BRADYARRHYTHMIA & TACHYARRHYTHMIA

Barret Bulmer, DVM, MS, DACVIM (Cardiology)

Cummings School of Veterinary Medicine at Tufts University

BRADYARRHYTHMIA (DOGS, <60-70 BPM; CATS, <120-140 BPM)

P waves present?

NO YES

DIAGNOSIS INVESTIGATION
Atrial standstill P wave for every QRS complex?

TREATMENT NO YES
h D etermine serum
electrolytes in dogs and
treat underlying causes
h A rtificial pacing (atrial
standstill secondary to
DIAGNOSIS INVESTIGATION
Sinus arrest may represent Associated QRS complex for every P wave?
idiopathic disease/AV
SSS (variable with presence
myopathy)
or absence of
supraventricular or
ventricular escape foci;
sinus pauses often present) NO YES

TREATMENT DIAGNOSIS DIAGNOSIS

h R ule out electrolyte Second- or Sinus bradycardia
imbalances, metabolic third-degree AV block (uncomplicated
disease (eg, GI, respiratory, by AV block)
CNS), athleticism
h A tropine response test may
be indicated
• If symptomatic and heart TREATMENT

rate increases, may h O ften idiopathic TREATMENT
administer anticholiner- h P acemaker likely h M ay resolve with
gics and/or sympathomi- indicated exercise, excitement,
metics h W ithdraw offending atropine
• If symptomatic and heart drugs (eg, digoxin) h Withdraw offending


rate does not increase, h C orrect identifiable drugs
may require pacemaker underlying causes h Correct identifiable
AV = atrioventricular

implantation h C RI isoproterenol or underlying causes
h E mergency cases may
SSS = sick sinus syndrome temporary pacing for h Increase heart rate

require CRI of isoproterenol short-term with anticholinergics,
SVT = supraventricular tachycardia or temporary pacing until emergency treatment sympathomimetics,
permanent pacemaker is h D o not use drugs that or artificial pacing
VT = ventricular tachycardia
implanted suppress ventricular (rare)
escape beats (eg,
procainamide,
lidocaine, atenolol,
sotalol)
 DIAGNOSTIC/MANAGEMENT TREE  h  CARDIOLOGY  h  PEER REVIEWED

TACHYARRHYTHMIA (DOGS, >160 BPM; CATS, >220 BPM)

Regular rhythm?

NO YES

DIAGNOSIS Supraventricular or ventricular complexes?

Atrial fibrillation

Supraventricular complexes Ventricular complexes

TREATMENT
h D ecrease heart rate with
agents (eg, digoxin,
calcium-channel blockers,
β-blockers) that increase h P waves are visible  P waves abnormal or
DIAGNOSIS
refractoriness of AV node (or less commonly not visible; abrupt Ventricular tachycardia
and number of impulses embedded in onset and termination
reaching ventricles preceding T wave) of arrhythmia
h Consider rhythm control h Progressive ramp

(conversion to sinus rhythm) up/slow down of

via transthoracic electric arrhythmia
TREATMENT
cardio-version
Immediate therapy indicated:
DIAGNOSIS h I f VT is rapid, multiform, and
h S ustained SVT
produces clinical signs—IV
(atrial/junctional
lidocaine or procainamide (bolus,
DIAGNOSIS tachycardia)
may require CRI)
Sinus tachycardia h P aroxysmal SVT
h  I dentify and treat underlying heart
(if abrupt onset/
disease
termination) h Treat underlying systemic diseases
h  W ithdraw possible offending drugs
(eg, digoxin)
TREATMENT h Correct electrolyte imbalances
Treat underlying h  S otalol, mexiletine, or less
causes TREATMENT commonly amiodarone for
Acute termination: long-term maintenance therapy
h Vagal maneuvers (eg, h  24-hour Holter monitoring to
carotid sinus massage, determine therapeutic efficacy
ocular pressure,
precordial thump)
h I V boluses of
procainamide, diltiazem, For heart rate control or prevention
esmolol (less commonly, of recurrence: Attempt prophylaxis
digoxin, amiodarone) with oral digoxin, diltiazem,
h  Transthoracic electrical atenolol, sotalol, or amiodarone
cardioversion
DIAGNOSTIC/MANAGEMENT TREE h CARDIOLOGY h PEER REVIEWED

 
 
 
 
COMMON CARDIAC ARRHYTHMIAS
Barret Bulmer, DVM, MS, DACVIM (Cardiology)
Cummings School of Veterinary Medicine at Tufts University

NORMAL HEART RATE (DOGS, 70–160 BPM; CATS, 140–220 BPM)

INVESTIGATION
Are all QRS complexes supraventricular?

NO YES

INVESTIGATION
Normal P wave preceding all QRS complexes?
DIAGNOSIS DIAGNOSIS
Underlying sinus Accelerated
rhythm with VPCs idioventricular rhythm

NO YES
TREATMENT TREATMENT
h Rule out cardiac/ Identify and treat
systemic disease underlying cause
h Rule out infectious
agents producing
DIAGNOSIS INVESTIGATION
Underlying sinus rhythm Does the underlying R-R interval vary by >10%?
myocarditis
h Treat underlying cause
with supraventricular
h 24-hour Holter
premature complexes
monitoring to determine
need for treatment and/
or therapeutic efficacy
h Rapid suppression
achieved via IV lidocaine TREATMENT NO YES
or procainamide (bolus, h I dentify and treat
may require CRI) underlying heart disease
h O ral maintenance h In patients with paroxysms

therapy via sotalol, of SVT, treatment with
mexiletine (± atenolol), digitalis, calcium-channel
Sinus rhythm (normal DIAGNOSIS
for dogs and cats) Sinus arrhythmia
or less commonly blockers, or β-blockers may
amiodarone be required to slow heart (usually normal,
rate; sotalol or amiodarone especially in dogs)
may resolve arrhythmia

TREATMENT
No treatment required;
P wave morphology
may vary in patients
displaying wandering
pacemaker

SVT = supraventricular tachycardia

VPC = ventricular premature complex
HEART MURMURS IN CATS
Brian A. Scansen, DVM, MS, DACVIM (Cardiology)*
The Ohio State University

CAT WITH HEART MURMUR1

INVESTIGATION Young cat (ie, <1 year of age), Adult Cat

or never previously auscultated
Check PCV

<7 years of age

h PCV >28% DIAGNOSIS I NVESTIGATION INVESTIGATION

h No significant (PCV <28%) Systolic grade IV/VI Continuous murmur

anemia Anemia or louder; all murmurs

Return to Cat TREATMENT DIAGNOSIS DIAGNOSIS INVESTIGATION INVESTIGATION

with heart h Correct anemia Congenital heart Patent ductus Systolic grade III/VI Systolic grade IV/VI

murmur h Investigate disease likely arteriosus likely or softer or louder
underlying h M ost common h C
 onfirm with
causes defect in cats is echocardiogram
h Recheck ventricular septal

murmur when defect
PCV normalizes h M itral and
INVESTIGATION
tricuspid valve h E
 chocardiogram recommended
dysplasia are also h M
 easure NT-proBNP (semiquantitative
common
h Echocardiogram is
[cage-side ELISA] or quantitative)
advised

A physiologic (nonpath- Quantitative NT-proBNP <100 Quantitative NT-proBNP

ological) cause is likely pmol/L or semiquantitative >100 pmol/L or
and can be common; (cage-side ELISA) = normal semiquantitative
can be confirmed by (cage-side ELISA) = abnormal
echocardiogram

DIAGNOSIS DIAGNOSIS
h  eart disease less likely
H h  eart disease more likely
H
• Further testing may not • Confirm severity


be necessary and cause with
echocardiogram

NT-proBNP = N-terminal pro-B type natriuretic peptide

PCV = packed cell volume
T4 = thyroid hormone assay *Byline reflects author information on original publication. On publication of this collection,

the author’s current affiliation is Colorado State University.
 DIAGNOSTIC/MANAGEMENT TREE h CARDIOLOGY h PEER REVIEWED

 
 
 
 
Any age with fever,
>7 years of age infection, new murmur

INVESTIGATION DIAGNOSIS
Evaluate thyroid hormone status h  lthough rare, consider endocarditis
A
• Confirm with echocardiogram

Normal T4 Elevated T4

TREATMENT
h Treat hyperthyroid state

and reassess murmur
after establishment of
euthyroidism
h S econdary cardiac
DIAGNOSIS disease may be present;
Organic heart disease is the likely echocardiogram can
cause of this grade murmur evaluate degree of
h H ypertrophic cardiomyopathy
cardiac remodeling from
is the most common acquired thyroid disease
heart disease of the cat
• Thoracic radiographs are

advised to evaluate heart size
and presence or absence of
congestive heart failure
• Echocardiogram is helpful

for definitive diagnosis, to
assess left atrial size, and
to evaluate risk for arterial
thromboembolism

Reference
1. Côté E, Edwards NJ, Ettinger SJ, et al. Management of incidentally detected heart murmurs in dogs and

cats. J Am Vet Med Assoc. 2015;246(10):1076-88.
HEART MURMURS IN DOGS
Brian A. Scansen, DVM, MS, DACVIM (Cardiology)
Ohio State University*

DOG WITH HEART MURMUR

Young or never previously auscultated

Systolic Diastolic Continuous

Left apex Left base Right

Mitral valve Subaortic Tricuspid valve

dysplasia or stenosis or dysplasia or Diastolic murmurs are Patent ductus
regurgitation pulmonary regurgitation;

uncommon arteriosus is most likely
stenosis or ventricular septal h Considerations include h Echocardiography is
functional defect


aortic or pulmonary valve helpful to confirm
murmur or insufficiency; mitral or
atypical VSD tricuspid stenoses are
even rarer
h Confirm with

echocardiography

In general, if the murmur Soft (grade I-II/VI),

is grade III/VI or higher, ejection-type murmurs
semilunar valve stenosis is at the left base may be
likely functional or represent
h I t is helpful to evaluate mild semilunar valve
pulse quality, as the pulse stenosis
in severe subaortic stenosis
is weak; it is normal in pul-
monary stenosis or func-
tional murmurs
h Confirm with

echocardiography
DIAGNOSTICS
Diagnostic tests to help separate these differentials
include radiography, ECG, or echocardiography
h Echocardiography is most likely to provide a definitive

diagnosis for congenital heart disease; radiography or
ECG can be supportive

*Byline reflects author affiliation on


original publication. On publication
of this collection, the author’s
VSD = ventricular septal defect current affiliation is Colorado State
University.
 DIAGNOSTIC/MANAGEMENT TREE h CARDIOLOGY h PEER REVIEWED

 
 
 
 
Middle aged and older

<15 kg >15 kg Any size with

fever, lameness,
new murmur

Systolic Diastolic Systolic Diastolic

DIAGNOSIS
Consider
endocarditis as a
differential;
Aortic insufficiency or Aortic insufficiency or
echocardiography


pulmonary insufficiency pulmonary insufficiency
required to confirm
most likely most likely
h Causes are rare; h Causes are rare;


infectious endocarditis, infectious endocarditis,
congenital malforma- congenital malforma-
tion, or severe degenera- tion, or severe degenera-
tion are considerations tion are considerations

Left base Left apex Right Left base Left apex Right

If grade III/VI or Mitral valve Tricuspid regurgita- If grade III/VI or Dilated cardiomyop- Tricuspid regurgitation is
less and with no degeneration (eg, tion is the most likely less and with no athy or mitral valve the most likely differential
clinical signs, a endocardiosis) differential clinical signs, a degeneration h Consider degenerative

functional murmur is the most likely h Consider degener- functional mur- (eg, endocardiosis) tricuspid valve disease

is possible differential ative tricuspid mur is possible are both possible and/or pulmonary
h For any grade, h Thoracic radio- valve disease (eg, h For any grade, h Consider echo- hypertension
endocardiosis)




consider undiag- graphy or echo- consider undi- cardiography to h A heartworm antigen
and/or pulmonary

nosed congeni- cardiography agnosed con- differentiate test should be evaluated
tal heart disease can help evalu- hypertension genital heart h Thoracic radio- h Consider previously
h A heartworm anti-


such as subaor- ate overall disease such graphs may also undiagnosed VSD if

gen test should be
tic or pulmonary heart size and as subaortic or be pursued to a left basilar systolic
evaluated
stenosis or VSD evidence of h Consider previ-
pulmonary ste- evaluate overall murmur is also present
h Confirm with congestive nosis or VSD heart size and h Confirm with

ously undiagnosed


echocardio- heart failure VSD if a left basilar
h Confirm with any evidence of echocardiography

graphy h Confirm with
systolic murmur is echocardio- congestion

echocardio- also present graphy
graphy h Confirm with

echocardiography
PULSE ALTERATIONS
Elisa Mazzaferro, DVM, MS, PhD, DACVECC
Cornell University Veterinary Specialists
Stamford, Connecticut

PALPABLE PULSE?

NO

INVESTIGATION
Auscult the heart; perform ECG

DIFFERENTIALS Small amplitude of Normal Dysrhythmia

h Pulseless electrical QRS complex;
electrical alternans

activity
h Asystole

h Ventricular

fibrillation
INVESTIGATION DIFFERENTIALS DIFFERENTIALS
Perform TFAST h Thromboembolism h Fever


h Pericardial effusion h Hyperthermia


Initiate CPR h Hypovolemia h Increased


h Hypothermia sympathetic tone

h Hypothyroidism h Myocardial


h Depressed myocardial dysfunction

contractility h Hyperthyroidism
DIFFERENTIAL Results inconclusive

h Obesity (cats)
or negative

h Pericardial fluid h Pheochromocytoma


If pericardial INVESTIGATION
effusion is Perform AFAST to
confirmed, perform check for abdominal
pericardiocentesis effusion

DIFFERENTIALS
h Hypovolemia

h Hypothermia

h Hypothyroidism

h D epressed myocardial contractility

AFAST = abdominal focused assessment using sonography for trauma

CPR = cardiopulmonary resuscitation
SIRS = systemic inflammatory response syndrome
TFAST = thoracic focused assessment using sonography for trauma
 DIAGNOSTIC TREE  h  CARDIOLOGY   h  PEER REVIEWED

YES

Dyssynchronous Synchronous

INVESTIGATION
Perform ECG

Bradycardia Normal Tachycardia Hyperdynamic Normal Hypodynamic

DIFFERENTIALS DIFFERENTIALS DIFFERENTIALS DIFFERENTIALS DIFFERENTIALS DIFFERENTIALS

h Sinus bradycardia h Atrial tachycardia h Sinus tachycardia h Fever/hyperthermia h Tachycardia h Hypovolemia
h  A trioventricular h  S inus arrhythmia h  P remature h Exercise • Pain h 
M yocardial
block h P remature ventricular h Stress/anxiety • Anxiety dysfunction
h Hypothyroidism ventricular contractions h Pain • Sepsis h Hypothermia
h H ypothermia contractions h  Ventricular h Early sepsis/SIRS • Dehydration h Hypothyroidism
h I dioatrial/ tachycardia h 
P atent ductus h Sinus arrhythmia

idioventricular h S upraventricular arteriosus

rhythm tachycardia h Hyperthyroidism
h Sinus arrest h Atrial fibrillation h A nemia
h H ypoglycemia

INVESTIGATION
INVESTIGATION h ECG
h CBC h CBC
h 
S erum chemistry h 
S erum chemistry
profile profile
h E lectrolyte/venous h E lectrolyte/venous
blood gas blood gas
measurements measurements
h ± thyroid panel h ± thyroid panel
h ± abdominal h ± abdominal
ultrasonography ultrasonography
h ± echocardiogram h ± echocardiogram

cliniciansbrief.com  19
ACUTE ABDOMINAL PAIN
Justine A. Lee, DVM, DACVECC*
Pet Poison Helpline
Minneapolis, Minnesota

SIGNS OF ACUTE ABDOMINAL PAIN

INVESTIGATION
Obtain complete history:
h S ignalment
h Presenting complaint

h Previous history, surgery, trauma

h Diet (eg, normal diet, recent ingestion, fatty meals, table food)

h Vaccine and medication status

h Toxin exposure

h Travel history

h Progression

h Systemic and metabolic signs (eg anorexia, coughing, sneezing, vomiting,

diarrhea, regurgitation, polyuria, polydipsia, polyphagia, weakness)
h Foreign body

h Indoor or outdoor status (cats)

INVESTIGATION
Perform physical examination:
h H ydration: skin turgor, tacky mucous membranes, sunken eyes
h O ral: string under tongue, ulcerations, erosions, halitosis, foreign body, ptyalism
h C ardiorespiratory: lung sounds, heart rate, pulse quality, capillary refill time
h A bdominal: organomegaly, ascites, pregnancy, pain localization, fluid-filled loops,
borborygmi, foreign body, masses
h I ntegumentary: petechiae, ecchymoses
h M usculoskeletal/neurologic: mentation, cranial nerves, ataxia, dysautonomia, decreased
rectal tone, ambulatory
h R ectal: prostatomegaly, fecal evaluation, melena
h U rogenital: bladder evaluation, neuter status, vaginal discharge, pain on kidney palpation

Evaluate if signalment, history, presenting complaint, and

examination findings help rule in or out differential diagnoses

BG = blood glucose
FAST = focused assessment with DIAGNOSIS
h D igestive: gastric or duodenal ulcer, gastritis, gastroenteritis, GD, GDV, GI obstruction,
sonogram for trauma
intussusception, ileus, pancreatitis, intestinal parasitism, protein-losing enteropathy, inflammatory
FIC = feline idiopathic cystitis disease, neoplasia, hepatic disease
h M etabolic: acute renal failure, hepatopathy, hyperadrenocorticism, hypoadrenocorticism, diabetes
GD = gastric dilatation h P eritoneal cavity: trauma, septic peritonitis, GI tract perforation, foreign body, splenic torsion,
GDV = gastric dilatation-volvulus ruptured abdominal abscess, uroabdomen, penetrating trauma, bile peritonitis, hemoabdomen,
liver lobe torsion
PCV = packed cell volume h U rinary: ureteral, urethral, or cystic calculi; acute nephritis; pyelonephritis; urethral obstruction;

PLI = pancreatic lipase immuno- acute renal failure; uroabdomen

h R eproductive: pyometra, labor or dystocia, uterine or testicular torsion, prostatic disease
reactivity
h M usculoskeletal: intervertebral disk disease, abdominal muscular trauma, referred orthopedic pain
TLI = trypsin-like immunoreactivity h I nfectious disease: infectious canine hepatitis, leptospirosis, parvovirus, panleukopenia, FIP,
Giardia spp infection, Salmonella spp infection, Clostridium spp infection, vector-borne diseases
TS = total solids h O ther: toxicity, bezoar, caustic or corrosive ingestion, nausea secondary to ileus (opioid therapy,

VBG = venous blood gas postoperative)

 DIAGNOSTIC TREE h CRITICAL CARE h PEER REVIEWED

 
 
 
 
INVESTIGATION
Complete initial diagnostics:
h P CV/TS/BG, electrolytes, BUN, VBG
h CBC and blood smear evaluation

h Serum chemistry profile

h Abdominal radiography

h FAST ultrasonography

INVESTIGATION
Complete additional diagnostics:
h F ecal ± smear to evaluate bacterial overgrowth
(Clostridium spp, Campylobacter spp)
h Urinalysis ± culture

h Thoracic radiography

h FeLV/FIV

h Pancreatic evaluation (eg, TLI, cPLI, fPLI)

h Abdominal ultrasonography

h Coagulation panel

h Advanced GI testing (eg, bile acids, cobalamin, folate)

INVESTIGATION
Complete advanced diagnostics:
h A bdominocentesis
h Cytology evaluation (eg, intracellular bacteria)
h F luid analysis (eg, culture; comparison of
serum:abdominal fluid ratios for creatinine,
bilirubin, glucose, lactate)
h B arium series
h F luoroscopy
h P neumocolonography

Reevaluate and repeat examination

Continuing signs of pain

*Byline reflects author


TREATMENT TREATMENT information on original
publication. On publi-
Nonsurgical cause: Surgical cause:
h F luid therapy (eg, crystalloids, colloids, blood transfusions)† h F luid resuscitation or stabilization before anesthesia and surgery
cation of this collec-
h A ntiemetic therapy h C orrection of underlying cause for abdominal pain†
tion, the author’s
h G I protectants† h F eeding tube placement †
current credentials
h A nalgesic therapy h B iopsy †
and affiliation are
h N utritional support h P ostoperative care
Justine A. Lee, DVM,
h A ntidiarrheal therapy
DACVECC, DABT, at
• Heat support
h Treatment for underlying metabolic disease
VETgirl, St. Paul,
• Antiemetic therapy
h D eworming
Minnesota.
• Fluid therapy
h R eevaluation of clinicopathologic analysis
†If appropriate
• Analgesia

h A ntibiotic therapy † • Antibiotic therapy †
h S ymptomatic supportive care • Symptomatic supportive care
h M onitoring • Nutritional support
ACUTE BREATHING DIFFICULTY: INITIAL MANAGEMENT
Rebecca Kirby, DVM, DACVIM, DACVECC*
Elke Rudloff, DVM, DACVECC†
Animal Emergency Center
Glendale, Wisconsin

IS THE ANIMAL BREATHING? YES INVESTIGATION

Primary survey

NO

Pleural space
TREATMENT h C hest/abdomen opposite
Begin CPR h M uffled lung sounds

Barrel chest? No lung sounds? YES Catastrophic? Cyanotic?

YES NO NO

TREATMENT TREATMENT TREATMENT

Convert tension to Chest tube Pleurocentesis
open pneumothorax

Improvement
observed?

NO YES
TREATMENT
h A nesthetize
h I ntubate, ventilate (100% O 2)
h S uction
TREATMENT
h A nesthetize
h I ntubate,
ventilate
(100% O 2)

CPR = cardiopulmonary resuscitation

*Byline reflects author information on original publication. On publication


of this collection, Rebecca Kirby, DVM, DACVIM, DACVECC, is retired.
†Byline reflects author information on original publication. On publication

of this collection, the author’s affiliation is Lakeshore Veterinary Special-
ists in Glandale, Wisconsin.
‡In some cases, extant murmurs cannot be heard over lung sounds or

because of true left congestive heart failure. However, furosemide can be
associated with hypovolemia and dehydration; thus, consequences of
furosemide may outweigh benefits in initial stabilization.
 DIAGNOSTIC/MANAGEMENT TREE h CRITICAL CARE h PEER REVIEWED

 
 
 
 
INVESTIGATION
Respiratory rate increased NO Rule out nonrespiratory
disease (pain, anemia,
with increased effort?
CNS, systemic disease)

YES

TREATMENT
h M inimize stress Large airway
h O 2 supplementation (loud breathing heard without
h ± sedation use of a stethoscope)

h IV catheter

h Observe breathing

Catastrophic?
Cyanotic?

Parenchyma Small airway

h S mooth breathing h S hort inspiration
h C hest/abdomen h L ong exhalation/
together push NO YES
h W heezing

TREATMENT TREATMENT
Catastrophic? Catastrophic? h S edation h A nesthetize
YES Cyanotic? Cyanotic? h S uction h I ntubate,ventilate
oropharynx (100% O 2)
h Suction trachea
h ± tracheostomy

NO NO YES

Improvement
observed?
NO
h Murmur TREATMENT TREATMENT

h Gallop h Bronchodilator h E pinephrine (IV/IM)


h Arrhythmia h Glucocorticoid h Bronchodilator



h History of heart disease h Glucocorticoid

YES

h ± intubate, ventilate

(100% O2)

NO YES

TREATMENT TREATMENT
± furosemide ‡ h Furosemide

h Nitroglycerin

INVESTIGATION
Secondary survey & continued treatment
ACUTE BREATHING DIFFICULTY: INITIAL MANAGEMENT
Rebecca Kirby, DVM, DACVIM, DACVECC*
Elke Rudloff, DVM, DACVECC†
Animal Emergency Center
Glendale, Wisconsin

IS THE ANIMAL BREATHING? YES INVESTIGATION

Primary survey

NO

Pleural space
TREATMENT h C hest/abdomen opposite
Begin CPR h M uffled lung sounds

Barrel chest? No lung sounds? YES Catastrophic? Cyanotic?

