assessing the stability of the fractures, the
degree of spinal cord compression should be assessed.
Advanced imaging may be required for this assessment to
be performed accurately. In this case, despite the severe
fractures, there was minimal overt spinal cord
compression and the dog was managed by surgical
stabilization of the fracture alone.

 68 Lateral radiograph (a) and sagittal T2-weighted

MR image (b) of a 9-month-old Husky with a 3-month
history of progressive ataxia and tetraparesis. The radio-
graph shows dorsal subluxation of C3 relative to C2. Even
without performing myelography or MRI, it is clear that
there is significant narrowing of the vertebral canal.
 IMAGING OF NEUROLOGICAL EMERGENCIES 93

a  69 Lateral radiograph (a), transverse CT image (b)

and sagittal reformatted CT image (c) of the lumbar spine
of a Cavalier King Charles Spaniel with back pain due to
lymphoproliferative disease. The radiograph shows
multifocal lysis of the vertebral bodies and spinous
processes. In comparison, the CT images show much
more extensive bone destruction. Radiography often
underestimates the extent of bone destruction. Note the
loss of the normal thin, sharply marginated dorsal surface
of the affected vertebral bodies. This is often a sensitive
feature of vertebral body destruction.

b
 70 Lateral radiograph of an 8-year-old Irish Setter
with severe back pain. There is incidental spondylosis
deformans visible at L5/6 and L6/7, which has all the
characteristics of benign new bone: smooth and sharply
marginated with no bone destruction. In contrast, at
L7/S1 there is ill-defined wispy mineralization (arrows)
that extends into a region of soft-tissue swelling ventral to
the lumbosacral junction. This is indicative of a very active
bone lesion most consistent with neoplasia.
Ultrasound-guided fine needle aspiration confirmed
lymphoma. The caudal lumbar spine is a predilection site
for bone metastases from prostatic and bladder tumours.

c
 94 ADMISSION AND NEURODIAGNOSTIC TESTS

a  71 Lateral radiograph (a) and sagittal plane

T2-weighted MR image (b) of the lumbar spine of a dog
with acute intervertebral disc extrusion at L4/5. The
radiograph shows typical features of acute disc disease,
with narrowing of the disc space, reduction in size of the
foramen and increase in opacity of the foramen. There is
also vacuum phenomenon within the disc space (arrow).
This is an uncommon but relatively specific feature of
acute disc disease. Despite the high suspicion of disc
b disease based on the radiographic changes, localization
prior to surgery needs to be confirmed with either
myelography or advanced imaging. The MR image shows
the typical appearance of an acute disc extrusion, with
amorphous hypointense extradural material lying ventral
to the spinal cord and compressing the spinal cord
dorsally. Note that on the MR image the vacuum
phenomenon is difficult to identify, as mineralization and
dense fibrous tissue have similar signal intensity to gas.

 72 Lateral radiograph of the lumbosacral junction

of a dog with discospondylitis of the lumbosacral disc.
Note the sclerosis and irregular, ‘chewed out’ appearance
to the endplates and, as a consequence, widening of the
disc space. There is soft-tissue swelling ventral to the
lumbosacral junction.

Alterations in vertebral alignment before changes are visible radiographically (73). Focal
It cannot be assumed that the degree of any subluxation bone lysis is easier to detect than generalized osteopenia
or misalignment on a radiograph correlates with spinal and is most commonly a feature of aggressive bone
cord injury (unless severe). Often, subluxation/luxation is disease (neoplasia or, less commonly, infection). Gener-
dynamic and during injury the degree of displacement alized reduction in bone opacity is most usually seen with
may have been more marked than is seen on later radio- metabolic bone disease (e.g. nutritional secondary to
graphs. Alteration in alignment may occur due to con- hyperparathyroidism) and may result in pathological
genital malformations (e.g. hemivertebrae), fractures, fractures. Myeloproliferative disease, especially multiple
luxations, AA subluxation, scoliosis secondary to syringo- myeloma, may result in ‘punched-out’ lysis of multiple
hydromyelia and caudal cervical spondylomyelopathy. vertebrae, commonly affecting the spinous processes
(69). Focal increases in vertebral opacity are usually the
Alterations in opacity result of periosteal new bone and careful evaluation of
Radiographs are relatively insensitive for the detection of the periosteal reaction is required to determine the
bone lysis, since at least 50% of mineral must be lost degree of bone activity (74) (also 70).
 IMAGING OF NEUROLOGICAL EMERGENCIES 95

a b

 73 Lateral radiograph (a) and sagittal T1-weighted a

MR image (b) of the cranial thoracic spine of an elderly
crossbred dog with severe neck pain. The dog has a
vertebral tumour at T2. Note the reduced signal on the
MR image (asterisk) and the presence of abnormal
extradural tissue extending dorsally from the bone (arrow)
into the vertebral canal and displacing the spinal cord. On
the corresponding radiograph the vertebral body at T2
(arrow) appears largely normal. Radiographs are relatively
insensitive for showing bone destruction or infiltrate.
b

 74 Lateral radiograph (a) of the lumbar spine of a

middle-aged dog. Spondylosis deformans is present at the
L2/3 disc space. Note the smooth, sharply marginated
new bone arising from the ventral aspects of the vertebral
endplates (arrow). The new bone production is benign
and is usually an incidental finding of no clinical signifi-
cance. (b) Sagittal T2-weighted MR image of another
middle-aged dog with spondylosis deformans. Note that
despite the presence of spondylosis the intervertebral
discs are normal. The normal intervertebral disc has a
hyperintense nucleus pulposus and hypointense annulus.
 96 ADMISSION AND NEURODIAGNOSTIC TESTS

Disc space narrowing irregularly marginated, in contrast to pressure atrophy,

Narrowing of the disc space usually indicates a in which remodelling is often smoothly marginated,
reduction in disc volume due to disc disease or, less com- although there can be some overlap.
monly, a congenitally small disc. The accuracy of disc Interpretation pitfalls are:
space narrowing as a sign of disc herniation is only ~70% • Cervical foramina can only be seen clearly on
and false positives are common. False positives may be oblique views.
due to divergence of the x-ray beam, anatomical variants, • Foramina in the mid-lumbar region are naturally
positioning effects or disc disease not resulting in spinal larger than those at the thoracolumbar and
cord compression. The width of the disc should be lumbosacral junctions.
assessed by comparison with adjacent disc spaces and
care taken with interpretation of disc spaces at the edge of Endplate changes
the radiograph. Normal discs have soft-tissue opacity. The normal vertebral endplates are smooth and sharply
Chondroid degeneration of the disc nucleus results in marginated and the more opaque subchondral bone
early degeneration and mineralization of the disc, which should be uniform in width. Sclerosis of the endplates
can be considered a normal feature of chondrodystro- often occurs with chronic Hansen type II disc disease. In
phic dogs and does not indicate clinically significant disc severe, chronic disc disease with collapse of the disc space
disease. Dorsal displacement or extension of a calcified there may be remodelling of the endplates, which can
disc into the vertebral canal indicates disc herniation, but become flared and slightly irregular. Differentiation
myelography or advanced imaging is required to assess from aggressive disc disease (discospondylitis) can be
the clinical significance. In non-chondrodystrophic dogs, difficult in these cases. Lysis of the endplates with devel-
discal mineralization is pathological and a feature of disc opment of an irregular ragged appearance is typical of
degeneration, but it may be non-significant. Gas may be discospondylitis (72). In young, large breed dogs, osteo-
present within the disc space. This is known as the chondrosis dissecans (OCD) lesions may affect the lum-
‘vacuum phenomenon’ and is a specific but insensitive bosacral joint. OCD lesions occur most commonly on
feature of acute disc herniation (71). the dorsal aspect of the cranial sacral endplate or, rarely,
Interpretation pitfalls are: the caudal L7 endplate, resulting in a focal defect in the
• Normally narrowed disc spaces exist at C2/C3. endplate with a separate osteochondral fragment. Sacral
• Disc spaces in the thoracic spine are most narrow at OCD may result in compression of the cauda equina.
T10/11 and get gradually wider from T11/12 The usually sharp margination of the lesion, separate
caudally. OCD fragment adjacent to the endplate defect and
• Wedge-shaped disc spaces can be normal in cats. involvement of only one endplate helps differentiate
• Disc space at L7/S1 is normally wider than other at OCD from discospondylitis.
lumbar discs.
Incidental findings
Intervertebral foramina There are a large number of anatomical and degenerative
A reduction in the size of the intervertebral foramina changes that affect the spinal column and which may be
commonly occurs secondary to disc herniation. As the mistaken for significant pathology. Congenital anomalies
disc reduces in width, the vertebrae move closer are common and often of no clinical significance. Radi-
together, resulting in reduction in foraminal size. An ographic changes that are unlikely to be clinically
increase in opacity of the foramina may be seen if a min- significant include:
eralized disc extends dorsally into the vertebral canal • Transitional vertebrae at the thoracolumbar
where it overlies the foramen. Enlargement of the junction; however, these are important if the last rib
foramina is rare and can occur secondary to bone is being used as a surgical landmark.
remodelling due to pressure from enlarging peripheral • Spondylosis deformans (unless it extends dorso-
nerve tumours/masses or bone lysis due to vertebral laterally to impinge on the intervertebral
tumours. Lysis due to a vertebral tumour is usually foramen) (74).
 IMAGING OF NEUROLOGICAL EMERGENCIES 97

• Roughening of the ventral aspect of the vertebral a

bodies of L3/4 due to normal attachment of
diaphragmatic crura. May be mistaken for
periosteal reaction.
• Abnormal number of vertebrae.
• Senile osteopenia (cats).
• Block vertebrae, although these may predispose to
disc disease at adjacent sites.
• Transitional lumbosacral vertebrae. May predispose
to degenerative lumbosacral disc disease.
• Hemi/wedge vertebrae. Common in screw-tailed b
breeds and often not clinically significant, but can
be associated with vertebral stenosis (75).
• Dural ossification.

Radiological assessment of spinal trauma

Diagnostic imaging is performed in patients with acute
onset of neurological signs or signs following known (or
suspected) trauma resulting in neurological signs in order
to try and determine the following:
• Whether there are systemic diseases/injuries that
require emergency treatment prior to specific
investigation of neurological signs (e.g. severe active  75 Lateral radiograph (a) and sagittal T2-weighted
haemorrhage, pneumothorax, airway obstruction, MR image (b) of a French Bulldog with acute-onset
pleural fluid) (58). paraplegia. Note on the radiograph the wedge vertebra at
• Whether there are severe injuries with a hopeless T13 (arrow), resulting in kyphosis. In this case the wedge
prognosis (e.g. spinal fracture/dislocation with vertebra did not result in vertebral stenosis (compare with
severe overriding of the vertebrae in a patient with b) and the clinical signs were due to an acute disc
absent nociception) (76). extrusion at L2/3 (arrow in b).
• Whether there are any surgical indications and if
so, what would be the best surgical option.
• What the prognosis is.

 76 Lateral radiograph of the thoracolumbar spine of a

dog following external trauma (hit by car). There is a
severe, complete fracture-luxation of the spine at the
thoracolumbar junction. Due to the degree of overriding
it can be assumed that the spinal cord will be transected.
Further advanced imaging to assess the spinal cord is not
required in this case.
 98 ADMISSION AND NEURODIAGNOSTIC TESTS

a b c

 77 Transverse plane CT image (a) of a lumbar vertebra. The three-compartment model (red lines) can be used to
determine if an injury is unstable. Damage to two or more compartments means that the injury should be considered
unstable. Sagittal plane reformatted (b) and transverse (c) CT images of a dog with a spinal fracture. All three compart-
ments can be seen to be damaged, indicating that surgical stabilization is required.

Traumatic spinal injuries in small animals can be assessed tive predictive values (48%) for detecting all vertebral
using a three-compartment model based on a human fractures in spinal trauma cases. In particular, there is
classification scheme (77). The dorsal compartment poor sensitivity for the detection of bone fragments
comprises the articular processes, laminae, pedicles, within the vertebral canal (57%) and vertebral canal
spinous processes and supporting soft-tissue structures. narrowing (58%), with a negative predictive value of only
The middle compartment involves the dorsal longitu- 35% for identification of spinal cord compression.
dinal ligament, dorsal aspect of the annulus and dorsal Spinal fractures occur most commonly at the junction
aspect of the vertebral bodies. The ventral compartment of mobile and less mobile joints (usually at the cervico-
contains the ventral aspects of the vertebral body, lateral thoracic, thoracolumbar and lumbosacral junctions).
and ventral annulus, disc nucleus and ventral longitudinal They may result in compressive and/or non-compressive
ligament. If two of the three compartments are disrupted cord injuries (concussion, contusion, intraparenchymal
or damaged, the injury is considered unstable (see haemorrhage, laceration). Compressive lesions may be
also 67). In addition to determining whether the lesion visualized on radiography, but non-compressive spinal
is unstable, the degree of spinal cord compression or cord injury requires advanced imaging (60, 61). Survey
narrowing of the vertebral canal needs to be considered. radiographs should be taken of the entire spine, as multi-
A stable fracture with spinal cord compression due to a ple fractures may be present. Significant soft-tissue
bone fragment will require decompression. Survey radi- swelling may be associated with cervical spinal trauma,
ography has relatively poor sensitivity (72%) and nega- which can result in upper airway obstruction.
 IMAGING OF NEUROLOGICAL EMERGENCIES 99

MYELOGRAPHY

Myelography may be used for the diagnosis of the site, to myelography (79). Advanced imaging should be
type and severity of spinal cord compression and, less considered if infectious/inflammatory or vascular
commonly, cord swelling. Myelography is technically diseases are suspected.
demanding and artefacts are common (78), which can The risks associated with myelography include:
make interpretation difficult or impossible. It is relatively • Seizures post myelography (common; up to 21% in
invasive compared with MRI and carries a risk of one study and more prevalent in dogs >20 kg body-
significant side-effects. weight, with cerebellomedullary injections and with
The indications for myelography are to: increasing contrast medium concentration).
• Confirm site, lateralization and severity of • Exacerbation/progression of neurological status
suspected disc disease seen on survey films. (usually temporary).
• Localize the number and site(s) of spinal cord • Iatrogenic injury to the CNS.
compression or swelling. • Cardiac arrhythmias.
• Determine the effect of traction, flexion or • Respiratory arrest.
extension on spinal cord compression. • Death.

Myelography allows assessment of the entire spinal cord, The contraindications for myelography are:
but as it only allows direct visualization of the subarach- • Coagulopathy, including thrombocytopenia and
noid space rather than the spinal cord, it provides limited thrombocytopathia.
information on the nature of any compressive lesions or • Spinal instability (relative contraindication; depends
cord swelling and minimal or no information on the on site of fracture and whether myelography can be
nerve roots/cauda equina. If the neurolocalization is performed without destabilizing the spine).
brachial plexus (focal peripheral C6–T2), cauda equina • Cloudy/turbid cerebrospinal fluid (CSF) suggestive
or a mononeuropathy, advanced imaging is preferred of an inflammatory/infectious process.

 78 Lateral myelogram following lumbar injection of  79 Normal lateral myelogram of a large breed dog.
contrast. The contrast has gone into the epidural space, The spinal cord appears as a filling defect between the
resulting in a thick undulating appearance to the contrast dorsal and ventral contrast columns. The contrast
and accumulations of contrast at the intervertebral columns should be assessed for any deviation or changes
foramina. Epidural contrast leakage or injection is more in width. There are breed and species differences in
common with lumbar injections and often results in a myelographic appearance, in addition to differences in
non-diagnostic myelogram. appearance within a spinal cord region.
 100 ADMISSION AND NEURODIAGNOSTIC TESTS

Myelographic technique myelographic technique is essential. Following contrast

Prior to injection of the contrast medium, a CSF sample injection, VD, left and right lateral obliques and lateral
should be taken and examined visually. A cloudy/turbid projections should be taken. Lateral obliques are
CSF sample is a contraindication to myelography, which obtained by positioning the animal for a VD projection
can exacerbate inflammatory CNS disease. If the CSF then tilting the animal to the left or right by approxi-
sample is contaminated by blood during sampling, myel- mately 45°. The contrast medium is denser than CSF,
ography may still be performed. Iatrogenic blood con- therefore positioning the animal in lateral recumbency,
tamination is usually obvious, as the sample generally with the affected side being dependent, may improve
starts clear, then a stream of blood is seen swirling within visualization of the lesion on the lateral projection.
the CSF. If there is doubt as to whether haemorrhagic The contrast medium rapidly disappears from the sub-
CSF is the result of iatrogenic blood contamination or arachnoid space and so the radiographs should be taken
due to pathology, then myelography should not be as soon as possible after injection.
performed until the results of CSF cytology and a white Only non-ionic low-osmolar iodinated water-soluble
blood cell (WBC) count are available. If the patient may contrast medium should be used (e.g. iohexol). The use
need more immediate treatment based on its clinical of ionic contrast media is contraindicated and their injec-
signs, a diagnosis should be sought using MRI. tion into the subarachnoid space may be fatal. A con-
Prior to myelography the contrast medium should be centration of 240–300 mg iodine/ml should be used;
warmed to body temperature to reduce viscosity and higher concentrations are associated with an increased
minimize side-effects. Survey radiographs should be risk of side-effects. The dose of contrast used varies
taken and injection sites should be clipped and aseptical- depending on the site of injection, lesion localization and
ly prepared. GA is mandatory for myelography. Spinal the size of the animal, with larger animals requiring a
needles must be used for myelography, the size of needle relatively lower dose. The minimum volume of contrast
depending on the size of the animal, with 22–20g needles medium is 2 ml and the maximal dose of contrast
most commonly used. medium is 0.45 ml/kg. For regional examinations, a dose
To obtain a diagnostic myelographic study with of 0.3 ml/kg is normally used and 0.45 ml/kg for examin-
maximal information, a careful and comprehensive ation of the entire spine.

Table 17 Advantages/disadvantages of the two contrast injection sites used for myelography

INJECTION SITE ADVANTAGES DISADVANTAGES

Atlanto–occipital • Easier to perform • Failure of contrast to outline thoracolumbar lesions more

cisternal injection • CSF collection easier and often less common than with lumbar injection
blood contamination of the • High cervical lesions increase the risk of contrast in the brain
sample • Risk of iatrogenic brainstem injury
• Fewer myelographic artefacts • Requires an assistant to position the head

Lumbar injection • Can inject with controlled • Artefacts (especially epidural leakage) more common
(L5/6 for dogs, pressure • Technically harder to perform, with greater chance of blood
L6/7 for cats) • Position of the needle and contrast contamination
can be checked at all times with • CSF flow can be limited in some patients
fluoroscopy
• Iatrogenic spinal cord injury can occur if needle passes through
• No need for an assistant spinal cord, but this appears to be less of a clinical issue than
one would expect; can cause transient LMN dysfunction at
the level of the injection
• Risk of injection of contrast into the central canal can be
clinically significant
 IMAGING OF NEUROLOGICAL EMERGENCIES 101

Myelographic interpretation
Table 18 Normal myelographic appearance
At least two radiographic projections are required to
assess the spinal cord. If the cord is compressed in one
Normal myelographic variants
plane, the contrast columns may diverge on the orthogo-
• The ventral contrast column normally elevates dorsally at nal view. Interpretation of the myelogram is based on
the cervicothoracic junction classifying the lesions into one of three patterns.
• The ventral contrast column is normally narrower as it
passes over C2/3 disc and this should not be mistaken for
ventral compression Extradural compression
• In small breed dogs the ventral contrast column may
This results in axial displacement of one or more contrast
conform to the ventral part of the vertebral canal and columns, with narrowing/compression of the spinal
narrow as it passes over the disc space cord. On orthogonal views there may be divergence
• Breed variation in size of spinal cord relative to vertebral of the contrast columns if compression is severe enough
canal (small dogs have relatively larger spinal cords) (80, next page). Contrast columns are usually thin or par-
• Spinal cord/vertebral canal ratio larger in cervical spine tially interrupted at the site of compressions and cord
• Position of dural sac further caudal in small breed dogs and swelling may occur proximal or distal to compression.
cats compared with large breed dogs
The extradural compression pattern is the most
• Dorsal subarachnoid space larger than ventral column in common myelographic lesion. Causes include any
large breed dogs in thoracolumbar spine (79)
extradural mass such as disc herniation, vertebral
stenosis, vertebral subluxation, neoplasia, haemorrhage,
epidural inflammation/infection, foreign bodies and
vascular malformations. Myelography determines the
Spinal cord swelling secondary to large compressive location and severity of a compression. Establishment of
lesions often prevents the passage of contrast following the differential diagnosis list is based on the additional
cisternal injections, which may prevent determination of information provided by survey radiographic findings,
the length of the lesion. Following cisternal injection of history and signalment, clinical examination and other
contrast the head should be elevated and the x-ray table ancillary diagnostic tests. Intervertebral disc herniation is
tilted if possible (lowering the caudal part of the animal) the most common cause of extradural compression.
to promote caudal flow of contrast. Following lumbar Compared with surgery, myelography has a reported
injection the caudal end of the animal can be elevated to accuracy of 91–100% for the localization of the correct
promote cranial flow of contrast. If the cranial and site of disc herniation. Correct lateralization of disc
caudal ends of a lesion cannot be assessed, a second herniation based on the myelographic appearance is less
contrast injection more cranially or caudally may be accurate than longitudinal localization, with sensitivity
required. The choice between cisternal (cerebello- reported to be between 70 and 99%.
medullary) and lumbar injection sites depends on the sus-
pected site and nature of the lesion. Epidural leakage is a Intramedullary swelling
common artefact with lumbar injections. If contrast is This results in divergence of the contrast columns, which
injected entirely into the epidural space, then waiting 15 appear thin on all views due to enlargement of the
minutes will often result in enough resorption of contrast underlying spinal cord (81, page 103). Causes include
to allow the injection to be repeated. intramedullary mass lesions and any cause of spinal cord
The advantages and disadvantages of the two contrast swelling (spinal cord neoplasia, acute ischaemic myelo-
injection sites used for myelography are shown in pathy, traumatic cord contusion or haemorrhage, syrinx
Table 17. The normal myelographic appearance varies formation and myelitis). MRI is required to characterize
with species and patient size (Table 18). Care should be the cause of the cord swelling.
taken to avoid misinterpreting normal variants as
pathology.
102 ADMISSION AND NEURODIAGNOSTIC TESTS

a  80 Lateral (a), ventrodorsal (b), right ventral–left

dorsal oblique (c) and left ventral–right dorsal oblique
(d) myelograms of a dog with intervertebral disc hernia-
tion at L1/2. Extradural compression with narrowing of
the spinal cord is seen on the ventrodorsal and right
ventral–left dorsal oblique projections ([b, c], arrows) and
divergence of the contrast column on the lateral
projection. Note that the right ventral–left dorsal oblique
projection shows the maximal cord compression and
b shows the lesion most clearly. The site of maximal cord
compression is dorsal to the disc space and there are radi-
ographic changes consistent with disc disease (narrowed
disc space [a], arrow). Given the location, the probable
diagnosis is disc herniation, but other extradural masses
will result in a similar myelographic appearance.

Intradural/extramedullary lesions
Intradural masses cause filling defects within the dilated
contrast columns, resulting in a so-called ‘golf tee’
sign (82), but concurrent epidural and subarachnoid con-
trast surrounding an extradural lesion may look similar.
The splitting or divergence of a contrast column seen
with small focal or asymmetrical extradural lesions
should not be mistaken for an intradural mass. Localized
dilation of the subarachnoid space due to an intra-
arachnoid ‘cyst’ or diverticulum formation results in
c focal widening of the subarachnoid space and narrowing/
compression of the spinal cord. These ‘cysts’ usually have
a characteristic teardrop shape (83).
Intradural/extramedullary lesions are usually neo-
plastic, with meningioma and peripheral nerve sheath
tumour occurring most frequently, although benign and
inflammatory masses can also occur.

Other myelographic lesions

d Extension of contrast medium into the spinal cord may
occur with myelomalacia and is a poor prognostic sign. If
syringomyelia is present, the syrinx may fill with contrast
following direct injection or contrast flowing out along
the needle tract.
Epidural leakage of contrast medium from the sub-
arachnoid space into surrounding epidural tissue and
adjacent soft tissues may occur following dural laceration
secondary to spinal trauma or poor technique.
 IMAGING OF NEUROLOGICAL EMERGENCIES 103

a a

b b

 81 Lateral (a) and ventrodorsal (b)  82 Lateral (a) and ventrodorsal (b) radiographs taken
myelograms of a dog with an following myelography of a Cavalier King Charles Spaniel
intramedullary tumour. This is an with an intradural/extramedullary mass. Note the splitting
example of an intramedullary myelo- of the contrast column on the right (arrow [b]) and
graphic pattern with divergence of the compression of the spinal cord. The unusual location
contrast columns on both projections. (dorsal), history and signalment (aged dog) make
neoplasia the most likely diagnosis.

 83 Lateral myelogram of a dog with an intra-arachnoid

‘cyst’. The finding of a teardrop-shaped dilation (arrow) of
the subarachnoid space is pathognomonic for this
condition.
104 ADMISSION AND NEURODIAGNOSTIC TESTS

ADVANCED IMAGING Wolfhounds) may not fit into the scanner in dorsal
recumbency, but may be scanned in lateral recumbency
Advanced imaging is relatively expensive, but should be using a torso coil. If the patient has to be imaged in lateral
performed if: recumbency, then careful positioning is vital and the
• Other imaging studies are non-diagnostic. spine will need to be padded as for radiography. It is
• Radiography is unlikely to give a diagnosis (brain, absolutely vital that the spine is straight. If it is rotated,
soft-tissue lesion or peripheral nerve lesion). the patient should be removed from the scanner and
• A more definitive diagnosis is required for repositioned.
prognosis or treatment. As a general rule, T2-weighted MR images are often
the most useful for neuroimaging, as they provide the
MRI is the imaging modality of choice for neuroimaging, best soft-tissue contrast. On a T2-weighted image, fluid
especially for brain and most spinal lesions, but CT can and fat are hyperintense. As most pathology results in an
provide useful information and, potentially, a diagnosis in increase in water content, pathology is often hyper-
many cases. The physical basis and techniques for intense (bright) on a T2-weighted image.
performing MRI and CT are beyond the scope of this A routine brain protocol includes transverse pre- and
chapter and the reader is referred to more comprehen- post-contrast T1-weighted, T2-weighted, T2-weighted
sive reviews (see Further reading, p. 623). fluid attenuated inversion recovery (FLAIR), sagittal
and dorsal T2-weighted images. In some cases, T1-
Imaging technique weighted (post-contrast) images may be useful in the
Correct neurolocalization and the establishment of a sagittal and dorsal planes (e.g. assessment of the pituitary
differential diagnosis list are vital before performing gland and extra-axial masses). The T2-weighted FLAIR
advanced imaging to ensure both that the scan is required sequence suppresses the signal from CSF and allows
and that the correct area is being imaged. GA is required assessment of periventricular changes difficult to see on
for MRI in all but the most stuporous patients. If the T2-weighted images. This sequence has a high sensi-
animal is a high anaesthetic risk, it should be stabilized tivity for inflammatory CNS disease. FLAIR images are
prior to scanning. Multislice CT scanners allow fast particularly useful if there is hydrocephalus or an intra-
scanning times, which means that some animals can be cranial cyst. T2* gradient-echo (GRE) images are very
imaged under sedation. Ideally, remote anaesthetic useful for evaluation of haemorrhage or bony changes. In
monitoring should be used for small animal MRI. If this some cases, diffusion-weighted imaging (DWI) may be
is not available, the anaesthetist will need to be in the helpful in the assessment of ageing infarcts and in the
scanning room to monitor the patient. identification of small infarcts in the peracute stage.
To accurately assess spinal cord compression, CT is Images acquired with fat suppression (short-tau inver-
often combined with myelography, with a lower dose of sion recovery [STIR] or post-contrast T1-weighted with
contrast being used. Multislice CT scanners allow high- fat saturation) are useful for showing pathology in the
quality reformatting of the CT images into oblique extracranial soft tissues, particularly orbital disease and
planes comparable with the multiplanar capabilities of pathology affecting the bone marrow. In unstable
MRI. MRI allows assessment of the spinal cord paren- patients, the sequences most likely to give a diagnosis and
chyma, but with CT this information is limited due to the assess secondary effects of increased ICP should be
inferior soft-tissue contrast. As with radiography, careful obtained first (transverse and sagittal T2-weighted
positioning of the patient is important, as oblique images images), in case the MRI study needs to be ‘aborted’.
may be difficult to interpret or completely misleading. For spinal imaging, dorsal plane and sagittal T2-
For spinal imaging, animals are best positioned in weighted images should always be obtained. If any
dorsal recumbency. A plastic radiographic positioning abnormalities are seen, then transverse T2-weighted
trough may be helpful to prevent the animal from rotat- images are acquired through the area of interest. If there
ing. Alternatively, the body can be supported by foam is any reason to suspect infectious, inflammatory
wedges or bean bags. Very deep chested dogs (e.g. Irish or neoplastic disease, T1-weighted images (pre- and
 IMAGING OF NEUROLOGICAL EMERGENCIES 105

post-contrast) should be obtained. T2* GRE images are Advanced imaging can also aid in determining a progno-
useful for demonstrating bony changes and haemor- sis in conjunction with the neurological examination.
rhage. In cases of back pain, and as a screening sequence, Ideally, CT and MR images should be viewed on a
some form of T2-weighted image with fat suppression/ computer work station rather than on hard copy
saturation should be obtained. The STIR image is a film. The entire film should be read, taking care to look
useful screening sequence, as most pathology results in additionally at the peripheral soft tissues. CT images
an increase in signal on T2-weighted images and with fat should be reconstructed using bone and soft-tissue algo-
suppression any lesions within the paraspinal soft tissues rithms and viewed on both bone and soft-tissue windows.
or vertebral bodies are more obvious. Intravenous contrast (water-soluble iodinated con-
trast medium [e.g. iohexol]) should be used for most
Interpretation and assessment of CT CT brain studies and is often useful for CT studies
and MR images of neoplastic and inflammatory/infectious diseases of
As with all imaging modalities, the images should be the spine.
evaluated for technical quality to see if the study is diag- Once images have been evaluated for positioning and
nostic and to identify artefacts. The following questions diagnostic quality, they can be critically assessed. The
should be answered before interpretation: interpretation of CT and MR images is similar to that for
• Was the correct area imaged (especially if the image radiography and is based on classical Röentgen signs (size,
is normal)? shape, number, alignment, margination) plus signal
• Were the correct sequences, planes and slice intensity or tissue attenuation. Comparison of signal
thickness used? intensity on different pulse sequences allows identifi-
• For CT, have the images been reconstructed to look cation of properties of the tissue (e.g. fatty, cystic) (84, next
at the bones and soft tissues in different planes? page; Table 19, page 107). With CT, tissue contrast is
• Are any artefacts evident? largely due to differences in tissue density. Suspected
• Did contrast enhancement occur as expected? lesions should be cross-referenced with different imaging
planes and sequences, as most genuine lesions are visible
The questions that advanced imaging and especially on more than one plane. Partial volume averaging is
MRI can answer include: common and can be mistaken for pathology (e.g. appar-
• Is there a compressive spinal cord or brain lesion ent defects of skull bones) (85, p. 108). The pitfalls in MRI
that can be corrected by surgery? interpretation are detailed in Table 20, p. 109.
• Is there pathology that can be treated medically
(e.g. presence of oedema, inflammatory or
infectious disease)?
• How extensive is the lesion?

The questions that advanced imaging may provide some

help with include:
• Is there evidence of increased ICP?
• What is the nature of the underlying pathology
(e.g. oedema, haemorrhage)?
 106 ADMISSION AND NEURODIAGNOSTIC TESTS

a b c

d e

 84 Transverse T2-weighted (a), T1-weighted (b), T1-weighted post-contrast (c), T2-weighted FLAIR (d) and
T2* GRE (e) images of a Boxer with a presumed glial cell tumour within the left piriform-occipital lobe. T2-weighted
images have the greatest contrast (fluid is hyperintense) and most pathology is hyperintense on a T2-weighted image.
By comparing the lesion on different sequences, information on the tissue characteristics can be obtained. In this case
the mass has small cystic regions (hyperintense on the T2-weighted image, which suppress on the FLAIR, and hypo-
intense on the T1-weighted images). There are also regions of probable haemorrhage within the mass (hypointense on
the T2* GRE image and mid-hyperintense on T1-weighted images). The FLAIR image shows sediment within the
dependent part of the lateral ventricles and an increase in signal within the periventricular tissue that is not visible on
the T2-weighted image. This illustrates the value of the FLAIR sequence in cases with pathology affecting the
ventricles. In this case the post-contrast images show only minimal/mild enhancement, which is not unusual with intra-
axial masses. Contrast medium gives information on the vascularity of lesions and integrity of the blood–brain barrier
and post-contrast T1-weighted images should be obtained in all MRI studies of the brain.
 IMAGING OF NEUROLOGICAL EMERGENCIES 107

Table 19 Comparison of MRI pulse sequences

PULSE SEQUENCE UTILITY ADVANTAGES DISADVANTAGES

T2-weighted High. Should be part of every High. Tissue contrast means very May be difficult to differentiate
brain and spine protocol sensitive for detecting pathology masses from very extensive
oedema. Small lesions adjacent to
sulci and ventricles may be missed

T1-weighted Pre- and post-contrast images Good anatomical imaging. Usually Little soft-tissue contrast
are essential for brain studies. used in combination with MR
Essential in spine if contrast medium (gadolinium
inflammatory/infectious/ chelates). Comparison of pre- and
neoplastic disease is suspected post-contrast images allows
and for post-surgical evaluations assessment of vascularity of lesions
and presence of damage to
blood–brain barrier

PD Not useful in comparison with In man may be useful for showing Time consuming to obtain and
other available sequences multiple sclerosis plaques. Good offers no significant advantage
anatomical detail, but little over T1W
advantage over T1W

T2-weighted FLAIR Essential if hydrocephalus, Suppression of CSF signal allows May be time consuming to obtain.
inflammatory/infectious CNS visualization of periventricular Relatively low signal to noise ratio.
disease or intracranial cystic lesions, which may be missed on CSF flow artefacts may be
lesions. Should be part of routine T2W images. Useful for characteri- confused for solid tissue
brain protocols. Rarely useful for zation of cystic lesions (will
spinal imaging (occasionally suppress if similar to CSF). More
useful to assess cystic spinal cord sensitive than T2W images in
lesions) revealing meningeal disease and
may identify small infarcts/inflam-
matory lesions more clearly than
T2W

T2*GRE Useful if haemorrhage is Most sensitive sequence for Susceptibility artefacts at air/bone
suspected. Very useful in spine to detecting intraparenchymal interfaces and due to microchips/
show bony malformations, bone haemorrhage. Small spurs of bone, implants are more marked than
destruction and production mineralization and bone with spin echo sequences. This may
destruction often seen better than prevent evaluation of some areas
on other sequences of brain/spine

STIR/FatSat images Most useful in spinal and Allows suppression of hyperintense Time consuming and low spatial
orthopaedic imaging. Rarely fat signal. This allows visualization resolution with STIR images. Flow
useful in brain (as limited free of lesions within fatty tissue that within blood vessels may be
fat). Spectral FatSat often used may be missed on T2W images (fat mistaken for lesions (nerve root
instead of STIR sequence with and water are both hyperintense, masses)
high-field MR systems therefore may not detect oedema
within bone marrow/fat). Good
screening sequence, as quite
sensitive for showing lesions in
paraspinal soft tissues and
vertebrae. Spectral FatSat useful in
conjunction with post-contrast T1W
images, as allows visualization of
enhancement within fat-containing
tissues (Continued)
 108 ADMISSION AND NEURODIAGNOSTIC TESTS

Table 19 Comparison of MRI pulse sequences (continued)

PULSE SEQUENCE UTILITY ADVANTAGES DISADVANTAGES

DWI Occasionally useful to determine Most sensitive sequence for Susceptibility artefacts at air/bone
age of infarcts within brain. Not detecting hyperacute infarcts, interfaces and eddy currents result
useful for spinal imaging which may not be visible on T2W in marked distortion of image
images

T2W = T2-weighted; T1W = T1-weighted; PD = proton density; FLAIR = fluid attenuated inversion recovery; T2* GRE = T2* gradient echo;
STIR = short-tau inversion recovery; FatSat = fat saturation; DWI = diffusion-weighted imaging.

Assessment of the brain

Assessment of brain images on CT and MRI is mainly
based on changes in symmetry (mass effect, loss of
parenchyma), changes in the ventricular system, shape
and size of the cerebellum and the cranial spinal cord.
CT may be of limited value for evaluation of caudal fossa
lesions, especially in larger dogs, due to a beam harden-
ing artefact resulting in hypoattenuating streaks, which
can obscure pathology. It is important to recognize MRI
alterations in signal intensity (grey matter, white matter).
CT images should be evaluated for alterations in attenu-
ation of tissues.
The extracranial soft tissues should be evaluated for:
 85 Transverse T1-weighted MR • Muscle volume.
image of the brain of a normal dog. • Muscle signal.
Note the blurring and apparent loss of • Nasal or orbital lesions.
normal cortical bone adjacent to the • Lymph nodes.
ventral aspect of the temporal lobes • Changes in skull bones – loss of signal, erosion.
(arrows). The apparent bone loss is
artefactual, due to partial volume Following administration of MR contrast medium
averaging, and should not be mistaken (gadolinium chelates), the images should be assessed to
for skull fractures. ensure that normal contrast enhancement has occurred.
With CT, the normal contrast enhancement pattern is
similar to that seen on MRI, with contrast evident in
larger blood vessels and in tissues outside the blood–
brain barrier. The choroid plexuses, large veins, pituitary
gland, nasal mucosa, salivary glands and trigeminal nerve
ganglia/periganglionic vascular plexuses should all
enhance in a normal animal. Failure of a lesion to
enhance post-contrast may be due to lack of a blood
supply or an intact blood brain–barrier, but it may also
be due to failure of administration of contrast medium
 IMAGING OF NEUROLOGICAL EMERGENCIES 109

Table 20 Possible pitfalls in MRI

interpretation

Ageing changes
Older animals undergo reduction in brain volume and this
results in mild widening of the sulci and dilation of the
ventricles. Neonatal animals have reduced grey/white matter
contrast compared with adult animals due to incomplete
myelination at birth
Anatomical variants
Asymmetry of the cranial vault is not uncommon and may lead
to distortion of the brain. This can hinder evaluation, but is not
significant. It may also make positioning of slices difficult.
Mineralization of the falcine meninges may be mistaken for
haemorrhage or a small mass lesion
Breed/species variation
There is marked variation in shape and thickness of the
calvarium in dogs. Boxers, Mastiffs and other heavily muscled
dogs may have dramatically thicker bone compared with  86 Transverse T2-weighted MR image of a normal
smaller dogs. This should not be mistaken for calvarial hyper- Boxer. Ventricular enlargement and asymmetry and
ostosis. In cats the olfactory/frontal lobes often appear
absence of the septum pellucidum are common normal
‘pinched’ by the medial orbital walls. On sagittal plane images
in cats there is often a pointed appearance to the cerebellar anatomical variants and should not be mistaken for
vermis. This should not be mistaken for pathological vermal pathological hydrocephalus.
herniation

Ventriculomegaly
Dilation and asymmetry of the lateral ventricles is commonly
seen, especially in brachycephalic and toy breeds.
Brachycephalic dogs often lack a complete septum pellucidum, (e.g. contrast still in catheter, leakage from catheter).
resulting in extensive communication between the lateral The mechanism of contrast enhancement is different on
ventricles (86). These dogs are also predisposed to hydro-
cephalus and the cut-off point where normal ventricular size CT and MRI. CT contrast enhancement is the result of
ends and hydrocephalus begins is unclear. Specific ratios are direct visualization of the contrast agent, whereas with
described, but are rarely used. A rounded appearance to the MRI the contrast agent is not directly visualized;
ventricle and a periventricular halo (seen on FLAIR images) enhancement occurs due to the effect of the contrast
indicates that the ventricular enlargement is pathological
(87, next page). Dilation of the 3rd and 4th ventricles is
agent on the immediately adjacent tissues.
abnormal and close examination for an obstructive lesion
should be made. Dilation of the olfactory recesses of the Brain masses
lateral ventricles is often seen with significant hydrocephalus Most brain masses are readily identified on MRI or CT
Fluid within bullae images (see also Chapter 26). They are often hyperin-
Fluid or tissue in the bullae is not uncommon in brachycephalic tense on T2-weighted MR images and are associated
dogs (especially Cavalier King Charles Spaniels). This is with a mass effect (midline shift, compression of ventri-
probably due to primary secretory otitis and is often seen as an cles and adjacent parenchyma). Much of the mass effect
apparent incidental finding. Lack of significant enhancement
is often due to perilesional oedema. The presence of
of the bulla wall and involvement of adjacent structures helps
differentiate from otitis media oedema is easier to appreciate on MRI than on CT. On
CT, oedema results in reduced attenuation of the brain
tissue. On MRI, oedema is hyperintense on T2-weight-
ed images, poorly marginated, usually most severe within
the white matter and tends to follow the white matter
tracts (especially the corona radiata).
110 ADMISSION AND NEURODIAGNOSTIC TESTS

a The differential diagnosis of brain masses is based on

classification into extra-axial or intra-axial location.
Extra-axial masses arise from outside the neuraxis
(e.g. meninges, skull bone) (88). Intra-axial masses arise
from within the neuraxis (e.g. glial cell tumours) (84).
Intraventricular masses are classified as extra-axial. The
imaging features of masses are non-specific. A mass
lesion is not necessarily neoplastic and other causes
(e.g. granuloma, haematoma) should be considered.
Definitive diagnosis requires tissue biopsy (stereotaxis,
free-hand or open surgical biopsy).
The diagnosis of a brain tumour relies on diagnostic
imaging. The aims of imaging an animal with a suspect
brain tumour are to confirm the diagnosis, to screen for
b metastases either to or from the brain and to aid thera-
peutic planning. MRI also allows identification of the
secondary pathological effects of intracranial masses and
inflammation (e.g. hydrocephalus, vasogenic oedema,
bleeding or brain herniation) (89).
Most primary brain tumours in dogs result in no
changes to the skull and are not visible on plain radiogra-
phy. Meningiomas in cats can be associated with hyper-
ostosis of the calvarium, which can be visualized on
radiographs, as can areas of mineralization of the tumour.
As with any suspected tumour, it is advisable to obtain
thoracic radiographs to screen for pulmonary metastases.
While primary brain tumours rarely spread to the lungs,
metastasis does occur, with consequences for treatment
 87 Transverse T2-weighted (a) and FLAIR (b) MR and prognosis. It is more common for tumours to metas-
images of a Flat-coated Retriever with obstructive hydro- tasize to the brain than vice versa. Metastases to the brain
cephalus secondary to an intraventricular mass (not are less common than primary brain tumours. When
visible). Note on the FLAIR image the hyperintense they do occur, they are usually multiple, small, located at
periventricular halo and rounded appearance to the lateral the junction between grey and white matter (i.e. water-
ventricles (arrows). These features are often seen with an shed zone) and surrounded by marked oedema.
acute increase in intraventricular pressures. The periven- Most intra-axial tumours (and other types of brain
tricular halo is clearly visible on the FLAIR image, but is pathology) result in an increase in water content, which
difficult to visualize on the T2-weighted image due to the appears hyperintense on T2-weighted images and
similar signal intensity of the CSF and the periventricular hypointense on T1-weighted images. Extra-axial masses
changes. are variable in appearance depending on cellularity and
mineralization. Most extra-axial masses are associated
with marked contrast enhancement. The contrast uptake
by intra-axial masses is variable (from none to marked).
While the mass effect produced by brain tumours is
obvious, delineating the mass is not always easy. In some
cases of diffuse neoplasia (e.g. lymphoma or gliomatosis
cerebri) the changes may mimic inflammatory disease.
Definitive diagnosis may require brain biopsy.
 IMAGING OF NEUROLOGICAL EMERGENCIES 111

a b

* *

 88 (a) Transverse T2-weighted MR image of a dog

with an extra-axial mass (asterisk) at the left mesen-
cephalon. Extra-axial masses are typically broad based
and lie superficial to the brain and result in displacement
of the brain away from the inner surface of the cranium.
Note the cleft of CSF between the mass and the brain-
stem (arrow). (b) The post-contrast T1-weighted image
shows dense homogeneous contrast enhancement of the
*
mass (asterisk). The diffuse area of increased signal
adjacent to the mass seen on 88a is likely to represent
peritumoural oedema.

In addition to identifying the primary lesion, the  89 Sagittal T2-weighted MR image of the brain of
brain should also be evaluated for secondary pathological a Greyhound with severe meningoencephalitis. As a
effects. Hydrocephalus is commonly seen with masses consequence of the increased intracranial pressure there
within the caudal fossa (e.g. brainstem masses) due to is subtentorial herniation (yellow arrow) and herniation
compression of the CSF pathways or due to the increased of the cerebellum through the foramen magnum. Note
CSF production and protein concentrations seen the rostrocaudal compression of the cerebellum and
with choroid plexus masses. With certain tumours protrusion of the cerebellar vermis through the foramen
(e.g. choroid plexus tumours) treatment may need to be magnum (red arrow). Assessment of brain herniation is
directed to treating the secondary pathological effects. usually most easily appreciated on sagittal T2-weighted
Any disease that increases ICP may result in brain images. Due to the caudal fossa overcrowding, the brain-
herniation. This is easiest to see on T2-weighted sagittal stem is displaced ventrally and compressed and there is
images, where displacement of the occipital lobes under swelling and increased signal within the cranial cervical
the osseous tentorium or caudal displacement of the cord (asterisk) due to early syringomyelia/oedema or
cerebellum through the foramen magnum may be seen. inflammation.
There are many treatments for intracranial neoplasia
and CT or MRI is required in most for accurate treat-
ment planning.
112 ADMISSION AND NEURODIAGNOSTIC TESTS

Brain haemorrhage to man. Most brain haemorrhage seen in dogs and cats
CT is exquisitely sensitive for the detection of acute is intraparenchymal. Haemorrhage is commonly seen
haemorrhage, which is evident as increased density due in association with tumours, but the MRI appearance is
to attenuation of x-rays by the globin portion of blood. predominately of a solid mass rather than a haematoma.
The attenuation gradually decreases until the Haemorrhagic tumours are often complex masses with
haematoma is isodense at about 1 month after the onset. solid, contrast enhancing parts (84). Lack of a distinct,
The periphery of the haematoma enhances with contrast complex hypointense rim and bleeding of different
at 6 days to 6 weeks due to revascularization. Until durations within the lesion are suggestive of neoplasia.
recently, CT was the preferred imaging modality in In some cases, repeat MRI is required to monitor pro-
human patients to determine the presence of haemor- gression of the lesion. The presence of oedema at a later
rhage in early stroke. Recent developments in MRI mean stage, regression in size of the lesion and failure to
that CT now offers no advantage in the diagnosis of follow the expected evolution of a haematoma are
stroke. indicative of neoplasia.
The appearance of haemorrhage on MRI is variable Large haematomas may show distinct fluid lines. If
and depends on the age of the haemorrhage, pH, oxy- there is intraventricular bleeding, alterations in signal
genation, size of bleed and magnetic field strength (see intensity (decreased signal on T2-weighted and increased
also Chapter 17). on T1-weighted and FLAIR images) and layered
T2* GRE sequences are the most sensitive for visual- fluid–fluid levels within ventricular CSF will be seen. The
izing haemorrhage, which always appears as a signal void presence of high signal on a T1-weighted image within
(black). On spin echo sequences, the appearance depends the brain and very low signal on a T2-weighted image is
on the degree of conversion of haemoglobin (Table 21). suggestive of recent haemorrhage. T2* GRE images are
In small animals the main causes of intraparen- the most sensitive for showing small haemorrhages
chymal haemorrhage are coagulopathy (e.g. primary (which are hypointense). Hyperintensity on a T1-weight-
or secondary to Angiostrongylus vasorum infection), ed image is not 100% specific for haemorrhage and may
neoplasia and trauma. Subdural and subarachnoid be seen with melanin, high protein, flow artefacts and
haematomas are rare in small animals (90) compared paramagnetic effects (e.g. due to manganese).

Table 21 MRI signal characteristics of intracranial haemorrhage based on duration of disease

BIOCHEMICAL FORM CLINICAL STAGE DURATION OF INTENSITY ON INTENSITY ON

OF HAEMORRHAGE HAEMORRHAGE T1-WEIGHTED T2-WEIGHTED

Oxyhaemoglobin Hyperacute Immediate to few hours Isointense Hyperintense

in RBCs

Deoxyhaemoglobin Acute Hours to days Iso- to hypointense Hypointense

in RBCs

Methaemoglobin Early subacute First few days Hyperintense Hypointense

in RBCs

Extracellular Subacute to chronic Days to months Hyperintense Hyperintense

methaemoglobin

Ferritin and Remote Days to indefinitely Iso- to hypointense Hypointense

haemosiderin
 IMAGING OF NEUROLOGICAL EMERGENCIES 113

a b c

d e f

 90 Transverse T2-weighted (a) and T1–weighted Brain infarct

(b) MR images of a dog with a subdural haematoma Brain infarcts in dogs are usually ischaemic with little/no
secondary to thrombocytopenia. Transverse T1-weighted haemorrhage. They are usually arterial and have charac-
(c), T2-weighted (d) and T2* GRE (e) MR images and teristic imaging findings (see Chapter 17).
CT image (f) of a Labrador Retriever with a subdural CT images are frequently normal during the acute
haematoma secondary to Angiostrongylus vasorum phase of ischaemia, therefore the diagnosis of ischaemic
infection. Hyperintensity on the T1-weighted images and stroke using CT relies on the exclusion of ‘mimics’ of
hypointensity on the T2* GRE sequences should raise the stroke. Early CT signs of ischaemia can be subtle and
suspicion of haemorrhage. Haemorrhage has a fairly difficult to detect, even for experienced readers, and
predictable evolution on MRI, which can indicate its age. include parenchymal hypodensity, loss of grey/white
The presence of extensive oedema, contrast enhancement matter differentiation, subtle effacement of the cortical
and haemorrhage of different ages failing to follow normal sulci and local mass effect.
evolution are features of bleeding secondary to neoplasia Lesions are most obvious on MR T2-weighted and
(84a–e). Acute haemorrhage is hyperattenuating on CT. FLAIR images, where they are usually hyperintense.
The MR images show the subdural haematoma clearly They have minimal/no mass effect and are usually
(best seen on the T2-weighted image) and the intra- homogeneous and sharply marginated, with clear
parenchymal bleed (best seen on the T2* GRE). The T2* demarcation from adjacent parenchyma. Grey matter is
GRE sequence is the most sensitive sequence for showing most severely affected and lesions are usually confined to
haemorrhage on MRI. Most haemorrhage is hypointense one vascular territory.
on a T2* GRE image, though there are other causes of
hypointensity on a T2* GRE image, such as
mineralization or gas.
 114 ADMISSION AND NEURODIAGNOSTIC TESTS

Territorial infarcts occur with large artery disease and Metabolic/toxic diseases
result in large rectangular/wedge-shaped lesions. They Many metabolic/toxic diseases result in no abnormalities
are most commonly seen in the cerebellum (small breeds, on MRI, therefore a normal MRI examination does not
with Cavalier King Charles Spaniels being predisposed). rule out the possibility of a metabolic or toxic brain
Large territorial infarcts in the vascular territory of the disease. Diagnosis relies on biochemical testing. Bilater-
middle or rostral cerebral arteries are occasionally seen in ally symmetrical abnormalities within the grey or white
sight-hounds, among other breeds. matter are suggestive of a metabolic or toxic aetiology
Lacunar infarcts are small infarcts affecting end arter- (91). The MRI changes most commonly seen with meta-
ies within deep grey matter structures (e.g. thalamus and bolic diseases are hyperintensity on T2-weighted images,
caudate nucleus). They are most commonly seen in with minimal/no mass effect and no abnormal contrast
larger dogs and may be multiple. Chronic lacunar enhancement. The distribution of the lesions is diagnos-
infarcts are sometimes seen as an incidental finding. tic for some diseases (e.g. thiamine deficiency). Cortical
DWI is useful in determining the age of the infarct atrophy and hyperintensities within the lentiform nuclei
with acute (<9 days old) infarcts appearing hyperintense on T1-weighted images (due to abnormal manganese
on the DW image and hypointense on the apparent dif- accumulation) may sometimes be present in animals with
fusion coefficient (ADC) map. After 7–9 days the DW congenital portosystemic shunts. Many metabolic dis-
image pseudonormalizes. DWI may be helpful in giving eases occurring in young animals are, however, poorly
some prognostic information if there are multiple characterized and the MRI changes may be non-specific.
infarcts by showing if they are occurring at different time
periods. MRI and CT angiography of intracranial arter- Imaging findings associated with seizure activity
ies is usually of limited or no value for the diagnosis of Idiopathic epilepsy is a diagnosis of exclusion, therefore a
canine and feline brain infarcts due to the small size of the normal MRI study is to be expected. If seizures are due to
blood vessels affected, which are often not visible even in underlying gross structural brain disease, lesions on the
normal animals. MRI examination will usually be obvious (see specific
Radiography and ultrasonography are useful in diseases for appearance). There are a number of MRI
looking for the underlying systemic causes of strokes changes that are thought to be caused by seizure activity.
(renal disease and adrenal disease most commonly). In some dogs with severe seizures an increased signal
within the grey matter of the piriform lobe and extending
Head trauma into the hippocampal gyrus may be seen (92, page 116).
Even mild neurological signs following head trauma have Similar changes in the cingulate gyrus are occasionally
a high incidence of lesions detectable on CT. Most cases seen. The changes in the piriform lobes may be
of head trauma resulting in neurological signs will have symmetrical or asymmetrical and are best seen on trans-
changes on MRI and the imaging study needs to deter- verse plane T2-weighted FLAIR images. (Note: The
mine if there is significant brain compression due to frac- piriform lobes have slightly higher signal intensity when
ture fragments or haematoma formation or mass effect. compared with adjacent parenchyma in normal dogs.)
A CT examination will clearly show the presence of skull The piriform lobe is also a predilection site for gliomas,
fractures (62, p.88) and allow detection of depressed which can resemble post-seizure changes. Careful exam-
fractures that may need surgical decompression. MRI, ination should be made for any mass effect. The presence
while not showing such clear bone detail, gives more of a mass effect/swelling of the piriform lobe is more
information on the extent of brain injury and allows suggestive of a tumour than a post-seizure effect.
identification of shearing or contusive injuries. In some cats with seizures, T1-weighted images obtained
 IMAGING OF NEUROLOGICAL EMERGENCIES 115

a b c

d e

 91 Transverse MR image of a Staffordshire Bull Terrier with L2-HGA (L2-hydroxyglutaric aciduria) (a), an English
Springer Spaniel with fucidosis (b), and a dog with thiamine deficiency (c–e). Despite the differences in location of the
lesions, they all share the characteristics of being symmetrical, hyperintense on T2-weighted images, with minimal or no
mass effect, and do not show contrast enhancement. When seen on MRI these features are suggestive of toxicoses or an
underlying metabolic disorder. Note that post-seizure changes may resemble a metabolic disorder (92, next page) and
bilateral symmetrical hyperintensity may be seen in the white matter of the occipital lobes as an apparent ageing change.
116 ADMISSION AND NEURODIAGNOSTIC TESTS

a b c

 92 Transverse T2-weighted MR images of the brain of two different Staffordshire Bull Terriers with post-seizure
changes. Note the bilateral hyperintensity within the piriform lobes (arrows) in dog 1 (a) and within the hippocampus
(arrows [b]) and cingulate gyrus (arrow [c]) of dog 2. Typically, post-seizure changes are most severe within the
superficial grey matter and have no mass effect. The changes may be bilateral or unilateral. CSF analysis +/- repeat
MRI scanning is required to rule out inflammatory CNS disease.

several minutes post administration of contrast may show for the hydrocephalus. In most cases of congenital
abnormal diffuse enhancement of the hippocampus. hydrocephalus, only the lateral ventricles +/- the 3rd
This may also represent a post-seizure change, but the ventricle are affected. Dilation of the mesencephalic
cause is unknown. In some dogs with a long-standing aqueduct and 4th ventricle often indicates obstruction to
history of seizures, there may be mild atrophy of the CSF flow at the lateral apertures of the 4th ventricle or
piriform lobes/hippocampus. There is no known associ- the foramen magnum. Mild hydrocephalus is commonly
ation between severity and duration of seizures and pres- seen in association with occipital malformation (Chiari-
ence of post-seizure MRI changes. These changes can be like malformation), but intracranial signs are not usually
detected for up to 10 weeks post seizure in some cases. seen. In older animals, hydrocephalus is often secondary
to inflammatory or neoplastic disease. In such cases it is
Hydrocephalus essential that FLAIR images are obtained to identify
In severe cases the diagnosis of hydrocephalus is periventricular lesions. In dogs with choroid plexus
straightforward on MRI, with obvious marked dilation of tumours and cats with feline infectious peritonitis (FIP)
the lateral ventricles and thinning of the overlying cortex there may be intraventricular masses arising from the
if congenital in origin. The fontanelle is usually open in choroid plexuses. Seeding along the CSF pathways with
toy breed dogs with congenital hydrocephalus, which lesions in multiple parts of the ventricular system may be
allows ultrasonography of the brain to identify the seen with choroid plexus carcinomas and FIP. Choroid
enlarged lateral anechoic ventricles. However, this is not plexus masses normally exhibit marked contrast
always the case, especially if the hydrocephalus is not a enhancement. Dilation of the olfactory recesses of the
congenital lesion. Although the diagnosis may be made lateral ventricle and a periventricular halo of increased
with ultrasound in some cases, MRI is indicated to signal (seen on FLAIR images) are suggestive of
confirm the diagnosis and identify any underlying cause increased intraventricular pressure (87).
 IMAGING OF NEUROLOGICAL EMERGENCIES 117

Compensatory hydrocephalus (hydrocephalus ex between the skull and the surface of the brain. This needs
vacuo) is seen secondary to loss of brain parenchyma, to be differentiated from subdural/extradural haemor-
with widening of the sulci in addition to the ventriculo- rhage (by assessing signal intensity of the fluid), which
megaly. This is most commonly due to chronic inflam- can provoke a chemical meningitis. Differentiating pat-
matory/vascular disorders and degenerative disease. It is terns of meningeal enhancement does not aid diagnosis,
often seen in older animals and is not associated with as this is a non-specific finding. Diffuse meningeal
thinning of the calvarium. tumours (lymphoma most commonly) may appear iden-
tical to inflammatory disease on MR images. Meningitis
Inflammatory diseases is not usually visible on CT without the use of intra-
Inflammatory CNS disease may be associated with a venous contrast unless it is very severe or if there are
normal MRI examination. In one study, 6 of 25 dogs with extra-axial fluid accumulations. The appearance of
inflammatory CSF had a normal MRI examination. meningitis on CT is similar to that on MRI, with abnor-
Investigation of suspected inflammatory/infectious mal contrast enhancement seen in severe cases.
disease therefore requires CSF analysis.
Encephalitis
Meningitis The appearance of encephalitis on MRI is variable and
In many cases of meningitis the CT or MRI images will there can often be concurrent meningeal involvement.
be normal, with the diagnosis requiring CSF analysis. Most commonly there are multifocal patches of ill-
Unless the meningitis/encephalitis is severe, there may defined hyperintensity on T2-weighted and FLAIR
not be changes on T2-weighted images, but FLAIR images, with a variable mass effect (from none to marked)
images may show a thin rim of increased signal repre- (see Chapter 19). In some cases it is impossible to differ-
senting abnormal meninges. On MR T2-weighted entiate inflammatory disease from diffuse or infiltrative
images the chemical shift artefact can mimic meningitis neoplasia. Conditions such as granulomatous menin-
due to the presence of linear hyperintensities at the goencephalitis (GME) have a predilection for the white
meningeal/skull boundary. Chemical shift artefact occurs matter as well as cerebellum and brainstem. Necrotizing
at fat/soft-tissue interfaces and is due to errors in spatial meningoencephalitis occurs in several small breed dogs
localization resulting from differences in resonant fre- (Pugs, Maltese) and preferentially affects the cerebrum,
quencies of fat and water. In cases of meningitis there is with areas of cavitation and cyst formation. Mengingo-
often involvement of the pia, which extends between the encephalitis secondary to extension of disease from
sulci. Increased signal of the pia on FLAIR images is outside the skull (usually middle ear disease) occurs occa-
abnormal and helps differentiate genuine meningeal sionally, but with extensional disease the extra-axial MRI
changes from chemical shift artefact (chemical shift arte- changes are evident (63). The sensitivity of CT for diag-
fact does not extend into the sulci). Post-contrast T1- nosing encephalitis is lower than that of MRI. Multifocal
weighted images are the most sensitive MR sequence for hypoattenuating lesions with variable enhancement may
diagnosing meningitis. Abnormal enhancement of the be seen with encephalitis, but mild cases of encephalitis
meninges is often seen, but is subjective, and the normal may have a normal CT scan. In severe cases a mass effect
appearance of the meninges varies with the MR machine, and areas of reduced attenuation due to oedema may be
the contrast medium used, imaging parameters and visible. Cats with FIP affecting the brain commonly have
the timing of image acquisition following contrast obstructive hydrocephalus due to marked inflammation
administration. It is helpful to have a normal image to of the meninges and periventricular tissues/ependyma.
compare, as meningeal enhancement may be subtle. Two These changes are clearly visible on MR images, with
patterns of meningeal enhancement are described: dural dilation of the ventricular system and abnormal enhance-
(no extension into the sulci) and pial (enhancement of ment of the meninges and periventricular tissues/
meninges extending into the sulci). It is abnormal for the ependyma. Abnormal CSF signal (increased on T1-
pia to enhance significantly. In severe cases of meningitis, weighted and FLAIR images) may be also be seen on MR
subdural/subarachnoid fluid accumulation may occur images due to elevated protein levels within the CSF.
118 ADMISSION AND NEURODIAGNOSTIC TESTS

Advanced spinal imaging • Epidural tissues. Evaluate the epidural fat and
Interpretation of spinal CT and MR images epidural blood vessels for pathological changes.
Interpretation of all imaging modalities is based on the
classical ‘Röentgen signs’ of shape, size, number, opacity Advanced imaging can provide high-quality images,
(or signal intensity) and margination. In addition, for the which means that a large number of incidental degener-
spinal column attention should be paid to the alignment ative changes may be seen. The significance of imaging
of the vertebral canal as a whole. Due to the complex findings can only be determined by careful correlation
geometry of the spine, the importance of high-quality with the neurological and clinical findings. Generally, if
images cannot be overemphasized. Myelography is often there are neurological deficits, then it is more likely that
required to assess the spinal cord accurately with CT. a gross structural lesion will be found. Key questions to
Intravenous iodinated contrast medium is useful for out- answer with spinal CT or MRI include: (a) is there spinal
lining spinal masses and opacifying the spinal blood cord compression? (b) what is the severity of compres-
vessels, which may delineate compressive lesions. sion? and (c) what is the cause of the compression? If the
The following areas should be evaluated on spinal clinical signs are milder or if pain is the only sign, then
images: lesions may be subtle. Spinal pain may be associated with
• Paraspinal soft tissues. As for the head, assess any diseases affecting one of many structures, so it is vital to
changes in muscles and other soft tissues. evaluate the entire spinal column and paraspinal soft
• Vertebral bodies, pedicles, laminae. Assess the tissues carefully.
number, shape, size, alignment. Is there any
alteration in signal intensity and presence of any Intervertebral disc disease
cortical destruction? MRI is extremely sensitive for detecting degenerative
• Appearance of the intervertebral discs. Assess changes of the spinal column, but assessing the signifi-
intensity and size of the nucleus, cance of any protrusions can be difficult in some cases
disruption/protrusion of the annulus and any (Table 22). In chondrodystrophic dogs with acute disc
changes (erosion, signal changes) in the endplates. extrusion, CT of the spine without the use of intrathecal
• Intervertebral foramina/nerve roots. Any changes contrast is as accurate as conventional myelography.
in size, position and signal intensity of spinal nerve,
as well as presence of periradicular fat, should be MRI findings
assessed on dorsal, sagittal and transverse planes. The normal intervertebral disc has a hyperintense (on
• Foraminal stenosis. Frequently associated with loss T2-weighted images) nucleus with a subtle slightly
of periradicular fat (often seen on parasagittal hypointense central cleft seen in some animals. The
images). Spinal nerves frequently appear swollen, annulus is hypointense on all sequences; the dorsal
mildly increased in their signal intensity and longitudinal ligament merges with the dorsal annulus
contrast enhancing with chronic compressions and cannot be differentiated from it. The vertebral
(should not be mistaken for nerve root/spinal nerve endplates are smooth and hypointense on all sequences.
tumour). Entrapment of spinal nerve by spondylosis With chondroid degeneration seen in chondrodystroph-
occurs occasionally and this can best be seen on ic dogs, there is early dehydration (decreased signal on
dorsal plane images. It is often difficult with MRI to T2-weighted images) of the nucleus. In non-chondro-
determine whether the stenosis is due to new bone dystrophic dogs, ageing changes do not occur until
or soft-tissue hypertrophy. middle age. The exception is the lumbosacral disc, which
• Articular processes. Assess for degenerative joint shows signs of degeneration at an earlier age. Calcifi-
disease or associated synovial cysts. cation of the disc nucleus is difficult to differentiate from
• Spinal cord. Assess size (any swelling/atrophy), dehydration on MRI unless severe (in which case the
position, any compression and signal intensity. affected nucleus appears as a signal void). Chronic disc
• Subarachnoid space. Evaluate as for myelography disease is often associated with changes in vertebral end-
and note any narrowing/divergence of the plates and subchondral bone.
subarachnoid space.
 IMAGING OF NEUROLOGICAL EMERGENCIES 119

a b

 93 Sagittal (a) and transverse (b) T2-weighted MR Disc extrusion

images of a middle-aged Cavalier King Charles Spaniel Acute extrusions are normally clinically significant and
with acute-onset neck pain. There is severe syringo- seen as amorphous extradural mass lesions of mid-low
hydromyelia (abnormal fluid accumulation within the signal intensity, extending dorsally from the disc space
spinal cord parenchyma) (arrows). The spinal cord (71). It is difficult to differentiate extruded disc material
changes are chronic and in cases where there is acute from haemorrhage; a combination of the two can occur.
onset of signs and obviously chronic pathology, alternative If vertebral sinuses are damaged, there may be extensive
reasons to explain the signs should be investigated. Acute epidural haemorrhage, which can extend for large dis-
decompensation of chronic compressive spinal lesions is tances from the site of disc extrusion. This is seen mainly
commonly seen due to concussion, instability or further in larger dogs and in the lumbar spine. Epidural haemor-
compression of neural structures. In this case there was a rhage appears as amorphous mid-signal tissue, often
concurrent foraminal disc extrusion (b). Assessment of the globular and discontinuous in distribution. Usually the
intervertebral foramina in the cervical spine is difficult on site of the disc disease is obvious and GRE images are
sagittal and dorsal plane images. If no lesions are found on helpful to confirm haemorrhage. Haematomas do not
these imaging planes, transverse plane images through the usually enhance following contrast administration, but
disc spaces should be considered. acute disc extrusions may.
Most disc disease is easily seen on sagittal plane
images. Foraminal extrusions/protrusions may be missed
if only sagittal plane images are acquired, particularly
in the cervical spine (93). Acute non-compressive nucleus
pulposus extrusion may occasionally occur secondary to
trauma (60, 61), resulting in severe focal parenchymal
changes with minimal or no compression.
Table 22 Evaluation of disc disease on MRI

• Position of disc material

• Degree of cord compression
• Nerve root/spinal nerve involvement
• Presence of cord atrophy
• Spinal cord changes – oedema/contusion, gliosis,
intraparenchymal
• Complicating factors – subluxation, concurrent
syringohydromyelia, vertebral stenosis
120 ADMISSION AND NEURODIAGNOSTIC TESTS

Disc protrusions
Protrusions are common in older dogs and are character-
ized by nodules of low-signal disc material protruding
through the annulus into the ventral aspect of the verte-
bral canal and indenting/displacing or compressing the
spinal cord. Chronic protrusions are often asymptomatic
and are especially common at the lumbosacral junction in
older dogs, but they can occur at multiple sites. Spinal
cord atrophy is commonly seen on MRI associated with
chronic disc protrusions and results in a reduced diame-
ter of the spinal cord (94). On myelograms and CT myel-  94 Sagittal T2-weighted MR image of an old Golden
ograms, preservation of the subarachnoid space may be Retriever with multiple chronic disc protrusions. The dog
recognized with spinal cord atrophy. Spinal cord atrophy presented with acute clinical signs of paraparesis. The
needs to be differentiated from overt spinal cord com- image shows chronic disc protrusions with spinal cord
pression due to an acute disc protrusion. With spinal atrophy. Note the focal increased signal within the spinal
cord atrophy there is often well-defined focal increased cord and relative preservation of the epidural fat/CSF
signal within the spinal cord (primarily affecting grey dorsally despite the severe reduction in spinal cord
matter) on T2-weighted MR images and no compression diameter (arrow).
of the dorsal subarachnoid space and epidural fat at the
site of reduced spinal cord diameter. With acute spinal
cord compression, the epidural fat and subarachnoid
spaces are compressed in addition to the spinal cord.
MRI signal changes seen with acute spinal cord compres- spine there are often subtle changes to a nearby disc
sive lesions are usually ill-defined, hyperintense on (often subtle reduction in volume of the nucleus, hyper-
T2-weighted images and often affect grey and white intense cleft in the dorsal annulus and mild bulging of the
matter. There may be swelling of the spinal cord annulus). With acute non-compressive nucleus pulposus
cranial/caudal to the site of compression. extrusion the spinal cord changes are similar (although
usually they are located over a disc space) and there is
Ischaemic myelopathy (fibrocartilaginous often subtle extradural material adjacent to the cord
embolism) without associated cord compression. GRE images do
Radiography of ischaemic myelopathy is usually normal. not show haemorrhage within the cord, which helps dif-
In severe cases there may be mild swelling of the spinal ferentiate intramedullary disc extrusions. Post-contrast
cord, resulting in an intramedullary pattern visible on T1-weighted images show variable contrast enhance-
myelography. The majority of cases have a focal asym- ment within the cord (usually none or mild). Chronic
metrical increased signal within the spinal cord (see cases of ischaemic myelopathy have more sharply mar-
Chapter 18). In severe cases there may be mild swelling ginated areas of hyperintensity, with no associated
of the spinal cord. The hyperintensities are irregular in swelling representing gliosis or ‘cyst’ formation on
shape and often dorsally located within the spinal cord. MR images. The majority of animals with suspected
The hyperintensity is mainly located within the central ischaemic myelopathy have abnormalities on MRI,
grey matter, but may extend into the white matter; although occasionally some dogs may have a normal
however this is difficult to visualize. Within the adjacent MRI examination.
 ADMISSION AND NEURODIAGNOSTIC TESTS Chapter 5

CEREBROSPINAL FLUID ANALYSIS

121

Amy Wood,
Laurent Garosi
& Simon Platt

INTRODUCTION
Table 23 Contraindications for CSF collection

Cerebrospinal fluid bathes the entire CNS and plays • Patient unstable for general anaesthesia
a vital role in its nourishment and protection. CSF • Evidence of coagulopathy
originates from a number of sites. Sites of production • Instability or pathology suspected at the site of collection
include: the choroid plexuses of the lateral, third and (e.g. atlanto-axial instability)
fourth ventricles; the brain by way of the ependymal • Severe hydrocephalus
lining of the ventricular system and the pial–glial • Recent head trauma
membrane covering its external surface; and the blood • Imaging evidence of intracranial mass lesion or
vessels in the pia-arachnoid. It is produced both by ultra- oedema/haemorrhage causing mass effect
filtration from the blood plasma and by active transport • Clinical indication of increased intracranial pressure
mechanisms that utilize energy. CSF is primarily
absorbed passively at the arachnoid villi found in venous
sinuses and cerebral veins.
CSF normally has a low protein content and contains
few cells. Pathology in the CNS is often reflected in the
CSF when there is compromise of the blood–brain General anaesthesia is mandatory for CSF collection.
barrier, the blood–CSF barrier or the CSF’s interface Inherent risks of the procedure include iatrogenic
with the brain and spinal cord. Abnormalities in the CSF trauma to the brainstem or spinal cord by needle punc-
during disease are usually limited to changes in the ture and introduction of infectious agents if there is a
number and distribution of cells present and increased break in aseptic technique. Specific contraindications for
protein content, making analysis of CSF a sensitive but CSF collection are listed in Table 23.
rarely specific indicator of CNS disease. Because of this, During a spinal tap, the subarachnoid space
the results of CSF analysis must be interpreted in light of becomes continuous, via the lumen of the needle, with
all other clinical findings and, ideally, advanced imaging. the outside environment, and the pressure between the
Ancillary tests that can be performed on CSF to provide two spaces will quickly equilibrate. In the presence of
more specific results are covered in the final section. increased ICP, CSF will flow out at a higher rate. This
In the emergency setting, CSF analysis may be indi- can lead to transtentorial or foramen magnum hernia-
cated in the absence of advanced imaging in cases of tion of neural tissues and acute signs of midbrain and/or
suspected inflammatory disease. Additionally, if myelo- brainstem compression. There is not a decreased risk of
graphy is to be performed, CSF should be collected prior herniation with a lumbar tap compared with cisternal,
to contrast injection and preserved for analysis in the as the subarachnoid space is continuous between these
event that the myelogram is non-diagnostic. two sites of collection.
 122 ADMISSION AND NEURODIAGNOSTIC TESTS

COLLECTION TECHNIQUE Cerebellomedullary cistern collection

The animal is anaesthetized and a rigid endotracheal
The site of collection depends essentially on the site of tube is used to avoid occlusion of oxygen flow during the
the suspected pathology. As CSF flows predominantly in neck flexion required for CSF collection from the CMC.
a cranial to caudal direction, abnormal CSF is more likely The CMC is reached by inserting a spinal needle at the
to be present caudal to a lesion. An exception to this gen- junction of the horizontal line between the occipital pro-
eralization is in the case of cervical lesions, where a cis- tuberance and the arch of the axis (C2 vertebra) and the
ternal tap may be of higher yield than a lumbar tap, vertical line that runs along the cranial edges of the wings
because the proximity of the cerebellomedullary cistern of the atlas (C1 vertebra) (95). A 22 or 20 gauge 1.5 inch
allows affected CSF to reach it via bidirectional flow. spinal needle will reach the CMC in most dogs and cats,
Collection from the cerebellomedullary cistern although in large dogs over 30 kg a 2.5 inch needle may
(CMC, or cisterna magna) is easier and less likely to be needed.
produce a sample contaminated with blood. This is the The region is clipped and aseptically prepared. With
most common site of collection in dogs and cats. Lumbar the animal in lateral recumbency, an assistant holds the
sampling is technically more difficult and more likely to head in ventral flexion (96) so that the nose is parallel to
produce blood contamination, but is also more likely to the table, while also ensuring that respiration is unen-
be diagnostically useful for lesions in the thoracolumbar cumbered. The animal has to be observed for adequate
spine. ventilation during the whole procedure, and positive-
A minimum of 0.5 ml (approximately 11 drops out pressure ventilation is often required. Adequate depth of
of a 22 gauge needle) of CSF is needed for standard anaesthesia should be confirmed before beginning the
analysis by most laboratories. One millilitre of CSF per procedure. The needle is positioned directly on the
5 kilograms of body weight can safely be removed at a midline perpendicular to the neck. Once the skin has
time. If CSF is to be sent for analysis to a distant labora- been penetrated, the stylet can be removed. The needle
tory, two aliquots should be obtained to allow for preser- is then slowly and carefully advanced 1–2 mm at a time.
vation of one sample (see Sample handling, p. 125). The puncture of the dura mater and atlanto-occipital

C2 vertebra
C1 vertebra
Atlanto-occipital space

Spinal needle Occipital crest

 95 The anatomical landmarks for cerebellomedullary  96 Manual flexion of the head and neck is essential to
cisternal CSF acquisition. obtain CSF from the cistern magna. The head is flexed at
approximately 90º to the neck in this dog, with the nose
parallel to the edge of the table.
 C E R E B R O S P I N A L F L U I D A N A LY S I S 123

membrane may be felt as a slight ‘pop’, but often this is L5

not the case. Resistance will decrease when the dura is Dorsal interarcuate
penetrated and CSF flow is observed into the hub of the space L5/L6

needle. The flow of CSF is the only reliable sign of a suc-

cessful puncture. The first two drops of CSF are allowed L6
to drip freely to remove any debris collected during Wing of ilium
needle insertion, and the following drops are collected L7
into a sterile collection tube. CSF should never be aspi- Sacrum
rated with a syringe, as this creates negative pressure in
the subarachnoid space and increases the risk of
herniation.
If the needle hits bone while being advanced, it may
be redirected cranially or caudally, moving the needle off
the bone into the atlanto-occipital space. If the nose is
not exactly parallel to the table, one of the vertebral
sinuses will be entered and blood will be obtained instead
of CSF. Hitting a vertebral sinus will not prevent getting
a clear CSF sample on a subsequent attempt, as these
structures are extradural. If blood-tinged CSF is
observed initially, it may clear after several drops if it is  97 The anatomical landmarks for lumbar CSF
due to injury to a subarachnoid vessel; it can then be acquisition. The L6 spinous process can be found just
collected. If the blood tinge does not clear, it is probably cranial to the wings of the ilium. For an L5/L6 lumbar
a result of the disease process and the CSF should be col- puncture, the needle is inserted craniomedially towards
lected for analysis. Once an adequate amount of CSF has the L5/L6 interarcuate space delineated by the caudal
been collected, the needle can be slowly withdrawn. edge of the L5 lamina and the cranial edge of the L6
Certain disease processes can obliterate the CMC or lamina.
increase the viscosity of the CSF to the extent that it will
not flow and may not even appear in the hub of the
needle. The clinician must be aware of this possibility and
not insert the needle too far while waiting for the CSF to
appear in the hub. In cases where a CMC sample cannot
be obtained, a lumbar puncture can be performed instead.

Lumbar collection
Lumbar puncture is technically more difficult than that its dorsum is close and parallel to the edge of the
CMC puncture and is more often associated with blood table. The hindlimbs are flexed as much as possible. The
contamination. The site for lumbar puncture is L5/L6 L6 spinous process is palpated just cranial to the wings of
(or L4/L5) in dogs and L6/L7 (or L5/L6) in cats. The the ilium. It is much more prominent than the smaller L7
area is clipped and aseptically prepared. The patient spinous process caudally (97).
should be positioned in right lateral recumbency (can be The needle is inserted, with the stylet left in place,
in left lateral recumbency for a left-handed person) so over the centre of the spinous process of L6 if attempting
 124 ADMISSION AND NEURODIAGNOSTIC TESTS

a b

c d

to reach the L5/L6 space and advanced until it hits the  98 Placement of the spinal needle into the lumbar sub-
spinous process (98a). The needle tip is then moved arachnoid space is depicted in this sequence. (a) The
slightly laterally so that it can be ‘walked’ down the spinal needle is positioned on top of the dorsal spinous
spinous process until it hits the dorsal lamina (98b). It is process of L6 following manual localization of this process
subsequently advanced at a 45º angle with the needle using the wings of the ilium. (b) The spinal needle is
point directed cranially remaining against the spinous ‘walked down’ the lateral aspect of the spinous process
process (98c). When correctly positioned, the needle typ- until it reaches the dorsal lamina of the vertebra. (c) The
ically passes through the interarcuate and yellow liga- needle is then angled cranially and slightly medially while
ment; this feels as if the needle is going through rubber. advancing cranioventrally. (d) The needle will move
This step is performed ‘by feel’ and multiple attempts through the soft tissues of the interarcuate ligament and
may be necessary to achieve the correct angle of inser- should be advanced until it hits bone, which should be the
tion. If the needle hits bone while being advanced, it may floor of the vertebral canal.
be redirected cranially or caudally, moving the needle off
the bone into interarcuate space while remaining along-
side the spinous process. This may lead to bending of the
needle, so a 20-gauge needle is often required in larger lumbar subarachnoid space. If CSF does not appear, the
dogs (2.5 or 3.5 inch). If it is no longer possible to visual- needle can be withdrawn slightly off the floor of the canal
ize the tip of the needle in relation to the anatomy, the or carefully turned while in place.
needle should be withdrawn for a new attempt. If blood appears, the needle should be withdrawn
The needle will pass through the yellow ligament and and a new attempt made. If blood-tinged CSF appears,
the cauda equina/caudal spinal cord. The latter often it may clear in a few drops. If the blood tinge does not
results in a tail or leg twitch seen or felt by the holder. clear, it is probably part of the disease process and the
The needle is advanced to the floor of the vertebral canal CSF should be collected. Complications of passing the
(98d). When the stylet is removed, CSF flow is observed, needle through the caudal spinal cord and nerve roots
which is the only reliable sign of a successful puncture. are occasionally reported, but this procedure can cause
CSF may be collected from either the dorsal or ventral intradural or intramedullary haemorrhage.
 C E R E B R O S P I N A L F L U I D A N A LY S I S 125

SAMPLE HANDLING STANDARD ANALYSIS TECHNIQUES

CSF should be collected into an empty sterile container. Standard tests performed on CSF include its gross
If infection is suspected, CSF can be collected into physical appearance (colour and turbidity), quantita-
culture medium or a culturette swab can be used to take a tive analysis (RBC count, total nucleated cell count
sample out of a sterile container. (See Standard analysis [TNCC] and protein concentration) and cytological
techniques, for samples that are to be analysed in-house analysis (leukocyte distribution and characterization in
rather than sent to a commercial laboratory.) addition to the presence of other cells or infectious
If analysis is going to be delayed by more than an agents). Normal values for these tests are given in
hour, ideally at least two aliquots of CSF should be Table 24. Ideally, CSF should be sent to a commercial
collected: one for analysis of protein, other analytes and laboratory with the necessary equipment to perform
cell counts; and one for cytological analysis. Because of these tests, established reference intervals and clinical
the typically low protein content of CSF, the cells in a pathologists experienced at interpreting cytological
sample are labile and short-lived once collected, which preparations. However, if this is not possible, many if
can significantly alter the differential cell count and not all of these tests can be approximated using stan-
reduce the usefulness of the test. Samples with a high dard equipment in most clinics, with the caveat that
protein content (>50 mg/dl) are unlikely to be affected cell counts and cytological analysis of CSF require
by 8–12 hours of storage without a stabilizing agent, but practice. The cytological appearance of various cell
because the protein content is unknown at the time of types is beyond the scope of this book, so the reader is
collection, a stabilizing agent is recommended. Alterna- directed to other sources (see Further reading).
tively, slides can be prepared using one of the tech-
niques described below and mailed to a laboratory for Macroscopic evaluation
staining and evaluation. The gross examination of CSF involves assessing it for
Autologous serum (added to achieve a concentration clots and holding the tube against a white background to
of 10%), hetastarch (added 1:1) and EDTA (added 1:1) assess it for colour change; black print should be read
are recommended as stabilizing agents to preserve cell easily through the tube as a test of clarity. Turbidity can
integrity for up to 48 hours after collection. Formalin is occur once the TNCC is in excess of 500/μl.
not recommended as a preservative if cytological analysis
is to be performed; added 1:1 it will suffice for cell count
and protein analysis. If too little CSF is collected to Table 24 Expected normal parameters for CSF
submit two separate aliquots, hetastarch should be used analysis
to preserve the sample. Protein analysis will not be
PARAMETER NORMAL FINDING
affected by the addition of hetastarch as it would by the
addition of autologous serum or EDTA. Colour/clarity Clear and colourless
Samples should be clearly labelled when sent to the
Total protein <25 mg/dl (cisternal)
laboratory so that the dilutional effects of the stabilizing <45 mg/dl (lumbar)
agent can be taken into account when necessary. All
samples should ideally be sent at a refrigerated tempera- Red blood cells Not normally found (excluding
iatrogenic blood contamination)
ture (4ºC).
Total nucleated cell count <5 cells/μl

Differential cell count Small lymphocytes (60–70% in

dogs; 15–30% in cats); monocytes
(30–40% in dogs; 50–80% in
cats); non-degenerated neutrophils
and eosinophils (<2%); other
non-pathologic cells (rare)
126 ADMISSION AND NEURODIAGNOSTIC TESTS

Table 25 Interpretation of urine dipstick Cell counts

readings for CSF protein analysis Erythrocyte counts and TNCCs are most commonly
performed using the standard haemocytometer tech-
DIPSTICK READING PROTEIN CONCENTRATION (mg/dl)
nique. This technique is described in Table 26. The
0 or trace <30 layout of a haemocytometer chamber is shown in 99.
Though the data have not yet been published, coating
+ 30–100
the cells with new methylene blue (100), as described in
++ 100–300 steps 1 to 5 of Table 26, does not affect the cell counts and
+++ 300–2000
makes distinguishing RBCs from WBCs easier. This
creates a very practical and feasible approach to a rapid
++++ >2000 approximation of RBC and WBC counts on an emer-
gency basis.
Leucocytes have a granular, stippled appearance and
are usually larger than erythrocytes. Erythrocytes are
Protein concentration translucent and biconcave; they lack any internal struc-
The concentration of protein in CSF (sometimes tures and may have crenated, spiculated edges. Small
called the microprotein concentration) is very low and lymphocytes can easily be mistaken for erythrocytes by
is comprised almost entirely of albumin. It is normally the untrained eye.
higher in the lumbar sample than the CMC one (see Though it remains the gold standard, the reliability
Table 24). Unlike the cytological analysis, the protein and repeatability of the haemocytometer technique
analysis is not time dependent. Because of its low are not known, as neither the range of possible cell
concentration, specialized techniques and reagents counts obtained from a single sample with repeated
(Coomassie blue or pyrogallol red) are needed for quan- counting nor the inter-observer variability has been
titative protein analysis. The protein concentration in specifically investigated. Newer haematology analysers,
CSF is too low to be quantified using refractometry,
but in-house semi-quantitative approximation of the
protein content of CSF can be performed using a stan-  99 Haemocytometer chamber. (a) A schematic drawing
dard urine dipstick protein pad. (See Table 25 for the of one side of a haemocytometer showing the 9 large
interpretation of urine dipsticks, bearing in mind that squares. (b) Photograph taken at × 20 magnification of the
dipsticks are more efficient at detecting albumin and yellow square seen in 99a. (c) Photograph taken at × 20
may give a false-negative result in cases of increased magnification of part of the red square in 99a; note the
globulins.) Protein can reliably be considered elevated unstained red blood cells seen here (arrows).
based on a dipstick reading of 2+ or greater. (Photos courtesy M Camus)

a b c
 C E R E B R O S P I N A L F L U I D A N A LY S I S 127

a Table 26 Standard haemocytometer technique

for CSF cell counts

Materials required

New methylene blue, non-anticoagulated microhaematocrit

tube, gauze sponges, saline, Neubauer haemocytometer with
cover slip, Petri dish, microscope
b Technique

1 Draw up new methylene blue into a microhaematocrit

tube by capillary action, allowing it to fill one-third of the
tube
2 Blot the loaded end of the tube on a gauze sponge to
empty it, leaving one-third of the tube coated with new
methylene blue
c
3 Fill the non-coated end of the tube by capillary action with
undiluted CSF to about halfway
4 Rock the tube back and forth gently to distribute the stain
5 Incubate the sample in the dye for 1–5 minutes prior to
loading the haemocytometer
6 Fill both chambers of the haemocytometer with CSF
d 7 Allow the cells to settle by placing the haemocytometer in
a humidified Petri dish (a wet gauze included inside a
closed Petri dish will suffice) for 5–15 minutes prior to
counting
8a Examine using the 40x objective lens; count the RBCs and
WBCs separately in all nine squares on the haemocyto-
meter (99) and multiply by 1.1 to obtain the number of
e RBCs and WBCs per microlitre. Do this in both chambers
and average the two results
8b Alternatively, count the RBCs and WBCs separately within
five squares (the four corner squares and the centre
square) in each chamber or side, for a total of ten squares
counted (99). Add up the number of cells in each
chamber to obtain the number of RBCs and WBCs per
microlitre.
f
(From Fry MM, Vernau W, Kass PH et al. (2006) Effects of time,
initial composition, and stabilizing agents on the results of canine
cerebrospinal fluid analysis. Vet Clin Pathol 35:72–77.)

 100 Methylene blue technique (see Table 26). (a) Once

the microhaematocrit tube has taken up the dye, blot the
loaded end of the tube onto a gauze sponge to empty it,
leaving one-third of the tube coated with new methylene
blue. (b) Fill the non-coated end of the tube with
undiluted CSF to about halfway (arrow shows where the
column of CSF ends). (c–f) Rock the tube gently back and
forth to distribute the stain evenly.
128 ADMISSION AND NEURODIAGNOSTIC TESTS

Table 27 Creation of a sedimentation a

technique for cytological analysis
of CSF

Materials required

Standard hole puncher, two binder-type clips, filter paper, glass

microscope slide, 1 ml syringe (plunger removed, cut in half)
(101)
Technique

1 Punch a hole in the middle of the filter paper and place it

on the glass slide
2 Centre the flanged end of the syringe over the hole in the
filter paper
b
3 Clamp the flanges of the syringe barrel onto the
microscope slide using the clips
4 Load 0.25–0.5 ml of CSF into the open end of the barrel
5 Allow the fluid to diffuse for 30 minutes
6 Air dry the slide (do not heat fix)
7 Send the slide to a commercial laboratory or stain with
Romanowsky-type stain (such as Wright–Giemsa) for
in-house examination
c

 101 Sedimentation chamber preparation.

(a) The materials required for sedimentation include
two binder-type clips, filter paper, a glass microscope
slide and a 1 ml syringe (plunger removed and cut in
half). (b) Punch a hole in the middle of the filter paper
and place it on the glass slide. (c) Centre the flanged
end of the syringe over the hole in the filter paper, then
clamp the flanges of the syringe barrel onto the
microscope slide using the clips.

such as the Advia 2120 (Siemens Medical Solutions) and have abnormalities in cell distribution, type or morphol-
Cell-Dyn 4000 (Abbott Diagnostics Division), are ogy. Due to the relatively low numbers of leucocytes in
currently being investigated for their ability to count and CSF, cells must be concentrated in order to make
differentiate the low numbers of cells in CSF. Their slides for microscopic examination. Commercial labora-
results correlate well in most respects with manual tech- tories use cytocentrifugation to concentrate cells,
niques and are less labour intensive. which requires expensive equipment. Sedimentation
techniques are an inexpensive way to prepare slides with
Cytological analysis good cell retrieval, although they do not preserve cell
Every sample of CSF that is collected should be morphology as well as cytocentrifugation. Many tech-
evaluated cytologically, regardless of the TNCC, as a sig- niques for creating a sedimentation chamber have been
nificant percentage of samples with normal cell counts described; one is outlined in Table 27 (101).
 C E R E B R O S P I N A L F L U I D A N A LY S I S 129

NORMAL CEREBROSPINAL FLUID AND Recently, the effect of blood contamination on CSF
IATROGENIC ALTERATIONS samples with a normal TNCC (<5 cells/μl) was studied.
Blood contamination (>500 RBCs/μl) was found to
Normal findings increase significantly the percentage of neutrophils, the
See Table 24 for normal findings of CSF analysis, bearing TP concentration and the presence of eosinophils. It
in mind that reference intervals, especially for protein did not, however, affect the presence of activated macro-
concentration, often vary among laboratories. phages or reactive lymphocytes, suggesting that the pres-
Other cells that may be observed in normal CSF ence of these cells may be a more specific indicator of
include elements of the CNS such as ependymal lining neurological disease in patients with a normal TNCC
cells, choroid plexus cells, meningeal lining cells and, and blood contamination.
rarely, neurons themselves. Haematopoietic cells can
occasionally be present after performing a lumbar punc- Effects of recent myelographic study
ture. These are probably collected from the bone Interpretation of CSF analysis can be challenging when
marrow as the needle is advanced along the vertebra and CSF is collected following the injection of intrathecal
are not a significant finding. Squamous epithelial cells contrast for a myelogram, as the presence of the contrast
can also be seen as a contaminant from the skin. material itself in the subarachnoid space causes a mild
aseptic meningitis. Metrizamide has been shown to cause
Effects of blood contamination a rapid rise and decline in the TNCC count over
CSF normally does not contain erythrocytes; however, 72 hours following myelography, with a large range of
its collection, especially from the lumbar site, commonly peak TNCCs among dogs (from normal to >140 cells/μl)
results in contamination of the sample with peripheral that probably is a reflection of individual variability in the
blood. This may result in grossly red-tinged fluid that reaction to the agent. A study comparing the effects of
clears on centrifugation. Other indicators of pathological iopamidol and metrizamide myelography at 90 minutes
haemorrhage are discussed below (see Interpretation of post myelogram found that both agents caused lepto-
abnormal CSF results, p. 130). meningeal irritation, resulting in a mild neutrophilic/
Contamination with peripheral blood inevitably mixed pleocytosis (median leucocyte count following
affects the quantitative CSF analysis by increasing the iopamidol injection: 12 cells/μl) and little change in TP
erythrocyte count, TNCC and TP concentration. concentration.
Although various ratios have been proposed to account
for the extra leucocytes and protein in the CSF con-
tributed by iatrogenic haemorrhage, one study has
shown these to be unreliable. Typically, no leucocytes
and little to no protein will accompany the many thou-
sands of RBCs resulting from iatrogenic haemorrhage.
However, when the haemorrhage contributes erythro-
cytes in excess of 10,000/μl, these values may be altered
and it is preferable to repeat the procedure. The tap can
be repeated in 24 hours to obtain a new sample.
130 ADMISSION AND NEURODIAGNOSTIC TESTS

Table 28 Gross appearance of CSF

CHANGE POTENTIAL CAUSES

Colour Pink or red Iatrogenic contamination; recent subarachnoid haemorrhage

(within a few hours)

Yellow or yellow-orange Erythrocyte breakdown products from previous haemorrhage

(xanthochromia) (within past 8–14 days); bilirubin from hyperbilirubinaemia or
disrupted blood–brain barrier; markedly increased TP

Clarity Turbid TNCC >500 cells/μl

INTERPRETATION OF ABNORMAL CSF RESULTS Table 29 Causes of CSF albuminocytological

dissociation
Abnormal gross appearance • Intervertebral disc disease or other extradural
See Table 28. compressive lesion*
• Trauma*
Increased total protein • Degenerative myelopathy (normal to mildly increased
Elevation in CSF protein concentration is a sensitive protein)
indicator of CNS disease, but it is the least specific • Ischaemic injury (such as fibrocartilaginous embolism)
causing infarction*
change observed on CSF analysis and accompanies
• Vasculitis or vascular lesion with haemorrhage
increased leucocyte counts virtually every time that
abnormality is seen. The concentration of protein in • Intrathecal globulin production caused by infection
(e.g. canine distemper, FIP)
the CSF can be increased due to abnormalities in
• Neoplasia* (due to intrathecal globulin production,
the blood–brain barrier or to intrathecal globulin interference with blood vessel integrity or necrosis of
production. Albuminocytological dissociation is the term the adjacent parenchyma)
used to describe an elevation in the microprotein • Recent seizure activity
concentration with a normal leucocyte count. This • Polyradiculoneuritis
occurs with diseases that cause intrathecal production of • Inflammatory CNS disease following corticosteroid
protein, obstruct the flow of CSF and allow protein treatment (which decreases the TNCC)*
accumulation, or disturb the blood–brain barrier enough
* Indicates conditions in which the neutrophil percentage of the
to allow protein from peripheral blood to enter the CNS. differential cell count may be increased.
These conditions tend to be non-inflammatory in aetiol-
ogy, though there are exceptions to this generalization.
(See Table 29 for potential causes of albuminocytological Table 30 Differential diagnoses based on total
dissociation.) nucleated cell count alone

Increased total nucleated cell count 5–25 cells/μl Vascular*, trauma*, neoplasia, IVDD*,
syringomyelia, recent seizure activity*
(See Table 30 for a summary of the expected ranges of
TNCC with various categories of disease.) Note 25–50 cells/μl Trauma*, neoplasia, +/- vascular*, IVDD*,
that there is significant overlap and that the differential inflammatory
cell count must be considered in order to maximize the >50 cells/μl Inflammatory (infectious or sterile),
diagnostic yield of CSF analysis. Abnormalities in the less commonly IVDD*, trauma*
differential cell count are described individually below,
* Pleocytosis should resolve by 2–7 days following insult
and potential causes are listed in Table 31. in these conditions.
IVDD = intervertebral disc disease.
 C E R E B R O S P I N A L F L U I D A N A LY S I S 131

Table 31 Disease differentials to consider based on the cytological interpretation of the CSF

Mixed pleocytosis Lymphocytic pleocytosis Neutrophilic pleocytosis Eosinophilic pleocytosis

• GME • Viral encephalitides (other than • Bacterial meningoencephalo- • EME (can be >90%
• Infectious diseases FIP) myelitis eosinophils)
(protozoal, rickettsial, • NME/NLE • SRMA (often >80% • Cryptococcosis (up to
less commonly fungal) • GME neutrophils) 80% eosinophils
• Neoplasia • FIP (can be >70% neutrophils) reported)
• Neoplasia, especially
• Trauma lymphoma • Neoplasia (can be >90% • Protozoal infections

• Intervertebral disc disease • Protozoal or fungal infections neutrophils) • Parasitic migration

• Fungal infection (Baylisascaris, Cuterebra,
• Fibrocartilaginous • Infarction Angiostrongylus)
embolism • Intervertebral disc disease • Infarction
• Intervertebral disc
• Less commonly, other infectious • Protozoal infections
disease
diseases (Ehrlichia canis or • Trauma/haemorrhage
• Uncommonly, GME
bacterial infection, especially • Acute intervertebral disc
following antibiotic therapy), disease
SRMA, parasitic migration or
• Rarely, GME (>60% neutrophils
feline polioencephalomyelitis
have been reported)

GME = granulomatous meningoencephatitis; FIP = feline infectious peritonitis; NME = necrotizing meningoencephalitis;
NLE = necrotizing leucoencephalitis; SRMA = steroid responsive meningitis–arteritis; EME = eosinophilic meningoencephalomyelitis.

In a mixed pleocytosis, no single cell type predomi-

nates (102); it contains a mixture of mostly lymphocytes
and large mononuclear cells, with smaller numbers of
macrophages, neutrophils and, occasionally, plasma cells
and eosinophils. Numerous conditions can be associated
with a mixed pleocytosis, the most notable being GME,
in which the cell counts are often markedly elevated
(average 800 cells/μl in one study).
A lymphocytic pleocytosis is characterized by an
elevated TNCC with >50% lymphocytes. It is the most
common form of mononuclear pleocytosis and usually
consists of a majority of small, mature lymphocytes, with
smaller numbers of reactive lymphocytes and larger
monocytoid cells. It occurs commonly in cases of viral
disease, notably canine distemper virus, in which the cell
count is typically <50 cells/μl, but it can also be associat-
ed with other chronic CNS infections. Necrotizing  102 Mixed pleocytosis. Small lymphocytes (red arrow),
meningoencephalitis (NME) and necrotizing leuco- monocytes (yellow arrow) and a neutrophil (black arrow)
encephalitis (NLE) cause a strongly lymphocytic (>80%) can be seen. (Wright–Giemsa; × 100 objective)
pleocytosis with a moderately to markedly elevated cell (Photo courtesy M Camus and E Cienava)
count. Rather than being mixed, the pleocytosis in GME
frequently has a predominance of lymphoplasmacytic
cells.
 132 ADMISSION AND NEURODIAGNOSTIC TESTS

A neutrophilic pleocytosis is defined as an elevated neutrophilic pleocytosis, but various other tumour types
TNCC with a predominance of neutrophils (103). can cause this change. Degenerate neutrophils may
However, diseases known to cause neutrophilic pleocy- or may not be observed in cases of bacterial infection
tosis should be considered when neutrophils constitute (104).
>2% of the nucleated cells whether or not neutrophils are While the presence of eosinophils in the CSF in the
the predominant cell type. In general, when there is a absence of significant peripheral blood contamination
very high nucleated cell count and neutrophils are the is not normal, it is often a non-specific change.
predominant cell type present, suppurative inflammatory A differential cell count with >10–20% eosinophils is
processes (e.g. steroid responsive meningitis–arteritis considered an eosinophilic pleocytosis (105). This
[SRMA], bacterial or fungal meningoencephalitis/ is an uncommon finding and has been associated with
meningoencephalomyelitis) must be considered. A mild an eosinophilic meningoencephalomyelitis (EME) of
to moderate neutrophilic pleocytosis can be associated unknown aetiology in both dogs and cats, aberrant para-
with acute inflammatory disorders, including trauma, sitic migration, various infectious agents (particularly
post-myelographic aseptic meningitis, encephalitis of protozoa and fungi) and, rarely, intervertebral disc
unknown aetiology, haemorrhage, necrosis, infarction disease (IVDD). The TNCC can be markedly elevated
and neoplasia. Historically, meningiomas (especially (>1000 cells/μl) in cases of EME, cryptococcosis and
those in the caudal fossa) have been associated with a Baylisascaris migration.

b
 103 Neutrophilic pleocytosis. (Wright–Giemsa; × 40
objective) (Photo courtesy R Di Terlizzi)

 104 (a) Degenerative neutrophilic pleocytosis in CSF,

with intracytoplasmic organisms evident (arrows). (× 40;
Photo courtesy M Camus and E Cienava); (b) Atlanto-
occipital CSF from a dog with bacterial meningitis. The
cytocentrifuge sample revealed a degenerate neutrophil.
Associated with the karyolitic neutrophil, small rod-shaped
bacteria are present intracellularly and often within intra-
cytoplasmic phagosomes. (Wright–Giemsa; × 100
objective) (Photo courtesy R Di Terlizzi)
 C E R E B R O S P I N A L F L U I D A N A LY S I S 133

Other cytologic abnormalities

Macrophages can be found in CSF and represent a
non-specific reaction to inflammation, haemorrhage or
degeneration. They may be vacuolated and may contain
phagocytosed cells or infectious agents. The presence of
erythrophagocytosis indicates pathological rather than
iatrogenic haemorrhage (106). Plasma cells can also rep-
resent a non-specific inflammatory response. They are
most often seen in cases of GME, but can also be present
in NME and various infectious diseases.
Infectious agents themselves can occasionally be
visualized on a cytospin preparation. These include bac-
 105 Eosinophilic pleocytosis. Three eosinophils teria, fungal elements, Ehrlichia morulae, protozoa and
and one erythrocyte are present in this image from a distemper inclusion bodies. Cryptococcus, being a gen-
dog with immune-mediated eosinophilic meningitis. erally surface-oriented fungus, has reportedly been
(Wright–Giemsa; × 40 objective) (Photo courtesy observed in the CSF in the majority of cases of CNS
R Di Terlizzi) infection; if suspected, India ink preparations aid in the
visualization of the organism (107).

b
 106 Erythrophagocytosis. The cell in the centre of
the field contains red blood cells. (Wright–Giemsa; × 40
objective) (Photo courtesy M Camus and E Cienava)

 107 (a) This sample contains a cluster of

basophilic-staining extracellular yeast forms consistent
with Cryptococcus spp. (Wright–Giemsa; × 100 objective)
(b) Same sample stained with India ink. (Photos courtesy
R Di Terlizzi)
 134 ADMISSION AND NEURODIAGNOSTIC TESTS

It is uncommon to find neoplastic cells in the CSF. Glucose and protein assays
Neoplasia reported to exfoliate into the CSF includes Depending on the reference laboratory, CSF glucose
lymphoma (108), choroid plexus carcinoma and malig- concentration may be measured as part of a routine
nant histiocytosis. Neural elements can also occasionally analysis; it can also be measured using a standard gluco-
be seen in the CSF. Myelin may be seen (either phago- meter. The concentration of glucose in the CSF depends
cytosed inside macrophages or as free myelin, also called in large part on the serum glucose concentration, so this
myelin fragments) in cases of myelomalacia or demyeli- should be measured simultaneously. Glucose levels in the
nating conditions such as degenerative myelopathy. CSF should be between 60% and 80% of the serum
In cases of lysosomal storage diseases, large inclusions glucose, although there is an approximately 1–2 hour
can be found in CSF mononuclear cells; the appearance delay before acute changes in serum glucose are reflected
of the inclusions depends on the accumulated metabolic in the CSF. Decreased glucose concentration in the CSF
product. (hypoglycorrhachia) is observed most commonly in cases
of bacterial meningitis.
ADDITIONAL TESTS Increases in CSF protein result from increased
permeability of the blood–brain barrier, intrathecal glob-
An increasing number of supplemental tests is available ulin production, or both. To discern the mechanism, the
to perform on CSF. This includes tests for CSF glucose protein in CSF can be further analysed for the albumin
and globulin levels, tests for specific infectious diseases quotient, which detects disruptions in the blood–brain
and newly developed tests whose clinical usefulness is still barrier, and for increased globulins, which indicates
to be determined. intrathecal production. The percentages of albumin and
alpha-, beta- and gamma-immunoglobulins (Ig) in CSF
can be measured by protein electrophoresis. These tech-
niques and the interpretation of the results are discussed
in detail elsewhere. Enzyme-linked immunosorbent assay
(ELISA) tests have also been developed to quantify the
IgG, IgA and IgM content of the gammaglobulin fraction
within the CSF, and accumulation of these substances has
been associated with inflammatory CNS conditions. Of
particular interest is that CSF levels of IgA are highest in
patients with SRMA. These levels remain elevated during
treatment and in the event of remission. While not entire-
ly specific, the combination of elevated CSF and serum
IgA is a very sensitive indicator of SRMA and may be a
useful diagnostic test if clinical suspicion of the disease is
high, but the standard CSF analysis is normal.

Infectious disease testing

Screening for infectious diseases is often a critical step in
the assessment of neurological disease, especially since
the clinician frequently has to decide in the face of an
inflammatory process between treating a patient with an
immunosuppressive or an antimicrobial drug regimen.
 108 Atlanto-occipital CSF from a 9-year-old Labrador Based on the signalment, history, geographic location,
Retriever. Medium to large lymphocytes can be seen with physical and neurological examination findings and
immature chromatin, prominent nucleoli and basophilic, results of other diagnostic tests, a list of possible infec-
often vacuolated, cytoplasm. (Wright–Giemsa; × 100) tious diseases can be made and the appropriate tests
(Photo courtesy R Di Terlizzi) selected (see Chapter 19).
 C E R E B R O S P I N A L F L U I D A N A LY S I S 135

Table 32 Infectious disease testing on CSF samples

INFECTIOUS AGENT ANTIBODY TITRES ANTIGEN TITRES PCR

Canine distemper virus + +

Feline infectious peritonitis + + (low sensitivity)

Brucella canis + + +

Ehrlichia canis + +

Rickettsia rickettsii + +

Toxoplasma + +

Neospora + +

Cryptococcus + (highly sensitive and specific)

Blastomyces +

Aspergillus + (false negatives possible;

many dogs are seropositive)

Coccidiomyces + (low sensitivity)

Histoplasma + (low sensitivity and specificity)

In general, aerobic and anaerobic culture of CSF is Antibody coefficient

performed if there is a suspicion of bacterial meningoen- disease-in-question antibody in CSF
=
cephalomyelitis; however, this is an insensitive test, as disease-in-question antibody in serum
false-negative results occur in over 70% of cases. Fungal
culture (especially for Cryptococcus) and virus isolation non-CNS disease antibody in serum
×
can also be performed on CSF, but have largely been non-CNS disease antibody in CSF
replaced by antigen or antibody titres and polymerase
chain reaction (PCR) testing. CSF antibody titres are Coefficients >1 provide evidence for intrathecal produc-
thought to be more reliable than serum titres for diag- tion of antibodies against the disease in question. PCR
nosing infectious disease within the CNS. To distinguish assays have been developed for many infectious agents
true intrathecal antibody production from contamina- affecting the CNS, and while these are valuable tests,
tion of the CSF with antibodies from the peripheral they are neither 100% sensitive nor specific and should
blood that may be present in the event of a compromised be used in combination with other diagnostic tests when
blood–brain barrier, the antibody coefficient can be possible. (See Table 32 for currently available diagnostic
calculated. This allows for the presence of blood-derived tests that can be performed on CSF for the detection of
antibodies by normalizing the titre for the disease under common CNS pathogens.)
investigation against the titre for a disease that does not
affect the CNS (e.g. canine adenovirus or parvovirus).
 136 ADMISSION AND NEURODIAGNOSTIC TESTS

Table 33 CSF analytes of possible future clinical significance

CSF ANALYTE RELEVANCE

Myelin basic protein Used as a marker of demyelination; may be useful in antemortem diagnosis of
degenerative myelopathy

Glutamate Elevated in dogs with acute and chronic spinal cord compression caused by IVDD;
excitotoxicity may play a role in secondary spinal cord injury and therefore become a
therapeutic target. Elevated in dogs with idiopathic epilepsy; may indicate that chronic
overexcitation caused by elevated glutamate levels contributes to the pathogenesis of
idiopathic epilepsy

Matrix metalloproteinase-9 Elevated during the first 24 hours following acute spinal cord injury caused by IVDD and
varies directly with severity of neurological deficits; may have prognostic significance or
present a therapeutic target

Beta-2-microglobulins Sensitive indicator of inflammation in IVDD; may be useful as a prognostic marker.

Markedly elevated in dogs with inflammatory CNS disease; may be useful for diagnosing
the cause of inflammation or monitor disease progression

IVDD = intervertebral disc disease; CNS = central nervous system.

Assays under investigation

Many CSF analytes are being studied both for their performed on tissues such as bone marrow, cavity fluids,
potential to expand our understanding of the pathogene- peripheral blood and lymph node, the reported
sis of various diseases and injuries and for their potential sensitivity is 75% for dogs and 65% for cats, and the
clinical usefulness. Several of these analytes and their reported specificity is 94%. However, the sensitivity and
area of relevance are listed in Table 33. One test that has specificity for this test when performed on CSF are
recently been validated and is commercially available is currently unknown and may be lower than for other
the PCR for antigen receptor rearrangement (PARR) for tissues because of the typically low cellularity of CSF.
the detection of lymphoid neoplasia. The goal of this test An inadequate number of cells in a sample may prevent a
is to distinguish a clonal neoplastic population of clonal arrangement from being detected, leading to a
lymphocytes from a genetically diverse population (as false-negative result, and an insufficient number of
could occur with lymphoid hyperplasia or response to an lymphocytes may make a heterogeneous population
antigenic stimulus). PCR primers direct replication of appear clonal, leading to a false-positive result. It is also
surface portions of the T-cell and B-cell receptors on not known how or whether the TNCC of a CSF sample
lymphocytes. The test can be performed on a variety of affects the test’s reliability. Further research is needed to
tissue samples, including CSF; however, its sensitivity understand the utility of this test in detecting lympho-
depends on the nature and cellularity of the tissue. When proliferative diseases in the CNS.
PART 2

DECISION MAKING 137

CHAPTER 6 Obtundation, stupor and coma

CHAPTER 7 Seizures

CHAPTER 8 Exercise-associated weakness and collapse

CHAPTER 9 Ataxia

CHAPTER 10 Acute paresis and paralysis

CHAPTER 11 Spinal pain

CHAPTER 12 Acute blindness

CHAPTER 13 Acute tremors and involuntary movements

CHAPTER 14 Head tilt and nystagmus

CHAPTER 15 Acute disorders of the head and face

CHAPTER 16 Monoparesis and neurological causes of lameness

This page intentionally left blank
 DECISION MAKING Chapter 6

OBTUNDATION, STUPOR AND COMA

139

Peter Dickinson

INTRODUCTION abnormal, within that environment. As such, familiarity

with the range of normal responses of cats versus dogs,
Assessment of the level of consciousness of an animal is young animals versus old animals and highly active
one of the most important and, often, most neglected, breeds such as terriers versus less active giant breeds is
components of the neurological examination. Alterations important in the assessment of mentation.
in consciousness are usually reflective of diseases, or Inappropriate behaviour or a decreased level of
exposure to substances, that result in dysfunction of the consciousness is a strong indicator of intracranial disease;
brainstem and/or the cerebrum. Alterations may be acute however, severe systemic disease, such as cardiorespira-
or chronic in nature and may vary from subjectively tory insufficiency, metabolic disease and exposure to
subtle alterations to profound dysfunction. Alterations exogenous toxins, can also result in secondary effects
may also result in changes in quality of mentation that produce similar if not identical clinical signs. When
(e.g. inappropriate behaviour) as well as changes in combined with other findings of the neurological exami-
absolute levels. Assessment of consciousness is based on nation, appropriate localization of neurological disease
an animal’s responses, either appropriate or inappropri- and formation of an appropriate differential list and diag-
ate to its environment, and stimuli, both normal and nostic plan become possible (Table 34).

Table 34 Differential diagnoses for obtundation, stupor and coma

DISEASE MECHANISM DOGS CATS

Vascular Brain infarct Brain infarct

Brain haemorrhage Brain haemorrhage
Hypertension Hypertension
Feline ischaemic encephalopathy
(Cuterebra migration)

Inflammatory/infectious Infectious encephalitis (distemper, Toxoplasma, Infectious encephalitis (Toxoplasma,

Neospora, fungal, bacterial, rickettsial, rabies)* bacterial, FIP, Cryptococcus, rabies)*
Meningoencephalitis of unknown aetiology Meningoencephalitis of unknown aetiology
(GME, necrotizing)* (presumed immune mediated); rare

Trauma Head trauma* Head trauma*

Toxic Anticoagulants (secondary haemorrhage) Anticoagulants (secondary haemorrhage)

Ivermectin Ivermectin
Hexachlorophene Hexachlorophene
* Common cause

(Continued)
140 DECISION MAKING

Table 34 Differential diagnoses for obtundation, stupor and coma (continued)

DISEASE MECHANISM DOGS CATS

Toxic Barbiturates Barbiturates

Ethylene glycol* Ethylene glycol
Lead Lead
Metaldehyde Metaldehyde
Theobromine (chocolate)* Theobromine (chocolate)
Opioids Opioids
Phenothiazine tranquilizers Phenothiazine tranquilizers
Recreational drugs Recreational drugs
Anticonvulsants Anticonvulsants

Anomalous Hydrocephalus* Hydrocephalus

Metabolic Hypoxia/ischaemia* Hypoxia/ischaemia*

Syncope (transient) Syncope (transient)
Excitotoxicity (post ictal) Excitotoxicity (post ictal)
Hepatic encephalopathy* Hepatic encephalopathy
Uraemia Uraemia
Hyperthermia Hyperthermia
Osmotic abnormalities (Na+ imbalance) Osmotic abnormalities (water intoxication)
Hypoglycaemia* Hypoglycaemia
Ketoacidosis* Ketoacidosis
Hypoadrenocortical crisis
Hypothyroidism

Idiopathic Narcolepsy

Neoplastic Primary or metastatic brain tumour* Primary or metastatic brain tumour*

Nutritional Thiamine deficiency Thiamine deficiency

* Common cause

NEUROANATOMICAL BASIS both the spinal cord and the brainstem, and projects this
information diffusely to the cerebral cortex via the thal-
The reticular formation is composed of a network of amus (109). The ascending reticular formation arouses
both ascending and descending neurons and forms both all areas of the cerebral cortex, resulting in a normal level
the most primitive, and the most extensive, component of consciousness. Because of this the ascending reticular
of the neuraxis in all mammals. On an evolutionary basis, formation is referred to as the reticular activating system
it corresponds to the basic nerve networks of inverte- (RAS). The true seat of consciousness is the cerebral
brates and primitive vertebrates. The ascending compo- cortex; however, the RAS is critical for adjusting the level
nent of the reticular system forms a diffuse midline of cerebral activity, and damage to either area or inter-
system and receives input from all sensory modalities ruption of the communication between the RAS and the
(except muscle and joint proprioception) at the level of cerebrum will result in abnormal levels of mentation.
 O BTUNDATION , S TUPOR AND C OMA 141

The rostral pons and caudal midbrain in the NEUROLOGICAL EVALUATION

brainstem are particularly important areas in their
contribution to the RAS and are important in mediating The first component of a complete neurological
the effects of CNS depressants and stimulants. examination consists of general observations, including
Sleep, which represents a physiologically normal assessment of the level of mentation and behaviour
decrease in the level of consciousness, is a complex exhibited by the animal. If possible, an animal should be
process involving neuronal systems in the medulla, pons allowed to move around the examination room freely so
and midbrain that under normal circumstances have that its response to both the local environment and the
generally inhibitory actions on the RAS. Normal sleep people present can be assessed. This may be accom-
can be characterized, in some phases, by the presence of plished while the examiner is obtaining the pertinent
synchronous neuronal activity of cortical neurons on an history and presenting problems from the owner.
electroencephalogram (EEG). Input from the RAS Mental status may be categorized as:
typically disrupts this synchrony (i.e. desynchronizes the • Bright and alert (normal).
cortex), resulting in arousal. • Obtunded: conscious, but with reduced activity and
responsiveness to environmental stimuli. There
may be an increased tendency to sleep when not
stimulated. This is a non-specific finding, as it may
result from systemic disease as well as CNS disease.
• Stuporous: sleeps or is unresponsive to innocuous
stimuli such as noise, but will respond to painful
stimuli. Both obtundation and stupor may be
further classified subjectively as mild, moderate or
 109 Schematic representation of the ascending severe. This results from a disease diffusely
reticular activating system (ARAS). The spinal cord affecting both hemispheres and/or the brainstem.
somatosensory pathways, as well as the sensory • Comatose: state of unconsciousness. Cannot be
component of cranial nerves I, II, V, VIII, IX and X, aroused even with painful stimuli, although some
project onto the brainstem reticular formation. simple reflexes may be present. This also results
The latter, in turn, diffusely activates the cerebral from a disease diffusely affecting both hemispheres
cortex to maintain a state of consciousness. and/or the brainstem.

Ascending neural radiations Cerebral cortex

to cerebral cortex Corpus callosum
Thalamus
Cerebellum
Reticular formation

Neural input Spinal cord

CN I somatosensory pathways

CN II
CN V Brainstem
CN VIII
CN IX & X
 142 DECISION MAKING

Terms such as depression and delirium should generally loss of placing reactions and seizures. Mild tetraparesis
be avoided when describing animals with altered menta- may be present; however, animals are often non ambula-
tion, since their definition requires an assessment of cog- tory. Common causes reflect the diffuse localization and
nition and emotion. include metabolic disease, hypoxia/ischaemia (e.g.
Additional observations that can be made during this secondary to status epilepticus or hyperthermia) intoxi-
period include inappropriate behaviour (aggression, cations and any severe focal disease that results in
fearlessness, ignoring specific stimuli), compulsive secondary global increases in ICP (e.g. a space-occupying
behaviour, pacing, circling and head pressing (110, 111). mass with peri-lesional oedema or hydrocephalus).
Any or all of these findings are suggestive of intracranial
disease affecting the forebrain (cerebrum and thalamus), Disease restricted to one cerebral hemisphere
and may be found coincidentally with a decreased level Any disease predominantly affecting one cerebral hemi-
of consciousness. sphere usually results in obtundation +/- contralateral
visual and menace deficits, contralateral loss of placing
Diffuse or multifocal disease of the cerebral cortex reactions, mild contralateral hemiparesis, circling
In general, diffuse or multifocal disease of the cerebral towards the side of the lesion and seizures. The more
cortex results in obtundation or stupor, although very focal localization resulting in the lateralizing signs is
severe disease with an acute onset may occasionally result suggestive of less diffuse disease processes including
in coma. Additional neurological deficits reflect the intracranial neoplasia, trauma, focal infectious/inflam-
diffuse cortical localization and may include bilateral matory disease and focal vascular disease such as
visual and menace deficits with normal PLRs, bilateral infarction or haemorrhage.

 110 Head pressing and getting ‘stuck’ in corners are  111 A decreased gag reflex is commonly seen in
typical signs in animals with extensive forebrain lesions severely stuporous and comatose animals and intubation
and elevated intracranial pressure. to protect the airways is recommended. Intensive nursing
may be required.
 O BTUNDATION , S TUPOR AND C OMA 143

a b

 112 Signs of brainstem damage. (a) Decerebrate

posture in a cat with rigid extension of the neck and limbs.
(b) Sagittal T2-weighted MR image. This intracranial
meningioma is causing raised intracranial pressure, which
has resulted in caudal transtentorial herniation with
compression of the cerebellum and underlying brainstem,
as well as herniation of the cerebellar vermis through the
foramen magnum. (c) Transverse T2-weighted MR image
of the brain showing a large rostrotentorial meningioma,
which has caused a dramatic mass effect with deviation of
midline structures.

Disease affecting the brainstem

Brainstem disease may result in altered consciousness Brainstem lesions are more likely to result in signifi-
ranging from obtundation to coma depending on the cant paresis compared with cerebral disease, and if
severity of the disease. Most cases of coma result from lesions are severe and involve the midbrain, a decerebrate
damage to the brainstem, particularly the rostral brain- posture may be seen. Decerebration typically results
stem, with disruption of the RAS or its projections to the from functional separation of the cerebrum from
cerebrum. Structural disease affecting the rostral brain- the brainstem, but may occur less commonly due to
stem will also often result in pupillary abnormalities, diffuse destruction of the cerebrum bilaterally. Signs
including anisocoria (see Chapter 15), and, as severity include coma, rigid extension of all limbs and opistho-
increases, pupils often progress from miotic to unrespon- tonus (extension of the neck and spine) (112). Common
sive and mydriatic. Loss of physiological nystagmus and causes of brainstem disease reflect the more focal local-
decreased gag reflex are commonly seen; however, these ization and include trauma, transtentorial herniation sec-
may also be present with more diffuse disease, particular- ondary to elevated ICP, neoplasia, vascular disease and
ly when there is elevated ICP. inflammatory/infectious disease.
144 DECISION MAKING

Examination pitfalls associated with altered levels • Behaviour and mentation should be interpreted in
of consciousness the context of age and species-dependent normals.
Assessment of altered consciousness can be a subjective • Animals with severe pain and/or fear may present
process, particularly when animals are only minimally for apparently altered mentation.
affected and are judged to be mildly or moderately • Acute loss of vision and/or hearing will often result
obtunded. It is not always possible to determine in apparently altered mentation and decreased
whether an animal is truly obtunded or has an appar- interaction with the animal’s environment.
ently altered level of consciousness due to other factors, • Post-ictal animals can exhibit a wide variety of
some of which are listed below. It is important to abnormalities including altered levels of conscious-
remember that there may be primary neurological ness. (However, prolonged status epilepticus may
disease resulting in altered consciousness (e.g. trauma result in diffuse cortical necrosis secondary to a
or neoplasia), systemic disease resulting in secondary hypermetabolic state and hypoxia.)
alteration of neurological function (e.g. metabolic/toxic • Always be aware of potential exposure to
disease) and, importantly, other conditions where the medications/drugs, either prescribed or otherwise,
outward behavioural manifestations may mimic an that can have profound effects on levels of
altered level of consciousness. There may also be a consciousness.
combination of these factors. Additional neurological • Transient alterations in level of consciousness
abnormalities may help to confirm a primary neurolog- may be seen with specific conditions
ical disease in origin; however, it is often necessary to (e.g. narcolepsy/cataplexy) and with syncope and be
rule out systemic disease and other potential causes of associated with systemic tumours such as
‘lethargy’ rather than true obtundation. Repeating the insulinomas and pheochromocytomas.
neurological examination over a period of time in dif-
ferent environments will help to define the true origin SPECIFIC DIAGNOSTIC TESTS
of the abnormal findings.
The following factors should be considered when Systemic and metabolic diseases are a major cause of
assessing animals with apparently decreased responsive- either true or apparently decreased levels of mentation in
ness to external stimuli: many animals. A thorough physical examination and
• Animals with debilitation due to severe systemic minimum database should be done in these patients prior
disease such as sepsis, uraemia, hypoglycaemia and to pursuing specific neurodiagnostic procedures.
other severe metabolic or endocrine disorders may The choice of specific neurodiagnostic techniques
present with lethargy rather than true decreased depends on the most likely underlying cause and location
levels of consciousness, although concurrent of the lesion (113). Although some diagnostic techniques,
secondary neurological effects are possible. such as advanced imaging, may be indicated to investi-
Similarly, post-traumatic complications, such as gate potential intracranial disease, the overall medical
hypotension, hypothermia and hypoxia, may result condition of the patient must be assessed and the risks
in apparent or true alterations in consciousness. and benefits calculated, particularly when GA is required
Correcting any underlying systemic abnormalities is (e.g. head trauma patients). Advanced imaging and other
essential before specifically investigating primary diagnostic procedures may be possible in the non-
neurological causes. anaesthetized animal if they are already stuporous or
comatose.
 O BTUNDATION , S TUPOR AND C OMA 145

 113 Stepwise diagnostic approach to altered

Decreased level of level of consciousness.
consciousness

Other deficits consistent

NO YES
with neurological disease

Rule out non-neurological

causes: debilitating systemic
disease, cardiorespiratory Focal, localizing
disease, pain, fear, behavioural NOT PRESENT neurological signs
abnormalities, (blind/deaf),
post ictal

PRESENT YES NO

Consider structural CNS disease:

Consider metabolic/toxic disease,
trauma, neoplasia, vascular,
hypoxia, elevated ICP,
infectious or inflammatory
diffuse cerebral disease
CNS diseases

Minimum database
(toxic history)

NO
METABOLIC/TOXIC METABOLIC/
DISEASE TOXIC DISEASE

Advanced imaging,
CSF analysis, EEG, BAER,
serology

Treat underlying structural Treat metabolic/toxic disease

Address alternative cause brain disease (medical, (endocrine, renal, hepatic,
surgical) electrolyte, nutritional)
 146 DECISION MAKING

a b

 114 (a) A comatose 1-year-old Domestic Shorthair cat presented following head trauma secondary to a dog attack 2
days previously. There was no response to a painful stimulus applied to the digit, and the cat had fixed and dilated pupils
that were unresponsive to light. T1-weighted transverse (b), T2-weighted transverse (c), T2*-weighted transverse (d)
and T2-weighted sagittal MR images (e) revealed a large poorly circumscribed lesion within the midbrain, consistent
with haemorrhage and perilesional oedema associated with vermal herniation (arrows). The imaging characteristics of
T1 isointensity, T2 hypointensity and marked T2* hypointensity would be consistent with deoxyhaemoglobin, typically
seen around 1–3 days post haemorrhage. Diffuse damage to the RAS and CN III (oculomotor) nuclei are consistent with
the loss of parasympathetic input to the eyes and the altered level of mentation. Fluid and soft tissue accumulation
present within the left bulla was reflective of haemorrhage from the external ear at presentation (arrows in b and d).
 O BTUNDATION , S TUPOR AND C OMA 147

The specific diagnostic tests for obtundation, stupor In a comatose animal:

and coma are described below: • ‘Flat’ EEG plus loss of BAER/SSEP and MLAER
• Magnetic resonance imaging. MRI is the imaging is evidence of cerebral and brainstem death (115,
modality of choice in most cases to help elucidate see next page).
structural disease of the CNS parenchyma resulting • ‘Flat’ EEG with loss of SSEP/MLAER and preser-
in decreased mentation (114). vation of BAER suggests cerebral disease with
• Computed tomography. CT is particularly useful preservation of brainstem function.
for investigation of head trauma where calvarial • Normal EEG with loss of BAER/SSEP and
fractures are suspected. It is also the imaging MLAER suggests brainstem disease with preserva-
modality of choice for determining the presence of tion of cerebral function.
acute haemorrhage (e.g. subdural haematoma),
although most MRI scanners are able to detect this COMMON CAUSES OF OBTUNDATION,
with gradient echo (T2*) sequences by the time STUPOR AND COMA
imaging is undertaken.
• CSF analysis. This should be undertaken with great Cerebrovascular accidents (Chapter 17), meningo-
care in animals with suspected intracranial disease, encephalitis (Chapter 19), head trauma (Chapter 20),
but it may help to determine underlying causes of brain tumours (Chapter 26), metabolic encephalopathies
disease. Collection is preferably done following (Chapter 27) and toxic encephalopathies (Chapter 28)
advanced imaging so that the presence of mass are described in detail elsewhere in the book.
lesions and/or brain herniation can be assessed.
• Brainstem auditory evoked response (BAER). Hydrocephalus
Assessment of the central auditory pathway allows Overview
indirect assessment of overall brainstem function. Hydrocephalus is active distension of the ventricular
Complete loss of BAER is a poor prognostic system of the brain resulting from inadequate passage of
indicator in comatose animals (assuming peripheral CSF from its point of production within the ventricles to
hair cells are functional). Middle latency auditory its point of absorption in the systemic circulation. Loss of
evoked responses (MLAERs) recorded from the brain parenchyma may result in a secondary increase in
cortex may be used to assess cortical function in ventricle size, which has been termed compensatory
addition to brainstem function. hydrocephalus or hydrocephalus ex vacuo. A congenital
• Electroencephalography. EEG allows for predisposition exists in many miniature breed dogs,
assessment of cortical function. Low amplitude or Bulldogs and Boston Terriers. The condition may be con-
flat trace (0.5 mV) following auditory and painful genital due to obstruction of ventricular drainage (often at
stimuli carries a poor prognosis in comatose the level of the mesencephalic aqueduct) or decreased
animals. absorption of CSF due to dysfunction of the arachnoid
• Somatosensory evoked potentials (SSEPs). villi, or it may be the result of secondary obstruction due
Recording of potentials from the head following to acquired disease (e.g. neoplasia, infection or inflamma-
stimulation of sensory nerves in a limb may be used tion). Hydrocephalus may be secondary to CSF over-
to assess conduction of information to the cortex production (e.g. choroid plexus tumour [rarely]) or
through the brainstem. increased viscosity of CSF due to elevated CSF protein
content seen with some tumours and the ‘dry-form’ of
FIP in cats.
148 DECISION MAKING

a Hypoxia/global brain ischaemia

b
 O BTUNDATION , S TUPOR AND C OMA 149

 115 Electrophysiological findings from a comatose

10-year-old Yorkshire Terrier that failed to recover from
anaesthesia. (a) Video EEG demonstrates essentially flat
line tracings consistent with diffuse loss of cortical
neuronal function. The ECG tracing can be seen at the
bottom of the tracing. A normal EEG from a dog in slow
wave sleep is inset for comparison. (b) BAER is also flat
line consistent with loss of brainstem function (compare
with normal animal, bottom right); however, damage to
the peripheral hair cells could also result in similar
recordings. The findings were consistent with a comatose
animal with no brainstem reflexes.

Clinical presentation  116 A 5-month-old Chihuahua with congenital

Hydrocephalus results in diffuse cerebral and/or brain- hydrocephalus. Clinical signs of decreased mentation,
stem signs due to cortical compression and elevated ICP. absent menace responses and postural reaction deficits in
Most commonly, animals have altered mentation, inap- all limbs were consistent with diffuse loss of cortical tissue
propriate behaviour, cortical blindness and seizures. secondary to the hydrocephalus. A marked doming of the
A ventrolateral strabismus is common. Hydrocephalus skull is apparent, as well as a typical ventrolateral deviation
may be asymptomatic in milder cases. Congenitally of the eyes. A persistent fontanelle was also palpable.
affected animals often have skull deformity (dome-
shaped) and persistent fontanelles (116).

Diagnosis  117 Ultrasound examination of the brain is possible

Pneumo/contrast venticulography has been superseded when persistent fontanelles are present. Typically,
by alternative diagnostic techniques. Ultrasound can be enlarged lateral ventricles (V) are easily imaged with
used to define ventriculomegaly if a persistent fontanelle variable loss of overlying cerebral cortex. Brainstem
is present, and it has been used to assess the likelihood of structures such as the thalamus (Th) usually appear
developing clinical signs (117). CT and, particularly, relatively unremarkable.
MRI (118, next page) are the diagnostic modalities of
choice. EEG may be suggestive of the diagnosis. Collec-
tion of CSF to aid in diagnosis of underlying diseases
should be done with care due to the potential for brain
herniation secondary to elevated ICP. Aspiration of CSF
from an enlarged ventricle (via a fontanelle or hole made
with a trochar), rather than from the cerebellomedullary
cistern, may help to reduce this risk. Use of hyper-
osmolar agents immediately prior to collection may also
be beneficial in this regard.
150 DECISION MAKING

a  118 (a, b) Transverse fluid-attenuated inversion

recovery MR image and corresponding gross necropsy
image from a 2-year-old Golden Retriever with a low-
grade astrocytoma invading the 3rd ventricle. Secondary
hydrocephalus involving the lateral ventricles probably
resulted in the animal presenting with signs of altered
behaviour and decreased level of mentation. (c) Sagittal
T2-weighted MR image obtained after the dog acutely
decompensated and exhibited opisthotonus, rapid decline
in mentation and respiratory arrest. Herniation of the
cerebellum through the foramen magnum is present
(arrow), resulting in compression of the underlying
brainstem with compromise of the reticular activating
system and the respiratory centres.

Management
Glucocorticoids may decrease CSF production, among
other less well-defined effects, and provide long-term
b management in some cases (prednisolone, 0.25–0.5
mg/kg PO q12h). Other drugs that decrease CSF
production, such as acetazolamide (0.1 mg/kg PO q8h)
(carbonic anhydrase inhibitor) or furosemide (1–2 mg/kg
PO q12h), are less well evaluated for the treatment of this
condition. Osmotic agents (mannitol, hypertonic saline)
may be used to decrease ICP as a short-term therapeutic
measure. Seizure treatment may be necessary in many
cases on a chronic and acute emergency basis.
Surgical treatment involves either resection of
space-occupying mass lesions or placement of ventricu-
loperitoneal (VP) shunts. Optimal indications for man-
agement of VP shunts for dogs has not been well
documented; infection, migration and obstruction of
c shunts are common complications, and no evidence of
consistent long-term benefits over medical management
has been published for dogs.
The prognosis is dependent on severity of neuro-
logical signs and rapidity of progression at presentation,
as well as the ability to treat any underlying diseases.
Specific and/or symptomatic treatment of mass lesions
and oedema can result in marked clinical improvement in
the short term. The prognosis for severe congenital
hydrocephalus is usually guarded, as clinical signs (corti-
cal atrophy) are often severe at presentation and
medical/surgical management has limited benefit in
many cases.
 O BTUNDATION , S TUPOR AND C OMA 151

Hypoxia/global brain ischaemia Common causes of hypoxia include anaesthetic-

Overview related accidents (cardiac arrest, inadequate oxygena-
Ischaemia is a deficiency of blood flow to an organ or tion, hypotension), near drowning, prolonged seizure
tissue resulting from diminished blood flow through a activity, smoke inhalation/carbon monoxide poison-
regional artery (i.e. infarct) or throughout the circu- ing and ischaemia. Cardiovascular and respiratory
lation. Hypoxia represents inadequate tissue oxygen disease may lead to transient hypoxia causing syncope.
supply for normal physiological function. It is often
associated with ischaemia and hypoglycaemia, with Clinical presentation
resultant failure in energy supply. The brain (particu- Clinical signs may be localized following local ischaemia
larly neurons) has the highest energy requirement of or infarction. Generalized hypoxia/ischaemia results in
any organ and minimal capacity for anaerobic meta- generalized pathology and symmetrical clinical signs.
bolism. Global brain ischaemia usually affects a dense Decreased levels of consciousness are common, as are
area of selectively vulnerable neurons in brain tissue. other signs referable to diffuse cortical disease such as
Lack of oxygen/cessation of blood flow results in seizures, blindness, menace loss, postural deficits and
unconsciousness within 5–10 seconds. inappropriate behaviour.
Neuronal cell death involves failure of energy
metabolism and secondary effects of excitatory neuro- Diagnosis
transmitters, such as build-up of glutamate and aspar- Diagnosis is often based on clinical signs and history.
tate, free radical formation and calcium influx. Specific MRI may reveal symmetrical and often diffuse lesions
anatomical areas, including the cerebral cortex, hip- involving ‘vulnerable’ structures such as the cerebral
pocampus, certain basal nuclei (e.g. caudate nuclei), cortex, hippocampus and other grey-matter areas (119).
thalamus and cerebellar Purkinje cell layers, are more Assessment of carbon monoxide toxicity requires a
susceptible to hypoxic injury. CO-oximeter.

a b

 119 Transverse T1-weighted MR images at the level of the caudate nuclei (a) and at the level of the midbrain (b).
This 4-year-old Labrador Retriever presented for obtundation and inappropriate behaviour following an episode of
prolonged status epilepticus and hyperthermia. Diffuse lesions involving the caudate nuclei bilaterally and specific
laminae within the cerebral cortex (arrows) can be seen. Altered metabolism of highly vulnerable neurons in these
grey-matter areas can result in diffuse cortical laminar and basal nuclei necrosis, with signs of diffuse cerebral disease.
 152 DECISION MAKING

Management
Treatment depends on addressing underlying diseases, 120 (a) Transverse FLAIR MR image at the level of the
seizure control if appropriate, oxygen supplementa- thalamus from a cat with hypertensive encephalopathy.
tion/ventilation and general supportive care. The prog- Diffuse hyperintensity within the white-matter tracts is a
nosis following global ischaemic damage is guarded, typical MRI finding and is reflected in typical clinical signs
particularly if neurological deficits are severe, although such as decreased level of mentation. (b) Sagittal T1-
some deficits may be reversible. Signs resulting from weighted post-contrast MR image showing herniation of
neuronal necrosis are almost always permanent. Recov- the cerebellum. Herniation with subsequent brainstem
ery can take days to weeks and may be accompanied by compression was suspected to have resulted in an
severe behavioural abnormalities, which most probably observed acute decrease in mentation from obtundation to
reflect damage to cerebral cortical tissue. stupor. The presenting obtundation was presumed to have
been caused by the diffuse cerebral disease seen on the
Hypertension FLAIR image. (c) Gross pathology showing herniation of
Overview the cerebellar vermis (red arrow) through the foramen
Hypertension is represented by a consistently elevated magnum (yellow arrows), with compression of the
BP (sustained systolic pressure >160 mmHg). It is most brainstem (asterisk). (d) Sustained systolic blood pressure
often secondary to underlying disease including renal over 200 mmHg resulted in multiple organ pathology,
disease, hyperadrenocorticism/glucocorticoid adminis- including retinal separation. There are multiple areas of
tration, diabetes mellitus, pheochromocytoma, hyper- haemorrhage (arrows) throughout the fundic layers and
thyroidism, primary hyperaldosteronism and hepatic separation of the retina (predominantly dorsally). (c, d
disease. Autoregulatory mechanisms (mostly arteriolar) courtesy UC Davis Ophthalmology Service)
regulate intracranial blood flow and protect local micro-
circulation up to approximately 180 mmHg. Beyond this
level, microvascular hypertension/hyperperfusion results
in interstitial oedema, with resultant elevations in ICP
and hypertensive injury. Haemorrhagic infarcts may also Management
occur. Cats are more sensitive than dogs to developing Treatment is usually aimed at addressing the underlying
hypertensive encephalopathy, particularly with rapidly cause (if identified) and symptomatic treatment of sys-
developing hypertension. temic hypertension, which may be continued indefinite-
ly. Amlodipine (a calcium channel blocker) (0.1–0.25
Clinical presentation mg/kg PO q12–24h) is the most commonly recommend-
Clinical signs include seizures, ataxia, tremors, blind- ed antihypertensive drug for cats, and amlodipine or an
ness, decreased mentation and abnormal behaviour angiotensin-converting enzyme inhibitor such as
(e.g. head pressing). Oedema may result in brain herni- enalapril (0.25–0.5 mg/kg PO q12h) (alone or in combi-
ation (120), which is often fatal. Signs of other organ nation) is recommended for dogs. Beta and alpha adren-
dysfunction secondary to the hypertension are likely, ergic blockers are used less commonly.
including retinopathy (retinal detachment and/or In severely neurological animals with rapid decom-
haemorrhage) (120d) and renal disease. pensation, hyperosmolar agents, such as mannitol, may
be beneficial in reducing cerebral oedema and ICP.
Diagnosis Ideally, these agents should not be used until BP has been
Diagnosis depends on documentation of consistently normalized, as they can cause transient increases in BP.
elevated systemic BP with appropriate neurological signs Correction of hypertension can result in rapid improve-
+/- compatible advanced imaging evidence. MRI may ment of neurological function.
reveal evidence of generalized oedema and/or ischaemic/ The long-term prognosis is often dependent on the
infarctive disease. Identification of underlying diseases is ability to manage both the hypertension and the underly-
essential for appropriate management. ing disease process.
 O BTUNDATION , S TUPOR AND C OMA 153

a b

c d

*
Narcolepsy/cataplexy stimuli, particularly food, and may last from seconds to
Overview minutes. Collapses may be complete or result in stagger-
Narcolepsy/cataplexy is a chronic sleep disorder charac- ing. Animals may remain conscious or fall into rapid eye
terized by excessive daytime sleepiness and cataplexy movement (REM) sleep (particularly with prolonged
(sudden loss of muscle tone in response to emotional attacks). Muscles are always flaccid, in contrast to seizure
stimuli). Both familial and sporadic narcolepsy occur in disorders where increased muscle tone is often present.
dogs and both are associated with defective hypo- Autonomic signs such as urination, salivation and defeca-
cretin/orexin neurotransmission. It is rarely reported tion are not seen.
in cats.
Diagnosis
Clinical presentation Diagnosis is based on clinical signs; EEG is useful to
Clinical signs include excessive sleepiness, with disrupted show that attacks are associated with recordings
sleep/wake patterns (difficult to document in most dogs typical of wakefulness or REM sleep rather than slow-
since frequent sleeping is common normally), and, more wave sleep. EEG is also important in ruling out the
clinically important, pronounced attacks of cataplexy. presence of paroxysmal activity such as abnormal
Cataplectic episodes are usually triggered by emotional spikes and waves consistent with a seizure disorder.
154 DECISION MAKING

Animals with familial narcolepsy (typically Dober- CNS stimulants, such as D-amphetamine and
manns, Labradors, Dachshunds) have defects in the modafinil, may decrease daytime sleepiness; however,
hypocretin-1 receptor 2 gene with normal CSF hypo- management of cataplectic attacks using drugs that
cretin-1 levels. Dogs with acquired narcolepsy have inhibit adrenergic reuptake, such as the tricyclic anti-
decreased CSF hypocretin-1 levels (less than 80 pg/ml; depressants clomipramine (3.0–6.0 mg/kg PO q24h),
reference 250–350 pg/ml). imipramine (0.5–1.0 mg/kg PO q8–12h), desipramine
(3 mg/kg PO q12h) and the alpha-2 antagonist yohim-
Management bine (0.05–0.3 mg/kg PO q12h), is clinically more
Narcolepsy is not life threatening; however, the cata- important.
plectic attacks can be debilitating and frustrating for A recent report has described the successful use of
owners. Common sense precautions, such as provision of venlafaxine (2.5 mg/kg PO q24h), which is an arylalka-
elevated water and food bowls, should be taken. Simple nolamine serotonin-norepinephrine reuptake inhibitor.
modification of daily routines, such as not allowing Intrathecal delivery of hypocretin-1 has not been
competition during feeding, can reduce frequency of shown to be effective in sporadically occurring narco-
attacks. lepsy in dogs.
 DECISION MAKING Chapter 7

SEIZURES
155

Simon Platt

INTRODUCTION The phenotypic nature of epileptic seizures

The stages of seizure activity
Epileptic seizures are sudden onset (paroxysmal) clinical There are four recognizable stages of seizure activity,
events that represent an abnormality of forebrain neuro- which can be vital when trying to differentiate a seizure
transmission. Epilepsy is characterized by recurrent event from other episodic activity such as syncope or
epileptic seizures and therefore implies a less transient neuromuscular weakness. The more seizure events that
aetiology. The underlying abnormality can be due to the dog or cat exhibits, the more likely it is that the owner
structural or chemical interference with the normal will be able to recognize these stages. The stages consist
‘balance’ that exists in the brain between neuronal excita- of the prodrome, aura, ictus and post-ictal period:
tion and inhibition. Disruption of this balance may result • The prodrome is a behavioural phenomenon that
in other clinical signs referable to forebrain dysfunction, precedes the onset of a seizure by hours to days and
such as behavioural and visual abnormalities, but this is is manifested by hiding, restless activity or fearful
not necessarily the case and the affected dog or cat could behaviour.
be completely neurologically normal apart from the • An aura is a subjective sensation that marks the
seizure activity. onset of a seizure. This is obviously difficult to
Unfortunately, a disturbance of the electrical circuitry recognize in dogs and cats unless it is presumed that
in the nervous system, whether structural or functional vomiting, salivation or inappropriate urination seen
(neurochemical), may result in other paroxysms that can prior to an obvious seizure event is classed as the
closely resemble seizure activity. These include narco- aura. Subtle changes in behaviour before a seizure
lepsy, cataplexy, movement disorders (dyskinesias), sleep may be indicative that the animal is experiencing
disorders and tremor syndromes. Tremors and involun- an aura.
tary movements are further discussed in Chapter 13. • The ictus is the seizure event itself (see below).
Further to disorders of the CNS, disorders of peripheral • The post-ictal period is characterized by atypical
nerves and muscles, the respiratory and cardiovascular behaviour that immediately follows the seizure. The
systems and systemic metabolism may result in parox- behaviour seen may include restlessness, aggression,
ysmal ‘collapses’, which must also be considered when delirium, lethargy, confusion, visual loss, thirst,
the possibility of a seizure event has been raised. hunger and inappropriate urination. This may last
It is extremely important to distinguish the nature of for hours in some animals regardless of the
the paroxysm, as this will determine the most appropriate underlying cause of the seizure. It is essential to
diagnostic and therapeutic actions and, in the case of discuss this period with the owner, as it is not seen
seizure activity, immediately confirm a forebrain localiza- with narcolepsy/cataplexy, neuromuscular collapse
tion. It is therefore necessary to ask the question: what is a or movement disorders. Short periods of confusion
seizure? The answer lies in the description of the event, and visual dysfunction may be apparent after a
which is often only seen by the owner, as well as the cir- syncopal event, depending on the severity of the
cumstances that surround its onset (Table 35, next page). It underlying cardiovascular cause.
is therefore important to know the typical clinical charac-
teristics (phenotypes) of seizures, so that the owner can be
asked the most appropriate questions about the event.
 156 DECISION MAKING

Table 35 Differentiation of non-epileptic paroxysmal events from epileptic seizures

PAROXYSMAL PRECIPITATING LEVEL OF FLACCID OR SPASTIC

EVENT FACTORS CONSCIOUSNESS COLLAPSE

Narcolepsy Excitement/feeding Absent Usually accompanied by

cataplexy

Cataplexy Excitement/feeding Normal, if not accompanied by Flaccid

narcolepsy

Neuromuscular collapse Activity/exercise Normal unless impaired by Often flaccid (e.g. myasthenia
respiratory compromise gravis). Can appear spastic in
some cases of myopathy

Syncope Exercise, excitement, cough Reduced to absent Flaccid

Movement disorder None, to excitement/activity/ Normal Often spastic

exercise

Metabolic collapse May be related to feeding Variable; Often flaccid. Can be spastic in
(e.g. hypoglycaemia) times/excitement long lasting some cases (e.g. hypocalcaemia)

Sleep disorder Sleep Absent (REM sleep) and may Either

progress to apparent wake-
fulness during event

Vestibular event Variable Normal to depressed Usually spastic

The ictal event Generalized seizures

The description of the ictus can go a long way to Generalized seizures indicate involvement of both
confirming that the animal is indeed exhibiting seizure cerebral hemispheres simultaneously (121). Conscious-
activity as opposed to syncope or neuromuscular col- ness is often impaired and motor manifestations are bilat-
lapse. The ictal event usually lasts for 60–90 seconds. eral. Generalized seizures may have one or several of the
Should this event last for longer than 5 minutes, then it is following phases, with a combination of tonic–clonic
termed status epilepticus (see Chapter 23). However, it is activity being the most common:
not unusual for the owner to be unable to determine the • Tonic: sustained, increased muscle contraction;
length of the event itself and to frequently overestimate the animal usually becomes recumbent in this
this experience. The event should be peracute in its onset phase (122).
and stereotypical (i.e. its characteristics are identical each • Myoclonic: sudden, brief, involuntary, single or
time it occurs). This is obviously different from neuro- multiple contractions of muscles or muscle groups.
muscular collapse. Most ictal events also have no identi- • Clonic: regularly repetitive myoclonus, which
fiable precipitating event, occurring most commonly involves the same muscle groups, and is prolonged.
from sleep or at rest. This distinguishes seizure activity • Atonic: sudden loss of muscle tone, usually lasting
from narcolepsy/cataplexy, which is precipitated by 1–2 seconds or more.
excitement, and from syncope and neuromuscular col-
lapse, which are precipitated by activity.
The ictus can be classified into two major phenotypic
categories: generalized and focal.
 SEIZURES 157

INVOLUNTARY MOVEMENT DURING POSSIBLE HISTORICAL POSSIBLE PHYSICAL

EVENT FINDINGS EXAMINATION FINDINGS

No Often purebred dog with early age onset Normal

No As for narcolepsy Normal

May appear to be present when May be accompanied by dysphagia, May be normal or may be muscle atrophy,
attempting to stand dysphonia, regurgitation muscle pain and/or reduced reflexes

No May be accompanied by cough, Arrhythmia, pulse deficits, murmur,

increased respiratory noise abnormal lung auscultation, cyanosis

Yes; exacerbated by attempts to stand May be purebred with early age onset Normal

No, except facial twitching in some cases Anorexia, depression, polyuria, polydipsia, May be normal; weight loss
of hypoglycaemia or hypocalcaemia vomiting, weight loss

Yes; REMs during event Never occurs during periods of normal Normal
consciousness

Attempts to stand; nystagmus Periods of head tilt and/or ataxia; Normal to nystagmus, head tilt,
head tremor; ear disease ataxia, vomiting

 121 Generalized seizure activity results from a

synchronized electrical discharge from the whole
of the forebrain.

 122 Generalized seizures most commonly

present with the animal in lateral recumbency
exhibiting tonic–clonic movements. The limbs
are most consistently in rigid extension (tonic),
as seen in this Bull Terrier, with the inter-
mittent involuntary muscle contractions super-
imposed appearing to cause a flexor ‘paddling’
Seizure activity (affecting
both cerebral hemispheres
motion.
simultaneously)
 158 DECISION MAKING

Focal seizures Seizure activity

A focal seizure is due to initial activation of only one part Seizure focus
of one cerebral hemisphere or specific region in the fore-
brain, such as the hippocampus (123). Compared with
dogs, cats more commonly exhibit focal seizures. Any
portion of the body can be involved during a focal
seizure, depending on the region of the brain affected
(124). The focal clinical signs may be associated with a
higher incidence of focal intracranial pathological
change in cats, but are apparently quite often associated
with idiopathic epilepsy in dogs. If there is an alteration
in the animal’s awareness during the event, it is called a
complex focal seizure (previously termed psychomotor
seizures).
The various forms of focal seizure depend on where
in the forebrain the neurotransmission abnormality
occurs. These forms include:
• Focal motor seizures. These are (1) elementary  123 Focal seizure activity results from an abnormal
motor events, which consist of a single type of electrical discharge in a single area of the brain. The area
stereotyped contraction of a muscle or group of from which the focus originates determines the clinical
muscles or (2) automatisms. Automatisms are characteristics of the focal seizure.
movements that resemble voluntary motor
movements and include chewing activity and
rhythmic contractions of a single limb.
Consciousness is often unaffected during focal
motor seizure activity, but it is difficult to assess
whether this is the case in many patients.
• Focal sensory seizures. These are behavioural
seizures involving the limbic system. They may
present as rage, aggression without provocation, fly-  124 Focal motor seizure activity can be manifested by
catching, running in circles, floor licking, vocaliza- rhythmic contractures of the muscle of a single limb, as
tion and tail chasing. An aura that does not evolve seen in the right hindlimb of this cat, which exhibited this
into loss of consciousness is a focal sensory seizure. form of seizure activity frequently throughout the day.
• Focal autonomic seizures. These seizures are
apparently rare and cause predominantly autonomic
signs such as vomiting, diarrhoea and abdominal
pain. A syndrome characterized by drooling,
dysphagia and painful enlargement of the
mandibular salivary glands is probably a form of
focal autonomic seizure.

A seizure may start focally and ultimately spread

throughout both cerebral hemispheres, resulting in sec-
ondary generalization, which the owner may not notice
until the animal has exhibited several such events.
 SEIZURES 159

 125 An action potential is generated by a

flow of positively charged sodium ions across the neuronal +40 Action potential
membrane, triggered by environmental stimuli or the +20

Membrane potential (mV)

release of neurotransmitters. This causes the membrane

zation
0

Repolariza
to depolarize, bringing the membrane from the resting
-20

Depolari
potential (about -70 mV) up to the threshold potential
-40 Threshold potential

tion
(about -55 mV). As the action potential is triggered, the
-60 Resting potential
membrane potential abruptly rises and then falls, often
below the resting level, as a compensatory flow of -80
Stimulus
potassium ions leaves the cell. Action potentials can occur
1 2 3 4 5 6 7
10–100 times per second. Time (ms)

Neuroanatomical basis of seizure activity In neurons, action potential generation (125) results
An epileptic seizure definitively implies a disorder of the primarily from changes in the membrane permeability to
forebrain. Therefore, it is extremely important to be four ions: sodium (Na+), chloride (Cl-), calcium (Ca++)
sure that a seizure is suspected, as the underlying causes and potassium (K+). These ions enter and exit neurons by
and subsequent investigations are vastly different from way of voltage-dependent channels. The maintenance of
those considered for cardiovascular and neuromuscular membrane potential and transient changes in ion flux
‘events’. Their causes may originate outside (extra- that culminate in the generation of an action potential are
cranial) or inside (intracranial) the brain. Intracranial entirely dependent on the tight regulation of the above
causes may be further subdivided into functional disor- mentioned ions into neurons. Thus, changes or abnor-
ders (where no gross structural changes are evident in the malities in the regulation or activity of these ions could
brain and the cause is probably a neurochemical dysfunc- have a dramatic impact on the excitability and ‘epilepto-
tion) and structural disorders (where there is a gross genicity’ of individual neurons. Because virtually all
structural cause within the brain [e.g. a brain tumour or neurons have the ability to fire in a rapid, repetitive
hydrocephalus]). Extracranial causes include toxicities fashion, it is clear that generating a recurrent cycle of
and metabolic disturbances that either interfere with membrane depolarizations and action potentials may be
CNS function or are directly neurotoxic. critical to the initiation and propagation of a seizure
discharge.
Pathophysiology of seizure activity Seizure propagation may be especially likely in
Irrespective of the fact that epilepsy can be caused by a neurons with intrinsic firing (bursting) abilities (such as
variety of intracranial structural, cellular or molecular those in the cortex and hippocampus) if the balance
conditions and manifest itself in different ways, the between excitatory or inhibitory inputs is altered. In the
epileptic seizure always reflects abnormal hypersynchro- absence of appropriate inhibitory regulation, these pop-
nous electrical activity of neurons in the forebrain. ulations of neurons may begin to fire synchronously,
How electrical and neurochemical events within leading to a seizure. It is hypothesized that a population
neurons culminate in a seizure, and what events are of neurons within an epileptic focus in the cortex under-
responsible for the termination of a seizure, are questions goes paroxysmal synchronous depolarization, termed a
with no definitive answers. It is, however, clear that paroxysmal depolarizing shift (PDS), which results in an
seizures are linked, at the lowest level, to membrane abnormal burst of action potentials that continue in syn-
potentials, ionic fluxes and action potential generation. chronous volleys without appropriate inhibition.
It has been suggested that seizure activity is ultimately As neuronal action potentials result from the action
due to an imbalance between excitation and inhibition, of neurotransmitters, such as glutamate and gamma-
with increased excitation or decreased inhibition leading aminobutyric acid (GABA), released by presynaptic
to epileptiform activity in the brain. terminals, abnormalities of these neurotransmitters and
160 DECISION MAKING

Mitochondrion

Glutamine
Glutaminase PRESYNAPTIC NEURON
Glutamate vesicle
Vesicular transporter
GABA vesicle
Exocytosis Glutamine transporter

Glutamate
Synaptic cleft Glutamate transporter

Glutam
GABA receptor Glutamate receptor
ne

i
Gl u

tam e
at
Gl
u

ta
mine
ASTROCYTE PROCESS
Gl Glutam
uta ate
ma te

Glutamine synthetase

GABA agonist binding site POSTSYNAPTIC NEURON

GABA antagonist binding site
Benzodiazepine binding site
Barbiturate binding site  126 Glutamate and GABA neurotransmission and
Chloride channel metabolism. Glutamate is secreted by the presynaptic
terminals in many pathways in the central nervous system,
β α as well as in many areas of the cerebral cortex. It is
synthesized from glutamine by the mitochondrial enzyme
β
γ glutaminase. Synaptic glutamate is recycled through
α
astrocytes, which metabolize it to glutamine, from where
it is transported back to the presynaptic neuron.
Glutamate transmission is predominantly excitatory.
The chief inhibitory neurotransmitter in mammals is
gamma-amino butyric acid (GABA), which is synthesized
from glutamate and taken up by receptor proteins in the
membrane of the postsynaptic neuron. GABAA receptors
are ligand-gated ion channels (also known as ionotropic
receptors) that allow chloride to pass through into the
cell, resulting in inhibition. Binding of GABA occurs at
the interface between the α and β subunits of the GABAA
receptor and triggers the opening of the channel, allowing
the rapid influx of Cl- into the cell. Other binding sites
Transmembrane domains
(TM1–4) include those for benzodiazepine and barbiturates.
 SEIZURES 161

their receptors have been implicated in the generation of Studies in idiopathic epileptic dogs have confirmed
seizures. Glutamate is the main excitatory neuro- there to be significantly less GABA and more glutamate
transmitter and GABA is the main inhibitory neuro- in the CSF compared with normal controls. However,
transmitter in the brain (126). Normally, the excitatory CSF neurotransmitter concentrations do not necessarily
post-synaptic potentials in neurons are followed immedi- correlate with the synaptic concentration in the brain.
ately by inhibitory transmission due to GABA. If excita- The mechanisms responsible for the ‘arrest’ of seizure
tory mechanisms dominate, initiated by either increased activity are poorly described, but supposedly relate to the
excitation or decreased inhibition, neurons become accumulation of lactic acid during the seizure. A break-
hypersynchronized, capturing more and more neurons down in the mechanisms of seizure arrest, in addition to
and generating an epileptic seizure (127). Perpetuation of the evolution of seizure-induced excitotoxicity, forms the
the seizure activity is possibly due to a vicious cycle basis of the pathophysiology of status epilepticus.
whereby glutamate initiates widespread neuronal excite-
ment, which can lead to neuronal damage and death, NEUROLOGICAL EVALUATION
which contributes to further glutamate release. It is OF THE SEIZURE PATIENT
widely believed that the neurotoxic effects of glutamate
stem in part from alterations in Ca++ permeability, which Seizures are aetiologically categorized as idiopathic,
result in an increase in intracellular Ca++ levels. Dramat- symptomatic or reactive. Regardless of their cause, they
ic elevations in Ca++ concentrations may induce a cascade all ultimately represent dysfunction of the forebrain.
of Ca++-dependent intracellular events, such as activation Recognizing this aetiological classification scheme can
of proteases and lipases, influx of other cations, such as help with interpretation of the neurological examination
sodium, and osmotic swelling of neurons that culminates of the seizure patient.
in cell death. These cellular pathways are almost certain- • Idiopathic seizures. The term idiopathic implies
ly responsible for the seizure-induced excitotoxicity a suspected genetic basis for the seizure activity
present in prolonged seizures and ultimately enlarge the for which the underlying disorder is frequently
seizure focus, potentiating more frequent and severe suspected to be a transient functional or neuro-
seizures, such as status epilpeticus and clustering. chemical abnormality. There are no identifiable
structural abnormalities of the forebrain.

Cerebrocortical neuron Seizure focus

Paroxysmal depolarization
at neuronal membrane

 127 Propagation of seizure activity from an

abnormal neuronal focus is possible via local capture
of neighbouring, spontaneously discharging
neurons.
 162 DECISION MAKING

• Symptomatic seizures. This term is often used to

describe seizures resulting from a structural intra-
cranial cause (e.g. brain tumours [128], inflamma-
tion or hydrocephalus [129]), which causes
structural damage to the forebrain. A seizure focus
that is not compatible with an idiopathic origin, but
is not readily identifiable as a structural defect on
MRI and CSF analysis, is referred to as cryptogenic.
• Reactive seizures. This term is often used to
describe seizures resulting from an extracranial
cause and includes metabolic and toxic disorders. As
mentioned above, these ultimately cause seizure
activity due to secondary interference with cerebral
metabolism or, more directly, as primary neurotoxic
insults. There are no identifiable structural abnor-
 128 A transverse T2-weighted MR image of a malities of the brain, but the functional impairment
7-year-old dog with a hyperintense heterogeneous is global and exists as long as the aetiology exists.
lesion in the piriform lobe, which was confirmed to be
an astrocytoma. Normal and abnormal forebrain function
The forebrain is important for normal behaviour, inter-
preting conscious sensory stimuli, vision and maintaining
normal alertness. In addition to seizure activity, lesions of
the forebrain may result in:
• Altered behaviour.
• Contralateral conscious sensory deficits. These
include decreased contralateral facial sensory
awareness (facial hypalgesia), contralateral
conscious proprioceptive deficits and the so-called
‘hemi-neglect’.
• Central blindness (blind with intact PLRs).
• Decreased levels of consciousness, typically to the
level of a stupor, coma in animals usually being
associated with brainstem lesions.

 129 A dorsal sectioned gross view of the brain

from a 3-month-old Chihuahua that was euthanized
following frequent seizures. Note the marked bilateral
ventricular dilation compatible with hydrocephalus.
(Photo courtesy Raquel Rech)

 130 Marked lateral body curvature and a head turn in

a young dog with a lateralized forebrain lesion.
 SEIZURES 163

• Circling. In the majority of cases this is ipsilateral, clinical signs may represent transient functional distur-
but can be contralateral with certain cerebral bances related to the seizure itself (see below).
lesions. Focal/asymmetrical forebrain abnormalities are sug-
• Head turn (i.e. not a head tilt, as the ears are still gestive of a structural intracranial cause of the seizures
horizontal). This usually occurs ipsilateral to the (symptomatic epilepsy).
lesion (130). Multifocal CNS abnormalities are also suggestive of
symptomatic epilepsy, but essentially narrow the differ-
Aims of the neurological examination in the entials down to inflammation and metastatic neoplasia.
seizure patient
A thorough neurological examination is essential to Neurological deficits arising as a consequence
detect abnormalities other than the seizures; it will help of seizures (post-ictal signs)
with an aetiological classification and development of a One of the features of idiopathic epilepsy is the absence
differential diagnosis list. The examination may reveal (1) of neurological deficits in the inter-ictal period. There-
no abnormalities; (2) diffuse/symmetrical forebrain fore, where abnormalities are present in the inter-ictal
abnormalities; (3) focal/asymmetrical forebrain abnor- period this would usually exclude idiopathic epilepsy
malities; or (4) multifocal CNS abnormalities. from the differential diagnosis list. However, there are
A completely normal neurological examination is two exceptions to this:
compatible with idiopathic epilepsy. Symptomatic epi- • Depression of forebrain activity occurs during the
leptic patients may also have a normal neurological exam- period immediately following an epileptic seizure
ination if the causative lesion is located in the ‘clinically (so-called post-ictal depression). During this period,
silent’ areas of the forebrain, such as the olfactory bulbs. subtle neurological deficits, including conscious
During the early stages of a slowly enlarging mass in such proprioceptive deficits, may be evident. Post-ictal
a region, seizures may be the only clinical signs, but in depression lasts a variable amount of time, but most
time other neurological deficits related to the site will cases return to normal a few hours (up to a day)
develop. Occasionally, metabolic disease may wax and following the seizure episode.
wane, resulting in a normal neurological examination. • Neurological deficits may also result secondary to
However, many such patients will have concurrent sys- severe or prolonged seizures due to hypoxic injury
temic signs such as weight loss, polyuria or anorexia. or the so-called excitotoxicity phenomenon. Such
Diffuse, symmetrical forebrain abnormalities should lesions are particularly evident in the N-methyl-
prompt consideration of an extracranial cause (reactive D-asparate (NMDA)-rich regions of the brain, such
epileptic seizures) (e.g. a metabolic encephalopathy such as the hippocampus, in the piriform lobes and, in
as hypoglycaemia or hepatic encephalopathy). If the severe cases, in the grey matter adjacent to the
patient is examined shortly after a seizure, such abnormal hippocampus (131).

a b  131 (a) Transverse T2-weighted

MR image of a dog 24 hours after a
protracted generalized seizure. The
piriform lobes bilaterally exhibit
hyperintensity (arrows) suggestive of
oedema secondary to the seizure
activity. (b) Normal transverse T2-
weighted MR image for comparison.
 164 DECISION MAKING

DIFFERENTIAL DIAGNOSES An epileptic seizure can be suspected based on:

FOR EPILEPTIC SEIZURES • The peracute and unexpected onset and offset.
• Stereotypical pattern of each event.
Prior to consideration of the differentials of forebrain • Presence of involuntary motor activity and/or
disease as the cause of seizure activity, the clinician should abnormal mentation and behaviour and/or
be as comfortable as possible that the event described by autonomic signs (salivation, urination and/or
the owner, or witnessed first-hand, is actually a seizure defecation). There is also notably increased muscle
rather than one of the several clinical ‘mimics’ of seizure tone accompanying limb movement or collapse in
activity (Table 35). This will dramatically affect the most cases, which helps to differentiate seizures
subsequent diagnostic investigation and further thera- from other forms of collapse such as syncope.
peutic interventions. This determination is based on the
phenotypic characterization of the event and historical Absolute confirmation of the epileptic nature can only be
confirmation of the potential precipitating events. obtained by observing simultaneously the characteristic
Detailed questioning of the owner will be necessary. EEG changes and physical manifestation of the seizures.
Although generalized tonic–clonic seizures have a The differential diagnosis for epileptic seizures is
fairly unequivocal description, recognition of a focal based on the signalment and history and the neurological
seizure can pose a real challenge to the clinician. For this examination suggesting idiopathic, symptomatic or reac-
reason, video footage obtained by the owner of the tive disease. The age of the patient may indicate the likely
paroxysmal event can be of tremendous help. combination of differentials (Tables 36, 37 and 38).

Table 36 Differential diagnosis of seizure activity in patients <6 months old

DISEASE MECHANISM DOGS CATS

Vascular Rare Rare

Inflammatory/infectious Infectious encephalitis (distemper, Toxoplasma, Infectious encephalitis (Toxoplasma, bacterial,

Neospora, fungal, bacterial, rickettsial, rabies)* FIP, Cryptococcus)*
Meningoencephalitis of unknown aetiology Meningoencephalitis of unknown aetiology
(GME, necrotizing, idiopathic)*; rare at this age (presumed immune mediated); rare

Trauma* Frequent Frequent

Toxic* Frequent Frequent

Anomalous Hydrocephalus* Infrequent

Metabolic Hepatic encephalopathy* Hepatic encephalopathy

Hypoglycaemia*
Hypocalcaemia

Idiopathic Very rare at this age Very rare at this age

Neoplastic Very rare at this age Very rare at this age

Nutritional Thiamine deficiency Thiamine deficiency

Degenerative Lysosomal storage disease Lysosomal storage disease

Intrinsic metabolic disorders (e.g. L-2-hydroxy-
glutaric aciduria)

* Common cause
 SEIZURES 165

Table 37 Differential diagnosis of seizure activity in patients 6 months to 6 years old

DISEASE MECHANISM DOGS CATS

Vascular Ischaemic/haemorrhagic stroke, infrequent Rare

Inflammatory/infectious Infectious encephalitis (distemper, Toxoplasma, Infectious encephalitis (Toxoplasma, bacterial, FIP,
Neospora, fungal, bacterial, rickettsial, rabies)* Cryptococcus)*
Meningoencephalitis of unknown aetiology (GME, Meningoencephalitis of unknown aetiology
necrotizing)* (presumed immune mediated); rare

Trauma* Frequent Frequent

Toxic* Frequent Frequent

Anomalous Hydrocephalus Infrequent

Metabolic Hepatic encephalopathy Hepatic encephalopathy

Hypoglycaemia
Hypocalcaemia

Idiopathic Frequent Rare

Neoplastic Infrequent Infrequent

Nutritional Thiamine deficiency Thiamine deficiency

Degenerative Rare late-onset disease Rare late-onset disease

* Common cause

Table 38 Differential diagnosis of seizure activity in patients >6 years old

DISEASE MECHANISM DOGS CATS

Vascular Ischaemic stroke Rare

Inflammatory/infectious Infectious encephalitis (distemper, Toxoplasma, Infectious encephalitis (Toxoplasma, bacterial,

Neospora, fungal, bacterial, rickettsial, rabies)* FIP, Cryptococcus)*
Meningoencephalitis of unknown aetiology Meningoencephalitis of unknown aetiology
(GME, necrotizing)* (presumed immune mediated); rare

Trauma* Frequent; may be chronic response to earlier Frequent; may be chronic response to earlier
trauma trauma

Toxic* Frequent Frequent

Anomalous Rare Rare

* Common cause

(Continued)
 166 DECISION MAKING

Table 38 Differential diagnosis of seizure activity in patients >6 years old (continued)

DISEASE MECHANISM DOGS CATS

Metabolic Hepatic encephalopathy (acquired) Hypoglycaemia

Hypoglycaemia (insulinoma*, extrapancreatic
insulin-like producing neoplasia, insulin overdose)
Polycythaemia

Idiopathic Occasional; consider cryptogenic* Rare; consider cryptogenic

Neoplastic Primary/metastatic brain tumour* Primary/metastatic brain tumour*

Nutritional Rare Rare

Degenerative Rare Rare

* Common cause

DIAGNOSIS OF EPILEPSY AND ITS CAUSES • Describe the event? Generalized seizures (132)
are commonly associated with extracranial causes
The importance of the history of seizures or inherited epilepsy and are occasional-
Often an owner may describe an event that gives rise to ly associated with symptomatic and cryptogenic
suspicion of an epileptic seizure, but the animal may be epilepsy. Focal seizures and focal seizures that
normal. It is vital that the clinician asks very specific ques- generalize secondarily are more often associated
tions, which will help to determine whether the event with an intracranial disorder such as symptomatic
could have been a seizure and what the underlying cause epilepsy or cryptogenic epilepsy. Focal seizures that
may be. begin in the facial muscles and then generalize with
• Was the first seizure within the past few weeks or little motor movement are seemingly more
months ago? Extracranial disorders and common in cats than in dogs.
symptomatic epilepsy may be considered higher on
the differential diagnosis list if the seizures began
recently. Idiopathic and cryptogenic epilepsy may
be more likely in an animal that has had inter-
mittent seizures for many months and is normal
in between episodes.
• Are there signs notable prior to the possible
seizure event? Consistent signs exhibited by the
animal prior to the event, such as behavioural
abnormalities, are more suggestive of seizures than
other possible abnormalities such as narcolepsy or
syncope.

 132 Generalized seizure activity is often tonic–clonic.

The owners should describe evident rigidity in the limbs,
as seen in this 10-week-old dog, in addition to involuntary
movement.
 SEIZURES 167

Table 39 Toxins associated with seizure activity in dogs and cats

TOXIN CLINICAL SIGNS ONSET SPECIFIC ANTIDOTE

Rodenticides

Alpha-chloralose Ataxia, seizures, aggression, Acute None

coma

Bromethalin Seizures, paralysis Delayed None

Strychnine Seizures Acute None

Zinc phosphide Seizures Acute None

Anticoagulants Rare seizures, rare paralysis Delayed Vitamin K1 (2.5 mg/kg PO or

SC q24h)

Cholecalciferol Rare seizures Delayed None

Metals

Lead Seizure, hysteria, ataxia, tremors, Acute if high dose CaNa2-EDTA (25 mg/kg SC
blindness, megoesophagus q6h for 5 days)

Thallium Rare seizures, tremors, ataxia, Acute Dithizone (50 mg/kg PO q8h
depression, paresis for 5 days)

Organic mercury Ataxia, hypermetria, tremors, Delayed D-Penicillamine

seizures, blindness (10–30 mg/kg PO q6h
for 1–2 weeks)

Lithium Tremors, ataxia, coma, seizures Acute None

Pesticides

Insecticides: Miosis, salivation, lacrimation, Acute Pralidoxime chloride for

organosphosphates (OPs) tetany, seizures, coma neuromuscular signs, but only
or carbamates if OP (20–50 mg/kg IM);
atropine for both (0.2 mg/kg
IM) if muscarinic signs

Pyrethroids: permethrin, Hyperexcitability, tremors, Acute/delayed None

imiprothrin, bifenthrin, seizures
allethrin

Molluscicides, metaldehyde Tachycardia, salivation, tremors, Acute None

vomiting, hyperaesthesia,
nystagmus, ataxia, seizures,
hyperthermia, diarrhoea,
respiratory failure

Household products

Ethylene glycol Depression, seizures, ataxia, Acute 4-Methylpyrazole

coma

Methyelxanthines: caffeine, Hyperactivity, ataxia, rare Acute None

chocolate, tea seizures
 168 DECISION MAKING

 133 Diagnostic investigation of

seizure activity. GENERALIZED SEIZURES

Normal clinicopathological tests

Normal clinicopathological tests
Normal or abnormal neurological
Abnormal clinicopathological tests Normal neurological examination examination
Normal CSF analysis, CT and/or MRI Abnormal CSF analysis, CT and/or MRI

Extracranial disorder Symptomatic epilepsy

(i.e. intoxications, hypoglycaemia, Idiopathic epilepsy or cryptogenic (i.e. encephalitis, head trauma,
hepatic encephalopathy) epilepsy (residual damage) neoplasia or hydrocephalus)

FOCAL SEIZURES OR FOCAL SEIZURES

WITH SECONDARY GENERALIZATION

Normal clinicopathological tests

Normal clinicopathological tests
Normal or abnormal neurological
Normal neurological examination
examination
Normal CSF analysis, CT and/or MRI
Abnormal CSF analysis, CT and/or MRI

Idiopathic or cryptogenic epilepsy Symptomatic epilepsy

(residual damage) (i.e. encephalitis, head trauma,
neoplasia or hydrocephalus)

• Seizure length? Most seizures last a few seconds or • Is the animal normal between the seizures? If the
minutes. Focal seizures may be brief, but can occur animal’s behavior is abnormal between well spaced
in clusters. seizure events, then seizures from extracranial
• Is there any abnormality evident after the possible disorders or symptomatic epilepsy are more likely.
seizure event? Identification of a post-ictal phase • Are the seizures associated with sleeping, feeding,
can be important to confirm seizures, as this activity fasting, exercise or stressful situations? Some dogs
is not seen with syncope, narcolepsy or REM sleep with idiopathic epilepsy or cryptogenic epilepsy may
behaviour disorder. In rare instances the animal seizure while sleeping, but cannot be awakened like
may have to be sedated because of prolonged animals with REM sleep behaviour disorder.
hyperactivity during the post-ictal phase. Seizures following feeding may be associated with
Occasionally it may become aggressive and should hepatic dysfunction. Seizures during fasting, exercise
not be handled until this phase resolves. or stress may be associated with hypoglycaemia.
Stressful situations may precipitate seizures in a few
dogs with idiopathic or cryptogenic epilepsy.
 SEIZURES 169

• Has there been exposure to other drugs or toxins?

See Table 39, page 167.
• Has the animal been sufficiently vaccinated for the
local endemic infections?
• Has there been a recent or past illness?
• Recent or past head injury? Seizures may occur at
the time of a head injury or up to several years later
from residual brain scarring.
• Is there any familial history of seizures? If the
parents, siblings or other relatives have epilepsy, an
inherited problem should be suspected.
• What is the diet? Although rare, thiamine
deficiency can cause seizures in dogs and cats.  134 Electroencephalogram traces from a dog with
Inadequate nutrition leading to hypoglycaemia can seizure activity recorded while the dog was under
cause seizures in toy breed dogs. anaesthesia. Multiple spike (arrows) and wave discharges
• What previous medications or treatments have are noted, compatible with abnormal synchronized
been given for seizures? Current antiepileptic discharges from multiple cerebrocortical neuronal cells.
medications or other therapies and their
effectiveness should be documented to help develop
an effective strategy for long-term seizure • Electroencephalography can confirm seizure
management if necessary. activity in the brain, but is not specific in most cases
as to the underlying cause (134).
Specific investigations (133)
Suspected extracranial causes Idiopathic epilepsy
• Complete haematology. Overview
• Comprehensive biochemistry, including pre- and Idiopathic (inherited) epilepsy has been documented in
post-prandial bile acids. Beagles, German Shepherd Dogs, Belgian Tervurens,
• Urinalysis. Keeshonds and Dachshunds and is also suspected in
• Toxicity screening: serum lead levels; serum Saint Bernards, Australian Shepherd Dogs, Labrador
cholinesterase levels; ‘recreational’ drug exposure Retrievers, Golden Retrievers, Irish Setters, Standard
testing may be available through the local general Poodles, Springer Spaniels, Cocker Spaniels, Lhasa
hospital, or even some pharmacies. Apsos, Border Collies and many other purebred dogs.
• Infectious disease (IgM and IgG) serology and Idiopathic epilepsy has not yet been documented in cats.
PCR.
Clinical presentation
Suspected intracranial causes Generalized seizures with loss of consciousness are very
• Thoracic radiographs. common and usually begin at between 1 and 3 years of
• MRI or CT of the brain. age, but in a few dogs seizures begin at between 6 months
• CSF analysis (protein quantification, complete and and 1 year of age or between 3 and 7 years of age. The
differential cell count). onset of seizures is almost always insidious, beginning
• In those cases with inflammatory CSF or with a seizure every few weeks or months, but then
compatible CNS imaging findings, consideration becoming progressively more frequent. Many dogs even-
should be give to performing serology/PCR and/or tually develop cluster seizures or status epilepticus and, in
CSF-PCR for all infectious diseases reported in the rare cases, this may be the first known seizure activity.
region/country. German Shepherd Dogs, Australian Shepherd Dogs,
Belgian Tervurens, Springer Spaniels, Labrador Retriev-
ers and Saint Bernards are prone to cluster seizures.
170 DECISION MAKING

Diagnosis
The diagnosis is suspected in a purebred dog with gener- • No abnormalities in the inter-ictal period.
alized seizures and normal findings on physical and • If these cases later develop additional clinical signs
neurological examinations between seizures and all diag- to suggest an alternative diagnosis or if the seizure
nostic tests including MRI and CSF analysis. Breeding control is poor, then further investigation would be
trials may be needed to confirm the diagnosis if no other justified.
dogs in the lineage have had seizures. Unless animals are
presented with severe cluster seizures or status epilepti- Management
cus, therapy is aimed at controlling the seizures with The treatment of seizure activity on an emergency basis
maintenance anticonvulsant therapy. is detailed in Chapter 23. Unless idiopathic or crypto-
It would not be unreasonable to make a diagnosis of genic epilepsy is considered to be the primary differential
idiopathic epilepsy in a dog (and to a lesser extent a cat) for the seizure activity, specific treatment of the under-
demonstrating: lying cause is essential and the success of this will
• The right age and signalment (particularly in a determine the need for symptomatic seizure therapy.
breed with a high incidence of idiopathic epilepsy). The aims of seizure treatment are:
• A normal haematological and biochemical • To reduce the frequency and severity of seizures.
evaluation. (It is important to explain to the owner that the
• History and seizure characteristics consistent with animal may still seizure despite the therapy.)
idiopathic epilepsy (generalized tonic–clonic • To minimize potential side-effects.
seizures from rest and with the seizure onset at • To maximize the owner’s and dog’s quality of life.
between 1 and 3 years of age). (Note: From
6 months to 6 years is acceptable.)