YES NO NO

TREATMENT TREATMENT TREATMENT

Convert tension to Chest tube Pleurocentesis
open pneumothorax

Improvement
observed?

NO YES
TREATMENT
h A nesthetize
h I ntubate, ventilate (100% O 2)
h S uction
TREATMENT
h A nesthetize
h I ntubate,
ventilate
(100% O 2)

CPR = cardiopulmonary resuscitation

*Byline reflects author information on original publication. On publication


of this collection, Rebecca Kirby, DVM, DACVIM, DACVECC, is retired.
†Byline reflects author information on original publication. On publication

of this collection, the author’s affiliation is Lakeshore Veterinary Special-
ists in Glandale, Wisconsin.
‡In some cases, extant murmurs cannot be heard over lung sounds or

because of true left congestive heart failure. However, furosemide can be
associated with hypovolemia and dehydration; thus, consequences of
furosemide may outweigh benefits in initial stabilization.
 DIAGNOSTIC/MANAGEMENT TREE h CRITICAL CARE h PEER REVIEWED

 
 
 
 
INVESTIGATION
Respiratory rate increased NO Rule out nonrespiratory
disease (pain, anemia,
with increased effort?
CNS, systemic disease)

YES

TREATMENT
h M inimize stress Large airway
h O 2 supplementation (loud breathing heard without
h ± sedation use of a stethoscope)

h IV catheter

h Observe breathing

Catastrophic?
Cyanotic?

Parenchyma Small airway

h S mooth breathing h S hort inspiration
h C hest/abdomen h L ong exhalation/
together push NO YES
h W heezing

TREATMENT TREATMENT
Catastrophic? Catastrophic? h S edation h A nesthetize
YES Cyanotic? Cyanotic? h S uction h I ntubate,ventilate
oropharynx (100% O 2)
h Suction trachea
h ± tracheostomy

NO NO YES

Improvement
observed?
NO
h Murmur TREATMENT TREATMENT

h Gallop h Bronchodilator h E pinephrine (IV/IM)


h Arrhythmia h Glucocorticoid h Bronchodilator



h History of heart disease h Glucocorticoid

YES

h ± intubate, ventilate

(100% O2)

NO YES

TREATMENT TREATMENT
± furosemide ‡ h Furosemide

h Nitroglycerin

INVESTIGATION
Secondary survey & continued treatment
BLOOD GAS ANALYSIS This algorithm reflects canine normals.
For cats, substitute feline normals for pH,
BE (or HCO3–), PCO2, and PO2 values (Table 1).

Lori S. Waddell, DVM, DACVECC

University of Pennsylvania

SELECT ANALYZER

INVESTIGATION
Determine if arterial or venous
h Venous: Jugular sample provides the best idea of whole-body status. Peripheral

samples may represent local tissue bed and not whole body.
h Arterial: Dorsal metatarsal artery, femoral artery, auricular artery, or caudal artery

INVESTIGATION INVESTIGATION
Arterial sample (to assess respiratory function) Venous sample (pulse oximetry can be used with venous blood gas to assess
h PaCO 2 assesses ability to ventilate oxygenation)

h PaO 2 assesses ability to oxygenate h PvCO 2 can suggest ventilation (usually about 5 mm Hg higher than PaCO2 )


INVESTIGATION
INVESTIGATION Evaluate pH to determine if acidemia or alkalemia present INVESTIGATION
Acidemia = pH <7.35 Alkalemia = pH >7.45

INVESTIGATION
INVESTIGATION Evaluate PCO2 and BE for masked INVESTIGATION
Determine if metabolic disturbances if pH = 7.35-7.45 Determine if metabolic
or respiratory in origin or respiratory in origin

Metabolic = BE INVESTIGATION Respiratory = PaCO2

Respiratory = <−4 mmol/L (or Assess for compensation <35 mm Hg Metabolic = BE
PaCO2 >45 mm Hg HCO3− <21 mEq/L) (see Rules of >4 mmol/L (or HCO3−
Compensation) >27 mEq/L)

DIFFERENTIAL DIFFERENTIAL DIFFERENTIAL

Respiratory acidosis Metabolic acidosis Respiratory alkalosis DIFFERENTIAL
h Depressed respiratory center h Increased anion gap: h Hypoxemia Metabolic alkalosis



h Cervical spinal cord disease • Ketones h Pulmonary disease h GI obstruction with loss



h Neuromuscular disease • Lactate h CNS disease (eg, of H +, K+, and especially
• Uremia


h Pleural space disease stimulating respiratory Cl− in vomitus
• Toxicity (eg, ethylene

h Airway obstruction center) h Loop diuretics

glycol, salicylates)


h Rarely severe pulmonary h Exercise, pain, stress h NaHCO 3 administration
h Normal anion gap:



parenchymal disease

h Respiratory muscle fatigue
• HCO3− loss through kidneys

or intestinal tract

TREATMENT TREATMENT TREATMENT TREATMENT
h   orrect underlying problem
C h   orrect underlying cause
C Correct underlying disease h H ypokalemic
h R elieve airway obstruction/ h L acate: Improve oxygen hypochloremic
restrictive disease (pleural delivery to the tissues metabolic alkalosis:
space) h K etones: Insulin therapy Volume expansion with
h I ntubate, begin PPV h N aHCO 3 (if needed) 0.9% NaCl
• HCO3− deficit = BE × body h L oop diuretic or

weight (kg) × 0.3 HCO3− therapy: No
• Give 1/4 to 1/3 of dose and treatment, usually

recheck blood gas self-limiting
 MANAGEMENT TREE h CRITICAL CARE h PEER REVIEWED

 
 
 
 
TABLE 1 TABLE 2

NORMAL VALUES FOR BLOOD GASES EXPECTED COMPENSATORY CHANGES

Arterial Venous Disorder Primary Compensatory

Change Response
CANINE
Metabolic acidosis ↓ HCO3− 0.7 mm Hg decrease in PCO2 for
pH 7.35-7.45 7.35-7.45 each 1 mmol/L decrease in HCO3−

PO2 (mm Hg) 90-100 30-42 Metabolic alkalosis ↑ HCO3− 0.7 mm Hg increase in PCO2 for
each 1 mmol/L increase in HCO3−
PCO2 (mm Hg) 35-45 40-50
Acute respiratory acidosis ↑ PCO2 1.5 mmol/L increase in HCO3− for
HCO3− (mmol/L) 20-24 20-24 each 10 mm Hg increase in PCO2
BE (mmol/L) −4-+4 −4-+4 Chronic respiratory acidosis ↑ PCO2 3.5 mmol/L increase in HCO3− for
FELINE each 10 mm Hg increase in PCO2

Acute respiratory alkalosis ↓ PCO2 2.5 mmol/L decrease in HCO3− for

pH 7.34 ± 0.1 7.30 ± 0.08
each 10 mm Hg decrease in PCO2
PO2 (mm Hg) 102.9 ± 15 38.6 ± 11 Chronic respiratory alkalosis ↓ PCO2 5.5 mmol/L decrease in HCO3− for
each 10 mm Hg decrease in PCO2
PCO2 (mm Hg) 33.6 ± 7 41.8 ± 9

HCO3− (mEq/L) 17.5 ± 3 19.4 ± 4

BE (mmol/L) −6.4 ± 5 −5.7 ± 5 Continues h

Rules of Compensation
1. Change in respiratory or metabolic component of the acid-

base status will normally induce opposite, compensatory
change in the other to return pH toward normal.
2. Lungs compensate rapidly by changing minute ventilation

(eg, respiratory rate/tidal volume/both) within minutes.
3. Metabolic compensation occurs via the kidneys and is much BE = base excess

slower, starting after a few hours and requiring 4 to 5 days for HCO3− = bicarbonate
maximum compensation. NaCl = sodium chloride
4. Absence or presence and degree of compensation for respi- NaHCO3 = sodium bicarbonate

ratory disturbance can give an idea of chronicity (Table 2). PaCO2 = partial pressure of arterial carbon dioxide
5. Overcompensation does not occur. PaO2 = partial pressure of oxygen

6. If expected compensation is absent, a mixed disturbance is PCO2 = partial pressure carbon dioxide

present. For example, if metabolic acidosis is not accompa- PO2 = partial pressure oxygen
nied by compensatory respiratory alkalosis (CO2 is normal or
PPV = positive-pressure ventilation
increased), a mixed disturbance is occurring with both meta-
PvCO2 = partial pressure of venous carbon dioxide
bolic acidosis and respiratory acidosis.
MANAGEMENT TREE h CRITICAL CARE h PEER REVIEWED

 
 
 
 
BLOOD GAS ANALYSIS ALTERNATIVES
If blood gas analysis is not available, some information can be obtained through other tests. Pulse oximetry can be
used to assess a patient’s oxygenation. It must be remembered that pulse ox saturation and PaO2 are not directly
correlated; a pulse ox of 93% corresponds with a PaO2 of 80 mm Hg and a pulse of 90% corresponds with a PaO2 of
60 mm Hg. If the patient is intubated, end tidal CO2 (ETCO2) can be used to assess for hypercarbia or hypocarbia.
ETCO2 usually corresponds well to PaCO2, with ETCO2 ≈5 mm Hg lower than PaCO2 in normal patients. In medium
and large dogs, the end tidal tubing can be placed just inside the nostril of an awake, compliant patient to estimate
ETCO2.

If anion gap measurement is available on a chemistry screen, it can be used to detect some causes of metabolic
acidosis, including those caused by ketones, lactate, and exogenous acids (eg, toxins, phosphates, sulfates). These
will cause an increase in the anion gap. If the anion gap is normal but the corrected chloride is elevated (see
equation below), loss of bicarbonate via the kidneys or the large bowel may be causing a metabolic acidosis.

In addition, the patient’s ketones may be measured via either ketone strips for use with urine or a ketometer to
measure serum ketones. A handheld lactate meter can be used to measure ketones. These are relatively
inexpensive, small pieces of equipment similar to a glucometer and give results in a few minutes. Although they do
not give information about pH, they can help guide fluid therapy and potentially help prognosticate in patients
that are presented with a high lactate and do not respond to therapy. To detect metabolic alkalosis, the patient’s
chloride concentration should be evaluated. If the corrected chloride is low, a metabolic alkalosis is likely.

Corrected Cl– = (normal Na+/measured Na+) × measured Cl–

This equation helps determine if the chloride concentration is abnormal in comparison to the sodium
concentration, as normally the 2 ions will change in the same direction and to the same degree. Changes in the
corrected chloride can indicate metabolic derangements.

Cl = chloride
ETCO2 = end tidal CO2
Na = sodium
PaCO2 = partial pressure of arterial carbon dioxide
PaO2 = partial pressure of oxygen
COLLAPSE
Vincent Thawley, VMD*
Deborah Silverstein, DVM, DACVECC
University of Pennsylvania

PATIENT COLLAPSE

INVESTIGATION
Obtain complete history:
h Signalment

h Signs: loss of consciousness, weakness with exercise, vomiting, diarrhea,

coughing, sneezing, polyuria, polydipsia, appetite, weight change
h Date/time when patient was last normal

h Progression

h Previous medical history

h Preventive care & medications

h Travel history

h Exposure to toxins, human medications, and/or sugar-free products

INVESTIGATION
h E pisode is brief with recovery and INVESTIGATION
YES minimal to no tonic–clonic motor signs
NO Episode involves:
h A bnormal motor or autonomic activity
or abnormal autonomic activity
h L asts >30 seconds
h E pisode follows exercise, barking,
h A bnormal behavior
coughing, straining, or vomiting
DIAGNOSIS
Syncope

YES NO

DIAGNOSIS Complete physical examination

Seizure

System-specific abnormalities revealed?

INVESTIGATION
Assess for system-specific abnormalities:
h N eurologic: altered mentation, cranial nerve deficits, abnormal reflexes
or gait, flaccid/spastic paresis
h C ardiovascular: abnormal heart rate or rhythm, murmur, muffled sounds, NO YES
weak or bounding pulse quality, pulse deficits, abnormal mucous
membrane color, rapid or prolonged CRT, jugular venous distention
h R espiratory: increased rate or effort, stertor or stridor, abnormal
ACTH = adrenocorticotropic
pulmonary auscultation
hormone
h Urogenital: increased bladder size and turgidity, painful bladder or INVESTIGATION

CRT = capillary refill time kidney palpation, intact or altered Complete initial diagnostics:
h Eyes, ears, nose, throat: oral lesions, pupil asymmetry, delayed or absent h S erum chemistry profile and
CSF = cerebral spinal fluid

pupillary light response, fundic lesions electrolytes
h Abdomen: painful palpation, organomegaly, fluid wave h C BC and blood smear
ECG = electrocardiogram

h Musculoskeletal: lameness; muscle atrophy; bone, spinal, neck pain; h Venous blood gas and acid–base

LDDS = low-dose dexamethasone joint effusion or crepitus; reduced ROM parameters
suppression h Lymphatics: peripheral lymphadenopathy h U rinalysis ± culture

h Rectal: sublumbar lymphadenopathy, prostatic enlargement, anal sac or h T horacic or abdominal radiography
ROM = range of motion

rectal abnormalities (eg, masses, hematochezia, melena) h T hyroid testing

UC:Cr = urine cortisol:creatinine h Integument: petechiae, ecchymoses, alopecia, ectoparasites h H eartworm, rickettsial testing

ratio h Rectal temperature: hyperthermia, hypothermia h F eLV/FIV testing

Go to Cause revealed?
 DIAGNOSTIC TREE h CRITICAL CARE h PEER REVIEWED

 
 
 
 
Cause
YES revealed?
NO

TREATMENT Repeat examination

Treat as indicated

System-specific
YES abnormalities suggested? NO

INVESTIGATION
If following abnormalities are present, complete ancillary diagnostics:
h O rganomegaly, abdominal pain, peritoneal effusion: abdominal ultrasonography
h C ardiac murmur, muffled heart sounds, arrhythmia, enlarged pulmonary arteries on thoracic radiographs: ECG
h A rrhythmia, pulse deficits: ECG ± Holter monitor
h P etechiae, ecchymoses, thrombocytopenia: coagulation profile
h S uspicion of hypercoagulability: thromboelastography or D-dimers
h J oint effusion, pain, redness, warmth on palpation: arthrocentesis
h N euromuscular weakness, flaccid paresis: acetylcholine receptor antibody titer ± edrophonium response
h N a:K ratio <27, lack of stress leukogram: testing for hypoadrenocorticism (eg, UC:Cr, ACTH stimulation testing,
LDDS testing)
h L iver enzyme elevations or evidence of decreased liver function on serum biochemistry profile: fasting and
postprandial serum bile acids or resting ammonia
h H ypoglycemia (blood glucose <60 mg/dL): insulin:glucose ratio
h I onized hypercalcemia: parathyroid hormone/parathyroid-related protein assay
INVESTIGATION h A bnormal gait or mentation, spinal or cervical pain, segmental reflex deficits: MRI or CT ± CSF tap
Complete system-specific diagnostics: h P eripheral lymphadenopathy: lymph node aspiration
h N eurologic: spinal or cervical
h A bnormal CBC: bone marrow aspiration
radiography h P ossibility of illicit drug exposure: screening
h Cardiopulmonary: ECG, blood

pressure, pulse oximetry, arterial
blood gas analysis, thoracic
radiography
h Abdominal: radiography,
YES System-specific abnormalities revealed? NO

ultrasonography, abdominocentesis
and fluid cytology
h Musculoskeletal: bone or joint

radiography, infectious disease (eg,
rickettsial) titers h Repeat examination

h Home monitoring recommended;

video of events may help

TREATMENT
Consider hospital admission

*Byline reflects author information on original publication.


On publication of this collection, the author’s current
credentials are Vincent Thawley, VMD, DACVECC.
ANTICOAGULANT RODENTICIDE INGESTION
Lori S. Waddell, DVM, DACVECC
University of Pennsylvania

ACUTE INGESTION

INVESTIGATION
Confirm ACR ingestion (ie, not bromethalin, cholecalciferol, zinc phosphide)

<1/10 LD 50 ≥1/10 LD 50 or unknown

TREATMENT 4-6 hours since ingestion?

h C lose observation
h P T 48 hours
postingestion
h D o not give vitamin
K1 before checking PT YES NO OR NOT SURE

PT normal?
TREATMENT
Induce emesis if no contraindications:
h D ogs: apomorphine (0.03 mg/kg IV or 0.04 mg/kg IM)
h Cats: xylazine (0.44 mg/kg IM or SC) then reverse with yohimbine

(0.25-0.5 mg/kg IM or SC) or dexmedetomidine (0.002-0.015 mg/
kg IV, IM, or SC), then reverse with equal volume of atimepazole
h IV administration is preferred, but if no IV access is available, IM
YES NO

or SC are options

TREATMENT TREATMENT TREATMENT

N o treatment needed If PT is prolonged, give vitamin K1 Activated charcoal (1-4 g/kg PO) and cathartic (sodium
(2.5 mg/kg PO q12h) for 4 weeks sulfate, 250 mg/kg or 70% sorbitol solution, 1-2 mL/kg PO)

Recheck PT 48 hours after TREATMENT

last dose of vitamin K1 h C heck PT at 48 hours postingestion
or
h Start vitamin K1 (2.5 mg/kg PO q12h) for 4 weeks

TREATMENT
Treat for 2 more weeks if COMMON ANTICOAGULANT RODENTICIDES
prolonged; repeat as needed

Agent LD50 (mg/kg) in Dogs1 LD50 (mg/kg) in Cats1

Brodifacoum 0.2-4 25
Bromadiolone 11-15 >25
Chlorophacinone 3-20 15
Diphacinone 0.9-8 15
 DIAGNOSTIC/MANAGEMENT TREE h CRITICAL CARE h PEER REVIEWED

 
 
 
 
The EPA has banned public use of brodifacoum, bromadiolone, difenacoum, and difethialone. These products were manufactured for home use until
December 31, 2014, and shipped until March 2015. The newer products contain diphacinone, and 4 weeks of vitamin K1 therapy is recommended at
the time of this publication to treat this anticoagulant rodenticide (ACR). These changes may decrease ACR toxicities and increase cases of other
rodenticide toxicities, particularly bromethalin, which can cause neurotoxicity.

CLINICALLY AFFECTED (ACTIVELY BLEEDING)

TREATMENT INVESTIGATION
Stabilize with IV fluids ± supplemental oxygen Common signs:
h L ethargy
h A norexia
h Increased RR/RE

h Hemoptysis

h Lameness
INVESTIGATION

Determine PCV/TS, PT, PTT, platelet count

INVESTIGATION
Examination findings:
INVESTIGATION h A bnormalities consistent
Confirm ACR exposure:
Unable to confirm ACR h P resent in environment ACR confirmed with location of bleed
h Dull lung or heart sounds
h C oagulopathy consistent

h Abdominal distension
with ACR (PT more

h Episcleral hemorrhage
prolonged than PTT or

h SC hematoma
both out of range)

DIAGNOSIS h A CR toxicology screening TREATMENT
Consider other (can be submitted to Vitamin K1 (5 mg/kg SC) once as soon as diagnosis is
differential diagnoses: most veterinary school suspected and coagulation panel has been drawn
h L iver failure diagnostic laboratories
h Disseminated and even some

intravascular commercial veterinary
coagulation diagnostic laboratories)
h Hemophilia Is patient anemic?

h Immune-mediated

thrombocytopenia
h Neoplasia
YES NO

TREATMENT TREATMENT
h Fresh frozen plasma (10-20 mL/kg IV) given over 1-2 hours to provide Fresh frozen plasma, frozen
active clotting factors immediately and pRBCs if needed plasma, or cryo-poor plasma
or (10-20 mL/kg IV) given over 1-2
h I f
only fresh whole blood is available, fresh whole blood (20-40 mL/kg) hours to provide active
to give equivalent dose of clotting factors (watch for volume overload) clotting factors immediately

ACR = anticoagulant rodenticide

LD = lethal dose TREATMENT
h C ontinue vitamin K1 at 2.5 mg/kg SC (until able to take PO) or PO q12h for 4 weeks
PCV = packed cell volume h C onvert to oral vitamin K1 as soon as patient is able to take oral medication (better bioavailability)

pRBCs = packed red blood cells

PT = prothrombin time
PTT = partial thromboplastin time
TREATMENT
RE = respiratory effort h M onitor PT at 48 hours after last dose of vitamin K1 Reference
h Treat for 2 more weeks if prolonged 1. MJ. Rodenticides. Vet Clin
RR = respiratory rate


h Repeat treatment as needed North Am Small Anim Pract.

TS = total solids 2002;32(2):469-484.
GASTRIC DILATATION-VOLVULUS
Lisa L. Powell, DVM, DACVECC*
University of Minnesota

Triage immediately (suspected GDV patients

SUSPECTED GDV may be cardiovascularly unstable)

Is patient stable?

NO YES

TREATMENT INVESTIGATION
Stabilize patient Obtain complete history:
h P lace IV cephalic catheters (2) h R etching or vomiting attempts
h Extract blood for MDB and blood lactate levels. h ± distended abdomen

h Fluid resuscitation (30 mL/kg crystalloid fluid bolus [≤3 h A gitation, restlessness, discomfort, anxiety

doses]; if very unstable, consider 4 mL/kg hypertonic saline h ± recent stressful event
with 10 mL/kg synthetic colloid) h R ecent large meal or water intake
h Monitor therapy response: heart rate (arrhythmias), h P rogressive weakness ± collapse

respiratory rate, blood pressure, pulse quality, mucous
membrane color, CRT, PCV/TP, urine output
h ± opioid pain management

INVESTIGATION
Check signalment
h U nderweight
h Fearful temperament
h Eating 1 meal/day
h L arge breed, deep chested
POSSIBLE COMPLICATIONS h A dvanced age

h Cardiac arrhythmias often begin within 24 hours of surgery. Continuous ECG monitoring

is ideal. Factors include poor myocardial perfusion, electrolyte disturbances, acidosis,
myocardial-depressant factor, and DIC. Antiarrhythmic drugs should only be considered INVESTIGATION
Perform examination
if volume has been adequately replaced and arrhythmia is life threatening or causing h C ardiopulmonary: tachycardia,
poor perfusion. tachypnea, poor pulse quality, pale
mucous membranes
h M entation: responsive or agitation,
h DIC can persist after surgery. Factors include blood pooling in portal circulation and the
minimally responsive or comatose

caudal vena cava, sepsis, vascular thrombosis, endotoxemia, acidosis, tissue hypoxia, h A bdomen: bloated abdomen†
h A mbulatory (eg, depending on severity
and splenic congestion. Diagnosis may be confirmed by prolonged activated clotting
of shock or pain)
time or abnormalities in platelet, FSP, and PTT values. Treatment should target
underlying cause; microvascular thrombosis should be prevented with adequate tissue
perfusion via IV fluid therapy.
h Sepsis can occur postoperatively; aspiration pneumonia is a frequent cause (vs gastric

leakage). Thoracic radiography and peritoneal lavage can help identify origin. *Byline reflects author information on original

publication. On publication of this collection,
h Recent studies have shown that lactate clearance is a much better indicator of the author’s current affiliation is BluePearl Pet

Hospital, Eden Prairie, Minnesota.
prognosis versus a single, baseline lactate at presentation.1-3 A lactate decrease of †Abdomen may vary from remarkable, distended, and
≥42% was found to be an indicator of improved outcome.1-3 A baseline lactate should

firm to tympanic. If stomach is contained in rib cage or
if there is gastric torsion with minimal air, visual bloat
be obtained, then serial lactates after adequate fluid resuscitation, and postoperatively, (ie, distention) may not be present.
should be performed and compared.
 DIAGNOSTIC/MANAGEMENT TREE h CRITICAL CARE h PEER REVIEWED

 
 
 
 
DIAGNOSIS
GDV suggested?

YES NO

INVESTIGATION INVESTIGATION
Diagnostics & imaging Assess for other abdominal disease
h A bdominal radiography
h E lectrolytes
h B lood glucose curve
h P CV/TP
h C BC, serum chemistry profile,
DIFFERENTIALS
± coagulation profile h G astric bloat (no volvulus)
h L actate (shown to be associated with h G astroenteritis
morbidity and mortality in dogs with h A bdominal effusion References
GDV); repeat lactate following bolus h P ancreatitis 1. De Papp E, Drobatz KJ, Hughes D.
fluid administration (30-45 minutes)

h A bdominal neoplasia Plasma lactate concentration as a
h B lood gas analysis h I ntestinalvolvulus predictor of gastric necrosis and
h S plenic torsion survival among dogs with gastric
h H emorrhage dilatation-volvulus: 102 cases
(1995-1998). J Am Vet Med Assoc
1999;215:49-52.
2. Zacher LA, Berg J, Shaw SP, et al.

Association between outcome
TREATMENT and changes in plasma lactate
Gastric decompression concentration during presurgical
h G astric paracentesis (eg, trocarization) treatment id dogs with gastric
• 14-gauge catheter preferred dilatation-volvulus: 64 cases
• Palpate for most tympanic area; avoid splenic laceration (2002-2008). J Am Vet Med Assoc
• Abdominal ultrasound (eg, focused ultrasound) to direct centesis 2010:236:892-897.
h P assage of orogastric tube
3. Green TI, Tonozzi CC, Kirby R,
• Sedate (eg, opioid with benzodiazepine)

Rudloff E. Evaluation of initial
• Intubate to prevent aspiration pneumonia plasma lactate values as a
• Orogastric tube for decompression and subsequent gastric lavage predictor of gastric necrosis and
h ± anesthetic induction for exploratory laparotomy, passage of orogastric tube after induction
initial and subsequent plasma
lactate values as a predictor
of survival in dogs with gastric
dilatation-volvulus: 84 dogs
(2003-2007). J Vet Emerg Crit Care
TREATMENT 2011;21(1):36-44.
Emergency surgery
h (Full) abdominal exploratory
h Stomach derotation
CRT = capillary refill time

h Assess for gastric necrosis

• Gastric resection if necessary DIC = disseminated intravascular

h Assess for splenic viability coagulation

• Splenectomy if necessary
h Gastropexy FSP = fibrin split products

GDV = gastric dilatation-volvulus
MDB = medulloblastoma
PCV = packed cell volume
PROGNOSIS
Poor prognostic indicators PTT = activated partial

h G as within gastric wall (ie, indicating gastric wall compromise) thromboplastin time
h Free gas in abdominal cavity (ie, indicating gastric rupture)
h Plasma lactate levels >6 mmol/L at presentation
TP = total protein
h Increased lactate with adequate fluid resuscitation and therapy
h L actate does not decrease by ≥42% with appropriate fluid resuscitation, surgery, and therapy1-3
 MANAGEMENT TREE h CRITICAL CARE h PEER REVIEWED

 
 
 
 
HYPOTHERMIA
Lysa Posner, DVM, DACVAA
North Carolina State University

BODY TEMPERATURE*

Temperature <82°F Temperature 82°F-92°F Temperature 93°F-101°F Temperature 102°F-104°F

(<28°C) (28°C-33°C) (34°C-38°C) (39°C-40°C)

TREATMENT TREATMENT TREATMENT TREATMENT

h C over exposed skin h C over exposed skin h C over exposed skin h C over exposed skin
h P
 rovide multiple active heat h Provide multiple active heat h Provide active heat source h Discontinue heat source



sources sources
h P  rovide warm IV fluids h Provide warm IV fluids

h P  rovide warm environment h Provide warm environment

INVESTIGATION
Continue monitoring

TREATMENT INVESTIGATION
Administer emergency h Monitor ECG

treatment: h Monitor coagulation

h Abdominal lavage

h Thoracic lavage

*As patient warms, treatment strategies change to suit current body temperature.
RESPIRATORY DISTRESS
Elizabeth Rozanski, DVM, DACVIM (SAIM), DACVECC
Cummings School of Veterinary Medicine at Tufts University

INVESTIGATION
h  T horacentesis
h T-FAST if available

TRAUMA? h Chest radiography

NO YES TREATMENT
Provide oxygen; assess for shock YES

INVESTIGATION
NO
Short or shallow respiration?
TREATMENT
Provide oxygen, low-stress/stress-free
environment
INVESTIGATION
Labored or obstructive breathing?

NO YES
INVESTIGATION Continue monitoring
Loud sounds?

YES NO
INVESTIGATION
Short/shallow
respiration?
Suspect upper airway disease YES NO

Dogs
Cats Dogs Consider pleural
space disease

INVESTIGATION INVESTIGATION Cats

Evaluate nose & larynx h  I f brachycephalic, suspect
h C onsider nasal tumor, elongated soft palate, stenotic
stenosis, polyp (young cat) nares, pharyngeal swelling,
h C onsider nasal CT scan, everted laryngeal saccules, INVESTIGATION INVESTIGATION
radiography, or rhinoscopy, laryngeal collapse h S creening ultrasonography Thoracentesis
including retroflexed view h I f older large breed, suspect if available h R emove all fluid; evaluate

h C onsider laryngeal mass laryngeal paralysis, mass lesions h C hest radiography for exudate, infection, FIP,
(eg, carcinoma, lymphoma, h C heck for foreign bodies h D iagnostic thoracentesis modified transudate, CHF,
granuloma) h C heck temperature neoplasia (lymphoma,
Bronchial infiltrates other),
chylothorax

INVESTIGATION
TREATMENT TREATMENT Bronchial infiltrates
h Airway disease
Emergent tracheostomy h H yperthermic: cool,

possible; sedation will supplemental oxygen, sedation h Ask about cough; rule out INVESTIGATION

affect airflow or intubation, glucocorticoids heartworm, lungworm Echocardiography
h Consider tracheal wash
for inflammation

h Consider palliative surgical
intervention
 MANAGEMENT TREE h CRITICAL CARE h PEER REVIEWED

 
 
 
 
DIFFERENTIAL DIFFERENTIAL
Pneumothorax Pulmonary contusion
h Open wound: stabilize and close wound, h S upportive care
consider thoracic exploration, place chest h S upplemental oxygen
tube at closure h F or isolated contusions, antibiotics DIFFERENTIAL
h Closed wound: thoracentesis as warranted not indicated Diaphragmatic hernia

h Recurrent pneumothorax, no negative h A void steroids, diuretics


h Prompt surgical correction, if


pressure, large volume: thoracostomy h I mprovement in 2-3 days
identified
(chest) tube h Ventilator (severe cases) h If unclear, repeat radiographs


h Referral and transport, if possible,
to confirm; look for blurring of

when severe diaphragm, intestines, or liver
in thorax
h Ultrasonography may help
INVESTIGATION

Chest radiography
DIFFERENTIAL
Rib fracture DIFFERENTIAL
h A nalgesics (local, systemic) warranted
Interstitial lung disease
h M ost treatments are nonsurgical
h Pulmonary fibrosis
h Flail chest with unstable fragment


h Early CHF
indicates

h Diffuse metastatic disease

h Older dogs

INVESTIGATION Dogs
Consider lower airway/ Chest radiography
parenchymal disease DIFFERENTIAL
B ronchial lung disease
h  C hronic/eosinophilic bronchitis

INVESTIGATION Cats
h  S
 creening
ultrasonography DIFFERENTIAL
h C hest radiography A lveolar lung disease
Mass lesion DIFFERENTIAL

h I f isolated, consider removal
Alveolar/interstitial
h  C HF
h B ronchial disease may look h Pneumonia

infiltrates

metastatic h Noncardiogenic edema
h C HF

M etastatic disease
h 
INVESTIGATION h Infectious disease
Diagnostic h Pneumoniaedema
thoracentesis
INVESTIGATION
h   racheal wash, culture, cytology
T
h B reath-activated inhaler

Air Exudate Modified transudate




h C T scans (referral) h P yothorax h Chylothorax INVESTIGATION

h S pontaneous h Neoplasia Echocardiography
h 

pneumothorax h Heart failure (right) Cytology, culture
h 

(exploratory) h Lung lobe torsion

h S ee Trauma
CHF = congestive
heart failure
FELINE RESPIRATORY DISTRESS TIPS
h Hypothermic cats often have heart disease. FIP = feline
CANINE RESPIRATORY DISTRESS TIPS

h History of cough is likely signal of airway disease, but infectious
h Loud murmur and weight loss often signal heart disease.
peritonitis

h Eosinophilic disease may be idiopathic or parasitic. not all cats with airway disease cough.

h Fever may be present with pneumonia. h Severe heart disease may exist with soft/absent T-FAST = thoracic-

focused

h Dorsal caudal infiltrates are commonly noncardiogenic. murmur; loud murmur may be innocent flow murmur.
assessment with

h Consider endemic fungal disease based on geographic h Isolated lung masses should not cause shortness of
sonogram for


location and travel. breath; if breathing labored, interstitial fibrosis possible. trauma
 MANAGEMENT TREE h CRITICAL CARE h PEER REVIEWED

 
 
 
 
STATUS EPILEPTICUS: EMERGENCY MANAGEMENT
Andrew Linklater, DVM, DACVECC
Lakeshore Veterinary Specialists
Glendale, Wisconsin

STATUS EPILEPTICUS*

TREATMENT
h D iazepam† (0.5-1 mg/kg IV)
h M idazolam (0.2-0.5 mg/kg IV, IM, or double-dose
†

PR, if client is administering); may repeat 3×

Seizure does not stop or recurs Some response Seizure stops

TREATMENT TREATMENT TREATMENT

Propofol infusion‡ at 2-8 mg/kg IV induction, then 0.1-0.6 CRI diazepam Begin long-term AED
mg/kg/min ± benzodiazepine CRI; phenobarbital load (0.5-1 mg/kg/h) or
midazolam (0.1-0.5 mg/kg/h
IV) and either phenobarbital
load (2-4 mg/kg IV q0.25-4h
[loading dose, 16-20 mg/kg
once total]), titrated to
effect (may have light
Seizure stops Seizure does inactivation and plastic
not stop or recurs adherence), or levetiracetam
30-60 mg/kg IV administered
over 5 to 15 minutes.

TREATMENT TREATMENT
Begin long-term AED Begin one of
the following: Seizure stops
h L evetiracetam (20-60
mg/kg IV)
h Isoflurane ‡

(0.5-2% for 1-6 hours)
h Dogs only: NaBr (IV, over TREATMENT

8 hours, diluted in sterile Begin long-term AED
water) or KBr divided PO
or PR (400-800 mg/kg)

Seizure stops

TREATMENT
AED = antiepileptic drug Begin long-term AED

CRI = constant rate infusion

* Airway, breathing, and circulatory disturbances should be treated first. Prolonged seizures may result

KBr = potassium bromide in cerebral edema, necessitating furosemide (1-2 mg/kg IV), 20% mannitol (0.5-1 g/kg, over 15-20 min IV),
and/or dexamethasone NaP (0.05-0.3 mg/kg IV). Underlying disease must be treated.
NaBr = sodium bromide †Patients on phenobarbital may require higher doses because of hepatic enzyme induction; blood AED levels

PR = per rectum should be collected. Patients on phenobarbital may receive a small load of 4 mg/kg IV.
‡Endotracheal intubation ± oxygen and ventilation is necessary.

DIAGNOSTIC/MANAGEMENT TREE h DENTISTRY h PEER REVIEWED

 
 
 
 
ACUTE FACIAL SWELLING & DENTAL DISEASE
Linda J. DeBowes, DVM, MS, DACVIM (SAIM), DAVDC

ACUTE FACIAL SWELLING

Swelling ventral & rostral to Swelling lateral to Unilateral periorbital swelling Reluctance and pain
medial canthus of eye bridge of nose upon opening mouth

Consider maxillary Consider maxillary Consider maxillary first

fourth premolar canine tooth and second molars

INVESTIGATION
Intraoral dental radiographs of suspected tooth/teeth

Periapical lucency of 1, 2, or 3 Periapical lucency of Periapical lucency of 1, 2, or 3

roots of maxillary fourth premolar canine tooth roots of first and/or second molar

DIAGNOSIS
Periapical abscess or granuloma
DENTAL WEAR: ATTRITION & ABRASION
Donald E. Beebe, DVM, DAVDC
Apex Dog & Cat Dentistry
Englewood, Colorado

TOOTH WEAR

No pulp exposure Pulp exposure

No radiographic evidence of endodontic pathology Radiographic evidence of TREATMENT TREATMENT

endodontic pathology Extraction h Root canal


h ± crown


placement

h C hronic gradual wear h E xtensive wear—structural weakness h R apid or acute wear
h V
 ery smooth surface h Smooth or rough surface h S mooth or rough surface
h R
 eparative dentin h ± reparative dentin h N o reparative dentin

TREATMENT TREATMENT TREATMENT TREATMENT

h P eriodic reassessment Extraction h Composite Dentin bonding agent


h ±follow-up restoration h ± odontoplasty to smooth
radiography every h ± crown any rough surfaces

6-12 months placement h ± composite restoration

Address or correct underlying source

DIFFERENTIAL DIFFERENTIAL DIFFERENTIAL DIFFERENTIAL

Orthodontic Chewing on excessively Abrasion (ie, external Dermatitis
malocclusion hard objects source of wear)

TREATMENT TREATMENT TREATMENT DIAGNOSIS

h Strategic extraction(s) h Eliminate access h Limit or eliminate source Investigate and treat



h Orthodontic movement h Substitute with soft chew item h Substitute with less dermatologic disorder



h Behavior modification abrasive item

TREATMENT
h Periodic reassessment

h Follow-up radiographs every 6-12 months

 DIAGNOSTIC/MANAGEMENT TREE h DENTISTRY h PEER REVIEWED

 
 
 
 
TOOTH WEAR TYPES FAST FACTS
h Abrasion is mechanical wear of teeth from external forces h Dental explorers have a sharp tip that helps determine


(eg, brushing, dental instruments), also defined as wear whether a worn surface is smooth from gradual wear or
from chewing on abrasive objects (eg, tennis balls, hair). rough from minor fractures; it can also probe for pulp
exposure. Its use is mostly reserved for anesthetized
h Attrition is gradual physiologic wear resulting from
patients; diligent caution should be used with

natural mastication.
nonanesthesized patients.
h Pathologic attrition is excessive wear caused by heavy
Reparative dentin is denser than regular dentin, lacks

h
chewing, biting, or grinding against other teeth

organized tubules, is produced during tooth wear, and
(eg, orthodontic malocclusion).
acts as a protective barrier. Pulp recedes behind the
deposited mineralized layer and remains shielded from
exposure.
h Intraoral radiographs are essential for evaluating

compromised teeth.
h Odontoplasty is the adjustment of tooth contours. Sharp

edges can be smoothed with hand or powered
instrumentation. Small surface defects can be restored
with dental composite.
h Signs of endodontic pathology may include wider-than-

normal pulp canals from odontoblast death and delayed
maturation, strictured or obliterated pulp canals from
accelerated calcification (can occur during pulpitis),
periapical radiolucency, or internal or external root
resorption.
 DIAGNOSTIC/MANAGEMENT TREE h DENTISTRY h PEER REVIEWED

 
 
 
 
DIAGNOSING ORAL ULCERATION IN DOGS & CATS
Jan Bellows, DVM, FAVD, DAVDC, DABVP
All Pets Dental
Weston, Florida

ORAL ULCERATION* OBSERVED

Acute (ie, abrupt onset, short duration [<3 weeks])

or chronic (ie, ≥3 weeks) presentation?

Acute Chronic

Obtain clinical history (eg, trauma, exposure to chemicals, radiation), See Chronic,
and conduct physical and oral examination and diagnostic tests next page
(eg, CBC, serum chemistry profile, cytology, histopathology)

Exogenous (ie, mechanical) or endogenous (ie, organic) cause?

Exogenous Endogenous

Conduct further diagnostic evaluation Conduct further diagnostic evaluation (eg, viral testing [eg, calicivirus in cats], biopsy)

DIAGNOSIS DIAGNOSIS DIAGNOSIS DIAGNOSIS DIAGNOSIS DIAGNOSIS

Traumatic ulceration Local irritation with Stomatitis Acute Calicivirus Erythema
h Thermal plaque sensitivity h Areas of marked necrotizing (in cats) multiforme


h Electrical (ie, contact mucositis inflammation and ulcerative

h Chemical with ulceration) ulceration, often gingivitis

h Mechanical located caudally (in dogs)

in cats
TREATMENT TREATMENT
h S upportive h E liminationof
TREATMENT care the primary/
See Chronic, next page h A ntibiotics to inciting cause
control h Treatment as
secondary recommended
infections

TREATMENT TREATMENT
h R emoval of offending cause h E xtraction of all teeth affected with
h M edical therapy via direct injection stage 3 or 4 periodontal disease
(eg, triamcinolone) into lesion h S trict daily plaque prevention at home
Continues h
h I f ulcer is still present after treatment and
removal of outside source, biopsy is indicated
*Oral ulceration is a full thickness breach of the epithelial continuity of the oromucosal surface, which may
extend into the tissues underlying the epithelium, including the submucosa, muscle, and/or periosteum.
 CHRONIC

Obtain clinical history (eg, trauma, exposure to chemicals, radiation), and conduct physical and oral
examination and diagnostic tests (eg, CBC, serum chemistry profile, cytology, histopathology)

Exogenous (ie, mechanical) or endogenous (ie, organic) cause?

Exogenous Endogenous

Conduct further diagnostic evaluation Conduct further diagnostic evaluation

DIAGNOSIS DIAGNOSIS DIAGNOSIS DIAGNOSIS

Persistent irritation from Local irritation with plaque Stomatitis Malignancy
malpositioned teeth sensitivity (ie, contact h Areas of marked inflamma- h In cats, poor prognosis if


mucositis with ulceration) tion and ulceration, often noted sublingually
located caudally in cats

TREATMENT TREATMENT TREATMENT TREATMENT

Elimination of tooth to mucosa Dental scaling and polishing, h E xtraction of multiple teeth, h S urgicalexcision, with ≥2
contact through crown followed by daily application followed by daily plaque cm clean margins
reduction and restoration or of wax gel after daily plaque control at home h D aily home care (eg, daily
extraction control h F ull-mouth extraction tooth brushing, application
h I f patient does not respond of wipes to control plaque
to treatment, administer and calculus accumulation)
pentoxifylline (dogs, 20 mg/
kg PO q12h [extra-label];
cats, 100 mg PO q12h
[extra-label]) with
doxycycline (5 mg/kg PO
q12h) and niacinamide
(dogs, 200-500 mg PO q12h;
cats, 125 mg PO q12h1)
h I f patient remains
unresponsive to treatment,
perform full-mouth
extractions

40 cliniciansbrief.com
 
 
 DIAGNOSTIC/MANAGEMENT TREE h DENTISTRY h PEER REVIEWED

 
 
 
 
References
DIAGNOSIS DIAGNOSIS DIAGNOSIS 1. Charlier C. Feline gingivostomatitis:

Uremia Eosinophilic granuloma h Pemphigus vulgaris what we know and how we treat it.

(due to marked azotemia) h Located under the lips, hard h Bullous pemphigoid Paper presented at: CVC East; 2015.


palate, or soft palate in cats http://www.dvm360storage.com/cvc/
h Commonly located in the proceedings/dc/Feline%20Medicine/

caudal oral cavity in dogs Charlier/Charlier,%20Cindy_Feline_
h Cats and certain dog breeds gingivostomatitis_STYLED.pdf. Accessed

TREATMENT (ie, Cavalier King Charles Perform biopsy December 1, 2018.
Treat underlying cause spaniels, Norwegian breeds) 2. Bonello D, Roy CG, Verstraete FJM. Non-
of uremia predisposed 2

neoplastic proliferative oral lesions. In:
Verstraete FJM, Lommer MJ, eds. Oral
and Maxillofacial Surgery in Dogs and
TREATMENT Cats. Elsevier Saunders; 2012:411-423.
h I mmunosuppressive
TREATMENT drugs (eg, prednisolone,
h C ats: flea control, azathioprine in dogs)
corticosteroids, laser
ablation/vaporization to
decrease bacterial load,
excision, immunosuppres-
sants (eg, cyclosporine)
h Dogs: laser ablation/

vaporization to decrease
bacterial load, antimicrobi-
als, corticosteroids,
immunosuppressants
(eg, cyclosporine)
h If poor response, biopsy is

indicated

cliniciansbrief.com 41
 
HALITOSIS
Jan Bellows, DVM, FAVD, DAVDC, DABVP
All Pets Dental
Weston, Florida

HALITOSIS OR ORAL MALODOR

History of No history of ingesting

coprophagy or foul-smelling substance or food
ingesting
foul-smelling
substance or food

INVESTIGATION INVESTIGATION
Extraoral assessment Intraoral assessment:
h R adiography

TREATMENT h P eriodontal probing depth and mobility

Cease coprophagy examination

h H alimeter measurement
or ingestion of
foul-smelling Check for lip fold
substance or food pyoderma

TREATMENT TREATMENT
Lip fold Clip hair, cleanse, Normal examination Abnormal oral examination
excision surgery apply steroid (normal probing
ointment daily depth: medium-sized
for 10 days, as dog, <2 mm;
needed cat, <1 mm)
Tooth mobility1

DIFFERENTIALS INVESTIGATION
h A utoimmune  etabolic assessment:
M
diseases of oral h C BC
cavity h S erum chemistry profile
h Eosinophilic h T hyroid evaluation
DIAGNOSIS DIAGNOSIS DIAGNOSIS
h U rinalysis
Stage 1 (M1): Stage 2 (M2): Stage 3 (M3):
granuloma complex
Mobility Mobility Mobility
increased over increased increased over
distance of over distance of distance of
>0.2-0.5 mm >0.5-1 mm >1 mm in any
direction
DIFFERENTIALS
TYPES OF HALITOSIS h D iabetes

CAUSED BY LOCAL h Uremia

h GI issues (eg, megaesoph-
AND METABOLIC CONDITIONS

agus, neoplasia, foreign
body)
TREATMENT TREATMENT
Remove Surgical
h Rare causes include small
h Fetor oris/fetor ex ore: offensive odor arising plaque/calculus extraction

intestinal bacterial

from sources in the mouth overgrowth, hepatic
disease, inflammatory
h Ozostomia: putrid smell detected in the mouth bowel disease

but derived from upper respiratory tract (eg,
nasal passages, sinus cavities, pharynx, larynx)
h Stomatodysodia: foul breath originating from

local areas in lower respiratory tract, particu-
larly below the carina from the bronchi, bron-
chioles and alveoli, or other contiguous parts of
VOHC = Veterinary Oral Health Council
the lung (eg, pleura)
 DIAGNOSTIC/MANAGEMENT TREE h DENTISTRY h PEER REVIEWED

 
 
 
 
Periodontal disease

DIAGNOSIS DIAGNOSIS DIAGNOSIS DIAGNOSIS

Stage 1: Stage 2: Stage 3: Stage 4:
h G ingivitis h < 25% probing depth or attachment loss h 2 5%-50% support loss h > 50% support loss
(measured from root apex to h F urcation involvement h F urcation exposure
cementoenamel junction) (F2; probe extends greater (F3; probe extends
h Furcation involvement (F1; probe extends than halfway under crown through-and-

less than halfway under crown of of multirooted tooth with through crown of
TREATMENT multirooted tooth with attachment loss) attachment loss) multirooted tooth)
Remove plaque/calculus

TREATMENT TREATMENT TREATMENT TREATMENT DIAGNOSIS

TREATMENT TREATMENT h R emove plaque Infrabony Suprabony pockets Surgical Oronasal
Home treatment: If home and calculus if pockets (extend (extend above crest extraction fistula
h Weekly dental treatment is not pocket apical to of alveolar bone):

hygiene chew an option, apply h Administer local alveolar crest): h Local antibiotics


h Twice daily plaque dental sealant antibiotics in h Mucogingival h Gingivectomy



control with wipes pocket or surgery h Apical reposition

h Surgical flap
or brushing pocket defects TREATMENT

h Weekly application extraction h Surgical extraction
Surgical


of plaque extraction
prevention gel to
help create a
barrier between
plaque and mucosa
h VOHC-accepted

products decrease
the accumulation PROGNOSIS
of plaque/tartar Frequent reexamination and prevention; encourage client use of VOHC-accepted products