Table 40 Maintenance anti-epileptics for use in cats

DRUG T1⁄2 (hours) RECOMMENDED DOSE MAJOR POSSIBLE SIDE-EFFECTS

Phenobarbitone 34–43 2–5 mg/kg/day PO (divided Sedation; ataxia; polyphagia with weight gain;
q12h) thrombocytopenia; swelling of feet; facial
pruritis; cutaneous eruption; lymphadenopathy

Diazepam 15–20 0.5–2.0 mg/kg/day PO (divided Acute hepatic necrosis; sedation; ataxia
q12h or q8h)

Potassium bromide 10 days 30 mg/kg/PO q24h Bronchial asthma

Gabapentin 5–10 mg/kg PO q24h Sedation; ataxia

Levetiracetam 3 10–20 mg/kg PO q8h Sedation; decreased appetite

Zonisamide 33–35 5–10 mg/kg PO q24h Sedation; anorexia; vomiting; diarrhoea

Pregabalin 5–10 mg/kg PO q12h Sedation

(Modified from Podell M (2005) Seizures. In: BSAVA Manual of Canine and Feline Neurology. (eds. SR Platt, NJ Oldby)
British Small Animal Veterinary Association, Gloucester.)
 SEIZURES 171

Table 41 Maintenance anti-epileptics for use in dogs

DRUG T1⁄2 (hours) TSS (days) SUGGESTED SERUM RECOMMENDED POSSIBLE

THERAPEUTIC RANGE DOSE SIDE-EFFECTS

Phenobarbitone 32–89 10–18 20–35 mg/dl 2–3 mg/kg PO Sedation; ataxia; polydipsia/
q12h polyuria; polyphagia; hyper-
excitability; hepatotoxicity;
induces P450 system; bone
marrow dyscrasia; pancreatitis

Potassium bromide 21–24 2.5–3.0 1–3 mg/ml 20–40 mg/kg PO Sedation; weakness;
days months q24h polydipsia/poyuria; polyphagia;
pancreatitis; pruritis;
behavioural changes

Felbamate 5–6 1–2 25–100 mg/l 15–70 mg/kg PO Blood dyscrasias; liver disease;
q8h dry eye

Topiramate 20–30 3–5 2–25 mg/l 2–10 mg/kg PO Vomiting; diarrhoea; sedation
q12h

Clorazepate 5–6 1–2 20–70 μg/l 0.5–1.0 mg/kg PO Sedation

(nordiazepam) q8–2h

Zonisamide 15–20 3–4 10–40 μg/ml 2.5–10.0 mg/kg Sedation; loss of appetite;
PO q12h dry eye; ataxia

Gabapentin 3–4 1 4–16 mg/l 10–20 mg/kg PO Sedation; ataxia

q8h

Levetiracetam 3–4 1 Not known 10–20 mg/kg PO Sedation; ataxia

q8h

Pregabalin 7 2–3 >2.8 μg/ml 3–4 mg/kg PO Sedation; ataxia

q8h–12h

TSS = approximate time to steady state

(Modified from Podell M (2005) Seizures. In: BSAVA Manual of Canine and Feline Neurology. (eds. SR Platt, NJ Oldby)
British Small Animal Veterinary Association, Gloucester.)

Although largely arbitrary and greatly dependent on • The seizures are increasing in frequency or severity.
owner demands and compliance, the following would be • An underlying progressive intracranial disorder has
a reasonable guide as to when to start treating seizures: been identified as the cause of the seizures.
• When more than one seizure occurs per month • Post-ictal signs are objectionable (e.g. aggression).
and/or the owners object to their frequency.
• If the animal has a very severe seizure or cluster of Specific drugs for seizure treatment in cats and dogs can
seizures, irrespective of the frequency of the be found in Tables 40 and 41, respectively.
seizures or seizure clusters.
This page intentionally left blank
 DECISION MAKING Chapter 8

EXERCISE-ASSOCIATED WEAKNESS
AND COLLAPSE 173

Arianna Negrin
& Simon Platt

INTRODUCTION the three major differential diagnoses of collapse in

addition to NM disease: seizures, syncope and
Exercise- or activity-associated weakness and collapse narcolepsy–cataplexy. Metabolic diseases (including
and exercise intolerance are distinct entities. They may Addisonian crisis) and paroxysmal disorders (i.e.
represent different clinical expressions of a primary Scotty cramp/Cavalier King Charles Spaniel hyper-
neuromuscular (NM) disease or can be secondary to tonicity/sleep disorders) also need to be considered
cardiovascular, metabolic/systemic or primary CNS as differentials in the collapsed patient.
conditions, including narcolepsy/cataplexy. • Exercise intolerance can be considered as
The NM system is composed of motor units, intermittent weakness or collapse, associated with
consisting of the neuronal cell body situated in the different levels of activity, which improves with rest.
ventral horn of the spinal cord, its axon, the NM junction Respiratory and cardiovascular dysfunction, as well
and the muscle unit composed of muscles fibres. In as orthopaedic disease, need to be considered as a
addition to motor units, there is a sensory component potential cause of exercise intolerance in addition to
existing as receptors, peripheral sensory axons, which are those diseases responsible for collapse.
associated with motor axons in most nerves, and dorsal • Narcolepsy and cataplexy are disorders in
root ganglions. The NM system has been referred to as sleep/wake control that may cause acute weakness,
the LMN system and in this chapter the two terms will sometimes associated with physical activity.
be considered synonymous. Narcolepsy, defined as excessive daytime sleepiness
In the clinical approach to the weak patient, it is with alteration of nocturnal sleep patterns, has been
important to define the specific terminology used: reported in many canine breeds and in some of
• Weakness, or paresis, is the inability to generate them (Labrador Retrievers and Doberman
voluntary movement and/or to support weight due Pinschers) an autosomal recessive inheritance has
to a lesion affecting the upper or lower motor been demonstrated. Cataplexy is characterized by
pathway. Signs of NM weakness relate to a lesion sudden flaccid muscular weakness, ranging from
of the LMN pathway. They include flaccid dropping of the jaw or head to complete collapse
paresis/paralysis, often manifested as a short- without loss of consciousness, frequently induced
strided gait and a progressive reluctance to walk or by excitement, such as eating or playing, and
run. Additional signs accompanying NM weakness often manifesting as muscular weakness (see
include ventroflexion of the neck, hyperflexion of Chapter 6). The pathophysiology is still unclear;
the joints, a plantigrade posture, a generalized however, recent studies have suggested that
decrease in muscle tone, occasional muscle deficiency of some hypothalamic neuropeptides
tremors and, in chronic cases, muscle atrophy. (hypocretins) and/or their receptors may play an
• Collapse is an acute event that may be a important role in the development of these sleep
manifestation of more chronic and progressive disorders.
NM diseases; however, it is important to consider
174 DECISION MAKING

Table 42 Key questions regarding episodic weakness, collapse or paroxysmal events

QUESTION IMPLICATIONS

What did the event look like? It may be difficult to distinguish the event from seizure activity,
and some may be seizures, but it will be important to establish that
these events are not due to a metabolic or cardiovascular crisis

Has this happened before? Episodic or paroxysmal events that warrant investigation should
be recurrent

How often has this happened? The answer will provide an insight into the progressive nature of the
disease and will serve as a marker for response to therapy

Has it always had the same characteristics? Paroxysmal events are usually stereotypical

Is the animal ‘normal’ immediately after these events? A seizure may be followed by a period of confusion, visual
dysfunction, compulsion or even aggression. NM disorders,
movement disorders and syncopal events usually have no such
associations

Is there any type of trigger factor that can be identified? Excitement or eating, which often causes a loss of consciousness
and/or collapse, should prompt the thought of narcolepsy/cataplexy.
Several documented events occur during sleep, such as the REM
sleep disorder. Exercise/excitement may be the trigger for the
syndromes described in Cavaliers and Scotties as well as many NM
diseases and hypoglycaemic-related collapse. Rarely, seizure events
will be triggered by a specific noise or action. Events seen more than
8 hours after last feeding may suggest hypoglycaemic collapse

Is the animal normal in between the events? Any abnormalities described in between the episodes could indicate
a structural CNS or neuropathic or myopathic disease. Metabolic and
cardiovascular diseases may be associated with a waxing and
waning clinical course, with some abnormalities detectable in
between the acute events

Are any other littermates known to be affected? Breed-associated events may be seen in related siblings; however,
underlying infectious diseases and toxicities should not be ignored

Is the animal stiff or floppy at the time of the event? Stiffness at the time of the event would often imply either a seizure
event, a movement disorder or a myopathy. A floppy animal at the
time of the event could also be a myopathy, but could also indicate
a cardiovascular or metabolic disease

Are the gums pale at the time of the event? Mucous membrane pallor could well indicate a cardiovascular
disease; however, metabolic diseases, such as Addison’s disease,
should also be considered
 E X E R C I S E - A S S O C I AT E D W E A K N E S S AND COLLAPSE 175

• Paroxysmal breed related disorders (Scotty

ACUTE
cramps, hypertonicity in Cavalier King Charles WEAKNESS/COLLAPSE
Spaniels, paroxysmal dyskinesia in Chinooks and
‘cramping’ in Norwich Terriers) are characterized
Organ dysfunction,
by sudden and transient onset of neurological signs electrolyte imbalance,
Ascites, hepatomegaly,
often elicited by stress or exercise and most likely splenomegaly,
endocrine disorders,
miscellaneous disorders,
due to abnormal CNS neurotransmission. The pale/cyanotic mucous erroneous medical
membranes, YES
neurological scenario is usually characterized by therapies
decreased/increased
initial progressive stiffness of the forelimbs, body temperature
followed by the hindlimbs, and it may progress to METABOLIC DISEASE
recumbency without loss of consciousness. These
NO
episodes usually resolve spontaneously within
10 minutes (see Chapter 13).
Polyarthritis, bone
The approach to a patient with acute exercise- or Joint effusion, fractures, degenerative
activity-associated weakness or collapse may be very lameness, pain and joint disease
reduced joint YES
challenging for the clinician, as numerous aetiologies movements
can potentially be responsible. A complete physical and ORTHOPAEDIC DISEASE
neurological examination, combined with the informa-
tion on the signalment and anamnesis, represents the NO
first and one of the most important steps in deciding if
the weakness/collapse originates from a primary neuro- Cardiac arrhythmias,
logical condition (including NM or CNS diseases) or hypotension, reduced
is caused by cardiovascular, respiratory, metabolic or Pale/cyanotic mucous cardiac output,
membranes, weak and vasovagal syncope,
orthopaedic disorders (Table 42). arrhythmic pulse, YES laryngeal paralysis,
The main differential diagnoses for neurological abnormal chest sounds, pulmonary diseases
dyspnoea, cough
causes of exercise- or activity-associated weakness/ CARDIORESPIRATORY
collapse depend on the lesion localization (i.e. CNS and DISEASE
the three main subdivisions of the NM system: neuro- NO
pathies, junctionopathies and myopathies).
The systemic causes of exercise- or activity-associated
weakness or collapse, such as orthopaedic, metabolic and
Seizures, narcolepsy
cardiorespiratory conditions, should be ruled out prior to Loss of consciousness
YES
investigating the NM system (135). Most metabolic during episodes
CENTRAL NERVOUS
disorders may have an effect on the functions of other SYSTEM DISEASE
systems, including the NM system and CNS, creating a
complex mixture of clinical signs. For this reason, evalu- NO
ation of the real neurological component of weakness in
these animals may be very difficult or, sometimes, impos-
sible until the metabolic imbalance has been addressed.
Reduced spinal
reflexes, ± cranial NEUROMUSCULAR
YES DISEASE
nerve dysfunction

MOVEMENT
DISORDER/
NO
 135 Systemic approach to an acutely collapsing PAROXYSMAL
DYSKINESIA
animal.
 176 DECISION MAKING

• Step 1. Rule out orthopaedic diseases, including peripheral pulses, bradycardia, hepatomegaly,
polyarthritis, degenerative joint disease, develop- splenomegaly, pale/cyanotic mucous membranes,
mental bone disorders and bone fractures. Physical decreased/increased body temperature and
examination may detect a stiff gait associated with vomiting/diarrhoea. Diagnosis may be reached
joint effusion and pain in dogs with polyarthritis; through the use of multiple standard diagnostic
this can be confirmed by synovial fluid analysis and tests (see Specific diagnostic tests, p. 184).
joint radiographs (136). Radiographs are useful in • Step 3. Rule out cardiorespiratory diseases,
the detection of appendicular bone fractures, devel- including arrhythmia, hypotension, reduced cardiac
opmental bone disorders (panosteitis, metaphyseal output, vasovagal syncope, thromboembolism,
osteopathy) and in degenerative arthropathies. laryngeal paralysis, pulmonary disease and
Blood tests, serology for infectious agents (Ehrlichia pleural/pericardial effusion. Pale/cyanotic mucous
spp., Borrelia burgdorferi, Mycoplasma spp., FeLV), membranes, weak and irregular pulse, abnormal
synovial fluid culture and an antinuclear antibody chest sounds, dyspnoea and coughing should alert
test are some of the tests often required to the clinician to investigate the potential for
investigate the aetiology of polyarthritis. cardiorespiratory diseases. Chest radiographs,
• Step 2. Rule out metabolic diseases, including ECG and echocardiography are mandatory in every
electrolyte imbalance, endocrine diseases patient with a history of collapse and signs of
(addisonian crisis, insulinoma, hypoglycaemia, cardiorespiratory disease.
diabetic ketoacidosis), erroneous dosage of • Step 4. Rule out CNS disorders, including seizures,
treatments (insulin) and miscellaneous disorders narcolepsy and paroxysmal movement disorders.
(anaemia, shock, acidosis, pyrexia). Physical CNS lesions may cause a sudden generalized
examination may detect signs of ascites, weak collapse/weakness with a loss of consciousness and
may be associated with excitement or exercise. CNS
lesions may be associated with visual deficits,
abnormal behaviour and/or levels of consciousness
as well as CN deficits. Sometimes, history,
signalment and clinical examination may not help
rule out a CNS lesion or related event and so the
clinician needs to rely on diagnostic tests, video
footage provided by the owner and treatment trials.

NEUROANATOMICAL BASIS OF NEURO-

MUSCULAR CAUSES OF WEAKNESS
AND COLLAPSE

Knowledge of the basic physiology of nerve and muscle

function is essential for comprehending their dysfunc-
tion. The physiology of the NM system can be divided
into two main areas:
• Ion function. Ions such as sodium, potassium
and calcium are essential for impulse generation
and transmission and for the mechanism of muscle
contraction.
• Energy metabolism of myofibres. Normal energy
 136 Lateral carpal radiograph of a dog that exhibited reserves and metabolism are required for adequate
weakness due to polyarthritis. Soft tissue swelling and muscle contraction and relaxation.
periosteal proliferation are evident.
 E X E R C I S E - A S S O C I AT E D W E A K N E S S AND COLLAPSE 177

Na+ channel Myelin sheath

Axon Depolarization

Action potential
Node 1 Node 2 Node 3
K+ channel

Depolarization

Action potential

Ion function  137 Saltatory conduction is the mechanism by which

Normal skeletal muscle fibres are stimulated by the signals travel in myelinated nerves. As sodium ion
LMN via the creation of electrical action potentials channels open at the unmyelinated nodes of Ranvier, that
generated at the NM junction (motor endplate). A pre- section of the membrane is depolarized, resulting in an
synaptic action potential is generated by movement of action potential that is conducted from node to node as
sodium and potassium ions along the nerve-cell subsequent channels are triggered. Electrical current
membrane and is influenced by calcium. An electrical flows through the surrounding extracellular fluid outside
potential exists in all cells, called the membrane potential the myelin sheath, as well as through the axoplasm inside
(resting potential), whereby the inside of the cell is the axon.
negatively, and the outside is positively, charged. The
membrane potential of nerve and muscle cells is capable
of abrupt change into an action potential providing a
capacity for ‘excitement’. In the resting state, sodium the interior of the axon, with an increase in the
concentration is high outside the nerve cell (in the extra- membrane potential (depolarization). Once the potential
cellular fluid), while potassium concentration is high attains positivity (+35 mV), the sodium channels begin
inside the cell (intracellular compartment); this is regu- to close and potassium ions diffuse to the exterior,
lated by the sodium–potassium pump, which exchanges 3 re-establishing the normal negative resting membrane
sodium ions for 2 potassium ions, leaving a net deficit of potential (repolarization) (see 125). The axon is sur-
positive ions on the inside and maintaining a stable mem- rounded by a myelin sheath; every 1–3 mm along the
brane potential at -70 mV. Nerve signals are transmitted length of the myelin sheath is a node of Ranvier. This is a
by action potentials, which are rapid changes to a positive junction between two Schwann cells, which form the
potential (depolarization) with a rapid return to a nega- myelin around the axon. The depolarization process
tive potential (repolarization). During depolarization the travels along the entire nerve from node to node to the
cell membrane becomes very permeable to sodium ions, NM junction (motor endplate); this is termed saltatory
allowing a large number of sodium ions to diffuse into conduction (137).
 178 DECISION MAKING

 138 The neuromuscular junction Skeletal muscle

connecting a large, myelinated nerve Muscle fibre
fibre to a skeletal muscle fibre. The Spinal cord
nerve fibre forms a complex of Ventral horn
branching nerve terminals that Motor neuron
invaginate into the surface of the Myelin sheath
muscle fibre, but lie outside the plasma
membrane. The entire structure is
called the motor endplate. It is covered
by one or more Schwann cells that
insulate it from the surrounding fluids.
Acetylcholine is released into the
synaptic cleft and binds to receptors on
the highly folded membrane.

Motor endplate

Mitochondrion
Vesicle containing acetylcholine
Muscle fibre
Junctional fold
Acetylcholine receptor

The nerve-fibre terminals invaginate into the surface When an action potential spreads over the terminal
of the myofibres, forming a structure called the motor of the nerve fibre, voltage-gated calcium channels open,
endplate or NM junction (138). The space in between allowing calcium ions to diffuse from the synaptic space
the muscle membrane (postsynaptic membrane) and the into the nerve terminal. The calcium ions serve to
nerve fibre membrane (presynaptic membrane) is called modulate the subsequent release of ACh at the motor
synaptic space and it represents the site where transmis- endplate, stimulating ACh vesicles to fuse with the neural
sion of impulses between nerve and muscle takes place, membrane.
mediated by the neurotransmitter acetylcholine (ACh).
 E X E R C I S E - A S S O C I AT E D W E A K N E S S AND COLLAPSE 179

Activation of ACh-gated ion channels in the muscle- Table 43 Electrolyte abnormalities and
fibre membrane allows large numbers of positive ions neuromuscular weakness
(Na+, K+ and Ca++), in particular sodium ions, to diffuse
ABNORMALITY PRIMARY CAUSES CLINICAL SIGNS
inside the myofibre, creating a local positively-charged
potential, called an endplate potential, which secondarily Hyperkalaemia Acute renal failure Muscle weakness
spreads along the muscle membrane. Once ACh is Hypoadrenocorticism Cardiac arrhythmia
released into the synaptic space it is rapidly removed by K+ sparing diuretics
acetylcholinesterase, an enzyme that degrades ACh, thus Metabolic acidosis
avoiding continuous stimulation of the post-synaptic Iatrogenic
membrane.
Hypokalaemia Renal loss Muscle weakness
Once depolarization reaches the muscle fibre, the
Intestinal loss Hypovolaemia
sarcoplasmic reticulum releases large quantities of stored
calcium ions, which become responsible for myofibre Metabolic alkalosis

contraction and subsequent relaxation. In summary, Hypocalcaemia Primary hypo- Muscle weakness
ionic imbalances, particularly of calcium or potassium, parathyroidism
may produce severe alterations of nerve and muscle Hyperphosphataemia Tetany
function, resulting in episodic weakness. Eclampsia Mental depression
Iatrogenic Seizures
Energy metabolism
Hypercalcaemia Malignant tumours Muscle weakness
Contraction of myofibres essentially requires energy.
Primary hyper- Mental depression
Two main substrates supply energy to the muscle: parathyroidism Polydipsia/polyuria
glycogen and fatty acids, through glycolysis and Hypervitaminosis D Constipation
β-oxidation, respectively. During intense exercise the
primary source of energy for muscle is glycogen via Hyponatraemia Intestinal loss Muscle weakness
anaerobic glycolysis, in which glycogen is converted to Hypoadrenocorticism Lethargy
pyruvate, which is transported to mitochondria where it Inappropriate anti- Seizures
is incorporated into the tricarboxylic acid (TCA) cycle diuretic hormone Coma
secretion
for energy production.
Iatrogenic
Lipids, on the other hand, in the form of fatty
acids, are the major substrates for energy production Hypernatraemia Water deprivation Muscle weakness
during aerobic muscle contraction via mitochondrial Excess salt gain Muscle rigidity
β-oxidation during sustained exercise. Carnitine plays a Pure water loss Tremors
major role in modulating transport of fatty acids into Seizures
mitochondria for β-oxidation; it also acts as a buffer Coma
against accumulation of organic acids, transferring them
outside the mitochondria to be excreted in the urine.
Therefore, disorders of muscle metabolism can cause
acute weakness associated with exercise.

Neuromuscular system causes of weakness

and collapse
Potential NM abnormalities causing acute generalized NM junction transmission, while muscle contraction
weakness/collapse can be due to dysfunction at one of depends highly on energy metabolism. However, ionic
the three levels into which the NM system is functionally balance, especially between calcium and potassium, is
divided: nerve transmission (neuropathies); NM trans- also essential in normal muscle contraction, and elec-
mission (junctionopathies); and muscle contraction trolyte abnormalities are associated with a wide range of
(myopathies). Ion disorders mainly affect nerve and signs (Table 43).
 180 DECISION MAKING

In nerve transmission, disorders affecting the axon ACh receptor dysfunction (congenital or acquired MG).
structure (139) or the myelin organization affect the A complete differential diagnosis for NM junction disease
velocity and/or amplitude of action potentials trans- in dogs and cats affected by exercise- or activity-associated
mitted along the nerve fibre, resulting in muscular weak- acute weakness and collapse is listed in Table 46.
ness. The clinical signs and differential diagnosis of a Efficient muscle contraction requires ionic balance
peripheral neuropathy are listed in Tables 44 and 45, (in particular between potassium and calcium ions),
respectively. intact myofibre structure and contraction coupling, and
The major NM junction abnormalities causing acute efficient energy metabolism. The clinical signs and dif-
collapse are ion disorders, altered ACh release (botulism, ferential diagnosis of myopathy are detailed in Tables 44
tick paralysis) or degradation (OP/carbamate toxicity) and and 47, respectively.

 139 Peripheral nerve anatomy. Each nerve is covered

by a sheath of connective tissue (the epineurium)
containing bundles of nerve fibres wrapped in a second
layer of tissue (the perineurium) while a further layer (the
endoneurium) surrounds the individual nerve fibres or
axons. In myelinated nerves, Schwann cells create a
myelin sheath around the axons.

Epineurium
Perineurium Myelin sheath
Endoneurium Axon

Table 44 Differentiation of neuropathy from myopathy on the neurological examination

PERIPHERAL NEUROPATHY MYOPATHY

Mental status Normal Normal

Posture/gait Plantigrade stance; flaccid paresis or paralysis; ataxia Stiff and paretic gait; exercise-induced
may be present if the sensory nerve is affected (rare) weakness/stiffness

Postural reactions Decreased (sensory) Decreased only in severe weakness

Cranial nerves May be involved Rarely affected

Spinal reflexes Decreased to absent Decreased only in chronic muscle disease

Muscle tone Decreased (motor) Normal to decreased (rarely increased)

Sensation Decreased to absent unless pure motor Normal

nerve disease

Muscle atrophy Present; often severe and rapid in onset and Atrophy or hypertrophy; muscle contracture
progression may be present in chronic cases
 E X E R C I S E - A S S O C I AT E D W E A K N E S S AND COLLAPSE 181

Table 45 Differential diagnosis for exercise-associated weakness and collapse due to

peripheral nerve disease

DISEASE MECHANISM EXAMPLES

Vascular Ischaemic neuromyopathy (see note)

Vascular anomalies compressing the nerve roots (rare)

Inflammatory/infectious Acute idiopathic polyradiculoneuritis*

Infectious polyneuropathies (Neospora caninum, feline leukaemia virus, feline
immunodeficiency virus)
Brachial plexus neuritis

Toxic Toxic/drug-induced neuritis (vincristine, organophosphates)

Metabolic Diabetes mellitus (D, C)

Hypothyroidism (D)*
Electrolyte imbalance* (see Table 43)
Hypoglycaemia-associated neuropathy

Idiopathic Distal denervating disease

Neoplastic Neoplastic (lymphoma, peripheral nerve sheath tumour, malignant sarcoma)

Paraneoplastic immune-mediated polyneuropathy (insulinoma, lymphoma, pulmonary
carcinoma, haemangiosarcoma)

* Common cause; D = dog; C = cat.

Note: Ischaemic neuromyopathy usually affects the hindlimbs and is characterized by acute onset and static progression, but can
infrequently be exercise/activity related and intermittent. It is important to assess peripheral pulses and abdominal vasculature in
dogs and cats presented with intermittent weakness.

Table 46 Differential diagnosis for exercise-

NEUROLOGICAL EVALUATION associated weakness and collapse
due to disorders of the neuro-
In a patient with activity-associated weakness or collapse muscular junction
and where a neurological condition is suspected rather
DISEASE MECHANISM EXAMPLES
than abnormalities of other systems, a detailed history
(see Table 42) and neurological examination are manda- Toxic Botulism*
tory. A thorough description of the weakness or collapse, Tick paralysis*
especially if supported by video footage, can provide Organophosphate/
important information about the speed of onset of carbamate toxicity
neurological signs, potential loss of consciousness during Snake bite
the events and type of activity the patient was perform- Anomalous Congenital myasthenia gravis*
ing at the time of the ‘episode’.
The neurological examination aims to localize the Idiopathic Acquired myasthenia gravis*
lesion within the nervous system in order to list appro- Neoplastic Paraneoplastic myasthenia gravis
priate differential diagnoses and establish what further
tests might be necessary. * Common cause
182 DECISION MAKING

Table 47 Differential diagnosis for exercise- Activity-associated weakness is the most typical
associated weakness and collapse clinical sign of NM disease. Interpretation of the neuro-
due to disorders of the muscles logical examination may be challenging in these patients.
At the time of examination they may appear normal or
DISEASE MECHANISM EXAMPLES
only mildly affected; additionally, if weakness is
Vascular Ischaemic neuromyopathy exhibited, it is rarely specifically indicative of nerve, NM
(see note) junction or muscle disease. In a patient with a NM disor-
Inflammatory/infectious Immune-mediated der, observation and gait analysis may detect ventro-
inflammatory myopathies (D)* flexion of the neck, a short-strided gait with overflexion
Infectious polymyositis* of the joints (often more evident in the hindlimbs),
(Toxoplasma gondii, Neospora a plantigrade stance at rest (140) and a generalized
caninum), (Ehrlichia spp.,
decreased muscle tone. In general:
bacterial, very rare)
• In contrast to UMN diseases, disorders of the
Metabolic Diabetic ketoacidosis LMN do not cause ataxia, only paresis. Due to their
(hypokalaemic myopathy close anatomical relationship within the caudal
in cats)*
brainstem and spinal cord, most gait abnormalities
Hypothyroidism (D)*
involving the UMN pathways necessary for gait
Hyperthyroidism (C)*
generation also cause some degree of proprio-
Hyperadrenocorticism*
ceptive ataxia. Diseases affecting the LMN system
Hypoadrenocorticism (D)*
are, by definition, not ataxic. If ataxia is present in
Electrolyte imbalance (see Table the collapsing patient, a lesion affecting the
43) (hypokalaemic myopathy
in cats)* cerebellum, the vestibular system or the ascending
Hypoglycaemia (D, C)* general proprioceptive pathways in the spinal cord
Myopathy related to
should be considered.
glucocorticoid excess • NM disease can be asymmetrical in presentation.
Heat stroke rhabdomyolysis (D, C) • The hindlimbs can be affected without obvious
Mitochondrial myopathy (D) signs in the forelimbs in patients with acute-onset
Lipid storage myopathy (D) NM disease.

Idiopathic Exertional rhabdomyolysis (D)

Breed specific exercise-induced
collapse (D)
Necrotizing polymyositis (D)

Neoplastic Neoplastic (lymphoma, peripheral

nerve sheath tumour,
rhabdomyosarcoma, metastatic
neoplasia)
Paraneoplastic polymyositis
(lymphoma)

Nutritional Vitamin E deficiency (D)

* Common cause
D = dog; C = cat.
Note: Ischaemic neuromyopathy usually affects the hindlimbs
and is characterized by an acute onset and static disease, but it
can infrequently be exercise/activity related and intermittent.

 140 A plantigrade stance suggestive of peripheral

nerve disease.
 E X E R C I S E - A S S O C I AT E D W E A K N E S S AND COLLAPSE 183

A neurological evaluation should follow the following • Step 3. Is the disease focal versus diffuse? In a
steps: patient affected by generalized weakness associated
• Step 1. Confirm the exercise/activity relationship to with exercise intolerance, the neurological
the problem described. Exercise testing is examination should aim to detect any other
mandatory and represents a good tool in evaluating peripheral nerve dysfunctions. Diffuse NM disease
metabolic pathways. From rest to maximal exercise, often causes the spinal reflexes in all limbs to be
energy demand progressively exacerbates clinical reduced to absent. In more generalized NM
signs due to the increased muscle metabolism. The diseases, specific dysfunctions, such as dysphagia
relationship of the primary complaint to activity (pharyngeal paralysis), dysphonia (laryngeal
may be obvious in some patients after a few steps, paralysis), regurgitation (oesophageal abnormalities)
but in some it may require a few minutes of activity and extraocular muscle paresis, as well as intercostal
to assess the potential effects on the gait. This is and diaphragmatic muscle weakness, may be
obviously very difficult in the cat. A protracted observed. Focal LMN disease may represent early-
period of observation may be essential in a room onset disease, especially in the acute stages, with the
where the cat cannot seek a hiding place. The main potential for rapid deterioration, but it may also
purpose of this step is to further confirm the represent a focal lesion in the spinal cord affecting
suspicion of a peripheral neurological abnormality the cell bodies of the LMNs.
by determining whether the characteristics of the • Step 4. Is the disease affecting peripheral nerve,
gait are compatible with NM disease. Additionally, muscle or NM junction? From a clinical point of
this will give the observer a chance to assess the view, in the majority of cases, distinguishing a
severity of the problem, the onset of pain with neuropathy from a junctionopathy or a myopathy is
activity (which may not be present at rest) and the not possible. However, some parts of the
effects of activity on the cardiorespiratory system. neurological examination, including evaluation of
• Step 2. Is the lesion UMN or LMN? Once a gait, postural reactions, spinal reflexes and
neurological abnormality has been observed, the sensation, can be particularly helpful in
paresis must be determined to be either UMN or distinguishing a muscular from a peripheral nerve
LMN in origin, although spinal localization is very disorder (see Table 44). In summary:
unlikely for neurological presentation exacerbated • Postural reaction deficits (knuckling) are
by or exclusively present at exercise. Disorders of usually only present with peripheral nerve
the UMN system result in spastic paresis and problems and not NM junction and muscle
normal to increased spinal reflexes, while NM disease. However, it may be difficult to evaluate
conditions (LMN system disorders) are character- very weak patients and to discern whether the
ized by flaccid paresis and decreased spinal reflexes. postural reaction abnormalities are real or not.
However, many NM conditions may actually
manifest with an apparent increase in tone, or
stiffness, at the time of the exercise- or activity-
associated weakness or collapse. Segmental spinal
reflexes should be evaluated before and after
exercise or activity.
184 DECISION MAKING

DIFFERENTIAL DIAGNOSIS FOR

NEUROMUSCULAR WEAKNESS AND COLLAPSE

The differential diagnoses to be considered depend on

the lesion localization in addition to the signalment,
history and response to previous treatment attempts. For
this reason, the potential NM causes of acute generalized
weakness and collapse need to be considered separately
by dividing them into:
• Neuropathies.
• Junctionopathies (NM transmission diseases).
• Myopathies.

Specific diagnostic tests

The tests listed below and in Table 48 (p. 186) should be
considered in any case of acute exercise-associated weak-
ness or collapse, although the diagnostic plan needs to be
specifically addressed after taking into consideration the
suspected underlying cause (142).
 141 Profound muscle atrophy in the
muscles supplied by the sciatic nerve Rule-out systemic aetiologies
suggests neurogenic atrophy. • Routine blood tests and urine analysis.
Haematology, complete serum biochemistry and
urine analysis should all be considered as the
• The flexor withdrawal reflex is usually intact minimum essential database, together with chest
with NM junction disease and acute-onset radiography and abdominal ultrasound.
muscle disease, but multiple rapid repetition • Serum CK levels. Evaluation of serum CK
may cause its progressive decrease. These concentration should be a part of the NM
reflexes are often reduced with peripheral nerve minimum database and may be indicative of active
disease and with chronic muscle disease. muscle disease in canine and feline patients.
• Muscle atrophy will be seen with nerve and The serum half-life of CK is very short, lasting only
muscle disease after 7–10 days, but not with 6 hours; a persistent elevation of 4–5 times the
NM junction disease (141). normal level in two tests carried out between 24 and
48 hours of each other is an indication of a recent
Additionally, there are some specific diagnostic tests and active muscle lesion. CK may be normal in the
that may help better define the lesion localization (e.g. presence of muscle disease, therefore muscle disease
CK serum levels, electrophysiology and an edrophonium should not be ruled out based on a normal CK
test) (see below). concentration. Serum CK may also be mildly
elevated in the absence of NM disease related to
factors such as exercise, recumbency, trauma such as
intramuscular injections, or markedly elevated in
anorexic cats. Elevations of CK are most dramatic
in the muscular dystrophies or with myonecrosis
(× 100 normal), moderately elevated in inflamma-
tory myopathies (× 10 normal) or normal or only
mildly elevated in other diseases such as myotonia
congenita.
 E X E R C I S E - A S S O C I AT E D W E A K N E S S AND COLLAPSE 185

 142 Diagnostic approach to Step 1 MINIMUM DATABASE

exercise-associated weakness. • Glucose • PCV and total solids
• Creatine kinase • Abdominal ultrasound
• Thoracic radiographs

Step 2 EDROPHONIUM OR NEOSTIGMINE

CHALLENGE TEST AND ANTI-ACETYLCHOLINE
RECEPTOR ANTIBODY TITRE

Step 3 ELECTROPHYSIOLOGICAL ASSESSMENT

(EMG, MNCV, repetitive stimulation, F waves)

Step 4 Step 4
MUSCLE BIOPSY NERVE BIOPSY

Neuropathic Infectious or
Inflammation
Rule out findings paraneoplastic cause?
endocrine disease,
long-term glucocorticoids,
NO
paraneoplastic,
Labrador Retriever
centronuclear myopathy Type II fibre
atrophy Treat for immune-mediated
neuritis

Rule out Rule out endocrine disease

Inflammatory Demyelination
infectious disease or paraneoplastic cause

NO NO

Treat for polymyositis Consider degenerative

(immune-mediated disease) or toxic

Consider toxins, metabolic

Axonal disease, motor neuron
Muscular dystrophy Dystrophic changes disease, axonopathy of
degeneration
undetermined cause

Lactate/pyruvate,
carnitine serum, muscle Mitochondrial Reconsider anatomical
abnormality/lipid storage Normal diagnosis
and urine analysis

Lumbar CSF tap

Consider infections, drug/ Necrosis without
toxin, metabolic defects, lymphocytic infiltration
muscular dystrophy,
heat stroke Muscle biopsy
186 DECISION MAKING

Table 48 Specific laboratory tests and associated diseases

LABORATORY TEST ABNORMALITY SUSPECTED DISEASE

Thyroid hormone testing Decreased fT4, tT4 and increased TSH (D) Hypothyroidism (hypothyroid
neuropathy/myopathy)

Serum glucose and serum insulin level Hypoglycaemia Hypoglycaemia-associated neuropathy

Inappropriately increased insulin levels Insulinoma

Cerebrospinal fluid Albumino-cytological dissociation Nerve root disorders

(increased protein associated with (polyradiculoneuritis)
normal TNCC)

Serum Neospora caninum and Elevated titres or positive PCR Neospora and Toxoplasma infection
Toxoplasma gondii titres or PCR

Plasma cholinesterase Decreased plasma levels Organophosphate toxicity

Serum glucose level or fructosamine Persistent hyperglycaemia Diabetes mellitus (diabetic neuropathy)
and glycosylated haemoglobin levels

Plasma lactate and pyruvate Elevated concentrations of resting Metabolic, mitochondrial myopathies
and post-exercise lactate and lactate:
pyruvate ratios

Plasma, urine and Reduced plasma and muscle carnitine, Metabolic, mitochondrial, lipid storage
muscle carnitine concentration increased urine excretion of myopathies
carnitine esters

Serum anti-AChR antibody Antibody titre >0.6 nmol/l (D) Acquired myasthenia gravis
Antibody titre >0.3 nmol/l (C)

Serum CK Severely elevated CK (x100 normal) Muscular dystrophies or myonecrosis

Moderately elevated CK (x10 normal) Inflammatory myopathies

D = dog; C = cat.
Modified from Glass EN, Kent M (2002) The clinical examination for neuromuscular disease.
Vet Clin North Am Small Anim Pract 32:1–29.

• Radiography and ultrasound. May reveal primary and acquired MG, may be considered; antibodies
cause of NM dysfunction, such as other major against the AChR need to be measured in all cases
organ diseases, neoplasia and major blood vessel of exercise-induced weakness, especially if megaoe-
abnormalities, and the consequences of NM sophagus is present.
diseases, including megaoesophagus or aspiration
pneumonia (143, 144). Neuromuscular system function
• Thyroid function testing (total T4, free T4, TSH) • Electrophysiology. Although diagnosis of a specific
and ACTH stimulation test. These tests should NM condition is rarely obtained by
always be considered, as NM disease may be the electrophysiological testing, it can be essential to
only sign of endocrine diseases. classify the NM condition as a junctional, axonal,
• Serology/PCR for infectious agents or myelin or myopathic disorder and to define the dis-
autoimmune conditions. Serology for autoimmune tribution and severity of the disease in order to
conditions, such as systemic lupus erythematosus better define the differential diagnosis (145).
 E X E R C I S E - A S S O C I AT E D W E A K N E S S AND COLLAPSE 187

a  143 (a) Doppler ultrasonography of the femoral artery

reveals an intraluminal mass compatible with a thrombus
(arrow). (b) Doppler ultrasonography confirms the altered
blood flow around this lesion (arrows).

 144 Lateral radiograph demonstrating mega-

oesophagus. The arrows mark the dorsal and ventral
boundaries of the caudal thoracic oesophagus.
b

 145 Needle electromyography can reveal the presence of positive sharp waves (black arrows) and fibrillations
(red arrows), which are compatible with axonal or muscle disease and tend to rule out neuromuscular junction diseases.
 188 DECISION MAKING

• Quantitative urinary organic acid analysis. Organic

aciduria can be due to inborn metabolic errors
causing accumulation of non-metabolizable organic
acids in tissues such as muscle and brain. Their
excess can be detected in urine. Organic aciduria
can result in intermittent weakness and collapse.
• Carnitine evaluation in blood, muscle and urine.
Primary or secondary carnitine metabolism
disorders are diagnosed by a complete evaluation
of the carnitine status in the body. This is done by
measurement of carnitine in urine, blood and
muscle in its three different forms: total, free and
esterified.
• Cerebrospinal fluid analysis. Rarely useful in the
evaluation of a primary NM condition; a lumbar
 146 A muscle biopsy should be performed in a routine CSF tap may be performed if a diffuse
sterile manner. Once a linear incision has been made in inflammatory condition affecting the nerve roots
the skin overlying the muscle of choice, the subcutaneous (polyradiculoneuritis) is suspected. Specific PCR for
fat is dissected to reveal the shiny muscle fascia. infectious agents may be performed on CSF if a
diffuse inflammatory condition is suspected.

COMMON NEUROMUSCULAR CAUSES OF

EXERCISE-INDUCED WEAKNESS AND COLLAPSE

Myasthenia gravis is described in detail elsewhere in this

• Muscle and nerve biopsy. Necessary to provide a book (Chapter 24).
specific diagnosis; requires interpretation in
conjunction with clinical signs and results of other Exercise-induced collapse
tests including electrophysiology (146). Overview
Young (7 months–2 years old) Labrador Retrievers of
Specific tests either sex have been reported with acute weakness and
Many of the tests outlined below are only performed at collapse during heavy training. The condition has also
selected laboratories. The clinician is advised to contact been described in Chesapeake Bay Retrievers, Curly-
the laboratory prior to acquiring and submitting the coated Retrievers, Border Collies and Welsh Pembroke
samples for details. Corgis.
• Evaluation of lactate and pyruvate levels. Lactic
acid is the product of anaerobic metabolism of Clinical presentation
glucose, therefore it may be increased in normal Affected animals are normal at rest and have normal
animals after anaerobic exercise. Lactic acidosis, levels of physical activity. Acute and progressive general-
however, can result from a defect in anaerobic ized weakness, ataxia and eventually collapse during exer-
metabolism, secondary to pyruvate deficiency. cise activity of variable duration (5–15 minutes) are most
Plasma lactate (L) and pyruvate (P) and their L:P commonly seen in affected animals. Animals affected
ratio in blood are evaluated in metabolic often show severe hyperthermia (>41.5°C [106.7°F])
myopathies and are essential for the diagnosis of during episodes, although comparable severe hyper-
mitochondrial diseases characterized by high serum thermia is also recorded in normal exercising Labrador
lactate and pyruvate concentrations with a high L:P Retrievers. Affected animals usually fully recover after
ratio compared to normal. 10–20 minutes of rest, but the condition can be fatal.
 E X E R C I S E - A S S O C I AT E D W E A K N E S S AND COLLAPSE 189

Recently a mutation of the Dynamin 1 gene (DNM1), Clinical presentation

responsible for a molecule essential in synaptic vescicle Progressive intolerance to exercise, with acute and gen-
endocytosis, has been associated with the syndrome of eralized weakness, is the most common presentation.
exercise-induced collapse. This mutation has been Marked weight loss is relatively common, while myalgia
observed in Labrador Retrievers, Chesapeake Bay is not a consistent finding.
Retrievers, Curly-coated Retrievers and Welsh Pem-
broke Corgis. Clinical signs are observed in the homo- Diagnosis
zygous state; 30–40% of pure Labrador Retrievers have Diagnosis is based on specific clinical signs, marked ele-
been noted as carriers of the mutation, without any vation of CK concentration, compatible electrophysio-
clinical importance. logical findings, histopathology and negative infectious
agent titres (Toxoplasma gondii, Neospora caninum and
Diagnosis tick-related disease when appropriate in dogs; T. gondii,
Diagnosis is exclusional and based on clinical findings, as feline leukaemia virus and feline immunodeficiency virus
laboratory, electrophysiological and histopathological in cats).
tests are normal. Severe alkalosis during the event may be
the only laboratory finding. Genetic testing has recently
become available at the Veterinary Diagnostic Labora-
tory, University of Minnesota.

Management
No specific treatments have as yet been proven
beneficial. Exercise restriction is necessary to avoid
relapse. The prognosis is good when providing exercise
restriction.

Idiopathic immune-mediated inflammatory

myopathy (polymyositis)
Overview
The condition affects dogs and rarely cats. No breed, sex
or age predispositions exist, although breed-specific vari-
ants are reported in Newfoundlands, Boxers and Vizslas.
This generalized inflammatory myopathy is not associ-
ated with any infectious disease and is histologically char-
acterized by a predominantly lymphocytic infiltration
within skeletal myofibres (147). Sarcolemma-specific
autoantibodies have been identified in a population of
dogs with polymyositis, particularly in the Boxer and
Newfoundland breeds. Cancer may be associated with
canine and feline inflammatory myopathies (lymphoma,
anaplastic round cell tumour or plasmacytoma).
Skeletal muscles are usually diffusely affected,
although focal forms involving pharyngeal, laryngeal
or oesophageal muscles have been described. Other
organs and systems may be involved in canine polymyo-
sitis, including the heart (myocarditis), gastrointestinal  147 Histopathology confirming a marked mono-
tract (inflammatory bowel disease), thyroid (thyroiditis) nuclear cell infiltration of the muscle compatible with
and skin. polymyositis. (H&E)
 190 DECISION MAKING

Infectious/inflammatory myopathies/polyneuritis
Overview
Protozoal (Toxoplasma gondii, Neospora caninum, Leish-
mania infantum, Hepatozoon canis), rickettsial (Ehrlichia
canis) and, less commonly, bacterial (Clostridium spp.,
Leptospira icterohaemorrhagiae) infections may cause
acute and generalized weakness in patients as part of a
multisystemic infection. No specific breed is overrepre-
sented. Immunocompromised animals, including young
patients or older dogs with concurrent disorders, are pre-
disposed.

Diagnosis
Diagnosis depends on identification of the infectious
agent in muscle tissue with molecular or immunohisto-
 148 Physiotherapy, including the use of electrical chemical methods. Elevation of CK concentration and
muscle stimulators, is vital for promoting the best an electromyogram (EMG) examination are not specific.
possible recovery. Positive serological titres sometimes cannot differentiate
between an exposed versus an infected animal, as a
mild/moderate positive titre can be seen in animals
previously exposed to the organism, while false negatives
Management are observed in acute stages or in severely immunocom-
Therapy with prednisolone at immunosuppressive promised patients.
dosages (2 mg/kg PO q12h in dogs; 3 mg/kg PO q12h in
cats), with tapering of the dose every 2–4 weeks, may Management
result in clinical resolution. Addition of oral azathioprine Protracted treatment with specific antibiotics or anti-
(2 mg/kg q24h until remission, then 0.5– 2 mg/kg q48h) monials is often required: trimethoprim-sulphadiazine
can be considered if there is failure to respond with pred- (15 mg/kg PO q12h for 4 weeks); clindamycin (15 mg/kg
nisolone only or in cases of relapse. PO q12h for 4 weeks); pyrimethamine (1 mg/kg PO
All cases that clinically relapse should have repeat q24h for 2 weeks in dogs).
muscle biopsy, as some cases demonstrate neoplastic pro- The prognosis is guarded, depending on clinical stage
gression. Serum CK concentration is a good marker of and time of diagnosis. If treatment has been initiated
treatment response and should be monitored during early, loss of function may be partial; physiotherapy is
therapy. mandatory to reduce muscle atrophy.
Opioid analgesia should be considered in the first
days in the few cases that exhibit severe muscle pain. Sup- (Exertional) rhabdomyolysis
portive care, including nutritional management and Overview
physiotherapy (148), is essential to control muscle Rhabdomyolyis is a clinical syndrome characterized by
wastage in non-ambulatory dogs. Oesophageal or gas- acute muscle necrosis with muscular pain, weakness/
trostomy tubes may be necessary to support nutritional collapse, marked increases in CK levels and myoglobin-
management. uria. Common causes include excessive exertion, as
The prognosis with early and aggressive initial treat- described in racing dogs, trauma, severe hyperthermia
ment may be good unless concurrent megaoesophagus (heat stroke), toxins and drugs, and salt and water imbal-
or pharyngeal paralysis is observed. Early diagnosis and ances resulting in severe electrolyte imbalance and infec-
treatment limit the severe myofibre loss and fibrosis tious diseases. In some cases the primary cause may be
associated with a poor prognosis. Relapse is possible and difficult to diagnose.
is associated with a poor prognosis.
 E X E R C I S E - A S S O C I AT E D W E A K N E S S AND COLLAPSE 191

Clinical presentation PO q24h) and decrease lipid storage in muscle by

Direct sarcolemmal injury or failure of muscular energy administration of riboflavin (100 mg PO q24h).
supply leads to increased intracellular calcium levels, Treatment should aim at maintaining good urinary
with secondary necrosis of myofibres. Severe myoglobin output through fluid therapy and diuretics (mannitol
release from myofibre injury may cause acute renal or/and furosemide). Muscle relaxation can be achieved
tubular necrosis with acute renal failure. Myocardial and by targeting the calcium movement at the sarcoplasmic
respiratory failure have been recently reported due to reticulum with dantrolene administration (1.5 mg/kg IV
cardiac and intercostal/diaphragmatic myonecrosis. q8h). Muscle pain should be controlled with either
fentanyl or gabapentin administration.
Diagnosis The prognosis is guarded. With early and appropriate
Muscle biopsy is mandatory for a diagnosis. Histology is supportive therapy, acute rhabdomyolysis can be a
characterized by a necrotizing myositis. reversible disorder.

Management Hypokalaemic myopathy

Therapy aims to control electrolyte imbalance, support Overview
muscular oxidative metabolism with L-carnitine Hypokalaemic myopathy is observed in cats and, very
(50 mg/kg PO q12h), increase activity of mitochondrial rarely, in dogs. It results from reduced potassium intake,
enzymes through coenzyme Q10 administration (100 mg increased potassium loss (chronic renal failure) and con-
genital predispositions (Burmese cat). Hypokalaemia
affects myofibres, which become progressively refractory
to depolarization. The muscle cell membrane increases
its permeability to sodium ions, causing hypopolarization
and acute weakness or collapse.

Clinical presentation
Generalized weakness with ventroflexion of the neck is
often seen (149). In severe stages, weakness may progress
to acute collapse.

Diagnosis
Diagnosis is reached by measurement of serum potas-
sium levels (≤3.5 mmol/l [3.5 mEq/l]). Chronic renal
failure with potassium loss in the urine and hyper-
thyroidism should be immediately ruled out. CK levels
may be increased due to muscle fibre necrosis, which is
visible on muscle biopsy.

Management
Supplementation with potassium gluconate (2–4 mmol
[mEq] q12h) orally can be used; however, in severe weak-
ness, intravenous potassium chloride supplementation
(0.2–0.4 mmol [mEq]/kg/hour) is required with cardiac
monitoring.
In general, the prognosis is good if potassium levels
are supplemented and the primary cause of the hypo-
 149 Cervical ventroflexion in a cat. kalaemia is treated.
192 DECISION MAKING

Mitochondrial myopathy • Muscle biopsy is characterized by massive prolifera-

Overview tions of mitochondria in myofibres, called ‘ragged-
Mitochondrial myopathy is a rare metabolic myopathy red’ fibres due to their red staining with the
reported in various canine breeds. Mitochondrial myo- Gömöri modified trichrome stain.
pathies are a group of disorders characterized by abnor- • Definitive diagnosis is obtained by biochemical and
malities of mitochondrial enzyme function. These cause molecular testing, and is difficult to perform.
a defect in the anaerobic metabolism of pyruvate in the
muscle, leading to severe lactic acidaemia. Management
No specific treatments are currently available. Support-
Clinical presentation ive care and treatment to support muscular oxidative
Combinations of brain and muscular signs, in particular metabolism, such as L-carnitine (50 mg/kg PO q12h) and
exercise intolerance and weakness, are often observed. coenzyme Q10 (100 mg PO q24h) may temporarily
improve muscular strength.
Diagnosis
Diagnosis can be challenging and is based on:
• Documentation of high serum lactate and pyruvate
concentrations, with high L:P ratios pre- and post-
exercise and pre- and post-food intake.
 DECISION MAKING Chapter 9

ATAXIA
193

Jonathan Levine

INTRODUCTION NEUROANATOMICAL BASIS

Ataxia is defined as incoordination that results from The processes involved in gait initiation, generation and
either insufficient proprioceptive (sensory) input to gait coordination are still poorly understood in veterinary
centres in the CNS or failure of the central regulators of species. Gait is believed to be initiated in midbrain nuclei,
motor function, such as the cerebellum. Paresis (weak- which signal, through UMN projections, to local gait-
ness) due to UMN or LMN lesions often accompanies generating neurons within the spinal cord. Sensory
ataxia and in many cases contributes to the observed gait system input is essential in coordinating these motor
deficits. Animals with ataxia may exhibit crossing of the responses. GP receptors are located within joints,
limbs, falling, leaning and overreaching, as well as disor- muscles and tendons. Changes in body position result in
ganized range and rates of movement, as single signs or receptor discharge and the stimulation of primary affer-
in combinations. ent (sensory) neurons. These primary neurons project to
Limb movement associated with ataxia can be the spinal cord, where signals ascend through the dorsal
described as follows: columns and lateral funiculi to brainstem structures.
• Dysmetria. An aspect of ataxia in which the ability Vestibular (special proprioceptive) receptors located in
to control the distance, power and speed of an the inner ear are also essential in gait coordination.
action is impaired. Usually used to describe Fibres associated with these receptors interact with the
abnormalities or movement associated with vestibular nuclei in the brainstem to help maintain the
cerebellar disorders. position of the eyes, neck, trunk and limbs with respect to
• Hypermetria. Ataxia characterized by overreaching the position and movement of the head.
a desired object or goal. Usually seen with In addition to appropriate proprioceptive input, gait
cerebellar disorders. coordination relies on interaction between the cerebel-
• Hypometria. Ataxia characterized by lum and motor systems. The cerebellum controls the
underreaching an object or goal. Usually seen rate, range and force of movements, without actually ini-
with cerebellar disease. A similar gait is seen more tiating motor activity. It receives sensory input from
often with LMN paresis. proprioceptive, visual and auditory systems. UMNs also
project to the cerebellum and the cerebellum provides
In veterinary medicine, ataxia is typically classified as GP, feedback information to UMNs in the brainstem and
vestibular or cerebellar in origin. Although some animals cerebral cortex via deep cerebellar nuclei. Because of its
may exhibit ataxia that reflects a combination of these close association with the brainstem vestibular nuclei
subclasses, accurate lesion localization is essential in (see Chapter 14), the cerebellum also functions in the
establishing an appropriate list of differential diagnoses maintenance of equilibrium. Ultimately, the complex
and a diagnostic plan. interaction between the cerebellum, motor systems and
 194 DECISION MAKING

sensory systems serves to ‘smooth’ voluntary movements of the UMN pathways necessary for gait generation. The
induced by the UMNs, regulate muscle tone and pre- change in the gait therefore generally reflects a combined
serve equilibrium (150). dysfunction of both UMN paresis and GP ataxia, with
delayed onset of protraction of the limb and lengthened
General proprioceptive ataxia stride. From a lesion localization point of view, UMN
GP ataxia is probably the most common form of ataxia paresis and GP ataxia visible in the gait can occur as
recognized in domestic species. It results from lesions a consequence of a lesion affecting the brainstem or
affecting the primary afferent neuron or the ascending spinal cord.
proprioceptive tracts within the spinal cord and brain- Compared with UMN paresis, disorders of the
stem (midbrain, pons, medulla). Therefore, animals with LMNs usually cause paresis and not ataxia. The degree
GP ataxia may have additional neurological signs reflect- of paresis varies from a short stride to a complete inabili-
ing a spinal cord or brainstem localization. Although ty to support weight, causing collapse of the limb when-
lesions within the thalamus and cerebral cortex will cause ever weight is placed on it. Although most peripheral
GP ataxia in humans, in domestic species the ataxia gen- neuropathies are likely to affect both motor and sensory
erated from lesions within these structures is usually too axons, gait dysfunction principally reflects LMN paresis.
subtle to be detected on gait evaluation. The pathways of The exception is with the so-called sensory neuropathies,
the GP sensory system are anatomically adjacent to most which initially can present primarily with ataxia.

General proprioceptive structures

Cerebellar structures Proprioceptive fibres
UMN feedback
Spinocerebellar pathways

Vestibular structures
Brainstem vestibular nucleus
Vestibulocochlear nerve
Semicircular canals
Utricle
Saccule

 150 Schematic drawing illustrating structures that can be affected in animals with ataxia. General proprioceptive
ataxia is most frequently seen with spinal cord lesions, due to disruption of ascending projections in the dorsal and
lateral funiculi. It is also recognized in some animals with caudal brainstem and peripheral nervous system diseases.
Vestibular ataxia may result from lesions within the inner ear or vestibular nuclei, which are located in the medulla
oblongata. Head tilt, leaning, falling and a broad-based gait are characteristic. The cerebellum receives proprioceptive
and upper motor neuron projections. It serves to smooth movements via modulating upper motor neuron tone. Lesions
within the cerebellum can lead to ataxia, characterized by dysmetria and hypermetria.
 ATA X I A 195

a b c

 151 Serial photographic images of a cat with severe cerebellar and vestibular ataxia. Note the presence of falling and
head tilt to the right (b) and as the cat attempts to stand, the ataxia results in a roll to the side. Complete body rolls can
be seen with vestibular ataxia.

Vestibular ataxia
Vestibular ataxia occurs with lesions affecting either the Cerebellar ataxia
peripheral or central vestibular apparatus. In addition to Cerebellar ataxia can be seen in animals that have lesions
ataxia, animals will often have concurrent neurological within the cerebellar cortex. Other signs of cerebellar
signs that reflect a vestibular disorder (e.g. head tilt or disease, such as intention tremors, are often present.
head sway, pathological nystagmus or positional strabis- Cerebellar ataxia is characterized by hypermetria and
mus). Animals with vestibular ataxia often have a broad- dysmetria. Hypermetria associated with cerebellar ataxia
based gait (especially in the hindlimbs), with leaning consists of overflexion during limb protraction and
towards the side of decreased vestibular tone. Some is therefore distinct from the overreaching, long-strided
animals may have substantial swaying when walking and gait noted in animals with combined GP ataxia/
will occasionally fall; recumbent animals may be seen to UMN paresis. Dysmetria is a component of cerebellar
roll (151). Weakness or paresis is only seen with central ataxia and is manifest by a loss of synchronous limb
vestibular disease and is not a feature of peripheral movements.
vestibular disease.
 196 DECISION MAKING

NEUROLOGICAL EVALUATION Step 1. Is the animal ataxic?

Lameness is defined as a reluctance to bear weight on a
At the outset of the neurological evaluation, the examin- limb, and is often the result of orthopaedic conditions or,
er must first determine whether the gait abnormalities less commonly, diseases affecting afferent (sensory)
seen are truly indicative of ataxia (152). Lameness, neurons. Lameness, unlike ataxia, may be episodic and
various orthopaedic gait disturbances and weakness due should not be characterized by dragging, scuffing or
to non-neurological disease must be excluded (see crossing over of the limbs. However, lameness and ataxia
Chapter 16). can exist concurrently, especially in older dogs that have
neurological and orthopaedic disease.
 152 Various forms of neurological gait disturbance. Other gait disturbances are possible with orthopaedic
(a) Dog with a left cerebellar ischaemic territorial infarct. disease in addition to lameness, especially short striding.
Hypermetria is seen best in the left forelimb. Note the This can occur in animals with hip dysplasia, elbow
preservation of carpal flexion in frames 2 and 3, with arthritis or polyarthritis (typically all limbs) and is related
sudden overreaching seen in frame 4. Dysmetria can also to joint pain. Again, crossing over of the limbs, dragging
be appreciated as a lack of synchrony between limbs. and knuckling should not be present. Orthopaedic
(b) Dog with C4/C5 spinal cord compression due to disease can interfere with certain elements of the neuro-
spondylomyelopathy. Note the long-strided gait in all four logical examination. For example, the hopping assess-
limbs, with a relative lack of flexion at the carpal and hock ment may be falsely diminished in animals that have joint
joints. These findings suggest upper motor neuron paresis or bone pain. Joint pain may also result in false reduction
and general proprioceptive ataxia affecting all the limbs. of flexor withdrawal reflexes.
(c) Dog with C6/C7 spinal cord compression due to disc
extrusion. The forelimb gait is markedly short strided,
indicating lower motor neuron paresis associated with
C6–T2 spinal cord segment involvement.

c
 ATA X I A 197

Finally, systemic illnesses (e.g. cardiac disease) and Step 2. Is the ataxia cerebellar, vestibular or
metabolic derangements can appear to cause gait dys- general proprioceptive in origin?
function similar to that seen with structural neurological If ataxia is present, the next step is to determine the
disease. For example, cardiac failure can lead to hypoper- portion of the nervous system that is affected and
fusion and hypoxia, both of which may result in poor contributing to the observed gait disturbance (153,
oxygen delivery to CNS structures. Addison’s disease can Table 49). In this regard it is often useful to try and
induce profound weakness due to low circulating cortisol characterize which classification(s) of ataxia is/are
levels, hyperkalaemia and hypovolaemic shock. Typical- contributing to the gait pattern. The presence of
ly, weakness resulting from systemic illness will not lead ataxia should suggest a lesion of the spinal cord,
to ataxia. However, some systemic illness can cause struc- brainstem, cerebellum or vestibular system as dis-
tural nervous system lesions. For example, animals with cussed above. Multifocal disease with involvement
sepsis may develop ischaemic infarction within the CNS of at least two of these regions should also be a con-
secondary to hypercoagulability and the release of sideration. Correct anatomical diagnosis is crucial
inflammatory mediators. The interrelationship between in establishing a differential list, as some causes of
systemic illness and the nervous system underscores the ataxia are specific to certain regions of the nervous
necessity to correlate neurological examination findings system. Additionally, the choice of ancillary diag-
with a standard physical examination and screening nostic tests is guided by lesion localization and the
ancillary diagnostics. differential list. Table 49 and the flowchart 153
(next page) are provided as a quick reference to
correlate gait and neurological examination char-
acteristics with lesion location.

Table 49 Types of ataxia and associated localizing signs

TYPE OF ATAXIA ANATOMICAL DIAGNOSIS NEUROLOGICAL SIGNS

Proprioceptive General proprioceptive pathways: Abnormal postural reactions. Concurrent UMN paresis in limbs
• Spinal cord and normal to increased spinal reflexes. No effect on the eyes
or head posture
• Brainstem

Vestibular Vestibular apparatus: Unilateral lesion. Head tilt, leaning, falling or rolling to one
• Vestibular nuclei (central) side, abnormal nystagmus, strabismus, normal (peripheral) or
abnormal (central) postural reactions
• Vestibular portion of CN VIII or
vestibular receptors (peripheral) Bilateral lesion. Crouched posture, reluctance to move and
wide head excursion

Cerebellar Cerebellum Diffuse lesion. Broad-based stance, symmetrical ataxia,

hypermetria, truncal ataxia, intention tremor of the head,
vestibular deficits, delayed and then exaggerated response to
postural reaction testing, menace deficit with normal vision, no
paresis and normal mentation
Unilateral lesion. Ipsilateral deficits except for vestibular
deficits, which are contralateral
 198 DECISION MAKING

ATAXIA

Vestibular General Cerebellar

proprioceptive

Postural Cranial nerve

CEREBELLUM
reaction deficits abnormalities

NO YES YES NO

CENTRAL GENERALIZED
PERIPHERAL BRAINSTEM SPINAL CORD OR
(medulla) PERIPHERAL NERVE

C1–C5:
LMN
CN III–IV (midbrain) UMN thoracic
Thoracic and pelvic
and pelvic

C6–T2:
CN V (pons) LMN thoracic,
UMN pelvic

T3–L3:
CN VI–XII (medulla) UMN pelvic
 153 Flow chart outlining an
approach to localizing the lesion
L4–S3:
responsible for ataxia. LMN pelvic

DIFFERENTIAL DIAGNOSIS Specific diagnostic tests

Appropriate diagnostic test selection is dependent on the
A differential diagnosis list should be established based region of the nervous system affected.
on the neuroanatomical origin of the ataxia. Table 50
(p. 201) outlines common causes of ataxia, listed by lesion Spinal cord disease (154, 155)
localization (spinal cord, caudal brainstem, cerebellum • CBC and serum biochemistry.
and vestibular system). Diseases that affect the alpha • Screening thoracic and abdominal radiography and
motor neuron, NM junction and muscle will result in ultrasonography to rule out metastatic diseases.
paresis without ataxia and therefore have not been • Vertebral column radiographs as a cost-effective
included (for further information, see Chapter 10). Dif- screening test to identify obvious vertebral
ferentiating ataxia from paresis based on gait and postur- fractures, luxation, osseous lytic tumours and disco-
al testing can be challenging; therefore, the clinician spondylitis.
must be willing to consider including all possibilities • Advanced imaging, preferably MRI rather than CT.
when generating differential lists if the animal does not • CSF analysis.
have a gait that is easy to define.
 ATA X I A 199

a a

b b

 154 Sagittal T2-weighted MR image (a) and  155 T2-weighted sagittal (a) and T1-weighted
3-dimensional bone-windowed CT reconstruction (b) transverse (b; at the C3/C4 articulation) MR images from
of a dog with proprioceptive ataxia in all limbs. The MR a 5-year-old Cocker Spaniel with ambulatory tetraparesis
image shows severe atlantoaxial subluxation as evidenced and general proprioceptive ataxia in all limbs. There is
by dorsal displacement of C2 and widening of the C1/C2 marked ventral extradural spinal cord compression due to
articulation (yellow arrow). The spinal cord is severely hypointense extruded disc material (arrow, a) that pre-
compressed by the displaced dens and is focally hyperin- dominantly overlies the body of C4.
tense. There is also a moderate-sized quadrigeminal cyst
(red arrow) resulting in compression of the rostral
cerebellum, tenting of the 4th ventricle and subtle
compression of the caudal cerebellum due to Chiari-like
malformation (these findings are probably incidental). The
CT image shows a defect in the occipital bone and dorsal
displacement of C2.
 200 DECISION MAKING

 156 Transverse T2-weighed MR image from a 4-year-  157 Transverse T2-weighed MR image from a 6-year-
old Cairn Terrier with cerebellar and vestibular ataxia. old Cocker Spaniel with progressive cerebellar ataxia.
Within the right cerebellum, caudal cerebellar peduncle There is a well marginated, round, high signal lesion
and medulla there is a poorly marginated hyperintense within the cerebellum. Biopsy identified the lesion as an
lesion. Further diagnostics suggested granulomatous anaplastic astrocytoma.
meningoencephalitis as the likely aetiology.

Brainstem and cerebellum (156, 157) • MRI of the brain and peripheral vestibular
• CBC and serum biochemistry. apparatus is suggested, as it may be challenging to
• Screening thoracic and abdominal radiography and discriminate central from peripheral vestibular
ultrasonography to rule out metastatic diseases. disease based on physical examination. CT provides
• MRI of the brain is suggested, as CT is less inferior imaging of the caudal fossa due to beam
sensitive for detecting soft tissue changes within the hardening artefacts.
caudal fossa due to beam hardening artefacts. • Myringotomy for cytology and culture of lesions
• CSF analysis. extending into the middle ear.
• Infectious disease titres. • CSF analysis if concurrent involvement of central
• Free T4 by equilibrium dialysis, total T4, thyroid structures is possible.
stimulating hormone and other thyroid function • Free T4 by equilibrium dialysis, total T4, thyroid
testing. stimulating hormone and other thyroid function
testing.
Vestibular system
• CBC and serum biochemistry.
• Screening thoracic and abdominal radiography and
ultrasonography to rule out metastatic diseases.
• Otoscopy ± ear swabs.
• Pharyngeal examination (to rule out polyps).
• Bullae radiographs.
 ATA X I A 201

Table 50 Differential diagnoses of ataxia by neuroanatomical localization

SPINAL CORD
DISEASE MECHANISM DOGS CATS

Vascular Fibrocartilaginous embolism* Fibrocartilaginous embolism*

Vascular malformations Vascular malformations
Spinal cord haematoma or haemorrhage Spinal cord haematoma or haemorrhage

Inflammatory/ Infectious meningomyelitis/myelitis (Toxoplasma*, Infectious meningomyelitis/myelitis (Toxoplasma*,

infectious Neospora*, rickettsial, fungal, canine distemper*, feline leukaemia virus myelopathy, FIP*, fungal,
rabies) rabies)
Discospondylitis and spinal epidural empyema Meningomyelitis/myelitis of unknown aetiology
Meningomyelitis/myelitis of unknown (very rare)
aetiology (GME)*

Trauma Spinal fracture/luxation* Spinal fracture/luxation*

Traumatic disc herniation * Traumatic disc herniation*

Toxic N/A N/A

Anomalous Atlantoaxial subluxation (C1–C5)* Spina bifida (especially Manx)

Spina bifida Myelodysplasia
Hemivertebra
Myelodysplasia
Syringo(hydro)myelia*
Sub(intra)arachnoid cyst*

Metabolic N/A N/A

Idiopathic N/A N/A

Neoplastic Primary or metastatic spinal column or spinal cord Primary or metastatic spinal column or spinal cord
tumour* tumour*

Nutritional B12 deficiency

Hypervitaminosis A

Degenerative Intervertebral disc disease* Intervertebral disc disease (especially caudal

Degenerative myelopathy (T3–L3) lumbar segments)
Cervical spondylomyelopathy* Storage diseases

* Common cause
FIP = feline infectious peritonitis
N/A = not applicable

(Continued)
202 DECISION MAKING

Table 50 Differential diagnoses of ataxia by neuroanatomical localization (continued)

BRAINSTEM (including central vestibular)

DISEASE MECHANISM DOGS CATS

Vascular Brain infarct* Brain infarct*

Brain haemorrhage* Brain haemorrhage*

Inflammatory/ Infectious encephalitis (distemper, Toxoplasma, Infectious encephalitis (Toxoplasma, bacterial, FIP,
infectious Neospora, fungal, bacterial, rickettsial, rabies)* rabies)*
Meningoencephalitis of unknown aetiology Meningoencephalitis of unknown aetiology
(GME, necrotizing, idiopathic)* (presumed immune mediated) (very rare)

Trauma Head trauma* Head trauma*

Toxic Metronidazole toxicity* Metronidazole toxicity*

Anomalous Intracranial intra-arachnoid cyst Intracranial intra-arachnoid cyst

Dermoid/epidermoid cyst Dermoid/epidermoid cyst
Dandy–Walker syndrome Hydrocephalus
Chiari-like malformation
Hydrocephalus

Metabolic Hypothyroidism N/A

Idiopathic N/A N/A

Neoplastic Primary or metastatic brain tumour* Primary or metastatic brain tumour*

Nutritional Thiamine deficiency Thiamine deficiency

Degenerative Storage diseases Storage diseases

Other neurodegenerative disease Other neurodegenerative disease

CEREBELLUM
DISEASE MECHANISM DOGS CATS

Vascular Brain infarct* Brain infarct

Brain haemorrhage Brain haemorrhage

Inflammatory/ Infectious encephalitis (distemper, Toxoplasma, Infectious encephalitis (Toxoplasma,

infectious Neospora, fungal, bacterial, rickettsial, rabies)* bacterial, FIP, rabies)*
Meningoencephalitis of unknown aetiology Meningoencephalitis of unknown aetiology (presumed
(GME, necrotizing)* immune mediated) (very rare)

Trauma Head trauma Head trauma

Toxic Marijuana Marijuana

5-fluorouracil 5-fluorouracil

Anomalous Chiari-like malformation* Cerebellar hypoplasia*

Intracranial intra-arachnoid cyst Intracranial intra-arachnoid cyst
Cerebellar hypoplasia Dermoid/epidermoid cyst
Dermoid/epidermoid cyst
Dandy–Walker syndrome
(Continued)
 ATA X I A 203

Table 50 Differential diagnoses of ataxia by neuroanatomical localization (continued)

CEREBELLUM
DISEASE MECHANISM DOGS CATS

Metabolic N/A N/A

Idiopathic N/A N/A

Neoplastic Primary or metastatic brain tumour* Primary or metastatic brain tumour*

Nutritional N/A N/A

Degenerative Storage diseases Storage diseases

Cerebellar abiotrophy Other neurodegenerative disease
Other neurodegenerative disease

PERIPHERAL VESTIBULAR SYSTEM

DISEASE MECHANISM DOGS CATS

Vascular None None

Inflammatory/ Otitis media/interna* Otitis media/interna*

infectious Nasopharyngeal polyp*

Trauma Head trauma Head trauma

Toxic Aminoglycosides* Aminoglycosides*

Topical iodophors* Topical iodophors*
Loop diuretics Loop diuretics
Topical chlorhexidine* Topical chlorhexidine*

Anomalous Congenital vestibular disease Congenital vestibular disease

Metabolic Hypothyroidism* N/A

Idiopathic Acute idiopathic peripheral vestibular disease* Acute idiopathic peripheral vestibular disease*

Neoplastic Middle and/or inner ear tumour Middle and/or inner ear tumour

Nutritional N/A N/A

Degenerative N/A N/A

* Common cause
FIP = feline infectious peritonitis
N/A = not applicable
 204 DECISION MAKING

COMMON CAUSES OF ATAXIA Diagnosis

Diagnosis is based on a combination of brain MRI
The most frequently identified aetiologies responsible (bilateral symmetrical brainstem nuclear lesions) (158),
for acute-onset ataxia in dogs and cats have been listed in erythrocyte transketolase levels (where available) and/or
the previous Tables in this chapter and will be reviewed urinary organic acid profile (high lactate, 2-hydroxyiso-
elsewhere in this book. Thiamine deficiency, an often valeric acid, 2-hydroxyadipic acid concentrations).
overlooked cause of brainstem signs, will be briefly Response to treatment can be considered diagnostic in
discussed here. most cases.

Thiamine deficiency Management

Overview Treatment consists of thiamine supplementation (oral or
Thiamine deficiency is identified in cats, and, less com- intramuscular at 25–50 mg q12h for dogs; 10–25 mg
monly, in dogs. In these species, thiamine deficiency q12h for cats) for at least 1 month after clinical signs
results in polioencephalomalacia, haemorrhage and have regressed and potential diseases affecting utiliza-
necrosis within brainstem nuclei (especially the caudal tion/absorption have been corrected. Intramuscular
colliculi and vestibular nuclei). Potential causes include delivery may be preferable in animals with gastrointesti-
decreased thiamine intake (dietary insufficiency, pro- nal disease that limits thiamine absorption. Resolution of
longed anorexia, vomiting) and diseases affecting normal signs will occur in days to weeks.
intestinal absorption or interfering with utilization (liver
disease, pancreatic disease).

Clinical presentation
Thiamine deficiency is acute to subacute in onset, with
progressive, usually bilateral, neurological deficits
including blindness, mydriasis, cervical ventroflexion
and vestibular dysfunction. Vestibular and GP ataxia
are observed in most cases. Some animals may have
additional signs relating to involvement of other body
systems (e.g. vomiting and weight loss).

a b c

 158 T2-weighted MR images of a crossbreed dog with thiamine deficiency showing bilateral symmetrical nuclear
hyperintensities (arrowed) at the level of the red nuclei (a), caudal colliculi (b) and vestibular nuclei (c).
 DECISION MAKING Chapter 10

ACUTE PARESIS AND PARALYSIS

205

John McDonnell

INTRODUCTION

Paresis and paralysis (plegia) are common neurological In general:

problems requiring emergency evaluation and treat- • Paresis is defined as loss of ability to support weight
ment. Determining the neurological basis for the paresis and/or inability to generate a gait; it can be
and paralysis is an essential goal for the clinician and is manifested as weakness or decreased strength of
necessary to guide the diagnostic and therapeutic voluntary motor movement (159), most commonly
decision-making process. seen with spinal cord diseases and NM diseases.
As a general rule, initial evaluation of an animal with a The term paresis implies that some voluntary
gait abnormality should be done with the aim of deter- movement is still present, as compared with
mining if the animal is ataxic (uncoordinated), paretic paralysis, which refers to a more severe paresis with
(weak) or lame (from either NM disease or an complete (-plegia) loss of voluntary movement
orthopaedic disorder) and which limb(s) is/are involved. (160). Paresis can be an ambulatory or a non-
Ataxia is covered in Chapter 9. ambulatory presentation.

 159 Paresis is suggested in this dog by a reduced  160 Reduced to absent motor function (paresis to
ability to bear weight in the hindlimbs. paralysis) is suggested by the posture of this dog.
206 DECISION MAKING

• Modifying prefixes are used to describe the abnor- • GP ataxia and UMN paresis are often seen together
malities seen. Monoparesis is weakness associated with spinal cord disorders due to the close
with one limb (161), while paraparesis is used to anatomical relationship of the respective sensory
describe weakness confined to the hindlimbs. and motor pathways.
Tetraparesis (or quadriparesis) is used to describe • Lameness usually presents with a short stride on the
weakness in all four limbs (162). Hemiparesis is affected limb and a long stride on the contralateral
weakness confined to a single side of the body (163). limb and is commonly associated with pain from
• Paralysis (plegia) is substituted for paresis when orthopaedic disease. It can also be associated with
complete loss of voluntary motor ability is nervous system dysfunction, referred to as nerve
identified. root signature. Lameness can be difficult to differ-
entiate from paresis caused by dysfunction of the
lower motor unit. Careful neurological and ortho-
paedic evaluation is therefore critical to confirm or
rule out a neurological basis for the lameness (see
 161 A 7-year-old mixed breed with left hindlimb Chapter 16).
monoparesis due to a nerve sheath tumour affecting the
lumbar plexus.

 162 A 4-year-old Greyhound cross with weakness in

all four limbs due to ischaemic myelopathy.

 163 A young Beagle with left-sided motor dysfunction

due to a lateralized cervical disc.
 A C U T E PA R E S I S AND P A R A LY S I S 207

Postural reaction testing should be performed to differ- NEUROANATOMICAL BASIS

entiate between neurological and orthopaedic causes of
lameness (164). Animals with orthopaedic lameness Paresis and paralysis localize the underlying disease to
should not have deficits in proprioceptive placing, within the neuraxis and/or lower motor units. Within the
hopping, hemistanding or placing reactions. Support nervous system, the problem should be further localized
may be necessary if significant pain is a component of the as an intracranial problem, spinal cord problem or gener-
presenting complaint. As an example, a dog with a alized lower motor unit disease.
humeral fracture may attempt to replace its paw to the The lower motor neuron (LMN) unit is the final
normal position after the paw is knuckled over if the common pathway for motor control. It includes the
animal is given enough support. ventral horn cell within the spinal cord or within the CN
The finding of paresis or paralysis requires accurate nucleus of the brainstem and the axon. The ventral root,
lesion localization within the nervous system before an spinal nerve, peripheral nerve and the individual nerve
appropriate differential diagnosis can be established and fibres that innervate the muscle fibres represent the
further testing ordered. anatomical portions of the axon. The final portion of the
LMN unit is the NM junction and the muscle fibres
innervated by the axon (see 138). Activation of the LMN
causes contraction of the muscle which it innervates.
The UMN systems include the corticospinal,
rubrospinal, reticulospinal, tectospinal and vestibulo-
spinal systems that control the LMN unit, which is the
final common pathway of voluntary movement. All
of these systems, except the vestibulospinal tract, tend
normally to inhibit the LMN. Therefore, when the
 164 Hopping can assist in the detection of postural UMN systems are activated, the LMN is inhibited and
reaction abnormalities, confirming neurological disease the innervated muscle relaxes.
rather than orthopaedic disease, as long as the dog’s body The generation of gait is a complex and delicate
weight is well supported during the procedure. balance of the UMN pathways, the LMN system and
feedback provided by the GP system. The two major
components of gait generation are the postural and pro-
traction phases. Activation or facilitation of the nerves to
the anti-gravity extensor muscles provides the postural
phase of gait generation. These muscles provide weight
support. Protraction is accomplished by facilitation of
the neurons that innervate the flexor muscles to initiate
movement, in addition to facilitation of the neurons that
innervate the extensor muscles to complete the move-
ment. The GP (sensory) system monitors the range, rate
and position of the limbs by receptors that are diffusely
located throughout the body in muscles, tendons and
joints.
Central gait generators modulate motor neuron
activity through a network of interneurons in the spinal
cord grey matter. In domestic animals these central gait
generators are located in the spinal cord intumescences.
A normal gait requires UMN activation and inhibition of
the spinal reflex mechanism of the LMN unit. These
spinal cord gait generators drive ambulation in domestic
208 DECISION MAKING

animals as opposed to the corticospinal and cerebral Table 51 Differentiation between LMN and
motor cortices in primates. This results in a relatively UMN signs in the neurological
normal gait in dogs and cats with significant forebrain examination
lesions such as tumours or infarctions. EXAMINATION LMN SIGNS UMN SIGNS
Voluntary motor movement differs from reflexive FINDINGS
movement and muscle tone. It is very important to Motor function Paresis or paralysis Paresis or paralysis
understand that complete spinal cord transection will
leave the LMNs below the site of injury intact and reflex- Reflexes Reduced or absent Normal to increased
ive motor movements can occur. A spinal cord lesion that Muscle tone Reduced Normal to increased
causes paresis or paralysis can affect both the UMN and
Hypoaesthesia/ Distribution With complete
LMN systems. Other signs, including muscle tone,
anaesthesia isolated to lesions, there is a
myotatic stretch spinal reflexes, withdrawal or flexor autonomous zones more diffuse and
reflexes and autonomous zone mapping (165), allow of the spinal generalized
more accurate localization than gait evaluation alone nerves affected anaesthesia of the
(165) limbs affected
(Table 51). In animals with LMN paresis and paralysis
there is typically reduced tone, reduced strength of Muscle atrophy Rapid and Mild, slow atrophy
reflexes and hypoaesthesia or anaesthesia in the severe atrophy, due to disuse
specifically of
autonomous zone of the spinal nerve’s cutaneous
muscles
innervation. (For further information the reader is innervated by
directed to Chapter 16.) UMN paresis and paralysis affected nerves
usually result in increased tone, normal or increased
reflexes and complete anaesthesia of the affected limbs.

Hindlimb nerves
Caudal cutaneous femoral
Genitofemoral
Lateral cutaneous femoral
Common peroneal
Saphenous
Sciatic
Tibial

Medial Lateral Caudal Cranial

Forelimb nerves
Axillary
Radial
Musculocutaneous
Ulnar
Brachiocephalic

 165 Approximate representation of the cutaneous autonomous zones of innervation in dogs and cats.
 A C U T E PA R E S I S AND P A R A LY S I S 209

NEUROLOGICAL EVALUATION 1. Gait evaluation

Initial evaluation of an animal with a gait abnormality
The finding of paresis or paralysis in the absence of should be done with the aim of determining whether the
intracranial signs indicates spinal cord disease or general- animal is ataxic, paretic or lame (from either NM disease
ized LMN unit disease. Brainstem injury is unlikely to or an orthopaedic disorder) and which limb(s) is/are
cause paralysis without obvious additional signs such as involved. The locomotor status should be evaluated on a
altered states of consciousness, vestibular ataxia, cerebel- non-slick surface with support if needed (166). Asymme-
lar ataxia or CN dysfunction. Apart from acute disease try should be assessed and graded. Assessing weakness
processes (i.e. infarct, haemorrhage and head trauma), can be done by describing whether the animal can rise,
lesions affecting the forebrain cause contralateral paresis stand or walk unassisted. Other semi-quantitative
that is so mild it is usually not apparent in the gait. descriptors could include how far it can walk without
The next goal for the clinician is to further localize the falling, how much support the animal needs to rise or
problem, as diagnostic approaches, differential diagnoses stand, and how much support is needed for purposeful
and treatment options differ for each possible disease ambulation. Noting the involvement of forelimbs is
location. important, as some animals with tetraparesis may have
The neurological evaluation of patients with paresis marked weakness in the hindlimbs and minimal weak-
and paralysis focuses on several critical points. ness in the forelimbs.
• What is the motor status of the patient: weak or In ambulatory animals, gait analysis can help differen-
paralysed? tiate LMN from UMN paresis. LMN dysfunction typi-
• Are signs confined to the hindlimbs or are the cally results in a short-strided gait with decreased ability
forelimbs also involved? to support weight. Dysfunction of the descending UMN
• Is one side worse than the other? system results in a long-strided, ‘reaching’ and stiff gait.
• Are the postural reactions in each limb intact or Animals with a caudal cervical lesion are often described
reduced? as having a ‘two-engine gait’ with a short, choppy gait in
• In the abnormal limbs, identify whether the signs the forelimbs and a long-strided, floating gait in the
are consistent with LMN or UMN dysfunction hindlimbs.
(Table 51).
• Is spinal column manipulation associated with
discomfort?
• What is the sensory status of the patient? Is there a
behavioural response to noxious stimulation of the
superficial and deep limb tissues?

The neurological evaluation should be done system-

atically in a relaxed setting using a neurological exam-
ination form to ensure that it is completely undertaken,
a permanent record exists and comparisons of serial
examinations are possible. Gait and postural reactions
identify which limbs are affected, while reflexes, tone and
muscle mass evaluation help identify LMN versus UMN
signs (Table 51).

 166 Sling support, as shown here, may be needed to

assess motor function effectively in large and weak dogs.
 210 DECISION MAKING

2. Postural reaction testing 5. Sensory testing

Postural reactions should be evaluated in all animals pre- Nociception testing is performed with a small haemostat
senting for paresis and paralysis. Each limb should be systematically over the surface of the affected limbs.
evaluated and the results noted on the neurological exam- Application of pressure should only be escalated when
ination form. The aim of postural reaction testing is pri- the initial stimulus fails to elicit a behavioural response
marily to detect subtle abnormalities that were equivocal such as turning of the head, vocalizing or an escape
or not obvious on gait evaluation. The results of gait eval- behaviour.
uation and postural reaction testing help to identify
which limbs are involved. Muscle tone and segmental
spinal reflexes are then tested on each abnormal limb to
determine if the lesion is UMN or LMN in nature. Spe-
cific postural reaction tests can be selected based on the
size and cooperation of the patient (see Chapter 1).

3. Evaluation of muscle tone and segmental spinal

reflexes
Muscle tone should be assessed by flexing and extending
the limb and joints (167). Although increased resistance
is indicative of UMN signs, it can also be seen in animals
that are fractious, excitable or in pain, as well as in associ-
ation with LMN paresis affecting the flexor system.
Diminished tone is a hallmark of LMN signs.
Segmental spinal reflexes should be performed in
lateral recumbency with the non-dependent limb being
tested. Responses graded as absent or depressed indicate
LMN dysfunction, while responses graded as normal or
exaggerated indicate UMN dysfunction. Specific spinal
reflexes that should be examined include the patellar,  167 Increased muscle tone of the forelimbs is seen in
flexors (withdrawal) and perineal reflexes. Anal tone this dog, but is best appreciated by attempting to flex and
should be evaluated by rectal palpation. Other spinal extend all the joints of each limb.
reflexes, such as the triceps, biceps, and gastrocnemius,
may be tested, but it should be remembered that these
reflexes are inconsistent and therefore unreliable, even in
normal animals.

4. Evaluation of tail, bladder and anal sphincter

Tail function is evaluated by assessment of voluntary tail
movement, tail tone and sensation. Bladder and urethral
function are evaluated by assessment of bladder size,
resistance to manual expression and presence of urine
dribbling. The bladder is often large, firm and difficult to
express with UMN lesions (i.e. lesions cranial to the S1
spinal cord segment), while the bladder is large, flaccid
and easily (but incompletely) expressed with LMN
lesions (Table 52). The anal sphincter is evaluated by
assessment of anal tone on digital rectal palpation, pres-  168 Reduced anal tone is evident in this dog, which
ence of anal reflex and sensation (168). had a severe lumbosacral lesion.
 A C U T E PA R E S I S AND P A R A LY S I S 211

6. Cutaneous trunci reflex and spinal Table 52 Anatomical and clinical

palpation/manipulation characteristics of UMN and LMN
The cutaneous trunci reflex enables accurate localization bladder dysfunction
within the T3–L3 UMN spinal cord segments, and addi- UMN BLADDER LMN BLADDER
tionally assesses the C8–T1 region of the brachial plexus
Lesion cranial to the S1 Lesion caudal to the S1
(efferent arm of the reflex) via the lateral thoracic nerve segment segment
from spinal cord segment C8 or T1. The cutaneous
trunci reflex can be decreased or absent caudal to a lesion Conscious voiding attempts Conscious voiding attempts
usually absent absent
anywhere in this pathway. In the occasional normal
animal the cutaneous trunci reflex is either unreliable or Bladder expression difficult Bladder easily expressed
totally absent. This test is conducted by stimulating the
Large bladder Half-full to large flaccid
skin with a pinprick or by pinching with a pair of bladder
haemostats, starting at the iliac crest, about 2.5 cm
(1 inch) lateral to the midline. This should result in a Perineal tone and reflex Perineal tone and reflex
present reduced to absent
bilateral contraction (or twitch) of the cutaneous trunci
muscles. In the absence of such muscle contraction, the May get overflow incontinence Frequent urine dribbling
point of skin stimulation should be moved cranially until when the bladder becomes
over-distended
a normal reflex is observed (i.e. cut-off point).
Paraspinal palpation is performed near the end of
the examination to ensure the continued cooperation
of the patient. The clinician should palpate down the • Animals with suspected or documented displaced
spine, feeling for focal pain, muscle spasm and heat. If spinal fractures should be immediately stabilized
the dog does not react to light palpation, then moderate externally using a backboard (see Chapter 21).
pressure is applied. The neck is flexed from side-to-side, Immediate evaluation of the patient should be
dorsally and ventrally, if no pain is elicited on palpation. confined to reflexes and sensory evaluation prior to
The lumbosacral junction is flexed and extended while imaging.
trying not to flex other joints. A repeated behavioural • Spinal pain when present can be a helpful localizer,
reaction to what should be an innocuous stimulation can although some stoic animals may not show obvious
be interpreted as pain. Concurrent administration of pain on palpation. In some of these animals,
anti-inflammatory or analgesic medications should be abdominal ‘splinting’ (thoracolumbar localization)
noted, as these may influence the results of the sensory or resistance to flexion/extension (cervical or
examination. cervicothoracic localization) is noted in response to
After collecting and recording the data above, the palpation and manipulation. Other potential causes
likely region of the nervous system affected can be of pain on palpation can include intra-abdominal
identified and specific differential lists can be assembled pathology and orthopaedic pain from the shoulder
for appropriate further testing (Table 53 and 169, next and hip.
page). • Nociception testing requires observation of a
behavioural response to a noxious stimulus. It is
Lesion localization for paresis and paralysis tested by pinching the digits with the fingers or
• Generalized NM junction diseases and myopathies with haemostats, heavy needle holders or even
rarely cause postural reaction deficits because GP pliers. The response seen may be a turn of the head
pathways are unaffected. Often, decreased strength or vocalization or an escape behaviour. The
of the flexor reflex may be the most prominent sign. withdrawal reflex must not be mistaken for a
• Complete paralysis or non-ambulatory paresis behavioural response. To avoid confusion, the
without evidence of intracranial signs, such as withdrawal reflex should be evaluated first and then
mental dullness and CN deficits, is typically due to increased pressure applied to evaluate pain
spinal cord disease. perception.
 212 DECISION MAKING

Table 53 A summary of neurological examination findings related to spinal cord localization

SPINAL CORD SEGMENT AFFECTED

C1–C5 C6–T2 T3–L3 L4–S3 S1–3 DIFFUSE LMN

DISEASE

Gait Tetraparesis/ Tetraparesis/ Paraparesis/ Paraparesis/ Typically Normal to

plegia; plegia; plegia; plegia; normal generalized
hemiparesis/ hemiparesis/ monoparesis/ monoparesis/ weakness
plegia; plegia; plegia plegia
monoparesis/ monoparesis/
plegia plegia

Forelimb reflexes Normal to Decreased Normal Normal Normal Decreased

increased (especially
withdrawal)

Hindlimb reflexes Normal to Normal to Normal to Decreased to Typically Decreased

increased increased increased absent normal

Urethral and anal Normal Normal Normal Normal to Decreased Normal to

sphincter tone decreased decreased

Bladder function UMN bladder UMN bladder UMN bladder Variable LMN bladder Variable

Hindlimb paresis or paralysis (as evidenced by gait

and/or postural reaction deficits)

Forelimb gait or postural

reactions

Hindlimb reflexes NORMAL ABNORMAL Forelimb reflexes

NORMAL OR DECREASED NORMAL OR

DECREASED
INCREASED INCREASED

T3–L3 Brainstem or
L4–S3 Hindlimb reflexes
C1–C5

NORMAL OR
INCREASED DECREASED
 169 Algorithm for the diagnosis of paresis or paralysis
in the absence of intracranial signs such as cranial nerve
deficits, abnormal mentation, nystagmus or cerebellar
ataxia. (Spinal localization given in terms of spinal cord C6–T2 Generalized LMN
diseases
segment affected.)
 A C U T E PA R E S I S AND P A R A LY S I S 213

• The presence or absence of nociception and Specific diagnostic tests

duration of this sign provide valuable prognostic The choice of neurodiagnostic tests in animals with
information about compressive spinal cord lesions. paresis and paralysis depends on the neurolocalization,
Function often deteriorates with increasing severity of signs and, often, the availability of diagnostic
compression, but this is also related to the speed modalities. Many tests require specialized skills and
and chronicity of compression. Loss of function equipment to perform and interpret. They are also not
develops in a predictable manner in the following without risks to the animals and these risks should be
sequence: (1) loss of postural reactions, (2) loss of discussed with the animal’s owner.
voluntary motor function, (3) loss of superficial pain
sensation and (4) loss of deep pain perception. Spinal cord localization (C1–S3)
Animals with loss of nociception after disc • Minimum database including CBC, serum
herniation are reported to have an approximately chemistry analysis and urinalysis. Based on the
60% chance of recovery if surgically decompressed results of the physical examination, a thyroid
within 48 hours of onset. Animals with loss of deep evaluation may be needed.
pain perception following exogenous trauma have a • Spinal radiographs: ventrodorsal and lateral
much worse prognosis. radiographs of the previously identified neuro-
• In non-compressive spinal cord lesions, such as seen anatomical spinal location. Animals should be
with infiltrative spinal cord tumours, vascular sedated prior to radiographic examination. In
infarctions or inflammatory/infectious myelo- animals with suspected vertebral fractures or
pathies, there is not the same predictable loss of luxations, extreme care should be exercised.
function as seen with compressive spinal cord • Spinal imaging, such as myelography, CT or MRI,
lesions. Loss of function is expected to be related to requires anaesthesia and specialized skills and
the part of the spinal cord affected by the lesion. equipment for performance (see Chapter 4).
Some focal spinal cord lesions, such as fibrocarti- • CSF collection and analysis. CSF needs to be
laginous embolic myelopathy, have shown some collected prior to injection of myelographic
anatomical correlation with functional spinal cord contrast into the subarachnoid space and should be
areas. analysed rapidly to prevent degradation of the cells.
This should usually be avoided if trauma cannot be
DIFFERENTIAL DIAGNOSIS ruled out.

The differential diagnosis list depends on the neuro- Lower motor neuron unit disease
anatomical localization and the presence of a painful • Minimum database consisting of CBC, chemistry
focus, as well as the history and signalment of the patient. profile, urinalysis and T4.
Although a presumptive diagnosis may be made based on • Further laboratory work may be indicated based on
the most common disease to affect a specific patient, it is results of the examination and minimum database
best to develop a complete differential list to confirm or (endocrine testing, infectious disease titres, toxin
exclude less likely diseases. Any time that a patient is not screening).
progressing as expected, the differential list should be • Edrophonium testing if MG suspected (see
revisited and re-evaluated. Chapter 24).
Diseases and conditions commonly necessitating the • Serum testing for anti-acetylcholine receptor
emergency evaluation of a dog or cat with paresis and antibodies if MG suspected (see Chapter 24).
paralysis are outlined in Tables 54–56 (pp. 214–216). • Electrodiagnostic testing, such as EMG, motor
nerve conduction studies, sensory nerve conduction
studies, repetitive nerve stimulation testing,
single-fibre EMG and F-waves studies. These tests
require anaesthesia, special equipment and
specialized skills to perform and interpret.
214 DECISION MAKING

Table 54 Causes of acute paresis and paralysis

TETRAPARESIS/PLEGIA LOCALIZED TO C1–T2 PARAPARESIS/PLEGIA LOCALIZED TO T3–L3

DISEASE MECHANISM EXAMPLES EXAMPLES

Vascular Fibrocartilaginous embolism* (D, rare C) Fibrocartilaginous embolism* (D, rare C)

Vascular malformations Vascular malformations
Spinal cord haematoma or haemorrhage Spinal cord haematoma or haemorrhage

Inflammatory/infectious Meningo(encephalo)myelitis (viral, bacterial, Meningomyelitis (viral, bacterial, rickettsial,

rickettsial, protozoal, fungal or immune mediated)* protozoal, fungal or immune mediated)*
Discospondylitis*/osteomyelitis Discospondylitis*/osteomyelitis
Spinal epidural empyema Spinal epidural empyema

Trauma Spinal fracture/luxation* Spinal fracture/luxation*

Traumatic disc herniation* Traumatic disc herniation*

Toxic None None

Anomalous Atlanto-axial subluxation* Syringo(hydro)myelia

Syringo(hydro)myelia

Metabolic None None

Idiopathic None None

Neoplastic Primary or metastatic spinal column or spinal cord Primary or metastatic spinal column or spinal cord
tumour* tumour*

Nutritional Hypervitaminosis A (C) Nutritional hyperparathyroidism

Hypervitaminosis A (C)

Degenerative Intervertebral disc disease* Intervertebral disc disease*

Cervical spondylomyelopathy* (D)

LOWER MOTOR NEURON UNIT CAUSES

OF ACUTE PARESIS AND PARALYSIS This disease is probably immune mediated, although
treatment with corticosteroids does not influence the
(See Part 3, Chapters 17 to 28, for the specific causes of course of the disease.
UMN paresis and paralysis.)
Clinical presentation
Polyradiculoneuritis or Coonhound paralysis There is an acute onset of a flaccid paraparesis rapidly
Overview ascending to involve the forelimbs. CNs are typically
Polyradiculoneuritis is seen in dogs and rarely in cats. It normal, although facial weakness and dysphonia can be
can be seen 7–10 days following a raccoon bite or expo- noted. Megaoesophagus is not a feature of this disease.
sure to other immunological stimulus. The lesion involv- The perineal reflex is normal and urinary continence is
ing the ventral roots and peripheral nerves is composed maintained. In the early stages of the disease, hyper-
of demyelination and mononuclear interstitial infiltrate. aesthesia can be seen. Recurrent episodes are possible.
 A C U T E PA R E S I S AND P A R A LY S I S 215

Table 55 Causes of generalized or diffuse

neuromuscular diseases seen on
PARAPARESIS/PLEGIA LOCALIZED TO L4–S3 emergency evaluation**

EXAMPLES DISEASE MECHANISM EXAMPLES

Fibrocartilaginous embolism* (D, rare C) Vascular None

Aortic thromboembolism
Inflammatory/infectious Polyradiculoneuritis*
Vascular malformations
Myasthenia gravis*
Spinal cord haematoma or haemorrhage
Polymyositis
Ascending and descending haemorrhagic myelomalacia
Polyneuritis
Meningomyelitis (viral, bacterial, rickettsial, protozoal, fungal or
immune mediated)* Trauma None
Discospondylitis* Toxic Tick paralysis* (D)
Botulism*
Spinal fracture/luxation* Aminoglycoside toxicity
Traumatic disc herniation* Coral snake envenomation
Organophosphate toxicity
None
Anomalous None
Syringo(hydro)myelia
Metabolic Endocrine polyneuropathies

None Idiopathic Acquired myasthenia gravis

Necrotizing myopathy (D)
None
Neoplastic Paraneoplastic polyneuropathy
Primary or metastatic spinal column or spinal cord
tumour* Nutritional None
Endocrine neuropathies Degenerative None
Hypervitaminosis A (C)

Intervertebral disc disease*

* Common cause; C = cats; D = dogs
* Common cause; C = cats; D = dogs ** See also Chapter 8

Diagnosis Management
Diagnosis is based on clinical signs and exclusion of other Excellent supportive care, including cleaning, frequent
acute LMN diseases (e.g. botulism, MG and tick para- turning, physical rehabilitation and expressing the
lysis ± adrenal insufficiency and electrolyte imbalance). bladder, is required for animals that have severe signs.
Electrodiagnostic tests, such as EMG and motor nerve Vigilant monitoring for urinary tract infections, pneu-
conduction velocity (MNCV), are abnormal, but these monia and bed sores, with immediate aggressive treat-
changes are not evident until 5–7 days after onset. CSF ment, will assure good outcomes. Respiratory paralysis
analysis may show elevated protein and a normal cell may result if the phrenic nerve and intercostal nerves are
count and cytology (albumino-cytological dissociation). severely affected and may require ventilatory support.
The overall course of the disease is typically 6 weeks,
although cases lasting 4–6 months are not uncommon.
The prognosis for recovery is good if respiratory
failure does not occur and supportive care is aggresive.
216 DECISION MAKING

Table 56 Differentiaton of the most common causes of acute diffuse neuromuscular diseases

POLYRADICULO- TICK PARALYSIS BOTULISM MYASTHENIA

NEURITIS GRAVIS–ACQUIRED

Signalment and history Any breed or age. Any breed with Any breed or age. Congenital (3–8
Some dogs have a potential exposure to History includes weeks). Acquired
history of raccoon bites ticks. Signs occur 5–7 rubbish or carcass (bimodal age distribu-
(hunting dogs) or other days after tick bite. Tick ingestion with onset of tion). Can be acute in
immunostimulation. is typically still attached signs hours to days. onset, but more
Can be acute onset or at time of clinical sign Multiple cases are typically episodic or
progress from hind- suggestive exercise-induced
limbs to forelimbs weakness

Clinical signs Typically progresses Rapid progression from Rapid progression of Acute signs (fulminant)
from a hindlimb paresis first signs to clinical signs. Can be or exercise-induced
to tetraparesis/ recumbency accompanied by gas- weakness (fatigable)
tetraplegia over 4–5 (24–48 hours). trointestinal signs. involving palpebral
days. Does not involve Rarely involves cranial Cranial nerve deficits reflexes, facial nerve,
tail, sphincters or nerves including gag, facial weak gag, laryngeal
cranial nerves except droop, swallowing and paresis or paralysis,
for some dogs showing megaoesophagus are dysphagia and mega-
mild facial paresis and common oesophagus. Spinal
voice changes. Animals reflexes are often
can have severe flaccid preserved
paralysis, but mental
status is normal, often
wagging tail

Electrodiagnostics EMG. Fibrillation EMG usually normal. EMG usually normal. EMG usually normal,
potentials and positive Conduction velocity Conduction velocity but minor changes can
sharp waves 3–7 days normal or slightly normal. Evoked be seen. Conduction
after signs develop. decreased. Evoked potentials reduced. velocity normal, but
Conduction velocity potentials reduced Repetitive nerve decremental response
reduced and dispersed. stimulation can with repetitive nerve
Increased F-wave be slow stimulation. Single-fibre
latency and F-ratio EMG shows typical
‘jitter’

Diagnosis Diagnosis by Identification and Toxin in stomach Anti-acetylcholine

exclusion removal of tick should contents, serum or receptor antibody titre.
result in clinical signs faeces can be identified Edrophonium (Tensilon)
resolving with a bioassay test can be supportive

Treatment and prognosis Supportive care; may Complete resolution of Supportive care; may Anticholinesterase
require ventilator signs 24–72 hours after require ventilator drugs ± immuno-
support. 4–6 weeks tick removed support. 1–3 week suppressive drugs and
recovery is typical recovery supportive care.
Prognosis guarded, but
worsens dramatically if
aspiration pneumonia
and megaoesophagus
develop
 A C U T E PA R E S I S AND P A R A LY S I S 217

Aortic thrombosis or ischaemic neuromyopathy

secondary to aortic thromboembolism
Overview
This condition occurs commonly in cats with hyper-
trophic cardiomyopathy and occasionally in dogs with
hypercoagulable states.

Clinical presentation
The typical presentation is a middle-aged to geriatric
animal with an acute onset of hindlimb pain and paralysis
with no progression. The exact clinical signs relate to the
region of circulatory obstruction. Other signs of circula-
tory compromise are typically seen, including cool, pale
or cyanotic extremities and lack of arterial pulses.
A history of ongoing signs of hypertrophic cardiomyo-
pathy in cats is usually evident.

Diagnosis  170 A 3D reconstructed CT scan in cross-section at

Other conditions, such as sepsis, neoplasia, heart disease the level of the pelvic inlet of a dog with aortic trifurcation
including heartworm infection, immune-mediated thrombosis. Absence of femoral artery structure detected
haemolytic anaemia and protein-losing nephropathy or by the CT can easily be seen on one side (arrow).
enteropathy, are uncovered with a basic investigation (Photo courtesy Davies Veterinary Specialists)
including a minimum database. Advanced imaging, such
as CT (170) and MRI, as well as Doppler ultrasono-
graphy, is necessary to identify vascular compromise.
Tick paralysis
Management See Chapter 28.
Treatment is aimed at treating the primary cause of the
thrombus formation, removing the obstruction and Snake envenomation
decreasing the continued accumulation of the thrombus. See Chapter 28.
A recent report on the use of tissue plasminogen
activator in 11 cats with arterial thromboembolism doc- Botulism
umented a high rate of side-effects (11/11) and a low rate See Chapter 25.
of hospital discharge (3/11). Although some animals will
functionally recover, recurrence is likely if treatment of Acquired myasthenia gravis
the underlying disease is not addressed. See Chapter 24.
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 DECISION MAKING Chapter 11

SPINAL PAIN
219

Ronaldo da Costa

INTRODUCTION NEUROANATOMICAL BASIS OF SPINAL PAIN

Spinal pain is a common clinical sign associated with a Spinal pain reflects the involvement of at least one of
variety of neurological conditions. In some diseases it is three main structures: meninges, vertebrae (vertebral
the most prominent feature, while in others it is less periosteum) and nerve roots or spinal nerves (171). The
obvious, but equally important. The approach to a presence of spinal pain is relatively consistent when a
patient with spinal pain is similar to that for other neuro- disease process affects these structures. However, many
logical presentations. First, a physical examination is different disease mechanisms can cause pain when these
performed to investigate the presence of systemic signs, structures are affected. In dogs and cats the most
such as fever, followed by a neurological examination to common mechanisms leading to spinal pain are inflam-
allow identification of other neurological problems and mation (e.g. meningitis, discospondylitis), compression
to localize the lesion(s). With this information, the clini- (e.g. intervertebral disc extrusion compressing the nerve
cian can then establish the differential diagnoses and roots) and destruction or lysis (e.g. vertebral neoplasia).
select the most appropriate test(s) to rule in or rule out a
specific diagnosis. The presence of spinal pain associated
with neurological deficits helps the clinician narrow  171 Cranial cervical spine of a dog demonstrating the
down the list of differential diagnoses, because some three most common structures (meninges, nerve roots,
spinal diseases can be broadly classified as painful diseases and periosteum) responsible for causing spinal pain in
(e.g. meningitis, disc extrusion, discospondylitis or extra- dogs and cats: (a) representation of inflamed meninges as
medullary spinal tumour) or as non-painful diseases (e.g. seen in cases of meningitis; (b) lateralized intervertebral
ischaemic myelopathy). The presence of neurological disc protrusion causing nerve root compression;
signs is important to rule out joint disease (polyarthritis) (c) periosteal changes secondary to discospondylitis.
and muscle disease (polymyositis). (Image courtesy Ohio State University)

Meninges a

Nerve root Vertebra

 220 DECISION MAKING

Other less common sources of spinal pain in small a

animals are intervertebral disc degeneration (discogenic
pain), arthritic changes affecting the vertebral facet joints
and dysplasia of the caudal vertebral facets. Unlike in
humans, disc degeneration and arthritis rarely cause
spontaneous spinal pain in dogs and cats. Before attribut-
ing spinal pain to disc degeneration or to spinal arthrosis
or arthritis, it is necessary to rule out other more
common causes of pain affecting the meninges, vertebrae Epidural space
or nerve roots. Spondylosis is a non-inflammatory b
degenerative process affecting the bone (vertebral body);
it is rarely associated with spinal pain and should not
cause neurological signs. Disseminated idiopathic skele-
tal hyperostosis (DISH) is a more severe form of spondy-
losis, but should also not cause spontaneous pain or
neurological deficits. Spondylosis or DISH should never
be considered to be the cause of spinal pain or neurolog-
ical deficits without a thorough diagnostic work-up
ruling out all other causes of spinal pain.  172 Magnetic resonance imaging of a 7-year-old,
Spinal pain in the thoracolumbar area is frequently clinically normal male Doberman Pinscher. (a) Cervical
associated with neurological deficits, while in the cervical spinal cord at C2/3. Observe the bright signal around
region it can commonly be the only clinical sign. The the spinal cord (arrow) within the larger vertebral canal.
reason for this clinical difference is that there is a larger (b) Cervical spinal cord at C6/7. Observe the spinal cord
vertebral canal in the cervical region in comparison with (arrow) and the smaller epidural space surrounding it
the thoracic or lumbar regions. This allows a larger area compared with the C2/3 region.
for the cervical vertebral canal to accommodate com-
pressive lesions. The so-called ‘cord-to-canal’ ratio is
also different between the cranial and caudal cervical
regions. The caudal cervical vertebral region has the cer- pain usually improves with the use of anti-inflammatory
vicothoracic enlargement of the spinal cord and, as such, drugs. Neuropathic pain is characterized by abnormal
less space to accommodate compressive lesions. Thus, somatosensory processing in the PNS or CNS. It is
caudal cervical lesions tend to be associated more com- usually manifested as paraesthesia (abnormal sensation
monly with neurological deficits (e.g. cervical spondy- without any physical cause) or allodynia (increased pain
lomyelopathy) in comparison with cranial cervical from stimuli that are not normally painful). One of the
lesions (e.g. intervertebral disc disease) (172). best examples of a cause of neuropathic pain in veterinary
While the meninges, periosteum and epineurium medicine is Chiari-like malformation and syringomyelia,
have a high density of nociceptors, the spinal cord particularly in dogs with a large syrinx and dorsal horn
parenchyma does not contain nociceptors. Because of involvement.
this, strictly myelopathic diseases, such as degenerative Rarely, intracranial diseases can cause cervical pain.
myelopathy or fibrocartilaginous embolic myelopathy, The neck pain seen in these cases may reflect the involve-
are not associated with spinal pain. ment of thalamic structures (thalamic pain syndrome) or
There are basically three types of pain: physiological, distension of the meningeal nerve endings caused by a
inflammatory and neuropathic. Physiological pain serves space-occupying intracranial lesion. Other signs sugges-
as a protective mechanism, warning animals of damaging tive of thalamocortical dysfunction (abnormal behaviour,
stimuli. Inflammatory pain occurs in response to tissue decreased menace response and/or nasal sensation) can
damage and stimulation of mechanosensitive, chemosen- be very relevant for the purpose of lesion localization in
sitive and thermosensitive nociceptors. Inflammatory these cases.
 S P I N A L PA I N 221

NEUROLOGICAL EVALUATION location of the spinal pain. The neurological examination

is then aimed at confirming the presence of spinal pain,
Dogs and cats with spinal pain may present with or localizing it precisely (either focal or multifocal) and
without neurological signs. Lesion localization and diag- assessing the extent, if any, of neurological involvement
nostic approach are facilitated when the patient shows (173). Occasionally, spinal pain may be episodic, with the
obvious signs of spinal pain (e.g. kyphosis, patient only showing signs of pain for a few seconds or
ventroflexed neck) or when the owner is aware of the minutes. On neurological examination, there may be no

 173 Diagram demonstrating a SPINAL PAIN

diagnostic approach to dogs and cats with
spinal pain and showing the most common
Neurological deficits
diseases affecting each spinal region.

YES NO

Localize the lesion

Consider multifocal
(gait, posture, postural MULTIFOCAL
or systemic diseases
reactions, reflexes)

C1–5 C6–T2 T3–L3 L4–S3

IVDD; atlantoaxial
subluxation; IVDD; wobbler IVDD;
Meningitis; polyarthritis;
spinal neoplasia; disease (CSM); IVDD; Lumbosacral
discospondylitis;
spinal trauma; spinal neoplasia; spinal neoplasia; stenosis;
multifocal neoplasia;
meningomyelitis; spinal trauma; spinal trauma; spinal neoplasia;
polymyositis; spinal trauma
syringomyelia; meningomyelitis; discospondylitis; spinal trauma;
Chiari-like syringomyelia empyema discospondylitis;
malformation empyema

Consider orthopaedic examination ±

Perform CBC, biochemistry profile and
joint taps, routine blood work, thoracic
urinalysis, and select the most
and abdominal radiographs, serum CK,
appropriate diagnostic test(s)
infectious disease titres, EMG, survey
according to your primary
spinal radiographs, CSF, advanced
differential(s)
imaging, IgA levels, in this order

Compressive diseases Meningitis/meningomyelitis

Discospondylitis
(e.g. IVDD, CSM, neoplasia)
Spinal radiographs
Spinal radiographs CSF culture and analysis
Myelography, CT or MRI
CT or MRI Serum and CSF IgA levels
Thoracic radiographs and abdominal
ultrasound if neoplasia Blood and urine cultures Titres or PCR in the serum and CSF for
infectious diseases (fungal, protozoal,
Biopsy (fine needle, core, surgical) Serology for Brucella and Aspergillus
rickettsial, viral)
if neoplasia
 222 DECISION MAKING

evidence of spinal pain detected. It is best to re-evaluate logical examination to ensure patient cooperation during
these patients after a few hours to days, depending on the the initial parts of the examination. Proper technique is
duration of presentation, and/or ask the owner for a essential to obtain reliable results (174). The patient
video recording of these episodes at home before pro- should be supported under the pelvic region and pressure
ceeding with further diagnostics. Frequently, these should be applied in a downward fashion between each
events of severe episodic pain are due to cervical disease. spinous process, with two fingers equidistant on each side
Dogs with thoracolumbar and lumbosacral pain have of the process. The goal is to place pressure at the level of
more consistent signs of pain that can often be elicited on the intervertebral foramina, where the spinal nerves exit.
spinal palpation. In a dog with a disease that causes nerve-root compres-
A complete neurological examination (evaluation of sion (e.g. intervertebral disc herniation), applying pres-
mental status, gait and posture, CNs, postural reactions, sure in this manner should consistently elicit focal spinal
spinal reflexes and spinal palpation) should always be per- pain. Since spinal problems occur less frequently in the
formed in patients with spinal pain to establish the loca- cranial thoracic region in comparison with the lum-
tion(s) of the lesion(s). Gait evaluation is the most bosacral and lumbar regions, the clinician can establish
important component of the examination with regard to the patient’s tolerance to spinal palpation by starting the
establishing the presence of neurological deficits. Propri- palpation in the cranial thoracic region between the
oceptive ataxia associated with spinal pain indicates the scapulae. This technique often allows specific identifica-
concurrent presence of spinal cord disease (myelopathy). tion of the painful area when pain is present within
Care should be exercised in the interpretation of postur- regions T2 to L7/S1. The lumbosacral region can be
al reactions (hopping, proprioceptive positioning) in additionally evaluated specifically by lifting the base of
dogs and cats with severe spinal pain, since they may the tail and pushing it cranially. This manipulation is sug-
appear to have delayed responses due to severe pain and gested to change the angle of the sacrum and the L7 joint
thus exhibit an unwillingness to respond appropriately. and it allows pain to be confirmed in the lumbosacral area
The same may hold true for the CN tests that evaluate without manipulation of the hip joint. Evaluation of the
thalamocortical function. Severe pain often causes a patient in lateral recumbency may also reduce the con-
decreased nasal sensation response and/or menace founding effects of concurrent joint pain in the limbs.
response, but if this is truly related to pain and stress, it The cervical spine can be evaluated by applying bilateral
should always be bilateral and symmetric, because both digital pressure to the transverse processes and inverter-
are cortically mediated responses. Spinal palpation tebral foramina. Voluntary range of motion can be
should be performed (carefully) at the end of the neuro- assessed if no pain is detected.

 174 (a) Transverse image of the lumbar spine demon-

a b
strating the position of the fingers for thoracolumbar
spinal palpation. Both fingers should be equidistant and
pressure should be applied in a downward fashion. The
fingers should be positioned close to the midline, aiming
for pressure at the level of the intervertebral foramina.
(b) Lateral image of the lumbar spine demonstrating that
pressure is applied between the spinal processes where
the intervertebral foramina and nerve roots are located.
Lateralized intervertebral disc protrusion is seen on both
images causing lateralized nerve-root compression.
(Image courtesy Ohio State University)
 S P I N A L PA I N 223

 175 Typical posture of a Beagle-cross with cervical  176 Kyphotic thoracolumbar posture of a mixed breed
spinal pain secondary to aseptic suppurative dog with intervertebral disc extrusion between vertebrae
meningoarteritis. L2 and L3.

SPECIFIC FEATURES OF SPINAL PAIN

ACCORDING TO LOCATION

Cervical pain It is not uncommon for cervical pain to have an

The presence of cervical pain can often be established by episodic character. It is the author’s impression that these
the patient’s posture. Dogs and cats with neck pain have episodic presentations of neck pain are usually associated
restricted cervical movement and a head-down posture with nerve root/spinal nerve involvement. Another cause
(175). They have a tendency to follow objects with their of spontaneous pain is the neuropathic pain seen in dogs
eyes rather than with the head. Reluctance to walk with Chiari-like malformation and syringomyelia. These
may also be observed. If neck pain is evident, cervical episodic presentations are in contrast to the more con-
manipulations (flexion, extension) are not necessary to stant and less episodic pain seen when meninges and
ascertain the presence of pain, and can lead to neurolog- osseous structures are affected.
ical deterioration if spinal instability is present.
Cervical palpation (digital palpation over the vertebral Thoracolumbar pain
bodies and intervertebral foramina) can be used to Owners of small breed dogs can usually perceive the
localize areas of pain or muscle spasms and are safer to presence of spinal pain when they pick up their dogs, or
perform than manipulations. The author prefers to use by their dog’s reluctance to go upstairs or jump up or
food to assess the voluntary range of motion in all four down. Thoracolumbar pain may be more difficult to
directions (dorsal, ventral, right and left lateral) rather detect in large breed dogs. Acute thoracolumbar pain
than use forced cervical manipulations. usually leads to a kyphotic (arched) thoracolumbar
Occasionally, a combination of cervical pain and fore- posture (176). The location of the kyphotic region
limb lameness is observed. This has been called ‘nerve (thoracic, thoracolumbar or lumbar) can facilitate local-
root signature’ and usually is seen with lesions in the ization of the area of spinal pain by the clinician. Chronic
caudal cervical spine involving the nerve roots or spinal thoracolumbar pain does not usually lead to a kyphotic
nerves. posture.
224 DECISION MAKING

Table 57 Possible causes of spinal pain in dogs and cats

DISEASE MECHANISM DOGS CATS

Vascular Epidural haemorrhage Epidural haemorrhage

Inflammatory/infectious Discospondylitis (bacterial or fungal)* Discospondylitis

Meningitis (aseptic suppurative meningo- Meningitis
arteritis* or bacterial meningitis) Infectious meningomyelitis
Infectious meningomyelitis (bacterial, fungal, Non-infectious meningomyelitis
rickettsial, viral)*
Vertebral osteomyelitis
Non-infectious meningomyelitis (GME)*
Polyarthritis
Spinal epidural empyema
Polymyositis
Vertebral osteomyelitis
Polyarthritis
Polymyositis

Trauma Spinal trauma (fracture/luxation)* Spinal trauma (fracture/luxation)*

Traumatic atlantoaxial subluxation Traumatic atlantoaxial subluxation
Traumatic disc herniation Traumatic disc herniation

Toxic None None

Anomalous Atlantoaxial subluxation* Atlantoaxial subluxation

Chiari-like malformation and syringomyelia Multiple cartilaginous exostoses
Multiple cartilaginous exostoses
Sacrocaudal dysgenesis
Dermoid sinus

Metabolic None None

Idiopathic Arachnoid cyst Arachnoid cyst

Neoplastic Primary or secondary spinal tumours* Primary or secondary spinal tumours*

Intracranial tumours (rare) Intracranial tumours (rare)

Nutritional Pathological fractures due to metabolic bone Hypervitaminosis A

disease Pathological fractures due to metabolic bone
disease

Degenerative Intervertebral disc degeneration* Intervertebral disc degeneration

Cervical spondylomyelopathy* Degenerative osteoarthritis of articular facets
Degenerative lumbosacral stenosis* Degenerative lumbosacral stenosis
Osteochondrosis dissecans of lumbosacral joint Extradural synovial cysts
Degenerative osteoarthritis of articular facets
(facet dysplasia)
Extradural synovial cysts
Calcinosis circumscripta

* Common cause
 S P I N A L PA I N 225

Lumbosacral pain • Thoracic and abdominal imaging. Useful to rule out

The presence of lumbosacral pain often is perceived by primary or secondary neoplastic processes.
the owners, but sometimes can be confused with • CSF analysis. Essential to confirm an inflammatory
orthopaedic (hip) pain. Historically, evidence of lumbo- process in the CNS. Aim to collect the CSF caudal
sacral pain includes difficulty getting up or sitting down, to the location of the lesion. The type of pleocytosis
a reluctance to jump up into the car or go upstairs, and can assist the clinician in establishing an aetiological
pain when touched in the caudal lumbar region. In diagnosis (see Chapters 4 and 19).
addition, the tail may be ‘down’ and the dog may not wag • Arthrocentesis and joint fluid analysis. May confirm
its tail as it used to. A guarded lumbar/lumbosacral the presence of polyarthritis. Young, large breed
posture with kyphosis may be seen in more acute cases. dogs may have concurrent immune-mediated poly-
Occasionally, the pain may be worse after exercise, a arthritis and meningitis.
feature not seen with cervical or thoracolumbar pain. • Myelography. Outlines the spinal cord structure. It
Lumbosacral pain may be the only clinical sign or it may allows indirect visualization of extradural,
be associated with other signs such as weakness (paresis) intradural/extramedullary and intramedullary
or lameness, which can be suggestive of nerve root or lesions.
spinal nerve compression. Many dogs with lumbosacral • CT. Can be used alone or with intravenous or
disease have concurrent orthopaedic problems, such as subarachnoid contrast (myelography) to enhance
hip dysplasia or cranial cruciate ligament rupture. It is visualization of lesions.
very important to evaluate the lumbosacral region specif- • MRI. Is the gold standard technique for investigat-
ically by lifting the tail and pushing it cranially, isolating ing diseases affecting the spinal cord. Allows visuali-
it from the hip joint. zation of the spinal cord parenchyma and provides
superior sensitivity when compared with other
DIFFERENTIAL DIAGNOSIS imaging techniques.
• Scintigraphy. May be used in cases of non-localized
Conditions to be considered when evaluating a dog or pain.
cat presented with spinal pain are listed in Tables 57 • Biopsy. Surgical biopsy of muscle or bone can assist
and 58. in the identification of neoplastic or inflammatory
conditions.
Diagnostic tests • Serum and CSF titres/PCR for infectious diseases.
The ancillary tests should be selected according to lesion Used to confirm specific infectious diseases causing
localization and differential diagnoses. For example, myelitis/meningomyelitis.
spinal radiographs can sometimes be very useful, but are • Blood and urine culture. Potentially useful for cases
not recommended for cases of suspected meningitis. of discospondylitis.
• CBC and biochemistry profile. May reveal evidence
of inflammatory (infectious or non-infectious)
diseases and changes suggestive of neoplasia, but
can all be completely normal in the presence of a
markedly inflammatory CNS process. Table 58 Conditions that may mimic
• Urinalysis/urine culture. Can allow identification spinal pain
of a source of chronic infection and the infectious
• Polyarthritis
agent in cases of discospondylitis or empyema.
• Polymyositis
• Survey radiographs. Allows assessment of osseous
spinal structures. It is useful to rule out major • Paraspinal muscle abscess

structural lesions as seen with discospondylitis, • Abdominal conditions (pyelonephritis, pancreatitis)

osteomyelitis or vertebral tumour. Absence of • Pelvic conditions (prostatic abscess)
abnormalities cannot rule out spinal lesions. • Bilateral cranial cruciate ligament rupture
Proper positioning is essential.
 226 DECISION MAKING

COMMON CAUSES OF SPINAL PAIN Radionuclide bone imaging can be used when a defin-
itive diagnosis cannot be reached on survey radiographs.
Discospondylitis and vertebral osteomyelitis It is usually abnormal before bone lysis becomes evident
(spondylitis) on survey radiographs. Changes consist of increased
Overview uptake of radiopharmaceutical at the affected disc space
Discospondylitis and vertebral osteomyelitis (spondy- and endplates. However, caution should be used when
litis) are infections of the intervertebral disc and adjacent interpreting the natural age-related degeneration seen
endplates (discospondylitis) or vertebral body (spondy- particularly at the LS joint, which will also result in
litis). The most commonly encountered infectious increased radiopharmaceutical uptake.
agents are coagulase-positive staphylococci (S. aureus, Investigation of a potential systemic infectious focus
S. intermedius), Streptococcus spp., Brucella canis and should be considered in all cases. This may involve dental
E. coli. Fungal (Aspergillus spp., Blastomyces dermatitidis, examination, thoracic radiographs and heart and abdom-
Histoplasma capsulatum, Coccidioides immitis, Paecilo- inal ultrasound for endocardial and prostatic or renal
myces) or Actinomyces spp. (secondary to grass awn) are disease, respectively.
rare in comparison. The conditions are more common in Culture of blood, urine or disc/bone material should
male, large and giant breed dogs and are rare in cats and be performed to identify the causative organism. Serolo-
small, chondrodystrophic dogs. gy for Brucella also should be performed, especially in
Haematogenous spread from distant sources (e.g. intact animals in endemic regions.
skin, heart valves, oral cavity, urinary tract, testes,
prostate, uterus) is the most common form of infection. Management
It can be secondary to penetrating wounds, foreign Treatment of discospondylitis is difficult and prolonged
bodies (grass awn migration, gunshot pellets), epidural (2–4 months); relapses are not uncommon. Ideally, treat-
analgesia or disc fenestration during spinal surgery. ment should be guided by the results of culture and sen-
sitivity. Cephalosporin antibiotics are a good empiric
Clinical presentation choice initially. Intravenous antibiotics should be consid-
Clinical signs consist of severe (sometimes diffuse) spinal ered if severe neurological compromise is present.
pain, often without neurological deficits initially. Affect- Empirical treatment can be initiated after all samples
ed dogs and cats may present with systemic illness, but (urine, blood, disc aspirate) have been taken for culture
can be normothermic and systemically normal. The con- and sensitivity. If there is no response within 5 days, the
ditions can occur anywhere along the spine, but are more antibiotics should be changed or a better sample should
common at the L7–S1 and T13–L1 regions, and the be obtained from the infected disc either at surgery or
thoracic spine. under fluoroscopy.
With progression of the disease, degeneration of Cage rest is important to minimize the risk of patho-
the disc can lead to disc protrusion/extrusion, causing logical fracture or luxation. Analgesia should be provided
signs of myelopathy. Less commonly, infection spread- using non-steroidal and/or other analgesics. Cortico-
ing to the epidural space can cause spinal epidural steroids are contraindicated.
empyema; infection spreading to the meninges can also Surgery is indicated if there is no response to medical
cause meningitis. treatment or to provide decompressive surgery in
patients with substantial neurological deficits and com-
Diagnosis pression identified on imaging. Surgical stabilization
Diagnosis is based on the radiographic features of col- may be necessary in some cases and can prove to be suc-
lapse of disc space with endplate lysis and sclerosis. cessful even when infection has not been completely
Radiographic changes may not occur for 10–14 days after resolved.
onset of infection. CT or MRI can be used and are more
sensitive for earlier stages of infection, with MRI also
assisting with the identification of soft tissue changes and
investigation of associated foreign bodies.
 S P I N A L PA I N 227

Spinal epidural empyema (epidural abscess) Chiari-like malformation and syringomyelia

Overview (caudal occipital malformation syndrome)
Epidural empyema or abscess is a suppurative, septic Overview
process within the epidural space of the vertebral canal. Chiari-like malformation is a disease characterized by a
It can be the result of haematogenous spread, vertebral congenital malformation of the occipital bone, resulting
osteomyelitis, discospondylitis, paraspinal muscle absces- in overcrowding of the caudal fossa, abnormal CSF
sation or direct inoculation of bacteria (e.g. following a dynamics and subsequent syringomyelia. The most com-
bite or spinal surgery). monly affected breeds are the Cavalier King Charles
Spaniel, Brussels Griffon, Yorkshire Terrier and Toy
Clinical presentation Poodle, with affected dogs usually between 6 months and
Systemic signs, such as anorexia, lethargy and fever, are 3 years old, but the disease is seen in many small and toy
common. Most dogs and cats present with spinal pain breeds of any age.
and neurological deficits.
Clinical presentation
Diagnosis Cervical pain (hyperaesthesia) is the most consistent sign,
Diagnosis is based on haematological findings (neu- although sometimes the pain may be difficult to localize.
trophilia), CSF changes (typically neutrophilic pleocyto- Scratching of the neck and/or shoulder area, typically on
sis with increased protein) and imaging finding of one side, is a common sign. Scoliosis, paresis and ataxia
extradural spinal cord compression. Cultures from may also be seen.
blood, CSF and surgical material should be performed.
A variety of organisms have been reported. Blood and Diagnosis
surgical cultures offer the highest diagnostic yield. Diagnosis is established by MRI of the caudal fossa and
the cervical spine (177).
Management
Treatment is based on antibiotic therapy along with Management
emergency surgical decompression and abscess drainage. Medical treatment consists of corticosteroids (pred-
The prognosis is guarded and depends on the degree of nisone, 0.5 mg/kg PO q24–48h), furosemide (2 mg/kg
neurological impairment and how quickly treatment is PO q12h), omeprazole (0.5–0.1 mg/kg PO q24h) and/or
instituted. gabapentin (10–20 mg/kg PO q8–12h). For refractory
cases, pregabalin (2–4 mg/kg PO q8–12h) can be given.
Surgical treatment (suboccipital decompression and
C1 dorsal laminectomy) is indicated for dogs that
respond poorly to medical treatment.

Spinal neoplasia
Overview
Spinal tumours can be located in the extradural,
intradural–extramedullary or intramedullary regions.
The most common tumours are osteosarcoma and fibro-
sarcoma in dogs, lymphoma and osteosarcoma in cats.
Spinal neoplasia occurs in any breed or age, but large
breed dogs (>18 kg) >5 years of age are overrepresented.
 177 Sagittal MR image of Chiari-like malformation Lymphoma tends to occur more commonly in young
and syringomyelia in a 2-year-old Cavalier King Charles cats (median 4.2 years), while all other feline spinal
Spaniel. Note the cerebellar herniation (red arrow) and tumours are seen in older cats (median 9.9 years). Spinal
syringomyelia (yellow arrows) within the cervical tumours can affect any spinal region, but commonly are
spinal cord. found in the cranial thoracic and cervical regions.
228 DECISION MAKING

Clinical presentation Feline hyperaesthesia syndrome

Clinical signs vary according to tumour location, but Overview
spinal pain is a common feature with most spinal neo- Feline hyperaesthesia syndrome (FHS), also known as
plasms. Affected dogs may appear with a chronic pro- ‘rippling skin disease’, is a poorly understood condition
gressive history, although subacute presentations (fast of cats that may have neurological, NM or behavioural
deterioration over 1–3 days) are very common. The causes. Cats of any age or breed may be affected.
majority of cats have a chronic progressive history. Occa-
sionally, acute onset of spinal pain and myelopathy may Clinical presentation
result from pathological fracture. Affected cats are extremely sensitive to touch in the
lumbar and lumbosacral regions, and may exhibit rip-
Diagnosis pling of the skin over the thoracolumbar area, muscle
A minimum database with CBC, biochemistry profile, spasms, compulsive licking and biting at the back, flank
thoracic radiographs and abdominal ultrasound should and tail, and abnormal erratic behaviour. Neurological
always be performed to investigate for systemic primary deficits are not observed in these cats.
lesions. Diagnosis is confirmed using spinal radiographs,
myelography, CT or MRI (178). Biopsy is necessary to Diagnosis
establish the tumour type and plan appropriate treat- A presumptive diagnosis is based on history and physical
ment. and neurological examination findings. Other spinal dis-
eases need to be ruled out. EMG and muscle biopsies
Management from epaxial muscles can be performed. A behavioural
Chemotherapy, radiation therapy and surgery can be evaluation is often recommended.
used alone or in combination, depending on the tumour
type, with varying prognosis. Median survival ranges Management
from a few months (e.g. spinal osteosarcoma) to almost 2 Treatment should be directed at the underlying cause,
years (e.g. multiple myeloma with chemotherapy). if identified. Usually, cats are treated with anticonvulsants
(phenobarbital, 2–3 mg/kg PO q12h or gabapentin,
10–15 mg/kg PO q12h), corticosteroids (prednisolone,
0.5 mg/kg q12–24h), non-steroidal anti-inflammatory
drugs (NSAIDs; e.g. meloxicam or piroxicam) or behav-
iour-modifying drugs (fluoxetine, 0.5–4.0 mg/cat PO
q24h; amitriptyline, 2 mg/kg PO q24h; clomipramine,
1–5 mg/cat PO q12–24h). Environmental enrichment
may be helpful.

Atlantoaxial subluxation
See Chapter 21.

Acute disc disease

See Chapter 22.

Meningomyelitis, meningitis
See Chapter 19.

Spinal trauma
 178 Dorsal MR image of a 7-year-old mixed breed dog See Chapter 21.
with a spinal meningioma. Observe the circular contrast-
enhancing mass (arrow) at C2/C3 on the right side.
 DECISION MAKING Chapter 12

ACUTE BLINDNESS
229

Peter Nghiem
& Scott Schatzberg

INTRODUCTION RELEVANT NEUROANATOMY

Acute visual loss or blindness is a relatively uncommon, The visual system is a special sensory system used to relay
but important, clinical syndrome of dogs and cats. information to the higher centres of the brain for pro-
Bumping into walls or inanimate static objects and an cessing and interpretation. This system consists of the
inability to recognize moving objects are classic signs of retina, optic nerves, optic chiasm, optic tracts, LGNs,
visual loss that typically are noted by owners of animals optic radiations and visual cortices (occipital cortices).
with bilateral blindness. However, unilateral blindness Visual stimuli initiate impulses by specialized cells
may be more difficult for owners to recognize. Depend- (e.g. photoreceptor cells, bipolar cells) within the retina
ing on the aetiology, visual loss initially may be partial or that are transmitted subsequently to retinal ganglion
complete. Partial visual loss may progress to complete cells. The axons of retinal ganglion cells transmit
blindness over days to weeks. Visual loss may be due to a impulses to the brain via the optic nerves, which course
lesion of the retina, optic nerve, optic chiasm, optic tract, caudally in the orbit surrounded by meninges, extra-
lateral geniculate nucleus (LGN), optic radiations or ocular muscles and periorbita. The optic nerves enter the
visual cortices. Although the entire visual pathways are skull via optic canals of the presphenoid bone and join at
part of the CNS, in this chapter they are divided into: the optic chiasm, ventral to the rostral aspect of the
• Peripheral visual pathways: visual pathways that are hypothalamus and rostral to the pituitary gland. At the
shared with the PLR pathways (i.e. retina, optic optic chiasm, the majority of axons in each optic nerve
nerve, optic chiasm, proximal optic tract). cross (75% in the dog, 60% in the cat) to form the
• Central visual pathways: distal optic tract, LGNs, contralateral optic tract. These axons ultimately influ-
optic radiations, visual cortices. ence the contralateral occipital lobes of the cerebral
hemispheres. The optic tracts course caudodorso-
An animal with acute visual loss requires a complete laterally over the side of the diencephalon to the LGN of
neurological examination to help localize the problem to the thalamus. When the optic tract reaches the level of
either the peripheral or the central visual pathway. An the LGN, two basic pathways continue: a pathway for
accurate neuroanatomical localization allows the clini- conscious visual perception (~80% of optic tract axons)
cian to formulate an appropriate differential diagnosis and a separate pupillary reflex pathway (~20% of optic
list, to select diagnostic tests and, ultimately, to imple- tract axons).
ment targeted therapies for the disorder responsible for
the blindness.
 230 DECISION MAKING

CONSCIOUS PUPILLARY LIGHT

VISION REFLEX

Dorsal view Dorsal view

1 Retina 1 Retina
2 Optic nerve 2 Optic nerve
3 Optic chiasm 3 Optic chiasm
4 Optic tract 4 Optic tract
5 Lateral geniculate 5 Parasympathetic
nucleus branch of CN III
6 Optic radiation 6 Pretectal nucleus
7 Occipital cortex in most rostral
part of midbrain
(rostral colliculus)
7 Parasympathetic
nucleus of CN III

Sagittal view Sagittal view

Optic radiation, contralateral Pretectal nucleus,
Occipital cortex, contralateral contralateral

Lateral geniculate Oculomotor nucleus

nucleus, contralateral
Oculomotor nerve
Thalamus, contralateral
Optic chiasm
Optic tract, contralateral
Optic chiasm

 179 Neuroanatomical pathway for conscious vision.  180 Neuroanatomical pathway for the pupillary light
The visual stimulus enters through the retina (1), travels reflex (PLR). A bright light stimulus enters the retina (1)
through the optic nerve (2) and optic chiasm (3) – where and travels through the optic nerve (2), optic chiasm (3)
the majority of fibres (65–75%) cross over – and continues and optic tract (4). The stimulus is relayed to the pretectal
along the optic tract (4). The stimulus is relayed from nucleus within the rostral colliculus (6). The parasympa-
here to the lateral geniculate nucleus of the thalamus (5), thetic nucleus of cranial nerve III (7) is stimulated and the
then travels through the optic radiations (6), synapsing in signal is transmitted through its parasympathetic branch
the visual cortex (7). A lesion in any part of this pathway (5), resulting in contraction of the iris sphincter muscle
can affect conscious vision. and constriction of the pupil. A lesion in any part of the
pathway can disrupt the PLR.
 ACUTE BLINDNESS 231

For the conscious visual pathway (179), axons from NEUROANATOMICAL LOCALIZATION
neuronal cell bodies of the LGN project caudally as the
optic radiations, which terminate in the cerebral (visual) Clinical evaluation of a suspected blind animal
cortex of the occipital lobe. The occipital cortex is where Since animals with visual deficits may have a lesion any-
integration and interpretation of visual stimuli occur. where along the peripheral or central visual pathway, it is
Two reflex pathways also exist, one for the PLR and imperative that the clinician performs a neurological and
another associated with somatic motor responses to fundoscopic examination. In order to localize blindness
retinal activity. as peripheral or central, the clinician should carefully
• For the PLR, approximately 20% of the optic tract evaluate the following:
axons bypass the LGN and synapse on the pretectal • A fundoscopic examination may disclose changes in
nucleus (PTN) of the midbrain. Some of these retinal reflectivity, vasculature and the optic discs
fibres synapse on the ipsilateral parasympathetic (neuritis or papilloedema). Optic neuritis may result
oculomotor nucleus (CN III), but the majority of in unilateral or bilateral changes to the optic nerve
the PTN axons cross to synapse on the contralateral head (papillitis), including ill-defined edges and dis-
parasympathetic oculomotor nerve nucleus placement of the optic disc. Retinal haemorrhage,
(ipsilateral to stimulated eye). Thus, light entering vascular attenuation, increased tapetal reflectivity
one eye will allow for constriction of both pupils, and exudates also may be visualized. Lesions in the
stronger in the stimulated eye (180). retina or optic disc are consistent with a peripheral
• For somatic responses to retinal activity, some optic visual problem. Fundoscopic examination may also
tract axons synapse on cell bodies located in the reveal papilloedema, which results from oedema
rostral colliculi of the midbrain. Some of these tracking down the optic nerve to the optic disc.
neurons send axons to CNs III, IV and VI and Optic nerve tumours, although uncommon, may be
influence ‘reflex movement’ of the eyes in response appreciated as an enlarged optic disc and may also
to visual input. In addition, other neurons of the be accompanied by retinal haemorrhage or
rostral colliculi send axons down the spinal cord detachment.
(tectospinal tract) that influence the LMNs of the • The palpebral reflex should ideally be evaluated
cervical spinal cord. The tectospinal tracts are before the menace response. The lateral and medial
important in activation of muscles concerned with canthus of each eye should be touched separately
orientation of the head and neck in response to and a blink response with complete closure of the
visual input. palpebral fissures should be expected. An intact
facial nerve is required for the menace response,
palpebral reflexes and dazzle reflex, as it is
responsible for orbicularis oculi muscle contraction
closing the palpebral fissures.
232 DECISION MAKING

• The menace response (181) is performed with a • PLRs are tested by directing a bright light towards
menacing gesture of the hand towards one eye, the lateral retina, which should result in constric-
while the other eye is covered; immediate closure of tion of both pupils. PLR testing evaluates the visual
the eyelid is the normal response. This learned pathway up to the level where optic tract axons
response requires the entire peripheral and central bypass the lateral geniculate nucleus to synapse on
visual pathway in addition to connections from the the PTN (i.e. peripheral visual pathways) and the
cerebrum (through several theoretical pathways parasympathetic nuclei of CN III, bilaterally. No
involving the ipsilateral cerebellum) to the involvement of any component of the cerebrum
ipsilateral brainstem facial neuron. occurs in this reflex (180). However, testing the
PLRs is important to help distinguish if the lesion is
affecting the peripheral or central visual pathways
(182, 183).

Dorsal view
 181 Neuroanatomical pathway for the menace
response. The menacing stimulus is detected by the retina
1
11 (1) and a resulting impulse travels through the optic nerve
(2) and optic chiasm (3) to the contralateral optic tract.
2 The stimulus is relayed to the lateral geniculate nucleus of
the thalamus (4), travels through the optic radiation and
synapses in the occipital cortex (5). The signal then travels
3
6 rostrally in association with interneurons and synapses in
the motor cortex (6) and continues within projection
fibres through the internal capsule, crus cerebri and longi-
10
4 tudinal fibres of the pons and synapses in the pontine
nucleus (7). It then proceeds within transverse fibres of
the pons, through the middle cerebellar peduncle and
5
synapses in the cerebellar cortex (8). The signal travels
through the efferent cerebellar pathway and synapses on
both facial nuclei (9). It is finally relayed through the left
8 and right facial nerves (only one shown in diagram, 10),
7
synapsing on facial muscles (orbicularis oculi) (11) to
cause muscular contraction of the eyelids. A lesion in any
part of the pathway can disrupt this response.
9

Sagittal view
1 Retina
2 Optic nerve
6 5
3 Optic chiasm
4 Lateral geniculate nucleus
8
5 Occipital cortex
4
6 Motor cortex
7 Pontine nucleus
1 8 Cerebellar cortex
2 7 9
3 9 Facial nucleus
11 10 Facial nerve (CN VII)

10 11 Orbicularis oculi
 ACUTE BLINDNESS 233

Retina
Optic nerve
Optic chiasm
Rostral optic tract
Pretectal nucleus
CN III nucleus
Caudal optic tract
Lateral geniculate
nucleus
Optic radiations
Occipital cortex

 182 Peripheral visual pathways (outlined in red).  183 Central visual pathways (outlined in red). These
These include the retinas, optic nerves, optic chiasm and include the caudal aspects of the optic tracts, the lateral
the rostral portions of the optic tracts. geniculate nuclei and the occipital cortices.

• Conscious vision can be tested by having the Systematic approach to the blind animal
patient negotiate an obstacle course, or track objects Step 1. Is the animal unilaterally or bilaterally blind ?
and/or by utilizing the visual placing responses (see This question is primarily answered by evaluating the
Chapter 1 for details of these tests). Conscious menace response in each eye separately. If the menace is
vision requires intact peripheral and central visual absent or delayed, the eyelids must be assessed for their
pathways (see 179, 182, 183). ability to close by eliciting the palpebral reflex. If facial
• The dazzle reflex (squint reflex) is evaluated by paralysis is present, eyeball retraction, elevation of the
directing an extremely bright light source towards third eyelid and head retraction may help in the assess-
the retina. This reflex involves optic tract axons that ment of vision. If facial paralysis is present or if there is
synapse in the midbrain and subsequently project doubt about the result of the menace response testing,
onto the facial nucleus, eliciting eyelid closure. This the patient’s ability to navigate an obstacle course and/or
reflex pathway does not involve the cerebrum. the visual placing response should be evaluated (if the
• Mentation or behaviour, response to nasal animal’s size allows it to be lifted) (184, 185, pages 234
stimulation and postural reactions should be and 235).
evaluated in all patients with visual loss. If
abnormal, these may help localize the lesion to the
central visual pathways. However, normal
mentation, behaviour, nasal sensation and postural
reactions do not exclude a central lesion.
 234 DECISION MAKING

 184 Approach to bilateral blindness using BILATERAL BLINDNESS

pupillary light reflex, electroretinogram
(ERG) examination and ophthalmoscopic
examination to determine lesion localization.
The red lines represent possible locations of
lesions along visual and pupillary light
reflex pathways.

Pupillary light reflex

NORMAL ABSENT

Electroretinogram (ERG) Ophthalmoscopic

examination + ERG

NORMAL ABNORMAL NORMAL ABNORMAL

Sudden acquired retinal Bilateral optic nerve or

Diffuse/multifocal Ocular media
degeneration syndrome optic chiasm
forebrain or retinal disease
(SARDS)
 ACUTE BLINDNESS 235

 185 Approach to a case with unilateral UNILATERAL BLINDNESS

blindness (left eye) using the pupillary light
reflex and ophthalmoscopic examination to
determine lesion localization. The red lines
represent possible locations of lesions along
visual and pupillary light reflex pathways.

Pupillary light reflex

NORMAL ABSENT

Ophthalmoscopic
examination

NORMAL ABNORMAL

Contralateral forebrain Ocular media

Ipsilateral optic nerve
or retinal disease
 236 DECISION MAKING

Step 2. Is the blindness peripheral or central? The pupils should be assessed for symmetry in
Following the menace response, the clinician should ambient light and in a dark room. A bright light source
evaluate the pupil size and PLRs to determine if the should then be directed into each eye individually;
lesion is affecting portions of the peripheral or normal patients have rapid constriction of the pupil into
central visual pathways (see 182–185). With a lesion of which the light is directed (direct PLR) and the opposite
the peripheral visual pathways the PLR is expected to be pupil also should constrict (indirect or consensual PLR).
absent, while it is intact with lesions of the central In addition to optic and oculomotor nerve lesions, there
visual pathways. It should be noted that the PLR are several possible localizations for PLR deficits. If a
requires fewer intact axons than conscious perception of direct PLR is not elicited in one eye, the clinician should
vision and, therefore, partial lesions of the peripheral direct the light as close to that eye as possible and direct it
visual pathways may cause loss of vision while sparing the around all aspects of the ocular fundus. If there is still no
PLR, creating the illusion of a lesion affecting the response present, the clinician should swing the light to
central visual pathways. In general, central blindness may the other eye and the non-responsive pupil should be
be accompanied by other forebrain signs such as assessed for constriction. If the non-responsive pupil is
abnormal behaviour, seizures, sensory (facial/nasal the result of an ocular or optic nerve lesion, it will con-
hypalgesia) deficits and postural reaction deficits. These strict when the light is directed into the contralateral eye
sensory and postural reaction deficits, as for the visual (i.e. positive indirect PLR). Such testing may need to be
deficits, are all contralateral to the side of the forebrain repeated multiple times to differentiate between a
lesion. Therefore, careful attention should be given to retinal/optic and oculomotor nerve problem.
CN function, mentation and postural reaction evaluation
(see Chapter 1). Step 3. Is the lesion focal, multifocal or diffuse
within the visual pathways?
See Table 59.

Table 59 Lesion localization within the conscious visual pathway

UNILATERAL OR INTACT PLR? PERIPHERAL OR LESION DISTRIBUTION

BILATERAL BLINDNESS? CENTRAL BLINDNESS?

Unilateral No Peripheral Focal lesion of the ocular media, retina or

optic nerve

Yes Central Focal lesion in the contralateral distal part

of the optic tract, lateral geniculate
nucleus, optic radiation or visual cortex
(i.e. contralateral forebrain)

Bilateral No Peripheral Multifocal lesion of the ocular media, retina,

optic nerves or focal lesion of the optic chiasm

Yes Central Multifocal or diffuse lesion in the optic tracts,

lateral geniculate nuclei, optic radiations or
visual cortices (i.e. bilateral forebrain)
 ACUTE BLINDNESS 237

DIFFERENTIAL DIAGNOSIS • Electroretinogram (ERG) detects retinal response

to various intensities and frequencies of light. This
Conditions to be considered when evaluating a dog or is the diagnostic of choice in suspected cases of
cat presented with acute blindness are listed in Tables 60 SARDS.
and 61. • Imaging of the optic nerves with CT or MRI for
optic neuritis and optic nerve tumours.
DIAGNOSTIC APPROACH • CSF analysis may disclose a mononuclear
pleocytosis in cases of optic neuritis.
The diagnostic approach taken for the patient with acute • Serology and PCR on serum and/or CSF for
visual loss depends on the neuroanatomical diagnosis regional infectious diseases.
(see 184, 185). If the neuroanatomical diagnosis is
unclear, the patient should be evaluated for both periph- Central blindness
eral and central blindness. • Metabolic profile (CBC, serum biochemistry, bile
acid stimulation test, urinalysis) if neurological
Peripheral blindness examination suggests diffuse forebrain anatomical
• Ophthalmic examination to check for lens luxation, diagnosis.
hyphaema, glaucoma, uveitis, retinal detachment, • Advanced brain imaging (CT or MRI).
chorioretinitis and papilloedema. • CSF analysis.
• Imaging of the lens and retina with ultrasound if • Serology and PCR on serum and/or CSF for
direct visualization is not possible due to turbidity regional infectious diseases.
of the ocular media or cataract.

Table 60 Causes of unilateral acute blindness

DISEASE MECHANISM PERIPHERAL BLINDNESS CENTRAL BLINDNESS

Vascular Brain infarct*

Brain haemorrhage

Inflammatory Retinitis/chorioretinitis Infectious encephalitis (viral, protozoal, fungal,

Retrobulbar abscess/cellulitis bacterial, rickettsial)*
Infectious or non-infectious optic neuritis Meningoencephalitis of unknown aetiology
(GME, necrotizing, idiopathic)*

Traumatic Trauma to the globe and orbit* Head trauma*

Anomalous Hyphaema, anterior uveitis, glaucoma, Intracranial intra-arachnoid cyst

lens luxation, corneal oedema Porencephaly/hydranencephaly

Neoplastic Neoplasia of the optic nerve or neoplasia Primary or secondary brain tumour*
compressing the optic nerve*
Ocular lymphoma
* Common cause
238 DECISION MAKING

Table 61 Causes of bilateral acute blindness

DISEASE MECHANISM PERIPHERAL BLINDNESS CENTRAL BLINDNESS

Vascular Retinal detachment and/or haemorrhage Brain haemorrhage

secondary to arterial hypertension*

Inflammatory/infectious Retinitis/chorioretinitis Infectious encephalitis (viral, protozoal,

Infectious or non-infectious optic neuritis* fungal, bacterial, rickettsial)*
Meningoencephalitis of unknown aetiology
(GME, necrotizing, idiopathic)*

Traumatic Trauma to the globes and orbits Head trauma*

Toxic Enrofloxacin toxicity (cats) Lead poisoning

Ivermectin toxicity (dogs)

Anomalous Hyphaema, anterior uveitis, glaucoma, Intracranial intra-arachnoid cyst

lens luxation Porencephaly/hydranencephaly
Hydrocephalus

Metabolic Hypoxia/ischaemia/excitotoxicity (e.g. post ictal)

Hepatic encephalopathy*
Osmotic abnormalities (Na+ imbalance)
Hypoglycaemia*
Ketoacidosis*

Neoplastic Tumour of the optic chiasm or in the vicinity Primary or secondary brain tumour*
of the optic chiasm (meningioma, pituitary
macroadenoma)

Degenerative Sudden acquired retinal degeneration

syndrome (SARDS)*

* Common cause

COMMON CAUSES OF PERIPHERAL BLINDNESS stages. Some dogs with SARDS have been reported
as having autoantibodies against neuron-specific enolase
See Tables 60 and 61 (NSE), although it is unclear whether these play a
causative role in SARDS or whether they are the result of
Sudden acquired retinal degeneration syndrome retinal destruction by another mechanism.
Overview
SARDS is an acute, progressive retinal disorder resulting Clinical presentation
in bilateral visual deficits to complete vision loss occur- Ocular examination commonly reveals conjunctival
ring over days to weeks; occurs in middle aged to older hyperaemia, bilateral mydriasis and decreased to absent
dogs (≥8 years of age). The aetiology is unknown, but PLRs bilaterally. Note: PLR can initially be normal,
several theories exist. Dachshunds, Miniature Schnau- creating the illusion of a more central lesion. A fundic
zers, Beagles and Brittanys are overrepresented. There is examination may be normal in the early stages; a hyper-
an initial apoptosis of the photoreceptor layer in the reflective fundus and vascular attenuation can be seen in
retina n the acute stages; retinal atrophy is seen in later the later stages.
 ACUTE BLINDNESS 239

Diagnosis Papilloedema
ERG is required to distinguish SARDS from other Overview
lesions responsible for acute blindness. Dogs diagnosed Papilloedema is a process secondary to increased ICP or
with SARDS are commonly presented with concurrent compression of optic nerve fibres causing ‘back up’ of
clinical, physical and historical findings consistent with CSF surrounding optic nerve fibres and secondary
hyperadrenocorticism at the time of vision loss, but any oedema of the optic disc. It can also be seen with condi-
association between the diseases is unknown at this time. tions causing widespread myelin oedema (e.g. some
Routine ACTH stimulation testing to evaluate cortisol metabolic or toxic disorders such as hexachlorophene
and sex hormones, BP screening and urinalysis for poisoning) and orbital space-occupying lesions. Papil-
protein/creatinine ratio are recommended in these loedema needs to be differentiated from hypermyelina-
animals. tion of the optic disc (pseudopapilloedema). Increased
ICP can be due to trauma, a cerebrovascular accident
Management (CVA) (see Chapter 17), meningoencephalitis or, most
There is no treatment. The prognosis is grave for return commonly, an intracranial tumour (meningioma, glioma,
of vision. Cushing’s-like signs usually resolve within pituitary macroadenoma, metastatic brain tumour).
months.
Clinical presentation
A fundic examination reveals loss of visualization of
optic disc margins and changes in the calibre of super-
ficial retinal blood vessels; neurological deficits will
reflect the location of the lesion (186).

Diagnosis
Diagnosis is made by determining the underlying cause:
• Advanced brain imaging for CVAs and
malformations.
• Advanced brain imaging +/- CSF analysis/biopsy
for brain tumours and meningoencephalitis.

Management
Treatment of the underlying cause is essential. For
increased ICP, mannitol (0.5–2.0 g/kg IV) can be given
over 15 minutes and repeated in 30 minutes. Furosemide
(0.5–1.0 mg/kg IV) can be given following mannitol
administration. For increased ICP in a normotensive
animal, 1–2 ml/kg of 7% hypertonic saline can be given
IV over 5–10 minutes and repeated if needed. For
increased ICP in a hypotensive animal, 4 ml/kg 7%
hypertonic saline can be given IV over 5–10 minutes.
Corticosteroids (dexamethasone, 0.05–0.1 mg/kg IV
q24h; prednisone, 0.5–1 mg/kg PO q24h) can be admin-
istered to decrease peri-tumoural oedema if present.
The prognosis is dependent on the aetiology.
 186 Photograph of the fundus of a dog with optic
nerve oedema. Note the blurred edges of the optic disc
(yellow arrows) and changes in the calibre of superficial
vessels (red arrow).
 240 DECISION MAKING

Optic neuritis Management

Overview Treatment is dependent on the underlying cause:
Optic nerves are covered by meninges and may be • GME or MUA. Corticosteroids (2–4 mg/kg PO
affected by similar disease processes that affect the CNS. q24h tapered over 4 months until 0.5 mg/kg
Optic neuritis is an acute, progressive inflammation of q48h depending on neurological signs); may need
the optic nerves. There are several causes of optic neuri- second immunosuppressive agent (e.g. cytosine
tis including ocular GME, meningoencephalitis of un- arabinoside, cyclosporine). (See Chapter 19.)
known aetiology (MUA) and infectious disease (viral, • Antibiotic therapy for 4–6 weeks if there is an
rickettsial, fungal). (See Chapter 19 for further details on infectious aetiology. (See Chapter 19.)
these diseases.)
The prognosis for return of vision is guarded to poor for
Clinical presentation infectious causes; the prognosis is fair for GME, but
Bilateral blindness is often seen. A fundic examination relapses and permanent vision loss may occur.
reveals loss of visualization of optic disc margins, dilata-
tion of retinal veins and elevation of optic disc(s) and/or Retrobulbar abscess
haemorrhage and/or tapetal reflective changes (187). Overview
A retrobulbar abscess is on occasion an acute, progressive
Diagnosis condition causing unilateral visual deficits to complete
Diagnosis is made by advanced brain imaging (CT, blindness. The abscess can be due to a penetrating
MRI), CSF analysis, titres and PCR. Biopsy is rarely foreign body caudal to the last upper molar tooth, usually
performed in an antemortem setting. through the oropharyngeal region.

Clinical presentation
Physical examination reveals fever and exophthalmos
due to a firm, painful mass in the retrobulbar space.
Dysphagia and/or pain when opening the mouth may be
present. Ocular examination reveals unilateral visual
deficits and a diminished ipsilateral PLR and menace
response, conjunctival hyperaemia, decreased retropul-
sion of the globe and third eyelid protrusion.

Diagnosis
Diagnosis is based on leukocytosis with neutrophilia,
advanced imaging (CT, MRI), ultrasound and fine-
needle aspiration with cytology and microbiological
culture.

Management
The abscess should be drained through the oral cavity.
Anti-inflammatories and broad-spectrum antibiotics
(e.g. amoxicillin and clavulanic acid, 15 mg/kg PO q12h
for 4–6 weeks) should be given until bacterial culture and
sensitivity results are available. Soft food should be fed
 187 Photograph of the fundus of a dog with optic for 3–4 days. The prognosis is guarded to good for return
neuritis. Note the poor demarcation associated with the of vision.
oedema and discoloration of the optic disc (arrows) caused
by the inflammation of the optic nerve.
 ACUTE BLINDNESS 241

Optic nerve tumours Diagnosis

Overview Diagnosis is made by advanced imaging (CT, MRI) (188)
Optic nerve tumours can present as acute, progressive, +/- CSF analysis. A definitive diagnosis is made by biopsy
unilateral visual loss. They most commonly occur in and histopathology of the affected optic nerve at the time
geriatric patients (≥9 years old), but can occur in younger of enucleation (189).
patients. Meningioma is the most common tumour
affecting the optic nerve, followed by gliomas; Management
lymphoma and metastatic haemangiosarcoma have been If the tumour is close to the retrobulbar space, enucle-
reported. ation with surgical excision of the affected portion of the
optic nerve can result in a cure. The prognosis is guarded
Clinical presentation to poor if the tumour is not completely excised, as recur-
Clinical signs include unilateral vision loss, which can rence and progression are likely to occur.
progress to bilateral vision loss. Physical examination
findings reveal a retrobulbar mass with exophthalmos
(more commonly with meningiomas), retinal haemor-
rhage (more commonly with gliomas), secondary papil-
loedema, absent PLR and menace response ipsilateral to
the lesion, and retinal detachment (more commonly with
gliomas).

 188 T2-weighted MR image in the dorsal plane of an  189 Gross image of an eye with an optic nerve
optic nerve meningioma (arrow). Note the enlarged optic meningioma (arrow) severed from its attachment to the
nerve as compared with the normal side. optic chiasm.
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 DECISION MAKING Chapter 13

ACUTE TREMORS AND

INVOLUNTARY MOVEMENTS 243

Marc Kent

INTRODUCTION • Tetany is defined as variably intermittent

contractions of the extensor muscles. The most
Involuntary muscle movements refer to a group of well-known syndrome example of tetany occurs
clinical syndromes in which sustained or episodic muscle secondary to hypocalcaemia.
contractions occur involuntarily in the conscious animal. • Myoclonus is the sudden contraction followed
In veterinary medicine the subject of involuntary muscle immediately by relaxation of a specific muscle
movements has received little attention. This may reflect group. One of the most common syndromes
their relatively infrequent occurrence in practice. Com- associated with myoclonus occurs secondary to
pounding this lack of study is a lack of standard, well- infection with canine distemper virus. With
accepted terminology to describe the various syndromes rapid and repeated cycles, repetitive myoclonus
of involuntary muscle movements. Not only does this manifests as a tremor.
make classification arduous, but it also creates difficulty • Myokymia. Simultaneous or sequential
in comparing various clinical manifestations. This spontaneous contractions caused by depolar-
chapter is founded on a proposed classification scheme ization of multiple motor units manifesting as a
derived from appropriate medical definitions. rippling of the muscle.
Involuntary muscle movements may originate from a • Movement disorders are sudden, involuntary
disturbance in either the muscle or the LMN. contractions of specific muscle groups that may
• Disturbance of muscle. When originating from persist over a period of time either at rest or
muscle, altered muscle membrane excitability during activity in an awake, conscious animal.
results in sustained muscle contraction called
myotonia. Myotonia can be congenital or A selection of involuntary muscle movements that may
acquired. For example, congential myotonia has be encountered in small animal emergency practice
been reported in the Miniature Schnauzer. are described in this chapter; these include constant
Acquired myotonia can occur secondary to repetitive myoclonus, idiopathic generalized tremor
hyperadrenocorticism. syndrome, intermittent head bobbing and myokymia, as
• Disturbance of the LMN. When originating as a well as breed-specific movement disorders.
result of spontaneous discharges of the LMN, the
following terms are applied: tetanus, tetany, NEUROANATOMICAL BASIS
myoclonus, myokymia and movement disorder:
• Tetanus is defined as constant contraction of The neuroanatomical basis for most of these involuntary
the extensor muscles and is discussed in detail muscle movements is unknown. In most instances these
in Chapter 25. The most common cause of conditions are rarely life threatening or incapacitating to
tetanus occurs secondary to the toxin produced the affected animal, therefore large-scale studies with
by Clostridium tetani. thorough histological evaluation of the nervous systems
of affected animals have not been performed. Where
investigations have been done, a functional disorder,
probably involving abnormal neurotransmitters or their
receptors, has been speculated.
 244 DECISION MAKING

NEUROLOGICAL EVALUATION DIFFERENTIAL DIAGNOSIS

Many involuntary muscle movement disorders are Creating a differential diagnosis list for many involuntary
episodic in nature. Consequently, at the time of presenta- muscle movement disorders is challenging. Given their
tion neurological evaluation may be normal. Even in episodic nature in many instances, clinicians are often
animals with constant involuntary muscle movements, a faced with providing an assessment, diagnosis, treatment
neurological examination may reveal few deficits. There- plan and prognosis based solely on a description of
fore, a thorough anamnesis is crucial in the evaluation of the event provided by the owner. Moreover, some
affected animals. Paramount to establishing the existence involuntary muscle movement disorders are diagnosed
of an involuntary muscle movement is ensuring that the based on pattern recognition (i.e. diagnosed simply from
affected animal maintains a normal mental state (normal observation and the knowledge of a disorder in a specific
consciousness) during the episode. Descriptions of the breed with a unique characteristic presentation). In a few
involuntary muscle movement should include whether it disorders a more typical orderly differential diagnosis list
was limited to an isolated anatomical area, such as a single and diagnostic plan can be made. In the end, an accurate
limb or the head (focal), or involved the body and all and thorough description, combined with a systematic
the limbs (generalized). Knowing whether the move- classification of involuntary muscle movement disorders,
ment persists during relaxation or sleep is also helpful. is essential in establishing a diagnosis.
Questioning owners about a possible trigger for the Consideration of the differential diagnoses and their
movement can also provide important information. typical characteristics can assist with their investigation
When possible, owners should be asked to provide a and differentiation. Some of these differentials have spe-
video recording of an episode to assist the clinician with cific clinical characteristics rather than diagnostic test
the evaluation of the affected animal. results, and these are outlined below.
When signs are present, affected animals often • Focal seizures. The most important differential
display tremors that vary in amplitude (fine to coarse) and diagnosis for involuntary muscle movement
frequency (slow to rapid). Tremors may wax and wane disorders is simple, focal seizures. Focal seizures are
with excitement and relaxation. Movements may affect recognized in animals with stereotypic, episodic
isolated areas (focal) or involve the body and limbs muscle movements. As such, focal seizures can be
(generalized). Along with tremors, increased extensor easily misconstrued as an involuntary muscle
tone is often present in generalized disorders. In some movement. Given the difficulty in the clinical
disorders, hypertonicity is the predominant or sole man- differentiation from simple focal seizures, along
ifestation. Gait analysis may be difficult to evaluate in with a lack of a defined diagnostic algorithm for
animals with generalized tremors and increased extensor involuntary muscle movement, diagnostic testing
tone. Despite this, weakness and ataxia are largely absent. should be aimed at eliminating structural disease of
However, affected animals can be incapacitated by an the CNS from consideration. Consequently,
inability to move their limbs because of sustained con- performing an MRI scan of the brain, along with
traction of extensor or flexor muscle groups. Postural CSF analysis, is recommended. In some cases,
reactions and spinal and CN reflexes are generally implementing a therapeutic trial of anticonvulsants
normal. As a result of a lack of definitive deficits, defining may be appropriate (see Chapter 7).
a neuroanatomical diagnosis is difficult. • Sleep disorders. Animals may have abnormally
excessive movements during sleep. Such
movements may be limited to the limbs and appear
as if the animal is trying to run. Additionally, more
complex behaviour, such as barking, crying,
growling and biting, sometimes along with the
animal standing up, can occur during REM sleep.
 ACUTE TREMORS AND I N V O L U N TA RY M O V E M E N T S 245

These movements can be differentiated from Head bobbing and idiopathic generalized tremors
involuntary muscle movements, as animals with are most frequently misinterpreted as a cerebellar
excessive movements during sleep have cessation of disorder. With head bobbing, the gait is normal and
the activity when woken. the movement can be interrupted with voluntary
• Intention tremors. Another important differential changes in head and neck posture. In general, ataxia
diagnosis for involuntary muscle movement is minimal or absent with idiopathic generalized
disorders is intention tremors resulting from tremors. Additionally, tremors tend to be fine and
cerebellar disease. Intention tremors due to do not increase in amplitude or rate with voluntary
diffuse/multifocal lesions involving the cerebellum movement.
occur only with voluntary movements and are
absent at rest. They are most evident in the head Differential diagnoses for generalized tremor syndromes
movement observed when the animal is eating or are presented in Table 62.
drinking. They appear as gross, jerky movements of
varying amplitude. Importantly, animals with DIAGNOSTIC APPROACH
cerebellar disease display a cerebellar ataxia
described as a dysmetria (most evident as The diagnostic plan will vary depending on the clinical
hypermetria), a truncal sway and a broad-based presentation of the affected animal. Often, the aim of the
posture when standing. Postural reactions, such as plan is to eliminate from consideration other disease
hopping, may be slightly delayed and display a processes that could mimic similar clinical signs (190,
‘burst-like’ quality as the animal tends to slap the next page).
foot to the ground; signs are not intermittent.
Idiopathic generalized tremors
• CBC, biochemical evaluation and urinalysis to
exclude underlying metabolic (especially fasting
Table 62 Differential diagnoses for
glucose and electrolytes), endocrine or toxicological
generalized tremor syndromes causes of generalized tremors.
• Toxicological screening may be pursued based on
DISEASE MECHANISM EXAMPLES
clinical suspicion and supportive history.
Vascular • MRI of the brain.
• CSF analysis.
Inflammatory/ Infectious and sterile
infectious meningoencephalitis*
Head bobbing
Toxic Pyrethrins*, organophosphate*, • If classical movement is observed in the typically
metaldehyde*, mycotoxin*,
drug induced
affected breed of dog, diagnostic testing is not
performed unless the dog is showing other
Anomalous Congenital hypomyelinogenesis neurological signs.
Metabolic Electrolyte imbalance (calcium, • Similar presentations have been seen due to focal
magnesium)*, hypoglycaemia*, thalamic lesions, suggesting an MRI could be
hypothermia*, hyperthyroidism* useful.
Idiopathic Idiopathic generalized tremors*
Myokymia
Degenerative Lysosomal storage disease, • CBC, biochemical evaluation and urinalysis to
cerebellar abiotrophy, peripheral
exclude underlying metabolic or endocrine
nerve diseases (including benign
postural tremors of older dogs) disorders that could affect peripheral nerves or
muscles.
* Common cause • CK activity.
246 DECISION MAKING

 190 Diagnostic
INVOLUNTARY MUSCLE
approach to involuntary
MOVEMENTS
muscle movements.

Normal consciousness;
Sleeping animal Altered consciousness
awake animal

Consider normal sleep

movements versus REM Consider a seizure
sleep disorder disorder: focal seizure;
generalized (tonic/clonic)
Diagnostics: CBC,
chemistry profile, UA
Toxicology (as indicated)
Brain MRI
CSF evaluation
CONTINUOUS EPISODIC

Abates with rest Persists during rest/sleep Head and neck Generalized

Idiopathic generalized Myokymia Head bobbing Breed-specific paroxysmal

tremors Generalized or focal English Bulldog, movement disorders
Signalment vermiform movements Doberman Pinscher, Boxer, Scottie cramp
Fine, rapid generalized May progress to collapse French Bulldog Hypertonicity in
tremors Occurs during relaxation CKCS/Dalmatian/Border
Typically normal Resolves with change in Terrier/Norwich Terrier/
examination, but may be head and neck posture Bichon Frise/Boxer/Chinook
ataxic /Irish Wolfhound

Diagnostics:
Diagnostics: CBC, chemistry profile, UA Diagnostics:
Diagnostics:
CBC, chemistry profile, UA CK None; based on signalment,
None; based on signalment
CSF evaluation Electrophysiology appearance and exclusion
and appearance
MRI Nerve/muscle biopsy of other diseases
Consider MRI

Treatment: Treatment:
Treatment: Phenytoin Benzodiazepines
Glucocorticoids Carbamazepine Treatment: Acetazolamide
Diazepam Procainamide None Phenobarbital
Propranolol Mexiletine hydrochloride Dantrolene
Prednisone Clonazepam

Prognosis: Prognosis: Prognosis: Prognosis:

Good Guarded to good Good Good to guarded
 ACUTE TREMORS AND I N V O L U N TA RY M O V E M E N T S 247

• Electrophysiology (EMG and motor nerve COMMON CAUSES OF ACUTE TREMORS AND
stimulation studies). INVOLUNTARY MOVEMENTS
• Consider MRI of the brain (if myokymia is limited
to the face) or spinal cord (if myokymia observed in The emergency treatment of a general acute tremor case
the limbs). is outlined in 191 (next page). More specific condition
• Consider muscle and motor nerve fascicular treatments are detailed below and in 190.
biopsies.
Idiopathic generalized tremor syndrome
Movement disorders Overview
• CBC, biochemical evaluation and urinalysis to Idiopathic generalized tremor syndrome is an acquired,
exclude underlying metabolic (including organic action-related repetitive myoclonus in dogs. It is also
acidurias) or endocrine disorders. known as ‘little white shaker disease’. The most common
• Discontinue any drugs associated with movement breeds affected are the West Highland White Terrier,
disorders. Cocker Spaniel and Maltese. The condition typically
• Consider therapeutic trial of oral diazepam, affects dogs between 1 and 5 years of age, weighing
clonazepam, acetazolamide or dantrolene in animals <15 kg and with a white coat, but it can affect any breed
with dystonia. regardless of age, size and coat colour.
• In an attempt to exclude simple focal seizures The syndrome is occasionally associated with
related to structural disease of the brain, vestibulocerebellar signs such as head tilt and abnormal
consideration should be given to the following nystagmus or tremor of the eyeball (opsoclonus).
options:
• MRI of the brain. Clinical presentation
• CSF analysis. There is acute onset of clinical signs – generalized rapid,
• EEG. fine tremors of the head and body – which may be pro-
• Serum and CSF serology, PCR testing or gressive over several days.The condition worsens with
microbiology where indicated. excitement, reduces with relaxation and is absent during
• Consider therapeutic trial of anticonvulsants, sleep. Rarely, cases have an associated absent menace
especially levetiracetam and zonisamide. response, inability to walk, weakness and seizures.
Differential diagnoses include disorders of myelin-
ation, CNS disease (degenerative), toxicity (pyrethrin/
organophosphate, lead, metaldehyde, mycotoxins),
physiological tremors (fear, pain, hypothermia), hypo-
glycaemia, hypocalcaemia and drug-induced dyskinesia
(abnormal movement).

Diagnosis
Diagnosis is based on clinical suspicion after considering
signalment, exclusion of similarly appearing disorders,
MRI of the brain and CSF analysis.

Management
Treatment consists of immunosuppressive therapy with
glucocorticoids (1–2 mg/kg PO q12h, then tapered over
several months). Affected dogs usually respond to
therapy in 2–3 days, but it may take up to 10 days to see
an effect. Dogs not responding to glucocorticoids may
require additional medications:
248 DECISION MAKING

Idiopathic/inflammatory
generalized tremors Suspected intoxication

Mycotoxins Insecticides
Metaldehyde Pyrethrins; carbamates;
Penitrem A; roquefortine
organophosphates (OP)

Diazepam (0.5–1.0 mg/kg IV bolus)

ONCE
DIAGNOSIS Administer antidote
Prednisone (1–2 mg/kg PO q12h) ESTABLISHED (if known)
or
2-PAM for OP toxicity causing
Dexamethasone (0.2 mg/kg IV neuromuscular signs
over 5 min) if unable to take oral
medication Anticholinergics to control
autonomic signs associated with OP

Induce vomiting
Reduce GI absorption
Activated charcoal (1–3 g/kg PO,
repeat up to q4–8h at 1⁄2 initial
dosage)
IF If topical exposure, bathe to
REFRACTORY remove drug

Phenobarbital (20 mg/kg slow IV

over 10 min to effect, followed by
3 mg/kg PO q12h, repeat to effect
Monitoring and
and to limit sedation)
supportive care:
Maintain normal ventilation
and oxygenation
IF
Maintain normothermia REFRACTORY
Maintain normoglycaemia
Maintain normal blood pressure
Provide appropriate fluid
therapy Diazepam CRI (0.5–1.0 mg/kg/hr)
or
Propofol CRI (0.1–0.6 mg/kg/min
to effect)

IF
REFRACTORY

 191 Emergency treatment of generalized Propanolol (0.02–0.06 mg/kg

slow IV over 5–10 minutes);
tremor syndromes. Monitor for bradycardia
can be repeated q8h then
2.5–10 mg/dog q12h
 ACUTE TREMORS AND I N V O L U N TA RY M O V E M E N T S 249

• Diazepam (0.5–1.0 mg/kg PO or IV q8h). Myokymia

• Propranolol (dog: 2.5–10.0 mg/dog PO q8–12h). Overview
Myokymia is an episodic, non-postural repetitive myo-
The prognosis is excellent, with most dogs returning to clonus that can involve any muscle group(s). A specific
normal. Recurrence is possible if the glucocorticoids are phenomenon, myokymia is the clinical observation of
tapered too rapidly. rhythmic, undulating, vermiform (worm-like) or wave-
like movements of the skin overlying contracting muscle
Head bobbing fibres. It affects both dogs and cats and there is an acute
Overview onset and a progressive course.
Head bobbing is a postural, repetitive myoclonus syn- Myokymia is the clinical manifestation of motor
drome involving the head and neck, characterized by axon or motor nerve terminal hyperexcitability (known
acute onset with variable frequency of occurrence. The as neuromyotonia). In humans, myokymia occurs sec-
most common breeds affected are the English Bulldog ondary to Guillain–Barré syndrome, multiple sclerosis,
and Doberman Pinscher. Other breeds include the radiation plexopathy, brainstem tumours, timber rattle
Boxer, French Bulldog and mixed-breed dogs. Head snake envenomation and a variety of autoimmune dis-
bobbing typically affects dogs between 1 and 5 years of eases, in particular one directed against voltage-gated
age. The pathophysiology is unknown, but it appears to potassium channels. Underlying causes have not been
be related to positioning of the head and neck, which identified in animals.
suggests a defect in the stretch reflex of the intrafusal Myokymia may occur in isolated muscle groups
muscle spindle. (focal) or affect body and limbs (generalized) simultan-
eously. The most common focal presentation involves
Clinical presentation facial muscles controlled by CN VII (facial nerve); some-
Episodes can last minutes to hours. Rapid coarse tremors times it also affects the muscles of mastication. When
of the head and neck are directed horizontally or verti- generalized, myokymia is also known as continuous
cally as if shaking the head and neck to say ‘yes’ or ‘no’, muscle fibre activity. One suggestion is that the condition
respectively. Head bobbing often occurs hours after is related to peripheral nerve hyperexcitability syndrome
heavy exercise while the animal is quiet and relaxed. in Jack Russell Terriers, with an underlying ion channel
Mentation and awareness are normal and the dog is able disorder as the cause.
to walk and function normally during an episode.
Clinical presentation
Diagnosis In Jack Russell Terriers signs begin at a mean age of
Diagnosis is based on observation of typical clinical signs 8 months. Movements are continuous and, importantly,
in commonly affected breeds. persist during sleep and general anaesthesia. Animals
with generalized disease may develop hyperthermia,
Management progressive stiffness, limb contractures and collapse.
During episodes, movement can be stopped when the Jack Russell Terriers with this disease frequently present
dog rests its head on a surface, thereby not using the neck with concurrent signs of hereditary ataxia and neuro-
muscles to support the head. Movements can also be myotomia (generalized muscle stiffness).
stopped by getting the dog to alter its head and neck posi- Differential diagnoses include disorders that result
tion by offering a treat or calling the dog’s attention. in muscle fasciculations and tremors, such as those
There is no known treatment. The prognosis is excel- observed in toxicities (pyrethrin/organophosphate, lead,
lent for this syndrome, as discernible structural lesions metaldehyde, mycotoxins), physiological tremors (fear,
are absent and affected dogs are not bothered by the pain, hypothermia), hypoglycaemia, hypocalcaemia and
movement. drug-induced dyskinesia.
250 DECISION MAKING

Diagnosis BREED-SPECIFIC PAROXYSMAL MOVEMENT

Diagnosis is based on the characteristic appearance of the DISORDERS
movement of the overlying skin. A definitive diagnosis is
based on EMG identification of myokymic and neuro- Various terms have been used to describe clinical obser-
myotonic discharges: vations in affected animals:
• Myokymic discharges are short, rhythmic or • Dyskinesia is a general term to describe
semi-rhythmic bursts of doublet, triplet or hyperkinetic movement disorders.
multiplets of motor unit potentials (MUPs) • Dystonia is an involuntary sustained contraction of
occurring at an interburst frequency of 5–62 Hz a group of muscles producing abnormal posture.
and an intraburst frequency of 150–280 Hz. • Chorea is an abrupt, unsustained contraction of
• Neuromyotonic discharges are long bursts of different muscle groups.
MUPs occurring at rates of 150–300 Hz that wax • Athetosis is a prolonged contraction of the trunk
and wane in amplitude. muscles resulting in bending and writhing of the
body.
Affected animals have an elevated serum CK activity. • Ballism is an abrupt contraction of the limb
muscles, which results in flailing movement of
Management the limbs.
Treatment involves drugs that stabilize muscle mem-
brane potentials: Movement disorders encompass a wide range of abnor-
• Phenytoin (dog: 15–30 mg/kg PO q8h; cat: mal movements. In an affected animal, such movements
2–3 mg/kg PO q24h). may not be stereotypic, varying not only in duration and
• Carbamazepine (dog: 4–8 mg/kg PO q8–12h; cat: frequency, but also in affected muscle groups. The most
2–6 mg/kg PO q12–24h). common clinical presentation is dystonia involving the
• Procainamide (dog: 6–8 mg/kg PO q6–8h). hindlimbs, which clinically appears as increased extensor
• Mexiletine hydrochloride (dog: 4–8 mg/kg tone of the limbs. While all four limbs may be affected,
PO q8h). the hindlimbs are often affected to a greater degree than
the forelimbs. Episodes are often triggered by excite-
Animals with focal syndromes may not require treatment ment or exercise.
unless the tremors are affecting the animal’s quality of Functional deficiencies in neurotransmitters or their
life. The prognosis is variable depending on severity of receptors are implicated in the pathogenesis of these dis-
clinical signs and response to therapy. The prognosis for orders. Structural lesions are usually absent. Loss of con-
focal syndromes is good, while generalized syndromes sciousness and awareness is not a feature of these
may not respond to therapy. conditions, which may help to differentiate them from
some epileptic seizure activities.

Breed-associated dystonia and chorea

(primarily of the hindlimbs)
Scottie cramp
Overview
Scottie cramp is a syndrome observed in Scottish
Terriers consisting of involuntary sustained muscle con-
tractions primarily affecting the hindlimbs. Signs begin
within the first 1–3 years of age. The disease has a pre-
sumed autosomal recessive inheritance pattern, with
variable expression of the clinical signs.
 ACUTE TREMORS AND I N V O L U N TA RY M O V E M E N T S 251

A functional deficiency in serotonin modulation of A syndrome involving hypertonicity of the hindlimbs,

motor neuron function has been postulated: similar to that observed in the Scottish Terrier and
• Expression of the disease varies inversely with CNS Cavalier King Charles Spaniel, has also been reported in
serotonin levels (i.e. more severe signs with the Dalmatian, Irish Wolfhound and Norwich Terrier.
decreased CNS serotonin levels and less severe with
increased serotonin levels). Clinical presentation
• Drugs that decrease CNS serotonin result in The clinical signs are very similar to those seen in
increased clinical signs (e.g. methionine). Scottish Terriers. Excitement and exercise are associated
with the development of clinical signs.
Clinical presentation
With excitement, the hindlimbs assume a hypertonic, Diagnosis
extended position or they may occasionally display exag- Diagnosis is based on signalment and characteristic clin-
gerated flexion of the limbs. The forelimbs become ical signs. A genetic test exists for Irish Wolfhounds.
abducted and develop increased extensor tone. Affected
dogs progressively develop a stiff stilted gait over a few Management
minutes. Severely affected dogs assume an arched Treatment reduces the severity and duration of the clini-
posture over their back and may fall into lateral recum- cal signs. Oral acetazolamide (4–8 mg/kg PO q8–12h)
bency with their head and tail flexed. usually results in complete resolution of clinical signs.
Clonazepam (0.5 mg/kg PO q8–12h) can be used as an
Diagnosis add-on to acetazolamide in refractory cases, but its
Diagnosis is based on signalment and characteristic clin- effects may not be lifelong, as functional tolerance tends
ical signs. Signs can be induced with exercise 2 hours to develop.
after administering methysergide (0.3 mg/kg PO), a The prognosis is good, as affected dogs are generally
serotonin antagonist. not incapacitated.

Management Breed-associated movement disorders

Treatment is aimed at muscle relaxation or increasing (with generalized signs)
serotonin levels. Treatment also reduces the severity and Although the specific breeds described below have been
duration of clinical signs (e.g. diazepam, 0.5–1.0 mg/kg reported to be affected with movement disorders, any
PO or IV; acepromazine, 0.075–0.1 mg/kg PO or IM). breed could exhibit a similar abnormality. For instance,
Although not currently documented, serotonin reup- the editors have seen several Labrador Retrievers
take inhibitors may be useful for the treatment of this con- exhibiting clinical signs similar to the Chinooks
dition. The prognosis is generally good; however, severely described below.
affected dogs may be incapacitated without treatment.
Bichon Frise
Hypertonicity in Cavalier King Charles Spaniels Overview
Overview A movement disorder has been observed in young
Hypertonicity in Cavalier King Charles Spaniels is Bichon Frise dogs. Episodes occur randomly and can
also known as episodic falling, deer stalking, collapsing be associated with excitement and activity or occur at
Cavalier and tetany. Affected dogs range in age from 1–4 rest. There are variable severity, duration and frequency.
years old. Candidate gene analysis has recently identified Consistent observations are:
a microdeletion affecting the brevican gene (BCAN), • Unilateral facial dystonia resulting in a grimacing
which encodes the brain-specific extracellular matrix expression.
proteoglycan brevican. This will allow the development • Dystonia of a single limb appearing as sustained
of rapid genotyping tests for this condition. hyperflexion of the affected limb.
252 DECISION MAKING

• Flexion of the thoracic vertebral column causing Border Terrier

the dog to assume a kyphotic posture. Overview
• Chorea-like movement of a limb consisting of rapid A syndrome known as canine epileptoid cramping
flexion and extension of the limb. syndrome (Spike’s disease) has been observed in Border
Terriers. Episodes consist of gait abnormalities ranging
Boxer from ataxia to an inability to stand, contractions of
Overview abdominal and lumbar muscles and contractions of
A movement disorder has been observed in young Boxer the appendicular muscle resulting in extensor rigidity
puppies. Episodes may be induced with excitement or or flexion of the limbs. Increased intestinal motility is
stimuli such as loud noise. Involuntary movements suspected based on hearing borborygmus. Affected
differ between episodes in a single pup as well as between dogs may be in pain during the episode. A genetic basis
pups. There are variable severity, duration and frequen- for the syndrome is suspected. Hypoallergenic dietary
cy. Both male and female pups are affected. A genetic therapy has been proposed by some breeders (http://
basis is suspected. www.borderterrier-cecs.com/index.htm).
Consistent observations are:
• Dystonia of the facial muscles resulting in a Drug-induced movement disorders
grimacing expression. Phenobarbital
• Athetosis of the neck musculature resulting in Overview
torticollis. Dyskinesia has been associated with phenobarbital
• Chorea-like movements of the limbs consisting of administration. Clinical signs consist of whole body
holding an extended limb off the ground, banging it jerking movements, severe enough to cause the affected
on the ground in rapid succession, or sustained dog to fall, and intermittent fine tremors of the facial,
hyperflexion of a limb. neck and shoulder musculature. Agitation and restless-
ness have also been reported. Signs gradually diminish
Chinook and resolve as phenobarbital is tapered and discontinued.
Overview
A disorder referred to as episodic dyskinesia has been Propofol
observed in Chinook dogs. Episodes consist of an inabil- Overview
ity to stand or walk, head tremors and involuntary flexion A variety of abnormal movements can occur on recovery
of one or multiple limbs. Dogs maintain normal con- from propofol administration. Clinical signs consist of
sciousness during the episode. Episodes last from opsoclonus (rapid abnormal eye movements) and myo-
seconds to hours. Affected dogs may also have general- clonus. Clinical signs resolve with discontinuation of
ized seizures, raising the possibility that this syndrome the drug.
represents a seizure disorder rather than a movement dis-
order. An autosomal recessive pattern of inheritance is
suspected.
 DECISION MAKING Chapter 14

HEAD TILT AND NYSTAGMUS

253

Laurent Garosi

INTRODUCTION

Head tilt and nystagmus are frequent clinical manifesta- Medial rectus
tions of a vestibular disorder, although a head tilt alone Lateral rectus
may be observed with otitis externa or other causes of Abducens nerve
aural irritation. The vestibular system is essential in Oculomotor nerve
maintaining balance and preventing the animal falling Oculomotor nucleus
over by keeping and adapting the position of the eyes, Abducens nucleus
head and body with respect to gravity. It is therefore not Cerebellum
surprising that disease of the vestibular system results in
some of the most dramatic and distressing neurological Medial longitudinal
signs. In addition to head tilt and abnormal nystagmus, fasciculus

positional strabismus, falling, rolling, leaning, circling, Flocculonodular lobe

and ataxia commonly result. Clinical signs of vestibular Vestibular nucleus

disease may be a result of lesions involving either the Vestibulocochlear nerve

receptor organs in the inner ear or the vestibular portion Vestibulospinal tract

of CN VIII (i.e. peripheral vestibular disease) or lesions

involving the brainstem vestibular nuclei or vestibular
centres in the cerebellum (i.e. central vestibular disease).
If an animal is presented with a head tilt and nystagmus,
a lesion must be localized to these particular sections of
the vestibular apparatus before an appropriate differen- Inhibit contralateral
extensor muscles
tial diagnosis list can be established and further testing
Facilitate ipsilateral
conducted. extensor muscles;
inhibit ipsilateral
flexor muscles
NEUROANATOMICAL BASIS

The vestibular system is a sensory system. Its main func- Inner ear
tion is to control balance and prevent the animal from Semicircular canals
falling over by maintaining and adapting the position of Vestibular nerve
the eyes, head and body with respect to gravity. The Utricle
vestibular system (192) consists of a receptor organ Saccule
within the petrous temporal bone (inner ear), the Cochlea
vestibular nerve and a balance control centre at the back
of the brain (four brainstem nuclei located in the rostral
medulla oblongata on each side of the fourth ventricle).  192 Schematic anatomy of the vestibular system.
 254 DECISION MAKING

The receptor organ (macular receptors of the saccule and

utricle located within the vestibule and crista ampullaris
of the semi-circular duct located within the semi-circular
canals) detects the position and movement of the head in
space while the animal is standing at rest or when it is
moving. The information on the position of the head is
converted into electrical signals, which are sent via the
vestibular nerve to the brain. The balance control centre
in the brainstem processes this information and sends
messages to the rest of the body to keep the animal
upright (facilitatory effect on the ipsilateral extensor
muscles of the limb via the vestibulospinal tract).
 193 Head tilt in a cat with central vestibular Messages are also sent to the muscles controlling move-
syndrome. ment of the eyes (via medial longitudinal fasciculus and
CNs III, IV and VI) to change the position of the eyes
according to the position of the head. Finally, the brain-
stem vestibular nuclei receive some influence from
higher vestibular centres in the thalamus and from
vestibular centres in the cerebellum (flocculonodular
lobe and fastigial nuclei). The latter have an inhibitory
effect, mainly on the brainstem vestibular nuclei.
Through these pathways, the vestibular system controls
the position of the eyes, trunk and limbs based on the
position and movement of the head.

Head tilt
Head tilt is described as a rotation of the median plane of
the head along the axis of the body resulting in one ear
being held lower than the other one (193). It occurs in
vestibular disease as a result of the loss of anti-gravity
muscle tone on one side of the neck. Head tilt must be
differentiated from a head turn, where the median plane
 194 Head and body turn (pleurothotonus) in a of the head remains perpendicular to the ground, but the
10-year-old Boston Terrier with a right-sided forebrain nose is turned to one side (194). Such head turn is usually
tumour. Compared with a head tilt, the median plane of associated with a body turn (pleurothotonus) and cir-
the head remains perpendicular to the ground, but the cling. A head turn does not indicate a vestibular disorder
nose is turned to one side. and is usually towards the side of a forebrain lesion.
 H E A D T I LT AND N Y S TA G M U S 255

Nystagmus In the absence of any head movement, nystagmus

Nystagmus is an involuntary rhythmic movement of the should never be present in a normal animal. Two types of
eyeballs. Physiological (or vestibular) nystagmus is a nys- pathological nystagmus can be observed with vestibular
tagmus that occurs in normal animals, while pathological disorders:
nystagmus reflects an underlying vestibular disorder • Spontaneous (observed when the head is in a
(195). In both instances the nystagmus has a slow and fast normal position at rest), and/or
phase (i.e. jerk nystagmus). A physiological nystagmus • Positional, which occurs when the head is held in
can be induced in normal individuals by rotation of different positions (e.g. to either side, dorsally or by
the head from side to side (oculovestibular reflex). It is placing the animal upside down on its back).
best performed on a cat by holding the animal at arm’s
length and rotating it from side to side. It may only be Nystagmus is usually classified on the basis of its
seen at the end of the movement. This nystagmus stabi- direction (the fast movement) and may be horizontal,
lizes images on the retina during head movement. It is vertical or rotatory. By convention, the direction of the
always observed in the plane of rotation of the head and nystagmus is described according to the direction of its
consists of a slow phase in the direction opposite to that fast phase. This can be confusing, because the lesion is
of the head rotation, with a fast phase in the same direc- present on the side of the slow phase of the nystagmus
tion as the head rotation. (i.e. a horizontal nystagmus with the fast phase to the
right side is usually indicative of a left-sided lesion of the
vestibular system).
As opposed to jerk nystagmus, in which the
 195 Pathological jerk nystagmus results from a nystagmus has a slow and fast phase, pendular nystagmus
unilateral disturbance in the normal bilaterally tonic is characterized as a continuous oscillation of both globes
influences provided by vestibular neurons to the motor without slow or fast components; less commonly, it may
nuclei of the extraocular muscles (CNs III, IV, VI). be characterized as random eye movements (amaurotic
Spontaneous or positional horizontal or rotatory jerk or ‘searching’ nystagmus). This type of nystagmus is not
nystagmus can be seen with either central or peripheral associated with vestibular disease and may occur second-
vestibular syndrome. Spontaneous or positional vertical ary to congenital abnormalities of the visual pathways in
nystagmus or nystagmus that changes direction indicates Siamese, Birman and Himalayan cats, as well as in
the presence of central vestibular syndrome. Belgian Shepherd Dogs.

Horizontal nystagmus Rotatory nystagmus Vertical nystagmus

Central or peripheral vestibular syndrome Central vestibular syndrome

 256 DECISION MAKING

 196 Positional strabismus in the left eye of a

Rottweiler with a central vestibular syndrome. This
strabismus was only visible by placing the head in
extension, indicating a sensory dysfunction (vestibular
apparatus) rather than a motor one (abnormal innervation
of the extraocular muscles by CNs III, IV and VI).

Other clinical signs of vestibular disease include: Animals with acute vestibular disease may additionally
• Positional strabismus, which can be seen associated display vomiting associated with dysequilibrium.
with vestibular disease when the head is placed in an
abnormal position (extended dorsally or the animal NEUROLOGICAL EVALUATION
placed on its back). Vestibular disease often causes a
ventral or ventrolateral positional strabismus in the The presence of a head tilt and jerk nystagmus is indica-
eye ipsilateral to the vestibular lesion (196). tive of vestibular disease. The primary goal for a clinician
• Ataxia is caused by a lack of vestibular input to examining a patient with head tilt and jerk nystagmus
the ipsilateral limb extensor muscles. This results is to determine whether the patient has evidence of
in swaying of the trunk and head, leaning, falling peripheral or central vestibular disease, as the differential
and rolling to one side with a unilateral lesion. diagnoses, diagnostic and treatment considerations and
The animal may tend to circle towards the affected prognoses differ.
side. These circles are usually small, which will
appear as though the patient is falling in that Is it a peripheral or a central vestibular disease?
direction. The laterally recumbent animal prefers to Both peripheral and central vestibular disease can cause a
lie on the side of the body with the lesion and the head tilt, horizontal or rotatory nystagmus, positional
ipsilateral limb often has decreased extensor tone. strabismus and ataxia. Most lesions causing vestibular
With bilateral vestibular disease, affected animals disease affect a region rather than a specific nerve or
tend to fall to either side and they often show wide nucleus, so accompanying neurological abnormalities
excursions of the head from side to side. can often be used to localize the lesion to the peripheral
• Leaning, falling and a wide-based stance. The or central vestibular system.
vestibular system affects limb tone via the vestibu- Correctly identifying central vestibular disease
lospinal tract, which facilitates the ipsilateral requires identification of clinical signs not attributable
extensor muscles and is a source of inhibition of the to diseases of the peripheral vestibular system. However,
contralateral extensor muscles. With unilateral even if such signs are not present, a central lesion cannot
vestibular disease, the lack of vestibular input can be excluded. Lesions that affect the central vestibular
result in the animal leaning and falling on the system typically have additional clinical signs suggestive
affected side as a result of the ipsilateral limb having of brainstem involvement. Such lesions often involve
decreased extensor tone and the contralateral side the reticular formation as well as ascending and
limbs having increased extensor tone. With bilateral descending motor and sensory pathways to the ipsilater-
vestibular disease, the animal falls to either side and al limbs. Therefore, abnormal mental status (depres-
often adopts a wide-based stance. The latter is also sion, stupor, coma), ipsilateral UMN hemiparesis and
seen with cerebellar disease. GP ataxia, and conscious proprioceptive deficits are
 H E A D T I LT AND N Y S TA G M U S 257

commonly associated with central vestibular disease. Identification of ear disease (197), facial nerve para-
Deficits of CNs V to XII (other than VII and VIII) can lysis and/or Horner’s syndrome (198) is suggestive of
also be associated with central vestibular disease. The peripheral vestibular disease due to the proximity of
presence of spontaneous or positional jerk nystagmus CN VII (facial nerve) and the ocular sympathetic nerve
indicates vestibular dysfunction but does not further supply, with the vestibular nerve in the region of the
localize the lesion to the peripheral or central vestibular petrous temporal bone.
system. However, vertical nystagmus and nystagmus
that changes in direction on changing position of the Pitfalls of lesion localization in vestibular disease
head (i.e. variable nystagmus) are features of central Occasionally, intracranial vestibular lesions can result
vestibular lesions. The rate of nystagmus (number of initially in signs indicative of a peripheral lesion. This is
beats per minute with the head in a neutral position as most commonly seen with extra-axial masses that com-
well as with the animal in dorsal recumbency) can press CN VIII as it exits the brainstem and lesions that
further assist with differentiation between central involve solely the vestibular nuclei. In the absence of
vestibular disease and peripheral vestibular disease. involvement of the UMN and GP systems adjacent to
According to one study, the median rate of resting and the central vestibular nuclei in the caudal brainstem,
positional nystagmus appears to be significantly faster these lesions cause ipsilateral clinical signs similar to all
for dogs with peripheral vestibular disease with a resting the lesions that affect the peripheral components of the
nystagmus ≥66 bpm, providing the highest combined vestibular system. If in doubt about the localization of the
sensitivity and specificity in diagnosing peripheral lesion, the clinician should investigate the animal for
vestibular disease. In this study, the median rates for central vestibular disease as well as peripheral vestibular
resting and positional nystagmus in dorsal recumbency disease. Conversely, animals with acute, severe peripher-
were 0 and 30 bpm for dogs with central vestibular al vestibular disease may be so incapacitated that accurate
disease and 90 and 120 bpm for dogs with peripheral interpretation of neurological examination findings may
vestibular disease, respectively. not be possible.

 197 Left-sided facial nerve paralysis in a Boxer with  198 Horner’s syndrome (miosis, enophthalmos,
otitis media. Because of the close association of the facial protruded third eyelid on the left side of this dog with
and vestibulocochlear nerves, they often are affected middle ear disease) can be seen with peripheral vestibular
simultaneously by the same lesion. disease due to the proximity of the sympathetic nerve
supply to the eye to the vestibular nerve and receptor in
the region of the petrous temporal bone.
 258 DECISION MAKING

With both central and peripheral vestibular disease, DIFFERENTIAL DIAGNOSIS

the head tilt, circling and nystagmus typically occur ipsi-
lateral to the side of the lesion. Less frequently, lesions The differential diagnosis list is entirely dependent on
affecting the caudal cerebellar peduncle, the fastigial the anatomical diagnosis. A lesion must therefore be
nucleus and/or the flocculonodular lobes of the cerebel- localized to a particular section of the vestibular appara-
lum can cause central vestibular disease, resulting in a tus (i.e. peripheral or central vestibular apparatus) before
paradoxical head tilt. The syndrome is described as ‘para- an appropriate differential diagnosis list can be estab-
doxical’ because the head tilt and loss of balance occur lished and further testing conducted. The differential
contralateral to the side of the central lesion. There is diagnosis list can be further developed taking into
also usually some evidence of a cerebellar disorder, such account historical findings. A thorough history should be
as a cerebellar ataxia (e.g. ipsilateral hypermetria) or a obtained to gain information with respect to the onset
truncal sway. In this situation, the lesion occurs ipsilater- and progression of the disease, any history of trauma,
al to the UMN paresis and/or hypermetria. vaccination history, presence of other clinical signs,
Bilateral vestibular disease is characterized by a head history of ear disease and whether potentially ototoxic
sway from side to side, loss of balance on either side drugs or drugs that can affect the function of the central
and symmetrical ataxia with a crouched posture closer vestibular system have been administered.
to the ground surface. A physiological nystagmus cannot Disease mechanisms and conditions commonly seen
usually be elicited and a head tilt is not observed. Bilater- in an emergency evaluation of a dog or a cat with vestibu-
al vestibular disease can occur as a result of a lesion affect- lar disorder are outlined in the Tables 63 and 64.
ing both peripheral vestibular components or, less
commonly, both central vestibular components. As with
unilateral vestibular disease, the presence of signs that
cannot be attributed to diseases of the peripheral vestibu-
lar system (abnormal mental status, postural reaction
deficits, paresis, vertical or variable nystagmus) can be
used to differentiate bilateral central vestibular disease
from bilateral peripheral vestibular disease.
In very rare cases, vestibular disease may be part of a
diffuse polyneuropathy or cranial polyneuropathy. Other
CN dysfunction, such as dysphagia, tongue weakness,
jaw weakness and/or facial paralysis, as well as limb
weakness with depressed segmental spinal reflexes, may
be seen.
Lesions of the thalamus (199), extrapyramidal basal
nuclei and rostral mesencephalon may also cause head tilt
and signs of central vestibular disease, with involvement
of the vestibular thalamic area (ventromedial thalamic
nucleus, thalamic reticular nucleus and ventral lateral
geniculate complex) and its afferent connections with the
brainstem vestibular nuclei (medial longitudinal fascicu-
lus). Head tilt in the absence of other signs of vestibular  199 Dorsal plane T2-weighted MR image of the brain
disease may also be seen with lesions affecting the rostral of a 7-year-old Greyhound with a rostromedial thalamic
aspect of the brainstem or caudal aspect of the thalamus. lacunar infarct (arrow) simultaneously affecting the
Although the mechanism is unclear, such lesions may internal capsule. This region is supplied by the proximal
cause an increase in activity of the major ipsilateral dorsal perforating artery. This dog presented acutely with signs
neck muscles and in contralateral obliquus capitis cau- of ataxia, with leaning and falling to the contralateral side
dalis muscles. of the lesion.
 H E A D T I LT AND N Y S TA G M U S 259

Table 63 Causes of peripheral vestibular disease

DISEASE MECHANISM DOGS CATS

Inflammatory/infectious Otitis media*/interna* Otitis media*/interna*

Nasopharyngeal polyps (rare) Nasopharyngeal polyps*

Trauma Head trauma* Head trauma*

Toxic Aminoglycosides*, topical iodophors or Aminoglycosides*, topical iodophors or

chlorhexidine* chlorhexidine*

Anomalous Congenital vestibular disease

Metabolic Hypothyroidism

Idiopathic Acute idiopathic peripheral Acute idiopathic peripheral

vestibular disease* vestibular disease*

Neoplastic Middle and/or inner ear tumour Middle and/or inner ear tumour

* Common cause

Table 64 Causes of central vestibular disease

DISEASE MECHANISM DOGS CATS

Vascular Brain infarct* Brain infarct

Brain haemorrhage Brain haemorrhage

Inflammatory/infectious Infectious encephalitis (distemper, Toxoplasma, Infectious encephalitis (Toxoplasma, bacterial,

Neospora, fungal, bacterial, rickettsial)* FIP, Cryptococcus)*
Meningoencephalitis of unknown aetiology Meningoencephalitis of unknown aetiology
(GME, necrotizing, idiopathic)* (presumed immune mediated)

Trauma Head trauma* Head trauma

Toxic Metronidazole toxicity* Metronidazole toxicity

Anomalous Intracranial intra-arachnoid cyst Intracranial intra-arachnoid cyst

Dermoid/epidermoid cyst Dermoid/epidermoid cyst
Dandy–Walker syndrome
Chiari-like malformation (rare)
Hydrocephalus

Neoplastic Primary or metastatic brain tumour* Primary or metastatic brain tumour

Nutritional Thiamine deficiency Thiamine deficiency

* Common cause
 260 DECISION MAKING

Specific diagnostic tests Peripheral vestibular disease

The choice of neurodiagnostic tests in patients with • Otoscopic and pharyngeal examination under GA
vestibular disease depends essentially on where the lesion (particularly to check for possible inflammatory
is suspected to be on the basis of the neurological exami- polyps in cats).
nation. If in doubt about the localization of the lesion, the • Swabs for cytology and culture (aerobic, fungal
animal should be evaluated for both peripheral and and yeast) from the middle ear if the tympanic
central vestibular disease (200). membrane is ruptured.

 200 General diagnostic approach VESTIBULAR SIGNS

to vestibular signs. Head tilt, nystagmus, positional
strabismus, ataxia

Signs not attributable to

peripheral vestibular disease?
Abnormal mentation, postural reaction
deficits, paresis, vertical or variable
nystagmus, involvement of CNs other
than CN VII or VIII.
Cerebellar or forebrain signs?

YES NO

Aminoglycosides or topical
Metronidazole administered? chlorhexidine administered?

Evaluate for causes of central Aminoglycosides or topical

NORMAL
vestibular disease chlorhexidine administered?

• Idiopathic Otoscopic examination;

Advanced imaging (CT, MRI); skull radiographs; CT or MRI for
CSF analysis; evaluation of middle/inner ear;
infectious disease titres ± BAER thyroid profile; electrophysiology

• Brain infarct • Idiopathic • Otitis media/interna

• Brain haemorrhage • Ear foreign body
• Inflammatory CNS disease • Polyps
• Head trauma • Middle ear tumour
• Anomalous • Hypothyroidism
• Brain tumour • Inflammatory or infectious
• Thiamine deficiency neuropathy
 H E A D T I LT AND N Y S TA G M U S 261

COMMON CAUSES OF ACUTE PERIPHERAL

VESTIBULAR DISEASE

Acute idiopathic peripheral vestibular syndrome

Overview
This syndrome affects both cats and dogs. It is most
prevalent in geriatric dogs and is rarely observed before
5 years of age. It has been reported in the late summer in
young cats with access to the outdoors in the northeast-
ern US, where it has been hypothesized (with no defini-
tive proof) that this condition is caused by migration of
Cutebra spp. larvae through the nasal cavity and cribri-
form plate of the ethmoid bone to enter the cranial cavity.
 201 Cerebellar infarct is a potential cause of acute There is no known cause in dogs.
central vestibular syndrome. This T2-weighted MR image
of the caudal fossa shows a border zone cerebellar infarct Clinical presentation
(arrow) at the junction between the median and inter- Animals present with acute and non-progressive signs of
mediate rostral cerebellar arteries. peripheral vestibular disease. Affected animals tend to
appear extremely disabled in the first 48–72 hours,
making a neurological examination very difficult. No
• Myringotomy with a 20-gauge spinal needle to other neurological signs are observed.
obtain samples for cytology and culture if the
tympanic membrane is intact, but bulging or of an Diagnosis
abnormal colour. Diagnosis is made by exclusion of other causes of acute
• Imaging of the tympanic bullae with radiographs, peripheral vestibular disease.
CT or MRI to assess for otitis media/interna and
polyps. Management
• Thyroid function testing. Serum T4, free T4 and Affected animals usually improve dramatically in 1–3
endogenous canine serum TSH determinations, weeks from the onset of signs. The nystagmus usually
and if these are suggestive but inconclusive for resolves quickly (within the first few days). Improvements
hypothyroidism, they can be followed by a TSH in posture and walking occur within 7 days, whereas a
stimulation test. head tilt tends to be the last sign to improve and may be
• BAER test to help differentiate central from residual. The recovery probably occurs as a combination
peripheral vestibular disease if needed. of substitution of visual and somatosensory cues for the
• EMG and motor nerve conduction study indicated lost vestibular cues and adaptation of the vestibular system
in patients suspected of cranial polyneuropathy or by modulation of activity in the brainstem and cerebellum.
of a more diffuse polyneuropathy. No treatment has been proven beneficial. Meclizine
(12.5 mg PO q12h in dog; 6.25 mg PO q12h in cats),
Central vestibular disease diazepam (0.1–0.5 mg/kg PO q8h in dogs; 1–2 mg PO
• Advanced brain imaging (CT or MRI) (201). q12h in cats) and/or maropitant (1 mg/kg SC q24h or
• CSF analysis (nucleated cell count, cytology and 2 mg/kg PO q24h in dogs) are sometimes helpful in
total protein concentration). decreasing signs associated with acute vestibular disorder
• Serum and CSF infectious titres (serology and/or (nausea, anorexia, anxiety and, in some instances, the
PCR) for various infectious organisms (Toxoplasma severity of the head tilt and ataxia).
gondii, Neospora caninum, canine distemper, Some animals may be left with episodic ataxia or a
coronavirus, rickettsial, Cryptococcus and persistent head tilt. Recurrence occasionally occurs after
Aspergillus). a variable period of weeks to months.
262 DECISION MAKING

Otitis media/interna
Overview
Otitis media/interna is usually associated with chronic
otitis externa/media, nasopharyngeal infection extending
through the auditory tube or haematogenous dissemin-
ation from a bacteraemia. The condition may arise in the
absence of external ear canal inflammation.

Clinical presentation
Clinical signs can be acute or chronic in onset and
progressive and can be associated with ipsilateral facial
paralysis and/or 3rd order Horner’s syndrome.
 202 CT scan at the level of the temporomandibular
Diagnosis joint displayed in a bone window, showing bilateral
Diagnosis is based on otoscopic examination and marked thickening of both tympanic bulla walls (arrows).
imaging studies (bullae radiographs, CT [202] or The normally air-filled tympanic bullae are partially (right
MRI [203]) and/or exclusion of other causes of peripher- side) and completely (left side) occupied by soft
al vestibular disease. Myringotomy (for culture and sen- tissue/fluid material. These findings are strongly
sitivity) is indicated if fluid is present in the middle ear. suggestive of bilateral chronic otitis media.

a b c

 203 MR images of a 5-year-old Cocker Spaniel with right-sided otitis media/interna with secondary meningo-
encephalitis causing central vestibular signs. (a) On the transverse T2-weighted image, the right bulla contains tissue
(red arrow) that is mostly hyperintense to neural tissue. Fluid within the membranous labyrinth of the normal left inner
ear is visible as a curved structure with a high signal (yellow arrow), while there is a partial lack of the high fluid signal
from the right inner ear. (b) On the transverse T1-weighted image, the normal left bulla is visible as a signal void
because it contains air. The right bulla contains tissue that is isointense to neural tissue (arrow). (c) Following
intravenous administration of gadolinium-DTPA, the tissue filling up the bulla shows marked uptake of contrast in its
periphery (red arrow). There also is marked enhancement of the vestibulocochlear nerve (white arrow) and meninges
overlying the cerebellum (yellow arrow).
 H E A D T I LT AND N Y S TA G M U S 263

Management
Treatment consists of systemic antibiotics for a minimum
of 4–6 weeks. The choice of antibiotic is dictated by
results of culture/sensitivity if available; if not, amoxi-
cillin/clavulanate, cephalosporin or fluoroquinolones
are reasonable choices to consider. Potentiated sulphon-
amides should be avoided if there is associated facial
paralysis due to the development (however limited) of
keratoconjunctivitis sicca.
Surgical drainage and debridement via bulla oste-
otomy may be required if the patient is refractory to
medical treatment.
The prognosis is good for resolution of the infection,  204 Nasopharyngeal polyp removed from the
but neurological deficits such as mild head tilt, facial tympanic bulla via ventral bulla osteotomy in a cat with
paralysis or Horner’s syndrome may persist despite effec- peripheral vestibular syndrome and facial nerve paralysis.
tive therapy because of permanent damage to the neural (Photo courtesy Jonathan Bray)
structures. The presence of persistent nystagmus is sug-
gestive of an active disease process.
Occasionally, an infection can extend into the cranial
vault from the middle and inner ear, causing central
vestibular disease rather than peripheral vestibular
disease.
COMMON CAUSES OF ACUTE CENTRAL
Nasopharyngeal polyps in cats VESTIBULAR DISEASE
Overview
Nasopharyngeal polyps are frequently seen in young Brain infarct
adult cats. They originate from the auditory tube or See Chapter 17.
lining of the bulla. Evidence of otitis externa is often
present. Otitis media/interna can be a complication. The Metronidazole toxicity
polyps can also be associated with facial nerve paralysis Overview
and/or 3rd degree Horner’s syndrome. Metronidazole neurotoxicosis is mostly seen with long-
term administration, usually at high doses (exceeding
Diagnosis 60 mg/kg/day in dogs and cats, although doses as low as
Diagnosis is based on visualization of the polyp in 30 mg/kg/day have been responsible) and occasionally as
the external ear canal or nasopharynx and imaging in soon as 3 days after starting treatment.
refractory otitis media/interna. Histopathology is neces- Anorexia and vomiting are frequent initial clinical
sary to confirm the diagnosis. signs. The condition progresses rapidly to bilateral
central vestibular disease with symmetrical or asymmet-
Management rical signs. Spontaneous recovery occurs within 3–14
Treatment consists of polyp removal with simple days following drug withdrawal. Diazepam (initially
traction or surgery via ventral bulla osteotomy (204). 0.5 mg/kg IV bolus then PO q8h for 3 days) may enhance
Antibiotics are usually not recommended unless an the speed of recovery.
associated bacterial infection is identified based on
results of culture/sensitivity. The prognosis is good, but Meningoencephalitis of unknown aetiology
recurrence is possible. See Chapter 19.
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 DECISION MAKING Chapter 15

ACUTE DISORDERS
OF THE HEAD AND FACE 265

Lara Matiasek
& Alberta de Stefani

INTRODUCTION ANISOCORIA

Acute disorders of the head and face can range in Introduction

severity from benign to life threatening. Their recogni- The pupil is an important indicator of the neurological
tion, based on typically characteristic signs, can help health of the central and peripheral nervous systems. The
define a lesion localization and identify a differential pupil regulates the amount of light that reaches the retina
diagnosis list. via the sympathetic and parasympathetic nerve pathways
The majority of such disorders are due to diseases that innervate the iris. The pupil size is in a constant state
affecting the CNs in either their peripheral or their of flux, a result of a labile, dynamic equilibrium between
central (brainstem) location. Some of the disorders are the sympathetic and parasympathetic innervations.
manifestations of more diffuse NM diseases. Although When presented with an animal with pupils of unequal
the recognition of a CN abnormality may be achieved size (anisocoria) or shape (dyscoria), a primary or second-
rapidly following visual inspection of the patient, the ary anatomical or mechanical pupil abnormality must be
precise location of the disease can only be determined by investigated before consideration is given to a neuro-
a thorough neurological examination. Such localization logical dysfunction. Examples of primary or secondary
is necessary to ensure consideration is given to the most anatomical or mechanical disorders include iris atrophy,
appropriate diagnostic tests. uveitis, glaucoma, subluxated lenses and synechiae.
Some of the conditions affecting the head and face
are described in other chapters. These include vesti- Neuroanatomical basis
bular abnormalities causing head tilt and nystagmus Two systems are implicated in the control of pupil size:
(Chapter 14), ophthalmological abnormalities causing the parasympathetic system and the sympathetic system.
blindness (Chapter 12) and tetanus and botulism causing
trismus and multiple cranial neuropathies, respectively Parasympathetic innervation of the eye and pupil
(Chapter 25). The acute abnormalities affecting the constriction
head and face discussed in this chapter include aniso- The ocular parasympathetic tract is a two-neuron
coria, trismus, dropped jaw, masticatory muscle atrophy, pathway mediated by the parasympathetic component of
facial paralysis, stridor/dysphonia and dysphagia/ the oculomotor nerve (CN III) (see 181), which is
regurgitation. involved in the control of pupillary constriction. The
motor portion of the oculomotor nerve is responsible for
innervation of the levator palpebrae superioris (respon-
sible for elevation of the upper eyelid) and the ipsilateral
dorsal, ventral and medial recti, as well as the ventral
oblique muscle (extraocular muscles responsible for
movement of the eyeball).
Parasympathetic denervation of the pupil (internal
ophthalmoplegia) can occur with or without disturbing
the motor innervation of the oculomotor nerve (external
ophthalmoplegia).
 266 DECISION MAKING

Internal ophthalmoplegia Sympathetic innervation of the eye and

The clinical signs of internal ophthalmoplegia include a pupil dilation
widely dilated pupil that is non-reactive to direct and The ocular sympathetic tract is a three-neuron pathway
indirect light stimulation. The associated anisocoria is (205). The central, or UMN, pathway begins in the
particularly obvious in ambient light, while maximal and hypothalamus and descends in the spinal cord through
equal dilation of both eyes occurs on dark adaptation. the lateral tectotegmentospinal tract to synapse on the
Common causes include pharmacological blockade with LMN at the level of the T1–T3 spinal cord segments.
atropine or atropine-like compounds, middle cranial The LMN is divided into a pre-ganglionic and post-
fossa syndrome (also known as cavernous sinus syn- ganglionic neuron. The pre-ganglionic axons leave the
drome), mesencephalic lesions, ipsilateral cerebellar spinal nerve in the segmental ramus communicans,
lesions and orbital diseases. which joins the thoracic sympathetic trunk inside the
thorax ventrolaterally to the vertebral column. It then
External ophthalmoplegia continues cranially along the cervical sympathetic trunk,
Clinical signs of external ophthalmoplegia include ptosis where it is part of the vagosympathetic trunk within the
of the upper eyelid and lateral strabismus with an inabil- carotid sheath. It then synapses with the bodies of the
ity to move the globe dorsally, ventrally or medially, post-ganglionic cells in the cranial cervical ganglion,
plus/minus signs of internal ophthalmoplegia. Common which lies caudal to the tympanic bulla. Post-ganglionic
causes include middle cranial fossa syndrome, extra- axons enter the middle ear and then the middle cranial
ocular myositis, fibrosing esotropia, trauma and retro- fossa, where they join the ophthalmic branch of the
bulbar lesions. trigeminal nerve running to the orbit. The sympathetic
nervous system innervates and provides tone to the
smooth muscle of the eye and eyelids. This tone keeps
the eyeball protruded, the eyelids opened and third
eyelid retracted, causing the palpebral fissure to widen
and the third eyelid to be pulled ventromedially. The
tone of the iris dilator muscle is also maintained by the
 205 Schematic representation of the neuroanatomy of sympathetic system, which keeps the pupil partially
the sympathetic nerve supply to the eye (Horner’s dilated under normal conditions and dilates it during
pathway). periods of darkness, stress, fear and painful stimuli.

Tectotegmentospinal tract
T1–T3 spinal cord segments
Sympathetic trunk ganglion
Ramus communicans

Ophthalmic branch of
trigeminal nerve
Cranial cervical ganglion
Vagosympathetic trunk
 ACUTE DISORDERS OF THE HEAD AND FA C E 267

Table 65 Pharmacological tests of lesion level in parasympathetic/sympathetic denervation

DRUG AFFECTED EYE NORMAL EYE

Parasympathetic denervation PRE-GANGLIONIC LESION POST-GANGLIONIC LESION

Pilocarpine 0.1% Constriction occurs more Rapid constriction of the pupil 20–30 minutes in dogs/cats
slowly, similar to the normal compared to normal eye due to
eye denervation hypersensitivity

Physostigmine 0.5% Rapid constriction of the pupil No effect on pupil size Constriction in 40–60 minutes
compared to normal eye

Sympathetic denervation FIRST ORDER SECOND ORDER THIRD ORDER

(PRE-GANGLIONIC) (POST-GANGLIONIC)
Phenylephrine 1% Dilation in Dilation in Dilation in less Dilation in about 90 minutes
60–90 minutes 20–45 minutes than 20 minutes in dogs. Minimal effect in cats

Note: A complete absence of pupillary response after administration of pilocarpine 0.1% in the pathological eye (pupil continues to be
mydriatic) probably suggests a non-neurological cause (i.e. iris atrophy).

Sympathetic denervation of the eye results in Neurological evaluation

Horner’s syndrome. Clinical signs include miosis, droop- The clinical approach to anisocoria involves the fol-
ing of the upper eyelid (ptosis), enophthalmia and pro- lowing steps:
trusion of the third eyelid. Damage anywhere along the • Ophthalmological examination to rule- out
sympathetic pathway can cause Horner’s syndrome. non-neurological causes (primary or secondary
This syndrome is most commonly observed with anatomical or mechanical pupil abnormalities).
lesions affecting the post-ganglionic fibres (secondary to • Determining which pupil is abnormal by checking
otitis media, middle ear neoplasia, orbital disease and the PLR and determining if the asymmetry in pupil
idiopathic dysfunction) or pre-ganglionic fibres (brachial size increases in bright light or in darkness.
plexus tumour or injury, cranial mediastinal mass, neck • Determining if the lesion is pre-ganglionic or
injury). Horner’s syndrome is usually described as first post-ganglionic by pharmacological testing
order (central pathways), second order (pre-ganglionic) (Table 65) and looking for other neurological signs
or third order (post-ganglionic) according to the level of (see Table 66, next page).
the lesion along the sympathetic pathway.
Differential diagnosis
The differential diagnosis and disease mechanisms often
encountered in dogs or cats with anisocoria are listed in
Table 66.
268 DECISION MAKING

Table 66 Features of anisocoria in dogs and cats

Lesion localization Pupil abnormality Associated signs Differential diagnoses Diagnostic tests

Sympathetic supply Ipsilateral miosis, Anisocoria most obvious • Middle ear disease • Pharmacological test
to the eye intact PLR bilaterally in darkness; third eyelid • Idiopathic with phenylephrine 1%
(Horner’s syndrome) protrusion; enophthal- • Cervical/rostral thoracic • First order: CT/MRI
mos; ptosis of upper spinal lesions brain and cervical area
eyelid; normal vision • Brachial plexus lesion • Second order: CT/MRI
• Injuries to soft tissues cervical area and
of the neck brachial plexus, chest
• Skull fractures radiographs
• Retrobulbar lesion • Third order: otoscopic
examination, CT/MRI
of bullae

Parasympathetic Severe ipsilateral Anisocoria most obvious • Dysautonomia • Pharmacological test

component of mydriasis, absent in light; narrowing of the • Cerebrovascular with pilocarpine 0.1%
oculomotor nerve direct and indirect palpebral fissure due to accident or physostigmine 0.5%
(CN III) PLR ptosis of upper eyelid; • Inflammatory disease • CT/MRI of brain
normal vision – ventro- • Neoplastic disease
lateral strabismus and
reduced ocular mobility if
motor component of CN
III involved

Unilateral retinal Partial ipsilateral Pupils symmetrically • Inflammatory disease • Fundoscopic

lesion mydriasis, absent dilated in darkness, • Neoplastic disease examination
direct PLR, normal fundoscopic examination • Retrobulbar contusion • ERG
indirect PLR and ipsilateral vision • Congenital abnormalities • Ocular ultrasound
abnormal (optic nerve hypoplasia)
• Degenerative diseases

Unilateral optic nerve Partial ipsilateral Pupils symmetrically • Neoplastic disease • Fundoscopic
lesion mydriasis, absent dilated in darkness, • Inflammatory disease examination
direct PLR, normal ipsilateral vision • ERG
indirect PLR abnormal • CT/MRI of orbit and
brain
• CSF analysis

Optic chiasm Absent PLR in both Absent vision bilaterally, • Neoplastic disease • CT/MRI of brain
eyes also likely forebrain signs • Inflammatory disease • CSF analysis
(e.g. depression, • Cerebrovascular accident
compulsive gait, proprio- (rare)
ceptive deficits)

Unilateral optic tract Contralateral pupil Homonymous hemianopia • Inflammatory disease • CT/MRI of brain
(rostral/proximal to remains more dilated (loss of medial visual field • Neoplastic disease • CSF analysis
the lateral geniculate during swinging in one eye and of the • Cerebrovascular accident
nucleus) flashlight test. Both lateral visual field in the • Trauma
pupils dilate other eye). Vision is
normally in the dark mostly affected in the eye
opposite the lesion. Other
forebrain signs are
probably associated

(Continued)
 ACUTE DISORDERS OF THE HEAD AND FA C E 269

Table 66 Features of anisocoria in dogs and cats (continued)

Lesion localization Pupil abnormality Associated signs Differential diagnoses Diagnostic tests
Unilateral visual Normal PLRs in both Homonymous hemianopia • Cerebrovascular accident • CT/MRI brain
cortex eyes. Normal ability or complete blindness in the • Inflammatory disease • CSF analysis
to dilate pupil in eye opposite the lesion. • Neoplastic disease
darkness Other forebrain signs are
probably associated

Cerebellar lesion Ipsilateral miosis or Menace response deficit • CT/MRI brain

contralateral with normal vision, • CSF analysis
mydriasis intention tremor, hyper-
metric gait, vestibular signs

Common causes of anisocoria Horner’s syndrome is usually classified based on the

Horner’s syndrome level of the lesion along the sympathetic pathway (first,
Overview second and third order). Phenylephrine eye drops 1%
Horner’s syndrome is a condition caused by a decreased can be helpful in testing this level (Table 65). Pharmaco-
sympathetic supply to the eye. It has been described in logical testing should always be performed in both eyes,
dogs and cats. Due to its very long pathway, many disease using the normal eye as a comparison.
processes may affect the sympathetic supply to the eye. Neurological signs present in association with
Among the most common causes of Horner’s syndrome Horner’s can help localize the lesion:
are the idiopathic form, middle ear diseases, trauma to • First-order Horner’s syndrome (rare). Signs
the neck or brachial plexus and mediastinal masses. associated with the intracranial portion: altered
mental status; changes in behaviour; abnormal
Clinical presentation temperature regulation; endocrine disturbances;
Typical clinical signs include a miotic pupil, ptosis of the visual deficits. Signs associated with the cervical
upper eyelid, protrusion of the third eyelid, enophthal- intramedullary portion: ataxia, paresis/plegia
mos and conjunctival hyperaemia (206). (usually mono- or hemi-paresis/plegia); postural
reaction deficits ipsilateral to the Horner’s
syndrome in one limb, in limbs on the same side,
or in all four limbs.
• Second-order Horner’s syndrome. Signs associated
with the intramedullary/brachial plexus portion:
weakness, paresis/plegia affecting one limb (mono-
paresis/plegia), all four limbs (tetra-paresis/plegia),
or only the limbs on the side of the Horner’s
syndrome (hemi-paresis/plegia); postural reaction
deficits (usually) in the forelimb ipsilateral to the
Horner’s syndrome; reduced reflexes in the fore-
limb (usually) ipsilateral to the Horner’s syndrome
or in both forelimbs; depressed or absent ipsilateral
cutaneous trunci reflex. Signs associated with the
cervical portion: laryngeal dysfunction (rare).
 206 Mixed-breed dog with right-sided miosis, third • Third-order Horner’s syndrome. Can commonly
eyelid protrusion and ptosis compatible with Horner’s see facial paralysis and/or peripheral vestibular
syndrome. signs.
270 DECISION MAKING

Diagnosis dogs with co-existing autoimmune MG and dysauto-

Diagnosis of Horner’s syndrome is based on clinical nomia. Evidence of Clostridium botulinum type C toxin
signs. Further investigations are warranted to identify the and antibodies to both the toxin and the surface antigens
underlying cause. The following diagnostic tests can be of C. botulinum were identified in a group of cats affected
performed in dogs or cats: by dysautonomia. This supports the implication of
• First-order Horner’s syndrome. MRI of the brain C. botulinum type C/D in the pathogenesis of dysautono-
and cervical spine to T4; CSF analysis. mia. In dogs the only identified risk factors for develop-
• Second-order Horner’s syndrome. CT or thoracic ing dysautonomia include living in rural areas and
radiographs, MRI of the brachial plexus and spending more than 50% of time outdoors.
CT/MRI/ultrasound of the cervical area.
• Third-order Horner’s syndrome. Clinical presentation
Radiographs/CT/MRI of the tympanic bullae and Clinical abnormalities typically reflect signs of auto-
MRI of the brain. nomic nervous system (sympathetic and parasympa-
thetic) dysfunction. Common clinical signs in cats
Management include vomiting/retching, depression, anorexia, third
Treatment and prognosis for Horner’s syndrome are eyelid protrusion, dilated non-responsive pupils, dry eyes
generally dependent on the underlying cause, though the and nose, constipation (sometimes with faecal impaction)
prognosis is generally excellent for the idiopathic form. and dehydration (207, 208). Urinary and faecal incontin-
ence have been observed. Bradycardia and mega-
Dysautonomia oesophagus are often present.
Overview Common clinical signs in dogs include lethargy,
Dysautonomia is due to autonomic nervous system anorexia, retching, regurgitation/vomiting, hypersaliva-
failure and has been described in both dogs and cats. tion and diarrhoea or, occasionally, constipation. Dry
While in the 1980s this condition was mainly document- mucous membranes, dry eyes and nose are often seen, as
ed in the UK, its distribution is now worldwide. The well as dilated or anisocoric pupils. Other signs include
aetiopathogenesis of this disease is not entirely clear. megaoesophagus, decreased anal tone and distended,
A possible autoimmune basis has been suspected in some atonic urinary bladder and bradycardia.

 207 A young cat with bilateral third eyelid protrusion.  208 A young dog with bilateral mydriasis and
third eyelid protrusion.
 ACUTE DISORDERS OF THE HEAD AND FA C E 271

Diagnosis TRISMUS
Diagnosis in vivo is based on the presence of typical clin-
ical signs. Several pharmacological tests can be per- Introduction
formed to support the clinical diagnosis. The ocular Trismus (also called ‘lockjaw’) describes a limited ability
pharmacological test using pilocarpine 0.1% is very to open the mouth due to spasm of the jaw muscles, as
helpful in confirming a post-ganglionic parasympathetic typically seen with tetanus (see Chapter 25), or, more
lesion. In dysautonomic patients there is rapid develop- rarely, with other CNS diseases. However, ‘mechanical’
ment of miosis (due to denervation hypersensitivity) after abnormalities of the temporomandibular joint (TMJ)
instillation of 1 or 2 drops of pilocarpine 0.1%. (ankylosis due to fracture, luxation, dysplasia, osteo-
In patients exhibiting dysuria, the bethanechol chal- arthritis) or fibrosis of masticatory muscles secondary to
lenge test can be performed; after subcutaneous adminis- chronic masticatory muscle myositis (MMM) may also
tration of a low dose (0.04 mg/kg), dysautonomic lead to trismus. Acute-onset MMM, craniomandibular
patients often show an improved ability to urinate. Other osteopathy, osteomyelitis or tumours affecting the jaw
(less common) pharmacological tests include assessing a bones or in the vicinity of the TMJ can also lead to severe
flare response to intradermally administered histamine pain and a reluctance to open the mouth. Dogs are more
or monitoring the heart rate response to intravenous or frequently affected by diseases causing a ‘lockjaw’ than
subcutaneous atropine injection. In both cases a dimin- cats, with the majority of affected dogs being adult.
ished response is expected in dysautonomic patients.
Decreased urinary catecholamine measurements can Neuroanatomical basis
also support a diagnosis of dysautonomia, as it is indica- The TMJ of the dog and cat is a transversely elongated
tive of denervation hypersensitivity. Documenting condylar synovial joint. The insertion line of the mas-
orthostatic hypotension can highlight failure of the sym- seter muscle reaches the ventral and rostral aspects of the
pathetic heart innervation and has been used in dogs to joint capsule. Medially, the lateral pterygoid muscle,
diagnose autonomic failure. which inserts in the region of the TMJ, supports trans-
The diagnosis can be confirmed by histopathology. verse joint movements and strengthens the joint capsule.
The lesions primarily involve the neuronal cell bodies of The masseter, pterygoid, temporal and digastricus
the autonomic ganglia of both the sympathetic and muscles are all innervated by the mandibular branch of
parasympathetic systems. These lesions are character- the trigeminal nerve (209).
ized by chromatolytic changes in the autonomic neurons,
neuronal degeneration and loss, neuronophagia and,
occasionally, mild mononuclear perivascular cuffing.

Management Temporalis
Therapy for dysautonomia is only supportive. Correc-
tion of hypovolaemia and/or electrolyte abnormalities is
recommended. Metoclopramide (0.2–0.5 mg/kg IM, SC
or PO q6–8h) enhances gastrointestinal motility and
bethanechol (2.5–25 mg/dog orally q8h and 1.25–5.0
mg/cat or 0.1–0.2 mg/kg PO q8h) can be used to help
evacuate the bladder. Gastrostomy tubes need to be con-
sidered for long-term nutrition in patients with mega-
oesophagus. The administration of ocular pilocarpine
can improve lacrimal and oral secretion. The prognosis Masseter
in both dogs and cats is guarded to poor. Digastricus

 209 The main muscles of mastication.

272 DECISION MAKING

Masticatory muscles contain a unique muscle fibre Specific diagnostic tests for trismus
(type 2M) that differs both histochemically and bio- If trismus is the only presenting sign:
chemically from the fibre types present in limb muscles • Type 2M antibody titres in dogs to investigate
(types 1A and 2A). for MMM.
The presence of ‘lockjaw’ can be due to ‘genuine’ • CK serum measurement to investigate for a
trismus caused by spasm of the jaw muscles or can arise myopathy.
from disease affecting the muscles of mastication or the • EMG to exclude a generalized myopathy.
TMJ itself. Spasms of the jaw muscles reflect a UMN • Muscle biopsy in case of an abnormal EMG.
defect, where UMNs or interneurons lose their inhibi- • Radiographs to assess the TMJ, mandible and
tory effect on the LMN, which results in increased bullae.
muscle tone. • Otoscopic examination to assess for middle ear
With diseases affecting the TMJ or mandible, ‘lock- disease causing referred pain and reluctance to open
jaw’ is either due to a mechanical restriction or is pain the jaw.
associated. Moreover, any painful conditions of the skull • Advanced diagnostic imaging of the head (CT or
that cause referred jaw pain can make animals reluctant MRI) ± CSF tap to exclude other causes of trismus
to open their mouth. and aid in selection of sites for muscle biopsy.

Neurological evaluation If additional neurological deficits are present and there is

A complete physical and neurological examination is suspicion of structural brain disease:
important to distinguish neurological from non- • Advanced brain imaging (CT or MRI).
neurological causes of trismus (210). Patients should • CSF analysis (nucleated cell count and cytology, TP
be closely examined for evidence of trauma that could concentration); infectious disease titres and PCR as
have resulted in TMJ luxation/subluxation. Thorough appropriate (see Chapter 19).
oral and ophthalmic examinations should be performed.
Retrobulbar masses often cause visible swelling or If additional signs of a generalized myopathy are present:
drainage behind the carnassial teeth. Animals with • CK serum measurement.
trismus caused by tetanus often show a characteristic • EMG.
facial expression (‘risus sardonicus’) resulting from an • Infectious titres.
increase in facial muscle tone. With disease affecting • Muscle biopsy of the masticatory muscles as well as
the TMJ or mandible itself, the neurological examina- limb muscles.
tion will not reveal any deficits, even though masticatory
muscles can become severely atrophied over several If myotonic signs are present (e.g. additional muscle
weeks (disuse atrophy). On an acute basis, there will be stiffness without cramping, muscle dimpling, percussion
no evidence of muscle atrophy. Limb muscle mass, myotonia after being struck with a reflex hammer):
tone and segmental spinal reflexes should be evaluated • EMG – myotonia is characterized by trains of
to investigate the possibility of a more generalized repetitive discharges, which wax and wane in
myopathy. frequency, producing an audible ‘dive-bomber’ or
motorcycle sound. These myotonic discharges are
Differential diagnosis independent of neural control and persist even
The list of differential diagnoses for trismus is depend- under GA.
ent on the overall clinical and neurological evaluation, as • Genetic tests for myotonia congenita in certain
well as on signalment, history and course of the disease. breeds (Miniature Schnauzer, Australian
The differentials for dogs and cats with trismus are listed Cattle Dog).
in Table 67, p. 274. • Exclude hyperadrenocorticism and intoxications
(e.g. cholesterol-lowering agents, drugs that block
chloride channels) as an underlying cause.
 ACUTE DISORDERS OF THE HEAD AND FA C E 273

TRISMUS

Presence of additional
neurological signs?

NO
YES (but jaw pain Serum 2M
possible) antibody titre (dog)

Risus sardonicus
Rigidity of limbs +/– Altered mentation,
epaxial muscles seizures,
and tail Stiff gait, postural reaction
NEGATIVE POSITIVE
percussion myotonia deficits, cranial
No jaw pain
nerve deficits
Possible history of
No jaw pain
previous injury

Electromyography MRI or CT brain Masticatory muscle

Electromyography
Muscle biopsy CSF analysis myositis

NORMAL ABNORMAL

Skull radiographs Muscle biopsy

MRI or CT of head Infectious titres

• Tetanus
• Brain tumour • Craniomandibular • Generalized
(Differential diagnosis: • Myotonia (rare) osteopathy (dog)
• Meningo- inflammatory
strychnine (Other myopathies) myopathy
encephalitis • Inflammatory,
intoxication)
neoplastic or
traumatic processes
of the TMJ, mandible,
middle ear or
retrobular area
• TMJ dysplasia or
osteoarthritis
• Extraocular myositis
(dog)

 210 Diagnostic approach to a patient with trismus.

274 DECISION MAKING

Common causes of trismus Clinical presentation

Masticatory muscle myositis Two types of clinical presentation are seen: the acute
Overview painful form and the chronic atrophic form. The acute
MMM is an autoimmune inflammatory myopathy of the form presents with bilateral masticatory muscle swelling,
masticatory muscles in dogs. Circulating autoantibodies occasional ocular signs (exophthalmos, conjunctivitis),
against masticatory muscle type 2M fibres (fibre type- pyrexia, mandibular lymphadenopathy and an inability
specific autoantibodies) can be detected in more than to open the mouth, primarily due to pain. The signs may
80% of dogs with MMM and are the basis of serological initially be unilateral without concurrent trismus.
testing for this condition. MMM can be seen in any The chronic form is a progression of the acute form
breed of dog, with no apparent gender predilection. The and results in marked bilateral masticatory muscle
average age of onset is 3 years. The condition has been atrophy (211). Fibrosis of the muscles can lead to an
reported in dogs as young as 3 months of age (Cavalier inability to open the mouth. Forceful opening of the jaw
King Charles Spaniels). must be avoided, even under sedation or GA.

Table 67 Causes of trismus

DISEASE MECHANISM DOGS CATS

Inflammatory/infectious Masticatory muscle myositis* Inflammatory processes of the TMJ,

Inflammatory processes of the TMJ, middle ear or retrobulbar area
middle ear or retrobulbar area Meningoencephalitis (rare)
Meningoencephalitis (rare) Generalized inflammatory myopathies:
Generalized inflammatory myopathies: immune-mediated polymyositis, infectious
immune-mediated polymyositis, infectious aetiology (Toxoplasma), para-neoplastic
aetiology (Toxoplasma, Neospora, Borrelia, syndrome
rickettsial, hepatozoon), para-neoplastic
syndrome, breed associated (Newfoundland,
Boxer and Hungarian Vizsla)
Extraocular myositis (rare)

Trauma Ankylosis due to fracture or luxation Ankylosis due to fracture or luxation

of the TMJ of the TMJ
Foreign bodies Foreign bodies

Toxic Tetanus* Tetanus*

Strychnine Strychnine

Anomalous TMJ dysplasia Myotonia congenita (rare)

Myotonia congenita (rare)

Idiopathic Craniomandibular osteopathy*

Neoplastic Tumours of the mandible or TMJ Tumours of the mandible or TMJ

Paraneoplastic polymyositis Brain tumours (rare)
Brain tumours (rare)

Degenerative TMJ osteoarthritis TMJ osteoarthritis

Muscular dystrophy (rare) Muscular dystrophy (rare)

* Common cause
 ACUTE DISORDERS OF THE HEAD AND FA C E 275

a b

Diagnosis  211 (a) A young Cavalier King Charles Spaniel with

Diagnosis is based on the presence of serum antibodies bilateral masticatory muscle atrophy due to masticatory
against masticatory muscle type 2M fibres. This serum myositis. (b) Muscle mass loss associated with masticatory
antibody titre is 100% specific, with a sensitivity of myositis can be profound, revealing underlying bony
85–90%. Previous corticosteroid medication can result conformation.
in false-negative results. Some cases of end-stage MMM
may also be associated with negative serum results. CK
may be elevated in acute stages of the disease. Masticatory muscle biopsies of dogs with MMM are
EMG can help to confirm the selective involvement characterized by intense multifocal lymphocytic and
of masticatory muscles and differentiate MMM from plasmacytic perivascular infiltration, occasional eosino-
polymyositis. However, EMG may be normal in dogs phils, and necrosis and phagocytosis of type 2M
with end-stage disease because of severe fibrosis and myofibres.
myofibre depletion. Evaluation of muscle biopsy taken MRI and CT are mainly helpful for excluding other
from the masticatory muscles can also provide diagnostic causes of trismus, but may be an aid in the selection of
confirmation of the disease, as well as provide prognostic sites for muscle biopsy (212). MRI is not routinely
information by determining the stage of the disease. performed to diagnose MMM.

 212 Transverse T1-weighted FLAIR MR image post

contrast of the head of a 4-year-old Boxer with
masticatory myositis. Note the bilateral hyperintensity
within the temporalis muscles secondary to contrast
enhancement (arrows). Identification of these areas
enabled a more targeted muscle biopsy to be performed,
which confirmed the pathology.
276 DECISION MAKING

Management Tetanus
Therapy for acute cases consists of immunosuppression Tetanus should be considered when evaluating any
with prednisolone (starting at 1–2 mg/kg PO q12h until animal with acute onset of head and face abnormalities,
serum CK and jaw function return to normal, gradually especially when trismus is present. Further details can be
tapering off to the lowest alternate-day dose), which found in Chapter 25.
should be maintained for 4–6 months. Serum antibody
titres can be used as a treatment guide. Other immuno- Craniomandibular osteopathy
suppressive agents, such as azathioprine (1–2 mg/kg Overview
PO q24h), are indicated in dogs that fail to respond to Craniomandibular osteopathy (CMOP) is a non-
corticosteroids or that relapse when the dose is tapered. neoplastic, developmental bone disease affecting the
In chronic cases, prednisolone should be adminis- mandible, tympanic bullae and temporal region of
tered at an anti-inflammatory dose for 1 month and young, growing dogs (4–8 months of age). Lesions are
physical therapy is recommended. The latter can be mostly bilateral and consist of irregular enlargement of
performed by encouraging the dog to play with tennis the affected bones due to cyclical resorption of normal
balls or chew rawhide; adequate nutrition is essential at bone and replacement by immature bone. CMOP is
all times. inherited in West Highland White Terriers and
The prognosis is good if MMM is identified and common in other terrier breeds, but various breeds can
treated aggressively during the early phase, but persistent be affected. Canine distemper virus and E.coli have also
muscle atrophy is a common manifestation. (Note: been indicated as possible causes.
Aggressive corticosteroid therapy alone can result in
masticatory muscle atrophy, therefore atrophy does not Clinical presentation
necessarily indicate a progression of the disease.) Typical clinical signs include firm swelling of the jaw,
difficulty eating, pain on opening the mouth, sometimes
an inability to open the mouth, cyclic fever, atrophy of
masticatory muscles and lymphadenopathy.

Diagnosis
Diagnosis is usually made via radiographs, which reveal
irregular bone thickening (213). Rarely, a biopsy is neces-
sary for confirmation.

Management
Pain relief and anti-inflammatory medication (pred-
nisolone) can make the dog more comfortable. Appro-
priate nutrition needs to be assured. The abnormal bone
growth usually ceases by 1 year of age, and lesions may
then regress (partially or completely). If the TMJ is
severely affected, a permanent inability to move the jaw
may result. Surgery may partially correct the problem.

 213 Lateral skull radiograph of a 5-month-old West

Highland White Terrier that presented with pain on
opening the jaw due to craniomandibular osteopathy.
Note the osseous proliferation present in the region of
the bullae (arrow).
 ACUTE DISORDERS OF THE HEAD AND FA C E 277

DROPPED JAW nose. The ophthalmic branch innervates the medial

aspect of the eyelids, the cornea, the nasal mucosa and the
Introduction skin of the nose. The maxillary and ophthalmic branches
‘Dropped jaw’ is a manifestation of dysfunction (usually also contain post-ganglionic parasympathetic fibres that
bilateral) of the motor component of the trigeminal innervate the lacrimal gland. The sympathetic fibres that
nerve (LMN disorder). The descriptive terminology for supply the pupil also follow the course of the ophthalmic
this condition derives from the characteristic clinical branch.
presentation (i.e. an inability to close the mouth
[mandibular paralysis]). Typically, dogs or cats presenting Neurological evaluation
with dropped jaw also show hypersalivation, with diffi- The first step in the evaluation of a patient presenting
culty eating and drinking. Additionally, anorexia, weight with dropped jaw is to decide if the cause is neurological
loss, lethargy, oral ulceration and masticatory muscle (bilateral trigeminal nerve LMN) or non-neurological
atrophy have been observed. While the cause of the (mechanical) (214, next page).
‘dropped jaw’ is usually attributed to a motor dysfunction
of the trigeminal nerve, some dogs may also present with Non-neurological causes of dropped jaw
altered facial sensation (sensory component of the • The jaw cannot be closed due to mechanical
trigeminal nerve), deficits of other CNs (such as the problems or pain (e.g. TMJ luxation, mandibular
facial nerve) and Horner’s syndrome. It is important to fracture, presence of oral foreign bodies).
remember that an inability to close the mouth can also • Anamnesis (history of trauma), physical
be due to non-neurological causes. The possibility of examination (presence of pain on manipulation
mechanical obstruction due to bilateral luxation of the of the jaw), oral cavity inspection and, ultimately,
TMJ, fracture of the mandible or oral foreign bodies has radiographs of the skull should help in the investi-
to be considered in each patient. gation of non-neurological causes of dropped jaw.

Neuroanatomical basis Neurological causes of dropped jaw

The trigeminal nerve (CN V) is the largest CN and has • Central/brainstem lesion: usually associated with
both sensory and motor functions. The mandibular depressed mentation, ataxic/paretic gait and deficits
branch contains both motor and sensory fibres. The affecting other CNs (e.g. rabies). This is a rare
motor fibres innervate the masseter, temporalis and localization.
pterygoid muscles, which are muscles of mastication, as • Cranial neuropathy: the trigeminal nerve may be
well as the mylohyoid muscle, the rostral belly of the the only CN affected or other CNs may also have
digastricus muscle, the tensor tympani and the tensor veli abnormal function. Generally, mentation and
palatine muscles. The sensory fibres innervate the buccal reflexes in all four limbs remain normal.
cavity, tongue, teeth of the lower jaw, skin of the • Generalized polyneuropathy: trigeminal nerve
mandible, caudal buccal region and craniolateral pinna. deficits are accompanied by generalized weakness
The maxillary and ophthalmic branches contain only affecting all four limbs and probably by deficits
sensory fibres. The maxillary branch innervates the in other CNs. Mentation should also remain
lower eyelid, nasal mucosa, upper teeth, upper lip and normal.
278 DECISION MAKING

DROPPED JAW
(Caution: rabies in endemic
regions)

History of trauma
or oral foreign body

YES NO

Careful examination of the

NORMAL Neurological examination
mandible and oral cavity

ABNORMAL

Only motor ± Trigeminal nerve + other

sensory trigeminal nerve cranial/spinal nerves

Brain MRI; CSF; electrophysiology; Chest radiographs;

Oral examination under GA; electrophysiology; CSF; brain MRI;
direct fluorescent antibody test on
skull radiographs; MRI or CT of direct fluorescent antibody test on
suitable brain tissue (postmortem)
head for foreign body identification skin biopsy or suitable brain tissue
for rabies diagnosis
(postmortem) for rabies diagnosis

• Bilateral luxation of the TMJ • Idiopathic trigeminal • Idiopathic cranial

neuropathy polyneuropathy
• Fracture of the mandible
• Lymphoma • Idiopathic generalized
• Neurapraxia polyneuropathy
• Trauma
• Oral foreign body • Lymphoma
• Rabies
• Myelomonocytic tumours
• Idiopathic hypertrophic
pachymeningitis
• Infectious diseases (Neospora,
botulism, rabies)

 214 Diagnostic approach to a patient with dropped jaw.

 ACUTE DISORDERS OF THE HEAD AND FA C E 279

Table 68 Differential diagnosis of dropped jaw

DISEASE MECHANISM DOGS CATS

Inflammatory/infectious Idiopathic hypertrophic pachymeningitis* Rabies

Rabies
Polyradiculoneuritis
Neospora

Trauma Prehending large, heavy objects Rare

(historically reported)

Toxic Botulism Rare

Idiopathic Idiopathic trigeminal neuropathy* Idiopathic trigeminal neuropathy

Idiopathic cranial polyneuropathy
Idiopathic polyneuropathy

Neoplastic Multicentric lymphoma* Multicentric lymphoma*

Myelomonocytic tumours Myelomonocytic tumours
* Common cause

Differential diagnoses Common causes of dropped jaw

Disease mechanisms and conditions responsible for Idiopathic trigeminal neuropathy/neuritis
acute dropped jaw are listed in Table 68. Overview
Idiopathic trigeminal neuropathy/neuritis (ITN) is the
Specific diagnostic tests for dropped jaw most common benign, neurological cause of sudden
• Thoracic radiographs to evaluate for inability to close the mouth. It is common in dogs, espe-
megaoesophagus in patients with suspected cially Golden Retrievers, and rare in cats. The aetiology
polyneuropathy. remains unknown. A non-suppurative inflammatory
• Sedated examination of larynx to assess for neuritis in the motor branches of the trigeminal nerve
laryngeal paresis in patients with suspected and its ganglion has been confirmed in some cases;
polyneuropathy. however, it is unknown whether this inflammatory
• EMG and motor nerve conduction study are process occurs in all cases.
indicated in patients suspected of multiple CN
involvement or of a more diffuse polyneuropathy.
• CSF analysis to investigate the possibility of an
inflammatory or neoplastic process (lymphoma).
• CT or MRI of the brain to assess for specific CN
enlargement and/or contrast enhancement, as well
as meningeal thickening and/or contrast
enhancement (215).

 215 Transverse T1-weighted contrast enhanced MR

image depicting bilateral enlargement and hyperintensity
of CN V due to lymphoma (arrows).
280 DECISION MAKING

Diagnosis
ITN is a diagnosis of exclusion and cannot be confirmed
antemortem. The only tests that are abnormal in most
dogs are EMG and CSF analysis. EMG often reveals
positive sharp waves and/or fibrillation potentials in the
masticatory muscles unless the dog is tested too soon
after the onset of mandibular paralysis (up to 7 days after
the onset). CSF analysis is often normal or it can reveal a
mild mononuclear pleocytosis, frequently with a normal
or mildly elevated protein content.

Management
Treatment is mainly supportive, assisting the animal to
eat and drink. Corticosteroid administration appears not
to affect the clinical course of the disease. The use of tape
muzzles has been recommended to improve ingestion of
food, as these dogs are unable to grab food, but can
 216 A Greyhound with an obvious dropped jaw, swallow normally. Aspiration pneumonia and dehydra-
which was acute in onset. tion are concerns associated with ineffective supportive
care. An oesophagostomy tube can be placed to support
nutrition in severely affected animals.
Application of artificial tears or eye lubricants several
times daily may be necessary in dogs or cats with evi-
dence of dry eyes to prevent severe corneal injuries and
conjunctivitis.
The mean time for recovery ranges from 2–10 weeks.
Dogs with a more protracted recovery frequently show
marked atrophy of the masticatory muscles caused by
prolonged denervation. Dogs with dropped jaw should
be encouraged to chew (on natural/synthetic chews).
Owners can also be instructed to perform a gentle,
passive range of movements of their pet’s jaw as part of a
physiotherapy plan. The main aim of the physiotherapy
is to limit masticatory muscle atrophy and consequent
 217 A Labrador Retriever with left-sided Horner’s muscle fibrosis.
and dropped jaw, both of which were sudden in onset.
Idiopathic hypertrophic chronic pachymeningitis
Overview
This condition is a recently recognized cause of multiple
Clinical presentation CN deficits. ‘Dropped jaw’ is the most common com-
Onset of dropped jaw is usually acute (216). Horner’s plaint associated with this condition; however, most dogs
syndrome (217), some degree of sensory loss in the also have other CN deficits. Greyhounds and crossbred-
sensory distribution of the trigeminal nerve and facial sight hounds seem to be predisposed. The condition is
nerve paralysis can occasionally be associated with the characterized by diffuse thickening of the dura mater
dropped jaw. The affected animal struggles to prehend caused by a fibrosing inflammatory process of the pachy-
food and water, but retains the ability to swallow. meninges. The aetiology is unknown.
 ACUTE DISORDERS OF THE HEAD AND FA C E 281

Diagnosis result in decreased tear secretion and neuro-

CSF analysis reveals inflammatory changes in most tropic keratitis secondary to the loss of the
cases, but can be normal. MRI is key to the diagnosis of afferent portion of the lacrimal reflex. Other
this disorder, with thickening, diffuse or localized hyper- neurological signs (e.g. hemiparesis, facial nerve
intensity on T2-weighted and T2-weighted FLAIR paralysis, circling, mydriasis) may be seen as the
images and marked contrast enhancement of the pachy- result of expansion of a mass lesion within the
meninges. cranial cavity and subsequent damage to adjacent
brainstem structures.
Management • Underlying causes for this unilateral CN V
Treatment consists of administering immunosuppres- dysfunction commonly include trigeminal nerve
sive doses of corticosteroids (prednisolone, 1–2 mg/kg sheath tumours and neuritis. In comparison to
PO q12h until remission, followed by tapering dosages). nerve sheath tumours, inflammatory diseases
The addition of other immunosuppressants, such as restricted to individual cranial nerves are
cytosine arabinoside, seems to help achieve a better uncommon in dogs. Possible causes of cranial
control of the disease. Although most dogs achieve clini- neuritis include autoimmune and infectious
cal remission, a cure is more difficult to obtain. processes.
• MRI allows an earlier diagnosis of these
MASTICATORY MUSCLE ATROPHY trigeminal nerve lesions, but it must be
remembered that this specific CN will
Introduction normally enhance following paramagnetic
Masticatory muscle atrophy can occur unilaterally or contrast administration due to its associated
bilaterally. It can result from impaired innervation due to vascularity (218).
lesions of the motor branch of the trigeminal nerve,
lesions affecting the masticatory muscles themselves or
systemic disorders. Systemic disorder is not often a cause
of unilateral muscle atrophy.

Unilateral masticatory muscle atrophy

• Due to muscle disorders:
• Unilateral masticatory muscle atrophy is
uncommon with myositis and, when present, a
trigeminal nerve disorder should be suspected.
However, acute presentations should prompt
consideration of a muscle disease.
• Due to unilateral trigeminal nerve disorders:
• Unilateral involvement of the motor part of CN
V causes ipsilateral masticatory muscle atrophy
secondary to neurogenic atrophy and decreased
jaw tone.
• Enophthalmia and protrusion of the third eyelid
can be observed in the ipsilateral eye (passive
retraction of the eyeball secondary to loss of  218 Transverse T1-weighted, contrast-enhanced MR
temporalis and digastricus muscle mass). image of a dog with masticatory muscle atrophy (red
Decreased or complete loss of facial sensation arrow) due to an ipsilateral nerve sheath tumour of CN V
may be seen with associated involvement of (yellow arrow). Note the contralateral normal CN V is
trigeminal sensory nerve branches. Involvement usually hyperintense secondary to contrast enhancement
of the ophthalmic branch of CN V can also (white arrow).
282 DECISION MAKING

FACIAL PARALYSIS

Introduction
Facial paresis or paralysis is often featured as a sole
sign, as seen with idiopathic facial paresis/paralysis.
However, it can also occur with more complex diseases
of the middle/inner ear or CNS, and can occasionally
reflect part of a generalized peripheral neuropathy.
Muscles that regulate facial expression and maintain a
physiological appearance of the mouth, ear position and
palpebral fissure are innervated by the facial nerve
(CN VII). A thorough neurological examination will
help to localize the problem, establish an appropriate list
of differential diagnoses and determine the choice of
diagnostic tests.
 219 A Dachshund with bilateral masticatory muscle
atrophy due to chronic steroid administration. Neuroanatomical basis
The facial nerve is motor to the muscles of facial expres-
sion and sensory (providing the sense of taste) to the
Bilateral masticatory muscle atrophy rostral two-thirds of the tongue and hard palate. Its
Bilateral masticatory muscle atrophy can be caused by parasympathetic component innervates the lacrimal
the following diseases: gland and the mandibular and sublingual salivary glands.
• Bilateral involvement of the motor branches of CN Neurons innervating the muscles of facial expression are
V (see Dropped jaw, above), which is usually located in the facial nucleus in the rostral medulla oblon-
associated with reduced jaw tone, a dropped jaw gata. The axons pass in the internal acoustic meatus of
and/or an inability to close the mouth voluntarily. the petrosal bone on the dorsal surface of the vestibulo-
• Systemic disorders (cachexia, hyperadrenocorticism cochlear nerve and leave the skull through the stylo-
or exogenous steroid administration) (219). mastoid foramen. The facial nerve courses through the
• Chronic MMM. In cases of chronic MMM, the middle ear before branches are distributed to the muscles
atrophy is caused by destruction of myofibres and of facial expression (ear, eyelids, nose, cheeks and lips) as
fibrotic scarring. It is usually associated with a well as the caudal portion of the digastricus muscle (220).
reduced ability to open the jaw (see Trismus, Motor dysfunction of CN VII produces the follow-
above). ing signs: drooping and inability to move the ear and
• Idiopathic condition – poorly documented. lip, drooling, widened palpebral fissure, absent sponta-
neous and provoked blinking, absent abduction of the
As with unilateral atrophy, bilateral masticatory muscle nostril during inspiration and deviation of the nose
atrophy may cause enophthalmia and protrusion of the towards the normal side due to the unopposed muscle
third eyelid. tone on the unaffected side (221). With chronic denerva-
tion, the lips are retracted further than normal and the
nostril is deviated to the affected side as a result of muscle
fibrosis. Lesions of the individual branches of the facial
nerve produce paresis or paralysis of the specific muscle
they innervate. Involvement of the parasympathetic
supply of the lacrimal and nasal glands produces kerato-
conjunctivitis sicca and a dry nose (222), respectively.
 ACUTE DISORDERS OF THE HEAD AND FA C E 283

Neurological evaluation
The neurological evaluation should help to localize the
problem as a central CN disease or a peripheral CN
disease (223, next page):
• Central cranial nerve disease/brainstem
disorder causing facial paralysis. If the brainstem
is affected, hemiparesis and/or postural reaction
deficits are usually present. These occur on the Trigeminal n.
same side as the facial paresis/paralysis. Moreover, Major petrosal n.
brainstem signs can include the involvement of Facial n.
further CNs, altered mentation or presence of Vestibular n.
vestibulocerebellar signs. Cochlear n.
Glossopharyngeal n.
Hypoglossal n.
Vagus n.
Stylomastoid foramen

 220 The intracranial anatomical course of the

facial nerve once it has left the brainstem.

• Peripheral nerve disease causing facial paralysis:

• Middle/inner ear disease. If there is evidence of
ipsilateral vestibular signs (see Chapter 14)
and/or Horner’s syndrome without any postural
reaction deficits, a middle/inner ear neurolocal-
ization must be suspected based on the close
proximity of CN VIII and the cranial cervical
 221 A Boxer with acute-onset left- ganglion/post-ganglionic sympathetic neurons.
sided facial paresis. • Polyneuropathy. If spinal reflexes are reduced,
the facial paresis/paralysis may be part of a
more generalized peripheral neuropathy
(see Chapter 10). Facial weakness, in particular a
decrementing blink reflex, may be seen with
junctionopathies, such as MG, or, more rarely,
botulism (see Chapters 24 and 25, respectively)
and tick paralysis, especially in Australia.
• Idiopathic facial nerve dysfunction. If facial
paresis/paralysis occurs as the sole sign,
idiopathic facial paresis is the most likely
diagnosis. However, even though hypothy-
roidism commonly causes polyneuropathies,
facial paresis may be the only clinical sign.
 222 Some patients with facial nerve
dysfunction can present with an ipsi-
lateral dry nose.
 284 DECISION MAKING

 223 Diagnostic approach to a patient

with facial paresis. The neurological FACIAL PARESIS/
PARALYSIS
evaluation should help to localize the
problem as a central or peripheral CN
disease.
Presence of additional
neurological signs?

YES NO

Abnormal mentation Hypersensitivity to

Reduced spinal reflexes, ± Horner’s syndrome Involvement of other cranial potentiated sulphonamides
postural reaction deficits ± Vestibular signs nerves (dog)?
Normal postural reactions Postural reaction deficits or Possibility of peripheral
cerebellar signs trauma?

Diffuse polyneuropathy/ Middle ear disease Brainstem disease or

junctionopathy multifocal CNS disease

Thyroid profile (dog) Otoscopic and Advanced diagnostic imaging

pharyngeal examination (CT, MRI)
AChR AB titre Thyroid profile (dog)
Advanced diagnostic imaging CSF evaluation
Electrodiagnostic (CT, MRI) superior to skull
investigations radiographs Infectious titres
Nerve biopsy
CSF evaluation
Infectious titres
Thoracic radiographs
Abdominal ultrasound
NORMAL ABNORMAL

Otoscopic and pharyngeal • Hypothyroidism

• Inflammatory, idiopathic, examination
metabolic, paraneoplastic • Otitis media/interna
neuropathies • Middle ear polyp (cat)
• Myasthenia gravis • Neoplasia
• Botulism • Trauma
•Tick paralysis • Idiopathic facial
NORMAL paresis/paralysis most likely
 ACUTE DISORDERS OF THE HEAD AND FA C E 285

Differential diagnosis Specific diagnostic tests for facial paresis

Disease mechanisms and conditions responsible for facial If facial paresis/paralysis is the only presenting sign:
paralysis/paresis are listed in Table 69. • Thyroid function testing (dog): total T4 and TSH
Facial muscle weakness can be seen in conjunction determinations as minimum screening; if inconclu-
with MG, botulism or tick paralysis; facial paresis/ sive, free T4, T3 and antithyroid antibody levels
paralysis (often bilateral, but may be asymmetrical) may should be analysed.
theoretically occur as part of any acute-onset peripheral • Otoscopic and pharyngeal examination (particularly
neuropathy; however, more generalized neuropathic to check for possible inflammatory polyps in cats)
signs should also be present. should be performed under GA if necessary.
• If otitis media/interna is suspected from the history,
see below.

Table 69 Causes of facial paresis/paralysis

DISEASE MECHANISM DOGS CATS

Vascular Brain haemorrhage/infarct (rare cause) Brain haemorrhage/infarct (rare cause)

Inflammatory/infectious Otitis media/interna* Otitis media/interna*

Meningoencephalitis of unknown aetiology Middle ear polyps
(e.g. GME) Meningoencephalitis of unknown aetiology
Infectious encephalitis (distemper, rabies, (presumed immune mediated) (rare)
Toxoplasma, Neospora, fungal, Infectious encephalitis (Toxoplasma, FIP,
bacterial, rickettsial) rabies, bacterial, fungal)
Acute canine polyradiculoneuritis
(Chronic demyelinating polyradiculoneuritis)

Trauma Head trauma/peripheral facial trauma Head trauma/peripheral facial trauma

Iatrogenic following bulla osteotomy Iatrogenic following bulla osteotomy

Toxic Hypersensitivity associated with potentiated Tick paralysis

sulphonamides
Tick paralysis (see Chapter 10)

Anomalous Chiari-like malformation (mild facial paresis,

possibly bilateral)**

Metabolic Hypothyroidism*

Idiopathic Idiopathic facial nerve paresis/paralysis* Idiopathic facial nerve paresis/paralysis

Acquired myasthenia gravis* Acquired myasthenia gravis

Neoplastic Primary or metastatic brain tumour Primary or metastatic brain tumour

Middle ear tumour Middle ear tumour
* Common cause
**If Chiari-like malformation is associated with syringomyelia, neck/flank scratching, neck pain
and postural reaction deficits due to the latter are the most common signs.
 286 DECISION MAKING

If otitis media/ interna is suspected (history, concurrent If a polyneuropathy or more generalized neuromuscular
vestibular signs and/or Horner’s syndrome): disease is suspected (reduced spinal reflexes, postural
• Otoscopic and pharyngeal examination should be reaction deficits, other CN involvement):
performed, if necessary under GA. • EMG and motor nerve conduction studies are
• Swabs for cytology and culture (aerobic, fungal and indicated in patients suspected of a more diffuse
yeast) from the middle ear cavity if the tympanic polyneuropathy or multiple CN neuropathy.
membrane is ruptured. • Search for an attached tick.
• Myringotomy with a 20-gauge spinal needle to • Consider botulism intoxication.
obtain samples from the middle ear cavity for • Thyroid function testing (dog).
cytology and culture if the tympanic membrane is • If electrodiagnostic testing is abnormal: chest
intact, but bulging, or of an abnormal colour. radiographs and abdominal ultrasound to exclude
• Imaging of the tympanic bullae with radiographs, paraneoplastic polyneuropathy; muscle and nerve
CT or MRI to assess for otitis media/interna (224). biopsy may aid in definitive diagnosis.
• Anti-AChR antibody titre to rule out focal MG in
If CNS involvement is suspected (postural reaction cases showing facial paresis.
deficits, altered mental status, other CN deficits, cere- • CSF analysis (nucleated cell count and cytology, TP
bellar or forebrain signs): concentration).
• Advanced brain imaging (CT or MRI). • Serum and CSF infectious disease titres and/or
• CSF analysis (nucleated cell count and cytology, TP PCR for various infectious organisms, and CSF
concentration). culture if indicated.
• Serum and CSF infectious disease titres and/or
PCR for various infectious organisms, and CSF Common causes of facial paresis/paralysis
culture if indicated. Idiopathic facial nerve paresis/paralysis
Overview
Most common cause of facial nerve paresis/paralysis in
dogs and cats. Cocker Spaniels and Boxers are predis-
posed. The aetiology is unknown.

Clinical presentation
Occurs mostly as unilateral dysfunction, but may occur
bilaterally. Other neurological deficits are usually absent,
although some animals might develop concurrent idio-
pathic vestibular syndrome.

Diagnosis
Diagnosis is made by exclusion of other possible causes.
Even in the absence of other neurological deficits, a thor-
ough investigation for ear disease, as well as blood tests
for hypothyroidism (dog), is recommended. CSF evalua-
tion can help exclude CNS inflammatory causes of facial
paresis. MRI revealing lack of contrast enhancement of
the intratemporal part of the facial nerve may be associ-
 224 Transverse T2-weighted MR image at the ated with a better outcome in dogs with idiopathic facial
level of the tympanic bullae of a cat with otitis media. paralysis.
Fluid accumulation can be noted in both the ventro-
medial (yellow arrow) and dorsolateral (red arrow)
compartments of the feline bulla.
 ACUTE DISORDERS OF THE HEAD AND FA C E 287

Management Inherited laryngeal paresis

No specific treatment exists. Even though tear produc- The hereditary form of laryngeal paresis/paralysis has
tion is expected to be normal with idiopathic facial been described in many different breeds including
paresis/paralysis, corneal lesions may occur because of Bouvier des Flandres, Siberian Huskies, white-coated
exposure due to reduced eyelid closure, and this should German Shepherd Dogs, Dalmatians, Rottweilers,
be addressed. The prognosis for complete recovery is Leonbergers, Bull Terriers and Pyrenean Mountain
guarded; recovery can take weeks to months, but may Dogs. Laryngeal paresis/paralysis has also been
not occur at all. Occasionally, this disorder progresses reported in a young Afghan Hound, Cocker Spaniel,
to affect both facial nerves. Chronicity may result Dachshund and Miniature Pinscher. In some of these
in muscle contracture and deform the facial expression breeds (Bouvier des Flandres, Dalmatians, Rottweilers,
permanently. Leonbergers and Pyrenean Mountain Dogs) laryngeal
paralysis is part of a more generalized NM disorder that
STRIDOR AND DYSPHONIA is referred to as laryngeal paralysis/polyneuropathy
complex.
Introduction
Respiratory stridor and/or dysphonia are characteristic Acquired laryngeal paresis
signs of laryngeal dysfunction (paresis or paralysis). Acquired laryngeal paralysis seems to affect mainly older,
Laryngeal paralysis is an important cause of upper respi- large/giant breed dogs with Labrador Retrievers being
ratory airway obstruction in dogs and it is increasingly overrepresented. Some reports found male dogs more
being recognized in cats. Clinical signs of laryngeal affected than females (3.7:1). The cause of this acquired
paralysis in dogs typically include stridor, exercise intol- form is most often described as idiopathic. Other causes
erance, respiratory distress, dysphonia, cyanosis, cough include thyroid neoplasia, surgical trauma to the vagus
and collapse. Cats manifest similar clinical signs, but can nerve and inflammatory or neoplastic brainstem diseases.
also show tachypnea, dysphagia, weight loss, anorexia Laryngeal paralysis has also been described in association
and fever. The age of dogs presenting with laryngeal with more generalized NM disorders such as MG and
paralysis has a bimodal distribution, with immature or acquired polyneuropathies. Hypothyroidism has also
young dogs usually less than 1 year of age and older dogs been implicated as a cause , but the relationship between
(mean age ranging from 9.5–12.2 years) being most these two conditions is still unclear. Laryngeal paralysis
affected. Both inherited and acquired diseases are recog- in cats does not seem to have any sex or breed predisposi-
nized. Young dogs usually suffer from inherited laryngeal tion. The median age of cats reported with laryngeal
paralysis, while older animals may have the acquired paralysis is 11 years, with a very broad range from 4
form of this disease. months to 17 years of age.

Posterior crico-
Neuroanatomical basis
arytenoid muscle The larynx is a very complex structure that is controlled
Arytenoid cartilage by both intrinsic and extrinsic muscles (225). Innervation
Lateral cricoarytenoid of three of the four intrinsic laryngeal muscles is supplied
muscle by the recurrent laryngeal nerve (dorsal and lateral
cricoarytenoid muscle and thyroarytenoid muscle). The
fourth muscle (cricothyroid muscle) is supplied by the
cranial laryngeal nerve. Both the recurrent laryngeal
nerve and the cranial laryngeal nerve originate from the
Cricothyroid muscle vagus nerve. The cranial laryngeal nerve leaves the vagus
Cricoid cartilage nerve at the level of the distal ganglion (ventral and
Thyroid cartilage
Thyroarytenoid
muscle  225 Anatomy in cross section of the laryngeal muscles.
288 DECISION MAKING

 226 Diagnostic approach to a patient presenting

STRIDOR/DYSPHONIA with stridor.

Visible and/or palpable mass

YES NO
in laryngeal/pharyngeal region

Complete neurological
Careful inspection of the examination
region under anaesthesia Careful inspection of region
under sedation/light
anaesthesia

ABNORMAL NORMAL

Consider radiographs,
Decreased segmental
ultrasound or
spinal reflexes
MRI of larynx/pharynx

NO YES

• Infection (abscess) Consider if breed at risk for

Other cranial nerve hereditary
• Foreign body polyneuropathy/laryngeal
abnormalities?
• Neoplasia paralysis

YES NO NO

MRI of brain, larynx/pharynx EMG of laryngeal and

and cervical region; appendicular muscles;
CSF analysis; Postural reactions MNCV of tibial and ulnar
Anti-AChR antibody titre; abnormal? nerves; repetitive nerve
thyroid profile stimulation

ABNORMAL NORMAL

• Neoplasia • Myasthenia gravis Anti-AChR antibody titre;

• Inflammation • Diffuse myopathy nerve and muscle biopsy; • Idiopathic laryngeal
• Vesicular disease • Diffuse polyneuropathy thorax and abdominal paralysis
• Polyradiculoneuritis imaging; ± CSF analysis
 ACUTE DISORDERS OF THE HEAD AND FA C E 289

medial to the tympanic bulla), while the vagus nerve gives Differential diagnosis
rise to the recurrent laryngeal nerve at the level of the The list of differential diagnoses in dogs or cats that
thoracic inlet. The cell bodies of these somatic efferent present with stridor/dysphonia varies enormously
fibres are located in the nucleus ambiguus in the medulla depending on the signalment and history, as well as the
oblongata. physical and neurological examination findings. Disease
mechanisms and conditions commonly associated with
Neurological evaluation the emergency evaluation of a dog or a cat with stridor or
The neurological examination should aim to identify dysphonia are outlined in Table 70 (next page).
non-neurological causes of stridor/dysphonia and other
neurological deficits (226). This may help to differentiate Specific diagnostic tests for stridor/dysphonia
between peripheral CN disease (NM) versus central CN Electrophysiological tests, such as EMG, MNCV evalu-
disease (brainstem). ation and repetitive motor nerve stimulations, should be
performed in every patient presenting with laryngeal
Non-neurological causes of stridor/dysphonia paralysis to investigate the possibility of a generalized
• Laryngeal trauma (foreign body). NM disorder. Intrinsic laryngeal muscles as well as
• Mass effect on the larynx (neoplastic lesion, axial and appendicular muscles should be thoroughly
abscesses or granulomatous lesions). evaluated with EMG, and MNCV studies should be per-
• Local inflammatory/infiltrative processes formed on both the tibial and ulnar nerves. These elec-
(laryngitis, polyps). trophysiological tests are invaluable for investigating
concomitant or underlying NM disorders such as
In the above scenario the neurological examination polyradiculoneuropathies, polymyopathies or MG. If a
should be completely normal and inspection of the larynx generalized NM disorder is identified, further diagnostic
under sedation/light anaesthesia should reveal normal tests (endocrine testing, anti-AChR antibody titre,
laryngeal function or restricted movement due to mass muscle and nerve biopsy, thorax and abdominal imaging,
effect on this structure. Occasionally, external palpation ± CSF analysis) should be carried out to identify a specif-
of the larynx may identify a mass lesion at this level with ic cause.
or without associated discomfort.
Common causes of stridor/dysphonia
Neurological causes of stridor/dysphonia Idiopathic laryngeal paralysis
• Central/brainstem lesion: usually associated Overview
with other neurological signs such as depressed Idiopathic laryngeal paralysis affects mostly middle-aged
mentation, ataxic/paretic gait and deficits affecting and older large or giant breeds dogs such as Labrador
other CNs. Retrievers, Chesapeake Bay Retrievers, Irish Setters,
• Cranial polyneuropathy: other CNs may have Afghan Hounds, St Bernards and Rottweilers. Sporadi-
abnormal function. Generally, mentation, gait and cally, medium and small/toy breeds can be affected.
segmental spinal reflexes in all four limbs remain Laryngeal paralysis classically results from unilateral or,
normal. more commonly, bilateral denervation of the laryngeal
• Part of a generalized polyneuropathy: dysphonia is abductor muscles (dorsal cricoarytenoid).
accompanied by generalized weakness affecting all
four limbs and probably by deficits in other CNs.
Mentation should remain normal.
290 DECISION MAKING

Table 70 Differential diagnosis of stridor/dysphonia

DISEASE MECHANISM DOGS CATS

Inflammatory/infectious Meningoencephalitis of unknown Meningoencephalitis of unknown

origin origin (rare)
Rabies Rabies
Trypanosomiasis (rare)

Trauma Cervical/thoracic traumas Cervical/thoracic traumas

Iatrogenic after cervical/thoracic surgery Iatrogenic after cervical/thoracic surgery
Iatrogenic after aggressive attempts at Iatrogenic after aggressive attempts at
external jugular venipuncture external jugular venipuncture

Toxic Lead poisoning

Metabolic Hypothyroid polyneuropathy

Idiopathic Idiopathic laryngeal paralysis* Idiopathic laryngeal paralysis*

Polyradiculoneuritis* Polyradiculoneuritis*
Acquired myasthenia gravis Acquired myasthenia gravis

Neoplastic Mass effect on laryngeal nerves Mass effect on laryngeal nerves

Lymphoma

Degenerative Hereditary laryngeal paralysis

(breed specific)

* Common cause

Diagnosis Management
Diagnosis is based on clinical examination, laryngoscopy While conservative treatment of laryngeal paralysis is
showing impaired abduction of the larynx and EMG generally ineffective in halting the disease progression, it
evidence of denervation potentials in the intrinsic may help prevent acute exacerbation of the clinical signs
laryngeal muscles. EMG is also helpful in detecting more (cyanosis and collapse). Guidelines for the conservative
generalized LMN disorders. Motor nerve conduction management of laryngeal paralysis include exercise
velocity studies of the recurrent laryngeal nerve can be restriction, avoiding stressful situations and encouraging
performed to more specifically define the origin of the owners to keep their dog/cat lean and not overweight.
EMG abnormalities (neuropathy versus myopathy). A variety of surgical techniques have been successfully
used for the treatment of laryngeal paresis/paralysis;
these include ventriculocordectomy, partial arytenoid-
ectomy, laryngeal tieback, modified castellated laryngo-
fissure and neuromuscular pedicle grafting. Of all these
techniques, arytenoid tieback surgery appears to give the
best overall results.
Idiopathic laryngeal paralysis in older dogs can have a
favourable prognosis if appropriately treated. In dogs
that have concurrent conditions, such as megaoesopha-
gus, the prognosis is generally poor.
 ACUTE DISORDERS OF THE HEAD AND FA C E 291

DYSPHAGIA AND REGURGITATION Neuroanatomical basis

Normal swallowing and dysphagia
Introduction Normal swallowing relies on a very complex, well-
Dysphagia is defined as difficulty in swallowing. coordinated function between the tongue, hard and soft
Regurgitation refers to emitting already swallowed food palates, pharynx, oesophagus and gastro-oesophageal
or drink and should be distinguished from vomiting; it is junction. It is coordinated by CNs V (trigeminal; motor
mostly associated with megaoesophagus (227), which innervation of masticatory, mylohyoid and soft palate
describes a dilation of the oesophagus. muscles; sensory fibres from oral cavity), VII (facial;
Dysphagia and regurgitation can result from func- motor innervation of stylo- and jugulohyoid muscles;
tional or morphological abnormalities of the oropharyn- sensory fibres from soft palate and nasopharynx), IX
geal area or oesophagus. They can occur as a sole sign or (glossopharyngeal; motor fibres to pharyngeal muscles;
be part of a more complex disease of neurological/NM sensory fibres from pharynx and tongue), X (vagus;
origin. In some NM diseases, such as MG, dysphagia and motor fibres to pharyngeal muscles and oesophagus;
regurgitation may be the only clinical signs. sensory fibres from pharynx, tongue and oesophagus)
Dysphagia and regurgitation often compromise and XII (hypoglossal; motor fibres to tongue) and their
nutrition and hydration and may lead to aspiration pneu- nuclei in the brainstem, which in turn are controlled
monia and dehydration. It is therefore important to rec- by areas of the reticular formation referred to as the
ognize these signs early and to try to establish the swallowing centre.
underlying cause as soon as possible to initiate appropri- Swallowing disorders (dysphagias) can arise from
ate treatment. functional or morphological abnormalities of any of the
structures involved. They may be classified as:
• Oropharyngeal dysphagia (impaired bolus
formation or passage from the mouth to the cranial
oesophagus).
• Oesophageal dysphagia (impaired bolus passage
from the cranial oesophagus to the gastro-
oesophageal junction).
• Gastro-oesophageal dysphagia (disturbance in the
passage from the oesophagus into the stomach).

The oropharyngeal phase of swallowing can be further

subdivided into oral, pharyngeal and cricopharyngeal
stages:
• Oral dysphagia is associated with disorders of
initiation of swallowing (bolus accumulation at the
base of the tongue).
• Pharyngeal dysphagia describes a disorder in
propulsion of the bolus across the pharynx (rostral
to caudal pharyngeal contractions propel the bolus
from the base of the tongue to the cricopharyngeal
passage).
• Cricopharyngeal dysphagia describes failure of
relaxation (achalasia) or closure (chalasia) of
the cricopharyngeal sphincter and lack of
 227 Lateral thoracic radiograph of a dog with mega- coordination of sphincter relaxation with
oesophagus. The dorsal border of the dilated oesophagus pharyngeal or oesophageal contraction.
is clearly visible (arrows).
 292 DECISION MAKING

In this section, dysphagia will refer to disorders affect- Larynx Vagus nerve
ing the pharyngeal and cricopharyngeal phases of Distal vagal
ganglion
swallowing. Disease causing oesophageal and gastro-
Cranial laryngeal
oesophageal dysfunction will be listed under Regurgita- nerve
tion and megaoesophagus, below.
An intact gag reflex (pharyngeal reflex) is a prerequi-
site for intact swallowing. The gag reflex is elicited by the Vagosympathetic
glossopharyngeal and vagal nerves, which both arise trunk

from the caudal brainstem where they share their sensory

Right recurrent Left recurrent
(solitary nucleus) and motor (nucleus ambiguus) nuclei. laryngeal nerve laryngeal nerve
Therefore, lesions of the caudal brainstem, or CNs IX
and X themselves, can result in reduced pharyngeal tone
and dysphagia. However, more generalized neuropathies
must not be overlooked. Oesophagus Left vagus nerve
Disorders of NM transmission are frequently associ-
ated with dysphagia and reduced pharyngeal tone.
Dysphagia can also occur due to disease that leads to Dorsal vagal Ventral vagal
spasms of the pharyngeal musculature, such as tetanus trunk trunk

(Chapter 25). Furthermore, dysphagia is a common

clinical sign of generalized myopathies (Chapter 8), in
particular those of inflammatory origin. With dystrophin
deficient muscular dystrophy, hypertrophy of the pha-
ryngeal muscles may be pronounced and lead to marked
dysphagia.
Simple physical obstructions in the head and neck  228 Anatomical representation of the vagus nerve.
area, such as foreign bodies or neoplastic masses, may
be the underlying cause of dysphagia. Animals with
pharyngitis or tonsillitis may have difficulty swallowing
as well.
In some cases, no underlying cause for dysfunction of vagus nerve. The oesophagus of the dog consists entirely
the swallowing reflex can be found (idiopathic dyspha- of striated muscle, whereas in the cat the distal third is
gia). If the cricopharyngeal muscle fails to open during composed of smooth muscle.
swallowing, the condition is also called cricopharyngeal Megaoesophagus can be congenital or acquired and
achalasia, which predominantly occurs as an idiopathic may be primary/idiopathic or occur secondarily to a
disease in young dogs. number of causes. Underlying causes of congenital
megaoesophagus include congenital idiopathic megaoe-
Regurgitation/megaoesophagus sophagus, megaoesophagus as a consequence of a persist-
Regurgitation is the result of oesophageal motility ent right aortic arch or as an aspect of congenital MG
dysfunction or is due to structural abnormalities. It may (Chapter 24). Recent studies suggest that the main
or may not be associated with overt megaoesophagus. underlying cause of congenital idiopathic megaoesopha-
Megaoesophagus occurs more commonly in dogs than gus is a selective rather than an afferent dysfunction of
in cats. the vagus nerve. Acquired megaoesophagus can be seen
The oesophagus is innervated by the vagus nerve with brainstem disease or be a sign of a more generalized
(228). The cervical part is innervated by the pharyngeal polyneuropathy or myopathy, especially the generalized
and recurrent laryngeal branches and the thoracic inflammatory myopathies. Megaoesophagus is frequent-
portion is innervated by vagal branches. In addition, CN ly seen with junctionopathies and occurs in 80% of dogs
XI (spinal accessory nerve) sends a few fibres to join the with acquired MG. Regurgitation may be the sole sign or
 ACUTE DISORDERS OF THE HEAD AND FA C E 293

it may be associated with generalized weakness. The inci- Clinically, it is difficult to distinguish whether regur-
dence of oesophageal dilation in cats with acquired MG gitation is a functional disorder or whether a structural
is lower. Moreover, feline and canine dysautonomia is abnormality could be responsible. Thorough palpation
frequently associated with megaoesophagus and regurgi- of the ventral neck area is recommended to assess for any
tation. In dogs, megaoesophagus has also been associat- obvious masses. If the neurological examination reveals
ed with metabolic diseases, such as hypothyroidism and any further deficits, a functional disorder is more likely.
Addison’s disease, or with systemic lupus erythematosus.
Apart from functional causes, structural abnormalities Assessment of a neuroanatomical cause
such as tumours in the neck or chest area, foreign bodies Idiopathic cause
or oesophagitis with possible secondary strictures may be If further neurological examination is unremarkable and
underlying causes of megaoesophagus and regurgitation. structural diseases have been excluded, idiopathic
However, in many cases of acquired megaoesophagus or megaoesophagus/idiopathic dysphagia must be consid-
dysmotility of the oesophagus, the underlying cause ered. It is, however, important to bear in mind that
remains unclear (acquired idiopathic megaoesophagus or megaoesophagus and regurgitation or dysphagia may be
dysmotility). the only clinical sign of a more generalized disease. For
example, 43% of dogs with MG have only focal manifes-
Neurological evaluation tations of diseases such as megaoesophagus or dysphagia.
A full clinical and neurological evaluation is important to
decide whether dysphagia and/or regurgitation results Central/brainstem cause
from a functional disorder or a structural abnormality With brainstem lesions (e.g. tumour or encephalitis),
and occurs as the sole clinical sign or as part of a more additional neurological deficits, such as altered menta-
complex disease involving the NM, central or autonomic tion, postural reaction deficits and multiple CN deficits,
nervous system (229, next page). In addition, prehension are usually present. Spinal reflexes, however, will be
disorders must be distinguished from dysphagia and normal or increased.
regurgitation must be distinguished from vomiting. If dysphagia is due to spasms of the pharyngeal
muscles, tetanus must be considered; however, further
Assessment of a functional versus typical signs, such as risus sardonicus (tetanus), rigidity of
a structural disorder limbs and trismus, are usually evident.
If the cause of dysphagia or regurgitation is structural or
mechanical (e.g. tumour or foreign body, stricture due to Neuromuscular cause
inflammatory processes, regurgitation due to persistent If generalized LMN signs are present (reduced or
right aortic arch), the neurological examination will be absent spinal reflexes), a polyneuropathy or botulism
unremarkable. (Chapter 25) must be considered as the underlying cause
In the case of functional dysphagia, the pharyngeal for dysphagia and/or regurgitation. If generalized weak-
tone will mostly be decreased and the gag reflex will be ness and exercise intolerance are present, MG should be
weak or absent. However, dysphagia can also be due to high on the list of differential diagnoses. Generalized
spasms of the pharyngeal muscles (tetanus, myotonia). weakness, together with a stiff gait, often indicates a gen-
The gag reflex can be tested by applying external pres- eralized myopathy. In cases of myotonia, spasms of the
sure to the hyoid bones or by stimulating the pharynx pharyngeal muscles can occur; however, further typical
directly with a finger. Alternatively, pharyngeal function signs, including muscle dimpling (percussion myotonia),
can be indirectly assessed by observing the animal eat or are usually evident.
drink or by opening its mouth wide, which is normally
followed by closing the mouth, licking the nose and swal- Autonomic cause
lowing. The pharyngeal/laryngeal area, as well as the If regurgitation is due to dysautonomia, additional signs
mouth, should be thoroughly assessed for structural of autonomic dysfunction are likely to be present (see
abnormalities. section above).
294 DECISION MAKING

 229 Diagnostic approach to a patient DYSPHAGIA/

presenting with dysphagia/regurgitation. REGURGITATION
Caution: rabies!

Presence of additional
neurological signs? Radiographs to assess for
megaoesophagus (young
animal: look for evidence of
persistent right aortic arch)
YES NO and aspiration pneumonia

Age and breed suggestive of

Autonomic signs congenital idiopathic
megaoesophagus?

NO

• Dysautonomia

YES Positive anti-AChR antibody

titre?

Abnormal mentation or Generalized weakness, stilted • Focal myasthenia gravis NO

posture, involvement of other gait, exercise intolerance, (acquired)
cranial nerves, postural reduced spinal reflexes,
reaction deficits ± postural reaction deficits
Normal thyroid profile and
NO ACTH stimulation test (dog)?

Intracranial (brainstem) • Hypothyroidism YES

lesion Neuromuscular disease
• Addison‘s disease

Normal electrodiagnostic
investigations?
NO
Anti-AChR antibody titre Normal radiograph/
Edrophonium-chloride MRI/CT of pharyngeal area,
Advanced diagnostic brain challenge test neck and chest?
imaging (CT, MRI) ACTH stimulation test • Neuromuscular disorders
CSF evaluation Thyroid profile • Foreign body
Infectious disease titres or Electrodiagnostic • Soft tissue tumours YES
PCRs investigations (muscle and
nerve biopsy)
CSF analysis
Contrast radiography
(barium sulphate) or
fluoroscopy
• Myasthenia gravis
• Encephalitis (brainstem) • Idiopathic functional
• Botulism pharyngeal disease
• Brain tumour
• Tick paralysis (Australia) • Idiopathic mega-
• Cerebrovascular accident
• Generalized myopathy oesophagus or oesophageal
• Caudal fossa malformation
• Polyneuropathy dysmotility
 ACUTE DISORDERS OF THE HEAD AND FA C E 295

Distinguishing prehension disorders from dysphagia • Electrolyte assessment and ACTH stimulation test
Taking a thorough history will help to distinguish the to exclude Addison’s disease (dog).
inability to prehend (trigeminal or hypoglossal nerve • Serum CK to investigate for generalized
dysfunction) from dysphagia (glossopharyngeal and/or inflammatory myopathies or muscular dystrophy.
vagal nerve dysfunction). If animals have a problem with • Anti-AChR antibody titre to exclude acquired MG.
prehension, they often seemingly spend a lot of time • Electrodiagnostic investigations (EMG, nerve
drinking without success; however, owners might report conduction velocity, repetitive nerve stimulation)
polydipsia. With dysphagia, coughing after drinking and to exclude generalized myopathies or neuropathies
eating will be common and there will be excessive saliva and to assess for junctionopathies.
in the pharynx. As the vagus also innervates the larynx, • Positive contrast radiography (barium sulphate) and
dysphonia and inspiratory stridor might be present in fluoroscopy can help determine which part of the
addition to laryngeal paralysis. swallowing phase is disturbed and demonstrate
abnormal oesophageal motility.
Distinguishing regurgitation from vomiting • MRI or CT of the pharyngeal area, neck and chest
Regurgitation (vagus nerve dysfunction) must be distin- helps to evaluate soft tissue structures and
guished from vomiting. This can be achieved with a investigate for masses or foreign bodies (especially
detailed description by the owners and measurement of stick injury).
the pH of the regurgitated or vomited material (vomit
will have an acidic pH and regurgitated material a more If there are additional generalized neuromuscular signs
basic pH). (weakness, exercise intolerance, stilted gait, reduced seg-
mental spinal reflexes, reduced postural reactions):
Differential diagnosis • Thyroid panel (dog; see above).
The list of differential diagnoses for dysphagia and • ACTH stimulation test to investigate for
regurgitation is dependent on the overall clinical and hypoadrenocorticism.
neurological evaluation, as well as on signalment, • Serum CK to investigate for generalized inflamma-
history and course of the disease. Disease mechanisms tory myopathies or muscular dystrophy.
and conditions commonly associated with the emergency • If generalized weakness/exercise intolerance is
evaluation of a dog or a cat with dysphagia and regurgita- present, edrophonium chloride challenge test and
tion/megaoesophagus are outlined in Tables 71 and 72 anti-AChR antibody titres to assess for MG.
(pages 296, 297). • Electrodiagnostic investigations (see above).
• If electrodiagnostic testing is abnormal: thoracic
Specific diagnostic tests for dysphagia radiographs and abdominal ultrasound to exclude
In any animal with a history of dysphagia, a thorough oral paraneoplastic polyneuropathy or para- or pre-
and pharyngeal examination should be performed, if neoplastic myopathy; CSF analysis and muscle
necessary under GA. Extreme care should be taken, as and nerve biopsy.
these animals may have rabies. Every animal with regur-
gitation should have conscious thoracic radiographs to If additional neurological deficits are present suggesting
investigate whether megaoesophagus or aspiration pneu- a structural brain disease:
monia is visibly present. • Advanced brain imaging (CT or MRI).
• CSF analysis (nucleated cell count and cytology,
If dysphagia/regurgitation is the only presenting sign: TP concentration).
• Thyroid function testing (dog): total T4 and TSH • Serum and CSF infectious titres and/or PCR for
determinations as minimum screening; if inconclu- various infectious organisms, and cultures if
sive, also consider free T4, T3 and antithyroid indicated.
antibodies.
296 DECISION MAKING

Table 71 Causes of dysphagia

DISEASE MECHANISM DOGS CATS

Inflammatory/infectious Generalized inflammatory myopathies: Generalized inflammatory myopathies:

immune-mediated polymyositis; infectious immune-mediated polymyositis; infectious
aetiology (Toxoplasma, Neospora, Borrelia, aetiology (Toxoplasma)
rickettsial, hepatozoon), paraneoplastic Meningoencephalitis of unknown aetiology
syndrome (presumed immune-mediated; rare)
Dermatomyositis Infectious encephalitis (rabies, FIP, Toxoplasma,
Sensory ganglioneuritis; protozoal bacterial, fungal)
polyradiculoneuritis (Neospora) Tonsillitis and pharyngitis (mostly bacterial)
Meningoencephalitis of unknown aetiology
(e.g. GME)
Infectious encephalitis (rabies, distemper,
Toxoplasma, Neospora, fungal, bacterial,
rickettsial)
Tonsillitis and pharyngitis (mostly bacterial)

Trauma Foreign bodies* Foreign bodies*

Toxic Botulism* Tick paralysis (rare)

Tetanus
Tick paralysis

Anomalous Congenital myasthenia gravis Congenital myasthenia gravis

Myotonia congenita
Hyoid bone abnormality (very rare)

Metabolic Hypothyroidism
Addison’s disease

Idiopathic Acquired myasthenia gravis* Acquired myasthenia gravis

Cricopharyngeal achalasia

Neoplastic Tumours of the neck/throat area Tumours of the neck/throat area

Brainstem tumours Brainstem tumours

* Common cause

Common causes of acute/subacute dysphagia Newfoundlands, Shar Peis and Greyhounds and is inher-
and regurgitation ited in Wire-haired Fox Terriers (autosomal recessive)
Idiopathic megaoesophagus and Miniature Schnauzers (autosomal dominant or 60%
Overview penetrance autosomal recessive). In cats there seems to
Idiopathic megaoesophagus occurs as congenital and be a predisposition for Siamese and Siamese-related
acquired forms in dogs and is rare in cats. Congenital breeds. In many cases of acquired megaoesophagus the
canine idiopathic megaoesophagus has been reported in cause is unknown and therefore the megaoesophagus is
Great Danes, German Shepherd Dogs, Irish Setters, termed idiopathic.
 ACUTE DISORDERS OF THE HEAD AND FA C E 297

Table 72 Causes of acute/subacute regurgitation/megaoesophagus

DISEASE MECHANISM DOGS CATS

Inflammatory/infectious Generalized inflammatory myopathies: Generalized inflammatory myopathies:

(see Table 71) immune-mediated polymyositis; infectious
Dermatomyositis aetiology (Toxoplasma)
Sensory ganglioneuritis Meningoencephalitis of unknown aetiology
(see Table 71; rare)
Meningoencephalitis of unknown aetiology
(see Table 71) Oesophagitis
Oesophagitis

Trauma Foreign bodies* Foreign bodies*

Toxic Botulism* Lead or thallium intoxication

Lead or thallium intoxication
Tiger snake envenomation
Tetanus
Acrylamide

Anomalous Persistent right aortic arch Persistent right aortic arch

Congenital myasthenia gravis
Myotonia congenita (only regurgitation)

Metabolic Addison’s disease

Hypothyroidism

Idiopathic Idiopathic megaoesophagus* Idiopathic megaoesophagus

Acquired myasthenia gravis* Acquired myasthenia gravis
Idiopathic oesophageal dysmotility without Idiopathic oesophageal dysmotility without
megaoesophagus megaoesophagus
Dysautonomia* Dysautonomia*

Neoplastic Tumours of the neck/chest area Tumours of the neck/chest area

Brainstem tumours Brainstem tumours

* Common cause

Clinical presentation Diagnosis

The most common clinical sign is regurgitation of undi- Underlying neurological/NM disease and structural
gested food. Neurological examination is normal with lesions must be excluded by thorough clinical and neuro-
idiopathic megaoesophagus. The congenital form is logical evaluation and further diagnostic work-up before
usually apparent at the time of weaning and seems to be making a diagnosis of idiopathic megaoesophagus.
associated with developmental immaturity of the inner- Diagnosis is based on the history of regurgitation
vation and/or musculature. For both congenital and and radiographic evidence of oesophageal dilation.
acquired idiopathic forms, a selective vagal afferent dys- A normal oesophageal motility can be demonstrated by
function seems to play a major role. contrast radiography and fluoroscopy. Concurrent aspi-
ration pneumonia must be excluded radiographically.
298 DECISION MAKING

Management Clinical presentation

The management of animals with idiopathic mega- Initial clinical signs in dogs and cats may be non-specific
oesophagus includes feeding and drinking from a height and include temperament change and excessive saliva-
and/or with a gastrostomy tube. Appropriate nutrition tion. After 2–5 days, signs will progress to either the
and hydration need to be assured at all times. furious form (aggression, restlessness, howling, saliva-
Aspiration pneumonia needs to be addressed if present. tion, sometimes convulsions) or the dumb-paralytic form
Certain medical therapies have been advocated for characterized by progressive ascending paresis/paralysis,
stimulating oesophageal peristalsis (e.g. metoclopramide dropped jaw, pharyngeal and hypoglossal paralysis with
or cisapride) or diminishing lower oesophageal sphincter subsequent dysphagia and drooling of saliva, and facial
tone (e.g. anti-cholinergics or calcium channel antago- paralysis. Regurgitation is not a typical sign, but can
nists); however, the results have been rather disappoint- occur as well if the brainstem is affected.
ing. Metoclopramide and cisapride are smooth muscle
prokinetic agents and therefore not likely to have much Diagnosis
of an effect on the oesophagus, especially in dogs, and Diagnosis is confirmed post mortem. Most animals will
risk too many side-effects (e.g. calcium channel antago- reveal typical inclusions (Negri bodies); however, defini-
nists have potent hypotensive effects). tive diagnosis depends on positive results of additional
The prognosis for congenital idiopathic mega- tests such as immunohistochemistry and PCR.
oesophagus is usually guarded. Acquired idiopathic
megaoesophagus generally has a poor prognosis for Management
recovery, although spontaneous recovery has been There is no treatment for rabies. Animals exposed to
reported sporadically. rabies that have not been vaccinated must be euthanized.
If animals are currently vaccinated and have been
Rabies exposed, they should be re-vaccinated and closely con-
Overview fined under observation for at least 3 months. If humans
Rabies, a notifiable disease in certain countries, is the are exposed to rabies and they are unvaccinated, post-
most important zoonotic infection and is caused by a exposure prophylaxis with immunoglobulins must be
rhabdovirus (genus Lyssavirus). (See also Chapter 19.) implemented.
It is characterized by a non-suppurative polioencephalo-
myelitis and craniospinal neuritis. All warm-blooded Myasthenia gravis
species are susceptible to rabies. Rabies occurs in many See Chapter 24.
countries, even though transmission through dogs and
cats plays a much lower role in developed countries due Dysautonomia
to vaccination regimes. Transmission occurs through See Anisocoria, above.
bite wounds (rarely other wounds), via the saliva of
infected animals. After local replication in the muscle, Botulism
the highly neurotrophic virus travels to the CNS via the See Chapter 25.
peripheral nerves. Once the CNS is infected, the virus
spreads centrifugally via peripheral nerves to other Generalized inflammatory myopathies
organs (including the salivary glands). Incubation time See Chapter 8.
may be anything from 2–3 weeks to up to 6 months,
depending on the site of inoculation, the amount of virus
transmitted, the viral strain and the animal’s immune
status.
 DECISION MAKING Chapter 16

MONOPARESIS AND NEUROLOGICAL

CAUSES OF LAMENESS 299

Toby Gemmill
& Malcolm McKee

INTRODUCTION NEUROANATOMICAL BASIS

Animals with dysfunction of a limb can be broadly The UMN system is confined to the CNS. It is responsi-
divided into cases exhibiting lameness and those suffer- ble for the initiation and maintenance of normal move-
ing paresis and/or ataxia. In general, most causes of ments and for the maintenance of tone in extensor
lameness are orthopaedic in origin, whereas most causes muscles to support the body. UMN cell bodies lie within
of paresis are neurological. However, these distinctions the cerebral cortex, basal nuclei, brainstem or spinal
are not clear-cut and diagnosing the cause of limb dys- cord. Axons travel through the brain and/or spinal cord
function can be challenging in some cases. For example, white matter and synapse indirectly via an interneuron
apparent paresis can on occasion be due to orthopaedic with an LMN to modulate its activity.
conditions such as hip dysplasia or an avulsion fracture. The LMN system connects the CNS with the muscle
In contrast, lameness in some patients can be attributed to be innervated. Its cell bodies lie mainly within the
to neurological conditions such as radiculopathies or ventral horn of the spinal cord grey matter in the cervical
peripheral nerve lesions. Furthermore, it is not uncom- and lumbar intumescences (spinal cord segments C6–T2
mon to encounter cases with concurrent orthopaedic and and L4–S3, respectively). Axons exit the spinal cord via
neurological conditions (e.g. animals with fractures and the ventral nerve roots and coalesce with sensory dorsal
concurrent peripheral nerve injuries). It is vital in such nerve roots to form a spinal nerve. These spinal nerves
cases to make an accurate diagnosis and to establish the then course into the brachial or lumbosacral plexus,
relative importance of different lesions as they relate to where they form peripheral nerves, which then innervate
management options and prognosis. specific regions of the limbs (230; 231, next page).

 230 Spinal and C8 C7

peripheral nerves associated T1 C6
with the brachial plexus: C5
lateral thoracic; ulnar;
median; radial; axillary; and
musculocutaneous nerves.
The subscapular and supra- Musculocutaneous n.
scapular nerves arise Axillary n.
immediately cranial to the Radial n.
musculocutaneous nerves. Lateral thoracic n.
Median n.
Ulnar n.
 300 DECISION MAKING

L6
L7

Femoral n.
Obturator n.
Sciatic n.
Pudendal n.

 231 Spinal and peripheral nerves associated with the  232 Ventrodorsal view of a cervical myelogram.
lumbosacral plexus: femoral; obturator; sciatic; and Compression of the spinal cord over the C2/C3 disc space
pudendal nerves. compatible with disc extrusion can be seen (arrow). The
dog was presented with left forelimb paresis. On clinical
examination very subtle left hindlimb proprioceptive
deficits were also apparent.

Spinal cord lesions are less likely to produce true dysfunction include rapid and pronounced muscle
monoparesis and/or lameness as opposed to lesions atrophy, hypotonia, hyporeflexia, paresis and/or lame-
affecting the nerve roots, spinal nerves, plexi and periph- ness (see Chapter 10). It is often possible to localize a
eral nerves. Lesions affecting spinal cord segments lesion to a specific peripheral nerve based on loss of spe-
C1–C5 (232) tend to cause UMN paresis and GP ataxia, cific spinal reflexes, involvement of specific muscle
which can occasionally appear to affect the function of groups and/or cutaneous sensory testing of specific
just one forelimb. Lesions affecting C6–T2 segments regions of the limbs. Knowledge of the motor and
may cause LMN paresis in a forelimb, although fre- sensory functions of different peripheral nerves is there-
quently UMN paresis and GP ataxia can be appreciated fore essential in lesion localization.
affecting the ipsilateral hindlimb. Lesions located at
T3–L3 segments may cause UMN paresis and GP ataxia Forelimb innervation
in one or both hindlimbs. Lesions affecting L4–S1 seg- The brachial plexus is derived from spinal cord segments
ments may cause LMN paresis affecting one or both C6–T1, with minor contributions from C5 and T2
hindlimbs. (see 230). The important nerves of the plexus, from
Sensory deficits are also observed in most cases cranial to caudal, include the suprascapular, musculo-
involving the LMN, and these may help in mapping out cutaneous, axillary, radial, median and ulnar nerves
the area of denervation. The clinical signs of LMN (Table 73). The median and ulnar nerves exit the plexus as
 M O N O PA R E S I S AND NEUROLO GICAL CAUSES OF LAMENESS 301

Table 73 Limb innervation

NERVE SPINAL CORD MUSCLES INNERVATED CUTANEOUS SEGMENTAL SPINAL

SEGMENTS SENSORY FIELD REFLEX

THORACIC LIMB
Suprascapular C6, 7 Supra- and infraspinatus Lateral aspect of None
shoulder

Subscapular C6, 7 Subscapularis None None

Musculocutaneous C6, 7, 8 Biceps brachii, brachialis, Medial aspect of Biceps reflex,

coracobrachialis proximal antebrachium withdrawal reflex
and first digit (flexion of elbow)

Axillary C7, 8 Deltoid, teres major and None None

minor

Radial (C6) C7, 8, T1, Triceps brachii, extensors Cranial aspect of Triceps reflex (proximal)
(2) of carpus and digits antebrachium, dorsal and extensor carpi
aspect of paw radialis (distal)

Median and ulnar C8, T1, (2) Flexors of carpus and Caudal aspect of Withdrawal reflex
digits antebrachium, palmar (flexion of carpus and
aspect of paw, lateral digits)
aspect of 5th digit

HINDLIMB
Femoral L4, 5, 6 Quadriceps group Medial aspect of thigh Patellar reflex
Psoas group and crus, first digit

Obturator (L4), 5, 6 Adductors None None

Sciatic nerve L6, 7, S1, (2) Biceps femoris, Entire limb (via tibial Withdrawal reflex (stifle
gastrocnemius, cranial and peroneal branch) flexion)
tibial, semitendinosus, except for medial aspect
semimembranosus and first digit

Tibial nerve L6–S1 Tarsal extensors, digital Plantar aspect of Gastrocnemius reflex
flexors metatarsus and paw

Peroneal nerve L7–S1 Tarsal flexors, digital Dorsal aspect of Cranial tibial reflex,
extensors metatarsus and paw withdrawal reflex (hock
flexion)

Pelvic nerve S1–S3 Parasympathetic supply to None None

pelvic viscera

Pudendal nerve S1–S3 External anal sphincter Perineum, external Perineal reflex
genitalia
302 DECISION MAKING

a single bundle, but separate into two distinct nerves at Hindlimb innervation
the level of the mid-humerus. The lateral thoracic nerve, The lumbosacral plexus is derived from the L4–S2 spinal
originating from spinal cord segments C8–T1, supplies cord segments, with a small contribution from the S3
motor innervation to the cutaneous trunci muscle. segment (see 231). Because of the foreshortening of the
Pre-ganglionic sympathetic fibres supplying innervation spinal cord with respect to the lumbar spine, these spinal
to the eye originate from the T1–T3 spinal cord cord segments lie between the L3 and L5 vertebral
segments. These pre-ganglionic neurons destined for the bodies. In cats and smaller dogs the spinal cord can
head leave the spinal cord in the segmental ramus terminate slightly further caudally, with the S3 segments
communicans, which joins the thoracic sympathetic lying adjacent to the cranial border of the vertebral body
trunk (see Chapter 15). of L6. Peripheral nerves arising from the lumbosacral
plexus include the femoral, obturator, sciatic, pelvic and
pudendal nerves (Table 73). The sciatic nerve divides at
the level of the distal femur into the peroneal and tibial
nerves.

Table 74 Neurological causes of monoparesis Table 75 Acute and subacute orthopaedic

and lameness causes of lameness

DISEASE MECHANISM DOGS AND CATS DISEASE MECHANISM DIFFERENTIAL DIAGNOSES

Vascular Ischaemic myelopathy Inflammatory/infectious Osteomyelitis

Ischaemic neuromyopathy Septic arthritis
(aortic or brachial artery Immune-mediated arthritis
thromboembolism)
Trauma Fractures, luxation, joint
Inflammatory/infectious Hypertrophic neuritis instability, soft tissue sprains and
Plexus neuritis strains
Discospondylitis
Toxic Snake bite
Myelitis/meningomyelitis
Neosporosis radiculitis/myositis Anomalous Incomplete ossification of the
humeral condyle or radial carpal
Trauma Plexus avulsion bones
Peripheral nerve trauma
Metabolic Pathological fracture secondary
Toxic Localized tetanus to metabolic bone disease

Neoplastic Peripheral nerve sheath tumour Idiopathic Panosteitis, metaphyseal

osteopathy, Legg–Perthes
Local invasion of nerves by
disease, fibrotic myopathy
adjacent tumours
Lymphoma Neoplastic Primary or secondary neoplasia
of bone or soft tissues
Degenerative Lateralized intervertebral disc
extrusion or protrusion Nutritional Pathological fracture secondary
Foraminal stenosis to nutritional hyperpara-
thyroidism

Degenerative Hip dysplasia, cranial cruciate

ligament deficiency, patellar
luxation, degenerative
tendinopathy
 M O N O PA R E S I S AND NEUROLO GICAL CAUSES OF LAMENESS 303

DIFFERENTIAL DIAGNOSIS ORTHOPAEDIC AND NEUROLOGICAL

EXAMINATION
The differential diagnoses depend implicitly on the
anatomical localization of the problem. However, A detailed history and thorough clinical examination are
specific neurological deficits may not be apparent in essential (233; 234, next page). The signalment of an
some cases presented for lameness. Furthermore, these animal can be suggestive of particular problems; for
patients can sometimes be in significant discomfort, example, forelimb lameness in a young Rottweiler might
making accurate localization of a source of pain chal- raise an index of suspicion for elbow dysplasia. On the
lenging. Differential diagnoses for acute monoparesis or other hand, rapid-onset lameness in a middle-aged
neurological causes of lameness are detailed below and Cocker Spaniel could be suggestive of IVDD causing a
outlined in Table 74. Common orthopaedic causes of foraminal compression. Features that can be associated
acute-onset lameness are listed in Table 75. with neurological conditions include a history of

 233 Neurological examination of a

monoparetic animal. MONOPARESIS

YES Other limbs neurologically NO

normal

Segmental spinal reflexes in Suspect CNS lesion or generalized

affected limb neuromuscular disorder

Decreased Normal
or absent or increased

Specific nerve involvement:

• Segmental spinal reflexes
• Cutaneous sensory fields Suspect lateralized
spinal cord lesion
• Horner’s syndrome
• Cutaneous trunci reflex

Electrophysiology; Spinal radiographs;

spinal radiographs; MRI myelography; MRI; CT

• Foraminal stenosis • Disc extrusion/protrusion

• Neoplasia • Ischaemic myelopathy
• Plexus avulsion/trauma • Neoplasia
• Peripheral nerve trauma • Myelitis/meningomyelitis
• Neuritis • Syringomyelia
304 DECISION MAKING

 234 Examination of an animal

LAMENESS AFFECTING
with a single limb lameness. SINGLE LIMB

Orthopaedic examination

Orthopaedic examination Pain with no clear Pain with clear

normal orthopaedic cause orthopaedic cause

Neurological examination
normal
Neurological deficits?

NO YES
Orthopaedic work-up

Pain on neck or back

Treat as monoparesis
manipulation

NO YES

Suspect neural lesion distal Suspect foraminal stenosis or

to exit foramen nerve root inflammation

Electrophysiology; MRI Electrophysiology;

CT; MRI; CSF analysis

• Disc extrusion/protrusion
• Neoplasia
• Juxtafacet cyst
• Neoplasia
• Benign soft tissue or bony
• Neuritis
proliferation
• Neuritis
• Discospondylitis
 M O N O PA R E S I S AND NEUROLO GICAL CAUSES OF LAMENESS 305

Table 76 Clinical signs suggestive of

Orthopaedic examination
neurological causes of lameness Following gait analysis, each limb should be systemati-
cally examined. Limbs should be palpated to assess
• Unprovoked vocalization
muscle mass and symmetry. LMN lesions often lead to
• Arching of the back dramatic muscle atrophy (235); this can be very specific
• Low head carriage depending on the peripheral nerves involved. Each limb
• Reluctance to lower head to eat from the floor should then be evaluated, working distally to proximally.
• Reluctance to allow manipulation of the neck Each joint, ligament, tendon and bone should be careful-
• Pain on palpation of the spine ly assessed for evidence of pain, restricted range of
motion, instability and swelling. To help localize a source
of pain it can be helpful in excitable patients to repeat this
examination following administration of a mild sedative
(e.g. using a combination of acepromazine/butorphanol).
An animal exhibiting lameness, but with a normal
stumbling or ataxia, low head carriage, an arched back orthopaedic examination, should immediately raise an
and holding an affected limb high off the ground rather index of suspicion for a possible neurological lesion. For
than exhibiting a weight-bearing lameness (Table 76). It is the forelimb, deep palpation of the axilla may help local-
important to question owners carefully to ensure these ize discomfort to the brachial plexus. Discomfort on trac-
features are not overlooked. tion of the limb (pulling the limb distally) can be
Following a general clinical examination, detailed suggestive of a lesion affecting neural structures of the
orthopaedic and neurological examinations should then proximal limb. Arterial pulses should be palpated proxi-
be performed. In most cases this will allow the clinician mally and distally to exclude vascular lesions. Finally, a
to establish whether a problem is orthopaedic or neuro- rectal examination can be performed, which may allow
logical in nature and to establish the anatomical origin of palpation of a mass affecting the lumbosacral trunk.
the problem. If a neurological lesion is suspected, it is
important to identify whether it is UMN or LMN in
nature, and whether it is originating from the brain, the
spinal cord, the nerve roots or a peripheral nerve.
Initial assessment of the gait allows the clinician to
determine which limb or limbs is/are affected and to gain
an impression of the severity of the problem. It is possi-
ble in most cases to establish from observing the gait
whether the principal problem is lameness, which often
suggests an orthopaedic problem, or weakness, which is
more suggestive of neurological disease.
Shortened stride length is frequently associated with
decreased muscle tone or pain, which would be more
commonly associated with LMN lesions or orthopaedic
disease, respectively. In contrast, UMN lesions can be
associated with increased stride length or hypermetria.
Compared with UMN paresis, disorders of the LMN
often only result in paresis and not in ataxia. Although
most peripheral neuropathies affect both motor and
sensory axons, the gait dysfunction principally reflects
LMN paresis. The degree of paresis varies from a short  235 Severe supra- and infraspinatus muscle atrophy in
stride to complete inability to support weight, causing a dog, secondary to a peripheral nerve sheath tumour
collapse of the limb whenever weight is placed on it. (cranial to left of picture, caudal to right).
 306 DECISION MAKING

Neurological examination
The neurological examination consists of assessment of
gait, posture, mentation, CN function, postural reactions
and segmental spinal reflexes. Cutaneous sensation of
different peripheral nerves of the dysfunctional limb
should be tested, although this is accepted to be a subjec-
tive behavioural assessment in many dogs (see Chapter
10). The eyes should be assessed for evidence of Horner’s
syndrome, which can be caused by a lesion affecting the
caudal part of the brachial plexus (T1–T3 nerve roots).
The C8 and T1 nerve roots supplying the lateral thoracic
nerve can also be affected in these cases, leading to ipsi-
lateral loss of the cutaneous trunci (panniculus) reflex.
Any paresis should be characterized as UMN or
LMN in origin where possible. Most neurological
lesions causing monoparesis or lameness affect spinal
nerve roots or peripheral nerves rather than the CNS.
Therefore, any deficits tend to be LMN in nature. It
should be borne in mind that lateralized spinal cord
lesions (236) can also produce monoparesis, although in
most cases involvement of more than one limb can be
appreciated.
For the forelimbs, the triceps and extensor carpi
radialis reflexes are helpful for assessing the radial nerve
proximally and distally, respectively. These reflexes are  236 Ventrodorsal view of a thoraco-
often considered subjective tests, especially in small dogs. lumbar myelogram of a dog presented
Weakness in elbow flexion, suggesting a musculocuta- with right hindlimb paresis. An extra-
neous deficit, and weakness in carpal flexion, suggesting dural compressive lesion caused by
median nerve dysfunction, can be assessed using the neoplasia is identified at the level of L4
withdrawal reflex. (arrow).
For the hindlimbs, the femoral nerve can be assessed
using the patellar reflex or extensor tone of the quadri-
ceps. The sensory zone innervated by this nerve is the
medial aspect of the proximal limb. The cranial tibial
reflex is useful in assessing the peroneal nerve; the tibial
nerve can be tested using the gastrocnemius tendon
reflex. The withdrawal reflex is useful in assessing the
sensory function of different nerves as well as sciatic
motor function. This can be accompanied by a neuro-
genic atrophy and an altered stance (237). Obturator
nerve dysfunction leads to a failure to maintain adduction
of the limb on slippery surfaces, although this can be dif-
ficult to appreciate, as dogs and cats can adapt their gait
surprisingly well to accommodate for obturator deficits.  237 Sciatic nerve dysfunction causing
Although not a cause of paresis or lameness, pudendal plantigrade stance and loss of muscle
nerve dysfunction can be tested with the anal reflex and mass in the proximal limb.
by assessment of perineal sensation.
 M O N O PA R E S I S AND NEUROLO GICAL CAUSES OF LAMENESS 307

DIAGNOSTIC TESTS Ultrasonography

• May allow identification of brachial plexus tumours
Once the anatomical source of a particular problem and subsequent investigation with fine-needle
has been established, further investigations can be con- aspiration.
sidered. It is important that any abnormalities are inter-
preted in the light of the original history and clinical Electrophysiological studies
examination; it is common to identify multiple abnor- • EMG is helpful in some cases to support neurologi-
malities on diagnostic tests, many of which may not be cal involvement, particularly in cases of occult
clinically significant. lameness where an orthopaedic cause cannot be
identified.
Plain radiographs • Spontaneous electrical activity often develops in
• Orthogonal radiographs are useful to assess denervated muscles 7–10 days after the nerve injury
vertebral structures and disc spaces. has occurred.
• Oblique projections of the spine can be useful to • EMG alone does not differentiate primary
identify foraminal disc extrusions. This is especially muscular disease from peripheral nerve disease.
true for the cervical spine if extruded material is • Nerve conduction studies can be used to assess
mineralized. specific spinal nerves. F-waves and cord dorsum
• Occasionally, neoplastic lesions can cause potentials can give information on ventral and
enlargement of the intervertebral foramen due to dorsal nerve roots, respectively.
pressure atrophy of the bone.
• Thoracic radiographs are useful as part of tumour CSF analysis
staging. • Useful to exclude inflammatory CNS disease.
• Collection distal to the site of the suspected lesion
Myelography is more likely to reveal any significant changes.
• Useful to assess spinal cord morphology, but is • Nerve root compression may result in increased
frequently unhelpful for identifying foraminal CSF protein levels.
stenosis or nerve root or peripheral nerve • CSF PCR and evaluation of antibody titres can be
lesions (236). useful to assess for specific conditions such as
neosporosis or toxoplasmosis.
Computed tomography
• Can be helpful to assess the spinal cord or identify Histopathology
mineralized disc extrusions. • Can be used to make a definitive diagnosis of a
• Especially useful for assessing spinal cord lesion.
compression when combined with myelography. • Biopsies should be guided by the results of previous
Transverse views help to evaluate foraminal imaging studies.
stenosis. • Biopsy of neural tissue must be considered carefully
• Resolution is generally not good enough to assess with respect to the potential iatrogenic morbidity.
peripheral nerves unless they are enlarged due to
neoplasia or are associated with osseous lysis. Synovial fluid analysis
• Useful to exclude inflammatory arthritis.
Magnetic resonance imaging • Can also help support a diagnosis of osteoarthritis,
• Imaging modality of choice for spinal cord, nerve although results should be interpreted with caution
root, plexus and peripheral nerve lesions. since this is frequently an incidental condition.
 308 DECISION MAKING

COMMON ACUTE/SUBACUTE CAUSES

OF FORELIMB MONOPARESIS

Brachial plexus avulsion

Overview
Brachial plexus avulsion is the most common traumatic
peripheral neuropathy in the dog. It results from forced
abduction of the forelimb and subsequent stretching or
tearing of nerve roots, often following a road traffic acci-
dent or a fall. The condition may affect the cranial (C6/7)
or caudal (C8/T1) nerve roots in isolation or can involve
the entire brachial plexus. It is more commonly unilateral
than bilateral. Three types of lesion can be distinguished
depending on the degree of nerve damage:
• Neurapraxia is a transient, physiological failure of  238 Carpal flexion in a dog secondary to a caudal
nerve transmission in the absence of structural brachial plexus avulsion.
damage.
• Axonotmesis is disruption of the axons, with the
endoneurial and Schwann cell myelin sheaths
remaining intact. Complete avulsion of all plexus roots (C6–T2 nerve
• Neurotmesis is complete severance of all structures roots) causes a flaccid limb with an inability to bear
of the nerve (axons, Schwann cells and supporting weight and loss of cutaneous sensation in the entire limb.
connective tissue). Ipsilateral Horner’s syndrome and/or loss of the cuta-
neous trunci reflex is often seen if the caudal brachial
Damage most often occurs at the level of the spinal plexus is affected.
nerve roots where resistance to stretch is less than in
peripheral nerves owing to the lack of perineurium. Diagnosis
Diagnosis can be primarily based on historical and
Clinical presentation clinical findings. EMG helps to document the extent of
Clinical signs vary depending on which peripheral nerves muscle denervation and confirms the distribution of
are involved and the severity of the injury. They relate to nerve injury, although changes may not be seen for
LMN paresis with or without associated cutaneous 7–10 days after the injury. CT evaluation would assist in
sensory loss. Avulsion of the cranial plexus roots (C6/C7 ruling out associated traumatic vertebral lesions. MRI
nerve roots) results in a loss of shoulder movement and may help rule out other causes if a traumatic aetiology
elbow flexion, although the animal can still bear weight cannot be confirmed, and it can identify nerve root
on the limb as elbow extension is spared. Cutaneous sen- abnormalities secondary to trauma.
sation may be lost over the craniomedial aspect of the
antebrachium. Management
Avulsion of the caudal plexus roots (C8–T2 nerve Treatment is usually conservative and relies mainly on
roots) results in carriage of the limb with the elbow and aggressive physiotherapy. Patients should be monitored
shoulder flexed. The animal cannot bear weight because for complications such as self-mutilation, excoriation of
of triceps brachii muscle paralysis. The elbow is dropped the digits, trophic ulcers and muscle contractures.
and the carpus knuckled (238). Cutaneous sensation may Gabapentin (10–20 mg/kg PO q8–12h) can be
be lost distal to the elbow and over the caudolateral considered to control neuropathic pain if self-mutilation
aspect of the antebrachium. is seen.
 M O N O PA R E S I S AND NEUROLO GICAL CAUSES OF LAMENESS 309

Tendon transposition procedures can be considered

to restore elbow or carpal function. Careful case selection
is essential and any muscle to be transposed should
have its function assessed using electrophysiology
prior to surgery. Pancarpal arthrodesis, to prevent carpal
collapse secondary to loss of radial nerve function, is
rarely appropriate since in most cases elbow function is
also absent. Amputation should be considered in more
severely affected cases or if complications develop. As
this is a ‘salvage’ procedure, it is prudent in most cases
to wait 2–3 months after the injury before such a decision
is made.
The prognosis depends on the extent of the avulsion.
Nerve transection has a poor prognosis, whereas dogs
suffering neurapraxia can recover. Clinically poor prog-  239 Intraoperative image of a forelimb amputation
nostic indicators include evidence of a caudal or com- demonstrating grossly thickened spinal nerves secondary
plete avulsion, loss of nociception and no evidence of a to proximal extension of a peripheral nerve sheath tumour
return of function within 1–2 months. The outcome is (arrows).
often acceptable for animals with cranial avulsions that
are able to bear weight and maintain sensation over the
distal part of the limb. Serial evaluation of radial motor
nerve conduction velocity may be a useful prognostic
indicator. Early decreased conduction velocity is associ-
ated with a poor outcome.

Peripheral nerve sheath tumours

Overview
Peripheral nerve sheath tumours arise from cells sur-
rounding the axons in peripheral nerves or nerve
roots and are frequently malignant. Tumours spread
proximally towards the spinal cord (239). They usually
present with severe, progressive lameness, marked
muscle atrophy and pain. They rarely present with acute
monoparesis (240). Neurological deficits are seen late in
the clinical course, if at all. Deep palpation of the axilla
can allow identification of a mass in some cases. Electro-  240 Right forelimb proprioceptive deficits in a dog
physiological studies, and in particular EMG, can be sup- with a peripheral nerve sheath tumour.
portive of neural involvement, but may be unremarkable
early in the disease.
310 DECISION MAKING

a b

 241 MR images showing a peripheral nerve sheath tumour (arrows): T2-weighted (a); post contrast
T1-weighted (b).

Diagnosis Clinical presentation

Diagnosis is usually confirmed with MRI (241). Ultra- The elbow is ‘dropped’ and the animal walks with the
sound can help to identify more peripherally located carpus and digits knuckled over. Elbow function may be
lesions (e.g. axilla) and may allow fine-needle aspiration preserved with injury located distal to the branches that
of the lesion. supply the triceps muscle. Clinical signs in these cases
include knuckling of the paw, carpal collapse and loss of
Management cutaneous sensation in the cranial aspect of the limb
Local excision is usually unrewarding due to postopera- distal to the injury.
tive brachial plexus dysfunction and tumour recurrence.
Forelimb amputation with proximal excision of nerve Diagnosis
roots is the treatment of choice in many cases. This can Diagnosis is usually made on clinical grounds.
be combined with a hemilaminectomy, durotomy and
rhizotomy if there is evidence of spinal nerve and/or Management
nerve root involvement. Appropriate treatment of any orthopaedic injuries
The prognosis is guarded as invasion of the spinal should be carried out. Treatment of the neurological
cord often occurs prior to diagnosis. Recurrences are injury is conservative in most cases and based on aggres-
common following resection of peripherally located sive physiotherapy to preserve joint motion and delay
tumours and in one report the average time to recurrence muscle atrophy. If nerve dysfunction is persistent, and
was 5 months. triceps function is retained, tendon transposition proced-
ures or carpal arthrodesis can be considered.
Radial nerve injury The prognosis for distal lesions depends on the sever-
Overview ity of the neural injury. Neurapraxia is more common
Proximal injury to the radial nerve is usually associated and most cases recover within 1–2 months. Neurotmesis
with fractures of the first rib and leads to loss of elbow, leads to complete loss of cutaneous sensation over the
carpal and digital extension. Distal injury is often caused cranial antebrachium and foot and carries a poor
by humeral fractures. prognosis.
 M O N O PA R E S I S AND NEUROLO GICAL CAUSES OF LAMENESS 311

Foraminal stenosis Surgery may be required for more severe cases or

Overview those refractory to conservative management. Direct
Pressure on neural structures within intervertebral decompression (via dorsal laminectomy plus facetectomy
foramina can lead to lameness or paresis. Causes of or foraminotomy) or indirect decompression via verte-
foraminal stenosis include: bral distraction–fusion can be considered.
• Lateralized disc extrusion or protrusion. Many cases respond well to conservative therapy.
• Juxtafacet cysts. Neoplasia carries a poor prognosis.
• Joint capsule hypertrophy of articular facets.
• Benign new bone formation around the margins of Brachial plexus neuritis
the foramen. Overview
• Discospondylitis. Brachial plexus neuritis is a rare, usually bilateral, sym-
• Any neoplasm causing relative stenosis of the inter- metrical condition. It is thought to be immune mediated
vertebral foramen. and has been occasionally associated with modified live
rabies vaccination, Mycobacterium infection in cats or
Clinical presentation eating horse meat. The condition may be part of a more
Animals may be presented with acute or chronic history. diffuse polyneuropathy.
Clinical features may include: pain on manipulation of
the neck; LMN paresis localizing to one or more Clinical presentation
nerves; sensory signs such as conscious proprioceptive Clinical signs are usually very acute and LMN in nature,
deficits and areas of cutaneous hypoaesthesia or leading to flaccid paralysis. A less severe form has been
analgesia; and/or ‘nerve root signature’ manifested as reported with clinical features including a shifting fore-
pain on manipulation of the limb, lameness or non- limb lameness.
weight bearing on the affected limb.
Diagnosis
Diagnosis A presumptive diagnosis is based on MRI findings.
Diagnosis often requires advanced imaging modalities to Brachial plexus neuritis can be difficult to distinguish
assess the intervertebral foramina and epidural spaces. from neoplasia and therefore histopathology is neces-
EMG may reveal spontaneous electrical activity in the sary for a definitive diagnosis. CSF changes may be seen
muscles innervated by the affected nerve; however, this is in some cases (elevated protein and pleocytosis). Electro-
non-specific. physiology can confirm axonal dysfunction.

Management Management
Conservative treatment is successful in mild cases. Milder cases may respond to corticosteroid treatment at
This consists mostly of strict rest for 4 weeks and decreasing doses. The prognosis is poor.
anti-inflammatory drugs (steroidal or non-steroidal)
to help alleviate signs of radicular pain. Other pain man-
agement modalities include acupuncture, gabapentin
(10–20 mg/kg PO q8–12h) and muscle relaxants such as
methocarbamol (20–45 mg/kg PO q8–12h).
312 DECISION MAKING

Lymphoma Spinal cord lesions

Overview Overview
Lymphoma has been reported to affect the brachial Rarely, spinal cord conditions can appear predominantly
plexus and is most commonly seen in cats (242). It can be to affect one forelimb. Spinal cord lesions usually cause
unilateral or bilateral and is usually chronic in onset. paresis. Lameness is usually due to concurrent foraminal
nerve compression. Neurological examination will often
Diagnosis reveal clinical signs involving more than one limb,
Diagnosis is based on MRI and fine-needle aspirate although these signs can be subtle. Differential diagnoses
cytology ± CSF analysis (243). include disc extrusion or protrusion (compressive),
traumatic (minimally compressive) disc herniation,
Management ischaemic myelopathy, syringomyelia, inflammatory
The prognosis is poor, as most cases fail to respond to CNS disease and spinal cord neoplasia.
chemotherapy.
COMMON ACUTE/SUBACUTE CAUSES
OF HINDLIMB MONOPARESIS

Spinal cord and cauda equina lesions

Overview
As with the cervical spine, thoracolumbar spinal cord
lesions can appear to affect predominantly one limb.
This is more common with vascular disorders such as
ischaemic myelopathy.

Clinical presentation
Clinical signs include paresis or lameness associated with
individual nerves. Cauda equina lesions may affect other
regional nerves, leading to associated signs such as tail
paresis, loss of perineal sensation and urinary and/or
faecal incontinence. Lesions at T3–L3 tend to produce

 242 Right forelimb proprioceptive deficits in a cat

with lymphoma affecting the brachial plexus.

 243 Cerebrospinal fluid cytology demonstrating a

homogeneous lymphocytic pleocytosis characteristic of
lymphoma.
 M O N O PA R E S I S AND NEUROLO GICAL CAUSES OF LAMENESS 313

Sciatic nerve injury

Overview
Sciatic nerve injury can be associated with trauma
(femoral or pelvic fracture), impingement from a femoral
intramedullary pin, entrapment by a suture following
perineal herniorrhaphy, intramuscular injections in the
caudal thigh and, less commonly, with neoplasia. It can
also be seen following total hip replacement or acetabu-
lar fracture stabilization. These are usually neurapraxic
injuries as a result of surgical retraction or thermal
damage from bone cement.

 244 Right pelvic nerve root signature in a dog Clinical presentation

with degenerative lumbosacral stenosis. Foraminal Affected animals may present with lameness or LMN
compression of the L7 spinal nerve was identified using paresis. Lesions at, or proximal to, the lumbosacral trunk
MRI and confirmed at surgery. lead to complete loss of sciatic function. Affected animals
are unable to extend the hip, flex the stifle or flex or
extend the tarsus. Sensation is absent over digits 3, 4
UMN paresis and GP ataxia; those at L4–S2 produce and 5. Proprioceptive deficits are marked and the with-
LMN paresis. Differential diagnoses are similar to those drawal reflex is weak or absent.
of cervical spinal lesions. In addition, lumbosacral disco- With lesions distal to the greater sciatic notch, gluteal
spondylitis can cause paresis/lameness of one hindlimb. function is preserved. Animals can extend their hip,
although this can be difficult to appreciate clinically. For
Foraminal stenosis lesions distal to the greater trochanter, hamstring muscle
Overview function is maintained (biceps femoris, semimembra-
Foraminal compression of nerves forming the lumbo- nosus, semitendinosus). Affected animals can flex the
sacral plexus (essentially femoral and sciatic nerve stifle, but the limb distal to the stifle is paralysed.
contributors) can cause paresis or lameness. In animals with fractures, segmental spinal reflexes
can be difficult to assess. Cutaneous sensory testing can
Clinical presentation give an indication of neurological damage.
Clinical signs relate to the specific nerve roots or spinal
nerves involved. Lesions affecting L4–L6 tend to cause Management
femoral nerve deficits; those at L7–S2 tend to cause If a neuropathy is due to impingement from an
sciatic deficits. The L7/S1 intervertebral foramen is the intramedullary pin, retrieval of the pin often leads to clin-
most commonly affected site, often associated with ical improvement; additional fracture stabilization may
degenerative lumbosacral stenosis (244). Differential be required. Following pelvic trauma, standard treat-
diagnoses are the same as for cervical foraminal stenosis. ment of fractures should be performed, but owners
should be made aware that the prognosis may be less
Management favourable. Neurapraxia as a result of trauma will often
Conservative treatment is reserved for mild cases and resolve over 1–2 months; distal limb sensation is usually
consists of the same modalities as described for cervical intact at presentation in these cases. Subsequent to an
foraminal stenosis. Surgical decompression via hemi- injection-associated injury, the prognosis for complete
laminectomy (+/- facetectomy or foraminotomy) may be recovery may be guarded, but it depends on the degree of
necessary for more severe cases. Treatment by lumbo- underlying pathology.
sacral fusion or distraction–fusion has also been suggest-
ed in dynamic lesions of these lumbosacral vertebrae.
314 DECISION MAKING

Regardless of the cause of the injury, extensive Tibial nerve injury

physiotherapy is necessary to assist with the maintenance Overview
of muscle mass and tone. The prognosis depends on the Tibial nerve injury is less common than peroneal nerve
underlying cause and the severity of the nerve injury. injury. It can be associated with trauma and intramuscu-
Loss of nociception in the digits innervated by the sciatic lar injections.
nerve indicates a poor prognosis. Failure to recover
sensory or motor function after 3 months is associated Clinical presentation
with a poor prognosis. Limb amputation may be Clinical features include loss of tarsal extension, loss of
required. sensation on the plantar aspect of the paw and proprio-
ceptive deficits. Trophic ulceration of the plantar aspect
Peroneal nerve injury of the paw may be observed. Differential diagnoses
Overview include Achilles tendon rupture and subtalar tarsal
Peroneal nerve injury can be associated with trauma, hyperextension.
following surgery on the lateral aspect of the stifle or
following inadvertent intraneural injection. Diagnosis
Diagnosis is usually made on clinical grounds. Electro-
Clinical presentation physiology can be useful in some cases to determine the
Clinical features include weak hock flexion and decreased presence of neurological abnormalities and to further
sensation on the dorsal aspect of the paw. Proprioceptive map out the extent of denervation.
deficits are often apparent.
Management
Diagnosis Most cases are managed conservatively initially. Pan-
Electrophysiological studies can be helpful after 7–10 tarsal arthrodesis may be helpful in cases that fail to
days to confirm neurological involvement and map out improve. Complications due to trophic ulceration are
the area of denervation. not uncommon and may necessitate limb amputation.
The use of orthotic devices to support the tarsus has been
Management described (245).
Treatment is usually conservative. Peroneal deficits have Neuropathy secondary to intraneural injection is
been seen following inappropriate placement of fabello- associated with a poor prognosis. The outlook following
tibial sutures in the management of cranial cruciate liga- trauma is more variable.
ment deficiency, and treatment in such cases involves
removal of the offending suture. Femoral nerve injury
The prognosis is variable depending on the under- Overview
lying cause. Neoplasia and injuries due to inappropriate Femoral nerve injuries are less common than sciatic
intramuscular injections are associated with a poor nerve injuries, as the nerve is well protected within the
prognosis. Neurapraxia is more common following sublumbar musculature. Femoral nerve injury can be
trauma or entrapment from a suture and carries a better associated with trauma, iliopsoas myopathies, retroperi-
outlook. toneal abscess, haematoma and neoplasia. Neurapraxia
may be seen secondary to positioning of a dog in ventral
recumbency with the hips extended as for perineal
herniorrhaphy.
 M O N O PA R E S I S AND NEUROLO GICAL CAUSES OF LAMENESS 315

a Clinical presentation
Clinical features include monoparesis with severe gait
abnormality. The patient cannot bear weight on the
affected limb and carries it flexed. Stifle extension and
patellar reflexes are lost. Neurogenic atrophy of the
quadriceps muscle rapidly develops and cutaneous sensa-
tion to the medial aspect of the limb and medial digit may
be lost.

Diagnosis
Electrophysiological studies can be useful to confirm
b neurological involvement and determine which muscles
and nerves are affected. MRI can be useful to diag-
nose neoplastic lesions, retroperitoneal abscesses or
haematomas.

Management
Treatment is mainly supportive and consists of physio-
therapy as well as measures to protect the foot from
injury. Exploratory surgery to evaluate the nerve damage
visually and perform neurorrhaphy (anastomosis) or
neurolysis (debriding inflammatory adhesions) can be
attempted in cases of severe nerve damage.
The prognosis is guarded, but depends on the
 245 Tibial nerve deficits following inappropriate severity and level of the injury with neurapraxic lesions.
intramuscular injection into the hamstring muscle group. Lesions closest to the muscle innervated have a more
Conscious proprioceptive deficits are evident (a) and the favourable prognosis. If no improvement is seen within
dog is unable to bear weight on the tarsus. The tarsus and 6 months, recovery is unlikely and amputation of the
paw are maintained in a weight-bearing position using an affected limb should be considered.
orthotic device (b).
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PART 3

SPECIFIC EMERGENCIES 317

CHAPTER 17 Cerebrovascular accidents

CHAPTER 18 Ischaemic myelopathy

CHAPTER 19 Infectious and inflammatory diseases of the CNS

CHAPTER 20 Head trauma

CHAPTER 21 Spinal trauma

CHAPTER 22 Acute disc disease

CHAPTER 23 Status epilepticus

CHAPTER 24 Myasthenia gravis

CHAPTER 25 Tetanus and botulism

CHAPTER 26 Intracranial neoplasia and secondary pathological effects

CHAPTER 27 Metabolic encephalopathies

CHAPTER 28 Neurological toxicities

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 SPECIFIC EMERGENCIES Chapter 17

CEREBROVASCULAR ACCIDENTS
319

Laurent Garosi

INTRODUCTION AETIOLOGY AND PATHOPHYSIOLOGY

Cerebrovascular diseases are the underlying cause Ischaemic stroke

of cerebrovascular accidents (CVAs). Pathological Ischaemic strokes have been reported infrequently in the
processes that may result in cerebrovascular disease veterinary medical literature when compared with the
include the following: human medical literature. Most reports have been based
• Occlusion of the lumen by a thrombus or embolus. on postmortem results in dogs that died or were eutha-
• Rupture of a blood vessel wall. nized because of the severity of the ischaemic stroke
• A lesion or altered permeability of the vessel wall. and/or the suspected underlying cause of the stroke. This
• Increased blood viscosity. may affect the putative prevalence and type of underlying
causes, as it is likely that only the most severely affected
CVA, also known as stroke, is the most common clinical dogs, or dogs in which infarction occurred secondary to
presentation of cerebrovascular disease. CVA is defined a disease with a poor prognosis, would die or be eutha-
as a sudden onset of non-convulsive and non-progressive nized. Suspected underlying causes identified in histo-
focal brain signs secondary to cerebrovascular disease. By pathologically confirmed cases include:
convention, these signs must remain for more than • Septic thromboemboli associated with bacterial
24 hours to qualify for the diagnosis of CVA, which is endocarditis or other sources of infection.
usually associated with permanent damage to the brain. If • Atherosclerosis associated with primary
the clinical signs resolve within 24 hours, the episode is hypothyroidism and Miniature Schnauzers with
called a transient ischaemic attack (TIA). hypertriglyceridaemia.
CVAs are caused by an abrupt disruption of blood • Aberrant parasite migration (Cuterebra spp.) or
flow to the brain due to blockage of an artery, thus parasitic emboli (Dirofilaria immitis).
depriving brain tissue of oxygen and glucose (ischaemic • Embolic metastatic tumour cells.
stroke), or to rupture of a blood vessel, which results in • Intravascular lymphoma.
haemorrhage into or around the brain (haemorrhagic • Fibrocartilaginous embolism.
stroke). • Aortic or cardiac embolism.
Ischaemic strokes result from occlusion of cerebral
blood vessels by a thrombus or embolism. Haemorrhagic
strokes result from rupture of blood vessel walls within
the brain parenchyma or subarachnoid space.
 320 SPECIFIC EMERGENCIES

 246 Lacunar infarct results from obstruction of a small  247 Territorial infarct results from obstruction of a
superficial or deep perforating artery. major artery of the brain or one of its branches.

In the author’s MRI-based imaging study of dogs with a

brain infarct, a concurrent medical condition was
detected in just over 50% of dogs. The most commonly
encountered conditions were:
• Hyperadrenocorticism.
• Chronic kidney disease.
• Hypothyroidism.
• Hypertension.

Chronic kidney disease and hyperadrenocorticism were

the most commonly suspected underlying causes for the
hypertension. No underlying cause could be identified
antemortem in nearly half of the dogs; this type of infarct
of unknown origin is referred to in humans as crypto-
genic. No age, sex or breed predisposition has been  248 Severe stenosis of the middle cerebral artery
identified, but Cavalier King Charles Spaniels and secondary to an atheromatous plaque in a dog with severe
Greyhounds appear to be overrepresented. hypothyroidism. (Photo courtesy Kaspar Matiasek)
Reports of ischaemic strokes in cat are scarce. The
term feline ischaemic encephalopathy has been used to
describe cases of peracute onset of clinical signs consist-
ent with a unilateral cerebral or brainstem problem
caused by ischaemia. Although the cause remains
unknown in most cases, some of them have been linked
to Cuterebra spp. migration. It is believed that the
migrating parasite, or the host response to it, leads to
vasospasm in the cerebral vasculature (typically middle
cerebral artery).
 C E R E B R O VA S C U L A R A C C I D E N T S 321

With limited stores, the brain relies on a permanent Penumbra

supply of glucose and oxygen to maintain ionic pump Core
function. When perfusion pressure falls to critical levels,
ischaemia develops, progressing to infarction if it persists
long enough and/or it is severe enough. An infarct is an
area of compromised brain parenchyma caused by a focal
occlusion of one or more blood vessels. It may be due
either to vascular obstruction that develops within the
occluded vessels (thrombosis) or to obstructive material
that originates from another vascular bed and travels to
the brain (thromboembolism). Depending on the size of
vessel involved, infarcts can be seen as being the conse-
quence of small vessel disease (i.e. superficial or deep
perforating arteries), which gives rise to a lacunar infarct
(246), or of large vessel disease (i.e. a major artery of the
brain or its main branches), which gives rise to a terri-  249 In contrast to the core, where ischaemia is severe
torial infarct (247, 248). and infarction develops rapidly, areas surrounding the core
Two distinct regions of an infarct can be distin- (called the penumbra) show a more moderate decrease in
guished: the core, where ischaemia is severe and infarc- cerebral blood flow and can tolerate longer durations of
tion develops rapidly, and the penumbra surrounding the ischaemic stress. In the penumbra neurons are still viable,
core, which shows a more moderate decrease of cerebral but at risk of becoming irreversibly injured.
blood flow (CBF) and allows longer durations of
ischaemic stress to be tolerated (249). The relative
volume of these two pathological regions changes as the
infarct evolves. The factors causing evolution of the
penumbra to irreversible injury are multiple and
complex. The time window during which the penumbra
is no longer viable depends on the degree of blood flow
reduction, the region of the brain involved and the indi-
vidual. In the penumbra, neurons are still viable, but are
at risk of becoming irreversibly injured. Tissue within the Haemorrhagic stroke
penumbra has the potential for recovery and therefore is In contrast to the high incidence in man, intracerebral
the target for interventional therapy in cases of acute haemorrhage resulting from spontaneous rupture of
ischaemic stroke. At the cellular level, the ischaemic vessels is considered rare in dogs. Secondary haemor-
neuron becomes depolarized as ATP is depleted and the rhage has been reported in dogs in association with:
Na+/K+ ATP pump, along with other ionic membrane • Rupture of congenital vascular abnormalities.
pumps, fails leading to loss of fluid–electrolyte home- • Primary and secondary brain tumours.
ostasis. This leads to loss of ionic gradients and a net • Inflammatory disease of the arteries and veins
translocation of water from the extracellular to the intra- (vasculitis).
cellular compartment, causing cells to begin swelling • Intravascular lymphoma.
(cytotoxic oedema). Over time, the ischaemic cascade • Brain infarction (haemorrhagic infarction).
progresses, with cell lysis, increased macrophage activity • Impaired coagulation.
and disruption of the blood–brain barrier leading to the
development of vasogenic oedema. This type of oedema Non-traumatic subarachnoid haemorrhage has been
typically takes between 4–6 hours to develop once blood reported in dogs, but remains very rare when compared
flow decreases to critical ischaemic levels and may con- with its occurrence in man, where aneurysmal rupture is
tinue to progress over 24–48 hours. the most common underlying cause.
322 SPECIFIC EMERGENCIES

 250 Intraparenchymal haematoma.  251 Subdural haematoma.

In haemorrhagic stroke, blood leaks directly into the CLINICAL PRESENTATION

brain, forming a haematoma within the brain paren-
chyma (250), or into the subarachnoid or subdural space Neurological signs seen in stroke patients are character-
(251), leading to physical disruption of the tissue and istically peracute or acute in onset and non-progressive
pressure on the surrounding brain. This alters CNS or regressive in their evolution. Initially, deficits observed
volume/ pressure relationships, with the possibility of are usually focal, often asymmetrical and ultimately
increasing ICP and decreasing CBF. As a haematoma related to the area of the brain involved.
develops, ICP may remain constant due to a system of In all forms of stroke (ischaemic or haemorrhagic)
compensation. Within the skull, a change in the volume the dominating feature is the temporal profile of
of one intracranial constituent (brain tissue, arterial neurological events. It is the abruptness with which the
blood, venous blood and CSF) will be balanced by a com- neurological deficits develop that is highly suggestive of
pensatory change in another. This is the basis of the a vascular disorder. This is then followed by an arrest and
Monro–Kellie doctrine (see Chapter 20), which explains then regression of the neurological deficit in all except
why some animals with large intracranial bleeds may fatal strokes. Worsening of oedema (associated with the
develop substantial increases in ICP at the time of herni- secondary injury phenomena) can result in progression
ation. Exhaustion of the compensating mechanisms for of neurological signs for a short period of 24–72 hours.
an intracranial space-occupying lesion results in further Intracranial haemorrhage can be an exception to this
increases in the volume of the haematoma, producing description, presenting with a more progressive onset
massive elevations in ICP. Due to mechanical autoregu- over a very short period of time. Clinical signs usually
lation, CBF remains constant even though CPP may vary regress after 24–72 hours. This is attributable to dimin-
between 40 and 120 mmHg. The normal autoregulation ution of the mass effect secondary to the haemorrhage
of CBF may be impaired following CVAs, causing blood and reorganization or oedema resorption.
flow to damaged regions to become directly dependent Neurological deficits usually refer to a focal anatom-
on systemic BP. Such animals may be unable to compen- ical diagnosis and depend on the neurolocalization of the
sate for reductions in MAP, causing decreased CPP in the vascular insult (telencephalon, thalamus, midbrain, pons,
presence of increased ICP. This emphasizes the import- medulla, cerebellum). Infarction of an individual brain
ance of maintaining systemic BP. In these circumstances, region is associated with specific clinical signs that reflect
systemic hypotension can result in inadequate perfusion the loss of function of that specific region. With haemor-
of the brain, which leads to cerebral ischaemic and sec- rhagic stroke, the total clinical picture is different, as the
ondary neuronal injury. haemorrhage usually involves the territory of more than
 C E R E B R O VA S C U L A R A C C I D E N T S 323

one artery and pressure effects cause secondary signs. DIAGNOSIS

Neurological signs are largely related to elevated ICP,
which gives rise to non-specific signs of forebrain, brain- Imaging studies of the brain (CT, conventional and func-
stem or cerebellar disturbance. tional MRI) are necessary to confirm stroke, define both
Fundus examination should be considered in all the vascular territory involved and the extent of the
animals and may reveal changes such as the presence lesion, as well as distinguish between ischaemic and
of tortuous vessels (suggestive of systemic hyperten- haemorrhagic disease. Imaging studies are also necessary
sion), haemorrhage (suggestive of coagulopathy or to rule out other causes of neurological deficit such as
systemic hypertension) or papilloedema (suggestive of tumour, head trauma and encephalitis.
elevated ICP).
Ischaemic stroke
DIFFERENTIAL DIAGNOSIS Computed tomography
CT images are frequently normal during the acute phase
Head trauma; decompensation from primary or meta- of ischaemia, therefore the diagnosis of ischaemic stroke
static brain tumour; infectious and non-infectious using CT relies on exclusion of the clinical mimics of
encephalitis; neurotoxicity. stroke. Early CT signs of ischaemia can be subtle and dif-
ficult to detect even by very experienced clinicians and
include parenchymal hypodensity, loss of grey-white
matter differentiation, subtle effacement of the cortical
sulci and local mass effect.
a
Conventional magnetic resonance imaging
Conventional MRI can be used to depict ischaemic
stroke within 12–24 hours of the onset and to distinguish
haemorrhagic lesions from infarction. T2-weighted and
FLAIR images are particularly useful for imaging
ischaemic stroke. They give a more anatomical image of
the brain and depict oedema, old infarcts, microangio-
pathic changes, tumours and other pathology. With
b these sequences, ischaemic infarction appears as a
hyperintense lesion. Differentiation of ischaemic
core from penumbral tissue is, however, not possible.
T2*-weighted (gradient echo) images are used to show
the presence of, or exclude, intracranial haemorrhage.
Although infarcts can sometimes be difficult to differen-
tiate from other pathological processes such as inflam-
matory diseases, they tend to have certain distinguishing
characteristics on conventional MR images (252–254).
The conformity of an infarct to a vascular territory is
an important element in the diagnosis and helps in
distinguishing these lesions from brain tumours, inflam-
mation and trauma. Ischaemia/infarcts are caused by
 252 Sagittal (a) and transverse T2-weighted (b) MR occlusion of a cerebral blood vessel. They therefore
images of the brain showing a cerebellar territorial infarct occur in and are limited to the region of the brain vascu-
(arrows) in the vascular territory of the rostral cerebellar larized by the affected vessel, with resultant borders
artery. The sharp demarcation, lack of mass effect and sharply demarcated from the surrounding normal brain
grey matter involvement are typical of an infarct. tissue and minimal to no mass effect.
 324 SPECIFIC EMERGENCIES

Infarcts are caused by blood perfusion failure and,

therefore, energy depletion. The consequence for the
cell is failure of the Na+/K+ pump and accumulation of
Na+ and water within the cell (i.e. cytotoxic oedema).
The MRI changes seen in ischaemic parenchyma rely
on an increase in tissue water content. Gradually, the
T2-weighted or FLAIR images (253) become more
hyperintense in the ischaemic region, particularly over
the first 24 hours (i.e. T2 prolongation, which produces
higher signal intensity in areas of increased tissue water
content).
MRI changes are best appreciated in the grey matter
and are well visualized in deep grey matter structures,
 253 Transverse T2-FLAIR MR image of the brain such as the thalamus and basal nuclei, due to their selec-
showing a telencephalic lacunar infarct in the vascular tive vulnerability to ischaemia. Contrast enhancement
territory of the striate arteries at the level of the caudate (associated with reperfusion) is not usually seen until at
nucleus (arrow). Compared with the standard T2- least 7–10 days.
weighted image, FLAIR images suppress the signal from
cerebrospinal fluid and may allow better visualization of a Functional magnetic resonance imaging
periventricular lesion, as seen in this dog. Functional MRI techniques have been developed for
the early diagnosis of stroke in, and follow-up stroke
treatment of, humans. These techniques include diffu-
a sion and perfusion imaging and magnetic resonance
angiography (MRA). Diffusion and perfusion MRI are
new techniques that monitor water transport in the
microenvironment at cellular or capillary level. They
provide complementary information about the patho-
physiological processes following cerebral ischaemia.
DWI is used commonly in humans to improve the
sensitivity and specificity for the diagnosis of acute
stroke, making it an ideal sequence for positive identifi-
cation of hyperacute stroke and excluding the clinical
mimics of stroke (254, 255). The temporal evolution of
the DWI signal also allows discrimination of acute versus
chronic lesions.
b

 254 Dorsal T2-weighted (a) and DW (b) MR images

of the brain of a dog with a territorial telencephalic infarct
in the vascular territory of the middle cerebral artery. DW
images allow earlier detection of infarction. The lesion on
this dog appears more extensive on the DW image
(b) (arrows) compared with the T2-weighted image (a).
Acute infarction results in water trapping within the cells
and causes reduced diffusion. This phenomenon of
decreased diffusion and cytotoxic oedema produces a
regional hyperintensity on DWI.
 C E R E B R O VA S C U L A R A C C I D E N T S 325

 255 Dorsal DW image (a) and apparent diffusion a

coefficient (ADC) map (b) of a dog with a cerebellar
territorial infarct. Hyperintense lesions within the
cerebellum by DWI may be attributable to restricted
diffusion or artefactual due to ‘T2 shine through’. To
differentiate between true restricted diffusion and ‘T2
shine through’, bright lesions on DWI should always be
confirmed with ADC maps, which exclusively measure
diffusion. The ADC map helps to remove the effect of
T2-weighted hyperintensity (associated with cytotoxic
oedema), which can contribute to DW hyperintensity.
The classic appearance of acute infarction is
hyperintensity on DWI and reduced ADC.
b

In addition to DWI, MR perfusion-weighted

imaging is employed to depict regions of hypoperfusion
in the brain and can document tissue ‘at risk’ (i.e.
penumbra) by comparing the results with the findings
on DWI.
In addition to its use for tissue evaluation, MRA can
non-invasively assess the intracranial vascular status of
stroke patients (256). Two techniques can be used: time
of flight MRA and contrast-enhanced MRA. One of the
main limitations of MRA is its lower resolution com-
pared with conventional angiography. This limitation
becomes progressively worse as the luminal size of the
vessels decreases. In humans, angiographic techniques
are especially used for screening of carotid artery
stenosis, vascular malformations (e.g. arteriovenous
malformation, venous angioma) and aneurysms. The
use of MRA in dogs has been described and may allow
identification of underlying vascular lesions in cases of
canine stroke.

256 Time-of-flight magnetic resonance angiography of

the carotid arteries.
326 SPECIFIC EMERGENCIES

 257 Transverse CT scan of the brain of a dog  258 Transverse CT scan of the brain of a dog with
with intraparenchymal haemorrhage (arrow) within the subdural haemorrhage at the level of the left occipital lobe
right parietal lobe. Acute haemorrhage is evident (arrow) secondary to Angiostrongylus vasorum infestation.
as hyperdensity on CT due to the hyperattenuation of
x-rays by the globin portion of haemoglobin.

 259 Transverse T2-weighted MR image of the brain  260 Transverse T2*-gradient echo MR image of the
of a dog with subdural haemorrhage (arrow). As the brain of a dog with intraparenchymal haemorrhage
haematoma ages, oxyhaemoglobin in blood breaks (arrow).
down sequentially into several paramagnetic products:
first deoxyhaemoglobin (1–3 days), followed by
methaemoglobin (3–14 days). These each have different
MR signal intensities. Compared with oxyhaemoglobin
and deoxyhaemoglobin, methaemoglobin appears as
hyperintense on T1-weighted images.
 C E R E B R O VA S C U L A R A C C I D E N T S 327

Haemorrhagic stroke proven to be the most accurate of all of the MR pulse

Computed tomography sequences, and more accurate than CT, in predicting the
CT is exquisitely sensitive for the detection of acute extent of haemorrhage on pathological examination in a
haemorrhage. Acute haemorrhage is evident as a hyper- dog model. Compared with other sequences, gradient
density on CT due to hyperattenuation of x-rays by the echo scans demonstrate readily detectable hypointensity
globin portion of blood (257, 258). The attenuation regardless of the time from ictus, the source and location
decreases until the haematoma is isodense at about of haemorrhage or the field strength (260). Due to the
1 month after the onset. The periphery of the haema- progressive centripetal increase in the deoxyhaemoglobin
toma contrast enhances from 6 days to 6 weeks after the concentration, the periphery of the haematoma is often
onset, due to revascularization. initially more hypointense on susceptibility-weighted
images than on T2-W images. Hypointensities on
Conventional magnetic resonance imaging gradient echo images are, however, not specific for
The MR signal intensity of intracranial haemorrhage is haemorrhage and may also be seen with calcification, air,
influenced by several intrinsic (time from ictus, source, iron, foreign bodies and melanin. However, air, calcifica-
size and location of haemorrhage) and extrinsic (pulse tion and often foreign bodies would also normally be
sequence and field strength) factors (259). The causes of hypointense on all the pulse sequences.
these variations in haematoma intensity are difficult to
evaluate with clinical studies since it is frequently impos- Cerebrospinal fluid analysis
sible to ascertain precisely the interval between haemor- CSF analysis is unlikely to confirm a diagnosis of CVA,
rhage and MR imaging. As the haematoma ages, but may help to rule out inflammatory CNS disease.
oxyhaemoglobin in blood sequentially breaks down into CSF is variable in dogs and cats with CVA. In most cases
several paramagnetic products: first deoxyhaemoglobin, it is either normal or reflects a mild mononuclear or
followed by methaemoglobin and, finally, haemosiderin. neutrophilic pleocytosis. CSF proteins are occasionally
The two most important biophysical properties in the elevated.
generation of MR signal intensity patterns seen in evolv-
ing intracranial haematomas are: (1) the paramagnetic IDENTIFICATION OF UNDERLYING
effects of iron associated with the changing oxygenation CAUSES OF STROKE
states of haemoglobin, and (2) the integrity of red blood
cell membranes that, when intact, compartmentalize the In the case of presumptive or confirmed ischaemic
paramagnetic iron. stroke, ancillary diagnostic tests should focus on evaluat-
The earliest possible detection of haemorrhage ing the animal for hypertension (and its potential under-
depends on the conversion of oxyhaemoglobin to deoxy- lying causes), endocrine disease (hyperadrenocorticism,
haemoglobin, which is believed to occur after the first hypothyroidism, hyperthyroidism, diabetes mellitus),
12–24 hours. In contrast to oxyhaemoglobin, where iron kidney disease (especially protein-losing nephropathy),
is shielded from surrounding water molecules, resulting heart disease and metastatic disease (261, next page).
in an MR signal similar to that of normal brain paren- Diagnostic tests in presumptive or confirmed cases of
chyma, the iron exposed to surrounding water molecules haemorrhagic stroke should focus on screening the
in the form of deoxyhaemoglobin creates a signal loss, animal for a coagulopathy or hypertension (and potential
making it easy to identify on T2-weighted and suscepti- underlying causes) as well as metastatic disease (particu-
bility-weighted sequences. Gradient echo sequences have larly haemangiosarcoma).
328 SPECIFIC EMERGENCIES

 261 Summary of the stepwise

approach to the diagnosis of stroke. STROKE
Is there suspicion of stroke?

Peracute/acute onset,
focal non-progressive and
non-convulsive brain signs

Confirmation of stroke?

• Imaging of the brain (MRI or CT)

Ischaemic stroke Haemorrhagic stroke
• CSF analysis

Test for underlying causes

of stroke

• Serial blood pressure measurements

• Complete blood count
• Serum biochemistry profile including
cholesterol and triglycerides • Serial blood pressure measurements
• Urinalysis • Complete blood count
• Urine protein/creatinine ratio • Serum biochemistry profile
• Serum antithrombin III activity • Buccal mucosa bleeding time
• D-dimers • Prothrombin time
• Thromboelastography • Activated partial thromboplastin
• Endocrine testing for hyperadreno- time
corticism, thyroid diseases and • Thoracic radiographs
pheochromocytoma • Abdominal ultrasound
• Thoracic radiographs
• Abdominal ultrasound
• Echocardiography and ECG

TREATMENT
of a recumbent dog will be vital to the success of more
Once the diagnosis of a stroke has been made (261), any specific therapies. Such management includes attention
potential underlying or associated disease should be to the prevention of decubital ulceration, aspiration
identified and treated. Generally, treatment of these pneumonia and urine scald, in addition to physical
patients aims to provide supportive care, maintain ade- therapy and enteral nutrition provision. More specific
quate tissue oxygenation and manage neurological and therapies are aimed at preventing further neurological
non-neurological complications. Nursing management deterioration.
 C E R E B R O VA S C U L A R A C C I D E N T S 329

Ischaemic stroke Monitoring and correction of basic

Most cases of ischaemic stroke recover within several physiological variables
weeks with only supportive care. Potential underlying Fortunately, the vast majority of ischaemic stroke
causes should be investigated and treated accordingly to patients have no major difficulty maintaining their
limit the risk of recurrence (262). airways, breathing efforts or circulatory competence
Treatment revolves around three principles: (1) mon- early in their clinical course. Some controversies exist
itoring and correction of basic physiological variables surrounding the management of hypertension in the
(e.g. oxygen level, fluid balance, BP, body temperature); setting of an ongoing acute ischaemic stroke. As well as
(2) inhibition of the biochemical and metabolic cascades being a potential risk factor, hypertension can occur as a
subsequent to ischaemia to prevent neuronal death (the physiological response to a stroke to ensure an adequate
concept of neuroprotection); and (3) restoration or CPP in the penumbra of the infarct for up to 72 hours
improvement of CBF by thrombolysis in the presence after onset. Maintenance of systemic arterial BP within
of a thrombus. The potentially salvageable portion of the the physiological range is essential, and aggressive lower-
ischaemic zone (ischaemic penumbra) is the presumed ing of BP should be avoided during the acute stages
therapeutic target for both thrombolytic and neuro- unless the patient is at a high risk of end-stage organ
protective stroke therapy. The time period during which damage (systolic BP remaining >180 mmHg). In such
injury may be reversible is called the therapeutic window. cases, hypertension can often be controlled with an ACE
It is estimated that this ‘window of opportunity’ is inhibitor such as enalapril (0.25–0.5 mg/kg q12h) or
approximately 6 hours before irreversible neurological benazepril (0.25–0.5 mg/kg q12h) and/or calcium
damage occurs. channel blockers such as amlodipine (0.1–0.25 mg/kg
q24h), which tend to be more effective.