Contact mucosal Normal-appearing periodontium

ulceration
(lesions
secondary to
mucosal
contact-bearing
irritant, allergen, DIAGNOSIS DIAGNOSIS DIAGNOSIS DIAGNOSIS DIAGNOSIS
antigen) h F oreign
h Petechiae Oral tumors causing Orthodontic body Cogenital cleft

h Chronic oral blood bleeding, tissue necrosis malocclusion h Trauma (eg, electric cord injury, palate defect

h Putrefaction causing food open jaw fracture, caustic

impaction agents damaging oral cavity)
TREATMENT
h Weekly oral hygiene INVESTIGATION

chew Fine-needle aspiration for
h Strict q12h plaque INVESTIGATION
Coagulation and cytopathology; tissue TREATMENT TREATMENT

control sample for histopathology
h Weekly application of platelet tests h Orthodontic Treat causes/signs

movement to

plaque prevention gel to
help create a barrier alleviate
between plaque and crowding
h Surgical
mucosa TREATMENT

h VOHC-accepted products extraction(s)
Surgery:

decrease the accumula- h Benign = 1 cm margins

tion of plaque/tartar h Malignant = 2 cm

or margins (all directions)
h Surgical extraction

DIAGNOSTIC/MANAGEMENT TREE h DENTISTRY h PEER REVIEWED

 
 
 
 
ORAL INFLAMMATION IN CATS
Judy Rochette, DVM, FAVD, DAVDC
West Coast Veterinary Dental Services
Vancouver, British Columbia

ORAL INFLAMMATION

INVESTIGATE
CBC, serum chemistry profile, FeLV/FIV testing

Juvenile Adult

DIAGNOSIS DIAGNOSIS DIAGNOSIS DIAGNOSIS DIAGNOSIS

Infected dental sac Eruption gingivitis FCGS h TR Systemic disease


h Periodontal disease


TREATMENT COHAT
h Operculectomy Unable to perform Able to perform
COHAT TREATMENT

h Antibiotics home care/plaque home care/plaque Treat underlying

control control disease

TREATMENT
h Plaque control TREATMENT

h Gingivectomy h Extractions


(as needed)
h Plaque control

TREATMENT TREATMENT TREATMENT
Extraction Extraction of Extraction of
of all teeth all teeth caudal compromised
to canines teeth
Resolution Persistence
TREATMENT
Interval
professional
care
Resolution Incomplete TREATMENT
TREATMENT Go to FCGS resolution Interval
Annual professional professional
care care

TREATMENT TREATMENT
Plaque control Extraction of
and annual any remaining
professional teeth
care (if any
teeth remain)

Incomplete
resolution

COHAT = comprehensive oral health

assessment and treatment
FCGS = feline chronic gingivostomatitis
TREATMENT
TR = tooth resorption h Feline ω-interferon

h Cyclosporine

h Supportive care/adjunct therapy

 DIAGNOSTIC/MANAGEMENT TREE h DENTISTRY h PEER REVIEWED

 
 
 
 
PERIODONTAL STAGING:
ASSOCIATED TREATMENT OPTIONS
Mark M. Smith, VMD, DACVS, DAVDC*
Virginia Tech

h N o attachment loss TREATMENT

STAGE 0 h Typical plaque and calculus accumulation
h A nnual professional teeth cleaning
• No prophylactic antimicrobial†
h No systemic antimicrobial

h Home care

h N o attachment loss TREATMENT
STAGE 1 h G ingivitis,plaque, and calculus accumulation
h A nnual professional teeth cleaning
• No prophylactic antimicrobial†
h No systemic antimicrobial

h Home care

h B eginning (<25%) attachment loss TREATMENT
STAGE 2 h P eriodontal pockets 3-5 mm
h A nnual professional teeth cleaning
h G ingivitis, plaque, and calculus accumulation • No prophylactic antimicrobial†
• Local doxycycline or clindamycin


gel in periodontal pockets ≥4 mm
h Systemic antimicrobial for 14 days

• Clindamycin
• Amoxicillin–clavulanic acid
h Home care

h M oderate (25%-50%) attachment loss TREATMENT
STAGE 3 h P eriodontal pockets 5-7 mm
h S emiannual professional teeth
h G ingivitis, plaque, and calculus accumulation cleaning
• No prophylactic antimicrobial†
h Systemic antimicrobial for 14 days

• Clindamycin
• Amoxicillin–clavulanic acid
h Local doxycycline or clindamycin gel

in pockets ≥4 mm
h Home care beginning 14 days

following treatment

h S evere (>50%) attachment loss TREATMENT

STAGE 4 h P eriodontal pockets >7 mm
h S emiannual professional teeth
h G ingivitis, plaque, and calculus accumulation cleaning
• No prophylactic antimicrobial†
h Systemic antimicrobial for 14 days

• Clindamycin
• Amoxicillin–clavulanic acid
h Open surgical debridement in

periodontal pockets ≥7 mm
h Local doxycycline or clindamycin gel

in periodontal pockets ≥4 mm
*Byline reflects author information on original publication. On publication of this or
h Root planing and apically

collection, the author’s current affiliation is the Center for Veterinary Dentistry

& Oral Surgery, Gaithersburg, Maryland. repositioned flap to eliminate pocket
†Preoperative IV antimicrobial therapy using a broad-spectrum bactericidal or
h Tooth extraction

agent (eg, sodium ampicillin) is recommended for use in high risk patients with

advanced periodontitis, immunosuppression secondary to metabolic disease,
h Home care beginning 14 days

primary immunopathies, artificial implants, or cardiac disease. following treatment
APPROACH TO TOOTH FRACTURE*
Kendall Taney, DVM, DAVDC, FAVD
Center for Veterinary Dentistry & Oral Surgery
Gaithersburg, Maryland

TOOTH FRACTURE

INVESTIGATION
Obtain thorough history:
h D uration of tooth injury
h D ifficulty eating, drinking, playing with toys
h A ssociation of injury with inappropriate object
chewing, trauma, cage biting
h Types of chew objects offered; instruct clients
on which chew objects to avoid (eg, bones,
antlers, cow hooves, hard plastic toys)

INVESTIGATION INVESTIGATION
Perform physical examination: Perform oral examination and assess with patient awake:
h G eneral attitude h Facial symmetry
h Facial pain and swelling h O cclusion
h P alpebral reflex h S oft tissue (ie, gingiva, oral mucosa, sublingual mucosa)
h P atency of nares h P resence of deciduous, permanent, or mixed dentition
h R egional lymph node palpation h I ntrinsic teeth staining
h A uscultation of heart and lungs h Type of tooth fracture (ie, uncomplicated, complicated)

Perform with patient anesthetized:

h P eriodontal probing, charting
h F ull-mouth intraoral radiography
h A ssessment and confirmation of clinically missing teeth
h R adiographic evaluation of intrinsically stained teeth to determine vitality

Suggested Reading
[Articles and step-by-step editions.] J Vet Dent. jov.sagepub.com.
AVDC Nomenclature Committee. Recommendations adopted by the AVDC board. American Veterinary
Dental College website. http:// www.avdc.org/nomenclature3.html#toothfracture. Published October
2009. Accessed November 21, 2016.
Girard N, Southerden P, Hennet P. Root canal treatment in dogs and cats. J Vet Dent. 2006;23(3):148-160.
Luotenen N, Kuntsi-Vaattovaara H, Sarkiala-Kessel E, Junnila JJ, Laitinen-Vapaavuori O, Verstraete FJ.
Vital pulp therapy in dogs: 190 cases (2001-2011). J Am Vet Med Assoc. 2014;244(4):449-459.

*Originally published as “Tooth Fracture in a Pediatric Patient”

 MANAGEMENT TREE h DENTISTRY h PEER REVIEWED

 
 
 
 
DIAGNOSIS
Uncomplicated crown fracture (no pulp exposure)

Permanent tooth Deciduous tooth

TREATMENT TREATMENT
h  ule out root fracture and document pulpal width on radiographs
R h  valuate root and developing permanent
E
• Perform and/or repeat dental radiography in 6-12 months to evaluate tooth tooth buds on radiographs

vitality by confirming decreasing pulp chamber width and/or root development h No treatment necessary if no evidence


h C ontour acute sharp fractures; seal with bonding agent and/or unfilled resin of disease is present
• Take care to avoid thermal injuries to the pulp during tooth preparation,

especially after an acute injury

DIAGNOSIS
Complicated crown fracture

Permanent tooth Deciduous tooth

INVESTIGATION TREATMENT
h  ssess amount of functional crown remaining
A h  xtraction is recommended to avoid periapical infection that could
E
h A ssess whether periodontal tissue is normal affect unerupted developing permanent tooth buds
h Development
 of a mucoperiosteal flap allows for suffic ient
h D etermine via radiography whether apex is open or closed
visualization to avoid potential damage to permanent tooth buds and
careful extraction of the entire tooth root

Severely damaged Minimal functional crown Open apex Closed apex

periodontal tissue and/or root fracture present

TREATMENT TREATMENT
Fracture occurred: Fracture occurred:
TREATMENT h ≤ 48 hours prior h ≤ 48 hours prior

Extraction • Vital pulp therapy † with yearly • If patient is <18 months of age,


radiographic monitoring vital pulp therapy † with
• Extraction yearly radiographic monitoring

h > 48 hours prior • If patient is >18 months of age,

• Apexification (ie, forced closure standard root canal therapy †

†
Endodontic training required to perform procedures
of the apex) followed by standard • Extraction


successfully. Refer to the American Veterinary Dental College root canal therapy † h >48 hours prior

(avdc.org) for local specialists. • Extraction • Standard root canal therapy †


• Extraction

CANINE PRURITIC DERMATITIS
Rosanna Marsella, DVM, DACVD
University of Florida

MIDDLE-AGED OR OLDER DOG YOUNG DOG (1–3 YEARS)

History of skin disease? YES Seasonal?

NO
NO YES

DIFFERENTIAL
h Parasitic (eg, Demodex spp) DIFFERENTIAL DIFFERENTIAL

h Allergic (eg, food,* contact) h Parasitic/infectious (eg, flea/tick, contagious mite, Demodex spp) h Allergic (eg, atopy,

Metabolic/autoimmune/


h
h Infectious (eg, dermatophytosis, bacteria/yeast overgrowth) flea, contact [eg,

endocrine (± infection)

h Allergic plants])
Neoplastic (eg, cutaneous

h
• Food, environmental, flea

epitheliotropic lymphoma) • Indoor contact allergy (eg, carpets)

INVESTIGATE INVESTIGATE
h Deep skin scrapings h Skin scrapings

h Cytology ± culture

h Cytology ± culture

h CBC, serum

h Aggressive flea control (if fleas are endemic)

chemistry profile, UA

h Fungal culture via dermatophyte test medium ± trichogram
h Biopsy

h Food trial (if not seasonal), hydrolyzed ± novel protein source when appropriate


h Confine to indoors

Sarcoptes spp Sarcoptes spp Demodex spp Demodex spp Bacteria/yeast
positive negative positive negative on cytology

TREATMENT TREATMENT TREATMENT TREATMENT TREATMENT

Treat patient and all Therapeutic trial Treat patient and all Consider biopsy for Treat skin infection;
in contact (if severe pruritus) in contact shar-peis or suspected consider culture if long
deep pyoderma or history of antibiotic
fibrotic lesions use or poor response

Food trial successful Complete improvement Improvement or resolution

(ie, improvement/resolution in with aggressive with 10-day indoor
8-12 weeks1) flea control confinement

ID = intradermal
SL = sublingual DIAGNOSIS DIAGNOSIS DIAGNOSIS
Rechallenge to confirm food allergy Flea allergy Rechallenge (indoor/outdoor)
UA = urinalysis to confirm contact allergy
 DIAGNOSTIC/MANAGEMENT TREE h DERMATOLOGY h PEER REVIEWED

 
 
 
 
No resolution after secondary infection treatment
(when appropriate) and diagnostic trials

DIAGNOSIS DIAGNOSIS INVESTIGATE

Atopic-like dermatitis (no Atopic dermatitis, usually triggered Consider testing at
allergen-specific IgE) by environmental allergies another time of year

TREATMENT TREATMENT
Symptomatic approach Causative and symptomatic
for older patients or short approach for younger patients
allergy season or long allergy season

Reference
1. Rosser EJ Jr. Diagnosis of food

allergy in dogs. J Am Vet Med Assoc.
1993;203(2):259-262.
TREATMENT TREATMENT
h Glucocorticoids (topical or Allergy test to prepare allergy vaccine (SL/SC)
Suggested Reading

systemic)
h Cyclosporine (if glucocorticoid Jackson H, Marsella R, eds. BSAVA

contraindicated/for long-term Manual of Canine and Feline
symptomatic relief) Dermatology. 3rd ed. Quedgeley,
h Frequent topical therapy Gloucester: BSAVA; 2012.

• Remove allergen Marsella R, Sousa CA, Gonzales AJ,
• Decrease pruritus INVESTIGATE INVESTIGATE Fadok VA. Current understanding
• Improve skin barrier ID skin test Serology of the pathophysiologic

h Requires h Continuation of
• Interleukin-31 inhibitors mechanisms of canine atopic


• Pentoxifylline (adjunctive) discontinuation of symptomatic treatment dermatitis. J Am Vet Med Assoc.
• Essential fatty acids and symptomatic treatment permitted 2012;241(2):194-207.
h Requires resolution of h Does not require

antihistamines (adjunctive)


h Oclacitinib for dogs older than infection resolution of infection
h Immediate results h Results available in days

1 year *Unlike food allergies, environmental


h More specific than h Less specific than ID
h Lokivetmab for younger dogs or

and flea allergies do not commonly


serology skin test

dogs with history of demodex develop later in life; therefore,
or neoplasia; also to be used environmental and flea allergies are
proactively to prevent flares or unlikely in middle-aged dogs unless
decrease their severity the patient has a history of geographic
movemement or environmental
change.
DIAGNOSING NASAL PLANUM DISEASE IN DOGS
Darren Berger, DVM, DACVD
Iowa State University

NASAL PLANUM DISEASE EVIDENT

Clinical signs of inflammation (eg, erythema, swelling, crusting,

erosion, ulceration, loss of normal cobblestone-like architecture)?

NO

Excessive keratin formation?

YES NO

Is the patient a Labrador retriever? Nasal planum depigmented?

YES NO YES NO

DIFFERENTIAL DIFFERENTIAL Changes to nasal planum architecture? Reevaluate patient for other
Hereditary nasal parakeratosis Idiopathic nasodigital clinical signs of inflammation
of Labrador retrievers hyperkeratosis*

YES NO
TREATMENT
Soften and/or remove keratin with
petroleum jelly or a natural skin-
restorative balm Reevaluate patient for inflammatory Other areas of leukoderma or
h For fissuring, topical therapy with disease of nasal planum leukotrichia present?

topical antibiotic/steroid

YES NO

DIFFERENTIAL DIFFERENTIAL
Vitiligo Idiopathic nasal depigmentation
*Labrador retrievers may also be affected by this (eg, snow nose, Dudley nose)

condition. For a discussion of differences in
presentation, see Suggested Reading, page 55.
TREATMENT
h Biopsy, if needed to confirm TREATMENT

h No treatment required No treatment required

 DIAGNOSTIC TREE h DERMATOLOGY h PEER REVIEWED

 
 
 
 
YES

Perform cytology

Etiologic agents observed?

YES NO

Proceed to Biopsy for nasal

Fungal Bacterial planum disease, next page

TREATMENT
DIFFERENTIAL DIFFERENTIAL Treat with systemic first-tier antibiotic (eg, cephalexin,
Deep or systemic mycotic infection Dermatophytosis clindamycin, amoxicillin–clavulanic acid) for at least 3
(eg, blastomycosis, cryptococcosis) weeks, with follow-up before end of treatment course

TREATMENT TREATMENT Clinical signs resolved?

Treat per disease-specific guidelines h Culture to verify

causative species
h Treat per published

consensus guidelines
YES NO Repeat cytology
Proceed to Biopsy for nasal
planum disease, next page

DIFFERENTIAL Bacteria still present?

Mucocutaneous pyoderma
NO YES

TREATMENT YES NO
h Perform bacterial culture and susceptibility testing

• Culture swabs usually sufficient
Clinical signs • Cytology results should correspond to culture results
resolved? h Treat for at least 3 weeks with appropriate antimicrobial

based on susceptibility or with topical antiseptic Proceed to Biopsy for nasal
planum disease, next page

Continues h
 BIOPSY FOR NASAL PLANUM DISEASE

Clinical signs or diagnostic test results consistent with uveitis?

YES NO

DIFFERENTIAL Focal, well-demarcated linear or circular

Uveodermatologic syndrome ulceration of the nasal philtrum?

TREATMENT YES NO
Systemic and topical therapy to
prevent ocular complications

DIFFERENTIAL Biopsy the nasal

Dermal arteritis of the planum
nasal philtrum

TREATMENT
Systemic immunosuppressive
medications and/or topical
steroids or tacrolimus

DIFFERENTIAL DIFFERENTIAL DIFFERENTIAL DIFFERENTIAL Biopsy report

Pemphigus foliaceus or vulgaris Subepidermal bullous Epitheliotropic Cutaneous histiocytosis reveals
disease (ie, mucous membrane lymphoma lymphocytic-
pemphigoid) to-plasmacytic
interface
dermatitis with
basal cell
apoptosis and
TREATMENT TREATMENT TREATMENT TREATMENT pigmentary
h Systemic immunosuppressive Systemic immunosuppressive h Chemotherapy h Immunosuppressive incontinence



therapy therapy with lomustine therapy
h Topical therapy may be h Possible h Consider further



beneficial in reducing overall radiation diagnostic tests to
systemic dosing if disease is therapy ensure patient does
confined to nasal planum not have systemic
histiocytosis
 DIAGNOSTIC TREE h DERMATOLOGY h PEER REVIEWED

 
 
 
 
Repeat cytology

Bacteria still present?

YES NO

DIFFERENTIAL Presence of protozoal amastigotes; patient travel history to

Mucocutaneous pyoderma or from southern Europe, Middle East, northern Africa,
Asia, or Central or South America; or patient from a region
of Texas where leishmaniasis is endemic?

TREATMENT
h Perform bacterial culture and

susceptibility testing
• Culture swabs usually sufficient YES NO

• Cytology results should correspond to

culture results
h Treat for at least 3 weeks with

appropriate antimicrobial based on Screen patient for leishmaniasis Patient showing systemic clinical signs of fever,
susceptibility polyarthritis, lymphadenopathy, renal disease,
blood dyscrasias, myopathy, or neuropathy?

YES NO

DIFFERENTIAL DIFFERENTIAL
Systemic lupus erythematosus Discoid lupus erythematosus
Suggested Reading
Miller WH, Griffin CE, Campbell KL. Muller and Kirk’s Small Animal
Dermatology. 7th ed. St. Louis, MO: Elsevier Mosby; 2013.
Perform further diagnostic TREATMENT
UV = ultraviolet tests to confirm h Systemic and/or topical

immunomodulatory therapy
h UV protection/avoidance

PERIORAL DERMATITIS IN DOGS
Jennifer Schissler Pendergraft, DVM, MS, DACVD*
Colorado State University

PERIORAL DERMATITIS

INVESTIGATION
Deep skin scrape or pluck

INVESTIGATION
Demodex spp present? NO

YES

INVESTIGATION
Demodex spp in >5 locations, body region, or feet?

YES NO

DIAGNOSIS DIAGNOSIS
Generalized demodicosis Focal demodicosis

INVESTIGATION INVESTIGATION
Bacteria or yeast >3/HPF on cytology? Bacteria or yeast >3/HPF on cytology?

YES NO YES NO

TREATMENT TREATMENT TREATMENT

Treat demodicosis, secondary infection Treat demodicosis No treatment

TREATMENT
TREATMENT h C ontinue to treat generalized demodicosis until 2
Topical therapy plus oral YES negative scrapes/plucks
antimicrobial therapy for: h Treat infection as needed until demodicosis resolution

h M ultifocal infection
h E rosions/ulcers Resolution of infection
h Crusts after 3 weeks of treatment?
h D epigmentation

TREATMENT
NO h B acterial
infection: culture and susceptibility testing,
then treat accordingly for 21 days
*Byline reflects author information on original publication. On publication of this h Malassezia spp infection: change empirical therapy

collection, the author’s current information is Jennifer Schissler, DVM, DACVD.
 DIAGNOSTIC/MANAGEMENT TREE h DERMATOLOGY h PEER REVIEWED

 
 
 
 
INVESTIGATION
Vesicles or bullae present?

YES NO

DIFFERENTIALS INVESTIGATION
h E pidermolysis bullosa Severe dental disease?
acquisita
h B
 ullous pemphigoid
h M
 ucous membrane NO YES
pemphigoid
h P  emphigus vulgaris

INVESTIGATION TREATMENT
Bacteria or yeast >3/HPF on cytology? Treat as needed, assess response
INVESTIGATION
Biopsy to confirm YES NO

TREATMENT TREATMENT NO INVESTIGATION

Immunomodulation Topical therapy plus oral Pruritus ± erythema only?
antimicrobial therapy for:
h M ultifocal infection
h E rosions/ulcers NO YES
h Crusts DIAGNOSIS
h D epigmentation Redundant lip
fold with
complete clinical
resolution? DIAGNOSIS DIFFERENTIALS
Redundant lip fold h F ood allergy
with moist h A topy
dermatitis (no
INVESTIGATION crusts, ulcers, or
Cytologic resolution of depigmentation)?
infection after 3 weeks
of treatment?
NO YES YES YES NO TREATMENT
h 8 -12 week diet
trial
h I f response, food
allergy
DIAGNOSIS TREATMENT TREATMENT Lesions remain h I f no response,
h B acterial infection: Topical drying h Topical drying agent despite lack of atopic dermatitis
culture susceptibility and antimicrobial for management infection, or
testing, then treat agents for h If no response, resolution of

accordingly for 21 maintenance consider cheiloplasty infection
days
h Malassezia spp

infection: change
empirical therapy
DIFFERENTIALS
h U veodermatologic syndrome
h P emphigus foliaceus and erythematosus
DIAGNOSIS h Epidermolysis bullosa acquisita, bullous

Biopsy and treat pemphigoid, mucous membrane pemphigoid
as needed h Juvenile cellulitis

h Cutaneous epitheliotropic lymphoma

h Zinc-responsive dermatosis

h Superficial necrolytic dermatitis

PSEUDOMONAS AERUGINOSA OTITIS EXTERNA & MEDIA
Susan Paterson, VetMB, MA, DVD, DECVD, MRCVS
Virtual Vet Derms
Kendal, United Kingdom

This article is an updated version of a previously published article from January 2016.

OTITIS

INVESTIGATION
Cytology

Bacilli identified on cytology with modified Wright’s stain

INVESTIGATION
Suspected P aeruginosa infection

Investigate primary (eg, allergy, endocrine disease, ectoparasites), Mild disease or first Severe or recurrent
predisposing (eg, conformation, swimming), and perpetuating (eg, presentation disease
otitis media, chronic change to ear anatomy) factors

TREATMENT
Culture, flush, and begin first-line antimicrobial therapy pending culture and susceptibility results

INVESTIGATION TREATMENT
Recheck in 10 days; conduct cytology Flush ear with tris-EDTA to
and culture and susceptibility testing INVESTIGATION evaluate eardrum integrity
Eardrum ruptured?
h If integrity unclear, assume ruptured

NO YES

TREATMENT INVESTIGATION TREATMENT

Tris-EDTA + chlorhexidine (<0.2%) flush in Recheck in 10 days; conduct Tris-EDTA flush in combination with topical*
combination with topical* ear drops for 10 days cytology and culture and antibacterial agents for 10 days pending
pending culture and susceptibility results. susceptibility testing culture and susceptibility results. Use
Use first-line topical licensed ear drops extra-label aqueous solution of first-line
containing aminoglycosides (eg, gentamicin) antimicrobial (eg, gentamicin) before
or topical compounded silver sulfadiazine second-line topical fluoroquinolones
before second-line topical fluoroquinolones
INVESTIGATION
Other bacilli (eg, E coli) cultured

Treat based on culture and susceptibility results

12 cliniciansbrief.com October 2019

 
 
 MANAGEMENT TREE h DERMATOLOGY h PEER REVIEWED

 
 
 
 
INVESTIGATION
Culture, flush, and begin first-line antimicrobial
therapy pending culture and susceptibility results.
Consider anti-inflammatory steroids if severe
inflammation or stenosis is present

TREATMENT
Flush ear with tris-EDTA to evaluate eardrum integrity. Consider
flushing with patient under anesthesia for more effective removal
of infectious material and better examination of the ear canal

INVESTIGATION
Eardrum ruptured?
h If integrity unclear, assume ruptured

NO YES

INTERMEDIATE TREATMENT
Flush to disrupt potential bacterial biofilm
(eg, N-acetylcysteine with tris-EDTA) before topical
antimicrobial application

TREATMENT TREATMENT
If eardrum is not ruptured, flush with tris-EDTA + If eardrum is ruptured, flush with tris-EDTA in
chlorhexidine (<0.2%) in combination with topical ear combination with topical antibacterial agent for 10
drops for 10 days pending culture and susceptibility days pending culture and susceptibility results. Use
results. Use first-line topical licensed ear drops containing extra-label aqueous solution of first-line antimicrobial
aminoglycosides (eg, gentamicin) or topical compounded (eg, gentamicin) before second-line fluoroquinolones
silver sulfadiazine before second-line fluoroquinolones

INVESTIGATION EDTA = ethylenediaminetetraacetic acid

Recheck in 10 days; conduct cytology and culture
and susceptibility testing (see next page)
*Many topical drugs are ototoxic to the

middle ear.

October 2019 cliniciansbrief.com 13

 
 
MANAGEMENT TREE h DERMATOLOGY h PEER REVIEWED

 
 
 
 
INVESTIGATION
Recheck in 10 days; conduct cytology and culture and susceptibility testing

INVESTIGATION INVESTIGATION
h P aeruginosa cultured Other bacilli (eg, E coli) cultured

h Reassess with cytology

Treat based on culture and
susceptibility results
Improving (eg, reduced Not improving
organisms, reduced (ie, no change on cytology)
inflammatory infiltrate)

Switch antibacterial agent

TREATMENT based on culture and
Continue with combination of susceptibility results, using tiered
flushes and topical antibacterial prioritization of drugs
agent until negative cytology

Use tiered topical antibacterial agents as

INVESTIGATION labeled or extra-label as needed:
h Tier 1: aminoglycosides (gentamicin, neo-
Investigate primary, predisposing,

and perpetuating factors to try to mycin), compounded silver sulfadiazine
h Tier 2: fluoroquinolones, polymyxin
prevent recurrence

h Tier 3: compounded ticarcillin, amikacin,

tobramycin, ceftazidime, piperacillin

Recheck in
10 days with cytology

Not improving
(ie, no change on cytology)
Suggested Reading
Buckley LM, McEwan NA, Nuttall T.
Tris-EDTA significantly enhances
antibiotic efficacy against
multidrug-resistant Pseudomonas
Chronic irreversible change aeroginosa in vitro. Vet Dermatol.
may be present in ear canal or 2013;24(5):519-e122.
tympanic bulla; patient may be a Nuttall T, Cole LK. Evidence-based vet-
candidate for advanced imaging erinary dermatology: a systematic
and possible total ear canal review of interventions for treat-
ablation and bulla osteotomy ment of Pseudomonas otitis in dogs.
Vet Dermatol. 2007;18(2):69-77.

14 cliniciansbrief.com October 2019

 
 
REFRACTORY DERMATOPHYTOSIS:
5 KEY EVALUATIONS WHEN TREATMENT FAILS
Ann M. Trimmer, DVM, DACVD
Animal Allergy and Dermatology Specialists
Las Vegas, Nevada

DERMATOPHYTOSIS IDENTIFIED

Refractory to treatment

Was treatment duration adequate? Was a proper treatment

h Were 2 negative cultures achieved protocol followed?

1 week apart?

NO YES
NO YES

TREATMENT
Reinstitute therapy Evaluate possible Evaluate possible TREATMENT
failure points of failure points of Institute combination therapy
systemic therapy topical therapy if not previously used

TREATMENT Lack of Proper dilution TREATMENT

h Compliance in compliance of lime If long-haired patient,
sulfur dip

administration of or low consider shaving or
medication application clipping coat
• Evaluate frequency frequency

• Evaluate ease of

administration (eg,
solution vs tablets)
h Medication

intolerance TREATMENT
• V omiting and/or If unable to
diarrhea can lead use lime sulfur
to poor absorption dip or bathing,
– If present, change try medicated

oral medication wipes, sprays,
h Compounded or mousses

medication daily
• Azoles difficult to

compound
• Avoid compounded

formulations
 DIAGNOSTIC/MANAGEMENT TREE h DERMATOLOGY h PEER REVIEWED

 
 
 
 
Was environmental Is there underlying illness or Was the original
decontamination adequate? environmental stress? diagnosis correct?

NO YES YES NO NO YES

TREATMENT Evaluate in Evaluate h Concurrent INVESTIGATION INVESTIGATION


Consider contact disinfectant immunosuppression h Repeat culture with Restart evaluation
animals for (eg, from medications,

confinement if species and examination
not previously possible endocrinopathies, identification
done subclinical neoplasia) h Perform biopsy
infections or Behavioral or

h
with PAS or silver

carrier state household stressors stains to screen for
fungal organisms

INVESTIGATION
h Reassess type of

disinfectant used
• Debris should be

removed before
disinfecting
• Ensure surface type

is compatible with
disinfectant used SUGGESTED READING
h Evaluate whether Moriello K. Feline dermatophytosis: environmental

there are unad- decontamination—it’s not as hard as we thought.
dressed fomites (eg, In: Proceedings of the North American Veterinary
in brushes, toys, cat Dermatology Forum; 2014b; Phoenix, AZ.
trees, furniture; from Moriello K. Feline dermatophytosis: treatment—getting
human interactions) to “cured” with less smell and mess. In: Proceedings
h Ensure disinfectant of the North American Veterinary Dermatology Forum;

is properly diluted 2014a; Phoenix, AZ.
h Determine whether

contact time was
adequate
PAS = periodic acid-Schiff
SUSPECTED CUTANEOUS DRUG REACTION
Alison Diesel, DVM, DACVD
Texas A&M University

CUTANEOUS ADVERSE DRUG REACTION

Probable Possible

INVESTIGATION
h O btain complete medical history
Is reaction life-threatening (eg, Stevens–Johnson Is patient receiving multiple therapeutics and conduct physical
syndrome, toxic epidermal necrolysis)? (eg, drugs, supplements, nutraceuticals)? examination
h O btain complete list of
medications (including
supplements and nutraceuticals)
currently being administered
• Include duration and any recent


dosage changes
YES NO YES NO h O btain thorough drug exposure
history
h D etermine any past suspected or
confirmed adverse reactions
h D etermine any acute or chronic
TREATMENT Is patient receiving TREATMENT diseases or comorbid conditions
Discontinue all medications Withdraw h D etermine toxin exposure
medications and refer necessary for offending agent
case for intensive care survival?
support

Clinical signs
resolved? NO
YES NO

YES
TREATMENT TREATMENT
h C ontinue Withdraw all
essential medications and
medications supplements DIAGNOSIS
h D iscontinue, 1 Probable
at a time, single adverse drug
medications reaction
most likely to
cause adverse Clinical signs
drug reaction resolved?
(eg, antibiotics,
NSAIDs)* TREATMENT
h A void offending agent for duration of patient’s life
h I f possible, identify and avoid drugs with similar
structure and/or same drug class (eg, NSAIDs,
NO YES cephalosporins, other β-lactam antibiotics)
h R eport adverse reactions to FDA ‡
h I f patient had been receiving multiple
medications, reintroduce, 1 at a time, those least
likely to cause adverse reactions
h Monitor closely for return of clinical signs

 MANAGEMENT TREE h DERMATOLOGY h PEER REVIEWED

 
 
 
 
Is adverse reaction strictly dermatologic?

YES NO

Is reaction a type 1 hypersensitivity INVESTIGATION

(eg, urticaria, angioedema, pruritus)? h A dditional diagnostic evaluation (eg, CBC, serum chemistry profile,
urinalysis) according to observed clinical signs recommended
h Perform careful examination of eyes, mucocutaneous junctions,

joints
• Monitor for erosions and ulcers and evidence of joint pain, which

may be indicative of a more systemic immune-mediated reaction
YES NO

TREATMENT
TREATMENT INVESTIGATION h P rovidesupportive care (eg, fluids, oncotic support,
h A dminister antihistamines h B iopsy skin to assess disease hepatoprotectants) as needed for clinical signs observed
(H1 ± H 2)† patterns (eg, pemphigus foliaceus, h C onsider referral to internal medicine specialist
h ± administer anti-inflammatory erythema multiforme, vasculitis,
corticosteroids if indicated due toxic epidermal necrolysis)
to severity of reaction†

TREATMENT AUTHOR INSIGHT

Clinical signs h Immunosuppressant therapy (eg,

resolved? corticosteroids, cyclosporine) may be Adverse drug reactions can be highly variable:
warranted
h Consider consultation with or referral h May be idiosyncratic or dose dependent

to veterinary dermatologist

h  ay occur at any time during treatment, even if
M
YES NO patient has tolerated the medication in the past
Clinical signs h Clinical appearance from one animal to

resolved?
another can be highly variable.

Although several classes of medication (eg,

antibiotics, NSAIDs, parasiticides) have been
YES NO reported to commonly cause adverse drug
reactions, any medication (including
supplements) has the potential to do so.1

TREATMENT Pursue consultation

Slowly taper with or referral to Reference
immunosuppressant treatment veterinary dermatologist 1. Voie KL, Campbell KL, Lavergne SN. Drug hypersensitivity

reactions targeting the skin in dogs and cats. J Vet Intern
Med. 2012;26(4): 863-874.
*If clinical signs of adverse drug reaction are life-threatening, withdraw all drugs.

†If initial treatment attempt was ineffective, use different medications than were previously used.
‡1-888-FDA-VETS
SUSPECTED FOOD ALLERGY IN DOGS
Elizabeth R. Drake, DVM, DACVD
University of Tennessee

SUSPECTED FOOD ALLERGY

(CUTANEOUS ADVERSE REACTION TO FOOD)

Is the patient pruritic?

NO YES

Recurrent skin or ear infections? GI signs?


h Regurgitation/vomiting/nausea


h Diarrhea

h ≥3 bowel movements per day

NO YES

NO YES
DIAGNOSIS
Not allergic

DIFFERENTIAL DIFFERENTIAL DIFFERENTIAL DIFFERENTIAL

Sarcoptic mange Flea allergy dermatitis Atopic dermatitis Food allergy
h Lesion distribution h Seasonal pruritus or h Nonseasonal pruritus



caudodorsal nonseasonal pruritus h Recurrent secondary

with seasonal flare skin infections (eg,
otitis externa/
pyoderma)

TREATMENT TREATMENT DIAGNOSIS TREATMENT

h S elamectin (FDA h Topical parasite Diagnosis of exclusion Treat and resolve
approved) preventive secondary infection
h M oxidectin, h A ntipruritic
imidacloprid (FDA treatment
approved) h Treat secondary
h L ime sulfur dip (FDA pyoderma
approved)
h I soxazolines
(extra-label)

22 cliniciansbrief.com June 2021

 
 
 DIAGNOSTIC TREE h DERMATOLOGY/NUTRITION h PEER REVIEWED

 
 
 
 
INVESTIGATION
Choose which elimination diet trial (eg, hydrolyzed, novel protein, home-cooked) will be given
h Diet should be readily available and easy to obtain (to minimize trial interruptions)

h Diet should be palatable

h Diagnosis can be made with any of these diet types, providing all potential variables (eg, no

flavored medications, prevent ingestion of other animals’ feces) are addressed
h Subsequent diet trial with a different type of diet may be needed if the first trial fails but food

allergy remains a top differential diagnosis
h Diet should also be based on life stage (eg, growth formula for young dogs)

h Treat options

• Vegetables (choose only one)

TREATMENT
Topical heartworm/intestinal helminth/flea/tick preventive

Pruritus/clinical signs improved ≥50% after 4 weeks?

NO YES

Continue diet trial Diet challenge with prior diet

Follow up after 4 weeks Patient pruritic?

Pruritus/clinical signs improved ≥50%?

NO YES

NO YES DIAGNOSIS
Cutaneous adverse food
reaction
h C onsider which individual
ingredient to challenge
Continue diet trial DIAGNOSIS
Cutaneous adverse food
reaction
h C onsider which individual
ingredient to challenge
DIAGNOSIS
After 12 weeks, not food allergy/
cutaneous adverse food reaction
OR
Diet trial is not valid
h I dentify reason for
lack of improvement

June 2021 cliniciansbrief.com 23

 
 
VEHICULAR TRAUMA
Cassandra Gilday, DVM
Adesola Odunayo, DVM, MS, DACVECC
University of Tennessee

PATIENT EXPERIENCES VEHICULAR TRAUMA

INVESTIGATION
h Perform a rapid evaluation of cardiovascular, respiratory, and CNS systems

h Place IV catheter as soon as possible

h Perform initial diagnostics (ie, PCV, TP, lactate, blood gas, electrolytes, SpO2 , ECG1,2)

Patient breathing?
NO YES

INVESTIGATION Signs of respiratory distress

Airway clear? (eg, tachypnea, cyanosis,
NO increased respiratory effort)? YES

Signs of shock? Consider pulmonary

YES NO contusions and
pleural space
disease
YES NO
TREATMENT TREATMENT
h Begin CPR h Clear the airway


h Provide (possibly blood/ See Signs of shock, Arrhythmias? TREATMENT

intubation, hematoma) page 24 Initiate basic
oxygen, and h Begin CPR respiratory support

positive pressure h Provide intubation, h Oxygen, sedation,


ventilation1 oxygen, and analgesia (see
positive pressure Analgesia in
ventilation1 Trauma, page 29)
YES NO h ± intubation and

positive pressure
ventilation

INVESTIGATION Signs of brain and/or

ECG spinal injury?

VPCs, ventricular tachycardia

YES NO

TREATMENT
h Lidocaine, oxygen, MgCl, See Brain See
and/or Stabilized

analgesia for sustained
ventricular tachycardia1,3 spinal patient,
(Table 1, page 29) injury, page 25
h Single VPCs do not need to page 24

be treated in most cases

22 cliniciansbrief.com March 2021

 
 
 DIAGNOSTIC/MANAGEMENT TREE h EMERGENCY MEDICINE & CRITICAL CARE h PEER REVIEWED

 
 
 
 
INVESTIGATION
h Characterize breathing pattern (rapid and shallow, inspiratory stridor vs paradoxical breathing)

h Thoracic auscultation

h POCUS1,2

RESULTS RESULTS RESULTS RESULTS
h Mixed breathing pattern h Restrictive (ie, rapid, shallow) breathing h Restrictive (ie, rapid, h Restrictive (ie, rapid, shallow)




h ± crackles, ± moist lung pattern shallow) breathing breathing pattern

sounds h Absent/decreased lung sounds (dorsal) pattern h Decreased lung/heart sounds


h ± B-lines/comet trails h Absent glide sign h Absent/decreased lung (ventral), thoracic borborygmi



and heart sounds (ventral) h ± effusion and abdominal


h Effusion (ventral) organs

DIFFERENTIAL DIFFERENTIAL DIFFERENTIAL DIFFERENTIAL
Consider pulmonary Pneumothorax Pleural effusion Diaphragmatic
contusions 1,2 (hemothorax) hernia1,2,4

TREATMENT TREATMENT TREATMENT TREATMENT

h Oxygen Basic respiratory support Basic respiratory support Basic respiratory support

h Analgesia (see Analgesia h Closed: thoracocentesis (see h Thoracocentesis 1,2,4 h Abdominal exploratory




in Trauma, page 29) Thoracocentesis, page 29). Monitor for h Monitor PCV/TS for surgery indicated

h Conservative fluid therapy repeated episodes of pneumothorax. repeated effusion

h Referral for mechanical Chest tube may be required if negative

ventilation if respiratory suction unattainable or recurrent
signs do not improve or pneumothorax
patient is clinically worse h If open: Apply seal to wound with sterile

lubricant and bandage chest. Thoracic
exploratory surgery to close wound1,2,4

CPR = cardiopulmonary resuscitation

MgCl = magnesium chloride
PCV = packed cell volume
POCUS = point-of-care ultrasound
SpO2 = oxygen saturation
TS = total solids
VPC = ventricular premature contraction

Continues h

March 2021 cliniciansbrief.com 23

 
 
 Signs of shock Brain and/or spinal injury

INVESTIGATION INVESTIGATION
MM, CRT, heart rate, BP, temperature, AFAST Cursory neurologic examination
(see AFAST, page 26), TFAST, mentation

Possible results
h Pale mucous membranes RESULTS RESULTS
Nonambulatory; Abnormal level of

h h
h Prolonged CRT


potentially altered pain consciousness, cranial

h Tachycardia
perception nerves, brain stem

h Bradycardia (cats)
reflexes, motor responses

h Hypotension

h Weak femoral pulses

h Hypothermia

h Lactate >22.5 mg/dL (>2.5 mmol/L)
DIFFERENTIAL

h Altered mentation
DIFFERENTIAL

h Cold extremities h Spinal cord injury, pelvic limb


h Free abdominal fluid fracture Traumatic brain injury

h Free thoracic fluid h Assume unstable spinal cord


injury

TREATMENT
DIFFERENTIALS h 
Oxygen, hypertonic saline/
h Hypovolemic (secondary to hemorrhage) shock TREATMENT mannitol (Table 2, page 30)

h Distributive shock h Analgesia (see Analgesia in h Head elevation 15-30



h Septic shock possible if hollow viscus organ rupture present Trauma, page 29) degrees, analgesia (see

h Temporary immobilization Analgesia in Trauma,

until further diagnostics page 29)
performed 7,8 h Steroids contraindicated 9-11

TREATMENT
h Oxygen, analgesia (see Analgesia in Trauma, page 29)

h Fluid therapy: Isotonic replacement fluid bolus, ± colloid, ±

hypertonic saline, ± blood product transfusion1 (Table 1, page 29)
h Investigate sources of hemorrhage and use external pressure/

ligation as needed
h Active warming for hypothermic animals (especially in cats)1,2,5,6

AFAST = abdominal focused assess- POCUS = point of care ultrasound
ment with sonography for trauma
PT = prothrombin time
Resuscitation endpoints (see Table 2, page 30) met? BP = blood pressure
PTT = partial thromboplastin time
CK = creatine kinase
RR = respiratory rate
CRT = capillary refill time
SAP = serum alkaline phosphatase
Hct = hematocrit
SIRS = systemic inflammatory
YES NO LRS = lactated Ringer’s solution response syndrome
MAP = mean arterial pressure TFAST = thoracic focused assessment
with sonography for trauma
MM = mucous membrane
TP = total protein
TREATMENT TREATMENT MODS = multiple organ dysfunction
Decrease fluids to h Repeat fluid bolus
PE = pericardial effusion

maintenance levels1 h Consider vasopressor support

24 cliniciansbrief.com March 2021
 
 
 DIAGNOSTIC/MANAGEMENT TREE h EMERGENCY MEDICINE & CRITICAL CARE h PEER REVIEWED

 
 
 
 
Therapeutic plan Discharge criteria
STABILIZED PATIENT h Fluid therapy with isotonic crystalloids h Eating and drinking well



(40-90 mL/kg/day) h No longer oxygen dependent


h Continue analgesia with opioids. (based on primary clinical signs,


Consider NSAIDs (eg, robenacoxib, 2 mg/ respiratory rate, effort)
kg PO every 24 hours) if normotensive h Pain well-managed with oral


INVESTIGATION and ideally eating on own analgesics
Admit to hospital for at least 24 hours h Provide oxygen if oxygen dependent h Adequate plan for follow-up care


h Closely monitor RR, respiratory effort, demeanor, h Address any cutaneous wounds depending on injuries sustained


and level of pain h Antibiotic therapy as indicated for

h Perform serial PE, AFAST, TFAST (every 15 wounds, open fractures, or septic

minutes to 12 hours as needed) peritonitis
h CBC, serum chemistry profile, ± PT/PTT (repeat h Monitor Hct, BP, oxygenation, level of


as necessary) pain, mentation, and cranial nerve signs
h Monitor urine output (at least 1-2 mL/kg/hour)7 h Recumbency care if not moving on own


h See Systemic Consequences of Trauma, page 30

Perform diagnostic evaluations

INVESTIGATION INVESTIGATION INVESTIGATION INVESTIGATION

Thoracic radiography See Orthopedic radiography, page 26 See Abdominal radiography, page 26 See POCUS (AFAST), page 26

RESULTS RESULTS RESULTS RESULTS RESULTS

h Incomplete diaphragmatic h Silhouette effect h Widened radiolucent h Interstitial to h Fractures(s)





silhouette h Retraction of lung lobes pleural space alveolar (see Fracture[s]

h Obscured cardiac silhouette h Fissure lines h Atelectasis pulmonary under Orthopedic



h ± gas filled loops/stomach h Atelectasis h Elevation of heart infiltrates radiography



in thorax from the sternum page 26)

DIFFERENTIAL DIFFERENTIAL DIFFERENTIAL DIFFERENTIAL

Diaphragmatic hernia Pleural effusion Pneumothorax Pulmonary
(hemothorax) contusions

TREATMENT TREATMENT TREATMENT TREATMENT

Surgery h Typically resolves with h Thoracocentesis h Supportive care



Ideally delayed 3-5 days to supportive care. h If thoracocentesis is h Rest, monitor for


allow improvement of Thoracocentesis may be needed twice within 24 hours
pulmonary contusions if required if large volume of a very short period h May not be

present. Indications for effusion. Oxygen support (ie, patient with appreciable on
emergency surgery: and blood transfusion recurrent radiographs for 24
h Herniated stomach may also be required. pneumothorax) or hours1,4

h Strangulated bowel/organ h Assess coagulation times. negative suction


h Inability to oxygenate Rarely requires surgical cannot be obtained,

properly despite intervention, but consider
appropriate treatment emergent surgery may be thoracostomy
h Ruptured viscera required if large-volume tubes1,4

bleed present 1,4,12 Continues h

March 2021 cliniciansbrief.com 25

 
 
DIAGNOSTIC/MANAGEMENT TREE h EMERGENCY MEDICINE & CRITICAL CARE h PEER REVIEWED

 
 
 
 
INVESTIGATION INVESTIGATION INVESTIGATION
Orthopedic radiography Abdominal radiography POCUS (AFAST)

RESULTS RESULTS RESULTS

h Free gas
h Fracture(s) h Free abdominal fluid



RESULTS DIFFERENTIAL
h Pelvic, appendicular, rib fractures Pneumoperitoneum INVESTIGATION

Abdominocentesis
h Compare PCV/TS, creatinine/


potassium, bilirubin, glucose,
and lactate of effusion to
TREATMENT TREATMENT peripheral blood and
h Pain management Stabilization and emergency cytology

h External coaptation when abdominal exploratory surgery

possible
h ± internal fixation

h Cage rest

h Flail chest: place affected side

down1,7,8
RESULTS RESULTS RESULTS RESULTS
h Peripheral blood h Effusion:serum h PCV/TS of effusion ≈ h Effusion:serum




to abdominal bilirubin ratio >2 PCV/TS of peripheral creatinine ratio >2
RESULTS fluid glucose h Cytology: bile blood h Effusion: serum


Spinal fracture(s) difference pigments potassium ratio
h Minimally displaced ≥20 mg/dL >1.9 (cats) >1.4 (dogs

h Minimal neurologic deficits h Effusion lactate


h Cervical trauma ≥22.5 mg/dL

h See Three Compartment Model, (≥2.5 mmol/L)

page 30 (dogs)
h Cytology: DIFFERENTIAL DIFFERENTIAL DIFFERENTIAL

Neutrophils Biliary rupture Traumatic Uroabdomen
(often hemoabdomen
degenerate),
TREATMENT presence of
h Pain management intracellular

h External coaptation bacteria TREATMENT

h Cage rest h Place urinary
TREATMENT TREATMENT


h Refer for CT ± MRI catheter. An
Emergency Most respond to

h
h ± surgery7,8 abdominal drain may

abdominal supportive care, fluid

be needed if urinary
exploratory surgery therapy, blood
DIFFERENTIAL to evaluate and transfusion, and
catheter is not fully
Septic abdomen draining the
repair possible restricted activity.
RESULTS damage as soon as May consider
abdomen.
Spinal fracture(s) h Consider contrast
patient is stable 1 abdominal

h Significant neurologic deficits study to identify
compression wrap,

h Penetrating injury source of leakage (eg,
but it must be done

h 2 of 3 spinal compartments urethra, urinary
TREATMENT correctly to be

affected indicates patient is bladder, ureter).
Stabilize, initiate valuable. Surgical
unstable (see Three h Surgery can be
broad spectrum intervention is rarely