 262 Summary of the treatment

approach to ischaemic stroke.
ISCHAEMIC STROKE
SBP = systemic blood pressure

Monitor vital parameters Investigate and treat potential

(airway, breathing, circulation) underlying causes

SBP >180 mmHg on serial blood

pressure evaluation and/or severe Proven cardiac or iliac
ocular manifestations of source of embolism
hypertension

Anti-hypertensive treatment: Low-dose aspirin

enalapril, benazepril, amlodipine or low-molecular-weight heparin
330 SPECIFIC EMERGENCIES

Neuroprotection Haemorrhagic stroke

There is no evidence that glucocorticoid treatment pro- The most important consideration in haemorrhagic
vides any beneficial neuroprotection in cases of stroke. stroke is maintenance of cerebral perfusion by treatment
Aside from the lack of proven benefit in veterinary stroke of hypotension and elevated ICP, as well as treating the
patients, the use of glucocorticoids may increase the risk underlying cause if one has been identified (263).
of gastrointestinal complications and infection. Treat- The medical management of dogs with intracranial
ment strategies for ischaemic stroke considered in man, haemorrhage commonly includes: (1) stabilization of the
utilizing other neuroprotective agents (N-methyl-D- patient (airway protection, monitoring and correction of
aspartate antagonists, Ca2+ channel blockers, sodium vital signs); (2) assessment and monitoring of the neuro-
channel modulators) or anti-platelet and thrombolytic logical status; (3) determination and treatment of
therapy, remain to be evaluated clinically in dogs. potential underlying causes of the haemorrhage; and
Although some of the neuroprotective agents have (4) assessment of the need for specific treatment meas-
resulted in a dramatic decrease in the size of stroke ures including management of raised ICP. The risk of
lesions in experimental animal models, these agents neurological deterioration and cardiovascular instability
either have failed to prove their efficacy in clinical is highest during the first 24 hours after the onset of an
trials or are awaiting further investigation. intracranial haemorrhage, as the space-occupying lesion
slowly expands and cerebral vasogenic oedema develops.
Thrombolytic therapy The initial approach to treatment of the animal with
At the time of writing, there are no definitive data in haemorrhagic stroke should focus on extracranial stabi-
humans or animals to confirm a significant improvement lization, closely followed by therapies directed towards
in clinical outcome in patients with acute ischaemic intracranial stabilization and treatment of the potential
stroke treated with unfractionated heparin as thrombo- underlying cause if one is identified. Careful monitoring
lytic therapy. Despite conflicting results regarding its is essential during the initial period and should include
efficacy, intravenous recombinant tissue plasminogen assessment of vital parameters as well as the neurological
activator is sometimes used in human stroke patients if status.
it can be given within the first 3 hours. This critical
time window makes the use of thrombolytic treatment Extracranial stabilization
unrealistic in veterinary neurology. Furthermore, this Extracranial stabilization involves careful monitoring of
type of treatment carries a significant risk of intracranial vital parameters (e.g. oxygen levels, fluid balance, BP,
haemorrhage following treatment. Anti-platelet therapy body temperature) and correction of any deviation from
with low-dose aspirin (0.5 mg/kg PO q24h) or clopido- normal. As with any other intracranial disease, hypoxia
grel (2–4 mg/kg PO q24h) can be used prophylactically should be avoided, but there is no evidence in humans to
to prevent clot formation in proven cardiac sources of an support the routine use of oxygen for the treatment of
embolus. haemorrhagic stroke, in the absence of hypoxia.
Hypoventilation may occur as a result of damage to
the respiratory centre in the brainstem following raised
ICP in the caudal fossa. The impaired respiratory drive
results in elevation in PaCO2 and resultant vasodilation,
which in turn aggravate intracranial hypertension.
PaCO2 should be maintained within a normal range and
not allowed to exceed 40 mm Hg. Immediate intubation
and ventilation should be considered if PaCO2 cannot be
maintained within an acceptable range.
The correction of tissue perfusion is an important
stabilizing therapy in any patient with haemorrhagic
stroke. The primary goal of fluid therapy is rapid
restoration of BP, such that CPP is maintained at
 C E R E B R O VA S C U L A R A C C I D E N T S 331

 263 Summary of the treatment

approach to haemorhagic stroke. HAEMORRHAGIC STROKE

Monitor vital parameters Intracranial stabilization Investigate and treat potential

(airway, breathing, circulation) (monitor neurological status) underlying causes

Imaging evidence of raised ICP

and/or deterioration in MGCS

PaO2 = oxygen arterial partial pressure

Mannitol 0.25–1.0 g/kg over PaCO2 = carbon dioxide arterial partial pressure
10–15 minutes SBP = systemic blood pressure
Hyperventilation to achieve PaCO2 ICP = intracranial pressure
of 30 mmHg
MGCS = modified Glasgow coma scale
Consider surgical evacuation
if subarachnoid location

SBP >180 mmHg on serial

blood pressure evaluation
PaO2 <80 mmHg PaCO2 >45 mmHg Hypovolaemia and/or severe ocular
manifestations of
hypertension

Anti-hypertensive treatment:
Hypertonic saline (7.5%)
Nasal or mask oxygenation Intubate + ventilate enalapril, benazepril,
or artificial colloids
amlodipine

>70 mm Hg. Hypovolaemia should be recognized and of 7.5% sodium chloride for volume expansion is
treated with volume expansion, preferably using artifi- 2–4 ml/kg (cats) and 4–6 ml/kg (dogs) given over
cial colloids or hypertonic saline (7.5%) to achieve 5–10 minutes. The use of glucose-containing solutions
rapid restoration of blood volume and pressure while is discouraged as hyperglycaemia has been shown to
limiting the volume of fluid administered. Hypertonic correlate with poor outcome in human stroke patients.
saline has many properties that may make it a superior As such, blood glucose levels should be monitored
rescucitation fluid for patients with intracranial disease from the time of presentation. Hypotonic fluid should
such as haemorrhagic stroke. The recommended dose also be avoided.
332 SPECIFIC EMERGENCIES

As with ischaemic stroke, attempts to lower and Cerebral blood volume is another intracranial com-
normalize BP should be reserved for animals at a high ponent that contributes to ICP. In a rapidly deteriorating
risk of end-stage organ damage (systolic BP remaining animal, hyperventilation can temporarily be used to
>180 mmHg) and/or animals with severe ocular manifes- reduce ICP. The aim of hyperventilation is to reduce
tations of hypertension such as retinal detachment or cerebral blood volume, and hence ICP, by causing a
intraocular haemorrhage. However, moderate levels of hypocapnic vasoconstriction. However, excessive hyper-
hypertension should not be treated, as systemic hyper- ventilation can be accompanied by a reduction in global
tension may be secondary to the intense reflex sympa- CBF, which may drop below ischaemic thresholds.
thetic response to intracranial hypertension, which is a Therefore, it is not a recommended therapy unless the
compensatory mechanism to maintain cerebral perfu- PaCO2 can be closely monitored with capnography or
sion. Treatment recommendations for lowering BP are arterial blood gas analysis.
detailed in the section on treatment of ischaemic stroke. Elimination of the space-occupying mass within the
cranial vault is the third method by which ICP reduction
Intracranial stabilization can be obtained. Surgical evacuation of the haematoma
Once initial assessment and extracranial stabilization can therefore be employed in dogs with large haema-
have occurred, medical intervention to address tomas (mostly subarachnoid) and a deteriorating neuro-
intracranial issues should be considered, with the main logical status.
focus being on decreasing ICP. Three principles can be
applied: (1) reducing cerebral oedema associated with PROGNOSIS
intracranial haemorrhage; (2) optimizing cerebral blood
volume; and (3) eliminating the space-occupying mass. The prognosis for ischaemic or haemorrhagic stroke
Osmotic diuretics, such as mannitol, are very useful depends overall on the initial severity of the neurological
for treating cerebral oedema and resultant intracranial deficit, the initial response to supportive care and the
hypertension associated with pathologies such as head severity of the underlying cause if one has been identi-
trauma, brain tumours and encephalitis. There is insub- fied. Fortunately, most cases of ischaemic stroke recover
stantial evidence to suggest that mannitol exacerbates within several weeks with only supportive care. In a
intracranial haemorrhage, therefore osmotic diuretics recent retrospective study of 33 dogs with MRI or
are routinely used in the control of ICP in human necropsy evidence of brain infarction, there was no
patients with known intracranial haemorrhage. Mannitol association between the region of the brain involved
therapy (0.25–2.0 g/kg IV over 10–20 minutes up to (telencephalic, thalamic/midbrain, cerebellum), the type
q4–8h) may be initiated to treat suspected elevated ICP of infarction (territorial or lacunar) and the outcome.
secondary to haemorrhagic stroke. Mannitol’s main However, dogs with a concurrent medical condition had
effect is to enhance CBF by reducing blood viscosity. It a significantly shorter survival time than those dogs with
should, however, be avoided in hypovolaemic patients. no identifiable medical condition. Dogs with a con-
current medical condition also were significantly more
likely to suffer from recurrent neurological signs due to
subsequent infarcts.
 SPECIFIC EMERGENCIES Chapter 18

ISCHAEMIC MYELOPATHY
333

Luisa De Risio

INTRODUCTION AETIOLOGY AND PATHOPHYSIOLOGY

Ischaemic myelopathy is a vascular disease of the spinal The intraparenchymal (intrinsic) spinal cord arteries are
cord caused by embolization or, less commonly, throm- functional end arteries and their occlusion leads to
bosis of spinal cord blood vessels. Vascular spasm can also ischaemia of the territory supplied. The arterial and
occur secondary to acute traumatic events (for further venous blood supply of the spinal cord is shown (264).
details see Chapter 21). The abrupt disruption of blood The most common cause of ischaemic necrosis of the
flow to an area of the spinal cord results in ischaemic spinal cord parenchyma is embolization of spinal arteries
necrosis and associated peracute (<6 hours) or acute or veins, or a combination of both, by fibrocartilaginous
(6–24 hours) neurological signs, with distribution and material. Arteriovenous anastomoses have been demon-
severity referable to the site and extent of the infarction. strated in the spinal cord vasculature and could explain
Fibrocartilaginous emboli are the most commonly the presence of emboli on either side of the circulation
documented cause of spinal blood vessel occlusion in regardless of whether the entry point is arterial or
histologically confirmed cases of ischaemic myelopathy. venous.
Hence this condition is called ‘fibrocartilaginous embol-
ism’ (FCE) or ‘fibrocartilaginous embolic myelopathy’
(FCEM).  264 The arterial and venous supply to the lumbar
spinal cord.

Dorsal spinal a. Dorsal spinal v.

Radial a. Dorsolateral v.
Dorsal radicular a. Dorsal radicular v.
Muscular branch Ventral radicular v.
Spinal branch Intervertebral v.

Ventral radicular a. Ventral spinal v.

Irregular arterial ring Ventrolateral v.
Lumbar a. Ventral internal
Central spinal a. venous plexus

Ventral spinal a. Basivertebral v.

Aorta Caudal vena cava

334 SPECIFIC EMERGENCIES

Histological and histochemical studies have shown • Neovascularization of the degenerated interverte-
that the embolized fibrocartilage has the same collagen bral disc. In man and non-chondrodystrophic dogs
type as that of the intervertebral disc nucleus pulposus. with disc degeneration, ingrowth of blood vessels
The fact that this type of embolism occurs primarily in within the degenerated annulus fibrosus has been
the spinal cord further supports the involvement of the documented. A sudden rise in intervertebral disc
nucleus pulposus as the source of the fibrocartilage. pressure exceeding arterial BP may result in
Additionally, it has been hypothesized that fibrocartilage penetration of nucleus pulposus fibrocartilage into
may arise from metaplasia of the vascular endothelium, the newly-formed intervertebral disc vessels (or into
which later ruptures into the lumen and embolizes within the embryonic remnant vessels) and progression
the spinal cord vessels. Vertebral growth plates may rep- into the intrinsic spinal cord vessels. The presence
resent the source of the fibrocartilage in immature dogs. of fibrocartilage within newly-formed blood vessels
Ischaemic myelopathy may also result from material in the degenerated intervertebral disc has been
other than fibrocartilage that obstructs the intrinsic reported in two dogs with histologically confirmed
spinal blood vessels, such as thrombi or bacterial, ischaemic myelopathy.
parasitic, neoplastic or fat emboli. Pre-existing medical
conditions (e.g. cardiomyopathy, hypothyroidism, hyper- The ischaemic injury caused by the arterial obstruction
thyroidism, hyperadrenocorticism, chronic renal failure, initiates a series of biochemical and metabolic events
hypertension) that may predispose to embolization or (similar to the secondary injury phenomenon described
thrombosis should be considered and investigated, par- in Chapter 21), which result in neuronal and glial cell
ticularly in cats. death. The grey matter, due to its greater metabolic
The pathophysiology of this condition is still unclear. demand, is affected more severely than the white matter.
Several hypotheses have been proposed to explain how
the fibrocartilaginous material, originating from the CLINICAL PRESENTATION
intervertebral disc nucleus pulposus, enters the vascular
system. These include: The typical clinical presentation is characterized by per-
• Direct penetration of nucleus pulposus fragments acute (<6 hours) onset of non-painful, non-progressive
into the spinal cord vessels or into the vertebral (after the first 24 hours) and often asymmetric myelo-
vessels. Extrusion of degenerated disc material into pathy (265).
the adjacent ventral internal vertebral venous plexus Ischaemic myelopathy has been reported commonly
has sometimes been observed during postmortem in dogs and sporadically in several other species including
examinations. Increased intrathoracic and intra- cats, humans, horses, pigs, turkeys, sheep, a calf, a tiger, a
abdominal pressure during coughing, straining, tayra and a pigtail macaque. Ischaemic myelopathy due to
exercise or trauma (Valsalva’s manoeuvre) could fibrocartilaginous embolization has been reported most
generate retrograde venous propulsion of the fibro- commonly in large breed dogs; however, this disorder has
cartilage into the spinal arteries. also been described in small breed dogs and, particularly,
• Mechanical herniation of nucleus pulposus into the in Miniature Schnauzers. Ischaemic myelopathy is,
vertebral bone marrow, with subsequent retrograde however, very rare in chondrodystrophic breeds. Either
entrance into the ventral internal vertebral venous gender can be affected, but a few studies on dogs have
plexus. documented a male to female ratio of about 2.5:1.
• Presence of embryonic remnant vessels within the Dogs and cats of any age can be affected. Ischaemic
nucleus pulposus (which is normally avascular in myelopathy has been confirmed histologically in young
adults). (8–13 weeks of age) Irish Wolfhounds of either gender
(but especially males). In the author’s MRI-based study
on 52 dogs the median age at diagnosis was 6 years
 I S C H A E M I C M Y E L O PAT H Y 335

Neurological deficits refer to the spinal cord seg-

ments involved (C1–C5, C6–T2, T3–L3 or L4–S3) and
are often asymmetric. Lateralization of signs is the result
of asymmetric branching of the intrinsic spinal cord
vasculature, particularly of the central branches of the
ventral spinal artery, and has been reported in 53–86% of
dogs. The most commonly affected spinal cord segments
have been reported to be L4–S3 (43–47%) and C6–T2
(30–33%) in dogs with a histologically confirmed diag-
nosis, and L4–S3 (44–50%) and T3–L3 (37–42%) in
dogs with a presumptive diagnosis. Some dogs with
ischaemic myelopathy affecting the T3–L3 spinal cord
segments and causing severe motor dysfunction have
been reported with decreased flexor withdrawal reflexes
in the hindlimbs in the acute stages of the disease. In the
author’s study, three (6%) paraplegic dogs with a T3–L3
 265 Spinal cord arteriole is obstructed with pale blue lesion on MRI had an interruption of the cutaneous
material consistent with fibrocartilaginous nucleus trunci reflex consistent with the site of the lesion on MRI,
pulposus (× 20). (Photo courtesy Victoria Watson) but also exhibited a decreased flexor withdrawal reflex in
the hindlimbs, a normal to increased patellar reflex,
normal perineal reflex and normal nociception. It has
(range, 3 months to 11 years and 11 months). The been suggested that the transient decrease of the hind-
median age reported in other studies on dogs with histo- limb flexor reflex in dogs with acute thoracolumbar
logically confirmed ischaemic myelopathy ranged from spinal cord injury is due to sudden interruption of
5–6 years. Age at onset of signs in cats with ischaemic descending supraspinal input on motor neurons and
myelopathy has been reported between 4 and 12 years interneurons, fusimotor depression and increased seg-
and the majority were Domestic Shorthair cats. mental inhibition. This phenomenon has important
In addition to the typical clinical presentation, some clinical implications, as it may lead to an erroneous
dogs can show spinal hyperaesthesia at the onset of neuroanatomical localization, site of diagnostic investi-
neurological signs and occasionally this can be identified gation and prognosis.
at clinical examination performed within 24 hours of Rarely, multiple ischaemic lesions within different
onset. Rarely, neurological dysfunction progresses for regions of the CNS have been reported following
48 hours due to worsening of spinal cord ischaemia, fibrocartilaginous embolization. Concurrent brainstem
oedema and malacia (associated with secondary injury and spinal cord fibrocartilaginous emboli have been
phenomenon). However, most commonly, maximal documented histologically in a sheep and a dog, and in
neurological deficits occur within the first 12–24 hours humans.
of disease and are followed by gradual improvement or
stabilization of signs depending on the extent and sever- DIFFERENTIAL DIAGNOSIS
ity of the ischaemic lesion. In the study of 52 dogs
mentioned above, onset of neurological signs was pera- Acute non-compressive nucleus pulposus extrusion;
cute or acute (<24 hours) in all dogs. Within the first intervertebral disc extrusion; intra-/extramedullary
24 hours after onset, according to the owners, neurolog- haemorrhage (coagulopathy, trauma); infectious and
ical signs were static in 34 dogs (65%) and progressive in non-infectious myelitis; intramedullary neoplasia.
18 dogs (35%).
336 SPECIFIC EMERGENCIES

a b

 266 (a) Mid-sagittal T2-weighted FSE image of C2–T1 vertebrae in an 8-year-old male neutered Staffordshire Bull
Terrier with acute-onset right-sided tetraparesis and Horner’s syndrome. The spinal cord overlying the C6 vertebral
body is swollen and has a focal intramedullary hyperintensity (arrow). (b) Transverse T2-weighted FSE image through
the intramedullary hyperintensity depicted in 266a. The focal and relatively sharply demarcated intramedullary
hyperintensity (arrow) involves predominantly the grey matter and is lateralized to the right.

DIAGNOSIS The MRI features suggestive of ischaemic myelo-

pathy include (266):
The antemortem diagnosis of ischaemic myelopathy • A focal, relatively sharply demarcated
is based on the typical clinical presentation (peracute/ intramedullary lesion (oedematous infarcted tissue),
acute non-progressive, non-painful, usually asymmetric predominantly involving the grey matter that
myelopathy), exclusion of other causes of peracute/acute appears:
myelopathy (by means of myelography, CT or MRI, and • Hyperintense to spinal cord grey matter on
CSF analysis) and visualization of a lesion compatible T2-weighted fast spin echo (FSE) and FLAIR
with spinal cord ischaemia on MRI. images and iso- or hypointense to spinal cord
grey matter on T1-weighted FSE images.
Magnetic resonance imaging • Sometimes, contrast enhances (usually mild and
MRI is the diagnostic imaging modality of choice to heterogeneous) as early as 48 hours after onset
attain an antemortem diagnosis of ischaemic myelo- of signs and becomes apparent by the fifth to
pathy. In addition to excluding other causes of myelopa- seventh day after onset of signs.
thy (similar to myelography and CT), it allows • MRI imaging performed within 24–48 hours
visualization of signal intensity changes suggestive of following onset of neurological signs may be
ischaemic infarction. normal.
 I S C H A E M I C M Y E L O PAT H Y 337

In the human literature it is widely accepted that conven- technically challenging because of the relatively small
tional MRI may not allow detection of the ischaemic size of the spinal cord, low spatial resolution and the
spinal cord lesion in the first 48 hours after onset of magnetic susceptibility to artefacts caused by vascular
neurological signs. Indeed, repeated MRI is commonly and CSF pulsation.
used in people with suspected ischaemic myelopathy. In MRI can help to differentiate between ischaemic
the author’s MRI-based study, 11 of 52 dogs imaged with myelopathy and acute non-compressive nucleus pulpo-
a 1.5 Tesla MRI scanner between 12 and 72 hours sus extrusion, whose clinical presentation can be very
(median, 12–24 hours) after onset of signs had normal similar. The MRI findings of acute non-compressive
MR images. In another study, ischaemic myelopathy was nucleus pulposus extrusion include (267):
confirmed histologically in dogs with normal MRI per- • Presence of a focal intramedullary hyperintensity
formed in the acute stages of the disease. The degree of overlying an intervertebral disc, with reduced
ischaemic insult, the size of the infarction and the avail- volume and signal intensity of the nucleus pulposus
ability of high-contrast resolution MRI influence the on T2-weighted FSE images.
ability to detect signal changes during the first 24–48 • Narrowed intervertebral disc space.
hours of ischaemic myelopathy. • Presence of extraneous material or signal change
DWI is used in humans to improve the sensitivity and within the epidural space dorsal to the affected
specificity of ischaemic myelopathy diagnosis in the disc, with absent or minimal spinal cord
acute phase of the disorder. However, in animals, DWI is compression.

 267 (a) Mid-sagittal T2-weighted FSE image of

a
T10–L1 vertebrae of a 3-year-old male neutered Lurcher
with acute-onset left hindlimb paresis while playing.
The nucleus pulposus of T11/T12 intervertebral disc (red
arrow) is smaller than the nucleus pulposus of adjacent
intervertebral discs. There is moderate ill-defined
intramedullary hyperintensity within the spinal cord
overlying the T11/T12 intervertebral disc space and
caudal half of T11 vertebral body (yellow arrow). (b)
b Transverse T2-weighted FSE image at the level of the
caudal end-plate of T11. The ill-defined intramedullary
hyperintensity is worse on the left side (red arrow).
Within the epidural space, dorsolaterally to the spinal
cord on the left side, there is focal disruption of the
epidural fat (yellow arrow) and presence of material
isointense to the intervertebral disc nucleus pulposus.
There is no spinal cord compression.
338 SPECIFIC EMERGENCIES

a b

Cerebrospinal fluid analysis  268 (a) Transverse section of the cervical spinal cord
CSF analysis may be normal or may reveal non-specific (C5) of an adult female mongrel dog. Note the bilaterally
abnormalities including xanthochromia, elevated protein asymmetric cavitation/malacia of spinal grey matter
concentration and mild pleocytosis. PCR for different (arrows). (b) Low-power field image of the cervical spinal
infectious agents in CSF may help to rule out specific cord transverse section showing focal disruption of the
aetiologies of meningomyelitis (e.g. canine distemper lateral and dorsolateral grey-white matter transition zone
virus, Toxoplasma gondii and Neospora caninum). and lateral fascicle (red arrows) next to an occluded
arterial blood vessel with a pink fibrocartilaginous
Myelography embolus (yellow arrow). PAS stain. (Photo courtesy
The main value of myelography in the diagnosis of Kaspar Matiasek)
ischaemic myelopathy is the exclusion of other causes of
peracute/acute myelopathy and in particular of those
resulting in spinal cord compression (e.g. intervertebral
disc extrusion, epidural haemorrhage). In dogs and cats
with ischaemic myelopathy, the myelogram may be Histology
normal or may reveal an intramedullary pattern sugges- A definitive diagnosis of ischaemic myelopathy can be
tive of spinal cord swelling in the acute stage of the reached only by histological examination of the affected
disease. However, this latter finding may also be spinal cord segment(s). Histological examination reveals
observed with other causes of myelopathy including necrosis within the affected spinal cord segment(s)
acute non-compressive nucleus pulposus extrusion. The (268). Commonly, grey and white matter are both
width of the underlying intervertebral disc spaces has involved, with the former being more severely affected
to be assessed carefully on good quality radiographs than the latter. The distribution of the lesion reflects the
with optimal patient positioning. The presence of a col- territory of the embolized vessel(s) and, therefore, is fre-
lapsed intervertebral disc space beneath the area of spinal quently asymmetric. The margins of the lesion tend to be
cord swelling should raise the suspicion of acute non- well delineated from normal tissue.
compressive nucleus pulposus extrusion. Lesion evolution occurs in three stages: (1) ischaemic
necrosis; (2) resorption; and (3) cavitation and gliosis.
Computed tomography The type and spatial distribution of the lesion are diag-
CT can also help to rule out other causes of acute nostic for an ischaemic myelopathy. However, proof of
myelopathy. An intramedullary pattern of spinal cord an embolic aetiology relies on the histological evidence
swelling may be seen on a CT myelogram in the acute of cellular or acellular material in one or more spinal cord
stage of ischaemic myelopathy. vessel(s) (arteries, arterioles and/or veins) within or near
 I S C H A E M I C M Y E L O PAT H Y 339

the lesion or, occasionally, in nerve root vasculature. severely impaired. Nursing care includes bladder and
In the majority of cases reported in the literature, the bowel management, adequate bedding, regular turning,
embolized material had histological and histochemical skin care to prevent decubital ulcers and urine scalding,
staining characteristic of fibrocartilage that is most prob- care of the respiratory system (prevention/treatment of
ably derived from the nucleus pulposus. Infarcted areas hypoventilation, aspiration pneumonia, pulmonary
are usually initially ischaemic, but sometimes may be atelectasis) and adequate nutrition. Physiotherapy
accompanied by haemorrhage. stimulates neuronal plasticity and therefore maximizes
functional recovery mediated by spared neural tissue.
TREATMENT In addition, physiotherapy plays an important role in
limiting and reversing disuse and immobilization
Treatment of ischaemic myelopathy includes reducing changes such as muscle atrophy and muscle and joint
secondary spinal cord injury (maintenance of spinal cord contractures. Nursing care and physiotherapy are
perfusion, neuroprotection), nursing care and physio- described in detail in Chapter 32 (Postoperative support-
therapy. ive care and physical rehabilitation).
Maintenance of spinal cord perfusion usually does not
require any intervention in patients with ischaemic PROGNOSIS
myelopathy as systemic BP, ventilation and oxygen-
ation are usually normal. However, in patients with con- The prognosis depends on the severity of the ischaemic
current cardiovascular or respiratory disease or with insult and the extent of the ischaemic injury. The latter
neurological impairment of ventilation (e.g. severe cer- can be assessed clinically (severity of neurological dys-
vical spinal cord lesions affecting phrenic nerve function) function) and by means of MRI (longitudinal and trans-
it is important to monitor and maintain systemic BP, verse extent of the lesion).
ventilation and oxygenation within normal limits. In the author’s MRI-based study, severity of neuro-
Neuroprotective agents, such as methylprednisolone logical signs at the time of initial examination was signifi-
sodium succinate and polyethylene glycol, could help to cantly associated with the extent of the lesion on MRI
minimize the secondary injury phenomenon triggered and with outcome. The extent of the lesion on MRI was
by the ischaemic insult. However, the clinical benefits of defined as the ratio between the length of the
these drugs require further investigation and there are intramedullary hyperintensity on mid-sagittal T2-
increasing concerns about the adverse effects of methyl- weighted images and the length of the vertebral body
prednisolone sodium succinate. These and other neuro- (referred to as the lesion length:vertebral length
protective agents are described in detail in Chapter 21 ratio) of C6 (in dogs with cervical lesions) or L2 (in dogs
(Spinal trauma). with thoracolumbar lesions), and as the cross-sectional
To date, there is no evidence that administration of area of the largest intramedullary hyperintensity on
either methylprednisolone sodium succinate, other types transverse T2-weighted images expressed as a percent-
of glucocorticoids or NSAIDs improves outcome in dogs age of the cross-sectional area of the spinal cord at the
with ischaemic myelopathy. However, no prospective same level (referred to as percentage cross-sectional area
randomized controlled clinical trial has been performed of the lesion). The lesion length:vertebral length ratio
to investigate the value of these or other drugs in patients and the percentage cross-sectional area of the lesion were
with ischaemic myelopathy. both significantly associated with outcome. The sensitiv-
Excellent nursing care and physiotherapy play an ity of using a lesion length:vertebral length ratio >2.0 or
essential role in the management of neurological a percentage cross-sectional area of the lesion *67% to
patients and particularly of those that are recumbent and predict an unsuccessful outcome was 100%.
 340 SPECIFIC EMERGENCIES

Other negative prognostic factors reported in previ- large number of dogs with ischaemic myelopathy have
ous studies on canine ischaemic myelopathy include the reported a favourable outcome in 42/50 (84%) dogs and
presence of LMN signs, symmetrical neurological 49/75 (65%) dogs, respectively.
deficits and loss of nociception. The latter is the most Most dogs and cats show an improvement within the
consistent and significant negative prognostic factor in first 2 weeks of onset of neurological signs. This rapid
different clinical studies on ischaemic myelopathy as well improvement is most probably due to the resolution of
as traumatic spinal cord injury. Another factor that influ- oedema surrounding the infarcted area of the spinal cord.
ences the prognosis in dogs with ischaemic myelopathy is In the author’s MRI-based study, mean time intervals
the owner’s commitment to pursue nursing care and between onset of neurological signs and recovery of vol-
physiotherapy, which can be quite extensive and intense, untary motor activity, unassisted ambulation and
especially in large breed dogs. maximal recovery were 6 days (range, 2.5–15 days), 11
Two studies have suggested that the presence of CSF days (range, 4–136 days) and 3.75 months (range, 1–12
abnormalities (increased protein concentration +/- pleo- months), respectively. In another study the mean time to
cytosis) may be associated with a poorer outcome in dogs recovery of unassisted ambulation was 12 ± 9.77 days in
with ischaemic myelopathy. However, in the author’s 49 dogs. To date no statistically significant association has
MRI-based study there was no association between the been identified between recovery times and neu-
presence of CSF abnormalities and outcome or the roanatomical localization, severity of motor dysfunction,
extent of the intramedullary lesion on MRI. involvement of an intumescence and site or extent of the
Success rates vary among studies, probably depending lesion on MRI.
on differences in inclusion criteria, severity and distribu- Even though reported cases are limited, it is likely that
tion of ischaemic lesions, definition of outcome and the prognosis for cats receiving adequate nursing care is
owner’s commitment. The two most recent studies on a as good as for dogs.
 SPECIFIC EMERGENCIES Chapter 19

INFECTIOUS AND INFLAMMATORY

DISEASES OF THE CNS 341

Scott Schatzberg
& Peter Nghiem

INTRODUCTION Aetiology/pathophysiology
MEM may be caused by an infectious agent or associated
Animals with meningoencephalomyelitis (MEM) typi- with an idiopathic inflammatory condition of the CNS.
cally are presented for acutely progressive, focal to multi- Canine and feline MEM have been reported throughout
focal neurological signs. Patients should be stabilized the world. However, infectious MEMs are more preva-
initially if systemic derangements (cardiovascular or res- lent in certain geographical locations (Table 77).
piratory) or evidence of increased ICP are/is present.
When the patient is stable, the clinician should attempt
to differentiate between infectious and idiopathic MEM Table 77 Global prevalence of
based on the signalment, physical examination findings, infectious MEM*
the presence/absence of systemic signs, and infectious
REGION INFECTIOUS AGENTS
disease testing. Differentiation between infectious and
idiopathic MEM is critical, and may require CSF analy- North A. platys, Aspergillus spp., Babesia spp.,
sis and advanced neuroimaging. Once an infectious or America B. dermatitidis, CDV, C. immitis,
C. neoformans, E. canis, FIPV, H. capsulatum,
idiopathic differential diagnosis list is generated, the N. caninum, rabies virus, R. rickettsii, T. gondii
most appropriate diagnostic plan can be implemented.
Central B. dermatitidis, CDV, C. immitis, FIPV,
America N. caninum, rabies virus, T. gondii
MENINGOENCEPHALOMYELITIS
South CDV, C. immitis, C. neoformans, FIPV,
Overview America H. capsulatum, N. caninum, rabies virus,
R. rickettsii, T. gondii
MEM is defined as inflammation of the meninges (dura,
arachnoid and pia mater) and the neuroparenchyma (e.g. Europe Aspergillus spp., B. dermatitidis, CDV,
forebrain, brainstem, cerebellum and/or spinal cord). C. neoformans, E. canis, FIPV, N. caninum,
Clinical signs of encephalitis reflect the location of the rabies virus, R. rickettsii, T. gondii
lesion(s) (forebrain, brainstem or cerebellum). Clinical Northern CDV, C. neoformans, E. canis, FIPV,
signs of myelitis reflect whether the spinal cord lesion(s) Asia rabies virus, T. gondii
are within the UMN or LMN system, or both. Pain
Southeast B. dermatitidis, CDV, C. neoformans,
and/or hyperaesthesia is/are most common with menin- Asia E. canis, FIPV, rabies virus, T. gondii
gitis (brain or spinal cord).
Due to the typical acute and progressive nature of Africa B. dermatitidis, CDV, C. neoformans,
E. canis, FIPV, rabies virus, T. gondii
MEM, animals are commonly presented for emergency
evaluation. Based on the neuroanatomical localization, it Australia A. platys, Aspergillus spp., CDV,
is imperative to formulate an accurate differential diag- C. neoformans, E. canis, FIPV, rabies virus,
T. gondii
nosis in order to institute the correct diagnostic recom-
mendations and therapies. *Risk of exposure to the most common diseases in these areas.
Great Britain, Scandinavia, New Zealand, Japan and much of
Australia are considered rabies ‘free’.
342 SPECIFIC EMERGENCIES

Table 78 Infectious agents known to cause acute meningoencephalomyelitis

AGENT DOGS CATS

Bacterial Aerobic Aerobic

Anaerobic Anaerobic

Rickettsial Rickettsia rickettsii

Ehrlichia spp.
Anaplasma spp.

Viral Canine distemper virus (CDV) Feline infectious peritonitis virus (FIPV)
Rabies virus Feline leukaemia virus (FeLV)
West Nile virus (North America) Borna disease virus (Europe and Japan)
Tick-borne encephalitis virus (Europe and Asia)
Borna disease virus (Europe and Japan)
Eastern equine encephalitis virus (North America; rare)

Protozoal Neospora caninum Toxoplasma gondii

Toxoplasma gondii Babesia spp.
Sarcocystis canis (rare) Leishmania spp. (Mediterranean basin and Portugal)
Encephalitozoon cuniculi (rare)
Trypanosoma cruzi (rare)
Acanthomoeba spp. (rare)
Babesia spp. (rare)
Leishmania spp. (Mediterranean basin and Portugal)

Fungal Cryptococcus spp. Cryptococcus spp.

Coccidioides immitis Coccidioides immitis
Blastomyces dermatitidis Blastomyces dermatitidis
Histoplasma capsulatum (rare) Histoplasma capsulatum (rare)
Aspergillus spp. (rare) Aspergillus spp. (rare)

Parasitic Cuterebra larva migration (rare) Cuterebra larva migration (rare)

Dirofilaria immitis – abberant migration (rare) Dirofilaria immitis – abberant migration (rare)

Infectious meningoencephalomyelitis factors including: the status of the animal’s immune

Infectious agents are confirmed uncommonly in cases system at the time of inoculation; strength of the animal’s
of MEM, but are important differentials nonetheless. immune response during active infection; nutritional
Pathogens that may cause canine or feline MEM include status of the animal; strain and virulence factors of the
bacteria, viruses, protozoa, fungi, and parasites. MEM infectious agent; and environmental factors. Clearance of
most commonly occurs in young or immuno- the infectious agents is dependent on these factors as
compromised animals; however, any dog or cat may well; however, some pathogens may enter a dormant
develop a CNS infection. Some infectious agents are stage within the host without producing clinical disease.
capable of affecting multiple organ systems in addition to Recrudescence of such organisms may occur with or
the CNS, which may prove helpful in distinguishing without clinically apparent disease.
CNS infections from an idiopathic meningoencephalitis Infectious agents known to cause acute MEM in the
(ME). The severity of infection is dependent on several dog and cat are listed in Table 78.
 INFECTIOUS AND I N F L A M M AT O RY D I S E A S E S OF THE CNS 343

Bacterial and rickettsial meningoencephalomyelitis a

Bacterial meningitis and CNS abscesses are among the
most important differentials for MEM that may lead to
an emergency presentation. Bacterial meningitis may
result from several different mechanisms including:
haematogenous spread from other foci within the body;
direct inoculation from traumatic wounds or needles
following CSF acquisition; or direct extension from
other structures of the head (eyes, ears, cribriform plate).
Bacteria that have been reported in association with
meningitis include Staphylococcus spp., Pasteurella spp., b
Escherichia coli, Actinomyces spp., Nocardia spp., Klebsiella
spp., Peptostreptococcus spp., Eubacterium spp. and Bac-
teroides spp. Pathological findings include infiltration of
mononuclear and polymorphonuclear (PMN) cells into
the leptomeninges. If the underlying neuroparenchyma
is affected, necrosis of the grey and white matter may
occur due to direct neuronal injury or thrombosis.
CNS abscesses and empyema, similar to bacterial
meningitis, may result from haematogenous spread from
other foci within the body, direct inoculation or direct
extension from other structures of the head (nasal cavity  269 Transverse T1-weighted post-contrast (a)
and sinuses, eye, ear). Immature and immunocompro- and T2-weighted (b) images of the brain of a cat with
mised animals are at a greater risk for the development of subdural empyema (arrows) causing severe mass effect
CNS abscesses. Similar organisms to those responsible with marked displacement of the falx cerebri.
for bacterial meningitis have been reported including (Photo courtesy Laurent Garosi)
Staphylococcus spp., Streptococcus spp., Nocardia spp.,
Pasteurella spp., Actinomyces spp., Fusobacterium spp.,
Bacteroides spp. and Peptostreptococcus spp. Occasionally,
fungal organisms may produce CNS abscesses. The pro-
gression of abscess formation includes inflammation of
the associated anatomical structure (i.e. encephalitis,
myelitis) followed by capsular formation. Oedema and
significant mass effect are often features of this disease in
the brain (269). Additional pathological findings include
rings of organisms with infiltration of mononuclear and Viral meningoencephalomyelitis
PMN cells, diffuse leptomeningitis, reactive astrocytes, Recently, there have been sporadic reports of flavivirus
gliosis and cerebral oedema outside the capsule. (tick-borne encephalitis virus, west Nile virus), borna-
Rickettsial organisms, including Rickettsia rickettsii virus and Eastern equine encephalitis infection in dogs,
and Ehrlichia canis, are transmitted to dogs via tick suggesting that canine viral ME is more prevalent than
vectors. Once rickettsiae infect a dog or cat, they enter currently accepted. However, the aetiologies for the
endothelial cells, leading to a vasculitis of multiple organ majority of cases of canine ME remain elusive, potential-
systems including the CNS. Lymphoplasmacytic menin- ly because of current limitations for pathogen detection
gitis predominates; however, MEM occurs occasionally in routine diagnostic testing. The most common viral
when the underlying neuroparenchyma (forebrain, causes of acute MEM appear to be rabies and canine dis-
brainstem and cerebellum) is affected. temper virus (CDV).
 344 SPECIFIC EMERGENCIES

Rabies infections have been reported more frequent- coronavirus. FIP occurs in two clinical forms: the effusive
ly in cats than in dogs in the US, with infection being uni- (wet) form and the non-effusive (dry) form. The more
formly fatal in both species. Rabies virus is considered common effusive form causes systemic disease secondary
endemic in most of the world except Great Britain, to an exuberant humoral immune response, character-
Scandinavia, New Zealand, Japan and much of Australia. ized by a fibrinous peritonitis and pleuritis. The non-
After the virus is introduced through a bite of an infected effusive form results from a combined humoral immune
animal, it then replicates and travels within peripheral and partial cell-mediated immune response. This ‘eye
nerves to the brain, resulting in a non-suppurative polio- and brain’ form affects the meninges, CNS neuro-
encephalomyelitis and craniospinal ganglionitis. The parenchyma and uvea. Pathological findings within the
incubation period is 2 weeks to 6 months. Areas of the CNS include perivascular pyogranulomatous infiltration
CNS affected are widespread and commonly include the of the leptomeninges, neuroparenchyma of the brain and
brainstem and cerebral hemispheres. Occasionally, dogs spinal cord, choroid plexus and ependyma. Other
and cats can develop post-vaccinal rabies if the vaccine common findings include subependymal necrosis, ven-
is given during times of stress (e.g. boarding, surgery, tricular dilatation, hydrocephalus, panophthalmitis and
systemic illness). vascular degeneration.
CDV, in contrast to rabies, is not uniformly fatal.
Three forms of CDV occur in dogs, with enceph- Protozoal meningoencephalomyelitis
alomyelitis in immature dogs (3–6 months of age most Protozoal organisms are important causes of MEM in
frequently) presenting most commonly as an acute dogs and cats. Dogs and cats are the definitive hosts for
neurological emergency. The other forms occur in adult Neospora caninum and Toxoplasma gondii, respectively.
to geriatric dogs, which are rarely presented for acute Transmission of T. gondii occurs by carnivorous inges-
neurological signs. Dogs are inoculated with the virus via tion (most common), orofaecal contamination or trans-
exposure to infected respiratory droplets. An infected placentally. Multiple organ involvement, including
dog with CDV can transmit the virus up to 60–90 days ocular, pulmonary, liver and CNS, is often present
post infection. The virus spreads haematogenously to concurrently. A mixed cell infiltrate predominated by
other organ systems including skin, endocrine and lymphocytes is typically present. Clinical toxoplasmosis
exocrine glands, epithelium of the gastrointestinal, res- most commonly affects dogs <1 year of age and immuno-
piratory and genitourinary tracts, and the CNS. Direct compromised geriatric dogs. Toxoplasmosis may be
viral replication results in neuronal injury and necrosis, associated with CDV or other infections, such as ehrli-
with multifocal lesions in grey and white matter. In the chiosis, or with glucocorticoid therapy. Neurological
subacute stages, white matter tends to be more affected signs associated with T. gondii infection include MEM
than grey matter. CNS lesions generally consist of and/or myositis–polyradiculoneuritis.
varying degrees of lymphoplasmacytic inflammation, The life cycle of N. caninum is not completely under-
demyelination and necrosis. Post-vaccinal canine dis- stood, but infection during the neonatal period is sus-
temper encephalitis typically occurs in dogs <6 months of pected. In addition to encephalomyelitis, multiple organ
age and is associated with administration of a live virus. system involvement may also occur with N. caninum
The pathogenesis is speculative, but may involve infection. In juvenile dogs <6 months of age, myositis,
immunosuppression of the dog, latent CDV infection, ascending polyradiculoneuritis and encephalomyelitis
inadequate attenuation of the vaccine or other vaccine predominate. Rigid limb contracture and arthrogryposis
component interactions. may occur as a result of the myositis. Severe MEM tends
FIP virus is the causative agent of CNS FIP, a syn- to be rare with N. caninum infection in young dogs. In
drome that is uniformly fatal in cats. FIP virus is a dogs >1 year of age, MEM (commonly cerebellitis) is the
mutated strain of the non-pathogenic feline enteric more typical presentation (270).
 INFECTIOUS AND I N F L A M M AT O RY D I S E A S E S OF THE CNS 345

a b c

 270 Transverse T2-weighted (a), T1-weighted (b) and T2-weighted FLAIR (c) images of the caudal fossa of a
9-year-old West Highland White Terrier with Neospora infection. The diffusely atrophied cerebellum is surrounded
by a thick T2-weighted hyperintense and T1-weighted hypointense signal that does not suppress on FLAIR sequences
(red arrow). Additionally, there are bilaterally symmetrical FLAIR hyperintensities within the cerebellar white matter
(yellow arrows). (Photo courtesy Laurent Garosi)

Fungal and parasitic meningoencephalomyelitis Idiopathic meningoencephalomyelitis

Mycotic agents sporadically cause MEM in dogs and Idiopathic MEM occurs commonly in the dog, but seems
cats. Cryptococcus neoformans is the most common CNS to be extremely rare in the cat. GME, NME, NLE,
fungal infection in cats and dogs. Blastomyces dermatitidis, SRMA and idiopathic tremor syndrome comprise the
Coccidioides immitis, Histoplasma capsulatum and Asper- most common inflammatory conditions of the canine
gillus spp. have also been reported to cause CNS infec- CNS. While each disease has unique histopathological
tion in dogs. The most common route of inoculation for features, these canine MEMs collectively seem to be
fungal organisms is inhalation. Morphological conver- aberrant immune responses directed against the CNS.
sion to the yeast form occurs in the animal and haemato- The aetiopathogenesis of GME, NME and NLE is
genous or lymphatic spread to other organ systems, probably multifactorial: familial predisposition, infec-
including the respiratory, skeletal, integument, ocular tious agents and immunopathologic mechanisms all may
and musculoskeletal systems, may occur. Fungal organ- play a role in disease pathogenesis. GME is responsible
isms may cause an acute, focal or multifocal-diffuse for up to 25% of canine CNS disease. Three morpho-
MEM with a mixed cell parenchymal infiltrate (granulo- logical forms of GME have been described: disseminat-
matous or pyogranulomatous). Aberrant migration of ed, focal and ocular. Typical histopathological lesions
parasitic larvae to the CNS, including Cuterebra spp. include concentric proliferation of inflammatory cells
(common in cats) and Dirofilaria immitis, may also around blood vessels, predominantly of the white matter
produce MEM in dogs and cats. of the CNS (271, next page). Clinical signs reflect the
location of the lesions, and GME typically is fatal if not
treated aggressively with immunosuppression.
 346 SPECIFIC EMERGENCIES

a b

 271 Disseminated granulomatous meningoencephalitis. (a) Transverse T2-weighted MR image at the level of the
midbrain and cerebral hemispheres. Multiple, infiltrative hyperintensities (arrows) are scattered throughout the central
white matter. These hyperintense lesions probably represent a combination of oedema and inflammation. (b) Subgross
GME lesions seen here in the cerebrum and midbrain. (c) The cells in the perivascular cuffs include lymphocytes,
plasma cells and large, pale histiocytic cells. The left panel shows coalescing cuffs. When several cuffs coalesce, a
grossly visible lesion will be evident. Despite the density of the cuffs, there is little tendency for cells to infiltrate the
parenchyma. (d) High-magnification view of lymphocytes and large histiocytoid cells in a perivascular cuff. Plasma cells,
rare in this image, may also be present. (From Talarico LR, Schatzberg SJ (2010) Idiopathic granulomatous and
necrotizing inflammatory disorders of the canine central nervous system: a review and future perspectives.
J Small Anim Pract 51:138–149, with permission.)
 INFECTIOUS AND I N F L A M M AT O RY D I S E A S E S OF THE CNS 347

a b

c d

 272 Necrotizing meningoencephalitis. (a) Transverse T2-weighted MR image at the level of the thalamus and
cerebral hemispheres. Note the asymmetric, hyperintense, infiltrative lesions affecting the prosencephalon (arrows).
The demarcation between grey and white matter is obscured and no evidence of cavitation is seen. (b) Transverse
section of the brain at the level of the diencephalon. Inflammation dulls the white matter and characteristically effaces
the junction of grey and white matter in the cerebrum (red arrow). Note also the asymmetric swelling, midline shift,
slight ventricular enlargement and focal cavitation (yellow arrow). (c) Occipital lobe of a Pomeranian dog. A diffuse infil-
trative lesion is present extending from the cortical surface through the grey matter and multifocally entering the white
matter. This was a substantially unilateral disease. (d) Cerebral cortex. Meningeal mixed inflammatory infiltrates, which
include large and small mononuclear cells and plasma cells. (From Talarico LR, Schatzberg SJ (2010) Idiopathic granulo-
matous and necrotizing inflammatory disorders of the canine central nervous system: a review and future perspectives.
J Small Anim Pract 51:138–149, with permission.)
 348 SPECIFIC EMERGENCIES

a b

c d

 273 Necrotizing leucoencephalitis. (a) Transverse T2-weighted MR image at the level of the frontoparietal lobes.
Multiple, asymmetric bilateral forebrain lesions, mainly affecting the subcortical white matter, are present (arrows).
(b) Asymmetric, cavitating lesions in the corona radiata (red arrows), internal capsule (black arrow) and thalamocortical
fibres. (c) Low-magnification view. Corona radiata with intense oedema, dissolution of white matter, early cavitations
and residual perivascular cuffing. (d) Corona radiata, high magnification. Left panel: lymphoid and histiocytoid cells
cuffing a vessel. Right panel: large reactive astrocytes (gemistocytes). (From Talarico LR, Schatzberg SJ (2010)
Idiopathic granulomatous and necrotizing inflammatory disorders of the canine central nervous system: a review and
future perspectives. J Small Anim Pract 51:138–149, with permission.)
 INFECTIOUS AND I N F L A M M AT O RY D I S E A S E S OF THE CNS 349

NME and NLE are CNS inflammatory disorders SIGNALMENT AND HISTORY
with similarly elusive aetiopathogeneses to that of GME.
Historically referred to as ‘Pug Dog encephalitis’ and Infectious meningoencephalomyelitis
‘necrotizing encephalitis of Yorkshire Terriers’, respec- Signalment and history may aid in prioritizing infectious
tively, these idiopathic MEs have now been reported in MEM over idiopathic MEM. For example, an inappro-
many other toy breed dogs. Although notable differences priate vaccination history may raise the index of suspi-
in lesion topography exist between them, the hallmarks cion for CDV or rabies MEM. Similarly, a history of
of both diseases include non-suppurative ME and vari- travel to endemic areas or recent tick exposure may
able degrees of cerebral necrosis (272 page 347, 273). suggest fungal or rickettsial disease, respectively. The
Clinical signs typically are progressive, reflect the loca- most common age group in which FIP occurs in cats is
tion of cerebral lesions and include seizures, lethargy, cir- between 6 months and 2 years of age, followed by geri-
cling, visual deficits and ultimately death. atric cats >14 years of age. There are no breed predispos-
Recently, the authors evaluated pedigree informa- itions for FIP; however, intact male cats and those in
tion on a large cohort of Pugs and demonstrated a stressful environments (e.g. catteries) may be at an
strong familial inheritance pattern for NME. While this increased risk.
transmission pattern is not surprising, a simple
Mendelian inheritance pattern could not be demon- Idiopathic meningoencephalomyelitis
strated. The latter suggests that NME is a multifactorial Breed and age are particularly important for the
disorder. Previous screens for viral aetiologies revealed recognition of the idiopathic MEMs. GME is most
negative results. Molecular studies are ongoing to assess common in females and toy and terrier breeds, but
for genetic susceptibility loci and a diverse group of both sexes and all breeds may be affected. For GME, the
potential infectious triggers that may lead to immune mean age of onset of neurological signs is 5–6 years
dysregulation in GME, NME and NLE. (range: 6 months to 12 years). NME and NLE have been
SRMA is a systemic immune disorder characterized reported in various toy breeds including the Pug,
by inflammatory, stenosing lesions of the meninges Maltese, Chihuahua, Yorkshire Terrier, Pekingese, West
and the associated arteries. The characteristic lesion Highland White Terrier, Boston Terrier, Japanese Spitz
associated with SRMA is a necrotizing fibrinoid arteritis and Miniature Pinscher. The age of onset of neurological
consisting predominantly of neutrophils and scattered signs associated with NME varies from 6 months to 7
lymphocytes, plasma cells and macrophages. Vasculitis is years of age and most commonly occurs in young dogs,
more common in the leptomeninges of the spinal cord with a mean age of 29 months. NLE typically manifests
than around the brain, and lesions are occasionally between 4 months and 10 year of age, with a mean age of
present in the thyroid, heart and mediastinum. Extensive onset of 4.5 years.
leptomeningeal haemorrhages and meningeal plaques SRMA may occur in any breed of dog, although
may be apparent grossly. Acute thrombosis of the vascu- young Beagles, Boxers, Bernese Mountain Dogs,
lature may create ischaemic changes. German Short-haired Pointers and Nova Scotia Duck
Idiopathic tremor syndrome is a mild, diffuse, non- Tolling Retrievers are overrepresented. The age of
suppurative encephalomyelitis, with perivascular cuffing onset of neurological signs associated with SRMA is
by lymphoplasmacytic mononuclear cells. The lesions commonly between 6 and 18 months, with a range from
affect the CNS diffusely, including the ascending sensory 4 months to 7 years.
tracts, descending motor tracts and, occasionally, the Idiopathic tremor syndrome affects predominately
cerebral and cerebellar hemispheres. CNS myelin is small breed dogs, most commonly Maltese, Cocker
unaffected. The exact aetiopathogenesis is unknown, but Spaniels and West Highland White Terriers. Affected
an autoimmune disorder affecting neurotransmitter syn- dogs typically present between 1 and 5 years of age, may
thesis has been considered. Other potential triggers be any colour (although often are white) and typically
include pathogens or endogenous epitopes associated weigh <15 kg.
with neurotransmitters or cell membrane receptors.
 350 SPECIFIC EMERGENCIES

CLINICAL PRESENTATION • A source or foci (e.g. liver abscess, pneumonia,

bacterial endocarditis) or evidence of direct
General meningoencephalomyelitis extension from the eyes, ears or nasal cavity with
The clinical presentation of infectious or idiopathic bacterial MEM and bacterial abscesses.
MEM is variable, as any part of the neuraxis may be • Pulmonary, gastrointestinal, ocular and integumen-
affected by inflammation. MEM may be focal, multifocal tary abnormalities with CDV infection.
or diffuse in nature and patients often present with • Focal haemorrhages (secondary to vasculitis), fundic
symmetric neurological signs (274). As mentioned previ- abnormalities (haemorrhage, exudate), fever,
ously, clinical signs of encephalomyelitis reflect the loca- peripheral oedema, thrombocytopenia,
tion of the lesion(s). Animals with meningitis may be lymphadenopathy, renal disease and arthropathy
presented for discomfort in the acute stage of disease, but with rickettsial infections.
may progress to manifest obvious neurological deficits in • Multisystem involvement, including pulmonary,
the later stages (if the underlying neuroparenchyma skin, musculoskeletal, ocular, and internal organ
becomes inflamed). involvement, with fungal and protozoal disease.
• Fever, hyperglobulinaemia and chorioretinitis
Infectious meningoencephalomyelitis with FIP.
Neurological signs caused by infectious agents are
extremely variable and are dependent on the neuro- Idiopathic meningoencephalomyelitis
anatomical location of the lesion(s). Although the neuro- As with the infectious MEMs, the neurological signs of
logical signs alone should not form the basis of a the idiopathic disorders tend to be reflective of the
diagnosis of infectious MEM, some infectious agents neuroanatomical locations of the lesion(s). Disseminated
cause ‘classic’ neurological signs. For example, CDV GME often presents as an acutely progressive, multifocal
often produces generalized flexor spasms of the muscles neurological disease that may be fatal if left untreated.
of the limbs, neck and/or masticatory muscles, so-called Neurological deficits referable to the caudal cranial fossa
CDV myoclonus. Rabies infection may cause ‘paralytic (vestibulocerebellar signs) and cervical spinal cord, in
(dumb)’ or ‘furious’ variants of disease, caused by addition to seizures and visual deficits, have been
ascending LMN paresis and limbic system involvement, reported most frequently. Neurological signs associated
respectively. Toxoplasmosis and neosporosis often affect with the uncommon, focal form of GME may be acute or
puppies with a combination of LMN signs and MEM. slowly progressive and they are suggestive of a single
Cats with CNS FIP typically are presented for acutely space-occupying mass lesion. Forebrain signs were
progressive, multifocal to diffuse neurological signs reported most frequently with focal GME in one study,
including seizures, behavioural abnormalities, cere- although the brainstem or spinal cord may be affected.
bellovestibular signs, GP ataxia and various degrees of The ocular form of GME manifests with an acute
fore- and hindlimb paresis to paralysis. onset of visual impairment, variable pupillary changes
The typical presentation for bacterial meningitis (commonly dilated and unresponsive), variable degrees
and/or CNS abscesses is an acutely progressive condition of optic nerve oedema and occasionally chorioretinitis,
with variable neurological deficits. Clinical signs of especially in the non-tapetal fundus. Dogs with ocular
meningitis include cervical hyperaesthesia, low head car- GME may concurrently have, or progress to develop,
riage and pain on palpation. In addition, vomiting, disseminated CNS lesions.
bradycardia and seizures may occur. CNS abscesses often
lead to a focal localization; however, a multifocal local-
ization may be present with multiple abscesses. If an
infectious MEM is suspected, systemic signs should be
evaluated carefully. Infectious CNS diseases are
associated with systemic signs more frequently than the  274 Algorithm for diagnosis of acute meningo-
idiopathic MEMs, including: encephalomyelitis.
 INFECTIOUS AND I N F L A M M AT O RY D I S E A S E S OF THE CNS 351

UMN: upper motor neuron

CSF: cerebrospinal fluid Acute, focal to multifocal
CT: computed tomography progressive signs?
MRI: magnetic resonance imaging Seizures, mentation changes,
cranial nerve deficits,
PCR: polymerase chain reaction
blindness, ataxia and UMN
ELISA: enzyme-linked immunosorbent assay paresis
IHC: immunohistochemistry
IFA: immunofluorescent antibody test
AGID: agar gel immunodiffusion
CBC: complete blood count
Other systemic signs?
CHEM: serum chemistry panel
UA: complete urinalysis

YES NO

Evaluate for infectious Evaluate for non-infectious

causes causes

Inappropriate vaccine
history

YES NO

Recent travel history or tick

exposure?

YES NO

AGID Advanced imaging (CT, MRI);

Antibody titre; ELISA; PCR; CBC, CHEM, UA; Advanced imaging (CT, MRI); CSF analysis;
IHC; IFA radiographs; cytology; infectious titres; CSF analysis; imaging-guided biopsy;
infectious titres; PCR CSF culture; urine culture; PCR infectious titres

• Rickettsia rickettsii • GME

• Ehrlichia canis • Toxoplasma gondii • NME
• Distemper • Coccidioiodes immitis • Neospora canis • NLE
• Rabies • Cryptococcus neoformans • Bacterial meningitis • MUA
• Aspergillus spp. • CNS abscess • SRMA
• Blastomyces dermatitidis • FIP • Idiopathic tremor
• Histoplasma capsulatum syndrome
 352 SPECIFIC EMERGENCIES

Dogs with both NME and NLE commonly manifest DIFFERENTIAL DIAGNOSIS
forebrain signs due to the predominance of lesions in the
prosencephalon. NLE may also cause mid to caudal Metabolic derangements; congenital anomalies (decom-
brainstem signs. The signs associated with NME and pensating hydrocephalus, Chiari-like malformation);
NLE typically are rapidly progressive and most com- tumours of the meninges (histiocytosis, lymphoma,
monly include seizures, depression, circling, vestibulo- meningioma); intervertebral disc disease; atlantoaxial
cerebellar signs, visual deficits and ultimately death. subluxation; cerebrovascular accident; head trauma;
Clinical signs with SRMA are characterized by mycotoxin and neurotoxin ingestion (for idiopathic
episodes of profound cervical hyperaesthesia, depression tremor syndrome and occasionally disseminated GME).
and pyrexia. Two forms of SRMA exist, i.e. the ‘classic’
acute form and the chronic protracted form. In acute DIAGNOSIS
SRMA, dogs most commonly present with hyperaesthe-
sia along the vertebral column, cervical rigidity, stiff gait Key diagnostic tests for MEM include molecular and
and fever. Affected animals often manifest a hunched advanced imaging diagnostics (Table 79).
posture with profound guarding of the head and neck,
sometimes mimicking a cervical intervertebral disc pro- General meningoencephalomyelitis
trusion. Dogs may be in so much pain that any manipula- The differential diagnosis for dogs presented for an acute
tion elicits a painful response. The chronic form of onset of multifocal CNS signs includes decompensating
SRMA most often occurs following relapses of acute congenital abnormalities, metabolic derangements,
disease and/or inadequate treatment. Involvement of the infectious and idiopathic MEM, neoplasia and toxin
motor and proprioceptive systems may lead to variable exposure. Differentiating these disorders may be chal-
degrees of paresis and ataxia. Other neurological signs, lenging. Diagnostic testing typically includes a minimum
such as menace deficits, anisocoria or strabismus, may database (CBC, chemistry panel and urinalysis), survey
occur with severe disease. radiographs of the thorax (+/- abdominal ultrasound) to
Idiopathic tremor syndrome typically causes fine rule out systemic disease and metastatic neoplasia,
tremors affecting all four limbs, the head and sometimes advanced cross-sectional imaging via CT or MRI and
the eyes. The tremors tend to worsen with exercise, stress CSF collection and analysis. Although more often uti-
and excitement, but disappear with sleep. Neurological lized for suspected brain tumours, CT-guided brain
examination typically is normal, although absent menace biopsy and histopathological evaluation of brain tissue
responses, nystagmus, dysconjugate eye movements, may be considered in cases of suspected ME.
head tilt, nondescript ataxia, hypermetria, body swaying, CSF analysis is a key component of the neuro-
varying degrees of paresis and, rarely, seizures have been diagnostic work-up and typically includes cytological
reported. Neurological signs manifest sporadically, often evaluation, differential cell counts and TP measurement
progress over several days and typically remain static if (Table 80). While pleocytosis is commonly present in
untreated. Clinical complications associated with pro- cases of MEM, cytology rarely provides definitive differ-
longed tremors include severe hyperthermia, hypo- entiation among idiopathic, infectious and neoplastic
glycaemia, dehydration and anorexia. disorders. On occasion, bacteria, fungi, protozoa or para-
Although the idiopathic MEMs are restricted to the sites may be identified on microscopic examination of
CNS, the severity and location of the CNS lesions CSF (see Chapter 5); however, this is extremely rare. One
occasionally produce profound systemic changes must be especially cautious not to ‘overinterpret’ the
(e.g. autonomic changes with brainstem lesions). Due to CSF profile. For example, in confirmed cases of MEM,
the acute, progressive nature of the majority of the con- CSF analysis occasionally reveals no abnormalities.
ditions causing MEM, dogs and cats often present for Despite its limitations, the CSF WBC differential may
emergency evaluation, therefore it is essential to formu- help the clinician to narrow down the differential diag-
late an accurate differential diagnosis in order to perform nosis, especially when combined with cross-sectional
the correct diagnostic investigations. imaging of the CNS.
 INFECTIOUS AND I N F L A M M AT O RY D I S E A S E S OF THE CNS 353

Table 79 Diagnostic tests for In both acute and chronic SRMA, blood work may
meningoencephalomyelitis show a neutrophilia with a left shift, an increased ery-
throcyte sedimentation rate and an elevated alpha2-
DISEASE DIAGNOSTIC TESTS
globulin fraction. The majority of affected dogs have
Infectious MEM elevated IgA levels in both the CSF and serum, a
Bacterial meningitis CSF analysis/culture; eubacterial finding that is probably secondary to dysregulation of
PCR; urine culture the immune system. Elevated serum and CSF IgA
CNS abscess CSF analysis/culture; eubacterial levels help differentiate SRMA from other idiopathic
PCR; urine culture; CT/MRI and infectious canine meningoencephalitides; how-
ever, elevated IgA levels may be associated with
Canine distemper virus PCR of CSF, urine or conjunctival
primary or secondary inflammation. Elevated IgM
scraping; IHC of skin biopsy; CSF
and serum IgM and IgG ratios and/or IgG levels in the CSF have also been docu-
mented. More recently, acute phase proteins (APPs),
FIP CSF analysis; RT-PCR of CSF or
including C-reactive protein (CRP) and alpha2-
cavitary fluid; CT/MRI, biopsy
macroglobulin, have been shown to be elevated con-
Rickettsia rickettsii Antibody titres; CSF analysis; PCR sistently in the serum of dogs with SRMA. However,
elevation of APPs is not pathognomonic for the dis-
Ehrlichia canis Antibody titres; CSF analysis; PCR
order and other systemic inflammatory diseases
Rabies virus IFA – postmortem examination should be included in the differential diagnosis when
Toxoplasma/Neospora Antibody titres; CSF analysis; PCR it is present. Once SRMA has been confirmed, elevat-
ed CRP serum concentrations may be used reliably to
Cyrptococcus neoformans Latex agglutination antigen test; monitor response to therapy, rather than repeated
CSF analysis/culture
CSF collection and analysis.
Coccidioides immitis Complement fixation or AGID The presence of anti-astrocytic and glial fibril-
(antibody); CSF analysis/culture lary acid protein (GFAP) autoantibodies has been docu-
Blastomyces dermatitidis Urine antigen assay
mented in the CSF of affected NME dogs. However,
similar antibody levels occur in the CSF of dogs with
Aspergillus spp. Latex agglutination antigen test GME, brain tumours and even some clinically normal
Parasitic MEM dogs. The diagnostic utility of autoantibodies in moni-
Dirofilaria immitis Antigen ELISA, antibody titres toring response to therapy is limited, since anti-GFAP
(cat), microfilaria identification autoantibodies can even be detected during clinically
successful immunosuppressive therapies.
Cuterebra larva Advanced imaging, postmortem
examination While CT may have diagnostic utility in some cases
of inflammatory brain disease, MRI is the gold standard
Idiopathic MEM neuroimaging modality for MEM. MRI may be espe-
GME, NME, NLE, MUA CSF analysis and lymphoma PCR; cially helpful for differentiating among the idiopathic
CT/MRI; biopsy
meningoencephalitides, as it often discloses lesions that
SRMA CSF analysis; CSF culture to rule are reflective of the gross neuropathologies associated
out infection; CT/MRI with each disorder. Although there are overlapping clin-
Idiopathic tremor CSF analysis; CT/MRI ical and histopathological features among the menin-
syndrome goencephalitides, the topographical distribution of the
lesions (e.g. NME versus NLE) and presence or absence
of necrosis (e.g. NME versus GME) may be imaging
features that help direct a presumptive antemortem diag-
nosis. In a recent MRI study, 17/18 Pug dogs with NME
had forebrain lesions, with 16/18 having a lesion in the
parietal, temporal and occipital lobes. Also, all the Pugs
 354 SPECIFIC EMERGENCIES

had asymmetric lesions in both the grey and white matter culture, serological antibody titres, immunohisto-
of the neuroparenchyma. MRI also has several advan- chemistry (IHC), immunofluorescent antibody (IFA),
tages over CT as it provides excellent anatomical detail ELISA and agar gel immunodiffusion (AGID). Identifi-
(especially of the caudal fossa) and allows for acquisition cation of infectious organisms on cytology is rare; micro-
of images in multiple planes (sagittal, transverse, dorsal). bial culture should be considered in cases with systemic
Despite the limited soft tissue detail provided by CT, signs, potential sources of infection (e.g. otitis media/
when coupled with CSF analysis it may help to provide interna) and CBC/biochemistry abnormalities (e.g. fever,
evidence of MEM. leucocytosis). CSF fungal culture may also be considered
in cases with concurrent systemic signs (skin, bone,
Infectious meningoencephalomyelitis ocular, internal organ involvement).
Traditional techniques to diagnose infectious CNS dis- Serology and/or PCR should be performed when
eases in dogs and cats include CSF analysis, microbial infectious agents are suspected to be the cause of MEM.

Table 80 CSF analysis findings in canine and feline CNS disease

TOTAL PROTEIN LEVEL NUCLEATED CELL COUNT CYTOLOGY

Viral meningoencephalitis Normal–markedly elevated Normal–moderate pleocytosis Mononuclear

(CDV and other)

Bacterial meningoencephalitis Mildy–markedly elevated Moderate–marked pleocytosis Predominantly neutrophilic

Protozoal meningoencephalitis Mildy–markedly elevated Moderate pleocytosis Mixed, occasionally eosinophilic

Fungal meningoencephalitis Markedly elevated Moderate–marked pleocytosis Mixed, occasionally eosinophilic

CNS parasites Mildy–markedly elevated Mild–moderate pleocytosis Mixed, often eosinophilic

Granulomatous Mildy–markedly elevated Normal–marked pleocytosis Variable: mononuclear, mixed,

meningoencephalitis occasionally eosinophilic

Eosinophilic Mildy–markedly elevated Mild–marked pleocytosis Eosinophils

meningoencephalitis

Steroid-responsive Mildy–markedly elevated Moderate–marked pleocytosis Acute: neutrophilic; Chronic:

meningitis–arteritis mononuclear

Necrotizing Mildy elevated Mild–marked pleocytosis Mononuclear

meningoencephalitis, or
necrotizing leukoencephalitis

Feline infectious peritonitis Markedly elevated Moderate–marked pleocytosis Mixed, occasionally eosinophilic
infection

Neoplasia Variable: normal–markedly Variable: normal–marked Variable: mononuclear, neu-

elevated pleocytosis trophilic (e.g. meningioma),
occasionally eosinophilic or
neoplastic cells (e.g. lymphosar-
coma)

Degenerative disorders Normal–moderately elevated Normal —

Necrosis Normal–markedly elevated Variable: normal–marked Mixed pleocytosis (often

pleocytosis neutrophilic)
 INFECTIOUS AND I N F L A M M AT O RY D I S E A S E S OF THE CNS 355

a b c

 275 (a) Sagittal T2-weighted image of the brain of an 8-month-old cat with the CNS form of FIP. There is marked
dilatation of the 3rd and 4th ventricles, with secondary dorsal displacement of the cerebellum and cerebellar vermal
herniation through the foramen magnum. The proximal part of the cervical spinal cord appears swollen and hyper-
intense. (b) Transverse T1-weighted and (c) T1-weighted post-contrast images of the spinal cord at the level of C1.
There is marked thickening and contrast enhancement of the meninges surrounding the spinal cord (arrows), which
probably accounts for the secondary obstructive hydrocephalus. FIP is a surface-related disease affecting mostly the
leptomeninges and ependymal lining of the CNS. (Photo courtesy Laurent Garosi)

IgM and IgG antibodies reflect acute and chronic diagnosis can be achieved with CSF analysis and MRI.
infections, respectively, and can be evaluated in the CSF analysis typically reveals protein levels of 2 g/l (200
serum and/or CSF. Although positive antibody titres mg/dl) or greater and a moderate to marked neutrophilic
reflect direct exposure to an organism, a positive titre pleocytosis. MRI may reveal periventricular contrast
does not confirm active infection. Serology results must enhancement, ventricular dilatation and/or hydro-
be interpreted in light of the patient’s signalment, history, cephalus (275). Reverse transcription PCR of FIP virus
neurological and systemic signs, CSF analysis and in infected macrophages has been reported; however,
imaging results. Serum and CSF serology and PCR may false positives may occur in healthy cats .
be pursued for Toxoplasma gondii (IgG and IgM ELISA, Since CSF and MRI findings are highly variable with
PCR), Neospora caninum (IgG indirect IFA, PCR), CDV infection, diagnostic techniques with greater
Ehrlichia spp. (IgG indirect IFA, PCR) and Rickettsia rick- specificity must be utilized. Immunohistochemical
ettsii (IgG IFA, PCR). AGID panels and panfungal PCR testing for CDV antigen on biopsies of nasal mucosa,
are available for Cryptococcus, Blastomyces, Coccidioides, footpad epithelium and the haired skin of the dorsal neck
and Histoplasma spp. Eubacterial PCR detection of has been reported to be a relatively sensitive and specific
16S ribosomal subunits is currently being investigated. test. Similarly, reverse transcription PCR applied to
Biopsy and IHC are required for the definitive diag- RNA extracted from whole blood, urine, CSF, tonsilar or
nosis of FIP. However, a presumptive antemortem conjunctival specimens is a sensitive and specific assay.
356 SPECIFIC EMERGENCIES

Idiopathic meningoencephalomyelitis
A definitive antemortem diagnosis of the specific variants
of idiopathic MEM is challenging, since histopathologi-
cal confirmation is required (276). In most cases a pre-
sumptive antemortem diagnosis is achieved via a
multimodal approach that includes assessment of case
signalment, neurological signs and neuroanatomical
localization, CSF analysis, cross-sectional imaging of the
CNS and negative infectious disease testing. The ante-
mortem diagnosis is often complicated by an overlap in
the neurodiagnostic profiles (especially between GME
and the necrotizing encephalitides). Therefore, the ter-
minology meningoencephalitis of unknown aetiology  276 Histopathology of the brain and meningeal tissue
(MUA) may be preferable on an antemortem basis in from a canine case of GME (× 20), which demonstrates
cases of idiopathic ME where histopathology is lacking. the cellular accumulation within the meninges often
The following points regarding CSF analysis (see also evident in these cases. (Photo courtesy Victoria Watson)
Table 80) and cross-sectional imaging may help with pre-
sumptive diagnoses of the idiopathic MEMs:
• The CSF profiles for GME, NME, NLE and
chronic SRMA overlap, with a mononuclear
(lymphocytes, monocytes) pleocytosis and TP
elevations being most common. may be observed as displacement of surrounding
• The CSF profile for acute SRMA is typified by a brain tissue. Some lesions may be associated with
neutrophilic pleocytosis, TP elevation and elevated hypoattenuating vasogenic (white matter) oedema.
IgA (CSF and serum). • The focal form of GME may be identified on CT
• The CSF profile for idiopathic tremor syndrome is or MRI as a nonspecific, single, space-occupying
typified by a lymphocytic pleocytosis and TP mass lesion.
elevation. • In ocular GME, the optic nerves may be hyper-
• Although not specific for GME, the most common intense on T2-weighted images and may show
MRI findings for the disseminated form include contrast enhancement on T1-weighted images.
multiple hyperintensities on T2-weighted or The optic chiasm also may appear enlarged,
FLAIR sequences scattered throughout the CNS reflecting the gross pathology.
white matter. These lesions typically assume an • Mild NME, infectious ME, CNS lymphosarcoma
infiltrative appearance and have irregular margins. and glial and metastatic neoplasms may present
• Despite the predilection of the GME for white with similar clinical and MRI findings to dissemi-
matter, MRI lesions are often distributed through- nated GME, and discriminating among these differ-
out both grey and white matter. Compared with entials may be challenging unless tissue biopsy is
cerebral parenchyma, the lesions are hyperintense obtained.
on T2-weighted images, variable intensity on T1- • Typical MRI lesions associated with NME include
weighted images and have variable degrees of asymmetric, multifocal prosencephalic lesions
contrast enhancement. Vasogenic oedema in the affecting the grey and white matter, with variable
white matter is commonly appreciable on T2- contrast enhancement on T1-weighted imaging.
weighted and T1-weighted images as hyper- and Loss of grey/white matter demarcation also may be
hypointense to cerebral parenchyma, respectively. discernible. Lesions appear hyperintense on
• Both focal and disseminated forms of GME may be T2-weighted images and isointense to slightly
associated with contrast enhancement of the hypointense on T1-weighted images, with slight
parenchyma and meninges on CT, and mass effect contrast enhancement.
 INFECTIOUS AND I N F L A M M AT O RY D I S E A S E S OF THE CNS 357

• In NLE, multiple, asymmetric bilateral pros- For toxoplasmosis or neosporosis, clindamycin

encephalic lesions mainly affecting the subcortical (10–25 mg/kg IV initially, then PO q12h for 3–4 weeks)
white matter have been described. The NLE may lead to a favourable outcome. Trimethoprim
lesions are hyperintense on T2-weighted and sulphonamide (15 mg/kg PO q12h) in combination with
FLAIR images and often include multiple cystic pyrimethamine (1 mg/kg/day PO) may also be effective.
areas of necrosis. These lesions are hypointense or Folinic acid or brewers yeast supplementation should be
isointense on T1-weighted images, and contrast considered (5 mg/dog q24h) in animals receiving this
enhancement is variable. latter therapy. However, bradyzoite cysts may not be
• Although leptomeningeal enhancement may be affected by antibiotics, resulting in disease recrudescence
appreciated on CT or MRI with SRMA or during periods of immunosuppression, with possible
idiopathic tremor syndrome, cross-sectional initiation of clinical signs. Rickettsial organisms should
imaging typically is normal for both disorders. be treated with doxycycline (5–10 mg/kg q12h for 4–6
weeks). Fungal MEM may be treated with voriconazole
MANAGEMENT (40–60 mg/kg PO q24h). Cryptococcal infections are
often treated with a combination of fluconazole (2.5–5.0
Infectious meningoencephalomyelitis mg/kg PO) and amphotericin B (0.5–0.8 mg/kg SC
Treatment of bacterial meningitis and CNS abscesses [diluted in 0.45% NaCl with 2.5% dextrose]) 2–3 times
necessitates the selection of an antibiotic that effectively per week (277, next page).
crosses the blood–brain/CSF barrier. Antibiotic selec- Anti-inflammatory doses of corticosteroids can be
tion should be based on culture and sensitivity results if given in some cases of infectious MEM in which
available. Empirical antibiotics should initially be given vasogenic oedema and/or an immune-mediated compo-
intravenously for 2–3 days to reach therapeutic levels in a nent of the disease process is present. Dexametha-
timely manner. Antibiotic choices include trimethoprim sone (0.05–0.1 mg/kg IV q24h for the first 24–48 hours)
sulphonamide (30–60 mg/kg q24h) and metronidazole followed by prednisolone (0.5–1.0 mg/kg PO q24h
(10–15 mg/kg q12h). Other choices include third-gener- for 1–2 weeks) can be used in the acute setting of
ation cephalosporins and fluoroquinolones such as enro- infectious MEM.
floxacin (5–10 mg/kg q24h). Antibiotics should be
continued for 3–4 weeks after clinical signs have Idiopathic meningoencephalomyelitis
resolved. Intravenous dexamethasone (0.05–0.1 mg/kg (GME, NME, NLE, MUA)
q24h) can be given for the first 24–48 hours to decrease The primary therapy for idiopathic MEM is immuno-
vasogenic oedema. Increased ICP may be seen with large suppression with corticosteroids and secondary
CNS abscesses (see below for treatment of increased immunosuppressive agents.
ICP). Abscesses of the CNS may be refractory to treat- Once an infectious aetiology has been ruled out and a
ment due to the fibrous capsule. Surgical decompression presumptive or definitive diagnosis of idiopathic MEM
by craniotomy, burr holes or laminectomy may be indi- reached, treatment should be instituted as soon as pos-
cated in cases of cranial subdural or spinal epidural sible. The patient should initially be stabilized if neuro-
empyema. logical derangements have produced respiratory or
To date, there is no definitive treatment for viral ME. cardiovascular abnormalities (e.g. seizures or brainstem
Supportive treatment and broad-spectrum antibiotics are lesions causing secondary autonomic changes). Supple-
given to prevent secondary bacterial infections in cases of mentary oxygen should be given for hypoxaemia and
CDV and FIP infection. Anti-inflammatory cortico- crystalloid/colloid support for perfusion and hypoten-
steroids may reduce inflammation in dogs or cats with sion, as needed. Once systemic parameters are stabilized,
any suspected viral ME. Euthanasia is recommended for therapy should be instituted (1) to prevent neurological
all animals with a history and clinical signs supportive of deterioration, (2) to halt the immune response with
rabies infection. In addition, rabies is a notifiable disease immunosuppressive therapy and (3) to provide support
in some countries and appropriate measures to inform for a recumbent patient if needed (278, page 359).
the relevant authorities should be taken.
358 SPECIFIC EMERGENCIES

 277 Treatment algorithm for

infectious MEM. INFECTIOUS MEM

Monitor vital parameters Intracranial stabilization

(airway, breathing, circulation) Antimicrobial therapy
(monitor neurological status)

Seizures

Diazepam 0.5–2.0 mg/kg

CRI 0.1–0.5 mg/kg/hour
Midazolam 0.06–0.3 mg/kg IV
Propofol bolus 1–2 mg/kg IV
CRI 0.1–0.6 mg/kg/minute

Bacterial meningitis/
Protozoal Rickettsial Fungal CDV and FIP
CNS abscess

Chloramphenicol Voriconazole
40–50 mg/kg q8h 40–60 mg/kg q24h
Metronidazole Voriconazole >>>
10–15 mg/kg q12h Clindamycin
itraconazole for Broad-spectrum
10–25 mg/kg q12h
Enrofloxacin Doxycycline Aspergillus spp. antibiotic, supportive
5–10 mg/kg q24h Trimethoprim– 5–10 mg/kg q12h Fluconazole 2.5–5.0 Consider prednisone
sulphonamide
Trimethoprim– mg/kg q24h and 0.5–1 mg/kg/day
15 mg/kg q12h
sulphonamide amphotericin B
30 mg/kg q12h 0.5–0.8 mg/kg q24h
Third-generation for 2–3 times/week for
cephalosporins Cryptococcus spp.
 INFECTIOUS AND I N F L A M M AT O RY D I S E A S E S OF THE CNS 359

 278 Treatment algorithm for

GME, NME, NLE and MUA. IDIOPATHIC MEM
(GME, NME, NLE, MUA)

Immunosuppressive Supportive care

Monitor vital parameters Intracranial stabilization
therapy Recumbency, urinary and
(airway, breathing, circulation) (monitor neurological status)
faecal management

Imaging or clinical Seizures

evidence of raised ICP

Mannitol 0.5–2.0 g/kg over

15 minutes (crystalloid fluid
replacement first) followed by Diazepam 0.5–2.0 mg/kg
Corticosteroids (prednisone)
0.5–1 mg/kg furosemide IV CRI 0.1–0.5 mg/kg/hour
2–4 mg/kg/day
7% hypertonic saline 1–2 Midazolam 0.06–0.3 mg/kg
Cytosine arabinoside
ml/kg IV over 5–10 minutes in IV
200–600 mg/m2SC
normotensive animal Propofol bolus 4–8 mg/kg IV or IV over 24 hours
7% hypertonic saline 4 ml/kg CRI 1–5 mg/kg/hour
IV over 5–10 minutes in
hypotensive animal

Preventing neurological deterioration Halting the immune response with

If seizures are present, diazepam or midazolam may be immunosuppressive therapy
given. (For control of emergency seizures see Chapter At present, immunosuppression is the mainstay of
23.) If neurological status progressively worsens and therapy for MUA. Most clinicians treat MUA with
increased ICP is suspected, mannitol may be given corticosteroids (prednisone or dexamethasone). In a
through an in-line filter. Some clinicians recommend large study of dogs with GME, radiation therapy
mannitol dosing every 30 minutes until the desired effect appeared to be the only independent predictor of patient
has been achieved. Intravenous furosemide may also be survival. However, these results may be biased, as patient
given following mannitol administration. The patient inclusion was based on only necropsied GME dogs.
must be adequately hydrated before mannitol is given in Depending on the severity of signs and the index of sus-
order to prevent hypovolaemia and potential renal picion for infectious disease, some specialists will initiate
damage. An alternative to mannitol is hypertonic saline. therapy with anti-inflammatory steroids (prednisone,
(See Chapters 20 and 26 for management of elevated 0.5–1.0 mg/kg PO q24h) and await serology and PCR
ICP.) results for screening of regional infectious diseases.
360 SPECIFIC EMERGENCIES

If the index of suspicion is extremely high for idiopathic

Table 81 Cytosine arabinoside regimen for
inflammatory disease (e.g. Pug with MRI lesions consis- idiopathic meningoencephalomyelitis
tent with NME), the authors immediately initiate
immunosuppressive therapy. Response to corticosteroids Intervals between Dosages given on Number of
treatment* consecutive days treatments
is variable and may be temporary, but dogs often have a
favourable initial response to steroid monotherapy. Addi- 3 weeks apart 50 mg/m2 SC 4
tional immunosuppression is considered on a case-by- q12h x 2 days
case basis, but the authors typically use secondary 4 weeks apart 50 mg/m2 SC 4
immunomodulatory agents on review of negative serol- q12h x 2 days
ogy and PCR results.
5 weeks apart 50 mg/m2 SC 4
In a clinical setting, steroid monotherapy may resolve q12h x 2 days
signs associated with MUA in some dogs, but insuf-
ficiently or only transiently provide resolution in 6 weeks apart 50 mg/m2 SC Indefinitely
q12h x 2 days
others. Moreover, long-term, high-dose corticosteroid
therapy often causes adverse effects including polyuria/
Intervals between doses can be adjusted based on clinical
polydipsia, polyphagia, weight gain, hepatotoxicity, response and occasionally repeat CSF analysis and MRI.
gastrointestinal ulceration, pancreatitis and iatrogenic * Treatment interval should only be extended if the patient
hyperadrenocorticism. These combined factors have led remains in clinical remission. If clinical signs recur, the last
to a recent focus on additional immunomodulatory drugs effective treatment interval should be used indefinitely. At the
to treat MUA (e.g. cytosine arabinoside [CA], 50 mg/m2 6-week stage, an attempt to take the dog off CA can be made
based on clinical response.
SC q12h for 2 days [see Table 81]; procarbazine,
25–50 mg/m2 PO q24h; cyclosporine, 5–10 mg/kg PO
q12h; azathioprine, 2 mg/kg PO q24h; mycophenolate,
10–20 mg/kg PO q12h; and leflunomide, 2–4 mg/kg PO
q24). In a recent study, patient survival times and
adverse effects were compared between a prednisone/
vincristine/cyclophosphamide protocol and a pred-
nisone/CA protocol. There was no significant difference
between survival times between the two groups. Adverse Treatment is monitored by clinical response and
effects were seen more often in the cyclophosphamide regression of neurological deficits and occasionally
group. The authors commonly use CA as an adjunctive repeated CSF analysis and MRI. In our experience, side-
therapy for MUA in combination with prednisone using effects have been minimal and dogs with MUA have a fair
the following protocol: long-term prognosis with combined CA/prednisone
• 1.5 mg/kg q12h for 3 weeks; therapy. However, CBCs are evaluated 10–14 days after
• 1.0 mg/kg q12h for 6 weeks; the first dosing regimen, then every 2–3 months to
• 0.5 mg/kg q12h for 3 weeks; monitor myeloid cell lines.
• 0.5 mg/kg q24h for 3 weeks;
• 0.5 mg/kg q48h indefinitely (may reduce Providing support for a recumbent patient
to 0.25 mg/kg q48h). Recumbent patients need to be properly managed
to prevent bed sores and urine scald. Ideally, the recum-
Intravenous rescue CA protocols (IV CRI at 200 mg/m2 bency of the patient and appropriate urinary and faecal
over 48 hours) have been described for the initial management need to be addressed every 4–6 hours.
treatment of severe idiopathic MEM. The authors have Urine and faeces must be cleaned off the patient as soon
also used a higher intravenous dose regimen (600 mg/m2 as possible in order to prevent dermatitis. Occasionally,
over 24–48 hours), which seems to be useful for severe recumbent and, sometimes, demented patients may need
relapses. It is recommended that intravenous rescue CA fluid therapy to support base fluid requirement and com-
protocols are used in severely affected dogs. pensate for corticosteroid-induced polyuria.
 INFECTIOUS AND I N F L A M M AT O RY D I S E A S E S OF THE CNS 361

Idiopathic meningoencephalomyelitis disease within 3–10 days of initial neurological signs. The
(presumptive SRMA and idiopathic tremor mortality rate for cats affected with CNS FIP is nearly
syndrome) 100%, with survival times ranging from weeks to
Immunosuppressive doses of corticosteroids form the months.
cornerstone of therapy for SRMA and idiopathic tremor
syndrome. For SRMA, the following protocol has been Idiopathic meningoencephalomyelitis
recommended for a minimum of 6 months: The prognosis for GME is considered to be poor
• Prednisone (2 mg/kg PO or IV initially q12h). After without aggressive immunosuppression. The largest
2 days the dose is reduced to 1 mg/kg PO q12h for study of histopathologically confirmed GME cases
1–2 weeks, followed by 0.5 mg/kg PO q12h. included 42 dogs with survival times ranging from 1 to
• Dogs are re-examined every 4–6 weeks; CSF >1,215 days. The major factors affecting survival were
analysis and haematology can be repeated every neuroanatomical localization and focal versus multifocal
4–6 weeks. neurological signs. Dogs with focal GME were reported
• When clinical signs and/or CSF are normal, the to survive longer (median 114 days) than those with
dose is reduced by half until a dose of 0.5 mg/kg the disseminated form, which died within a few days to
q48–72h is reached. weeks (median 8 days) of diagnosis. This large study sug-
• Treatment is stopped 6 months after clinical gests that GME has a poor prognosis, with most dogs
examination and CSF evaluation are normal. succumbing to the disorder or being euthanized within a
• For chronic or refractory cases, other immuno- few weeks to months after diagnosis, despite steroid
suppressive drugs, such as azathioprine treatment. However, the study was limited to post-
(1.5–2.0 mg/kg PO q48h), may be used in mortem confirmed disease, so survival times and the
combination with steroids (e.g. alternating each associated prognosis may be biased towards dogs with
drug every other day). severe GME.
A recent epidemiological study of Pugs with NME
The majority of dogs with idiopathic tremor syndrome disclosed a median survival of 93 days (range, 1–680
respond to corticosteroid immunosuppression within days), with dogs receiving any form of treatment living
3 days. The duration of steroid therapy may range from significantly longer than those that were not treated. The
4 weeks to several months. For refractory cases of idio- prognosis for SRMA is fair to good, especially for dogs
pathic tremor syndrome, diazepam (0.5 mg/kg PO q8h) with acute disease that are treated with aggressive
or propanolol (2.5–10 mg/dog PO q8–12h) may be insti- immunosuppression. Untreated dogs typically have a
tuted. The rationale for propanolol treatment is based on relapsing and remitting disease course. The prognosis
the observation that catecholamines enhance physio- for idiopathic tremor syndrome is generally favourable.
logical tremors in humans; therefore, beta-adrenergic Tremors typically abate in most dogs by the end of the
antagonism of receptors in muscle and CNS may first week of therapy. Some dogs relapse at the end of the
ameliorate tremors. Cyclosporine has also been reported treatment, requiring continued or adjunctive immuno-
anecdotally to be a useful adjunctive therapy for idio- suppressive therapy. Occasionally, relapses may occur
pathic tremor syndrome. after several months or years. Re-institution of pred-
nisone therapy typically results in resolution of tremors
PROGNOSIS within 5 days in relapsing cases.
Previous reports of combined prednisone and CA
Infectious meningoencephalomyelitis treatment protocols for MUA showed survival times of
The prognosis for infectious MEM (bacterial, CDV, pro- 46–1,025 days. In a more recent study comparing pred-
tozoal, fungal) is dependent on the aetiology, duration, nisone/vincristine/cyclophosphamide with prednisone
recrudescence of disease and severity of neurological /CA protocols for treatment of MUA, median survival
signs. Rabies MEM is associated with a grave prognosis, times did not differ between the groups and were both
as animals infected with rabies typically succumb to the >12 months. Side-effects with the cyclophosphamide
362 SPECIFIC EMERGENCIES

protocol were greater and more severe than with the CA time of 40 dogs with presumed MUA treated with pred-
protocol. Cyclosporine has also been evaluated for the nisone and azathioprine was 1,834 days (range, 50–2,469
treatment of MUA, with an overall median survival time days). Finally, in a study of dogs with MUA comparing
(10 dogs) of 930 days (range, 60–1,290 days). Side-effects dogs treated with procarbazine and prednisone with dogs
were minimal and included excessive shedding, gingival not receiving any treatment, median survival time was
hyperplasia and hypertrichosis. The median survival 14 months and 0.73 months, respectively.
 SPECIFIC EMERGENCIES Chapter 20

HEAD TRAUMA
363

Courtenay Freeman
& Simon Platt

INTRODUCTION • Compliance is the ability of the intracranial

contents to decrease in volume in an attempt to
Head trauma is an important cause of morbidity and maintain normal ICP.
mortality in both humans and animals. Immediate and • Concussion is a reversible traumatic paralysis of
appropriate treatment is critical to potentiate an accept- nervous system function and is immediate in onset.
able recovery. Although treatment recommendations in The effects of concussion on brain function may
veterinary medicine remain controversial, there are last for a variable amount of time. This term does
several guidelines for head trauma management. Accur- not describe underlying brain pathology.
ate and frequent assessment of both systemic and neuro- • Contusion is a common result of severe head injury,
logical injuries can allow for a successful outcome. often associated with a concussion. It represents a
Additionally, treatment strategies should remain flexible, bruising of the brain surface without rupture of the
adjusting to the patient’s needs and changes in neuro- pia-arachnoid and/or interruption of the brain
logical status. A complete understanding of intracranial architecture.
physiology and the effects of injury will aid in the man-
agement of dogs and cats with head trauma. AETIOLOGY AND PATHOPHYSIOLOGY
The following definitions are useful when discussing
head trauma in small animals: Traumatic brain injury in veterinary patients occurs most
• ICP is the pressure exerted within the skull by the commonly secondary to road traffic accidents. Other
intracranial contents. Normal ICP in a dog is common causes of traumatic brain injury include kicks to
between 5 and 12 mmHg. the head, falls, gunshot wounds and animal bites.
• CPP, the pressure of blood flowing to the brain, is
reliant on a balance between MAP and ICP: CPP = Normal physiology
MAP minus ICP. Elevations in ICP can have a The brain receives 15–20% of the total cardiac output
significant impact on CPP, leading to decreased with each cardiac cycle. The high metabolic rate and
brain perfusion. dependence of the brain on adequate circulation for
• CBF is the rate of blood delivery into the brain and nutrients demonstrate the need for adequate blood flow.
is driven predominantly by CPP. CBF is regulated CBF is driven by systemic arterial pressure, but is
by cerebral metabolic activity, partial pressure of dependent on several factors. BP, cerebral metabolic
oxygen and partial pressure of carbon dioxide. rates, blood oxygen levels and carbon dioxide levels have
The relationship between CPP, CBF and cerebral a significant effect on CBF.
vascular resistance (CVR) is CBF = CPP/CVR. The brain has an intrinsic ability to maintain CBF
CVR depends primarily on blood viscosity and despite fluctuations in CPP. This ability is known as
vessel diameter. autoregulation. Autoregulation is mediated through
• Autoregulation is the intrinsic ability of the brain to myogenic, chemical and neurogenic mechanisms main-
maintain cerebral perfusion. taining tight control over CVR. Myogenic factors
 364 SPECIFIC EMERGENCIES

Systemic
100 hypotension;
PaO2 PaCO2 hypovolaemia

80 CPP

60
CBF

CPP = MAP – ICP

40 Blood pressure

20
CVR
CBF Haemorrhage,
0 50 100 150 (CPP/CVR) oedema
MAP (mmHg)

 279 The relationship between cerebral blood flow  280 The relationship between cerebral perfusion
(CBF), arterial oxygen and carbon dioxide levels and mean pressure (CPP), mean arterial blood pressure (MAP) and
arterial blood pressure (MAP). CBF is maintained at a intracranial pressure (ICP) is tightly regulated, but can be
constant throughout wide variations in MAP (autoregula- affected by various pathologies and systemic disturbances.
tion), which is primarily due to an inverse relationship CPP is shown here to be responsible for CBF, which can
between cerebral perfusion pressure (CPP) and cerebral only be kept constant by alteration of the cerebral vascular
vascular resistance (CVR) or vascular diameter. resistance (CVR).

describe the ability of the vascular smooth muscle to con- occur with a CPP <40 mmHg. The relationship between
tract or dilate in response to arterial pressure; a constant CPP, CBF and CVR is CBF = CPP/CVR. CVR depends
CBF occurs between MAPs of 50 and 150 mmHg (279). primarily on blood viscosity and vessel diameter, there-
Outside of this range, blood flow to the brain will be fore CBF is kept constant by fluctuations in CVR to
dependent on systemic arterial circulation. Chemical compensate for alterations in CPP, which can occur due
factors mediating autoregulation include: oxygen, with a to MAP changes (279).
decrease in arterial concentration resulting in vasodila-
tion and vice versa; carbon dioxide, with an increase in Injury-related physiology
arterial concentration resulting in vasodilation and vice Following injury, CBF is often significantly reduced due
versa; and nitric oxide. Finally, the sympathetic and to associated elevations in ICP (≥12–20 mmHg). Specif-
parasympathetic innervations of the vasculature allow for ic factors that decrease CBF include the presence of
further neurogenic control over blood flow to the brain. oedema, haematomas, compression of vessels from mass
A functional and intact blood–brain barrier is required effect and vasospasm. Additionally, trauma significant
for proper function of autoregulation. Therefore, loss of enough to cause brain injury probably causes some
autoregulation following head trauma is related to dis- degree of systemic shock and hypotension. The presence
ruption of the blood–brain barrier and a decline in CPP. of hypotension further reduces cerebral blood flow (280).
Failure of autoregulation allows CBF to passively follow Reduction in CBF due to raised ICP can lead to brain
arterial pressure and be less responsive to changes in ischaemia. A series of physiological responses, when CBF
oxygen delivery. declines, are in place to prevent this. Reduced blood flow
CPP is defined as the difference between MAP and to the vasomotor centres in the brainstem leads to
ICP and an elevation in ICP and/or a drop in MAP leads reduced carbon dioxide removal. Subsequent elevation
to decreased CPP. Ischaemia and a loss of autoregulation in local carbon dioxide concentrations stimulates the
 HEAD TRAUMA 365

sympathetic nervous system to increase MAP. The result

Reduced Reduced
is systemic hypertension in an effort to maintain blood CPP CBF
flow to the brain. However, as the baroreceptors located
in the aorta and carotid sinus both detect systemic hyper- Raised Raised
tension, a signal is sent to the vagal centres of the brain- ICP PaCO2
stem. A reflex bradycardia occurs as a consequence. This
phenomenon is referred to as the Cushing reflex (281). Carotid Medullary
baroreceptor vasomotor
Therefore, concurrent systemic hypertension and brady- centre
cardia can indicate elevated ICP in head trauma patients. Bradycardia
Additionally, an elevation in ICP and the subsequent
Sympathetic
reduction in CPP stimulate the release of cate- stimulation
cholamines. This catecholamine surge can lead to the
Vagal Arterial
brain–heart syndrome, which causes arrhythmias and stimulation hypertension
myocardial ischaemia.

Primary and secondary brain injury  281 The Cushing reflex creates a hypertensive and
After trauma, the brain parenchyma is susceptible to two bradycardic response to raised intracranial pressure (ICP)
types of injury: primary injury and secondary injury. as reduced cerebral perfusion pressure (CPP) and cerebral
blood flow (CBF) result in elevated CO2 concentrations.
Primary injury
Primary, or biomechanical injury, describes the injury to
the brain tissue from direct trauma and the forces applied Open (compound) comminuted depressed
to the brain at impact. An impact to the skull exerts the fracture following penetrating injury

following forces on the brain: acceleration, deceleration Closed comminuted depressed

fracture
and rotational forces. The brain is unable to tolerate these
Linear fracture
forces because of its composition and lack of internal
support. The superficial grey matter is most susceptible
to the forces of acceleration, leading to haemorrhage or
contusion and tearing of neuronal tissue. The rotational
forces have more of an impact on the deeper white matter
of the brain, causing concussive injuries and axonal
damage. The roughly spherical shape of the skull and the
propagation of rotational forces after injury direct these
forces into the deeper tissues of the brain. Additionally,
penetrating injuries can cause fractures, haemorrhage
and direct damage to the brain parenchyma.  282 Fracture classification of the calvarium.

Skull fractures
Skull fractures are described based on pattern (depressed,
comminuted, linear [282]), location and type (open however, fractures in these locations are difficult to
versus closed). A depressed fracture is one where the evaluate. Bullae fractures can result in neurological
inner shelf of bone is driven into the brain to a depth signs such as vestibular syndrome, facial paresis/paralysis
equivalent to the width of the skull. Depressed fractures and Horner’s syndrome on the side of the fracture.
are most common on the dorsal and lateral aspects of Fractures of the temporomandibular joint, mandible and
the skull. Fractures may also occur at the base of the skull, zygomatic arch may require additional treatment, but are
the middle ear and the temporomandibular joint; unlikely to cause neurological signs alone.
366 SPECIFIC EMERGENCIES

Haemorrhage Brain oedema

Haemorrhage following trauma may be located in an Oedema develops after primary brain injury and con-
extra-axial or intra-axial location. Extra-axial haemor- tinues to develop as secondary brain injury ensues. Typi-
rhage may occur in the epidural, subarachnoid or sub- cally, brain oedema is most severe 24–48 hours after
dural space. The most common location of haemorrhage injury. There are two main types of oedema: vasogenic
following trauma is within the brain parenchyma (intra- and cytotoxic (intracellular) (283).
axial) or in the subarachnoid space. Epidural haemor- • Vasogenic oedema occurs secondary to failure of
rhage is frequently secondary to bleeding from the blood–brain barrier and vasodilation (284).
meningeal arteries, resulting in blood between the skull Vasodilation is frequently secondary to
and dura. Haematomas located in the subdural space hypercapnea, which is often associated with head
(between the arachnoid and dura) are typically secondary injury. Initially, the brain is able to compensate for
to venous bleeding, resulting in slow accumulation of this increase in fluid through the compliance
blood. strategies discussed above.
Haemorrhage into the cranial cavity has several dele- • Cytotoxic oedema occurs secondary to failure of
terious effects. The presence of haematomas contributes cellular ion pumps and damage to cellular
to elevations in ICP and reduction in CBF. In addition, membranes; it can lead to cellular death.
haemorrhage provides a substrate for oxygen free radical
formation and promotes inflammation. Finally, haemor-
rhage promotes the release of excitatory amino acids,
which exacerbate secondary brain injury. Normal
Capillary
Secondary injury endothelial cell

After impact, a cascade of biomolecular events occurs Tight junction

causing continued and progressive brain pathology. The Astrocyte foot

presence of haematomas and oedema from the primary

injury distorts normal brain parenchyma and decreases
CBF. In addition, a series of cellular reactions begins at Vasogenic oedema
the time of impact and continues after the injury. This Vesicular transport
secondary brain injury has a significant effect on outcome across cell

and can lead to continued death of neurons and glial cells. Open junction

The primary mediators involved in secondary brain Escape of plasma

injury include oxygen free radicals, excitatory amino

acids (i.e. glutamate) and nitric oxide.
Following trauma, neurons release excitatory amino
acids, particularly glutamate. Glutamate causes wide- Cytotoxic oedema
spread neuronal depolarization and cellular influx of Oedematous
calcium. Excessive intracellular calcium leads to cellular endothelial cells

damage and promotes the production of oxygen free rad- Oedematous

astrocyte
icals. The combination of increased intracellular calcium
and oxygen free radicals stimulates the production of
nitric oxide and additional excitatory amino acid release.
The presence of nitric oxide perpetuates oxygen free
radical reactions and lipid peroxidation of cellular mem-
branes, causing further release of excitatory amino acids.
This process results in a self-perpetuating vicious cycle
leading to ischaemia, infarction, brain oedema and sub-
sequent elevations in ICP.  283 Vasogenic and cytotoxic oedema.
 HEAD TRAUMA 367

Decreased CPP

Increased ICP
Normal Compliance

Vasodilation

Oedema
Venous outflow

Increased CBV CSF outflow

 284 The vasodilatory cascade and its relationship with  285 The Monro–Kellie doctrine describes the ability
oedema. Vasodilation occurs in response to a decreased of the intracranial cavity and its contents to maintain a
cerebral perfusion pressure (CPP). This increases cerebral relatively constant intracranial pressure when its volume
blood volume (CBV), which in turn exacerbates oedema increases. This is possible due to compliance, whereby
and increases intracranial pressure (ICP). CSF is shunted out of the intracranial cavity and, subse-
quently, vasoconstriction decreases cerebral blood volume.

Intracranial pressure
The brain is protected within the bony confines of the 70
Intracranial pressure (mmHg)

skull, where it exists in equilibrium with CSF and blood.

60
The pressure exerted between the brain and the skull is
the ICP, which is normally between 5 and 12 mmHg in 50
dogs and cats. The skull is relatively inelastic, limiting the 40
volume that can exist within the cranial cavity. The space 30 ⌬P2
within the cranial vault is occupied primarily by three
20
components: brain parenchyma, CSF and blood.
The Monro–Kellie doctrine describes the relation- 10 ⌬P1

ship between these components and their ability to com- 0

Intracranial volume
pensate for increases in volume within the cranial cavity
(285). After head trauma, the volume of the intracranial
contents within the skull may increase due to haemor-  286 As intracranial volume increases, compliance
rhage, oedema or CSF accumulation. The brain has the ensures that the intracranial pressure (ICP) remains
capacity to tolerate small increases in volume by adjust- constant until a point when small increases in volume
ing the size of one of the three components, primarily cause exponential increases in ICP.
CSF. Shunting CSF to the spinal subarachnoid space,
decreasing CSF production and increasing CSF absorp- compensation, the patient’s clinical signs will remain rel-
tion can rapidly decrease the intracranial CSF volume. atively normal, unless the trauma primarily injured the
CSF production does not typically effect elevations in parenchyma (e.g. laceration, puncture wounds). Once
ICP unless its drainage is obstructed, leading to obstruc- compliance is exhausted, small increases in volume will
tive hydrocephalus. Additionally, venous blood can be result in dramatic elevations in ICP, which will be accom-
redirected out of the cranial cavity and CBF will decrease panied by a rapid decline in the patient’s neurological
to compensate for ICP elevation. The ability of the brain status (286). This ability to compensate is more effective
to adjust for increases in ICP by decreasing the volume of if the increase in volume occurs slowly. With continued
CSF and blood is called compliance. During this time of elevation of ICP, brain herniation can result.
 368 SPECIFIC EMERGENCIES

Caudal transtentorial herniation CLINICAL ASSESSMENT

Expanding haematoma
The ability to recognize signs consistent with elevated
ICP or a declining neurological status is critical in the
management of dogs and cats following head trauma.
Trauma significant enough to cause brain injury will
have systemic effects, which may be life threatening, and
systemic injuries and shock will cause continued decline.
Therefore, complete systemic evaluation and stabiliza-
tion are required in addition to a thorough neurological
assessment (Table 82).

Foramenal herniation Systemic assessment

Initial assessment should involve evaluation of the
 287 Caudal transtentorial herniation occurs when the patient’s respiratory and cardiovascular systems. An
parahippocampal gyrus of the occipital lobe herniates airway must be established, if necessary through endo-
underneath the osseous tentorium. In foramenal tracheal intubation. Breathing patterns may be affected
herniation the cerebellar vermis herniates caudally by thoracic trauma, but may also be secondary to brain
through the foramen magnum. injury. Auscultation of the thorax may detect pulmonary
pathology or cardiac arrhythmias. Oxygen support
should be given as necessary and mechanical or manual
ventilation may be required with severe pulmonary
injuries. Traumatic pneumothorax may require thoraco-
centesis or chest tube placement to allow proper ventila-
tion. The cardiovascular system should be evaluated by
There are four types of brain herniation: monitoring heart rate and BP and by electrocardiogra-
• Falcine herniation: herniation of one cerebral phy. An ECG may demonstrate cardiac arrhythmias sec-
hemisphere ventral to the falx cerebri. ondary to traumatic myocarditis, systemic shock or brain
• Transtentorial herniation (287): herniation of the injury. Arterial blood analysis and lactate concentrations
parahippocampal gyrus below the tentorium may provide additional information regarding systemic
cerebelli, which causes compression of the perfusion and respiratory function.
midbrain and leads to mydriatic, unresponsive Temperature assessment on a frequent basis is
pupils and loss of consciousness. A sign of important in all head trauma patients. Cerebral meta-
developing transtentorial herniation is asymmetric bolic rate is proportional to body temperature and
mydriasis followed by symmetrical mydriasis as the increases by 5–7% per Celsius degree (approximately 3%
parasympathetic portion of the CN III nucleus is per Fahrenheit degree). Hyperthermia should be
compressed. Transtentorial herniation can be life avoided in all patients and cooling techniques should be
threatening, leading to sudden cardiopulmonary considered if this is noted. Hypothermia reduces the
arrest. cerebral metabolic rate and decreases the CBF by
• Foramenal herniation: cerebellar herniation into approximately 5% per degree of reduction in body tem-
the foramen magnum (287). This is frequently fatal, perature. Although this may be advantageous to the
causing respiratory arrest by compressing the injured brain, it also increases the risk of cardiac abnor-
respiratory centres of the medulla. malities. Temperature instability in the brain-injured
• Calvarial herniation: the brain can also herniate patient may be a grave prognostic sign. (Further infor-
through a defect in the skull. mation is available in Chapter 2.)
 HEAD TRAUMA 369

Once the patient is stable, radiographs of the chest A delayed onset of scleral haemorrhage (12–24 hours)
and abdomen are recommended to evaluate for pulmon- has been noted in dogs with head trauma. This usually
ary contusions, pneumothorax and abdominal injuries. resolves in 7–10 days, but the presence of subarachnoid
Pulmonary contusions are common following trauma haemorrhage should be strongly suspected.
and may not be at their most severe until 24 hours later. In the days and weeks following head trauma, a few
The abdomen should be evaluated through radiography patients may develop endocrine disease related to hypo-
and ultrasonography for the presence of free fluid, blood thalamic/pituitary damage. Signs can be related to hypo-
or urine, which may require additional therapy. Radi- adrenocorticism and inappropriate antidiuretic hormone
ographs of the cervical vertebrae should also be consid- secretion. (Further details on the detection and manage-
ered, as head trauma can often be accompanied by ment of these conditions can be found in Chapter 3.)
fractures and luxations of these bones.

Table 82 Monitoring parameters for the cat and dog following head trauma

MONITORING PARAMETER SUGGESTED GOAL SUGGESTED TREATMENT

Neurological examination MGCS >15 • Ensure head elevation (30º)

• Ensure all points below are addressed
• Consider mannitol (see below)
• Consider surgery (see text)

Blood pressure MAP 80–120 mmHg • Adjust fluid therapy

• Pressor support (dopamine,
2–10 μg/kg/minute)

Blood gases PaO2 *90 mmHg • Oxygen supplementation

PaCO2 between 35 and 40 mmHg • Consider active ventilation

Pulse oximetry (SpO2) SpO2 *95% • Oxygen supplementation

• Consider active ventilation

Heart rate and rhythm Avoid tachy- and bradycardias; • Adjust fluid therapy
avoid arrhythmias • Treat for pain
• Address ICP
• Treat arrhythmias specifically

Central venous pressure 5–12 cm H2O • Adjust fluid therapy

Respiratory rate and rhythm 10–25/minute • Ventilate if necessary

Body temperature 37–38.5ºC (98.6–101.3ºF) • Passive warming or cooling

• NSAIDs if hyperthermic

Electrolytes (See individual laboratory normal values) • Adjust fluid therapy

Blood glucose 4–6 mmol/l (72–108 mg/dl) • Adjust fluid therapy

• Consider dextrose administration

Intracranial pressure 5–12 mmHg • As for MGCS abnormalities

MGCS = Modified Glasgow Coma Scale.

 370 SPECIFIC EMERGENCIES

Neurological assessment
Table 83 Modified Glasgow Coma Scale
A neurological assessment should be undertaken on
any animal that has experienced a trauma. Assessment SCORE
of neurological status in a patient after head trauma Motor activity
should initially be performed every 30–60 minutes. Normal gait, normal spinal reflexes 6
Frequent assessment allows for monitoring efficacy
Hemiparesis, tetraparesis or decerebrate activity 5
of treatment and early recognition of deterioration. Pri-
marily, neurological evaluation of the patient serves to Recumbent, intermittent extensor rigidity 4
determine whether there are neurological deficits sug-
Recumbent, constant extensor rigidity 3
gesting structural neurological lesions, where the lesions
are located (i.e. at least intracranial, spinal and peripher- Recumbent, constant extensor rigidity 2
al nerve) and the severity of the lesion(s). Detection of a with opisthotonus
spinal and/or peripheral nerve (e.g. brachial plexus) Recumbent, hypotonia of muscles, depressed 1
lesion can affect the prognosis of any patient with head or absent spinal reflexes
trauma. Without any extracranial lesions, the prognosis
Brainstem reflexes
associated with head trauma is dependent on the location
Normal pupillary light reflexes and 6
and severity of the parenchymal lesions.
oculocephalic reflexes
The assessment should include evaluation of state of
consciousness, motor function and reflexes, pupil size Slow pupillary light reflexes and normal 5
to reduced oculocephalic reflexes
and responsiveness, position and movement of the eyes
and breathing pattern. The evaluation of pupil and eye Bilateral unresponsive miosis with normal 4
function is the most accurate manner in which brainstem to reduced oculocephalic reflexes
function can be assessed, and this is the most important
Pinpoint pupils with reduced to absent 3
part of the examination prognostically. A scoring system oculocephalic reflexes
has been developed in veterinary patients to provide an
Unilateral, unresponsive mydriasis with reduced 2
objective assessment and allow for rational diagnostic
to absent oculocephalic reflexes
and treatment decisions.
Bilateral, unresponsive mydriasis with reduced 1
Modified Glasgow Coma Scale to absent oculocephalic reflexes
The Glasgow Coma Scale is used in human medicine to Level of consciousness
assess head trauma patients by evaluating eye, verbal and Occasional periods of alertness and responsive 6
motor responses. This scale has been modified and to environment
applied to veterinary patients. The Modified Glasgow
Depression or delirium, capable of responding 5
Coma Scale (MGCS) evaluates motor activity, brainstem but response may be inappropriate
reflexes and the level of consciousness in veterinary
patients, thus enabling initial and serial monitoring Semicomatose, responsive to visual stimuli 4
following injury. The three categories evaluated using Semicomatose, responsive to auditory stimuli 3
the MGCS provide objective standards for scoring a
patient between 1 and 6, with lower scores assigned to Semicomatose, responsive only to repeated 2
noxious stimuli
more severe clinical signs (Table 83). The scores from
each category are added together to determine a patient’s Comatose, unresponsive to repeated 1
coma score, ranging from 3 to 18, and may be used to noxious stimuli
guide treatment decisions and prognosis (288).
 HEAD TRAUMA 371

 288 The Modified Glasgow Coma Scale score is

1.0
determined from the neurological examination. The score
0.9
given can be anywhere between 3 and 18, with the lowest
0.8 score representing the worst neurological situation. The
Probability of survival

0.7 score is almost linearly related to prognosis in terms of the

0.6 probability of survival in the first 72 hours.
0.5
 289 (a) Decrebrate rigidity seen in this 3-year-old
0.4
Domestic Short hair cat is associated with coma, extensor
0.3
rigidity in all four limbs and, occasionally, opisthotonus.
0.2
This posture reflects a lesion of the midbrain.
0.1 (b) Decerebellate rigidity, which is often associated with
0 normal consciousness, hyperextension of the forelimbs
2 4 6 8 10 12 14 16 18 and spastic flexion of the hips, is seen here. This posture
MGCS Score
reflects a lesion of the rostral part of the cerebellum.

Assessment of limb function a

The first category of the MGCS describes motor activity,
limb tone and posture. Voluntary motor activity is char-
acterized as normal, paretic or recumbent. Patients typi-
cally maintain some degree of voluntary motor activity
even in altered states of consciousness unless they are
comatose. Abnormal motor function usually reflects
either brainstem injury or spinal cord injury; the latter
may complicate the assessment of head trauma.
Tone is evaluated by placing the limbs through a
passive range of motion. Increased tone can be seen fol-
lowing cranial trauma, as CNS inhibitory modulation to
the LMNs is lost. However, severe brain injury leading to
coma will be associated with decreased tone in all limbs.
Spinal reflexes are tested primarily to assess nerve func-
b
tion, but may provide some information on cerebral
activity. Animals may have exaggerated reflexes following
cerebral injury and absent reflexes when comatose.
An animal’s posture can also provide information
about the location and degree of brain injury following
trauma. Decerebrate rigidity (289a) can occur following
cerebral trauma and suggests severe brain injury and a
poor prognosis, as this posture reflects loss of communi-
cation between the cerebrum and the brainstem. Animals
with decerebrate rigidity have opisthotonus with hyper-
extension of all four limbs and are stuporous or coma-
tose, with abnormal pupillary light reactions.
Decerebellate rigidity suggests acute cerebellar damage
and may cause either flexion or extension of the hind-
limbs (289b); however, consciousness may be normal.
372 SPECIFIC EMERGENCIES

R L Normal
Sympathetic nucleus
Parasympathetic nucleus

Normal mid-range bilateral pupil size

Early severe trauma
Sympathetic nucleus
dysfunction

Bilateral miosis with left pupil pinpoint

Progressive trauma
Parasympathetic nucleus
dysfunction

Asymmetric left-sided mydriasis

Assessment of brainstem reflexes  290 Pupil size following head trauma can progress
Pupil size, the PLR and the oculocephalic reflex should from normal and reactive to light through miotic and
be immediately evaluated in all head trauma patients. pinpoint to dilated and unresponsive as the pathology
Pupil size, symmetry and reactivity can provide valuable progresses. The onset of miosis is related to brain injury
information about severity of brain injury and the prog- causing damage to the sympathetic system responsible for
nosis. These parameters should be assessed frequently, as pupil dilation. As the injury progresses and causes
they can signal a deteriorating neurological status. transtentorial herniation, the oculomotor nucleus
Response of the pupils to a bright light indicates suffi- becomes affected and results in pupil dilation.
cient function of the retina, optic nerves, optic chiasm
and rostral brainstem. The presence of miosis may indi-
cate a lesion in the diencephalon, as the sympathetic
innervation to the eye originates in the hypothalamus.
The peripheral sympathetic innervation to the eye can decreased cerebral perfusion, postictal changes, trauma
also be affected by injury anywhere along its pathway to the iris or retina, periorbital trauma or haematoma and
through the brachial plexus, cranial mediastinum, cervi- previous ocular abnormalities.
cal soft tissues and tympanic bulla, which often causes Progression from miosis to mydriasis indicates a
concurrent third eyelid elevation, enophthalmos and deteriorating neurological status and is an indication for
ptosis as part of Horner’s syndrome. A miotic pupil may immediate, aggressive therapy. Unilateral changes in
also be seen with ocular injury and spasm of the ciliary pupil size may be seen early in deterioration. Paralysis of
muscles of the iris; therefore, an ocular cause of miosis CN III can lead to mydriasis, loss of direct PLR, ptosis
should be investigated. and ventrolateral strabismus. The CN III nucleus is
Bilateral mydriasis that is unresponsive to light can located in the midbrain, therefore damage to this nucleus
indicate permanent midbrain damage or brain herniation can be seen as a result of midbrain injury or compression
and a poor prognosis. Other causes of mydriasis include secondary to transtentorial herniation (290).
 HEAD TRAUMA 373

The oculocephalic reflex (physiological nystagmus) is Assessment of respiration

tested by moving the animal’s head in vertical and hori- Although assessment of respiratory patterns does not
zontal planes to assess brainstem function and function of form part of the MGCS, intracranial trauma may lead to
the CN nuclei innervating the extraocular eye muscles. abnormal respiratory patterns and these should be
If the animal’s head cannot be moved without risk, a assessed. Their associations with specific lesion localiza-
visual stimulus such as food or the owner should be tions have not been confirmed in veterinary patients and
moved or move around the animal. Absence of the oculo- so much of what we suspect is taken from the human lit-
cephalic reflex reflects injury to the brainstem. This erature. Hyperventilation may occur as a result of central
reflex may also be delayed with cerebral injuries. mediation secondary to cerebral acidosis, cerebral
hypoxia, mesencephalic injury or transtentorial hernia-
Assessment of consciousness tion. A period of hyperventilation followed by apnoea is
A patient’s level of consciousness provides information referred to as Cheyne–Stokes respiration, which is
regarding function of the cerebral cortex and the ARAS usually secondary to diencephalic injury and reduced
of the brainstem (see Chapter 6). Consciousness can be responsiveness to partial pressure of arterial carbon
described as normal, depressed or obtunded, stuporous dioxide. Respiration may also be classified as ataxic,
or comatose. An animal in a stupor is partially or which is indicative of severe brainstem damage and
completely unconscious, but will respond to noxious carries a grave prognosis. This breathing pattern is char-
stimuli. A patient in a coma is unconscious and cannot be acterized by an irregular rate, rhythm and depth of respi-
roused with noxious stimuli. Coma typically indicates ration and is frequently accompanied by the Cushing
severe cerebral injury or brainstem damage, which reflex (i.e. hypertension and bradycardia), forming the
carries a guarded prognosis. These terms describe differ- Cushing triad.
ent levels or ‘quantities’ of consciousness and provide
information regarding the degree of cerebral impair- DIAGNOSIS
ment. The quality of consciousness may be more difficult
to evaluate objectively. Inappropriate activity suggesting A diagnosis of head trauma is based primarily on a com-
confused or exaggerated responses to routine stimuli patible history and clinical signs of intracranial neuro-
often confirms prosencephalon damage. It is important logical dysfunction. However, additional tests can be
to note that the patient’s BP, oxygenation status and tem- used to confirm the location and the extent of the injury.
perature may all affect the animal’s level of consciousness Advanced imaging of the brain (CT and MRI) should be
and so the latter should be re-evaluated after correction reserved for patients who do not respond to initial treat-
of the former vital parameters. ment or for patients who deteriorate despite aggressive
After evaluation, a patient should be assigned a score therapy. Both of these imaging modalities require anaes-
for each category to determine their overall coma score. thesia, which can destabilize the head trauma patient
This score can be used to monitor for improvement or unless the patient is in a coma on presentation.
deterioration of neurological status, guide diagnosis and Significant injury to the brain, leading to neurological
treatment decisions (see below) and provide information signs, can occur without causing skull fractures or
about prognosis (see 288). haematoma formation. Advanced imaging of the brain
may be performed to evaluate for fractures, haemorrhage
or parenchymal lesions; however, changes may not be
seen even in a patient with severe neurological deficits.
 374 SPECIFIC EMERGENCIES

 292 Transverse CT scan (soft tissue window) of a

7-year-old mixed breed dog 8 days after a head trauma.
b There is a large hypoattenuating lesion (arrows) in the
temporal lobe, which was found to be a cystic lesion
secondary to haemorrhage on postmortem examination.

Radiography
Skull radiography may reveal calvarial fractures, but pro-
vides no information regarding the brain parenchyma
(291). Radiographs of the skull require anaesthesia for
accurate positioning, which may be contraindicated in
 291 (a) Dorsoventral skull radiograph of a 3-year- the acutely injured patient, and they can be difficult to
old Chihuahua that had been attacked by another dog. interpret due to the irregularity of the skull bones.
A linear fracture of the temporal bone is evident (arrows). Radiography should not be limited to the skull following
(b) Lateral radiograph of a 2-year-old Chihuahua that head trauma. Radiographs of the vertebral column,
was also attacked by another dog. There are comminuted thorax and abdomen are indicated to evaluate for evi-
fractures of the parietal bone (arrows), which could be dence of other injuries.
depressed, but two views would be necessary and,
possibly, advanced imaging to make an accurate Ultrasonography
assessment of injury. The dog was positioned carefully Ultrasonography can be used to evaluate the brain
with flexion of the cervical spine in order to evaluate parenchyma crudely through a bony defect. Haemor-
for the potential of vertebral abnormalities such as rhage within the brain is hypoechoic in the acute stages,
atlantoaxial subluxations, which were not present. but may become hyperechoic over time. Doppler ultra-
sonography may be used to detect blood flow and indi-
rectly assess ICP by evaluating the basilar artery.
 HEAD TRAUMA 375

a b  293 (a) Transverse CT scan at the

level of the caudal fossa demonstrates
a beam-hardening artefact (arrows),
due to the dense bone surrounding
the parenchyma. This artefact
interferes with lesion assessment in
the brainstem. (b) Transverse T2*-
weighted (gradient-echo) MR image
at the level of the caudal fossa. This
allows identification of a parenchymal
lesion (arrow) secondary to trauma
within the brainstem.

a b  294 Transverse T2-weighted (a)

and transverse T2-weighted FLAIR
(b) MR images of a dog bite. The
penetrating lesion can be identified
on both images, but the hyperinten-
sity on the FLAIR image more clearly
indicates the surrounding oedema.
FLAIR MRI is more sensitive to
oedematous lesions as it can suppress
signals from free water such as CSF.

Computed tomography Magnetic resonance imaging

CT allows superior evaluation of bony structures and is MRI allows superior soft tissue detail and is preferred for
preferred over conventional radiography, especially con- evaluation of the brain, especially the caudal fossa, which
sidering the 3D reconstruction capabilities. In addition, does not image well with CT (293). MRI can detect more
CT can be used to diagnose intracranial haemorrhage, subtle parenchymal changes that may be missed on CT
alterations in ventricular size or shape, midline shift of and may provide information about the prognosis.
the falx cerebri and oedema. CT does not provide good Haematomas or haemorrhage, parenchymal contusions
soft tissue detail of the brain parenchyma, but is fre- and oedema are readily apparent on MR images (294;
quently the preferred modality for evaluation of human 295, next page). Although CT is preferred for evaluation
head trauma patients for surgical intervention because of of bony structures, fractures can also be identified on
the speed of image acquisition. Typically, haemorrhage is MRI (296, next page), most proficiently using STIR and
hyperattenuating (hyperdense) on a CT scan in the acute gradient echo sequences (see Chapter 4 for further
stages. Over time, the density decreases with clot resorp- details).
tion, creating a hypoattenuating lesion similar to oedema Typically, CT and MRI are only pursued in patients
(292). CT can provide images for surgical planning, but who fail to respond to aggressive medical therapy or
should only be pursued in patients who are severely patients who deteriorate and may require surgical inter-
affected or are deteriorating and require surgical inter- vention. MRI findings were recently correlated with
vention. prognosis in veterinary head trauma patients, therefore
its use may be of specific additional benefit (see below).
 376 SPECIFIC EMERGENCIES

a b  295 Transverse (a) and dorsal

T2*-weighted (gradient-echo) (b) MR
images of a Jack Russell Terrier
following a head trauma. The hypo-
intense (signal void) or black areas
within the parenchyma (red arrows)
are compatible with haemorrhage.
The dorsal image (b) also reveals a
linear skull fracture (yellow arrows),
which can be best seen on T2*
images.

a b  296 (a) Transverse T2-weighted

MR image of a Labrador Retriever
revealing a comminuted depressed
fracture of the frontal bone. (b)
Sagittal T2*-weighted (gradient-
echo) MR image of a Corgi revealing
a depressed occipital bone fracture, as
well as hyperintensity within the
cranial cervical spinal cord (arrow),
compatible with oedema secondary to
the compressive fracture.

Intracranial pressure monitoring

ICP may be monitored through placement of a pressure
transducer or fibre-optic transducer into the epidural,
intra-axial or intraventricular space (297). ICP monitor-
ing is frequently pursued in human head trauma patients,
but it may have limitations in veterinary patients. ICP
monitoring is not without risk and may lead to the devel-
opment of oedema, haemorrhage, parenchymal damage
and infection.

 297 An intracranial pressure (ICP) monitor often

relies on a fibre-optic transducer placed within the
cerebral parenchyma to record fluctuations in ICP.
 HEAD TRAUMA 377

MANAGEMENT normalization of MABP, mentation and CVP if

monitored, and giving additional fractions if needed.
Treatment strategies should be directed towards both Unfortunately, crystalloid solutions will extravasate into
systemic and neurological stabilization in an effort to the interstitium within 1 hour of administration, thus
minimize secondary damage. Several aspects of treat- requiring additional fluid resuscitation.
ment exist. Systemic stabilization involves correction of Hypertonic and colloid fluid therapy can rapidly
systemic shock and respiratory abnormalities with fluid restore blood volume using low-volume fluid resuscita-
therapy and oxygen therapy/management of ventilation, tion; in addition, colloids remain in the vasculature
respectively. The second aspect of treatment involves longer than crystalloid fluids. These fluids should be
measures to reduce elevations in ICP and cerebral meta- used with caution as without concurrent administration
bolic rate. Finally, some animals require surgical inter- of crystalloid solutions, hypertonic and colloid solutions
vention because of lack of improvement or a declining can lead to dehydration. Other benefits of hypertonic
neurological status. fluids include the ability to improve cardiac output,
Corticosteroids are no longer recommended in restore normovolaemia and reduce inflammation after
head trauma patients. Their use has been extensively trauma. Hypertonic saline may be preferred in hypo-
evaluated in people, which has shown no beneficial effect volaemic, hypotensive patients with increased ICP.
and may even result in worse morbidity and mortality Hypertonic saline improves CPP and blood flow by
rates. Detrimental effects of corticosteroids include rapidly restoring intravascular blood volume. Also, the
immunosuppression, hyperglycaemia and gastrointesti- high sodium content of hypertonic saline draws
nal disturbances. fluid from the interstitial and intracellular spaces, subse-
Treatment of head trauma is proposed in a progres- quently reducing ICP. Contraindications to administra-
sive, tiered system, based on the severity of injury and the tion of hypertonic saline include systemic dehydration
success of the initial therapy (298, next page). Tier 1 and hypernatraemia. Hypertonic saline only remains
treatments are administered to all patients; Tier 2 treat- within the vasculature for about 1 hour, therefore it
ments are administered to all patients with an MGCS of should be followed by colloids to maximize its effects.
<8 and failure of Tier 1 treatments; Tier 3 treatments are A dose of 5–6 ml/kg (dogs) and 2–4 ml/kg (cats) of 7.5%
administered to all patients with an MGCS of <8 and NaCl should be given over 5–10 minutes.
failure of Tier 2 treatments. Colloids (e.g. Hetastarch, Dextran-70) allow for low-
volume fluid resuscitation, especially if total protein
Tier 1 therapy concentrations are below 50 g/l (5 g/dl). These fluids
Fluid therapy also draw fluid from the interstitial and intracellular
The goal of fluid therapy in the head trauma patient is to spaces, but have the added benefit of staying within the
restore a normovolaemic state. It is deleterious to dehy- intravascular space longer than crystalloids. Hetastarch is
drate an animal in an attempt to reduce cerebral oedema. typically given as 5–6 ml/kg boluses in dogs and 2–4
Aggressive fluid therapy and systemic monitoring are ml/kg in cats over 5–10 minutes, with frequent patient re-
required to ensure normovolaemia and so maintain ade- evaluation. A total dose of 20 ml/kg/day may be given. In
quate CPP. Detailed descriptions of fluid therapy indica- addition to volume resuscitation, oxygen carrying capac-
tions and techniques are provided in Chapter 31. ity should be considered, especially if the PCV is <0.3 l/l
Crystalloid, hypertonic and colloid fluids should be (<30%). Further information on blood transfusions and
given concurrently to help restore and maintain blood the use of oxyglobin can be found in Chapter 31. The use
volume following trauma. Crystalloids are usually given of oxyglobin and other haemoglobin-based oxygen carri-
initially for the treatment of systemic shock. These ers has not been well evaluated in head trauma, but initial
balanced electrolyte solutions may be given at shock studies suggest that they could play a valuable role.
doses (90 ml/kg for dogs; 60 ml/kg for cats). Typically, Systemic BP may require management to maintain
it is recommended that the shock dose be given in frac- adequate CPP. An MAP of 80–100 mmHg should be the
tions starting with one-third to one-fourth of the calcu- target BP. Hypotension should initially be treated with
lated volume, frequently reassessing the patient for fluid resuscitation, but if persistent may need treatment
 378 SPECIFIC EMERGENCIES

HEAD TRAUMA
Administer anticonvulsant
therapy*
1. Diazepam
0.5–2.0 mg/kg IV
2. Phenobarbital YES Seizures? NO
2–3 mg/kg IV or IM
3. Levetiracetam
20–60 mg/kg IV
Immediate systemic
evaluation and ABC
emergency therapy, then
neurological evaluation
*See Chapter 23 for further details (MGCS)

TIER 1
Improvement or stable 1. Fluid therapy Survey spine, thorax and
and MGCS >8 2. Oxygenation and abdomen radiographs
management of ventilation

Monitor over next 72 hours;

repeat neurological Deterioration or no
examination q6h improvement and MGCS <8

TIER 2
1. Mannitol 0.5–2.0 g/kg IV
over 15 minutes
2. Furosemide 0.7 mg/kg IV

Deterioration or no
improvement and MGCS <8
Consider advanced imaging

TIER 3
1. Surgical decompression
2. Hyperventilation
298 Algorithm for the
3. Hypothermia
management of head trauma.

with vasoactive agents (e.g. dopamine, 2–10 g/kg/ Head trauma patients should be positioned to maxi-
minute). Systemic hypertension may occur as a sequela to mize arterial circulation to the brain and improve venous
intracranial hypertension as a result of the Cushing drainage. This goal is best achieved by elevating the
reflex. Raised ICP leading to systemic hypertension animal’s head at a 30° angle. It is important to ensure
should be treated aggressively. The use of additional that the jugular veins are not occluded and that no
drugs to modulate the BP should be avoided unless all restrictive collars are placed around the neck, which
attempts to lower ICP have been exhausted. would elevate ICP.
 HEAD TRAUMA 379

Oxygen therapy and management of ventilation There are no contraindications to the use of PEEP in
Oxygen supplementation is recommended in all patients hypoxaemic patients. With adequate volume resuscita-
following head trauma. Control of PaO2 and PaCO2 is tion, PEEP does not increase ICP nor does it lower CPP,
mandatory and will affect both cerebral haemodynamics and it may actually decrease ICP as a result of improved
and ICP. Permissive hypercapnea should be avoided cerebral oxygenation. Assessment of adequacy of ventila-
because of its cerebral vasodilatory effect, which increas- tion can be made by measurement of arterial CO2 or,
es ICP. Hypocapnea can produce cerebral vasoconstric- alternatively, by using capnography. Details on capno-
tion through serum and CSF alkalosis. Reduction in graphy and blood gas analysis, as well as details on the
CBF and ICP is almost immediate, although peak ICP indications and techniques associated with ventilating
reduction may take up to 30 minutes after PaCO2 has patients, can be found in Chapter 2.
been changed.
The amount of oxygen within the blood (SpO2) can Tier 2 therapy
be assessed with a pulse oximeter, measuring the PaO2 Diuretics
with blood gas analysis in conjunction with measurement ICP can be addressed aggressively with the administra-
of circulating haemoglobin concentration. Calculation tion of osmotic diuretics (e.g. mannitol); however, they
of oxygen delivery to the tissues requires measurement of should not be given to any patient without being certain
both arterial oxygen content and cardiac output. Mea- that the patient has been volume resuscitated. If not,
surement of mixed venous oxygen can provide an indi- their use can precipitate acute renal failure. For this
rect measure of adequacy of oxygen supply to the tissues. reason they are reserved as Tier 2 therapies.
The amount of CO2 within the blood can also be Mannitol improves CBF and reduces ICP by decreas-
assessed by arterial blood gas analysis, as well as via ing oedema. After administration, mannitol expands the
capnography. Capnography provides breath by breath plasma volume and reduces blood viscosity, which
assessment of the adequacy of ventilation assuming improves CBF and delivery of oxygen to the brain. In
normal cardiovascular function. This technique meas- addition, mannitol assists in scavenging free radicals,
ures CO2 in the expired patient gases (P’ETCO2), which which contribute to secondary injury processes. Vaso-
approximates to the CO2 tension in the alveoli. As alveo- constriction occurs as a sequela to the increased partial
lar gases should be in equilibrium with arterial blood, pressure of oxygen, leading to an immediate decrease in
P’ETCO2 can be used to approximate PaCO2 unless ICP. Also, the osmotic effect of mannitol reduces extra-
severe pulmonary dysfunction is present. cellular fluid volume within the brain.
The goal of oxygen therapy and management of Mannitol (0.5–2.0 g/kg) should be given as a bolus
ventilation is to maintain PaO2 greater than or equal to over 15 minutes to optimize the plasma expanding effect.
90 mmHg and PaCO2 between 35 and 40mmHg. If the Continuous infusions of mannitol increase the perme-
patient is able to ventilate spontaneously and effectively, ability of the blood–brain barrier, exacerbating oedema.
supplemental oxygen should be delivered via ‘flow-by’; Lower doses of mannitol are as effective at decreasing
confinement within an oxygen cage prevents frequent ICP as higher doses, but may not last as long. Mannitol
monitoring. Face masks and nasal catheters should be reduces brain oedema over about 15–30 minutes after
avoided if possible as they can cause anxiety, which may administration and has an effect for approximately 2–5
contribute to elevation in ICP. hours. Repeated dosing with mannitol can cause diuresis,
Patients with severe head injury require mechanical leading to reduced plasma volume, increased osmolarity,
ventilation to maintain these arterial blood gas concen- intracellular dehydration, hypotension and ischaemia.
trations at their optimal levels. The absolute indications Therefore, adequate isotonic crystalloid and colloid
for mechanical ventilation include loss of consciousness, therapy is critical to maintain hydration. Administration
a rising PaCO2 of >50 mmHg and falling SpO2 despite of mannitol should be reserved for critical patients
appropriate treatment. (MGCS of <8), a deteriorating patient or a patient failing
380 SPECIFIC EMERGENCIES

to respond to other treatment. Administration of furose- Tier 3 therapy

mide (0.7 mg/kg) prior to administration of mannitol Failure of fluid therapy, oxygenation and ventilation
may have a synergistic effect at lowering ICP. Currently, strategies and osmotic diuretics to stabilize the patient
there is no evidence to support the view that mannitol is and/or improve the neurological status significantly war-
contraindicated in the presence of intracranial haemor- rants radical therapy and such cases should be considered
rhage, as has been suggested. for advanced imaging such as MRI. The treatments
discussed below have not been evaluated in veterinary
Seizure therapy medicine in terms of their efficacy and they remain
Seizures should be treated aggressively to prevent wors- controversial or unproven in human head trauma.
ening of the secondary effects in the brain parenchyma
due to associated brain hypoxia and subsequent develop- Hyperventilation
ment of oedema. Seizure activity may occur immediately Hyperventilation has been suggested as a method of low-
following trauma or may be delayed in onset. The need ering ICP quickly. Hypercapnea causes vasodilation and
for antiseizure prophylaxis after severe brain trauma subsequent increases in ICP, therefore hypoventilation
remains controversial in human medicine. Human should be avoided. Mechanical or manual ventilation
patients treated in the first 7 days after head trauma with may be used to lower PaCO2 (<35 mmHg) and reduce
anticonvulsants have a significantly lower risk of post- ICP in deteriorating patients responsive to no other
traumatic seizures within this time period than if not treatment and with no surgical lesions. The prolonged
treated. Beyond 7 days from injury there appears to be no use of hyperventilation should be avoided, as a reduction
benefit to prophylactic treatment. in cerebral PaCO2 of less than 30–35 mmHg causes vaso-
Diazepam (0.5–2.0 mg/kg) can be given intravenous- constriction, which ultimately leads to decreased CBF
ly to treat seizures. Phenobarbital (2–3 mg/kg IV or IM) and ischaemia.
may also be given and continued parenterally, following
a loading dose (18–24 mg/kg IV over a 24–48 hour Hypothermia
period), if necessary. Recently, the use of intravenous At the time of writing, hypothermia is an experimental
levetiracetam (20–60 mg/kg) has been described for treatment that has not been validated in veterinary med-
emergency seizure treatment, as it may be effective for up icine and remains controversial in human medicine. Fol-
to 8 hours without needing hepatic metabolism. Refrac- lowing trauma, the cerebral metabolic rate may be
tory seizures at the time of head trauma may require increased, leading to exacerbating secondary effects.
additional therapy such as a continuous infusion of Controlled hypothermia and induction of coma reduce
diazepam (0.5–1.0 mg/kg/hour) or propofol (4–8 mg/kg the cerebral metabolic rate and have been reported in
bolus to effect followed by 1–5 mg/kg/hour CRI). human head trauma patients and, recently, in a veterinary
Emergncy seizure treatment is discussed in greater detail patient. Hypothermia can be achieved by cooling a
in Chaper 23. patient to a rectal temperature of 32–35°C
Some patients may require long-term management (89.6–95.0°F), which reduces cerebral metabolic rate and
of seizure activity with antiepileptic medications. oxygen consumption and leads to decreased CBF and
However, if maintenance therapy is continued beyond ICP. However, reduction of core body temperature
7 days and seizure activity is not noted over a 3–6 month carries risks and may lead to the development of cardiac
period, antiepileptic treatment may be slowly withdrawn. arrhythmias, coagulopathies, electrolyte disturbances,
Therapy should be reinstituted if seizures return with an hypovolaemia and insulin resistance. Coma may also be
unacceptable frequency. induced using barbiturates, but this prevents neurologi-
cal evaluation and requires induction of mechanical ven-
tilation.
 HEAD TRAUMA 381

Progesterone therapy Intracranial hypertension should be treated initially

Progesterone therapy has been used experimentally in with the therapies discussed previously. However, in
rats and humans to reduce cerebral oedema and for its about 20% of human head trauma patients, additional
neuroprotective effects. Systemic injections of proges- decompressive surgery is also required. Surgery is bene-
terone decrease excitotoxicity by reducing the effects ficial in deteriorating patients before irreversible brain
of glutamate and enhancing the effects of GABA. damage, indicated by bilateral pupillary dilation, occurs.
Administration of progesterone to rats following trau- Surgical intervention for intracranial hypertension
matic brain injury has been shown significantly to involves the creation of a large craniectomy over the
improve functional outcome following injury, decrease most affected site, followed by a durectomy or duraplas-
neuronal loss, reduce accumulation of astrocytes, reduce ty to allow the brain to swell.
inflammation by blunting cytokine generation and Typically, skull fractures do not require surgical
improve vasogenic and cytotoxic oedema. Additionally, intervention. However, significantly contaminated,
progesterone has antioxidant effects and reduces lipid comminuted fractures may require surgical débride-
peroxidation and oxidative stress by decreasing free ment, especially if open (299). In dogs, such fractures of
radical generation and enhancing endogenous free the frontal sinus may be associated with traumatic
radical systems. pneumocephalus and this should be considered in any
dog deteriorating despite aggressive medical therapy. If
Surgery surgical intervention is pursued, aggressive débridement
Surgical intervention is reserved for patients that do not should include removal of all devitalized tissues and bone
improve or deteriorate despite aggressive medical and should be guided by imaging. Large bone fragments
therapy. Advanced imaging (CT or MRI) is necessary for may be spared and replaced after thorough débridement,
surgical planning and is also used in medically refractory cleaning and soaking in an antibiotic solution.
patients. Surgery may be indicated to remove haema-
tomas, relieve ICP or address skull fractures. Ventricular
obliteration and mass effect identified on advanced
imaging should be considered strong indicators for
surgical treatment in any animal that does not improve
with medical therapy.
Extra-axial haematomas can be removed through a
generous craniectomy. Surgery in these patients may lead
to significant haemorrhage that requires blood transfu-
sions. Removal of haematomas may exacerbate bleeding
as compression of bleeding vessels is removed, leading to
re-accumulation of blood even after surgery. Intra-axial
haematomas are typically managed conservatively.
Surgery may be indicated in a deteriorating patient with
subacute enlargement of a previously small haematoma.
Haemorrhagic parenchymal contusions can cause
severe neurological signs depending on their location.
They are typically managed conservatively. Cerebellar
contusions causing 4th ventricle and brainstem compres-  299 Intraoperative view of the dorsal calvarium of a
sion are an indication for surgery in humans in an effort 4-year-old Dachshund that was kicked by a horse. There
to reduce continued compression and the risk of hernia- are multiple linear fractures evident (arrows). Surgery was
tion. Surgery for cerebellar contusions may be indicated only necessary because the fractures were associated with
prior to neurological deterioration because these signs extra-axial haemorrhage, which warranted removal due to
are less reversible with conservative management. the deteriorating neurological status.
382 SPECIFIC EMERGENCIES

Following surgery, seizure and antibiotic prophylaxis PROGNOSIS

are recommended. Phenobarbital (2–3 mg/kg IV q6–8h
for 48 hours, followed by maintenance parenteral The prognosis is dependent on the severity of neuro-
therapy) is advised. An alternative approach is the use logical signs and the response to treatment. The associa-
of levetiracetam (20–60 mg/kg IV q8h, followed by tion between a patient’s score using the MGCS and
20 mg/kg PO q8h). prognosis has been evaluated. This showed an almost
linear correlation between score and probability of sur-
General supportive care vival within the first 72 hours (see 288). Patients with
Urinary catheters should be placed to provide proper high MGSC scores had a high probability of survival,
bladder management in recumbent patients and to while patients with low scores were unlikely to survive.
monitor urinary output. Adequate urine output is A score of 8 on the MGSC was associated with about a
between 1 and 2 ml/kg/hour, but it should match the 50% chance of survival. The MGCS has recently been
volume of fluid given to the patient. Reduced urine evaluated with long-term survival at 1 and 6 months
output could indicate continued dehydration, hypo- following injury. Again, a linear trend between MGCS
volaemia or reduced renal function. Increased urine and survival at 1 and 6 months was demonstrated. An
output may be seen secondary to osmotic diuretic association between the MGCS and long-term patient
therapy as well as central diabetes insipidus, which can outcome could allow a prediction of acceptable patient
occur as a sequela to intracranial trauma. recovery and aid in decision making at the time of injury.
Adequate nutrition is critical to the recovery of In humans with head trauma, hyperglycaemia on
patients following brain injury; however, hyperglycaemia admission is a frequent component of the stress response
should be avoided, as it increases the cerebral metabolic to the injury, a significant indicator of severity of injury
rate and promotes anaerobic metabolism, leading to and a potent predictor of the patient’s outcome. A recent
cerebral acidosis. Initially, nutrition may be supplement- study in dogs and cats suggests that head trauma in these
ed through naso-oesophageal feeding tubes. Placement species may be associated with hyperglycaemia and that
may be contraindicated in patients with elevated ICP, as the degree of hyperglycaemia can be associated with the
placement can stimulate sneezing, which causes transient severity of the head trauma. However, the degree of
increases in ICP. In patients with proper oesophageal hyperglycaemia does not seem to be associated with
function, oesophagostomy tubes allow medium- to long- outcome for dogs and cats with head trauma. Because
term management of feeding. Gastrotomy tubes offer hyperglycaemia can potentiate neurological injury, iatro-
nutritional support in patients with poor oesophageal genic hyperglycaemia should be avoided in patients with
function and allow long-term nutritional support. head trauma.
Recumbent patients require proper bedding and MRI evaluation of head trauma patients has also been
monitoring to prevent the development of decubital assessed in conjunction with the MGCS to determine
ulcers. Bedding should be well padded and evaluated fre- patient outcome. MRI changes were graded (I–IV) with
quently to maintain a clean and dry surface. Patients increasing severity of injury and evaluated with patient
require alternation of recumbency every 4–6 hours and outcome at 1 and 6 months following injury. Grade was
frequent evaluation of pressure points for development significantly associated with patient outcome. A higher
of decubital ulcers. MRI grade correlated with reduced likelihood of sur-
vival. In addition, the presence of a midline shift on MRI
was significantly associated with prognosis, with dogs
without a midline shift more likely to survive to 1 month.
Severely affected animals can achieve a functional
recovery with proper patient assessment and monitoring,
appropriate aggressive treatment and time.
 SPECIFIC EMERGENCIES Chapter 21

SPINAL TRAUMA
383

Natasha Olby

INTRODUCTION  300 Various types of vertebral and spinal cord trauma.

(a) Lateral radiograph of the thoracolumbar spine showing
Spinal trauma implies external trauma to the vertebral subluxation at T12/T13 (arrow) (caused by flexion and
column. The consequences include vertebral fractures, rotation of the spine). There is no evidence of a fracture.
luxations and subluxations, acute disc herniations and (b) Lateral radiograph of the cervical spine. The articular
soft tissue injuries. Spinal cord contusion, laceration and facets at C5/C6 have become luxated, causing a syndrome
compression, and nerve root entrapment can all occur as called ‘locked facets’ (caused by flexion and rotation of the
a result of spinal trauma. spine). The inset is a sagittal T2-weighted MR image
showing compression of the spinal cord at the site of the
AETIOLOGY AND PATHOPHYSIOLOGY luxation. (c) Displaced vertebral body fracture of L7
(caused by flexion and rotation of the spine). (d) Sagittal
The most common cause of spinal trauma is a road traffic and transverse T2-weighted MR images of the lumbar
accident. Other causes include falls, dog fights, gun shots, spine showing a traumatic disc herniation (caused by
falling objects (e.g. trees) and accidental owner-induced hyperflexion). There is a small amount of disc material in
injuries (especially cats and toy breeds of dog). the canal (red arrow) and the affected nucleus (yellow
The clinical signs associated with spinal trauma are arrow) is less hydrated than the adjacent nuclei.
caused by injury to the spinal cord, the spinal nerves as
they exit the vertebral canal and the vertebral column
itself. The various injuries resulting from trauma include
vertebral fractures, subluxations and luxations, flexion/
extension injuries and traumatic disc herniations (300).

a b

c d
 384 SPECIFIC EMERGENCIES

Subluxation and luxation can occur in combination with Spinal cord contusion
a vertebral fracture or be due to soft tissue disruption Contusive injury to the spinal cord causes primary
only, without evidence of vertebral injury. These injuries mechanical injury to the parenchyma and vasculature,
occur most frequently at the lumbosacral, thoracolumbar and secondary damage that is responsible for an expand-
and atlantoaxial junctions. Cats are more likely to suffer ing zone of necrosis and apoptosis. The majority of the
from sacrocaudal fractures than dogs and typically have a secondary damage occurs in the 24–48 hour period after
combination of fracture and luxation, whereas approxi- the initial injury, but ongoing apoptotic cell death can be
mately 20% of dogs suffer a luxation only. detected months and even years later. Primary damage to
Several different types of vertebral fracture and luxa- the spinal cord can be devastating, resulting in transec-
tion can occur dependent on the combination of loading tion of the spinal cord. Indeed, displaced vertebral frac-
forces applied and the location along the spine. Forces tures coupled with the clinical finding of paralysis and
can be divided into axial loading, flexion and extension, loss of nociception indicates an extremely poor progno-
and rotational, with each producing a different type of sis for recovery of neurological function.
vertebral column injury. Combinations of these forces Secondary injury develops because of biochemical
also produce characteristic injuries (Table 84). This type and metabolic events that interact to produce cell death.
of classification can be useful in the development of a The mechanisms can be summarized as energy failure,
treatment plan when used in combination with informa- changes in membrane permeability, excitotoxicity, oxida-
tion on the severity of spinal cord compression. tive damage and inflammation (301). Damage to the vas-
These events can cause spinal cord contusion and culature by the initial impact causes energy failure in
laceration and can result in compression by bone, soft neurons and glia, which in turn causes failure or reversal
tissue or blood (haematomas). Ongoing instability can of ion pumps, loss of membrane polarization and entry of
result in repeated contusive injuries, additional laceration sodium and calcium into cells, producing cytotoxic
of the cord and increasing severity of compression. oedema. Reactive oxygen species (ROS) (free radicals)

Table 84 Loading forces in spinal trauma

LOADING FORCE VERTEBRAL COLUMN INJURY THERAPEUTIC CONSIDERATIONS

Flexion Traumatic disc herniation May be stable

May require decompression

Extension Fracture of articular facets May be stable

Fracture of dorsal lamina and spinous May require decompression
processes

Flexion and rotation Luxation/subluxations (soft tissues of Typically unstable

vertebral column disrupted) Realignment may provide adequate decompression
Fracture/luxations (vertebral body and Additional decompression may be necessary
articular facets fractured)
Significant spinal cord laceration may be present

Flexion and axial loading Wedge compression fractures Variable stability

(vertebral body) May require decompression
Burst fractures

Flexion, extension, rotation, Transverse fracture Often stable

axial loading May require decompression
 SPINAL TRAUMA 385

 301 Diagrammatic representation of the changes that

occur following contusive injury to the spinal cord.

Energy failure
Change in membrane
• Mechanical injury to vasculature permeability
• Free radical-induced injury to • Mechanical injury
vasculature
• Energy failure
• Trmp4 expression
• Glutamate release
• Failure of autoregulation
• Free radical damage
• Increased intraspinal cord pressure

Reduction of perfusion Entry of Na+ and Ca++

NECROSIS AND APOPTOSIS

Enzyme activation Bystander damage Membrane peroxidation

Inflammation Oxidative damage

Excitotoxicity
• Ca++ entry and activation of Production of ROS due to:
• Increased release of glutamate
phospholipase A2 • Ischaemia
• Decreased removal of glutamate
• Microglial activation • Haemorrhage
• Activation of glutamate receptors
• Influx of neutrophils and • Inflammation
• Na+ and Ca++ entry into cells macrophages • Mitochondrial damage
386 SPECIFIC EMERGENCIES

produced as a result of haemorrhage, ischaemia and stances that are toxic to adjacent intact tissue, causing
mitochrondrial failure cause damage to cell membranes demyelination and axonal damage; a reduction in
and ongoing destruction of the microvascular bed, macrophage influx has been associated with an
increasing the zone of ischaemia. Intraparenchymal improved outcome. However, the inflammatory reac-
haemorrhage has also been linked to a rapid increase in tion plays an important role in tissue repair, revascular-
expression of Trmp4, a gene that encodes monovalent ization and axonal sprouting.
cation channels. Although the mechanism of this
phenomenon is poorly understood, prevention of Trmp4 Spinal cord compression
expression results in reduced haemorrhage and improved Compression of the spinal cord reduces perfusion,
outcome. Finally, local perfusion is reduced by increased potentially causing neuronal and glial cell death by
intraspinal cord pressure due to cytotoxic oedema the secondary injury mechanisms described above.
and haemorrhage and by a failure of autoregulatory Demyelination is a common finding histopathologically,
mechanisms. as a result of both direct damage to myelin and death of
The importance of decreased perfusion in initiating oligodendrocytes. Physical deformation of axons can
and perpetuating secondary damage is clear. It is critical, cause failure of ion channels, changing membrane
therefore, to maintain BP and oxygenation within permeability and producing a conduction block that
normal limits. Both hypotension and hypoxaemia can rapidly reverses when decompressed. Ongoing spinal
greatly exacerbate injury severity. cord compression can also cause development of
Membrane permeability is increased by the initial syringohydromyelia cranial to the compression site,
mechanical injury, thus exacerbating the imbalance of potentially causing neuropathic pain in addition to
intra- and extracellular ions. In addition, extracellular further neurological deterioration.
concentrations of the excitotoxin glutamate (and, to a
lesser extent, aspartate) are elevated. This results from Instability
neuronal release caused by the initial mechanical injury Instability of the vertebral column can have devastating
and energy failure, and by failure of astrocytic uptake. consequences for the patient. Sudden luxation of an
Activation of NMDA, alpha-amino-3-hydroxy-5- unstable vertebral unit can cause spinal cord transection,
methyl-4-isoxazole propionic acid (AMPA) and kainate contusion and compression (302). Sometimes, apparent-
receptors by glutamate increases sodium and calcium ly stable fractures/luxations have just enough movement
entry into neurons. Calcium entry causes cell death by to cause repeated small spinal cord contusions, produc-
activation of apoptosis-inducing proteases such as ing a deterioration in neurological status. Stability is
calpain and caspase, initiation of an inflammatory produced by the interaction of the vertebrae with each
response by activation of phospholipase A2 and further other via intervertebral discs and synovial joints at the
diminishing energy sources by binding intracellular articular facets. The dorsal and ventral longitudinal liga-
phosphates. ments, interarcuate ligaments and spinal musculature
The inflammatory response has both beneficial and provide further support. While there are different
detrimental effects. Early production of thromboxane methods of predicting instability, the most commonly
and prostaglandins by activation of phospholipase A2 used method divides the spine into three compartments
and microglial production of cytokines, such as inter- (303). Compartment one contains the ventral three-
leukin-1 (IL-1) and tumour necrosis factor-alpha quarters of the vertebral body and disc, and the ventral
(TNF-α) initiate the inflammatory response. There is longitudinal ligament; the second compartment consists
massive recruitment of neutrophils to the injured tissue of the dorsal one-quarter of the vertebral body, the disc
within a few hours, followed by macrophage recruit- and the dorsal longitudinal ligament; and the third
ment that peaks around 5 days after injury. Necrotic compartment includes the articular facets, lateral pedi-
tissue is removed eventually, leaving a cystic cavity cles, dorsal laminae, interarcuate ligaments and dorsal
(syrinx). Activated phagocytic cells can release sub- spinous processes. Disruption of any two of the three
 SPINAL TRAUMA 387

CLINICAL PRESENTATION

Animals with spinal trauma can present with a range of

signs depending on the location and severity of the injury.
Mild injuries may just cause spinal pain, but more severe
injuries cause neurological deficits related to the location
(see Chapter 1). The aneurological examination aims to
localize the neurological injury and to grade its severity.
Special attention should be paid to determining the pres-
ence of voluntary motor function and nociception in
 302 Lateral radiograph and sagittal T2-weighted MR each limb. In cases of suspected sacrocaudal fracture or
image (inset) of the thoracolumbar spinal column of a dog luxation, nociception in the tail base and perineal region
that was hit by a car. The fracture and displacement of the should be assessed. It is not unusual for there to be more
first lumbar vertebra have caused severe mechanical than one site of injury and so neurological signs can be
damage to the spinal cord. multifocal, and peripheral nerve injury, such as brachial
plexus avulsion, can complicate the clinical assessment.
A full neurological assessment should be performed
cautiously, as clinical deterioration is possible due to ver-
tebral instability. Such a deterioration can be catastroph-
3 ic, particularly in patients that have suffered an
atlantoaxial injury. It should be remembered that toy
breeds can develop atlantoaxial instability secondary to
2 minor trauma due to congenital malformations of the
dens and associated ligaments.
Patients who have suffered trauma can have other
1 soft tissue injuries. It is not uncommon for spinal
trauma victims to have significant thoracic trauma
causing pneumothorax, pulmonary contusions and
traumatic myocarditis with their attendant signs. In
addition, cervical spinal cord injury may affect motor
 303 Lateral radiograph of the lumbar spine showing control of the intercostal and diaphragmatic muscles.
the three compartments that are evaluated when The ability to ventilate should therefore be assessed
determining stability of the spine. carefully. Abdominal trauma can result in a ruptured
bladder and splenic and hepatic injury. Finally, neuro-
logical signs can be masked by appendicular fractures
and complicated by head injury.

compartments is suggestive of instability. Sometimes, DIFFERENTIAL DIAGNOSIS

muscle spasm or impaction of fracture fragments into
each other renders a potentially unstable injury stable for In the absence of a history of trauma, the following dif-
practical purposes. It is also important to remember that ferentials should be considered: acute intervertebral disc
disruption of the soft tissues of the intervertebral disc, herniation; vascular disease of the spinal cord or affecting
the dorsal and ventral longitudinal ligaments and the the blood supply of the limb (ischaemic neuromyopathy);
synovium of the articular facets disrupts all the compart- pathological fracture associated with neoplasia, infection
ments and causes instability. or metabolic disease.
 388 SPECIFIC EMERGENCIES

DIAGNOSIS respiratory and cardiovascular systems. CT and MRI

are the preferred modalities and both have advantages
Diagnosis is confirmed by imaging of the spine. Imaging and disadvantages. CT provides excellent detail of
also provides information on the number and location of fracture fragments and can identify fractures that are
lesions and on the type of injuries that are present not visible on plain radiographs. Moreover, three-
(compression, contusion, instability), thus allowing the dimensional reconstruction of images is possible,
clinician to make an appropriate treatment plan. Follow- greatly facilitating surgical planning (304). However,
ing systemic stabilization of the injured patient, the first CT provides less information on the soft tissue compo-
diagnostic step is to obtain spinal radiographs. The entire nents of the injury and might therefore miss compres-
spine should be radiographed, notwithstanding the pre- sive lesions due to haematomas or intervertebral disc
senting signs, because of the possibility of clinically silent material. MRI provides excellent soft tissue detail,
lesions and an LMN-type lesion masking the effect of a identifying spinal cord contusions, disc herniations and
UMN lesion. Thoracic and abdominal radiographs epidural haemorrhage, but it can be more difficult to
should also be obtained to identify additional soft tissue identify fracture lines in vertebrae, which is important
injuries. information when planning ‘corridors’ for implant
Great care should be taken with moving and posi- placement (305). Both CT and MRI are useful for
tioning the patient because of the possibility of instabil- measuring vertebral body size from the transverse
ity. Two people should always be present so that the views, essential when considering the maximum depth
patient can be moved while providing adequate support of surgical implants to be used.
to the spine. Sedation is needed to position adequately
and for pain control (see Chapter 30 for further details),
but should be administered cautiously as muscle relax-
ation increases the risk of further instability. Lateral
views are taken first and evaluated for evidence of
fractures or luxations. Orthogonal views should always
be obtained. Ideally, a horizontal beam is used to obtain
the ventrodorsal views. If this is not possible, the patient
should be rolled onto its back very carefully with
adequate support. The radiographs are evaluated for
evidence of fractures, luxations, subluxations and
collapsed disc spaces. The presence of displaced frac-
ture fragments is important to note, as this indicates
compression is likely. The radiographs should be
evaluated for evidence of instability based on the three
compartment model (see above). In the case of suspect-
ed AA instability, if a subluxation is not visible on lateral
radiographs, the cervical spine can be flexed carefully
while fluoroscoping the procedure to identify instabil-
ity. Flexion of the neck without fluoroscopic monitor-
ing is not appropriate, as it could result in catastrophic
failure of the AA junction.
Further evaluation of the injured spinal cord follow-  304 A three-dimensional reconstruction of a cervical
ing trauma requires advanced imaging. This is vital if column CT scan demonstrating a locked facet on the
surgery is planned, but not necessary in mildly affected left side of the subluxated C5/C6 vertebrae (arrow).
animals that are going to be managed conservatively. Such images are crucial for the correct surgical planning
Advanced imaging will require anaesthesia and this will of many spinal fractures and luxations. (Photo courtesy
require that the patient is stable with respect to its Simon Platt)
 SPINAL TRAUMA 389

a b

c d e

 305 CT and MR images of a dog with a C2/C3 spinal luxation and traumatic disc herniation. The sagittal recon-
struction of the CT image (a) shows a collapsed disc space at C2/C3 with mild dorsal displacement of the cranial end
of the C3 vertebral body (arrow). The sagittal T2-weighted MR image (b) shows hyperintensity in the spinal cord
parenchyma centered on C2/C3 and extending for the length of both vertebrae, indicative of a spinal cord contusion.
The transverse T2-weighted image at the C2/C3 disc interspace (c) shows herniated disc material causing
compression of the overlying spinal cord (arrow). The transverse and sagittal T2-weighted images at the level of
C1/C2 (d, e) show that the transverse ligament of the dens is intact, although it contains a region of hyperintensity,
perhaps indicative of a tear (arrow) (d) and that the apical ligament of the dens is also intact (arrow) (e).
 390 SPECIFIC EMERGENCIES

a MANAGEMENT

Treatment of spinal trauma is focused on contusion,

compression and instability. The decision to manage
spinal trauma medically or surgically for these issues
depends on the systemic and neurological examinations,
as well as the findings of imaging investigations (307).
• Contusion. As with any trauma patient, the first
step is to check airway patency, breathing
b and circulation. Hypotension and hypoxaemia
will worsen the outcome of spinal cord injury and
should be corrected if present. Further medical
management is contentious. Corticosteroids may be
indicated for shock, but are not indicated to treat
spinal cord injury. Methylprednisolone sodium
succinate (MPSS) has been advocated as a free
radical scavenger. Prospective placebo-controlled
trials in humans with spinal cord injury (the
National Acute Spinal Cord Injury Study [NASCIS]
trials) suggested that high doses of MPSS (30 mg/kg
 306 (a) Lateral myelogram of the thoracolumbar spine IV followed by a CRI of 5.4 mg/kg/hour for 24–48
of a patient with a traumatic injury at T10/T11. Note the hours) improved outcome slightly if treatment was
slight collapse of the disc space, with thinning of the initiated within 8 hours of injury. Since the
contrast columns at T10/T11 and over the body of T11. publication of the NASCIS trials, the validity of the
(b) Lateral CT myelogram of the lumbar spine of a dog statistical analysis and conclusions of the study have
following a trauma that caused an L5/L6 subluxation. been questioned and the results remain contentious.
Dorsal and ventral attenuation of the subarachnoid MPSS did not improve outcome in dogs with an
contrast columns is notable at the site of the luxation, experimentally induced spinal cord injury, and there
suggestive of a circumferential compressive lesion. are no controlled data on its effect in a clinical
(Photo courtesy Simon Platt) setting. There is currently no clear evidence that
MPSS will improve outcome of spinal cord injury in
dogs. Polyethylene glycol (PEG) has also been
Myelography as a diagnostic technique has largely advocated as a therapy for acute spinal cord injury.
fallen out of favour because of the potential to cause This hydrophilic polymer is a surfactant that can
deterioration in neurological signs and potential side- seal defects in cell membranes. Following injury,
effects such as seizures. Because patients with spinal membrane damage causes an increase in perme-
fractures and luxations frequently have vertebral in- ability that plays a large role in secondary injury.
stability, the potential for causing additional injury It is proposed that administration of PEG can
during positioning to obtain orthogonal views in myel- reverse this change, thus improving outcome.
ography is of real concern. However, historically, myel- A study in dogs with disc herniations showed that
ography has been used to identify spinal cord it is a safe drug and may improve outcome, but the
compression, and it can be used when CT and MRI are outcomes reported in this study were similar to
not available. Myelography can also be combined with those in other published case series in which PEG
CT to enhance the ability to identify soft tissue com- was not administered. The drug is not commercially
pression of the spinal cord (306). available in a medical grade at the time of writing,
therefore it requires specialized pharmacy
 SPINAL TRAUMA 391

SPINAL TRAUMA

Stabilize patient
• Assess and treat A, B, C
• Treat hypotension and hypoxaemia

Neurological examination

Localize signs and grade severity

• Presence of motor function
• Presence of nociception
• Respiratory function

Obtain radiographs
• Spinal
• Thoracic
• Abdominal

• Good motor function • Non-ambulatory status

• Controllable pain • Severe pain
• Systemically unstable patient • Unstable spine
• Limited owner finances

CONSERVATIVE MANAGEMENT Change in patient status Advanced imaging

SURGICAL MANAGEMENT
 307 Approach to the patient with spinal cord trauma.
 392 SPECIFIC EMERGENCIES

a b  308 Schematic representations of

approximate pin or screw placement
angles in (a) the body of the cervical
vertebrae, (b) the body of the thoracic
vertebrae, (c) the body of the lumbar
vertebrae and (d) in the joint
processes.The last represents a
temporary fixation technique securing
vertebral alignment prior to more
appropriate implant use in the bodies
of the vertebrae.

c d

preparation and administration through a filter. The Decompressive procedures could produce or
recommended dose is 2 ml/kg of PEG (3500 exacerbate instability in the injured spine, thus
Dalton, 30% w/w in saline) given intravenously over requiring surgical stabilization.
15 minutes and then repeated 4 hours later. New • Instability. Instability can be addressed surgically,
adjunctive medical therapies are constantly being by placement of an external splint or simply by cage
tested: minocycline and erythropoietin show rest (Table 85). Surgical stabilization is the most
promise, but they have yet to be evaluated clinically. effective method of stabilizing an unstable spine,
• Compression. Compression of the spinal cord can but it is associated with significant surgical risks.
be addressed surgically. Compression can be due to A variety of different techniques are used. In one of
displaced vertebral fragments, a herniated interver- the most easily adaptable techniques, screws or pins
tebral disc or haematomas. Decompression may be are placed in the vertebral bodies adjacent to the
achieved by realignment of vertebrae alone; a injury and cement is applied to hold the structure in
laminectomy or hemilaminectomy may be neces- alignment (308, 309). Another popular technique,
sary to remove material from the vertebral canal. sometimes known as ‘spinal stapling’ or ‘segmental
 SPINAL TRAUMA 393

Table 85 Advantages and disadvantages of different stabilization techniques

TECHNIQUE ADVANTAGES DISADVANTAGES INDICATIONS

Cage rest Inexpensive No stability provided Stable fracture (articular

No anaesthetic or surgical risk No decompression facet, dorsal spinous and
transverse processes)
No spinal cord compression
Mild neurological deficits

External splint Inexpensive Splint complications Unstable fracture

No anaesthetic or surgical risk Limited protection against axial Limited spinal cord
or rotational forces compression
No decompression Mild neurological deficits

Screws/pins and PMMA; Excellent stabilization Cost Unstable fractures

plates Can combine with decompression Risk of iatrogenic injury during
implant placement
Infection
Implant failure

Segmental stabilization Good stabilization against flexion Suboptimal protection against Unstable lumbosacral/
and extension rotational and axial forces caudal lumbar fractures
Reduced risk of iatrogenic injury Implant failure/migration
Readily applied in the lumbosacral Infection
region

PMMA = polymethyl methacrylate cement

a b

 309 Lateral (a) and ventrodorsal (b) radiographs of the cervical spine following surgical stabilization. The cervical
luxation has been stabilized using screws and polymethyl methacrylate cement. K wires have been placed in the cement
as rebars to strengthen the cement.
 394 SPECIFIC EMERGENCIES

stabilization’, uses pins wired to articular facets and

dorsal spinous processes to stabilize dorsally (310).
Different plates can be used. Difficulty contouring
plates to the vertebral bodies limits options, but
more recently, locking plates, such as the String of
Pearls plate, have been described that can offer
more flexibility (311).

Sacrocaudal luxations in cats are typically addressed by

amputation of the tail if it is paralysed and has no noci-
ception. Prompt removal of the tail may limit any
ongoing damage to the sacral nerve roots that could
result from inadvertent movement of the tail.
Surgical complications from any spinal stabilization
procedure can be serious and include iatrogenic injury
to the spinal cord, damage to the vasculature immedi-
ately ventral to the vertebral column and infection. The
timing of surgery is often dictated by the severity of
 310 Ventrodorsal radiograph demonstrating other systemic injuries (e.g. lung contusions, traumatic
segmental stabilization of an L7 fracture. (Photo courtesy myocarditis), which might affect the ability to perform
Karen Muñana) general anaesthesia. Typically, spinal stabilization is
performed as soon as it is safe for the patient. However,
animals with cervical injuries that are hypoventilating
need surgery as soon as possible to avoid the use of, or
reduce the amount of time spent on, a ventilator.
If surgery is not an option, patients can still make a
successful recovery with conservative management.
This involves strict confinement to a cage for 4–6 weeks
combined with controlled rehabilitation exercises. If
there is an unstable fracture or luxation, an external
splint can be placed. The fore- and hindlimbs need to
be included in the splint in order to immobilize the
thoracolumbar junction, and the head and forelimbs
must be included to immobilize the cranial cervical
spine (312). Placement of the splint is achieved by wrap-
ping the appropriate part of the body in cast padding.
A splint is then formed (e.g. from Vetcast [3M]) to cover
the dorsal aspect of the thoracolumbar spine or the
ventral aspect of the neck (from below the chin to the
sternum). Following padding of the splint to ensure
that there are no sharp edges, it is incorporated into the
bandage with a cover of bandaging material such as
Vetwrap. Pressure points, particularly between the
 311 Ventrodorsal radiograph of the thoracolumbar fore- and hindlimbs, should be checked and padded
spine showing use of String of Pearls plates to repair an carefully. The patient should always be hospitalized
L1 fracture. (Photo courtesy Peter Early) overnight after the first placement of a splint to ensure
that it is tolerated and to allow adjustment for any initial
 SPINAL TRAUMA 395

 312 Application of an external splint for a caudal  313 A partial thickness decubital ulcer present over
lumbar fracture luxation. (Photo courtesy Simon Platt) the ischiatic protuberance (arrow) in a dog that had been
recumbent for 2 weeks.

splint movement. Splints should be checked daily by the integrity of joints and muscles. Ideally, patients are
owner for development of decubital ulcers. They managed initially at a rehabilitation centre or a rehabili-
should be checked and potentially changed by the vet- tation plan is developed for the owner to perform at
erinarian after the first 3–5 days, then on a weekly basis home. If the patient is unable to urinate, the owner must
for 6 weeks. Splints do not protect from compressive be able to express or catheterize their pet 3 times a day.
loading of the spine and offer poor protection against The addition of phenoxybenzamine (0.25–0.5 mg/kg PO
rotatory forces. In addition, it is not possible to stabilize q8–12h) or prazosin (dog: 1 mg if less than 15 kg body
the lumbosacral spine with an external splint. Splints weight or 2 mg if over 15 kg PO q8–12h; cat: 0.25–0.5
are inappropriate if there are open wounds affecting mg PO q12–24h) and diazepam (0.5 mg/kg PO 20
areas that would be incorporated into the bandage. minutes prior to expression) may help to reduce urethral
Aftercare of all patients is similar whether managed sphincter tone and facilitate expression. Since marked
surgically or conservatively. Pain relief should be pro- hypotension can result from prazosin, patients should
vided. An appropriate regimen includes: be monitored for lethargy, collapse, pallor, syncope or
• An NSAID such as carprofen (contraindicated seizures. The skin should be kept clean and dry and
if large doses of corticosteroid have been checked regularly for development of urine scald or
administered). decubital ulcers over pressure points (313). Patients
• An opioid (e.g. intravenous hydromorphone in the should be rechecked by the veterinarian at least once a
first 24–48 hours, then oral tramadol or transdermal week if a splint has been applied; they are expected to
fentanyl). make a steady recovery. Any deterioration in neurologi-
• A drug active against neuropathic pain cal status should be investigated using spinal radiography
(e.g. gabapentin). and, potentially, advanced imaging if deterioration con-
tinues. At 6 weeks, the splint can be removed and the
Animals should be confined to a small, well-padded owner instructed to gradually increase the amount of
cage so that they cannot fall. They should be taken out controlled exercise that the patient performs over the
3–4 times a day to urinate (or have their bladder manual- next 3 months. Vigorous exercise that involves jumping
ly expressed) and defecate and for limited controlled and and twisting should be avoided permanently, especially in
supported exercise. Massage and PROM exercises the case of luxations, which will only demonstrate fibrous
should be performed on affected limbs to maintain the union rather than osseous union.
 396 SPECIFIC EMERGENCIES

a b

 314 Lateral (a) and ventrodorsal (b) radiographs of surgical correction of an atlantoaxial instability using two screws
placed transarticularly between C1 and C2. The cartilage between C1 and C2 was removed and an autologous
cancellous bone graft placed to produce bony fusion. A splint was placed for 6 weeks postoperatively.

Management of atlantoaxial subluxation intensive care unit in which they can be monitored
AA subluxations pose a particular set of therapeutic prob- closely and placed on a ventilator if needed. The progno-
lems that include extremely small and soft bones due to sis for recovery following surgery is affected by the sever-
breed and age, high risk of mortality associated with the ity and duration of signs at presentation and the age of
consequences of a C1/C2 spinal cord injury and a diffi- the dog. It is also important to note that surgical experi-
cult surgical approach. Cases can be managed surgically ence and skill can critically affect the outcome, and this
or conservatively, but in general, surgery is recom- surgical procedure should not be attempted without
mended for any patient with a severe luxation (and there- appropriate training.
fore instability) and neurological deficits. A variety of Conservative therapy of AA subluxation is indicated
different surgical techniques have been advocated. A in dogs that are extremely young, in order to postpone
ventral approach is used most commonly nowadays, surgery until a time when their skeleton is more mature,
although great care should be taken of the soft tissue in dogs with a fracture and mild signs (pain, paresis
structures (the larynx, pharynx, oesophagus and thyroid only), and in cases where the owner is reluctant for
glands) retracted to give access to the ventral aspect of the surgery to be performed. An external splint is placed
cervical spine. Screws or threaded pins can be placed that extends from in front of the ears to include the
transarticularly between C1 and C2 (314), although it forelimbs. The neck is placed slightly in extension. The
can be difficult to achieve the necessary angle and bone splint in kept in place for 6–12 weeks. An animal with a
failure may also occur in young toy breeds. An alternative fracture can develop a bony union within 6 weeks and
is to place screws vertically in the body of C1 and C2 may have the splint removed at that time if radiographs
and encase them in polymethyl methacrylate cement show fusion. Animals with congenital instability may
(315). Using the latter approach, placement of the screws not be able to stabilize their AA junction permanently
still requires careful consideration of the implant corri- with conservative therapy. It is hoped that scar tissue
dors, but it is more straightforward than placing transar- will form between the dorsal aspect of C1 and C2 (the
ticular screws. The disadvantage is that the cement lying dorsal AA ligament) and potentially around the dens
ventral to C1/C2 can cause compression of the underly- while in the splint. However, although most dogs will
ing pharynx and airways, resulting in swallowing difficul- improve while the splint is in place, this fibrous repair
ties. The immediate postoperative period carries a high will always be prone to further damage and a relapse in
risk of respiratory failure and cases should recover in an signs is possible.
 SPINAL TRAUMA 397

a PROGNOSIS

The prognosis associated with spinal cord injury is influ-

enced by the severity of the spinal cord injury and the
presence of injuries to other organs (e.g. lungs, heart,
bladder). The form of treatment (surgical versus conser-
vative) does not appear to influence outcome, although in
published case series the more severely affected patients
b tend to be treated surgically, and so a true comparison is
difficult. Prognostic indicators based on the neurological
examination are somewhat different for different regions
of the spine:
• Thoracolumbar injuries carry a guarded to grave
prognosis for recovery of hindlimb function and
faecal and urinary continence if the animal is
paraplegic with loss of nociception to its hindlimbs.
If nociception is still present, these animals do have
a good chance of recovery.
• Cervical injuries are associated with a guarded to
grave prognosis if the animal is tetraplegic and
unable to ventilate adequately. If treated surgically,
the risk of perioperative death can be as high as
36% in cervical injuries. Note that it is extremely
unusual to see tetraplegic animals that lack
nociception, because cervical spinal cord transection
usually causes death by respiratory failure and brad-
 315 Lateral (a) and ventrodorsal (b) radiographs of yarrhythmias. Delaying referral, diagnosis and
surgical correction of an atlantoaxial instability using two treatment does worsen the prognosis. Less severe
screws placed in the ventrum of C1, two screws in the injuries carry a much better prognosis, with the
cranial body of C2 and one screw placed in the caudal majority of cases making a recovery if managed
body of C2. The caudal screw was placed to aid in the appropriately.
reduction of the subluxation. A wire was placed around • The prognosis for recovery of faecal and urinary
the screw and retracted caudally to hold the vertebrae in continence in lumbosacral and sacrocaudal fractures
alignment while the polymethyl methacrylate cement was is approximately 50% if there is absent anal tone
placed and hardened around the screw heads. As in 314, and no nociception in the perineal region or the tail
the cartilage between C1 and C2 was removed and a bone at the time of presentation. A recent study suggests
graft was placed to produce bony fusion. There is no need that positive tail base sensation is useful for
for a postoperative splint using this technique. identifying cases that will definitely recover within
30 days of the injury, but it is not very useful for
identfying cases that will recover despite not having
tail base sensation. Because the cauda equina is
largely composed of peripheral nerves, displace-
ment of fracture fragments is less likely to cause
complete transection, but severe pain due to nerve
root entrapment is common and can be a reason for
euthanasia.
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 SPECIFIC EMERGENCIES Chapter 22

ACUTE DISC DISEASE

399

Joan Coates

INTRODUCTION AETIOLOGY AND PATHOPHYSIOLOGY

Degenerative disc disease represents clinical signs related The intervertebral disc permits stable motion of the
to degenerative changes in the intervertebral disc. spine while supporting and distributing loads under
Fibroid degeneration of the disc is a normal age-related movement. The annulus fibrosus is a multilaminated
change associated with progressive decrease in proteo- ligament that encompasses the periphery of the disc and
glycans and glycosaminoglycans. These degenerative attaches to the hyaline cartilage of the vertebral end
changes are accelerated in the chondrodystrophic plates. Its outer collagen lamellae blend with the ventral
breeds. and dorsal longitudinal ligaments, while the inner lamel-
Intervertebral disc disease (IVDD) is often divided lae blend with the nucleus pulposus. The nucleus pul-
into two distinct categories, referred to as Hansen type I posus, an embryologic remnant of the notochord, is the
and Hansen type II: central portion of the disc and is highly hydrated.
• Hansen type I IVDD results in herniation of the The major molecular components of the discs are col-
nucleus pulposus through the annulus fibrosus and lagenous and non-collagenous proteins, proteoglycan
extrusion into the vertebral canal, and is usually aggregates and glycoproteins. Glycosaminoglycans
associated with chondroid metaplasia. (GAGs) are proteoglycans composed of repeating units
• Hansen type II IVDD results in annular protrusion of hexosamines: chondroitin sulphate (CS), dermatan
caused by shifting of central nuclear material and is sulphate, keratan sulphate (KS) and hyaluronic acid. One
associated more with fibroid degeneration. of the functions of GAGs is to imbibe water. Concentra-
tions of these GAGs are highest in the nucleus pulposus.
Acute IVDD is characterized by rapid extrusion of Age-related or pathological change is associated with a
nucleus pulposus into the vertebral canal causing spinal progressive decrease in GAG content coinciding with a
cord compression and extradural haemorrhage. As such, decrease in water and proteoglycans within the nucleus
acute disc disease is usually synonymous with type I and annulus. The proportion of non-collagenous pro-
IVDD, but it can occur either without preceding disc teins also increases with age: the structure of the aggre-
degeneration (traumatic non-compressive nucleus pul- can changes, the core protein and GAG chains shorten
posus extrusion) or following type II IVDD. This type of and there is an increase in the ratio of KS to CS. CS syn-
clinical presentation is caused by a combination of thesis differs from KS synthesis in the requirement of
primary and secondary spinal cord injury. The spinal oxygen during the constituent sugar formation. Thus,
cord is the ‘innocent bystander’ and neurological dys- the increased KS:CS ratio is a consequence of the change
function is a secondary consequence of disc herniation. from an aerobic to an anaerobic environment.
The cervical and thoracolumbar spinal cord are com- These degenerative changes occur earlier in chondro-
monly affected by acute-onset Hansen type I IVDD. dystrophic breeds. The intervertebral discs of these dogs
The presence of nociception in the limbs is a positive undergo chondroid metamorphosis as early as 2 months
indicator for recovery from acute IVDD. after birth. Chondrification involves a decrease in GAGs
and an increase in collagen. Studies on structural compo-
sition of the nucleus pulposus and the transitional zone
suggest a genetic predisposition for IVDD.
400 SPECIFIC EMERGENCIES

a b

Hansen first classified IVDD as type I and type II.  316 T2-weighted MR mid-sagittal (a) and transverse
Hansen type I IVDD is herniation of the nucleus pulpo- (b) images of a cervical spine from a Pomeranian with
sus through the annular fibres and extrusion of nuclear acute-onset tetraparesis from a suspected acute non-
material into the vertebral canal. The extrusion causes compressive nucleus pulposus extrusion. An area of intra-
dorsal, dorsolateral or circumferential compression of parenchymal hyperintensity (arrows) suggestive of
the spinal cord. Acute disc extrusion is characterized by oedema or ischaemia extends from C3 to C4. There is
extradural haemorrhage and soft disc material. Hansen dorsal displacement of the nucleus pulposus within the
type II IVDD is characterized by annular protrusion interspace and minimal spinal cord compression.
caused by shifting of central nuclear material and is com-
monly associated with fibroid disc degeneration associat-
ed with age-related changes in the disc constituents.
Acute-onset disc disease is less common with Hansen
type II IVDD. A third type of IVDD has been described Acute and severe disc extrusions cause pannecrosis of
as acute non-compressive nucleus pulposus extrusion the grey and white matter. Sequential haemorrhage,
(ANNPE). Other terms include high-velocity–low- oedema and neuronal necrosis depend on severity and
volume disc extrusion, intervertebral disc ‘explosion’ and type of injury. Acute spinal cord injury initiates a cascade
traumatic disc extrusion. However, the term ANNPE of vascular, ionic and biochemical events, associated with
describes the main features of the disease and helps dif- ischaemia, that contributes to secondary spinal cord
ferentiate it from the more common type of disc extru- injury and irreversible neuronal damage. Myelopathic
sion that occurs following intervertebral disc changes initially involve the grey matter, with centrifugal
degeneration (Hansen type I IVDD) and that typically spread to the white matter.
results in spinal cord contusion and compression (316). The most severely affected dogs (paralysis with absent
Extrusion of the nucleus or protrusion of the annulus nociception) develop ascending and descending haemor-
causes primary spinal cord injury and associated neuro- rhagic myelomalacia, which is an auto-destructive
logical signs by concussion, compression, laceration and myelopathy. This type of myelomalacia is suspected to
ischaemic events. Spinal cord damage is usually most be an end-stage result of ischaemic and circulatory
severe at the site of intervertebral disc protrusion or processes. Its pathogenesis is unknown, but it is thought
extrusion. Pathological changes are characterized as to reflect extensive compromise of the intramedullary
compressive myelopathy and myelomalacia with vasculature with haemorrhagic or non-haemorrhagic
demyelination of the ventral, lateral and dorsal funiculi. infarction. Haemorrhage is often present in the
Wallerian degeneration occurs in the spinal cord seg- extradural and subarachnoid spaces and spinal cord
ments above and below the lesion in the ascending and parenchyma. Myelomalacia extends from the site of
descending pathways, respectively. An inflammatory impact to ascend or descend the spinal cord. Associated
reaction subsequently develops as a result of the neu- neurological signs include analgesia, areflexia, ascending
rodegenerative and injury processes. cutaneous trunci reflex loss and respiratory dysfunction.
 ACUTE DISC DISEASE 401

The incidence rate of focal and ascending/descending Cervical intervertebral disc disease
haemorrhagic myelomalacia has been reported to be as Cervical spinal pain is the most common clinical sign of
high as 10% in dogs with acute thoracolumbar IVDD acute-onset cervical IVDD. Low head and neck carriage,
and loss of nociception. Myelomalacia is also not an neck guarding, stilted gait, radicular pain and spasms of
uncommon scenario with traumatic non-compressive the cervical spinal muscles are common clinical manifes-
disc extrusions where the extruded nucleus spreads along tations of cervical spinal pain. Due to the greater ratio of
the epidural space for a distance and may completely the vertebral canal diameter to spinal cord diameter in
surround or penetrate the dura mater. The prognosis for the cervical spine, Hansen type I cervical disc disease
ascending and descending haemorrhagic myelomalacia is commonly presents with pain only even if a large amount
generally poor; however, there have been reports of of nucleus is extruded. Pressure from disc material on the
improvement in neurological function in cases of focal nerve root can cause nerve root ischaemia and severe
malacia. pain. Pain is often intermittent and manifests as forelimb
Hoerlein determined that IVDD accounted for lameness (root signature or radicular pain). Radicular
2.02% of all diseases diagnosed in dogs. Thoracolumbar pain also can be elicited by manipulation of the affected
IVDD accounts for approximately 80–85% of all disc limb. Gait evaluation is assessed as normal, GP ataxia
lesions, with the highest incidence being at the thoraco- (more severe in the hindlimbs) and hemi- or tetra-
lumbar junction (T12/T13 to L1/L2) in chondrodys- paresis/plegia. Neurological dysfunction can be asym-
trophic dogs. The Dachshund has the highest frequency metric based on lateralization of the extruded disc. In
followed in succession by the Pekingese, Welsh Corgi, general, forelimb spinal reflexes are normal to hyper-
Beagle, Lhasa Apso and Miniature Poodle. Large non- reflexic with a C1–C5 spinal cord lesion and normal to
chondrodystrophic breeds of dog (e.g. Doberman hyporeflexic with a C6–T2 lesion. However, spinal reflex
Pinscher, German Shepherd Dog, Dalmatian and evaluations may not be reliable for neuroanatomical
Labrador Retriever) are also affected with Hansen type I localization within the cervical spinal cord region follow-
IVDD. The most common site in large breed dogs is the ing acute disc disease. A decreased withdrawal reflex does
disc interspace between L1 and L2. The age at onset for not always indicate a lesion from C6–T2 and it can also
clinical signs of thoracolumbar IVDD peaks at 4–6 years occur with lesions at the C1–C5 spinal cord level. Non-
of age in chondrodystrophic breeds and at 6–8 years in ambulatory tetraplegia is an infrequent clinical manifes-
non-chondrodystrophic breeds. Cervical IVDD tation of cervical IVDD. A study of 32 dogs summarized
accounts for approximately 15–20% of all intervertebral that fewer than one-third of dogs that are non-ambulato-
disc extrusions. The most common sites for Hansen ry secondary to cervical disc herniation experience com-
type I IVDD in the cervical spine are C2/C3 and C3/C4 plete loss of voluntary motor function; sensory deficits
in small breed dogs and C6/C7 in larger breed dogs. are encountered even less frequently. Horner’s syndrome
can be a clinical manifestation caused by disruption of the
CLINICAL PRESENTATION tectotegmental spinal tract with severe cervical spinal
cord injury. Loss of nociception is rare in dogs with acute
Neurological signs seen in dogs with IVDD may be cervical IVDD, but is associated with severe spinal cord
peracute (<1 hour), acute (<24 hours) or subacute damage, myelomalacia, cardiac arrhythmia and respira-
(>24 hours). Hansen type I IVDD is the most common tory dysfunction.
cause for the peracute and acute clinical presentations
of IVDD. Clinical signs of intervertebral disc extrusion Thoracolumbar intervertebral disc disease
are variable and determined by the rapidity and severity Clinical signs of thoracolumbar IVDD vary from spinal
of spinal cord injury and neuroanatomical localization. hyperaesthesia only to paraplegia with or without noci-
The presence or absence of nociception determines the ception. Dogs with back pain only are reluctant to walk
prognosis. and may show kyphosis. Dogs with back pain alone or
minimal neurological deficits can have imaging evidence
of substantial spinal cord compression. Lateralization of
the extruded disc and spinal cord compression will often
402 SPECIFIC EMERGENCIES

cause asymmetry of neurological deficits. Neuroanatom- Ascending and descending haemorrhagic myelo-
ical localization of thoracolumbar spinal lesions is deter- malacia should be suspected in dogs with thoracolumbar
mined by normal to hyperreflexic (T3–L3) or IVDD that have an ascending loss of the cutaneous
hyporeflexic (L4–S3) spinal reflexes and by site of trunci reflex. Other neurological signs of myelomalacia
paraspinal hyperaesthesia. Dogs presented with peracute include loss of nociception caudal to the lesion, ascend-
or acute thoracolumbar disc extrusions often manifest ing and descending flaccidity and areflexia, tetraplegia,
initial clinical signs of ‘spinal shock’ and/or Schiff– hyperthermia and respiratory distress. Death results
Sherrington postures. Spinal shock is usually manifested from asphyxia associated with intercostal and diaphrag-
as flaccidity distal to the lesion. Likewise, the spinal matic muscle paralysis. Clinical signs of ascending and
reflexes are depressed to absent and the bladder may be descending myelomalacia may manifest in hours to
flaccid, with urine retention and sphincter hypotonia. several days from the onset of paraplegia.
The cause of spinal shock is unclear. A transient decrease
in limb tone may be due to loss of descending supraspinal DIFFERENTIAL DIAGNOSIS
input on the alpha-motor neurons and interneurons,
along with an increase in segmental inhibition. Spinal A differential diagnosis for acute disc disease is based on
shock is important to recognize in order to prevent erro- speed of onset, lesion symmetry and presence of
neous lesion localization. These transient phenomena paraspinal hyperaesthesia. Paraspinal hyperaesthesia
indicate acute and severe spinal cord injury, but do not usually indicates a compression and/or inflammation to
determine the prognosis. pain-sensitive structures, which include the periosteum
A classification scheme adapted from Griffiths of the vertebrae, meninges, nerve roots and superficial
describing hyperaesthesia, sensory and motor dysfunc- layers of the annulus fibrosus. Disorders that typically
tion and loss of micturition has been used as a functional do not manifest paraspinal pain include intramedullary
grading system to provide treatment guidelines for tho- neoplasia and fibrocartilaginous embolic myelopathy
racolumbar IVDD: (FCEM).
0 = Normal. • Vascular. FCEM thrombosis, infarction.
1 = Paraspinal hyperaesthesia only. • Inflammatory. Infectious: meningitis/myelitis (viral,
2 = General proprioceptive ataxia and/or ambulatory fungal, bacterial, rickettsial, protozoal, algal), spinal
paraparesis. epidural empyema, discospondylitis (bacterial,
3 = Non-ambulatory paraparesis. fungal), vertebral physitis. Noninfectious: MEM of
4 = Paraplegia (intact nociception). unknown aetiology (granulomatous MEM,
5 = Paraplegia with loss of nociception. necrotizing encephalomyelitis), steroid-responsive
meningitis, vasculitis.
Complete loss of nociception is the most important • Trauma. Vertebral fractures/luxations, AA
prognostic indicator for acute spinal cord injury. Noci- subluxation.
ception by definition is perception of a noxious stimulus. • Neoplasia. Primary: extradural (vertebral,
Classically, a ‘superficial’ pain response is elicited on lymphoreticular), intradural extramedullary
pinching a skin fold and a ‘deep’ pain response is elicited (lymphoreticular, meningioma, nerve sheath
on use of a noxious stimulus, most commonly a bone of a tumour), intramedullary (oligodendroglioma,
digit. Distinguishing between superficial and deep ‘pain’ astrocytoma, ependymoma). Secondary: metastatic
perception may not be reliable because of individual (lymphoreticular, haemangiosarcoma, meningeal
animal differences in perception of a ‘painful’ stimulus. carcinomatosis, undifferentiated sarcomas).
Moreover, differences between these two nociceptive • Degenerative. Degenerative lumbosacral stenosis.
pathways are poorly defined.
 ACUTE DISC DISEASE 403

DIAGNOSIS
Presumptive
diagnosis of IVDD
Imaging studies of the spinal cord (myelography and/or
CT and MRI) are necessary to confirm the presence and
extent of the lesion (317).
Anaesthetized
survey spinal
radiography Survey radiography
Survey radiography identifies in-situ intervertebral disc
mineralization associated with the presence of degenera-
Myelography CT alone MRI tive disc disease, rules out other differentials causing
bony lesions and assists with confirmation of anatomical
landmarks. One study determined that in-situ disc min-
Site of eralization in the thoracolumbar spine of Dachshunds at
compression
ascertained
2 years of age was a significant predictor of future clinical
disc herniation. Survey radiography, however, lacks accu-
racy in identifying the exact location of the extruded disc.
NO NO NO
Accuracy for determining the site of thoracolumbar
intervertebral disc extrusion using survey radiography
ranged from 51–61% in one study. Roentgen findings of
suspected disc extrusion (318) include the following:
Consider other
differentials • Narrowing of the disc space.
• Altered shape of the intervertebral foramen.
• Wedging of the disc space.
Consider • Presence of mineralized material in the vertebral
Consider
CT or MRI
CT-myelography CSF analysis canal or superimposed over the intervertebral
or MRI
foramen.

 317 Neurodiagnostic technique decision-making

scheme for diagnosis of acute intervertebral disc disease.

 318 Lateral radiograph of the thoracolumbar junction demonstrating radiographic signs of intervertebral disc
disease. There is presence of in-situ mineralization (red arrows) at T10/T11, T13/L1 and L1/L2. The intervertebral disc
space at T11/T12 is wedged (yellow arrows) and the space between the articular processes is collapsed (black arrow),
which is suggestive for the site of the disc extrusion.
404 SPECIFIC EMERGENCIES

Myelography
Myelography has served as a standard for diagnosing subarachnoid space attenuation of contrast flow can be
spinal cord compression in dogs with IVDD. A non- seen with haemorrhage and/or spinal cord swelling. The
ionic, radiographic contrast medium is injected into the extent of spinal cord swelling seen with myelography
subarachnoid space at the cerebellomedullary cistern or may assist in establishing a prognosis. Dogs with absent
caudal lumbar (L4/L5, L5/L6) region. Attenuation nociception have a significantly worse outcome if the
of contrast flow within the subarachnoid space occurs at extent of spinal cord swelling is greater than five times
sites of compression and subarachnoid space occlusion; the length of L2. Myelomalacia is suspected when there
such patterns are described as extradural, intradural is leakage of contrast medium into the spinal cord
extramedullary and intramedullary (319). Lateral, parenchyma during myelography.
ventrodorsal and oblique views are useful for determin- Common technical problems associated with myel-
ing the circumferential and longitudinal location and ography include difficulties during injection and poor
extent of the extradural compression. Longitudinal distribution of contrast medium. Anatomical problems
lesion localization by myelography in thoracolumbar include atypical displacement of disc material and the
IVDD has nearly 90% accuracy. An intramedullary presence of spinal cord swelling. Systemic complications
pattern associated with spinal cord oedema is more of myelography include seizures, worsening of neurolog-
common with acute extrusions and may obscure the site ical status, apnea, cardiac arrhythmias, meningitis, sub-
of extradural compression (320). Extensive longitudinal arachnoid haemorrhage and death.

 319 Lateral radiograph of the

caudal thoracic and lumbar spine after
injection of contrast medium. There
is an extradural myelographic pattern
(arrow) at L2/L3 characterized by
dorsal deviation of the ventral
contrast column caused by Hansen
type I intervertebral disc disease.

 320 Lateral radiograph of the

thoracolumbar spine after injection
of contrast medium. There is an
intramedullary pattern (arrows)
extending from T12/T13 to L1/L2
and obscuring the site of extradural
compression.
 ACUTE DISC DISEASE 405

 321 Transverse CT images. (a) An acute disc extrusion a

over the body of T13 demonstrating heterogeneous
attenuation (arrow). (b) A chronic disc extrusion over the
body of L1 demonstrating homogeneous attenuation.

 322 T2-weighted mid-sagittal image of the cervical

spine. Hansen type I disc degeneration, recognized by loss
of signal intensity within the nucleus pulposus (arrow),
can be seen at C6/C7. Notice also the area of extruded
disc causing ventral spinal cord compression. b

Computed tomography chronic lesion often will not have associated spinal cord
CT is an adjunctive procedure to myelography to further swelling. Spinal cord swelling or oedema may also be
delineate lateralization of the extruded disc material or it identified using MRI based on identification of an area of
can be used as the sole technique for detecting interver- high signal intensity on T2-weighted images associated
tebral disc extrusion. Imaging the spine using CT alone with disc compression.
is non-invasive and performed more quickly and with
fewer complications than myelography. The lesion Magnetic resonance imaging
extent and lateralization of disc material are more distinct MRI is superior in the recognition of intraparenchymal
on CT than with myelography. Mineralized disc material pathology and has become the standard for the assess-
and acute haemorrhage can be identified in the verte- ment of acute spinal cord injury in human patients. Stan-
bral canal using non-contrast-enhanced CT. Acutely dardized MRI protocols for intervertebral disc disease
extruded disc material typically is recognized as a hetero- often use T1- and T2-weighted sagittal and transverse
geneous hyperattenuating extradural mass (321). The (axial) images over the areas of interest. MRI also is con-
attenuation of the disc material increases with the degree sidered the best method for early recognition of in-situ
of mineralization. Chronically extruded disc material has disc degeneration based on a decrease in signal intensity
a more homogeneous hyperattenuating appearance. If within the nucleus pulposus on T2-weighted images
more than one site has extruded disc material, a myelo- (322). The hypointensity seen with degenerative disc
gram may be necessary to identify the site of the lesion disease is linked with changes in proteoglycan concentra-
based on a corresponding area of cord swelling. A more tions. Focal signal void within the intervertebral disc
 406 SPECIFIC EMERGENCIES

a space or vertebral canal may represent a free fragment of

mineralized nucleus pulposus (323). Acute pathologies
of spinal cord tissue seen as high signal intensity on
T2-weighted images include necrosis, myelomalacia,
intramedullary haemorrhage, inflammation and oedema.
However, it is difficult to distinguish between these spe-
cific types of pathology. Areas of focal high signal inten-
sity on T2-weighted images in chronic spinal cord
disease are suggestive of focal myelomalacia and
b
syringohydromyelia. MRI studies of myelomalacia in
dogs with intervertebral disc extrusion and acute-onset
paraplegia have demonstrated parenchymal high signal
intensity on T2-weighted images and diffuse hypointen-
sity on gradient echo images, cranial and caudal to the
compressive extradural lesion (324).
MRI may provide better clarity than other imaging
techniques in detecting haemorrhage associated with
intervertebral disc extrusion. However, timing of MRI in
relation to onset of the lesion can confound the interpre-
tation of signal intensity since rapid changes can occur
within areas of haemorrhage in the early stages after
injury. The presence of an extradural mass of low signal
intensity on T1- and T2-weighted images near the
 323 T2-weighted MR images of an extruded disc at mineralized disc material may be suggestive of recent
C4/C5. (a) Sagittal image with signal void suggestive of haemorrhage or haematoma (325). A haematoma that is
mineralization causing ventral spinal cord compression hours to several days of age typically appears hypointense
(arrow). (b) Transverse image of the same disc as in 323a on T2-weighted and gradient echo images until
with areas of signal void of the extruded disc material conversion of deoxyhaemoglobin to methaemoglobin.
(arrow) right of midline and displacing the spinal cord to Intracellular methaemoglobin causes pronounced short-
the left. Note the hyperintensity in the spinal cord from ening of the T1 relaxation times of tissues because
presumptive oedema. its paramagnetic properties alter proton interactions.

 324 T2-weighted sagittal thoracolumbar MR image

demonstrating homogeneous hyperintensity within the
swollen lumbar spinal cord (arrows) becoming more
heterogeneous towards the unaffected thoracic spinal
cord. This dog demonstrated clinical and pathological
features of myelomalacia.
 ACUTE DISC DISEASE 407

 325 T2-weighted transverse MR image of the  326 Sagittal T2-weighted MR image of the cervico-
thoracolumbar spine at the T12/T13 disc space. A large thoracic spine demonstrating extensive intramedullary
extradural mass of low signal intensity is present (arrow) swelling and hyperintensity (arrow) from C5–C7
lateral to the spinal cord. Note that the spinal cord is associated with a traumatic non-compressive disc
displaced. Surgery confirmed that the low signal was extrusion.
epidural haemorrhage.

Thus methaemoglobin appears hyperintense on T1- length of the L2 vertebral body was 10% (1/10 dogs). As
weighted images. The presence of deoxyhaemoglobin expected, the degree of cord compression noted on MRI
does not cause T1 shortening and appears isointense to of thoracolumbar disc disease has not been associated
the spinal cord on T1-weighted images. with prognosis.
MRI has been used to predict prognosis in paraplegic
dogs caused by intervertebral disc extrusion. Results Cerebrospinal fluid analysis
suggest that dogs with an area of hyperintensity at least as CSF analysis is unlikely to confirm a diagnosis of IVDD,
long as the L2 vertebral body seen on pre-operative T2- but may help to rule out primary inflammatory CNS
weighted sagittal MR images of the spinal cord have a disease. Moderate to marked lymphocytic CSF pleo-
poorer prognosis for functional recovery (326). The cytosis (>5 cells/μl) is seen in dogs with Hansen type I
success rate following surgery in dogs without hyperin- IVDD, especially in those with chronic presentation or
tensity of the spinal cord was 100% compared to 55% in in an acute presentation of chronic IVDD. Protein con-
those with areas of hyperintensity. Moreover, the success centration elevations have been associated with acute-
rate reported for dogs with areas of hyperintensity and onset disease and clinical severity. Albuminocytological
loss of nociception was 31%, and the success rate in dogs dissociation is also a common clinicopathological finding
with no nociception and hyperintensity >3 times the in IVDD.
408 SPECIFIC EMERGENCIES

MANAGEMENT See Chapter 21 for more information on the treat-

ment of spinal injury and Chapter 30 for a more detailed
Medical management discussion of patient analgesia.
Indications for medical management of IVDD include
first time incidence of spinal pain only, mild to moderate Cervical intervertebral disc disease
paresis and financial constraints of the pet owner. In Conservative therapy can be attempted while the dog is
general, conservative therapy consists of pain control and monitored for reduction of pain and improvement in
strict cage rest. Strict cage confinement enforced for a neurological status. In dogs with cervical IVDD,
minimum of 4–6 weeks is an essential aspect of successful conservative therapy alone is often ineffective. A possible
conservative management. reason for lack of response to strict cage rest is that total
immobility of the cervical spine is difficult to maintain.
General concepts Additionally, dogs with cervical spinal pain as the primary
Dogs with initial pain or minimal motor dysfunction can presenting sign may have a significant amount of
be managed by strict cage rest for 4–6 weeks combined extruded disc present within the spinal canal.
with pain management using anti-inflammatory drugs In the author’s experience, surgical management is
(NSAIDS, opioids and muscle relaxants). The impor- recommended when pain is refractory to standard pain
tance of cage rest is that it allows for annular and liga- management for longer than 1–2 weeks or if there is pro-
mentous healing and prevention of further disc gression of neurological deficits. There is limited infor-
herniation. Fluid therapy is important at the time of the mation available on the success of medical therapy for
injury in order to maintain spinal cord perfusion. MPSS cervical IVDD in dogs, but the recurrence rate has been
(30 mg/kg IV slow bolus) administered within the first 8 reported to be as high as 36%. More recently, a success
hours from onset of trauma has been advocated as an rate of nearly 50% has been reported, with 33% having
adjunctive treatment of acute disc herniation causing recurrence of clinical signs and 18% having therapeutic
paraplegia and loss of nociception. Dexamethasone failure. This study also suggested that duration of cage
(0.5–1.0 mg/kg IV once) or prednisone (0.5–1.0 mg/kg rest was not significantly associated with success or
PO q12–24h for 5 days, then taper) has also been advo- ‘quality of life’ scores. It was stated that an initial period
cated to reduce spinal cord oedema. However, adminis- of strict cage confinement may be beneficial, but that
tration of corticosteroids is controversial from the prolonged (>2 weeks) strict rest at the expense of physical
standpoint of countering pathophysiological mecha- rehabilitation may not have any benefit.
nisms and efficacy still remains to be proven. Corticos-
teroid use in dogs with acute IVDD can increase rates of Thoracolumbar intervertebral disc disease
postoperative complications (which include gastroin- Indications for medical treatment of dogs with thoraco-
testinal disease) and financial cost to the client. NSAIDs lumbar IVDD include first time incidence of spinal pain
should not be used in combination with corticosteroids only, mild to moderate non-progressive paraparesis and
as gastric ulceration and potentially fatal perforation can financial constraint of the client.
result. Gastrointestinal protection may be necessary if Success rates for conservative management of ambu-
anti-inflammatory therapies are used. Dogs treated con- latory dogs with thoracolumbar pain only and/or mild
servatively should be assessed daily for pain level, paresis range from 82–100%. Recovery rates in non-
comfort, bladder emptying, evidence of decubital ulcer- ambulatory dogs with thoracolumbar disease are lower
ation and neurological status. Acupuncture and muscle and recurrence rates are higher in studies following con-
relaxants have also been advocated as treatments for pain servative treatment. More recent retrospective studies of
management. Cases with recurrent episodes of neck or conservatively managed dogs with thoracolumbar disc
back pain uncontrolled by medication and/or worsening disease documented 30–50% recurrence rates in dogs
of neurological status should have decompressive with minimally affected ambulatory status. Recurrence
surgery. Physical therapy, weight control and avoidance of spinal hyperpathia in dogs with thoracolumbar IVDD
of jumping activities may reduce recurrence rates. that are conservatively managed usually occurs within
6 months to 1 year from onset of the initial clinical signs.
 ACUTE DISC DISEASE 409

Surgical management (also termed mini-hemilaminectomy). The primary

Decisions for emergency surgery in dogs with acute purpose of decompressive surgery is to allow for ade-
IVDD should take into account the severity of the neu- quate exposure for removal of disc material while mini-
rological status, the rapidity of deteriorating neurologi- mizing spinal cord manipulation. There are advantages
cal signs and the patient’s overall health status. Patients and disadvantages of each decompressive technique.
presenting with plegia and absent nociception need
emergency surgical decompression (327). Cervical intervertebral disc disease
Goals for surgical management of dogs with spinal Indications for surgical treatment of cervical interverte-
cord injury include decompression, removal of extruded bral disc extrusion include pain refractory to medical
disc and haemorrhage, and visual observation of the management and/or severe and progressive neurological
spinal cord. Chronicity of disc extrusion at the time of deficits.
surgery may influence the ease with which extruded disc In cervical IVDD, decompressive procedures via a
material can be removed. Decompressive procedures for ventral, lateral or dorsal approach are the techniques of
IVDD include ventral slot, dorsal laminectomy, hemi- choice for removal of extruded disc. The selection of the
laminectomy, partial corpectomy and pediculectomy decompressive procedure is usually determined by the

Neurological examination

GRADES 1 OR 2 GRADES 3 OR 4 GRADE 5

Recurrence or refractory Elective Emergency

First episode
to pain management neuroimaging neuroimaging

Confined rest (6 weeks) Surgical Surgical

and pain management decompression decompression

Recovery and physical

rehabilitation

 327 Decision-making algorithm with respect to the

surgical management of a dog with thoracolumbar disc
herniation.
 410 SPECIFIC EMERGENCIES

Outer cortical bone Interarcuate Dorsal

Cancellous bone space lamina

Inner cortical bone Spinal cord Epaxial

musculature

Venous sinus
Dorsal longitudinal
ligament

 328 Ventral slot procedure after drilling. The slot is  329 Dorsal laminectomy in the cervical spine: shown
more extensive in the vertebra cranial to the disc. Drilling here is the epaxial musculature attached to articular
depth is judged by recognition of the outer cortical bone, process; the edge of the laminectomy defect; the inter-
cancellous bone and inner cortical bone. Other structures arcuate space; and the spinal cord. (Adapted from Coates
not easily visualized are the paired venous sinuses and the JR, Hoffman A, Dewey CW (2003) Surgical approaches to
dorsal longitudinal ligaments. (Adapted from Coates JR, the spine. In: Textbook of Small Animal Surgery, 3rd edn.
Hoffman A, Dewey CW (2003) Surgical approaches to the (ed. D Slatter) WB Saunders, Philadelphia, pp. 1148–1162.)
spine. In: Textbook of Small Animal Surgery, 3rd edn. (ed.
D Slatter) WB Saunders, Philadelphia, pp. 1148–1162.)

location of the disc material in relation to the cord. The Dorsal laminectomy involves dissection of the epaxial
ventral slot technique is commonly performed for disc musculature and removal of the dorsal spinous processes
displaced ventral to the spinal cord (328). Using the iden- and the laminae (329). Dorsal procedures provide spinal
tifiable landmarks of the ventral prominence of C1 and cord decompression and access for laterally extruded disc
the transverse processes of C6 to identify the disc inter- material, but access is limited to extruded disc located
space of interest, a slot is cut into the ventral aspect of the beneath the spinal cord. A lateral approach has been
cervical vertebrae using a high-speed surgical drill. described for lateral or intraforaminal disc extrusions at
Advantages of the ventral decompressive technique the C4/C5 and C5/C6 interspaces. Excessive haemor-
include minimal muscle dissection and exposure for rhage from muscle dissection and damage to the internal
prophylactic fenestration of adjacent cervical discs. Dis- vertebral venous plexus or vertebral artery and incom-
advantages may include excessive venous sinus haemor- plete removal of disc material can be complications of
rhage, lack of spinal cord decompression and inadequate dorsal decompression. The risk for spinal instability is
exposure for lateral or intraforaminal disc extrusion. considered less when compared with the ventral slot
If the width of the slot is >30% of the size of the vertebral technique.
body, dogs may suffer from instability or subluxation at
the surgery site.
 ACUTE DISC DISEASE 411

Thoracolumbar intervertebral disc disease The type of decompressive procedure may not affect
Indications for surgical management of thoracolumbar outcome; however, the ability to retrieve the disc mate-
IVDD include spinal pain or paresis refractory to rial depends on the type of decompressive procedure
medical therapy, recurrence or progression of neuro- selected. Hemilaminectomy provides the same degree of
logical deficits, paraplegia with intact nociception and decompression as dorsal laminectomy and is less fre-
paraplegia with loss of nociception for less than quently associated with a postsurgical constrictive
24–48 hours. Prolonged loss of nociception (>48 hours) laminectomy membrane. Radical bilateral dorsal
carries a poorer prognosis and owners should be made laminectomy (removal of pedicle – Funkquist A) has an
aware of this prior to surgery. increased risk of constrictive laminectomy membrane
Decompressive procedures for thoracolumbar IVDD formation. Studies have reported retrieval of disc materi-
include dorsal laminectomy, hemilaminectomy and pedi- al in 93% of dogs that had hemilaminectomy compared
culectomy. Hemilaminectomy significantly improves with 40% of dogs that had dorsal laminectomy, but the
retrieval of extruded disc material, with minimal spinal initial neurological recovery after hemilaminectomy was
cord manipulation (330). Pediculectomy is the least inva- not significantly different compared with dorsal laminec-
sive and least destabilizing technique and can be used as an tomy. Surgical complications include excessive haemor-
adjunctive technique in cases requiring a bilateral rhage, incomplete removal of extruded disc (331),
approach to the vertebral canal. An accurate 3D depiction constrictive fibrosis and, rarely, instability.
of the disc location is necessary prior to pursuing this sur-
gical technique due to the small surgical field that it pro-
vides. Biomechanical studies have shown that unilateral
facetectomy and fenestration do not significantly destabi-
lize the spine during lateral bending.

 330 Location and extent of a typical left-sided hemi-  331 Transverse CT image of an incomplete hemi-
laminectomy. (Adapted from Coates JR, Hoffman A, laminectomy with pedicle (arrow) still remaining and
Dewey CW (2003) Surgical approaches to the spine. preventing adequate visualization of the vertebral canal
In: Textbook of Small Animal Surgery, 3rd edn. (ed. ventral to the spinal cord.
D Slatter) WB Saunders, Philadelphia, pp. 1148–1162.)
412 SPECIFIC EMERGENCIES

commonly predisposed to disc herniation. Reasons for

not performing fenestration include surgical complica-
tions (which include extruding further disc), increased
anaesthetic time and increased costs to the pet owner.
Fenestration is not recommended in large non-
chondrodystrophic dogs due to the potential for under-
* lying spinal instability as a predisposing factor for
annular protrusion.

Role of fenestration
Prophylactic fenestration typically is performed from
T11/T12 to L3/L4. Published studies suggest recur-
rence rates of 0–24% with prophylactic fenestration and
2.7–42% without prophylactic fenestration. Dogs
undergoing prophylactic fenestration tend to have lower
 332 Intraoperative photograph demonstrating recurrence rates. One study determined a 4.7% recur-
myelomalacia (asterisk) after durotomy over the cranial rence rate after multiple disc fenestrations in 265 dogs,
aspect of the exposed spinal cord. (Photo courtesy but commented that prophylactic fenestration could
Robert Bergman) promote disc extrusion at an adjacent non-fenestrated
disc. These findings provide further support for addi-
tional therapeutic interventions such as prophylactic
fenestration and disc ablative procedures.

If the patient has absent nociception prior to surgery, PROGNOSIS

a durotomy can be considered for visualization of the
spinal cord parenchyma to determine the extent of Cervical intervertebral disc disease
swelling and the presence of myelomalacia (332). Prediction of recovery outcomes in dogs with cervical
However, durotomy is ineffective as a treatment for acute IVDD based on site of herniation, ambulatory status and
compressive spinal cord trauma caused by IVDD. breed size is controversial (Table 86). In a study of
Absence of visual evidence of myelomalacia does not 190 dogs with cervical IVDD treated surgically, out-
guarantee functional recovery; conversely, recovery may comes were no different for the ambulatory versus non-
still occur despite the presence of focal myelomalacia. ambulatory dogs with intact nociception. After surgery,
Although controversial, intervertebral disc fenestra- 99% of those dogs had resolution of cervical spinal
tion has been advocated as a prophylactic procedure to hyperaesthesia and were able to ambulate unassisted.
prevent future extrusions at adjacent spaces. Prophylac- Other previous studies have reported that dogs with
tic intervertebral disc fenestration was recommended caudal cervical disc extrusions respond less favourably
after similar recurrences were noted in patients that and are more severely affected than dogs with cranial cer-
underwent spinal decompression and those that were vical disc extrusions. A study that also included dogs with
managed conservatively. Fenestration of the herniated Hansen type II IVDD associated with caudal cervical
disc at the time of spinal decompression is recommended spondylomyelopathy reported only a 66% success rate
to prevent continued extrusion of disc material. Surgical following surgery in large breed dogs. Recently, a study
approaches for disc fenestration include dorsolateral, in 32 dogs with non-ambulatory tetraparesis reported
lateral and ventral. Power-assisted and manual methods that 62% had a complete recovery. Small dogs were 6
have been described for disc fenestration. The effective- times more likely to recover than large breed dogs and
ness of fenestration is related to the amount of nucleus dogs that regained the ability to walk within 96 hours
pulposus removed. Multiple disc fenestrations are after surgery were 7 times more likely to recover than
performed from T11/T12 to L3/L4, sites more those not ambulating within 96 hours. If given more
 ACUTE DISC DISEASE 413

Table 86 Reported recovery outcomes in dogs with cervical IVDD

NEUROLOGICAL STATUS SUCCESS OF MEDICAL MANAGEMENT SUCCESS OF SURGICAL MANAGEMENT

Pain, mild paresis 50% (Levine et al., 2007) 66% (large breed) (Chambers et al., 1986)
87% (Fry et al., 1991)
99% (Cherrone et al., 2004)

Non-ambulatory tetraparesis Unknown 62% (Hillman et al., 2009)

Recurrence rate 33% (Levine et al., 2007) 6% (Russell and Griffiths, 1968)
36% (Russell and Griffiths, 1968) 10% (8% small breed; 13% large breed)
(Cherrone et al., 2004)
33% (Toombs, 1992)

time, however, recovery of ambulatory function can success may consist of improvement in the patient’s neu-
occur, but residual deficits are likely. In contrast to prev- rological grade, but still may not translate to complete
ious studies, the site of disc herniation was not a signifi- normality. It has been reported that approximately 40%
cant predictor of complete recovery. Compared with of dogs that recovered from loss of nociception (grade 5)
thoracolumbar IVDD, the severity of neurological continued to have faecal incontinence. Additionally,
deficit was not a robust predictor of outcome. recurrent urinary tract infection can occur in dogs recov-
Recurrence of clinical signs after surgery in dogs with ering from non-ambulatory neurological status. Residual
cervical IVDD has been reported to range from 10–33% signs such as faecal and urinary incontinence can be
(Table 86). The most common clinical sign during recur- unacceptable to some pet owners.
rence was cervical spinal hyperaesthesia. A second disc Dogs with thoracolumbar IVDD and ambulatory
extrusion at a site distinct from the initial lesion was the dysfunction will often have concomitant UMN urinary
most common reason for recurrence. bladder dysfunction. These dogs will require manual
bladder expression and intermittent or indwelling
Thoracolumbar intervertebral disc disease urinary bladder catheterization. Incomplete bladder
Differences in recovery rates of non-ambulatory dogs evacuation and use of urinary catheters may predispose
with thoracolumbar IVDD vary with the severity of neu- dogs to urinary tract infection (UTI). A prospective study
rological dysfunction (neurological grade), time interval in dogs with thoracolumbar IVDD determined that the
from initial clinical signs to surgery and speed of onset of prevalence of UTI was 30%, with a higher incidence in
signs (Table 87, pp. 414–415). Overall success rates after dogs that were female and had lower intraoperative body
decompressive surgery range from 58.8–95%. However, temperatures. However, intermittent urinary catheteri-
the success of a surgical approach may depend on what zation has a lower risk of inducing a UTI over indwelling
criteria are used to define it and how long after the closed-system urinary catheterization techniques. If an
surgery the patient is assessed, as well as the outcome that indwelling system is selected, minimizing the duration of
the owners are willing to accept. In other words, surgical use is important for reducing the risk of UTI.
414 SPECIFIC EMERGENCIES

Table 87 Reported recovery outcomes in dogs with thoracolumbar IVDD

NEUROLOGICAL STATUS SUCCESS OF MEDICAL MANAGEMENT SUCCESS OF SURGICAL MANAGEMENT

Pain, ataxia, paraparesis 75–85% (Hoerlein, 1978; Funkquist, >95% (Davies and Sharp, 1983; Forterre et al.,
1978; Davies and Sharp, 1983); 2008);
55% (Levine et al., 2007) 96% (pain only) (Sukhiani, 1996); 96% (Schulman
and Lippincott, 1987);
65–83% (Brown et al., 1977)
Paraplegia with superficial 51% (Funkquist, 1970) 79% (Schulman and Lippincott, 1987);
nociception 81% (Funkquist, 1970);
82% (Ruddle et al., 2006);
86% (Forterre et al., 2008);
91% (Brisson et al., 2004);
96% (Davies and Sharp, 1983)

Paraplegia with deep 50% (Davies, 1983) 86% (Ferrira, 2002);

nociception 89% (Gambaredella, 1980)
Absent deep nociception 5–10% (Davies, 1983) 47% (Brown et al., 1977);
<12 hours 50% (Gambaredella, 1980);
58% (Olby et al., 2003);
60% (Loughin et al., 2005);
62% (Scott, 1997);
69% (Ruddle et al., 2006);
76% (Anderson et al., 1992)
Absent deep nociception 5–10% (Davies, 1983) 6.7% (Loughin et al., 2005);
>48 hours 33% (Scott and McKee, 1999)

(Continued)

In general, dogs with more severe motor dysfunc- Patient age and weight also have an association with the
tion tend to have longer recovery times for regaining time required for ability to ambulate. Moreover, dogs
ambulatory function. Reported mean time from that undergo physical rehabilitation may have shorter
surgery to a pain-free ambulatory status varies from times to return of ambulation.
10 days for dogs presenting with spinal pain only to There are many contradictory studies on the effect of
52 days for paraplegic dogs. Other long-term studies rate of onset and duration of signs prior to surgery on
reported the recovery times as 2–14 days for dogs that speed of recovery and final outcome. It is agreed that
were either ambulatory or nonambulatory paraparetic rapid removal of extruded disc material facilitates a more
and up to 4 weeks for paraplegic dogs. In a recent report complete and rapid recovery. Dogs with shorter duration
on 218 nonambulatory dogs with intact nociception, of signs and gradual onset of neurological dysfunction
42% were ambulatory by 2 weeks and 79% ambulatory (<48 hours) have a quicker recovery. However, a study of
by 4 weeks following decompression. This same study 71 paraplegic dogs with intact nociception demonstrated
also reported that dogs with disc extrusions caudal to that although a shorter duration of signs was indeed asso-
L3–L4 are likely to achieve ambulatory status sooner ciated with a shorter recovery time, the rate of onset of
than dogs with disc extrusions between T10 and L3. clinical signs did not influence the recovery time, but it
 ACUTE DISC DISEASE 415

Table 87 Reported recovery outcomes in dogs with thoracolumbar IVDD (continued)

NEUROLOGICAL STATUS SUCCESS OF MEDICAL MANAGEMENT SUCCESS OF SURGICAL MANAGEMENT

Recurrence rate 48% (Funkquist, 1978); Without fenestration:

34% (Davies, 1983); 3% (Brown et al., 1977);
40% (Levine, 1984); 5% (Muir, 1995);
33% (Ferreira, 2002); 6% (Dhupa et al., 1999);
50% (Mann, 2007) 6% (Olby et al., 2003);
15% (Necas, 1999);
16% (Brisson et al., 2004);
19% (Mayhew et al., 2004);
23% (Black, 1988);
27% (Levine and Caywood, 1984);
17% (Funkquist, 1978);
32% (McKee, 1992);
42% (Funkquist, 1970)
With single site fenestration:
15% (Ferreira, 2002);
13% (Scott, 1997)
With multi-site fenestration:
0% (Black, 1988);
4% (McKee, 1992);
4.4% (Brisson et al., 2004);
3.5% (Bartels, 2003);
6.25% (Olby et al., 2003);
16% (Levine and Caywood, 1984);
24% (Knapp, 1990)

did influence the final outcome. Similarly, peracute onset absence of nociception prior to surgery as a prognostic
of signs indicated a poorer prognosis for dogs with no indicator is controversial. In general, dogs with loss of
nociception. One study compared the outcome of dogs nociception for longer than 24–48 hours prior to surgery
after hemilaminectomy with duration of clinical signs have a poorer prognosis for return of function. Recovery
and concluded that delay before surgery does not influ- rates for dogs with thoracolumbar IVDD and absent
ence outcome in dogs with mild neurological dysfunc- nociception range from 0–76%. Recovery of nociception
tion, but does affect better functional recovery in within 2 weeks after surgery has been associated with a
paraplegic dogs when performed within 12 hours. successful outcome to ambulatory status. In a study of
Nociception is considered the most important prog- 87 dogs with loss of nociception, 58% regained noci-
nostic indicator for functional recovery. In general, the ception and the ability to walk. In summary, dogs with
majority of dogs with intact nociception, whether para- absent nociception that have surgery within 12 hours
plegic or paraparetic, have an excellent prognosis, have a better chance of more rapid and complete recov-
particularly if treated surgically. Without surgery, or with ery than those with delay of surgery. The prognosis is
delayed surgery, dogs with absent nociception have an considered poor if nociception does not return within
extremely guarded prognosis, although duration of 2–4 weeks after surgery.
416 SPECIFIC EMERGENCIES

Recurrence of clinical signs after decompressive Hansen type II IVDD is a common incidental age-
surgery in dogs with thoracolumbar IVDD is a common related change in older cats. The cervical spinal region
clinical entity, with incidence rates reported from 2–42% has been reported as the most common site for disc pro-
(Table 87). Risk factors determined for recurrence trusion followed by the mid to caudal lumbar region.
include presence of radiographic mineralization of mul- The onset of type I IVDD in cats is usually acute.
tiple discs at the time of first surgery (5–6 opacified Clinical signs of thoracolumbar IVDD include para-
discs = 50% risk) and if the breed is a Dachshund. The spinal hyperaesthesia, paraparesis/plegia and inconti-
time for recurrence is usually between 1 month and 2 nence. Commonly reported signs for lumbosacral IVDD
years after surgery. Early recurrence clinical signs within are reluctance to jump, low tail carriage, paraparesis,
1 month after surgery are probably related to residual urinary incontinence and constipation.
compression at the original disc site; recurrence more Lesions of Hansen type I herniations occur most
than 1 month after surgery is usually caused by a disc commonly in the thoracolumbar region, with a predilec-
herniation at a site distinct from the initial lesion. The tion to the caudal lumbar and lumbosacral regions. The
prognosis for functional recovery is not affected by a more frequently reported sites were between the
second surgery. Subclinical recurrence noted on MRI is T11/T12 and L1/L2 disc spaces and at the L4/L5 disc
reported to be as high as 60% in dogs after thoracolum- interspace. Cats have tendencies to jump while applying
bar decompression. increased biomechanical loads on their lumbar spine,
which may predispose to caudal lumbar disc extrusions.
FELINE INTERVERTEBRAL DISC DISEASE Similar techniques for diagnosis of spinal cord disease
in dogs also apply for use in cats. Treatment includes
Intervertebral disc disease in cats occurs less frequently both conservative and surgical methods based on neuro-
than in dogs, with a reported incidence of 0.02–0.12%. logical status. Cats do not seem to respond as well to con-
Hansen type I IVDD usually occurs in middle-aged cats, servative treatments. In cats, decompressive surgical
with a mean age reported as 9 years and ranging between techniques allow for a more rapid and complete clinical
1.5 and 17 years. Cats with lumbosacral IVDD are often recovery and a definitive diagnosis. The long-term prog-
older, with a mean age of 12 years. Rarely, intervertebral nosis is considered good to excellent in the majority
disc extrusions have been reported in cats younger than of cases.
5 years of age. Postmortem studies have shown that
 SPECIFIC EMERGENCIES Chapter 23

STATUS EPILEPTICUS
417

Allison Haley
& Simon Platt

INTRODUCTION L-glutamate is an excitatory amino acid found in

elevated concentrations when associated with seizure
An epileptic seizure is defined as excessive and/or hyper- activity. GABA is the major inhibitory neurotransmitter
synchronous neuronal electrical activity in the cerebral of the CNS (333, next page and 126, page 160). It is
cortex resulting in paroxysmal episodes of abnormal con- believed that altered GABAergic function is a major part
sciousness, motor activity, sensory input and/or auto- of seizure pathophysiology.
nomic function. Essentially, seizure activity represents At the time of a seizure there is an extracellular eleva-
temporary abnormal forebrain function with clinical tion in potassium and decrease in calcium, which is
characteristics dependent on the location of the abnor- responsible for enhancing neuronal excitability and facil-
mality (see also Chapter 7). Status epilepticus (SE) is itating the spread of the seizure. If there is synchroniza-
defined as continuous seizure activity lasting 20–30 tion of the seizure discharge with other neurons, it may
minutes or longer. A clinically more practical definition propagate to other areas of the brain. It is hypothesized
would be a seizure lasting longer than 5 minutes, or two that a population of cortical neurons within an epileptic
or more seizures between which the patient does not focus undergo paroxysmal synchronous depolarization
completely recover consciousness. Cluster seizures are termed a paroxysmal depolarizing shift (PDS). This
defined as two or more seizures over a short period of results in an abnormal burst of action potentials that con-
time (minutes to 24 hours), between which the patient tinue in synchronous volleys without appropriate inhibi-
regains consciousness. tion. Although elevated extracellular potassium levels
may induce seizures, the occurrence of seizures is also
AETIOLOGY/PATHOPHYSIOLOGY dependent on intact synaptic inputs from the hippo-
campus, which appears to facilitate the transition from
Seizure pathophysiology normal to ictal cell firing.
In normal neurons, like other cells, an action potential is The basic pathophysiology of SE involves a failure of
created by changes in the cell membrane potential. The mechanisms that usually stop an isolated seizure. This
membrane potential is governed by the influx and efflux failure can arise from abnormal excessive excitation or
of ions through voltage-gated channels. At resting mem- ineffective recruitment of inhibition. It is likely that
brane potential the extracellular sodium concentration is numerous mechanisms are involved depending on the
much higher than the intracellular concentration. underlying cause. Recent experimental work has sug-
Distribution of potassium is just the opposite, with gested that the failure of inhibition may be caused by a
higher concentrations within the cell. An increase in shift in the functional properties of the GABA receptor
the membrane’s permeability to sodium results in depo- that occurs as seizures become prolonged. Repetitive
larization. As the action potential reaches an axon termi- neuronal firing imposes a massive metabolic demand,
nal, the influx of sodium into the cell results in opening of which is exacerbated by glutamate-mediated excito-
calcium channels (see 125, page 159). Calcium enters the toxicity and decreased GABA inhibitory neurotrans-
cell and causes release of the neurotransmitter. Many mission. This has become known as the excitotoxic
neurotransmitters have been identified within the CNS. theory of neuronal damage.
 418 SPECIFIC EMERGENCIES

Glutamine
Mitochondrion PRESYNAPTIC NEURON
Glutaminase
Cytosolic enzyme
Vesicular transporter

Glutamate
GABA vesicle
Exocytosis Glutamine receptor/transporter
GABA receptor/transporter GABA transporter/receptor

GABA
Glutamine synthetase

GA
BA
Glut
a m

ine
ASTROCYTE PROCESS
GA

ate
BA GA
SYNAPTIC CLEFT

am
BA

lut
G

GABA-transaminase

POSTSYNAPTIC NEURON

 333 GABA is formed by alpha-decarboxylation of

glutamate, a reaction catalysed by a cytosolic enzyme Glutamate binding site Calcium and sodium
(L-glutamic acid-1-decarboxylase). GABA is taken up into Magnesium binding site influx
storage vesicles, then released into the synaptic cleft by
exocytosis. It is also taken up into the glia via GABA
transporters where it is converted into glutamate by the
mitochondrial enzyme GABA transaminase.

 334 The N-methyl-D-aspartate (NMDA) receptor is

an ionotropic glutamate receptor, which is distributed
widely in the CNS. Each NMDA receptor consists of 4
transmembrane domains (TM1–TM4). The TM2 domain
forms a kink, which serves as a gate and does not fully
traverse the membrane. Magnesium binds to the receptor
at normal resting potentials or when the cell is hyperpo-
larized, and blocks the NMDA receptor channel. When
the cell is depolarized, the magnesium is dislodged,
allowing sodium and calcium to enter the cell and Transmembrane
potassium to leave. Potassium efflux domains (TM1–4)
 S TAT U S E P I L E P T I C U S 419

a b

 335 (a) Gross brain section of a dog with idiopathic epilepsy that experienced protracted status epilepticus unrespon-
sive to medication. Note the haemorrhagic oedema and associated swelling, which resulted in cerebral herniation.
(b) Histopathological section of thalamic grey matter in a dog that died following seizure activity. Multiple neurons are
shrunken, angular and hypereosinophilic. These microscopic changes indicate acute neuronal degeneration and
necrosis. These changes can occur as a result of seizure or ischaemic episodes. (Photo courtesy Raquel Rech)

Many molecular signals are triggered by SE, activat- neuronal necrosis in SE include the pyramidal cells of the
ing receptors in neuronal membranes. Activation of the hippocampus and the amygdala. Both these regions are
NMDA receptor (334) has been shown to play a key role rich in GABA, the major inhibitory neurotransmitter of
in neuronal signalling and delayed neuronal death. It has the brain, therefore destruction of these regions predis-
been shown that NMDA receptors become activated poses the animal to future episodes of SE and can make
during continuous neuronal stimulation, and in several long-term seizure control difficult.
animal models, NMDA receptor antagonists have been Brain injury, during prolonged seizure events, may
shown to block or delay seizure activity. However, little is also relate to a mismatch between substrate demand and
known about the receptor’s precise role. Excessive con- supply. Compensatory factors may be unable to meet the
centrations of the excitatory amino acid glutamate cause considerable metabolic demand placed on the brain
NMDA receptors to open cation channels to calcium. during seizures. SE lasting longer than 30 minutes can
Large amounts of calcium enter the neuron and then cause brain damage, especially in the limbic structures. In
induce a cascade of intracellular neurochemical events several animal models of SE, histopathological evidence
that can kill the cells. Other possible neurotoxic sub- of neuronal damage was identified within CA1 and CA3
stances released during SE include aspartate, free fatty sectors of the hippocampus; layers 3, 5 and 6 of the neo-
acids, arachidonic acid and free radicals. cortex; Purkinje cells within the cerebellum; the thala-
Certain areas of the brain are more sensitive to the mus; and the amygdala following prolonged seizure
detrimental effects of SE. The underlying biochemical activity (335). Animal models have also demonstrated
reason for this increase in sensitivity is complex and not the deleterious role that hyperthermia, hypoxia and
fully understood. One theory is that there is a mechanism hypotension play in creating further neuronal damage.
mediated through glutamate’s interaction with NMDA However, observation of neuronal changes in well-
receptors. Administration of exogenous glutamate ventilated animals in which adequate glucose levels have
results in a similar distribution of neuronal damage as been maintained suggests that ongoing seizure activity
that of seizure-induced damage. The areas sensitive to itself substantially contributes to neuronal damage.
 420 SPECIFIC EMERGENCIES

Systemic consequences
SE can be divided into an early phase (0–30 minutes) and probably in response to the increased metabolic demand
a late phase (beyond 30 minutes) based on the patho- of the neurons. Lactic acidosis occurs due to increased
physiological changes occurring. anaerobic metabolism resulting from the excessive
The body’s initial response to seizure activity is a muscle and neuronal activity.
release of large amounts of catecholamines, resulting in As the seizure activity continues, the body’s compen-
cardiovascular effects, which include increased systemic, satory measures fail and can no longer adequately meet
pulmonary and left atrial BP, CVP and heart rate, and the increased metabolic demands of the brain. The
an increased susceptibility to cardiac arrhythmias. The impaired respiratory function that occurs in the early
combination of the sympathetic response and increased phase results in hypoxia, which is responsible for most of
muscle activity from the convulsions occurring in SE the continued complications. Impaired cardiac ventricu-
results in a hyperthermic state, with the potential for lar function, cardiac output and hypotension occur. As
body temperature to rise to life-threatening levels. The cerebral autoregulation fails, CBF becomes dependent
sympathetic tone also causes increased bronchial secre- on systemic BP, thus the systemic hypotension results in
tions and salivation that, in combination with decreased inadequate cerebral perfusion. The end result is neuronal
ventilation, results in respiratory compromise. An ischaemia and cell death. The cumulative systemic
increase in CBF is also seen in the early phase of SE, hypoxia can result in multi-organ failure (336).

Bladder 336 Schematic overview

Urine production needs to of the systemic effects of
be monitored.
prolonged seizure activity.
Kidneys
Susceptible to poor
perfusion and in
combination with rhabdo-
myolysis can lead to acute
renal failure.

Brain
Ictal or seizure discharges
can occur without any
physical manifestation.

Skeletal muscle
Susceptible to rhabdo-
myolysis when the patient
becomes hyperthermic.

Heart
Arrhythmias can be due to
hypoxic damage as well as
systemic abnormalities
such as acidosis.
 S TAT U S E P I L E P T I C U S 421

CLINICAL PRESENTATION DIFFERENTIAL DIAGNOSIS

Most patients experiencing SE display obvious general- The precipitating factors in a case of SE must always be
ized seizure activity and marked alteration in conscious- vigorously sought and treated to facilitate seizure control
ness. The mean age of dogs at presentation has been and to be certain that the underlying cause is treated
estimated to be between 4.2 and 5 years (range 0.15– before it results in irreversible cerebral damage.
15 years). No statistical gender prevalence has been doc- Common disease processes associated with SE include
umented, although one study indicated a male predomi- tumours, CNS inflammatory disease (337), trauma,
nance. One study found the English Foxhound, Pug, metabolic disorders such as electrolyte disturbances, and
Teacup Poodle, Boston Terrier and Lakeland Terrier toxicities. Therefore, the presentation of a patient in SE
breeds to be overrepresented when considering SE due does not imply a specific underlying disease process. Of
to multiple causes. Another study investigating seizures all dogs experiencing generalized seizure activity due to
due to multiple causes found German Shepherd Dogs any cause, up to 30% may manifest SE. A recent study
had an increased risk of experiencing SE. documented the frequency of SE as ≤5% in dogs with
Non-convulsive SE has not been well documented in idiopathic epilepsy. However, idiopathic epilepsy has
veterinary medicine, but is recognized in human medi- been identified as the cause of SE in 27–37% of patients,
cine. In human medicine these patients are classified as some of which was associated with inappropriately low
having complex partial SE or absence SE and require therapeutic concentrations of antiepileptic drugs
electroencephalography for diagnosis. Focal motor (AEDs). Secondary epilepsy (e.g. brain tumours, inflam-
seizure activity has been documented in veterinary matory disease) has been identified in 32–40% of patients
patients and this activity may be prolonged enough to be presenting in SE, while reactive epilepsy (systemic meta-
classified as focal motor SE. Focal motor seizures may bolic abnormalities and toxicities) has been documented
also become generalized and progress to generalized SE. in 7–23% of these patients. For dogs with SE with no
Human patients who have electroencephalographic prior seizure history, toxicity should be the primary
evidence of SE with little or no visible motor activity are differential.
still at risk for CNS injury and require immediate atten- The differential diagnoses for primary, secondary
tion. Ongoing SE can produce neuronal death in experi- and reactive epilepsy are reviewed in more detail in
mental models of status, even when metabolic factors are Chapter 7.
corrected, and in animals that are ventilated and para-
lysed. Such damage has been seen in canine experimental
models of focal status as well, indicating a need for treat-
ment of this situation.

 337 Hippocampus of a cat. Distinct labelling for rabies

virus antigen within the perikaryon of several neurons.
(Note: This can be a cause of status in dogs and cats in
endemic regions.) (Photo courtesy Raquel Rech)
 422 SPECIFIC EMERGENCIES

DIAGNOSIS AND MANAGEMENT

The diagnosis, systemic management and seizure treat-

ment detailed in the sections below should, as much as
possible, be taking place simultaneously. This necessi-
tates a ‘team’ or multi-person approach to the emergency
seizure patient.

Diagnosis
The diagnostic protocol for a patient presenting in SE
includes a thorough history to determine if toxin expo-
sure or trauma is a possibility. On initial presentation of
the patient, it is prudent to examine the skull and spine
for any evidence of recent trauma (338). This should be
done by gentle palpation of the animal, paying particular  338 Lateral cervical spine radiograph of a dog that
attention to the head and spine, assessing for crepitus, presented in status epilepticus after trauma. An atlanto-
pain and asymmetry. axial subluxation was discovered, presumed to be related
Immediate assessment of glucose, sodium and to the initial trauma, but co-existent with the status.
calcium levels, renal and hepatic dysfunction and serum
cholinesterase levels should be performed in all SE
patients. (Note: Liver and muscle enzymes may be
increased shortly after seizure activity because of the
Table 88 Diagnostic investigation of status
effects of hypoxia, hypotension and convulsive activity in epilepticus patient
the case of muscle enzyme elevations.) At some point a
more complete minimum database (haematology, serum • Arterial blood gas. Marked metabolic acidosis is common
chemistry, urine analysis) will help to further evaluate the and will resolve when patient is stabilized; respiratory
acidosis needs immediate treatment.
patient for metabolic disturbances as an underlying cause
• Electrolyte analysis. Treat immediately with fluid therapy.
for SE (Table 88) and/or evaluate for systemic damage
• Glucose analysis. If hypoglycaemic, treat with 50%
produced by the SE event. Myoglobinuria can be seen
dextrose diluted to 25% (500 mg/kg IV) over 15 minutes or
associated with SE as a consequence of the muscle treat with oral glucose syrup.
damage mentioned above. If the patient has a chronic • Haematology/serum chemistry. Can be affected by
seizure disorder and is on maintenance AEDs, blood seizure activity so may need to repeat 48 hours after
levels of these medications should be assessed as soon as stabilization.
possible. • Urinalysis. Rule out myoglobinuria and monitor urine
output with indwelling urinary system.
If the patient is stable enough to be anaesthetized
once seizure activity has been controlled, advanced • Serum AED level. If patient has been on AED treatment.

imaging with CT or MRI is recommended to determine • ECG. Arrhythmias can occur up to 72 hours after the
seizures due to myocardial damage.
if there is an underlying structural disease responsible for
• Dynamic bile acid assessment.
the SE. Analysis of CSF should be performed to evaluate
• Toxicity screen. Immediate results will not be available,
the patient for encephalitis and consideration should be
but blood can be taken to submit for cholinesterase levels.
given to serum and CSF infectious disease titres and
• CSF tap. Rule out inflammatory disease.
PCR analysis.
• MRI/CT scan of the brain. Rule out structural brain
Abnormalities in imaging and CSF can be the result diseases.
of SE itself. MRI lesions have been described in the piri- • EEG. Documents continued seizure activity after the
form/temporal lobes. These lesions appear as variable physical manifestations have ceased (339).
hyperintense lesions on T2-weighted sequences and
hypointense on T1-weighted sequences (see 131).
 S TAT U S E P I L E P T I C U S 423

in the presence of extremely subtle convulsive move-

ments (339). Unfortunately, a large series evaluation of
EEG recordings in veterinary patients experiencing SE
has not been done. However, EEG recordings should be
utilized in those patients that are in a coma on presenta-
tion or after drug administration to evaluate the presence
of continuing SE. If clinical seizure activity stops and the
patient is clearly recovering consciousness, EEG moni-
toring is not necessary. Despite the many uses of the
EEG, therapy for SE should not be delayed by waiting
for electroencephalography results. After seizures have
terminated in dogs or cats with SE, an assessment can be
performed to identify the aetiological precipitating
factors (see Chapter 7).
 339 Reproduction of an EEG from an anaesthetized
dog that had been hit by a car 2 days earlier. The dog was Management
having seizure activity prior to anaesthesia. The trace An underlying disease must be identified if possible to
reveals diffusely abnormal electrical activity. Calibrations ensure adequate therapy and, ultimately, seizure control.
20μV:1 second. Treatment of the patient in SE should be focused on:
• Systemic stabilization.
• Correcting any underlying conditions.
These lesions completely or at least partially resolve with • Cessation of the seizure activity.
time (10 days to 18 weeks) in the absence of additional
seizure activity. The signal intensities on MRI represent These 3 areas need to be addressed at the same time, and
an increase in relative water content, suspected to be the concurrently with diagnostic investigations.
result of vasogenic and/or cytotoxic oedema. Recently,
the use of diffusion-weighted MRI has suggested that Systemic stabilization (Tables 89 and 90)
this may be a useful method for imaging SE dogs in terms All of the issues below are difficult to address during SE
of detecting underlying seizure-related pathology. and may improve after SE has stopped, but attempts
should be made to focus on these management areas,
The role of the electroencephalogram especially when multiple drug use has been necessary.
Although the initial diagnosis of SE is usually based on
clinical criteria, electroencephalography has an impor- Airway, breathing and circulation
tant role in the diagnosis and management of SE. Elimi- Hypoxia may be the result of, or precipitate, SE and thus
nation of seizure activity on the EEG is the goal in the must be corrected for recovery to occur. Airway manage-
management of SE, as seizure activity in the brain can ment in a patient actively having a seizure may be diffi-
continue even when its physical manifestations have cult; however, ensuring airway patency is crucial in an
ceased. Initially, discrete changes are seen, which may unresponsive patient. The level of intervention will
merge to form a waxing and waning pattern of rhythmic depend on the animal’s status. The airway may need to be
ictal discharges that ultimately continues. This continu- suctioned due to production of excessive amounts of
ous seizure activity, which may take the form of continu- saliva. Administration of 100% oxygen via either a non-
ous spike or spike-and-wave patterns, rhythmic sharp rebreathing mask or flow-by is recommended. If the
waves or rhythmic slow waves, is then punctuated by patient is unresponsive, not spontaneously breathing or
periods of relative flattening that become progressively not ventilating adequately (high end tidal CO2 or high
longer as the ictal discharges shorten. These patterns can PaCO2), intubation and/or mechanical ventilation is/are
be recognized in a comatose patient suggesting SE, even necessary.
424 SPECIFIC EMERGENCIES

A large-bore intravenous catheter should be placed followed by colloids if necessary (see Chapter 31). Acid-
for administration of fluids and drugs; this is obviously osis is far more common in SE patients than alkalosis,
not possible during SE, which initially limits the treat- therefore administration of balanced electrolyte solu-
ment possibilities. tions is appropriate.
While hypertension is usually present early in SE,
hypotension can occur as the event progresses and is Acid–base status
often exacerbated by the AEDs used. Therefore, obtain- Metabolic acidosis is common in SE patients during the
ing and monitoring systemic BP is important, but is convulsive episode. Resolution of the metabolic acidosis
completely impractical during the seizure event. Treat- usually occurs with cessation of the convulsions. Identifi-
ment of hypertension is directed at cessation of the cation of hypoxia or respiratory acidosis should result in
seizure activity. Hypotension should be treated as in any immediate attempts to improve oxygenation via oxygen
shock situation, starting with a bolus of crystalloids supplementation (340).

Table 89 Monitoring the SE patient Table 90 Managing the recumbent patient

• Heart rate/rhythm. Continuous monitoring with telemetry • Monitor vital parameters. See Table 89.
or a least audible Doppler monitoring is preferred. Target • Keep in well-padded cage. Bedding should be kept clean
ranges: dog, 60–120 bpm; cat, 140–180 bpm. and dry at all times. Bean beds, slings or hammocks, and
• Respiratory rate. Continuous monitoring with telemetry is mattresses can all be used to achieve adequate padding.
preferred. Target ranges: dog, 8–34 bpm; cat, 10–20 bpm. Well-padded caging helps to prevent pressure sores.
• Urine production/specific gravity. Placement of a closed • Turn every 4 hours. Helps to prevent pressure sores and
urinary collection system is preferred for hygienic reasons atelectasis of lungs on dependent side. If possible, keep
and to allow for appropriate quantifications of ‘in and outs’: chest sternal as much as possible and continue to turn hips.
 USG: over 1.030–1.035 is concentrated, higher may • Lubricate eyes. Ideally use artificial tears every 2–4 hours.
indicate inadequate fluid intake. Petroleum ophthalmic ointment is less good (due to build
 Normal urine production: 1–2 ml/kg/hour. up), but possible if availability of artificial tears is limited.
Prevents damage to cornea (ulceration).
• Blood pressure. Frequent monitoring with oscillometry or
Doppler would be appropriate. Continuous, direct arterial • Urination. Place indwelling urinary collection system using
blood pressure monitoring is not necessary, but can be used sterile technique. The collection bag should be emptied
if an arterial line is present. The goal is to maintain systolic aseptically every 4–6 hours as needed. Quantification of the
BP >90 mmHg (MAP 70–80 mmHg when available). urine allows calculation of patient ‘ins and outs’ and thus
monitoring of renal function and hydration status.
• Oxygenation/ventilation. Monitoring oxygenation with
pulse oximetery and end tidal CO2 is adequate, though • Feeding/watering. If patients are able to voluntarily
serial blood gases are more accurate: eat/drink, they should be in sternal recumbency when
offered food and water and ideally kept in a sternal position
 Pulse oximetry: above 95%.
for 5 minutes after eating/drinking. This is to prevent
 End tidal CO2: 35–40 mmHg. aspiration of oral contents. If unable to eat and drink fluid,
 PaO2: 75–100 mmHg (arterial; on room air). therapy and/or nutritional support should be addressed.
 PaCO2: 35–45 mmHg (arterial; on room air). • Thermoregulation. Additional heat support or cooling
• Body temperature. A rectal probe is tolerated by many should be provided, depending on body temperature.
patients due to the level of sedation. Target ranges: dog, • Pressure sores. Monitor integument 2–3 times daily.
36.9–39.2ºC (98.5–102.5ºF); cat, 37.8–39.2ºC Pressure sores most often occur along bony protuberances.
(100–102.5ºF). Areas of heat, pain, erythema, hair loss or softening of the
• Neurological examination. Imperative that these skin are suspicious and should be clipped, cleaned and
examinations are performed serially and recorded to monitored. If a pressure sore develops, it should be kept
allow for review and assessment of signs of clean and dry. The site should be padded (doughnut
improvement/deterioration. bandages are ideal, though in some anatomical locations
can be difficult) to prevent worsening.
 S TAT U S E P I L E P T I C U S 425

and, therefore, anaerobic metabolism with lactic acidosis

created by SE. Administration of thiamine (vitamin B1)
may help to counteract the detrimental side-effects of
hyperglycaemia. Thiamine is a coenzyme essential for
the entry of glucose into the Kreb’s cycle within the
brain. Giving thiamine (25–50 mg per animal IM) before
the administration of a dextrose bolus is recommended.
If intravenous therapy is difficult to perform, oral admin-
istration of a sugar-based syrup can be a useful substitute.
Administration of oral medications should be done with
caution and only attempted in a patient with an adequate
degree of consciousness.

Hypocalcaemia
If hypocalcaemia is confirmed in a patient in SE, imme-
 340 A dorsal pedal arterial catheter is placed to help diate therapy is indicated. Administration of 10%calcium
with repeat blood gas evaluations. gluconate (0.5–1.5 ml/kg IV slowly over 10 minutes)
should occur. During administration, the heart rate and
rhythm should be monitored, preferably with electrocar-
diography. The infusion should be stopped if there is any
evidence of bradycardia.
Longer-term maintenance of hypocalcaemia requires
oral calcium (25 mg/kg q8–12h) and vitamin D (cal-
Temperature regulation citriol, 2.5–10 ng/kg q24h; dihydrotachysterol, 0.02–
Hyperthermia occurs commonly in SE patients and can 0.03 mg/kg q24h for 3 days then 0.01–0.02 mg/kg
be life threatening. If the temperature exceeds 40oC q6–24h) supplementation. Serum concentration of
(104oF), passive cooling measures should be started. calcium should be monitored closely (every 1–3 days) and
Continuous rectal temperature monitoring should be adjustments made based on the calcium concentration.
pursued, particularly if cooling measures are performed
to prevent rebound hypothermia. Passive cooling should Sodium abnormalities
be stopped when the patient’s temperature reaches 39oC Abnormalities in sodium levels should be corrected
(102oF) in order to prevent rebound hypothermia. slowly if there is suspicion that they have been chroni-
cally present, as rapid correction may lead to further
Identify and treat underlying conditions neurological deterioration. (See Chapter 27 for further
A minimum database should be collected to include details on sodium abnormalities and their treatment.)
evaluations of glucose, electrolytes, renal and hepatic
function and, if indicated, AED serum concentration. Hepatic encephalopathy
Hepatic encephalopathy (HE) results when the meta-
Hypoglycaemia bolic and detoxification functions of the liver are
If hypoglycaemia is confirmed, administration of 50% severely impaired and/or bypassed from reduced hepatic
dextrose (500 mg/kg [1 ml/kg] IV) is indicated. This function, urea cycle enzyme deficiency or abnormal
bolus should ideally be diluted to 25% dextrose and shunting of portal blood around the liver. Some of the
administered over 15 minutes. Hyperglycaemia has been substances implicated include ammonia, amino acids
linked to exacerbation of the neuronal injury of SE, (especially the aromatic amino acids), short-chain fatty
therefore it is preferable that hypoglycaemia is evaluated acids, mercaptans and biogenic amines. Short-term
prior to administration of an intravenous bolus. This therapy of HE may include lactulose, enemas and anti-
neuronal injury is the result of the hypoxic environment biotics. (See Chapter 27 for more information.)
 426 SPECIFIC EMERGENCIES

 341 Stepwise approach to the

STATUS EPILEPTICUS
treatment of status epilepticus. Various
options are presented for the animal that
does not respond to standard parenteral
antiepileptic drugs. • Diazepam (O.5–2.0 mg/kg IV, IN
or PR)
• Midazolam (0.06–0.3 mg/kg IV, IN
or IM)

Have the seizures stopped?

NO YES
Phenobarbital (2 mg/kg IV/IM)
Repeat x 2–3 or
diazepam infusion
(0.1–0.5 mg/kg/hour IV diluted in
dextrose saline given as a
maintenance fluid requirement)
Further seizure activity over next
1–3 hours

YES

Repeat phenobarbital
administration x 2 or NO
levetiracetam, 20–60 mg/kg IV

Do the seizures stop after

15–30 minutes?

• Continue phenobarbital bolusing

• Propofol 1–2 mg/kg IV bolus or up to a maximum of 24 mg/kg in
0.1–0.6 mg/kg/min titrated to effect 24 hours IV inclusive of daily
(up to 6 mg/kg/hr as a CRI), or maintenance dose where applicable.
• Ketamine 5 mg/kg IV bolus NO YES • Start oral phenobarbital
followed by 5 mg/kg/hr CRI, or (2–3 mg/kg PO bid), or
• Isoflurane 1–2% MAC • Start oral levetiracetam
• Continue phenobarbital, 10–20 mg/kg q8hr
levetiracetam or bromide load • Investigate aetiology
 S TAT U S E P I L E P T I C U S 427

Cessation of the seizure activity (341)

Administration of intravenous antiepileptic medications
should be commenced immediately on attaining
intravenous access in an SE patient. As intravenous
access is frequently not initially possible, other routes of
administration should be considered. Immediate therapy
is indicated based on acceptance that the duration of SE
is linked to neurological morbidity and that SE may
become progressively less responsive to treatment with
diazepam.
 342 Intranasal administration of benzodiazepines can
Step 1: Benzodiazepines result in rapid cerebral concentrations of the drug due to
This class of drug includes diazepam, midazolam, the highly vascular nature of the turbinates. This avoids
lorazepam and clonazepam. They are injectable, potent the first-pass metabolism associated with intravenous
and fast-acting, making them the preferred initial administration.
therapy in SE. With their effects only being temporary,
a more long-acting anticonvulsant will be necessary fol- Intravenous administration of diazepam is preferred;
lowing their use. Respiratory depression, hypotension however, if intravenous access is not available, it may be
and reduced consciousness are all possible side-effects. administered rectally or intranasally (342). Intramuscular
Antiepileptic effects are thought to be the result absorption of diazepam is variable, therefore this route of
of benzodiazepine-receptor-mediated enhancement of administration is not recommended. Rectal administra-
both pre- and post synaptic GABAergic transmissions. tion results in adequate absorption, with peak plasma
This enhanced GABAergic transmission results in concentrations reached within 15 minutes. (Note:
increased movement of chloride ions into neurons and Patients on long-term phenobarbital therapy may
thus hyperpolarization of the neuron with decreased require higher doses of diazepam [2 mg/kg] due to acti-
ability to form an action potential. They also limit sus- vation of the liver’s hepatic cytochrome P-450 enzyme
tained repetitive neuronal firing at higher concentrations system resulting in increased metabolism of diazepam
by decreasing the spread of nerve impulses to other and its metabolites.) Target plasma concentrations are
neurons. It is thought that benzodiazepines prevent reached in approximately 10 minutes in animals that are
the spread of seizure activity rather than suppress the not being treated with phenobarbital and by 20 minutes
epileptic focus. in animals on chronic phenobarbital therapy.
If 1–2 doses of diazepam fail to control the seizure
Diazepam (0.5–2.0 mg/kg IV up to 20 mg manifestation, the addition of another, longer-acting
maximum dose) anticonvulsant medication should be immediately con-
Diazepam is metabolized in the liver by hepatic microso- sidered; however, it should be remembered that these
mal systems. The major metabolites (nordiazepam, drugs can take a short time to become effective. Contin-
oxazepam) have 33% of the activity of their parent drug. ued administration of diazepam, in the face of failure to
Diazepam has a short elimination half-life in the canine control seizure manifestation, may result in further
patient (3.2 hours), although the half-lives of the metabo- neurological compromise to the patient from the seizure
lites are slightly longer (oxazepam, 5.2 hours). Because of activity as well as toxicity from diazepam. Administration
its short elimination half-life it is not an appropriate of diazepam in cats has been associated with acute hepatic
choice for chronic management of seizure patients. necrosis; however, this complication has only been
Mean peak plasma concentrations are reached in less reported when diazepam was administered orally, there-
than 2 minutes when diazepam is administered intra- fore parenteral administration of diazepam in the emer-
venously. gency situation should not be withheld from feline
patients.
 428 SPECIFIC EMERGENCIES

If a bolus of diazepam does work, a CRI should be commonly used barbiturate for acute seizure control.
considered (0.1–0.5 mg/kg/hour) in the interim prior to Barbiturates are metabolized in the liver, predominantly
the longer-acting anticonvulsant becoming effective. A through hydroxylation. The post-synaptic enhancement
syringe pump can be used or the diazepam can be diluted of the inhibitory effects of GABA is the primary mecha-
in 5% dextrose in water (D5W) such that the total nism of action. This effect results in an increased seizure
volume administered is equal to the patient’s mainte- threshold as well as a reduction in spread of the seizure.
nance fluid requirement over the hour. Concerns regard- The loading dose of phenobarbital is 12–24 mg/kg IV.
ing aqueous solubility, formation of deposits and However, it is recommended that smaller boluses
adsorption onto polyvinyl chloride tubing have been (2–4 mg/kg) should be administered, repeating every
raised. Compatibility should be checked before combin- 20–30 minutes, to effect, but not exceeding 24 mg/kg
ing diazepam with any other medication or intravenous over 24 hours. The parenteral form of phenobarbital
fluid, as formation of precipitates is common. Drugs may also be used intramuscularly, which is useful in the
should never be administered if a precipitate forms. The initial treatment of a case that does not have intravenous
use of midazolam in lieu of diazepam circumvents many access. However, the distribution of phenobarbital to the
of these concerns, but this drug can be more expensive. If CNS and hence its effect may take up to 30 minutes due
diazepam is used, the administration set should be pro- to its low lipophilicity. Intramuscular administration may
tected from light and changed every 2 hours. Care should avoid the profound respiratory and cardiovascular
also be taken when administering other medications into depression experienced when phenobarbital is adminis-
this line, as many medications will cause precipitates to tered following benzodiazepines.
form when combined with diazepam. Side-effects of phenobarbital include respiratory
A high initial rate is used following a bolus dose and is depression, hypotension and sedation. In an SE patient,
usually continued for up to 6 hours before a gradual and whose respiratory and cardiovascular function may
tapered (50% every 6 hours) reduction is begun. This already be compromised, these side-effects could
approach is useful if SE is due to toxicity, where seizures become life threatening, thus monitoring of respiratory
will probably be present for a protracted time period, or and cardiovascular parameters must be continuously per-
while awaiting a loading dose of phenobarbital to formed.
become effective. Parenteral use of this drug should be followed as soon
as possible by the more routine twice daily oral adminis-
Midazolam (0.06–0.3 mg/kg IM or IV) tration, to ensure long-term control of seizure activity is
Midazolam’s peak plasma concentration in dogs after addressed.
intramuscular injection is 15 minutes and its half-life in
dogs is 1–2 hours. Midazolam’s superior absorption and Step 3: Levetiracetam
bioavailability with intramuscular injection when com- If the use of phenobarbital is not successful or is consid-
pared with diazepam make it a feasible alternative when ered inappropriate (e.g. underlying presence of liver
there is no intravenous access on initial presentation. disease), the next option is the use of levetiracetam.
Levetiracetam (20–60 mg/kg IV) is a newer anticonvul-
Step 2: Barbiturates sant and has a half-life of 3–4 hours in dogs. Its intra-
Following the successful use of benzodiazepines, barbi- venous use may be effective for 8 hours, at which time it
turates should be considered as long-term maintenance can be repeated. While the binding site of the drug, a site
anticonvulsants. They can be parenterally loaded to on a synaptic vesicle protein in neurons, has been identi-
achieve a rapid steady state serum concentration. fied, the exact mechanism of action is unknown. It is
Loading phenobarbital is usually only performed in thought to act by modifying calcium-dependent exo-
those patients that have not previously received this drug cytosis of neurotransmitters and may therefore be syner-
or are suspected to have low serum drug levels. If bolus gistic with phenobarbital or potentially effective where
doses of benzodiazepines did not stop the seizure activity phenobarbital has not been. When used with pheno-
or were only temporarily successful, barbiturates become barbital, a dose of levetiracetam at the upper end of the
the next therapeutic option. Phenobarbital is the most range may be necessary. Levetiracetam causes minimal
 S TAT U S E P I L E P T I C U S 429

sedation, making it desirable in treating more refractory In human medicine, a propofol infusion syndrome
SE patients that already have an altered consciousness. It has been reported when propofol has been used at
is not metabolized in the liver and so represents a more high doses (>4 mg/kg/hour) or for prolonged periods
suitable option than phenobarbital for dogs and cats with (>48 hours). Signs of this syndrome include metabolic
portosystemic shunts or liver disease. Excretion is purely acidosis, rhabdomyolysis, hyperkalaemia, lipaemia, renal
renal and therefore there are minimal interactions with failure, hepatomegaly and cardiovascular collapse. While
other anticonvulsant medications; however, caution this syndrome has not been reported in veterinary
should be used in patients with deficient renal function. patients, the possibility exists, especially in those patients
Levetiracetam may also have neuroprotective effects, maintained on a CRI long term. (Note: Propofol is a
reducing seizure-related brain damage. As with pheno- phenol and therefore capable of causing oxidative injury
barbital, the oral maintenance use of levetiracetam to RBCs of the cat, resulting in Heinz body formation
should follow its parenteral use once SE has been and haemolytic anaemia.)
controlled.
Ketamine (5 mg/kg IV bolus followed by 5 mg/kg/hour
Step 4: Short-acting anaesthetic agents CRI)
SE that does not respond to a benzodiazepine, pheno- Ketamine is an NMDA receptor antagonist. NMDA
barbital or levetiracetam is considered refractory and receptor antagonists, like ketamine, are able to end the
requires more aggressive treatment. Potential reasons for maintenance phase of chronic SE, sometimes called self-
resistant seizure activity include inadequate anticonvul- sustaining SE. NMDA receptor activation only occurs in
sant doses, an uncorrected metabolic abnormality or the the later phases of SE, perpetuating the seizure activity,
presence of an intracranial disease, such as a tumour. so NMDA antagonists are suspected to be beneficial
These patients often represent a difficult therapeutic during prolonged or refractory SE. Ketamine may also
problem. Short-acting anaesthetic drugs are the most have neuroprotective effects by inhibiting NMDA
commonly used agents for treating resistant SE, as they receptor-mediated excitotoxicity associated with pro-
have a rapid onset of action and short half-lives and cause longed seizure activity; however, there is also some evi-
reductions in cerebral metabolic rates. These drugs dence that excessive antagonism of the NMDA receptors
should be used only in an intensive care setting because can be detrimental. Although the use of ketamine has
of the need for continuous BP monitoring and, ideally, been documented in a dog with SE, there are currently
CVP monitoring. no clinical studies documenting the effectiveness or
safety of ketamine CRI in treating veterinary patients.
Propofol (1–2 mg/kg IV bolus or 0.1–0.6 mg/kg/
minute titrated to effect, up to 6 mg/kg/hour as a CRI) Step 5: Inhalant anaesthesia
Propofol acts on the GABA receptor in a similar way to Inhalant anaesthesia is considered a last resort in refrac-
both barbiturates and benzodiazepines and so has anti- tory SE. Not all volatile anaesthetics are appropriate in
convulsant actions as well as being an anaesthetic. It also managing the SE patient. For example, enflurane may
reduces the metabolic demand of the CNS. Its metabo- increase seizure activity. Isoflurane and sevoflurane may
lism is predominantly through hepatic mechanisms and attenuate seizure activity, as has been shown in cats with
is far more rapid than that of barbiturates. This drug can experimentally induced seizures. The utility of this
be successfully used in SE cases due to toxin exposure and approach is in the cessation of the physical manifestations
while awaiting more effective steady state levels of phe- of SE while a maintenance anticonvulsant takes effect.
nobarbital or bromide (see below). Maintaining a patient on an inhalant anaesthetic requires
The primary side-effect of propofol is apnoea, which intensive monitoring and mechanical ventilation.
may result in hypoxaemia if not treated appropriately. During this time, phenobarbital, levetiracetam or
Thus, if a CRI of propofol is used, adequate airway bromide should be given at a loading dose to achieve a
control, haemodynamic support and possible ventilatory steady state, at which time the inhalant anaesthetic can be
support should be available. withdrawn to assess seizure control.
430 SPECIFIC EMERGENCIES

Step 6: Recovery/maintenance Bromide

Dexmedetomidine Potassium bromide (KBr) is a recommended mainte-
Some patients will display marked agitation on recovery. nance AED in the dog. It is not used in the cat because of
The use of dexmedetomidine as a CRI (0.1–1.0 the risk of inducing allergic pneumonitis. The half-life of
μg/kg/hour) has been reported to help manage this issue. KBr after its oral administration in the dog is approxi-
However, caution must be used as dexmedetomidine mately 25 days, which has precluded its use in SE. Recent
may cause bradycardia, arrhythmia (AV block), decreased work has established that KBr is well absorbed after
respiration and hypothermia, which can be problematic rectal administration, with an estimated bioavailability of
in the SE patient, therefore the dose should be adjusted 57.7% and a mean half-life of 20.4 days. For a more rapid
following careful monitoring. effect than that obtained with oral maintenance dosing
Vital parameters, including heart rate, BP, ventilation regimens, a rectal loading protocol has been devised.
and body temperature, should continue to be monitored Intrarectal administration may be preferred in the
and serial neurological examinations performed until the patient that is heavily sedated from prior diazepam and
patient is mentally alert and mobile. The combination of phenobarbital administration. A loading dose of KBr
SE and the previously mentioned medications can result (600 mg/kg) can be administered over a 24 hour period as
in marked cardiovascular and respiratory depression as 6 per rectal boluses (100 mg/kg q4h). The side-effects
well as hypothermia. It is imperative that the clinician seen with the use of this regimen may be transient diar-
monitor parameters to ensure systemic support is contin- rhoea and sedation. The use of sodium bromide may be
ued as needed for a complete recovery. considered, as it can be administered intravenously at a
Once seizure activity has been controlled and sys- loading dose of 900 mg/kg over 24 hours and then con-
temic stabilization has been ensured, a maintenance tinued at 30 mg/kg/day orally.
AED will need to be considered. In a naïve patient,
phenobarbital may be used as the sole medication. It is Zonisamide
recommended that a patient with a history of SE be The exact mechanism of action of zonisamide is
loaded so that steady state serum levels are reached as unknown. It is thought to produce its antiepileptic effect
quickly as possible. Instructions for loading phenobarbi- by blocking sodium channels and reducing transient ion
tal have been given above. If the animal was on pheno- currents, thus stabilizing the membranes and suppressing
barbital prior to the episode of SE, two options exist: potential hypersynchronization. The half-life is 15
• If the animal’s serum phenobarbital level is low, an hours, therefore it can be used twice daily, reaching
increase in dose may be indicated. steady state within 3–5 days. It is a sulphonamide drug
• If the serum level is well within the therapeutic and should not be administered to a dog with a history of
range, is approaching toxic levels or if the patient is reactions to this class of drug. It is also a known teratogen
displaying adverse effects, an additional AED may and so should be avoided in breeding animals. Most of
be added. Add-on AED drugs include bromide the drug is excreted through the kidneys, with some
(20–30 mg/kg q24h, and can be loaded at hepatic metabolism. Minimal sedation is seen with this
600 mg/kg over 4 hours to 4 days; rapid administra- medication. Doses have been reported as 10 mg/kg PO
tion can result in coma), zonisamide (8–12 mg/kg q12h and 8–12 mg/kg PO q12h. It should be made clear
PO q8h), levetiracetam (7–20 mg/kg q8h), to owners that the use of this medication in veterinary
gabapentin (10–30 mg/kg q8h) and pregabalin medicine has been limited and therefore its effectiveness
(2–4 mg/kg q8–12h). and potential side-effects are not fully understood.

(See Chapter 7 for additional information on mainte-

nance seizure medications.)
 S TAT U S E P I L E P T I C U S 431

Levetiracetam be sufficient for most dogs). Sedation is the most com-

Levetiracetam’s supposed mechanism of action has been monly reported side-effect. Like zonisamide, levetirac-
discussed above. As a maintenance AED, administration etam and gabapentin, pregabalin has had limited use in
three times daily is required, potentially making this drug veterinary medicine.
less desirable to owners. A dose of 20 mg/kg PO q8h has
been reported. Like zonisamide, there is limited experi- PROGNOSIS
ence of using this medication in veterinary medicine.
Sedation is minimal. One study reported a 25% mortality rate for dogs pre-
senting with SE or cluster seizures, while another study
Gabapentin documented a 5% mortality rate and a 33% euthanasia
The mechanism of action resulting in gabapentin’s rate in dogs with SE of multiple causes while in hospital.
antiepileptic effects is not fully understood. While gaba- However, an unbiased mortality rate for dogs is unknown
pentin is structurally related to the neurotransmitter given that many patients are euthanized prior to aggres-
GABA, it does not appear to exert its effects through the sive treatment and diagnostic testing, and SE is due to
same mechanism. It does not alter GABA binding, reup- multiple types of brain disease (343). Dogs with SE of all
take or degradation, nor does it serve as a GABA agonist causes that die or are euthanized after discharge have a
within the body. The half-life in dogs is about 2–4 hours, survival time of 0.1–5.9 years (median 0.8 years).
making three times daily administration necessary, but Factors reported as negatively affecting outcome are
steady state serum levels are reached quickly (10–20 the diagnosis of symptomatic epilepsy (e.g. due to GME
hours). Gabapentin is eliminated by the kidneys or cerebral neoplasia) and failure to adequately control
unchanged. Administration of 10–20 mg/kg q8h for both the seizure activity within 6 hours of its onset. Dogs with
dogs and cats has been recommended. Side-effects are SE due to toxicosis have more favourable outcomes than
uncommon, with sedation the most likely. dogs with symptomatic epilepsy. No associations have
been made correlating breed and age with type of seizure
Pregabalin activity observed.
The mechanism of action of pregabalin is unknown, The mean hospitalization time for dogs with SE has
but its chemical structure is related to that of gabapentin. been reported as 51.6 ± 42.6 hours. Recurrent SE is a
It may modulate calcium influx into neurons, reducing possibility even after initial stabilization and hospitaliza-
excessive neurotransmitter release. The recommended tion. Both these factors have important financial implica-
oral dose is 2–4 mg/kg q8–12h (twice daily is thought to tions that the owner should be made aware of.

 343 Morbidity following prolonged status epilepticus,

such as the aspiration pneumonia evident on this lateral
radiograph, can be a reason for euthanasia.
 432 SPECIFIC EMERGENCIES

THE OUT-OF-HOSPITAL The use of diazepam administered rectally at home for

STATUS EPILEPTICUS PATIENT cluster seizures in dogs has been evaluated and it resulted
in fewer seizures per cluster, reduced owner cost for
In out-of-hospital situations there are often inadequate emergency room visits and good owner compliance.
resources to manage the potential complications of The effect of concurrent long-term oral phenobarbi-
intravenous therapy. In these situations, severe systemic tal administration on rectally delivered diazepam has
and cerebral damage may result, which can lead to death recently been evaluated. The mean peak concentration
in some dogs. However, if prompt pre-hospital seizure of benzodiazepine after rectal administration of diaze-
treatment can be given, fewer AEDs are required and pam in six dogs fell from 629 ng/ml to 274 ng/ml when
seizures tend to be shorter. Rectal, intranasal and the dogs were given phenobarbital (2.5 mg/kg every
buccal/sublingual routes of administration may be 12 hours for 30 days). These results demonstrate that
useful in these settings, especially as the absorbed drug dogs receiving chronic phenobarbital therapy may
bypasses the liver, thus avoiding the problem of first-pass require a higher dose (1–2 mg/kg) of rectally delivered
metabolism. As both intravenous and intramuscular injec- diazepam than those dogs that have not been previously
tions during SE can pose risks to the patient and the care- treated with this drug. This phenomenon is due to the
giver and are often difficult to achieve, per rectal and increased activity of the hepatic microsomal enzyme
intranasal routes of administration need to be considered. system caused by phenobarbital administration.
The use of benzodiazepines by the routes discussed Rectal administration of midazolam in humans has
below is not licensed, therefore they need to be used with been shown to be safe and effective, with peak plasma
caution. The at-home treatment of seizures is not meant concentrations occurring within 10 minutes after admin-
to avoid immediate veterinary attention for systemic istration.
stabilization, and this must be made clear to the owner.
Indications for immediate veterinary attention should be Intranasal administration
discussed with the owner and these may include: seizures In recent years, intranasal drug administration for systemic
that do not respond to the at-home therapy prescribed effects has received increased attention because of its con-
within 10 minutes; seizures that respond but recur within venience and reliability. Intranasal anticonvulsants have
24 hours; and systemic concerns such as depressed respi- been used successfully in human SE cases. Midazolam has
ratory effort, obtundation and blindness. The dangers of been shown to be quickly absorbed by the nasal mucosa
being in close contact with a seizuring dog should also be and to reach levels that equal or substantially exceed
emphasized to the owner. threshold levels for sedation in humans. The duration of
action following intranasal administration is similar to that
Rectal administration after oral dosing, although the onset of action is earlier.
Rectal administration of an AED is useful in emergency Peak plasma concentrations occur 10 minutes after admin-
situations, and it is relatively easy to carry out in the home istration in dogs; plasma concentrations of midazolam
environment. It has been well established that absorption exceeding therapeutic values were seen within 3 minutes
of lipid-soluble drugs by the membranes of the colon and after intranasal administration to children.
rectum is rapid and complete. Diazepam can be adminis- It has also been suggested that drugs instilled into
tered into the rectum using plastic administrators such as the nasal cavity may directly reach the brain via the crib-
tom-cat catheters with a water-soluble lubricant. The riform plate and that the concentration in the CNS
efficacy of rectally delivered diazepam in SE depends on may be higher than that reflected by measurements of
several factors: the time that it takes for the drug to reach plasma concentrations. Further studies to better under-
the therapeutic concentration and exactly what the thera- stand uptake and absorption from the nasal cavity are
peutic concentration is in an individual dog. The actual required.
therapeutic level in dogs has not been well documented
and may be anywhere from 300 to 1500 ng/ml.
 SPECIFIC EMERGENCIES Chapter 24

MYASTHENIA GRAVIS
433

Kerry Smith Bailey

INTRODUCTION AETIOLOGY/PATHOPHYSIOLOGY

Myasthenia gravis (MG) is literally defined as ‘serious Normal neuromuscular transmission

muscle weakness’ and is associated with failure of NM A clear understanding of the anatomy and physiology of
transmission. There are two types of MG: congenital the normal NM junction is imperative to understand
and acquired. MG’s pathophysiology. A motor unit consists of a motor
Congenital MG (CMG) is a rare disease and is neuron and the muscle fibres innervated by the axonal
defined as an inherited disorder in which the safety terminals of that neuron. The strength of a muscle con-
margin of NM transmission is compromised by one or traction depends on the number of motor units activated
more specific mechanisms; it can arise from presynaptic, within the muscle. The NM junction consists of three
synaptic or postsynaptic defects. Clinically, patients with components: the motor nerve terminal, the synaptic cleft
CMG present similarly to patients with acquired MG and the muscle end plate.
(AMG), with the chief complaints being exercise intoler- The release of ACh from the motor nerve terminal
ance and weakness. ensures a unidirectional conduction from the axon ter-
In its acquired form, MG is an immune-mediated minal to the muscle end plate. Located within the pre-
disorder in which antibodies are targeted against the synaptic axoplasm are vesicles, 300–500Å in diameter,
nicotinic acetylcholine receptor (AChR) of skeletal that contain ACh. Each vesicle contains one quantum
muscle. This results in muscular weakness and excessive of ACh, or 5,000–10,000 molecules. Approximately
fatigability. AMG is the most common NM disorder 1,000 quanta are located adjacent to the cell membrane
diagnosed in the canine patient, with three clinical syn- and are available for immediate release. Many more are
dromes: focal, generalized and acute fulminating: contained in store and move toward the membrane to
• Focal AMG presents as localized weakness of replace the liberated ACh. Each ACh quantum liberated
oesophageal, pharyngeal, laryngeal and/or facial from the nerve terminal contains a nearly equal number
muscle groups, with no clinical evidence of appen- of ACh molecules. The nerve endings contain high con-
dicular weakness. centrations of choline acetyltransferase, which synthe-
• Generalized AMG is defined by the presence of sizes ACh, and acetylcholinesterase (AChE), which
obvious appendicular weakness with or without hydrolyzes ACh.
megaoesophagus and facial, pharyngeal or laryngeal When the action potential reaches the nerve terminal,
weakness. the resultant depolarization of the distal region of the
• Acute fulminating AMG is characterized by a rapid axon initiates an influx of Ca2+ into the motor axons.
onset and progression of profound appendicular The increased amount of Ca2+ accelerates the fusion
muscular weakness, with varying degrees of facial, of the vesicle membranes with the nerve terminal mem-
pharyngeal, oesophageal and laryngeal weakness. brane, which leads to a large increase in the rate of ACh
This form is often rapidly fatal due to the release. The ACh molecules traverse the synaptic cleft to
progression of tetraparesis and respiratory failure reach the AChR, which is located in the end plate region
associated with diaphragmatic and intercostal of the skeletal muscle fibre (344, next page).
muscle weakness.
 434 SPECIFIC EMERGENCIES

 344 Sequence of events at the neuromuscular

junction leading to an action potential in the muscle
fibre plasma membrane. (1) Action potential increases
the permeability of the motor neuron terminals to Ca2+.
(2) Ca2+ enters the terminals and triggers exocytosis of
acetylcholine-containing vesicles. (3) Acetylcholine 1
diffuses to the muscle nicotinic acetylcholine receptors.
(4) Two molecules of acetylcholine bind to these
receptors, increasing the Na+ and K+ conductance of the
membrane. (5) The resultant influx of Na+ produces a
9
depolarizing potential – the end plate potential.
(6) The current sink created by this local potential
2
depolarizes the adjacent muscle membrane to its firing
level and the voltage-gated Na+ channels open, leading
to propagation of the action potential in the muscle
membrane. (7) The acetylcholine is then removed 8 NM JUNCTION
7 3
from the synaptic cleft by the enzyme acetylcholin- 4
esterase and hydrolysed to choline and acetate.
(8) Choline is actively taken up via a transporter into
6
the cholinergic axon terminal. (9) Acetylcholine is
synthesized from choline and acetyl-coenzyme A 5
(acetyl-CoA), catalysed by the enzyme choline acetyl-
MUSCLE FIBRE
transferase (CAT). Acetyl-coA is synthesized in the cell
mitochondria when the acyl group in acetate bonds to Choline
Ca2+
the carrier molecule Coenzyme A (CoA). Acetylcholine Acetate
Na+ Acetyl-coA
K+ CoA
Acetylcholinesterase CAT

Sodium channel
Acetylcholine
δ β binding site
 345 Schematic diagram of the nicotinic acetyl-
choline-gated ion channel. The receptor channel
consists of five subunits arranged around a central α γ α
cation (Na+) channel. When two molecules of acetyl-
choline bind to portions of the α-subunits exposed to
the membrane surface, the ion channel opens and Na+
enters the muscle cell. The subsequent depolarization
of the end plate region is referred to as the end plate
potential.

Transmembrane
domains (TM1–4)
 M YA S T H E N I A G R AV I S 435

The AChR is a nicotinic acetylcholine receptor. It is Pathophysiology of myasthenia gravis

a transmembrane glycoprotein with five subunits (α x 2, The fundamental difference between CMG and AMG
β, γ and δ) that form an ion channel (345). Binding of two lies in the pathophysiology. CMG is the result of a single,
ACh molecules to specific sites on each of the two α sub- or combination of, presynaptic, synaptic or postsynaptic
units opens the ion channel. This allows cations (specifi- defect(s). Presynaptic defects, such as mutations in the
cally Na+) to flow through the postsynaptic membrane choline acetyltransferase gene, or synaptic defects due
into the muscle cell. This depolarization of the end plate to mutation of the AChE-associated collagen gene
region is known as the end plate potential (EPP). When are occasionally the cause in human CMG. More com-
the EPP exceeds the excitability threshold of the muscle monly, the defect is related to the amount of AChR
cell, voltage-dependent Na+ channels open, leading to expressed on the postsynaptic region of the NM junc-
the generation of an action potential. This propagation tion. Proposed mechanisms for the AChR deficiency in
of the muscle potential activates the contractile elements canine CMG include deficient synthesis of AChR,
within the muscle cell through excitation–contraction defects in the membrane insertion of the receptor, accel-
coupling. eration of its degradation, decrease in its binding affinity
Excitation–contraction coupling links the electrical for ACh or a structural abnormality of the NM junction.
and mechanical activity of NM transmission and repre- An absolute deficiency of AChR molecules in the NM
sents the spread of the action potential from the motor junction, not just a failure of AChR to bind ACh and its
end plate to the transverse tubules, thus initiating muscle ligands, has been demonstrated in the Jack Russell
contraction. A molecular change of the depolarized Terrier and Springer Spaniel.
membrane results in a selective increase in Na+ conduc- In AMG the deficiency of AChR is due to a heter-
tance, followed by an increase in K+ conductance. ogeneous group of autoantibodies (mostly immuno-
Provided depolarization reaches the critical value, this globulin class G) produced against the receptor. A
molecular change (inherent in the muscle membrane) specific region of the α subunit on the AChR has been
occurs regardless of the nature of the stimulus. While the found to be the binding site for most of the antibodies in
action potential itself is an all-or-none phenomenon AMG; this region is known as the main immunogenic
(represented as amplitude), the latency of the action region (MIR). The MIR is separate and distinct from the
potential can change depending on the speed of the AChR binding sites. There is one MIR on each of the
initial depolarization. This variability forms the basis of 2 α subunits in an AChR and it is located on the extracel-
‘jitter’ in single-fibre electrodiagnostic studies, which lular surface of the AChR, making it readily accessible to
will be discussed in more detail in the diagnostic section. circulating antibodies. Mature AChRs are continuously
Jitter serves as a sensitive measure of subtle changes turned over by internalization and degradation and
within the end plate. replaced by new AChRs; they are not reused or recycled.
The muscle fibre membrane at the end plate is lined Antibody–receptor complexes may lead to impairment of
with a basal lamina containing the enzyme AChE. This the NM transmission by encouraging endocytosis of the
enzyme splits the unbound ACh molecule into choline AChR, activating complement-mediated destruction of
and acetate. It is located mainly in the troughs of the postsynaptic muscle cell membrane near the AChR,
junctional folds of the muscle membrane. The concen- decreasing synthesis and membrane incorporation of
tration of AChE is several-fold lower than the concentra- new AChR, and directly interfering with AChR function
tion of AChRs, but it is adequate to hydrolyse most of the by bound antibody. Regardless of the exact mechanism,
ACh released by the nerve terminal and to prevent repeat the result is a decreased number of functional AChRs,
binding of ACh to the AChRs. which results in decreased NM transmission. The
common clinical sign of exercise intolerance or fat-
igability is secondary to the depletion of the stores
of ACh, compounded by the reduced number of func-
tional receptors being bound with ACh molecules and
also being desensitized to further stimulation.
 436 SPECIFIC EMERGENCIES

CLINICAL PRESENTATION in the intercostal and diaphragmatic muscles. This can

lead to aspiration pneumonia and potentially respiratory
Acquired myasthenia gravis failure.
AMG has been reported in dogs ranging in age from Several conditions have been associated with canine
7 weeks to 15 years, with all breeds and both genders AMG, including other autoimmune disorders and neo-
potentially affected. Breeds with the highest risk for plastic disorders. Autoimmune disorders reported to
AMG are Akitas, several Terrier breeds, Scottish Terri- occur concurrently with AMG include hypothyroidism,
ers, German Shorthaired Pointers and Chihuahuas. hypoadrenocorticism, thrombocytopenia, haemolytic
German Shepherd Dogs, Golden Retrievers, Labrador anaemia, polymyositis and inflammatory bowel disease.
Retrievers and Dachshunds are most commonly docu- AMG has been linked to paraneoplastic syndromes sec-
mented, but this may reflect their popularity. A familial ondary to thymoma, osteosarcoma, cholangiocellular
predisposition has been suggested in Newfoundlands carcinoma, anal sac adenocarcinoma and cutaneous lym-
and Great Danes. A bimodal age of onset with peaks of phoma. Cranial mediastinal masses and thymomas have
incidence at approximately 3 and 10 years of age has been been associated with AMG in humans, dogs and cats.
reported in affected dogs. Rare cases of juvenile-onset Thymoma cells may express antigenic epitopes similar to
autoimmune MG have also been documented. those of nicotinic AChRs. The immune response to
The typical presentation of a dog with AMG is these epitopes results in the lack of functional AChRs in
episodic, generalized muscle weakness (most obvious in skeletal muscle.
the appendicular muscles) that is worsened by activity Third-degree heart block (346) has been detected in a
and might be relieved with rest. Some dogs present so limited number of dogs with AMG and potentially
profoundly weak that rest does not improve their condi- results from circulating autoantibodies directed against
tion, so this should not be a definitive criterion for diag- the cardiac conducting tissue. Since generalized weak-
nosis. At times, the weakness may be confined to the ness is a clinical sign of both AMG and third-degree
hindlimbs only, often mimicking an orthopaedic disorder heart block, both NM and cardiac diagnostic evaluations
or possibly a spinal cord disorder. Thorough neuro- are indicated in these patients.
logical and orthopaedic examinations are helpful in AMG is rare in cats. Purebred cats are overrepre-
differentiating between the three. In addition, dogs may sented, specifically the Abyssinian and Somali breeds.
present with regurgitation due to a megaoesophagus or Similarly to dogs, there is a bimodal distribution for the
dysphagia secondary to pharyngeal dysfunction. In dogs age of onset of clinical signs in cats, with peaks occurring
with focal MG, this might be the only clinical sign. at 2–3 and 9–10 years of age. The generalized form is
Megaoesophagus is a relatively common finding in the most common clinical presentation of AMG in
canine myasthenic patients (84% of all dogs with AMG cats. Approximately 40% of cats with AMG have a
present with megaoesophagus) since the majority of the megaoesophagus, a lower prevalence than seen in dogs;
canine oesophagus is skeletal muscle. Owners may note a this is probably due to the fact that the feline oesophagus
recent voice change as a result of laryngeal muscle weak- has a smaller skeletal muscle component. The three
ness. Urinary incontinence is occasionally seen because clinical syndromes of AMG (focal, generalized and acute
the external urethral sphincter also is skeletal muscle. fulminating) have all been reported in cats. Therefore,
Spinal reflexes and proprioceptive testing usually clinical signs can include regurgitation, dysphonia,
remain normal, but dogs with profound weakness might decreased palpebral reflex, decreased menace response
appear to have poor paw positioning and/or hopping and respiratory distress. Some cats present with cervical
response. Cranial nerve examination is usually normal, ventroflexion and a dropped jaw (347). Also unique to
although some dogs with AMG will exhibit a decre- cats is an association between the development of AMG
mental palpebral reflex, indicating facial muscle fatigue. and treatment of hyperthyroidism with methimazole.
Dogs with acute fulminating AMG can present This is known as acquired drug-induced MG. Feline
collapsed in respiratory distress. These dogs often AMG has been associated with the presence of a cranial
develop a rapid onset of oesophageal dilation, tetra- mediastinal mass, though this is not associated with an
paresis, pharyngeal dysfunction and loss of strength increase in severity of clinical signs.
 M YA S T H E N I A G R AV I S 437

 346 Electrocardiogram depicting a dog with third-

degree heart block. The p waves and QRS complex
bear no relationship to each other.

 347 Adult cat exhibiting extreme weakness and

cervical ventroflexion.

Congenital myasthenia gravis DIAGNOSIS

CMG has been reported in the Jack Russell Terrier,
Springer Spaniel, Smooth-haired Fox Terrier, Gammel Acquired myesthenia gravis
Dansk Honsehund breeds, two unrelated mongrel dogs, Diagnosing AMG in dogs and cats can prove to be a dif-
and the Miniature Short-haired Dachshund as well as ficult task. Signalment, history, clinical signs and exami-
several cats. Multiple cases often occur within a single litter nation findings may provide a strong index of suspicion
and a recessive mode of inheritance has been suggested. for a diagnosis of AMG; however, additional diagnostics
These dogs are young, between 6 and 12 weeks old, when are required for a more definitive diagnosis.
they present with clinical signs consistent with NM weak-
ness. Megaoesophagus occurs less commonly in CMG Initial diagnostic tests
when compared with AMG, having only been reported in Because AMG can mimic other NM diseases, diagnosis
the Smooth-haired Fox Terrier, where an early sign of begins with attaining a minimum database including a
disease typically is stiffening of the hindlimbs when CBC, chemistry profile and urinalysis. Although none of
walking. Affected dogs frequently sit with their stifles in these tests are definitive for AMG, other causes of gener-
extension. They may progress to the point where they are alized weakness may be ruled out (e.g. electrolyte distur-
unable to hold their head up, using their nose as support. bances or hypoglycaemia). In addition, the minimum
database will provide baseline health screening that will
DIFFERENTIAL DIAGNOSIS be helpful in guiding diagnostics requiring general
anaesthesia and designing therapeutic protocols. Occa-
Other NM disorders may mimic MG, including botu- sionally, serum CK is mildly to moderately elevated in
lism, polyradiculoneuritis, tick paralysis or infectious dogs with AMG, secondary to muscle cell damage as a
neuropathies/myopathies, and should be considered result of falling down or being recumbent.
when diagnosing MG.
438 SPECIFIC EMERGENCIES

Presumptive diagnostic tests Electrodiagnostic testing

Edrophonium challenge test Electrodiagnostic testing of the nerves and muscles
The edrophonium challenge test (Tensilon test) is a diag- is a common tool for determining the presence of NM
nostic test that is relatively easy to perform and may help disease. Motor and sensory nerve conduction studies are
to establish a clinical diagnosis of AMG while the results normal in patients with AMG. Electromyography
of antibody testing are pending. Edrophonium chloride studies can show normal to increased insertional activity
is an ultra-short-acting anticholinesterase agent that without spontaneous myofibre discharges. Occasionally,
allows more ACh to be available for binding to the func- chronic severe MG can give rise to abnormal sponta-
tional AChR present on skeletal muscle. The recom- neous electrical muscle activity. Because these ‘classic’
mended dose is 0.1–0.2 mg/kg IV in dogs and 0.25–0.5 electrodiagnostic tests are not specific for AMG, two
mg/kg IV in cats. The author recommends placement of additional electrodiagnostic studies are performed (348):
an intravenous catheter, as this test is not without risk. • Repetitive nerve stimulation testing in patients with
Overstimulation of the AChR can produce depolarizing AMG often reveals a decrement in the amplitude of
blockade and worsening of muscle weakness. This is the compound muscle action potential (CMAP).
known as a ‘cholinergic crisis’ and respiratory paralysis The CMAP is a summation of action potentials
may result. In addition, overstimulation of the mus- from numerous muscle fibres belonging to a
carinic AChR may lead to salivation, vomiting, defeca- number of motor units. A greater than 10%
tion, urination, bronchoconstriction and bradycardia. decrease in the amplitude and/or the area of
Therefore, it is recommended to ‘pre-treat’ with successive CMAPs during a train of 10 stimulations
atropine (0.02–0.04 mg/kg IM or SC) and be prepared to at a rate of 1–3 Hz is suggestive of AMG.
treat such a cholinergic crisis with intravenous atropine Unfortunately, this test lacks specificity and
(0.02–0.04 mg/kg). Because atropine is an antimuscarinic sensitivity and requires general anaesthesia, which
agent, it will not have any effect on the nicotinic AChRs might not be desirable in a critical patient.
at these doses and therefore will not interfere with the • Single-fibre electromyography (SF-EMG) investi-
edrophonium test. The dog should be exercised to the gates NM transmission and evaluates the extent to
point of detectable weakness. The test is considered which diseases directly affect the ability of the NM
positive when a patient demonstrates marked improve- junction to synthesize or release ACh or the ability
ment in muscle strength shortly after the administration of the postsynaptic membrane to respond to ACh.
of the edrophonium chloride. The improvement usually When muscle action potentials are recorded from a
lasts a few minutes, after which the patient returns to its single muscle fibre with an SF-EMG electrode, the
pre-treatment state. This is a subjective test and the latency from the stimulus to the response varies;
results are not always clear and definitive. Some ‘true’ this is known as jitter. Most jitter is produced by
myasthenic patients do not respond positively to intra- fluctuations in the time it takes for the end plate
venous edrophonium. These patients may not have potentials at the NM junction to reach the action
enough functional AChRs available to respond to the potential (depolarization) threshold. Jitter is a
abundance of ACh. This is particularly the case in dogs sensitive measure of the safety factor of NM trans-
with acute fulminating AMG. Conversely, false-positive mission. It becomes increased when the safety
results are possible. There can be subjective improve- margin is smaller than normal (or when the ratio
ment in muscle strength with other NM conditions, such between the depolarization threshold and the end
as polymyositis. When edrophonium chloride is not plate potential becomes increased). MG is the most
available, neostigmine methyl sulphate can be used (40 common disorder that reduces the safety factor of
μg/kg IM or 20 μg/kg IV). This challenge test is not NM transmission. SF-EMG is the most sensitive
useful for dogs with focal AMG. Because the edropho- test for diagnosing MG in humans. However, the
nium challenge test is a subjective test for AMG, other test requires a high degree of expertise and the cost
diagnostic options are required for a definitive diagnosis of the SF-EMG needle is substantial, therefore it is
of AMG. not commonly performed in veterinary medicine.
 M YA S T H E N I A G R AV I S 439

a Confirmatory diagnostic tests

Immunocytology
Immunocytochemical staining of muscle end plates is
another diagnostic test available to help diagnose AMG.
Immunoglobulin localized to the end plate regions of
skeletal muscle can be identified by an immunocyto-
chemical method. The reagent used is a staphylococcal
protein A (SPA) linked with horseradish peroxidase
(HRPO). This reagent is incubated with fresh muscle
tissue. The SPA binds to the Fc portion of the immuno-
globulin and the HRPO stains the region where the
binding occurs. SPA-HRPO conjugate is not specific for
the antibodies against the AChR, so false positives are
possible. However, a negative result will rule out a diag-
b nosis of AMG unless the patient has received prednisone
or other immunosuppressive drugs prior to testing.

Serum AChR antibody assay

The ‘gold standard’ diagnostic test for AMG in dogs and
cats is demonstration of circulating AChR antibodies
using 125I-labelled α-bungarotoxin bound to native
AChR in a radioimmunoassay. The assay is objective,
quantitative and specific, demonstrating an autoimmune
 348 (a) The Cadwell Sierra Wave, a multipurpose response to AChRs. Serum AChR antibody titres
electrodiagnostic machine that has the capability of >0.6 nmol/l are diagnostic for AMG in dogs; titres
performing single-fibre electromyography and repetitive >0.3 nmol/l are diagnostic in cats. The test detects
nerve stimulation tests, which are helpful in the diagnosis approximately 98% of dogs with AMG. Two percent of
of MG. (b) Supramaximal repetitive stimulation of the myasthenic dogs are categorized as ‘seronegative’.
distal ulnar nerve (carpal stimulation) and recording from Several mechanisms as to why the test does not identify
the palmar interosseous muscles in a dog with acquired all affected dogs have been proposed:
myasthenia gravis. Note the decremental response in • There might be a strong affinity of the antibody to
compound muscle action potential amplitudes over the the muscle end plate, resulting in undetectable
first four recorded waveforms; greater than 10% (24% in amounts of antibody in the serum.
this case) with low stimulation rate (3Hz in this case). • During solubilization of the AChR for the test
The scale applies to each individual waveform, but the probe, damage to certain antigenic epitopes of the
distance between them does not correspond to the AChR can occur and the test probe might therefore
stimulation frequency on this computerized representa- fail to recognize some antigenic variations of the
tion. Vertical double arrow represents 2mV and horizontal AChR antibodies.
double arrow represents 2ms. (Photo courtesy Nicolas • Some of the antibodies in AMG may be directed
Granger) against antigenic proteins of the end plate region
other than the AChR and these would not be
identified by the test.
• Dogs treated with prednisone or other immuno-
suppressive agents for at least 7–10 days prior to
testing have a decreased amount of circulating
antibody, which may not be detected by the test.
440 SPECIFIC EMERGENCIES

a Ancillary diagnostic tests

Thoracic radiographs should also be included in the
diagnostic plan. Radiographs should be evaluated for the
presence of a cranial mediastinal mass, megaoesophagus
and aspiration pneumonia (349). The presence of aspira-
tion should prompt collection of tracheal wash or bron-
choalveolar lavage for cytology and culturing to assist in
optimal antibiotic therapy. The relative oesophageal
diameter is of little diagnostic value in distinguishing
b dogs with megaoesophagus secondary to AMG versus
other causes of megaoesophagus. Therefore, other diag-
nostic options are needed to more definitively diagnose
AMG. When megaoesophagus is suspected and not
evident on radiographs, oesophagography with liquid
barium or fluoroscopy may be performed, but caution
must be taken as the risk of aspiration pneumonia in dogs
with megaoesophagus and AMG is high. Because other
autoimmune disorders such as hypothyroidism and
hypoadrenocorticism have been associated with AMG,
adrenal and thyroid testing are recommended in suspect-
ed myasthenics.

Congenital myasthenia gravis

Diagnosis of CMG begins with signalment, history and
presenting clinical signs. In addition, these animals often
 349 (a) Right lateral thoracic radiograph depicting display a positive response to the drophonium challenge
megaoesophagus and a cranial mediastinal mass test. The serum AChR antibody titre is normal. EMG
(thymoma). (b) Ventrodorsal radiograph depicting testing is normal. Diagnosis is supported by demonstra-
megaoesophagus and severe aspiration pneumonia. tion of a decremental response with repetitive nerve
stimulation, which may be reversed with administration
of edrophonium chloride. Definitive diagnosis is based
It is recommended that dogs and cats with negative titres on demonstration of decreased AChR content in a
be re-tested one month later to evaluate for seroconver- muscle biopsy. The intercostal muscles have the highest
sion. The titres tend to be lower in focal AMG than in concentration of AChR and are the muscles of choice
generalized or acute fulminating AMG, but there is no for the test. External intercostal muscle AChR content
direct correlation between severity of clinical signs and <0.1 pmol/g tissue is suggestive of CMG (normal refer-
the level of antibody titre in dogs. ence: 0.2–0.4 pmol/g tissue).
 M YA S T H E N I A G R AV I S 441

MANAGEMENT Anticholinesterase agents are useful in the treatment

of all forms of MG. Although they do not correct the
Therapy for AMG should be tailored to the individual underlying aberrant immune response, the natural
needs of the patient. The three main aspects of therapy course of canine AMG is to go into spontaneous remis-
for MG are anticholinesterase therapy, immunomodula- sion. If an optimal response is successfully achieved and
tory therapy and supportive care. muscle strength is regained, anticholinesterase agents
and supportive care may be all that is needed for treat-
Anticholinesterase therapy ment. However, for more refractory cases of AMG, the
Anticholinesterase therapy is the mainstay therapy for addition of immunomodulatory drugs is indicated.
treatment of both CMG and AMG. Anticholinesterase
drugs prolong the action of ACh at the NM junction by Immunomodulatory therapy
reversibly inhibiting AChE and thus enhancing NM The indications for immunomodulatory therapy are:
transmission. The agent that is used most commonly is • Dogs with persistently elevated AChR antibody
pyridostigmine bromide (1–3 mg/kg either PO or via a titres.
feeding tube q8–12h in dogs, 0.25 mg/kg q8–12h in cats). • Seropositive dogs that had a negative edrophonium
To avoid a cholinergic crisis, it is recommended to start at chloride challenge test.
the low end of the dose rate, three times daily, and • Dogs with less than optimal response to anti-
increase as needed. In dogs who cannot tolerate oral cholinesterase agents.
drugs and where a feeding tube is not available, • Dogs with unacceptable side-effects relating to
neostigmine bromide can be administered (0.04 mg/kg therapeutic anticholinesterase treatment.
IM q6h) because it has a rapid onset of effect, but shorter • Cats seem to respond better to combined immuno-
duration, when given parenterally than pyridostigmine. modulatory and anticholinesterase treatment.
For critical animals, a constant rate intravenous infusion • AMG and not CMG patients, as there is no
of pyridostigmine bromide (0.01–0.03 mg/kg/hour) may immune-mediated basis for CMG.
be given until oral feedings are resumed or a feeding tube
is placed. Common side-effects of anticholinesterase Corticosteroids and other immunomodulatory drugs
drugs include nausea, cramps, diarrhoea, salivation and should not be administered until the patient is stable and
lacrimation. These may be abated with concurrent aspiration pneumonia, if present, has resolved.
administration of atropine or administration of the drug
with a meal. Overdosing with anticholinesterase drugs Corticosteroids
will lead to an excess accumulation of ACh at the NM Corticosteroids, such as prednisone, show some benefit
junction, resulting in weakness as a result of depolariza- in the treatment of human MG, but they should be used
tion and desensitization of the postsynaptic membrane. with caution in dogs with MG. The main cause of death
An increase in anticholinesterase medication that does in canine myasthenic patients is aspiration pneumonia
not produce a dramatic increase in muscle strength associated with megaoesophagus, a complication not
should be quickly reversed in order to avoid a cholinergic commonly seen in human patients. Prednisone is contra-
crisis. The edrophonium chloride challenge test can be indicated in these patients because it has the potential to
used to monitor treatment for dogs on pyridostigmine as exacerbate pneumonia. In addition, corticosteroids may
well as help to differentiate between under and over- exacerbate weakness in dogs with MG. The worsening of
treatment. If treatment is inadequate, edrophonium clinical signs is a direct negative effect of glucocorticoids
chloride will provide immediate amelioration of signs of on excitation–coupling of the contractile elements within
weakness, whereas in a cholinergic crisis due to over- myofibres and altered function of the ion channel of the
treatment the signs will be temporarily aggravated. AChR. Consequently, lower initial corticosteroid doses
 442 SPECIFIC EMERGENCIES

(0.5 mg/kg q24h or q48h) gradually increased to higher hinder oral administration of drugs. In a recent case
doses (2 mg/kg q24h) in 0.5 mg/kg increments every 2–4 series, three dogs with generalized MG and concurrent
days have been recommended in canine AMG. Unlike ME were treated with intravenous mycophenolate
dogs, exacerbation of muscle weakness may not occur as mofetil. Signs of clinical remission were evident within
frequently in cats treated with high doses of cortico- 48 hours. Once resolution of the ME was achieved, oral
steroids. Once muscle strength has returned, the dosage administration replaced the intravenous administration.
of prednisone can be reduced very slowly while monitor-
ing carefully for relapse. Azathioprine
Azathioprine is a cytotoxic antimetabolite drug that is
Mycophenolate mofetil effective in treating humans with MG. Through its active
Mycophenolate mofetil is a lymphocyte-specific metabolite, 6-mercaptopurine, azathioprine decreases
immunosuppressive drug that has shown promise in the lymphocyte proliferation, with a subsequent decrease in
treatment of canine AMG. Mycophenolate mofetil’s immunoglobulin production. It is relatively specific for
active compound, mycophenolic acid, selectively inhibits T lymphocytes, but can cause bone marrow suppression.
the action of the enzyme inosine monophosphate dehy- Other adverse effects include gastrointestinal irritation
drogenase, which is necessary for the de novo synthesis of and hepatotoxicity. These adverse effects typically
guanosine triphosphate (GTP). A lack of GTP impairs a resolve with reduction of drug dosage or discontinuation
cell’s ability to synthesize DNA, RNA, proteins and of therapy. The initial dosage for azathioprine in dogs is
glycoproteins. Lymphocytes are preferentially targeted 2 mg/kg orally per day. The dosage is then tapered to an
by mycophenolic acid, while other leucocytes, such as every other day regimen after the desired clinical
neutrophils and macrophages, are unaffected. Mycophe- response is achieved. Periodic (every 1–2 weeks) moni-
nolate mofetil increases the clinical remission rate in toring of the haemogram is recommended in the initial
dogs with AMG. Additionally, because of the lack of non- stages of therapy and every 1–2 months thereafter to
specific immunosuppression, it can be used safely in monitor for bone marrow suppression. In a limited case
patients that have, or are at risk for developing, aspiration series, four of five dogs treated with azathioprine (four
pneumonia. In a recent study, the one year mortality rate dogs were concurrently treated with pyridostigmine; one
was 38% for dogs with AMG treated with pyridostig- was treated concurrently with prednisone) appeared to
mine alone, compared with 28% for dogs treated with have a positive clinical response to therapy with minimal
both pyridostigmine and mycophenolate. Mycopheno- side-effects; however, the exact efficacy of this drug and
late mofetil is initially administered at a dosage of its role in the treatment of canine AMG have not yet
20 mg/kg orally twice daily. After one month of therapy, been established. A major disadvantage of this medica-
the dosage is decreased to 10 mg/kg twice daily to avoid tion is the delay of 2–8 weeks before a clinical response is
cumulative adverse gastrointestinal effects. Side-effects observed.
of mycophenolate mofetil include bone marrow suppres-
sion and cumulative gastrointestinal irritation (vomiting Cyclosporine
and diarrhoea), which occur most commonly when the Cyclosporine, a calcineurin inhibitor, inhibits T-cell acti-
initial dosage is continued for longer than one month. vation and prevents synthesis of several cytokines includ-
The cost of the drug is high and may be prohibitive in ing interleukin-2 (IL-2). Without stimulation by IL-2,
large breed dogs. Because of its promising efficacy and further T-cell proliferation is inhibited and cytotoxic
limited side-effects, mycophenolate mofetil should be activity is decreased. Cyclosporine is specific for lympho-
considered in cases of AMG refractory to anti- cytes, and minimal bone marrow suppression is noted.
cholinesterase agents alone or in all cases of AMG where Side-effects include gingival hyperplasia and mild gas-
megaoesophagus is present. In addition to the oral trointestinal upset. Based on very limited clinical data,
formulation, an intravenous one is available. This formu- cyclosporine at a dosage of 4 mg/kg every 12 hours might
lation is useful in patients in the acute setting or patients be effective in cases of AMG where anticholinesterase
with severe megaoesophagus, where regurgitation may therapy alone fails.
 M YA S T H E N I A G R AV I S 443

Thymectomy
Surgical removal of hyperplastic thymic tissue is associ-
ated with long-term clinical improvement in humans
with generalized forms of AMG. The potential benefits
of thymectomy for canine MG patients is unknown;
however, complete removal of thymomas has been asso-
ciated with normalization of the AChR antibody titre
and resolution of clinical signs. Surgical removal of a
thymoma also resulted in rapid resolution of mega-
oesophagus in a dog with focal AMG.

Supportive care
Supportive care and nutritional support are critical
when treating a patient with MG. In those patients
with normal pharyngeal and oesophageal function (i.e.
without megaoesophagus), supportive care is minimal.
Oral feeding can continue normally because the risk of
aspiration pneumonia is low. In a patient with pharyngeal
dysfunction or megaoesophagus, a nutritional plan must
be devised. If the patient is able to consume food orally  350 Keeping the dog upright for a while after feeding
and is not continually regurgitating, oral feeding still in a Bailey chair, as here, or similar, is necessary to reduce
might be possible. The best consistency of food varies the potential for regurgitation. (Courtesy Roxie’s MEGA
depending on the individual and may be dry dog food, Mission)
gruel or canned food. Feeding the patient in an upright
position with elevated bowls, or holding the dog upright Tubes can be placed surgically or via endoscopic guid-
after eating, is helpful to encourage the passage of food ance (percutaneous endoscopic gastrostomy tube) (351).
from the oesophagus to the stomach (350). In patients In large breed patients (>25 kg body weight) the former
that continually regurgitate or present with megaoeso- is recommended to ensure proper placement and forma-
phagus and concurrent aspiration pneumonia, placement tion of an adequate seal with the body wall. Once a tube
of a gastric feeding tube is strongly recommended. is in place, all feedings, water and medications should be

 351 Placement of a
percutaneous endoscopic
gastrostomy tube in a patient
with megaoesophagus.
 444 SPECIFIC EMERGENCIES

given through the tube. Nothing should be allowed a

orally until clinical remission, including resolution of the
megaoesophagus, has been achieved. Placement of a
gastrostomy tube requires general anaesthesia, which
may present a significant risk in some myasthenic
patients. A ‘low-profile’ replacement gastrostomy tube
can be utilized long term for added convenience. In cases
of acute fulminating AMG, parenteral nutrition may be
the only feasible option and should be implemented as
soon as possible.
Aspiration pneumonia is a common complication
related to AMG and the main cause of death in these
patients. Early detection and aggressive treatment are
vital for a successful outcome. Radiography, pulse b
oximetry, arterial blood gas monitoring, body tempera-
ture monitoring and careful auscultation allow early
identification of pneumonia. Patients with aspiration
pneumonia should be treated with broad-spectrum anti-
biotics, ideally based on culture and sensitivity results
from tracheal wash specimens. In addition, respiratory
supportive care, including supplemental oxygen, nebu-
lization treatments and coupage exercises, is beneficial
(352). Certain antibiotics (i.e. aminoglycosides, ampi-
cillin, ciprofloxacin, erythromycin and imipenem)
should be avoided because they can have potentially
adverse effects on the NM junction. In cases of acute ful-
minating AMG, ventilatory support is usually required
due to weakness of the intercostal muscles and/or
diaphragm or severe aspiration pneumonia.

 352 Respiratory supportive care. (a) Patient with

severe aspiration pneumonia, intubated, receiving oxygen
and being monitored with pulse oximetry and a
capnograph. (b) Patient with myasthenia gravis and
aspiration pneumonia being treated with nasal oxygen.
(c) Coupage exercises being performed on a patient with
aspiration pneumonia and myasthenia gravis.
 M YA S T H E N I A G R AV I S 445

PROGNOSIS patients receiving immunomodulatory therapy, as false-

negative results can occur. Despite the overall guarded
Overall, the prognosis for AMG is guarded. Approxi- prognosis for dogs with AMG, especially for those with
mately 84% of patients have megaoesophagus, and aspiration pneumonia, there is a frequent occurrence of
aspiration pneumonia is the main cause of death in spontaneous remission among canine myasthenics.
canine patients with AMG. In dogs, the 1-year mortality A large percentage of dogs with AMG (88.7%), regard-
rate has been reported to be as high as 60%. German less of the form, enter a spontaneous immune and
Shepherd Dogs appear to have a more guarded progno- clinical remission at an average of 6.4 months after
sis. Because fewer cats develop megaoesophagus and diagnosis. Those dogs that do not enter spontaneous
aspiration pneumonia, the 1-year mortality rate for cats clinical remission are at an increased risk for developing
is only 15%. There is an inverse relationship between the neoplasia, including thymoma. The high incidence of
concentration of AChR antibodies in cats and the prog- spontaneous clinical remission makes it difficult to
nosis. Higher concentrations are associated with more evaluate the efficacy of various treatment protocols
acute and severe clinical signs (acute fulminating cases and establish a standard of care. A similar study evaluat-
have the highest AChR antibody titres), therefore this ing the natural course of the disease has not been
titre may be used to determine the prognosis for cats. performed in the cat.
A similarly strong correlation has not been established in Response to treatment of CMG is usually poor and
dogs; however, monitoring serial AChR antibody titres the complete resolution of clinical signs is uncommon.
in an individual is a good indicator of disease status. Weakness is usually progressive and death commonly
There is an excellent correlation between resolution of occurs within 1 year of age, although with treatment,
clinical signs and return of the AChR antibody titre some individuals might survive longer. In contrast with
below the normal level of 0.6 nmol/l in dogs. As long as a previously reported cases of CMG in dogs that are
patient has an elevated titre, therapy should be continued relentlessly progressive, spontaneous remission of clini-
despite any resolution of clinical signs. Care must be cal signs was recently reported in two Dachshunds with
taken when evaluating serial AChR antibody titres in CMG by 6 months of age without medical therapy.
This page intentionally left blank
 SPECIFIC EMERGENCIES Chapter 25

TETANUS AND BOTULISM

447

Jacques Penderis

INTRODUCTION AETIOLOGY/PATHOPHYSIOLOGY

Tetanus is a disease characterized by prolonged muscle Tetanus

contraction (either focal or generalized). It is caused by Tetanus is seen with moderate frequency in veterinary
production of the neurotoxin tetanospasmin, usually patients and is caused by the neurotoxin tetanospasmin,
within an anaerobic wound. There are marked differ- formed by the gram-positive, obligate anaerobe C. tetani.
ences in species susceptibility, with the horse being C. tetani is found around the world and C. tetani spores
highly susceptible, while the dog is much less susceptible are ubiquitous in the environment, in particular in soil,
(around 600 times less susceptible) and the cat even less faeces and dust. The spores are highly resistant (includ-
so. Tetanospasmin (tetanus toxin) is produced by the ing to heat and some disinfectants) and survive for
gram-positive, obligate anaerobic bacterium Clostridium prolonged periods in the environment, in particular in
tetani. The toxin binds irreversibly to presynaptic sites of soil with high moisture and organic content. Following a
inhibitory neurons and recovery from the clinical signs of contaminated wound, the spores gain entry to the body
tetanus requires the formation of new axonal terminals. and convert into the vegetative form. This process is
The toxin is usually degraded within the gastrointestinal made more likely in the presence of concurrent local
tract if ingested orally. tissue infection, abscessation, necrosis or a foreign body.
Botulism is a neuroparalytic disease characterized by However, in a substantial number of cases no evidence of
symmetrical flaccid (LMN) paralysis affecting motor a wound can be identified. Following germination into
and autonomic nerves and is caused by botulinum neuro- the vegetative form, local production of tetanus toxins
toxin. Botulism occurs occasionally in dogs, most com- occurs, in particular the neurotoxin tetanospasmin.
monly secondary to dietary ingestion of preformed toxin, Tetanospasmin is usually degraded within the gastro-
but has only once been demonstrated clinically in cats intestinal tract if orally ingested and does not cross the
(although it can be produced experimentally). Botulinum placenta. There are a variety of different strains of C.
toxin is the most potent known naturally-occurring acute tetani, but in all these strains the tetanospasmin toxin
toxin and is most commonly produced by the gram- produced has the same antigenic properties and there-
positive, anaerobic, spore-forming bacterium Clostridi- fore a single antitoxin is effective against tetanospasmin
um botulinum. Toxin within C. botulinum spores are heat produced by all strains of C. tetani.
resistant and the toxin is resistant to low pH and is not
denatured in the stomach. Botulinum toxin produced by
different strains of C. botulinum have different antigenic
properties (with seven recognized, of which type C is the
most common in dogs). Different strains of toxin require
different antitoxins.
 448 SPECIFIC EMERGENCIES

Botulinum vesicle Acetylcholine vesicle Glycine vesicles

Botulinum toxin Botulinum light chain Glycine receptor INHIBITORY
Botulinum SNARE proteins Synaptobrevin INTERNEURON
heavy chain Tetanospasmin
light chain
8
Tetanospasmin
vesicle

5 7
3

4 Acetylcholine vesicle
Acetylcholine
receptor

2 9
NEUROMUSCULAR JUNCTION

1
6

a MUSCLE
Acetylcholine receptor b MUSCLE

 353 The mechanism of action of (a) botulism and (b) tetanus neurotoxins. (1) Normal acetylcholine release
at the NM junction. (2) The botulinum toxin is haematogenously transported from the gut to the axon terminal
where it is absorbed via endocytosis. (3) The heavy chain of the toxin releases the light chain into the terminal
cytoplasm, where it cleaves specific SNARE proteins (4, 5) required for fusion of acetylcholine vesicles to the
presynaptic membrane, thus preventing their exocytosis. In contrast, the tetanus neurotoxin usually enters the
bloodstream through a wound. It, too, attaches to the presynaptic membrane (6), but is transported back through
the axon into the CNS (7). The toxin then binds to inhibitory interneurons and, as with botulism, the light chain
is freed. This targets the vesicle-associated membrane protein synaptobrevin, preventing the release of the
inhibitory neurotransmitters GABA and glycine (8) and leading to uncontrolled release of acetylcholine (9).

The toxin is spread haematogenously (or, in some pathways of neurons innervating these muscles (354).
cases, locally) and binds preferentially to NM junctions, All muscles are affected in generalized tetanus, but the
from where it undergoes retrograde axonal transport to clinical finding of extensor limb rigidity and trismus
the neuronal cell body (353). From there the toxin reflects the greater strength of the extensor muscle
spreads via synaptic junctions to adjacent motor and groups and the muscles that close the jaw, in comparison
autonomic neurons. Tetanospasmin cleaves synapto- with the flexor muscle groups and muscles that open the
brevin, one of the vesicle-associated membrane proteins jaw. The most common form of tetanus is generalized
required for neurotransmitter release. The main effect of tetanus, where the entire body is affected, but localized
tetanospasmin is on inhibitory pathways (in particular tetanus may also occur in a single limb in close proximity
interneurons inhibiting alpha motor neurons), where it to a wound.
prevents the release of glycine and GABA, resulting in Involvement of the autonomic nervous system tends
failure to inhibit motor reflexes. The consequence of this to occur later in the disease course, but may continue for
is dramatically increased muscle tone and rigidity. Early 1–2 weeks. The exact mechanism is unknown, but the
involvement of the facial muscles (‘risus sardonicus’ and most widely accepted theory involves impairment of
trismus [‘lockjaw’]) reflects the relatively short axonal inhibitory circuits in the autonomic nervous system.
 T E TA N U S AND BOTULISM 449

The clinical signs vary and reflect overstimulation of Botulism

either the sympathetic or parasympathetic nervous Botulism is relatively uncommon in veterinary patients
system. Dogs with naturally occurring tetanus appear to and the majority of cases can be linked to eating animal or
have more parasympathetic overactivity with fewer bird carcasses, food that has spoilt or food that has been
sympathetic signs. Increased parasympathetic tone com- stored inappropriately in anaerobic conditions, allowing
monly results in bradycardia, bradyarrhythmias and the growth of bacteria. Botulinum toxin is usually pro-
hypotension. Increased sympathetic tone results in vaso- duced by C. botulinum bacteria, but may also be pro-
constriction, tachycardia and hypertension. In some duced by some strains of C. baratii and C. butyricum. C.
cases, episodes of excessive catecholamine release occur botulinum bacteria are a heterogeneous group of gram-
secondary to adrenal stimulation, resulting in episodes of positive, anaerobic, spore forming, rod bacteria, which
tachycardia and hypertension, contrasted with periods of are all characterized by the production of botulinum
bradycardia and hypotension. toxin. Botulinum toxins produced by different C. botu-
Binding of tetanospasmin to neurons is irreversible linum bacteria have different antigenic properties, allow-
and recovery requires the generation of new nerve termi- ing them to be subdivided into seven distinct strains
nals. This explains the slow recovery in these cases. (types A, B, C1, D, E, F and G). All reported canine cases
to date have been caused by type C toxin, with the excep-
tion of two cases reported from Senegal caused by type D
toxin. Naturally occurring botulism has only been
reported once to date in cats, where a group of cats were
fed pelican carrion; however, the disease has been exper-
imentally produced in cats. Botulism is reported in man
and a variety of other animals, with different antigenic
strains responsible for disease in different species. Differ-
ent strain types produce identical clinical signs, but strain
type is important as strain-specific antiserum is required
for treatment. Botulism in man has been reported sec-
ondary to types A, B, E and F. Type C is also the most
common strain in other animals, although strain D is
sometimes also seen in cattle, strain B is reported in
horses and strains A and E occur in birds and mink.
C. botulinum is found worldwide and is a relatively
ubiquitous bacterium, present in the soil, marine and
freshwater sediments and the gastrointestinal tracts of
mammals and fish. C. botulinum is capable of producing
spores and these are resistant to heat, light, desiccation,
many chemical agents and radiation. Under anaerobic
conditions, combined with a high organic nutrient envi-
ronment, the bacterium produces botulinum toxin as it
grows. Vegetative cells contain higher levels of toxin than
spores; toxin is only released following cell or spore lysis.
 354 Generalized tetanus in an English Springer However, the toxin contained within spores is resistant to
Spaniel with a nail bed infection. Generalized tetanus heat denaturation. In most veterinary cases, botulism
is characterized by dramatically increased muscle tone occurs following ingestion of preformed toxin in food
of the limbs, body and head. The facial musculature that has spoilt (either food that has been poorly stored
demonstrates ‘risus sardonicus’, which is characterized or carrion), but in occasional cases botulism may
by the ears drawn together, lips drawn back and occur following colonization of anaerobic tissues by
wrinkling of the forehead. C. botulinum, with local toxin production. There is also
 450 SPECIFIC EMERGENCIES

some anecdotal evidence to suggest that in a multiple dog CLINICAL PRESENTATION

outbreak of botulism from a kennel environment, dogs
that did not have access to the contaminated diet may still Tetanus
have developed botulism, presumably by ingestion of Two forms of tetanus are described in domestic animals:
botulism toxin through coprophagia. Botulism second- localized tetanus and generalized tetanus. Localized
ary to ingestion of preformed toxin in spoilt food is also tetanus, where limb rigidity is seen close to a wound, is
the most common form in man, but two other clinical less common. Generalized tetanus results from haemato-
variants occur in man: infant botulism and infant-like genous spread of the tetanospasmin toxin. Clinical signs
botulism. Both of these forms are due to in-vivo botu- first become apparent 5–10 days after a wound in which
linum toxin production following intestinal colonization growth of C. tetani bacteria has occurred, and this delay
with botulinum toxin-forming clostridial bacteria. may explain why there is often no wound apparent when
Intestinal colonization causing botulism has been report- a case is presented with clinical tetanus. Wounds closer to
ed in a young dog. the head are associated with more rapid onset and more
Following cell or spore lysis in spoilt food (carrion is commonly present as generalized tetanus than wounds
the most common source in dogs) the toxin is released distally on the limbs. Generalized tetanus may also occur
and binds with other protein complexes to form progen- following a recent ovariohysterectomy in dogs. Local-
itor toxins. These progenitor toxins are extremely stable, ized tetanus with spasticity of one hindlimb and scoliosis
particularly at low pH, and pass through the stomach has been reported in cats following ovariohysterectomy.
into the small intestine, where the toxin is released and Cats are more resistant to tetanus, resulting in a
absorbed. decreased incidence and longer time to onset (up to 3
The toxin is absorbed from the small intestine by weeks); however, when it does occur in cats it is usually
endocytosis, enters the lymphatic system and from there associated with larger wounds producing larger amounts
the bloodstream. Botulinum toxin in the blood stream of toxin.
binds rapidly and with extremely high affinity to pre-
synaptic peripheral nerve terminals, affecting the limb, Localized tetanus
trunk and head muscles. Differences in toxin binding Localized tetanus is uncommon in human patients, but is
affinity explain the differences in species susceptibility. more common in cats and dogs due to their increased
The process of neuronal binding comprises: (1) binding innate resistance. Local muscular stiffness and rigidity
with neuronal cell surface receptors, (2) endosomal inter- develop in a single limb or the paraspinal muscles in asso-
nalization of the toxin, (3) membrane translocation and, ciation with a wound or in the hindlimbs in association
finally, (4) modification of target SNARE proteins with infection of the reproductive tract of females
required for exocytosis of ACh at the NM junction. or following ovariohysterectomy. The stiffness progres-
Botulinum toxin binds rapidly and irreversibly to the sively develops from the distal extremity to affect the
neuronal cell surface receptors and once it has been entire limb, before affecting the opposite limb and
internalized it is no longer vulnerable to antitoxin. At the then the entire body, with the head the last region to be
NM junction, SNARE proteins are required for docking affected. In some cases of localized tetanus there is no
and fusion of the synaptic vesicles with the presynaptic progression of the clinical signs.
cell membrane. Targeting of the SNARE proteins by
botulinum toxin prevents presynaptic release of ACh at Generalized tetanus
the NM junction, resulting in flaccid (LMN) paralysis In generalized tetanus the head and neck musculature is
and evidence of autonomic nervous system dysfunction. affected first, followed by the body and limbs. Affected
Botulinum toxin inhibits ACh release at the NM junc- animals have a stiff and stilted gait with difficulty stand-
tion following a motor action potential, as well as sponta- ing up or lying down due to the muscular stiffness. The
neous ACh release (353). limbs are usually held in extension and the tail may be
 T E TA N U S AND BOTULISM 451

held out straight or curved dorsally. Muscle stretch Muscle tetany occurs in response to auditory, visual or
reflexes are often exaggerated and may go into persistent tactile stimuli and may be generalized, resulting in
clonus following stimulation. The CNs are affected rela- opisthotonus or even progress to generalized seizures.
tively early in generalized tetanus, with the combination Consciousness is not impaired (unless seizures develop)
of trismus (‘lockjaw’) and the typical facial expression and the tetany may be extremely painful, with animals
(‘risus sardonicus’), which comprises the ears drawn exhibiting distress during the episodes. The presence of
together, lips drawn back and wrinkling of the forehead trismus makes prehension of food difficult; more severe
(355, 356). In addition, there may be protrusion of cases may have evidence of dysphagia and regurgitation.
the third eyelids, enophthalmos due to contraction of The effect of autonomic dysfunction means that
the retractor bulbi muscles and miosis. Autonomic insta- gastrointestinal and urinary dysfunction are common.
bility may be evident in more severe cases as tachycardia The constant muscle contractions may result in hyper-
or bradycardia, respiratory compromise and dysphagia. thermia. Death is usually the consequence of cardiac or
Urine retention/inability to void can also be noted as a respiratory failure. Respiratory failure usually arises due
result of a hypertonic urethral sphincter requiring con- to laryngospasm, rigidity of respiratory muscles or sup-
tinual or intermittent urinary catheterization. pression of the respiratory centre in the brainstem.

 355 Reflecting their shorter axonal length and  356 In contrast to tetanus, other conditions causing
therefore the decreased distance tetanus toxin needs to be contraction or abnormally increased tone of the cranial
transported retrograde, the cranial nerves are affected muscles, as in this left-sided facial nerve contraction
relatively early in generalized tetanus with the secondary to facial nerve irritation, do not result in the
combination of trismus (‘lockjaw’) and the typical facial characteristic ‘risus sardonicus’ expression.
expression (‘risus sardonicus’), which comprises the ears
drawn together, lips drawn back and wrinkling of the
forehead.
 452 SPECIFIC EMERGENCIES

Botulism DIFFERENTIAL DIAGNOSIS

Botulism is characterized by an afebrile, flaccid (LMN)
paralysis with additional involvement of the autonomic Tetanus
nervous system. The onset and severity of clinical signs The main differential diagnoses for generalized tetanus
are dependent on the total dose of toxin ingested and the include bacterial meningoencephalitis, epileptic seizures
individual susceptibility of the animal. Clinical signs typ- (however, these are usually episodic in nature and nor-
ically develop rapidly within 12 hours (but can be up to mally resolve with administration of diazepam), strych-
6 days) following ingestion of the toxin. The more nine poisoning, hypocalcaemic tetany and severe
rapidly the clinical signs develop, the more severe the generalized sepsis. Masticatory muscle myositis should
disease tends to be. Affected animals develop a progres- be considered in focal tetanus affecting the head. In
sive and symmetrical paresis, progressing to flaccid paral- endemic regions, cerebral canine babesiosis and rabies
ysis that typically first becomes evident in the hindlimbs should also be considered.
before extending to the forelimbs. Voluntary control of
the tail wag is often preserved. Reflexes and muscle tone Botulism
are decreased to absent, which is consistent with an The main differential diagnoses for flaccid (LMN) paral-
LMN lesion. ysis include acute fulminating MG and acute polyradicu-
In severe cases the respiratory musculature may be loneuritis. The following diseases may also need to be
affected with decreased abdominal tone and primary considered as part of the differential diagnosis list (either
diaphragmatic respiration. The diaphragm is more as less common differential diagnoses, or in endemic
resistant to botulism toxin and is only affected in very regions): tick bite paralysis (tick paralysis); neuroparalytic
severe cases. Death may result from paralysis of the res- snake envenomation; post-vaccination polyradiculoneu-
piratory muscles or be secondary to aspiration pneumo- ritis; organophosphate toxicity; blue-green algae (anatox-
nia and complications resulting from prolonged ins) and green algae (charatoxin); black widow spider
recumbency. envenomation (the latter stages of envenomation are
Sensory function, including pain perception, and characterized by flaccid paralysis, although this is preced-
level of consciousness are unaffected. Distinct from other ed by muscle fasciculation); and accidental administration
causes of diffuse LMN disease, in botulism there is more of NM blocking agents (e.g. vecuronium and succinyl-
frequently additional evidence of CN deficits (e.g. facial choline). Rabies should be considered in endemic regions,
nerve paralysis, depressed gag reflex, decreased jaw tone, particularly if CN deficits are dominant.
reduced vocalization and megaoesophagus), as well as (in
some cases) evidence of dysfunction of the cholinergic
neurons of the autonomic nervous system. The choliner-
gic signs include alterations of heart rate (increased or
decreased), pupil changes (mydriasis with depressed
pupillary light reflexes), keratoconjunctivitis sicca,
urinary retention and constipation.
 T E TA N U S AND BOTULISM 453

DIAGNOSIS Routine investigation

The results of routine investigation (including routine
Tetanus haematology, biochemistry and CSF analysis) are usually
Diagnosis of tetanus is based on the typical clinical pres- normal or reflect secondary complications of recum-
entation of persistent muscle rigidity or tetany (focal or bency and paralysis. Conscious thoracic radiography
generalized) and, in generalized tetanus, the additional should be performed to assess for evidence of megaoe-
involvement of the face (‘risus sardonicus’ and trismus sophagus and secondary aspiration pneumonia.
[‘lock-jaw’]) and autonomic instability (bradyarrhyth-
mias or tachyarrhythmias). A recent history of a wound Demonstration of botulinum toxin
or neutering of a female dog would support the diagno- Definitive diagnosis is based on the demonstration of
sis, but often a wound is not identified. botulinum toxin early in the course of the disease, either
To further substantiate the diagnosis, routine bio- in blood (10 ml of serum should be collected) or gas-
chemical and haematological testing is usually normal, trointestinal tract contents (50 g of faeces, vomitus or
excluding other causes; however, elevation of muscle food sample should be collected). The more rapidly the
enzymes may occur in response to prolonged muscle sample is collected after the onset, the higher the likeli-
contracture. If available, electromyography may be used hood of confirming the diagnosis. In human patients,
to confirm the presence of sustained muscle depolariza- samples collected within 24 hours of onset are positive in
tion in anaesthetized animals. In most animals the muscle over 50% of cases, but this drops to less than 25% in
contraction is reduced with anaesthesia, but usually does samples collected 3 days after onset. It is essential to
not totally resolve. Bacterial isolation is usually unre- discuss the diagnostic sample requirements with the lab-
warding and is not helpful in most cases. C. tetani is an oratory performing the investigation. The samples
obligate anaerobe and therefore culture must be per- should be refrigerated, but not frozen (freezing affects
formed under strict anaerobic conditions. Serological the vegetative form of C. botulinum, but does not affect
testing can be performed to demonstrate a titre against the toxin). The sample should be labelled as a biological
tetanospasmin toxin; however, this is not generally useful hazard, particularly as people are considerably more sus-
in the clinical setting and is probably only useful in ceptible than dogs or cats to botulism toxin. The gold
unusual cases of focal tetanus. Control animal samples standard test is a mouse biological assay, in which serum
would need to be submitted with the suspect case. or a sample of faeces, vomitus or food is inoculated into
two groups of mice, one group of which is protected with
Botulism antitoxin. The development of clinical signs consistent
Diagnosis of botulism is primarily based on the history with botulism in the unprotected mice provides confir-
and suggestive clinical presentation. Due to the dietary mation. However, the test is expensive and requires live
origin of the toxin, multiple cases may occur within the animals and is therefore not often performed in veteri-
same group of animals and there may be a history of nary patients. Alternatives to the mouse biological assay
exposure to carrion. In many cases of botulism in domes- include ELISAs and PCR to detect botulism toxin
tic animals and human patients the underlying organism in food, but many of these tests are still being validated at
is not identified. In part this relates to the ubiquitous the time if writing.
nature of the C. botulinum in the environment, and
culture of food or environmental samples is therefore Isolation of C. botulinum
usually of little use. As has already been discussed, culture from food or the
environment is not helpful, but culture of the organism
from a patient’s faeces or gastric contents may be very
helpful in supporting the diagnosis. C. botulinum can be
successfully cultured from the faeces or gastric contents
in around 60% of human patients.
454 SPECIFIC EMERGENCIES

a R. common peroneal – AH 30ms 2mV  357 (a) EMG of vecuronium-induced neuromuscular

block demonstrating the typical electrodiagnostic features
Normal
of decrease in transmission at the neuromuscular junction,
similar to that seen in botulism. Following stimulation of
the common peroneal nerve, intravenous vecuronium
administration results in marked reduction of compound
motor action potential amplitude during motor nerve
conduction, in the presence of normal nerve conduction
velocity and no evidence of temporal dispersion of the
compound motor action potential. The recordings were
Blockade
performed prior to vecuronium administration (top trace)
and intermittently over the 2 minutes immediately
afterwards. The reduction in amplitude reflects the
decrease in transmission at the neuromuscular junction.
(b) Recovery from vecuronium-induced neuromuscular
b L. common peroneal – EDB block similar to that seen in botulism. The increasing
amplitude of the resulting compound motor action
potential following stimulation of a motor nerve indicates
recovery of neuromuscular junction transmission.
AH = abductor halluci; EDB = extensor digitorum brevis.
Recovery

Electromyography and nerve conduction studies periods of paralysis (around 2 weeks), followed by posi-
Electrodiagnostic evaluation of muscle and nerve func- tive sharp waves on recovery, and subtly decreased motor
tion may assist in the diagnosis, but is not definitive. The nerve conduction velocities in some canine patients, but
typical electrodiagnostic feature of botulism is marked these findings are not reliably present and consideration
reduction in compound motor action potential ampli- should be given to an alternative cause. Repetitive nerve
tude during motor nerve conduction, in the presence of stimulation at low frequency (less than 5 Hz) may
normal nerve conduction velocity and no evidence of produce a small decrement in compound motor action
temporal dispersion of the compound motor action potentials; rapid stimulation (50 Hz) are likely to produce
potential (357). The reduction in amplitude reflects the an increment in successive compound motor action
decrease in transmission at the NM junction. In addition potentials, and this increment is highly supportive of bot-
to the reduction in amplitude, there are some reports of ulism. Evidence of increment on high-frequency stimu-
identification of mild fibrillation potentials and increased lation may only be evident in a few muscle groups,
insertional activity on electromyography after prolonged despite multiple muscle groups being weak or paralysed.
 T E TA N U S AND BOTULISM 455

MANAGEMENT Other supportive care considerations in tetanus cases

reflect the prolonged recumbency and the muscular
Tetanus rigidity and stiffness that these patients experience.
The management of generalized tetanus requires inten- These include decubital ulcers from prolonged recum-
sive treatment with frequent monitoring. Binding of bency, aspiration pneumonia due to the dysphagia and
tetanospasmin to neurons is irreversible and recovery recumbency, respiratory impairment, urinary and faecal
requires the generation of new nerve terminals. For this retention (which may require bladder catheterization
reason, improvement is usually only evident after about and enemas), hyperthermia from the sustained muscle
one week of treatment. Sudden death can occur due to contraction and acute renal failure secondary to rhab-
respiratory failure or aspiration. Facilities for respiratory domyolysis following a prolonged tetany.
support should be available and animals should be closely
monitored for respiratory distress. General monitoring Antitoxin administration
should include vital signs, arterial blood gases (especially Free circulating tetanus toxin should be neutralized with
PaCO2 levels), pulse oximetry and respiratory rate and tetanus antitoxin. Available tetanus antitoxins include
effort. antitetanus equine serum and human tetanus immuno-
globulin (HTIG). Bound tetanus toxin is not affected by
Supportive care antitoxin. All animals with acute tetanus should have the
The most important aspect of the treatment of tetanus antitoxin administered and this should be performed
cases is the quality of the supportive care. Patients should prior to wound débridement, as wound débridement
be kept in a dark and quiet area and any stimulation min- results in further tetanus toxin release. The route of
imized in order to reduce the risk of precipitating administration affects the availability of the antitoxin,
seizures or severe muscular contractions. Foam ear plugs with subcutaneously administered tetanus antitoxin
(or pieces of cotton wool) should be placed in the ears to taking 2–3 days to reach therapeutic levels. Intravenous
limit stimulation by sound. If the ears are kept occluded administration is therefore preferable. Following admin-
for a prolonged period (more than a couple of days), istration of tetanus antitoxin, effective therapeutic levels
there is the likelihood of developing a marked moist otitis are maintained for at least 2 weeks and repeated injec-
externa and the ears should be regularly cleaned and tions are not required (and are associated with a greater
allowed to dry, with the animal sedated with midazolam risk of adverse reactions). Adverse reactions to tetanus
or diazepam during the procedure. Because affected antitoxin administration are of concern, in particular
animals are recumbent, they should be kept on soft anaphylaxis, and this is more likely to occur following
bedding and kept clean and dry to avoid urine and faecal intravenous administration or repeated injections.
scald. In order to limit the potential for anaphylaxis, a test
Maintaining adequate nutrition and fluid intake is an dose of 0.1–0.2 ml is administered intradermally or sub-
important part of management. Weight loss is a signifi- cutaneously prior to administration of the full dose, and
cant problem due to the inability to open the mouth, dys- the injection site monitored for 30 minutes. The devel-
phagia, abnormal gastrointestinal function due to opment of a wheal or other reaction at the injection site
autonomic dysfunction and the increased metabolic indicates risk of an adverse reaction. If there is no
demands associated with the increased muscle tone. evidence of an adverse reaction, the full dose can be
Animals are also at risk of dysphagia and gastro- administered. There is little consensus on the correct
oesophageal reflux, with a concomitant risk of aspiration dose of tetanus antitoxin, with a total dose of
pneumonia. Consideration should be given to placing a 5,000–10,000 units of HTIG recommended in human
gastrostomy or oesophagostomy tube. If that is not pos- patients. The dose of antitetanus equine serum is
sible, although less ideal, animals can be carefully fed 100–1,000 units/kg (with a maximum of 20,000 units),
with soft food or a nasogastric tube can be placed; preferably given as an intravenous bolus over 30 minutes,
however, in all cases there is still the risk of gastro- but it can also be administered subcutaneously or intra-
oesophageal reflux and aspiration. muscularly. In focal tetanus, local injection of a total dose
456 SPECIFIC EMERGENCIES

a of 1,000 units in the proximal affected limb has been

reported to be effective. Epinephrine should be available
in case of anaphylaxis and if there is concern about an
adverse reaction, glucocorticoids and antihistamine can
be administered prior to injection of the antitoxin.
There is some evidence to suggest that intrathecal
administration of a lower dose (as low as 1% of the
intravenous dose; 1–10 units/kg), in addition to the
intravenous dose, is beneficial in dogs with generalized
tetanus. The intrathecal administration of antitoxin
means that it does not need to cross the blood–brain
barrier and there is a suggestion that it may partially
neutralize CNS-bound toxin. However, intrathecal
administration is no longer recommended in human
practice because a number of studies and meta-analyses
have shown that it has no benefit over parenteral
administration.

Wound débridement
Following the administration of tetanus antitoxin, any
identifiable wound should be thoroughly cleaned,
foreign material removed and necrotic tissue débrided. It
b is important to look for evidence of nail bed infections
and sepsis elsewhere, including mastitis and reproductive
tract infections (358). The identification and débride-
ment of a wound result in an improved prognosis.
Wound débridement most likely would require general
anaesthesia; hydrogen peroxide can be used to flush the
wound in order to reduce the anaerobic bacterial load.

Antimicrobial therapy
A wide range of antibiotics are effective against C. tetani,
with metronidazole (10–15 mg/kg IV q8h [dog] and
q12h [cat]) being the antibiotic of choice. A variety of
other antibiotics are viable alternatives, including eryth-
romycin, tetracyclines, chloramphenicol, clindamycin
 358 (a) A female intact English Springer Spaniel with and amoxicillin–clavulanate. In all cases the antibiotic
generalized tetanus secondary to mastitis. Generalized therapy is continued for at least 10 days. There is some
tetanus is frequently associated with a recent ovario- debate regarding the effectiveness of penicillin in cases of
hysterectomy, sepsis of the female reproductive tract generalized tetanus, with many texts recommending the
or mastitis. (b) Examination of the mammary glands use of penicillin G at a dose of 20,000–100,000 units/kg
confirmed them to be hot and painful, with discoloured slow IV or IM q8–12h. However, one randomized trial in
milk indicative of mastitis. The identification and human patients demonstrated a higher mortality in
resolution of an infectious focus are associated with patients treated with penicillin than in those treated with
a better prognosis in dogs with generalized tetanus. metronidazole (24% vs 7%). Metronidazole may also be
a better choice because it penetrates tissue with vascular
compromise, including abscesses, more effectively.
 T E TA N U S AND BOTULISM 457

Control of muscle rigidity (or tetany) and seizures cost and it may result in respiratory depression. Metho-
Muscle tetany, muscular rigidity and seizures require carbamol is a centrally acting muscle relaxant that can be
management with sedation. There are a large variety of used at a dosage of 20–45 mg/kg PO q8h. As metho-
agents that have been and can be used, but benzodi- carbamol is a CNS depressant, additive depression may
azepines are the initial treatment of choice as a continu- occur when it is given with other CNS depressants.
ous intravenous infusion. Either diazepam (IV bolus of Baclofen, a structural analogue of GABA, has demon-
0.5–1.0 mg/kg or as a continuous IV infusion at a start- strated a dramatic response in some human patients
ing dose of 0.2 mg/kg/hour, titrated upwards to effect) or when administered intrathecally. Following intrathecal
midazolam (IV bolus of 0.2–0.3 mg/kg or as a continuous administration, baclofen inhibits neuronal transmission
IV infusion at a starting dose of 0.3 mg/kg, titrated in the spinal cord, but it is associated with a significant
upwards to effect) can be used, usually at higher doses risk of respiratory depression. Baclofen can also be
than required for control of SE and titrated to effect. administered orally, after which it is rapidly and well
The benzodiazepines are usually combined with absorbed. Doses recommended are 1 mg/kg PO q8h up
phenothiazines in order to decrease hyperexcitability, to a maximum of 5–10 mg. This medication can cause
again titrated to effect as intermittent injections. vomiting, depression and vocalization in some dogs
Chlorpromazine (0.2–10 mg/kg IV as required or, in and should be used with care. Magnesium sulphate has
dogs, a total oral dose of 5–10 mg) is the agent of choice, been recommended in humans for control of muscle
although other phenothiazines, including acepromazine tetany in severe tetanus. Magnesium plays a crucial role
(0.01–0.06 mg/kg IV, 0.01–0.25 mg/kg IM or SC, in neurotransmission and excitability. Its dosage
1–3 mg/kg PO) and methotrimeprazine (0.5–1.0 mg/kg (0.2 mEq/kg/hour CRI) has unfortunately not been
IV), are also effective. Chlorpromazine is effective established for animals with tetanus and is extrapolated
and does not potentiate seizures in tetanus, but is not from human reports. Magnesium dosing should be
effective in other conditions associated with increased titrated to reduce rigidity to an acceptable level without
muscle tone. causing respiratory depression. ECG and systemic BP
If midazolam or diazepam is not effective in control- monitoring are advised while establishing the dose of
ling the seizures (in those animals demonstrating magnesium due to the associated risks of bradycardia and
seizures), longer-acting agents, in particular pheno- hypotension. Serum magnesium concentration should
barbital, can be used. Doses of barbiturates that suppress be maintained between 2 and 4 mmol/l.
respiration should be avoided, as should other drugs that In cases where the muscle tetany and rigidity are com-
may suppress respiration. Propofol is also effective, but pletely refractory to diazepam, the NM blocking agent
doses sufficient to cause muscle relaxation require atracurium or vecuronium can be used as a ‘final resort’,
ventilatory support and are not feasible for the length of but this requires mechanical ventilation, which is usually
management that is required. not feasible in most veterinary patients.
Other medications that may be considered include
morphine, dantrolene, methocarbamol, baclofen and Control of autonomic dysfunction
magnesium sulphate. Despite the risk of respiratory One of the more important causes of mortality in severe,
depression, morphine can be effective in alleviating generalized tetanus is cardiovascular failure secondary to
muscle tetany and rigidity due to a central action that involvement of the autonomic nervous system. The clin-
reduces the effect of tetanospasmin. It is also useful in ical signs of autonomic dysfunction are usually only
alleviating the effects of excessive catecholamine release. evident in severe tetanus and usually resolve once animals
The muscle relaxant dantrolene has been used success- start to improve and, in most cases, are effectively
fully in a few human patients, but its use is limited by controlled by sedation. One of the main problems is that
 458 SPECIFIC EMERGENCIES

of tachyarrhythmias, but bradyarrhythmias and sinus Supportive care

arrest may result from overstimulation of the Supportive care represents the mainstay of treatment in
parasympathetic system. Tachyarrhythmias most likely botulism, in particular the avoidance of problems associ-
result from elevated catecholamine levels and a direct ated with prolonged recumbency. This involves bladder
effect of tetanus toxin on the myocardium. Bradycardia is management (including prevention of retention cystitis),
probably due to a direct effect of tetanus toxin on the avoiding the development of pressure sores, access to
vagal nucleus. food and water, cleanliness, support while patients return
The first step in the management of autonomic dys- to normal exercise and physical therapy. In more severe
function is to sedate the animal. Morphine as part of the cases, respiratory support may also be required. In cases
sedative protocol is effective in decreasing catecholamine that have recently presented and where toxin may still be
release. Other medications that are frequently used in present within the gastrointestinal tract, an attempt
human patients include clonidine (α2-adrenergic should be made to remove the material, taking care to
agonist) and magnesium (with is particularly effective in avoid aspiration pneumonia. This may include using
reducing autonomic overstimulation by blocking cate- gastric lavage, enemas and cathartics.
cholamine release and reducing receptor sensitivity to Bladder management is important, as recumbent
catecholamines). Treatment with atropine or glycopyro- animals will tend to retain urine and may develop
late is usually effective in reversing bradyarrhythmias. retention cystitis; the bladder should be kept as empty as
possible to minimize the residual urine volume, either
Analgesia through support for urination, manual expression, inter-
Analgesics are recommended to address the pain associ- mittent catheterization or indwelling closed collection
ated with constant muscle rigidity or tetany. (For further systems. Intermittent catheterization is associated with
details, refer to Chapter 30.) the lowest incidence of urinary tract infection, followed
by manual expression and finally indwelling closed
Botulism urinary collection systems.
The treatment of botulism is largely supportive until new All recumbent patients should be maintained on soft
functional NM junctions have formed. Because of the bedding and turned frequently in order to avoid the
requirement for prolonged supportive care and the development of pressure sores. Physical therapy
potential for respiratory failure, hospitalization and fre- (massage and passive range of joint movement) will also
quent monitoring of animals are required. Respiratory help to maintain joint movement. The animal should
failure is the main cause of death and usually develops also be kept clean in order to avoid urine and faecal scald
relatively early in the disease, but a delayed onset of up to and contamination of any pressure sores with faecal
7 days after first presentation may occur. In more severe material. (Refer to Chapter 32 for further details on
cases, monitoring of respiratory function is important nursing care of the emergency neurological patient.)
and respiratory failure may occur without preceding evi- Recumbent animals are usually unable to reach their
dence of increased respiratory effort, respiratory rate or food or water bowls, therefore maintaining daily fluid
desaturation. As an indication of patients at risk of respi- and caloric requirements is important. Care should be
ratory failure, serial measurements of respiratory func- taken during oral feeding, particularly if dysphagia is
tion should be performed, although these are not widely present, as aspiration pneumonia is a risk. The use of
available in veterinary patients. In human patients this is feeding tubes and parenteral fluids should be considered.
best assessed by serial determination of forced vital Antibiotics may be required for secondary infections;
capacity or static inspiratory pressure. A decrease in static however, they should generally be avoided, unless neces-
inspiratory pressure of 15–20% indicates that a patient is sary, because of the possibility of altering the intestinal
likely to require mechanical respiratory support. (Refer microflora and risking overgrowth with C. botulinum. If
to Chapter 2 for further details on the management of antibiotics are required, then those that may impair NM
compromised respiration.) transmission should be avoided (in particular the
 T E TA N U S AND BOTULISM 459

aminoglycosides, but also lincomycin, penicillamine, PROGNOSIS

polymyxins and tetracyclines). Ophthalmic preparations
may be necessary to protect the cornea due to paralysis of Tetanus
the eyelids and potentially reduced tear production. The prognosis for recovery from tetanus is dependent on
the presenting severity and whether the animal is
Antitoxin administration demonstrating progression. Tetanus toxin binds irre-
Antitoxin administration is currently the only specific versibly to axonal terminals, resulting in disinhibition
therapy for botulism. Antitoxin is only effective in limit- and muscular rigidity or tetany. Recovery is dependent
ing the severity of the clinical signs if administered early on the synthesis of new pre-synaptic components and
in the disease course. Antitoxin administration will not their transport to the distal axon, typically leading to a
reverse established weakness or paralysis, therefore it 2 week delay before signs of clinical improvement.
should be performed early in the disease course before There is a grading scale for determining the progno-
the toxin has irreversibly bound to the nerve terminals. sis in human patients, but due to the infrequency of
Most canine cases are due to type C botulism and the canine and feline cases this is less useful. Localized
human trivalent antitoxin acts against types A, B and E, tetanus is less common than generalized tetanus, but is
therefore the available antitoxin is not effective. If type C associated with lower mortality and more rapid recovery.
antitoxin is available, anaphylaxis and other hypersensi- In human patients (where localized tetanus is less
tivity reactions are a potential risk. A small subcutaneous common than in canines and felines) the mortality asso-
or intradermal test dose should therefore be adminis- ciated with localized tetanus is approximately 1%.
tered first. Human botulism immune globulin is available A recent retrospective study identified a significant
and has been shown to be effective in reducing the sever- association between younger age and development of
ity and duration of disease in one of the human forms of more severe clinical signs and an inverse relationship
botulism, namely infant botulism, but this is unlikely to between development of severe clinical signs (including
be effective in dogs as it is not targeted against type C autonomic disturbance) and survival.
botulism. In generalized tetanus the owners should be made
aware of the costs of treatment, particularly as dogs will
Wound débridement in botulism only start to demonstrate an improvement after about a
Most cases of botulism are due to ingestion of preformed week of therapy. Dogs that are unable to stand or walk
toxin, but, less commonly, cases of wound-associated without support, demonstrating opisthotonus or demon-
botulism with local production of botulism toxin can strating seizures all have a poor prognosis for recovery.
occur. In these cases management comprises wound
débridement with concurrent antibiotic therapy. Botulism
Effective antibiotics include benzyl penicillin and Animals with botulism have the potential for complete
metronidazole. Antibiotics are contraindicated in food- recovery with no long-term deficits if they can be sup-
acquired botulism unless there are secondary infections. ported through the period of flaccid paralysis. Despite
Ideally, wound débridement is performed after antitoxin apparent full recovery, muscle weakness may still be
administration, but as human trivalent antitoxin only acts present for up to 1 year after recovery. The overall
against types A, B and E botulism, this may not be mortality in human patients with botulism is approxi-
effective. mately 7–10%, but this is doubled in patients over
460 SPECIFIC EMERGENCIES

60 years of age. There are substantial costs associated

with the duration of nursing required and the owner
should be made aware of these at the outset.
The more rapid the disease onset the more severe the
disease tends to be, therefore the worse the prognosis.
Different muscle groups have different susceptibility to
disease and this is reflected in the temporal progression
of the disease as it develops and the reversal of these clin-
ical signs as the animal recovers. The duration of disease
is approximately 2–3 weeks and respiratory, CN, neck
and forelimb function tends to return first.
One of the primary causes of death in severe cases is
respiratory failure or secondary aspiration pneumonia
(359). The more severe the disease (particularly with
 359 Lateral thoracic radiograph demonstrating involvement of the respiratory muscles) the worse the
megaoesophagus in a dog with evidence of severe prognosis. The prognosis is also worse in animals with
secondary aspiration pneumonia. Aspiration is a risk factor pre-existing respiratory disease. The development of
in both tetanus and botulism due to the dysphagia present secondary problems associated with prolonged paralysis
in both conditions, but particulaly in botulism where there or recumbency, in particular aspiration pneumonia, is
is usually a concomitant megaoesophagus. The presence associated with a worse prognosis.
of aspiration pneumonia is associated with a poor
prognosis in both conditions.
 SPECIFIC EMERGENCIES Chapter 26

INTRACRANIAL NEOPLASIA
AND SECONDARY PATHOLOGICAL EFFECTS 461

John Rossmeisl
& Theresa Pancotto

INTRODUCTION It stipulates that an increase in the volume of one of the

constituents requires a compensatory decrease in
Primary brain tumours (PBTs) are neoplasms arising another in order to maintain pressure–volume homeo-
from the constitutive parenchymal tissues of the CNS. stasis. In the case of intracranial neoplasia, the volume of
The most common PBTs in veterinary medicine are the brain parenchyma is increased by the presence of the
of mesodermal (meningiomas) or neuroectodermal tumour, which necessitates decreases in intracranial
(astrocytomas, oligodendrogliomas and choroid plexus intravascular and CSF volumes in order to maintain the
tumours) origin. Astrocytomas, oligodendrogliomas ICP within physiological ranges. This response is termed
and oligoastrocytomas (mixed gliomas) are the most intracranial compliance, and its adaptive abilities are
common tumours arising in intra-axial locations in the blunted as the ICP continues to rise (see also page 363).
brain and they cannot be differentiated with antemortem Histopathological examination of neoplastic tissue is
imaging techniques. These types of PBT are collectively the only method by which intracranial neoplasms can be
and clinically referred to as gliomas. definitively diagnosed.
Secondary brain tumours (SBTs) are neoplasms that
haematogenously metastasize to the brain parenchyma AETIOLOGY/PATHOPHYSIOLOGY
from a distant site in the body, or compress or invade
neural tissue by local extension from an anatomical site Acute and often severe clinical neurological deterioration
in proximity to the brain (e.g. nasal, orbital, osseous associated with PBTs and SBTs necessitating emergency
tumours of the skull, pituitary tumours). The prevalence treatment can usually be attributed to one of several
of SBTs has been shown to be higher than that of PBTs pathophysiological alterations including: (1) neural dys-
in necropsy-based canine studies, with haemangio- function induced by the presence of the neoplastic mass;
sarcomas, pituitary tumours and carcinomas being most (2) uncompensated intracranial hypertension; (3) para-
common. CNS lymphoma can rarely occur as a PBT, but neoplastic mechanisms; and (4) drop metastases.
is more commonly seen as an SBT in association with
multicentric disease. Tumour-associated brain dysfunction
ICP is generated from the sum total volumetric Damage to neurons, glia and vascular elements can occur
contributions from all resident tissues enclosed in the directly as a result of the mechanical effects of the tumour
calvarium, namely the brain parenchyma, blood and on parenchymal tissues or the subsequent inflammatory
CSF. The CPP is the mean arterial blood pressure less response that is generated as a result of the tumour itself.
the ICP. The CPP is the driving force behind mainte- Neurons and glia in proximity to mass lesions can
nance of CBF, which is the volume of blood coursing become dysfunctional via direct physical destruction,
through the intracranial circulatory bed per unit time. through multiple disturbances (synthesis, release, recy-
CBF must be preserved within physiological ranges in cling) in neurotransmitter-mediated cellular signalling
order to meet the minimal oxygen and nutritional and through vascular impairment. In the early stages of
requirements of the brain. tumour growth, compensatory autoregulatory mecha-
The Monro–Kellie doctrine describes the relation- nisms, such as shifting of CSF into the spinal subarach-
ships between pressure and volume within a closed, noid space and decreased CSF production, are effective
non-expansile system, such as the osseous calvarium. and ICP is maintained within physiological ranges
 462 SPECIFIC EMERGENCIES

according to the principles of the Monro–Kellie doc-

trine. With slowly growing neoplasms, pressure–volume
homeostatic regulatory mechanisms can remain intact
despite large tumour volumes and significant mass effect
(360). In these cases, clinical signs of neurological dys-
function are focal and referable to the neuroanatomical
origin of the neoplasm. With progressive increases in
tumour volume and the resultant secondary pathophysi-
ological changes, autoregulatory mechanisms become
overwhelmed and exponential and deleterious elevations
in ICP occur. This results in uncompensated intracranial
hypertension and dangerous decreases in CPP.

Uncompensated intracranial hypertension

Intracranial hypertension is the final pathophysiological
360 Axial/transverse post-contrast CT scan demon- common denominator underlying many of the mecha-
strating a large, markedly enhancing, extra-axial mass nisms of brain injury induced by the presence of an
lesion in the ventrolateral aspect of the right cerebral intracranial neoplasm. Acute and catastrophic clinical
hemisphere. Hyperostosis of the calvarium overlying the deterioration due to intracranial hypertension is usually
mass (yellow arrows) can be seen when compared with the caused by accumulation of brain oedema (361), obstruc-
contralateral side. Peritumoural oedema is visible as the tive hydrocephalus, abnormalities of CBF (ischaemia or
hypoattenuating region in the white matter dorsal to the haemorrhage), physical displacement of intracranial
mass (red arrow). Mass effect is manifested as lateral parenchymal structures (360, 362) or combinations of
ventricular compression and a falx cerebri shift to the left. these mechanisms.
The histopathological diagnosis was a grade I, transitional There are three main types of brain oedema that can
meningioma. often coexist in animals with brain disease: vasogenic,
cytotoxic and interstitial.
 361 Gross necropsy specimen from a 6-year-old mixed • Vasogenic oedema is common in animals with
breed dog with a high-grade (grade III) oligoastrocytoma intracranial neoplasms and results from physical or
of the right fronto-olfactory lobes (red arrows). Note the functional disruption of the vascular endothelium.
midline shift and white matter oedema (black arrows) in Studies of multiple tumour types in humans and
the right cerebrum. animals have shown that intratumoural neovascula-
ture can be morphologically and functionally
abnormal, e.g. lacking endothelium, having large
endothelial fenestrations, or overexpressing
receptors for pro-angiogenic proteins and vascular
permeability factors such as vascular endothelial
growth factor (VEGF). VEGF and its receptors are
overexpressed in canine intracranial neoplasms,
such as meningiomas, astrocytomas and oligoden-
drogliomas. These pathological alterations in
vascular permeability factors may contribute to the
oedema-forming potential of certain tumour types.
Rostrotentorial meningiomas and high-grade
gliomas are often associated with significant vaso-
genic oedema, which will often accumulate along
subcortical white matter tracts (360, 361, 363).
 INTRACRANIAL NEOPLASIA AND S E C O N D A RY P AT H O L O G I C A L E F F E C T S 463

 362 Dorsal planar, post-contrast T1-weighted MR

image from a dog with seizures from a multifocal intracra-
nial choroid plexus carcinoma. Both lateral ventricles
contain uniformly contrast-enhancing masses, and a falx
cerebri shift is present towards the right of the midline.

 363 (a) Transverse T2-weighted FLAIR MRI scan at a

the level of the mesencephalon from a dog with an
anaplastic (grade III) oligodendroglioma presented for
stupor and decerebrate rigidity. An elliptical, poorly
marginated and heterogeneously iso- to hyperintense
mass lesion is present in the left cerebral hemisphere (red
arrows), surrounded by a hyperintense rim compatible
with oedema (yellow arrows). The mass obliterates the left
lateral ventricle and causes a falx cerebri shift to the right.
Periventricular oedema is also present as hyperintensity
located in the dorsomedial aspect of the right lateral
ventricle. (b) Transverse post-contrast T1-weighted image
obtained at the same level as 363a. The mass demon-
strates mild, heterogeneous contrast enhancement, partic-
ularly at its periphery (yellow arrows). The rim of
b
peritumoural oedema appears hypointense. A left
unilateral transtentorial brain herniation is also more
apparent, resulting in compression of the mesencephalon
(red arrow).
464 SPECIFIC EMERGENCIES

• Cytotoxic oedema occurs when there is failure of

the Na+/K+ ATPase pumps to extrude intracellular
sodium, leading to an intracellular accumulation of
water. It is usually due to cellular energy substrate
deficiency from ischaemia/hypoxia, hypoglycaemia
or excitotoxicity, or from toxins that interfere with
cellular metabolism, such as reactive oxygen species
and nitric oxide. Progressive distension of the cell
eventually leads to cellular lysis and death. Grey
matter is preferentially affected, as this tissue is
more metabolically active and quantitatively
contains more Na+/K+ ATPase pumps per unit area
than white matter.
• Interstitial oedema often accompanies obstructive
 364 Transverse post-contrast CT scan demon- hydrocephalus. Obstructive hydrocephalus can
strating a well-demarcated, markedly enhancing, result from compression of any segment of the
choroid plexus papilloma in the interventricular ventricular system by the presence of an intracranial
foramen, causing enlargement of the lateral mass, intraventricular haemorrhage or ventricular
ventricles (obstructive hydrocephalus). occlusion by a drop metastasis that impedes CSF
flow pathways. Areas of normal narrowing of the
ventricular system are predisposed to obstruction by
intracranial tumours, including the mesencephalic
aqueduct and interventricular foramen. Tumours
a that form in intraventricular locations, such as
choroid plexus tumours, ependymomas and
meningiomas, are often associated with obstructive
hydrocephalus (364). In obstructed regions, as the
intraventricular pressure rises, compartmentalized
CSF will cross ventricular walls, resulting in
periventricular interstitial brain oedema (363a).