Compartment Model, page 30) delayed for 6-24
antibiotics and required
hours if the
emergency h Abdominal
abdominal cavity is

abdominal exploratory and
properly drained and
exploratory surgery to surgical intervention
there is no evidence
evaluate and repair required when
TREATMENT possible damage hemorrhage is
of septic peritonitis.
h Pain management h Urethral tears usually
profound and


h Immobilize heal on their own
ongoing and patient

h Refer for CT ± MRI without surgical
cannot be stablized1

h ± surgery as soon as possible7,8 intervention1

Continues h
26 cliniciansbrief.com March 2021
 
 
ANCILLARY MATERIAL TO VEHICULAR TRAUMA
Cassandra Gilday, DVM
Adesola Odunayo, DVM, MS, DACVECC
University of Tennessee

d FIGURE 1 AFAST: Anechoic free abdominal fluid (arrows) at


the diaphragmatico-hepatic view (A) and splenorenal site (B).
Images courtesy of Silke Hecht, DACVR, DECVDI

d FIGURE 2 Lateral thoracic radiograph of the pneumothorax in a d FIGURE 3 Thoracic radiographs of diaphragmatic hernia in a


dog. Increased gas opacity in the pleural space, retraction of the dog. Cranial displacement of abdominal viscera (circle), loss
lung lobes from the thoracic wall and diaphragm (arrowheads), of normal diaphragm outline (line), and displacement of
separation of the cardiac silhouette from the sternum (arrow), thoracic structures can be seen. Images courtesy of Silke
and diffusely increased opacity of the lungs due to atelectasis Hecht, DACVR, DECVDI
can be seen. Image courtesy of Silke Hecht, DACVR, DECVDI

28 cliniciansbrief.com March 2021

 
 
 DIAGNOSTIC/MANAGEMENT TREE h EMERGENCY MEDICINE & CRITICAL CARE h PEER REVIEWED

 
 
 
 
TABLE 1

GENERAL GUIDELINES FOR FLUID RESUSCITATION

& BLOOD TRANSFUSION IN PATIENTS WITH TRAUMA

Perfusion Parameters Normal Endpoints

Whole blood5 Dogs: 20-30 mL/kg given over 30 minutes to 4 hours, depending on how critical the
patient is
Cats: 50-60 mL/cat (NOT mL/kg) given over same time period as for dogs

Packed RBCs5 Dogs: 15 mL/kg given over same time frame as whole blood
Cats: 30-40 mL/cat (NOT mL/kg) given over same time frame as for dogs

Synthetic colloid (controversial)5 1-5 mL/kg given over 15 minutes

Fresh frozen plasma5 15-30 mL/kg for patients with coagulopathy and active hemorrhage

Isotonic fluid shock bolus (LRS, 10-25 mL/kg given over 15 minutes. End goals should be reassessed; may be
Norm-R, 0.9% sodium chloride, repeated until entire shock dose administered.
Plasma-Lyte)5,9 Dog shock dose: 90 mL/kg/hour; cat shock dose: 50-60 mL/kg/hour

Hypertonic saline5,9 4-6 mL/kg given over 15 minutes; may be repeated 2-3 times in 24 hours

Mannitol9 0.5-1.5 g/kg IV given over 15 minutes, may be repeated 2-3 times in 24 hours

Lidocaine3 2 mg/kg IV bolus, followed by 50-80 µg/kg/minute if rhythm converts

THORACOCENTESIS ANALGESIA IN TRAUMA

Thoracocentesis is often a Quick and effective analgesia is essential for patients with vehicular trauma. Opioids
life-saving treatment that are the drug of choice because of their efficacy and limited adverse effects. NSAIDs
should be performed during should be avoided until the patient is hemodynamically stable. In addition, butorpha-
initial stabilization, ideally nol has minimal analgesic effects and should not be used. IM or SC administration of
prior to radiographic pure µ-receptor agonists may cause vomiting; IV administration is strongly
confirmation of preferred.1,13
pneumothorax or pleural
h Morphine (0.1-0.5 mg/kg IV every 4 hours)
effusion to prevent patient
decompensation in h Hydromorphone (0.05-0.2 mg/kg IV every 4-6 hours)

radiology.1,2,4
h Methadone (0.1-0.5 mg/kg IV every 4-6 hours)

h Fentanyl (2-5 µg/kg bolus, then 2-6 µg/kg/hour IV CRI)

h Buprenorphine (0.01-0.03 mg/kg IV or IM every 6-8 hours) Continues h

March 2021 cliniciansbrief.com 29

 
 
DIAGNOSTIC/MANAGEMENT TREE h EMERGENCY MEDICINE & CRITICAL CARE h PEER REVIEWED

 
 
 
 
ANCILLARY MATERIAL TO VEHICULAR TRAUMA CONTINUED

TABLE 2
THREE COMPARTMENT MODEL
h Dorsal column: laminae, spinous processes and their RESUSCITATION ENDPOINTS
ligaments
h Middle column: dorsal longitudinal ligament, dorsal annulus,
dorsal cortex of the vertebral bodies Perfusion Parameters Normal Endpoints

h Ventral column: ventral longitudinal ligament, ventral Heart rate Dogs: 60-120 bpm
annulus, ventral cortex of the vertebral bodies Cats: 160-220 bpm

MM color Pink

SYSTEMIC CONSEQUENCES OF TRAUMA CRT 1-2 seconds

Temperature 99°F-102.5°F (37.2°C-39.2°C)

h Common metabolic consequences6,12
–Activation of the coagulation cascade Mentation Alert
–Hypothermia
–GI disturbance (eg, vomiting, diarrhea) SAP (systolic BP) >90 mm Hg
–Systemic inflammation (eg, SIRS, MODS) MAP (mean BP) >70 mm Hg
h Common clinical pathologic abnormalities2,6,12 Urine output 1-2 mL/kg/hour
–Hyperglycemia
–Hyperlactatemia Lactate <22.5 mg/dL (2.5 mmoL)
–Metabolic acidosis
–Hypoalbuminemia
–Anemia BP = blood pressure PT = prothrombin time
–Thrombocytopenia CRT = capillary refill time PTT = partial thromboplastin time
–Increased ALT
MAP = mean arterial pressure SIRS = systemic inflammatory
–Increased CK response syndrome
MODS = multiple organ dysfunction
–Prolonged PT/PTT n

References
1. Reineke EL. Trauma overview. In: Drobatz KJ, Hopper K, Rozanski E, Animal Critical Care Medicine. 2nd ed. Elsevier; 2015:431-436.

Silverstein DC, eds. Textbook of Small Animal Emergency Medicine. John 8. Jeffery ND. Vertebral fracture and luxation in small animals. Vet Clin North
Wiley and Sons; 2019:1039-1051.

Am Small Anim Pract. 2010;40(5):809-828.
2. Simpson SA, Syring R, Otto CM. Severe blunt trauma in dogs: 235 cases 9. DiFazio J, Fletcher DJ. Traumatic brain injury. In: Drobatz KJ, Hopper

(1997-2003). J Vet Emerg Crit Care (San Antonio). 2009;19(6):588-602.

K, Rozanski E, Silverstein DC, eds. Textbook of Small Animal Emergency
3. Reiss AJ. Myocardial contusion. In: Silverstein DC, Hopper K, eds. Small Medicine. John Wiley and Sons; 2019:107-117.

Animal Critical Care Medicine. 2nd ed. Elsevier; 2015:236-239. 10. Fletcher DJ, Syring RS. Traumatic brain injury. In: Silverstein DC, Hopper K,

4. Sauvé V. Pleural space disease. In: Silverstein DC, Hopper K, eds. Small eds. Small Animal Critical Care Medicine. 2nd ed. Elsevier; 2015:723-727.

Animal Critical Care Medicine. 2nd ed. Elsevier; 2015:151-156. 11. Sande A, West C. Traumatic brain injury: a review of pathophysiology and

5. Prittie J, Cazzolli D. Crystalloids versus colloids. In: Drobatz KJ, Hopper management. J Vet Emerg Crit Care (San Antonio). 2010;20(2):177-190.

K, Rozanski E, Silverstein DC, eds. Textbook of Small Animal Emergency 12. Lynch A, Goggs R. Trauma-associated coagulopathy. In: Drobatz KJ, Hopper
Medicine. John Wiley and Sons; 2019:1103-1114.

K, Rozanski E, Silverstein DC, eds. Textbook of Small Animal Emergency
6. Roa L, Streeter EM. Metabolic consequences of trauma. In: Drobatz KJ, Medicine. John Wiley and Sons; 2019:1060-1067.

Hopper K, Rozanski E, Silverstein DC, eds. Textbook of Small Animal 13. Wetmore LA. Opioids. In: Drobatz KJ, Hopper K, Rozanski E, Silverstein DC,
Emergency Medicine. John Wiley and Sons; 2019:1068-1071.

eds. Textbook of Small Animal Emergency Medicine. John Wiley and Sons;
7. Davis E, Vite CH. Spinal cord injury. In: Silverstein DC, Hopper K, eds. Small 2019:1250-1254.

30 cliniciansbrief.com March 2021
 
 
HEMOABDOMEN
Elizabeth A. Rozanski, DVM, DACVIM (Small Animal), DACVECC
Sarah E. Cudney, DVM
Cummings School of Veterinary Medicine at Tufts University

HEMOABDOMEN OBSERVED

Patient stable (ie, heart rate <120 bpm, blood lactate <18 mg/dL, alert and oriented)?

NO YES*

TREATMENT
h A dminister crystalloids (20-30 History of trauma?
mL/kg) and hypertonic saline
(3-5 mL/kg)
h P erform:
• ± blood transfusion
• ± thoracic and abdominal
YES NO

radiography and POCUS a
• ± urgent exploratory surgery,

splenectomy, liver mass
removal, or other mass
removal
h C onsider immediate referral for TREATMENT Mass observed on POCUS a?
ultrasonography and h Provide
 monitoring, treatment, a nd
stabilization supportive care
h R echeck peripheral PCV in 2-6 hours
h P erform imaging and diagnostics (eg, CBC,
serum chemistry profile, urinalysis,
coagulation testing) YES NO
h E valuate other body systems

TREATMENT See No Mass

h P erform thoracic radiography (eg, to Observed on
evaluate for metastatic disease) POCUS a
h C onsider exploratory surgery
h E valuate PT/aPTT; consider
performing thromboelastography
and/or VCM to evaluate for fibrinolysis

PT/aPTT <20% prolonged PT/aPTT >20% prolonged

*All stable hemoabdomen


patients have the potential to
decompensate. Heart rate,
TREATMENT TREATMENT
h P erform exploratory surgery, splenectomy, liver h Treat with plasma or fresh whole blood
mucous membrane color, blood h C onsider ε-ACA therapy (50-100 mg/kg IV every 6
mass removal, or other mass removal
pressure, packed cell volume/ h C onsider blood transfusion hours)
total solids, mentation, pulse h P rovide supportive care h P roceed to surgery after treatment
quality, and capillary refill time h M onitor for postoperative ventricular ectopy h P rovide supportive care
should be closely monitored. h M onitor for postoperative ventricular ectopy

28 cliniciansbrief.com July 2020

 
 
 MANAGEMENT TREE h EMERGENCY MEDICINE & CRITICAL CARE h PEER REVIEWED

 
 
 
 
NO MASS OBSERVED ON POCUSa

Evaluate PT/aPTT

Coagulation times increased Coagulation times normal

TREATMENT Gallbladder wall edema

h I ncreased PT and aPTT: (suggestive of anaphylaxis, a cause
Consider anticoagulant of hemoabdomen) present?
rodenticide toxicity (rare cause
of hemoabdomen)
h Increased aPTT: Consider DIC

h Perform transfusion with fresh

frozen plasma or fresh whole
blood YES NO
h Administer vitamin K (5 mg/kg

SC every 24 hours) if PT is
extremely elevated (eg, >2 times
the upper limit of the reference
range) TREATMENT TREATMENT
h Treat for anaphylaxis (epinephrine Pursue CT and advanced diagnostics
[0.005-0.01 mg/kg IM or 0.1-1 µg/kg/min IV])
h M onitor closely

ACA = aminocaproic acid

aPTT = activated partial thromboplastin time
DIC = disseminated intravascular coagulation
PCV = packed cell volume
POCUSa = point-of-care ultrasonography (abdomen)
PT = prothrombin time
VCM = viscoelastic coagulation monitoring

July 2020 cliniciansbrief.com 29

 
 
 MANAGEMENT TREE h EMERGENCY MEDICINE & CRITICAL CARE h PEER REVIEWED

 
 
 
 
SNAKE ENVENOMATION
Adesola Odunayo, DVM, MS, DACVECC
University of Tennessee

SNAKEBITE VICTIM PRESENTED

Snake seen and/or identifiable?

YES NO

Snake venomous?*

YES NO

Perform triage examination TREATMENT


h Evaluate airway, h Analgesia


respiration, circulation, h Anti-inflammatory medications; NSAIDs are acceptable in

blood pressure, and PCV/ patients with nonvenomous snakebites
TS/glucose/lactate, and h Cage rest

perform ECG1 h Antibiotics are generally only indicated in cases of infection;

h Provide analgesia (eg,
culture and susceptibility testing may be of benefit if indicated

opioids); NSAIDs should be
avoided, as many venoms
can lead to coagulopathy,
hypotension, and
pigmenturia1,2
h If necessary, administer Determine whether patient is stable or unstable based


diphenhydramine or on physical examination abnormalities
trazodone to keep patient h Stable: puncture wounds, pain, hemorrhage,

calm 3,4 neurologic signs, edema, bruising, tissue necrosis,
h Avoid tourniquets, ice petechiae, ecchymoses1-4

packs, hot packs, h Unstable: tachycardia, weak peripheral pulses,

incisions, and suction 2,4 hypotension, obtundation, seizures, arrhythmias,
h Limit patient activity as any findings noted for stable patients1,2,4

much as possible to slow
spread of venom 2,4

PATIENT STABLE PATIENT UNSTABLE

Go to Patient stable box, Go to Patient unstable

next page box, page 13

*Coral snakes and pit vipers (eg, rattlesnakes, copperheads, water

moccasins, cottonmouths) are among the venomous snakes found PCV = packed cell volume
in the United States.2,4
TS = total solids

May 2019 cliniciansbrief.com 11

 
 
MANAGEMENT TREE h EMERGENCY MEDICINE & CRITICAL CARE h PEER REVIEWED

 
 
 
 
PATIENT STABLE

Conduct diagnostic investigation (eg, CBC, serum chemistry


profile, urinalysis, ECG, blood pressure, coagulation profile) and
snakebite severity score evaluation (see Suggested Reading).
Diagnostic investigation findings may include:
h Echinocytes (may be present for up to 24-48 hours), thrombo-

cytopenia, and leukocytosis on CBC4-6
h Coagulation abnormalities on coagulation testing 4,7,8

h Alterations in ALT, ALP, GGT, AST, creatine phosphokinase,

creatinine, blood urea nitrogen, sodium, potassium, calcium,
chloride, and glucose on serum chemistry profile1-6
h Pigmenturia, glucosuria, and casts on urinalysis 2

Determine outpatient versus inpatient status

h Consider outpatient therapy in stable patients with minimal

pain and/or no clinical or blood work abnormalities (eg,
thrombocytopenia, evidence of coagulopathy or hypotension)
h Consider inpatient therapy in unstable patients and/or any

patient with significant pain, pigmenturia, casts, elevated
hepatocellular or cholestatic liver enzyme activity, azotemia,
and/or hypotension 4

OUTPATIENT INPATIENT

TREATMENT TREATMENT
h Analgesia (eg, buprenorphine, h Fluid therapy to treat hypovolemia and dehydration and provide daily


gabapentin, fentanyl patch) maintenance fluid requirement
h Shaving and cleaning area around h Antivenom, if indications (eg, hypotension, neurologic signs, coagulopathy,


puncture wounds, if able tissue necrosis, rapid progression of swelling; see Antivenom
h Providing specific monitoring Recommendations) persist 10,12

instructions to the pet owner h Analgesia (ie, opioids); NSAIDs should be avoided1,2,4

h Antibiotics are indicated only in h Shaving and cleaning area around puncture wounds, if able


patients with evidence of an h Hyperbaric oxygen treatment, 13,14 if available

infected wound 2,9 h Long-term antiepileptic medications (eg, levetiracetam) in patients with seizures

h Glucocorticoids are controversial h Packed RBC transfusion in bleeding anemic patients


and typically not recommended 2,4,10 h Passive range of motion and frequent changes in recumbency in patients with

h The efficacy of the rattlesnake muscle weakness and/or paralysis

vaccine is controversial and not h Mechanical ventilation in patients with upper airway obstruction and/or

indicated in the immediate hypoventilation1,5
treatment of a snakebite 5,11 h Antibiotics are indicated only in patients with evidence of an infected wound2,9

h Glucocorticoids are controversial and typically not recommended 2,4,10

Consider outpatient therapy when patient is clinically stable (eg, pain is under
control, patient has interest in food, wounds are clinically static)

ALP = alkaline phosphatase

ALT = alanine transaminase
AST = aspartate aminotransferase
GGT = gamma-glutamyl transferase

12 cliniciansbrief.com May 2019

 
 
 PATIENT UNSTABLE

TREATMENT
Address life-threatening abnormalities
h Fluid bolus of isotonic crystalloids (10-25 mL/kg over 15 minutes) in patients

with hypotension, then reassessment of patient.15 Vasopressors may be
required in certain patients
h Benzodiazepines in patients with active seizures

h Analgesia (ie, opioids); NSAIDs should be avoided1,2,4

h Antivenom (see Antivenom Recommendations)2,11

h Antiarrhythmics (eg, lidocaine, procainamide, amiodarone) as needed

h Oxygen supplementation as needed10

h Intubation and mechanical ventilation in patients with airway obstruction

and/or hypoventilation1,5
h Vasopressors in patients with hypotension unresponsive to fluid therapy

After patient is stable, go to Patient stable box

References
1. Mcalees TJ, Abraham LA. Australian elapid snake envenomation in cats: clinical priorities
ANTIVENOM RECOMMENDATIONS

and approach. J Feline Med Surg. 2017;19(11):1131-1147.
2. Armentano RA, Schaer M. Overview and controversies in the medical management of pit

h Clinicians should start with one vial of antivenom viper envenomation in the dog. J Vet Emerg Crit Care (San Antonio). 2011;21(5):461-470.

per patient; however, patients with a lower 3. McCown JL, Cooke KL, Hanel RM, Jones GL, Hill RC. Effect of antivenin dose on outcome

from crotalid envenomation: 218 dogs (1988-2006). J Vet Emerg Crit Care (San Antonio).
body weight may require more antivenom,1-5 as 2009;19(6):603-610.
smaller patients tend to receive a larger amount 4. Gilliam LL, Brunker J. North American snake envenomation in the dog and cat. Vet Clin North

Am Small Anim Pract. 2011;41(6):1239-1259.
of venom per kg of body weight when bitten (eg,
5. Wells RJ, Hopper K. Management of clinical snake bite in dogs and cats. In:
a Chihuahua vs a Great Dane injected with the

Gopalakrishnakone P, Vogel CW, Seifert SA, Tambourgi DV, eds. Clinical Toxinology in
same amount of venom).5 Australia, Europe, and Americas. Springer; 2018:487-503.
6. Goddard A, Schoeman JP, Leisewitz AL, Nagel SS, Aroch I. Clinicopathologic abnormalities

h If the antivenom is lyophilized, one vial should be associated with snake envenomation in domestic animals. Vet Clin Pathol. 2011;40(3):282-292.

7. Stanley MK. Viscoelastic Coagulation Changes in Dogs with Tiger Snake Envenomation
reconstituted with crystalloid fluids (100-250 mL).5

[master’s thesis]. Melbourne: University of Melbourne; 2018.
8. Lieblick BA, Bergman PJ, Peterson NW. Thromboelastographic evaluation of dogs bitten by
h Antivenom should be administered

rattlesnakes native to southern California. Am J Vet Res. 2018;79(5):532-537.

intravenously over 1 to 2 hours.2,3 9. Carr A, Schultz J. Prospective evaluation of the incidence of wound infection in rattlesnake

envenomation in dogs. J Vet Emerg Crit Care (San Antonio). 2015;25(4):546-551.
h Patients should be monitored for signs of 10. Hoose JA, Carr A. Retrospective analysis of clinical findings and outcome of cats with


anaphylactoid/anaphylactic reactions. suspected rattlesnake envenomation in southern California: 18 cases (2007-2010). J Vet
Emerg Crit Care (San Antonio). 2013;23(3):314-320.
h Diphenhydramine may be considered if 11. Witsil AJ, Wells RJ, Woods C, Rao S. 272 cases of rattlesnake envenomation in dogs:

demographics and treatment including safety of F(ab’)2 antivenom use in 236 patients.

anaphylaxis or a mild anaphylactoid reaction to Toxicon. 2015;105:19-26.
the antivenom is suspected, whereas epinephrine 12. Pashmakova MB, Bishop MA, Black DM, et al. Multicenter evaluation of the administration of

crotalid antivenom in cats: 115 cases (2000-2011). J Am Vet Med Assoc. 2013;243(4):520-525.
and intravenous fluids should be administered for
13. Birnie GL, Fry DR, Best MP. Safety and tolerability of hyperbaric oxygen therapy in cats and
severe anaphylaxis/anaphylactoid reactions.2

dogs. J Am Anim Hosp Assoc. 2018;54(4):188-194.
Administration of antivenom should be stopped in 14. Korambayil PM, Ambookan PV, Abraham SV, Ambalakat A. A multidisciplinary approach

with hyperbaric oxygen therapy improve outcome in snake bite injuries. Toxicol Int.
both instances.4 However, if the reaction is not 2015;22(1):104-109.
severe, administration of antivenom should be 15. Odunayo A. Fluid therapy. Clinician’s Brief. 2018;16(10):71-75.

slowly resumed after approximately 20 to 60
minutes.4 Additional support in patients with Suggested Reading
hypotension (eg, vasopressors) and/or respiratory Peterson ME, Matz M, Seibold K, Plunkett S, Johnson S, Fitzgerald K. A randomized multicenter
trial of Crotalidae polyvalent immune F(ab) antivenom for the treatment of rattlesnake
signs (eg, mechanical ventilation) may be required.1 envenomation in dogs. J Vet Emerg Crit Care (San Antonio). 2011;21(4):335-345.