 365 (a) Transverse CT scan from a dog with status

epilepticus, demonstrating a hyperattenuating intra-
ventricular mass lesion within the left lateral ventricle,
with hypoattenuating perilesional white matter oedema
(arrows) and mass effect. (b) Gross necropsy specimen
obtained from approximately the same level as the CT
scan, revealing intraventricular haemorrhage and
haematoma associated with choroid plexus carcinoma
(arrows).
 INTRACRANIAL NEOPLASIA AND S E C O N D A RY P AT H O L O G I C A L E F F E C T S 465

Neoplastic erosion into, or compression of, brain vascu-

lature can result in intracranial haemorrhage, intravascu-
lar neoplastic embolization or ischaemic brain infarction.
High-grade gliomas and choroid plexus carcinoma,
whose phenotypes are often defined by significant neo-
vascular proliferation, may haemorrhage spontaneously
in intratumoural, intraventricular, subarachnoid, epidur-
al or intraparenchymal locations. Haemorrhage can
result in acute neurological deterioration if it is severe
enough to cause a mass effect or obstructive hydro-
cephalus from resultant haematoma formation (365).
Ischaemic infarctions will result in the evolution of cyto-
toxic and vasogenic brain oedema, which will further
exacerbate intracranial hypertension; however, this is
dependent on whether the infarct is lacunar or territorial
in nature (see Chapter 17).
Brain herniations are the terminal effects of intracra-
nial hypertension. Three types of spontaneous brain  366 Transverse post-contrast CT scan at the level of
herniation are commonly observed in patients with the mesencephalon of an 8-year-old Boston Terrier dog
intracranial neoplasms. These are subfalcine, transtento- with a right forebrain anatomical diagnosis. A ring-
rial and foramenal herniation (360, 366, 367). enhancing mass (red arrows) is present in the right
• Subfalcine. A marked increase in volume of one occipital lobe of the cerebrum. Significant mass effect is
cerebral hemisphere from tumour mass, oedema, visible as a falx cerebri shift, compression of the mesen-
haemorrhage or ventricular obstruction can result cephalon by a transtentorial brain herniation (yellow
in subfalcine herniation, which is medial displace- arrows) with resultant shifting of the mesencephalic
ment of the affected cerebral hemisphere under the aqueduct to the left of midline. The histopathological
falx cerebri. Subfalcine herniations are commonly diagnosis was glioblastoma multiforme (grade IV
associated with, or preceded by, diagnostic imaging astrocytoma).
evidence of a falx or midline ‘shift’. In the axial
(transverse) and dorsal imaging planes, a falcine
shift appears as a displacement of the normally
sagittally located falx cerebri away from the
hemisphere containing the mass, across the midline
towards the contralateral cerebral hemisphere (360,
361, 362).
• Transtentorial herniation is the unilateral or
bilateral displacement of the cerebral hemisphere(s)
beneath the tentorium cerebelli, resulting in
compression of the mesencephalon and/or rostral
cerebellum (363, 366).
• Foramenal herniation (367) is characterized by
shifting of the caudoventral aspect of the cerebellar
vermis through the foramen magnum, with
secondary compression of the underlying  367 Sagittal, T2-weighted MR image from a comatose
medulla. dog demonstrating foramenal herniation (yellow arrow).
A caudal transtentorial herniation can also be seen (red
arrow).
 466 SPECIFIC EMERGENCIES

 368 Intraoperative herniation of the brain parenchyma  369 Transverse post-contrast T1-weighted MR
overlying a cerebral glioma through a parietotemporal image of a dog with seizures and pituitary-dependent
craniectomy defect following durotomy. The arrows hyperadrenocorticism associated with a pituitary
delineate the dorsal limits of the durotomy. macroadenoma (arrow).

The clinical signs associated with brain herniations are The most common examples of paraneoplastic syn-
discussed in the clinical presentation section below. Sub- dromes associated with functional pituitary tumours
falcine herniations may be clinically occult. The brain include dermatological and metabolic changes that fre-
parenchyma may also herniate through craniectomy quently accompany canine and feline pituitary-depend-
defects intraoperatively (368) or postoperatively. ent hyperadrenocorticism (PDH) and feline acromegaly
(370, 371). Cats with functional pituitary tumours are
Paraneoplastic syndromes more likely than dogs to present as an emergency for
A paraneoplastic syndrome is an alteration in the struc- extraneural signs. This can be attributable to sepsis
ture or function of an organ that is anatomically distant related to cutaneous wounds resulting from skin fragility
from the site of the tumour. With respect to the brain, in cases of PDH (371) or metabolic crises associated with
paraneoplastic syndromes are primarily the result of the concurrent insulin-resistant diabetes mellitus (PDH and
distant effects of hormones produced autonomously by acromegaly). Neurological emergencies associated with
functional and neoplastic pituitary glands (369) or from PDH can be the result of tumour-induced neuronal
hormonal deficiency secondary to neoplastic destruction dysfunction or from vascular encephalopathy, as hyper-
of the pituitary gland, both of which lead to systemic coagulability and hypertension are well-recognized com-
target organ dysfunction. It is important to recognize plications of PDH predisposing to cerebrovascular
paraneoplastic syndromes as potential premonitory signs accidents (see Chapter 17).
of underlying intracranial neoplasia. In addition, the clin- Less common examples of paraneoplastic pituitary
ical effects of these hormonal abnormalities on the syndromes include acquired central diabetes insipidus
quality of life of affected animals and their owners can be (CDI) and pituitary apoplexy. Animals with CDI result-
more devastating than the actual effects of the tumour. ing from neoplastic infiltration of the pituitary from a
 INTRACRANIAL NEOPLASIA AND S E C O N D A RY P AT H O L O G I C A L E F F E C T S 467

 370 Sagittal, post-contrast CT scan from a cat with  371 Cutaneous wound in the flank of a cat that
chronic, insulin-resistant diabetes mellitus and an acute occurred during routine restraint for venipuncture.
onset of circling to the right. The cat had a markedly The cat had insulin-resistant diabetes mellitus, a
elevated serum IGF-1 concentration and the pituitary dexamethasone suppression test consistent with
macrotumour visible in this image (arrow) is consistent hyperadrenocorticism and a pituitary macrotumour.
with a diagnosis of feline acromegaly.

variety of PBTs and SBTs have been reported. These empty sella syndrome (372, next page). Secondary empty
cases typically have histories of severe polyuria/poly- sella syndrome is the term used to describe a secondary
dipsia and hyposthenuria resulting from antidiuretic reduction in pituitary volume due to infarction, pituitary
hormone deficiency preceding the development of surgery or irradiation, cystic pituitary lesions, compres-
neurological signs. Acute and severe alterations in sion from adjacent intrasellar neoplasms or following
consciousness accompanied by seizures in animals with chemotherapy for pituitary tumours. In these instances,
acquired CDI are the result of hypertonic dehydration presenting signs are usually attributable to a secondary
and hypernatraemia. These neurological crises are often hypoadrenocortical crisis.
precipitated by restricted access to water, which can be
iatrogenic on the part of the owner in an attempt to pal- Drop metastases
liate severe polyuria and perceived urinary incontinence. Intracranial or spinal intradural, extramedullary tumour
Pituitary apoplexy is the peracute onset of neurological foci developing at sites remote from a primary neoplasm
impairment associated with infarction or haemorrhage of are called drop metastases. The mechanism of metastasis
a pituitary tumour, and has been rarely described in dogs. is exfoliation of neoplastic cells into the subarachnoid
Associated neurological signs can be non-specific space. Choroid plexus tumours, ependymomas and
(e.g. depression and behaviour change), but can also meningiomas have been rarely associated with drop
include visual deficits and seizures. In some instances the metastases, but virtually any intracranial tumour can
initial neurological dysfunction is mild enough that metastasize in this manner if it is contiguous with the
owners do not seek veterinary attention, and animals subarachnoid space. The development of drop metas-
present as an emergency from the delayed effects of tases may also be a result of seeding of the subarachnoid
partial or complete hypopituitarism and secondary space during surgical removal of intracranial tumours.
468 SPECIFIC EMERGENCIES

a  372 Transverse FLAIR (a), T2-weighted (b) and

sagittal T1-weighted (c) MR images from a dog with
previous clinical and biochemical evidence of pituitary-
dependent hyperadrenocorticism successfully managed
long term with trilostane. A CT scan of the brain
performed 8 months previously revealed a normal
pituitary gland. The dog presented for stupor, collapse,
vomiting and diarrhoea associated with a hypoadreno-
cortical crisis. The images demonstrate a fluid-filled
region occupying the central portion of the pituitary
(arrows). The presumptive diagnosis was secondary
empty sella syndrome secondary to infarction of the
pituitary gland.

b  373 (a) Sagittal T2-weighted MR image from the

lumbar spine of a 5-year-old Golden Retriever with
flaccid paraparesis and central vestibular signs. Multifocal,
heterogeneously iso- (yellow arrow) to hypointense
(red arrows) appearing, intradural-extramedullary drop
metastases from an intracranial choroid plexus carcinoma
are present in the L3/L4 and L5/L6 regions. (b) Gross
necropsy specimen obtained at the level of the cerebellum
from the same dog. The friable pink mass (arrows) at the
right cerebellopontomedullary angle is a choroid plexus
carcinoma.

L3 L4 L5 L6

c
b
 INTRACRANIAL NEOPLASIA AND S E C O N D A RY P AT H O L O G I C A L E F F E C T S 469

a b

 374 (a) Parasagittal, post-contrast, T1-weighted MR image from a dog presented for epistaxis, stertorous respiration
and seizures. A uniformly contrast enhancing mass lesion (arrow) is noted in the nasal cavity and fronto-olfactory
regions of the cerebrum. (b) Rhinoscopic photograph of the nasal portion of the mass; the histopathological diagnosis
was a poorly differentiated nasal carcinoma.

Clinical signs associated with drop metastases are reflec- ferential diagnosis in any dog or cat ≥5 years of age with
tive of the location(s) of the metastases, and may result in an onset of seizures. Historical evidence of seizure activ-
a multifocal CNS neurolocalization (373). Affected ity or behavioural change may be the only manifestation
animals have also been reported with acute, severe spinal of an underlying brain tumour, as rostral prosencephalic
cord dysfunction attributed to drop metastases whose neoplasms can often be associated with normal interictal
intracranial tumours have been clinically occult. neurological examinations. Central vestibular signs are
common in animals with caudotentorial intracranial
CLINICAL PRESENTATION tumours.
Primary complaints in cases presented as an emer-
If the neoplasm and any of its associated pathophysio- gency in association with intracranial neoplasms are typ-
logical effects are confined to a focal region of the brain, ically associated with acute and profound alterations in
the clinical signs should localize to that area during the consciousness, status epilepticus or cluster seizures, head
neurological examination. Although the majority of and body postural abnormalities or progressive gait and
PBTs occur as solitary intracranial masses, the clinical balance disturbances. When interpreted in conjunction
presentation is often consistent with a multifocal intra- with a complete neurological examination, head and
cranial disease process as a result of tumour-associated body postural abnormalities and gait disturbances may
pathophysiological alterations, especially in animals with provide additional neurolocalizing information, but in
uncompensated intracranial hypertension. Locally inva- many instances they are reflective of progressive, second-
sive SBTs may also cause neurological multifocal signs ary pathophysiological sequelae such as brain herniation.
secondary to bacterial meningoencephalitis, resulting Evaluation of neurological dysfunction and therapeutic
from a breach of the integrity of the calvarium, especial- progress are achieved through serial performance of the
ly seen with tumours arising from the oral and nasal MGCS in stuporous or comatose animals in which
cavities (374), or bullae. routine components of the neurological examination
Seizures and behavioural changes are very commonly cannot be interpreted. The components and interpreta-
reported clinical abnormalities with prosencephalic tion of the MGCS are discussed elsewhere in this book
neoplasms. A brain tumour should be considered as a dif- (see Chapter 20).
470 SPECIFIC EMERGENCIES

Performance of a complete and systematic physical tamponade, or other problems related to the presence of
examination, including a fundoscopic evaluation, is also a tumour in extraneural organs. Cases with pituitary
indicated to identify deleterious systemic consequences apoplexy may present with non-specific signs of lethargy,
of intracranial hypertension, extraneural sources of gastrointestinal distress or collapse secondary to a hypo-
primary tumours in dogs with an SBT, or other signifi- adrenocortical crisis.
cant concurrent diseases. Intracranial hypertension may In the absence of an identifiable cerebral ischaemic
result in visible papilloedema. Massive, acute rises in response, clinical detection of the terminal effects of
ICP have been associated with the development of the intracranial hypertension, such as brain herniation, can
cerebral ischaemic response. The cerebral ischaemic be difficult. In animals with altered levels of conscious-
response may be a premonitory sign of impending brain ness, the detection of depressed CN functions, or
herniation and death, and its identification warrants changes in body posture (see Chapter 20), provides the
immediate therapeutic intervention. In response to a most sensitive indication of impending or current brain
progressive and near terminal decrease in cerebral perfu- herniation. However, CN dysfunction is not often
sion as a result of intracranial hypertension, the brain present in the presence of brain herniation. A recent
triggers a massive sympathoadrenal-mediated release of study found that only 1/28 dogs with isolated caudal
catecholamines in a final attempt at preserving CPP. This transtentorial herniation seen on MRI had associated
response has evolved to increase the mean arterial BP and CN dysfunction. Forty percent of dogs with both caudal
promote blood flow to the ischaemic brain. However, the transtentorial and foramen magnum herniation had CN
catecholamine surge of the cerebral ischaemic response dysfunction on evaluation. A diminished or absent
can cause several deleterious pathophysiological conse- oculovestibular reflex, the development of unilateral or
quences, including: bilateral mydriasis and loss of the PLRs are suggestive of
• Severe systemic arterial hypertension that can transtentorial brain herniation. Nystagmus, head tilt, gag
result in end-organ damage (retinal detachments/ reflex deficits and tongue weakness are suggestive of a
haemorrhage) and reflexive bradycardia that occurs foramen magnum herniation.
following the detection of systemic hypertension Although numerous pathological respiratory alter-
induced by vascular baroreceptors (the Cushing ations (e.g. Cheyne–Stokes respiration, ataxic respira-
reflex). tions, central mesencephalic hyperventilation) have been
• Non-cardiogenic pulmonary oedema. described in association with injuries to brainstem venti-
• Brain–heart syndrome. Clinically, this will present latory centres as a result of brain herniations, their clini-
as a variety of cardiac arrhythmias, resulting from cal characterization can be difficult and they should not
myocardial ischaemia, that can have negative be relied on for localization of injury or considered
cardiovascular consequences. indicative of brain herniation.

In addition to neurological dysfunction, animals with an DIFFERENTIAL DIAGNOSIS

SBT may present for respiratory distress referable to the
upper respiratory system in the case of neuroinvasive Head trauma, cerebrovascular accident, infectious or
primary intranasal neoplasms (374), the lower respira- non-infectious meningoencephalitis/granuloma, toxic or
tory system in the presence of pulmonary metastases, metabolic encephalopathy.
cardiovascular collapse from haemoabdomen or cardiac
 INTRACRANIAL NEOPLASIA AND S E C O N D A RY P AT H O L O G I C A L E F F E C T S 471

Table 91 Neurological features of common veterinary intracranial neoplasms

NEOPLASM TYPE ANATOMICAL CT FEATURES MRI FEATURES PATTERN OF COMMENTS

FEATURES CONTRAST
ENHANCEMENT

Gliomas: Solitary, intra-axial Hypo- to hyper- T1-weighted: hypo- to Variable and Oligodendroglioma
oligodendroglioma, mass; well to poorly attenuating mass isointense; often hetero- has predilection for
astrocytoma, marginated; ovoid (366) T2-weighted: geneous; ‘ring- frontal lobes, more
mixed glioma to amorphous; isointense to hyper- enhancing’ (366) uniform shape and
infiltrates intense; FLAIR: contrast or ring
parenchyma hyperintense (363) enhancing

Meningiomas Solitary, extra-axial Iso- to T1-weighted: Usually marked, Occasionally

mass; broad based; hyperattenuating isointense or uniformly contrast multifocal masses,
well circumscribed; mass; can hypointense/cystic; enhancing especially in cats
dural tail sign; be cystic/ T2-weighted: (360, 381a); (375)
calvarial hyper- hypoattenuating isointense to hyper- occasionally ring
ostosis; compresses intense; FLAIR: enhancing
parenchyma hyperintense
(375, 381)

Choroid plexus Intraventricular or Hyperattenuating T1-weighted: hypo-, Moderate to Occasionally

tumours cerebelloponto- mass (364) iso- or hyperintense; marked, uniform multifocal masses
medullary angle, T2-weighted: iso- to to heterogeneous from drop
extra-axial mass; hyperintense enhancement metastases with
secondary, obstruc- (362) carcinomas (373)
tive hydrocephalus;
spherical or lobular
appearance

Pituitary neoplasms Pituitary fossa/sella Enlarged pituitary T1-weighted: Normal pituitary Irregular shape or
region, extra-axial gland (370) isointense; enhances; benign heterogeneous
mass; may displace T2-weighted: tumours have enhancement may
suprasellar isointense to uniform indicate carcinoma;
structures mixed iso- to hyper- enhancement dynamic pituitary
intense (369) imaging can
enhance detection
of microtumours

DIAGNOSIS Advanced neuroimaging (CT or MRI) of the brain is

the necessary first step in the antemortem diagnosis of
Definitive diagnosis of intracranial neoplasms is only intracranial neoplasia. Although diagnostic confirmation
possible following biopsy of representative neoplastic of a tumour can only be achieved after histopathological
tissue. However, contemporary, presumptive ante- examination (tumour biopsy), specific neuroimaging fea-
mortem diagnosis of intracranial neoplasia has been tures have been reported to correlate well with certain
revolutionized by the superior anatomical detail and tumour types (Table 91). The majority of PBTs are
spatial resolution afforded by MRI techniques. associated with imaging evidence of a solitary mass lesion
 472 SPECIFIC EMERGENCIES

within the brain, although both meningiomas (375) and

choroid plexus tumours (362) may be multifocal. The
diagnostic imaging characteristics of SBTs are more het-
erogeneous, and depend on their tissue of origin as well
as on the manner in which they involve the brain (i.e.
local extension [374a] or distant haematogenous
metastasis). Haematogenous brain metastases present as
multifocal ovoid to spherical lesions in the cerebral
watershed zone (i.e. the anatomical border between the
grey and white matter [376]). Advanced neuroimaging
may also offer additional information regarding the types
of secondary tumour-associated pathological effects con-
tributing to the clinical deterioration of the patient, such
 375 Transverse post-contrast T1-weighted image as brain oedema, obstructive hydrocephalus, haemor-
from a dog with multifocal intracranial meningiomas in rhage, infarction or brain herniation, that are helpful to
falcine and parasellar locations. A dural tail sign is evident guide therapeutic decision making.
in the parasellar location (arrow).
Computed tomography
Although less ideal for visualization of the neural paren-
chyma than MRI, newer-generation CT scanners are
capable of imaging the calvarium in seconds, thus offer-
ing the advantage of superior image-acquisition speed
and obviating the requirement for general anaesthesia in
patients who are in a critical clinical condition. The use
of CT imaging is common for the planning of radio-
therapeutic treatments in animals with intracranial
neoplasms. The CT features of common intracranial
neoplasms are provided in Table 91.

 376 Transverse CT scan revealing multiple, variably

hyperattenuating nodular lesions (arrows) throughout
both cerebral hemispheres from a dog with metastatic
splenic haemangiosarcoma.

 377 CSF cytology demonstrating a homogeneous

population of round cells compatible with lymphoma.
 INTRACRANIAL NEOPLASIA AND S E C O N D A RY P AT H O L O G I C A L E F F E C T S 473

Magnetic resonance imaging procedures can be safely performed using open free-
MRI provides excellent detail with respect to the size, hand surgical techniques, with minimally invasive stereo-
margination, tissue properties and neuroanatomical tactic CT guidance or with ultrasound assistance.
location of the tumour, as well as identification and dif- Definitive classification and grading of PBTs can be dif-
ferentiation of any concurrent secondary pathophysio- ficult in cases where the tumour is poorly differentiated.
logical effects caused by the tumour. MRI is the preferred
technique for the non-invasive antemortem diagnosis of Systemic screening for extraneural disease
intracranial neoplasms, as well as for surgical treatment Intracranial neoplasms often affect middle-aged to
planning. The MRI features of common intracranial geriatric animals, so routine haematology, serum bio-
neoplasms are provided in Table 91. chemical profiles and urinalysis are helpful for the
identification of significant concurrent systemic disease
Cerebrospinal fluid collection or secondary pathophysiological effects of the under-
In animals with intracranial neoplasia, analysis of CSF lying brain tumour. Thoracic radiography, echocardio-
commonly reveals non-specific abnormalities, particu- graphy and abdominal imaging (ultrasonography) are
larly an elevated TP concentration. Exfoliation of neo- all indicated in animals with clinical complaints referable
plastic cells into CSF is uncommon and is typically to organs in those body cavities, but should be considered
associated with CNS lymphomas and choroid plexus in all patients, especially prior to performance of thera-
carcinomas (377). Considering the overall low specificity peutic cytoreductive surgery or brain irradiation. Retro-
of CSF analysis for the diagnosis of intracranial spective studies have shown that concurrent, unrelated
neoplasia and the potential risks (rapid decrease in ICP neoplasms are commonly identified in geriatric dogs
resulting in brain herniation), CSF collection is best with PBTs, and extraneural tumour foci are frequently
performed after advanced neuroimaging procedures. present in the lung, heart and kidneys of dogs with SBTs.
This approach allows the clinician to best assess the Intracranial meningiomas have also been occasionally
comparative risks and benefits of the procedure in each reported to metastasize to the lung.
individual patient.
Electrophysiology
Cytological and histopathological examination Electroencephalography and BAER are electrophysio-
of brain tumour tissue logical techniques that have been used in animals with
A definitive diagnosis of intracranial neoplasia may only intracranial neoplasms. The information that they
be obtained via microscopic evaluation of tumour tissue. provide is complementary to the history, clinical, neuro-
Histopathological examination of tissue samples is the logical and neuroimaging examinations. Although these
most accurate and sensitive method, although intra- techniques are sensitive for the detection and occasional-
operative cytological preparations are also useful. Brain ly for the neurolocalization of pathological processes
tumour biopsy samples are most often procured during within the brain, the identification of any abnormality is
therapeutic craniotomy procedures, but brain biopsy non-specific for the underlying aetiology.
 474 SPECIFIC EMERGENCIES

 378 Emergency treatment Vital parameter assessment

algorithm for intracranial neoplasia. Airway, Breathing, Circulation

Intubate/ventilate Hypercapnea
Normocapnia O2 supplementation (PaCO2 >50 mm Hg)
Normoxaemia Low-volume IV resuscitation Hypoxaemia
Normovolaemia (7.5% hypertonic saline or colloid (PaO2 <80 mm Hg)
[hetastarch, dextran, pentastarch]) Hypovolaemia

Symptomatic treatment of emergent

neurological complications

Deterioration in MGCS score despite

SEIZURE correction/normalization
DISORDER of vital parameters;
(presumed uncompensated
intracranial hypertension)

20% Mannitol IV CRI

(0.5–2.0 g/kg over 10–20 minutes)
Diazepam IV bolus Furosemide
(0.5–2 mg/kg); see chapter 23 for (0.5–1.0 mg/kg IV bolus)
persistent seizure treatments
Temporary hyperventilation
(target PaCO2 of 30 mmHg)

Advanced neuroimaging of the MGCS

SEIZURES STATIC OR
brain (CT or MRI) consistent with
STOPPED DECREASING
intracranial neoplasm

Imaging evidence of elevated ICP

• Mass effect or brain herniation
• Obstructive hydrocephalus (OH)
Dexamethasone
Neoplasm amenable to surgery • Peritumoural brain oedema (0.25–0.5 mg/kg IV)

Non-operable mass
Therapeutic intent craniotomy +
tumour biopsy • Brain irradiation
(definitive or palliative)
• Palliative decompressive craniectomy
• Palliative CSF diversion if OH present
+/– diagnostic mass biopsy
AND/OR • Palliative, symptomatic
medical therapy; anti-inflammatory
+/– Postoperative radiotherapy corticosteroids + anticonvulsants
if indicated
 INTRACRANIAL NEOPLASIA AND S E C O N D A RY P AT H O L O G I C A L E F F E C T S 475

MANAGEMENT Brain oedema

Patients with evidence of mass effect (midline shift,
Assessment and stabilization of systemic vital parameters attenuation of ventricles, brain herniation, oedema) can
are the first priorities. A patent airway and normal venti- benefit from pharmacological therapies. Osmotic and
lation, normovolaemia,and normotension should be the loop diuretics are the mainstays of therapy for cerebral
initial treatment goals to optimize cerebral oxygenation oedema in the acute period. Vasogenic oedema is the
and CPP. Secondary goals include intervening for primary form of oedema treatable with diuretics.
emergent neurological complications, which include
tumour-related seizure disorders, clinical neurological Mannitol
deterioration secondary to uncompensated intracranial Mannitol may be given intravenously (0.5–2.0 g/kg) as
hypertension and paraneoplastic metabolic derange- a slow bolus infusion, every 4–6 hours as needed. It is an
ments. For animals with paraneoplastic metabolic osmotic diuretic that decreases ICP by drawing water
derangements, such as those seen with pituitary apoplexy out of the interstitial space; it is also a positive rheologic
and subsequent secondary hypoadrenocortical crisis or agent, decreasing the viscosity of blood and improving
hypertonic dehydration with CDI, parenteral fluid microvascular perfusion and CPP. It is recommended
therapy and medications should be administered as indi- that mannitol is given as a slow bolus over 10–20 minutes,
cated (see Chapter 31). Once the patient is systemically as a rapid bolus may increase intravascular volume before
stabilized, advanced neuroimaging studies are performed renal clearance, resulting in transiently but markedly
to prioritize the differential diagnoses and identify the increased ICP. Mannitol crystallizes at room temperature
appropriate ancillary diagnostic and therapeutic plans. and should be kept warm prior to administration through
A treatment algorithm is provided in 378. a filter to prevent injection of crystals.

Treatment of secondary pathophysiological Furosemide

alterations Furosemide (0.5–1.0 mg/kg IV) is given in conjunction
Seizures with mannitol, typically during the last 5 minutes of the
The first-choice anticonvulsant in emergency situations mannitol CRI. Furosemide is a loop diuretic that does
is diazepam (0.5–2.0 mg/kg IV). If prompt intravenous not require an intact blood–brain barrier to be effective.
access cannot be established, 1–2 mg/kg diazepam can Furosemide therapy is synergistic with mannitol in
be given per rectum. CRI of diazepam or propofol and patients with elevated ICP in that it decreases CSF pro-
intravenous loading doses of barbiturates may be consid- duction, prolongs the osmotic effect of mannitol and can
ered for recurrent seizures or SE. (See Chapter 23 for mitigate the transient rebound increment in ICP that
additional specific treatment recommendations regard- may occur following mannitol administration.
ing recurrent seizures or SE.) Patients with secondary
epilepsy due to intracranial neoplasm should be started Corticosteroids
on oral maintenance anticonvulsant drugs. If undesirable Corticosteroids (dexamethasone, methylprednisolone,
alterations in the patient’s behaviour or interactions with prednisone) are effective at reducing peritumoural brain
the owner are present as a result of the tumour, the oedema and can be used in the acute emergency
authors recommend the use of anticonvulsants that have situation and continued chronically as a palliative treat-
less potential to further exacerbate sedation, such as ment. The initially prescribed dose should approximate
levetiracetam (20 mg/kg PO or IV q8h) or felbamate an anti-inflammatory dose (equivalent to 0.5 mg/kg of
(15 mg/kg PO q8h) in lieu of more traditional anti- prednisone q12h), and can be titrated as necessary based
convulsants (i.e. phenobarbital or bromide). on the individual patient’s response. Individual patient
responses to corticosteroids can be highly variable. In
some instances, vasogenic oedema may be completely
refractory to steroid therapy. The lowest possible dose of
steroid that mitigates clinical signs should be used for
chronic outpatient therapy.
476 SPECIFIC EMERGENCIES

Uncompensated intracranial hypertension Palliative, decompressive craniectomy

Hyperventilation Removal of the skull with subsequent durotomy is a very
Many of these patients have loss of the normal pressure effective procedure for reducing ICP. Decompressive
and chemical vascular autoregulatory mechanisms in craniectomies are usually performed following intracra-
addition to some degree of respiratory depression due to nial imaging to optimize the surgical approach, and can
brainstem compression, resulting in hypercapnea and be combined with therapeutic intent cytoreductive
hypoxaemia. Hypercapnea stimulates cerebral vasodila- surgery or diagnostic brain biopsy procedures. However,
tion, which contributes to the increase in ICP by increas- palliative craniectomy can also be performed with the
ing cerebral blood volume. Transient hyperventilation to sole intent of lowering life-threatening intracranial
maintain a target PaCO2 of 30 mmHg (P’ETCO2 ~ 25 hypertension, particularly in cases where neoplasms are
mmHg) can be considered to maximize CPP and main- inoperable and future brain irradiation is being consid-
tain optimal cerebral blood volume in patients that have ered. In the absence of diagnostic information provided
not responded to diuretic administration. However, by advanced neuroimaging, the approach used for
since chemical autoregulatory mechanisms are often dis- decompressive craniectomy is dictated by lateralizing
rupted, the theoretical vasoconstrictive benefits of hyper- deficits identified during the neurological examination.
ventilation are probably non-uniform within the brain In the absence of localizing clinical signs, bilateral ros-
and so are associated with some degree of risk. Further- trotentorial craniectomy can be considered (379).
more, excessive or chronic hyperventilation can be
accompanied by a reduction in global CBF, which may CSF diversion (ventriculoperitoneal shunting)
drop below ischaemic thresholds. Therefore, it is not a Diversion of CSF can be an effective procedure for
recommended therapy unless the PaCO2 can be closely reducing ICP. This technique can be performed via ven-
monitored with capnography or arterial blood gas analy- triculostomy or ventriculoperitoneal shunting. Ventricu-
sis (see Chapter 20). lostomy involves insertion of a catheter into the
ventricular system of the brain for the purposes of with-
drawing CSF and/or implantation of an ICP monitoring
 379 Schematic representation of the intended calvarial device. Ventriculostomy is often performed in humans
defect (hatched area) when performing a bilateral rostro- with a minimally invasive burr-hole craniectomy tech-
tentorial craniectomy. nique, as anatomical landmarks for catheter placement
are well described. In veterinary patients, however,
patient size and skull conformational differences, as well
as pathological shifts in anatomical structures due to
intracranial mass effect, often hamper performance of
minimally invasive ventriculostomy. Ventriculoperi-
toneal shunting is occasionally indicated as an adjunctive
therapeutic procedure in animals with obstructive hydro-
cephalus, particularly in cases where the neoplasm
causing the obstruction is inoperable, and the patient
requires stabilization in preparation for other primary
therapy (radiation). Diversion of CSF from the ventricu-
lar system to the peritoneal cavity is efficacious at
improving clinical signs associated with intracranial
hypertension. Shunt-related complications (overshunt-
ing/slit-ventricle syndrome, obstruction, dislodgement)
can occur and generally require surgical shunt revision.
 INTRACRANIAL NEOPLASIA AND S E C O N D A RY P AT H O L O G I C A L E F F E C T S 477

Specific treatment of intracranial neoplasia

Cytoreductive craniotomy/craniectomy
The surgical approach employed in individual cases is
primarily dictated by the neuroanatomical location of the
neoplasm, which is identified with advanced neuroimag-
ing. In general, superficially located, rostrotentorial and
extra-axial tumours are the most amenable to surgical
removal. Intra-axial and caudotentorial neoplasms are
inherently more technically demanding, but can be sur-
gically treated in some instances, especially when involv-
ing the superficial aspects of the cerebellum. Although
somewhat intuitive, in the case of low-grade intracranial
neoplasms (e.g. many meningiomas), recent literature
suggests that the success of surgery appears to be related  380 Patient being positioned in the CT scanner for
to the completeness of the surgical excision. Devices that GammaKnife ™ stereotactic radiosurgical treatment
assist with gross total tumour removal by improving planning using a custom-modified Leksell headframe.
intraoperative visualization (e.g. intracranial endoscopy)
or techniques that facilitate removal of microscopic
disease at the tumour margin (e.g. ultrasonic surgical
aspirators or cortical resection) have been associated with
prolonged survival (2–3 years) in dogs with meningiomas Cytotoxic chemotherapy
treated surgically. To date, there have been no objective, data-based studies
investigating or demonstrating in-vivo efficacy for any
Radiotherapy systemically administered chemotherapeutic drug for the
Multiple types of brain irradiation have been used to treat treatment of veterinary intracranial tumours. Currently,
brain tumours in dogs and cats including orthovoltage, chemotherapy should be considered an empirical adjunc-
cobalt-60, megavoltage external beam radiotherapies tive therapy for intracranial neoplasms. Therapeutic
and interstitial brachytherapies. Irradiation of intracra- obstacles that may hamper the efficacy of systemic
nial tumours has been shown to be effective at improve- chemotherapy include large tumour burdens at diagnosis
ment of tumour-associated neurological dysfunction and and problems with effective delivery across the
prolongation of survival, especially when compared blood–brain barrier. Rare case reports have shown some
with palliative medical therapy. The current standard measurable therapeutic responses of intracranial
of care is delivery of external beam radiotherapy using tumours to nitrosourea drugs such as lomustine (60–90
fractionated dose prescriptions, but hypofractionated mg/m2 PO every 3 weeks in dogs; 50–60 mg/m2 PO
therapies and single session, stereotactically-delivered every 3 weeks in cats) and carmustine (50 mg/m2 IV
radiotherapy using conventional linear accelerators or every 6 weeks in dogs) that will cross the blood–brain
dedicated stereotactic radiosurgical systems (Gam- barrier. Hydroxyurea (50 mg/kg/day PO in dogs, 10
maKnife™, [380]; CyberKnife®) are currently being mg/kg/day PO in cats) has been shown to be cytotoxic to
used and investigated at a few veterinary centres. human meningioma cell lines in vitro, and has been used
Tumour-specific treatment planning techniques and as an adjunctive treatment for canine meningiomas.
dose prescriptions can vary considerably among veteri- These compounds are therefore prescribed by some cli-
nary radiation oncologists. Palliative radiation alone can nicians to treat intracranial neoplasms. CNS lymphoma
have a significant and rapid beneficial effect on neurolog- may respond to combination chemotherapy with multi-
ical status in some cases. agent protocols that include cytosine arabinoside.
 478 SPECIFIC EMERGENCIES

Obstacles to drug delivery have been mediated in PROGNOSIS

humans with brain tumours through topical infusion of
chemotherapeutics in tumour resection cavities via The prognosis for patients with PBTs and SBTs is
implantable catheters, convection-enhanced drug deliv- dependent on numerous factors such as tumour type and
ery strategies or interstitial implantation of chemo- grade, neuroanatomical tumour location, severity of
therapeutic impregnated wafers within the brain. neurological deficits and type of treatment(s) adminis-
tered. Symptomatic medical therapies, such as pred-
nisone and anticonvulsants, have had survival times of
6–56 days reported in dogs with brain tumours, although
survivals of > 6 months are possible in some mildly affect-
ed animals with forebrain tumours treated palliatively.
Multiple studies have reported that the severity of neuro-
logical dysfunction is negatively correlated with survival
in animals treated for intracranial neoplasms. Addition-
 381 (a) Preoperative, transverse post-contrast T1- ally, animals with rostrotentorial tumours survive longer
weighted MR image from a 12-year-old cat with circling than those with neoplasms in caudal tentorial locations if
and seizures. An extra-axial, markedly enhancing mass is treated with similar techniques.
present in the right parieto-occipital lobes of the In cats with meningiomas, median survivals of
cerebrum, resulting in compression of the right lateral >2 years have been reported following successful cyto-
ventricle. Hyperostosis of the calvarium can be seen reductive surgery (381), with presumed or confirmed
(arrows). (b) Transverse, post-contrast T1-weighted tumour recurrences documented in about 20% of oper-
image taken 2 years following craniectomy. The cat was ated cats.
clinically normal with no evidence of tumour recurrence. There is also evidence in the literature that survival of
The craniectomy defect in the calvarium is apparent. dogs with intracranial meningiomas is superior (median
survival, 16 months) when multimodal treatment, con-
a sisting of cytoreductive surgery and postoperative exter-
nal beam radiotherapy, is administered when compared
with surgical treatment alone (median survival,
7 months). Irradiation of intracranial masses has been
shown to be safe and associated with tolerable adverse
effects, and efficacious at improving clinical signs of brain
dysfunction and prolonging survival in animals in which
surgical resection was not possible or performed.
However, extrapolation of tumour-specific, evidence-
based prognostic information from these radiotherapeu-
b tic studies is hampered by the fact that histopathological
confirmation of the mass as an intracranial neoplasm was
not a universal inclusion criterion.
Transsphenoidal hypophysectomy and pituitary irra-
diation have also been shown to be safe and efficacious
treatments for functional pituitary adenomas in dogs
and cats. Studies investigating the efficacy of various
treatments and outcomes in dogs and cats with histo-
logically confirmed PBTs of neuroectodermal origin or
metastatic SBTs are sufficiently rare to preclude provi-
sion of any evidence-based prognostic information about
these types of tumours.
 SPECIFIC EMERGENCIES Chapter 27

METABOLIC ENCEPHALOPATHIES
479

Kate Chandler
& Robert Goggs

INTRODUCTION Common clinical signs of metabolic encephalopathies

include:
Metabolic encephalopathy is a clinical syndrome result- • Predominant forebrain signs (and/or brainstem):
ing from disorders of metabolism. It is characterized by • Seizures.
altered mental state and neurological deficits due to • Behaviour change: aggression, anxiety,
disruption of brain function and structure secondary dementia, mania.
to energy deprivation, derangements of electrolytes, • Obtundation/stupor/coma.
acid–base balance or accumulation of endogenous toxins. • Blindness with normal PLRs (amaurosis).
Metabolic encephalopathy is not a single entity, but a • Symmetrical neurological deficits.
heterogeneous and frequently multifactorial condition.
It is commonly encountered in the critical care setting The key to successful treatment in these patients is
and arises secondary to conditions such as liver dys- (1) rapid identification of underlying causes; (2) rapid
function, endocrinopathy or renal failure. Endogenous treatment of metabolic abnormalities; (3) effective mon-
metabolic diseases due to inborn errors of CNS meta- itoring to rapidly identify potentially life-threatening
bolism also occur occasionally. abnormalities. Effective symptomatic treatment is fre-
Metabolic encephalopathies typically cause diffuse, quently the difference between success and failure.
symmetrical forebrain signs. Onset may be acute or
chronic and signs may wax and wane. The earliest and ELECTROLYTE DISTURBANCES
most consistent signs are depression of consciousness
and generalized seizures. Other neurological signs vary Sodium disorders
with the type and severity of the metabolic disturbance. Most disorders of sodium concentration result from dis-
Common historic signs associated with metabolic orders of water balance. Both hyper- and hyponatraemia
encephalopathy include: can cause neurological dysfunction via alterations in neu-
• Waxing and waning neurological signs/behaviour ronal cell volume and function. Slow, gradual alterations
change. in sodium concentration are well tolerated until concen-
• Temporal relationship between feeding and neuro- trations become extreme. Small absolute changes that
logical signs. occur rapidly may cause more profound neurological
• Seizure activity. dysfunction than larger more gradual alterations.
• Altered mentation.
• Blindness. Hypernatraemia
• Gastrointestinal signs. Overview
• Increased or decreased appetite. Blood sodium levels reflect the ratio of sodium to water
• Pica. in the extracellular fluid and account for most of the
• Dermatological signs (e.g. alopecia). osmotically active particles in serum. Hypernatraemia is
• Tremor. indicative of an increase in total body sodium relative to
total body water. It occurs secondary to net solute gain,
sodium-free water loss or hypotonic fluid loss.
480 SPECIFIC EMERGENCIES

Aetiology/pathophysiology Clinical presentation

Causes of hypernatraemia include: The cells of the CNS are very intolerant of the volume
• Net solute gain: excess salt intake associated changes described above and this leads to clinical signs
with salt poisoning, administration of intravenous including obtundation, head pressing, seizures, ataxia,
hypertonic saline or sodium bicarbonate. Water tremors, blindness and coma. In addition, signs of
loss and salt gain can also occur with hyper- volume depletion are often present in hypernatraemia
aldosteronism and hyperadrenocorticism. secondary to hypotonic fluid losses, while signs of hyper-
• Sodium-free water loss: diabetes insipidus, primary volaemia (e.g. pulmonary oedema) may be present in
hypodypsia, water unavailable or patient unable to cases of net solute gain. Clinical signs typically develop if
drink, heat stroke. the sodium concentration alters at a rate of >1 mmol/l/
• Hypotonic fluid loss: gastrointestinal loss (vomiting, hour (>1 mEq/l/hour) or if the absolute sodium concen-
diarrhoea, small intestinal obstruction), third space tration exceeds 180 mmol/l (180 mEq/l). If sodium con-
loss (pancreatitis, peritonitis), osmotic diuresis centrations alter slowly, the brain adapts by producing
(mannitol infusion, hyperglycaemia), chemical idiogenic osmoles such as taurine, sorbitol and inositol.
diuresis (furosemide), non-oliguric renal failure, These molecules increase intracellular osmolality,
chronic renal failure, postobstructive diuresis. buffering cell volume against the increased extracellular
sodium concentration. Rapid correction of chronic
Hypernatraemia can be further divided into hypo- hypernatraemia (>0.5–1 mmol/l/hour [>0.5–1 mEq/l/
volaemic (hypotonic loss), normovolaemic (sodium-free hour]) can lead to osmotic gradient reversal, inducing
water loss) and hypervolaemic (net solute gain) forms. water to move into cells and causing cell swelling,
Hypernatraemia due to a gain of sodium results in cerebral oedema and clinical signs of intracranial
increased extracellular fluid (ECF) (hypervolaemic hypertension.
hypernatraemia). Pure water loss results in relative
preservation of ECF due to equilibration with ICF Management
(normovolaemic hypernatraemia), while hypotonic fluid Treatment of hypernatraemia
loss results in decreased ECF volume (hypovolaemic The underlying cause and sodium abnormality should be
hypernatraemia). With the latter, affected patients are identified and treated. There is no standard method of
therefore more likely to show signs of volume depletion correction to suit all situations, therefore treatment
(tachycardia, increased capillary refill time, weak pulse). should be individualized, aiming to replace the water
Evaluation of the volume status of the patient is therefore deficit and treat the underlying cause. Correction of
important in the process of identifying the underlying sodium concentration should occur at the same rate at
cause of hypernatraemia and the treatment approach. which it developed (i.e. rapid in cases of salt intoxication;
The increase in serum sodium creates a hypertonic slowly in cases of fluid loss). The rate of blood sodium
state in the ECF. Hypernatraemia leads to cell shrinkage change should not exceed 0.5–1 mmol/l/hour (0.5–1
secondary to osmotic water movement into the hyper- mEq/l/hour). If serum sodium concentrations are
osmolar interstitium. The decrease in brain volume lowered too quickly, cerebral oedema may result, with a
caused by cellular dehydration can cause tearing of small clinical deterioration in consciousness. Blood sodium
intracranial blood vessels and haemorrhage (subarach- concentration should be monitored every 4–6 hours
noid, subdural and/or intraparenchymal). during correction.
 M E TA B O L I C E N C E P H A L O PAT H I E S 481

Treating hypernatraemia secondary to fluid loss Treating hypernatraemia secondary to sodium gain
A hypovolaemic, hypernatraemic patient should be With hypernatraemia, patients are typically hyper-
volume resuscitated with a fluid containing a sodium volaemic, may have elevated systemic BP and are at risk
concentration equal to that of the patient. This can be of pulmonary oedema. Furosemide (1–2 mg/kg IV)
created by adding aliquots of a concentrated NaCl will facilitate loss of both sodium and excess fluid. Five
solution such as 7.2% saline (1.23 mmol [mEq] NaCl percent dextrose in water can be used to correct the
per ml) to an isotonic replacement crystalloid solution sodium concentration. Should the sodium concentration
such as 0.9% saline or Hartmann’s solution. For example, drop more rapidly than >0.5 mmol/l/hour (>0.5 mEq/
a patient with a plasma sodium concentration of 181 l/hour), this may need to be altered to 0.45% saline or
mmol/l (181 mEq/l) will need a solution that contains Hartmann’s solution. Frequent monitoring of blood
181 mmol/l (181 mEq/l) NaCl (equivalent to a 1.06% sodium concentrations will guide the use of furosemide
solution). This can be prepared by increasing the sodium and fluid therapy.
concentration of 0.9% saline (154 mmol/l [154 mEq/l])
by adding 27 mmol (27 mEq) of NaCl per litre. This is Hyponatraemia
achieved by adding 22 ml of 7.2% saline to 1,000 ml of Overview
0.9% saline. (Note: 1,000 ml fluid bags typically contain Hyponatraemia occurs primarily due to loss of salt,
an excess of 20 ml, which will need to be removed prior to gain of water, gain of hypotonic fluid or addition of hyper-
addition of the 7.2% saline.) The sodium concentration tonic solution without sodium (glucose or mannitol).
of the resultant solution should be checked using an Apart from hyperglycaemia and mannitol administra-
electrolyte analyser prior to bolus administration to the tion, which may lead to hyponatraemia and hyperosmo-
patient. lality, most hyponatraemic patients are hypo-osmolar.
Following volume resuscitation, the hypernatraemic Hyponatraemia with low plasma osmolality may be
patient’s free water deficit should be replaced slowly to accompanied by normal plasma volume (syndrome of
reduce sodium concentration at a rate of 0.5–1.0 mmol/ inappropriate antidiuretic hormone secretion [SIADH],
l/hour (0.5–1.0 mEq/l/hour). If a recent body weight is psychogenic polydypsia, hypotonic fluid infusion),
available, the following equation can be used to approxi- decreased plasma volume (Addison’s disease, gastro-
mate the free water deficit: intestinal and third space loss) or increased plasma
volume (congestive heart failure, severe liver disease,
Free water deficit (l) = 0.6 × body weight (kg) × nephrotic syndrome, advanced renal failure). As for
([measured Na+/normal Na+] – 1) hypernatraemia, determination of the volume status of
the patient is essential in the process of identifying the
The predicted change in blood sodium concentration underlying cause of the hyponatraemia and the treat-
from administration of one litre of fluid can be calculated ment approach.
using the following equation:
Aetiology/pathophysiology
Change in Na+ Hyponatraemia leads to cell swelling and cerebral
infusate Na+ – blood Na+ oedema secondary to osmotic water movement into cells.
=
(body weight (kg) × 0.6) + 1 A gradual change in sodium concentration allows cells to
adapt by expelling intracellular solutes to decrease intra-
Free water replacement can be achieved with a range of cellular osmolality and restore normal cell volume. Rapid
fluids. If significant ongoing losses such as diarrhoea are correction (>0.5–1.0 mmol/l/hour [>0.5–1.0 mEq/
occurring, the use of 0.9% saline or Hartmann’s solution l/hour]) of hyponatraemia can cause severe cell shrinkage
will be safer. Hypotonic fluids, such as 0.45% saline or as water moves into the increasing osmolality of the
5% dextrose in water, can be used if ongoing losses extracellular environment. This shrinkage can separate
are minimal. Hypotonic fluids will reduce the sodium the neurons from their myelin covering, leading to
concentration more rapidly than an equal volume of myelinolysis. In humans this occurs predominantly in
isotonic fluid (see Chapter 31 for further details). the pons (central pontine myelinolysis; also known as
482 SPECIFIC EMERGENCIES

a b c

 382 Transverse (a, b) and dorsal (c) T2-weighted MR images of a Collie-cross dog with osmotic demyelination
syndrome following rapid correction of hyponatraemia. Note the bilaterally symmetrical hyperintensities affecting the
thalamic and mesencephalic grey matter.

osmotic demyelination syndrome), while in dogs it which may take several days to become evident.
occurs principally in the thalamus (382). Sodium concentrations should be monitored every 4–6
hours during correction. The hypovolaemia should be
Clinical presentation corrected using 0.9% saline. The rate of sodium correc-
Mild to moderate hyponatraemia is typically occult. tion should not be >0.5 mmol/l/hour (>0.5 mEq/l/hour).
Severe hyponatraemia, where sodium concentrations are Hypertonic saline is rarely required for the treatment of
less than 120 mmol/l (120 mEq/l) or rapid decreases in hyponatraemia. An exception to these recommendations
sodium concentration (>1 mmol/l/hour [>1 mEq/ are patients with SIADH, who may require a combina-
l/hour]) occur, are associated with obtundation, head tion of water restriction and a slow continuous infusion
pressing, seizures and coma. In addition, hyponatraemic of hypertonic (3%) saline to normalize their sodium
patients may have signs of dehydration and hypo- concentration. Specific criteria should be used to diag-
volaemia (e.g. rapid and weak pulse, hypotension, cold nose this uncommon condition, including measuring
extremities, prolonged capillary refill time), while hyper- plasma sodium and plasma osmolality, measurement of
volaemic patients may be presented with ascites, pul- urine osmolality or urine sodium, assessment of renal,
monary oedema, peripheral oedema or jugular adrenal and thyroid function, and evaluation for ascites
distension. or oedema. Further information on the diagnosis and
treatment of SIADH can be found in Chapter 31.
Management (see Chapter 31 for further details) Hypoperfused patients may be depressed and this
Both the underlying cause and the sodium abnormality should not be confused with the neurological signs of
should be identified and treated. Hyponatraemia almost hyponatraemia (e.g. seizures, coma). Seizures due to
always develops slowly; therefore, hyponatraemia must sodium abnormalities should be treated with diazepam
be corrected slowly to avoid life-threatening neuro- (0.5 mg/kg IV or per rectum).
logical damage (osmotic demyelination syndrome),
 M E TA B O L I C E N C E P H A L O PAT H I E S 483

Parathyroid
Hypocalcaemia gland
Overview
Ca2+
Calcium homeostasis is based on a complex interplay of
parathyroid hormone (PTH), calcitriol and calcitonin.
Ionized calcium concentrations (iCa2+) are usually tightly PTH
controlled. PTH is responsible for minute-to-minute
changes and acts to increase iCa2+. Calcitriol (1,25 di-
hydroxyvitamin D) is synthesized in the kidney under the Kidney
influence of PTH. Calcitriol is responsible for day-to- 1,25
day changes and also acts to increase iCa2+. Calcitonin (OH)2D
Ca2+
acts to reduce postprandial increases in iCa2+ (383).

Aetiology/pathophysiology Extracellular
Gut Bone
Hypocalcaemia may result from renal failure, eclampsia, fluid
Ca2+ Ca2+
pancreatitis, ethylene glycol intoxication or primary
hypoparathyroidism. Iatrogenic hypocalcaemia occurs
following thyroidectomy or parathyroidectomy, phos-  383 Calcium physiology and the roles of parathyroid
phate enema administration or citrate anticoagulant hormone (PTH) and calcitriol (1,25(OH)2D) in calcium
overdose following transfusion. Hypocalcaemia lowers homeostasis. The principal action of PTH is to raise
the threshold for neuronal and muscle depolarization as calcium levels in extracellular fluid (ECF) by increasing
a result of alterations in sodium flux and membrane renal tubular resorption of calcium, mobilizing calcium
potentials. from bone and increasing intestinal (gut) calcium
absorption. Actions on bone and kidney are mediated
Clinical presentation directly through interaction with specific receptors.
Clinical signs of hypocalcaemia include facial rubbing, Action on gut is indirectly mediated by 1,25(OH)2D,
muscle twitching, cramping, tetanic tremors, ataxia and whose synthesis in the kidney is stimulated by PTH.
seizures. Hypotension and tachyarrhythmias may also Extracellular calcium feeds back to the parathyroid gland,
occur. inhibiting further secretion of the hormone.
(Adapted from Habener JF, Rosenblatt M, Potts JT (1984)
Diagnosis Parathyroid hormone: biochemical aspects of biosynthesis,
Diagnosis is based on recognition of characteristic clini- secretion, action, and metabolism. Physiol Rev
cal signs and confirmation of ionized hypocalcaemia, 64:985–1053.)
which is typically <1.0 mmol/l (<4.0 mg/dl). A number of
point-of-care technologies are available for rapid meas-
urement of ionized calcium. Serum biochemistry profiles Management
typically report total calcium, which is a poor indicator of Hypocalcaemia should be treated only if clinical signs
ionized calcium concentrations (the biologically active are present. Calcium gluconate 10% (0.5–1.5 ml/kg
fraction). Correction formulae exist, but their use is [providing 5–15 mg/kg calcium] as a slow IV bolus over
not recommended because their inaccuracy in predict- 10–30 minutes) can be administered. A continuous
ing iCa2+ precludes safe treatment of hypocalcaemia. ECG should be monitored because of the risk of cardio-
Primary hypoparathyroidism can be diagnosed by toxicity. There is significant risk of cardiac arrest during
radioimmunoassay determination of plasma PTH con- rapid administration. The infusion should be stopped
centration. immediately if bradycardia, increased P-R interval,
484 SPECIFIC EMERGENCIES

prolonged QRS complex, shortened QT interval on Clinical presentation

ECG or vomiting occurs. Subacute therapy for hypocal- Patients with this rare endocrine emergency may present
caemia is provided with 10% calcium gluconate solution with mental dullness, stupor or coma. In dogs, typical
at a dosage of 5–10 ml/kg given slowly intravenously in clinical signs include obesity, oedema, mental dullness,
lactated Ringer’s solution or isotonic (0.9%) NaCl main- hypothermia, bradycardia, hypotension and hypoventila-
tenance infusion over a 24-hour period. Serum calcium tion. Stupor and coma are less common. CN dysfunction
concentration must be monitored every 1–3 days and (especially facial and vestibular) can also be noted.
dosage adjustments made every 1–3 days based on serum
levels to avoid iatrogenic hypercalcaemia. Long-term Diagnosis
maintenance requires oral calcium (25 mg/kg q8–12h) Identification of profoundly low serum thyroxine levels
and vitamin D supplementation. (or free thyroxine levels by equilibrium dialysis) ±
increased thyroid-stimulating hormone (endogenous
ENCEPHALOPATHIES TSH) levels assists with diagnosis. Interference from
intercurrent disease must be considered when interpret-
Endocrine encephalopathy ing thyroid function tests in sick patients. Blood gases
Patients with endocrine encephalopathy may present may reveal hypoxaemia and hypercarbia. Patients may be
with numerous clinical abnormalities such as electrolyte hypoglycaemic and have other biochemical changes
disturbances or seizures, requiring specific treatment or consistent with hypothyroidism (e.g. hypercholesterol-
symptomatic therapy, respectively. The underlying aemia, hyponatraemia). Electrocardiography may iden-
disease must be identified and specific therapy initiated. tify bradyarrhythmias, and response to treatment may
Intravenous or rectal diazepam is an appropriate choice actually aid in diagnosis. Investigation must also be
for seizures in these patients. A phenobarbital loading directed towards identifying a predisposing cause such as
protocol is an appropriate second choice, providing infection, recent drug therapy or heart failure.
hepatic function is normal (see Chapter 23).
Management
Hypothyroid myxoedema coma The respiratory status must be assessed and oxygen and
Overview ventilatory support provided if required. Warmed intra-
Myxoedema coma is an extreme life-threatening form of venous fluid therapy ± supplementary glucose should be
canine hypothyroidism. given as appropriate, together with passive external
rewarming. L-thyroxine (1–5 g/kg IV q12h) should be
Aetiology/pathophysiology given. Resolution of abnormal mentation, ambulation
Myxoedema coma pathophysiology is incompletely and systolic hypotension should be expected within
understood. Doberman Pinschers seem to be over- 30 hours. Injectable levothyroxine may not be readily
represented. Thyroid hormones indirectly regulate available, in which case oral levothyroxine may be admin-
multiple cell functions affecting catabolism, metabolism istered via an orogastric tube. A liquid preparation is
and development. They also play permissive roles in available and may be sourced from a local hospital.
multiple organ systems. The altered mental status in this Care must be taken to avoid aspiration if the patient is
condition results from direct effects of reduced thyroid obtunded or stuporous. Serum thyroxine levels should be
hormone concentrations, and indirectly from decreased monitored daily and oral levothyroxine begun once
CBF, cerebral oedema and hyponatraemia. Myxoedema serum thyroxine levels are normal and appetite has
coma is typically precipitated by an event that over- resumed. This may take several days.
whelms normal homeostasis such as infection or concur-
rent administration of thyroid hormone-altering Prognosis
medication or surgery, although in dogs no single event The prognosis is guarded and is poor if intercurrent
has been repeatedly identified. disease is also present.
 M E TA B O L I C E N C E P H A L O PAT H I E S 485

Thyrotoxicosis/thyroid storm (0.1–0.5 mg/kg IV over 1 minute) may be required for

Overview treatment of supraventricular tachyarrhythmias, but care
Hyperthyroidism or thyrotoxicosis describes the condi- must be taken not to cause hypotension due to negative
tion of excess thyroid hormone concentrations, while the inotropy. Methimazole (2.5 mg/cat and 2.5–5.0 mg/dog
term thyroid storm refers to a life-threatening multi- PO q12h) is the drug of choice for thyroxine synthesis
systemic syndrome resulting from this condition. suppression. Investigation of an underlying precipitating
process should be undertaken concurrently with initial
Aetiology/pathophysiology stabilization.
Thyroid storm syndrome consists of pyrexia combined
with CNS, cardiovascular and gastrointestinal dysfunc- Prognosis
tion. This syndrome occurs due to the combination of The prognosis is guarded in the acute stages. The
high basal thyroid hormone concentrations coupled syndrome is poorly recognized, which may increase
with a rapid increase in hormone concentrations, mortality. With appropriate management patients may
sympathetic nervous system hyperactivity and increased be stabilized sufficiently to permit more definitive treat-
cellular response to thyroid hormones. This condition ment (e.g. thyroidectomy or 131I therapy).
may be precipitated by infection, surgery, non-thyroidal
illnesses, aggressive thyroid palpation, iodine adminis- Parathyroid disease
tration or abrupt cessation of antithyroid medication. Overview
Primary hyperparathyroidism (PHPTH) results from
Clinical presentation excessive PTH secretion by neoplastic chief cells.
Hyperthyroid cats may present with restlessness, hyper- The condition is characterized by high PTH concentra-
activity, anxiety, pacing, circling and occasionally focal or tions, hypercalcaemia, hypophosphataemia and hyper-
generalized seizures. Some cats may display a paradoxical phosphaturia.
apathy characterized by dullness and depression. Neuro-
logical signs include behavioural change, agitation, Clinical presentation
seizures and coma. Clinical signs include polyuria, polydipsia, vomiting,
weakness, abdominal pain, constipation and anorexia.
Diagnosis Approximately half of canine patients with PHPTH
A total thyroxine level above the reference interval is demonstrate listlessness, depression and lethargy. This is
diagnostic if appropriate clinical signs are present, partic- likely to be due to reduced CNS excitability secondary to
ularly if the history is consistent with a predisposing the effects of hypercalcaemia on the neuronal membrane
event. Hyperthyroidism with non-thyroidal illness may potential. In 10% of dogs, PHPTH causes muscle
have thyroxine values within the normal reference range. twitching and, more rarely, seizure activity secondary to
The clinician should suspect this if a goitre is present. hypercalcaemia, cerebral thromboembolic events or
vasospasm. These events are more likely to occur in
Management feline patients with ionized calcium concentrations >1.75
Treatment is directed at the provision of supportive mmol/l (>7.0 mg/dl). In canine patients a hypercalcaemic
therapy, the reduction of thyroid hormone production, crisis is likely in patients with ionized calcium concentra-
the systemic effects of excess thyroid hormones and the tions >1.88 mmol/l (>7.5 mg/dl).
identification and treatment of precipitating factors.
Careful assessment of cardiopulmonary function is vital. Differential diagnosis
Some patients may present in congestive heart failure In dogs the differentials include: lymphoma; anal sac
and thus supportive therapies, such as oxygen therapy, apocrine gland adenocarcinoma; multiple myeloma;
and diuretic and vasodilator administration may be acute and chronic renal failure; hypoadrenocorticism;
necessary. Judicious use of antiarrhythmics may be nec- vitamin D intoxication (cholecalciferol or calcipotriene);
essary. Atenolol (0.5–2.0 mg/kg PO q24h) or esmolol granulomatous disease.
 486 SPECIFIC EMERGENCIES

 384 Popliteal lymph node aspirate of a dog with

ionized hypercalcaemia. Cytology reveals numerous large
lymphoid cells with irregular nucleolated nuclei and
minimal basophilic cytoplasm, and a single atypical mitotic
figure, consistent with a large cell lymphoma.

Idiopathic hypercalcaemia and neoplasia are the most

common differentials in cats followed by renal failure
(elevation of total calcium but usually not ionized
calcium).

Diagnosis
The investigation of suspected PHPTH must focus on
a differentiating it from other causes of hypercalcaemia.
Investigations include assays of total and ionized calcium,
lymph node cytology (384), CBC, serum biochemistry,
urinalysis, spinal (385) and abdominal imaging, splenic
cytology (385), ACTH stimulation testing and assays of
PTH and parathyroid hormone-related protein
(PTHrP). Patients with PHPTH typically have total and
b ionized hypercalcaemia and inappropriately normal or
increased PTH with normal PTHrP concentrations.
Patients with only PHPTH will demonstrate an increase
in serum cortisol concentrations following ACTH
stimulation.

Management
Aggressive therapy will be required in patients with very
high calcium levels. High Ca:Phos ratio (>5.6 SI units
[>70 US units]) are unlikely in PHPTH, but are possible
with other causes of hypercalcaemia. Treatment for
PHPTH typically involves surgical resection of the
parathyroid mass.
 385 (a) Lateral radiograph of the cervical spine and The most important therapeutic measure is to
(b) splenic aspirate of a 8-year-old Doberman Pinscher rehydrate the patient. Isotonic NaCl is the fluid of choice,
presented with multifocal spinal pain, polyuria, polydipsia as 0.9% NaCl competitively inhibits renal tubular
and lethargy. Serum biochemistry revealed elevated absorption of calcium and urinary calcium excretion is
ionized hypercalcaemia and marked elevation in serum enhanced by saline infusion. Therapy for hypercalcaemia
globulin. The radiograph reveals multiple osteolytic consists of diuresis with 0.9% saline, furosemide (2 mg/kg
skeletal lesions scattered throughout the cervical IV q4–6h), calcitonin (4–6 IU/kg SC q8–12h) or bisphos-
vertebrae. The splenic aspirate shows numerous phonates (e.g. pamidronate, 1.3–2.0 mg/kg in 0.9% saline
pleomorphic plasma cells alongside low numbers of small as a CRI over 2 hours). The infusion rate of 0.9% saline
lymphocytes and rare neutrophils. The central plasma cell should be rapid enough to produce intense diuresis, but
shows aberrant mitosis, consistent with (multiple) care must be taken to avoid plasma overload. If possible,
myeloma. (Photo courtesy Roger Powell) CVP measurements should be taken intermittently and
the infusion slowed down or discontinued when the CVP
 M E TA B O L I C E N C E P H A L O PAT H I E S 487

Normal ammonia Abormal ammonia

metabolism Gut metabolism Gut
Brain
Muscle Portal vein PSS Increased
Muscle
glutamine

Liver Liver
dysfunction
Urea cycle
No urea cycle

Kidney Kidney

Ammonia
Urea
Glutamine

is >10 cm H2O. Once the plasma space is adequately  386 Ammonia metabolism. In an animal with normal
volume expanded (normal hydration and capillary refill hepatic function, ammonia synthesized in the gut is
time <2 seconds), repeated injections of furosemide can be transported to the liver via the hepatic portal vein.
given intravenously to enhance diuresis. Glucocorticoids Approximately 90% of ammonia delivered to the liver is
should not be used to treat hypercalcaemia until a diagno- converted into urea via the urea cycle. The remaining
sis is reached since they may worsen some disease process- ammonia exits the liver via the hepatic veins and is
es and hamper the identification of others. Total and distributed within the circulation. The heart, kidneys,
ionized calcium, serum phosphate, BUN and creatinine brain, skeletal muscle and intestine can also metabolize
levels should be serially monitored. ammonia. Ammonia and amino acids are also released into
the circulation following muscle damage and, similarly,
Prognosis will be metabolized in the liver. The urea is then excreted
PHPTH carries a good prognosis with appropriate through the kidneys. In an animal with liver dysfunction,
therapy. The prognosis for other causes of hyper- a urea cycle defect or a portosystemic shunt (PSS), the
calcaemia varies considerably, but is often guarded. ammonia is not sufficiently metabolized and enters the
systemic circulation and the brain tissues. In the brain,
Hepatic encephalopathy ammonia metabolism produces glutamine as well as urea.
Aetiology/pathophysiology This glutamine is degraded to the excitatory neurotrans-
HE is a complex neurological condition that occurs as a mitter glutamate. Increased brain glutamate will increase
consequence of acute or chronic liver disease, most fre- neuronal excitability and is one factor in the development
quently due to congenital portovascular anomalies, of hepatic encephalopathy.
hepatic microvascular dysplasia or liver failure from any
cause including intoxication or infection. Multiple
pathophysiological theories have been proposed and
these are briefly discussed here.

Ammonia much of the inconsistency in the results obtained.

Elevated blood ammonia is characteristic of HE, but the Ammonia (NH3) is produced primarily in the gastro-
role of ammonia in the pathogenesis of HE is contro- intestinal tract by bacterial metabolism of amino acids,
versial since the degree of correlation between HE urea and glutamine. NH3 diffuses through the intestinal
severity and blood ammonia concentration is variable. mucosa into portal blood and is delivered to the liver as
The labile nature of blood ammonia may be the origin of ammonium (NH4+) (386). The liver itself produces
 488 SPECIFIC EMERGENCIES

ammonium ions from amino acid deamination. In liver excreted via the hepatobiliary route and its concentration
failure, hepatic ammonia detoxification is ineffective, increases in liver disease. Patients with chronic liver
leading to hyperammonaemia. Ammonium ions are disease and HE have increased brain manganese concen-
detoxified predominantly in the liver via the urea cycle, trations, although whether this is causative or coinciden-
with resultant production of glutamine. The brain lacks tal is unknown. Increased manganese concentration may
a urea cycle and relies on production of glutamine for appear as a bright signal on T1-weighted MR images,
detoxification of ammonia, which is a direct neurotoxin which has been observed in the lentiform nuclei in a
acting via chloride channel inhibition. It has been sug- canine patient.
gested that the glutamine produced acts as the ‘Trojan
horse’ of HE pathogenesis by inducing oxidative stress. TNF-alpha
Much of the evidence supporting the ammonia theory Circulating levels of TNF-α, a proinflammatory cyto-
comes from the apparent efficacy of anti-ammonia thera- kine, are increased in liver failure patients and appear
pies such as lactulose, oral synbiotics, oral antimicrobials to correlate with HE severity. In liver failure, TNF-α
and enteral or parenteral L-ornithine–L-aspartate. production increases while TNF-α clearance may be
reduced. Pathological derangements of the brain in HE
GABA/benzodiazepine may be induced in part by TNF-α excess. The TNF-α
GABA is the principal inhibitory neurotransmitter in the hypothesis links a number of the other hypotheses
CNS and increased GABAergic tone results in impaired together. TNF-α increases CNS endothelial ammonia
motor function and decreased consciousness. The diffusion, enhances glutamate receptor-mediated neuro-
GABAergic theory suggests that HE is due to increased toxicity and is associated with significantly increased
circulating levels of GABA derived from the gastro- levels of GABA. Additionally, TNF-α increases periph-
intestinal tract, although the theory has been modified eral type benzodiazepine receptors and excess man-
to include the involvement of endogenous benzo- ganese potentiates in-vitro production of TNF-α.
diazepines, which are also increased in HE patients.
Activation of the GABA/benzodiazepine receptor Reactive oxygen species/reactive nitrogen species
complex causes chloride ion influx, membrane hyper- Oxidative and nitrosative stress may play a role in HE
polarization and neuronal inhibition. This theory is development. Hyperammonaemia, inflammatory cyto-
supported by the improvement in clinical signs in HE kines and benzodiazepines induce ROS production.
patients given the benzodiazepine receptor antagonist Oxidative stress is linked to astrocyte swelling, a key
flumazenil, although this drug appears to improve component of the pathophysiology of HE. Ammonia,
encephalopathic signs in less than half of HE patients. TNF-α , benzodiazepines and astrocyte swelling trigger
an NO-dependent Zn2+ mobilization, which modulates
Aromatic amino acids GABA function, peripheral benzodiazepine receptor
The concentrations of branched-chain amino acids expression and neurosteroid synthesis. ROS generation
in the brain decrease in liver disease, while those of and secondary astrocyte swelling may thus mechanisti-
aromatic amino acids increase. This increase in brain cally link the other theories together.
aromatic amino acid concentration may lead to false
neurotransmitter generation; however, branched-chain Clinical presentation
amino acid administration does not appear to be effective HE is well documented in both humans and small
for treatment of HE. animals and is characterized by changes in behaviour,
consciousness and NM function. Neurological signs may
Manganese include head pressing, hyperreflexia, rigidity, myoclonus,
This trace element is an essential constituent of multiple seizures and coma. Signs of hepatic dysfunction (weight
antioxidant metalloenzymes such as superoxide dismu- loss, polydipsia, anorexia and vomiting) may be present.
tase. Manganese-induced neurotoxicity causes astrocyte Ptyalism is another common sign, especially in cats.
dysfunction, neuronal loss and gliosis. Manganese is
 M E TA B O L I C E N C E P H A L O PAT H I E S 489

Management
HE therapy has three aims: stop the seizures; reduce
serum levels of neurotoxic metabolites; treat the under-
lying cause.

Stop seizures
If the patient is having seizures, antiepileptic drug treat-
ment will be necessary. Controversy exists over the use of
benzodiazepines for treatment of HE-associated
seizures; however, they remain the first-line drug of
choice. For maintenance therapy, ideally, a drug with no
effect on hepatic metabolism should be used. Potassium
bromide is theoretically a good choice and it can be given
 387 Ultrasound image of a 7-month-old female via a loading protocol over 1–6 days either orally or
Weimaraner through a dorsal right-sided intercostal rectally (see Chapter 23). Levetiracetam (20–60 mg/kg)
window demonstrating a large intrahepatic portosystemic may be effective when given intravenously, intramuscu-
shunt. (Photo courtesy Francisco Llabres-Diaz) larly or per rectum, although it has not yet been evaluat-
ed for efficacy in animals via these routes or at these
doses. In patients with SE secondary to HE, it may be
Diagnosis necessary to use anaesthetic drugs, some of which have
HE is diagnosed primarily by clinical signs in conjunc- potent anti-seizure properties, in order to terminate
tion with biochemical evidence of liver dysfunction. seizure activity. Propofol (1–4 mg/kg IV for induction,
Serum biochemistry evidence of liver dysfunction given to effect followed by CRI 0.1–0.6 mg/kg/minute)
includes hypoalbuminaemia, hypocholesterolaemia, low can be used for this. Once anaesthesia is induced patients
BUN and hypoglycaemia. Increased liver enzyme con- must be intubated to protect their airway and an inten-
centrations indicate hepatocellular damage or cholesta- sive protocol of monitoring and care of the recumbent
sis, which are commonly seen in patients with disease patient initiated. (Note: Electrical seizure activity may
processes causing liver dysfunction. Patients with con- continue despite the appearance of a cessation of tonic or
genital portovascular anomalies commonly have two-to- clonic activity.) Other measures to treat HE must also be
threefold increases in liver enzymes. Supportive findings initiated in patients with SE.
from specific liver function tests include hyperammon- Some patients develop neurological dysfunction
aemia, increased pre- and/or postprandial bile acids or following portosystemic shunt ligation. One study
clotting time prolongations. Microcytosis is an inconsis- reported postoperative neurological abnormalities in
tent haematological finding in liver disease. Abdominal 11/89 dogs within 6 days of surgical shunt attenuation.
imaging, and in particular ultrasound, may be useful in The cause of postoperative seizures is not known. Signs
identifying liver pathology such as biliary tract disease included disorientation, ataxia, generalized seizures and
or neoplasia. Identification of a portosystemic shunt is SE. The development of SE following surgical attenua-
possible by ultrasonography (387) or mesenteric porto- tion probably carries a poor prognosis. However, nine of
graphy. MRI of the brain may reveal cortical atrophy the 11 patients described in this study survived. The
characterized by widened sulci, and hyperintensity of the authors concluded that perioperative phenobarbital
lentiform nuclei on T1-weighted images. Hepatic biopsy therapy may not prevent such neurological sequelae, but
is rarely required. may reduce their severity.
490 SPECIFIC EMERGENCIES

Reduce neurotoxic metabolites Hypoglycaemia

Oral lactulose (0.5–1.0 ml/kg PO q8h) decreases gut Aetiology/pathophysiology
transit time, helps to prevent constipation and alters gut Hypoglycaemia may arise from numerous conditions.
flora, thus reducing colonic ammonia production. Once Hypoglycaemic neurological dysfunction has been
metabolized it produces an acid environment, trapping reported in patients with endogenous and iatrogenic
ammonia as ammonium. In stuporous or comatose hyperinsulinaemia, sepsis, liver failure, portosystemic
patients, lactulose can be administered by retention shunting, hypoadrenocorticism, neoplasia (insulinoma
enema (20 ml/kg, made of three parts lactulose diluted in or extrapancreatic insulin-like producing neoplasm),
seven parts warm water, q4–6h). neonatal hepatopathy and xylitol toxicity. Hypo-
Ampicillin (22 mg/kg PO q8h) or, if unavailable, glycaemic neurological dysfunction is also reported in
metronidazole (7.5 mg/kg PO q8h) or neomycin (20 toy breeds and in hunting dogs.
mg/kg PO q8h) can be used to reduce urea-splitting Despite constituting only 2% of total body mass, the
colonic bacterial numbers. Proximal gastrointestinal brain utilizes 25% of total body glucose due to its inher-
haemorrhage may exacerbate encephalopathic signs and ently high metabolic rate and limited local storage. Brain
should be treated with proton-pump inhibitors such as interstitial glucose concentrations are typically 20–30%
omeprazole. This drug can be given orally or intra- less than plasma, therefore glucose must be continuously
venously (1 mg/kg). Additionally, gastrointestinal bleed- transported into the brain. Blood glucose is closely mon-
ing in patients with liver dysfunction must be itored by glucose-sensing neurons in the hypothalamic
investigated to identify any underlying thrombocyto- ventromedial nuclei. Hypoglycaemia stimulates these
penia or coagulopathy that requires specific treatment. neurons, leading to increased sympathetic output and,
If appropriate, based on the patient’s mentation, the therefore, increased plasma epinephrine (adrenalin),
diet may be altered to a high-quality, low-protein one to norepinephrine (noradrenalin), cortisol, glucagon and
reduce ammonia production in the gastrointestinal tract. somatostatin concentrations. These counter-regulatory
Care must be taken not to limit protein intake excessive- hormones act to increase plasma glucose concentration,
ly since many patients with portovascular anomalies are increase glucose delivery to, and uptake by, the brain and
young, growing patients and such protein restriction may alter glucose metabolic pathways. Insulin is not required
be detrimental to their musculoskeletal development. for glucose uptake by the brain because of specific
glucose transporting transmembrane proteins.
Treat underlying cause If hypoglycaemia persists and mechanisms to increase
Surgical ligation of single, uncomplicated extrahepatic or glucose delivery and uptake are inadequate, the brain can
intrahepatic shunts is the most direct treatment. Dogs shift towards production of pyruvate via glycolysis, which
and cats with multiple extrahepatic shunts and those with is then shuttled to lactate. Astrocyte mobilization of
acquired shunts secondary to cirrhosis or acute fulminant glycogen stores and subsequent lactate production
hepatic failure are not candidates for surgery. In cases of provides a limited energy supply for neurons. Brain
acquired liver disease, specific therapy for any underlying glycogen stores appear to be consumed gradually during
cause should be instituted. hypoglycaemia. The exhaustion of these stores seems to
coincide with ATP depletion and the onset of EEG iso-
Prognosis electricity, suggestive of neuronal death and potentially
The prognosis for dogs and cats with HE is dependent irreversible brain injury. It also seems that brain function
on the degree of hepatic impairment and the severity of becomes impaired before ATP depletion is detectable,
the neurological signs. It is guarded in patients with concomitant with changes in brain monoamine concen-
seizures secondary to HE, poor in patients with liver trations, increased free fatty acid concentration and
failure and fair with surgical treatment in patients with impaired plasma membrane function. At the point of
portovascular anomalies. energy failure, where brain glucose has fallen by >97%,
ATP becomes abruptly depleted. ATP depletion causes
 M E TA B O L I C E N C E P H A L O PAT H I E S 491

Na+-K+-ATPase dysfunction, leading to transmembrane

Hypoglycaemia gradient dissipation. Neuronal cell swelling and mem-
brane disruption cause excitatory neurotransmitter
release (particularly glutamate and aspartate) into the
brain interstitium. High extracellular concentrations of
ATP depletion glutamate and aspartate activate glutamate receptors,
increasing intracellular calcium, stimulating neuronal
nitric oxide synthase activity and potentiating neuronal
death. Increased intracellular calcium and zinc concen-
Na+-K+-ATPase
trations lead to mitochondrial dysfunction, poly[ADP-
dysfunction
ribose] polymerase-1 activation and the opening of the
mitochondrial membrane megachannel (mitochondrial
permeability transition) leading to cell swelling and ROS
Na+ Into neurons generation. ROS damage DNA and initiate lipid peroxi-
CI– Ca2+
dation, causing cellular necrosis (388).

Neuronal cell
swelling Increased
[Ca2+]ic

Glutamate Increased PARP-1

Excitatory neuro-
receptor [Zn2+]ic activation
transmitter release
activation

Increased
iNOS

 388 Mechanism of cellular necrosis in the context

of hypoglycaemia. ATP depletion causes dysfunction Mitochondrial Opening of
of the transporter enzyme Na+-K+-ATPase, permeability MMC
transition
responsible for the exhange of sodium and potassium
ions across the cell membrane. A cascade of events
leads eventually to permanent brain injury. (Zn, zinc;
iNOS, ionized nitric oxide synthetase; PARP-1,
ROS generation Cell swelling
poly[ADP-ribose] polymerase-1; MMC, mitochondrial
membrane megachannel; ROS, reactive oxygen
species.)

DNA damage Lipid peroxidation

Cellular necrosis

Irreversible
brain injury
492 SPECIFIC EMERGENCIES

Clinical presentation
Clinical signs of cortical neuronal damage range from
hyperexcitability to tremors, blindness, cognitive dys-
function, seizures, coma and death. Nervousness,
tremors and weakness typically appear when plasma
glucose levels approach 3.6–3.8 mmol/l (64.8–68.4
mg/dl). When plasma glucose levels fall below 1 mmol/l
(18 mg/dl), seizures, severe brain damage, coma
and death may occur. However, as with many homeosta-
tically controlled parameters, the rate of change may be
more important than the absolute values in determining
the point of onset and severity of clinical signs. Early
recognition and therapy for hypoglycaemia are vital both
for early return of neuronal function and to diminish the  389 Intraoperative image of an insulinoma, which is a
risk of permanent damage. few millimetres across (black arrow) within the left limb
of the pancreas. A local lymph node appears enlarged
Diagnosis (yellow arrow). Histopathology of this affected lymph
A blood glucose measurement that is consistently node confirmed the presence of metastasis from the
less than the reference interval is diagnostic of hypo- insulinoma. (Photo courtesy Ronan Doyle)
glycaemia. (Note: False hypoglycaemia may result from
use of human point-of-care glucometers in haemo-
concentrated patients.) Falsely low glucose values may
also result from delayed separation of serum from RBCs Renal failure
as these cells continue to consume glucose for glycolysis. Aetiology/pathophysiology
This can be prevented by using a sodium fluoride tube. Patients with acute or chronic renal failure may develop
Once hypoglycaemia is identified, a thorough investi- encephalopathy due to uraemia, thiamine deficiency,
gation for an underlying cause must be undertaken. dialysis, transplant rejection, hypertension, fluid and
Principle rule-outs include sepsis, liver failure, hypo- electrolyte disturbances or drug toxicity. Uraemic
adrenocorticism, insulin overdose, xylitol toxicity, neo- encephalopathy is typically more severe in patients with
natal or toy breed hypoglycaemia, insulinoma (389) and acute renal failure. The pathophysiology of this
other paraneoplastic hypoglycaemias. encephalopathy is complex and poorly understood, but
metabolite accumulation, hormonal disturbances, meta-
Management bolic abnormalities and neurotransmitter imbalances
The underlying cause of the hypoglycaemia must be may all contribute. Renal failure results in accumulation
addressed. An intravenous dextrose bolus (0.5 g/kg 50% of numerous organic substances that possibly act as
dextrose diluted 1:4 with 0.9% saline) should be given uraemic neurotoxins, but no single metabolite has been
and continued with a CRI of 2.5–5% dextrose in an iso- identified as the sole cause of uraemia and the degree of
tonic fluid as required to maintain normoglycaemia. azotaemia correlates poorly with the degree of neuro-
Solutions of 2.5–5% dextrose can be readily prepared by logical dysfunction. Accumulation of urea, guanidine
adding aliquots of a solution of 50% dextrose to 0.9% compounds, uric and hippuric acids, amino acids, poly-
saline or Hartmann’s solution (e.g. 50 ml of 50% dextrose peptides, polyamines, phenols, phenolic and indolic
in 500 ml saline creates a 5% solution). Glucose syrup acids, acetone, glucuronic acid, carnitine, myo-inositol,
can be administered orally if intravenous access is not sulphates, phosphates and middle molecules has been
available; however, there needs to be caution using the reported. NMDA receptor activation and concomitant
oral route if the patient is actively seizuring. Frequent inhibition of GABAA neurotransmission have also been
small meals should be fed throughout the day. proposed.
 M E TA B O L I C E N C E P H A L O PAT H I E S 493

Hormonal disturbances, particularly PTH, have been Diagnosis

suggested to play a role in the pathogenesis of uraemic Serum biochemical analysis demonstrates very severe
encephalopathy. PTH may facilitate calcium entry into azotaemia, hyperphosphataemia ± accompanying alter-
tissues, altering the brain calcium balance and disrupting ations in total and ionized calcium levels. Urinalysis
cerebral function. Thiamine deficiency in uraemic before fluid therapy showing isosthenuria is compatible.
patients is rare, although dialysis patients are at increased Systemic hypertension and a non-regenerative anaemia
risk. Encephalopathy due to aluminium accumulation are common in chronic renal failure patients. Investiga-
secondary to use of aluminium-based phosphate binders tions must be directed towards identifying any reversible
has been reported in humans and in dogs. underlying cause.
Systemic hypertension commonly accompanies renal
failure. Chronic systemic hypertension has a variety of Management
pathological consequences, which is referred to as end- Reversible conditions (e.g. ureteric obstruction) should
organ or target organ damage (TOD). Important TOD be identified and treated. Fluid balance and electrolyte
is observed in the kidneys, eyes, heart and nervous disturbances are corrected with targeted fluid therapy
system. Hypertensive encephalopathy is thought to be (see Chapter 31). If the patient is anuric, an attempt
caused by vasogenic oedema due to impaired cerebro- should be made to establish urine output with fluid
vascular autoregulation, endothelial injury and elevated therapy and osmotic or loop diuretics. This should be
plasma natriuretic peptide concentrations. With acute monitored for signs of fluid overload. If the patient is
hypertension, the autoregulatory capacity of the brain polyuric, diuresis should be provided.
vasculature may be exceeded, which leads to hyperperfu- Systemic hypertension should be monitored and
sion, breakdown of the blood–brain barrier and cerebral treated if systolic BP is >200 mmHg, mean >140 mmHg
oedema. In chronic hypertension, brain vasculature may or diastolic BP is >110 mmHg, or if signs of end-organ
be chronically vasoconstricted, leading to hypertrophy damage exist (e.g. retinal haemorrhage). ACE inhibitors
and hyperplasia of the smooth muscle. As a result, fibrous (e.g. benazepril, 0.25–0.5 mg/kg PO q24h in the dog
changes develop allowing leakage of plasma, which or 0.25–1.0 mg/kg PO q24h in the cat; amlodipine,
ultimately causes degeneration of the vasculature, 0.1 mg/kg PO q24h; or hydralazine, 0.5–2.0 mg/kg PO
predisposing to vessel rupture and microhaemorrhages. q12h in the dog or 2.5 mg/cat PO q12h) are the drugs
Clinically, it is associated with lethargy, ataxia, blindness, of choice.
stupor and seizures. If renal failure is severe, or patients remain anuric,
Fluid and electrolyte disturbances, including hyper- peritoneal dialysis and haemodialysis are the only options
calcaemia, hypo- and hypernatraemia and hypo- and available to reduce azotaemia. Referral for dialysis should
hyperosmolality, are common in patients with renal be considered, but the clinician must be aware of dialysis
failure and may contribute to encephalopathy. Encepha- disequilibrium syndrome (DDS) in severely azotaemic
lopathy may also occur due to drug accumulation patients. DDS is a CNS disorder that is an important
secondary to renal insufficiency. Drugs implicated clinical problem in human dialysis patients. It is charac-
include metronidazole and cefazolin. Additionally, terized by neurological symptoms of varying severity that
altered drug–protein binding in renal failure may lead to are thought to be due primarily to cerebral oedema.
neurotoxicity associated with theophylline, diazepam, Predisposing factors include severe metabolic acidosis,
propranolol and cimetidine. older age, paediatric patients and the presence of other
494 SPECIFIC EMERGENCIES

CNS disease such as a pre-existing seizure disorder. Table 92 Canine systemic inflammatory
Classic human DDS refers to acute symptoms develop- response criteria
ing during or immediately after haemodialysis. Early
* Rectal temperature ≤37.8ºC or >39.7ºC
findings include headache, nausea, disorientation, rest- ()100.0ºF or >103.5ºF)
lessness, blurred vision and asterixis. More severely
affected patients progress to confusion, seizures, coma * Heart rate ≥160 bpm
and even death. It is now recognized that many milder * Respiratory rate ≥40 breaths/minute
signs and symptoms associated with dialysis, such as
muscle cramps, anorexia and dizziness developing near * Leucocyte count <4 x 109/l or >12 x 109/l WBCs
or band neutrophils >10%
the end of a treatment, are also part of this syndrome.
*3 out of 4 are necessary
Prognosis (Adapted from Okano S, Yoshida M, Fukushima U et al. (2002)
Patients with uraemic encephalopathy are typically in Usefulness of systemic inflammatory response syndrome criteria
as an index for prognosis judgement. Vet Rec 150:245–246.)
end-stage chronic renal failure or are anuric due to an
acute renal insult. Anuric patients have a poor prognosis
even with haemodialysis.

Sepsis
Overview
Sepsis-associated encephalopathy (SAE) is a well- Aetiology/pathophysiology
recognized, although ill-defined, entity in humans, SAE pathophysiology is incompletely understood and is
occurring in 23% of patients in one study. Definitive probably multifactorial. Brain dysfunction in sepsis may
identification of the condition is problematic because few be related to microbial toxins, inflammatory mediators,
criteria are both sensitive and specific. To date, SAE has metabolic and vascular abnormalities, mitochondrial
not been reported as a specific entity in small animals. dysfunction, oxidative stress and apoptosis. Bacterial
Given the similarities between canine and human sepsis toxins can exert CNS effects and induce brain dysfunc-
it is probable that dogs also suffer from SAE. SAE associ- tion. Endotoxin-induced inflammatory mediators and
ated with gram-negative sepsis appears to have a higher ROS cause endothelial, astrocyte and neuronal dysfunc-
mortality in people. Septic encephalopathic patients have tion. Plasma and CSF concentrations of ascorbate are
significantly higher mortality than those with normal significantly reduced in encephalopathic septic patients.
mentation. Pathologically, the cerebrum is most com- Endotoxin interferes with the hypothalamic–pituitary
monly involved. Multiple lesion types have been axis. Breakdown and enhanced permeability of the
described including ischaemic lesions, particularly in blood–brain barrier have been observed in SAE, leading
autonomic nuclei, purpura, central pontine myelinolysis, to alterations in cerebral monoamine concentrations and
multifocal necrotizing leucoencephalopathy, haemor- perivascular oedema formation. In patients with SAE,
rhage, microabscessation, perivascular oedema and dis- altered mental status has been related to aromatic amino
ruption of astrocyte foot processes. Neuronal damage acid excess and decreased levels of branched-chain amino
includes eosinophilic cytoplasm, shrunken nuclei and acids.
disruption of the nuclear membrane. Astrogliosis and
focal necrosis of cerebral white matter have been
described in experimental neonatal kittens following
intraperitoneal injection of E. coli lipopolysaccharide.
 M E TA B O L I C E N C E P H A L O PAT H I E S 495

Table 93 Feline systemic inflammatory THERMOREGULATORY DISORDERS

response criteria
Heatstroke
* Rectal temperature ≤37.8ºC or >39.7ºC ()100.0ºF or
>103.5ºF)
Overview
Heatstroke, the most severe form of heat-induced illness,
* Heart rate <140 bpm or >225 bpm has been defined as hyperthermia associated with a sys-
* Respiratory rate >40 breaths/minute temic inflammatory response leading to a syndrome
of multiorgan dysfunction in which encephalopathy
* Leucocyte count <5 x 109/l or >19.5 x 109/l WBCs predominates.
or band neutrophils >5%

*3 out of 4 are necessary Aetiology/pathophysiology

(Adapted from Brady CA, Otto CM, Van Winkle TJ et al. (2000) Heatstroke occurs when the thermal load exceeds the
Severe sepsis in cats: 29 cases (1996–1998). J Am Vet Med patient’s ability to dissipate heat and can be exertional or
Assoc 217:531–535.)
non exertional. The degree of injury is dependent on
both the magnitude and duration of core temperature
increase. Direct thermal injury and protein denaturation
occur at approximately 42.8°C (109.0°F). Experimental
evidence suggests that sustained temperatures as high as
40.6°C (105.1°F) may cause permanent brain damage,
Diagnosis although recovery is possible even when the temperature
Sepsis is defined as the systemic inflammatory response reaches 46.5°C (115.7°F). Severe hyperthermia results in
to infection. Sepsis is diagnosed on the basis of positive massive neuronal injury and cell death. Cerebral oedema,
systemic inflammatory response criteria (Tables 92 and haemorrhage, infarction and cerebellar dysfunction are
93) with suspected or confirmed infection. SAE should common consequences of severe hyperthermia in dogs.
be considered in any patient with sepsis who develops Although the exact mechanisms are unclear, dopamine,
clinical signs of encephalopathy. SAE should be consid- serotonin, glutamine and cytokines (e.g. IL-1, IL-6,
ered a diagnosis of exclusion and efforts should be made TNF-α) have been implicated as potential mediators.
to exclude other potential causes of metabolic encepha- The development of cerebral and cerebellar oedema and
lopathy such as hypoglycaemia. Confirmation of charac- localized areas of necrosis due to intracranial haemor-
teristic pathological findings requires postmortem rhage can lead to disorientation, seizures, coma and
examination. sometimes death. Excessive temperatures in the hypo-
thalamus may impair temperature regulation by damag-
Management ing the thermoregulatory centre. Arterial hypotension
No specific treatment for SAE exists. Once sepsis is diag- and cerebral ischaemia may also be involved in the devel-
nosed, treatment should focus on cardiovascular system opment of canine heatstroke.
support, rapid initiation of appropriate intravenous
antimicrobials, source control if appropriate and close Management
patient monitoring. Hyperthermia must be distinguished from pyrexia
through assessment of the patient’s history, signalment,
Prognosis physical examination findings and clinicopathological
Sepsis itself carries a guarded to poor prognosis, with data. Major body system abnormalities should be identi-
reported mortality rates varying between 20% and 70% fied and treated as appropriate and oxygen provided.
in small animals. It is likely that SAE will only occur in Room temperature intravenous fluids should be given as
those most severely affected and therefore the prognosis required to correct hypoperfusion. Sedation may be
is probably worse for this patient population. necessary to reduce stress. Only sedative agents with
 496 SPECIFIC EMERGENCIES

minimal effects on the cardiopulmonary system should between body temperature and clinical signs associated
be used in patients with heatstroke who may be suffering with secondary hypothermia, where comparable adverse
from shock (see Chapter 29). effects occur at higher temperatures. For secondary
Active cooling must be undertaken if the body tem- hypothermia, mild is classified as 36.7–37.7°C
perature is >39.5oC (>103.1oF). This can be achieved by (98.1–99.9°F), moderate as 35.5–36.7°C (95.9–98.1°F),
dousing the fur with tepid water and blowing air across severe as 33–35.5°C (91.4–95.9°F) and critical <33°C
the patient. In extreme cases where the body temperature (<91.4°F). Controlled hypothermia following return of
is >42oC (>107.6oF), additional measures, such as cool spontaneous circulation after cardiopulmonary arrest
water enemas or peritoneal lavage (10–20 ml/kg room may be neuroprotective. Severe CNS depression and
temperature sterile saline), may be required, although coma may occur with progressive hypothermia. Mild-to-
experimental studies suggest that evaporative cooling moderate hypothermia reduces CBF and impairs cere-
may be as effective as peritoneal lavage. Ice water must bral autoregulation. Cerebrovascular autoregulation is
not be used since this may cause vasoconstriction, reduc- lost below ~25°C (77°F) and in addition, CBF decreases
ing efficacy and potentially inducing shivering. Cortico- by 6–7% for each 1°C drop in body temperature.
steroids or NSAIDs should not be administered. They However, in severe hypothermia there is a markedly
will not reduce the patient’s temperature and are contra- reduced metabolic rate, conferring increased cerebral
indicated in patients with shock or gastrointestinal injury. ischaemic tolerance. The EEG becomes flat at body
Aggressive cooling efforts should be discontinued when temperatures below ~20°C (68°F) in people.
the patient’s temperature reaches 39.5°C (103.1oF)
to prevent overshoot hypothermia, which might be Management
detrimental. For mild hypothermia, passive external rewarming with
blankets to prevent further heat loss is appropriate. For
Hypothermia moderate hypothermia, active external rewarming is
Aetiology/pathophysiology appropriate. A forced air blanket is ideal. Direct applica-
Primary hypothermia results from exposure to low envi- tion of heat sources to skin must be avoided. External
ronmental temperatures, while the causes of secondary rewarming should be applied to the trunk and head, not
hypothermia are multifactorial and include underlying to the extremities. For severe hypothermia, active core
disease, trauma, toxins, immobility, surgery and anaes- rewarming by peritoneal lavage should be considered in
thesia. Primary hypothermia in dogs and cats is classified addition to other techniques. (Note: Beware of rewarm-
as mild 32–37°C (89.6–98.6°F), moderate 28–32°C ing shock [hypotension due to vasodilation] and after-
(82.4–89.6°F), severe 20–28°C (68.0–82.4°F) and pro- drop [falls in core temperature due to peripheral
found <20°C (<68°F). A different correlation exists vasodilation] during treatment.)
 M E TA B O L I C E N C E P H A L O PAT H I E S 497

Thiamine deficiency Diagnosis

Overview Diagnosis of thiamine deficiency is typically made on the
Vitamin B1 (thiamine) is an essential dietary component basis of signalment, clinical signs and a detailed dietary
in small animals. Thiamine pyrophosphate is a coenzyme history. Confirmation of the deficiency can be made by
for pyruvate dehydrogenase, alpha-ketoglutarate dehy- assays of thiamine metabolites in blood or by measure-
drogenase and transketolase, all of which are involved ment of erythrocyte transketolase activity. Presumptive
in carbohydrate metabolism. Thiamine deficiency diagnosis can be made on the basis of urinary organic acid
impairs oxidation of ketoacids, leading to impaired cere- profile analysis. Occasionally, a diagnosis is only con-
bral energy metabolism, focal lactic acidosis, NMDA firmed postmortem. Clinical sign resolution following
receptor-mediated excitotoxicity and blood–brain treatment with thiamine is supportive of the diagnosis.
barrier breakdown. CSF analysis does not appear to be discriminatory for
thiamine deficiency. MRI findings have been described
Clinical presentation in the dog and cat including non-contrast enhancing
Thiamine deficiency, termed Wernicke’s encephalopathy bilaterally symmetrical thalamic and brainstem nuclear
in people, causes polioencephalomalacia with bilaterally hyperintensity evident on T2-weighted and FLAIR
symmetrical spongiosis, necrosis and brainstem nuclei images (390).
haemorrhage. Thiamine-deficient dogs present with
dilated unresponsive pupils and mild ataxia progressing Management
to altered mentation, hyperaesthesia, tetraparesis, Thiamine deficiency can be treated with thiamine
seizures and opisthotonus. Cats, in contrast, display hydrochloride (5–50 mg/dog IV, IM or PO q24h or 1–20
central vestibular signs, head tremors, mydriasis and mg/cat by slow CRI). The underlying disorder should
cervical ventroflexion. Thiamine deficiency in dogs and also be investigated and managed appropriately.
cats has been reported secondary to feeding of sulphur
dioxide-preserved meat, feeding thiamine deficient Prognosis
diets or fresh fish diets containing thiaminase. Thiamine Provided the diagnosis is made early or presumptive
deficiency can occur due to decreased intake, impaired treatment is rapidly initiated, then the prognosis for
absorption due to intestinal disease, liver dysfunction, thiamine deficiency is good.
increased utilization secondary to fever or infection or
increased urinary loss.

a b  390 Transverse T2-weighted

FLAIR MR images of a Cocker
Spaniel with thiamine
deficiency. There is bilaterally
symmetrical hyperintensity at the
level of the rostral colliculus (a)
and vestibular nuclei (b).
498 SPECIFIC EMERGENCIES

a b

 391 Sagittal (a) and transverse (b) T2-weighted MR images of a Staffordshire Bull Terrier with L-2-hydroxyglutaric
aciduria. There is diffuse abnormal hyperintensity extending rostrally through the dorsal brainstem to the thalamus and
also affecting the grey matter of the cerebellum and cerebral hemispheres (a). Note the symmetrical hyperintensity in
the grey matter of the cerebral hemispheres and the thalamus (b).

Inborn errors of metabolism Diagnosis

Organic acidopathies: L-2-hydroxyglutaric aciduria Bilateral symmetrical hyperintensity is evident on
Overview T2-weighted MR images of the cerebral, cerebellar, thal-
L-2-hydroxyglutaric aciduria is an inherited disease amic and brainstem grey matter (391). CSF cytology and
of Staffordshire Bull Terriers and West Highland protein content are normal. L-2-hydroxyglutaric acid
White Terriers. It is an organic acidopathy characterized levels are increased in urine, plasma and CSF.
by raised L-2 hydroxyglutaric acid in plasma, urine A causative mutation in the canine homologue of the
and CSF. L-2-hydroxyglutarate dehydrogenase gene has been
identified. A genetic test is available commercially at the
Clinical presentation Animal Health Trust, Newmarket, UK. Histopathology
The condition has an acute or chronic onset and it is reveals diffuse polioencephalopathy.
progressive over 4 months to 7 years. Clinical signs
include seizures, ataxia, head tremor and subtle behav- Management
iour changes/dementia. Treatment is palliative and symptomatic (e.g. anti-
epileptic drugs).

Prognosis
The prognosis is poor, although some dogs can be
managed symptomatically for many months to years.
 SPECIFIC EMERGENCIES Chapter 28

NEUROLOGICAL TOXICITIES
499

Jennifer Pittman,
Ben Brainard
& Katrin Swindells

INTRODUCTION instead of frequent oropharyngeal suctioning.) Patients

should be intubated and ventilated if respiratory paraly-
Neurotoxicity is commonly encountered in emergency sis or other causes of hypoventilation are present and
veterinary practice. Toxins that cause neurological signs oxygen should be provided if the patient is cyanotic or
may be exogenous or endogenous in origin. Exogenous hypoxaemic (for further details see Chapter 2).
neurotoxins include plant and environmental toxins, Maintenance of adequate BP is essential for hepatic
envenomations, pesticides, herbicides, medications and and renal perfusion, which are important for the clearance
food. Endogenous neurotoxins are the result of meta- of many toxins. Systemic BP should be measured and nor-
bolic diseases or organ dysfunction (e.g. hepatic or malized, and cardiac arrhythmias should be evaluated and
uraemic encephalopathies) and are not discussed in this treated. BP may initially be measured using indirect
chapter (see Chapter 27). methods (e.g. Doppler probe or oscillometric machine);
Most toxins affect the neurological system directly; normal MAP should be near 75 mmHg and normal
some may have indirect effects due to the metabolic Doppler blood pressure should be >80 mmHg. Cardiac
effects of the toxin (e.g. HE due to a toxin that causes rhythm may be assessed using electrocardiography or by
hepatic failure). Toxins that have indirect effects on the simultaneous palpation and auscultation for pulse deficits.
neurological system will not be covered in depth in this Techniques for fluid resuscitation of the hypotensive neu-
chapter, but they should remain on the veterinarian’s dif- rological patient are covered in Chapter 31.
ferential diagnosis list where applicable. This chapter will
discuss the general management of exogenous neuro- Symptomatic treatment
toxicity. In addition, common toxins will be discussed Treatment of neuroexcitatory signs
with reference to mechanism of action, clinical signs, (See Chapters 13 and 23 for additional discussion, drug
treatment (if available) and prognosis. doses and administration rates.)

GENERAL TREATMENT PRINCIPLES

The main principles of treating neurotoxicity include the

following and are often performed simultaneously:
systemic stabilization; symptomatic treatment; deconta-
mination and prevention of absorption of further toxins;
providing antidotes if available.

Systemic stabilization
The patient’s airway should be protected using a cuffed
endotracheal tube if the patient is obtunded and/or at
risk of aspiration of gastric contents. Suction of the oro-
pharynx with a Yankauer suction tip (392) may be neces-
sary in patients who are unable to swallow. (These  392 A Yankauer suction tip may be useful for
patients may be more easily anaesthetized and intubated clearing secretions from the oropharynx.
500 SPECIFIC EMERGENCIES

Diazepam or midazolam is the first-line therapy for Maintenance of hydration and normovolaemia
seizures of unknown cause including toxicities. Occa- Following fluid resuscitation, hydration may be
sionally, benzodiazepine drugs can result in disinhibition maintained with any isotonic crystalloid fluid (e.g.
and worsening of hyperaesthesia in susceptible patients. Normosol R, lactated Ringer’s solution or Plasma-Lyte®
If benzodiazepines are ineffective at stopping seizure 148). In addition to maintenance needs, the effect of
activity, phenobarbital may be used. If these drugs are additional administered drugs (e.g. diuresis by mannitol
ineffective, anaesthesia may be induced with propofol or or furosemide) must be taken into account. Animals with
alfaxalone. In these cases it is imperative to maintain a diarrhoea or vomiting, or those that are panting exces-
protected airway with a cuffed endotracheal tube. sively, may have iso or hypotonic fluid losses that must
Patients who require prolonged anaesthesia can be main- be accounted for. If animals are anaesthetized for long
tained with volatile anaesthetics (isoflurane, sevoflurane), periods of time, free water loss from the respiratory
intravenous infusions of propofol or alfaxalone or inter- mucosa may occur, especially if the ventilator circuit
mittent injections or CRIs of pentobarbital, where this is is not humidified. In addition, the use of sorbitol or
available as a sterile solution for infection. Long-term other cathartics may result in fluid loss, and the use of
alfaxalone administration may result in accumulation in propylene glycol-containing activated charcoal suspen-
cats and requires gradual dose reduction in this situation. sion may result in serum hyperosmolarity and metabolic
Patients with severe muscle tremors, but not seizures, are acidosis. (Additional information about fluid therapy in
often best managed with methocarbamol, although the neurological patient can be found in Chapter 31.)
benzodiazepines may also be used to provide some
muscle relaxation. General nursing care
Recumbent animals should be turned every 4 hours and
Control of body temperature maintained on padded bedding to prevent pressure sores
Patients with hyperthermia (rectal temperature *40°C and muscle damage. Recumbent animals are also at risk
[104°F]) should be aggressively cooled until the rectal for atelectasis and subsequent hypoxaemia; this may be
temperature is 39.7°C (103.5°F). Convective cooling is prevented by supporting these patients in sternal recum-
the most effective way to cool a patient and involves bency if possible, and oxygenation should be monitored
wetting the fur and placing the animal near a fan. regularly. Daily physiotherapy of limbs is indicated for
Application of alcohol to the paw pads is usually animals that will have a prolonged period of recumbency
not adequate for cooling of hyperthermic patients, and (see Chapter 32). If the animal is unable to void urine,
direct application of ice packs may cause cutaneous vaso- bladder management protocols should involve regular
constriction and, paradoxically, slow cooling. The appli- expression or catheterization to prevent overdistension
cation of wet towels to the animal will also slow cooling of the urinary bladder. Animals with paralysis may also be
by impairing evaporative losses. Patients who have been unable to blink. If this occurs, lubricants, such as hyaluro-
hyperthermic for prolonged periods of time may develop nan, petroleum-based lubricants or artificial tears, should
and require treatment for heat stroke, in addition to their be applied at least every 4 hours.
primary neurological problem.
Patients presenting with hypothermia should be Decontamination and prevention of absorption of
warmed gradually, with frequent reassessment of tem- further toxin
perature, electrocardiography and BP, in addition to The methods used to prevent absorption of toxins, as
metabolic state (e.g. blood glucose concentration). well as those used for decontamination, will depend on
Forced warm air is the most effective way to warm a the route of entry of the toxin and the metabolic profile
hypothermic patient and many commercial products are of the toxin. Many methods both decrease absorption as
available that may be used for this purpose. Circulating well as decontaminate by encouraging elimination of the
warm water blankets may also be used, but are less effec- toxin.
tive than forced warm air.
 NEUROLOGICAL TOXICITIES 501

Cutaneous toxins
Table 94 Commonly used emetic agents
Most toxins that are absorbed by a cutaneous route are
lipid soluble. It is important to ensure that the patient is • Apomorphine
physiologically stable prior to bathing. Washing-up • 0.04 mg/kg IV or 0.06 mg/kg SC or IM
liquid may be more effective than shampoo at removing • 0.25 mg/kg of crushed tablet may be placed into the
fats and lipids. Multiple baths may be necessary to fully conjunctival sac
decontaminate the animal. Detergents should not • If administered subconjunctivally, eye should be rinsed
be used and medicated shampoos should be avoided. with artificial tear solution after vomiting
Persons handling animals should wear gloves for their • If profound depression results, reverse with naloxone
(0.04 mg/kg IV, IM, SC)
own safety while washing off cutaneous toxins.
• Less effective in cats

Inhaled toxins • Xylazine

Patients should be removed from the toxic atmosphere to • 0.4 mg/kg SC or IM in cats
a well-ventilated area and oxygen should be provided if • Sedation may be reversed with yohimbine
indicated. Animals that have inhaled caustic substances (0.25–0.5 mg/kg IM) or atipamezole
may require mechanical ventilation and aggressive sup- (0.03–0.05 mg/kg SC, IM)
portive care. • Hydrogen peroxide (3%)
• 1–2 ml/kg PO up to two times
Gastrointestinally absorbed toxins • Effective for at-home induction of emesis
Decontamination methods consist of emesis, gastric
lavage and colonic lavage. Activated charcoal and/or • Sodium carbonate (washing soda crystals)
cathartics can be used to decrease absorption of toxins. • 1 cm3 (1 teaspoon) per 20 kg body weight PO
• A relatively mild emetic, useful for at-home emesis
Emesis • Clinically it is safe so long as not repeatedly dosed
Emesis is most successful within 2 hours of toxin inges- • Acts as a mild gastric irritant
tion and rarely successful if >6 hours after ingestion. • Caution should be exercised to prevent accidental
aspiration of this product when administered by
Vomiting should continue until vomition is no longer
inexperienced individuals
productive to optimize gastric content evacuation. For
• DO NOT confuse washing soda with caustic soda, which
rapidly absorbed or small volume ingestions, and for will cause severe oropharyngeal chemical burns
exposures that occurred beyond the 4–6 hour window,
administration of activated charcoal is a more effective • Table salt
method of decontamination. Emesis is generally contra- • The administration of large amounts of oral table salt is
not a recommended method for induction of emesis due
indicated in cases of ingestion of caustics (risk of
to dangers of acute hypernatraemia and lack of
worsening oesophageal injury), hydrocarbons or other guaranteed efficacy
volatile substances (high risk of pulmonary aspiration).
It is also contraindicated in animals with obtundation, • Syrup of ipecac

pharyngeal paresis/paralysis, dysphagia or seizures due to • Syrup of ipecac is not recommended because of the
potential for arrhythmias due to cardiotoxicity if emesis
an inability to protect the airway during emesis. (See does not occur
Table 94 for commonly used emetic agents.)

Gastric lavage
Gastric lavage is used when the patient’s condition those that slow gastrointestinal (GI) motility, it may be
contraindicates emesis (e.g. profound CNS depression productive up to 6 hours postingestion. Gastric lavage is
or severe neuroexcitatory signs), but a significant volume contraindicated in cases of: ingestion of caustics and
of toxin is likely to still be present in the stomach. Gener- hydrocarbons; small-volume toxin, which could be
ally, it should be performed within 2 hours of toxin inges- decontaminated with activated charcoal; and moderate
tion; however, with large-volume toxin ingestions, or volume of toxin ingested more than 2 hours previously
502 SPECIFIC EMERGENCIES

Table 95 Procedure for gastric lavage

1 Induce anaesthesia with a short-acting intravenous agent 8 Repeat filling and emptying of stomach until the egress fluid
such as propofol or alfaxalone. The animal should be in is clear. Rotate the animal onto the other side and repeat
sternal recumbency with the head elevated and pressure lavage process until stomach contents run clear. Turn the
applied to the cricoid cartilage until it is intubated and the animal back onto the original side and lavage again.
endotracheal cuff is inflated to minimize the risk of aspiration. Stomach contents often become caught in the gastric tissue
Recheck the endotracheal cuff seal frequently during the folds and repeated turning and filling of the stomach gives
lavage process, especially when turning the animal. more effective decontamination. Gently rocking the
distended stomach by lifting it up from the ventral aspect
2 Maintain anaesthesia with gaseous anaesthetic (e.g. during egress can help swirl heavy grain-based toxins and
isoflurane, sevoflurane) or intravenous infusion of propofol improve the effectiveness of the lavage.
(0.1–0.6 mg/kg/min). These patients are high general
anaesthetic risks and require careful monitoring of respiratory 9 Allow water to exit around the tube(s) during lavage and
and cardiovascular function and anaesthetic depth. A light drain as much water from the stomach as possible at the end
plane of anaesthesia is adequate as the process is not painful. of the lavage.

3 Maintain body temperature. Unless the patient is hyper- 10 When finished, a charcoal +/– sorbitol mixture can be admin-
thermic, use lavage fluids at body temperature and minimize istered via the tube to decrease absorption of remaining
external heat loss. toxin and aid elimination. Use a small-bore stomach tube for
administration of activated charcoal. Administration of
4 Protect the airway. Any water present in the pharynx can activated charcoal under anaesthesia increases the risk of
enter the upper airway and leak past the endotracheal cuff. regurgitation and aspiration during anaesthetic recovery, but
The patient should be placed in lateral recumbency with the this is the most effective method of ensuring adsorption of
head lower than the rest of the body during lavage. any toxin that has passed into the small intestine.
Metoclopramide (0.2 mg/kg IM) can be given to increase the
5 Pre-measure a large-diameter tube (horse/foal stomach tube) lower oesophageal sphincter tone.
from the nose to the last rib and mark the tube at this length
with tape. Use the largest tube that can safely be passed. 11 Kink the gastric tube prior to removal to minimize fluid efflux
into the oesophagus.
6 Lubricate and pass the tube gently down the oesophagus to
the stomach. A single-lumen tube can be used for both 12 Suction or swab the pharynx and oesophagus prior to
ingress (pouring in warm water) and egress (draining). extubation. During recovery the animal should be monitored
Alternatively, double-lumen tubes or two smaller tubes can continuously until able to protect its airway. In dogs, keep a
be used. With double tubes, ingress and egress can occur cuffed endotracheal tube in place until the dog is conscious
continuously. The stomach should remain mildly to and can maintain sternal recumbency and lift its head, to
moderately distended to help remove toxin trapped in rugal minimize aspiration risk. Avoid delayed extubation in cats
folds. If in doubt that the tube has passed down the because of the risk of laryngospasm.
oesophagus, ideally visualize the pharynx with a laryngo-
scope or palpate the neck for the presence of the tube in the 13 If egress is not complete and the stomach remains distended,
oesophagus. the tube may be placed too far caudally and can be
obstructed by the stomach wall. Pulling the tube out of the
7 Attach a funnel onto the oral end of the tube. Using gravity mouth a small distance may re-establish egress flow.
fill the stomach with warm water until it is mildly distended
on manual palpation. (Do not connect a hose/tap directly
onto the orogastric tube, as this can result in intragastric
pressures high enough to cause gastric rupture.) Drop the
oral end of the tube below the patient and allow fluid to
siphon out. If the tube becomes blocked with gastric
contents, flush with water to clear. If this is a repeated
problem, try to place a larger tube.
 NEUROLOGICAL TOXICITIES 503

and probably no longer present in the stomach (activat- longer be present in the GI tract. It is also contra-
ed charcoal could be administered instead). A detailed indicated if the patient is judged to have a high risk of
description of gastric lavage is provided in Table 95. charcoal aspiration and the airway cannot be controlled
or the patient cannot be closely monitored postadminis-
Colonic lavage tration. Alcohols, petroleum products, strong acids or
Colonic lavage is indicated for toxins that may be alkalis, dissociable salts and metals, such as iron or
absorbed from the colon, or in patients who present lithium, are not adsorbed by activated charcoal. The rec-
with clinical signs more than 4–6 hours after ingestion ommended dosage ranges from 1 to 5 g/kg PO. This
of the toxin. It is generally considered of no benefit if initial dose may be a charcoal suspension with or without
performed within one hour of toxin ingestion except sorbitol (a cathartic) and may be combined with a small
with organophosphates and carbamates, which can amount of food, but additives may decrease the effective-
track rapidly through the GI tract secondary to the ness of the charcoal (393). In toxins with slow GI release
toxins’ effects. A narrow non-rigid lubricated tube is and absorption, and in toxins which undergo entero-
advanced from the anus to the level of the transverse hepatic recirculation, repeated dosing should be per-
colon and warm water is instilled into the colon under formed at a dose of 1–5 g/kg PO every 6–8 hours for 24
gravity flow. (Note: Avoid attaching the tube to a mains hours after exposure. With repeated dosing, the patient
water tap as this may result in excessive pressure and must be well hydrated to avoid constipation. The char-
colonic rupture.) Although this procedure may be per- coal preparation containing sorbitol should not be used
formed in obtunded animals, endotracheal intubation is for repeated dosing. Activated charcoal can be adminis-
recommended to provide a protected airway, as colonic tered by stomach tube after gastric lavage, if indicated, or
distension can stimulate emesis. syringe fed if the animal can swallow safely. Occasionally,
dogs will willingly drink the charcoal liquid. The efficacy
Activated charcoal of activated charcoal is altered by addition of mineral oils
Activated charcoal is indicated for adsorption of most or dairy products, but the effect of small amounts of dog
toxins, especially when toxin may still remain in the GI food or other additives is unknown. Activated charcoal is
tract or if toxin undergoes enterohepatic recirculation available as a suspension (with or without sorbitol as an
(i.e. excretion of toxins into bile and reabsorption via the additive) and a powdered form, which must be made into
intestines). It is contraindicated if the toxin is likely to no a suspension for administration.

a b c

 393 Activated charcoal is available with or without sorbitol as an additive (a). It may be administered directly via
dosing syringe (b) or mixed with a small amount of food if the animal will eat the food and charcoal together (c).
504 SPECIFIC EMERGENCIES

Cathartics lowed by a CRI of 4 ml/kg/hour for 4 hours. The dose

Cathartics are used to hasten bowel evacuation and may be repeated in 6–8 hours if clinical signs are still
reduce intestinal transit time, in order to minimize the present and the serum is not lipaemic. The dog in the
amount of toxin absorbed. They have no benefit in intox- case report received a second dose of 0.5 ml/kg/minute
ications when administered as sole therapy and activated for 30 minutes, 15 hours after the initial infusion. Even
charcoal should be administered as well. Carthartics are though propofol is formulated in a lipid emulsion, it is
contraindicated in cases of ingestion of caustic materials unlikely to provide a significant lipid sink without signif-
or in patients with hypovolaemia, dehydration or electro- icant systemic effects.
lyte disorders. (See Table 96 for details on the use of
cathartics.) Ion trapping
The concept of ion trapping involves purposeful acidifi-
Additional strategies to decrease toxin levels cation or alkalinization of the urine with the purpose of
Lipid infusions trapping the ionized form of the toxin in the urine and
A recent report in the veterinary literature described the encouraging excretion. The clinician is encouraged to
use of intravenous administration of a commercially assess the possible adverse effects of systemic pH modu-
available lipid solution to assist in the recovery of a lation on the patient and the severity of intoxication prior
patient with severe avermectin toxicity. The infused lipid to pursuing this route.
was postulated to act as a sink for lipophilic drugs, pre-
venting further tissue absorption as well as decreasing Haemodialysis
tissue levels. The infusions are well described in the Haemodialysis uses an artificial circuit to pass the sys-
human literature for therapy of bupivacaine overdose temic blood through either a filter or adsorbent mem-
and may have use for other lipophilic toxicants seen in brane that can act to remove certain toxicants from the
veterinary medicine. In the single veterinary case report, blood quickly and effectively. If haemodialysis is readily
20% soybean oil in water (Intralipid®) (394) was available, it may be an appropriate therapy for treating an
administered as an intravenous bolus of 2 ml/kg, fol- intoxicated animal.

Table 96 Cathartic solutions

• Sorbitol 70%
• 0.7–1.4 g/kg (1–2 ml/kg) PO once
• Repeated dosages risk severe osmotic diarrhoea and
hypernatraemia
• Can also be administered by orogastric tube following
gastric lavage
• Usually available in a solution with activated charcoal
suspension (the dose is based on the charcoal content)

• Sodium sulphate (Glauber’s salts) 40% solution

• 0.25 g/kg PO once, to a maximum of 5 g in cats and 25 g
in dogs
• Repeated dosages risk severe osmotic diarrhoea and
hypernatraemia
• Contraindicated in patients who cannot tolerate
elevations in serum sodium (e.g. those with heart or renal  394 Intravenous lipid may be administered to patients
disease)
using regular intravenous infusion pumps.
 NEUROLOGICAL TOXICITIES 505

SPECIFIC NEUROTOXINS Mechanism of action

Bromethalin leads to uncoupling of oxidative phospho-
Neurotoxins can be broadly categorized into neuro- rylation and a subsequent decrease in ATP production in
excitatory and neuroinhibitory according to the predom- the cell. Inhibition of ATP production leads to dysfunc-
inant neurological signs present (Table 97): tion of the Na+/K+ ATP-ase pump within the CNS and
• Neuroexcitatory toxins affect the CNS, causing an increase in intracellular sodium concentrations.
hyperexcitability and seizures, and/or affect the Water then moves into the cells and results in cerebral
peripheral nervous system causing muscle tremors oedema, increased volume of CSF and vacuolization of
and fasciculations. Ataxia may also occur. Possible myelin. This may result in increased ICP, axonal damage
systemic complications associated with neuro- and ultimately inhibition of neural transmission.
excitatory toxins can also include heat stroke (and The LD50 is 4.7 mg/kg in dogs and 1.5 mg/kg in cats.
subsequent complications such as DIC [395]), rhab- Standard packages contain between 15 and 45 g of 0.01%
domyolysis, aspiration pneumonia and secondary bromethalin.
neurological injury.
• Neuroinhibitory toxins either affect the CNS,
Table 97 Differential diagnosis of neuro-
causing obtundation, stupor and coma, and/or excitatory and neuroinhibitory toxins
affect the peripheral nervous system causing
NEUROEXCITATORY TOXINS Sodium monofluoroacetate
weakness or flaccid paralysis, which, at its most (1080; SMFA)
Amphetamines
severe, includes respiratory paralysis. Salicylates (overdose)
Avermectin
Bromethalin Strychnine
Neuroexcitatory toxins Tricyclic antidepressants
Brunfelsia
Bromethalin
Bufotoxins (toad toxicity) Zinc phosphide
Overview
Carbamates NEUROINHIBITORY TOXINS
Bromethalin is a rodenticide that was developed for use
Cocaine Aminoglycoside overdose
against warfarin-resistant rats and mice.
Diethyltoluamide (DEET) Amitraz
Ethylene glycol Avermectin
Ivermectin Botulism
Latrodectism (black Bromethalin
widow/red-back spider Coral snake/elapid
envenomation) envenomation
Lead Ethylene glycol
Marijuana Ivermectin
Metaldehyde Latrodectism (black
Methylxanthines widow/red-back spider
Mycotoxins (tremorgenic) envenomation)
Nicotine Macadamia nuts
Organochlorines Marijuana
Organophosphates Metronidazole
Permethrin Nicotine
Phencyclidine (PCP) Organophosphates (chronic
toxicity)
Pseudoephedrine
Tetrodotoxins
Salt (sodium chloride)
Tick paralysis
Tricylcic antidepressents
 395 This dog is suffering from disseminated intra-
vascular coagulation secondary to heat stroke. Note the Non-toxic causes should also be considered as differential
diagnoses
presence of petechiae on the skin in the inguinal region.
 506 SPECIFIC EMERGENCIES

Clinical presentation to maximize CPP. Care should be taken to avoid hyper-

Higher doses produce acute signs of hyperexcitability, thermia and hypercapnea. Bladder management, nutri-
hyperaesthesia, muscle tremors, focal or generalized tion supplementation and general nursing care should be
seizures and hyperthermia within 2–24 hours of inges- instituted in paretic patients. The use of corticosteroids
tion. Low to moderate doses produce the more common has previously been suggested for bromethalin toxicosis;
clinical presentation of hindlimb ataxia, extensor rigidity, however, there is no evidence to support this recom-
decreased conscious proprioception and paresis that can mendation and thus their use is not indicated.
progress to paralysis. CNS depression is also usually
present, with more severely affected animals becoming Prognosis
comatose. These signs may not manifest until 1–3 days The prognosis is guarded to grave due to the severity of
after exposure. In the later/terminal stages, animals may clinical signs seen at even low doses of exposure, as well as
develop seizures and a decerebrate posture. Cats may the lack of an antidote. Animals with mild clinical signs
experience a slower onset and longer duration of clinical can recover and full resolution of clinical signs may take
signs than dogs. several weeks; however, some will have permanent neu-
rological dysfunction.
Diagnosis
Antemortem diagnostics are not available. Bromethalin Brunfelsia spp.
or its metabolites can be detected in the liver, kidney and Overview
brain. Samples should be submitted frozen and protect- Brunfelsia spp. (also known as yesterday, today and
ed from light. tomorrow) (396) is related to other plants, such as
the Carolina jasmine (Gelsemium sempervirens), and
Management exposure to either causes similar clinical signs. It is found
No antidote is available. Decontamination is by induc- in coastal regions of the USA and Australia. Semi-shade
tion of emesis. Alternatively, gastric lavage should be per- conditions in rich acid soil with a generous water supply
formed to remove any bromethalin within the stomach. appear best for plant growth.
Repeated doses of activated charcoal (1–5 g/kg q6–8h)
should be administered for at least 48 hours after inges- Mechanism of action
tion to decrease absorption and reduce enterohepatic All species and all parts of the plant (flowers, leaves,
recirculation of the bromethalin and its metabolites. Use berries and seeds) are considered toxic to dogs. There are
of a cathartic (sorbitol) is recommended with the initial no reports of toxicity in cats. The toxic principle is
dose of activated charcoal. thought to be brunfelsamidine; however, multiple
Excessive muscle tremors can be controlled using biologically active compounds have been isolated. The
methocarbamol (initial dose 44–220 mg/kg IV, given in toxic component is water soluble and stable for up to
small boluses of 30–40 mg/kg until tremors have 4 months.
improved or ceased). Methocarbamol is a centrally-
acting muscle relaxant. It is stated to have a maximum Clinical presentation
24-hour dose of 330 mg/kg for cats and dogs. If injectable The GI tract and CNS are most commonly affected,
methocarbamol is unavailable, it may be administered with signs occurring within a few hours of ingestion. GI
orally or the tablets may be ground up, dissolved in water signs precede neurological signs and include vomiting,
and administered per rectum at the same doses used for hypersalivation and diarrhoea. CNS signs initially
intravenous administration. Diazepam (0.5 mg/kg IV) include agitation, nervousness or excitement, followed
can be used for seizures and mannitol (0.5–1.0 g/kg IV) by tremors, shaking, paddling and tonic–clonic seizures.
or 7% hypertonic saline (1–3 ml/kg IV) to help reduce Later signs closely resemble those of strychnine poison-
cerebral oedema. ing. Muscle rigidity in animals can result in a ‘sawhorse’
Supportive care should focus on maintaining normal stance. Symptoms may resolve within a few hours or last
cardiovascular parameters (heart rate and BP) in an effort for several days, despite therapeutic intervention.
 NEUROLOGICAL TOXICITIES 507

 396 The flowers and leaves of Brunfelsia spp. (also  397 Cane toad (Bufo marinus). (© Simon Lemin, used
called ‘yesterday, today and tomorrow’ due to its colour with permission.)
variation). (© Mary Pinké Neck, used with permission.)

Diagnosis Prognosis
Diagnosis is generally presumptive based on a history of Complete recovery may take several days or weeks.
ingestion or exposure to the plant. The presence of seeds,
seed pods or berries in the vomitus or stool can help to Bufotoxins (toad toxicity)
confirm suspicions. Overview
There are over 200 species of Bufo toads throughout the
Management world. One of the most common toads associated with
Induction of emesis or gastric lavage should be consid- intoxications around the world is Bufo marinus (cane
ered if the toxicity is recent and especially if large toad) (397). In the USA, this toad is found mainly in
amounts of seeds or berries have been ingested. Activated Florida, and it is found in the north and northeast of
charcoal is recommended every 4–6 hours after emesis Australia. This section is specific to toxicity from Bufo
for 24 hours or until resolution of clinical signs. A cathar- marinus except where otherwise specified. Toad toxicity
tic can be given with the first dose of activated charcoal, occurs most commonly during periods of high rainfall or
but should not be used in patients who already have diar- high temperatures and in the evenings when toads are
rhoea. Intravenous fluid administration for 1–2 days after active.
ingestion may be required to help promote excretion and
maintain hydration during recovery. Mechanism of action
Seizures may be treated with benzodiazepines or The severity of toxicity is determined by the dose
barbiturates, although variable success in control of received and the patient’s body size, therefore small dogs
seizures due to Brunfelsia toxicity has been noted with that mouth large toads tend to be more severely affected.
diazepam. Severely affected animals may require anaes- In endemic regions, canine intoxication is common; cats
thesia, intubation and mechanical ventilation. Metho- are rarely affected. Toxicity most commonly occurs in
carbamol may be used for muscle relaxation. Animals young small breeds of dogs, with Terriers overrepresent-
should be kept in a quiet, dimly lit area to decrease exac- ed. Some dogs will require repeated treatment secondary
erbations of nervousness or excitement. to toad-catching behaviour.
 508 SPECIFIC EMERGENCIES

Toxins are produced in large volumes in the parotoid Management

glands on the dorsum of the toad as well as in other Decontamination is performed by copious washing of
glands found throughout the skin of the toad. Dogs may the animal’s mouth to remove the secretions. Ocular
compress the parotoid glands when biting toads, thereby lavage may also be required. In the rare situation where
releasing venom into their mouth; alternatively, toads the toad has been ingested, emesis, gastric lavage or
may also squirt venom towards other animals. Venom is endoscopic removal may be required. Owners should not
tenacious and sticks to mucous membranes. Toad toxins be advised to hose their dog’s mouth as this has been asso-
are rapidly absorbed across oral mucous membranes, ciated with pulmonary aspiration of the water. Instead,
conjunctiva, gastric mucosa and open wounds. they should be advised to wipe secretions out of the
Components of toad venom include bufotenines, mouth with a wet cloth.
bufogenins (bufadienolides), bufotoxin and catechola- Intravenous fluids should be given to patients with
mines. Bufotenines have hallucinogenic effects due to significant cardiac effects, as bufogenins are excreted in
serotonin and 5-hydroxytryptophan. Bufogenins and the urine. Diazepam should be administered to control
bufotoxins have effects similar to those of digitalis (cardiac any seizures; if this is ineffective, the use of pentobarbital
glycosides) and inhibit Na+/K+ adenosine triphosphate or propofol is indicated. Phenobarbital can also be
enzymes, resulting in bradyarrhythmias and supra- administered for sedation or seizure control. Anti-
ventricular or ventricular tachyarrhythmias. Bufotoxins arrhythmic drug therapy should only be instituted if the
also have vasoconstrictive effects. Catecholamines,which arrhythmias are associated with decreased cardiac
include epinephrine, norepinephrine and dopamine, output. ECG analysis is required to decide on appropri-
cause tachycardia, hypertension and seizures. ate drug therapy, as bradycardias as well as tachycardias
Complications can include cerebral oedema second- may occur. Lidocaine, propranolol and verapamil have
ary to prolonged seizure activity, heat stroke and cardiac all been shown to decrease the incidence of ventricular
arrest. fibrillation secondary to toad toxin-induced ventricular
arrhythmias. Esmolol is another potential treatment.
Clinical presentation Propranolol may predispose to significant bradycardia in
Clinical signs occur within minutes to 1 hour after expo- anaesthetized patients.
sure. The most common clinical signs include salivation, Atropine should be avoided unless bradycardia is
brick-red mucous membranes, pawing at the mouth, associated with decreased cardiac output. Because of the
altered mentation, vomiting, extensor rigidity, nystag- potential for atropine-induced sinus tachycardia it
mus and seizures. Other signs include weakness, ataxia, should not be used to control salivation. Digoxin-
cardiac arrhythmias, muscle tremors, tachypnoea, aniso- specific Fab fragments have been used in humans suffer-
coria, mydriasis, opisthotonus and pulmonary oedema. ing significant cardiac effects secondary to ingestion or
Sinus arrhythmia and sinus tachycardia are the most inhalation of toad herbal products. Digoxin-specific
common ECG rhythms reported; however, sinus brady- Fab fragments are antibody fragments produced by
cardia and first- and second-degree heart block occur immunizing sheep with a digoxin derivative.
less commonly. Supportive care should also be instituted.
In the UK, Bufo vulgaris causes severe oral inflamma-
tion, profuse salivation, retching and vomiting for up to Prognosis
12 hours when mouthed by animals. Systemic signs have Up to 96% survival rates have been reported with appro-
only been reported in cats and take longer than 24 hours priate decontamination and supportive care. Small
to occur; these include abdominal pain, ataxia and tem- animals are more likely to be hospitalized, whereas large
porary blindness. Recovery may take up to 6 days. dogs may only require oral decontamination before dis-
charge.
Diagnosis
Diagnosis is based on confirmed contact with a toad and
appropriate clinical signs. Blood digoxin levels may be
elevated.
 NEUROLOGICAL TOXICITIES 509

Ivermectin and other macrolide parasiticides Diagnosis

Overview Diagnosis is based on a history of exposure or iatrogenic
This drug class, also known as avermectins or macro- administration of macrolide drugs. Testing for MDR1
cyclic lactones, includes ivermectin, moxidectin, sela- genotype can be carried out to assess for defective
mectin, milbemycin, doramectin, eprinomectin and p-glycoprotein in dogs who appear to have increased
abamectin. Toxicity may occur secondary to ingestion of susceptibility. These animals will probably have
large-animal deworming products or contaminated increased sensitivity to other drugs such as opioids. Some
faeces. Overdose may be iatrogenic if owners inappropri- laboratories will assay blood levels of macrolides.
ately administer topical products orally or give inappro-
priate doses of anti-parasitic medications. A high Clinical presentation
percentage of Collies and related herding breeds of dog Signs of toxicity in dogs and cats include ataxia, lethargy,
have an increased genetic susceptibility for toxicity due to tremors, mydriasis, blindness, hypersalivation, disorien-
ineffective blood–brain barrier efflux pumps. tation and seizures. This may progress to weakness,
stupor, coma and respiratory failure.
Mechanism of action
Macrolide antiparasitic drugs cause toxicity in mammals Management
by acting as agonists at the GABAA-gated chloride chan- In cases of recent ingestion, emesis may be induced as
nels in the CNS. Initially, this may result in neuroexcita- long as the animal is alert. If the animal is stuporous or
tion, but at higher doses can result in flaccid paralysis and comatose and a large amount of drug has been ingested,
coma. Collies, Border Collies, Shetland Sheepdogs, Aus- gastric lavage may be considered. Repeated doses of
tralian Shepherd Dogs and herding breeds of dogs have a activated charcoal (1–5 g/kg every 6–8 hours for 6
high incidence of a mutation in p-glycoprotein (MDR1), treatments) can be given. The use of intravenous lipid
which serves as an efflux pump for lipophilic compounds infusion may limit the duration or severity of clinical
in the CNS. This results in increased accumulation of signs.
the drug within the CNS and clinical signs of neurotoxi- Seizure control is achieved primarily using barbitu-
city at doses safe for dogs without this mutation. Occa- rate drugs such as phenobarbital. Historically, benzo-
sionally, dogs from breeds not previously reported to diazepines were thought to exacerbate clinical signs of
have increased susceptibility to avermectins may develop avermectin toxicoses due to proximity of binding sites on
signs of toxicity at low doses. the GABA receptor, and so were not recommended as
Toxicity in dogs is unlikely to occur at prophylactic first-line seizure control. It has been recently postulated
heartworm doses of ivermectin (6 mcg/kg), even in sus- that this may not be the case. If sedation or prolonged
ceptible breeds. Ivermectin toxicity in susceptible dogs anaesthesia is required, a propofol CRI is a better option
may occur at doses as low as 0.1 mg/kg, whereas non- than repeated benzodiazepine administration.
susceptible breeds may not develop toxicity until doses of Supportive care, which in severe cases may necessitate
2.5 mg/kg are exceeded. The LD50 for Beagles has been ventilatory support, should be given.
reported to be 80 mg/kg. Cats may be more sensitive to
ivermectin and 0.3–1.3 mg/kg subcutaneously may be Prognosis
enough to cause signs of toxicity. Many of these drugs The prognosis is guarded if the ivermectin dose received
have long half-lives for elimination; in dogs this ranges is >5 mg/kg. Recovery may be prolonged, especially in
from 2 days for ivermectin to 19 days for moxidectin. animals exposed to a longer-acting drug such as moxi-
Enterohepatic recirculation does occur. dectin, taking 2–3 weeks for full recovery.
 510 SPECIFIC EMERGENCIES

Lead blindness, tremors, polyneuropathy and seizures. Signs

Overview can be intermittent, with periods of normal behaviour.
Sources of lead can include lead-based paint (products Clinical signs may vary based on duration of exposure,
made prior to 1977), batteries, plumbing materials, lead amount ingested, the form of lead ingested and the age
sinkers, bullets or pellets, lead foil, lubricants (grease or of the patient (younger animals are more commonly
used motor oil), toys, golf balls or roofing materials. affected).
Owners of pets with suspected lead toxicity should be
advised to evaluate the environment, especially if small Diagnosis
children are present, as animals may manifest clinical In illness caused by chronic exposure, historical findings
signs prior to people who share the same environment. are not always reliable; however, a history of recent home
renovation and possible exposure to, or ingestion of,
Mechanism of action lead-containing paint may be relevant. The presence of
Lead binds to sulfhydryl groups and interferes with many high numbers of nucleated RBCs and basophilic stip-
sulfhydryl-containing enzymes, resulting in interference pling (especially in dogs, 398) can be found in cases of
of haem synthesis, increased RBC fragility and basophilic lead intoxication. Mild anaemia may be seen in chronic
stippling (398). Neurotoxic mechanisms are unclear, but lead poisoning, but generally is not present in acute cases.
postulated effects of lead on the CNS include interfer- Radiographs may be useful in identifying the pres-
ence with the action of GABA, capillary damage result- ence of metallic foreign objects either within the GI tract
ing in cerebral haemorrhage and neuronal necrosis, or subcutaneous tissue. Confirmation of poisoning can
competitive inhibition of calcium and interference with be made by analysis of whole blood lead levels. Samples
dopamine uptake. may be anticoagulated with heparin or EDTA; however,
contact with the laboratory should be made to determine
Clinical presentation the preferred anticoagulant, since certain methodologies
Vomiting, anorexia, abdominal pain and occasionally will be inaccurate with EDTA samples. Clinical signs
diarrhoea are the initial signs of intoxication. Other combined with blood levels that exceed 0.35 ppm or
clinical signs may include lethargy, polyuria, polydipsia, urine levels that are >0.75 ppm are consistent with acute
weight loss, pica or aggression. Neurological manifesta- intoxication.
tions include behaviour changes, ataxia, head pressing,
Management
Emesis should be induced to remove any lead product
present in the stomach. Endoscopic retrieval or surgical
removal, particularly for bullets or fragments present in
subcutaneous tissue, may be necessary. Magnesium
sulphate (250–500 mg/kg PO for dogs; 200 mg/kg PO
for cats) can be used as a cathartic and to reduce absorp-
tion by forming insoluble lead sulphate.
Chelation therapy is aimed at removing lead from the
blood and soft tissues. Succimer (meso-2,3-dimercapto-
succinic acid) (10 mg/kg PO q8h for 10 days) is
the preferred chelating agent. Succimer can be given
rectally in animals who are vomiting or in those unable to
take oral medication (i.e. seizuring or obtunded patients).
It has a wide margin of safety; however, side-effects may
include GI upset or a rebound in blood lead levels after
 398 Red blood cells in this blood smear display treatment, which may necessitate an additional 10-day
basophilic stippling characteristic of lead toxicity. course.
 NEUROLOGICAL TOXICITIES 511

Calcium EDTA (27 mg/kg SC q6h for 5 days) has Metaldehyde

commonly been used in dogs and cats to chelate lead. Overview
Injections should be diluted in saline to a final concentra- Metaldehyde is found in slug and snail baits and it is also
tion of 10 mg/ml (or less) to help reduce pain associated used as a camping fuel. Large volume ingestion of snail
with the injection. Renal tubular necrosis may result and slug pellets is common, as dogs are attracted to the
from administration of calcium EDTA and thus it should bran and molasses included in the pellet.
be avoided in patients with diminished renal function and
limited to a maximum of 5 consecutive days. It may be Mechanism of action
repeated in 2–3 weeks if blood lead concentrations Metaldehyde decreases levels of the inhibitory neuro-
remain elevated. It may also be administered slowly transmitter GABA, while increasing monoamine oxidase
intravenously (5 mg/kg/day divided q12h); however, this activity and decreasing levels of noradrenaline and sero-
should be used with caution as increases in ICP have tonin (5-hydroxytryptamine, 5-HT). Both aspects can
occurred in people with cerebral oedema after intra- have a pro-convulsive effect. The LD50 starts at 100
venous administration. mg/kg PO in dogs and 207 mg/kg PO in cats. Heat
D-penicillamine (33–55 mg/kg/day divided q6–8h) stroke and its associated complications are common in
may be used as an alternative to, or in conjunction with, metaldehyde toxicity.
calcium EDTA. Dosages up to 110 mg/kg/day have been
used; however, GI side-effects usually limit use to the Clinical presentation
lower dosage. Administration for 1 week, followed by Clinical signs develop rapidly after ingestion. Anxiety,
discontinuation for 1 week and a subsequent week of muscle tremors, muscle fasciculations, ataxia and then
therapy, has also been recommended. seizures appear in a progressive order. Tachypnoea,
Seizure activity should be treated with benzodiaze- hyperthermia and tachycardia are also often seen. Diar-
pines. Since cerebral oedema may contribute to seizures rhoea is rare unless the affected dog develops heat stroke.
in cases of severe intoxication, mannitol (0.5–1 g/kg IV Metabolic acidosis is common. Severe cases will present
given over 20 minutes) should be used in cases with in lateral recumbency, comatose and with generalized
severe or prolonged seizures. muscle rigidity.
Thiamine supplementation (1–2 mg/kg IM or 2
mg/kg PO q24h) has resulted in improvement in neuro- Diagnosis
logical signs associated with lead toxicosis in some Diagnosis is based on a history of witnessed ingestion
animals. Zinc supplementation (especially in patients or recent garden treatment with metaldehyde pellets,
receiving calcium EDTA) can help prevent chelation- combined with appropriate clinical signs. Bait may be
induced zinc deficiency. found in gastric contents, which should be frozen for
laboratory analysis if required.
Prognosis
Response to treatment is one of the best indicators of Management
prognosis, and is generally favourable for animals that Emesis should be induced for acute ingestion (≤3 hours)
undergo chelation therapy. Continuous or uncontrolled and only in those at minimal risk for aspiration (mildly
seizures may warrant a poorer prognosis and can result in affected, able to stand and walk with minimal ataxia). If
permanent neurological deficits. patients are recumbent or have severe ataxia, GA for
gastric lavage is indicated. Gastric lavage can be produc-
tive more than 3 hours after ingestion if a large volume of
bait has been consumed. Activated charcoal is effective
and should also be administered to prevent further
absorption.
512 SPECIFIC EMERGENCIES

Muscle tremors can be managed with methocar- Table 98 Estimated theobromine levels in
bamol. Generalized seizures are initially managed with chocolate products
short-acting injectable drugs such as benzodiazepines or
• Milk chocolate: 1.6–2.3 mg/gram (45–65 mg/oz)
phenobarbital, but may need prolonged therapy in the
• Semi-sweet chocolate: 5.3 mg/gram (150 mg/oz)
form of long-acting anticonvulsants or intravenous infu-
• Dark chocolate: 10.6 mg/gram (300 mg/oz)
sions of an anaesthetic such as propofol. GA using
inhalant anaesthetics has also been reported to control • Baker’s (unsweetened) chocolate: 14.1–15.8 mg/gram
(400–450 mg/oz)
intractable seizures in metaldehyde-poisoned canine
• Cocoa bean mulch: 10.6 mg/gram (300 mg/oz)
patients.
• Cocoa beans: 10.6–42.3 mg/gram (300–1,200 mg/oz)
With effective GI decontamination and limited clini-
• White chocolate: negligible content
cal signs, prolonged anaesthesia is generally not required.
If >4–6 hours of anaesthesia is required to control
seizures, then either inadequate GI decontamination or
another cause of seizures should be suspected. Support-
ive care is required for heat stroke and metabolic acido- in Table 98. The lethal toxicity for theophylline is
sis. Inadequate clearance of toxin from the stomach may reported to be 300 mg/kg PO in dogs and 700 mg/kg PO
be secondary to decreased gastric motility caused by the in cats.
metaldehyde.
Clinical presentation
Prognosis Clinical signs generally occur within 1–2 hours post
The prognosis is generally good if aggressive and rapid ingestion and initially include restlessness, hyperactivity
supportive care and GI decontamination are instituted and mild hyperreflexia. Vomiting and diarrhoea are also
early and heat stroke has not developed. Reported mor- among some of the first signs seen, especially if chocolate
tality rates for dogs with metaldehyde toxicoses range is the source. At higher doses, severe tachycardia
from 0% to 17%. The prognosis is guarded for patients (200–300 bpm), tachypnoea, polyuria, hyperactivity,
who present with temperatures >41.6oC (106.9oF) or muscle twitching and tonic to tetanic convulsive seizures
who have developed hypoglycaemia or complications are seen. Hyperthermia is also often seen. Clinical signs
associated with heat stroke, such as DIC. generally last for 12–24 hours, but can persist for up
to 72 hours.
Methylxanthines
Overview Diagnosis
This class includes caffeine, theobromine (found in A history of chocolate ingestion or of vomitus with
chocolate) and theophylline. chocolate is frequently seen and suggestive of toxicity
when accompanied by appropriate clinical signs.
Mechanism of action Stomach contents, serum, plasma or urine can be
Methylxanthines are phosphodiesterase inhibitors that analysed for methylxanthine levels. Theobromine may
cause an elevation in intracellular cyclic AMP (cAMP). be detected in serum 3–4 days after the initial ingestion.
Increased cAMP results in increased intracellular Levels are stable in plasma or serum for up to 7 days at
calcium, causing NM excitability as well as a positive room temperature and 14 days if refrigerated.
inotropic effect. Competitive inhibition of adenosine
receptors also results in CNS stimulation, as well as Management
further increases in intracellular cAMP, which may addi- Emesis should be induced in patients with known or
tionally contribute to the development of cardiac suspected exposure 2–4 hours prior to presentation.
arrhythmias. For caffeine and theobromine the LD50 is Activated charcoal every 3–4 hours may help to reduce
100–200 mg/kg. Animals ingesting 20 mg/kg may have further absorption and increase excretion. The use of
mild clinical signs and seizures may occur at 60 mg/kg. activated charcoal containing a cathartic (sorbitol) is
The theobromine content of specific sources is listed recommended for the first dose only.
 NEUROLOGICAL TOXICITIES 513

Intravenous fluid therapy can be beneficial in Mechanism of action

increasing urinary excretion of methylxanthines, as well The actual mechanism of toxicity is unknown, but is
as maintaining cardiovascular stability. Placement of a thought to be related to the inhibitory actions of glycine
urinary catheter will help to prevent reabsorption of in the CNS. It is possible that the toxin inhibits glycine
metabolites across the bladder mucosa. release or antagonizes the actions of glycine in inhibitory
Ventricular arrhythmias compromising cardiac func- neurons. There is also a possibility that some mycotoxins
tion should be treated with lidocaine in dogs. An initial result in increased pre-synaptic neurotransmitter release.
bolus of 1–2 mg/kg IV should be given, followed by an In one small study of intraperitoneal toxicity of penitrem
infusion of 30–75 mcg/kg/minute IV. In cats, a lower A in dogs, doses from 0.125 mg/kg resulted in tremors
bolus dose of 0.25–0.5 mg/kg IV and an infusion of and doses of 0.5 mg/kg to 5 mg/kg also resulted in inter-
10–20 mcg/kg/minute IV is recommended. Cats are mittent periods of seizure activity and finally death in the
susceptible to CNS toxicity secondary to lidocaine. Addi- majority of untreated dogs. Seizure length and severity
tional medications, such as procainamide (6–10 mg/kg appeared to worsen with higher doses.
IV slowly over 10–15 minutes) or calcium channel block- Both penitrem A and roquefortine are rapidly
ers (e.g. diltiazem, 0.1–0.2 mg/kg IV), may be beneficial absorbed after oral ingestion. They are excreted via bile
in cases of severe arrhythmias. Beta-blockers may be and enterohepatic recirculation may occur.
needed for persistent tachycardias; however, propranolol
reportedly delays renal excretion of methylxanthines, so Clinical presentation
esmolol may be more appropriate. Patients should be The onset of clinical signs can occur 30 minutes to
monitored carefully for hypotension and cardiac rhythm several hours postingestion. Signs include hyperaes-
while administering antiarrhythmic therapy. thesia, anxiety, restlessness, panting, vomiting, salivation,
Muscle tremors can be managed with methocar- mild to severe muscle tremors and fasciculations, seizures
bamol. Seizures generally are controlled with benzo- and SE. There is a potential for hyperthermia, heat
diazepines; however, additional use of barbiturates or stroke and rhabdomyolysis secondary to the tremors.
anaesthetics may be indicated for severe cases. Hyper-
thermic animals should be cooled appropriately. Diagnosis
Diagnosis is based on a history or suspicion of ingestion
Prognosis of mouldy food. Penitrem A or roquefortine can be iden-
The prognosis is generally good for animals that are tified in vomitus or food material via mass spectrometry,
treated early and aggressively or who have mild to mod- thin layer chromatography or quantitative analysis via
erate clinical signs. Animals that develop severe seizures high-pressure liquid chromatography. If toxin identifica-
or arrhythmias may have a more guarded prognosis. tion is unavailable, then culture of food or vomitus and
Animals that have ingested large amounts of milk choco- growth of Penicillium or other mycotoxin-producing
late may develop pancreatitis due to the high fat content fungus is compatible.
of the chocolate; it is prudent to alert owners to this
possible sequela. Management
Emesis or gastric lavage should be induced if there is
Mycotoxins (tremorgenic) recent or large volume ingestion. Activated charcoal
Overview should be administered q6h for 24 hours due to entero-
The most common tremorgenic mycotoxins are peni- hepatic recirculation of toxins. Benzodiazepines +/-
trem A (produced by Penicillium crustosum) and roque- methocarbamol can be used to control tremors and
fortine (produced by Penicillium roquefortine and other phenobarbital may also be used for tremor/seizure
Penicillium species). Other less common tremorgenic control. In severe cases, GA may be required. Supportive
mycotoxins have been reported. Mouldy foods (nuts, care should be provided as indicated.
garbage, soft cheeses) and compost may all be sources.
Penitrem A is most likely to be produced in food materi-
als that have a high moisture content.
514 SPECIFIC EMERGENCIES

Prognosis effects are seen. Seizures may be controlled with benzo-

The prognosis is generally good with appropriate diazepines or phenobarbital. In cases of hypoventilation
supportive care and effective GI decontamination. from respiratory paralysis, mechanical ventilation should
However, the prognosis is guarded if GI decontamina- be performed.
tion is incomplete in the face of a large dose of ingested Alkalinization of the stomach increases absorption,
mycotoxin. Recovery can be very rapid, but commonly therefore antacid medications such as H2-blockers and
occurs over 24–48 hours and occasionally is prolonged to proton pump inhibitors are contraindicated. The major-
up to 4–5 days. ity of ingested nicotine is eliminated within 16–20 hours.

Nicotine Prognosis
Overview The prognosis for ingestion of small amounts with mild
Sources of nicotine include tobacco products, smoking clinical signs is generally good. Larger intoxications and
cessation drugs and patches, and insecticides. increased severity of clinical signs generally warrant a
poorer prognosis.
Mechanism of action
Low doses of nicotine mimic ACh and result in stimula- Organochlorines
tion of the post synaptic nicotinic receptors. At high Overview
doses the initial stimulatory effects are followed by Organochlorines are potent pesticides that were used
blockade at the NM junction caused by persistent more frequently in the 1970s. Exposure from contami-
depolarization. Nicotine also directly stimulates the nated environments, old dump sites or stored supplies
emetic chemoreceptor trigger zone. The LD50 in dogs is are still occasionally seen.
9.2 mg/kg.
Mechanism of action
Clinical presentation The full mechanism of organochlorine toxicity is incom-
Rapid onset of hyperactivity, vomiting and salivation are pletely understood. Most organochlorines result in a
generally seen within 1 hour of ingestion. Miosis and persistent opening of sodium channels within neurons,
repeated defecation have also been reported. Bradycardia resulting in repetitive firing of action potentials and a
can result from vagal stimulation. Tremors and convul- slower repolarization. Some of the organochlorines are
sions may also be noted in the early phases of high-dose also inhibitors of GABA. Organochlorines are highly
intoxication. These may progress to depression, weak- lipid soluble. After ingestion, plasma levels peak then
ness, paralysis and death. Hypotension as a result of quickly decline as the compound redistributes into fat
vasodilation may occur. Death is primarily as a result of stores. Extensive enterohepatic recirculation can lead
respiratory paralysis. to prolonged clinical signs. The LD50 for mammals is
50 mg/kg.
Diagnosis
A detailed history, in combination with clinical signs, Clinical presentation
may reveal exposure to nicotine. It may be detectable in Initially, hypersensitivity, nervousness, agitation and
the stomach contents or urine. tremors may be seen. These signs may develop within a
few minutes after exposure or can be delayed for up to
Management 2 days. Other signs may include weakness, vomiting or
Emesis should be induced if ingestion was within 2 hours respiratory depression. Advanced signs include a spastic
of presentation. The administration of activated charcoal gait, continuous clamping of the jaws, abnormal posture
every 4–6 hours for 12–24 hours is recommended to or tonic–clonic seizures. Some animals may be depressed
prevent absorption. Intravenous fluid therapy is recom- between seizures, while others remain comatose. Seiz-
mended to help increase excretion. Atropine may be ures may last for up to 48–72 hours. Hyperthermia may
necessary in cases in which severe parasympathetic be present in patients with prolonged seizure activity.
 NEUROLOGICAL TOXICITIES 515

Diagnosis • Acute toxicity.

Organochlorines can be detected in multiple tissues, • Intermediate syndrome for which the underlying
including fat, blood, liver or brain. All tissue samples pathology has not been determined.
should be submitted in glass or metal containers (avoid • OP-induced delayed neuropathy (OPIDN), which
plastic containers). is a toxin-induced degeneration of the long motor
nerves.
Management
No antidote is available, and treatment is symptomatic Carbamates do not become permanently bound and they
and supportive. Emesis should be induced in acute inges- bind to AChE for a significantly shorter period, general-
tion. Gastric lavage can be useful if a large exposure is ly <40 minutes.
suspected. To prevent absorption, activated charcoal
should initially be given q4–6h after acute ingestion. Clinical presentation
Since pesticide residues can persist long term and Acute toxicity presents with a combination of muscarinic,
undergo extensive enterohepatic recirculation, daily nicotinic and CNS signs:
dosing of activated charcoal has been recommended for • Muscarinic clinical signs include hypersalivation,
1–2 weeks after exposure. Benzodiazepines, barbiturates lacrimation, urination, defecation, diarrhoea,
or levetiracetam can be given for seizure control. In vomiting, miosis, bradycardia, bronchospasm and
severe cases, GA may be required. Severe intoxications bronchorrhoea. Respiratory compromise may result
resulting in comatose states and respiratory depression in cyanosis. Tachycardia and mydriasis may be
may require ventilatory support. present secondary to catecholamine release.
• Nicotinic clinical signs include muscle fascicula-
Prognosis tions, muscle twitches and tremors. Weakness and
Patients with prolonged seizure activity or who remain paralysis can be a delayed NM sign.
comatose have a grave prognosis. • Central nervous system signs include anxiety, ataxia,
seizures, obtundation and coma.
Organophosphates and carbamates
Overview The intermediate syndrome develops 7–96 hours after
These toxins are commonly used in agriculture and for an acute OP toxicity. Clinical signs of severe NM weak-
domestic garden and household pest use. Additionally, ness are present, particularly affecting the cranial half of
they are used for external parasite control. Pets are gen- the body, with cervical ventroflexion, forelimb weakness
erally exposed by ingestion or dermal contact. and hypoventilation reported.
Chronic toxicity or exposure can cause OPIDN. This
Mechanism of action generally occurs 1–4 weeks after exposure to the OP.
OPs and carbamates inhibit the action of AChE, allow- Anorexia, lethargy, hindlimb paresis, hyperaesthesia and
ing ACh to accumulate at cholinergic synapses. Contin- cervical ventroflexion have been reported in cats.
ued stimulation at cholinergic synapses results in Anorexia is an early sign.
excessive stimulation of the distal neuron, gland or
muscle, causing (1) familiar cholinergic signs of mus- Diagnosis
carinic toxicity, which include salivation, lacrimation, Known contact with the toxin and appropriate clinical
urination and defecation, in addition to bronchospasm, signs are compatible with the diagnosis. Whole blood
(2) CNS toxicity (depression, decreased level of con- cholinesterase activity <25% of normal can be diagnostic.
sciousness and seizuring), and (3) nicotinic toxicity Values <50% of normal are suspicious in both acute tox-
(weakness and muscle tremors). OPs bind tightly to icity and the intermediate syndrome. Reference levels,
AChE and can become permanently bound, which is which are normally measured on heparinized whole
known as ‘ageing’ of the AChE. There are three syn- blood, are specific to the laboratory. Sample handling
dromes associated with OP toxicity: and transport should be confirmed with the laboratory.
 516 SPECIFIC EMERGENCIES

Cholinesterase activity testing can be problematic in administration of 2-PAM may worsen clinical signs,
carbamate toxicity due to the short half-life of carba- which is definitely the case with carbaryl toxicity.
mate’s binding to cholinesterase; the cholinesterase activ- Diazepam can be administered for seizures.
ity may normalize during transport. Gastric contents can
be tested for the specific toxin in acute ingestions. Intermediate syndrome
An atropine response test can be used in suspected cases Supportive care, including ventilation when required,
of acute OP or carbamate toxicity: 0.02 mg/kg atropine should be administered. 2-PAM may be useful if given
is given intravenously; if muscarinic signs resolve and before permanent ‘ageing’ of AChE occurs; however,
mydriasis and tachycardia develop, then acute OP or there have been anecdotal reports of death of cats in
carbamate toxicity is not present and no further atropine association with use of this drug.
should be administered.
Organophosphate-induced delayed neuropathy
Management OPIDN treatment involves removal of the source of the
Acute toxicity OP and supportive care. Diazepam should not be used as
If there is dermal exposure, decontamination is by an appetite stimulant in cats suffering from chronic
washing. If the exposure is oral, decontamination is by toxicity as it has occasionally been associated with the
emesis, lavage and activated charcoal. development of muscle tremors and muscarinic signs.
Atropine is the antidote for muscarinic signs; it has no The mechanism for this is unknown.
effect on nicotinic and central signs. If severe or life-
threatening muscarinic signs (cyanosis, bradycardia, Prognosis
bronchial secretions) are present, the use of atropine The prognosis for acute toxicity is good if the patient
is indicated. An initial dose of 0.02 mg/kg IV can be survives the initial toxicity. Potential complications
administered as an atropine response test if there is any include aspiration pneumonia, intussusceptions and the
uncertainty about the diagnosis. Rapid resolution of side-effects of heat stroke if severe hyperthermia devel-
muscarinic signs at this dose of atropine indicates that ops. The prognosis for the intermediate syndrome and
OP or carbamate toxicity is unlikely. Atropine doses of up OPIDN appears to be good if appropriate supportive
to 0.1–0.5 mg/kg can be administered slowly (1/4 slow care is provided, but weeks of support may be required
IV; remainder IM if required) to effect in confirmed cases for OPIDN and ventilation may be required for severe
until cyanosis, dyspnoea, salivation and bradycardia cases of intermediate syndrome.
are resolved. For carbamate toxicity lower doses are gen-
erally required because of the short half-life of carbamate Permethrin
toxicity and repeated doses of atropine are unlikely to be Overview
required. With OP toxicity, higher and repeated doses Permethrin is a lipid-soluble synthetic pyrethroid, a class
are frequently required. Atropine frequently causes gut of compound originally derived from chrysanthemum.
stasis (delaying GI transit times) and this should be taken This is a common toxicity in cats, generally resulting
into account when treating orally ingested OPs and from inappropriate topical administration of specific
carbamates with minimal muscarinic signs. ‘spot-on’ flea products or rinses by owners. Secondary
Pralidoxime (2-PAM) (10–20 mg/kg SC, IM or slow exposure may occur in cats that are in close contact with
IV up to q8h) acts to reactivate phosphorylated treated dogs or environments. Pyrethroids can also be
cholinesterase and is indicated for severe nicotinic signs found in medicated shampoos, some flea collars and
of OP toxicity. Atropine should be co-administered with environmental insecticidal treatments. Significant expo-
2-PAM. 2-PAM has anticholinesterase properties and sure in cats may also occur due to oral ingestion by
can cause clinical signs of OP toxicity if used when OP grooming behaviour. Cats have reportedly been exposed
toxicity is not present or when the OP has become per- by licking empty packets of spot-on products. Other
manently bound to AchE and can no longer be dislodged synthetic pyrethroids cause similar clinical effects.
by the 2-PAM. In carbamate toxicity there is a risk that
 NEUROLOGICAL TOXICITIES 517

Mechanism of action unlikely to result in hyperthermia or muscle damage.

Pyrethroids can slow both opening and closure of voltage Attempting to stop all muscle tremors with drug therapy
sensitive sodium channels, interfering with depolariza- may result in unnecessarily deep sedation/anaesthesia
tion of nerves and resulting in repetitive nerve discharges and respiratory depression. Methocarbamol (initial dose
or prolonged depolarization. Motor and sensory nerve 44–220 mg/kg IV, given in small boluses of 30–40 mg/kg
fibres are affected and the lipophilic character of the to a maximum of 330 mg/kg/day) should be used until
compounds encourages accumulation and persistence in tremors have improved or ceased. It is very efficacious for
neural tissues. muscle fasciculations secondary to permethrin toxicity.
Cats may have increased susceptibility due to defi- If injectable methocarbamol is unavailable, it may be
ciencies in hepatic glucuronidation, which slows initial administered orally or the tablets may be ground up,
detoxification of these compounds. The minimal toxic dissolved in water and administered per rectum at the
dose is unknown; toxicity in cats has been seen even with same doses used for intravenous administration.
exposure to small amounts. Hypothermia may exacer- Both benzodiazepines and phenobarbital may be used
bate the clinical effects of permethrin. to attenuate clinical signs of tremors or seizures in com-
bination with or instead of methocarbamol. Diazepam
Clinical presentation may be administered initially as IV bolus doses of
Almost all exposed cats will become symptomatic and the 0.25–0.5 mg/kg and it may also be administered as a
majority of these will display muscle tremors. Common CRI of 0.2–0.5 mg/kg/hour. Phenobarbital should be
clinical signs include muscle fasciculations, ear twitching, administered in small doses of 2–4 mg/kg IV or IM as
paw flicking, tremors, ataxia, seizures, hyperthermia and necessary, not to exceed 16 mg/kg/day. If necessary,
mydriasis. Effects on sensory nerves can result in hyper- propofol or alfaxalone CRI or gaseous anaesthesia may
aesthesia and hypersalivation (which may also be seen be used to anaesthetize the patient. NM blocking agents
after oral exposure). Clinical signs develop within 3 to are not indicated.
72 hours postexposure. Recovery takes from 2–3 days on Intravenous fluid therapy should be given to main-
average, but up to 5–7 days has been reported. tain hydration if the animal is unable to drink. More
aggressive fluid rates may be indicated in the pres-
Diagnosis ence of myoglobinuria to minimize the possibility of
Classic clinical signs are suggestive and owners should myoglobinuria-induced nephropathy. Measurement of
be questioned about exposure to flea treatments (either blood electrolytes will help to guide additional fluid
directly on the cat or on other animals in the household). therapy and choices (see Chapter 31).
The highly lipophilic nature of pyrethroids suggests
Management that intravenous lipid administration may be an effective
For dermal exposures, the pet should be washed with therapy to decrease the severity and duration of clinical
warm water and washing-up liquid. Activated charcoal signs.
(to prevent absorption) is only indicated in confirmed
oral exposures, as permethrin undergoes minimal Prognosis
enterohepatic recirculation (although other pyrethroids The prognosis is good unless clinical signs have been
may be more extensively recirculated). Hypothermia, present for a prolonged period prior to the institution of
especially after bathing, must be prevented as it may appropriate treatment; intensive supportive care may
exacerbate clinical signs by enhancing intracellular be necessary. Treatment delays or the presence of gener-
sodium movement. alized seizures is associated with a worse prognosis
The aim of drug therapy is to stop all seizure activity and increases the likelihood of death. Death has been
and decrease muscle tremors and fasciculations to a level reported to occur in 5–37% of cases.
 518 SPECIFIC EMERGENCIES

Salt toxicity (paintballs, play dough) Chapters 2 and 27). Rapid reduction in serum sodium
Overview levels can result in cerebral oedema and exacerbation of
Sources of excess sodium include table salt (especially neurological signs if toxicity is chronic. The deficit of
when used as an emetic), home-made play dough, paint- free water is calculated as:
balls, seawater and iatrogenic sources such as hypertonic
saline solutions and sodium phosphate enemas. Free water deficit (l) = 0.6 × body weight (kg)
× (patient’s Na/normal Na –1).
Mechanism of action
An increase in serum sodium creates an increase in The deficit should be replaced over the number of hours
plasma osmolality. Water shifts from the interstitium to calculated to maintain a safe and slow decrease in sodium
the vasculature, as well as from the intracellular fluid plasma levels, not to exceed 8–12 mmol/l (mEq/l) in a
(ICF) to the ECF to maintain equilibrium. The ECF 24-hour period. 5% Dextrose in water is the fluid of
expands to a state of hypervolaemia, and dehydration of choice for replacement of free water. Intravenous admin-
the cells results. istration of 5% dextrose at up to 3.7 ml/kg/hour, in addi-
The lethal dose of sodium chloride is reported to tion to regular isotonic maintenance fluids, should
be 4 g/kg PO, with clinical signs noted at dosages of decrease serum sodium by approximately 1 mmol/l/hour
approximately 1.9 g/kg PO. The level of resulting (mEq/l/hour). Serum sodium and other electrolytes
hypernatraemia seems to be a more accurate way of pre- should be monitored at least every 4 hours and adjust-
dicting clinical signs than the amount of sodium chloride ments to fluid therapy made as needed. Combination with
ingested, with one study reporting seizures in all animals other isotonic fluids (lactated Ringer’s solution, Nor-
with serum sodium levels greater than 180 mmol/l mosol-R) is usually needed to prevent the sodium from
(180 mEq/l). dropping too quickly. If the neurological signs worsen, or
sodium levels drop too quickly, free water supplementa-
Clinical presentation tion should be temporarily discontinued and mannitol
Sodium chloride is a gastric irritant and ingestion of large administered (0.5–1 g/kg IV) to treat cerebral oedema.
amounts can lead to acute gastroenteritis and dehydra- Increasing serum sodium concentrations can indicate
tion. Immediate clinical signs may include vomiting, inadequate decontamination. Repeat gastric lavage, or
polydipsia and polyuria. Ataxia, tremors, hyperthermia, even surgical removal in extreme cases, has been recom-
seizures and death may be seen as a result of ICF shifts. mended to remove ongoing sources of sodium. A loop
diuretic (furosemide, 1–2 mg/kg IV) can be used to
Diagnosis promote sodium excretion; however, it is important not
A history of ingestion of sodium chloride-containing to decrease sodium levels too quickly if this therapy
products and acute increases in serum sodium are is instituted.
strongly supportive. Frequent access to small amounts of water may
be sufficient to lower serum sodium levels in patients
Management showing no clinical signs and only mild elevations in
For recent exposure, induction of emesis is recom- serum sodium concentration. Animals should not be
mended. Activated charcoal is likely to be of little benefit allowed unlimited access to water at the risk of decreas-
and is not recommended. ing sodium too quickly.
Decreases in serum sodium must be monitored fre- Symptomatic and supportive care should be given as
quently and should not exceed 0.5–1.0 mmol/l/hour indicated.
(mEq/l/hour). Acute elevations in serum sodium (i.e.
within 2–4 hours) may be reduced more quickly than in Prognosis
animals with chronically elevated sodium, as the neurons The prognosis depends on the underlying cause, as well
have not had time to adjust osmolality. In the absence of as the degree of hypernatraemia and associated clinical
a known time of ingestion, all hypernatraemic animals signs. Most animals treated appropriately with slow
should be assumed to have chronic hypernatraemia (see decreases in serum sodium will fully recover.
 NEUROLOGICAL TOXICITIES 519

Sodium monofluoroacetate (1080) of exposure. Analysis of gastric contents can confirm

Overview exposure. Contents should be kept frozen until analysed
Sodium monofluroacetate is also known as fluoroacetate, to prevent bacterial breakdown of the toxin.
sodium fluoroacetate and SMFA. It is used for rodent,
rabbit and carnivore pest control. Its use is restricted to Management
authorized users in many countries; however, accidental Emesis should be induced and activated charcoal given if
poisonings do occur in baiting areas. Secondary poison- clinical signs have not yet developed. Patients who are
ing occasionally occurs from ingestion of regurgitated already showing clinical signs should be anaesthetized
baits or carcasses of baited animals. and gastric and colonic lavage performed. Activated
charcoal may be subsequently administered per os or via
Mechanism of action an orogastric tube and is an effective adsorbent for 1080.
Fluoroacetate is converted to fluorocitrate and blocks the To control seizures, patients should be kept anaes-
tricarboxylic acid or Kreb’s cycle. This impairs cellular thetized; pentobarbital or propofol CRI is often recom-
respiration and energy metabolism, resulting in a lactic mended for the prolonged anaesthesia required. Ten to
acidosis. The accumulation of citrate can bind serum 48 hours of anaesthesia may be required until the patient
calcium, resulting in low ionized calcium levels. The is no longer showing clinical signs. Recovery from intra-
main organ systems affected are the GI, neurological and venous anaesthesia with pentobarbital may be confused
cardiovascular systems. The toxin is rapidly absorbed with seizure activity, and it may be prudent to first wean
from the GI and respiratory tracts and may also be the patient onto a shorter-acting anaesthetic, such as
absorbed from mucous membranes and skin abrasions. propofol, prior to attempting anaesthetic recovery.
Heat stroke could result in multiorgan failure and DIC in One antidote treatment method, with a reported 83%
patients that survive the initial toxicity. The reported success rate (5 of 6 dogs), is to administer 300 mg/kg of
LD50 is 0.05–0.1 mg/kg in dogs and 0.2 mg/kg in cats. sodium bicarbonate IV (3.6 mmol/kg or 3.6 ml/kg of the
8.4% solution). Half is given as an intravenous bolus and
Clinical presentation the remainder over 20 minutes with intravenous fluids.
Clinical signs generally occur 30 minutes to 2 hours post This may result in the development of hypernatraemia. It
ingestion, although longer periods have been reported. is important, during this treatment, to monitor ventila-
Early signs include GI hypermotility (manifested by tion to avoid elevations in dissolved CO2 levels.
vomiting and diarrhoea), tenesmus, salivation, urination, Another antidote is acetamide; 15 g acetamide gran-
anxiety and hyperaesthesia. Subsequent signs include ules are dissolved in 1 litre of warmed 5% dextrose (con-
muscle tremors, barking, howling or screaming, running sider the need for sterilization and infusion through a
fits and then generalized seizures (which can be inter- filter if made up from a chemical grade). The initial
spersed with running fits) and eventually coma and dosage is 10 ml/kg IV over 15 minutes, followed by an IV
death. Cardiac arrhythmias can occur due to cellular infusion at 8 ml/kg/hour until resolution of clinical signs.
anoxia and hypocalcaemia. Hyperthermia may occur sec- Hyponatraemia may develop during this therapy second-
ondary to exertion, although hypothermia may occur in ary to the large volumes of free water administered, and
cats. Hypoxia and aspiration pneumonia may also be seen electrolytes should be closely monitored.
in exposed animals. In untreated cases death generally Calcium gluconate (5–15 mg/kg slow IV) should be
occurs within 2–12 hours from the onset of clinical signs. administered as necessary if ionized hypocalcaemia
develops. It is prudent to monitor for bradycardia (by
Diagnosis ECG) during administration.
Diagnosis is based on the history of ingestion or exposure In addition, supportive care should be instituted.
to an area that was recently (within 6 weeks) baited with
1080. Although 1080 is water soluble and broken down Prognosis
by many soil bacteria, dry, arid conditions may delay this The prognosis is guarded once seizures have developed.
breakdown and redistribution. Ionized hypocalcaemia The mortality rate in dogs has been estimated to be close
combined with appropriate clinical signs is suggestive to 75%, but early aggressive therapy may improve this.
 520 SPECIFIC EMERGENCIES

Strychnine severe clinical signs may require anaesthesia with CRI of

Overview propofol or pentobarbital.
Strychnine is used as a pesticide for small mammals. Mechanical ventilation and associated supportive care
Restricted access in many countries has decreased the may be required during treatment if deep anaesthesia or
incidence of unintended toxicity in companion animals. use of multiple muscle relaxants and sedatives is required
for patients with severe clinical signs.
Mechanism of action
Strychnine blocks the effects of the inhibitory neuro- Prognosis
transmitter glycine in the spinal cord and prevents the The prognosis is fair to guarded. If muscle spasms and
release of glycine from Renshaw cells. This loss of inhi- tetany can be controlled with drug therapy, and support-
bition leads to exaggerated neurological stimulation of ive care and mechanical ventilation can be provided, the
muscle and severe muscular spasms. Reported LD50 prognosis may be improved.
doses are 0.5–1.2 mg/kg in dogs and 2 mg/kg in cats.
Neuroinhibitory toxins
Clinical presentation Latrodectism (spider envenomation)
There is a rapid onset of clinical signs within 10–120 Overview
minutes after ingestion. Anxiety, tremors, muscular The Latrodectus genus of spiders is found throughout the
rigidity, muscular spasms, ‘saw horse stance’ of extensor world. The American black widow spider (L. mactans)
rigidity and opisthotonus, and contracture of facial (399) and the Australian red-back spider (L. hasselti) are
muscles may result in a ‘sardonic grin’ similar to that of the most notorious species. Females are significantly
patients with tetanus. Muscle spasms affect the respira- larger than males and responsible for envenomation.
tory muscles and diaphragm and death can occur from Female black widow spiders are easily recognized by the
secondary hypoventilation, hypoxia or heat stroke. red or orange ‘hourglass’ present on the ventral or dorsal
aspect of a shiny, dark abdomen and they can grow up to
Diagnosis 2.5 cm long. Males are 20 times smaller than females and
Baits may be specifically coloured in some countries and are unable to bite due to their small jaws. The red-back
recognizable during gastric decontamination, or the spider grows up to 1 cm in length and is black in colour
history may be strongly suggestive. A definitive diagnosis with a red or orange stripe running from the dorsum to
generally requires analysis of gastric contents or tissue the ventral abdomen.
samples for the presence of strychnine or its metabolites. The venom and clinical signs of envenomation are
very similar for all Latrodectus species.
Management
Emesis can be instituted if the animal has not yet devel- Mechanism of action
oped any clinical signs of toxicity. It is contraindicated The portion of the venom responsible for neurotoxic
once clinical signs are present, due to the risk of inducing effects in dogs and cats is alpha-latrotoxin, which induces
a generalized muscle spasm during the act of vomition, neurotransmitter release from nerve terminals. The net
which could result in aspiration of stomach contents. effect is a massive release of ACh, norepinephrine, dopa-
Patients showing clinical signs are best anaesthetized for mine, glutamate and enkephalins. At the pre-synaptic
gastric lavage and administration of activated charcoal, membrane, the toxin also irreversibly binds with the lipid
which is an effective adsorbent for strychnine. bilayer of the cell membrane. This results in a cation
To control seizures and muscle activity, patients selective channel and interferes with endocytosis of
should be kept under sedation or anaesthesia for 24–72 vesicle membranes. The LD50 of the black widow venom
hours until clinical signs resolve. For patients showing is 1.39 mg/kg, and a single bite can produce a fatal dose in
only mild clinical signs, benzodiazepines or pheno- companion animals. Studies show that the venom is
barbital may be control muscle spasms. For patients with capable of destroying local motor nerve terminals within
moderate signs, methocarbamol may be used alone or as 24 hours, with re-innervation and complete recovery
well as benzodiazepines and phenobarbital. Patients with occurring over the following 2–8 days.
 NEUROLOGICAL TOXICITIES 521

Diagnosis
There are no confirmatory diagnostic tests for black
widow or red-back spider envenomation. Historical
information regarding noting the presence of these
spiders in the environment can be supportive. Puncture
wounds are often difficult to find due to the hair coat,
small size and lack of a local tissue reaction. Diagnosis is
usually dependent on onset of systemic clinical signs.

Management
Antivenom for black widow spider bites is available and
provides the quickest relief of clinical signs (usually
within 30 minutes of infusion). Severe pain is appropriate
justification for the use of antivenom. Black widow
antivenom should be diluted (in up to 100 ml of saline
depending on patient size) and given IV over 30 minutes
to 1 hour. Close monitoring for anaphylactoid reactions
is imperative during infusion. Patients who develop a
fever, tachycardia, hyperaemia or other signs of a reac-
 399 A female black widow spider tion should have the antivenom temporarily stopped.
(Latrodectus mactans) showing the classic Treatment with diphenhydramine (2–4 mg/kg SC) and
hourglass marking. (© Steve Ryan, used with resuming the infusion at a slower rate will usually allow
permission.) for complete infusion of the antivenom.
Red-back spider antivenom is recommended for
intramuscular administration, though intravenous
administration is used in severe cases in humans. The
rate of adverse reactions is rare in humans, with an
Clinical presentation incidence of 0.5–0.8%.
Clinical signs are generally seen within 8 hours of One vial is the recommended dose to treat intoxica-
envenomation. In humans pain is the most significant tion by either spider; however, a second vial can be given
clinical sign and without antivenom has been reported to if clinical signs recur. Black widow antivenom is supplied
last from days to months. as a 2.5 ml vial (Merck) and red-back antivenom is sup-
In dogs regional numbness, progressive muscle pain plied as a 500 U vial (1.0–1.5 ml) (CSL Ltd).
and fasciculations or cramping may be seen. Abdominal Red-back spider antivenom is effective even with
rigidity is also common. Restlessness is common due to delayed treatment and it is recommended for use up to
the painful nature of the signs. Systemic signs can 2 weeks postbite if clinical signs are still severe. Alterna-
progress to hypertension, tachycardia, seizures and tively, supportive and symptomatic care to relieve clinical
paralysis. Vomiting and diarrhoea may also occur. signs should be performed.
Cats are more sensitive to spider venom and paralytic Administration of 10% calcium gluconate (1–3 ml/kg
signs are often noted early after the bite. Hyperexcita- slowly IV at 4–6 hour intervals) may help control muscle
bility, pain, vocalization, excessive salivation, and rest- cramping and fasciculations. If calcium infusion fails to
lessness are common. Vomiting and diarrhoea, muscle maintain the patient for more than 1.5 hours, additional
tremors, muscle fasciculations, cramping, ataxia and infusions are likely to be ineffective. Careful monitoring
eventual flaccid muscle paralysis occur. Death is common of heart rate and rhythm should be performed while
in cats, with one study citing a 91% mortality rate. administering calcium.
Approximately 15% of bites are ‘dry bites’, in which
no venom is injected.
 522 SPECIFIC EMERGENCIES

Pain medication (often opioids) is recommended to Diagnosis

control the pain associated with envenomation and There are no confirmatory tests available. Classic clinical
muscle cramping. Benzodiazepines are recommended signs are suggestive and questioning owners on potential
and are often more successful at relieving muscle cramps exposure will generally elucidate the cause.
and discomfort than are muscle relaxants (such as metho-
carbamol). BP should be monitored frequently, as Management
patients are at risk of developing severe hypertension. Decontamination via emesis may be indicated in known,
There is a risk of respiratory depression from the venom recent ingestion (within 2–4 hours). In general this is not
and ventilatory support should be instituted in patients indicated in patients who have already developed clinical
who are unable to ventilate adequately. Hospitalization signs. Supportive and symptomatic care should be insti-
and monitoring are recommended for a minimum of tuted. Intravenous fluid therapy and anti-emetics may be
48 hours. considered in vomiting dogs. Intravenous fluid therapy
Red-back spider antivenom has been shown to be and cooling measures should also be instituted in patients
effective for bites of the black widow spider and case whose temperature is >40oC (>104oF).
studies and in-vitro studies show Latrodectus antivenoms Methocarbamol may be used to control muscle
have the ability to neutralize venoms of different tremors and prevent further hyperthermia.
Latrodectus species.
Prognosis
Prognosis The prognosis is generally excellent, with most dogs
The prognosis for black widow envenomation is making a full recovery within 48 hours.
guarded. Clinical signs may persist for 3–7 days and
complete recovery in severe cases may take weeks. The Metronidazole
prognosis for red-back spider envenomation is fair to Overview
good if antivenom is administered. Metronidazole is commonly used to treat bacterial and
protozoal infections in small animals.
Macadamia nuts
Overview Mechanism of action
Macadamia nuts are cultivated in the USA (especially The exact mechanism for metronidazole’s neurotoxic
Hawaii) and Australia. They may be found in cookies effects is unknown; proposed mechanisms include inhi-
(biscuits), candies (sweets) or nut mixes. bition of neuronal protein synthesis by binding to RNA
and thiamine antagonism. Studies in dogs with metro-
Mechanism of action nidazole toxicity revealed axonal swelling and degenera-
The toxic mechanism is unknown and has been limited tion in vestibular nuclei, as well as leucomalacia of
to reports only in dogs. the brainstem. The toxic dose is generally stated as
>60 mg/kg/day; however, lower dosages have been
Clinical presentation reported to cause neurotoxicity even after just a few days
Clinical signs usually develop within 12–24 hours of of administration.
ingestion and most commonly involve hindlimb weak-
ness, stiffness or paresis and muscle tremors. Vomiting, Clinical presentation
hyperthermia and depression may also be seen. Clinical Ataxia and vestibular signs (mostly bilateral), tremors,
signs have been seen in dogs ingesting as little as 0.7 g/kg peripheral neuropathies and seizures are common mani-
of raw or roasted nuts and as much as 62.4 g/kg. festations of metronidazole toxicity. Vomiting, anorexia,
stomatitis and glossitis may also be noted.
 NEUROLOGICAL TOXICITIES 523

Diagnosis a
A history of administration of metronidazole with
consistent clinical signs provides supportive evidence of
toxicosis. Discontinuation of therapy followed by resolu-
tion of clinical signs is also supportive.