May 2019 cliniciansbrief.com 13

 
 
CANINE DIABETIC KETOACIDOSIS
Alice Huang, VMD*
J. Catharine Scott-Moncrieff, Vet MB, MS, MA, DACVIM, DECVIM
Purdue University

SUSPECTED CANINE DIABETIC KETOACIDOSIS

Physical examination Laboratory results:

(patient may have only 1 or h B G: hyperglycemia (>200 mg/dL)

more of the following signs): h B lood gas (venous or arterial): metabolic acidosis
h Polyuria h U rine dipstick: glucosuria; ketonuria or ketonemia
h Polydipsia (Serum ketones can be measured if urine is unavailable.)
h Polyphagia
h W eight loss
h Vomiting
h Lethargy
DIAGNOSIS
Diabetic ketoacidosis

TREATMENT
1. IV isotonic crystalloid therapy:
h Shock fluid therapy is warranted if hypovolemic or hypotensive shock are present: Start with 1/4

to 1/3 shock dose (90 mL/kg) and reassess until stable
h Correct dehydration, provide maintenance needs, and replace ongoing losses over 6-24 hours:

• % dehydration × body weight (kg) × 1000 plus

• 20 mL/kg/day (insensible losses) plus
• 20 to 40 mL/kg/day (maintenance sensible losses) plus

h Account for vomiting, diarrhea, and polyuria (ongoing sensible losses)

TREATMENT
2. Electrolyte supplementation (see Table 1, next page):
h Monitor serum potassium every 4-6 hours until within reference interval and stable; then every

12-24 hours
h Monitor serum phosphorus every 4-6 hours until >1.5; then every 6-24 hours

h When supplementing potassium and phosphorus concurrently, take into account the amount of

potassium contained in the potassium phosphate
h Consider magnesium supplementation in instances of refractory hypokalemia

TREATMENT
*Byline reflects author information on original 3. Regular insulin:

publication. On publication of this collection, 1
h CRI protocol :
the author’s current credentials and affilia-

• Start with 2.2 U/kg of regular insulin to 250 mL of 0.9% saline and increase concentration, if necessary
tion are Alice Huang, VMD, MS, DACVIM (SAIM),

at Seattle Veterinary Specialists, Kirkland, • Allow 50 mL of insulin solution to run through administration set because insulin adheres to plastic

Washington. • Administer solution as shown in Table 2, next page

h Intermittent low-dose IM protocol:

• Administer 0.2 U/kg regular insulin IM initially; 1 hour later begin IM injections of 0.1 U/kg every hour

BG = blood glucose • If BG <250 mg/dL, make 5% dextrose solution with hydration fluids and change dosage regimen

cPLI = canine pancreatic lipase immunoreactivity to 0.1-0.4 U/kg SC insulin every 4-6 hours
h For either protocol:

CRI = constant rate infusion • Monitor BG every 1-2 hours

NPH = neutral protamine Hagedorn • Goal for either protocol is to maintain BG between 200 and 300 mg/dL

• Do not decrease BG faster than 70-100 mg/dL/h
­

 DIAGNOSTIC TREE h ENDOCRINOLOGY h PEER REVIEWED

 
 
 
 
INVESTIGATION
It is essential to identify the underlying cause of the
increase in diabetogenic hormones (eg, catecholamines,
glucagon, glucocorticoids, growth hormone, estrogen)
that led to the ketogenic crisis:
INVESTIGATION h Physical examination


h Physical examination: respiratory rate/effort, heart rate, pulse quality h CBC



h Hydration: central venous pressure, weight, skin turgor, mucous h Serum chemistry profile



membrane quality h Urine culture


h Electrolytes: potassium, phosphorus, ± magnesium h cPLI



h Ketones: serum, urine h Abdominal radiography



h Blood glucose h Abdominal ultrasonography



h Blood gas and acid/base status h Thoracic radiography



h Appetite or emesis

h As needed: packed cell volume/total solids, serum chemistry profile,

blood pressure
Underlying cause of insulin resistance identified?

INVESTIGATION
h Hydrated? (Once the patient is hydrated, the route of regular insulin

administration can be switched from IM to SC, if desired. There is no
need to switch to SC administration if CRI protocol is chosen initially.) NO YES
h Acidemia and electrolyte abnormalities resolved?

h Underlying condition resolving?

TREATMENT
Treat any concurrent
conditions
h Pancreatitis
YES NO h UTI
h Renal failure
h Cholangiohepatitis
h Pyometra

INVESTIGATION TREATMENT h Skin disease

YES h Heart disease
Ketones present? h Continue IV fluids and electrolyte

h Neoplasia
supplementation
h Continue regular insulin administration,

either CRI or IM (can administer via SC
NO (OR TRACE) route if patient is hydrated)
INVESTIGATION
Hyperadrenocorticism
(see Hyperadrenocorticism:
INVESTIGATION why wait to test?, next page)
NO
Eating consistently?

TREATMENT TREATMENT
YES
Switch to SC intermediate-acting insulin Continue
h NPH or lente insulin (FDA-approved management for

veterinary formulation), 0.25-0.5 U/kg SC uncomplicated
every 12 hours initially; consider starting diabetes
at a higher dose if patient is expected to
have insulin resistance initially (eg, severe
pancreatitis)
DIAGNOSTIC TREE h ENDOCRINOLOGY h PEER REVIEWED

 
 
 
 
TABLE 1
HYPERADRENOCORTICISM:
ELECTROLYTE SUPPLEMENTATION WHY WAIT TO TEST?
Although hyperadrenocorticism
is one of the most frequent causes
Serum Potassium Concentration (mEq/L) Potasssium Chloride Dose of insulin resistance, it is not
appropriate to test for it during
>3.5 (maintenance) 0.05-0.1 mEq/kg/h a diabetic ketoacidosis crisis
3-3.5 because false positives would be
0.1-0.2 mEq/kg/h
expected. Diagnostic testing for
2.5-3 0.2-0.3 mEq/kg/h hyperadrenocorticism should not

­
be performed until the patient has
2-2.5 0.3-0.4 mEq/kg/h
been systemically healthy for at least
<2 0.4-0.5 mEq/kg/h 2 weeks. Appropriate regulation of

­
diabetes mellitus may be difficult
Serum Phosphorus Concentration (mg/dL) Potassium Phosphorus Dose to achieve prior to diagnosis of
concurrent hyperadrenocorticism.
2-2.5 0.03 mmol/kg/h

1.5-2 0.06 mmol/kg/h

1-1.5 0.09 mmol/kg/h Reference

1. DiBartola SP. Fluid, Electrolyte, and Acid-

<1 0.12 mmol/kg/h Base Disorders in Small Animal Practice, 3rd
ed. St. Louis, MO: Saunders Elsevier, 2005.

Suggested Reading
Boysen SR. Fluid and electrolyte therapy in
TABLE 2 endocrine disorders: diabetes mellitus and
hypoadrenocorticism. Vet Clin North Am
Small Anim Pract. 2008;38(3):699-717, xiii-xiv.
CRI INFUSION OF INSULIN DiTommaso M, Aste G, Rocconi F, Guglielmini
C, Boari A. Evaluation of a portable meter
to measure ketonemia and comparison
with ketonuria for the diagnosis of canine
diabetic ketoacidosis. J Vet Intern Med.
BG Concentration IV Hydration Fluids Rate of Insulin 2009;23(3):466-471.
(mg/dL) Solution (mL/h) Durocher LL, Hinchcliff KW, DiBartola SP,
Johnson SE. Acid-base and hormonal
abnormalities in dogs with naturally
>250 0.9% saline 10 occurring diabetes mellitus. J Am Vet Med
Assoc. 2008;232(9):1310-1320.
Greco, DS. Complicated diabetes mellitus. In:
200-250 0.9% saline + 2.5% dextrose 7 Bonagura JD, Twedt DC, eds. Kirk’s Current
Veterinary Therapy XIV. St. Louis, MO:
150-200 0.9% saline + 2.5% dextrose 5 Saunders; 2009:214-218.
Hume DZ, Drobatz KJ, Hess RS. Outcome of
100-150 0.9% saline + 5% dextrose 5 dogs with diabetic ketoacidosis: 127 dogs
(1993-2003). J Vet Intern Med. 2006;20:(3)
547-555.
<100 0.9% saline + 5% dextrose Discontinue
Panciera DL. Fluid therapy in endocrine and
metabolic disorders. In: DiBartola SP, ed.
Fluid, Electrolyte, and Acid-base Disorders in
Small Animal Practice. 3rd ed. St. Louis, MO:
Saunders; 2005:478-483.
Reineke EL, Fletcher DJ, King LG, Drobatz
KJ. Accuracy of a continuous glucose
monitoring system in dogs and cats with
diabetic ketoacidosis. J Vet Emerg Crit Care.
2010;20(3):303-312.
DIABETES REMISSION IN CATS
Thomas Schermerhorn, VMD, DACVIM (SAIM)
Kansas State University

DIABETIC CAT ON INSULIN THERAPY

INVESTIGATION
Client education

Educate about goals of treating diabetes; INVESTIGATION

possibility of achieving remission with intensive, Signs of hypoglycemia (eg, lethargy, odd behavior, weakness,
early treatment; and signs of remission. ataxia, hypersalivation, vomiting, dilated pupils, seizure, coma)?

YES

INVESTIGATION
Assess compliance

Hypoglycemia occurred after prescribed insulin dose INVESTIGATION

was given; no other cause for hypoglycemia identified Insulin overdose?

TREATMENT
Discontinue insulin
YES NO

INVESTIGATION
After discontinuation of insulin, findings suggestive of diabetic remission: Remission INVESTIGATION
h Euglycemia over most of the day unlikely h Hypoglycemia (either clinical or


h Hyperglycemia, if it occurs, is mild and typically does not exceed renal subclinical) detected on glucose curve

threshold (~250 mg/dL) h Hypoglycemia occurs after

h When cat is not hypoglycemic, glucose concentration often remains in pharmacologic doses of insulin

the low euglycemic range h When cat is not hypoglycemic, glucose

h Urine may test negative for glucose concentration often remains in the low

euglycemic range
h Urine may test negative for glucose

DIAGNOSIS
Remission likely
 DIAGNOSTIC TREE h ENDOCRINOLOGY h PEER REVIEWED

 
 
 
 
DIABETIC REMISSION AT A GLANCE
h Diabetic remission is achieved when insulin is no longer required to maintain normoglycemia.

h Other interventions (eg, diet) may still be used for blood glucose control.

h Likelihood of remission is highest in cats with newly diagnosed diabetes that receive intensive, early treatment.

h Some diabetic cats may alternate periods of overt diabetes with remission.

h Distinguishing diabetic remission from well-controlled diabetes may be difficult via history and clinical examination.

h Unless concurrent disease is present, well-controlled cats and cats in diabetic remission should not show signs typical

of diabetes (eg, polydipsia, polyuria, weight loss).

INVESTIGATION
NO Review history and signs; perform glucose curve assessment
± laboratory assessment (eg, fructosamine level)

Subclinical Glycemia Persistent

hypoglycemia within range hyperglycemia

Proper insulin dose

and no cause for
hypoglycemia INVESTIGATION
identified Reevaluate insulin
DIAGNOSIS DIAGNOSIS protocol
Diabetic Well-regulated
remission diabetes

DIAGNOSIS
Remission Remission unlikely
likely
INVESTIGATION INVESTIGATION
Findings suggestive of Findings suggestive of
diabetic remission: well-controlled diabetes:
h Euglycemia most of the h Hyperglycemia present
INVESTIGATION


day at least part of the day
Monitor as for typical diabetes h Hyperglycemia, if it h Hyperglycemia may


patient: occurs, is mild and approach or exceed the
h Diabetic cats in remission should renal threshold
typically does not

be considered as having diabetes exceed renal threshold (~250 mg/dL)
that does not require insulin for (~250 mg/dL) h Euglycemic periods

control h Glucose concentration followed by periods of

h Cats with a history of insulin- hyperglycemia, suggest-
is usually in the low

requiring diabetes should euglycemic range most ing need for insulin
be monitored by owners for of the day h Urine is usually positive

recurrence of signs consistent h Urine may test negative for glucose, although it is

with diabetes and evaluated by for glucose present in low amounts
a veterinarian at least every 3
months
h Return of signs does occur in some

cats previously in remission, and
insulin therapy may need to be Remission unlikely
reinstituted
INSULIN SELECTION IN DIABETIC DOGS & CATS
Thomas Schermerhorn, VMD, DACVIM (SAIM)
Kansas State University

HYPERGLYCEMIA DIAGNOSED

INVESTIGATION
Evaluate patient’s history, perform a physical examination, and
assess CBC, serum chemistry profile, and urinalysis results

Is persistent hyperglycemia present, along with

compatible clinical and laboratory findings?

NO YES

Diabetes mellitus (DM) not indicated DIAGNOSIS

Diabetes mellitus (DM)

INVESTIGATION
Assess patient for other
conditions that cause Insulin-independent Insulin-dependent
hyperglycemia: h Hyperglycemia may occur h Insulin formulations can be
h Laboratory error


despite normal or grouped by expected duration

h Physiologic hyperglycemia (ie,
elevated serum insulin of action:

stress/fear) concentration in patients – Ultra-short–action: Insulin
h Hyperadrenocorticism*

with prediabetes or aspart, insulin lispro

h Pancreatitis*
conditions that cause –Short-action: Regular insulin

h Acromegaly*

insulin resistance – Intermediate-action: Lente

h Drug effect (eg, glucocorticoids)

h Hyperglycemia may be insulin, NPH insulin

h Sepsis

treated by means other – Long-action: protamine zinc

h Trauma

than insulin (eg, diet, insulin, insulin glargine, insulin

h Pregnancy/diestrus
weight loss, oral detemir

hypoglycemic drugs) – Ultra-long–action: Insulin

h Uncommon in dogs and glargine U300, insulin

cats degludec
h Most dogs and cats h Insulin products


TREATMENT require insulin at the time – For human use, these

Pursue appropriate diagnosis of diagnosis products are marketed under
and treatment depending on various trade names and are
determined underlying cause available as U100 (100 Units
insulin/mL) preparations
– Concentrated preparations

(≥U300) are available for
specialized applications
DM = diabetes mellitus – Veterinary products are

available as U40 preparations
NPH = neutral protamine Hageman
PZI = protamine zinc insulin

*Hyperglycemia may be partly caused by DM in these conditions, as DM may be present at the

same time as or as a consequence of these disorders.

36 cliniciansbrief.com November/December 2020

 
 
 DIAGNOSTIC TREE h ENDROCRINOLOGY/INTERNAL MEDICINE h PEER REVIEWED

 
 
 
 
Does patient appear ill and possibly require hospitalization?

YES NO

Complicated DM Does patient maintain normal appetite and water intake?

h Hyperglycemia

h Associated metabolic disturbances,

such as:
– Hyperosmolality

– Ketosis

– Acidosis NO YES

– Electrolyte disturbances

h Diabetic ketoacidosis

h Hyperglycemia hyperosmolar syndrome

h DM with concurrent severe illness (eg,

necrotizing pancreatitis) Uncomplicated DM
h Hyperglycemia without major metabolic disturbances

TREATMENT
Early insulin therapy TREATMENT
h Goals:
Initial insulin therapy

– Immediate insulin replacement to control h Goals


hyperglycemia – Educate pet owners regarding insulin use, including appropriate
– Ability to rapidly manipulate glucose level

handling and administration techniques and potential for

h Ultra-short–action or short-action insulin
hypoglycemic complications

is indicated – Initiate intermittent insulin therapy
– Regular insulin CRI or IM can control

– Insulin duration sufficient to suppress hyperglycemia over an

hyperglycemia

extended time period
– Ultra-short–action insulin can be equally

effective, but experience is limited in
dogs and cats

INVESTIGATION
Insulin selection
h No insulin formulation or type is clearly indicated as the preferred
TREATMENT

choice in dogs or cats. However, expert guidelines provide a starting
Transitional insulin therapy point for beginning insulin treatment in diabetic dogs and cats.1
h Begins when patient is stable, hydrated, h Intermediate- and long-action insulin are most suitable for daily


and able to eat and drink at-home administration
h Goals
–Twice-daily administration is typical, but once-daily administration

– Control glycemia using intermittent

is possible in some dogs receiving PZI and some cats receiving

insulin administration insulin glargine or insulin detemir
– Insulin duration sufficient to suppress h Other considerations for at-home insulin selection include:


hyperglycemia over an extended time – Cost
period

– Product availability

– Preferred source for supplies (ie, veterinary clinic vs commercial

pharmacy)

See Chronic Insulin Therapy, next page

November/December 2020 cliniciansbrief.com 37

 
 
DIAGNOSTIC TREE h ENDROCRINOLOGY/INTERNAL MEDICINE h PEER REVIEWED

 
 
 
 
TREATMENT
Chronic insulin therapy
Long-term insulin therapy is guided by information obtained through periodic monitoring.
h Goals:

– Acceptable glycemic control and hypoglycemia avoidance

– Acceptable patient quality of life

–Treatment protocol balances patient needs and owner convenience

h Monitoring may include:

– Clinical assessment of DM signs, body weight, BCS, activity level, and general health

• Periodic use of urine glucose and ketone monitoring is occasionally recommended. Large changes in urine glucose and/or the appearance of

ketonuria may indicate deterioration of diabetes control in previously regulated dogs and cats. Absence of glucosuria can indicate hypoglycemia.
– Glycated protein assessment

• Serum fructosamine and/or blood hemoglobin A1c levels provide information on blood glucose concentrations over preceding several weeks and

months, respectively.
– Glycemic profile assessment

• Can be assessed using standard 12- or 24-hour glucose curve(s) or continuous glucose monitoring (eg, interstitial glucose monitoring device)

methods. These are the only routine methods that assess the pharmacodynamic profile of injected insulin in diabetic dogs and cats and are important
to evaluate before making a change in insulin formulation (eg, intermediate- to long-action insulin) or type (eg, insulin glargine to insulin detemir).
• Indications for performing a glucose curve include:

—Concern for hypoglycemia
—Requiring information not available through other assessments (eg, glycated protein measurement)
—Determining the time–action profile of insulin used
• Curve results can be markedly influenced by the circumstances under which the curve is performed. Steps taken to minimize stress and anxiety

(eg, performing measurements at home rather than in the clinic) may improve the reliability of information provided by the curve.

INVESTIGATION Re-evaluate 1-2 weeks after any

h DM signs persist or signs of hypoglycemia are noted? adjustment to the insulin protocol

h Laboratory assessments indicate persistent

hyperglycemia or frequent/intermittent hypoglycemia?
h Patient quality of life not optimal?

Insulin (ie, formulation, type) change
h Switch insulin based on:

– Evidence for insufficient insulin duration

–Substantial peak effect that produces hypoglycemia

NO YES – Whether reduction in administration frequency is

desired
h New insulin should have characteristics or features

that address the identified deficiencies
– For example, if NPH has abbreviated duration of

No change needed Dose change may be needed action in a dog, PZI may be selected as the new
insulin because of its generally longer duration of
action

Dose adjustment guidelines:

h Reduce insulin dose by 25%-50% if hypoglycemia associated with

clinical signs (eg, lethargy, weakness, seizure, among others) is noted
or if there is clear evidence for biochemical hypoglycemia
– Discontinue insulin if there is evidence of persistent hypoglycemia Reference

–Some cats receiving long-term insulin may develop persistent, often 1. Behrend E, Holford A, Lathan P, Rucinsky R, Schulman R.


subclinical hypoglycemia, which may indicate diabetes remission 2018 AAHA diabetes management guidelines for dogs and
h Dose increase is typically done in 10%-20% increments in dogs cats. J Am Anim Hosp Assoc. 2018;54(1):1-21.

h Minimal dose change in cats is usually 0.5 Unit because of difficulty in

accurately providing smaller volumes
h Switching to twice-daily administration is an option when patients on DM = diabetes mellitus

once-daily insulin administration require a dose increase due to
persistent hyperglycemia. Dividing the daily dose may reduce the risk NPH = neutral protamine Hageman
for hypoglycemia following a dose increase PZI = protamine zinc insulin

38 cliniciansbrief.com November/December 2020

 
 
HYPOGLYCEMIA
Thomas Schermerhorn, VMD, DACVIM (SAIM)
Kansas State University

HYPOGLYCEMIA

INVESTIGATION
Rule out laboratory error or spurious result (eg, delayed or lack of serum
separation from blood, especially in animals with severe polycythemia)

INVESTIGATION
Has animal received exogenous insulin?

YES

Diabetic Nondiabetic

Received prescribed Received insulin Emergency treatment of Incorrect diagnosis

insulin dose: overdose: hyperkalemia: of DM (eg, stress
h R esolution of DM h I mproper
storage of h U rinary obstruction hyperglycemia,
(primarily cats) insulin h O liguric renal failure pancreatitis, endocrine
h C hange in insulin h Technical error h H ypoadrenocorticism disease)

requirement h Incorrect syringe size h S evere acidosis

h C hange in insulin type h Inconsistency in

h I nappetence/ insulin product Patient not properly supplemented
decreased intake h Mistreatment or abuse with dextrose following exogenous

insulin administration

INVESTIGATION
Diagnostic plan INVESTIGATION
h R eview patient history Diagnostic plan
h E valuate for concurrent diseases affecting insulin h C onsider evaluating fructosamine level
requirements:
• CBC and serum chemistry profile

• Urinalysis and urine culture
• Abdominal ultrasound
h Redefine current insulin needs

h Determine fructosamine level

h Perform serial BG determinations:

• BG curve
• Continuous BG monitoring
h Review insulin handling and injection techniques

 DIAGNOSTIC/MANAGEMENT TREE h ENDOCRINOLOGY h PEER REVIEWED

 
 
 
 
NO

Adult Juvenile

Juvenile diseases that cause

hypoglycemia:
Excess production of Impaired glucose Increased glucose h Toy-breed hypoglycemia

insulin or insulin-like production: consumption: h Portosystemic shunt

growth factors: h E ndocrinopathy: h S evere leukocytosis or h Glycogen storage diseases

h I nsulinoma (islet cell • Hypoadrenocorticism polycythemia h Neonatal illness


neoplasia) • Hypopituitarism h S epsis/SIRS

h E xtrapancreatic tumor: (rare) h H unting dog hypoglycemia
• Hepatoma/carcinoma h H epatic cirrhosis h I nfectious disease:

• Leiomyoma/sarcoma h P ortosystemic shunt • Babesiosis

• Lymphoma h E nd-stage liver failure • Hepatozoonosis INVESTIGATION

Diagnostic plan
h Minimum database

• CBC and serum chemistry profile

• Urinalysis
INVESTIGATION

h Imaging studies

Diagnostic plan • Radiography

h M inimum database • Ultrasonography

• CBC and serum chemistry profile • Portography


• Urinalysis h Genetic testing (if available)


h Imaging studies

• Radiography

• Ultrasonography

• Portography

h Additional laboratory analysis

• Serum insulin levels

• Insulin-like growth factors*

• Resting cortisol level (to screen for hypoadrenocorticism)

• Bile acids (to assess liver function)

h Evaluation for sepsis
*Normal or elevated insulin with concurrent hypoglyce-

• Blood cultures

mia suggests insulin-secreting tumor

• Chest radiography

• Echocardiography

h Hepatic biopsy BG = blood glucose

h Infectious disease testing
DM = diabetes mellitus

SIRS = systemic inflammatory response syndrome
LACK OF DIABETIC CONTROL IN CATS
Thomas Schermerhorn, VMD, DACVIM (SAIM)
Kansas State University

SUSPICION FOR POORLY CONTROLLED DIABETES

INVESTIGATION
h P ersistent hyperglycemia/hypoglycemia for all or part of the day
h M ild hyperglycemia may only be evident on laboratory evaluation
h C linical signs related to magnitude of hyperglycemia:
• Polydipsia

• Polyuria (may produce incontinence)

• Weight loss

• Dehydration

h C hronic or intermittent hypoglycemia

INVESTIGATION
Direct (ie, fructosamine) and indirect (ie, glucosuria) evaluation of glycemia

Poor glycemic control Acceptable glycemic

control

INVESTIGATION
Evaluate compliance
h I nsulin protocol (type, dose, administration, storage)
h A ncillary therapy (eg, diet)

Noncompliance Compliance

TREATMENT INVESTIGATION
Client education Assess environment and lifestyle
h E ducate about h C hanges to home environment?
principles and goals h C hanges to daily routine?
of treating diabetes
h R eview insulin
handling (eg, storage),
preparation,
administration Recent changes No changes

INVESTIGATION TREATMENT
Reevaluate h M itigate negative environmental AUTHOR INSIGHT
after 7-10 days factors
h Adjust insulin dose as indicated Chronic poor control of diabetes may

h Adjust ancillary diabetic therapy as
increase risk for hypoglycemia, ketoacidosis,

indicated
h Evaluate response after 7-10 days and hyperosmolarity.