Management b
Discontinuation of metronidazole and supportive care
are generally all that is necessary for treatment. Diaze-
pam has been reported in dogs to hasten the recovery
response times. Treatment with an initial dose of 0.2–0.5
mg/kg IV followed by 0.3–0.5 mg/kg PO q8h for 3 days
can be considered in severely affected animals in an effort
to promote resolution of clinical signs. Treatment with
diazepam is not recommended in cats.

Prognosis c
Metronidazole intoxication generally has an excellent
prognosis, with most animals recovering completely
within 14 days. Animals with severe CNS signs may take
months to recover; however, this is very rare.

Snake bite envenomation

Overview
This section concentrates on Australian elapid enveno-
mations; however, North American coral snake enveno-
mation is also discussed. d
In Australia, identification of specific snake species by
members of the public is frequently inaccurate. Accurate
choice of antivenom is determined by knowledge of local
snakes, snake identification using a scale key or the most
appropriate choice of antivenom determined by use of
the Australian CSL Snake Venom Detection Kit. There
are at least 25 terrestrial species of snake within Australia
whose bite may require treatment with antivenom. The
most significant genera responsible for envenomation
include tiger snakes (Notechis) (400b), brown snakes
(Pseudonaja), black snakes (Pseudechis) (400c), copper-
heads (Austrelaps), death adders (Acanthophis) (400d) and
taipans (Oxyuranus).
Clinically significant North American coral snakes  400 Venomous snakes. (a) An American coral snake
include subspecies of the Micrurus genus, including the (M. fulvius fulvius). (© Justin Oguni, with permission.)
Eastern coral snake (M. fulvius fulvius) (400a), the South (b) A mainland tiger snake (Notechis scutatus). (c) A mulga
Florida coral snake (M. fulvius barbouri) and the Texas snake (Pseudechis australis), also known as the ‘king brown’
coral snake (M. fulvius tenere). These snakes have red, snake, though actually a member of the black snake family.
yellow and black bands and the red bands contact the (d) A common death adder (Acanthophis antarcticus).
yellow bands. (b, c and d © Brian Bush, with permission.)
 524 SPECIFIC EMERGENCIES

The basic principles of treatment of elapid enveno- Venom absorption occurs via the lymphatics and
mation are the same regardless of the snake species muscular activity can hasten the clinical signs of enveno-
involved. Antivenom, if available, should be administered mation.
if the patient develops clinical signs of envenomation.
The venom of elapid snakes is composed of multiple Clinical presentation
different toxins; however, all elapids have neurotoxicity Australia
(paralysis) as a common clinical sign. In general, it is rare Clinical signs vary according to the snake species:
to find the bite site in animals because of the snake’s small • Tiger snakes: paralysis, coagulopathy, rhabdo-
fangs and minimal local tissue damage associated with myolysis, mild haemolysis.
bites by these species in comparison with pit vipers • Brown snakes: paralysis and coagulopathy.
(rattlesnakes). In Australia, snake bites occur during • Death adders: paralysis.
the warmer months of the year and are rare in winter. • Black snakes and copperheads: haemolysis, rhabdo-
Specific antivenom is required for envenomation by indi- myolysis, paralysis (occasionally mild weakness
vidual snake species and an incorrect choice of antivenom only), bite site swelling +/- coagulopathy.
will not be efficacious. • Taipans: paralysis, rhabdomyolysis, coagulopathy.

Mechanism of action Lack of coagulopathy does not rule out envenomation by

Toxins from Australian venomous snakes have the fol- any of these species.
lowing effects:
• Neurotoxins. These cause neuromuscular paralysis Preparalytic signs
either presynaptically by preventing ACh release or Salivation, vomiting, dyspnoea, acute collapse, inappro-
postsynaptically by binding to AchRs. Eventually, priate urination or defecation may occur first. These
death occurs due to respiratory paralysis. temporary signs generally occur within 15 minutes of the
Presynaptic neurotoxins cause structural changes to snake bite, before being followed by a period of recovery.
the nerve terminal, which with time becomes unre- Dogs that develop preparalytic signs after a bite by a
sponsive to antivenom. highly venomous Australian snake generally go on to
• Procoagulants. These cause diffuse activation of develop life-threatening signs of envenomation. Anti-
coagulation, resulting in widespread thrombus venom should be administered to animals that have a
formation, which generally resolves by fibrinolysis. history of preparalytic signs post snake bite.
Clinically, a severe coagulopathy secondary to
consumption of clotting factors is seen; this affects Lower motor neuron paralysis
both intrinsic and extrinsic coagulation pathways. LMN signs commonly start with weakness of the palpe-
Coagulopathy is unresponsive to fresh frozen bral and gag reflexes and progress to weakness and ataxia
plasma until procoagulants have been effectively in the hindlimbs, then the forelimbs and finally the respi-
neutralized with antivenom. ratory muscles. Dyspnoea secondary to saliva pooling in
• Anticoagulants. Have a heparin-like effect and the paralysed pharynx is common, as is laryngeal paraly-
cause mild prolongations in aPTT without sis, and can occur before generalized paralysis develops.
development of clinical bleeding. Onset can be rapid, with some animals requiring intuba-
• Haemolysins. Damage red cell membranes, causing tion and ventilation within 30 minutes of being bitten;
intravascular haemolysis. however, in some animal reports, the development of
• Myotoxins. Damage striated skeletal muscle, NM paralysis may be delayed by up to 24 hours. Aspira-
resulting in diffuse rhabdomyolysis. tion pneumonia may occur as a sequela of pharyngeal and
laryngeal paralysis. Pupillary dilation and loss of PLR
North American coral snake venom contains several occur as later signs.
neurotoxins that cause postsynaptic blockade at the NM
junction.
 NEUROLOGICAL TOXICITIES 525

Coagulopathy Diagnosis
Prolongations in PT, aPTT and ACT can occur. In Bite sites are infrequently found due to the snake’s
humans, thrombocytopenia is also reported. Clinical small fangs, the lack of swelling and the animal’s hair
coagulopathies with overt bleeding are uncommon coat. Appropriate clinical signs of envenomation and
except in brown snake bites. However, patients may recent known contact with a snake, or a history of snakes
develop severe bleeding in any area of the body associ- in the animal’s environment, are highly suggestive of
ated with venipuncture (avoid jugular venipuncture and envenomation.
use peripheral veins when possible). Haematemesis and
haemorrhagic diarrhoea occasionally occur, as well as Management
haematuria, epistaxis and hyphaema. Spinal cord com- First-aid advice to owners is to keep animals quiet and
pression secondary to epidural haematoma has also been rested to slow the onset of clinical signs. Immediate
reported. transport to a veterinary hospital is indicated even if the
animal appears asymptomatic. Onset of respiratory
Rhabdomyolysis paralysis can be extremely rapid in severe envenoma-
Myoglobinuria may be severe and can result in acute tions. Owners should be advised to position paralysed
renal failure. Additionally, if insufficient antivenom is animals so as to maintain an open airway and with the
administered, there can be significant damage to skeletal head lowered to enable drainage of saliva. If cyanosis and
muscle. Megaoesophagus may occur in dogs, with recov- respiratory arrest develop, owner-administered mouth-
ery times of up to 5 weeks reported. CK levels may to-nose breathing may maintain life during transport.
increase to 10,000–1,000,000 U/l. If bites occur on a distal limb, a crepe pressure
bandage applied to the whole limb can significantly slow
Haemolysis the onset of clinical signs. Most animals are bitten on the
Red cell lysis results in haemoglobinuria. Clinically sig- head, neck or thorax, and these sites are not suitable for
nificant anaemia generally only occurs with black snake pressure bandage application.
bites; however, the presence of haemolysis can be used as On arrival at the veterinary hospital, animals must
an indication of envenomation. never be left unattended due to the occasional rapid onset
of paralysis and respiratory arrest. The bite site should
Acute renal failure not be washed, as it may help in identification of the
Acute renal failure may occur secondary to myoglobin- appropriate antivenom to administer. Bite site infection
uria, haemoglobinuria or ischaemia. is extremely uncommon. Intravenous catheterization
should be performed immediately. Blood is collected for
North America coagulation testing from the catheter where possible.
Coral snake envenomation results in generalized LMN Alternatively, a compression bandage should be applied
paralysis. The onset may be rapid or delayed up to at sites of blood collection. Animals should be strictly
18 hours. The neurological signs are the same as for confined and rested until recovered. Two weeks’ rest is
Australian snakes (see above). In dogs, haemolytic recommended after discharge.
anaemia, haemoglobinuria and elevations in CK also In Australia, a history of preparalytic signs provides an
occur. indication for antivenom administration even if there is
no other clinical evidence of envenomation. The appro-
priate antivenom in Australia can be determined by visual
identification of the snake using scale keys or by an expe-
rienced herpetologist. The Australian CSL Snake
Venom Detection Kit can be used on the bite site, urine
or blood. (Note: A positive response to this kit alone does
not indicate antivenom is required. The animal must also
have clinical signs of envenomation.) Knowledge of local
snake species can also help guide antivenom choices.
526 SPECIFIC EMERGENCIES

A neurological examination should be performed, taken to confirm the envenomating snake species if this
recorded and repeated hourly in asymptomatic animals. has not already occurred.
The development of any signs of weakness or paralysis is The correct antivenom is required for the specific
an indication for antivenom. Coagulation testing (PT snake species involved. The following is a list of snake
and aPTT or ACT) should be performed and repeated species venom treated by specific antivenoms:
every 2–6 hours. The development of a coagulopathy is • Tiger snake antivenom is used for the common
an indication for antivenom. Coagulopathies normally tiger snake (Notechis scutatus), black tiger snake
take at least 6 hours to start to improve after antivenom. (Notechis ater), common copperhead (Austrelaps
CK should be measured and repeated every 6 hours. Sig- superbus), highland copperhead (A.ramsayi), pygmy
nificant elevations of >1,000 U/l are an indication for copperhead (A.labialis), rough-scaled snake
antivenom. Myoglobinuria should start to clear after suf- (Tropidechis carinatus), broad-headed snake
ficient antivenom has been administered. (Hoplocephalus bungaroides), Stephens’ banded snake
Urine should be collected to check for casts, glucose, (Hoplocephalus stephansii), red-bellied black snake
haemoglobin/myoglobin and red cells. The presence of (Pseudechis porphyriacus) and the spotted black snake
casts or glucose (in a normoglycaemic patient) is an indi- (Pseudechis guttatus). It may also be suitable for
cation of renal damage and monitoring or treatment for North American coral snake envenomation.
acute renal failure may be required. The presence of • Brown snake antivenom is used for all members of
myoglobinuria/haemoglobinuria may be an indication of the brown snake family (Pseudonaja) including the
envenomation. Patients with dark red or brown/black eastern brown snake (P. textilis), western brown
urine should be closely monitored for the development snake (P. nuchalis), dugite (P. affinis), peninsula
of acute renal failure and treated aggressively if oliguria brown snake (P. inframacula), spotted brown snake
or anuria develops. (P. gutta) and Ingram’s brown snake (P. ingrami).
Patients that develop clinical signs should be placed • Black snake antivenom is used for only a few
on intravenous fluids at 2–3× maintenance to minimize members of the black snake family including the
the development of acute renal failure secondary to myo- mulga, also known as the king brown snake
globinuria or haemoglobinuria. Fluid diuresis should be (Pseudechis australis), Collett’s snake (P. colletii), and
instituted as snake venom toxins are excreted in the urine. Butler’s mulga snake (P. butleri). Some members of
Mannitol should be administered if oliguria or anuria the black snake genus (e.g. the red-bellied black
develops in well hydrated patients. Antivenom-induced snake) can be treated adequately by tiger snake
anaphylaxis may also require aggressive fluid therapy. antivenom.
Animals that present with or develop dyspnoea may • Death adder antivenom is used to treat envenoma-
require intubation, using anaesthesia as required. Mech- tions by the common death adder (Acanthophis
anical ventilation should be used in patients with elevat- antarcticus), northern death adder (A. praelongus),
ed P’ETCO2 or minimal respiratory excursions. Other desert death adder (A. pyrrhus), pilbara death adder
causes of dyspnoea, such as overhydration in the face of (A. wellsii) and the bardick (Echiopsis curta).
renal failure, should be ruled out. Shock may develop • Taipan antivenom is used to treat the common
secondary to hypoxia. taipan (Oxyuranus scutellatus) and the inland taipan
Antivenom is dosed according to the amount of (O. microlepidotus).
venom injected rather than the animal’s body weight. • Polyvalent antivenom treats all venomous
Each vial of antivenom has sufficient antibodies for an Australian snakes.
average bite. Animals with preparalytic signs or mild
signs generally only require 1 vial of antivenom. Animals Novel snake species causing clinically significant enven-
with respiratory paralysis generally require at least 2–4 omation are ideally treated with antivenom according to
vials of antivenom, which should be given within the first the CSL Snake Venom Detection Kit results or, alterna-
1–2 hours of treatment. If the animal continues to deteri- tively, with tiger snake antivenom or polyvalent anti-
orate, more antivenom should be administered and steps venom if available.
 NEUROLOGICAL TOXICITIES 527

Production of the coral snake antivenom (Antivenom Dogs most commonly become intoxicated by eating
[Micrurus fulvius] [Equine]) has been discontinued and fish discarded by fishermen on beaches and tidal river
there is currently no alternative product available in the banks. Cats become intoxicated when mistakenly fed fish
USA. Alternatives that show cross-reactivity include caught by their owners.
Australian tiger snake antivenom and Mexican coral
snake (Micrurus) antivenom. One to 4 vials of coral snake Mechanism of action
antivenom are recommended for treatment. The dose is Tetrodotoxin blocks sodium channels thus preventing
determined by symptom severity and amount of venom the generation of action potentials. Peripheral nerve
injected. Very small animals or animals that deteriorate fibres are mainly affected, but autonomic nerves, sensory
after initial treatment will require higher doses. nerves, skeletal muscles and, least commonly, cardiac
Supportive care should be instituted as described in muscle can also be affected. This results in generalized
the tick paralysis section below. LMN paralysis, hypoventilation or respiratory arrest,
vasodilation and hypotension. Stimulation of the chemo-
Prognosis receptor trigger zone causes vomiting.
In Australia, following treatment with antivenom, 91% The lethal oral dose in dogs is 70 μg/kg; when admin-
of cats and 75–92% of dogs have been reported to survive istered subcutaneously the lethal dose is 15 μg/kg; an
snake envenomation. intravenous dose of 0.3 μg/kg will result in emesis. In cats
the lethal intravenous dose is 2 μg/kg.
Tetrodotoxin
Overview Clinical presentation
Tetrodotoxin is found in fish of the family Tetraondonti- Onset of clinical signs can be within 10 minutes to 1 hour
dae (scaleless fish with four large teeth). These sea fish of ingestion, but may be delayed for hours after inges-
are found throughout the world. Various species of tion; one report documented a delay of 24 hours before a
tetrodotoxic fish may also be known as puffer fish, blow- dog exhibited paralysis.
fish, blowies, globefish, toadfish (401) and porcupine fish. In dogs, early signs include severe vomiting, which is
Some species have spines and inflate their bodies when often sufficient to cause adequate gastric decontamina-
startled. Tetrodotoxin is also found in the bite of the tion, probably preventing absorption of lethal levels of
blue-ringed octopus (Hapolochlaena) of Australia, central the toxin. However, if vomiting is ineffective at deconta-
American frogs of the Aetolopus genus, Californian newts mination or a high dose has been absorbed, dogs may go
of the Taricha genus and the Pacific goby, as well as on to develop salivation, weakness, ataxia, facial paralysis
various other marine animals. Tetrodotoxin levels vary and generalized muscle paralysis, which in the most
seasonally and between species. severe cases can include respiratory paralysis. Skeletal
muscle fasciculations have also been reported in a study
of the effects of tetrodotoxin in dogs.
In cats, cases of ataxia without respiratory failure, as
well as death, have been reported. Death is generally due
to respiratory paralysis and can occur as rapidly as
17 minutes after ingestion. Hypotension is uncommon.

Diagnosis
Diagnosis is based on a history of known or suspected
tetrodotoxic fish ingestion and a rapid onset of LMN
paralysis. Liquid or gas chromatography of gastric con-
tents, serum or urine will help confirm the diagnosis.

 401 Toadfish. (© Helena Lemin, used with

permission.)
528 SPECIFIC EMERGENCIES

Management Tick paralysis (Australia)

Emesis or gastric lavage is indicated in animals that have Overview
not vomited. Activated charcoal should be administered. Tick paralysis is a common problem affecting domestic
Supportive care is indicated if there is respiratory animals living along the east coast of Australia. Cases of
paralysis – oxygen if hypoxaemic, mechanical ventilation tick paralysis most commonly occur from spring to mid-
if hypoventilating. Generally, patients who require summer, although they can occur at any time of year.
supplemental oxygen will also require ventilation.
Hydration should be maintained with intravenous fluids Mechanism of action
if affected animals have evidence of pharyngeal or Neurotoxins (holocyclotoxins) are produced in the
oesophageal paralysis. Hypotension is initially treated salivary glands of female Ixodes holocyclus ticks (402)
with intravenous fluids and then inotropes or vasopres- and injected during feeding (403). The toxin prevents
sors if required. Ventilation may be required for up to release of ACh at the NM junction. Cardiotoxicity occa-
3 days, although most animals require ventilation for less sionally occurs and is clinically associated with diastolic
than 12 hours. dysfunction due to impaired myocardial relaxation. The
Humans frequently remain mentally aware during presence of additional ticks prevents recovery despite
severe paralysis, and sedation to minimize anxiety should administration of tick antitoxin serum. Clinical signs can
be used in paralysed animals during ventilation. Drugs continue to progress for up to 48 hours after tick removal
that could predispose to hypotension should not be used. if tick antitoxin serum is not administered. Immunity
develops in some dogs and tick antitoxin serum is pro-
Prognosis duced from serum collected from hyperimmune dogs.
The majority of animal cases recover within 2–3 days.
The prognosis is grave if respiratory paralysis develops Clinical presentation
and mechanical or manual ventilation is not rapidly The onset of clinical signs generally occurs within
provided. The prognosis is fair if animals develop para- 5–7 days (and rarely up to 2 weeks) of tick attachment; if
lysis without respiratory failure. The prognosis for sur- the ticks remain attached and no treatment is provided,
vival can be good if the animal is still breathing when it death occurs 18–32 hours later.
reaches veterinary care and appropriate intensive care is Animals with tick paralysis present with a combi-
provided. nation of LMN paralysis and respiratory depression.
Occasionally, animals will present with vomiting or
regurgitation as the only clinical sign. Several slightly
different scoring systems have been used to stage the
progressive deterioration of clinical signs:
• Gait score:
• No gait abnormalities or mild ataxia when
walked.
• Significant ataxia present, but ambulatory.
• Non-ambulatory, but can maintain sternal
position and manoeuvre into sternal position
from lateral recumbency.
• Laterally recumbent and unable to manoeuvre
into sternal recumbency; can weakly move all
limbs.
• Moribund.
 NEUROLOGICAL TOXICITIES 529

• Respiratory score:
• Normal. Normal character and rate
(<30/minute).
• Mild compromise. Increased rate (≥30/minute),
normal respiratory pattern or mild expiratory
effort.
• Moderate compromise with abnormal
respiratory expiratory grunt. Gasping and
cyanosis may be present. Respiratory rate may
be decreased (i.e. ≤12/minute).
• Severe compromise with dyspnoea and
 402 Tick (Ixodes holocyclus): ventral aspect on left and ‘grunting’ respiration due to vocal cord closure
dorsal on the right. (© Simon Lemin, used with during expiration.
permission.)
Focal neurological deficits, such as localized facial paral-
a ysis, can occur with ticks found ipsilaterally on the head
or neck. Other neurological signs include changes in the
sound of vocalization (bark or meow), pupillary dilation
and loss of PLR, palpebral paralysis, decreased gag reflex,
facial paralysis, bladder paralysis, gagging and retching.
Salivation and retching are common due to pharyngeal
and oesophageal dysfunction. Megaoesophagus is a
common finding on thoracic radiographs (70% of cases).
Vomiting also occurs. Hypoventilation secondary to res-
piratory paralysis occurs late in the disease. During the
final stages, hypoxaemia and hypercapnoea develop.
Hypoxaemia is not solely due to hypoventilation and can
be contributed to by either aspiration pneumonia or pul-
b monary oedema. Respiratory compromise is significant-
ly associated with mortality. Laryngeal paralysis may
cause clinically significant upper airway obstruction.
Reported cardiovascular abnormalities include pro-
longed QT intervals and altered T wave morphology on
ECG analysis. These changes temporarily persist after
apparent recovery. Rarely, increased systemic mean and
systolic arterial pressure is observed and in-vivo studies
have shown increases in pulmonary artery pressure.

Diagnosis
The presence of an Ixodes holocyclus tick and appropriate
clinical signs confirm the diagnosis. Even if no evidence
of a tick or tick crater (attachment site) is found, the pres-
 403 (a) Paralysis tick (Ixodes holocyclus) attached to ence of appropriate clinical signs in an animal that has
skin. (© Simon Lemin, used with permission.) (b) The been in an endemic area within the previous 2 weeks is
appearance of a tick bite on a dog after removal of the tick regarded as strongly suggestive of tick paralysis and an
(the ‘tick crater’). indication for treatment if no other cause is diagnosed.
 530 SPECIFIC EMERGENCIES

Management Supportive care for paralysis should include:

All ticks should be removed. The whole animal’s coat • Strict confined rest.
should be repeatedly searched for the presence of addi- • Recumbent animals should be kept on padded
tional ticks and insecticides effective against ticks should bedding and turned every 4 hours to prevent
be applied. In long-haired animals, close clipping of the pressure sores.
coat may be required (after treatment with antiserum and • Food and water should be withheld until animals
stabilization). Ticks are most commonly found around are fully recovered and have had no episodes of
the head, neck and shoulders, but they can be found any- vomiting or regurgitation for 24 hours.
where on the body or external orifices. • Hydration should be maintained with intravenous
Animals that have no clinical signs should be moni- fluids, but fluid overload must be avoided as there
tored closely and tick antitoxin serum administered if may be an increased risk of development of
required. Tick antitoxin serum should definitely be pulmonary oedema. Mild cases in healthy young
administered to animals that have significant ataxia, animals who recover within 24 hours may not
paralysis or any respiratory compromise. require intravenous fluids, provided no signs of
Clinical improvement generally lags at least 12 hours dehydration develop.
behind hyperimmune serum administration. In some • Normothermia must be maintained.
patients there is a mild deterioration in this period before • Bladder size should be monitored and the bladder
improvement is seen. Tick antitoxin serum should be should be expressed manually or catheterized to
warmed, diluted in saline and administered slowly IV prevent overdistension and subsequent bladder
(over 1 hour) while the animal is monitored closely for atony.
anaphylaxis. Antihistamines, corticosteroids or adrena- • Corneal hydration should be maintained with the
line (epinephrine) are administered as premedication at use of ocular lubricants if the blink reflex is
the veterinarian’s discretion. Because the antitoxin serum compromised.
is produced from the serum of hyperimmune dogs, there • Animals should be sedated if distressed: opioids,
is a potential risk of anaphylaxis or anaphylactoid benzodiazepines or acepromazine can be used.
reactions. The recommended dose of tick antiserum is • Animals should be positioned in sternal
generally 1 ml/kg, with a minimum of 5–8 ml and a recumbency wherever possible. In animals unable
maximum dose of 25 ml. The higher end of the dosage to maintain sternal recumbency the shoulders
rate is recommended for cases with severe clinical signs should be elevated above the stomach and the head
or multiple ticks present. positioned to optimize drainage of saliva and thus
Three percent of dogs and 6% of cats treated by minimize the risk of aspiration. Pharyngeal and
general practitioners have been reported to develop oesophageal suctioning is frequently required in
adverse reactions to the administration of tick antitoxin recumbent animals. Intubation with a cuffed
serum, with one study attributing the majority of reac- endotracheal tube should be considered in
tions to the Bezold–Jarisch reflex (bradycardia and severely paralysed patients at significant risk of
hypotension) rather than anaphylaxis. Slow administra- aspiration.
tion of antiserum minimizes the risk of non-anaphylactic • Metoclopramide CRI (1–2 mg/kg/day) can be
reactions developing. administered as a prokinetic to try to minimize
Adrenaline and possibly antihistamines or cortico- vomiting and aspiration.
steroids should be available for administration if anaphy-
laxis develops. Supportive care for respiratory signs should include:
After recovery, a 2-week convalescence period with • Oxygenation should be monitored and oxygen
minimal exercise is recommended, as exercise-induced administered if hypoxia develops, commonly by the
sudden death occasionally occurs. At discharge, owners intranasal route or oxygen cage.
should be counselled on tick preventive measures and • Mechanical ventilation will be required if
the importance of daily manual searching of the animal’s respiratory paralysis and hypoventilation occur.
coat for ticks in endemic areas.
 NEUROLOGICAL TOXICITIES 531

• Aspiration pneumonia is a common complication Clinical presentation

and should be treated appropriately with parenteral Ascending LMN paralysis develops within 5–9 days of
antibiotics (ideally based on culture and sensitivity tick attachment. One tick is sufficient to cause paralysis;
testing) and intravenous fluids. large numbers of ticks are associated with increased
• Pulmonary oedema may also occur secondary to severity of clinical signs and rapidity of onset. Early signs
congestive heart failure. Radiographs and echo- are hindlimb weakness and ataxia, which progress to
cardiography should be used to confirm congestive quadriplegia over 1–3 days. If ticks remain in situ, death
heart failure prior to treatment with diuretics. from respiratory paralysis may occur in 1–5 days. A
• Patients with laryngeal paralysis may develop change in the bark suggestive of laryngeal paralysis may
significant upper airway obstruction. Sedation occur, but otherwise CN paralysis rarely occurs.
may alleviate distress; however, intubation or
tracheostomy and oxygen insufflation will be Diagnosis
required in severe cases. Diagnosis is based on appropriate clinical signs and the
presence of an engorged tick, together with rapid
Prognosis improvement after tick removal.
Mortality rates following treatment with tick antitoxin of
5% in dogs and 0.6% in cats have been reported. Management
The entire tick, including the mouth parts, must be
Tick paralysis (North America) removed. Repeated searching of the whole body for
Overview further ticks should be carried out. Long hair should be
The ticks most commonly associated with tick paralysis clipped to improve the efficacy of tick searches. Applica-
in North America are the Rocky Mountain wood tick tion of topical insecticidal solution effective against ticks
(Dermacentor andersoni), the American dog tick (Derma- is indicated. Noticeable improvement occurs within
centor variabilis), the Lone star tick (Amblyomma ameri- 24 hours of tick removal and the majority of cases are
canum) and the Gulf coast tick (Amblyomma maculatum). fully recovered within 1–3 days if all ticks are removed.
Dogs are most frequently affected, whereas cats do not Supportive care for paralysis is described above in the
seem to develop signs of this disease in spite of tick section on tick paralysis in Australia.
attachment.
Prognosis
Mechanism of action The prognosis is good if all ticks are removed and
The toxin appears to inhibit ACh release at the NM animals do not require ventilatory support.
junction of motor nerves. Sensory nerve conduction may
also be affected.
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PART 4

SPECIFIC 533

MANAGEMENT ISSUES

CHAPTER 29 Emergency neuroanaesthesia

CHAPTER 30 Analgesia for patients with neurological disease

CHAPTER 31 Fluid therapy

CHAPTER 32 Postoperative supportive care and physical rehabilitation

APPENDICES
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 SPECIFIC MANAGEMENT ISSUES Chapter 29

EMERGENCY NEUROANAESTHESIA
535

Anthea Raisis
& Gabrielle Musk

INTRODUCTION

This chapter discusses the considerations and techniques

for anaesthetizing animals with neurological disease.
The chapter will cover intracranial disease, spinal disease
and NM disease. A thorough understanding of the
pathophysiology of diseases affecting these regions of the
nervous system is essential to select the most appropriate
anaesthetic technique and drug combination.

INTRACRANIAL DISEASE

Considerations
The main aim of anaesthesia in animals with intracranial
disease is to preserve neuronal function. Normal neuro-  404 Animals with intracranial disease are at risk of
nal function depends on maintaining adequate CBF. increased ICP and subsequent brain herniation (as shown
CBF regulation is complex and will not be described on this sagittal T2-weighted MR image [arrow]) if
in detail in this chapter (for more details see Further appropriate stabilization is not performed prior to
reading). Put simply, CBF is maintained if CPP is main- anaesthesia. (Photo courtesy Victoria Johnson)
tained. The CPP represents the difference between
MAP and ICP. The considerations for maintaining CBF
and minimizing neuronal injury during anaesthesia will
be discussed with reference to the stages of the anaes-
thetic procedure (stabilization, induction, maintenance
and recovery from anaesthesia). This is summarized in
Table 99 (p. 537). Specific management of increased ICP is indicated if
deterioration of neurological status occurs rapidly or
Stabilization prior to anaesthesia continues despite normal oxygenation, ventilation and
Any patient with increased ICP (404), regardless of the perfusion. (For management of increased ICP see
cause, requires stabilization before considering anaes- Chapter 20.)
thesia or sedation for further diagnostics.
Correction of hypoxaemia, hypercapnia and poor Sedation
perfusion are the most important strategies for reducing In animals with clinical signs of intracranial disease,
ICP and stabilizing the patient prior to anaesthesia. the performance of procedures under heavy sedation is
(For specific details on supporting the respiratory and generally avoided. Heavy sedation may lead to excessive
cardiovascular systems see Chapter 2.) depression of cardiovascular and respiratory function,
 536 SPECIFIC MANAGEMENT ISSUES

intracranial disease are detailed in Table 100 (p. 539).

Drugs such as acepromazine and medetomidine are best
avoided in animals with intracranial disease.
Opioids provide analgesia and varying degrees of
sedation without affecting cerebral perfusion or ICP.
Adverse effects associated with a decrease in heart rate
and respiratory depression can be avoided by using con-
servative doses. Morphine administration is best avoided
in patients with high ICP given its significant potential
for causing vomiting (and transient increases in ICP).
Benzodiazepines may be useful as anxiolytics in criti-
cally ill animals. These agents should be used cautiously
in animals with mild disease/minimal decreases in men-
tation, as the effects can be unreliable and excitement,
dysphoria and disinhibition can occur.
Phenobarbital is the drug most often used to control
 405 Heavy sedation, as seen in this Bull Terrier, is seizures. The authors have found that the administration
generally avoided in patients with intracranial disease, due of phenobarbital at 2–3 mg/kg intramuscularly can be a
to the risk of excessive cardiovascular and respiratory useful premedicant in anxious dogs when used in con-
depression. junction with an opioid 30 minutes prior to induction of
anaesthesia.

Adjustment of dose rates of sedative and

anaesthetic agents
In animals with intracranial disease, damage to the
which will exacerbate secondary neuronal injury (405). blood–brain barrier and concurrent CNS depression due
In addition, heavy sedation may interfere with accurate to the neurological injury will serve to exacerbate the
assessment of the neurological status of the animal and effects of a given dose of anaesthetic or analgesic agent.
delay initiation of appropriate therapy. As a result, the doses used in these patients should be
In these cases, anaesthesia performed carefully with lower than those used in healthy patients. As the agents
a good understanding of how to minimize detrimental have a rapid onset and short duration of action, the dose
effects is preferable, as this allows protection of the rate can be adjusted incrementally (i.e. titrated to effect)
airway and control of ventilation. In addition, many until the desired analgesic effect is achieved, while
anaesthetic agents, such as propofol and barbiturates, minimizing side-effects.
have the added benefit of reducing cerebral metabolic
rate, which helps reduce neurological injury. Induction of anaesthesia
A smooth and high-quality induction of anaesthesia is
Premedication essential. Minimizing stress and struggling and main-
The aims of premedication are to: taining oxygenation and ventilation during induction of
• Reduce stress and anxiety. anaesthesia is necessary to prevent adverse effects on the
• Decrease the amount of anaesthetic induction and CNS. The induction of anaesthesia using intravenous
maintenance agents required. agents minimizes struggling and allows rapid control of
• Provide analgesia. the airway.
Pre-oxygenation is performed by mask, if tolerated,
Agents used for premedication should have minimal or by flow-by (406) for 5–10 minutes prior to induction
effects on cerebral perfusion and ICP. The advantages to minimize hypoxaemia during and immediately
and disadvantages of different agents in animals with following induction of anaesthesia.
 EMERGENCY NEUROANAESTHESIA 537

Table 99 Considerations for anaesthetizing animals with intracranial disease

CONSIDERATION MANAGEMENT

Maintain adequate CPP Maintain MAP between 80 mmHg and 100 mmHg. Maintain normal
(CPP = MAP – ICP) circulating blood volume. Minimize depressant effects of anaesthetic agents
on cardiovascular function. Avoid/use carefully anaesthetic drugs that
interfere with CBF autoregulation (e.g. volatile anaesthetics)

Maintain haemodynamic stability Avoid sudden increases in MAP and associated increases in ICP caused by
stress, pain, surgical stimulation and laryngeal stimulation. Provide adequate
analgesia. Ensure adequate depth of anaesthesia before intubation

Ensure adequate ventilation and Avoid hypercapnia (PaCO2 >40 mmHg) and associated increased ICP.
normocapnia (PaCO2 35–40 mmHg) Use positive pressure ventilation during anaesthesia. Avoid hyperventilation
(PaCO2 <30 mmHg) except in an emergency to avoid brain herniation. Do
not decrease PaCO2 below 30 mmHg

Maintain adequate oxygenation Avoid hypoxaemia (PaO2 <80 mmHg) by providing oxygen supplementation
during induction, maintenance and recovery from anaesthesia

Decrease CMR Select anaesthetic agents that decrease CMR (e.g. propofol). Avoid increase
in CMR by preventing or controlling seizures, maintaining normothermia and
avoiding anaesthetic agents that increase CMR (e.g. ketamine)

Ensure adequate venous drainage Avoid interference with jugular venous blood flow and associated venous
congestion and increased ICP. Avoid jugular obstruction, excessive airway
pressure during ventilation and fluid overload. Mild head elevation (15–30
degrees) will encourage venous drainage

MAP = mean arterial blood pressure; ICP = intracranial pressure; CBF = cerebral blood flow; CMR = cerebral metabolic rate;
PaCO2 = arterial carbon dioxide partial pressure.

 406 ‘Flow-by’ oxygen therapy is useful for providing

oxygen supplementation to animals that will not tolerate a
mask over their face.
538 SPECIFIC MANAGEMENT ISSUES

Manual ventilation with a close-fitting mask during intracranial disease. The administration of ‘co-induction’
induction of anaesthesia (407) may be necessary to ensure agents with fewer depressant effects on the cardio-
normocapnia until the anaesthetic depth is sufficient to vascular and respiratory systems can be used to reduce
minimize reflex responses (i.e. cough, increased heart the dose of the more depressant induction drugs. Co-
rate and MAP) to endotracheal intubation. Once an oral induction agents (see Table 101, p. 540) are administered
ETT has been positioned and secured in place, ventila- immediately prior to the induction agent and are usually
tion via the tube is commenced. (Note: When ventilating given intravenously.
via a mask, oxygen can be forced into the stomach, To minimize coughing in response to endotracheal
leading to gastric distension. Should this occur, a intubation, it is important to ensure that the depth of
stomach tube can be passed once the animal is adequately anaesthesia is adequate. The depth of anaesthesia
anaesthetized and the stomach deflated.) required to prevent a response to intubation is compara-
To maintain adequate cardiovascular and respiratory ble to that required for major surgery. It is common prac-
function during induction of anaesthesia, the use of tice in cats to apply topical local anaesthetic (lidocaine) to
short-acting agents that can be carefully titrated to the larynx before intubation (408). This is particularly
effect without excitation is preferred. Drugs that effective for preventing the autonomic response to intu-
minimally interfere with regulation of cerebral perfusion bation and it is useful for canine patients as well. In
are also preferred. The advantages and disadvantages of canine patients, use of co-induction agents such as lido-
different intravenous anaesthetic agents in the neurolog- caine (1–2 mg/kg) and opioids (e.g. fentanyl, 1–5 μg/kg)
ical patient are provided in Table 100. Propofol is the intravenously can also help reduce stimulation of the
agent the authors most frequently use in animals with larynx during intubation.

 407 Ventilation via a tight-fitting mask may be

necessary during induction to ensure adequate CO2
removal and delivery of oxygen.

 408 Application of topical lidocaine to the cat’s larynx,

after an adequate depth of anaesthesia has been achieved.
 EMERGENCY NEUROANAESTHESIA 539

Table 100 Intravenous sedatives and induction agents for use in animals with
central nervous system disease

AGENT CBF DIRECT CMR ICP SEIZURE COMMENT DOSE

REGULATION CARDIOVASCULAR ACTIVITY RATE*
EFFECTS

Acepromazine NR ↓↓ BP NR ↑ ↑ Avoid in intracranial 0.01–0.05

disease. Useful anxiolytic mg/kg IM
in spinal disease.
Contraindicated in hypo-
volaemic patients

Alpha-2 ↓ Flow- ↑ BP then ↓BP ↓ - ↑ Avoid in intracranial Dogs: 2–10

agonists metabolic disease. Useful in fractious μg/kg IM
coupling animals. Care in Cats: 5–20
hypovolaemic patients μg/kg IM

Opioids Normal ↓ HR ↓ ↓ ↓ Reduce the required dose See Table 102

+/– ↓ BP of induction and and
maintenance agents. Chapter 30
Reduce response to
intubation and surgical
stimulus

Benzodiazepines Normal No direct ↓ ↓ ↓↓ Possible sedative/ Diazepam,

vascular effects anxiolytic. Reduce 0.1–0.5
induction agent. mg/kg IV;
Potentiate respiratory midazolam,
depression of other 0.1–0.5 mg/kg
agents IV or IM

Lidocaine Normal ↓ BP: VD and ↓ ↓ Low Reduce response to Co-induction:

↓ CO dose: ↓ intubation and extubation. 1 mg/kg IV
Decrease seizures.
High Analgesia (see Chapter
dose: ↑ 30)

Thiopentone Normal ↓ BP: VD and ↓↓ ↓↓ ↓ Excitement in unsedated Up to 10

↓CO animals. Accumulates with mg/kg IV
repeated dosing

Propofol Normal ↓ BP: VD and ↓↓ ↓↓ ↓ Excitement-free induction. Induction:

↓CO Suitable for maintenance up to 2–4
of anaesthesia in dogs mg/kg IV.
with intracranial disease Maintenance:
0.2–0.4 mg/kg/
minute

Ketamine Normal ↑ HR and BP ↑↑ ↑ ↑ Avoid in animals with 1–2 mg/kg IV

intracranial disease.
Avoid in animals at risk of
seizures (e.g. post
myelography)

CBF = cerebral blood flow; CMR = cerebral metabolic rate; ICP = intracranial pressure; NR = not reported; BP = blood pressure;
HR = heart rate; CO = cardiac putput; VD = vasodilatation; VC = vasoconstriction.
* Note: These dose rates are based on those used in normal animals and lower doses may be required in animals with CNS disease.
540 SPECIFIC MANAGEMENT ISSUES

Table 101 Co-induction agents for use in animals with central nervous system disease

AGENT DOSE* AND TIMING COMMENTS

Butorphanol 0.1–0.2 mg/kg IV 1–2 minutes Potent antitussive. Mild analgesia only: avoid in surgical
prior to induction or animals in pain. Antagonize effects of mu agonists

Fentanyl 1–5 μg/kg IV 5 minutes prior to Bolus administration can cause significant bradycardia.
induction Exacerbates respiratory depression of induction agent.
Capnography and appropriate manual or mechanical
ventilation should be commenced. Also useful for
reducing the autonomic response to endotracheal
intubation

Diazepam 0.1–0.2 mg/kg IV immediately Negligible cardiovascular depression. Can cause

or Midazolam prior to induction disinhibition and paradoxical excitement: follow with
induction agent immediately. May exacerbate respiratory
depression of induction agent. Capnography and
appropriate manual or mechanical ventilation should be
commenced

Lidocaine 1–2 mg/kg IV 1–2 minutes prior to DO NOT USE IN CATS. Can exacerbate cardiovascular
induction depression of other agents. Also useful for reducing the
autonomic response to endotracheal intubation

*Lower end of dose range is recommended in critically ill animals.

Table 102 Opioids used intraoperatively to control pain and stabilize anaesthesia

OPIOID ADVANTAGES DISADVANTAGES COMMON DOSE RATES*

Fentanyl Potent analgesia (full mu agonist). Marked respiratory depression at Bolus: 1–2 μg/kg IV
Short acting after bolus higher doses. Duration of action q15–20 minutes.
administration (15–20 minutes). increases with duration of infusion CRI: 0.2–0.7 μg/kg/min
Suitable for infusion

Alfentanil Potent analgesia (full mu agonist). Marked respiratory depression at 0.5–2 μg/kg/minute
Fast onset: 1 minute. Short duration doses used intraoperatively.
after bolus administration Duration of action increases with
(5 minutes). Suitable for infusion duration of infusion

Remifentanil Potent analgesia (full mu agonist). Marked respiratory depression at 0.2–0.7 μg/kg/minute
Very short acting (1–2 minutes). doses used intraoperatively. Very
Suitable for infusion. Duration of rapid recovery: additional
action is constant regardless of analgesia required before
duration of infusion stopping infusion

* Doses are a guide only and should be titrated on an individual patient basis.
 EMERGENCY NEUROANAESTHESIA 541

Maintenance of anaesthesia
Following induction of anaesthesia it is essential to select
drugs and apply techniques that will either decrease or
minimally increase ICP.

Total intravenous anaesthesia

Total intravenous anaesthesia (TIVA) with suitable agents
provides the best conditions for the maintenance of anaes-
thesia in the neurological patient, providing normocapnia
(P’ETCO2 30–35 mmHg [4–4.7 kPa]) and systemic BP
are maintained. TIVA can be achieved with variable rate
infusions of propofol (0.2–0.4 mg/kg/minute) or target
controlled infusion (TCI) of propofol (2.5–3.5 μg/ml of  409 Propofol can be administered by variable rate
blood) using specialized infusion equipment. Propofol is infusion where the rate is adjusted by the operator.
frequently infused in combination with short-acting
opioids (409) (see Table 102) to allow the dose of propofol
and, therefore, its associated side-effects to be reduced.
Additional information on TCI can be found in the
Further reading list for this chapter. Sevoflurane and isoflurane have the least effect on
The use of opioids (e.g. fentanyl (0.2–0.7 μg/kg/ ICP providing the dose is minimized and the animals are
minute, remifentanil 0.2–0.7 μg/kg/minute) in combina- ventilated to normocapnia. As described below, infusion
tion with propofol allows the dose of propofol required of short-acting opioids is a useful technique for reducing
for maintenance of anaesthesia and, in turn, the cardio- the required dose of inhalation agent. Despite efforts to
vascular side-effects, to be reduced. prevent herniation of the brain, there are still anecdotal
TIVA is the authors’ preferred technique for canine reports of this life-threatening complication occurring
neurosurgical patients and unstable patients requiring when these agents are used to maintain anaesthesia
diagnostic imaging. The TIVA protocol utilizing propo- during intracranial surgery in small animals. Other
fol in cats is less well established and less commonly prac- volatile agents, such as halothane, desflurane and N2O,
tised. Cats are inefficient metabolizers of propofol, have a marked effect on ICP and are best avoided.
predisposing to prolonged recoveries. Their RBCs are
also more prone to the oxidative effects of the propofol Maintain adequate ventilation and oxygenation
(this may cause a Heinz body anaemia). Alfaxalone may To maintain adequate ventilation and ensure normocap-
prove to be a suitable alternative, as it has a similar phar- nia (PaCO2 35–40 mmHg [4.7–5.3 kPa]; P’ETCO2
macokinetic profile to that of propofol, thus making it 30–35 mmHg [4–4.7 kPa]), the use of IPPV and meas-
ideal for infusion. Infusion rates of alphaxalone currently urement of end tidal CO2 concentration breath by breath
used clinically in healthy animals range from 0.07–0.1 are essential.
mg/kg/minute. However, appropriate dose rates for use To maintain oxygenation during diagnostic proce-
in neurological patients have not been determined and dures and surgery it is not uncommon to use high
the quality of recoveries in these patients is not known. inspired concentrations of oxygen during anaesthesia.
For long-term ventilation the FiO2 is ideally adjusted to
Inhalation anaesthesia the minimum required to maintain PaO2 >80 mmHg
Inhalation anaesthesia can be used for short anaesthetics in (10.7 kPa) and minimize the risk of lung damage. In
stable neurological patients. It is preferred by many anaes- animals with concurrent pulmonary pathology, ventila-
thetists for maintenance of anaesthesia in cats given the tion strategies employing PEEP may be required to
concerns about using propofol by infusion. The character- maintain oxygenation. (For more details on IPPV and
istics of inhalation agents are summarized in Table 103 PEEP see Chapter 2.)
(next page).
542 SPECIFIC MANAGEMENT ISSUES

Table 103 Inhalation agents for use in animals with central nervous system disease

AGENT CBF DIRECT CMR ICP SEIZURES COMMENT

REGULATION CARDIOVASCULAR
EFFECTS

Halothane Autoregulation: ↓↓ Cerebral VD ↓ ↑↑↑ None Avoid in neurological

Flow-metabolism ↓↓ MAP patients
coupling: ↓
Chemical regulation:
↓

Isoflurane Autoregulation: ↓ Cerebral VD ↓ ↑ None IPPV required. Rapid

Flow-metabolism ↓↓ MAP recovery. Use balanced
coupling: ↓ anaesthesia to reduce
Chemical regulation: dose and side-effects in
normal neurological patients

Sevoflurane Autoregulation: ↓ Cerebral VD ↓ ↑ Reported IPPV required. Very

Flow-metabolism ↓↓ MAP in humans rapid recovery. Use
coupling: ↓ balanced anaesthesia
Chemical regulation: to reduce dose and
normal side-effects in neuro-
logical patients

Desflurane Autoregulation ↓↓ Cerebral VD ↓ ↑↑ None IPPV required.

Flow-metabolism ↓↓ MAP Very rapid recovery.
coupling: ↓ Use balanced
Chemical regulation: anaesthesia to reduce
normal dose and side-effects in
neurological patients

Nitrous oxide Not reported Potent cerebral No ↑ None Avoid in patients with
vasodilator. effect increased ICP
Minimal systemic
effects

CBF = cerebral blood flow; CMR = cerebral metabolic rate; ICP = intracranial pressure; VD = vasodilation; MAP = mean arterial pressure;
IPPV = intermittent positive pressure ventilation.

Monitoring pulmonary function during anaesthesia is Maintain perfusion and cerebral perfusion pressure
essential to ensure normocapnia (PaCO2 35–40 mmHg To maintain CPP in patients with increased ICP, it is rec-
[4.7–5.3 kPa]) and adequate oxygenation (PaO2 >80 ommended that mean BP is maintained between 70 and
mmHg [10.7 kPa]). For short anaesthetic procedures, 80 mmHg and systolic BP above 100 mmHg. For short
such as for diagnostic imaging or CSF sampling, capnog- procedures in stable patients undergoing MRI or CT,
raphy and pulse oximetry are adequate for monitoring non-invasive BP monitoring is adequate. For unstable
ventilation and oxygenation. For unstable patients or patients or for monitoring during surgical procedures,
animals undergoing long procedures, such as surgery, invasive, direct monitoring of arterial BP and CVP is
analysis of serial arterial blood gas samples is essential. preferred. (For details on BP and CVP monitoring see
(For details on monitoring techniques, see Chapter 2.) Chapter 2.)
 EMERGENCY NEUROANAESTHESIA 543

Reduce cardiovascular depression associated with Maintain venous drainage from the head
maintenance agents Diagnostic imaging procedures and craniectomy are
As most anaesthetic agents cause dose-dependent invariably performed with the patient positioned in
decreases in BP, it is preferable to combine short-acting sternal recumbency with the head level with the spine
anaesthetic agents that can be titrated to effect with (410). This position is excellent for ensuring adequate
short-acting opioids that cause minimal cardiovascular lung expansion and also encourages venous drainage
depression. This will reduce the required dose of the from the head. However, it is important to ensure that
selected maintenance agent in a dose-dependent fashion. the jugular veins are not occluded when the animal is
The doses of opioids commonly used for maintenance of placed in this position, as this will lead to venous conges-
anaesthesia are provided in Table 102. Animals with tion within the brain and marked increase in ICP. For
severe neurological impairment may require lower doses. animals in lateral recumbency, mild head elevation
An expected side-effect of administration of these (15–30 degrees) is also recommended to encourage cere-
potent opioids is respiratory depression. Even at low bral venous drainage.
doses, significant hypoventilation may occur and IPPV Measurement of CVP is generally performed via a
may be required to maintain normocapnia. Both alfen- catheter inserted into the jugular vein. This may increase
tanil and fentanyl will accumulate after a period of infu- the risk of disturbance to venous return and increased
sion, so it may be prudent to terminate or reduce the ICP. Methods for reducing the interference with
infusion rate prior to the end of anaesthesia to ensure venous return are described in Chapter 2.
adequate ventilation on recovery. Remifentanil does The use of IPPV may also impede venous return
not accumulate and has a duration of action of approxi- from the head during the inspiratory phase of ventilation.
mately 3 minutes regardless of the duration of infusion. To minimize this adverse effect, the inflation pressures
required to maintain normocapnia can be reduced by
Maintenance of normal fluid balance administration of NM blockade using drugs such as
Providing animals have normal fluid and electrolyte atracurium. Atracurium is initially administered at
balance prior to anaesthesia, fluid therapy during anaes- 0.2–0.5 mg/kg IV. This is followed by increments of
thesia initially consists of isotonic, polyionic crystalloids 0.1 mg/kg, which is administered according to NM activ-
administered at 10 ml/kg/hour. Subsequent infusion ity assessed using a nerve stimulator.
rates and types of fluid will depend on losses and cardio-
vascular performance during anaesthesia. Measurement
of CVP, arterial BP and urine output (UOP) is the best
way to assess the response to fluid therapy. (For details on
selection of fluids and rates for varying conditions see
Chapter 31; for details of techniques for monitoring of
BP, CVP and UOP see Chapter 2.)

Avoid sudden/marked increases in blood pressure

Various stimuli during anaesthesia, including nocicep-
tion from surgical stimulation, can cause increases in BP,
which in a diseased brain may result in an increase in
CBF and ICP. To minimize sudden or marked increases
in BP during anaesthesia, the continuous infusion of an
opioid (as described above) can help minimize this sym-
pathetic stimulation and the haemodynamic responses to
surgery. This in turn will contribute to the maintenance  410 In animals with intracranial disease, venous
of stable BP and CBF. drainage from the head is maintained by positioning in
sternal recumbency with the head at the same level as
the spine.
544 SPECIFIC MANAGEMENT ISSUES

Maintain body temperature It is important to remember that head trauma (espe-

Body temperature should be maintained as close to cially if it involves the hypothalamus) can result in
normal as possible. Hypothermia has numerous adverse impaired thermoregulation. Close monitoring of the
effects on the patient including: temperature in these animals is imperative and appropri-
• Cardiovascular system depression with bradycardia ate therapy should be initiated when abnormalities arise.
and hypotension. Methods for maintaining normal body temperature in
• Suppression of the immune system and an increased animals with neurological disease will be discussed in
risk of infection. more detail in the NM disease section below.
• Delayed healing.
• Intra- and postoperative coagulopathy and Recovery from anaesthesia
increased blood loss. The aims during the recovery period are to achieve a
• Slow recovery. smooth emergence from anaesthesia with minimal
• Shivering on recovery, which increases oxygen excitement, coughing or straining, and adequate ventila-
demand when oxygen delivery may be tion (411). The timing of extubation is a compromise
compromised. between ensuring the animal can protect its own airway,
• Prolonged hospital stays. breathe spontaneously and maintain normocapnia, while
avoiding stimulation that can lead to increases in arterial
Hyperthermia, on the other hand, increases CMR, BP and coughing.
which increases CBF and can lead to increases in ICP and
further reductions in CPP. Ensure adequate ventilation
Reduce rates of opioid infusions
If high infusion rates of opioids have been used during
surgery, it is important that the infusion rate is reduced in
preparation for recovery. Once the patient is extubated
and IPPV can no longer be delivered, it is imperative that
the patient can breathe spontaneously. Extubation
should therefore only be performed when the patient can
spontaneously ventilate adequately (check the capno-
graph or blood gases).
When using either an alfentanil or fentanyl infusion,
the rate should be reduced approximately 30 minutes
prior to extubation. This will depend to some extent on
the duration of infusion and the total amount of drug that
has been delivered (the higher the dose and the longer
the infusion, the more time required to reduce serum
concentrations).
Remifentanil does not accumulate and activity rapidly
disappears after infusion is stopped, allowing prompt
return to spontaneous ventilation. The disadvantage is
that the analgesic activity is also rapidly terminated. If
continued analgesia is required, another opioid must be
administered prior to turning off the remifentanil infu-
 411 Following brain surgery, animals should be sion. This may be in the form of a long-acting opioid
recovered in a controlled, quiet manner. Extubation is a such as methadone. Alternatively, infusion of short-
balance between ensuring normal ventilation and acting opioids at a lower dose (see Chapter 30) can be
preventing coughing when the endotracheal tube is used to provide postoperative analgesia so long as the
removed. patient can breathe spontaneously.
 EMERGENCY NEUROANAESTHESIA 545

Assess adequacy of spontaneous ventilation SPINAL DISEASE

periodically
When preparing to extubate, the ETT tie is undone and Considerations
the cuff left inflated. As the depth of anaesthesia decreas- Anaesthesia in animals with spinal disease should be
es, trial periods of apnoea are performed. If spontaneous designed to maintain spinal perfusion and minimize
ventilation and maintenance of normocapnia occur, then further neurological injury. As a result, many of the prin-
the animal can be extubated; otherwise IPPV is reintro- ciples of anaesthesia for patients with intracranial disease
duced before P’ETCO2 exceeds 45 mmHg. Once extu- are relevant to patients with spinal disease. Considera-
bated, the patency of the airway needs to be assessed, tions for anaesthetizing animals with spinal disease are
particularly in animals with brachycephalic airway syn- outlined in Table 104 (next page).
drome. It is important to have ready access to an induc-
tion agent in case immediate reintubation is required. Stabilization
Animals with spinal trauma frequently have other
Minimizing coughing and hypertension on recovery injuries. Patients with spinal disease may have had
To minimize laryngeal stimulation, the administration of reduced access to water due to reduced mobility (412).
agents such as fentanyl or lidocaine can be used as Stabilization of pulmonary and cardiovascular functions
described for intubation. At the end of anaesthesia, the and correction of fluid and electrolyte deficits should be
drugs are given just prior to expected extubation. Alter- performed prior to anaesthesia. A full clinical examina-
natively, in animals requiring ongoing analgesia, a con- tion should be performed with particular attention paid
tinuous infusion of fentanyl (2–5 μg/kg/minute) can also to the function of the cardiovascular and respiratory
help reduce coughing on extubation. systems.
Hypertension in the recovery period despite ade-
quate analgesia can be treated by administration of β
receptor antagonists or blockers (e.g. esmolol, 50–200
μg/kg/minute CRI). More details on hypertension in
neurological patients can be found in Chapter 2.

Minimizing agitation in the perianaesthetic period

Agitation is not uncommon in animals with intracranial
disease. Administration of opioid analgesics will ensure
the agitation is not caused by pain. If it persists, then
sedative agents such as acepromazine or dexmedetomi-
dine will be required, but as these agents have adverse
effects on the CNS and the cardiovascular system, their
benefits for controlling agitation and calming the patient
need to be weighed against the adverse effects that may
occur. If administration of these agents is deemed neces-
sary, low doses should be used and blood volume and BP
should be normalized before administration. For
example, the authors have used acepromazine (5–10
μg/kg IM) to control agitation in dogs post craniectomy
when other methods of controlling the agitation have
failed and the animal is considered at risk of injury from  412 Spinal patients may have reduced access to water
the agitation. Trazodone hydrochloride, a triazolopyri- due to immobility. This may predispose to dehydration if
dine derivate and member of the phenylpiperazine class supplemental fluid is not provided. Dogs, such as the one
of drugs, can also be considered as an anxiolytic in these in this photograph, will need to be administered fluids
situations (see Further reading). intravenously or frequently ‘by hand’.
546 SPECIFIC MANAGEMENT ISSUES

Table 104 Considerations for anaesthetizing animals with spinal disease

CONSIDERATION MANAGEMENT

Maintain perfusion Correct deficits in circulating blood volume and body water. Use agents/techniques that
minimally depress cardiovascular function

Pain Most spinal diseases are painful and effective analgesia (e.g. full mu agonists) is necessary

Anxiety Anxiety is common in paralysed animals and decreases the pain threshold. Administering
anxiolytics is an important part of pain management in spinal patients

Mechanical instability Animals need to be moved carefully to minimize further trauma to the spinal cord,
particularly when a fracture or luxation is suspected. Intubation of animals with suspected
instability of the cervical spine should also be performed carefully. Flexion and extension of
the head should be avoided

Respiratory insufficiency Cervical spinal lesions can interfere with innervation of the diaphragm and intercostal
muscles, leading to inadequate ventilation and respiratory arrest. Sternal recumbency
during surgery restricts movement of the diaphragm and thus mechanical ventilation is
recommended during surgery to ensure adequate ventilation

Maintain airway Ventral approaches to the cervical spine require retraction of the trachea and may partially
or completely obstruct the endotracheal tube

Blood loss Blood loss during surgery can be significant and needs to be monitored closely by weighing
swabs and measuring fluid in suction bottles. Transfusion is indicated if >20% of
circulating blood volume is lost or if signs of hypovolaemia (increased heart rate without
increased MAP, pale mucous membranes) are observed

Guidelines for sedating and anaesthetizing

animals with spinal disease
Premedication
Premedication is important not only to provide analgesia be used in extremely anxious or fractious animals that are
and minimize the dose of induction agent required, but normally hydrated and cardiovascularly stable. Benzodi-
also to increase the ease of handling without the need for azepines are unpredictable and unreliable sedatives in
excessive physical restraint, which may be dangerous for healthy dogs and cats, but may provide useful sedation in
these patients. critically ill animals. Medetomidine and benzodiazepines
both cause skeletal muscle relaxation and should be
Choosing drugs and drug combinations avoided in animals with unstable spinal fractures (413).
Opioids form the basis for premedication of animals with Ketamine is another option in normovolaemic cats with
spinal disease and are generally administered on their normal renal function in combination with opioids, ace-
own to patients with other systemic abnormalities. promazine or benzodiazepines. However, ketamine is
A variety of other agents can be used in conjunction with extremely painful when injected intramuscularly. This
opioids to provide additional sedation if required. The may cause additional discomfort to animals already in
doses and advantages and disadvantages of these agents pain. In addition, sudden uncontrolled movement in
are outlined in Table 101. Acepromazine is useful in response to the injection may be detrimental in animals
anxious but otherwise stable animals. Medetomidine can with an unstable spinal fracture.
 EMERGENCY NEUROANAESTHESIA 547

 413 Handling and choice of premedication should be  414 For animals with cranial spinal lesions, such as the
performed carefully in animals with unstable spinal C2/C3 disc extrusion seen on this sagittal MR image
fractures, such as that noted on this lateral thoracolumbar (arrow), intubation should be performed with support of
radiograph (arrow). the head and neck.

Induction
Minimize further damage to spinal cord
A rapid and controlled induction of anaesthesia with
minimal struggling is best achieved with intravenous
agents. Endotracheal intubation should be performed
carefully with adequate support of the head and neck,
particularly in animals with cervical spinal cord injury
(414). Intubation is facilitated by the use of a laryngo-
scope (415). Excessive extension of the neck should be
avoided in dogs with caudal cervical lesions, while exces-
sive flexion should be avoided in animals with AA sublux-
ation or other cervical fractures.

Select induction agents that minimally interfere with

spinal perfusion  415 Intubation is best performed with the animal in
Selection of an appropriate induction agent is based on lateral recumbency. Use of a laryngoscope will aid visuali-
the same basic principles as those described for animals zation of larynx.
with intracranial disease. The characteristics of the intra-
venous agents and suggested doses are described in
Table 100. To decrease the required dose of intravenous
induction agent and to minimize cardiovascular depres-
sion, concurrent administration of a potent opioid, such
as fentanyl or a benzodiazepine, can be used during
induction (Tables 101 and 102).
548 SPECIFIC MANAGEMENT ISSUES

Maintenance of anaesthesia
Select agents that maintain spinal perfusion
Maintenance of anaesthesia is usually performed with
inhalation agents. As autoregulation of perfusion to the
spinal cord and chemoreceptor response to carbon
dioxide are better maintained with isoflurane and sevo-
flurane than halothane, these are the preferred inhalation
agents. Nitrous oxide is reported to increase ICP as a
result of cerebral vasodilation, so is best avoided in
patients with intracranial disease. Whether the same pre-
cautions are warranted in animals with spinal cord injury
and compression is not known.  416 Heat and moisture exchange devices can be placed
Infusion of short-acting opioids can also be used between the endotracheal tube and the breathing circuit
in conjunction with inhalation agents. These agents to help reduce heat and moisture loss from animal.
provide analgesia, which is essential in most animals with
spinal disease, and will help reduce the dose and thus the
amount of cardiovascular depression observed with
inhalation agents. Details of the use of these opioids are
described in the section on intracranial disease.
Maintenance of anaesthesia can also be performed blood-soaked swabs, weighing swabs (1 ml of blood
with a TIVA technique as described for intracranial weighs approximately 1.03 g) or measuring the volume of
disease. TIVA is especially useful for dogs requiring fluid in suction bottles (taking into account dilution from
surgery of the cranial cervical spinal cord where manipu- irrigation fluids).
lation of the cervical spinal cord and/or brainstem may Blood loss can also be estimated from the PCV of
occur (e.g. repair of AA instability). fluid in the suction bottle. This technique requires an
accurate measurement of the patient’s PCV at the time
Maintain adequate ventilation of blood loss. The PCV prior to anaesthesia may not be
IPPV is recommended during anaesthesia in spinal representative of the PCV during anaesthesia. The PCV
patients for several reasons. Firstly, the detrimental may decrease due to splenic sequestration of RBCs in
effects of inhalation agents on spinal blood flow response to anaesthetic agents (propofol, barbiturates)
regulation can be minimized by maintaining normo- and dilution by intravenous fluid therapy. If an accurate
capnia. Secondly, surgical access frequently requires that estimate of the PCV of the patient prior to haemorrhage
the animal is positioned in sternal recumbency, which is known, the amount of blood in the bottle can be
can interfere with diaphragmatic excursions and impair estimated using the following:
ventilation. Finally, the dose rates of the opioid agonists
recommended for intraoperative use produce marked Amount of blood lost (ml)
respiratory depression and therefore necessitate IPPV. PCV of flush in bottle × total volume of fluid in bottle
=
PCV of patient at time of haemorrhage
Maintain adequate perfusion
Intravenous fluid therapy is essential during anaesthesia A blood transfusion is indicated when blood loss exceeds
in all spinal cases to maintain fluid balance, adequate BP 20% of the circulating blood volume or haemoglobin
and perfusion of the spinal cord. In hypovolaemic concentration is <80 g/l (<8 g/dl). Blood loss of less than
animals, the volume deficit should be replaced before 20% can be managed by administrating crystalloids
anaesthesia. Intraoperative blood loss can be unpre- +/– colloids such as hetastarch (maximum dose
dictable and surprisingly high during spinal surgery. 20 ml/kg/day). (For more details on fluid therapy see
Blood loss should be estimated regularly by counting Chapter 31.)
 EMERGENCY NEUROANAESTHESIA 549

Maintain body temperature NEUROMUSCULAR DISEASE

Heat loss can be a problem, particularly when spinal cord
injury causes sympathetic nervous system imbalance and Considerations
peripheral vasodilation. Monitoring core body tempera- Considerations for anaesthetizing animals with NM
ture should be performed during anaesthesia. Heat loss disease are outlined in Table 105. The general principles
can be prevented during anaesthesia by heat pads, warm for anaesthetizing these patients are similar, with some
water beds or warm air blowers and ‘blankets’. Heat and differences depending on the type of NM disease
moisture exchange devices (416) can be placed between present. These principles are described in more detail in
the endotracheal tube and the breathing system to regard to premedication, induction, maintenance and
promote warmth and humidification of inspired gases. recovery of anaesthesia.

Monitoring Stabilization
During diagnostic imaging and surgery in animals with Fluid and electrolyte abnormalities are common in these
spinal disease, non-invasive monitoring of cardiopul- patients due to immobility and an inability to eat and
monary function with electrocardiography, non-invasive drink. These deficits need to be corrected prior to
BP measurement, capnography and pulse oximetry is anaesthesia when possible. Fluid and acid–base abnor-
generally adequate. In animals where cardiopulmonary malities associated with toxicities, such as metaldehyde,
dysfunction (e.g. cranial cervical surgery, trauma will also need to be corrected prior to anaesthesia (see
involving multiple organ systems) or excessive blood loss Chapter 28).
is expected, invasive BP measurement is recommended. Animals with aspiration pneumonia should be stabi-
Monitoring techniques have been discussed in detail in lized as much as possible prior to anaesthesia. Antibiotic
Chapter 2. and oxygen therapy forms the basis of symptomatic treat-
ment in these animals.
Recovery
It is essential that the provision of analgesia is continued Premedication
into the postoperative period to ensure a calm and com- The use of premedication in animals with peripheral
fortable recovery. In some cases the use of low-dose seda- NM disease will depend on the type of disease that is
tives, such as acepromazine (0.01–0.02 mg/kg IM or IV) present, how painful that disease is and how urgent the
or dexmedetomidine (0.5–1.0 μg/kg IV bolus or infusion need for anaesthesia is (e.g. an animal with airway
of 0.5–1.0 μg/kg/hour), may be required in extremely obstruction requires immediate anaesthesia). In anxious
stressed or agitated animals exhibiting signs of subopti- animals, the judicious use of sedatives may be needed to
mal emergence. However, these drugs should only be facilitate a smooth, stress-free induction. (Note: Sedation
used in animals with normal cardiovascular function. can interfere with the maintenance of a patent airway and
Trazodone (see p. 545) can also be used to treat postoper- increase the risk of upper respiratory tract obstruction
ative anxiety. (For details on possible postoperative anal- and aspiration. If used, low doses are recommended and
gesia see Chapter 30.) animals should be constantly monitored for any adverse
effects.)
In animals with painful NM disease (which is uncom-
mon), premedication should include an opioid, either
alone or in combination with other agents. Opioid pre-
medicants should also be given to animals requiring
muscle and nerve biopsies and animals undergoing
painful diagnostics such as electromyography.
 550 SPECIFIC MANAGEMENT ISSUES

Induction of anaesthesia Prevent regurgitation and aspiration

Maintain oxygenation Induction of anaesthesia should be performed with the
The patient should be pre-oxygenated for 5–10 minutes patient in sternal recumbency (417). If there is an
prior to induction when possible. If an animal objects to increased risk of regurgitation (e.g. megaoesophagus),
the placement of a face mask, the use of flow-by oxygen is cricoid pressure should be applied. Cricoid pressure is
recommended. Flow-by oxygen is preferred in animals maintained until the ETT is placed and secured in the
predisposed to hyperthermia, because masks encourage airway with the cuff inflated. Suctioning of the pharynx,
re-breathing of warm expired gases. Pre-oxygenation oesophagus and stomach should be performed as soon as
increases the concentration of oxygen in the func- the airway is secure to minimize the risk of aspiration
tional residual capacity of the lung and delays the onset of during anaesthesia (if the cuff becomes deflated). If vom-
hypoxaemia in the event of a difficult intubation or in iting or regurgitation occurs during induction of
patients with cardiovascular or respiratory compromise. anaesthesia and before the airway is protected by the
presence of an ETT, the animal should immediately be
positioned with its head over the edge of the table to
allow gravity-assisted drainage of the pharynx. The
pharynx and oesophagus should be suctioned before
intubation is performed.
Induction of anaesthesia should be performed with
short-acting intravenous agents that facilitate rapid
control of the airway. Furthermore, a prompt recovery
from anaesthesia is important in order for the patient to
regain control of its airway as soon as possible. Agents
such as propofol and alfaxolone allow rapid recovery;
however, in animals at risk of obstruction, titration of
these agents to effect can delay intubation. Furthermore,
bolus administration can lead to marked decreases
in BP. To reduce the dose and thus the side-effects,
co-induction agents (fentanyl + short-acting benzo-
diazepines) can be administered immediately prior to an
intravenous induction agent. This combination of agents
will invariably cause apnoea and therefore animals should
be ventilated as soon as intubation is performed.
Ketamine should be avoided in animals with tetanus and
increased muscle activity. Thiopentone allows rapid
control of the airway, but the recovery period is likely to
be prolonged.

Maintenance of anaesthesia
Selection of agent
Agents with a short duration of action, thus allowing
rapid recovery, are preferred. Inhalation agents, such as
isoflurane, sevoflurane and desflurane, all have physico-
chemical properties that ensure a rapid clinical response
 417 Animals that are at risk of regurgitation during to changes in vapourizer settings. In addition, recovery
induction should be maintained in sternal recumbency from anaesthesia is relatively rapid, with prompt return
with cricoid pressure applied until the endotracheal tube of airway reflexes.
is placed and cuff inflated.
 EMERGENCY NEUROANAESTHESIA 551

Table 105 Considerations for anaesthetizing animals with neuromuscular disease

CONCERN CONSIDERATIONS

Pain Presence and severity of pain will vary with the disease. Painful conditions include
polyradiculoneuritis, some myopathies and muscle and nerve biopsy patients

Dysphagia Weakness of pharyngeal muscles results in difficulty swallowing and predisposes

to aspiration

Airway obstruction Laryngeal paresis or paralysis. Laryngeal spasm (e.g. tetanus)

Impaired ventilation Mechanical ventilation frequently required due to:

• Weakness of respiratory muscles (e.g. snake envenomation, myasthenia gravis,
polyradiculoneuritis, tetrodotoxin, botulism).
• Spasm of diaphragm and intercostals (e.g. tetanus)

Impaired oxygenation Dysphagia, megaoesophagus and inability to protect the airway predisposes to aspiration.
Recumbency predisposes to atelectasis. Supplemental oxygen recommended in peri-
operative period

Impaired thermoregulation Laryngeal dysfunction and impaired ventilation reduce ability to pant and predispose to
hyperthermia during exposure to warm environments. Muscle fasciculations and tetany
increase metabolic rate and predispose to hyperthermia. Generalized weakness prevents
shivering and predisposes to hypothermia during exposure to cold environments

Dehydration and electrolyte Recumbent animals may have restricted access to water. Dysphagia impedes ability to eat
abnormalities and drink. Regurgitation associated with megaoesophagus increases loss of water and
bicarbonate (from saliva)

Ensure adequate ventilation Neuromuscular relaxation

Mechanical ventilation is recommended in all animals In animals with peripheral NM disease requiring surgery
with peripheral NM disease as there is likely to be a com- for other reasons (e.g. thoracotomy for thymoma
ponent of respiratory muscle involvement. IPPV should removal in animals with MG), NM relaxation may be
be delivered with close monitoring of CO2 concentration required to improve surgical access. Non-depolarizing
in the expired gas with a capnograph or serial arterial muscle relaxants can be used, but extreme care is required
blood gas analyses. Monitoring of the haemodynamic as prolonged duration of skeletal muscle weakness can
consequences of ventilation is also prudent. occur. Depolarizing muscle relaxants such as suxametho-
nium should be avoided.
Maintain normal body temperature Non-depolarizing NM blocking agents should be
Animals with NM disease may have difficulty maintain- administered in incremental doses with careful monitor-
ing normal body temperature (see Table 105). It is there- ing of peripheral nerve blockade with a nerve stimulator.
fore essential to monitor core body temperature There must also be facilities to provide either mechanical
perioperatively in these animals. Mild decreases in body or manual IPPV and assessment of adequacy of ventila-
temperature can be managed with passive warming tion (capnography or blood gas analysis). Shorter-acting
(e.g. warm air blankets or warm water beds). It is easier to NM blocking agents, such as atracurium or vecuronium,
prevent hypothermia than to treat it, so all efforts to pre- administered at one tenth of the usual dose, are the pre-
serve body temperature should be made. Although it is ferred agents. Infusions allow more precise control of the
unusual for animals to develop hyperthermia under degree of NM blockade than boluses, which create peaks
anaesthesia, increases in body temperature should be and troughs in plasma concentration and thus cause
managed by passive cooling. relative overdose and relative underdose, respectively.
 552 SPECIFIC MANAGEMENT ISSUES

Recovery Maintain a patent airway

Maintain adequate oxygenation and ventilation Animals with neuromuscular weakness or
As the animal recovers from anaesthesia, it is essential to post-gastric lavage
monitor end-tidal CO2 to ensure spontaneous ventila- In these animals extubation is delayed for as long as pos-
tion is sufficient to maintain normocapnia. These sible to ensure upper and lower respiratory muscle func-
animals will invariably have some degree of pulmonary tion is adequate. Recovery should be performed in a
pathology due to aspiration or atelectasis, so oxygenation quiet, dimly lit environment to minimize stimulation on
should be monitored throughout recovery and supple- recovery. The cuff of the ETT=endotracheal tube is left
mental oxygen provided until the animal can maintain inflated until the animal is ready to be extubated. Ade-
SpO2 >95% when breathing room air. Initially, this quate analgesia must always be provided in animals with
can be performed via the ETT; however, following painful diseases to optimize conditions for a smooth
extubation, oxygen can be provided by mask, oxygen emergence from anaesthesia. Low-dose infusions of
cage or nasal catheters. Where oxygenation is expected short-acting opioids can also help reduce stimulation
to be poor for prolonged periods (e.g. animals with pneu- from the ETT and help maintain a patent airway for
monia or animals expected to be recumbent following longer.
anaesthesia), nasal catheters should be placed before the
end of anaesthesia to provide a smooth stress-free transi- Animals with tetanus
tion from oxygenation via the ETT to the nasophar- Although tetanus does not cause NM pathology, it is
yngeal catheters. (Note: Animals that develop upper associated with severe muscle spasms. Extubation in
respiratory tract obstruction [e.g. laryngeal paralysis or patients with tetanus can stimulate laryngospasm. The
laryngeal spasm] following extubation may require a tra- safest approach is to recover these animals with a tra-
cheostomy to maintain adequate oxygenation and venti- cheostomy in place. If a tracheostomy is not performed,
lation [see below].) laryngospasm can be minimized by extubating early, as
long as the patient is ventilating spontaneously. Topical
Prevent aspiration lidocaine applied to the larynx may also help. In any
Suctioning of the oesophagus and pharynx should be case, it is essential to be prepared to perform an emer-
performed prior to recovery in order to minimize the risk gency tracheostomy should laryngospam occur and if
of regurgitation at extubation. The animal is best posi- reintubation is too difficult. Preparing the site before-
tioned in sternal recumbency with the head elevated to hand is recommended to save time should a tracheo-
maximize chest excursions and respiratory function. In stomy be required. The ability to provide oxygen
addition, elevation of the head will help prevent passive supplementation via an intratracheal needle or catheter
regurgitation. Should vomiting or regurgitation occur should also be available in case upper respiratory tract
during recovery, the animal’s head must be positioned obstruction occurs (see Chapter 2). (Note: This method
over the edge of the table to allow fluid or stomach con- of providing oxygen is only suitable for short periods, as
tents to flow out of the mouth. If the animal is still suffi- there is no concurrent ventilation, and overinflation of
ciently anaesthetized, the pharynx and mouth can be the lungs can occur because there is no outflow for the
cleared by suctioning and swabbing. To prevent oeso- insufflated oxygen.)
phagitis associated with regurgitation of gastric contents,
the oesophagus should ideally be carefully lavaged until
the fluid retrieved is clear. It is essential that the ETT is
secured in place with adequate cuff inflation when lavage
is performed.
 EMERGENCY NEUROANAESTHESIA 553

Table 106 Possible agents for sedating or anaesthetizing animals during long-term ventilation

DRUG DOSE COMMENTS

Inhalation agents: 1 minimum alveolar concentra- Not recommended for long-term ventilation in animals
isoflurane/sevoflurane tion equivalent or less with intracranial disease. Isoflurane can be irritant to
airway and therefore is best avoided. May have adverse
effects in airway disease or prolonged anaesthesia

Propofol 0.05–0.4 mg/kg/minute Ideal for animals with intracranial disease. Can be used
for any animal requiring sedation or anaesthesia for
ventilation

Midazolam 0.05–0.2 mg/kg/hour (do not Can be used in animals with intracranial disease that
dilute drug with Hartmann’s) require sedation for intubation. Dysphoria observed
with prolonged infusion may cause stressful recoveries.
Use cautiously in animals with neuro-
muscular weakness

Fentanyl 0.2–0.7 μg/kg/minute Can be used alone in paralysed animals or in

conjunction with other agents to provide
analgesia/sedation

SEDATION/ANAESTHESIA FOR CHRONIC short-acting agents that can be titrated to achieve the
INTUBATION AND MECHANICAL VENTILATION required level of sedation or anaesthesia in each individ-
ual are preferred.
The choice of agent used to maintain anaesthesia in
animals requiring ventilation will depend on the indi- Additional considerations for paralysed animals
cations for ventilation, the expected duration of ventila- The use of sedation or anaesthesia for ventilating para-
tion and whether the animal has an oral ETT or a lysed animals warrants special mention. Sedation or
tracheostomy. Ventilation techniques are discussed in anaesthesia is not required to tolerate the presence of an
Chapter 2. Examples of agents that can be used to ETT; however, as they recover from paralysis, sedation
provide sedation or anaesthesia for ventilation are listed or anaesthesia will be required to maintain intubation.
in Table 106. The reason for this is the differential recovery of differ-
ent skeletal muscles from paralysis, allowing these
Dose rates animals to move before being able adequately to ventilate
Maintenance of anaesthesia has ‘lighter’ requirements or protect their own airway. As a result, these animals can
than does surgical anaesthesia, and in some cases sedation start to struggle. Furthermore, it must be remembered
only may be needed. In animals intubated via tracheo- that even when a patient is fully paralysed they are con-
stomy, the depth of sedation/anaesthesia will be even scious and responsive to their environment, therefore
lower, as the stimulus associated with oral intubation is some sedation and/or analgesia is required to minimize
absent. Animals that are weak, paralysed or suffering stress and discomfort.
from CNS depression will also require much lower Nursing and airway management of the chronically
doses than those with normal CNS activity. Therefore, ventilated patient are covered in Chapter 2.
 554 SPECIFIC MANAGEMENT ISSUES

SPECIFIC CONSIDERATIONS FOR

DIAGNOSTIC PROCEDURES

Myelography
Myelography is associated with a risk of seizures on
recovery from anaesthesia and a variety of cardiopul-
monary abnormalities that can occur during anaesthesia,
particularly during/after contrast injection (418).

Seizure activity
Seizure activity is a recognized adverse effect of injection
of contrast agents into the subarachnoid space. The risk
of seizures is influenced by several factors including the
volume and rate of contrast injection, the site of injec-  418 Myelography is frequently performed to diagnose
tion, the size of the animal, duration of anaesthesia after intervertebral disc disease (as seen here). Performance of a
injection and the position of the animal during injection. myelogram requires special considerations for anaesthesia.
Seizures are more commonly observed after CMC myel- (Photo courtesy Victoria Johnson)
ography compared with lumbar myelography. Animals
weighing >20 kg are also observed to have a higher inci-
dence of seizures, possibly due to the relatively higher
volume of contrast injected.
To reduce the risk of seizures, the dose rate should be
calculated from surface area rather than body weight, the
speed of injection should be slow and the head should
be elevated as soon as injection is complete to promote
the flow of contrast away from the head. The use of a Cardiopulmonary disturbance
tilting table allows head elevation while keeping the Cardiopulmonary side-effects during or immediately
animal’s spine straight and supported. after the injection of contrast have been observed and
Pharmacological agents that decrease the seizure include apnoea, tachypnoea, bradycardia, tachycardia,
threshold should be avoided. Acepromazine, ketamine arrhythmias, hypotension and hypertension. Many of
and medetomidine have been previously reported to these effects are associated with the discomfort or pain of
decrease the seizure threshold, and most of the literature injection and can be minimized by slowing the injection
recommends that these agents are not used in animals rate and ensuring an adequate depth of anaesthesia
undergoing myelography. However, the association during injection. Transient increases in ICP may also be
between use of acepromazine and seizure activity has responsible, particularly with cisternal contrast injec-
become increasingly unclear and its effect may depend tions. Careful monitoring of cardiopulmonary function
on the cause of the seizure activity. The authors recom- is necessary during myelography to detect any problems
mend that its use be avoided whenever possible and if early and treat accordingly.
required for sedation/anxiolysis, it is used carefully and at
low doses. Magnetic resonance imaging
Seizures have been reported to occur up to 6 hours The main considerations for anaesthetizing patients with
after contrast injection, so these animals should be intracranial and spinal disease for MRI are described in
closely monitored during this time. If seizures occur, the relevant sections earlier in this chapter. In addition,
administration of diazepam (0.2–1.0 mg/kg IV) is recom- there are several important considerations unique to
mended as the first-line treatment. anaesthetizing a patient within a magnetic field.
 EMERGENCY NEUROANAESTHESIA 555

Equipment hazards ETTs reinforced with coiled wire resist kinking and
Ferromagnetic objects can become dangerous projectiles can be used to prevent airway obstruction when the neck
and may result in injury and/or death to the patient or is flexed for collection of CSF. As these tubes contain
personnel within the scanning room. It is essential that metal, they are not suitable for use in animals undergoing
these objects remain outside the 5 gauss line. Anaesthet- concurrent MRI imaging.
ic machines are required to be as close to the patient as In animals with increased ICP the collection of CSF
possible to minimize the length of the breathing system carries the risk of parenchymal herniation. When sam-
and should be composed of non-ferromagnetic materi- pling is essential for the diagnosis and treatment of the
als. If this is not possible, a non-rebreathing anaesthetic animal, pre-emptive use of mannitol (30 minutes prior to
circuit (e.g. Bain) can be used, as the length of the inspi- CSF collection) and reduction of PaCO2 to 30 mmH
ratory and expiratory tubes (which are coaxial) may be g (4 kPa) by hyperventilation during the sampling period
effectively infinite. Non-ferromagnetic objects within a may reduce the risk of herniation.
magnetic field (e.g. ECG leads) have the potential to
induce electric currents, leading to heating and burns. Electroencephalography
The risk of burns can be minimized by insulating the Electroencephalography records the spontaneous elec-
wires, separating the wires from the skin by padding, trical activity within the brain and may be performed
avoiding large loops of wire that allow the induction of in animals to identify areas of abnormal electrical
currents and applying sensors as far away from the activity responsible for seizures. Performance of electro-
imaged area as possible. encephalography in conscious animals is difficult, as
muscle movement causes artefacts, which affect the diag-
Monitoring nostic quality. Inhalational and intravenous anaesthetic
Monitoring of the anaesthetized patient during MRI has agents also alter the electrical activity within the brain in
inherent limitations. Equipment used for monitoring a dose-dependent manner, thus limiting the amount of
must be MRI safe and ideally MRI compatible. Equip- useful information that can be obtained from electro-
ment that is MRI safe has been demonstrated to present encephalography in anaesthetized animals. A sedative
no additional risk to the patient. Equipment that is MRI regimen used to perform electroencephalography in
compatible has been demonstrated to be both MRI safe conscious animals has been described. This regimen was
and to not reduce significantly the diagnostic quality of reported to limit spontaneous movement in conscious
the imaging procedure nor have its operation affected by animals, while reducing the effects of deep sedation or
the scanning procedure. MRI compatible equipment is general anaesthesia on the recorded EEG. However, this
currently available that allows distant monitoring of report describes the use of high doses of acepromazine, a
animals during MRI. Where cost is limited, some moni- drug that may decrease seizure threshold. As discussed
toring equipment, such as capnography, oesophageal above, the association between seizures and acepro-
stethosope and oscillometric methods of non-invasive mazine is still unclear and its use in animals with patho-
BP measurement, can be used if the electrical compo- logical causes of seizure activity should be performed
nents are outside the 5 gauss line. cautiously.

Cerebrospinal fluid collection

The collection of CSF may be performed by CMC or
lumbar puncture. CMC puncture requires flexion of the
neck, which can cause inadvertent kinking of the ETT
and respiratory obstruction. In addition, flexion of the
neck can obstruct jugular veins, impair venous drainage
and contribute to increased ICP. IPPV is essential during
CMC puncture to ensure adequate ventilation and
normocapnia.
This page intentionally left blank
 SPECIFIC MANAGEMENT ISSUES Chapter 30

ANALGESIA FOR PATIENTS WITH

NEUROLOGICAL DISEASE 557

Gabrielle Musk
& Anthea Raisis

INTRODUCTION a

Pain is defined by the International Association for the

Study of Pain as an unpleasant sensory and emotional
experience associated with actual or potential tissue
damage or expressed in terms of such damage. Recogni-
tion of the presence of pain and assessment of the severity
of pain are essential for optimal management and are
integral steps towards appropriate treatment of pain in
animals with (and without) neurological disease. Poorly
managed pain is a significant contributor to morbidity
and mortality, has adverse welfare implications and
delays the return to normal function. Good pain
management relies on regular pain assessment and
includes the administration of analgesic drugs (419).
The aims of pain treatment are to: b
• Inhibit the neuroendocrine stress response, which
may compromise recovery.
• Maintain tissue perfusion.
• Allow restful sleep.
• Encourage mobility.
• Improve appetite.
• Attenuate peripheral and central sensitization.

A plethora of drugs exist that can be used alone or in

combination to manage pain in animals with neurologi-
cal disease. Analgesic therapy must be tailored to each
individual animal based on the cause, duration and  419 (a) A dog following hindlimb amputation with
severity of pain, the level of consciousness, the presence inadequate analgesia. (b) The obvious difference in this
of coexisting diseases and the impact of expected animal’s behaviour is demonstrated after adequate
side-effects (420, p. 559). This chapter describes specific analgesia was provided.
considerations for selecting analgesic agents for pain
management of animals with acute neurological disease
and provides examples of analgesic regimens that may be
suitable for these patients. The physiology of pain and
the pharmacology of analgesic drugs are beyond the
558 SPECIFIC MANAGEMENT ISSUES

scope of this book, but a good understanding of both is Table 107 Neuropathic pain
vital to ensure optimal pain management (see Further
reading). Furthermore, familiarity with available drugs TERMINOLOGY DEFINITION
will guide the clinician’s decision making.
Allodynia A pain response to a non-painful
Painful stimuli may cause an acute pain response and stimulus. This is usually localized to the
poorly managed pain can lead to neurophysiological area of the initial injury
changes that are permanent. Furthermore, certain types
Hypersensitivity An exaggerated pain response to a
of pain are particularly difficult to manage and require a
painful stimulus. This phenomenon
multimodal approach. The clinician should be prepared occurs as a result of ‘sensitization’
to trial therapy and assess the response before commit-
Peripheral ‘Wind up’ of peripheral nociceptors
ting to a long-term plan. Neuropathic pain is particular-
sensitization leading to an exaggerated pain
ly difficult to manage and is often not responsive to response to stimulation
opioids. It is produced by peripheral and central sensiti-
zation and may be present as allodynia or hypersensitivi- Central ‘Wind up’ of central nociceptors
sensitization leading to generalized exaggerated
ty (Table 107). It may be continuous or sporadic and is pain response to stimulation
described as burning, shooting, tingling or electric in
nature.

Pain assessment Table 108 The multiple steps of the

Accurate assessment of pain in animals is difficult. In nociceptive pathway
animals with acute neurological disease it is even more
TERMINOLOGY DEFINITION
challenging, especially if a patient is moribund or
depressed. Conversely, physical examination may reveal Noxious stimulus A mechanical, chemical or thermal
tachycardia, tachypnoea and hypertension, which com- stimulus that causes pain. Pain is the
plicates objective assessment of autonomic nervous sensory and emotional experience
associated with actual or potential
system activity. These cases are easy to misinterpret tissue damage resulting from a noxious
and concern about the adverse effects of analgesic drugs stimulus
may influence clinical decision making. Given the scope
Transduction Processing the noxious stimulus from
and variability of responses to painful stimuli in human
the peripheral site to the sensory nerve
patients, every effort must be made to perform a thor- endings
ough pain assessment in each animal patient and treat
Transmission Signalling along sensory nerves to the
accordingly. Furthermore, assessment of the response to
central nervous system. Sensory nerves
therapy is essential to ensure that pain is adequately and may be small myelinated A fibres
continuously controlled. associated with sharp mechanical-type
In human medicine, self-reporting of pain is the gold stimuli or unmyelinated C fibres
standard method of pain assessment. In veterinary medi- associated with dull, burning or longer
lasting pain
cine, pain assessment has been performed somewhat
subjectively or by applying pain scales used in humans. Modulation Alteration of the incoming signal by
These include simple descriptive scales, numerical rating synapsing in the dorsal horn of the
spinal cord. Neurotransmitters are
scales and visual analogue scales. There are inherent lim-
involved in the propagation of ongoing
itations with each of these scales; they are one-dimen- impulses in the central nervous system.
sional and they have been shown to be unreliable in the Synapses within the grey matter of the
setting of acute postoperative pain in dogs. They have, spinal cord also connect with the
ventral horn to complete the reflex arc.
however, had their place in the evolution of pain assess-
This manifests as a withdrawal
ment in animals and have contributed to the understand- response to a noxious stimulus
ing of the complexity of the pain experience.
 ANALGESIA FOR P AT I E N T S WITH NEUROLOGICAL DISEASE 559

 420 The different classes of analgesic

drugs interfere with the pain process at
different points and a multimodal approach
is invariably most appropriate. The sites of
action of each class of medication are
highlighted. (See also Table 108.)
Perception
Opioids Transmission
Alpha-2 agonists Local anaesthetics
Tramadol
Transduction
Projection Opioids
NSAIDs
Modulation Alpha-2 agonists
Opioids Tramadol
NSAIDs
Alpha-2 agonists Noxious stimulus:
mechanical,
Tramadol
chemical, thermal

The only validated pain scoring system for acute pain pain score is 24 (or 20, if mobility is impossible to assess)
in dogs is the Glasgow Composite Measure Pain Scale and it is reported that a clinical decision point for
(GCMPS), which is a multidimensional scale taking into analgesia gave an intervention level of 6/24 (or 5/20 if
account not just the intensity of pain, but its conse- mobility could not be assessed).
quences. The GCMPS is based on psychometric princi-
ples that are well established in human medicine for the Analgesic drugs
measurement of complex constructs such as intelligence, Analgesic drugs fall into the following categories:
pain and quality of life. It categorizes and weights • Opioids.
spontaneous and evoked behaviour and interactive and • NSAIDs.
clinical observations (comfort, vocalization, mobility, • Local anaesthetics.
demeanour, posture, attention to surgical wound and • Alpha-2 adrenoceptor agonists (e.g. medetomidine).
response to touch), resulting in a composite score. It is • N-methyl-D-aspartate antagonists (e.g. ketamine).
practical in a clinical setting and easy to become familiar • Miscellaneous drugs (e.g. gabapentin, tramadol,
with and use. As it forces the assessor to evaluate behav- nitrous oxide).
iour that may be associated with pain and draw conclu-
sions about whether or not the animal requires additional Most analgesic drugs will diminish pain; they are
analgesia, it contributes to improved pain management. hypoalgesic in effect, rather than entirely abolishing it.
A short form of the GCMPS for dogs suffering acute The effects are usually dose dependent and an under-
postoperative pain has been developed for use in a clini- standing of nociceptive pathways, pain transmission,
cal setting where the emphasis is on speed, ease of use and modulation and perception, the chemical mediators of
guidance for provision of analgesia as opposed to precise pain and inflammation and their impact on pain
measurement of pain in a research environment. The processing will help the decision-making process (420
short form comprises six behavioural categories (vocal- and Table 108). The different classes of analgesics
ization, mobility, demeanour, posture, attention to interfere with the pain process at different points and a
surgical wound and response to touch). The maximum multimodal approach is invariably most appropriate.
560 SPECIFIC MANAGEMENT ISSUES

INTRACRANIAL DISEASE while pain may cause either hypoventilation if chest

excursions are uncomfortable or hyperventilation if
Overview the pain is poorly managed. Close monitoring of
Management of pain in animals with intracranial disease pulmonary function and careful adjustment of doses
is important from a welfare perspective and because pain are required to provide appropriate analgesia
itself may increase ICP. This occurs because of sympa- without respiratory depression.
thetic nervous system-modulated increases in BP. • Neurological assessment. Analgesic drugs often
cause tranquillization or sedation. Caution should
Considerations be exercised if these side-effects are likely to impede
• Cerebral perfusion. Selected analgesic drugs and assessment and mask neurological deterioration.
management techniques should have little impact Low doses of short-acting drugs are preferable and
on regulation of CBF. Minimal depression of the a neurological examination should be performed
cardiovascular and respiratory systems is important prior to the administration of any medication.
for maintaining adequate cerebral perfusion and • Severity of pain. As nociceptors are present in the
oxygenation while minimizing secondary neuronal meninges and skull, the severity of pain will depend
injury. Hypoventilation and consequent hyper- on involvement of these structures in the disease
capnia may increase CBF and therefore increase process. Animals with meningitis (421) or skull
ICP, while hyperventilation and hypocapnia may fractures (422) are expected to suffer from severe
cause cerebral vasoconstriction and compromise pain and should be treated accordingly. Animals
CBF. Higher doses of opioids may contribute to with concurrent trauma to other body systems are
hypoventilation through respiratory depression, also expected to suffer severe pain.

 421 Meningitis is suspected based on the meningeal  422 Radiograph of a frontal bone fracture (arrow) in a
enhancement present in this dorsal T1-weighted post- dog. This lesion would be expected to contribute to the
contrast MR image (arrows). This condition can be pain present in the animal following its head trauma.
extremely painful. (Photo courtesy Victoria Johnson) (Photo courtesy Victoria Johnson)
 ANALGESIA FOR P AT I E N T S WITH NEUROLOGICAL DISEASE 561

Drug selection Full mu agonist opioids can be reversed in the event

Opioids of undesirable side-effects. The potential complications
Opioids are often administered to patients with intra- of opioid administration, particularly important to
cranial disease. A summary of the characteristics and dose animals with intracranial disease, include bradycardia
regimes of commonly used opioids is presented in (with potential hypotension) and respiratory depression
Table 109. (with associated hypercapnia). Hypotension associated

Table 109 Opioid analgesic agents used for perioperative pain control in dogs and cats with
neurological disease

AGENT ADVANTAGES DISADVANTAGES DOSE

Morphine Excellent analgesia (full mu agonist). Nausea and vomiting may occur, but are 0.1–0.4 mg/kg IV/IM*
Can be infused intravenously more likely if given to a pain-free animal. q2–6h** CRI: 0.05–0.1
Histamine release is reported following mg/kg/hour
rapid IV injection

Methadone Excellent analgesia (full mu agonist). Pharmacokinetics in small animals unclear. 0.1–0.4 mg/kg IV/IM*
Moderate duration of action. May accumulate with repeated dosing q2–6h**
Antagonizes NMDA receptors

Oxymorphone Excellent analgesia (full mu agonist) Bradycardia, respiratory depression, 0.05–0.2 mg/kg
(US) sedation occur at conservative doses IV/IM

Hydromorphone Excellent analgesia (full mu agonist) Hyperthermia associated with >0.1 mg/kg. 0.05–0.2 mg/kg
(US) Vomiting (especially with SC injection) IV/IM

Pethidine Good analgesia (full mu agonist) Potent releaser of histamine when given 2–5 mg/kg IM/SC
(meperidine US) IV. Pain on IM injection. Large volume. q1–2h**
Short duration of action (1–2 hours)

Fentanyl Excellent analgesia (full mu agonist). High doses cause respiratory depression CRI: 3–24 μg/kg/hour;
Short duration of action (15–20 and bradycardia transdermal patches:
minutes). Suitable for infusion 2–5 μg/kg/hour

Remifentanil Excellent analgesia (full mu agonist). Short duration of action (3 minutes). CRI: 3–24 μg/kg//hour
Short duration of action (3 minutes). Higher doses cause respiratory depression
Suitable for infusion and bradycardia

Tramadol Analgesia for moderate pain. May cause nausea, vomiting, dizziness. 1–2 mg/kg PO/IM/IV
Capsules and syrup available for oral Increases risk of seizures in susceptible q6–12h
administration patients. Use cautiously with head injuries

Buprenorphine Long duration of action (6–8 hours). Analgesia for moderate pain (partial mu dog: 0.006–0.01 mg/kg
May provide more analgesia than agonist). Prolonged onset of action (30–60 IV/IM/SC* q6–8h;
morphine in cats minutes) cat: 0.005–0.01 mg/kg
IV/IM q4–8h.

Butorphanol Good sedative Analgesia for mild pain (kappa agonist). 0.05–0.4 mg/kg IV/IM*
Short duration of action (1–2 hours).
mu receptor antagonist

* Where a dose range is given, the lower doses are recommended for IV administration (where specified) or IM
injection in depressed animals and the higher doses for IM administration in alert animals/animals in pain.
** Cats may have slower metabolism and may require less frequent administration.
CRI = continuous rate infusion.
 562 SPECIFIC MANAGEMENT ISSUES

between adequate analgesia and minimal CNS, cardio-

vascular and respiratory depression (and increase in
PaCO2) must be achieved. Patients with high ICP may
be extremely sensitive to the sedative, cardiovascular and
respiratory depressant effects of opioids, so great care
should be taken and conservative doses should be admin-
istered in the first instance. The authors have observed
markedly reduced mentation using low infusion rates of
fentanyl. It is recommended that infusions of fentanyl
are started as low as 1 μg/kg/hour in animals with head
trauma and increased gradually to achieve the desired
level of pain management without causing further dete-
 423 Pupillary dilation in a cat after rioration in mentation. When analgesia cannot be
premedication with an opioid. achieved without respiratory depression, the application
of IPPV (manual or mechanical) will be required to
maintain normocapnia.

Animals with moderate to severe pain

(e.g. postoperative period), having received pre-
with opioid-induced bradycardia is not common in and intraoperative analgesia
normovolaemic patients with normal myocardial Intermittent dosing of full mu receptor agonists (e.g.
function. Often, the arterial BP remains stable or methadone, 0.1–0.4 mg/kg IM) may be adequate for
improves as the increased time during diastole associated animals with severe to moderate pain. However, pain
with the slight reduction in heart rate allows for management can only be achieved by maintaining a
improved ventricular filling and an increased stroke stable therapeutic plasma concentration of drug. This in
volume. Conservative doses of opioids are unlikely to turn ensures a stable, effective (e.g. brain or peripheral
cause significant respiratory depression in normal dogs nociceptor) concentration of drug. To achieve a stable
and cats, but in those with increased ICP the effects may plasma concentration of opioid, an infusion that can be
be more marked. Care should be taken and therefore the adjusted according to clinical effect is best. Intermittent
adequacy of ventilation should be closely monitored. ‘bolus’ dosing will cause periods of relative overdose and
Opioids are also reported to cause pupillary constriction periods of relative underdose. Morphine and other
in dogs and pupillary dilation in cats (423), which has the opioids that may induce emesis should not be used if
potential to interfere with neurological assessment. In there is any contraindication to vomiting (e.g. raised
conscious animals these side-effects do not appear to be a ICP). The use of tramadol for perioperative analgesia is
problem at the low doses used clinically. However, in currently popular, but there are only a few reports in the
animals with CNS depression, these side-effects can be literature documenting its use and efficacy in dogs.
exacerbated. While it may be appropriate for animals in moderate to
severe pain, it is the authors’ opinion that it should be
Animals in severe pain, without pre-emptive reserved for use as an adjunct to an analgesic protocol. A
analgesia (e.g. trauma) reported side-effect of tramadol in humans is seizures,
The use of short-acting reversible opioids, such as and while this seems to be a risk for veterinary patients as
fentanyl or remifentanil, is preferred in patients in severe well, it is unknown how significant a problem this may
pain. These drugs have a relatively fast onset and short be. If the patient is receiving other medication that affects
duration of action, giving them a pharmacokinetic profile the reuptake of serotonin, drug interactions should be
suitable for infusion. The infusion rate can therefore taken into account. In such cases a low dose of tramadol
be titrated to achieve the desired clinical effect. A balance or an alternative analgesic drug should be used.
 ANALGESIA FOR P AT I E N T S WITH NEUROLOGICAL DISEASE 563

Animals with mild pain Other agents

Mild pain can be managed with drugs such as buprenor- A summary of other agents available for use in animals
phine (0.01–0.02 mg/kg IM q4–6h) or pethidine (2–5 with neurological disease is presented in Table 110.
mg/kg IM q1–2h). The appropriate interval between NSAIDs are also useful, but if any contraindication is
drug administrations will depend on the anticipated identified (e.g. circulatory shock, coagulopathies, gastric
duration of action of an individual drug. It is always mucosal bleeding, corticosteroid administration, renal
better to aim for a continuum of pain control, so regular disease), they should be avoided. Ketamine should
dosing is important. To achieve a continuum, subsequent be avoided in patients with intracranial disease and
doses of drug should be administered before the plasma associated increased ICP, as they may be exacerbated by
concentration of the drug has decreased. Pethidine is a ketamine. Alpha-2 adrenoceptor agonists should be used
full mu agonist, but it does not produce analgesia compa- with extreme caution, as their vasoconstrictive effects
rable to morphine, methadone or other full mu agonists. may further compromise CBF. Corticosteroid adminis-
It is often associated with an increase in heart rate as it has tration may contribute to pain management in certain
an atropine-like structure. Pethidine should only be disease processes (e.g. meningitis or neoplasia associated
given intramuscularly as the potential for histamine with marked peritumoural oedema) through their anti-
release following intravenous injection is high. Further- inflammatory action. However, corticosteroids may
more, pain associated with intramuscular injection and potentiate neuronal ischaemia in a hypoxic environment
the frequent dosing required for continuous analgesia (see Chapter 20).
make pethidine a less desirable option for pain manage-
ment compared with other opioids.

Table 110 Non-opioids used as part of pain management in animals with spinal disease

AGENT ADVANTAGES DISADVANTAGES DOSE REGIMEN

Benzodiazepines: Muscle relaxation Disinhibition in healthy animals. Diazepam: 0.1–0.2 mg/kg

diazepam, Respiratory depression in animals with IV/PO. Midazolam:
midazolam underlying respiratory disease/ 0.1–0.4 mg/kg IV/IM
insufficiency

Phenothiazine Anxiolysis, sedation Hypotension; avoid in hypovolaemia. 0.01–0.05 mg/kg IV/IM

tranquillizers: Contraindicated in carbamate and
acepromazine organophosphate poisoning

Alpha-2 agonists: Sedation, muscle relaxation, Adverse cardiovascular effects: avoid in Medetomidine: bolus,
medetomidine, analgesia. Dexmedetomidine animals with heart disease, hypo- 1–2 μg/kg IV up to 3–5 μg/kg
dexmedetomidine is associated with fewer volaemia. Hyperglycaemia: avoid in IM; CRI, 0.5–3 μg/kg/hour.
cardiovascular side-effects diabetics and head trauma. High Dexmedetomidine: Bolus,
than medetomidine incidence of vomiting in cats 1 μg/kg IV; CRI, 0.5–1
μg/kg/hour

NMDA antagonists: Analgesia. May be useful to treat Dysphoria associated with accumulation Ketamine: CRI,
ketamine, neuropathic pain. Interferes with of norketamine with prolonged infusion, 5–10 μg/kg/minute (can be
amantadine central sensitization. Reverse therefore requires dose reduction with used with morphine or
tolerance associated with time. Arrhythmogenic: avoid in chest lidocaine CRI). Amantadine:
prolonged opioid administration trauma. Increased skeletal muscle tone 3–5 mg/kg PO q24h
may potentiate pain due to muscle
spasm. Pain on IM/SC injection. Cerebellar
dysfunction reported anecdotally in some
breeds of cat (Continued)
 564 SPECIFIC MANAGEMENT ISSUES

Table 110 Non-opioids used as part of pain management in animals with spinal disease (continued)

AGENT ADVANTAGES DISADVANTAGES DOSE REGIMEN

Tricyclic May be useful in the treatment of Vomiting and diarrhoea, excitability, 1–2 mg/kg PO q12h
antidepressants: neuropathic pain. Blocks nor- arrhythmias. Consider drug interactions if
amitriptyline adrenaline and serotonin reuptake using anaesthetics or antiepileptics.
in the brain, increasing the effect Enhanced sedation if used with other
of these neurotransmitters sedating drugs

Lidocaine Analgesia. May be useful in Sedation may interfere with mobility. Initial bolus of 2 mg/kg
neuropathic pain Myocardial depression can cause hypo- followed by 20–50
tension in unstable patients. Vomiting μg/kg/minute
reported. DO NOT USE IN CATS

Gabapentin Supplementary analgesia for Sedation and ataxia Titrate dose from 2 mg/kg up
neuropathic pain to 10–20 mg/kg PO q8–12h

SPINAL DISEASE • Anxiolysis. Anxiety in weak or paralysed animals

may decrease the pain threshold. The judicious
Considerations administration of anxiolytics is a useful part of pain
• Neuronal function. Aiming to preserve neuronal management in haemodynamically stable animals.
function by maintaining perfusion and oxygenation • Muscle relaxation. The administration of muscle
is vital. Agents that cause excessive depression of relaxants is useful in reducing pain associated with
cardiovascular and pulmonary functions should be muscle spasm. (Note: Do not use in animals with
avoided. Arterial BP and adequacy of ventilation unstable fractures.)
(using a capnograph) should be monitored closely. • Neuropathic pain. When present, neuropathic
• Pain. Pain associated with spinal disease (424) is pain is often resistant to opioid analgesia and
likely to be severe, necessitating the use of potent requires a multimodal analgesic regime.
analgesic drug combinations by continuous • Multimodal analgesia. A combination of analgesic
infusion. agents can be administered concurrently to
optimize pain management and minimize the
frequency and severity of side-effects associated
with individual agents.

Drug selection
Opioids
Due to the severity of pain in most animals with spinal
disease, opioid analgesics are often the best choice. The
advantages and disadvantages of commonly used opioids
and appropriate dose rates are described in Table109.

Animals in severe pain (e.g. spinal trauma)

As previously described for animals with intracranial
disease (see above), the use of short-acting reversible
 424 Animals with spinal disease, such as the one in this opioids, such as fentanyl or remifentanil, is preferred in
picture, will be in pain and require administration of animals with severe pain (e.g. trauma victims with multi-
analgesic agents. ple organ damage and orthopaedic injury).
 ANALGESIA FOR P AT I E N T S WITH NEUROLOGICAL DISEASE 565

a b

c d

 425 Steps for placement of a fentanyl patch. (a) Clip

the skin prior to placement of the patch. (b) Wipe the
skin with a dry swab only. (c) Wear gloves when
positioning the patch. In this case two patches are being
used (25 μg/hour and 50 μg/hour). (d) Ensure even
adherence to the skin with gentle digital pressure.
(e) Cover the patches with a light adhesive dressing and
label with the name of the drug and the time and date
of application.

Stable animals requiring intensive pain control The transdermal delivery of drug from a patch
During the immediate post-trauma or post-surgical applied to the skin (e.g. fentanyl patches, 425) may
period, the continuous infusion of opioids (e.g. fentanyl provide a useful adjunct to perioperative analgesia. It may
or morphine) is more likely to prevent breakthrough take up to 24 hours for therapeutic plasma concentra-
pain. Opioid infusions can be combined with other tions to be achieved, so analgesia will be required until
agents to achieve multimodal pain management (e.g. an this time. The delay is shorter in cats than in dogs.
opioid in combination with ketamine and/or lidocaine). Because there is also marked individual variation in
Infusion rates for each of the individual drugs are absorption and, therefore, plasma concentrations
provided in Tables 109 and 110. achieved, fentanyl patches should not be relied on as the
 566 SPECIFIC MANAGEMENT ISSUES

sole method of providing analgesia. Buprenorphine Muscle relaxants

patches are also available and should be used with the Benzodiazepines (diazepam or midazolam, 0.25–0.5
same caveats as fentanyl patches. Patches should not be mg/kg PO q6–8h) may provide a useful adjunct to pain
cut in half. If a lower dose is required, then creating a management in patients with stable spinal injury by alle-
barrier between the patch and the skin is most appropri- viating muscle spasm, which is commonly observed in
ate. It is best to place the patch on a clipped area of skin animals with spinal disease. In animals with unstable
out of reach of the patient. The lateral thorax, dorsum or spinal lesions (e.g. fractures), skeletal muscle relaxation
neck may be appropriate. may be detrimental as it reduces the splinting effects of
the epaxial muscle.
Stable animals requiring less intensive pain control Alpha-2 agonists, such as medetomidine, can also be
When less intensive management of the animal is used to provide muscle relaxation. In addition, these
required, intermittent administration of full mu opioids agents are analgesic. Because of sedative and cardio-
such as methadone or morphine can be used. Although vascular side-effects, these agents are generally limited to
vomiting is less likely in animals in pain, the use of mor- animals that do not have cardiovascular pathology. The
phine is generally avoided in animals with cervical injury authors have found that infusing medetomidine at
where violent movements associated with vomiting can 1–3.5 μg/kg/hour is useful in healthy dogs that have pain
cause further injury to an unstable spinal lesion. In or anxiety that is unresponsive to other drugs. As with
addition, recumbent animals that vomit may not be able benzodiazepines, these agents should be avoided in
to clear vomitus from the pharynx and mouth, predispos- animals with unstable spinal fractures.
ing to airway obstruction and aspiration.
Anxiolytics
Other agents Acepromazine is an extremely useful agent for anxious
A variety of other agents can be used in conjunction with animals with spinal disease. Due to its hypotensive
opioids to improve pain management. A summary of effects, the use of this agent should be limited to normo-
these agents can be found in Tables 110 and 111. volaemic and normotensive animals. The side-effects
are dose dependent; the authors use 0.01–0.05 mg/kg
Non-steroidal anti-inflammatory drugs to a maximum of 1 mg/kg. Acepromazine is also more
NSAIDs may be used to decrease inflammatory pain and effective if combined with an opioid (e.g. 0.03 mg/kg
they are potent analgesics in their own right. The cyclo- acepromazine with 0.3 mg/kg morphine for sedation).
oxygenase inhibitors carprofen, meloxicam and meclo- Trazodone can also be used for this function (see p. 545).
fenamic acid are registered for perioperative use (Table
111). The lipoxygenase and cyclo-oxygenase inhibitor N-methyl-D-aspartate antagonists
tepoxalin was available to the veterinary market, but it Ketamine is becoming increasingly popular as part of a
has been associated with an increased incidence of multimodal analgesic protocol in small animals. Keta-
adverse side-effects. mine interferes with the process of CNS sensitization
Concurrent administration of NSAIDs and cortico- (wind-up), which may manifest as hyperalgesia (exagger-
steroids is contraindicated due to increased risk of gastro- ated pain response to a painful stimulus) or allodynia
intestinal ulceration and haemorrhage, therefore the use (pain response to a non-painful stimulus) from peripheral
of NSAIDs is best delayed until it has been decided and central sensitization. It plays an extremely important
whether the patient will benefit from corticosteroid role in the management of animals with chronic pain,
therapy. For animals receiving either steroids or animals with direct nerve trauma, amputees and trauma
NSAIDs, concurrent administration of gastrointestinal patients. Care is required when using this agent in
protectants may help reduce the incidence of gastro- trauma patients where the arrhythmogenic effects of
intestinal ulceration. ketamine may exacerbate myocardial contusions or
 ANALGESIA FOR P AT I E N T S WITH NEUROLOGICAL DISEASE 567

Table 111 Non-steroidal anti-inflammatory drugs

DRUG SIDE-EFFECTS DOSE RATE: DOGS DOSE RATE: CATS

Carprofen Minimal. Vomiting 2 mg/kg PO, SC or IV q12h or 2 mg/kg SC once only

4 mg/kg q24h

Meloxicam Minimal. Diarrhoea 0.2 mg/kg PO, SC or IV q24h 0.1–0.2 mg/kg PO or SC

then 0.1 mg/kg q24h once only. 0.1 mg/kg q24h
thereafter for 3 days

Meclofenamic acid Vomiting and diarrhoea 1–2 mg/kg PO q24h Not used

ischaemia and associated arrhythmias. At higher doses and at lower doses than in dogs, as the former species is
the cardiovascular effects of ketamine can become prob- more sensitive to the neuroexcitatory effects of lidocaine.
lematic (increased heart rate and BP). The authors use Lidocaine patches are also available and may be useful
2–10 μg/kg/minute by infusion for analgesia (higher end for topical analgesia prior to attempting vascular access
of dose rate if intraoperatively and lower end if con- or for the management of incisional pain. The onset of
scious). A ‘bolus’ dose of ketamine may be incorporated action is relatively rapid. (The area should be clipped and
into a premedication for cats (5–10 mg/kg) and very dif- the patch secured in position to avoid inadvertent
ficult dogs (1–2 mg/kg). Dogs are more prone to the dis- ingestion by the patient. Care should also be taken to
sociative effects of ketamine, so lower doses should be avoid heating the area, as this may accelerate absorption
used in this species. As part of an induction combination, and increase the potential for side-effects.)
ketamine can be given at 5 mg/kg with a benzodiazepine
(e.g. diazepam or midazolam, 0.25–0.5 mg/kg). Tramadol
Methadone may also act as an antagonist at the Tramadol is an agent with weak mu opioid agonist and
NMDA receptor and this is thought to be especially non-opioid analgesic properties. The non-opioid effects
beneficial in the treatment of neuropathic pain that may are associated with increased noradrenaline (norepine-
otherwise be resistant to typical opioids. phrine) and 5-hydroxytryptamine (serotonin) at central
neuronal synapses, which reduces the excitability of
Lidocaine spinal nociceptive activity, partly via alpha-2 adrenergic
The effectiveness of this agent in spinal pain has not been activity. The activities of the opioid and non-opioid
determined. It should, however, be considered if pain is mechanisms are synergistic, resulting in greater analge-
unresponsive to other agents. It can be administered sia than that expected for each component acting
either alone or in combination with morphine and/or separately. The efficacy of tramadol postoperatively in
ketamine. Infusion of each drug is adjusted to optimize humans appears to be similar to that of μ opioid agonists.
analgesia but minimize sedation. Lidocaine can depress It can be administered parenterally and enterally. Com-
cardiovascular function and contribute to hypotension, prehensive clinical studies in animals are currently
therefore it is essential that animals are normovolaemic lacking. Tramadol has a wide therapeutic margin and
and that cardiovascular function is monitored during while most dosing is based on anecdotal reports it is
administration. It should also be used cautiously in cats common to use 1 mg/kg q12h or q8h.
568 SPECIFIC MANAGEMENT ISSUES

NEUROPATHIC PAIN Drug selection

Any of the drugs used for management of spinal pain can
Neuropathic pain (426) is classically less responsive to be used for management of animals with painful NM
opioids and difficult to manage. It may occur in patients disease. The choice will depend on the stability of the
with lumbosacral disease, neuropathy, nerve root trauma animal and the severity of the pain.
and a number of other conditions. Other agents that may
be useful in animals suffering neuropathic pain include Regional and local anaesthesia in animals with
ketamine, amantadine, medetomidine, lidocaine, tra- neurological disease
madol, gabapentin and tricyclic antidepressants. A While pain associated with intracranial disease and
summary of these agents and doses rates are found in generalized NM disease is not amenable to regional
Table 110. anaesthesia, this modality may be useful for managing
Gabapentin’s mode of action in the treatment of pain associated with trauma to other regions of the body.
neuropathic pain is thought to be by prevention of the Regional anaesthesia may also be used in certain spinal
release of glutamate in the dorsal horn via interaction diseases. Regional and local anaesthesia provide the ulti-
with the alpha-2/delta subunit of the voltage-gated mate in analgesia if the innervation of an area can be iso-
calcium channels. While gabapentin has been used safely lated and completely desensitized.
in dogs, only anecdotal reports of its efficacy have been In patients with chest wall trauma, intrapleural or
published. intercostal nerve blocks are effective as an adjunct to an
analgesic regime. A maximum dose of 2 mg/kg of bupi-
NEUROMUSCULAR DISEASE vacaine should be administered every 6 hours. For
intrapleural analgesia this dose may be diluted to increase
Considerations the volume or combined with NaHCO3 to minimize the
• Severity of pain. The type of NM disease will discomfort associated with the low pH of the solution.
influence the severity of pain and the choice of For intercostal nerve blocks, two intercostal spaces either
analgesic agents. Some conditions may not be side of the lesion or surgical wound should be blocked
painful, so careful pain assessment is essential. (five spaces in total). The intercostal nerves cross-inner-
• Ventilation. Animals with NM disease frequently vate, so it is essential to block at least five spaces. The
have impaired ventilation. This may be exacerbated nerve runs caudal to the rib. Epidural administration of
by drugs that depress spontaneous ventilation analgesic drugs will provide additional analgesia in
(e.g. opioids). animals with concurrent pelvic and abdominal trauma
• Vomiting. Animals with NM disease may not be (see Further reading). Epidurals have also been used to
able to protect their airway. In addition, vomiting provide analgesia in animals with spinal fractures,
may trigger laryngeal spasm in animals with although the use of local anaesthetic by this route, and
tetanus. Agents that predispose to vomiting (e.g. consequent motor (and sensory) blockade, should gener-
morphine) should be avoided. ally be avoided, as motor function is an essential part of
• Sedation. The use of analgesic agents with sedative neurological assessment. Local anaesthetic drug prepara-
properties may exacerbate recumbency and tions may be diluted to minimize motor blockade (e.g.
immobility in animals with NM weakness. In 0.25% bupivacaine can be diluted to 0.125%) or ropiva-
contrast, sedation can be useful in animals that are caine may be used. Epidural administration of local
hyperaesthetic (e.g. polyradiculoneuritis). (Note: anaesthetics should be avoided in haemodynamically
Acepromazine is contraindicated in methiocarb and unstable animals as sympathetic nerve blockade will
organophosphate poisoning.)
 ANALGESIA FOR P AT I E N T S WITH NEUROLOGICAL DISEASE 569

exacerbate hypotension. In these cases, epidural admin- Non-specific aspects of pain management in
istration of morphine alone (0.1 mg/kg diluted in sterile animals with neurological disease
saline to the desired volume) can still provide useful • Bedding should be well padded, able to wick
regional analgesia. The volume of injection is a factor moisture away from the patient, easy to clean and
that determines the degree of cranial spread of the drug easy to replace as often as required.
and, therefore, the clinical effect. Opioids are lipophilic, • A comfortable ambient temperature will help
so will spread cranially, but increasing the volume of prevent hypothermia or panting.
injection will facilitate this. As a rule of thumb, 1 ml • A urinary catheter may be necessary to prevent
of diluted drug per 4.5 kg to a maximum of 6 ml is urinary retention, especially if an epidural has been
appropriate. administered. Placement of a urinary catheter also
For infiltration of surgical or traumatic wounds, a facilitates the measurement of urine output, which
combination of lidocaine with NaHCO3 (1 mmol/ml) in is useful to ensure adequate fluid therapy and renal
a ratio of 9:1 will help reduce irritation on injection. function (see Chapters 31 and 2, respectively).
Lidocaine 2% can be combined with 0.5% bupivacaine Placement of the urinary catheter must be
in a 1:1 ratio to provide a more rapid onset and longer performed aseptically.
duration of action. • Any wounds should have regular dressing changes.
Prior to placement of an intravenous or intra-arterial If dressings are wet or odorous, they should be
catheter, a eutectic mixture of local anaesthetic (EMLA) changed immediately.
cream can be applied to the site at least 30 minutes • Patients that require exercise should be managed
beforehand. EMLA will facilitate painless placement of a carefully by skilled personnel with a good
catheter and is especially useful for arterial catheteriza- understanding of the individual patient’s history and
tion in conscious patients. Lidocaine patches are also treatments.
useful in this situation. For nasal cannula or urinary • ICUs can be busy places and animals may find it
catheter placement, topical application of a local anaes- difficult to sleep quietly and rest. It is important to
thetic, such as xylocaine or lidocaine spray, is helpful if provide quiet times with the lights out, so sleep
administered a few minutes beforehand. deprivation does not contribute to morbidity.

Spinothalamic tract  426 Neuroanatomy and neurotransmitters involved

Descending serotonin and in pain pathways. Descending pathways modulate the
norepinephrine tracts
incoming pain sensation, which stimulates glutamate
release.

Interneuron containing Dorsal root ganglion

enkephalin
Peripheral process
Opioid receptors
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 SPECIFIC MANAGEMENT ISSUES Chapter 31

FLUID THERAPY
571

Anthea Raisis
& Katrin Swindells

INTRODUCTION The first part of this chapter discusses general aspects of

fluid therapy, with specific reference to the considera-
Maintenance of normal circulating blood volume and tions in animals with neurological disease. Aspects of
hydration are essential to maintaining adequate perfu- fluid therapy that are described include types of fluid and
sion of the brain and spinal cord and form an essential rates that can be used in these patients and indications
part of the stabilization of animals with neurological and cautions associated with their use. The second part
disease. discusses some specific conditions that alter fluid and
The principles of fluid therapy in animals with neuro- electrolyte balance and require special fluid therapy as
logical disease are generally the same as those in animals part of the management of the condition. The final part
with normal neurological function. There are, however, presents guidelines for use of blood products.
some specific considerations that relate to animals with
intracranial disease. These include the following: GENERAL GUIDELINES
• Fluid restriction is associated with increased
mortality and is no longer recommended in the Types of fluid
management of head trauma patients. Intravenous fluids can be divided into two main types:
• Adequate oxygen carrying capacity (RBC count) is crystalloids and colloids. The characteristics of these
essential to ensure adequate cerebral oxygenation. types of fluid and the considerations for use of each fluid
An excessive RBC count is also detrimental to in animals with CNS disease are outlined in Tables 112
cerebral perfusion due to the increased blood and 113 (pp. 572/573).
viscosity.
• Hypotonic fluids should be avoided when large Administration of fluids
fluid volumes are required due to the potential for The rate and type of fluid administration will depend on
increases in brain tissue water. the clinical condition of the animal, red cell count and
• Fluid balance and BP should be carefully serum protein levels, electrolyte concentrations and
monitored. Overzealous fluid therapy associated acid–base status. Fluid therapy can be divided into an
with high CVP and arterial BP should be avoided, emergency (resuscitation) phase, a rehydration/replace-
as these will increase the risk of elevating the ICP. ment phase and a maintenance phase.
• Normoglycaemia is essential for normal neuronal Emergency fluid therapy is indicated if an animal is
function, but hyperglycaemia should be avoided. demonstrating clinical signs of circulatory shock caused
Glucose-containing fluids need to be administered by an absolute (hypovolaemic shock) or a relative
judiciously with close monitoring of blood glucose. (vasodilatory shock) reduction in circulating blood
• Normal electrolyte concentrations and acid–base volume. Shock is defined as inadequate delivery of
status are important for normal neuronal function. oxygen to the tissues. Thus, the aim of the emergency
• Maintenance fluid volume requirements in animals phase of fluid therapy is to restore adequate delivery of
receiving corticosteroids and osmotic diuretics, such oxygen and other nutrients to the tissues. Adequate
as mannitol, are frequently higher than normal. oxygen delivery should be restored within 1–2 hours.
572 SPECIFIC MANAGEMENT ISSUES

Table 112 Characteristics of commonly available crystalloid fluids

TONICITY TYPE OSMOLARITY COMPOSITION CONSIDERATIONS

(mosm/l)

Hypotonic 5% dextrose 252 Glucose ....50 g/l Administered at up to maintenance rates in

2.5% dextrose/ 280 Glucose ....25 g/l hypoglycaemic patients. Avoid hyperglycaemia,
0.45% NaCl Na ............77 mmol/l which increases secondary neuronal injury. Used
Cl ..............77 mmol/l to replace free water deficits in patients with
hypernatraemia. Hypotonicity increases brain
tissue water. Administer at maintenance rates
(except neurological disease secondary to acute
hypernatraemia). Blood glucose should be
closely monitored when administered

0.45% NaCl 154 Na ............77 mmol/l Hypotonicity increases intracellular brain tissue
Cl ..............77 mmol/l water. Used to replace free water deficits in
patients with hypernatraemia if ongoing losses
are minimal. Avoid in intracranial disease
(except secondary to hypernatraemia). (See also
chapter 27)

Isotonic Hartmann’s 272 Na ............131 mmol/l Relative hypotonicity may increase brain tissue
solution/lactated Cl ..............111 mmol/l water when administered in large volumes.
Ringer’s solution K ..............5 mmol/l Calcium may increase secondary neuronal
Ca ............28 mmol/l damage (theoretical). Calcium may combine with
Lactate citrate in blood products and cause microemboli
when coadministered through fluid lines. Lactate
will accumulate in liver insufficiency. Avoid in
hepatic encephalopathy

Plasma-Lyte 148 294 Na ............140 mmol/l Less likely to increase brain tissue water than
(also consider Cl ..............98 mmol/l Hartmann’s when given in large volumes.
Normosol R and K ..............5 mmol/l Magnesium may help reduce reperfusion injury
Plasmalyte-A) Mg ............3 mmol/l (theoretical). Bicarbonate precursors do not
Acetate ....27 mmol/l require hepatic metabolism. Can be coadminis-
Gluconate 23 mmol/l tered with blood products due to lack of calcium

0.9% NaCl 308 Na ............154 mmol/l Less likely to increase brain tissue water
Cl ..............154 mmol/l when given in large volumes. Hyperchloraemic
metabolic acidosis may develop when large
volumes administered

Hypertonic 7.5% NaCl 2564 Na ............1282 mmol/l Useful for rapid low-volume resuscitation
Cl ..............1282 mmol/l (2–5 ml/kg over 5–10 minutes). Osmotic effects
will help decrease cerebral oedema. Rapid
increase in osmolarity and serum sodium may
cause central pontine myelinosis in chronic
hyponatraemia

3% NaCl 1026 Na ............513 mmol/l Useful for treatment of hyponatraemia in SIADH

Cl ..............513 mmol/l

SIADH = syndrome of inappriate antidiuretic hormone secretion

 FLUID THERAPY 573

Table 113 Characteristics of commonly available colloids

TYPE PERIOD OF RELATIVE CONSIDERATIONS

VOLUME EXPANSION INCREASE IN
(relative duration) BLOOD VOLUME

Gelatins Gelofusine ++ +++ Rapid renal excretion. Anaphylactic reactions

Haemacel recorded. No reported coagulopathy

Dextrans Dextran 40 ++ ++ Should not be used. Renal failure reported.

Coagulopathy if exceed 20 ml/kg/day
Dextran 70 +++ Possible coagulopathy if exceed 20 ml/kg/day

Hydroxy- Voluven +++/+ ++/+ Larger molecules may help reduce vascular per-
ethylstarch Hetastarch 6% meability in SIRS (see Chapter 2). Voluven is
(Hextend®) less substituted on the starch molecule than
hetastarch or pentastarch. Hextend® is a
Pentastarch
balanced electrolyte solution that resembles the
(Pentaspan®)
composition of the principal ionic constituents
of normal plasma. Possible coagulopathy if
exceed 20 ml/kg/day

Hb-based Oxyglobin ++++ +++ NO scavenger; role in secondary neuronal injury

oxygen-carrying unknown. Discoloration of mucous membranes,
solutions skin, sclera and urine. Potential for excessive
volume expansion. Vomiting has been reported
in some patients. Interferes with biochemistry
tests, especially those that use colourimetric
techniques

Natural Plasma; FFP + + Inefficient colloid (COP = 20). Weak source

of albumin. Source of clotting factors, AT
(FFP only)

COP = colloid osmotic pressure; PVE = plasma volume expansion; AT = antithrombin; FFP = fresh frozen plasma; NO = nitric oxide.

This does not necessarily require correction of the entire have lost <20% of the circulating blood volume (where
fluid deficit. (For more detail on causes and clinical signs blood volume in dogs = 90 ml/kg and in cats = 60 ml/kg)
of circulatory shock see Chapter 2.) can usually compensate for this loss by reducing urine
The rehydration/replacement phase is indicated once output and shifting fluid from extravascular space to
emergency fluid therapy has restored adequate tissue intravascular space and, as such, do not have decreased
perfusion. This phase is also indicated in any animal that tissue oxygenation. However, in both these cases the fluid
presents with a deficit in total body fluid that is not deficit still needs to be replaced. The replacement phase
causing a significant reduction in circulating blood can be performed more slowly than the emergency
volume or delivery of oxygen to the tissues and thus is not phase, allowing the type of fluid and rate to be adjusted
associated with clinical signs of circulatory shock. For regularly according to changing patient requirements.
example, an animal that is mildly to moderately dehy- Maintenance phase is indicated once all fluid deficits
drated will have a reduction in total body water of have been replaced, but the animal is unable to maintain
5–10%, but sufficient circulating blood volume to main- fluid requirements orally. The three phases of fluid
tain adequate oxygenation of the tissues. Animals that therapy and the types of fluid used are described below.
 574 SPECIFIC MANAGEMENT ISSUES

EMERGENCY FLUID THERAPY • Start with volumes of up to 90 ml/kg in dogs or

(RESUSCITATION PHASE) 60 ml/kg in cats, to be administered in less than
1 hour.
Aims of emergency fluid therapy • Monitor mentation and heart rate continuously
The aims of emergency fluid therapy are to: (ECG is ideal for continuous monitoring of heart
• Rapidly restore adequate circulating blood volume rate) and reassess all vital signs every 10–15 minutes
and tissue perfusion (within 1–2 hours). (or after 1/4 of the dose has been administered) to
• Maintain adequate oxygen carrying capacity assess response to therapy.
(i.e. RBCs). • The rate of administration and planned bolus
• Maintain COP (COP >15; total solids (TS)>45 g/l volume is decreased as soon as signs of shock
[4.05 g/dl]; albumin >20 g/l [2.0 g/dl]). resolve (see end points of resuscitation below). The
• Avoid excessive increases in arterial BP and CVP. remaining fluid deficit can then be replaced more
gradually. (Note: Continue to monitor closely to be
Guidelines for fluid administration sure that the condition of the animal does not
during resuscitation deteriorate once fluid rates are decreased. If clinical
Replacement of circulating blood volume can be per- signs deteriorate and PCV and TS are still within
formed with a variety of fluid types, including isotonic acceptable ranges, resume crystalloid fluid adminis-
crystalloids +/– hypertonic crystalloids, colloids and tration at higher rates.)
blood products, depending on the type of fluid deficit • Monitor changes in PCV/TS every 30 minutes or
present. The types of fluid used for initial resuscitation, after 45 ml/kg and 90 ml/kg in the dog and
severe dehydration, loss of high-protein fluids and blood 30 ml/kg and 60 ml/kg in the cat has been given. If
loss are described below. significant decreases in PCV and/or TS occur in
animals with ongoing clinical signs of shock,
Initial resuscitation regardless of fluid deficit adjustment of the fluid type administered is
Immediate volume resuscitation of hypovolaemic required (see below).
animals is usually performed using a polyionic isotonic
fluid. Introduction or change to another fluid type can be Resuscitation of animals that fail to respond to initial
made if indicated following initial basic blood work fluid therapy
including PCV, TS and electrolytes. In animals with head When rapid administration of polyionic isotonic fluids
trauma, Plasma-Lyte 148 and 0.9% NaCl offer theoreti- fails to achieve any improvement in tissue perfusion
cal advantages over Hartmann’s and may be the preferred within 30–60 minutes, or the patient is deteriorating, the
fluids (see Table 112). introduction of other fluids that expand blood volume
The administration of excessively large volumes of more effectively may prove useful sooner rather than
isotonic crystalloids for resuscitation can predispose to later. Synthetic colloids can be effective even in animals
oedema if an excessive increase in hydrostatic pressure or with normal serum protein concentration. Hypertonic
decreases in COP occurs. In addition, if an animal has saline also provides rapid expansion of blood volume in
suffered significant blood loss (>30% blood volume), the animals with haemorrhagic shock. Blood transfusions
use of crystalloids alone will not compensate for the will help stabilize animals with severe blood loss that fail
reduction in oxygen carrying capacity due to the loss of to respond to initial fluid therapy (427). Vasopressors
RBCs. may be required in animals with vasodilatory shock after
To minimize the detrimental effects of large-volume initial intravenous fluid boluses. (For more details see
crystalloid administration, the following protocol is below and Chapter 2.)
recommended:
• Obtain baseline vital signs (mentation, heart
rate, respiratory rate, BP, body temperature),
PCV and TS.
 FLUID THERAPY 575

Resuscitation of animals with severe dehydration Polyionic crystalloids form the basis of fluid therapy
Dehydration may occur in any neurological patient that in animals with hypovolaemia caused by severe dehydra-
has reduced mobility and subsequently has not had access tion (>10–12% body weight). In these animals, polyionic
to water. In addition, animals with CN deficits may isotonic fluids described above are predominantly used.
appear to be drinking, but may be unable to swallow. The first priority is to restore tissue perfusion. Once this
Animals with prolonged increases in muscle activity and has been achieved, the choice of fluid will depend on
hyperthermia (uncontrolled seizures; snail bait toxicity) electrolyte and acid–base abnormalities. Baseline elec-
may also develop severe dehydration and associated trolyte levels should be assessed in dehydrated patients
circulatory shock. Dehydration will cause hypovolaemia when possible. (For management of specific electrolyte
once the fluid deficit exceeds >10% of body weight. abnormalities see below. More details on metabolic
derangements can be found in Chapters 3 and 27.)

Resuscitation of animals predisposed to oedema

The use of hypertonic crystalloids and colloids may be
useful for resuscitation of animals that are predisposed to
cerebral (head trauma) or pulmonary (contusions)
oedema (428). This will help reduce the volume of crys-
talloid required to restore blood volume and BP rapidly.
 427 If the patient does In addition, hypertonic saline has the advantage of reduc-
not improve with ing cerebral oedema due to its osmotic effect.
crystalloid fluid administra- Hypertonic saline 7.5% is administered at 2–4 ml/kg
tion and/or repeat packed (cats) or 4–6 ml/kg (dogs) over 5–10 minutes. As with all
cell volume and total solids other fluids, administration is monitored closely and
values (at 30 minutes) are stopped once signs of shock resolve to avoid over admin-
abnormal, addition of istration and excessive increase in circulating blood
another type of fluid is volume and BP. Serum electrolyte concentrations should
useful. With decreasing be measured to ensure excessive increases in sodium and
packed cell volume and osmolarity do not occur.
total solids values, blood It is important to remember that the effects of hyper-
products should be tonic saline are transitory and that the fluid deficit needs
considered. to be corrected with the appropriate fluid type according
to the type of fluid deficit present. In addition, adminis-
tration of hypertonic saline expands the circulating blood
volume by drawing fluid from the interstitial and intra-
cellular spaces. This fluid deficit needs to be included in
calculations of fluid rates and volumes required for
replacement fluid therapy (see below). In animals with
chronic dehydration, abnormalities in serum sodium and
osmolarity may already exist. In these cases, administra-
tion of hypertonic saline is contraindicated.

 428 In animals prone to pulmonary oedema, as shown

in this radiograph of a dog following pulmonary
contusions, the use of hypertonic saline or synthetic
colloids may be beneficial.
576 SPECIFIC MANAGEMENT ISSUES

Resuscitation of animals that have suffered Resuscitation of animals with hypoproteinaemia

blood loss Animals that are, or are expected to become, hypo-
Hypertonic saline 7.5% can be administered at 2–4 proteinaemic will require administration of colloids to
ml/kg (cats) or 4–6 ml/kg (dogs) over 5–10 minutes in maintain COP. Protein loss may occur in animals with
conjunction with polyionic isotonic solutions for initial neurological disease for the following reasons:
resuscitation of animals with haemorrhagic shock. This • Trauma may have resulted in large exudative
will help expand blood volume more rapidly. If the wounds or extensive bruising and tissue inflamma-
animal is not responding to crystalloids or the PCV tion (429). In these cases, protein will be normal at
decreases to <0.3 l/l (<30%), whole blood or packed the time of the accident; however, losses of large
RBCs should be administered (see Principles of blood amounts of protein-rich fluid can occur during
transfusion therapy, below). subsequent days following the trauma and if not
Haemoglobin glutamer-200 (bovine) (Oxyglobin®) treated appropriately, these losses can result in
has been used to replace blood volume in haemorrhagic circulatory shock and hypoproteinaemia.
shock, although the role of Oxyglobin® in resuscitation • Loss of protein-rich fluid may also occur from the
of hypovolaemic head trauma patients remains uncer- GI tract of any patient that presents with or
tain. Potential benefits include restoration of oxygen- develops circulatory shock. The GI tract is very
carrying capacity and COP. Potential adverse effects of susceptible to ischaemic damage, particularly in
Oxyglobin® include fluid overload due to the relatively dogs. Any delay in the correction of circulatory
high COP and impaired cerebral perfusion due to the shock can lead to GI tract damage and subsequent
vasoconstrictive effects of nitric oxide (NO) scavenging. loss of large amounts of protein-rich fluid.
Vasoconstriction causes an increase in afterload and asso-
ciated decrease in cardiac output, which decreases Administration of synthetic colloids is indicated when TP
oxygen delivery in some haemorrhagic animal models. is <45 g/l (4.5 g/dl), albumin is <20 g/l (2 g/dl) and/or
The effect of NO scavenging on cerebral perfusion COP is <15 mmHg. Synthetic colloids are preferred to
in brain injury is also unknown. The recommended plasma, as these are more efficient in restoring COP and
maximum dose of Oxyglobin® is 5–10 ml/kg in dogs and blood volume. To resuscitate a hypoproteinaemic animal,
2.5–5.0 ml/kg in cats. the rate of polyionic crystalloids is reduced from shock
rates to approximately 5–10 ml/kg (higher rates may be
required if cardiovascular function does not improve or
deteriorates despite introduction of colloid) and colloids
are administered at volumes of 10–20 ml/kg/day in dogs
and 5–10 ml/kg/day in cats. However, in dogs that are
continuing to lose large volumes of protein-rich fluid or if
>20 ml/kg/hour is required to stabilize blood volume and
prevent death due to hypovolaemic shock, the benefits of
administering larger volumes outweigh the risk:
• Fluid overload can occur if excessive volumes are
administered. To prevent volume overload, colloids
should be administered in increments (1/4 doses) to
effect. The rate of administration is reduced as soon
as signs of shock improve.

429 Loss of large amounts of protein can occur in

trauma patients with open wounds (as shown in this dog)
and large amounts of tissue bruising.
 FLUID THERAPY 577

• Coagulopathy has been associated with administra- [systemic hypertension and reflex sinus bradycardia in
tion of synthetic colloids. To minimize the risk of response to increased ICP] in animals with brain injury
coagulopathy the maximum recommended daily may complicate assessment of BP. Thus, increased ICP
amount is 20 ml/kg. Should significant coagulo- needs to be ruled out as a potential cause of hypertension,
pathy occur, then management includes cessation of particularly if the heart rate is lower than expected. [For
artificial colloids and administration of fresh frozen more details see Chapter 20.])
plasma (FFP) and/or fresh whole blood.
Laboratory assessment
End points of resuscitation There is increasing evidence that clinical assessment
During emergency fluid therapy, large volumes of fluids alone does not always provide accurate information
are administered rapidly to restore tissue oxygenation as about tissue oxygen delivery. Significant tissue hypox-
quickly as possible. Once tissue perfusion has been aemia has been observed despite the return of clinical
restored, fluid therapy needs to be reduced to prevent variables to normal. Certain laboratory measurements
adverse effects associated with continued rapid adminis- may provide a better indirect measure of the adequacy of
tration of large volumes. It is not possible to measure fluid therapy in restoring tissue oxygenation. Laboratory
tissue perfusion directly in the clinical environment. measurements that have been found to be useful for
Indirect assessment of tissue oxygenation can be per- assessing response to fluid therapy include serum lactate
formed using a variety of clinical variables. Certain concentrations, base deficit, mixed venous oxygen satu-
laboratory measurements can also provide additional ration and jugular venous oxygenation (see Further
information about adequacy of tissue oxygenation. reading).
• Serum lactate concentrations (normal <2.5
Clinical assessment mmol/l). Lactate concentrations increase during
Cardiovascular variables that can provide indirect assess- shock when the rate of production in the ischaemic
ment of tissue oxygenation include heart rate, mucous tissues exceeds the rate of elimination of lactate by
membrane colour and capillary refill time, peripheral the liver and kidneys. Changes in lactate concentra-
body temperature, pulse quality, BP and mentation. tion are considered more useful than the actual
Certain target values for these clinical variables have lactate concentration measured. Serial lactate meas-
been established as guidelines for the end of the resusci- urements can provide information about the
tation phase (see Further reading): resolution of tissue ischaemia in response to fluid
• Mentation: alert and responsive. therapy. If treatment of shock is adequate, serial
• Heart rate (bpm): small dogs <140; large dogs <120; measurements will show decreases in serum lactate
cats 160–200. concentrations. Measurements should be performed
• Mucous membrane colour: pink. prior to fluid resuscitation and then repeated at the
• Capillary refill time: <2 seconds. end of resuscitation as indicated by resolution of
• Urine output (UOP): >1 ml/kg/hour. cardiovascular signs of shock. Further increases in
• Body temperature increasing. lactate or failure to reduce by at least 50% with
• Arterial BP (in animals with intracranial disease): treatment indicates ongoing significant ischaemia
SAP >90 mmHg; MAP >70 mmHg. and either insufficient fluid administration and/or
the administration of the wrong type of fluid.
(Note: While adequate BP is required in these animals, Lactate measurements do have limitations in
high BP [SAP >140 mmHg, MAP >100 mmHg] should assessing oxygen delivery, particularly in the
also be avoided as this increases the risk of ongoing presence of conditions that interfere with lactate
haemorrhage and predisposes to increased ICP, reduced metabolism in the tissues or liver (e.g. sepsis, liver
CPP and herniation. The presence of the Cushing reflex insufficiency, lymphoma).
 578 SPECIFIC MANAGEMENT ISSUES

• Base deficit (normal -3 to +3). The measured ml/kg/day. Maintenance requirements are discussed in
deficit in the amount of base within the circulation more detail below. (Note: In animals receiving corticos-
can also provide information about adequacy of teroids or osmotic diuretics, higher than normal mainte-
oxygen delivery to the tissues. With decreasing nance fluid volume requirements may be warranted.
oxygen delivery, tissues become ischaemic. There is Fluid rates must be adjusted accordingly.)
increased production of hydrogen ions (metabolic
acidosis) and as these are buffered there is an Guidelines for replacement fluid therapy
associated decrease in the amount of base present The type and rate of fluid administered during this phase
(base deficit). The greater the base deficit the worse will depend on the type and severity of the fluid deficit
the impairment in tissue oxygenation. Improvement (e.g. blood, plasma, body water), the duration over which
in tissue oxygen delivery during fluid therapy will the loss has occurred and associated electrolyte and
be associated with a decrease in the base deficit. acid–base abnormalities.
• Mixed venous oxygen tension (normal 53 +/-
10 mmHg). Mixed venous oxygen tension can be Blood loss
useful for detecting the imbalance between oxygen As long as oxygen-carrying capacity and COP are/remain
delivery and oxygen consumption in the tissues that adequate (PCV >0.3 l/l [>30%]; Hb >80 g/l [8 g/dl]; COP
occurs during shock. In response to decreased >15 mmHg), crystalloids can be used to replace the
oxygen delivery, a greater uptake of oxygen occurs remaining deficit. The volume of crystalloid required is
in the tissues, resulting in lower venous oxygen 3–4 times the estimated remaining deficit in blood
tension. An improvement in venous oxygen tension volume, as only 1/4–1/3 of crystalloid remains within the
would be indicative of improved perfusion and vasculature after approximately 1 hour. In animals with
oxygen delivery. intracranial disease, failure to correct anaemia may reduce
• Jugular venous oxygen saturation. Can be cerebral oxygen delivery. Therefore whole blood is the
monitored as an assessment of the adequacy of preferred fluid to replace deficits in blood volume if the
brain oxygen delivery. Values below 50% suggest PCV is <0.3 l/l (30%). Details of transfusion therapy are
inadequate perfusion and oxygen delivery (see described at the end of this chapter.
Further reading). (Note: Overtransfusion can be detrimental due to
resultant increases in viscosity, which will decrease cere-
REPLACEMENT PHASE/REHYDRATION bral perfusion. In human patients with intracranial
disease, the ideal PCV is 0.3 l/l (30%), as this provides
During this phase the fluid deficit is replaced more adequate oxygen-carrying capacity and also produces
slowly, allowing more controlled correction of fluid and beneficial rheological properties that enhance cerebral
electrolyte abnormalities. The replacement phase of perfusion.)
fluid therapy is commenced when resuscitation is suc-
cessful in restoring adequate oxygen delivery to the Loss of protein-rich fluid
tissues. It is also indicated in animals that do not present Once the signs of shock have resolved, the type of fluid
in shock. This includes animals with mild to moderate used for ongoing replacement is determined by the COP
dehydration (<10% of body weight) (430) or blood loss in and TS values. Artificial colloids +/- plasma are used to
the absence of clinical signs of hypovolaemic shock. This maintain COP (>15 mmHg). In the absence of COP
generally occurs when <20% of circulating blood volume measurements, colloid administration is recommended if
is lost. As the animal compensates for this blood loss by TS are <45 g/l (4.5 g/dl) or albumin <20 g/l (2.0 g/dl).
reducing urine output and redistributing fluid from the (Note: Once administration of synthetic colloids has been
extravascular to the intravascular compartment, replace- performed, interference with refractometer readings will
ment of the fluid deficit is still required. prevent accurate measurement of TS. Therefore, assess-
During this phase, fluid must also replace ongoing ment of continued need for colloids is based on clinical
losses (e.g. vomiting/diarrhoea/polyuria) and supply signs [presence of oedema] or measurement of COP, TP
maintenance fluid requirements of approximately 50 or albumin.)
 FLUID THERAPY 579

Table 114 Clinical characteristics of

dehydration

DECREASE IN CLINICAL SIGNS

BODY WEIGHT

<5% No obvious clinical abnormalities

5–10% Decreased elasticity of skin, slight prolon-

gation of CRT, dry mucous membranes

10–12% Marked prolongation of skin tent and CRT,

dry mucous membranes, sunken eyes

12–15% Signs of circulatory shock: increased heart

rate, decreased pulse quality, cold
extremities, decreased BP
 430 When animals present with dehydration (<10% in
this dog) and normovolaemia, replacement of volume BP = blood pressure; CRT = capillary refill time.
deficit can be performed less rapidly.

MAINTENANCE PHASE
Maximum recommended doses of artificial colloids
are 20 ml/kg/day in dogs and 10 ml/kg/day in cats. In The maintenance phase begins when all fluid deficits
patients with severe oncotic deficits, doses of up to 40 ml/ have been replaced. Maintenance fluid requirements
kg/day in dogs and 20 ml/kg/day in cats may be required; provide fluid to replace the sensible (measureable losses
however, there is an increased potential for side-effects, such as urine output) and insensible (unmeasured losses
including coagulopathy, with such high doses. from respiratory tract, wounds, GI tract).

Body water (dehydration) Guidelines for maintenance fluid therapy

Rehydration replaces the estimated deficits in total body Typically, maintenance requirements are approximately
water. Estimating the deficit in dehydrated animals 50 ml/kg/day. Maintenance fluid requirements will be
depends on the clinical abnormalities present. Guide- higher if either sensible or insensible losses increase. For
lines for assessing fluid deficits (% body weight) are out- example, normal urine output is 1–2 ml/kg/day; however,
lined in Table 114. in animals that are receiving corticosteroids or diuretics,
It is generally recommended that rehydration is per- increased urine production will necessitate higher fluid
formed over half the time frame in which dehydration requirements. Ideally, the rate of fluid administration
occurred to prevent sudden correction of abnormalities should be based on measured urine output. Insensible
in osmolarity and electrolyte concentration. As a general loss cannot be measured clinically; however, in normal
guide, half the calculated deficit should be replaced over resting animals it is approximately 20 ml/kg/day.
the first 6 hours and the remaining deficit over the next Increases in insensible losses of up to 50 ml/kg/day are
18 hours. For patients who have taken 3 days or longer to associated with increased metabolism (fever, hyper-
develop dehydration, the deficit should be replaced at thermia) or increased respiratory losses (panting). Insen-
a slower rate to prevent marked changes in sodium sible losses can be higher due to gastrointestinal loss or
concentration. secondary to inflammation of the peritoneum or tissues.
 580 SPECIFIC MANAGEMENT ISSUES

For most animals, a polyionic, isotonic fluid, such as Magnesium supplementation

Hartmann’s solution or Plasma-Lyte 148, is suitable for Animals receiving diuretics and inappetent or critically
short-term maintenance. If an extended period of fluid ill animals may develop hypomagnesaemia, which neces-
administration is required, these fluids may cause gradual sitates supplementation. In addition, magnesium is
increases in Na+ and Cl– concentration. If this occurs, reported to help reduce secondary neuronal injury.
0.45% NaCl or 0.45% NaCl/2.5% glucose can be However, data on supplementation rates specific for
administered. Close electrolyte monitoring is required if neurological disease are lacking. It is reasonable to extra-
0.45% NaCl or 0.45% NaCl/2.5% glucose is admin- polate current critical care guidelines to maintain mag-
istered at greater than maintenance fluid rates. In nesium in normal ranges. If hypomagnesaemia is present
hypoproteinaemic, normovolaemic animals, synthetic or a total body magnesium deficit is suspected, the rec-
colloids (Voluven, Pentastarch, Hetastarch) can be ommended rate of magnesium supplementation is
administered at 20 ml/kg/day in dogs and 10 ml/kg/day 0.15–0.5 mmol/kg/day (0.3–1 mEq/kg/day), with daily
in cats to help maintain COP. monitoring of magnesium levels.

Potassium supplementation Assessment of fluid therapy during replacement

Inappetent animals will require potassium (K+) supple- and maintenance phases
mentation during replacement and maintenance phases Assessment of the adequacy of fluid therapy should
of fluid therapy (Table 115). The use of diuretics, particu- include a thorough clinical examination 2–3 times daily.
larly of loop diuretics, will increase renal losses of K+. Calculation of fluid balance and measurement of body
The amount of supplementation will depend on the weight should be performed at least once a day. In addi-
serum K+ concentration of the animal and the rate of tion, measurement of heart rate, respiratory rate, arterial
fluid administration, but should not exceed 0.5 mmol/ BP +/- CVP and body temperature should be recorded
kg/hour. Serum potassium concentrations should be frequently to determine changes that may reflect
maintained in normal ranges. Maintenance supplemen- improvements or deteriorations in blood volume and
tation of KCl for animals that are not eating or are receiv- hydration status. Trends in UOP and urine SG should
ing inadequate nutrition is 20 mmol/l in isotonic also be recorded on a regular basis. Guidelines for
crystalloid delivered at maintenance fluid rates. interpreting the response to fluid therapy using these
measurements are provided in Table 116. The frequency
with which all these measurements should be recorded
will depend on the condition of the animal and ongoing
Table 115 Guidelines for supplementation losses. In animals where hydration status and fluid
of potassium losses may be unpredictable, measurements should be
Serum Supplementation Maximum recorded every 2 hours, particularly if they were previ-
potassium (mmol KCl/l of infusion rate ously suffering from circulatory shock. Once the animal
(mmol/l) crystalloid) (ml/kg/hour) becomes more stable, measurements can be recorded
<2.0 80 6
every 4–6 hours.

2.1–2.5 60 8 Fluid balance calculation

2.6–3.0 40 12 Calculation of the fluid balance should be done at least
once daily in animals receiving fluid therapy. Fluid
3.1–3.5 30 16 balance is the difference between the estimated fluids
3.6–5.0 20 25 received and fluid losses.
Fluids received include all fluids administered includ-
(Adapted from Greene RW, Scott RC (1975) Lower urinary
ing water contained in the food fed to the animal (intra-
tract disease. In: Textbook of Veterinary Internal Medicine.
(ed. SJ Ettinger) WB Saunders, Philadelphia, p. 1572.) venous and oral, water content of food). Fluid losses
include all losses including UOP, GI tract losses (vomit-
ing/diarrhoea), insensible losses (see above) and losses of
 FLUID THERAPY 581

Table 116 Guidelines for assessing response to fluid therapy during replacement and
maintenance phases

CLINICAL SIGNS FLUID BALANCE BODY WEIGHT URINE OUTPUT USG* CVP CHANGES TO
FLUID PLAN

Dehydrated Ins < outs (ongoing losses) < Normal Low High Low ↑

Ins > outs (losses ceased, < Normal, Low High Low ↑
but not yet replaced) but increasing

Ins > outs (3rd space > Normal (3rd

fluid losses occurring) space losses)

Overhydrated Ins > outs ↑ Low (anuric or Low High ↓

oliguric renal failure)

Normal/high
(if excessive fluid
therapy)

Normal Ins = outs Normal Normal Normal Normal Maintenance +

hydration ongoing losses

USG = urine specific gravity; CVP = central venous pressure.

* assuming normal renal function, no diuretics and the patient is not currently receiving artificial colloids such as Voluven

fluid from the circulation into spaces such as body cav- If fluid received is more than fluid loss, one possible
ities (pleural/peritoneal effusion). The amount of fluid cause is an ongoing fluid deficit that has not been ade-
lost as oedema or into a body cavity (third space fluid quately replaced. Evidence of the body’s attempts to con-
losses) can be estimated from inappropriate increases in serve fluid (low UOP and high USG) and a low CVP
body weight (i.e. increases in body weight in excess of would support this finding. Continued fluid administra-
that expected with replacement of fluid deficit). It is tion at the planned rates or increased fluid rates if the dif-
important to remember that inappropriate increases in ference is still large would be required. The exception
body weight may also be caused by fluid retention in would be animals with anuric or oliguric renal failure,
anuric/oliguric renal failure. This represents an excess of where failure to produce urine is responsible for the
fluid and indicates that a reduction in administered fluid imbalance between fluid in and fluid out. Clinical
rate and volume is necessary. Insensible losses are respi- evidence of fluid retention (e.g. oedema) may help
ratory and normal GI tract losses. These cannot be meas- confirm this. In these cases, USG will be low and meas-
ured, but should be included in calculations of fluid urements of CVP will be high.
balance. For most animals resting quietly, insensible
losses are approximately 20 ml/kg/day. In animals that Serial body weight measurement
are panting excessively or have increased body tempera- Repeated measurement of body weight is a useful guide
ture, insensible losses can be up to 50 ml/kg/day. to assessing fluid therapy during the replacement and
If the calculated fluid received is less than ongoing maintenance phases. In uncomplicated cases, once to
fluid loss an increase in fluid administration may be twice daily measurement is recommended. For animals
required. Clinical and laboratory evidence of inadequate at risk of volume overload (reduced renal function, low
hydration should also be present to confirm the need for COP), more frequent monitoring (4–6 hourly) will
increased fluids. provide early detection of fluid retention.
582 SPECIFIC MANAGEMENT ISSUES

Weight loss during the replacement/maintenance

phases may represent dehydration due to inadequate
fluid administration. Humans with traumatic brain injury
have been shown to have significant negative nitrogen
balance and weight losses of up to 15% body weight per
week (see Further reading), therefore weight loss due to
inadequate nutrition should be taken into account when
interpreting decreases in body weight. Weight loss due to
inadequate nutrition may also mask expected weight gain
associated with replacement of fluid deficit.
Weight gain during this phase may reflect replace-
ment of a fluid deficit. If the fluid deficit has been accu-
rately estimated and the fluid therapy is adequate, then
 431 Inappropriate increases in body weight may weight gain should be consistent with replacement of the
reflect retention of fluid within the body. This cat has estimated fluid deficit. If weight gain is in excess of esti-
septic peritonitis secondary to traumatic damage to the mated water deficit, it is possible that the initial estimate
abdomen and intestine. was inaccurate. Alternatively, fluid retention/volume
overload may be responsible (431, 432). If the initial
deficit was underestimated, there should be no clinical
signs of overhydration. In contrast, clinical signs of
oedema (e.g. pitting oedema on limbs, increased respira-
tory rate, nasal discharge, pulmonary crackles) and a high
CVP are suggestive of fluid retention.

Serial packed cell volume/total solids, electrolyte and

acid–base measurement
Measurement of PCV, TS, electrolyte and acid–base
balance are useful for assessing the effectiveness of
volume replacement and also for assessing the appro-
priateness of the chosen fluid type and rate. During
the replacement phase, monitoring should be per-
 432 Accumulation of fluid within the peritoneum, as formed at least twice a day. For animals with severe
seen in this laparotomy, is associated with increased body electrolyte abnormalities, more regular monitoring is
weight. recommended (see below).

 433 Frequent monitoring of urine output and specific

gravity is also useful for determining fluid balance. Use of
an indwelling catheter and a closed collection system is
recommended in critical patients.
 FLUID THERAPY 583

Urine output and specific gravity measurement In animals that present without clinical neurological
Serial measurement of UOP and USG is also useful for abnormalities, free water restriction can be used to grad-
assessing correction of fluid deficits (433). UOP below ually increase serum sodium concentration. It is also
normal (where normal = 1–2 ml/kg/hour) in association essential that the underlying cause is corrected.
with a high USG is supportive of dehydration and In animals with neurological abnormalities associated
reduced renal perfusion. Generally, improvements in with hyponatraemia, more aggressive therapy is needed.
UOP together with a decrease in USG from highly con- As these animals are either normovolaemic or hyper-
centrated (>1.040) towards minimally concentrated volaemic, administration of fluids at or in excess of the
(<1.025) are indicators of improved renal perfusion and maintenance rate is not required. 0.9% saline was previ-
correction of fluid deficits during administration of ously considered a suitable fluid for correction of the
crystalloid fluids. sodium deficit in SIADH. However, due to the excessive
There are several situations when changes in UOP renal water reabsorption in response to ADH, and
and USG may not be as expected. Firstly, if large volumes sodium losses in response to hypervolaemia and natri-
of synthetic colloids have been administered, USG may uresis, administration of replacement fluids such as 0.9%
actually increase, as the excretion of the colloid mole- saline may result in worsening hyponatraemia and is no
cules will alter the refraction of the urine. Secondly, longer recommended. Administration of 3% saline as a
drugs that alter urine production and renal concentrating slow continuous infusion in conjunction with water
ability, such as diuretics or corticosteroids, can cause restriction is the recommended therapy for SIADH asso-
increased UOP and decreased USG despite ongoing ciated with clinically significant hyponatraemia.
dehydration. Therefore, when an animal with neuro- Administration of 3% saline should be calculated to
logical disease has recently received these drugs, UOP increase serum sodium by a maximum of 0.5 mmol/l/
and urine USG alone should not be used for assessment hour or 10–12 mmol/l/24 hours until a serum concentra-
of fluid therapy. (For more details of monitoring urine tion of 125–130 mmol/l is reached, at which time further
output see Chapter 2.) correction of serum sodium can be performed by water
restriction alone. Serum sodium should be initially mon-
Central venous pressure measurement itored every 1–2 hours to assess response and prevent
Measurement of CVP is particularly important for overcorrection.
assessing fluid therapy in animals at risk of increased ICP. The volume and rate of administration of 3% saline
(For more details on CVP monitoring see Chapter 2.) are calculated as follows:
• The total body sodium deficit is 0.6 × lean body
SPECIFIC FLUID AND ELECTROLYTE weight × (125 – serum sodium).
DISTURBANCES IN NEUROLOGICAL DISEASE • The calculated sodium deficit is divided by 513 (the
sodium content [in mmol/l] of 3% hypertonic saline
Metabolic abnormalities that accompany CNS injury are solution) to obtain the number of litres of 3% saline
most commonly associated with disorders of water and required.
sodium regulation. • The required sodium increase (i.e. sodium deficit)
in mmol/l is then multiplied by 2 to give the period
Syndrome of inappropriate antidiuretic of time over which the sodium should be infused to
hormone secretion ensure that replacement of the deficit occurs at
SIADH is caused by antidiuretic hormone (ADH)- 0.5 mmol/l/hour.
secreting neoplasias, excessive ADH release secondary to • The volume is then divided by the time period to
CNS or pulmonary pathology, drugs, stress and pain. It is calculate the rate of fluid administration.
characterized by hyponatraemia, hypo-osmolarity, nor- • Electrolytes should be monitored every 1–2 hours
movolaemia to hypervolaemia and urine sodium concen- initially to assess response.
tration >20 mmol/l (> 20 mEq/l). Treatment will depend
on the clinical presentation. For example, if a 10 kg dog presents with a serum sodium
concentration of 108 mmol/l:
584 SPECIFIC MANAGEMENT ISSUES

• The calculated total body sodium deficit is of 145 mmol/l (145 mEq/l) in dogs and 155 mmol/l
0.6 × 10 × (125 – 108) = 102 mmol sodium. (155 mEq/l) in cats is used.
• The deficit of 102 is divided by 513 to produce a • This calculated volume of water (administered as
volume of 0.199 l or 199 ml. 5% dextrose) should be infused gradually with the
• The time period over which this volume is infused aim of decreasing the sodium concentration by a
is (125 – 108) × 2 = 34 hours. maximum of 12 mmol/l/day or 0.5 mmol/l/hour.
• Therefore, the infusion rate of 3% saline is
199/34 = 5.8 ml/hour for 34 hours. For example, a dog with a serum sodium of 170 mmol/l
• Monitor electrolytes every 1–2 hours. If correction (170 mEq/l) ( i.e. 25 above normal) should have its free
occurs too rapidly, the infusion rate is decreased; if water deficit infused over 50 hours (25 mmol/l ÷
too slowly, the fluid rate is increased. 0.5 mmol/l/hour = 50 hours). Alternatively, 1.9 ml/kg/
hour of 5% dextrose will drop sodium by approximately
In some patients, furosemide may be required to increase 0.5 mmol/kg/hour.
water excretion. Antagonists of ADH receptors in the For patients showing severe neurological signs sec-
kidney (e.g. demeclocycline) are used in humans; ondary to hypernatraemia, sufficient free water should be
however, there is potential for renal toxicity and no spe- infused over 2–3 hours to decrease the serum sodium
cific recommendations for dosages in dogs and cats. concentration by 5–7 mmol/l (5–7 mEq/l), allowing
rapid improvement in the severity of clinical signs. Once
Central diabetes insipidus signs improve, the rate should be immediately reduced to
CDI is caused by pituitary and hypothalamic lesions sec- stay within the maximum recommended daily decrease
ondary to head trauma and intracranial surgery. It is in serum sodium of 12 mmol/l/day (12 mEq/l/day).
characterized by polyuria, dehydration, hypernatraemia,
low urinary sodium and low USG. Other causes of Abnormalities associated with treatment
hypernatraemia (see below) associated with treatment of of neurological disease
neurological disease need to be ruled out before a diag- A variety of medications used in neurological disease can
nosis of CDI is made. lead to fluid and electrolyte abnormalities. Administra-
Treatment includes exogenous replacement of ADH tion of corticosteroids interferes with the concentrating
with desmopressin or aqueous vasopressin and gradual ability of the kidneys and may result in nephrogenic dia-
replacement of the free water deficit with 5% dextrose betes insipidus. Diuretics can also predispose to excessive
(intravenously or orally with water). water losses. This is of little consequence in animals able
All the formulae for calculating the free water deficit to drink adequately. However, animals that have water
provide an approximate starting point for fluid rates of withheld or stop drinking for another reason are at risk of
5% dextrose (or oral water). However, the actual rate of developing dehydration accompanied by hyperna-
sodium decrease will depend on the patient’s underlying traemia.
pathology and ongoing water losses; therefore, sodium Diuretics can also result in increased urinary loss of a
levels should be monitored initially every 2–4 hours and variety of electrolytes from the body with long-term
fluid rates adjusted to maintain a decrease in sodium of administration including sodium (mannitol), potassium
approximately 0.5 mmol/l/hour. (loop diuretics), magnesium (mannitol and furosemide)
The free water deficit can be calculated as: and phosphate (carbonic anhydrase inhibitors).
• Body weight (kg) × 0.6 × ([measured sodium – Electrolytes, PCV and TS should be monitored at
normal sodium]/normal sodium – 1). For this least once daily in patients who are reliant on intravenous
calculation a normal serum sodium concentration fluid therapy to maintain hydration.
 FLUID THERAPY 585

PRINCIPLES OF BLOOD TRANSFUSION THERAPY

Administration of blood products is required in animals

that have suffered significant loss of blood or red cells in
order to maintain oxygen-carrying capacity and thus
oxygen delivery to vital organs such as the brain. In
animals with brain injury this is particularly important
for preventing secondary neuronal damage due to
ischaemia. Administration of blood products is also
required in animals that have disorders of primary or sec-
ondary haemostasis. Indications for different blood  434 Blood transfusions may be required when
products in neurological patients include: haemorrhage occurs during surgery. Significant blood loss
• Haemorrhage (434) (secondary to trauma or can occur during spinal surgery, so the suction bottles,
surgical losses): whole blood, packed RBCs. such as seen in this figure, should be regularly checked.
• Anaemia (435) (Heinz body anaemia in cats
secondary to propofol administration): whole blood
or RBCs.
• Decreased number or function of platelets (436)
(secondary to large volume [>50%
circulating blood volume] transfusion of stored
whole blood or packed RBCs): fresh whole blood,
platelet-rich plasma, or platelet conentrate.
• Decreased clotting factors (cerebral haemorrhage
secondary to coagulopathy [e.g. rodenticide]; DIC
secondary to prolonged circulatory shock, hypox-
aemia): fresh whole blood; fresh frozen plasma.

The following section describes methods for collecting

blood for transfusion and provides information on how  435 Anaemia may occur due to destruction of red
to determine rates and volumes of blood required to be blood cells, causing pale mucous membranes as seen in
administered. this cat. Treatment may include administration of packed
red blood cells.
Acquisition of blood products
Selection of donors
All donors should be healthy, fully vaccinated, free of
blood-borne diseases/parasites and have never previous-
ly received a transfusion. Each animal should receive an
annual physical examination, CBC, biochemistry and
urinalysis. PCV and TS should be checked prior to every
transfusion.

 436 Animals with reduced platelet numbers or

function, associated with clinical signs such as the
ecchymoses seen in this dog, can be treated with fresh
whole blood.
586 SPECIFIC MANAGEMENT ISSUES

Canine donors
Docile large breed dogs over 25 kg can donate 450 ml up
to once every 3 weeks. Greyhounds are considered ideal.
The main dog erythrocyte antigens (DEAs) include
DEA types 1.1, 1.2, 3, 4, 5, 6, 7 and 8. Dogs frequently
have more than one type of antigen on their red cells and
so can be positive for several blood types. Testing is not
available for all blood types. DEA 1.1 is the most anti-
genic blood type and is associated with acute haemolytic
reactions in previously sensitized individuals. Because
of the significant potential for stimulating immunoreac-
tivity in naïve dogs, the life span of DEA 1.1 red cells
transfused into DEA 1.1 negative dogs can be signifi-
cantly shorter than expected due to delayed haemolysis.  437 Blood is collected with the dog positioned in
Donors should be DEA 1.1 negative, unless the recipient lateral recumbency. The weight of the bag is monitored
is DEA 1.1 positive, in which case it can receive DEA during collection to determine the volume collected.
1.1-positive or DEA 1.1-negative blood. Other blood
types require prior exposure for reactions to occur. DEA
4 is present in approximately 98% of canines, therefore
donors who are positive for DEA 4 and negative for DEA
1.1 are considered ideal donors. Alternate jugular veins should be used in animals
donating regularly. Local anaesthesia with administra-
Feline donors tion of subcutaneous lidocaine can increase donor com-
Feline donors ideally should be over 5 kg in body weight. pliance. The collection site is surgically scrubbed.
Healthy felines can donate 10 ml/kg of blood. Collection into commercial blood collection bags con-
Feline blood donors should be blood typed. Feline taining anticoagulant is preferred. To minimize bacterial
blood types have historically been divided into A, B or contamination, care must be taken not to allow air to
AB, with the incidence of different types varying between enter the line or bag. During collection, the bag should
countries. Within Australia, the majority of cats are type be rocked continuously to prevent coagulation occur-
A; the incidence of type B varies geographically up to ring. The amount of blood in the bag can be measured
39% and type AB is <1%. Within Europe and America, during collection by weighing the bag. The collection is
type A is also most common, with type B being variable finished when the bag has gained 450 g in weight; over-
(reports of 1–6% in the USA) and type AB rare. filling bags will dilute the anticoagulant and increase the
risk of clots forming.
Collection of blood
Canines Felines
Ideally, dogs who donate regularly should be trained to Collection of blood from feline donors usually necessi-
lie in lateral recumbency on a table (437). However, for tates sedation. Possible sedative regimes include:
less cooperative donors, light sedation with butorphanol • Midazolam (0.2 mg/kg IM) + butorphanol
(0.2–0.4 mg/kg IV or IM) is often adequate. If not, small (0.2–0.4 mg/kg IM).
doses of acepromazine (0.01–0.02 mg/kg SC) can be used • Midazolam (0.1mg/kg IV) + butorphanol
but increase the risk of hypotension in the donor and (0.2 mg/kg IV).
should be avoided. If the donor requires acepromazine • Acepromazine (0.01–0.02 mg/kg IM) + butorphanol
sedation, a peripheral intravenous catheter should be (0.2–0.4 mg/kg IM).
placed in case rapid fluid replacement is required. • 1–2 mg/kg ketamine + 0.1–0.2 mg/kg diazepam IV.
 FLUID THERAPY 587

• Mask induction with sevoflurane or desflurane and Preparation of recipient

subsequent maintenance with an inhalation agent Blood typing and cross-matching: dogs
delivered using a mask is extremely useful in very Ideally, cross-matching should be performed in all recip-
uncooperative donors. ients if time allows. This is particularly important in
animals that have had a previous transfusion, as anti-
The cat is gently restrained in sternal recumbency with bodies to transfused blood types will develop within 4–14
its neck extended or in lateral recumbency. The jugular is days of the transfusion. Cross-matching is essential to
clipped and surgically prepared. Collection of blood into avoid blood transfusion reactions if repeat blood
syringes containing appropriate amounts of anticoagu- transfusions are required more than 4 days after the first
lant is the easiest way of drawing blood from donor cats. transfusion.
The amount of citrate phosphate dextrose adenine-1 Antibodies can also develop in animals that have not
(CPDA-1) or acid citrate dextrose-A (ACD-A) required been previously transfused. Antibodies to DEA 7 may
is 1 ml per 7 ml of blood. Blood is collected via a butterfly also occur after exposure to some bacteria. Therefore,
needle into either one 60 ml syringe or three 20 ml dogs should ideally have cross-matching performed even
syringes. Syringes should be rocked to ensure adequate on their first transfusion. However, in dogs that have
mixing with anticoagulant. Short extension sets on but- never previously received a transfusion, the use of non-
terfly needles provide sufficient distance from the needle cross-matched and non-typed canine blood has been
for the syringes to be rocked. Blood collected via syringes used as a life-saving measure. (For details regarding
should be used within 48 hours of collection, as there is cross-matching, see Further reading.)
increased risk of bacterial contamination.
Blood typing and cross-matching: cats
Administration of blood products Blood typing or cross-matching is essential for all feline
Ideally, blood products should be at room temperature. recipients (see Further reading for details). Type A cats
All blood products, including packed red cells and have weak, naturally occurring antibodies against type B
plasma, should be administered through a blood filter blood. Transfusion of type B blood into a type A cat will
(in general 170 μm filters should be used). Small volume result in a delayed transfusion reaction, with markedly
paediatric filters are best in cats. shortened RBC survival and potential for an acute
The preferred route for administration of blood is haemolytic reaction. Type A cats that received a second
intravenously (cephalic or jugular vein), although the type B transfusion would be at high risk for an acute life-
intraosseous route can be used in neonates. Selection of threatening haemolytic reaction. Type B cats have
catheter size will depend on the rate at which the blood strong, naturally occurring antibodies against type A
needs to be administered. A shorter catheter with a larger blood and transfusion of type A blood into type B cats
diameter should be selected for rapid administration. causes a rapid and potentially fatal transfusion reaction
Catheter size will also depend on the size of the animal (after as little as 1 ml of blood). Type AB cats do not have
and the vein used. For example, a 20 G catheter is proba- antibodies against either blood type, but should receive
bly the largest catheter that can be placed comfortably in either type AB blood or type A blood. There has been
the cephalic vein of an adult cat or small–medium dog, recent recognition of a new and probably rare feline
while an 18 G can be placed in a medium–large dog. If a blood type Mik, which is present in addition to the A, B
larger catheter is required, placement will need to be into and AB antigens. Mik-negative recipients are at risk from
the jugular vein. Absorption from the intraperitoneal acute haemolytic transfusion reaction if they receive
cavity is excessively slow, particularly with RBCs. Mik-positive blood, even if the blood is correctly typed
Blood can be administered in the same line as 0.9% for the A, B and AB system. Because of the possibility of
NaCl or Plasma-Lyte 148. It must not be administered Mik antigen reactions, all cats should ideally be cross-
with Hartmann’s solution (calcium can cause coagula- matched prior to transfusions, even if the donor and
tion) or hypotonic solutions such as 5% dextrose, which recipient blood type are the same.
can cause haemolysis.
 588 SPECIFIC MANAGEMENT ISSUES

Premedication In patients with heart disease or at risk of volume

Premedication can be administered, if desired, particu- overload, the administration rate should not exceed
larly if cross-matching has not been performed. Suitable 4 ml/kg/hour. Signs of volume overload include tachy-
premedicants include chlorphenamine (0.5mg/kg IM) pnoea/dyspnoea and a watery nasal discharge. If volume
and diphenhydramine (2 mg/kg IV). overload occurs, the transfusion should be stopped and
diuretics administered and, in cases of severe volume
Rate of administration overload where a marked increase in blood viscosity has
Emergency cases occurred, phlebotomy should be considered.
In an emergency (e.g. haemorrhagic shock, DIC with In normovolaemic animals (i.e. patients with anaemia
active bleeding) administration of any blood product or decreased clotting factors), infusion of blood products
(whole blood, packed RBCs, FFP) should be commenced (i.e. packed RBCs or FFP, respectively) at slow rates is
at rates of at least 10–20 ml/kg/hour. In cases of massive, recommended. Concurrent infusion of packed RBCs
acute haemorrhage, blood should be infused as rapidly as with a crystalloid solution such as 0.9% NaCl or Plasma-
possible until clinical signs of shock resolve. As with all Lyte 148 may be required to reduce the viscosity of the
resuscitative fluids, continual assessment of response is infusion.
required to prevent volume overload. As soon as signs of
shock resolve, rates of blood administration can be Quantities of blood/plasma to administer
reduced and the remaining deficit in blood volume Anaemia/haemorrhage
replaced at a slower rate. (Note: Patients who require The volume of whole blood or packed RBCs required
large volumes of blood products transfused in a short can be calculated using the following formula:
period of time are at risk of developing hypocalcaemia,
which may present as muscle fasciculations or hypoten- Actual amount of donor blood needed (ml) = [(desired
sion. If this occurs, 10% calcium gluconate is adminis- PCV – actual PCV)/donor PCV] × body weight × circu-
tered intravenously at a starting dose of 0.5 ml/kg.) lating blood volume (ml/kg) where:
• Desired PCV = PCV desired at the end of
Non-emergency cases transfusion. After acute haemorrhage a PCV of
In non-emergency situations, infusion of blood products 0.3 l/l (30%) is generally desirable.
should be started slowly in order to monitor for and min- • Actual PCV = PCV of recipient at start of
imize the severity of reactions. (For details on blood transfusion.
transfusion reactions see Further reading.) • Donor PCV = PCV of the dog that donated blood.
Typically, the infusion is started at 0.25–2 ml/kg/hour. • Circulating blood volume = 90 ml/kg in dogs and
Vital signs should be recorded (heart rate, respiratory 60 ml/kg in cats.
rate, arterial BP, temperature) prior to starting the trans-
fusion and then every 10 minutes for the first 30 minutes. As an alternative to the above formula, an estimate of the
If no reaction has occurred after 30 minutes, the transfu- volume of blood required can be made according to the
sion rate can be increased to up to 4–20 ml/kg/hour. Vital following rule of thumb (calculation based on conven-
signs should be monitored again 10 minutes after the tional units and not SI units):
increase in infusion rate and then every 30 minutes until
the end of the transfusion. An example of a form that can 1 ml/kg of packed RBCs or 2 ml/kg of whole blood
be used to monitor animals receiving blood transfusions should raise the PCV by approximately 1%. For
can be found in the appendices. example, to increase the PCV from 20% to 30% (i.e. an
increase of 10%) in a 20 kg dog, the amount of packed
RBCs required = 1 × 20 × 10 = 200 ml, while the amount
of whole blood required = 2 × 20 × 10 = 400 ml.
 FLUID THERAPY 589

Use of these formulae requires measurement of PCV

prior to infusion. In animals that have suffered acute
haemorrhage, the PCV changes very little initially and
can take several hours to reach the minimum value,
depending on the amount of fluid administered. There-
fore, the amount of blood/packed RBCs required must
be estimated from the severity of clinical signs. With loss
of <15–20% of circulating blood volume, sympathetic
stimulation and associated responses resulting in
increases in heart rate, peripheral vasoconstriction and
venoconstriction are usually able to maintain BP and
peripheral perfusion. As blood loss exceeds 20%, com-
pensatory mechanisms will be gradually overwhelmed
and reduction in BP and tissue perfusion will occur.  438 After collection, whole blood can be separated
Hypotension will generally occur when >30% of circu- into packed red blood cells and plasma. If frozen within
lating blood volume has been lost. However, patients 6 hours, the plasma is called fresh frozen plasma. This can
who have sustained severe trauma may decompensate at be used to treat coagulopathies.
lower volumes of blood loss. Therefore, patients who
present with hypotension after acute haemorrhage can
be estimated to have lost at least 30% of blood volume
and this can provide a starting point for calculating the
volume of blood required to be administered. Further Cryoprecipitate (one unit per 10 kg body weight)
volumes of blood are administered until signs of shock can be used for patients with haemophilia A or von
resolve. Willebrand’s disease. For animals with severe thrombo-
(Note: When large volumes [>50% circulating blood cytopenia, fresh whole blood, platelet concentrate or
volume] of stored blood are administered, dilution of platelet-rich plasma should be administered to effect to
clotting factors will occur, resulting in coagulopathy. correct the coagulopathy.
FFP or fresh whole blood should be administered to
replace clotting factors [see below].) Method of administration
As a general rule, blood products should be administered
Coagulopathy within 4–6 hours of starting the infusion (i.e. 4–6 hours
FFP (438) (10–20 ml/kg) should be administered to after the drip set was inserted in the bag) and leftover
animals with clotting factor deficiencies that are predis- blood products and administration lines should be dis-
posed to CNS haemorrhage. Patients with DIC may carded because of the risk of bacterial contamination.
require FFP every 8–12 hours to correct clinical haemor- Frozen plasma should be administered within 6 hours of
rhage. Fresh whole blood can also be used to correct thawing. Gravity administration is generally recom-
coagulopathies. However, as greater volumes are mended, as some infusion pumps may cause haemolysis.
required to correct the respective clotting defect, care is The fluid pump manufacturer’s recommendations must
required to avoid volume overload (see above). be checked before use.
This page intentionally left blank
 SPECIFIC MANAGEMENT ISSUES Chapter 32

POSTOPERATIVE SUPPORTIVE CARE

AND PHYSICAL REHABILITATION 591

Sebastien Behr
& Rebecca Green

INTRODUCTION treat Hansen type I disc herniation), an adequate physical

rehabilitation plan may prevent permanent disability and
A well-designed rehabilitation plan and a high standard medical complications; in addition, it will accelerate the
of nursing care will improve the quality of life for an functional recovery of the patient. Rehabilitation should
emergency neurological patient and reduce the com- be initiated as soon as stabilization of the neurological
plications associated with prolonged hospitalization. patient is achieved.
Failure to provide appropriate supportive care following This chapter will focus on the supportive care of the
an acute neurological injury or disease could compro- neurological patient during hospitalization and on the
mise greatly the chance of recovery due to the develop- simple fundamental techniques of rehabilitation that can
ment of life-threatening complications (e.g. aspiration be performed at the beginning of the recovery period.
pneumonia) or permanent disability.
Rehabilitation is a discipline dedicated to restoring SUPPORTIVE CARE
function to an injured or diseased body. Physical rehabil-
itation covers a wide variety of topics from physio- Bladder management
therapy, hydrotherapy and thermotherapy to ultrasound, Micturition problems can be seen in patients either with
acupuncture and electrical stimulation. a lesion of the sacral spinal cord segments, their respec-
Although clinical signs may improve with time, tive nerve roots and peripheral nerves, or with a spinal
assuming an appropriate diagnosis was achieved and cord lesion cranial to the sacral spinal cord segments
treatment provided (e.g. decompressive spinal surgery to (439). The former is described as an LMN disorder and

Pontine micturition centre Motor control from L2–L5 in cats

Afferent stimuli from cortex L1–L4 in dogs Pelvic nerve
bladder S1–S3 Detrusor muscle
Pudendal nerve

 439 Schematic illustration

depicting the neurological innervation
of the bladder. The storage phase
involves contraction of the urethral
sphincter (pudendal and hypogastric
nerves) coupled with detrusor
relaxation (hypogastric nerve).
Hypogastric nerve
During micturition, the pelvic nerve
Stretch receptor in
causes detrusor contraction. bladder wall
592 SPECIFIC MANAGEMENT ISSUES

the later as a UMN disorder. Patients with either Usually, the safest option when using bethanechol
a UMN or an LMN bladder may not be able to store in patients with UMN bladder dysfunction is to use
and/or eliminate urine effectively and voluntarily. The a concurrent indwelling urinary catheter. It
risks associated with bladder dysfunction include damage normally takes 3–5 days for bethanechol and phe-
to the detrusor muscle caused by overstretching, urinary noxybenzamine to be effective; their individual
tract infections, urine scalding and in severe retention dosages can be increased at these times if there has
syndromes, ureter and kidney damage. The patient’s not been a satisfactory clinical effect.
bladder should be checked at regular intervals (every
3–4 hours). Bladder size and urinary status should be Lower motor neuron bladder disorders
documented throughout the day and this should not be LMN bladder disorders are related to diseases of sacral
based solely on the presence of urine on the bedding. spinal cord segments or the sacral plexus and are usually
described as incontinence from urine overflow. Perineal
Pharmacological management reflex and sensation are usually decreased or absent. The
Upper motor neuron bladder disorders detrusor and the external urethral sphincter are hypo-
UMN bladder disorders are commonly associated with tonic. The smooth urethral sphincter tone is intact due to
thoracolumbar spinal cord lesions occurring alongside its hypogastric innervation. The bladder is usually easily
other neurological deficits (e.g. paraparesis/paraplegia, expressed, but resistance can be found due to the internal
hindlimb ataxia). These disorders are characterized by a sphincter tone (innervated by the hypogastric nerve,
continuous storage phase due to the lack of inhibition of which would be unaffected). Pelvic nerve damage is
the hypogastric nerve (which causes detrusor relaxation another cause of urinary incontinence and is commonly
and internal urethral sphincter contraction) and lack of the consequence of an external trauma. There is a lack of
inhibition of the pudendal nerve (which causes external conscious sensation of filling and the bladder is distend-
urethral sphincter contraction). Voluntary micturition ed. The external and internal sphincters are both con-
can be delayed or absent, leading to a distended detrusor stricted. The anal tone and perineal reflex are normal.
muscle while urethral sphincter tone is increased.
Manual expression of the bladder is usually difficult. Treatment
• Decrease residual internal sphincter resistance.
Treatment Phenoxybenzamine (0.25–0.5 mg/kg PO q12–24h).
• Decreasing the internal urethral sphincter tone. • Stimulate detrusor activity. Bethanechol for
Alpha-adrenergic antagonists such as phenoxyben- cholinergic stimulation (dog: 2.5–15.0 mg/dog PO
zamine (0.25–0.5 mg/kg PO q8–12h) or prazosin q8h; cat: 1.25–5.0 mg/cat PO q8h). It is important,
(dog: 1 mg if less than 15 kg body weight or 2 mg additionally, to empty the bladder regularly (every
if over 15 kg PO q8–12h; cat: 0.25–0.5 mg PO 2–4 hours) via catheterization or manual expression
q12–24h). to limit the risks of retention cystitis and over-
• Decreasing the external urethral sphincter tone. stretching of the detrusor muscle.
Skeletal muscle relaxants such as diazepam (dog/cat:
0.2–0.5 mg/kg PO q8h), methocarbamol (20–40 Urinary catheterization
mg/kg PO q8h) or dantrolene (dog/cat: 0.5–2.0 Patients with urinary incontinence should either have
mg/kg PO q12h). their bladder manually expressed or have a urinary
• Stimulating the detrusor muscle. Bethanechol for catheter placed. Manual expression or drainage of the
cholinergic stimulation (dog: 2.5–15.0 mg/dog bladder should be performed every 3–4 hours. Patients
PO q8h; cat: 1.25–5.0 mg/cat PO q8h). that have a urinary catheter placed should wear an Eliza-
Bethanechol should always be given with drugs that bethan collar to prevent interference and have their
decrease the sphincter muscle tone, and bladder size temperature checked at least twice daily, as unexpected
should be monitored closely every 2–4 hours. pyrexia may indicate a severe urinary tract infection.
 P O S T O P E R AT I V E S U P P O RT I V E C A R E AND P H Y S I C A L R E H A B I L I TAT I O N 593

Should a long or uncertain recovery of voluntary uri-

nation be expected, based on the patient’s neurological
status (i.e. absence of nociception in the hindlimbs
and/or tail and/or perineum), surgical placement of a cys-
totomy catheter can provide long-term management of
urinary retention/incontinence without interfering with
the potential recovery of voluntary urination. Several
types of cystotomy catheter can be used. These include
percutaneous catheters or Foley urinary catheters, which
are placed after laparotomy or a minimally invasive
inguinal incision.
If possible, patients should still be taken outside. The
change of surroundings is beneficial to their mental well-
being and may also promote voluntary urination. It is
useful to find out from the owners how frequently the
patient would normally urinate, any toileting commands
and if the patient has a preferred surface to urinate on.
 440 Urinary catheter and collection bag. Patients should be placed on suitable bedding material
The bag should always be kept lower than (see Bedding) and monitored daily for urine scald.
the animal.
Management of urine scalding
Urine scalding arises from prolonged contact of urine
with the skin (441). The onset appears as small erythe-
matous areas, but these can develop into much larger
areas. Urine scalding is a lot easier to treat if noticed early
in its course. Patients at risk should be monitored daily.
Urine scalding can be relieved by regular cleansing
with a mild antiseptic shampoo, clipping the hair around
Because of patient discomfort, regular catheterization the perineal/inguinal area, applying a barrier cream
is not ideal even if the risk of infection is not significantly (e.g. zinc oxide), catheterization if appropriate and using
higher than that of indwelling catheterization. Prefer- non-retentive bedding.
ably, Foley silicone catheters should be placed and left in
situ provided no complications occur; they should be
maintained in an aseptic manner (440). Nevertheless, the
risk of urinary tract infection will increase with increased
durations of catheterization, therefore the urinary
catheter should be removed as soon as voluntary urina-
tion is suspected (e.g. recovery of voluntary movement in
the hindlimbs).
Urine should be monitored daily for output (1–2 ml/
kg/hour), SG and sediment cytology as well as changes
in colour and odour. Prophylactic antibiosis for urinary
tract infection is not recommended when an indwelling
urinary catheter is placed, as it significantly increases the
chance of drug-resistant bacterial disease.

 441 Severe urine scalding on a paraplegic dog.

594 SPECIFIC MANAGEMENT ISSUES

Gastrointestinal problems are still able to defecate, even with severe spinal injury,
Diarrhoea and vomiting due to the reflex action of the GI when stimulated by
GI problems, such as diarrhoea and vomiting, are not distension.
unusual during the recovery period of neurological dis- It is essential that patients are cleaned as quickly as
eases due to possible development of colonic and gastro- possible to avoid formation of sores, infection of any
duodenal ulceration and pancreatitis. Administration of wounds, general discomfort and further soiling. Patients
corticosteroids (dexamethasone in particular) and/or that develop diarrhoea should have their perianal and
NSAIDs will increase the risk of GI problems. Further- perineal areas clipped, cleaned and protected using a
more, diarrhoea and vomiting will increase the risk of waterproof barrier cream (e.g. zinc oxide). Feeding a
complications such as urinary tract infections and aspira- low-residue, highly digestible food can assist in the care
tion pneumonia, respectively, emphasizing the impor- of these patients by decreasing stool volume and fre-
tance of preventing and treating rapidly such GI quency. As with urination, patients should be taken
disturbances. outside to encourage voluntary defecation. It is beneficial
Symptomatic treatment is recommended as a first-line to find out from the owners how many times a day
approach by discontinuing anti-inflammatory treatment, the animal would usually pass faeces, any toileting com-
withholding food for 24 hours, administering intravenous mands and if the animal has a preferred surface to
fluids and administration of gastric acid secretion defecate on.
inhibitors such as cimetidine, ranitidine, omeprazole,
misoprostol or sucralphate. Unfortunately, none of these Respiratory problems
drugs reduce the potential of haemorrhage due to GI Hypoventilation
ulceration subsequent to corticosteroid administration. Patients with brainstem lesions, C1–C6 spinal cord
Should initial medical management fail or should damage and diffuse NM disease can experience hypoven-
signs of haemorrhagic gastroenteritis be obvious tilation leading to hypercapnia. If hypoventilation is sus-
(e.g. presence of melena), diagnostic tests (haematology pected clinically, measuring the PaCO2 provides a
and biochemistry including electrolytes, abdominal quantitative evaluation of the efficiency of ventilation
ultrasound, endoscopy) are recommended to investigate (see Chapter 2). Oxygen supply by facial mask, nasal
for possible underlying causes (e.g. pancreatitis or GI catheter or flow-by delivery should be provided in
ulceration). patients where mild hypoventilation is confirmed, with
the method of delivery dependent on the particular cir-
Bowel management cumstances. In severe cases, mechanical ventilation will
Similar to micturition, defecation relies on UMN and be required.
LMN controlling systems. Most commonly, faecal Brachycephalic breeds can suffer from severe
incontinence arises from neurogenic sphincter inconti- breathing difficulty with NM conditions or during
nence secondary to diseases of the cauda equina postoperative/postanaesthetic recoveries due to the con-
(e.g. L7/S1 fracture/luxation, disc disease, neoplasia, formation of their upper airways. Should severe respira-
vertebral malformation) affecting the LMN system. tory compromise be noticed, surgical management
Damage to the cauda equina results in inability of the (e.g. rhinoplasty and/or palatoplasty) or placement of a
anal sphincter to retain faeces and loss of conscious tracheostomy tube is recommended.
recognition of the passage of faeces. Less frequently, Patients with respiratory difficulties should have their
UMN incontinence is present with cranial lumbar, temperature, mucous membrane colour, capillary refill
thoracic or cervical spinal cord lesions (e.g. ischaemic time, respiratory rate and respiratory effort checked
myelopathy, arachnoid cysts, neoplasia). These patients hourly and arterial blood gas checked at least twice daily.
 P O S T O P E R AT I V E S U P P O RT I V E C A R E AND P H Y S I C A L R E H A B I L I TAT I O N 595

 442 Lateral thoracic radiograph revealing aspiration  443 Feeding a Siamese cat with an oesophagostomy
pneumonia secondary to megaoesophagus. tube.

Aspiration pneumonia by aspiration, helping to reduce the risk of regurgi-

Aspiration pneumonia results from inhalation of tation. The use of a gastrostomy tube enables food
stomach/oesophageal contents and is associated with to enter the stomach directly, thus reducing the
high morbidity and mortality. Aspiration pneumonia risk of regurgitation. A gastrostomy tube is the
can affect the recumbent tetraparetic or tetraplegic ideal manner in which to feed animals with
spinal patient, but, even more commonly, patients with megaoesophagus; however, placing this type of
NM disease, megaoesophagus, regurgitation and dys- feeding tube involves GA, unlike the oesophagos-
phagia (442). tomy tube, which can be placed with sedation and
The most efficient approach to pulmonary aspiration analgesia, and the naso-oesophageal tube, which
of gastric contents is prevention, which can be achieved can be placed in conscious/sedated animals.
by following simple practices: • Rest. In all cases, exercise should be avoided for a
• Positioning. The risk of aspiration pneumonia can minimum of 4 hours post feeding.
be reduced by feeding the patient in a sternal
position. Animals with megaoesophagus should be Treatment
lifted into a sitting position, enabling gravity to • Pharyngeal/oesophageal suctioning. Should
assist the movement of food into the stomach. aspiration be witnessed or suspected, suction of
Animals fed in this sitting position should be held fluids and particulates is recommended.
for at least 20 minutes after feeding to prevent • Oxygenation. Humidified oxygen should be
‘pooling’ of food in the oesophagus. delivered by mask, nasal cannula or ‘flow-by’ tubes
• Feeding tubes. For patients that are regurgitating, to maintain a normal PaO2.
nothing should be fed by mouth until the regurgita- • Bronchodilation. Aspiration will induce broncho-
tion has stopped. Placing a naso-oesophageal or constriction and administering bronchodilators is
oesophagostomy tube enables food to enter the recommended (e.g. aminophylline or terbutaline).
oesophagus at a closer entry point to the stomach, • Nebulization and cupping/coupage. Nebulization
reducing the time spent in the oesophagus and con- and cupping/coupage (see below) should be
sequently the risk of pooling (443). The use of performed 3–4 times daily in patients suffering
naso-oesophageal and oesophagostomy tubes from aspiration pneumonia to humidify respiratory
enables the oesophagus to be emptied intermittently airways and promote coughing, respectively.
596 SPECIFIC MANAGEMENT ISSUES

• Fluid therapy. Intravenous fluids are required to to side every 4–6 hours. Patients that cannot stay in
correct hypoperfusion and expand intravascular sternal recumbency should be turned between left
volume. Care should be taken not to elevate and right lateral recumbency a minimum of every
capillary hydrostatic pressure too much, as leakage 2–4 hours.
of fluid into the alveoli will increase pulmonary Cupping/coupage (see below) should be performed
oedema. However, diuretic therapy is not 3–4 times daily over both lung fields to promote loosen-
recommended. ing of secretions developed while recumbent.
• Antibiotic therapy. Antibiotic administration after
aspiration without confirmed infection is contro- Bedding
versial in human literature, as secondary infection The most important aspects of the bedding are that it is
may not necessarily take place and carries the risk of non-retentive and will allow urine to drain away from the
resistant bacterial infection. However, aspiration of patient. This can be provided by a non-retentive bed
oesophageal content carries a high risk of infection (e.g. Vetbed®), a sling bed, a non-retentive bed in its own
and antibiotic therapy is usually recommended for a right, which is raised and allows urine to drain through,
minimum of 3–4 weeks. A tracheal wash submitted or a grate covered by a non-retentive bed that raises
for cytology, culture and sensitivity is indicated the patient off the kennel floor and allows urine to drain
before starting antibiotics. Cephalosporins, from the bed to the floor (444).
amoxicillin/clavulanate or trimethoprim- Recumbent patients require a well padded non-
sulphonamide are recommended as first-line retentive bed to prevent pressure sores (decubitus ulcers,
treatments of aspiration pneumonia while waiting see below). This can be provided by a waterproof foam
for culture/sensitivity results. In case of severe mattress, a memory foam orthopaedic mattress or multi-
infections with suspected resistant gram-negative ple thick blankets covered by a non-retentive bed.
bacteria, enrofloxacin can be added, but should not Incontinence pads can be placed under the patient’s
be used as a single agent. Patients should be treated hind end and disposed of once soiled, or under the non-
for at least 3–4 weeks and 1 week beyond resolution retentive bed to protect against any further soiling of
of clinical and radiographic changes. bedding. If the pads are placed under the patient’s hind
end, it is important that they are removed immediately,
All animals at risk of aspiration pneumonia should have as they are retentive and will hold the urine next to the
their body temperature and respiratory rate monitored skin, consequently risking urine scalding.
regularly. Thoracic radiographs are recommended to Patients that are not fully recumbent or mobile,
confirm and monitor aspiration pneumonia 5–7 days but trying to stand, should be provided with non-slip
after initiating treatment. Radiographic changes may not flooring and bedding that is not too soft so as to unbal-
be seen in the first 24–48 hours after aspiration pneumo- ance them.
nia and will usually lag behind clinical improvement.
Decubitus ulcers
Pulmonary atelectasis Decubitus ulcers are an ulceration of skin and underlying
Atelectasis refers to collapse of part of the lung. It tissue caused by pressure that limits the blood supply
may include a lung subsegment or the entire lung. It is to the affected area. They are caused by the prolonged
most commonly seen in patients where prolonged pressure and friction on the body surface due to the
recumbency prevents lung expansion. Patients showing underlying bed.
signs of atelectasis may be tachypnoeic, dyspnoeic and The most common places for decubitus ulcers to
cyanotic. develop are over bony prominences such as the olecra-
To prevent pulmonary atelectasis, patients should be non process of the ulna, cranial aspect of the iliac wing,
maintained in either complete sternal recumbency or coxofemoral joint, ischiatic tuberosity and the calcaneal
sternal at the front with the hindlimbs moved from side tuberosity.
 P O S T O P E R AT I V E S U P P O RT I V E C A R E AND P H Y S I C A L R E H A B I L I TAT I O N 597

 444 A grate kennel base providing non-retentive  445 Decubitus ulcer treated temporarily using circular
bedding and effective support should the patient be padding ‘doughnuts’.
moved.

Prevention of decubitus ulcers is easier than treat- Intravenous catheter management

ment; the following suggestions may help reduce their Patients may require intravenous fluids or a CRI for a
occurrence. Recumbent patients are at risk of developing variety of reasons (see Chapter 31). For incontinent
these ulcers and therefore require a well padded non- patients, intravenous catheter placement would ideally
retentive bed; the patient should be turned every 2–4 be in either of the cephalic veins, or in the jugular vein if
hours ideally and massage applied to the bony promi- long-term fluid therapy is anticipated. If placement of a
nences to help promote circulation. Areas at high risk of catheter in a saphenous vein is necessary in an inconti-
ulceration can be protected using circular padding or nent patient, it must be checked regularly to observe for
‘doughnuts’ of foam (445), cotton wool or bubble wrap. signs of infection and redressed as necessary to prevent
The ‘doughnut’ is placed and secured surrounding the ‘strike-through’ to the catheter.
at-risk area, elevating the area from the bedding and The patient’s temperature should be taken at least
thereby promoting circulation. Advanced ulceration will twice daily to observe for any unexplained pyrexia, which
require surgical management. Decubitus ulcers increase can indicate an intravenous catheter infection.
the risk of septicaemia and postsurgical infections, and so Jugular catheters should be checked and flushed with
they should be aggressively treated. heparinized saline every 4 hours and peripheral catheters
Recumbent patients, where possible, should be lifted at least twice daily; however, patients with sensory
into a normal standing position at least twice daily with deficits may need more regular checks, as they may not
the use of a hoist or sling; this will not only relieve pres- show the usual signs of discomfort if the catheter is dis-
sure from the bony prominences and encourage circula- lodged and fluid is administered perivascularly. Should a
tion to them, but will also help enhance mental status, catheter infection be suspected, a sample of the catheter
strength, endurance and proprioception and help NM tip should be sent for culture and sensitivity, especially in
awareness (see p. 605). postsurgical patients.
Hydrotherapy can also be of benefit. The use of a
water spa where the patient either stands or is assisted to
stand can increase blood flow to affected areas. Water
temperature of around 40ºC (104ºF) tends to increase
heart rate.
 598 SPECIFIC MANAGEMENT ISSUES

Hypothermia PHYSICAL REHABILITATION

Hypothermia is a common complication of anaesthesia
and surgery, seen mainly in small or toy breed dogs and It is essential that a thorough examination of the patient
cats. The initial rapid decrease in core temperature after is undertaken before starting any treatment to avoid
GA results from an internal redistribution of body heat deterioration of any pre-existing conditions and to detect
due to inhibition of vasoconstriction that maintains a any abnormalities that may contraindicate further treat-
large core-to-peripheral temperature gradient. Great ment. The clinical diagnosis should be discussed with the
care should be taken to maintain and monitor body therapist before starting any therapy.
temperature in patients undergoing GA and surgery.
The use of a forced-air warming blanket is recom- Massage
mended during surgery, as it is the most effective method The benefits of massage are many and it can make a sig-
of minimizing anaesthetic-induced hypothermia and nificant difference to recovery. The following section will
rewarming hypothermic patients. An incubator provides describe how to perform various massage techniques and
the appropriate immediate postoperative environment their effects. (Note: Massage in some patients may cause
for recovery in cats or small breed dogs; blankets and heat discomfort. Treatment should be adjusted according to
pads are recommended in large breed dogs. Direct the disease or the time since surgery.)
contact of the heat pad on the skin is prohibited due to The effects of and contraindications to massage are
the risk of developing skin burns. listed in Table 117. Techniques include stroking, effleur-
age, petrissage (kneading, compression, picking up,
Exposure keratitis wringing and skin rolling), friction (circular and trans-
GA and opioid administration will decrease tear produc- verse), percussion (clapping, cupping/coupage, hacking
tion for at least 24 hours after administration. Regular and pounding), shaking and vibration.
(every 2–4 hours) and effective eye lubrication is manda-
tory in patients undergoing GA and/or receiving opioids Stroking
to prevent development of exposure keratitis. Artificial This is a slow and superficial gliding movement over the
tears should be applied during anaesthesia, in the first 24 body using the entire palm of the hand, usually in the
hours following GA and for up to 24 hours after the use direction of the hair growth, from cranial to caudal and
of opioids. proximal to distal. Stroking is generally considered first
Breeds with a relative exophthalmic conformation as it helps relax the animal, increase blood flow and
(e.g. most brachycephalic dogs, Shih Tzu, Lhasa Apso reduce muscle tone. It can be conducted with the animal
and Cavalier King Charles Spaniel) are prone to lagoph- in a standing position or in lateral recumbency and can be
thalmos and, thus, increased risk of exposure keratitis. done both at the beginning and end of a massage session
In such breeds, a temporary tarsorrhaphy can be per- and also between techniques to help loosen tissues.
formed as well as regular lubrication with artificial tears.
Effleurage
Pain management This is a similar technique to stroking; however, it
A well designed analgesia regimen is mandatory, particu- is carried out in the opposite direction, from distal to
larly for the postsurgical management of patients. The proximal, and in a direction towards the heart and lymph
most common drugs used alongside NSAIDs to manage nodes (446). Effleurage increases venous and lymphatic
spinal or neurogenic pain include buprenorphine, mor- return by mechanical pressure towards the heart and
phine, methadone, fentanyl, ketamine, medetomidine, lymph nodes. It is particularly useful when swelling is
dexmedetomidine, lidocaine and gabapentin. The present and in between other techniques.
patient’s level of pain should be assessed every 2–4 hours Effleurage decreases muscle tone, stretches muscle
using an appropriate pain scoring system. (see Chapter fibres, increases the mobility of the superficial fibres and
30 for further details on pain management.) aids in the removal of chemical irritants.
 P O S T O P E R AT I V E S U P P O RT I V E C A R E AND P H Y S I C A L R E H A B I L I TAT I O N 599

Petrissage
Table 117 Massage therapy
Petrissage techniques are best used on large areas of
muscle and consist of five methods: kneading, compres- Benefits
sion, picking up, wringing and skin rolling. • Stimulates the lymphatic and circulatory systems, helping
All five methods have the same effect. They mechan- to remove metabolic waste products from the muscles and
ically assist venous and lymphatic return, thereby improve blood flow and oxygen supply to the tissues,
cleansing the tissues of waste products and assisting cir- consequently preparing the tissues for activity and
alleviating pain
culatory interchange; they increase the length and
• Increases tissue circulation, temperature and elasticity,
mobility of fibrous tissue; they restore mobility between
leading to accelerated muscle recovery
tissue surfaces; they aid tissue fluid mobility; and they
• Stimulates the production of endorphins, therefore providing
increase flexibility and strength of connective tissue. analgesia
If done at a faster rate, they will cause vasodilation and • Relieves muscle spasm, cramps and adhesions (scar tissue)
reddening (hyperaemia) of the treated area, and when • Improves muscle tone and sensory perception
used slowly they may reduce muscular tension, resulting • Promotes both relaxation and the relationship between the
in relaxation. Sessions of petrissage are best interspersed patient and the therapist
with plenty of effleurage, to help relax the tissues and
Contraindications
disperse any waste products released during the session.
• Fever or hyperthermia
Kneading • Infection and skin problems
This technique comprises rhythmical half circles, • Neoplasia
with the right hand moving clockwise and the left hand • Open wounds
anticlockwise (447). The skin in front of the motion is • Unstable fractures
wrinkled and the skin behind the motion is stretched as • Acute haematoma
compression is also applied to the motion. The palmar • Heart conditions
surface of the fingers or thumbs is used for smaller areas • Shock
and the palm of the hand for larger areas. Reinforced • Acute inflammation
kneading can be achieved by placing one hand over the
other to increase the depth of compression.

 446 Effleurage is carried out from distal to proximal,  447 Kneading comprises rhythmical half circles, with
and in direction towards the heart and lymph nodes. It is the right hand moving clockwise and the left hand anti-
particularly useful when swelling is present and in clockwise. The skin in front of the motion is wrinkled and
between other techniques. the skin behind the motion is stretched.
600 SPECIFIC MANAGEMENT ISSUES

 448 Compression uses the palm of the hand or a  449 ‘Picking up’ is mostly used to decongest and relax
clenched fist to apply direct pressure, with no movement muscles and is carried out by grasping, lifting and
of the hand over the muscles. squeezing the muscles.

Compression Skin rolling

This technique uses the palm of the hand or a clenched This technique also uses both hands and involves grasp-
fist, alternating between each hand rhythmically, apply- ing and lifting the skin and superficial tissues between
ing compression to the muscles and tissues (448). This is the fingers and thumbs and rolling them either forwards
direct pressure with no movement of the hand over or backwards by drawing the skin towards the thumbs.
the muscles. Compression should only be applied to Skin rolling is useful in detecting adhesions along
larger muscle areas of larger dogs; care should be taken the back.
not to overcompress the tissues and hurt the patient.
Friction
Picking up Friction comprises localized small, fast and deep move-
This technique is also known as ‘muscle squeezing’ and is ments given with the tips of the first two or three fingers
mostly used to decongest and relax muscles. It is carried or the thumb of one hand for smaller areas and both
out by grasping, lifting and squeezing the muscles hands for larger areas. It is used to increase blood flow,
between extended fingers and thumb or heel of the hand, remove toxins and restore movement between tissues by
maintaining contact at all times (449). Picking up is breaking down adhesions developing over or between
mostly used on the limbs and tail and along the crest of tissues as a result of injury or surgery. In combination
the neck with either one or two hands. It can also be used with kneading, friction can also be used to break down
in a stimulatory manner affecting the nervous system and haematoma formation. Friction may cause local hyper-
at a faster rate to help warm up cold muscles. aemia by increasing blood circulation and producing a
histamine-like substance.
Wringing It is essential that these tissues are warmed before
This technique involves using both hands and is mainly applying friction, as well as drained and kept warm using
used on the patient’s back, shoulders and hindquarters. effleurage and petrissage. Friction can be performed in a
With both hands placed on the patient with the palms circular or transverse direction, and when applied causes
against the skin, each hand should be moved in the oppo- the superficial tissues to move over the deeper ones. At
site direction so that one hand brings the tissue towards no time during friction is there any glide of the fingers or
the operator and the other away (450). thumb on the skin.
 P O S T O P E R AT I V E S U P P O RT I V E C A R E AND P H Y S I C A L R E H A B I L I TAT I O N 601

 450 Wringing involves using both hands in opposite  451 Hacking is done with the hand at right angles to
directions so that one hand brings the tissue towards the the muscles, using the ulnar border of the hand with the
operator and the other away. elbows flexed.

Friction, especially deep friction, can cause discom- Hacking

fort, therefore 2–3 minutes on any one area should not be Hacking is done with the hand at right angles to the
exceeded. Further inflammation is to be avoided. muscles, using the ulnar border of the hand with the
elbows flexed, the wrists extended and the fingers relaxed
Percussion (451). Hacking penetrates deep into the muscles in a
Percussion, or tapotement, is a soft, rhythmical hitting of gentle manner and is particularly useful for treating back
the body using alternating hands in a flexible and springy muscles and those of the hindquarters.
manner. The effects of percussion are an increase in
blood circulation, the release of histamine, warming and Pounding
relaxation of muscles, stimulation of muscle tone and, Pounding is performed using the ulnar side of a relaxed
when used over the lungs, it promotes the loosening of loosely clenched fist with the wrists held in extension.
secretions. Percussion consists of clapping, cupping, Pounding is only performed after several clapping,
hacking and pounding. cupping and hacking moves to ensure the tissues are
warmed beforehand and is usually only performed to
Clapping provide deep stimulation of the larger muscle groups.
Clapping is done with the elbows flexed, wrists alternat-
ing in flexion and extension and the palm of the hand flat Shaking
against the body. It is performed on muscle groups, not This technique stimulates circulation and can also help
on bony surfaces, apart from the chest. loosen and move pulmonary secretions. It can be per-
formed using either the fingers or the whole hand,
Cupping/coupage depending on the size of area to be treated. The hand is
Cupping/coupage is done with the elbows flexed, the placed on the skin then the skin is moved with the hand
wrists alternating in flexion and extension and the palm over the muscle structures. This is a highly stimulating
of the hand in a cupped/arched position against the body. technique, so care should be taken around surgical sites
Cupping can be used all over the body. The cupped area and areas of inflammation.
is used to accommodate bony prominences and the hand
shape to mould around curved areas, such as the chest.
602 SPECIFIC MANAGEMENT ISSUES

Vibrations Although the joint should be taken beyond its normal

This technique involves no movement of the hand or ROM to enable a stretch to occur, it is essential that the
fingers over the skin surface. The hand is placed on the tissues are not stretched beyond their limits; this will
skin and a trembling or quivering movement applied to lead to permanent elongation of the tissues, termed
the area under the hand. With increasing pressure these plastic deformation, which may then contribute to joint
vibrations will reach the deeper tissues or joints. instability and further immobilization. In older animals
Vibrations can reduce adhesions in well healed scar the collagen fibres in the muscles become less elastic, and
tissue, soothe swollen joints and arthritic joints and over
the lungs can aid in the loosening of pulmonary secre-
tions, making it easier for them to be removed by other
massage techniques such as cupping.

Passive range of motion and static stretching

Passive range of motion (PROM) is best described as
the full range that a joint or muscle can be moved
through with no muscle contraction, using an external
force (the therapist) to move the joint (452). Joint range
of motion (ROM) can be measured using a goniometer;
readings are taken of the angle at which the joint is
in full flexion and extension. The measurements are
re-evaluated at intervals to determine whether there is
any improvement or deterioration in the ROM.
ROM can be affected by the structure of the joint and
also the tissues that surround the joint; these tissues may  452 Passive range of motion of the stifle. The joint is
be normal or pathological. Paralysed patients, or those moved in its normal range of motion, in proper alignment,
with a reduced ambulatory status, are at risk of: with the proximal and distal bones supported.
• Joint contracture.
• Reduction in fluidity between the tissues contribut-
ing to the formation of adhesions. Table 118 Passive range of motion therapy
• Reduction in blood and lymphatic flow to the
Benefits
limbs, resulting in waste products building up in the
• Improves the flexibility of the tissues and consequently the
muscles, leading to muscle tension and pain.
flexion and extension of the joints
• Prevents contracture of muscles, tendons and ligaments and
While performing PROM movements, the joint can be consequential muscle weakness
taken beyond the normal ROM and stretched in flexion • Increases blood and lymphatic circulation, helping to reduce
and extension. Other joints, such as the hip and shoulder, oedema and remove metabolic waste products from tissues
can also be stretched in abduction and adduction. The and relieve any associated pain
effects of and contraindications to PROM exercises are • Prevents the formation of adhesions
listed in Table 118. • Increases synovial fluid production
PROM exercises and stretches will not prevent • Improves proprioceptive awareness
muscle atrophy or increase strength, as there is no active • Enhances awareness of neuromuscular structure and
contraction of the muscle. Even if performed regularly, function
they will also not eliminate the possibility of muscle con- Contraindications
tracture, which can only be prevented by the animal
• Fractures (risk of further injury postsurgery or trauma)
regaining functional NM control.
• Septic arthritis
 P O S T O P E R AT I V E S U P P O RT I V E C A R E AND P H Y S I C A L R E H A B I L I TAT I O N 603

so these patients are at a higher risk of overstretching and During all stages of the treatment it is vital that the
possible plastic deformation. Care should be taken not to patient is comfortable. At no time should the patient
stretch a muscle too quickly, as this will cause the muscle show any sign of pain by vocalizing or trying to bite. If
spindle fibre to contract (i.e. muscle shortening and not signs of discomfort are present, the treatment needs to be
relaxation), the opposite effect to that desired. altered, by reducing the frequency and/or the amount of
To achieve the most from the session and get the best motion applied to the joint.
results from the tissues, it is important that the patient is It may take several weeks of performing PROM
as relaxed as possible, usually in lateral recumbency on a exercises and stretches for any effects to be evident, even
well-padded mat, or, sometimes, in a standing position. when performed many times daily and especially if tissue
The muscles must have been warmed previously using contracture has occurred.
massage and/or thermotherapy, otherwise there is a risk
of tissue damage, especially during stretches. The joint to Flexor reflex exercise
be manipulated should be moved in its normal ROM, in Prevention of muscle atrophy can only be achieved with
proper alignment, with the proximal and distal bones active muscle contraction, which requires intact NM
supported, to reduce any abnormal stresses on the joint. control. The flexor reflex exercise can provide such active
PROM exercises should be performed 2–6 times muscle contraction and should be repeated 3–5 times
daily, depending on the ROM in the joint. The better the several times daily. Resistance can gradually be applied to
ROM the less frequent the need for the exercises. The the reflex to increase muscle tone and bulk. This exercise
movements can be repeated 10–30 times on any one is achievable as long as the animal is tolerant and has
joint. If ROM is normal, or is returning to normal, the reduced pain sensation; if it has normal limb pain sensa-
frequency can be nearer to 10 times. If the joint has tion, this exercise will probably not be tolerated.
reduced ROM due to contracture or immobilization, the
frequency should be nearer 20–30. In a paraplegic Walking/lifting aids
patient, PROM movements may be repeated more fre- Patients that lack or have reduced motor function of
quently on the hindlimbs than the forelimbs. All joints, either their fore- or hindlimbs will need aids to help
including the digits, on all limbs should be treated, espe- them be moved and lifted. This can be achieved by using:
cially if the animal is recumbent, as the normal level of • An abdominal sling (453). Provides support under
activity will be greatly reduced in all limbs and not just the abdomen in front of the hindlimbs; can cause
the affected ones. the spine to arch. A towel can be used in the same
Stretches should be performed 3–5 times daily and way as the sling.
repeated 2–3 times in any necessary position: flexion,
extension, abduction or adduction. The stretch is held
for 15–30 seconds. Care should be taken not to ‘bounce’
the joint while it is being held in the stretch, as this can
contribute to tissue damage. Stretches of abduction in
the hip will help to prevent ‘crossing over’ of the
hindlimbs, seen in paraparetic or paraplegic patients. As
ROM improves in the joint, due to an increase in the
flexibility of the surrounding tissues, the frequency of
the stretches can be reduced.

 453 Sling support of the hindlimbs of a Dachshund

after a hemilaminectomy.
604 SPECIFIC MANAGEMENT ISSUES

Therapeutic exercises
Assisted range of motion
Assisted range of motion (AROM) exercises are per-
formed on patients that have no voluntary motor func-
tion, active muscle contraction and/or not enough
muscle strength to move the limbs. The therapist has to
move the limbs in order to perform the exercise. AROM
exercises can be performed in either lateral recumbency
or assisted standing. Moving a limb through its normal
ROM, as though walking, is an AROM exercise.
These exercises can be performed after the PROM
exercises to incorporate the movement of multiple joints
in unison. They can be performed 5–10 times on each
limb, repeated 3–4 times daily, and have similar effects as
PROM. The exercises will assist with:
• Proprioceptive and gait pattern training.
• Neuromuscular re-education.
• Maintaining or improving joint ROM.
• Increasing sensory perception.

 454 Hindlimb harness preventing spinal arching. As with PROM, AROM will not prevent muscle atrophy
as no active muscle contraction is present. The con-
traindications for AROM are the same as those for
• A hindlimb harness (454). Provides support both PROM (see Table118).
in front of and behind the hindlimbs and prevents
spinal arching. Active assisted range of motion
• A forelimb harness. Provides support to the Active assisted range of motion (AAROM) is indicated
forelimbs. when the patient has regained some motor function,
• A body harness. Supports the entire body. Some muscle contraction is present, but assistance and support
harnesses are available with lateral supports down are still required. The therapist assists the patient to
the side to help keep the spine straight. perform a complete limb movement, where there may
be deficits, by assisting the limb to move at the appropri-
Patients should not be left in a harness when not being ate phase of the gait cycle. This may be while being sup-
moved, as it may rub and cause sores to develop. ported walking on the ground or in water, in lateral
Hoists can also be used. They usually have their own recumbency or swimming. As with AROM, it may be
integral harness. They are more expensive, but free the advantageous and more productive to perform AAROM
therapist to perform further treatment on the patient. exercises after PROM. These exercises will have all of
Boots can be used to protect the feet against abrasions the effects that AROM has, but they will also help to
and sores while being assisted to move, or, in some cases, prevent muscle atrophy and increase muscle strengthen-
self-mutilation while being treated. They should not be ing due to the presence of muscle contraction and NM
left on for long periods as the feet will become hot and control. The contraindications for AAROM are the same
sweaty. as for PROM (see Table 118).
 P O S T O P E R AT I V E S U P P O RT I V E C A R E AND P H Y S I C A L R E H A B I L I TAT I O N 605

Assisted and active assisted standing Active exercises

Assisted standing is performed when the patient has no Active exercises are considered when the animal is able to
ability, or little ability, to hold its own body weight. Active move all limbs and bear weight. The exercises will
assisted standing is performed when the patient only improve muscle strength, endurance and coordination
needs partial assistance and is able to hold the majority of and create more flexion and/or extension of a joint.
its body weight. This exercise can: These exercises do not usually form part of the rehabili-
• Encourage weight bearing. tation plan of the emergency patient, but are more part of
• Assist and enhance NM awareness. the plan for the recovering patient.
• Promote proprioception and proprioceptive
training. Hydrotherapy
• Prevent decubitus ulcers and atelectasis. Hydrotherapy is available in three main forms: hot spa,
• Encourage urination and defecation. pool and water treadmill. There are five main principles:
• Improve mental state. buoyancy, hydrostatic pressure, viscosity, resistance and
• Provide the correct posture for eating and drinking, surface tension. The effects and contraindications are
so reducing the risk of aspiration pneumonia. listed in Table 119. Hydrotherapy is normally not part of
• Prevent muscle atrophy and encourage muscle the immediate postoperative care. It is usually started
strengthening, as well as endurance if weight 4–6 weeks after spinal surgery. In conditions such as
bearing is evident. ischaemic myelopathy or NM diseases, hydrotherapy can
be initiated straight away assuming no respiratory com-
A towel, sling, harness or hoist can be used to perform plications are present.
assisted standing exercises, and for active assisted stand-
ing the use of Swiss balls and physio rolls can be added.

Balance and proprioceptive exercises

The aim of these exercises is to improve sensory percep-
tion, balance, strength and coordination. The principle is
Table 119 Hydrotherapy
to alter the animal’s centre of gravity, which encourages it
to shift its weight to maintain its balance. This can be Benefits
achieved by:
• Limb movement through decreased load bearing
• Weight shifting, which can be done in a cranio-
• Prevents muscle atrophy and assists with standing and
caudal and caudocranial direction using the physio therapeutic exercises
roll or Swiss ball. • Increases muscle mass, strength, tone and endurance
• It can also be done from side to side. The animal
• Increases sensory perception
should have some weight-bearing ability and stand
• Provides pain relief, relaxation and reduces oedema
squarely either with or without the support of a
• Provides thermotherapy
sling. The hands are placed on either side of the
body and the patient is pushed from side to side. Contraindications
If a sling is being used, this can help to shift the • Infection and/or skin disease
weight from side to side. • Open or draining wound
• Lifting a limb or gently nudging the animal to the • Faecal incontinence
side while walking will alter its centre of gravity and • Aquaphobia
cause weight shifting. Encouraging the animal to • Reduced cardiac function
follow a treat/ball with its head will also encourage • Caution with patients having respiratory disease
weight shifting. At all times care should be taken • Caution with brachycephalic breeds having higher risk of
not to cause the patient to fall; additional support overheating
may be needed while performing these exercises.
606 SPECIFIC MANAGEMENT ISSUES

Thermotherapy/cryotherapy Cryotherapy
Thermotherapy Cryotherapy is the application of cold to the body. Cold
Thermotherapy is the application of heat to the body. can be applied using ice packs, cold compression units or
There are several ways of applying heat: hot packs, heat ice massage. Cold can penetrate deeper than heat and
pads, hydrotherapy (hot spa) and heat lamps. However, lasts longer than heat due to the decrease in circulation
all of these methods have an effect only on the superficial caused by vasoconstriction.
tissues. Ice or ice packs should never be applied directly
Heat should be applied for 15–20 minutes in order to to the skin (except for ice massage); no form of cryother-
a obtain 3Cº (5.4Fº) increase in tissue temperature to apy should be applied to a surgical incision.
acquire a therapeutic effect. Once the heat is removed, Cryotherapy should be used in the acute stages of
tissue temperature rapidly decreases because of the inflammation, in the first 2–3 days after injury, trauma or
vasodilation and increase in circulation. Therefore, surgery, or after exercise as a precautionary measure. It
exercises/massage should be performed while heat is in should be applied for 15–20 minutes, but the area treated
place, while the patient is in the hot spa or immediately should be checked every 5–10 minutes for signs of frost-
after the removal of the heat source. bite and continually checked after treatment. The effects
Hot packs should never be applied directly to the and contraindications/disadvantages of cryotherapy are
skin; they should be wrapped in a towel or something listed in Table 121.
similar. Thermotherapy should not be used in the first
few days after injury, but can be used 3–5 days post-
surgery. The effects of and contraindications to ther-
motherapy are listed in Table 120.

Table 120 Thermotherapy Table 121 Cryotherapy

Benefits Benefits
• Provides pain relief, induces relaxation and reduces oedema • Reduces inflammation and haemorrhage
• Softens scar tissue • Reduces oedema and muscle spasm
• Increases flexibility of tissues • Decreases nerve conduction velocity
• Increases nerve conduction velocity • Provides analgesia by stimulating cold receptors and
• Accelerates healing numbing superficial nerve endings

Contraindications Contraindications

• Inflammation • Areas that have previously had frostbite

• Haemorrhage • Areas of vascular compromise or patients with poor/reduced
thermoregulation
• Tumours
• Do not apply ice to a surgical incision or open wound
• Decreased cardiac function
• Patients that are cold-sensitive. Perform a test area and
• Open wounds
observe for swelling and wheals on the skin caused by the
• Pyrexia/poor thermoregulation release of histamine; this indicates cold urticaria
• Decreased sensory awareness (patients may not be aware of • Care should be taken when applying cryotherapy over
the presence of the heat, therefore they are at risk of superficial nerves to prevent nerve palsy
developing burns)
 P O S T O P E R AT I V E S U P P O RT I V E C A R E AND P H Y S I C A L R E H A B I L I TAT I O N 607

Therapeutic ultrasound and increasing/maintaining muscle strength. This

This treatment should only be performed by a veterinary method of stimulation is useful for patients that
physiotherapist or other trained personnel. The ultra- have reduced or no voluntary motor function and
sound frequencies used are typically between 1 and are recumbent.
3 MHz and penetrate between 0 and 5 cm, affecting both • Transcutaneous electrical nerve stimulation
superficial and deeper tissues. Ultrasound can be applied (TENS). Does not induce any muscle contraction,
either directly onto clipped skin using a coupling but excites the sensory nerves. This provides
medium, or indirectly by placing the treatment area in analgesia to muscles, joints or the spine by
water. The effects and contraindications/disadvantages activating neural pain control systems. Analgesia is
of therapeutic ultrasound are listed in Table 122. also provided by the reduction in muscle tone,
increase in circulation, removal of metabolic waste
Electrical stimulation products and stimulation of endogenous opioids
Electrical stimulation should be performed only by a from the spinal cord.
veterinary physiotherapist or other trained personnel. • Electrical muscle stimulation (EMS) is used when a
The effects of and contraindications to electrical stimu- muscle is denervated and patients have secondary
lation are listed in Table 123. atrophy (neurogenic muscle atrophy). To achieve
Types of electrical stimulation include: muscle contraction in these patients, to prevent
• Neuromuscular electrical stimulation (NMES). atrophy or increase muscle mass and strength, the
Acts on motor nerves to achieve muscle muscle has to be stimulated. This will need to
contraction. Useful for preventing muscle atrophy continue until nerve regeneration has occurred.

Table 122 Therapeutic ultrasound Table 123 Electrical stimulation

Benefits Benefits
• Increases the elasticity of fibrous tissue • Increases ROM, muscle strength, tone and function
• Prevents joint contracture • Provides analgesia
• Softens scar tissue • Reduces muscle spasm
• Improves joint mobility • Decreases joint contracture
• Reduces muscle tension • Corrects gait abnormalities
• Provides analgesia • Enhances circulation

Contraindications Contraindications
• Avoid direct contact with the heart, eyes, gravid uterus, • Pacemaker placement
tumours, testes, infected wounds, acute injuries or inflam- • Neoplasia
mation, or growth plates
• Risk of further injury/instability
• Avoid areas over the spinal cord following a laminectomy
• Blood clots/haemorrhage
• Decreased sensory awareness
• Inflammation or infection of the area
• Haemorrhage/blood clots
• Patients at risk of seizure
• Open wounds or recent surgical sites to avoid dehiscence
• Decreased sensory awareness in the area
• Decreased cardiac function. Higher risk of burning as the
• Areas of thrombosis or thrombophlebitus
heat is not dissipated as effectively
• Pyrexia/poor thermoregulation
This page intentionally left blank
 APPENDICES
Amy Wood, 609
Laurent Garosi
& Simon Platt

APPENDIX 1: EMERGENCY DRUG USE

The table below provides selected information on the drug mechanism, dosage and adverse effects of commonly
used drugs in neuroemergency patients.

Drugs used in neurological emergencies

DRUG NAME DRUG MECHANISM DOSAGE ADVERSE EFFECTS AND PRECAUTIONS

Acepromazine Phenothiazine Dog: 0.01–0.02 mg/kg slow IV; Can cause significant hypotension.
tranquillizer 0.01–0.05 mg/kg IM, SC; No reversal agent available. Can cause
Antiemetic 1–3 mg/kg PO q8–12h paradoxical excitement, especially in aggressive
Cat: same dosage as in dog animals

Acetazolamide Systemic carbonic Dog: 5–10 mg/kg IV; 4–8 mg/kg Contraindicated in patients with significant
anhydrase inhibitor PO q8–12h hepatic or renal disease, Addison’s
Diuretic Cat: do not use disease, hypokalaemia, hyponatraemia or
hyperchloraemia

Amantadine NMDA antagonist Dog: 3–5 mg/kg PO q24h Adverse effects include GI upset, agitation and
(analgesic) Cat: Anecdotal use reported at sedation, especially early in therapy. Use with
dosages used in dogs caution in patients with renal or liver disease,
heart failure, narrow-angle glaucoma or seizure
disorders. Narrow safety margin; overdosage
can cause fatal cardiac arrhythmias, CNS
toxicity, hyperthermia, renal dysfunction, and
respiratory distress

Amitriptyline Tricyclic antidepressant Dog: 1–2 mg/kg PO q12–24h Do not use concurrently with monoamine
Cat: 0.5–2 mg/kg PO q12–24h oxidase inhibitors or anticholinergic drugs.
Contraindicated in patients with cardiac
arrhythmias, seizure disorders, thyroid disease
or adrenal tumours

Atropine Anticholinergic Dog: 0.02–0.04 mg/kg IV, IM Contraindicated in patients with tachyarrhyth-
(muscarinic antagonist) Cat: same dosage as in dog mias, narrow-angle glaucoma or suspected
autonomic neuropathy

Azathioprine Immunosuppressive Dog: 1–2 mg/kg PO q24h, taper Can cause bone marrow suppression (especially
drug to q48h in cats) and hepatotoxicity; hepatotoxicity is
Cat: not recommended idiosyncratic in dogs

(Continued)
610 APPENDICES

Drugs used in neurological emergencies (continued)

DRUG NAME DRUG MECHANISM DOSAGE ADVERSE EFFECTS AND PRECAUTIONS

Bethanechol Cholinergic Dog: 5–25 mg/dog PO q8h Do not use in patients with urethral obstruction
(muscarinic agonist) Cat: 1.25–5 mg/cat PO q8h or increased urethral outflow resistance. Do not
use concurrently with other cholinergic drugs or
drugs that increase urethral sphincter tone.
Adverse effects include salivation, lacrimation,
urination and defecation

Buprenorphine Opioid analgesic; Dog: 0.005–0.03 mg/kg IV, IM, SC, Will prevent efficacy of pure mu agonists for
partial agonist bucally/sublingually q6h 6–8 hours
Cat: 0.005–0.03 mg/kg IV, IM, SC,
bucally/sublingually q6h

Butorphanol Opioid analgesic, Dog: 0.1–0.6 mg/kg IV, IM, Do not use in patients with pneumonia or other
mixed agonist/ SC, PO q2–4h lower respiratory tract disease with copious
antagonist Cat: 0.1–0.8 mg/kg IV, IM, mucus production (suppresses cough)
SC, PO q2–4h

Carprofen Nonsteroidal anti- Dog: 2–4 mg/kg SC, slow Can cause GI ulceration; do not use in
inflammatory IV single dose; 2 mg/kg PO q12h combination with other ulcerogenic drugs
Cat: 2 mg/kg SC, slow (steroids, other NSAIDs, aspirin, methotrexate).
IV single dose Adverse effects include hepatic and renal
insults; do not use in dehydrated, hypovolaemic
Licensed at 4 mg/kg single or hypotensive patients or those with GI
dose in cats disease or blood clotting abnormalities

Charcoal, Adsorbent Dog: 1–4 g/kg PO (granule); Adverse effects include emesis (especially when
activated 6–12 g/kg PO (suspension) administered rapidly) and constipation.
Cat: same dosage as in dog Separate from other oral medications by at
least 3 hours. Administer cautiously in sedated
patients or those with reduced gag reflex

Clindamycin Antibiotic Dog: 5–33 mg/kg PO, SC, IM, IV q Use with caution in patients with severe liver or
Antiprotozoal 8–12h; for Neospora,10 mg/kg kidney disease and in neonates. GI upset is
q12h concurrently with trimetho- most common adverse effect. Can cause hyper-
prim/sulphonamide salivation following liquid administration in
Cat: 5–15 mg/kg PO, SC, IV cats. Recommend following pills with water to
q8–12h; for systemic toxo- avoid oesophageal injury
plasmosis, 12.5–25 mg/kg PO,
SC q12h

Clomipramine Tricyclic antidepressant Dog: 1–3 mg/kg PO q12h Do not use concurrently with monoamine
Cat: 0.25–1 mg/kg PO q12h oxidase inhibitors or anticholinergic drugs.
Contraindicated in patients with cardiac
arrhythmias, seizure disorders, thyroid disease
or adrenal tumours

Clonazepam Benzodiazepine Dog: 0.5 mg/kg PO q8–12h Contraindicated with severe liver disease.
Anticonvulsant Cat: 0.1–0.2 mg/kg PO q8–12h May lose efficacy after ~3 months. Taper rather
than discontinue abruptly after long-term use

(Continued)
 APPENDICES 611

Drugs used in neurological emergencies (continued)

DRUG NAME DRUG MECHANISM DOSAGE ADVERSE EFFECTS AND PRECAUTIONS

Clorazepate Anticonvulsant Dog: 0.5–2 mg/kg q8h for 24–96 Primary adverse effect is sedation, which can
hours (for management of cluster be profound. Recommend starting with lower
seizures at home) dose and repeating as necessary for cluster
Cat: use for seizures not reported seizures between doses. Rapidly induces
hepatic metabolism, so not useful as
maintenance drug. Contraindicated in patients
with severe liver disease or narrow-angle
glaucoma. May precipitate fear/aggression

Cyclosporine Immunosuppressive Dog: 5–10 mg/kg PO q12–24h Vomiting, anorexia, diarrhoea, gingival
drug Cat: 5 mg/kg PO q24h hyperplasia and papillomatosis. Avoid reaching
high blood levels in patients with renal or
hepatic disease. Atopica or Neoral (brand
names) recommended for reliable drug delivery

Cytarabine Immunosuppressive Dog: 50 mg/m2 SC q12h, for 4 Myelosuppression (especially leukopenia) has
(cytosine drug doses or 200 mg/m2 IV infusion been reported, with nadir 5–7 days after
arabinoside) over 24 hours then every 3 weeks treatment; recommend monitoring CBC.
Cat: 100 mg/m2 SC q12h, then Can also cause GI upset. Use appropriate
every 3 weeks precautions when handling. Excreted in urine
for 24 hours after administration

Dantrolene Skeletal muscle relaxant Dog: 1–5 mg/kg PO q12h; Can cause hepatotoxicity. Avoid use in patients
2–5 mg/kg IV single dose with liver disease. Adverse effects include
(prevention of malignant hyper- weakness, sedation, GI upset and increased
thermia); 3–10 mg/kg q8h (urine frequency of urination
retention disorder); 0.5–2.0
mg/kg PO q8h with diazepam
Cat: 0.5–2 mg/kg PO q12h

Dexamethasone Corticosteroid Dog: 0.1–0.2 mg/kg IV, IM, PO Causes iatrogenic hyperadrenocorticism
Anti-inflammatory agent Cat: same dosage as in dog (especially in dogs); effects include PU/PD,
polyphagia, weight gain, poor hair coat,
panting, elevated liver enzymes and insulin
resistance, among others. Can cause GI upset,
including ulceration, especially if given concur-
rently with other steroids or NSAIDs (con-
traindicated). Taper slowly after long-term use.
Immunosuppressive doses contraindicated in
patients with known or suspected infections

Dextrose Fluid replacement Dog: 40–50 ml/kg IV q24h Overdosage can lead to hyperglycaemia,
solution 5% (glycaemic control) dehydration and hyperosmolar syndrome
Cat: same dosage as in dog

Dextrose Fluid replacement Dog: 0.5 g/kg IV bolus, Must be diluted and given slowly to avoid
solution 50% diluted 1:1 with sterile water phlebitis. Overdosage can lead to hyper-
Antibiotic (hypoglycaemia) glycaemia, dehydration and hyperosmolar
Cat: same dosage as in dog syndrome

(Continued)
612 APPENDICES

Drugs used in neurological emergencies (continued)

DRUG NAME DRUG MECHANISM DOSAGE ADVERSE EFFECTS AND PRECAUTIONS

Diazepam Anticonvulsant Dog: 0.5–2.0 mg/kg IV to effect Contraindicated in patients with severe liver
Benzodiazepine (emergency management of disease. Can cause idiosyncratic hepatotoxicity
Tranquillizer seizures); 0.5–2.0 mg/kg/hour IV when given orally to cats. May cause thrombo-
in 0.9% NaCl as CRI (emergency phlebitis, especially if given as a CRI through a
Skeletal muscle relaxant
management of seizures); 0.25 peripheral vein. Can cause paradoxical
mg/kg PO q8–12h (skeletal excitement in both dogs and cats
muscle relaxant); 0.2–0.5 mg/kg
IV, IM (sedation or premedica-
tion); 1–2 mg/kg rectal
(emergency management of
seizures)
Cat: 0.3–2 mg/kg slow IV slow
(emergency management of
seizures); 0.5 mg/kg/hour IV in
0.9% NaCl as CRI (emergency
management of seizures); 0.25
mg/kg PO q8–12h (skeletal
muscle relaxant); 0.2–0.5 mg/kg
IV, IM (sedation or premedica-
tion); 0.5–1.0 mg/kg rectal
(emergency management of
seizures); 0.2 mg/kg IV (appetite
stimulant)

Doxycycline Antibiotic Dog: 3–11 mg/kg PO, IV q12h Adverse effects include GI upset (recommend
Cat: 3–11 mg/kg PO, IV q12h giving with food). Can cause oesophageal
stricture in cats (follow with water or give in a
slurry). Avoid use in pregnant or young animals
due to the potential for teeth and bone
abnormalities. Antacids affect absorption.
Phenobarbital can reduce half-life. Rapid IV
administration can cause significant cardiac
arrhythmias

Felbamate Antiepileptic Dog: 15 mg/kg PO q8h Adverse effects may include blood dyscrasias,
Cat: no data available dry eye, anxiety, inappetence and behaviour
changes. Avoid in patients with pre-existing
hepatic disease

Fentanyl Opioid analgesic Dog: 1–5 mcg/kg IV Adverse effects include sedation, dysphoria,
Pure agonist q15–20 minutes; 2–15 urine retention and constipation. Causes dose-
mcg/kg/hour CRI preceded related CNS, respiratory and cardiovascular
by loading dose; patch: depression (bradycardia) that can be profound.
3–5 mcg/kg/hour Patches may not provide consistent blood levels
Cat: 1–5 mcg/kg IV in veterinary patients; skin irritation at the
q15–20 minutes; 2–10 patch site has been reported. Do not use in
mcg/kg/hour CRI preceded by patients that have received a selective
loading dose; patch: 25 mcg/hour. serotonin reuptake inhibitor or monoamine
Kittens <3 kg: half a 25 mcg/hour oxidase inhibitor in the last 14 days
patch exposed (do not cut or
apply heat)

(Continued)
 APPENDICES 613

Drugs used in neurological emergencies (continued)

DRUG NAME DRUG MECHANISM DOSAGE ADVERSE EFFECTS AND PRECAUTIONS

Furosemide Diuretic Dog: 2–6 mg/kg IV, IM, SC, PO Do not use in dehydrated patients, patients
q8–12h with electrolyte imbalances or patients in
Cat: 1–4 mg/kg IV, IM, SC, PO anuric renal failure. Can cause hypona-
q8–24h traemia, hypokalaemia and dehydration.
High doses can cause ototoxicity, especially
in cats

Gabapentin Anticonvulsant Dog: 15–25 mg/kg PO q8–12h Sedation and ataxia are most common
Analgesic (antiepileptic);10–15 mg/kg PO adverse effects. Withdrawal seizures may
q8–12h (neuropathic pain, paraes- occur if discontinued abruptly after chronic
thesia) usage. Separate by at least 2 hours from
Cat: same dosage as in dog administration of oral antacids. Use with
caution in patients with impaired renal
function. Liquid formulation must be
compounded, as commercially available
liquid contains xylitol

Heparin Anticoagulant Dogs:100–200 IU/kg IV, then Do not use in patients with severe thrombo-
100–300 IU/kg SC q6–8h (arterial cytopenia, hypocoagulability (due to causes
thromboembolism, DIC);100 IU/kg other than DIC) or those that may undergo
SC q6–8h (thrombosis surgery. Overdosage can cause spontaneous
prevention) bleeding; reversal agent is protamine
Cat: same dosage as in dog sulphate

Hetastarch Colloid Dog: 1–10 ml/kg IV bolus, then Do not use in patients in heart failure or
1 ml/kg/h IV; maximum oliguric/anuric renal failure due to the risk of
50 ml/kg/24 hours IV as CRI volume overload. Use with caution in
Cat: 1–5 ml/kg IV bolus, then patients with thrombocytopenia (interferes
1 ml/kg/hour IV; maximum with platelet function). Can cause vomiting if
50 ml/kg/24 hours IV as CRI, always given too rapidly
administered to effect

Hydrocortisone Anti-inflammatory Dog: 0.5 mg/kg PO q12h (anti- See dexamethasone

inflammatory); 2–4 mg/kg IV,
IM q4–6h (acute addisonian crisis)
and 0.125 mg/kg PO q12h for
maintenance; 1–10 mg/kg
IV single bolus (shock)

Hydroxyurea Anti-neoplastic agent Dog: 50 mg/kg PO q24h Adverse effects include GI upset, stomatitis,
3 days/week alopecia, sloughing of nails, dysuria, bone
Cat: 25 mg/kg PO q24h marrow suppression and pulmonary fibrosis.
3 days/week Dosages >500 mg in cats can cause methe-
moglobinaemia. Use with caution in
Dalmatians or patients with a history of
urate stones

Imipramine Tricyclic antidepressant Dog: 2–4 mg/kg PO q12–24h See clomipramine

Cat: 0.5–1 mg/kg PO q12–24h

(Continued)
614 APPENDICES

Drugs used in neurological emergencies (continued)

DRUG NAME DRUG MECHANISM DOSAGE ADVERSE EFFECTS AND PRECAUTIONS

Ketamine Dissociative anaesthetic Dog: 10 mcg/kg/minute IV CRI Contraindicated in patients with hyperten-
Analgesic preceded by a 0.25 mg/kg loading sion, suspected increased intracranial
dose (intraoperative analgesia); pressure (e.g. patients with head trauma) or
2–5 mcg/kg/minute IV CRI preceded increased intraocular pressure. Also contra-
by a 0.25 mg/kg loading dose (post- indicated in patients with seizure disorders
operative analgesia); 2 mg/kg IV or those undergoing myelography. Can cause
(induction of anaesthesia in hyperthermia in cats. Adverse effects
combination with diazepam or reported with high dosages include
midazolam as part of volatile respiratory depression, vomiting, muscle
anaesthetic technique); 5–7 mg/kg tremors, convulsions and cardiac arrest
IV, IM combined with 40 mcg/kg IV,
IM medetomidine (induction general
anaesthesia)
Cat: same dosage as in dog for intra-
and postoperative analgesia;
5 mg/kg IM with 0.2 mg/kg IM
midazolam or diazepam (chemical
restraint)

Lactulose Laxative Dog: 10–20 ml/kg of a solution Adverse effects include flatulence, diarrhoea
comprising 3 parts lactulose to and abdominal cramping. Overdosage can
7 parts water per rectum as lead to dehydration. Contains free sugars
retention enema q6–8h (acute and may affect insulin requirements in
hepatic encephalopathy); diabetic patients. Do not combine with other
0.5–1 ml/kg PO q8–12h (hepatic laxatives
encephalopathy)
Cat: same dosage as dog for
retention enema; 2.5–5 ml/cat PO
q8–12h (hepatic encephalopathy)

Levetiracetam Antiepileptic Dog: 20–30 mg/kg PO q8h; Reported adverse effects include behaviour
20 mg/kg IV q8h (emergency changes and sedation. Patients receiving
treatment of seizures) phenobarbital may require higher doses than
Cat: 30 mg/kg PO q12h; 20 mg/kg those not on phenobarbital. Dosages up to
IV q8h (emergency treatment of 60 mg/kg q8h have been tolerated without
seizures) adverse effects

Levothyroxine Thyroid hormone Dog: 0.02 mg/kg PO q12–24h Use with caution in patients with hypo-
(adjust dose via monitoring) adrenocorticism, cardiac disease or diabetes.
Increases the action of catecholamines and
sympathomimetics and may alter insulin
requirements in diabetic patients

(Continued)
 APPENDICES 615

Drugs used in neurological emergencies (continued)

DRUG NAME DRUG MECHANISM DOSAGE ADVERSE EFFECTS AND PRECAUTIONS

Lidocaine Analgesic Dog: 25–75 mcg/kg/minute IV CRI Use with caution in patients with heart
Antiarrhythmic preceded by loading dose of 1 mg/kg block, heart failure, liver failure, respiratory
slow IV (intraoperative analgesia); depression or hypovolaemia. Rapid adminis-
2–4 mg/kg SC, perineural infiltration tration of an IV bolus can cause
(local, regional blockade hypotension. Adverse effects are dose
anaesthesia) related and progress from CNS abnormalities
Cat: 1–2 mg/kg SC, perineural infil- (depression, excitability, ataxia, muscle
tration (local, regional blockade tremors) to ECG abnormalities. Signs of
anaesthesia) toxicity include nystagmus, seizures,
bradycardia and cardiovascular collapse. Do
Do not exceed 4 mg/kg in dogs and
not give the formulation containing
2 mg/kg in cats whatever the route
epinephrine intravenously

Mannitol Osmotic diuretic Dog: 0.5–2.0 g/kg IV CRI over Contraindicated in patients with
15–20 minutes (acute cerebral dehydration, anuric renal failure or severe
oedema) pulmonary oedema. Adverse effects include
Cat: same dosage as in dog GI upset and tachycardia. Overdosage
causes sodium, potassium and chloride loss.
Must be warmed prior to administration and
given through a filter to avoid precipitation

Meclizine Antiemetic Dog: 12.5–25 mg/dog q24h (motion Can cause sedation or anticholinergic
sickness or vertigo) effects. Do not use in patients with
Cat: 12.5 mg/cat q24h (vertigo) glaucoma or urinary obstruction

Medetomidine Alpha-2 adrenoreceptor As supplemental analgesia and Contraindicated in patients with cardiac
agonist sedation: disease, renal disease or shock. May
Sedative and analgesic Dog: 1–2 mcg/kg/hour disinhibit aggressive dogs. Causes
Cat: 1–3 mcg/kg/hour bradycardia and pale mucous membranes.
For premedication in healthy Adverse effects include AV block, respiratory
animals: depression and hypoglycaemia. Do not
Dogs: up to 30 mcg/kg combine with anticholinergic drugs. Reversal
Cats: up to 50 mcg/kg agent is atipamezole (Note: Label dosage is
considered high)
Licensed dose for premedication
varies with country

Meloxicam Nonsteroidal anti- Dog: 0.3 mg/kg SC, IM, IV single Most common adverse effect is GI upset.
inflammatory injection; 0.1 mg/kg PO q24h Do not use in dehydrated patients, patients
Cat: 0.2–0.3 mg/kg SC, IM, IV single in renal failure or those with bleeding
injection; 0.05 mg/kg PO q24–48h disorders. Do not use concurrently with other
NSAIDs or steroids

Methadone Opioid analgesic Dog: 0.2–0.5 mg/kg IM, slow IV Can cause vomiting, constipation, sedation,
Pure OP3 agonist q3–6h bradycardia and respiratory depression.
Cat: 0.2 –0.3 mg/kg IM, slow IV; Overdosage can cause profound CNS and/or
may need longer dosing interval respiratory depression. Reversal agent is
than dogs naloxone

(Continued)
616 APPENDICES

Drugs used in neurological emergencies (continued)

DRUG NAME DRUG MECHANISM DOSAGE ADVERSE EFFECTS AND PRECAUTIONS

Methocarbamol Centrally acting muscle Dog: 20–45 mg/kg PO q8h Adverse effects include sedation, vomiting,
relaxant Cat: same dosage as in dog salivation, weakness and ataxia. Do not use
injectable product in patients with renal disease

Methylprednisol- Anti-inflammatory Dog: 30 mg/kg IV within 8 hours See dexamethasone

one sodium Immunosuppressive of spinal cord trauma, followed by
succinate drug 5.4 mg/kg/hour IV CRI for 24–48
hours or 15 mg/kg IV at 2 and
6 hours (spinal cord trauma), then
q8h for maximum of 48 hours
Cat: same dosage as in dog

Mexiletine Class 1b anti-arrhythmic Dog: 4–8 mg/kg PO q8–12h Use with caution in patients with AV block,
(myokymia) congestive heart failure, hypotension or seizure
disorders. Adverse effects include GI upset and
CNS abnormalities (trembling, dizziness,
depression). Signs of toxicity progress from CNS
abnormalities to cardiovascular depression

Midazolam Sedative Dog: 0.1–0.3 mg/kg IV, IM, PR Use with caution in patients with
Analgesic (emergency management of significant hepatic disease. May cause
Benzodiazepine seizures); 0.1–0.3 mg/kg/hour IV paradoxical excitation. Overdosage can cause
anticonvulsant CRI respiratory depression. Reversal agent is
Cat: same dosage as in dog flumazenil

Morphine Opioid analgesic Dog: 0.2–0.5 mg/kg slow IV, IM, Primary adverse effect is respiratory depression.
Pure agonist SC q3–6h; CRI: 0.1–0.2 Other adverse effects include vomiting,
mg/kg/hour preceded by loading sedation and hypothermia. Use with caution in
dose of 0.2 mg/kg patients with renal impairment, hypoadrenocor-
Cat: 0.1–0.2 mg/kg IM, SC; CRI: ticism, mast cell disease or elevated intracranial
0.1 mg/kg/hour preceded by pressure. Overdosage can cause profound CNS
0.1 mg/kg loading dose. May and/or respiratory depression. Reversal agent is
need longer dosing interval than naloxone. Do not use in patients that have
dogs received a selective serotonin reuptake inhibitor
or monoamine oxidase inhibitor in the last 14
days

Mycophenolate Immunosuppressive drug Dog: 10 mg/kg PO, IV q12h Not recommended for use concurrently with
(range: 5–20 mg/kg q12h) azathioprine due to similar mechanism of
Cat: 10 mg/kg q12h (limited action and increased risk of bone marrow
reported use) suppression. Must be given slowly IV. Adjust
dosage in patients with renal insufficiency. GI
upset is the most common adverse effect

(Continued)
 APPENDICES 617

Drugs used in neurological emergencies (continued)

DRUG NAME DRUG MECHANISM DOSAGE ADVERSE EFFECTS AND PRECAUTIONS

Neostigmine Anticholinesterase Dog: 0.01–0.1 mg/kg IM, IV, SC as Use with caution in patients with cardiac
bromide and needed depending on duration of arrhythmias, epilepsy, hyperthyroidism or
neostigmine response (myasthenic crisis); intestinal or urinary tract obstruction. Adverse
methylsulphate 0.1–0.25 mg/kg PO q4–6h effects are dose related and include cholinergic
Cat: use not reported in cats, but signs (vomiting, salivation, lacrimation,
extrapolation from dogs seems urination, defecation, miosis and agitation);
reasonable these can progress to cholinergic crisis
(hypotension, weakness, bronchospasm,
tachycardia or bradycardia). Atropine can be
used to reduce adverse effects

Oxymorphone Opioid analgesic Dog: 0.02–0.2 mg/kg IM, SC, IV Primary adverse effects are respiratory
Pure OP3 agonist Cat: 0.02–0.1 mg/kg IM, SC, IV depression and bradycardia. Other adverse
effects include vomiting, sedation and
hypothermia. Use with caution in patients with
renal impairment, hypoadrenocorticism or
elevated intracranial pressure. Overdosage can
cause profound CNS and/or respiratory
depression. Reversal agent is naloxone. Do not
use in patients that have received a selective
serotonin reuptake inhibitor or monoamine
oxidase inhibitor in the last 14 days

Pentobarbital Anaesthetic Dog: 2–15 mg/kg slow IV bolus to Do not use in patients with significant liver
effect, followed by 0.2–1 disease. Use with caution in hypovolaemic or
mg/kg/hour IV CRI (status anaemic patients. Primary adverse effect is
epilepticus or cluster seizures) respiratory depression; can also cause
Cat: same dosage as in dog hypothermia. Cats appear to be more sensitive
to adverse effects. Rapid IV administration can
cause respiratory depression. Perivascular
injection causes tissue irritation

Phenobarbital Antiepileptic Dog: 2–3 mg/kg PO q12h initial Do not use in patients with significant liver
dose; 10–20 mg/kg slow IV bolus disease. Use with caution in hypovolaemic or
to effect or divided into 2–4 anaemic patients. Primary adverse effects
mg/kg IV bolus q20–30 minutes include respiratory and CNS depression. Rapid
(status epilepticus, cluster IV administration can cause respiratory
seizures, tremors) depression. May cause tissue necrosis if given
Cat: 1–2 mg/kg PO q12h perivascularly. Idiosyncratic bone marrow
initial dose hypoplasia has been reported. Adverse effects
include ataxia, sedation (usually transient),
PU/PD and polyphagia. Hepatotoxicity is rare,
but may occur with long-term use in dogs at
high serum concentration or as idiosyncratic
reaction within 2 weeks of onset of treatment

Phenoxy- Alpha-adrenergic Dog: 0.25–1 mg/kg PO q8–24h Use cautiously in patients with heart disease.
benzamine antagonist Cat: 1.25–5 mg/cat PO q12–24h Adverse effects include hypotension and GI
upset

(Continued)
618 APPENDICES

Drugs used in neurological emergencies (continued)

DRUG NAME DRUG MECHANISM DOSAGE ADVERSE EFFECTS AND PRECAUTIONS

Phenylpropanol- Adrenergic agonist Dog: 1 mg/kg PO q8–12h Use with caution in patients with hypertension,
amine Cat: same dosage as in dog heart disease, hyperthyroidism, diabetes
mellitus or glaucoma. Adverse effects include
restlessness, irritability, hypertension and
anorexia; rarely, strokes and cardiotoxicity have
been reported

Potassium Antiepileptic Dog: maintenance dose 30–40 Often causes sedation during the first few
bromide mg/kg PO q24h; loading dose weeks of treatment. Other adverse effects
600–800 mg/kg PO divided over include PU/PD, polyphagia and GI upset.
5–6 days Pancreatitis has been reported. Signs of toxicity
Cat: use not recommended include sedation/stupor, tremors, ataxia,
paraparesis, hyporeflexia, anisocoria and
muscle pain. Can cause a potentially fatal
asthma-like syndrome in cats. Dietary intake of
chloride affects serum bromide levels: diets low
in chloride can cause bromide toxicity, while
diets high in chloride can reduce serum level
and may affect seizure control

Prednisolone Anti-inflammatory Dog: 0.5–1.0 mg/kg PO, IV, See dexamethasone

Immune modulator IM q12–24h then taper to
0.5–1 mg/kg PO q48h (anti-inflam-
matory); 1.1–3.3 mg/kg PO q12h
then taper to 0.5–2.2 mg/kg q48h
(immunosuppressive); 0.2–0.3
mg/kg PO q24h (replacement
therapy)
Cat: 1.1 mg/kg PO q12h then taper
to 1.1–2.2 mg/kg q48h (anti-inflam-
matory); 2.2–6.6 mg/kg PO q12h
then taper to 2.2–4.4 mg/kg q48h
(immunosuppressive)

Pregabalin Antiepileptic Dog: initially 2 mg/kg PO q8–12h Adverse effects include sedation, ataxia and
Analgesic gradually increased to 3–4 mg/kg weakness
PO q8–12h to effect
Cat: no data available in cats

Primidone Antiepileptic Dog: 5–20 mg/kg PO q12h Adverse effects include anxiety and depression
Cats: do not use at lower serum levels, PU/PD and polyphagia at
moderate serum levels and sedation and ataxia
at higher serum levels. Long-term use can cause
serious hepatic injury. Rarely reported adverse
effects include anaemia, dermatitis, hyperventi-
lation, urolith formation and anorexia

(Continued)
 APPENDICES 619

Drugs used in neurological emergencies (continued)

DRUG NAME DRUG MECHANISM DOSAGE ADVERSE EFFECTS AND PRECAUTIONS

Propofol Anaesthetic Dog: 2–6 mg/kg slow IV over Causes transient apnoea, especially if given
60 seconds to effect (anaesthesia rapidly. Overdosage can cause severe
induction); 0.1–0.6 mg/kg/minute respiratory and myocardial depression.
IV CRI preceded by 3–6 mg/kg Repeated daily use in cats can cause Heinz
slow IV bolus to effect (status body haemolytic anaemia
epilepticus, tremors)
Cat: 3–8 mg/kg for induction of
anaesthesia (Note: Care with
long-term CRI in the cat; not
recommended)

Propranolol Beta-1 adrenoceptor Dog: 0.5–1 mg/kg PO q8h Do not use in patients with heart failure,
antagonist (refractory idiopathic tremor bradyarrhythmias or conduction disturbances,
syndrome); 0.02–0.06 mg/kg slow diabetes mellitus, hypoglycaemia or significant
IV bolus over 10 minutes renal or liver disease. Adverse effects include
(emergency refractory idiopathic bradycardia, hypotension, AV block, hypo-
tremor syndrome) glycaemia and bronchoconstriction

Pyridostigmine Anticholinesterase Dog: 0.2–3 mg/kg PO q8–12h See neostigmine

bromide (titrate to effect)
Cat: same dosage as in dog

Selegiline Dopamine agonist Dog: 1 mg/kg PO q24h Adverse effects include vomiting, diarrhoea,
(narcolepsy); 0.5–1 mg/kg q24h anorexia and lethargy; restlesness, salivation,
for minimum 2 months (cognitive pruritus, tremors and decreased hearing have
dysfunction) also been reported. Separate use by 2 weeks
Cat: 1 mg/kg PO q24h from other antidepressants (selective
serotonin reuptake inhibitors or tri/tetracyclic
antidepressants); do not use concurrently with
opioids or amitraz

Sodium Antiepileptic Dog: maintenance dose 30 mg/kg See potassium bromide, although sodium
bromide (3%) PO q24h; loading dose bromide causes fewer GI adverse effects
900 mg/kg/24 hours CRI
Cat: use not recommended

Tetanus Antitoxin Dog: 100–1000 U/kg IV, IM, SC near IV administration highly associated with
antitoxin wound site once preceded by anaphylaxis; precede with test dose and have
0.1–0.2 ml SC, ID test dose epinephrine, dexamethasone and benadryl
(observe for 30 minutes for signs of on hand
anaphylaxis)
Cat: same dosage as in dog

Thiamine Vitamin Dog: 50–100 mg/dog IM, SC, Can cause soreness at the site of IM injection.
(vitamin B1) PO q12–24h Rarely, hypersensitivity has been reported
Cat: 25 mg/cat IM, SC, PO
q12–24h

(Continued)
620 APPENDICES

Drugs used in neurological emergencies (continued)

DRUG NAME DRUG MECHANISM DOSAGE ADVERSE EFFECTS AND PRECAUTIONS

Topiramate Antiepileptic Dog: 2–10 mg/kg PO q12h Adverse effect profile not well known; may
Cat: no data available cause ataxia, lethargy or abnormal
mentation. Avoid concurrent use with
carbonic anhydrase inhibitors

Tramadol Analgesic Dog: 2–5 mg/kg PO q8–12h Adverse effects include sedation and GI
Opioid agonist Cat: 2–4 mg/kg PO q12h upset. Naloxone is not effective in treating
overdose. Do not use in patients that have
Inhibitor of reuptake
received a selective serotonin reuptake
of serotonin and
inhibitor or monoamine oxidase inhibitor in
norepinephrine
the last 14 days

Trazodone Serotonin-2 Dog: Initial dose range for first 3 Do not use concurrently with monoamine
antagonist/reuptake days: <10 kg, <25 mg q8–24h; oxidase inhibitors. Adverse effects include
inhibitor >10–20 kg, 50 mg q12–24h; serotonin toxicity, GI upset, dry mouth and
Antidepressant, >20–40 kg, 100 mg q12–24h; >40 excessive sedation. Do not use in dogs with
anxiolytic kg, 100 mg q12–24h. glaucoma, a history of seizures or urinary
Target dose for long-term adminis- retention and severe liver disease.
tration: <10 kg, <50 mg q8–24h; Recommend lower dosage for patients also
>10–20 kg, 100 mg q8–24h; receiving tramadol
>20–40 kg, 200 mg q8–24h; >40
kg, 200–300 mg q8–24h. All doses
given PO
Cats: no information available on
use in cats
Valproic acid Antiepileptic Dog: 60–200 mg/kg PO q8h or Use with caution in patients with significant
25–100 mg/kg/day PO when liver disease or thrombocytopenia/pathia.
administered with phenobarbital Adverse effects reported in humans include
sedation, GI upset, hepatotoxicity, bone
marrow suppression and pancreatitis

Voriconazole Triazole antifungal Dog: loading dose 6 mg/kg IV or Increases risk of toxicity/adverse effects of
PO q12h for 2 days, followed by cyclosporine, phenytoin, phenobarbital and
3–4 mg/kg PO q12h benzodiazepines if given concurrently.
Photosensitization, hallucinations and liver
damage reported in humans

Zonisamide Antiepileptic Dog: 5 mg/kg PO q12h (single AED) Adverse effects may include sedation,
and 10 mg/kg PO q12h (add-on AED ataxia and GI upset
for dogs already receiving drugs
requiring hepatic metabolism)
Cat: 5–10 mg/kg PO q12–24h
 APPENDICES 621

APPENDIX 2: UNITS AND REFERENCE RANGES

(Note: All reference ranges provided are approximate and may differ slightly from those of the individual
laboratory used.)

Common conversion factors Selected biochemical parameters

Units provided Units desired Conversion factor

Parameter Dog Cat
lb kg 0.454
Calcium 2.45–2.92 mmol/l 2.27–2.8 mmol/l
kg lb 2.2 (9.8–11.7 mg/dl) (9.1–11.2 mg/dl)

mmol/l mg/dl × MW/10 Creatine kinase 46–467 U/l 49–688 U/l

mg/dl mmol/l × 10/MW Glucose 3.6–6.2 mmol/l 3.7–9.3 mmol/l

(65–112 mg/dl) (67–168 mg/dl)
mmol/l mEq/l × valence
Ionized calcium 1.25–1.50 mmol/l 1.1–1.4 mmol/l
mEq/l mmol/l /valence (5.01–6.01 mg/dl) (4.41–5.61 mg/dl)

% mg/ml × 10 Lactate (lactic acid) 0.5–2.0 mmol/l 0.5–2.0 mmol/l

(4.5–18.0 mg/dl) (4.5–18.0 mg/dl)
°C °F × 9/5 + 32
Potassium 3.9–4.9 mmol/l 3.5–4.8 mmol/l
°F °C –32 × 5/9 (3.9–4.9 mEq/l) (3.5–4.8 mEq/l)

Protein 54–71 g/l 66–86 g/l

(5.4–7.1 g/dl) (6.6–8.6 g/dl)

Sodium 140–150 mmol/l 146–157 mmol/l

(140–150 mEq/l) (146–157 mEq/l)

Coagulation test reference ranges Normal arterial blood gas values

Coagulation parameter Dog Cat Blood gas parameter Dog Cat

Prothrombin time (seconds) 6.8–10.2 9.6–13.2 pH 7.41 (7.35–7.46) 7.39 (7.31–7.46)

Partial thromboplastin 10.7–16.4 12.6–15.7 PaCO2 (mmHg) 37 (32–43) 31 (26–36)

time (seconds)
PaO2 (mmHg) 92 (80–105) 107 (95–115)
Fibrinogen degradation <5 <5
product (μg/ml) Bicarbonate (mmol/l) 22 (18–26) 18 (14–22)

D-dimers (μg/ml) <0.2 <0.2

Buccal mucosal bleeding 2–3 2–3

time (minutes)
622 APPENDICES

APPENDIX 3: BLOOD TRANSFUSION MONITORING SHEET

Label: Kennel No: ____________

Clinician in charge: Reason for transfusion:

Telephone number:
Other phone number:

Calculation area Possible transfusion reactions

Volume of blood to be transfused: _________________ (usually occur in first hour)
• Tachycardia
• Bradycardia (cats)
x x –
• Pyrexia
BW (kg) 90 (dog) Desired PCV Current PCV • Salivation, vomiting
70 (cat) • Tremors, agitation, vocalization
• Weakness, depression, recumbency
• Dyspnoea
PCV of donor
• Pale mucous membranes
Blood type: __________________________ • Weak pulse
• Seizures
Cross-matched donor?: Yes ❑ No ❑ • Skin changes (swelling/oedema)
Type of cross-match: __________________
If any suspected transfusion reactions are seen, STOP the
Previous transfusions?: Yes ❑ No ❑ transfusion and contact clinician immediately

Time

Initial transfusion rate Subsequent transfusion rate

Monitoring ❑ 0.25 ml/kg/hr ❑ 4–10 ml/kg/hr: ____________
❑ Other: ________ ❑ Other: ____________
Heart rate •
Monitor patient & TPR every 30–60 mins
Monitor patient & TPR every 5–10 mins

Respiratory rate
° 200
IABP >I<

NIBP >I<
150

100

50

Temp
PCV
Notes/observations
 FURTHER READING
623

CHAPTER 1: EXAMINING THE Mueller ER (2001) Suggested strategies for

NEUROLOGICAL EMERGENCY ventilatory management of veterinary patients
with acute respiratory distress syndrome.
de Lahunta A, Glass E (2008) Veterinary J Vet Emerg Crit Care 11:191–198.
Neuroanatomy and Clinical Neurology, 3rd edn.
Saunders/Elsevier, St. Louis. CHAPTER 3: METABOLIC EVALUATION OF
Dewey CW (ed.) (2003) A Practical Guide to Canine CRITICALLY ILL NEUROLOGICAL PATIENTS
and Feline Neurology. Iowa State Press, Ames.
Garosi LS (2004) The neurological examination. Hopper K, Silverstein D (eds.) (2009) Small Animal
In: BSAVA Manual of Canine and Feline Neurology. Critical Care Medicine. Saunders/Elsevier, St. Louis.
(eds. SR Platt, NJ Olby) British Small Animal Kube SA, Olby NJ (2008) Managing acute spinal cord
Veterinary Association, Gloucester, pp. 1–23. injuries. Compend Contin Educ Vet 30:496–504.
Garosi LS (2004) Lesion localization and differential Lu J, Goh SJ, Tng PY et al. (2009) Systemic inflam-
diagnosis. In: BSAVA Manual of Canine and Feline matory response following acute traumatic brain
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Animal Veterinary Association, Gloucester, Mellanby RJ, Jeffery ND, Gopal MS et al. (2005)
pp. 24–34. Secondary hypothyroidism following head trauma
King AS (1987) Physiological and Clinical Anatomy of in a cat. J Feline Med Surg 7:135–139.
Domestic Mammals. Vol. 1. Central Nervous System. Morrison JA, Fales-Williams A (2006)
Oxford University Press, Oxford. Hypernatremia associated with intracranial B-cell
Lorenz MB, Kornegay JN (eds.) (2011) Handbook of lymphoma in a cat. Vet Clin Pathol 35:362–365.
Veterinary Neurology, 4th edn. Elsevier/Saunders, Nielsen L, Thompson H, Hammond GJ et al. (2008)
St. Louis. Central diabetes insipidus associated with primary
focal B-cell lymphoma in a dog. Vet Rec
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CARDIOVASCULAR SUPPORT Palevsky PM, Bhagrath R, Greenberg A (1996)
Hypernatremia in hospitalized patients.
Aitkenhead AR, Rowbotham DJ, Smith G (eds.) Ann Int Med 124:197–203.
(2001) Textbook of Anaesthesia, 4th edn. Churchill Powner DJ, Boccalandro C, Alp MS, Vollmer DG
Livingston, Edinburgh. (2006) Endocrine failure after traumatic brain
Hopper K, Silverstein D (2009) Small Animal Critical injury in adults. Neurocrit Care 5:61–70.
Care Medicine. Saunders/Elsevier, St. Louis. Powner DJ, Boccalandro C (2008) Adrenal insuffi-
Morgan GE Jr, Mikhail MS, Murray MJ (eds.) (2005) ciency following traumatic brain injury in adults.
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Fluid and electrolyte disorders following surgery
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67:225–230.
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314:1535–1542. pathologic, and magnetic resonance imaging
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 INDEX
651

Page references in bold refer to figures; acute phase proteins (APP) 353 anaemia 585, 585
those in italic refer to tables or boxes acute respiratory distress syndrome acute 40
(ARDS) 39 blood transfusion 585
A adder, common death 523, 526 causes in neurological disease 40
AAROM, see active assisted range of Addison’s disease 197, 296, 297 chronic 40
motion adenosine triphosphate (ATP), management 40
abdominal injuries 369 depletion in hypoglycaemia 490–1 anaesthesia, general
abducens nerve (CN VI) 29, 32 adversive syndrome 18 animals requiring ventilation 553
abscesses (CNS) 343, 350, 353 AEDs, see anti-epileptic drugs body temperature management 544,
epidural 227 aerophagia 42 551, 551
management 357 agar gel immunodiffusion (AGID) 355 CSF collection 555
retrobulbar 240 agitation, post anaesthesia 545 imaging studies 83
Acanthomoeba spp. 342 airway intracranial disease 535–45
ACE inhibitors, see angiotensin- humidification 36, 50, 51 mechanical ventilation 48
converting enzyme (ACE) inhibitors status epilepticus 423 MRI 554–5
acepromazine 251, 457, 609 suctioning 47, 50 myelography 554
adverse effects and precautions 554, airway pressure, measurement 48 neuromuscular disease 549–52
609 albumin, serum 574, 578 in neurotoxicities 500, 502
contraindications 568 alfaxolone 500, 541, 550 pre-oxygenation 537, 539
dosage 609 alfentanil 540, 543 premedication 536, 567
felines 586 ALI, see acute lung injury SMFA toxicity 519
intracranial disease 539 alkalaemia 70–1 spinal disease 83, 545–9
pain management 563, 566 alkalosis 70 total intravenous (TIVA) 540, 541,
use in EEG studies 555 alpha-2 agonists 539, 559, 563, 563, 566 548
acetamide 519 medetomidine 563, 566, 615 anaesthesia, local/regional 568–9
acetazolamide 150, 251 alpha-2-macroglobulin 353 anaesthetic agents
adverse effects and precautions 609 alpha-adrenergic antagonists 55, 395, cardiovascular depression 53, 54
dosage 609 592, 617 ‘co-induction’ 538, 540, 550
acetylcholine (ACh) 433, 434 alphachloralose 167 inhalant 429, 541, 542, 548, 553
acetylcholine esterase (AChE) 515 alveolar recruitment 50 intracranial disease 538, 539
acetylcholine receptor (AChR) 434, 435 amantadine 563, 609 seizure control 429
antibody titres 186, 439–40, 445 Amblyomma americanum 531 short-acting 429
acid–base status 70–2, 424 Amblyomma maculatum 531 use in NM disease 550
acidopathies, organic 115, 498 amino acids, aromatic 488 anal sphincter tone 210, 212
acidosis, defined 70 amitriptyline 228, 564, 609 analgesic drugs 559
action potential 159, 159, 177, 417, 433, amlodipine 55, 152, 329, 493 categories 559
434 ammonia 76 sites of action 559
activated charcoal, see charcoal, ammonia metabolism 487–8, 487 spinal pain 395, 563–4
activated amoxicillin/clavanulate 596 anamnesis 15–16
activated clotting time (ACT) 76 D-amphetamine 154 anaphylaxis, tetanus antitoxin
active assisted range of motion amphotericin B 357 administration 455–6
(AAROM) 604 ampicillin 490 Anaplasma spp. 342
acute lung injury (ALI) 38–9 amputation, forelimb 309, 309, 310 angiography, MR 325, 325
acute non-compressive nucleus amygdala, seizure damage 419
pulposus extrusion (ANNPE) 400
 652 INDEX

angiotensin-converting enzyme (ACE) seizures/status epilepticus 80, 422 organophosphate toxicity 516
inhibitors 152, 329, 493 spinal cord injury 82 toad toxicity 508
anisocoria 30, 143, 265–71 tetanus 81 aura 155
common causes 269–70 arterial catheter, BP measurement 56, Australia
features in cats and dogs 268 57 snake bite envenomation 523–6
annulus fibrosus 399 arteriovenous anastomoses, spinal cord tick paralysis 528–31
protrusion 400 vessels 333 autoantibodies
anti-astrocytic antibodies 353 arthritis, spinal 220 GFAP 353
anti-epileptic drugs (AEDs) 421, 427–9 arthrodesis, pancarpal 309 MEM 353
cats 170 artificial airway myasthenia gravis 435
dogs 171 endotracheal tube 35–6 NSE 238
intranasal 427, 427, 432 humidification 36, 50, 51 autonomic dysfunction 270–1, 457
out-of-hospital patient 432 indications for 35 autonomous zones of innervation 208,
rectal administration 427, 432 intratracheal catheter 37 208
see also named AEDs tracheostomy 36–7 autoregulation 363–4
anti-platelet therapy 330 arytenoid cartilage 287 avermectin toxicosis 509
antibiotic therapy arytenoid tieback surgery 290 awareness 17
aspiration 596 ascending reticular activating system axillary nerve 208, 299, 301
botulism 458–9 (ARAS) 17, 140–1, 141 axonotmesis 308
C. tetani infection 456 aspartate 491 azathioprine
discospondylitis 226 Aspergillus spp. 341, 342, 345, 353 adverse effects and precautions 442,
hepatic encephalopathy 490 aspiration, prevention in anaesthesia 609
infectious myopathies 190 550, 552 dosage 609
MEM 357, 358 aspiration pneumonia 38, 431, 440, masticatory myositis 276
444, 460, 460 MEM 360, 362
see also named antibiotics
treatment 595–6 myasthenia gravis 442
antibodies
aspirin, low-dose 330 polymyositis 190
acetylcholine receptor (AChR) 186,
295, 439–40, 445 assisted range of motion (AROM)
exercises 604
CSF 135, 135 B
astrocytoma 162
see also autoantibodies Babesia spp. 341, 342
anaplastic 200
anticholinesterases 441, 617 baclofen 457
grade IV (glioblastoma multiforme)
anticoagulants 167, 613 bacterial meningitis 132, 342, 343
465
anticonvulsants clinical presentation 350
hydrocephalus 150
feline hyperaesthesia syndrome 228 diagnosis 353
neurological features 471
head trauma 380 treatment 357
ataxia 21, 182
hepatic encephalopathy 489 Bacteroides spp. 343
causes 198–200, 201–3, 204
see also antiepileptic drugs (AEDs) and BAER, see brainstem auditory evoked
cerebellar 195, 197, 200
named drugs response
definition 193
antidepressants 154, 228, 564, 609, 613 Bailey chair 443
general proprioceptive (GP) 21, 22,
anti-emetics 615 balance control centre 254
194, 197, 199, 206
antivenom balance exercises 605
neuroanatomical basis 193–5
black widow spider 521 barbiturates 428
neurological evaluation 196–7, 198
red-back spider 521 barotrauma 45
tick paralysis 528
snake bites 526–7 base deficit 578
vestibular 195, 197, 256
anuria 493, 494 bathing, toxin removal 501
atelectasis 38, 39, 596
anxiolytics 566 bedding 596
prevention 596
aortic thrombosis 217 bedside tests 61
atenolol 485
apomorphine 501 behaviour-modifying drugs 154, 228,
atherosclerosis 319
ARAS, see ascending reticular activating 564, 609, 613
atlanto-occipital space 122
system (ARAS) behavioural changes 17
atlantoaxial (AA) instability 91, 388, 199
ARDS, see acute respiratory distress brain tumours 469
syndrome management 396–7
atracurium 543, 551 interpretation 144
arterial blood gases 51, 70–2 behavioural-modifying drugs 228
head trauma 79, 369 atropine 438, 458
adverse effects and precautions 609 benanzepril 493
intracranial mass/lesions 80 benzodiazepines 427–8, 432
normal values 621 dosage 609
avermectin toxicosis 509
 INDEX 653

blood donor sedation 586 measurement 56, 57, 499 brain haemorrhage 112, 113
as co-induction agents 540 neurotoxicity 499 MRI 112, 112, 113
hepatic encephalopathy 489 renal failure 493 brain herniation 111, 111, 368, 368,
metronidazole toxicity 263, 523 status epilepticus 420, 424, 424 535
neurotoxicity 500 blood products 573, 576 calvarial 368
pain treatment 563, 566 collection 585–7 caudal transtentorial 143
permethrin toxicity 517 blood transfusion 40, 574, 576, 578, falcine 368
as premedicants 536, 539 585–9 foramenal 368, 465, 465
strychnine toxicity 520 indications for 548, 585 hydrocephalus 150
tetanus 455, 457 monitoring sheet 622 intracranial disease 465–6, 470, 535
toad toxicity 508 non-emergency 588 risk with CSF collection 121, 123
see also diazepam; midazolam PCV threshold 62 secondary to hypertension 152
beta-2-microglobulins, CSF 136 blood typing 587 signs 470
beta-blockers 54, 55, 248, 249, 361, blood–brain barrier, disruption 364, 494 subfalcine 465
508, 513, 545 BMBT, see buccal mucosal bleeding transtentorial 368, 465
bethanechol 271, 592 times brain infarcts 113–14, 320, 321
adverse effects and precautions 610 body temperature 77–8 cerebellar artery 19, 323, 325
challenge test 271 anaesthesia 544, 548, 549, 551, 551 brain injury
bicarbonate 66, 71 control in neurotoxicity 500 primary 365–6
intra/extracellular 67 head trauma 368, 369, 380 prolonged seizures 419
Bichon Frise, movement disorder 252 status epilepticus 420, 424, 425 secondary 366–8
bilirubin, urine 68 systemic inflammatory response see also head trauma
biochemical evaluation 79–82 494, 495 brain ischaemia, global 151–2
bisphosphonates 486 ventilated animal 48 brain masses
bladder see also hyperthermia; hypothermia differential diagnosis 110
function assessment 210 body turn 254, 254 imaging 109–11
innervation 591 body weight, fluid therapy 581–2, 581 see also brain tumours
bladder dysfunction 210 bone lysis 93, 94, 95, 486 brain oedema 324, 330, 332, 366, 367,
LMN 211, 212, 591–2 boots 604 377
UMN 211, 212, 592 Border Terrier, epileptoid cramping bromethalin toxicosis 506
bladder management 413, 458, 591–3 syndrome 252 cytotoxic 324, 366, 366, 464
Blastomyces dermatitidis 341, 342, 345, Borna disease virus 342, 342 fluid therapy 575
353, 355 botulism 216, 270, 296, 447 hypertension 152, 153
blindness aetiology/pathophysiology 449–50 hyponatraemia 481
bilateral 234, 238 clinical presentation 216, 452 interstitial 464
central 236, 236–7, 237, 237 diagnosis 216, 453–4 intracranial neoplasms 462–4, 462,
clinical evaluation 231–3 management 458–9 463, 475
neuroanatomy 229, 230, 231 prognosis 459–60 lead toxicity 511
peripheral 236, 236–7, 237, 237, bowel management 594 treatment 69, 152, 332
238–41 Boxer, movement disorder 252 vasogenic 356, 357, 366, 366, 367,
systematic evaluation 233–6 BP, see blood pressure 463–4
unilateral 235, 237 brachial plexus 27, 299, 299, 300–2, 301 brain parenchyma, contusion 363, 381
blood donor 585–7 avulsion 308–9 brain tumours 162, 162
blood loss lymphoma affecting 312, 312 aetiology and pathophysiology
clinical signs 589 neuritis 311 461–9
estimation 548 brachiocephalic nerve 208 causing blindness 238
fluid replacement 548, 576, 578 bradyarrhythmias 53, 54 causing facial paralysis 285
blood pressure (BP) 50, 51–3 bradycardia 458 clinical presentation 469–70
anaesthesia 542, 543 reflex 365, 470 diagnosis and imaging 109–11,
and cerebral blood flow 364, 364 brain 471–3
drugs to increase 53 glucose supply 63 differential diagnosis 470
elevation 152 imaging, MRI and CT 108–18 drop metastases 467–9
emergency fluid therapy 577 oxygen delivery 62, 63 hydrocephalus 150
head trauma 369, 377–8 penetrating injury 88 management 474, 475–8
management in CVA 329 see also index entries commencing with primary 461
‘cerebral’ prognosis 478
 654 INDEX

secondary 461, 469, 469, 470, 472 calcium channel blockers 55, 152, 329, cataplexy 153–4, 156–7, 173
systemic disease screening 473 513 catecholamines
brain–heart syndrome 365, 470 calcium channels 417 release 271, 365, 420, 470
brainstem calcium EDTA 511 toad venom 508
compression (Cushing reflex) 54, 55, calcium gluconate 483–4, 519, 521 cathartics 504, 504
365, 365, 373, 378, 470, 577 calvaria, hyperostosis 462, 478 catheter
fibrocartilagenous embolism 335 canine distemper virus (CDV) 341, 342 arterial 56, 57
vestibular nuclei 194, 204, 254 clinical presentation 350 intratracheal 36
brainstem auditory evoked response CSF testing 135 nasal 41–2
(BAER) 147, 149, 261, 473 diagnosis 353, 355 catheterization
brainstem disease management 357 intravenous 58, 424, 597
causing altered consciousness 143 post-vaccinal 344 urinary 424, 458, 569, 592–3
causing dropped jaw 277 canine epileptoid cramping syndrome cauda equina lesions 312–13, 594
causing dysphagia 293 (Spike’s disease) 252 caudal occipital malformation syndrome
causing stridor/dysphonia 289 capnography 49, 50–1, 379 227, 227
facial paresis/paralysis 283 carbamates 515–16 Cavalier King Charles Spaniel 251
brainstem reflexes 370, 372–3 carbamazepine 250 cavernous sinus (middle cranial fossa)
brevican (BCAN) gene 251 carbon dioxide syndrome 266
brewer’s yeast 357 expired (P’ETCO2) 50–1 CBF, see cerebral blood flow
bromethalin 167, 505–6 partial pressure (PaCO2) CDI, see diabetes insipidus, central
bromide 430 anaesthesia 542 CDV, see canine distemper virus
bronchodilation 595 haemorrhagic stroke 330, 331 central nervous system (CNS)
Brufelsia spp. toxicity 506–7, 507 head trauma 369, 379 effects of mechanical ventilation 45
buccal mucosal bleeding time (BMBT) lowering 380 overview 16
76, 76, 621 normal values 621 stimulants 154
Bufo marinus (cane toad) 507–8, 507 carbon monoxide toxicity 151 central venous pressure (CVP) 59
bufogenins 508 cardiac arrhythmias 52, 52, 53, 54 fluid therapy assessment 583
bufotenines 508 botulism 457–8 head trauma 369
bufotoxins (toad toxicity) 507–8 methylxanthine toxicity 513 hypercalcaemia 486–7
bulla osteotomy 263 thyrotoxicosis 485 measurement 58, 59, 59
bullae, soft tissue/fluid 89 toad toxicity 508 cephalosporins 357, 596
bupivacaine 568–9 cardiac failure 197 cerebellar artery, infarction 19, 323, 325
buprenorphine 561, 563, 566 cardiac output cerebellar ataxia 195, 197, 245
adverse effects and precautions 610 assessment 51 causes 202–3
patches 566 circulatory shock 52–3 cerebellomedullary cistern (CMC/cis-
butorphanol 540, 561, 586 and heart rate 53 terna magna), CSF collection 122–3,
adverse effects and precautions 610 mechanical ventilation 43 122, 555
CNS disease 540 cardio–pulmonary–cerebral cerebellum
dose 610 resuscitation (CPCR) 78 functions 193–4
cardiomyopathy, feline hypertrophic lesions, neurological signs 269
217 cerebral blood flow (CBF) 322, 363
C
C-reactive protein (CRP) 353 cardiopulmonary function autoregulation 363–4
Cadwall Sierra Wave 439 anaesthesia 549 definition 363, 461
caffeine toxicity 167, 512 myelography 554 hypothermia 496
cage cardiorespiratory disease, causing and pain treatment 560
weakness/collapse 176 relationship to ICP 55, 364–5
IVDD 408
cardiovascular system cerebral cortex disease 142
recumbent patient 424
assessment 15 cerebral hemisphere disease 142
spinal trauma 394, 395
effects of mechanical ventilation 45 cerebral ischaemic response 470
calcitonin 483, 486
support 51–60 cerebral metabolic rate (CMR),
calcitriol 425, 483
carmustine 477 anaesthesia 537
calcium
carnitine 179, 186, 188 cerebral oedema, see brain oedema
homeostasis 483, 483
L-carnitine 191, 192 cerebral perfusion pressure (CPP) 51,
intracellular 161, 366, 386, 491, 491
carotid arteries, MRA 325 52, 322, 364, 461
ionized serum 483, 485, 621
carprofen 395, 567, 610 in anaesthesia 537, 542
serum levels 179, 425, 483–6, 621
carpus, knuckling 308, 310 definition 363
 INDEX 655

cerebral vascular resistance (CVR) 364, clinical presentation 322–3 cisterna magna, CSF collection 122–3
364 diagnosis 323–7, 328 clapping 601
cerebrospinal fluid (CSF) differential diagnosis 323 clindamycin 190, 357, 610
collection 122–4 haemorrhagic 321–3, 326, 327, clomipramine 154, 228, 610
anaesthesia 555 330–2 clonazepam 251, 610
cisterna magna/CMC 122–3, ischaemic 319–21, 323, 329–30 clonidine 458
122, 555 management 328–32 clopridogrel 330
lumbar puncture 123–4, 123 metabolic evaluation 79 clorazepate 611, 170, 171
prior to myelography 100, 129 prognosis 332 Clostridium spp. 190
raised ICP 555 cervical spine Clostridium botulinum 270, 447, 453
decreasing production 150 caudal anatomy 219 Clostridium tetani 447, 453, 456
diversion (ventriculoperitoneal ‘cord-to-canal’ ratio 220 CMOP, see craniomandibular
shunting) 476 hyperaesthesia 227 osteopathy
hypocretin–1 levels 154 IVDD 206, 401 CMR, see cerebral metabolic rate
immunoglobulins 134, 353 medical therapy 408 ‘co-induction’ agents 538, 540, 550
intracranial volume 367 surgical decompression 409–10 coagulation cascade 75
neoplastic cells 134, 134 pain coagulation factors
neurotransmitter levels 161 assessment/clinical signs 223 deficiency 585, 589
overproduction 147 causes 219–20 reference ranges 621
protein levels 125, 126, 134, 354, management 566 coagulopathies 74–5, 74
407 radiography 91, 92, 95 blood product administration 589
red blood cells 125 trauma 91, 92, 388, 389, 393, 396, colloid fluid administration 573, 577
sample handling 125 397, 397 snake bite envenomation 524, 525,
sites of production 121 intubation 547, 547 526
total nucleated cell count (TNCC) cervical ventroflexion 191, 191 Coccidiodes immitis 341, 342, 345, 353,
125 cervicothoracic intumescence 24 355
cerebrospinal fluid (CSF) analysis 121 charcoal, activated 503, 506, 507, 512 cochlear nerve 283
altered consciousness 147 adverse effects and precautions 610 coenzyme Q-10 191, 192
assays under investigation 136, 136 dosage 503, 610 collapse 156–7, 173
blood contamination 129 chelation therapy 510–11 exercise-induced 188–9
brain tumours 472, 473 chemotherapy, intracranial neoplasms systemic approach 175
cerebrovascular accidents 327 477–8 colloid oncotic pressure (COP) 63, 573,
cytology 128, 354 Cheyne–Stokes respiration 373 574, 576
differential cell count 125 Chiari-like malformation 116, 199, 220, colloids 377, 573
exercise-associated weakness/ 223, 227 coagulopathy risk 573, 577
collapse 186, 188 Chinook dogs 252 maximum recommended doses 579
hydrocephalus 149 chlorpromazine 457 colonic lavage 503
ischaemic myelopathy 338, 340 chocolate coma 370, 373
IVDD 407 ingestion 167, 512–13 brainstem disease 143
lymphoma 136, 312, 312 theobromine content of products common causes 147–54
macroscopic 125, 125, 130 512 defined 141
MEM 352, 353, 354–5, 354 cholecalciferol, toxicity 167 diagnostic tests 144–7
monoparesis/lameness 307, 312 choline acetyl-transferase 433, 434 differential diagnosis 139–40
normal findings 125, 129 ‘cholinergic crisis’ 438 head trauma 146
nucleated cell count 354 cholinesterase, plasma 186 common peroneal nerve 208
pleocytosis 130–2, 133, 338, 340, chondrodystrophic breeds 334, 399 compliance, intracranial 363, 367
352, 354, 407 chondroitin sulphate (CS) 399 compression technique 600, 600
recent myelographic study 129 chorea-like movements, breed-specific computed tomography (CT) 104–5
risks and contraindications 121, 121 252 advantages/disadvantages 84
spinal cord lesions 213 chorioretinitis 238 altered consciousness 147
status epilepticus 422 choroid plexus tumours 463, 464, 465 aortic thombosis 217
trismus 272 drop metastases 468 brain 108–18
vestibular disease 261 neurological features 471 brain tumours 471, 472–3, 472
cerebrovascular accident (CVA) 79, 319 circling 17, 163, 256, 258 cerebrovascular accidents 323, 326,
aetiology and pathophysiology circulatory shock 52–3, 576 327
319–22 cisapride 298 head injury 88, 114, 375
 656 INDEX

imaging technique 104–5 coupage 444, 601 D

interpretation of images 105 CPCR, see cardio–pulmonary–cerebral D-dimers 76, 621
ischaemic myelopathy 338 resuscitation Dachshund 401, 416
IVDD 405, 405 CPP, see cerebral perfusion pressure dantrolene 191, 457, 592, 611
monoparesis/lameness 307 cramp, Scotty 175, 250–1 dark adaptation test 29, 30
otitis media/interna 262 cramping syndrome, canine epileptoid dazzle reflex 233
skull fracture 88 (Spike’s disease) 252 DDS, see dialysis disequilibrium
spinal 118–20 cranial cervical ganglion 266, 266 syndrome
spinal trauma 388, 389 cranial nerves, examination 28–33, 29 DEA, see dog erythrocyte antigens
concussion 363 craniectomy decerebellate rigidity 18, 19, 371, 371
consciousness level 17, 139, 162 cytoreductive 477, 478 decerebrate posture 18, 19, 143, 143,
assessment 139, 144 decompressive 476 371, 371
brainstem disease 143 craniomandibular osteopathy (CMOP) decontamination
decreased 274, 276 GI tract 500–5, 501, 512
common causes 147–54 cranium, see skull mouth 508
definitions 141 creatine kinase (CK) 184 skin/coat 501
diagnostic tests 144–7 elevation 184, 186, 191, 437, 526 decubitus ulcers 395, 395, 596–7, 597
differential diagnosis 139–40 reference ranges 621 defecation 594
head trauma 370, 372 cricothyroid muscle 287 dehydration 578, 579
systemic disease 144 cross-matching 587 clinical characteristics 579
transient alterations 144 cryoprecipitate 589 fluid therapy 575, 579
continuous positive airway pressure cryotherapy 606, 606 PCV/TP levels 62
(CPAP) 43, 44 Cryptococcus spp. 133, 342, 353, 354, 355 risk in spinal patients 545
adverse effects 45 treatment of infection 357 delirium 142
contrast media, myelography 99, 100, Cryptococcus neoformans 341, 345 demyelination
101, 129, 554 crystalloids 377, 572 CSF analysis 134, 136
conversion factors 621 polyionic 574, 575 osmotic syndrome 481–2, 482
cooling, methods 77, 496, 500 CSF, see cerebrospinal fluid spinal cord compression 386
Coonhound paralysis 214–15, 216 cupping technique 601 deoxyhaemoglobin 326, 327
COP, see colloid oncotic pressure Cushing reflex 54, 55, 365, 365, 373, depression 142
‘cord-to-canal’ ratio 220 378, 470, 577 post-ictal 144, 163
corneal reflex 29, 30 Cushing triad 373 Dermacentor andersoni 531
corticosteroids Cushing’s syndrome 67 Dermacentor variabilis 531
adverse effects 359 cutaneous toxins 501 desflurane 542
brain neoplasms 475 cutaneous trunci (panniculus) reflex 27 desipramine 154
bromethalin toxicosis 506 assessment 27, 211 detrusor muscle, stimulation 592
causing masticatory muscle atrophy loss 27, 211, 402 dexamethasone 357, 408, 475, 611
282, 282 neurological pathways 27, 27 dexmedetomidine 430, 545, 563
concurrent NSAIDs 566 Cuterebra spp. 319, 320, 342, 345, 353 dextrans 573
dexamethasone 357, 408, 475, 611 CVA, see cerebrovascular accident dextrose solutions 64, 65, 492, 572, 611
head trauma patient 377 CyberKnife ® 477 diabetes insipidus 480
hydrocephalus 150 cyclophosphamide 360, 361–2 central (CDI) 66, 466–7, 584
immunosuppressive 190, 360–1 cyclosporine 360, 361, 362, 442, 611 nephrogenic 67, 67, 584
masticatory muscle myositis 276 cystostomy catheter 593 diabetes mellitus 466
pachymeningitis 281 cytokines 386, 488 diagnostic testing 61
involuntary movement disorders cytosine arabinoside (CA/cytarabine) minimum database 61
247, 248 359–60, 360 dialysis disequilibrium syndrome (DDS)
IVDD 408 adverse effects and precautions 360, 493–4
MEM 357, 359–60 611 diarrhoea 594
myasthenia gravis 441–2 doses 360, 611 diazepam 357, 427–8
pain management 563 idiopathic MEM 360, 360, 361 adverse effects and precautions 612
polymyositis 190 cytotoxic oedema 324, 366, 366 blood donor sedation 586
in spinal trauma 390 bromethalin toxicosis 506
syringomyelia 227 as co-induction agent 540
coughing, minimizing on CRI 428
intubation/extubation 538, 545 dosage 612
 INDEX 657

feline epilepsy 170 dry nose 283 renal failure 493

generalized idiopathic tremor 248, dural tail sign 472 electrolytes 64–7
249 durotomy 412 electromyography (EMG)
head trauma 380 dysautonomia 270–1, 293, 457 botulism 454, 454
idiopathic tremor syndrome 361 clinical presentation 270 monoparesis/lameness 307
idiopathic vestibular syndrome 261 diagnosis 271 needle 187
intranasal 427, 427, 432 feline 270 neuromuscular disorders 186, 187
intravenous 427 management 271 repetitive nerve stimulation 438,
metronidazole toxicity 263, 523 dyscoria 30 439
movement disorders 251 dyskinesia, phenobarbital 252 single-fibre 438, 439
pain treatment 563, 566 dysmetria 193, 196, 245 tetanus 453
permethrin toxicity 517 dysphagia 32, 291–8 trismus 272, 273
and phenobarbital therapy 427, 432 anaesthesia 551 in vestibular disease 261
rectal 427, 432 causes 296–8, 296–7 electroretinography (ERG) 239
spinal trauma patient 395 definitions 291 ELISA tests, CSF 134
tetanus 457 diagnostic tests 295 emesis 501, 501
toad toxicity 508 myasthenia gravis 436 methylxanthine toxicity 512
DIC, see disseminated intravascular dysphonia 287–90 EMLA cream 569
coagulation dystonia 247, 252 empty sella syndrome, secondary 468
differential diagnosis 33, 34 dysuria 271 empyema
diffusion weighted imaging (DWI) 114, epidural 227
324–5, 324, 325, 337 subdural 343, 343
digoxin-specific Fab fragments 508 E
ear disease 257, 257, 262–3 EMS, see electrical muscle stimulation
dihydrotachysterol 425 enalapril 152, 329
Eastern equine encephalitis virus 342,
diltiazem 513 encephalitis
343
Dinamin 1 gene (DNM1) 189 imaging 117–18
ecchymoses 585
dipstick analysis 68 infectious 164, 165
ECF, see extracellular fluid
Dirofilaria immitis 319, 342, 345, 353 Encephalitozoon cuniculi 342
edrophonium challenge (Tensilon) test
discospondylitis 94, 226 213, 295, 438, 441 encephalopathy
disseminated idiopathic skeletal effleurage 598, 599 hepatic 164–6, 425
hyperostosis (DISH) 220 hypertensive 152
Ehrlichia spp. 133, 190, 341, 342, 343,
disseminated intravascular coagulation 353, 355 ischaemic 320
(DIC) 505, 505
elbow, dropped 308, 310 renal failure 492–4
diuretics 613
elbow flexion, weakness 306 sepsis-associated 494–5
hydrocephalus 150
electrical muscle stimulation (EMS) end plate potential (EPP) 435
hypercalcaemia 486 190, 190, 607 endocrine disorders 484–7
hypernatraemia 481 electrocardiogram (ECG) causing exercise-associated
osmotic 332 hyperkalaemia 65, 65 weakness/collapse 182
raised ICP 239 hypocalcaemia correction 483–4 following head trauma 369
salt toxicity 518 myasthenia gravis 436, 437 endoneurium 180
dobutamine 54 tachyarrhythmia 52 endotracheal intubation 35–6, 42
dog erythrocyte antigens (DEA) 586 electrodiagnostic testing gas humidification 36, 50, 51
dopamine 53, 54 dysphagia 295 indications 35
Doppler blood pressure 56, 56, 499 myasthenia gravis 438, 439 minimizing coughing 538, 545
Doppler ultrasonography 187 neuromuscular function 186, 187 in NM disease 550
dorsal laminectomy, cervical spine 410, see also electromyography (EMG); precautions 35–6
410 nerve conduction studies in spinal disease 546, 547
dorsal pedal artery, catheter placement electroencephalogram (EEG) endotracheal tube (ETT) 35–6
56, 57
altered consciousness 147, 148 heat and moisture exchange devices
‘doughnut’ dressing 597
brain neoplasms 473 50, 51, 548, 548, 549
doxycycline 612
epileptic seizure 169, 169, 423 prevention of kinking during CSF
DP-penicillamine 511 collection 555
narcolepsy/cataplexy 153
drop metastases 467–9 repositioning 36, 47
sedation 555
‘dropped jaw’ 277 size 35–6
sleep 141, 149
common causes 279–81 enema, cool water 496
electrolyte disturbances 245, 479–82
diagnostic tests 279 energy metabolism 179
causing weakness/collapse 179
differential diagnosis 279
 658 INDEX

enophthalmia 281 increased 480 injury 314–15

enrofloxacin 238, 357 extubation lateral cutaneous 208
eosinophilic meningoencephalomyelitis animal with tetanus 552 fenestration, intervertebral disc 412
(EME) 132, 354 following cranial surgery 544, 544, fentanyl 561
epidural anaesthesia 568 545 adverse effects and precautions 543,
epidural empyema 227 eye drops, phenylephrine 267, 268, 269 612
epidural haemorrhage 406, 407 eyes as co-induction agent 540
epilepsy care in recumbent patient 424 dose 561, 612
idiopathic 169, 169–70 function in head trauma 370 in head trauma 562
management 170, 170–1 movement/positioning 31–2 intraoperative 540
secondary to brain neoplasm 475 parasympathetic denervation 267 transdermal patch 561, 565–6, 565
see also epileptic seizures; status parasympathetic innervation 265–6 use in long-term ventilation 553
epilepticus ‘reflex movement’ 231 FFP, see fresh frozen plasma
epileptic seizures 19, 417 sympathatic innervation 266 fibrinogen degradation product 621
cluster 417 sympathetic denervation 267 fibrocartilagenous embolism 120, 333,
diagnosis 166–9 334, 338
differential diagnosis 155, 156–7, fibrosarcoma, spinal 227–8
F
164, 164–6 fish, tetrodotoxin 527–8
face mask 41, 538
focal 158 flaccid paresis 173
facetectomy 311
generalized 156–7 flavirus 342, 343
facial nerve (CN VII) 232
ictal event 156 flea products, spot-on 516–17
anatomy 282, 283
neurological evaluation 161–3 flexor reflex, see withdrawal reflex
assessment 29, 29, 31
pathophysiology 159, 160, 161, flexor reflex exercise 603
dysfunction 282, 283, 286–7
417–19 fluconazole 357
paralysis 257, 257
stages 155 fluid balance, calculation 580–1
facial nucleus 232
epinephrine 456 fluid loss
facial paresis/paralysis 19, 282–7
epineurium 180 hypernatraemia 480–1
blindness 233
epistaxis 74, 74, 469 hypotonic 480
causes 285, 285
equilibrium, maintenance 193–4 insensible 579, 581
diagnostic tests 285–6
erythrocytes, see red blood cells (RBCs) protein-rich 578–9
idiopathic 286–7
erythrophagocytosis 133, 133 fluid overload 576
facial sensation, loss 281
esmolol 54, 55, 485, 508, 545 fluid therapy 596
faecal incontinence 594
ethylene glycol toxicity 167 aspiration pneumonia 596
falling, vestibular disease 256
Eubacterium spp. 343 assessment of replacement/
falx cerebri, displacement 343, 462,
excitotoxicity phenomenon 163 rehydration 580–3
463, 465
exclusion, process of 17 blood loss 548
feeding
exercise intolerance 173 CDI 584
botulism 458
exercise testing 183 during anaesthesia 543
megaoesophagus 443, 443
exercise-associated weakness/collapse emergency 571, 574–8
reduction of aspiration risk 595
common neurological causes 188–92 haemorrhagic stroke 330–1
status epilepticus 424
definition of terms 173, 175 head trauma 377–8
feeding tubes 595, 595
diagnostic approach 185 hyperkalaemia 65–6
felbamate 171, 475, 613
diagnostic tests 184, 186–8, 186 hypernatraemia 481, 518, 584
feline hyperaesthesia syndrome (FHS)
differential diagnoses 175 228 hyponatraemia 482, 583–4
key questions 174 feline infectious peritonitis (FIP) 147, hypoproteinaemia 576–7
neuroanatomical basis 176–80 341, 344, 350 hypothyroid myxoedema coma 484
neurological evaluation 181–3 clinical forms 344 intravenous catheter management
orthopaedic causes 176, 176 clinical presentation 350 597
systemic approach 175 diagnosis 353, 354, 355, 355 maintenance 573, 579–83
exercises, therapeutic 604–5 management 357 neurotoxicities 500
exertional rhabdomyolysis 190–1 pathological findings 344 permethrin toxicity 517
exophthalmic conformation 598 prognosis 361 rehydration/replacement 573
exophthalmos 240 femoral artery, thrombus 187 replacement/rehydration 578–9
extensor carpi radialis reflex 306 femoral nerve 300, 301 SIADH 583–4
extracellular fluid (ECF) assessment 306 snake bite envenomation 526
electrolytes 67 caudal cutaneous 208 ventilated animals 49
 INDEX 659

fluids, intravenous 571 gag reflex 29, 292, 293 glycine 251, 520
colloids 377, 573, 579 absent/decreased 32, 142, 143 glycolysis 73
crystalloid 377, 572, 574, 575 testing 292 glycopyrolate 458
dextrose-containing 572, 611 gait abnormalities glycosaminoglycans (GAGs) 399
flumenazil 488 orthopaedic disease 196–7, 299, 302 GME, see granulomatous meningo-
fluoroquinolones 357 spinal cord compression 196, 199 encephalitis
fluoxetine 228 see also ataxia goby, Pacific 527
folinic acid 357 gait assessment 20–4, 26, 209, 305 ‘golf tee’ sign 102, 103
foraminal stenosis 311, 313, 313 exercise-associated weakness 183 granulomatous meningoencephalitis
foraminotomy 311 lesion localization 212 (GME) 19, 117, 200, 240
forebrain lesions 22, 142, 162–3 gait generation 20, 193, 207–8 clinical presentation 350
forelimb gamma-aminobutyric acid (GABA) diagnosis 354, 356
amputation 309, 309, 310 159–61, 160, 417, 418, 427, 488 histopathology 345, 346
increased muscle tone 210 GammaKnife ™ 477, 477 management 357, 358–61
innervation 299, 300–2, 301 gastric dilation 42 ocular form 356
monoparesis 308–12 gastric lavage 501–3, 502, 511 prognosis 361
neurological examination 306 procedures 502 signalment and history 349
reflexes 25, 212 gastric ulceration, risk with NSAIDs grate kennel 596, 597
fractures 408 grey matter, cavitation/malacia 338
skull 88, 89, 365, 365, 374, 374, 560 gastrocnemius tendon reflex 306
spinal 383, 384 gastrointestinal bleeding 490 H
cervical 92 gastrointestinal problems, management hacking 601, 601
imaging 90, 92, 98 594 haematoma, intracranial 366, 380
free radicals 366 gastrointestinal system, effects of haemocytometer 126, 126, 127
mechanical ventilation 45
free T4 levels 200 haemodialysis 504
gastrostomy tube 382, 443–4, 443
free water deficit 66, 481, 518 haemodilution 62
GCMPS, see Glasgow Composite
calculation 584 haemoglobin (Hb) 62, 63, 578
Measure Pain Scale
free water replacement 481, 518 glycosylated 186
gelatins 573
fresh frozen plasma (FFP) 573, 589 oxygen saturation 38
general proprioceptive (GP) ataxia 21,
friction massage 600–1 22, 194, 197, 199, 206 haemoglobin (Hb)-based oxygen-
frogs, Aetolopus spp. 527 carrying fluids 573, 576
general proprioceptive (GP) receptors
frontal bone, fracture 560 193 haemoglobinuria 67, 68
fructosamine levels 186 genitofemoral nerve 208 haemolysis, snake bites 525
fucidosis 115 GFAP, see glial fibrillary acid protein haemophilia A 589
fundoscopy 231, 323 Glasgow Coma Scale, Modified 370–3, haemoproteinuria 68
fungal disease 370, 371, 382, 469 haemorrhage
meningoencephalomyelitis 342, Glasgow Composite Measure Pain blood products administration
345, 354 Scale (GCMPS) 559 588–9
treatment 357 Glauber’s salts 504 circulatory shock 52–3, 576
furosemide 227, 239, 359, 475, 481 glial fibrillary acid protein (GFAP) clinical signs 589
adverse effects and precautions 613 autoantibodies 353 coagulopathy 74
dosage 613 glioblastoma multiforme 465 epidural 406, 407
hydrocephalus 150 glioma 465, 471, 478 extra-axial 366
hypercalcaemia 486 glossopharyngeal nerve (CN IX) 29, 32, fluid resuscitation 574–8
serum sodium reduction 518 283 intracranial 321–2, 322, 366
Fusobacterium spp. 343 glucometer 64 management 330
glucose PCV/Hb levels 62
blood 63–4, 186, 331, 425, 490 haemosiderin 327
G
GABA, see gamma-aminobutyric acid head trauma 369, 382 haemostasis, defects 74–5
gabapentin 227, 228, 308, 311, 431, 564, normal ranges 64, 621 halothane 542
568 brain consumption 490 hands-off examination 17–22
adverse effects and precautions 613 CSF 134 hands-on examination 22–33
cats 170 urine 68 harnesses 604, 604
dogs 171 glutamate 136, 159–61, 160, 366, 386, Hartmann’s solution 572, 580
417, 419, 491 head, palpation 33
glutamine 488 head bobbing 245, 249
 660 INDEX

head collar, oxygen delivery 40, 41 Horner’s pathway 266, 266 hyperparathyroidism, primary
head pressing 142 Horner’s syndrome 257, 257, 263, 306, (PHPTH) 485–7
head tilt 18, 19, 195, 253 401 hypertension, systemic 51, 55, 152, 153,
‘paradoxical’ 258 classification 269 320, 470
head trauma clinical signs 268, 269, 269 anaesthesia 543, 545
aetiology and pathophysiology diagnosis 267, 269, 270 head trauma 365
363–8 with dropped jaw 280, 280 renal failure 493
causing blindness 238 management and prognosis 270 see also intracranial hypertension
clinical assessment 368–73 human medicine, status epilepticus 421 hyperthermia 77–8, 188, 368, 420, 425,
decerebrate posture 18, 19 human tetanus immunoglobulin 495–6
definition of terms 363 (HTIG) 455 anaesthesia 551
diagnosis 373–6 humidification, ventilation gases 36, 50, cooling 500
fluid therapy 575 51 effects 544
hyperglycaemia 63 hydralazine 493 oxygen supplementation 40
imaging 86, 88, 88, 114 hydrocephalus 111, 147–50, 162, 164, hyperthyroidism 485
management 377–82 165 hypertonicity, Cavalier King Charles
prognosis 382 congenital 147, 149, 149 Spaniel 251
seizures 169 definition 147 hyperventilation 332, 373, 380, 476
thermoregulation 544 diagnosis and imaging 116–17, hypoadrenocortical crisis 467, 468
149–50 hypocalcaemia 179, 425, 483–4
head turn 18, 19, 162, 163, 254, 254
management 150 blood transfusion 588
hearing, acute loss 144
obstructive 464, 464 hypocretin–1, CSF levels 154
heart block, third-degree 436, 437
secondary 147, 150 hypogastric nerve 591
heart rate 53
hydrocortisone 613 hypoglossal nerve 283
fluid therapy 574
hydrogen peroxide 501 hypoglycaemia 63, 64, 164–6, 168, 169,
head trauma 369
hydromorphone 561 425, 490–2
systemic inflammatory response
494, 495 hydrotherapy 597, 605, 605 aetiology/pathophysiology 490–1,
hydroxl-ethylstarch 573 491
heat, application of 606, 606
hydroxyurea 477, 613 chronic 63
heat loss, during anaesthesia 548, 549
hyoid bone abnormality 296 clinical presentation 492
heat and moisture exchange (HME)
devices 50, 51, 548 hyperadrenocorticism 239 diagnosis and management 492
heatstroke 495–6 pituitary-dependent (PDH) 466 hypokalaemia 179, 191
heavy metal toxicity 167 hyperaesthesia hypomagnesaemia 580
hemi-neglect syndrome 18 cervical spine 227 hypometria 193
hemianopia, homonymous 268, 269 feline syndrome (FHS) 228 hyponatraemia 66, 179, 481–2, 583–4
hemilaminectomy 313, 411, 411 paraspinal 335, 352, 402, 413 hypoparathyroidism 483
hemiparesis 206 hyperalgesia 566 hypoproteinaemia 62, 63, 576
Hemocue 62 hypercalcaemia 179, 485–6 hypotension 50, 51, 52–3, 420, 424
heparin 613 hypercapnia 476, 594 blood loss 589
hepatic encephalopathy 164–6, 425, during oxygen supplementation 40 orthostatic 271
487–90 permissive 47 status epilepticus 420
Hepatozoon canis 190 respiratory failure 43 hypothalamus 77, 495
hetastarch 377, 613 hyperglobulinaemia 62 hypothermia 77–8, 368, 496, 598
hindlimb hyperglycaemia 63, 425 adverse effects 544
monoparesis 205, 206, 312–15 head trauma 382 anaesthesia 544
reflexes 24–5, 212, 335 hyperglycaemia–hyperosmolar head trauma 380
hippocampus syndrome 63, 64 induced 78
rabies virus 421 hyperkalaemia 65–6, 65, 179 management 78, 500, 598
seizure damage 419 hyperlactataemia 73 hypothyroidism 285, 287, 296, 297, 320
histamine flare response 271 hypermetria 193, 196, 245, 305 myxoedema coma 484
Histoplasma capsulatum 341, 342, 345, hypernatraemia 66, 179, 479–81, 518, hypoventilation 39, 330, 594
355 584 hypovolaemia 331
historical data 33 hyperosmolar agents 69, 70, 152 hypoxaemia
hoists 604 see also mannitol causes 38
holocyclotoxins 528 hyperostosis definition 38
hopping response 22, 23, 207, 207 calvarium 462, 478 management 39–42
DISH 220 respiratory failure 43
 INDEX 661

hypoxia 151–2 inhalation anaesthetics 429, 541, 542, causing cervical pain 220
causes 151 548, 553 clinical signs 142
diagnosis 151 long-term ventilated patient 553 fluid therapy 575, 578
management 152 maintaining spinal perfusion 548 metabolic aberrations 80–1
status epilepticus 151, 420 inner ear 194, 253–4, 253 pain treatment 560–3
inositol 480 see also brain tumours
inotropes 54 intracranial hypertension 142, 239,
I
ice packs 606 insecticide toxicity 167, 248 364–5
imaging insoflurane 542 anaesthesia 535
choice of modality 83 insulin 65, 186 brain mass 461–3, 470
comparison of modalities 84 insulinoma 492 compensation mechanisms 367
decision-making 85 intensive care units (ICUs) 569 CSF collection 555
head trauma 373–6 intention tremor 245 management 55, 239, 332, 357–8,
intermittent positive pressure 379–80, 475
patient handling 83, 84, 85
ventilation (IPPV) 43, 43–4 surgical 476
role of 83
adverse effects 45 uncompensated 476
survey radiography 86–9
anaesthesia 541, 548 intracranial pressure (ICP) 367–8, 461
see also individual imaging modalities
intervertebral disc 399 brain haematoma 322
imipramine 154, 613
components 300 and cerebral blood flow 55, 364–5
immunoglobulins (Ig), CSF 134, 353
degeneration 399 definition 363
immunohistochemistry (IHC) 354, 355
fibrocartilagenous embolism elevation, see intracranial
immunosuppressive drugs
120, 334, 335 hypertension
azathioprine 360, 362, 442, 609
extrusion 87, 119, 199 monitoring 376
corticosteroids 190, 360–1, 441–2
herniation 96, 383, 389 normal 367
cyclosporine 360, 361, 362, 442, 611
normal 95 reduction 332, 475
cytosine arabinoside (cytarabine)
protrusions 120 ventilated animal 47
359–60, 360, 611
intervertebral disc disease (IVDD) intramedullary pin, femoral 313
masticatory muscle myositis 276
aetiology and pathophysiology intratracheal catheter 36
MUA 359–60, 360
399–401 intravenous catheter 58, 424, 597
myasthenia gravis 441–2
breed susceptibility 401 involuntary movements 18–20
mycophenolate 616
cervical spine 206, 400, 401 definitions 243
pachymeningitis 281
clinical presentation 401–2 diagnosis 245–7, 246
polymyositis 190
diagnosis 403–7 differential diagnosis 244–5, 245
inborn errors of metabolism 498
CSF analysis 136, 407 neuroanatomy 243
incontinence pads 596
CT 405 neurological evaluation 244
infectious disease
MRI 118–20, 119, 405–7 iohexol 100
causing blindness 238
myelography 101, 102, 404 ion channels 417
causing exercise-associated
radiography 94, 96 ion trapping 504
weakness/collapse 182, 190
differential diagnosis 402 iopamidol 129
causing paresis/paralysis 214–15
feline 416 IPPV, see intermittent positive pressure
causing spinal pain 224, 226
functional grading 402 ventilation
causing tremor 245
Hansen type I 399, 400, 401, 404, iris dilator muscle 30
causing vestibular disease 259
405 irradiation, intracranial mass 477, 477,
CSF testing 134–5, 135
Hansen type II 399, 400, 401 478
differential diagnosis of epilepsy
management ischaemic encephalopathy, feline 320
164, 165
medical 408 ischaemic myelopathy 120
meningoencephalomyelitis 342–9,
342, 350 surgical 409–12 clinical presentation 206, 335
inflammatory disease prognostic factors 213, 412–16 diagnosis 336–9
causing paresis/paralysis 214–15 thoracolumbar 401–2, 408 differential diagnosis 335
causing vestibular disease 259 intervertebral foraminae, stenosis 311, pathophysiology 333–4
313, 313 treatment and prognosis 339–40
imaging 117–18
intra-arachnoid cyst 102, 103 ischaemic neuromyopathy 181, 182
inflammatory response
intracranial compliance 363, 367 isoflurane 541, 548
spinal trauma 385, 386
intracranial disease use in long-term ventilation 553
see also systemic inflammatory
response anaesthesia 535–45 ivermectin toxicity 238, 509
infraspinatus muscle, atrophy 305 causing alteration of consciousness Ixodes holocyclus 528–31, 529
142–3
 662 INDEX

J idiopathic 289–90 lower motor neuron (LMN)

Jack Russell Terrier, myokymia 249 inherited 287 paresis/paralysis 21–2, 21, 194, 208,
joints tick bites 529, 530 208, 300
pain 196–7 laryngospasm 552 acute 214–17
range of motion 602–3 larynx, anatomy 287, 287, 289 botulism 450
jugular vein, catheter placement 58 lateral geniculate nucleus (LGN) 30, diagnosis 213
jugular venous oxygen saturation 578 229, 230, 231 flaccid 452
junctionopathies, see neuromuscular latrodectism (spider envenomation) snake bites 525
(NM) disorders 520–2 tick paralysis 528–9
lead toxicity 167, 238, 510 lower motor neuron (LMN) system 20,
leaning, vestibular disease 256 20, 207, 299
K
keratan sulphate (KS) 399 leflunomide 360 lumbar plexus, nerve sheath tumour 206
keratitis, exposure 598 Leishmania spp. 190, 342 lumbar puncture 123–4, 123
ketamine 429, 563, 563 Leptospora icterohemorrhagiae 190 lumbosacral intumescence 24
adverse effects and precautions 614 lesion localization 16, 17 lumbosacral pain
blood donor sedation 587 gait 21–2, 21 causes 224
contraindications 550 spinal reflexes 24–7 evaluation 222
use in central nervous system disease leucocytes lumbosacral plexus 300, 301, 302
539 CSF 126 lumbosacral stenosis 313
ketonuria 68 systemic inflammatory response lung injury 38–9
Kirscher wires 393 494, 495 lungs
Klebsiella spp. 343 leucoencephalitis, necrotizing, see effects of mechanical ventilation 45,
kneading technique 599 necrotizing leucoencephalitis (NLE) 46
knuckling 183 levetiracetam 380, 428–9, 431, 475 tidal volume 37
Kreb’s cycle 73 adverse effects and precautions 614 see also entries beginning with
cats 170 ‘pulmonary’
kyphosis 223
dogs 171 lymphoma
head trauma 382 affecting brachial plexus 312, 312
L hepatic encephalopathy 489 CNS 279, 472, 473, 477
L-2-hydroxyglutaric aciduria 115, 498 CSF cytology 134
as maintenance AED 431
labetalol 55 large cell 486
levothyroxine 484, 614
Labrador Retriever, exercise-induced spinal 227–8
LGN, see lateral geniculate nucleus
collapse 188–9
lidocaine 54, 508, 513 lysosomal storage disease 164
lacrimal gland 31
adverse effects and precautions 615
lactate, plasma 72, 186, 188, 192, 577
arterial catheter placement 56 M
normal ranges 73, 621
intravenous 540 macadamia nuts 522
lactic acidosis 72–4, 420
local/regional anaesthesia 569 magnesium 418, 457, 458, 510, 580
classification and causes 74
spinal pain treatment 564, 567 magnetic resonance angiography
measurement 73
use in general anaesthesia 538, 539 (MRA) 325, 325
treatment 74
lifting aids 603–4, 603, 604 magnetic resonance imaging (MRI)
lactulose 490, 614
limbs advantages/disadvantages 84
lagophthalmos 598
innervation 301 anaesthesia 554–5
lameness 22, 196
palpation 33 brain 104, 106, 108–18
cervical pain 223
rigid extension 143, 143, 157 diffusion weighted (DWI) 114,
clinical signs 305
see also fore limb; hind limb 324–5, 324, 325, 337
intervertebral disc disease 401
lipid infusions 504, 517 FLAIR 104, 107, 356, 357
neurological 206
lipids 179 functional 324–5, 324, 325
neurological causes 299, 302
lithium toxicity 167 imaging technique 104–5
orthopaedic causes 196–7, 299, 302
‘little white shaker disease’ 247 interpretation of images 105, 109
orthopaedic examination 305
liver, ammonia metabolism 487–8, 487 pulse sequences 105, 107–8
laminectomy 311, 313, 392, 410, 411,
liver enzymes 488 in specific disorders
411
local anaesthesia 568–9 altered consciousness 143, 146,
hemilaminectomy 313, 411, 411
‘locked facets’ 383, 388 147
radical bilateral dorsal 411, 411
‘lockjaw’ (trismus) 271–6, 451, 451 brain neoplasms 468–9, 471, 473
laryngeal paresis/paralysis 35, 287–90,
lomustine 477, 478 brainstem disease 143
524
Chiari-like malformation 227
acquired 287
CVA 323–7
 INDEX 663

diffuse cerebral disease 151 meclizine 261, 615 management 357–61

empyema 343, 343 meclofenamic acid 567 prognosis 361
head trauma 375–6, 382 medetomidine 563, 566, 615 signalment and history 349
hydrocephalus 150 median nerve 299, 301, 306 mental status, categorization 141–2
intervertebral disc disease 405–7 megaoesophagus 270, 271, 291, 292–3, meperidine (pethidine) 561
ischaemic myelopathy 336–7, 436, 437, 460, 525 mercury toxicity 167
339 acquired 292 metabolic acidosis 424
L-2-hydroxyglutaric aciduria aspiration pneumonia 595 metabolic disorders
498, 498 congenital 292 causing blindness 238
MEM 353–7, 355 diagnosis and imaging 187, 440, 440 causing decreased consciousness 140
otitis media/interna 89, 262 idiopathic 296–8 causing dysphagia 296
peripheral nerve sheath tumour management 298, 443, 443 causing exercise-associated
310 meloxicam 567, 615 weakness/collapse 182
seizure activity 114, 116 MEM, see meningoencephalomyelitis causing regurgitation 297
spinal meningioma 228, 228 membrane potential (resting potential) causing tremor syndromes 245
spinal trauma 388, 389 177, 417 causing vestibular disease 259
status epilepticus 422–3 menace response 28, 29, 232 causing weakness/collapse 176
thiamine deficiency 497, 497 deficit 142, 269 collapse 156–7
spinal 104–5, 118–20 neuroanatomical pathway 232 differential diagnosis of epilepsy
STIR 104–5, 107 meninges 219 164, 165
main immunogenic region (MIR) 435 meningioma 102 imaging 114, 115
manganese 488 cats 110 metabolic encephalopathies 479
mannitol 239, 332, 379–80, 475 intracranial 143, 472, 478 clinical signs 479
adverse effects and precautions 615 neurological features 471 electrolyte disturbances 479–84
cerebral oedema 506 optic nerve 241, 241 endocrine 484–7
lead toxicosis 511 spinal 228, 228 hepatic 487–90
MEM 359 transitional 462 historic signs 479
maropitant 261 meningitis metabolism, inborn errors 498
mask ventilation 538 imaging 117 metaldehyde toxicity 167, 248, 511–12
mass effect 343, 462, 463, 465 pain management 560 metastases
massage therapy 598–602 meningoencephalitis brain tumours 467–9
benefits 599 eosinophilic (EME) 132, 354 to brain 110
contraindications 599 granulomatous (GME) 19, 117, 200, methadone 561, 567, 615
techniques 598–602 240, 345, 346, 348, 350 methaemoglobin 326, 327
masticatory muscles 271–2, 271 secondary to otitis media/interna methimazole 485
atrophy 281–2, 282 262 methocarbamol 311, 457, 506, 507, 517,
myositis (MMM) 271, 274–6, 274, unknown aetiology (MUA) 164, 592, 616
275 165, 238, 240, 356 methylene blue technique 126, 127, 127
mastitis, tetanus 456 meningoencephalomyelitis (MEM) methylprednisolone sodium succinate
matrix metalloproteinase-9 136 111, 341 (MPSS) 339, 390, 408, 475
mean arterial pressure (MAP) 51, 52, 55 aetiology and pathophysiology adverse effects and precautions 616
anaesthesia 537 341–9 dosage 616
and cerebral blood flow 364, 364 clinical presentation 350–2 methylsergide 251
head trauma 369 definition 341 methylxanthines 167, 512–13
mechanical ventilation 43–51 diagnosis 352–6 metoclopramide 271, 298, 530
adverse effects 44, 45, 46–7 idiopathic 345, 348, 350–2, 356, metrizamide 129
357–60
anaesthesia/sedation 48, 553, 553 metronidazole 357, 456, 490
infectious
general and nursing care 47, 47–8 toxicity 202, 263, 522–3
agents 342
guidelines 44, 46 mexiletine 250, 616
bacterial and rickettsial 132, 342,
head trauma 379 microcytosis 489
343, 353, 354
intracranial disease 47, 49 micturition problems 591–3
fungal 342, 345, 354, 357
in lung pathology 46–7 midazolam
global prevalence 341
modes 43–4 adverse effects and precautions 616
parasitic 342
monitoring 48–9, 49 as co-induction agent 540
protozoal 342, 344, 345, 354
NM disease 551, 551 dose 616
viral 341, 342, 343–4, 354, 355,
in ventilatory failure 46 357 felines 587
664 INDEX

long-term ventilation 553 energy metabolism 179 myelopathy, ischaemic, see ischaemic
MEM 357 mononuclear cell infiltration 189 myelopathy
pain treatment 563, 566 muscle fibres myeloproliferative disease 93, 94, 486
status epilepticus 428 injury 191 see also lymphoma
tetanus 457 masticatory muscles 272, 275 myocardial contractility 53, 54
middle cerebral artery, stenosis 320 nerve stimulation 177 myoclonus 18, 156
middle cranial fossa syndrome 266 muscle movements, involuntary, see defined 243
middle latency auditory evoked involuntary movements repetitive 18
responses (MLAERs) 147 muscle relaxants 551, 566, 611 sporadic 18
middle/inner ear disease 257, 283 ‘muscle squeezing’ 600, 600 myoglobinuria 67, 68, 190–1, 525
miosis 269 muscle tone myokymia 19, 243, 245, 247, 249–50
head trauma 372, 372 assessment 210 myonecrosis 184
induction 267, 271 increased forelimb 210 myopathy
mitochondrial membrane megachannel muscle tremors differential diagnosis 182
(MMC) 491 bromethalin toxicosis 506 differentiation from peripheral
mitochondrial myopathy 192 management 517 neuropathy 180, 183
mixed venous oxygen tension 578 neurotoxicty 517 hypokalaemic 191
MMM, see masticatory muscles, muscular dystrophies 184, 292 idiopathic immune-mediated
myositis musculocutaneous nerve 208, 299, 301 (polymyositis) 189–90
modafinil 154 myasthenia gravis (MG) 292–3, 296, infectious/inflammatory 182, 190
Modified Glasgow Coma Scale 297 mitochondrial 192
(MGCS) 370–3, 370, 371 acquired 216, 433, 436, 445 myotonia 19, 243, 293
brain tumours 469 clinical presentation 216, 436–7 acquired 243
and prognosis of head injury 382 clinical syndromes 433 congenital 243
molluscicides 167 congenital 433, 437, 440, 445 jaw muscles 272
monoparesis 206 diagnosis 216, 437–40 myotonia congenita 274
causes 302, 303 differential diagnosis 437 myringotomy 200, 261, 262, 286
diagnostic tests 307 management 441–4 myxoedema coma, hypothyroid 484
forelimb 308–12 megaoesophagus 292, 293, 436, 437
hindlimb 206, 312–15 pathophysiology 435 N
neurological examination 306 prognosis 445 N-methyl-D-aspartate (NMDA)
Monro–Kellie doctrine 322, 367, 367, mycophenolate mofetil 360, 442, 616 receptor 418, 419
461 mycotoxins 248, 513–14 antagonists 429, 563, 566–7
morphine 457, 458, 561, 562 mydriasis 268, 270, 372, 372, 470 Na-K-ATPase 490–1, 491
postoperative use 562 myelin, CSF 134 naloxone 54
as premedicant 536 myelin basic protein 136 narcolepsy 153–4, 156–7, 173
motor end plate, see neuromuscular myelinolysis 481–2, 482 nasal catheters 41–2
(NM) junction
myelography 99–103, 404 nasal sensation response 29, 31, 222
motor function
advantages/disadvantages 84 naso-oesophageal feeding tube 382
assessment 209
anaesthesia 554 nasopharyngeal polyps 263, 263
head trauma 370, 371
artefacts 99 neck pain, see cervical pain
reduced/absent 205
contraindications 99 necrotizing leucoencephalitis (NLE)
motor nerve conduction velocity 345
CSF analysis following 129
(MNCV) 215
indications 99 clinical presentation 352
mouth, decontamination 508
interpretation 101–3 diagnosis 353, 354, 356, 357
movement disorders 20, 243, 247
ischaemic myelopathy 338 histopathology 348
breed-specific paroxysmal 175,
monoparesis 306, 307 management 357, 358–61
250–2
normal appearance 99, 101 signalment and history 349
differentiation from seizures 156
risks associated with 99 necrotizing meningoencephalitis
drug-induced 252
spinal trauma 390, 390 (NME)
MUA, see meningoencephalitis,
technical problems 404 clinical presentation 352
unknown aetiology
technique 100–1 diagnosis 353, 354, 356
multiple myeloma 93, 94, 486
myelomalacia 102, 400–1, 402 histopathology 345, 347
muscarinic signs 515, 516
diagnosis 406, 406 management 357, 358–61
muscle
intraoperative photograph 412 signalment and history 349
atrophy 184, 184, 305, 305
neurological signs 402 Negri bodies 298
biopsy 188, 192
 INDEX 665

neomycin 490 neuron-specific enolase (NSE) nutrition

neoplasia antibodies 238 head trauma 382
causing dysphagia 296 neuronal cell death 151 tetanus 455
causing exercise-associated neuropathic pain 220, 558, 568 nutritional disorders
weakness/collapse 182 neuroprotective agents 330, 339, 390, causing paresis/paralyis 214–15
causing paresis/paralysis 214–15 392, 408 thiamine deficiency 114, 115, 164,
causing regurgitation/ neurotmesis 308, 310 165, 169, 204, 259, 497, 497
megaoesophagus 297 neurotransmitters 159, 161 nystagmus 31–2, 255, 257
causing vestibular disease 259 newt, Taricha spp. 527 classification 255
optic nerve 231, 237 nicardipine 55 pathological 32, 255, 255
spinal 93, 93, 94, 95, 101, 103, nicotine 514 physiological 31–2, 143, 255, 373
227–8, 402 nitric oxide 366
see also brain tumours nitric oxide scavenging 573, 576
O
Neospora caninum 186, 190, 341, 342, nitrosurea drugs 477 obtundation
344, 345 nitrous oxide 542, 548 assessment 144
neosporosis NLE, see necrotizing leucoencephalitis common causes 147–54
diagnosis 353, 355 NMDA, see N-methyl-D-aspartate definition 141
management 357 NME, see necrotizing meningo- differential diagnosis 139–40
neostigmine bromide 441, 617 encephalitis
obturator nerve 300, 301, 306
neostigmine methylsulphate 438, 617 NMES, see neuromuscular electrical
octopus, blue-ringed 527
nerve biopsy 188 stimulation
oculocephalic reflex (physiological
nerve conduction, physiology 177 Nocardia spp. 343
nystagmus) 31–2, 143, 255, 373
nerve conduction studies 261, 307 nociception
oculomotor nerve (CN III) 29, 30, 32,
nerve root signature 206, 223 loss 265
nerve sheath 180 ischaemic myelopathy 340 abnormalities 268, 372
nerve sheath tumour 102, 281, 305, IVDD 401, 402, 414, 415 parasympathetic nucleus 230, 231,
309–10, 309 testing 27–8, 211 372
lumbar plexus 206 nociceptive pathway 558 oculovestibular reflex 29, 31–2, 255, 470
trigeminal nerve 281, 281 nociceptors, spinal cord 220 oedema
neurapraxia 308, 310, 313, 314 node of Ranvier 177 cytotoxic 324, 366, 366, 464
neuritis, brachial plexus 311 nonsteroidal anti-inflammatory drugs pulmonary 39, 86
neurological examination (NSAIDs) 566, 567 vasogenic 356, 357, 366
aims 16–17 adverse effects 408 see also brain oedema
rational and principles 17 carprofen 395, 567, 610 oesophagostomy tube 382, 595
seizures 163 concurrent corticosteroids 566 oesophagus
neuromuscular collapse 156–7 intracranial disease 563 innervation 292
neuromuscular electrical stimulation IVDD 408 suctioning 552
(NMES) 607 meclofenamic acid 567 oligoastrocytoma, high-grade 462
neuromuscular (NM) blockade 543, 551 meloxicam 567, 615 oligodendroma, anaplastic (grade III)
neuromuscular (NM) disorders sites of action 559 463
anaesthesia 549–52 spinal pain 395, 566, 567 omeprazole 227, 490
causing stridor/dysphonia 289 noradrenalin (norepinephrine) 53 oncotic pressure 69
causing weakness/collapse 179–80, Normosol R 572 ophthalmoplegia 265–6
179 North America OPIDN, see organophosphate-induced
diffuse 183 snake bites 525–6 delayed neuropathy
dysphagia 292 tick paralysis 531 opioids 395, 561–3
generalized diffuse 215 nucleus pulposus 399 advantages and disadvantages 561
metabolic aberrations 81 extrusion 334, 337, 337, 400, 400 bradycardia 54
neurological evaluation 181–3 nursing care cardiovascular depression 540, 543,
pain management 568–9 head trauma 382 561–2, 561
neuromuscular (NM) junction 177, 178, ischaemic myelopathy 339 doses 561
433, 434 neurotoxicity 500 intraoperative 540, 541
action of botulinum and tetanus recumbent patient 360, 424, 458, as premedicants 536, 539
toxins 448, 448 596–7 short-acting 543, 548
neuromyopathy, ischaemic 181, 182, ventilated animal 47, 47–8 sites of action 559
217
see also supportive care spinal disease/trauma 395, 564–6
neuromyotonic discharges 250
see also named opioids
 666 INDEX

opsoclonus 247 myasthenia gravis 444, 444 hypoparathyroidism 483

optic chiasm 229, 230 nasal 444 primary hyperparathyroidism
tumours/lesions 238, 268 status epilepticus 423 (PHPTH) 485–7
optic nerve (CN II) 29, 230, 232 oxygen–haemoglobin dissociation curve parathyroid gland 483, 483
oedema 239, 239 38, 50 parathyroid hormone (PTH) 483, 483,
tumours/lesions 231, 237, 241, 241, oxygenation, in anaesthesia 537, 539, 485, 486, 493
268 541–2 parathyroid hormone-related protein
optic neuritis 231, 238, 240, 240 oxyhaemoglobin 326, 327 (PTHrP) 486
optic tract lesions 268 oxyhaemoglobin saturation (SpO2) 38, paresis 21
optic tracts 229, 230 48, 379 acute
orbicularis oculi 232 oxymorphone 536, 561, 617 differential diagnosis 213,
organochlorines 514–15 214–16
lesion localization 211–13, 212
organophosphate-induced delayed P
neuropathy (OPIDN) 516 pachymeningitis, idiopathic LMN causes 214–17
organophosphates 167, 248, 515–16, hypertrophic 280–1 neuroanatomical basis 207–8,
568 packed cell volume (PCV) 40, 377, 574, 208, 208
orthopaedic disease 578, 582 neurological evaluation 209–13
causing weakness 176, 176 assessment 62–3 definition 173, 193, 205
gait dysfunction/lameness 196–7, blood transfusion 62, 588–9 diagnostic tests 213
299, 302 estimation of blood loss 548 facial 19, 282–7
investigations 176, 305 normal ranges 63 flaccid 173
oscillometry 56 pain ischaemic myelopathy 335, 336, 337
osmolality, serum 69–70, 79, 80, 81 assessment 27–8, 557, 558–9 laryngeal 35, 287–90, 529, 530
osmolarity, serum 69 definition 557 LMN 21–2, 21, 173, 194, 208, 208,
osmoles, diogenic 480 neuropathic 220, 558, 568 213, 300
osmometer, cryoscopic 69 types 220 UMN 21–2, 21, 194, 300
osmotic demyelination syndrome pain treatment 598 paroxysmal breed related disorders 175,
481–2, 482 250–2
aims of 557
osteomyelitis, vertebral 226 paroxysmal depolarizing shift (PDS)
intracranial disease 560–3
osteosarcoma, spinal 227–8 159, 417
intraoperative 540, 541
otitis media/interna 257, 262–3 paroxysmal events, differentiation from
IVDD 408 epileptic seizures 156–7
clinical signs 18, 19 neuromuscular disease 568–9 partial thromboplastin time (PTT) 75,
diagnosis 262 neuropathic pain 568 76, 621
facial paresis/paralysis 283, 285–6 postoperative 549, 562 passive range of motion therapy 602–3,
imaging 89, 89, 262, 262 spinal trauma 395 602
management 263 palpation patellar reflex 25–6, 306, 335
owner questioning 33 head 33 patient handling, spinal imaging 83, 84,
involuntary movements 244 limbs 33 85
seizure history 156, 166, 168–9 spinal/paraspinal 33, 211, 222, 222 patient positioning
oxidative stress 488 palpebral fissure 266 head trauma 378
oxygen palpebral reflex 29, 30–1, 231, 233 spinal trauma 388
fractional concentration in inspired pamidronate 486 venous drainage 543
air (FiO2) 40, 42 pancarpal arthrodesis 309 ventilated animal 48
partial pressure (PaO2) 38, 48, 71 panniculus reflex, see cutaneous trunci paw replacement reaction 22
head trauma 369, 379 reflex PCR, see polymerase chain reaction
normal values 621 papilloedema 231, 239, 470 peak inspiratory pressure (PIP) 45, 47
oxygen delivery (DO2) 38 paralysis pediculectomy 411
calculation 51 definition 205 PEG, see percutaneous endoscopic
cerebral 62, 63 sedation/anaesthesia 553, 553 gastrostomy; polyethylene glycol
oxygen free radicals 366 tick bites 216, 296, 528–31 pelvic nerve 301, 592
oxygen supplementation 38–42 paraneoplastic syndromes 466–7 penicillins 456
cage 40 paraplegia, ischaemic myelopathy 335, penitrem A 513–14
‘flow-by’ 536, 537 336 pentobarbital 519, 617
head trauma 379 parasite migration 319, 320, 345, 353 Peptostreptococcus spp. 343
indications 38 paraspinal palpation 211 percussion (tapotement) 601
methods 40–2 parathyroid disease 485–7
 INDEX 667

percutaneous endoscopic gastrostomy physostigmine 267 low blood levels 179, 191
(PEG) 443–4, 443 picking up technique 600, 600 raised blood levels 65–6, 65, 179
perineal reflex 26 pilocarpine, ocular 267, 271 reference ranges 621
perineurium 180 piriform lobes, post-seizure oedema potassium bromide
peripheral nerve diseases 163 cats 170
differential diagnosis 180, 181, pituitary apoplexy 467, 470 dogs 171
182–3 pituitary gland tumours 80–1, 466–7, hepatic encephalopathy 489
nerve sheath tumours 102, 281, 281, 468, 471 pounding 601
305, 309–10, 309 pituitary-dependent hyperadreno- pralidoxine (2-PAM) 516
peripheral nerves, anatomy 180 corticism (PDH) 466 prazosin 395, 592
peripheral nervous system 16 plantigrade stance 182, 306 prednisolone
peritoneal lavage, hyperthermia 496 plasma volume expansion (PVE) 573 masticatory muscle myositis 276
permethrin 167, 516–17 Plasma-Lyte 148 572, 580 MEM 357, 361
peroneal nerve 301, 314 Plasmalyte-A 572 polymyositis 190
pesticide toxicity 167, 511–12, 514–17 platelet count 62, 76, 585, 585 prednisone
pesticides 519 pleocytosis 130–2, 133, 338, 340, 352, brain neoplasms 475
petechiae 74 354, 407
Chiari-like formation/syringomyelia
pethidine 561, 563 pleural fluid 86 227
petrissage 599 pleurothotonus 18, 19, 254, 254 immunusuppressive 360
pH, arterial 71, 621 PLR, see pupillary light reflex IVDD 408
pharyngeal muscles pneumocephalus 381 MEM 359, 361–2
spasm 293 pneumonia, aspiration 38, 431, 440, myasthenia gravis 441–2
tone 32, 292, 293 444, 460, 460
prednisone/vincristine/cyclo-
pharyngeal reflex 32 treatment 595–6 phosphamide protocol 360, 361–2
phenobarbital pneumothorax 39, 368 pregabalin 227, 431
adverse effects and precautions 428, polyarthritis 176 cats 170
617 polycythaemia 166 dogs 171
cats 170, 228 polyethylene glycol (PEG) 339, 390, prehension disorders 295
and diazepam therapy 427, 432 392
preliminary survey examination 15, 15
dogs 171 polymerase chain reaction (PCR) 354–5
premedication 539, 546, 567
dyskinesia 252 for antigen receptor rearrangement
in animals with NM disease 549
feline hyperaesthesia syndrome 228 (PARR) 136
blood transfusion 588
generalized tremor syndromes 248 polymethylmethacrylate (PMMA)
cement 393, 397 pressure ulcers 395, 395
head trauma 380, 382 pretectal nucleus (PTN) 230, 231
polymyositis 189–90
permethrin toxicity 517 procainamide 250, 513
polyneuritis, infectious/inflammatory
as premedicant 536 procarbazine 360, 361, 478
190
status epilpeticus 428 progesterone therapy 381
polyneuropathy 283
toxicities 500, 508, 517 prokinetic agents 298
causing facial paresis/paralysis 286
phenobarbitone, see phenobarbital propofol 489, 500, 502, 509, 550
causing stridor/dysphonia 289
phenothiazines 457, 563 cats 541
generalized 277
phenoxybenzamine 395, 592, 617 generalized tremor syndromes 248
polyradiculoneuritis (Coonhound
phenylephrine 53 paralysis) 214–15, 216 head trauma patient 380
eye drops 267, 268, 269 pontine nucleus 232 induced abnormal movements 252
phenytoin, myokymia 250 portosystemic shunt 489, 489, 490 intracranial disease 538, 539
physical therapy 598–607 positive end-expiratory pressure long-term ventilation 553
electrical stimulation 607 (PEEP) 43, 44 status epilepticus 429
exercises 604–5 adverse effects 45, 46–7 tetanus 457
hydrotherapy 597, 605, 605 anaesthesia 541 propranolol 248, 249, 361, 508, 513
ischaemic myelopathy 339 postural reaction testing 22–4, 26, 207, proprioceptive deficits
massage techniques 598–602 207, 210 forelimb 312
neurotoxicity 500 deficits 183 hindlimb 311
passive range of motion 602–3, 602 potassium 65–6, 67, 179, 191, 580 nerve sheath tumour 309
polymyositis 190, 190 extra/intracellular 417 proprioceptive exercises 605
thermo/cryotherapy 606 fluid therapy 580, 580 proprioceptive (paw) positioning 23
ultrasound 607 hypokalaemic myopathy 191
668 INDEX

protein radicular pain 401 respiratory support 594–6

CSF 125, 126, 134, 354, 407 radiography myasthenia gravis 444, 444
total plasma (TP) 62, 63, 576, 621 advantages/disadvantages 84 see also mechanical ventilation;
urine 68 head injury 374 oxygen supplmentation
protein-rich fluid loss 578–9 horizontal beam 90, 91 respiratory system, assessment 15
prothrombin (PT) 75, 76 monoparesis and lameness 307 reticular activating system (RAS) 140–1,
prothrombin time 621 myasthenia gravis 440, 440 141
proton pump inhibitors 490 spinal 90–7 retinal degeneration, sudden acquired
protozoal meningoencephalitis 342, assessment 91–7 syndrome (SARDS) 238–9
344, 345, 354 technique 90–1 retinal haemorrhage 231
pseudohyperreflexia 26 spinal injuries 87, 97–8, 388 retinal separation 152
PTH, see parathyroid hormone survey 86–9 retinitis 238
PTHrP, see parathyroid hormone- technique 90–1 retrobulbar mass 240, 272
related protein radiotherapy 477, 477, 478 rewarming 496, 500, 598
ptosis 266, 268, 269 ramus communicans 266, 266 rhabdomyolysis 190–1, 525
PTPTH, see hyperparathyroidism, range of motion (ROM), exercises riboflavin 191
primary 602–3 Rickettsia rickettsii 341, 342, 343, 353,
PTT, see partial thromboplastin time reactive oxygen species (ROS) 384, 386, 355
pudendal nerve 300, 301, 591 488, 491 rickettsial disease 190, 342, 342
‘Pug Dog encephalitis’ 349, 353–4 recumbent patient, care of 339, 360, diagnosis 353, 355
pulmonary atelectasis 38, 39, 596 382, 424, 458, 596–7 treatment 357
pulmonary contusions 39, 369, 575, 575 red blood cells (RBCs) 571 rigidity 18, 19, 143, 371, 371
pulmonary function, monitoring in basophilic stippling 510, 510 Ringer’s solution, lactated 572
anaesthesia 542 CSF 125, 126, 129 ‘rippling skin disease’ 228
pulmonary oedema 39, 86, 575 lysis 525 risus sardonicus 272, 449, 451, 520
pulse oximetry 48, 49, 50, 444 packed 588 rodenticide toxicity 167
head trauma 369, 379 refractometer 62, 69 roquefortine 513–14
status epilepticus 424 regurgitation 291–8, 436 rostral colliculus 230
pupil definition 291, 295
brainstem disease 143 prevention during anaesthesia 550, S
constriction 265–6 552 sacrocaudal spine, trauma 384, 387, 394,
dilation 266–7 rehabilitation, see physical therapy 397
evaluation 30 rehydration 579 saline
head trauma 372, 372 remifentanil 540, 541, 544, 561, 562 hypertonic 331, 357–8, 377, 572,
opioid use 562, 562 renal failure 492–4, 525, 526 576
unequal size (anisocoria) 30, 143, renal function, and mechanical hypotonic 572
265–71 ventilation 45, 49 isotonic 482, 572
pupillary light reflex (PLR) 29, 30 renal system, assessment 15 salt
deficits 236 repetitive nerve stimulation 438, 439, oral emesis 501
head trauma 370 454 toxicity 480, 518
indirect 236 respiratory depression, opioids 540, 543 saltatory conduction 177
neuroanatomical pathway 230, 231 respiratory distress, brain tumours 469, saphenous nerve 208
PVE, see plasma volume expansion 470 Sarcocystis canis 342
pyrethroids 167, 516–17 respiratory failure Schiff–Sherrington posture 18, 402
pyridostigmine bromide 441 botulism 458 Schirmer tear test 31
pyrimethamine 190, 357 causes in neurological disease 43 Schwann cells 177
pyruvate, plasma 186, 188, 192 hypercapnic 43 sciatic nerve 208, 300, 301
hypoxaemic 43 dysfunction 306, 313, 313
respiratory paralysis scintigraphy, spinal 226
R
snake bites 525 scleral haemorrhage 369
rabies 298, 341, 342, 344, 353, 421
tick paralysis 529, 530–1 Scotty cramps 175, 250–1
clinical presentation 350
respiratory pattern secondary injury phenomenon 335, 339
management and prognosis 357, 361
head trauma 368, 369, 373 sedation
post-vaccine 344
systemic inflammatory response blood donors 586–7
radial nerve 299, 301
494, 495
assessment of function 306 botulism 458
injury 310 EEG 555
 INDEX 669

hypotension 53 SMFA, see sodium monofluoroacetate myelography 101–2, 103

intracranial disease 535–6, 539 snake radiography 92
mechanical ventilation 48, 553, 553 American coral 523, 523, 525–7 see also laminectomy
neuromuscular disease 549, 568 death adder 526 spinal cord lesions
spinal disease/injury 83, 388, 546 mulga (King brown) 523 causing ataxia 201
tetanus 455 tiger 523, 526 causing hind limb monoparesis
sedimentation techniques 128, 128 snake bite envenomation 523–6 312–13
seizures SNARE proteins 450 localization 24–7, 211, 212
after myelography 99, 554 sodium non-compressive 213
brain imaging 114, 116 blood levels 66–7, 67, 425, 479–82 paresis/paralysis 208
brain neoplasms 469, 475 decreasing 584 spinal pain
focal 158, 244 elevated 66, 179, 479–81, 518, causes 224, 226–8, 387, 402
head trauma 380 584 differential diagnosis 225, 225
hepatic encephalopathy 489 increasing 583–4 neuroanatomical basis 219–20, 219
history 166–9 low 66, 179, 481–2, 583–4 neurological evaluation 221–2, 221
idiopathic 161 reducing 518 treatment 395, 563–4, 564–7
MEM 350, 352, 358 reference ranges 621 spinal reflexes 24–7, 26, 371, 401
metabolic aberrations 79–80 SIADH 583–4 depressed 24
metaldehyde toxicity 512 sources of excess 518 segmental 210
neurotoxins 167, 500, 506–13, 517, total body deficit 583, 584 spinal shock 402
519, 520 sodium bicarbonate 519 ‘spinal stapling’ 392
post-ictal state 144, 163 sodium carbonate (washing soda) 501 spinal trauma
reactive 162 sodium channels 434, 435 aetiology and pathophysiology
sodium abnormalities 482 sodium chloride (salt) 383–7
symptomatic 162 oral emesis 501 approach to patient 391
tetanus 457 toxicity 480, 518 assessment 211
see also epileptic seizures sodium monofluoroacetate (fluoro- cervical spine 388, 389, 393, 396,
sensory deficits 162, 281 acetate) 519 397, 397
sensory neuropathies 194 sodium nitroprusside 55 clinical presentation 387
sepsis-associated encephalopathy 494–5 sodium sulphate (Glauber’s salts) 504 contusion 384–6, 385
serotonin levels 251 sodium/potassium (Na+/K+) pump 177, diagnosis 388–90
sevoflurane 541, 542, 548, 553 321, 324 differential diagnosis 387
shaking 601 somatosensory evoked potentials management 390–7
shock (SSEPs) 147 metabolic aberrations 81–2
circulatory 52–3, 576 sorbitol 480, 503, 504 patient handling and imaging 83, 84,
obstructive 55 soybean oil, infusion 504 85
spinal 402 SPA-HRPO, see staphylococcal protein prognosis 397
A-horseradish peroxidase radiography 87, 97–8
short striding 196, 305
spider envenomation 520–2 sacrocaudal spine 384, 387, 394,
SIADH, see syndrome of inappropriate
antidiuretic hormone secretion spiders 397
signs, evolution 16 black widow 520, 521 thoracolumbar spine 387, 394,
red-back 520, 521 397
single-fibre electromyography 438, 439
Spike’s disease 252 spine, palpation 33, 211, 222, 222
skeletal muscle relaxants 551, 566, 611
spinal column splint, external body (spinal injuries)
skin rolling 600
instability 91, 386–7, 387, 392 394–5, 395
skull, radiography 86, 88, 89
luxation/subluxation 92, 94, 383, spondylomyelopathy 196
skull fractures 365, 374, 374
384, 389 spondylosis 220
classification 365, 365
spinal cord spondylosis deformans 93, 95, 96
pain management 561, 561
arterial and venous supply 333, squint (dazzle) reflex 233
surgical management 381–2
333, 335 SRMA, see steroid responsive
sleep 141 meningitis–arteritis
fibrocartilagenous embolism
EEG 149 120, 333, 334, 335 SSEPs, see somatosensory evoked
REM 153 spinal cord compression 386, 390 potentials
sleep disorders 156–7, 168, 244–5 decompression 392, 409–10 standing, assisted 605
sling support 603–4 extradural 199 staphylococcal protein A-horseradish
assessment of motor function 209 gait abnormalities 196, 199 peroxidase (SPA-HRPO) 439
slug/snail baits 511–12 Staphylococcus spp. 343
 670 INDEX

static inspiratory pressure, botulism 458 supportive care Tensilon (edrophonium challenge) test
status epilepticus (SE) botulism 458–9 438, 441
aetiology and pathophysiology gastrointestinal problems 594 tepoxalin 566
417–19 myasthenia gravis 443–4 tetanus 243, 272, 293, 296, 447
approach to management 426 pain control 569 aetiology/pathophysiology 447–9
brain neoplasms 464 recumbent patient 360, 382 anaesthesia 552
causing global ischaemia 151, 151 respiratory difficulty 594–6 clinical presentation 449, 450–1
clinical presentation 144, 421 tetanus 455 diagnosis 453
definition 417 tick paralysis 530 management 455–8
diagnosis 422–3 urinary incontinence 591–3 metabolic aberrations 81
differential diagnosis 421 see also nursing care prognosis 459
management 423–31 suprascapular nerve 301 tetanus antitoxin 455–6
non-convulsive 421 supraspinatus muscle, atrophy 305 tetany 243
out-of-hospital patient 432 swallowing 291 tetraparesis 206, 335, 336
prognosis 431 assessment 295 tetrodotoxin 527–8
systemic consequences 420 disorders (dysphagia) 291–8 thalamus 140, 141, 230, 232
stereotactic radiosurgery 477, 477 swinging flashlight test 268 lesions 258, 258
steroid-responsive meningitis-arteritis syncope (collapse) 156–7, 173 thallium toxicity 167
(SRMA) 349 exercise-induced 188–9 theobromine 512–13
clinical presentation 352 syndrome of inappropriate antidiuretic content of chocolate products 512
diagnosis 134, 353, 353, 354, 356, hormone secretion (SIADH) 481, theophylline 512
357 482 thermoregulation 77–8, 544
management 361 definition 583 thermotherapy 606
pathological lesions 349 fluid therapy 572, 583–4 thiamine 425
signalment and history 349 synovial fluid analysis 307 deficiency 114, 115, 164, 165, 169,
strabismus 32 syringohydromyelia 386, 406 259
lateral 266, 268 syringomyelia 102, 220, 223, 227 causes 204
positional 256, 256 syrinx 386 diagnosis 204, 497, 497
Streptococcus spp. 343 syrup of Ipecac 501 management 204
stress response 63, 382 systemic inflammatory response 53, supplementation 425, 497, 511
stretcher 84, 85 494, 495, 495 thiopentone 539, 550
stretching, static 602–3 systolic arterial blood pressure (SAP) 52, third eyelid, protrusion 268, 270, 281
stridor 287–90 55 thoracic injuries 369
stroke, see cerebrovascular accident thoracolumbar spine
(CVA) T IVDD 401–2, 408
stroke volume 53 tachyarrhythmias 52, 52, 53, 54 medical management 408
strychnine 167, 274, 520 botulism 457–8 prognosis 413–16, 414–15
stupor tactile placing response 23–4 surgical management 411–12
assessment 144 tail base sensation 397 pain 220, 223
common causes 147–54 tail function assessment 210 palpation 222, 222
definition 141 tapotement (percussion) 601 trauma 387, 394, 397
diagnostic tests 144–7 target organ damage (TOD) 493 thorax, survey radiography 86
differential diagnosis 139 taurine 480 thrombocytopenia 74, 74, 75
stylomastoid foramen 282, 283 tea 167 thrombolytic therapy 330
subarachnoid haemorrhage 321–2, 366 tear production 281, 287, 598 thymectomy 443
subarachnoid space, widening 102, 103 tears, artificial 424, 598 thymoma 436, 440
subdural empyema 343, 343 tectotegmental spinal tract 266, 266 thyroid cartilage 287
subdural haematoma 366 temozolamide 478 thyroid function testing 186, 200, 261,
subscapular nerve 301 temperature, see body temperature; 285, 295
succimer 510 hyperthermia; hypothermia thyroid hormone 484
suctioning temporalis muscles 271, 275 thyrotoxicosis/thyroid storm syndrome
airway 47, 50 temporomandibular joint (TMJ) 271–2, 485
oesophagus 552 274 thyroxine 484, 485
sudden acquired retinal degeneration tendon transposition 309 tibial nerve 208, 301
syndrome (SARDS) 238–9 TENS, see transcutaneous electrical injury 314, 315
nerve stimulation tibial reflex 306
 INDEX 671

tick-borne disease 216, 296, 342, 343, transient ischaemic attack (TIA) 319 urea cycle 487, 488
528–31 transsphenoidal hypophysectomy 478 urethral sphincter 591, 592
ticks traumatic brain injury urethral tone 210, 212
antitoxin serum 530 hyperthermia 77 urinalysis 67–9, 79, 80, 81
removal 530 metabolic abnormalities 77, 79 urinary catheterization 424, 458, 569,
tidal volume 37 see also head trauma 592–3
tissue perfusion, assessment 577–8 trazodone 545, 566, 620 cystostomy 593
tissue plasminogen activator 217 tremor 18, 243 urinary incontinence 592–3, 596, 597
TIVA, see total intravenous anaesthesia action-related 18 urinary tract infections (UTI) 413
TMJ, see temporomandibular joint intention 245 urine specific gravity (USG) 67–9, 71,
toad, cane 507–8, 507 resting 18 583
toad toxicity 507–8 tremor syndrome, idiopathic 245, urine collection 49, 60, 424, 458
toadfish 527–8 247–9, 345, 349 urine output 60
tone, assessment 371 clinical presentation 352 fluid therapy 579, 582, 583
tongue, innervation 33 diagnosis 353 head trauma patient 382
tonic–clonic movements 156, 157, 166 management 361 monitoring 60, 593
topiramate 171, 620 prognosis 361 normal 579
total intravenous anaesthesia (TIVA) triceps reflex 306 spinal trauma 395
540, 541, 548 tricyclic antidepressants 154, 564 status epilepticus 424
total protein (TP) 62, 63, 576, 621 amitriptyline 609 ventilated animla 49
total solids (TS) 574, 578, 582 imipramine 154, 613 urine scalding 593, 593
toxicities 499 trigeminal nerve (CN V) 29, 30–1, 277 urobilinogen 68
associated with seizure activity 167 disorders 277, 279–80, 281, 281 USG, see urine, specific gravity
causing acute blindness 238 ophthalmic branch 266, 281
causing ataxias 202, 203 trimethoprim/sulphadiazine 190 V
causing decreased consciousness trimethoprim/sulphonamide 357, 596 vacuum phenomenon 94, 96
139–40 trismus 271–6 vagosympathetic trunk 266
causing dysphagia 296 common causes 274–6, 274 vagus nerve (CN X) 29, 283, 292, 292
causing facial paralysis 285 diagnostic tests 272 valproic acid 620
causing involuntary movements 245, differential diagnosis 272 Valsalva’s manoeuvre 334
248 neuroanatomical basis 271–2 vascular diseases
causing regurgitation/mega- neuroanatomical evaluation 272
oesophagus 297 causing blindness 238
Trm4 gene 386 causing decreased consciousness 139
causing vestibular disease 259, 263
trochlear nerve (CN IV) 29, 32 causing paresis/paralysis 214–15,
cutaneous 501
Trypanosoma cruzi 342 217
decontamination 500–5, 501
tumour necrosis factor-alpha (TNF- causing vestibular disease 259
general treatment principles alpha) 488
499–504 vasodilatory shock 53
turning, recumbent patient 424 vasopressin 53
inhaled 501
tympanic bullae, imaging 261, 262, 286 vasopressors 574
neuroexcitatory 505–20, 505
neuroinhibitory 505, 520–31 vecuronium 551
Toxoplasma gondii 186, 190, 341, 342, U venlafaxine 154
344, 353 ulnar nerve 208, 299, 301 venous drainage, head 543, 543
toxoplasmosis ultrasonography (US) venous oxygen tension, mixed 578
diagnosis 353, 355 advantages/disadvantages 84 ventilation
management 357 head injury 374 anaesthesia 538, 541–2
TP, see total protein hydrocephalus 149, 149 animal with NM disease 551
tracheostomy 36–7 monoparesis/lameness 307 recovery 544
tramadol 559, 561, 562, 567, 620 portosystemic shunt 489 spinal surgery 548
doses 620 skull 88 see also mechanical ventilation
mode of action 559 therapeutic 607, 607 ventilator-induced lung injury (VILI) 46
side-effects 562, 620 upper motor neuron (UMN) paresis ventral slot technique 410, 410
transcutaneous electrical nerve 21–2, 21, 194, 206, 208, 208, 300 ventricular dilatation 355
stimulation (TENS) 607 diagnosis 213 ventriculoperitoneal (VP) shunt 150
transdermal patch, fentanyl 561, 565–6, upper motor neuron (UMN) system 20, ventriculostomy 476
565 20, 207, 299 ventroflexion, neck 191, 191
uraemic encephalopathy 492–4
 672 INDEX

verapamil 508 weakness

vertebra, wedge 97 assessment 209
vertebral canal definitions 173, 175
cervical spine 220 generalized 436, 437
radiographic assessment 91–2, 92 see also exercise-associated weak-
vertebral endplate, radiographic ness/collapse
changes 96 weight, see body weight
vertebral fracture 383, 384 West Nile virus 342, 343
vestibular disease 17, 32 wheelbarrowing 22, 23
acute idiopathic 261 wide-based stance 18, 256
ataxia 195, 203 wind-up 566
bilateral 258 withdrawal (flexor) reflex 24–5, 183,
central 254, 256–7, 256, 263 211, 306
differential diagnosis 258, 259 decreased 335, 401
peripheral wounds
common causes 261–3 débridement 456, 459
investigation 89 local anaesthetic infiltration 569
neurological evaluation 256–8
symptoms and signs 254–6 X
vestibular nerve (CN VIII) 29 xylazine 501
vestibular (special proprioceptive)
receptors 193
Y
vestibular system 253–4, 253 Yankauer suction tip 499
vestibulocochlear nerve 194, 283 yesterday, today and tomorrow 506–7,
vibrations 602 507
VILI, see ventilator-induced lung injury yohimbine 154
vincristine 360, 361, 478 Yorkshire Terrier, necrotizing
viral meningoencephalomyelitis 341, encephalitis 349
342, 343–4, 354, 355, 357
vision
Z
assessment 29, 29, 233
zinc
loss, see blindness
intracellular concentrations 491,
visual pathways 229, 230, 231 491
visual placing response 29, 29, 233 supplementation 511
vitamin B1, see thiamine zinc phosphide 167
vitamin D 425, 484 zonisamide 170, 171, 430, 620
VITAMIN D mnemonic 33, 34
vitamin E deficiency 182
volutrauma 45
vomiting
avoidance in pain control 566
distinguishing from regurgitation
295
induction (emesis) 501, 501
management 594
neuromuscular disease 568
von Willebrand’s disease 589
voriconazole 357, 620

W
walking aids 603–4, 603, 604
warming 496, 500, 598
washing soda (sodium carbonate) 501
water loss, sodium-free 480