 DIAGNOSTIC/MANAGEMENT TREE h ENDOCRINOLOGY h PEER REVIEWED

 
 
 
 
INVESTIGATION
Evaluate for concurrent disorders
h P hysical examination
h M inimum database (CBC, serum chemistry profile, urinalysis, urine culture)
h A dditional testing to confirm diagnosis

DIFFERENTIAL DIFFERENTIAL
Disorders that cause insulin resistance Disorders that mimic uncontrolled diabetes

DIFFERENTIAL DIFFERENTIAL
Consider: Consider:
h A cromegaly: Excess growth hormone production caused h R enal disease: Causes polyuria/polydipsia; early kidney disease
by pituitary neoplasia can cause severe insulin resistance. may be difficult to recognize with poorly controlled diabetes.
h O besity h H yperthyroidism: Loss of body condition with healthy appetite,
h B acterial infection: Includes severe urinary, skin, oral polyuria/polydipsia; possible but poorly documented cause for
infection insulin resistance.
h I atrogenic: Exposure to exogenous glucocorticoid (most h N eoplasia: Loss of body condition (eg, cachexia/chronic illness)
common) or progesterone compounds may produce may occur in diabetic cats with neoplasia.
insulin resistance. Glucocorticoids absorbed after h L ower urinary tract disorders: Pollakiuria associated with lower
application of topical ocular or otic medications or owner urinary tract disorders (eg, urolithiasis, UTI) may be mistakenly
hormone creams may contribute to insulin resistance. reported as polyuria by owners.
h P ancreatitis: Severe inflammation may produce insulin h H ypercalcemia: Causes polyuria/polydipsia; look for loss of
resistance; direct damage to pancreatic islet cells may body condition, inappetence.
result in loss of functional beta cells and decreased insulin
production.
h H yperadrenocorticism: Uncommon, but can produce
severe insulin resistance.
LACK OF DIABETIC CONTROL IN DOGS
Thomas Schermerhorn, VMD, DACVIM (SAIM)
Kansas State University

SUSPICION FOR POORLY CONTROLLED DIABETES

INVESTIGATION
h P ersistent hyperglycemia for all or part of the day
h M ild hyperglycemia may only be evident on laboratory evaluation
h C linical signs related to magnitude of hyperglycemia:
• Polydipsia

• Polyuria (may produce incontinence)

• Weight loss

• Dehydration

INVESTIGATION
Direct (ie, fructosamine) and indirect (ie, glucosuria) evaluation of glycemia

Poor glycemic control Acceptable glycemic

control

INVESTIGATION
Evaluate compliance
h Insulin protocol (eg, type, dose, administration, storage)

h Ancillary therapy (eg, diet)

Noncompliance Compliance

TREATMENT INVESTIGATION
Client education Assess environment and lifestyle
h E ducate about h C hanges to home environment?
principles and goals h C hanges to daily routine?
of treating diabetes
h R eview insulin
handling (eg, storage),
preparation,
administration Recent changes No changes

INVESTIGATION TREATMENT
Reevaluate h M itigate negative environmental AUTHOR INSIGHT
after 7-10 days factors
h Adjust insulin dose as indicated
Chronic poor control of diabetes may increase

h Adjust ancillary diabetic therapy as

indicated risk for hypoglycemia, ketoacidosis,
h Evaluate response after 7-10 days
hyperosmolarity, cataracts, and neuropathy.

 DIAGNOSTIC/MANAGEMENT TREE h ENDOCRINOLOGY h PEER REVIEWED

 
 
 
 
INVESTIGATION
Evaluate for concurrent disorders
h P hysical examination
h M inimum database (CBC, serum chemistry profile, urinalysis, urine culture)
h A dditional testing to confirm diagnosis

DIFFERENTIALS DIFFERENTIALS
Disorders that cause insulin resistance Disorders that mimic uncontrolled diabetes

DIFFERENTIALS DIFFERENTIALS
Common: Consider:
h H yperadrenocorticism h H ypercalcemia: Causes polyuria/polydipsia; look for loss of
h O besity body condition, inappetence.
h B acterial infection (eg, severe urinary, skin, oral infections) h R enal disease: Causes polyuria/polydipsia; early kidney disease
h P ancreatitis may be difficult to recognize with poorly controlled diabetes.
h Liver disease: Many liver disorders are associated with polyuria
and may cause hypoglycemia.
h I nsulinoma: Hypoglycemia secondary to insulin production by
an endocrine tumor; rare in diabetic dogs.
DIFFERENTIALS h N eoplasia: Loss of body condition (cachexia/chronic illness)

Less common: may occur in diabetic dogs with neoplasia. Lymphoid and other
h H ypothyroidism neoplasias that produce PTH-rP may also produce
h G estation: Gestational diabetes is partly mediated by hypercalcemia. Large tumors (hepatic neoplasms) may produce
progesterone. hypoglycemia.
h l atrogenic: Exposure to exogenous glucocorticoid (most h L ower urinary tract disorders: Pollakiuria associated with

common) or progesterone compounds may produce disorders (urolithiasis, UTI, urinary incontinence) may be
insulin resistance. Glucocorticoids absorbed after reported as polyuria. An increase in urine volume from loss of
application of topical ocular or otic medications or owner diabetes control can manifest as overflow incontinence.
hormone creams may contribute to insulin resistance.

PTH-rP = parathyroid hormone-related peptide

METHIMAZOLE INTOLERANCE IN A HYPERTHYROID CAT
Alex Gallagher, DVM, MS, DACVIM
University of Florida

ADVERSE EVENTS FROM METHIMAZOLE

Dose-dependent

DIFFERENTIAL DIFFERENTIAL
GI signs (eg, vomiting, diarrhea, anorexia) Azotemia

TREATMENT INVESTIGATION
Discontinue methimazole T4 levels less than
reference range?

Signs resolve?

YES NO

YES NO
TREATMENT Is patient clinical
Discontinue for azotemia?
or reduce
methimazole dose
TREATMENT Investigate further until T4 is within
Restart methimazole (eg, laboratory work reference range
at 50% dose [including fecal
examination] and YES NO
diagnostic imaging)

Reassess azotemia
GI signs recur?
TREATMENT TREATMENT
Discontinue Continue
or reduce treatment and
TREATMENT methimazole monitor
Initiate therapy for azotemia
CKD as indicated
YES NO

Reassess azotemia

TREATMENT
Titrate dose until hyperthyroidism is controlled
 DIAGNOSTIC/MANAGEMENT TREE h ENDOCRINOLOGY h PEER REVIEWED

 
 
 
 
Idiosyncratic

DIFFERENTIAL DIFFERENTIAL DIFFERENTIAL

Hepatotoxicity Blood dyscrasias Facial pruritus

TREATMENT TREATMENT TREATMENT

Discontinue Discontinue methimazole Discontinue
methimazole and provide and provide supportive methimazole and
supportive care care; if neutrophil count is provide supportive
<1000-1500/uL, initiate care; may require
antibiotic therapy anti- inflammatory
­
dose of steroids

INVESTIGATION
Does patient recover? TREATMENT
Alternative therapy
may include
h 131
 I therapy
h T hyroidectomy
h D ietary iodine
restriction
YES NO h Transdermal
methimazole if
vomiting is sole
adverse event

Investigate further
(eg, diagnostic imaging,
culture as indicated, biopsy)

I = radioiodine
131

CKD = chronic kidney disease

T4 = total thyroxine
LEPTOSPIROSIS
J.S cott Weese, DVM, DVSc, DACVIM
Ontario Veterinary College
Ontario, Canada

Patient presented with clinical signs consistent with leptospirosis (ie, classically renal ±
hepatic disease [eg, polyuria/polydipsia, oliguria, fever, anorexia, depression, vomiting/
diarrhea, icterus], uveitis) or with leptospiral pulmonary hemorrhagic syndrome

INVESTIGATION
h CBC

h Serum chemistry profile

h Urinalysis

h Blood pressure

h ± clotting profile

h ± urine protein:creatinine ratio

h ± thoracic radiography, if evidence of respiratory disease

h ± abdominal ultrasonography

h ± urine culture and susceptibility testing

INVESTIGATION
History of leptospirosis vaccination?

NO

Perform patient-side IgM test or LipL-32 ELISA

NEGATIVE POSITIVE

Other likely cause identified? DIAGNOSIS

Leptospirosis (see Leptospirosis
Management, page 28)

YES NO

POSITIVE
Pursue other Consider urine ± blood PCR* and/or repeat IgM
diagnosis or LipL-32 ELISA test in 48-72 hours Leptospirosis very unlikely.
Pursue other diagnosis; can
NEGATIVE consider submitting acute and
convalescent MAT titers to
lgM = immunoglobulin M further investigate
MAT = microscopic agglutination test
*Utility of PCR is low if antimicrobials were started before specimen collection.

26 cliniciansbrief.com April/May 2021
 
 
 DIAGNOSTIC/MANAGEMENT TREE h INFECTIOUS DISEASE h PEER REVIEWED

 
 
 
YES

≥3 months prior <3 months prior

Perform patient-side IgM test h Urine ± blood PCR


h MAT titers can be evaluated, but interpretation

can be challenging if vaccination was very
recent (ie, within 1 month)
h Ongoing antibiotic administration might affect

sensitivity of PCR testing
NEGATIVE POSITIVE

Perform urine ± blood PCR* ± Presumptive positive; more likely with NEGATIVE POSITIVE
repeat IgM test in 48-72 hours increased time since vaccination.
Consider confirmation via urine PCR

Leptospirosis unlikely.
If no other cause is
apparent, treat
NEGATIVE POSITIVE PCR POSITIVE IgM TEST empirically while
pursuing testing for
other causes

DIAGNOSIS
Leptospirosis (see Leptospirosis Management, next page)
Continued h

April/May 2021 cliniciansbrief.com 27

 
 
DIAGNOSTIC/MANAGEMENT TREE h INFECTIOUS DISEASE h PEER REVIEWED

 
 
 
Leptospirosis Management h Other care as needed based on clinical syndrome


Once leptospirosis diagnosis is confirmed, patients and patient response to treatment
should be treated with antimicrobials and support-
ive care as needed. During hospitalization, hydration status should be
carefully monitored (ie, measure “ins and outs,”
Antimicrobials thoracic auscultation, blood pressure), as should
h If the patient can tolerate oral medication: BUN/creatinine, acid-base/electrolytes, ± hepatic

Doxycycline (5 mg/kg PO every 12 hours) for enzymes (as often as every 24 hours initially). PCV
14 days1) should be rechecked as often as every 24 hours ini-
h If the patient cannot tolerate oral medication: tially, and CBC should be repeated as often as every

Ampicillin (20 mg/kg IV every 6 hours), then, if 48 hours if thrombocytopenia is present and/or in
possible, de-escalated to oral doxycycline (5 mg/ severe cases. Urine specific gravity should also be
kg PO every 12 hours) for an additional 14 days1 rechecked every few days once fluid therapy has
been discontinued, and clotting factors should be
Supportive Care rechecked if abnormal.
h IV fluids for replacement, diuresis, acid-base bal-

ance, and electrolyte maintenance Approximately 1 week after the patient is dis-
h Antiemetics charged, serum chemistry profile should be

h Nutritional support for renal or hepatic injury repeated, as should CBC if abnormalities were

h Renal replacement therapy can be considered in present at the time of discharge. Serum chemistry

oliguric dogs developing volume overload, profile should be rechecked again in 3 to 7 days if
severe hyperkalemia, or severe azotemia nonre- results are still abnormal. Urine specific gravity
sponsive to medical management.1 should be monitored regularly if abnormal. n

TABLE

LEPTOSPIROSIS TESTS & CONSIDERATIONS

Test Target Sample type Patient-side? Impacted by Impacted by

vaccination? antimicrobial
treatment?

MAT Antibody (IgM and IgG) Serum No Yes No

Lepto rapid test Antibody (IgM) Serum Yes Yes No

LipL-32 Leptospira Antibody (IgG>IgM) Serum Yes Yes No

PCR Antigen Urine, whole blood No No Potentially

28 cliniciansbrief.com April/May 2021

 
 
 www.facebook.com/Cheapebooks33

Elura ™

(capromorelin oral solution)

20 mg/mL
For oral use in cats only
CAUTION:
Federal (USA) law restricts this drug to use by or on the order of a licensed veterinarian.
Before using Elura, please consult the product insert, a summary of which follows:
INDICATION:
For management of weight loss in cats with chronic kidney disease.
DOSAGE AND ADMINISTRATION:
Administer ELURA orally at a dose of 2 mg/kg (0.9 mg/lb) or 0.1 mL/kg (0.045 mL/lb) body weight once daily.
CONTRAINDICATIONS:
ELURA should not be used in cats that have a hypersensitivity to capromorelin.
WARNINGS:
Not for use in humans. Keep this and all medications out of reach of children and pets. Consult a physician in case of
accidental ingestion by humans.
For oral use in cats only.
Do not use in cats with hypersomatotropism (acromegaly). ELURA may increase serum glucose for several hours after
dosing. Use in cats with current or historical diabetes mellitus has not been evaluated and use may not be appropriate.
PRECAUTIONS:
Use with caution in cats that may have cardiac disease or severe dehydration. ELURA causes transient decreases in heart
rate and blood pressure up to 4 hours following dose administration. Some cats may exhibit clinical signs
of bradycardia or hypotension following administration of ELURA. Use with caution in cats with hepatic dysfunction.
Reference Capromorelin is metabolized in the liver in humans and dogs and similar metabolism is expected in the cat.
The safe use of ELURA has not been evaluated in cats younger than 5 months old. The safe use of ELURA has not been
1. Sykes JE, Hartmann K, Lunn KF, Moore GE, Stoddard evaluated in cats that are pregnant, lactating, or intended for breeding.
RA, Goldstein RE. 2010 ACVIM small animal consensus ADVERSE REACTIONS:
statement on leptospirosis: diagnosis, epidemiology, Safety was evaluated in a 56-day field effectiveness study in 176 client-owned cats (118 administered ELURA, 58
treatment, and prevention. J Vet Intern Med. administered vehicle control) that received at least one dose. Cats enrolled had ≥5% unintended weight loss and a history
2011;25(1):1-13. of chronic kidney disease (CKD). Cats had a mean age of 15 years and at enrollment 11.4% of the cats were in Stage 1
CKD, 66.5% were in Stage 2, 21.0% were in Stage 3, and 1.1% were in Stage 4. Cats enrolled in the study had a variety of
comorbid conditions: dental disease (88.1%), moderate or severe muscle loss (43.2%), heart murmur (28.4%), history of
vomiting or underlying gastrointestinal disease (28.4%), hyperthyroidism (13.6%) and hypertension (9.7%).
Suggested Reading Table 1: Adverse Reactions in the Field Effectiveness Study
Barr SC, McDonough PL, Scipioni-Ball RL, Starr JK. Adverse Reaction ELURA Vehicle Control
Serologic responses of dogs given a commercial (n=118) (n=58)
vaccine against Leptospira interrogans serovar Vomiting 35 (29.6%) 13 (22.4%)
pomona and Leptospira kirschneri serovar Hypersalivation 25 (21.2%) 0 (0.0%)
grippotyphosa. Am J Vet Res. 2005;66(10):1780-1784. Inappetence 22 (18.6%) 7 (12.0%)
Curtis KM, Foster PC, Smith PS, et al. Performance Behavior Change a
17 (14.4%) 3 (5.2%)
of a recombinant LipL32 based rapid in-clinic Lethargy 16 (13.6%) 6 (10.3%)
ELISA (SNAP Lepto) for the detection of antibodies Anemia 11 (9.3%) 1 (1.7%)
against Leptospira in dogs. Intern J Appl Res Vet Med. Dehydration 11 (9.3%) 2 (3.4%)
2015;13(3):182-189. Stage of CKD Increased b 10 (8.5%) 3 (5.2%)
Diarrhea 9 (7.6%) 2 (3.4%)
Lizer J, Grahlmann M, Hapke H, Velineni S, Lin D, Kohn B.
Evaluation of a rapid IgM detection test for diagnosis of Urinary Tract Infection 8 (6.8%) 2 (3.4%)
acute leptospirosis in dogs. Vet Rec. 2017;180(21):517. Hyperglycemia 8 (6.8%) 2 (3.4%)
Upper Respiratory Infection 7 (5.9%) 1 (1.7%)
Lizer J, Velineni S, Weber A, Krecic M, Meeus P. Evaluation
Hypercalcemia 7 (5.9%) 0 (0.0%)
of 3 serological tests for early detection of Leptospira-
specific antibodies in experimentally infected dogs.
J Vet Intern Med. 2018;32(1):201-207. Adverse Reaction ELURA Vehicle Control
(n=118) (n=58)
Midence JN, Leutenegger CM, Chandler AM, Goldstein Facial Skin Lesion 6 (5.1% 3 (5.2%)
RE. Effects of recent Leptospira vaccination on whole Hyperkalemia 5 (4.2%) 0 (0.0%)
blood real-time PCR testing in healthy client-owned Ataxia 4 (3.4%) 0 (0.0%)
dogs. J Vet Intern Med. 2012;26(1):149-152. Diabetes Mellitus 1 (0.8%) 0 (0.0%)
Schuller S, Francey T, Hartmann K, et al. European Congestive Heart Failure 1 (0.8%) 0 (0.0%)
consensus statement on leptospirosis in dogs and Note: If an animal experienced the same event more than once, only the first occurrence was tabulated.
cats. J Small Anim Pract. 2015;56(3):159-179. a
Behavior change included hiding from the owner (8 ELURA, 1 vehicle control); owner reported difficulty administering
medication (7 ELURA, 1 vehicle control); and redirected aggression to another household cat (2 ELURA, 1 vehicle control).
b
Two ELURA and 1 vehicle control cat increased by two CKD stages; 8 ELURA and 2 vehicle control cats increased one
CKD stage. It could not be determined if the progressive renal disease was the natural course of the pre-existing disease or
IgG = immunoglobulin G treatment related.
Hypersalivation was generally associated with dosing and resolved within a few minutes.
lgM = immunoglobulin M Nine cats (8 ELURA and 1 vehicle control) either died or were euthanized during or shortly after the study. Six ELURA cats
were euthanized or died from decompensated CKD. One ELURA cat was euthanized after study withdrawal
MAT = microscopic agglutination test on Day 33 for declining quality of life and recent identification of a new mass. One ELURA cat acutely declined and was
euthanized for findings of nodules in both kidneys and diagnosis of sarcoma. The vehicle control cat was euthanized for
acute onset of right hindlimb paresis and suspected embolic event. Two additional cats were diagnosed with neoplasia
during the study (one ELURA cat with unspecified soft tissue sarcoma and one control cat with mammary adenocarcinoma)
but completed the study. In voluntary post-approval reporting for extra-label use of a capromorelin product for dogs, the
following adverse events have been reported in cats (listed in decreasing order of reporting frequency): bradycardia,
lethargy, hypersalivation, hypotension, behavior change, and vomiting.
To report suspected adverse events, for technical assistance or to obtain a copy of the Safety Data Sheet (SDS), contact
Elanco US, Inc. at 1-888-545-5973.
For additional information about adverse drug experience reporting for animal drugs, contact FDA at 1-888-FDA-VETS or
http://www.fda.gov/reportanimalae.
EFFECTIVENESS:
Effectiveness was demonstrated in a multicenter, prospective, masked, randomized, vehicle-controlled field study. The
study enrolled 176 client-owned cats with ≥5% unintended weight loss and a history of chronic kidney disease. The cats
enrolled included 96 females and 80 males of various breeds, 4.4 - 22.1 years old with a mean age of 15 years and
weighing 1.81 - 6.76 kg. CKD stage was determined based on creatinine at screening according to the International Renal
Interest Society (IRIS) 2015 guidelines. All stages were enrolled. Cats were administered ELURA at 2 mg/kg or a matched
volume of control once daily by mouth for 56 days. The control was the solution without capromorelin (vehicle control). The
primary effectiveness variable was the percent change in body weight from Day 0 to Day 55. Effectiveness was evaluated
in 112 cats: 71 cats administered ELURA and 41 cats administered vehicle control. There was a statistically significant
difference between the percent change in weight for the ELURA group (+5.2%) compared to the vehicle control group
(-1.6%) at Day 55 (p<0.0001). Secondary analysis for percent change in weight at Day 15 and Day 27 demonstrated cats
in the ELURA group gained weight throughout the study.
STORAGE CONDITIONS:
Store at or below 86˚F (30˚C)
HOW SUPPLIED:
20 mg/mL flavored oral solution in a 15 mL bottle with an oral dosing syringe.
Approved by FDA under NADA # 141-536.
Manufactured for: Elanco US Inc, Greenfield, IN 46140 USA
REV. DATE-10/2020
ELURA, Elanco and the diagonal bar logo are trademarks of Elanco
or its affiliates.
April/May 2021  cliniciansbrief.com  29 PA402828X W2a
FELINE INFECTIOUS PERITONITIS
Matthew Kornya, DVM, ABVP (Feline) Residency Trained, ACVIM (SAIM) Resident
Ontario Veterinary College
The Cat Clinic
Ontario, Canada

FIP SUSPECTED BASED ON

CLINICAL SIGNS AND DIAGNOSTICS

Determine organ-specific clinical signs

Cavitary effusion Uveitis Neurologic signs Nonspecific signs

h Pleural h Aqueous humour h CSF h Aspirates of spleen,




h Abdominal liver, kidney, lymph

h Pericardial node, whole blood

INVESTIGATION INVESTIGATION INVESTIGATION INVESTIGATION
Rivalta test Aqueous humor cytology CSF cytology FECV RT-PCR
h Whole blood


h Organ aspirates


h CSF


h Effusion


h Aqueous humor


Negative Positive

DIAGNOSIS INVESTIGATION Alternative diagnosis reached (ie, cytology Negative Positive

FIP unlikely Cytology confirms neoplasia or bacterial infection)?

YES NO

DIAGNOSIS
FIP unlikely

18 cliniciansbrief.com November/December 2020

 
 
 DIAGNOSTIC TREE h INFECTIOUS DISEASE h PEER REVIEWED

 
 
 
 
INVESTIGATION
S-protein gene PCR

Negative Positive

INVESTIGATION DIAGNOSIS
Seek other diagnoses and biopsy tissues FIP likely
for organ immunohistochemistry

Negative Positive
immunohistochemistry immunohistochemistry For an expert overview on FIP, see Consult the Expert:
Feline Infectious Peritonitis on page 11.

DIAGNOSIS DIAGNOSIS
FIP unlikely FIP
FECV = feline enteric coronavirus
RT = reverse transcriptase
S = spike

November/December 2020 cliniciansbrief.com 19

 
 
ISOLATION OF ENTEROCOCCUS SPP
J. Scott Weese, DVM, DVSc, DACVIM
University of Guelph

ENTEROCOCCUS FAECIUM OR FAECALIS DETECTED

Typically sterile site?

YES

Signs consistent with bacterial

infection?

YES NO

Other bacterial species isolated in TREATMENT

addition to enterococci? h R evisit
diagnosis
• E faecium or faecalis may not be cause

of infection
YES NO

TREATMENT Abscess?
h C onsidertreating only
other isolated bacterial
species YES NO
• Particularly if more

common pathogens (eg,
Escherichia coli) and if
antimicrobial options for
Enterococcus spp are TREATMENT INVESTIGATION
limited1 h I nciseand drain Possible underlying factor
h A ntibiotics (eg, foreign body, comorbidity)?
indicated only YES NO
with presence of
associated
cellulitis and/or
signs of systemic
disease (eg, fever, TREATMENT INVESTIGATION
depression) Address if possible Susceptible to antimicrobials on
culture and susceptibility panel? *,†
YES

TREATMENT
Choose drug based on patient factors, infection site,
and administration route and frequency †,‡
 DIAGNOSTIC/MANAGEMENT TREE h INFECTIOUS DISEASE h PEER REVIEWED

 
 
 
 
NO

TREATMENT
In nonsterile site (eg, skin,
I f no clinical response, further
eyes, GI tract, others)
investigation for underlying
factors and/or comorbidities
is indicated
h Further diagnostic testing


(ie, complete workup)
TREATMENT h Query owner compliance


Consider contamination vs infection h Consult with board-certified


based on: veterinary internist with
h P resence of other organisms infectious disease expertise
h A mount of growth h Consider referral


h S ampling site
h P revalence of enterococcal
infections at site

TREATMENT
Choose drug based on
YES patient factors, infection site,
and administration
TREATMENT route and frequency †,‡
h R equestextended
antimicrobial panel
INVESTIGATION
Is isolate susceptible to
NO • Consider consultation one or more antimicrobials

with board-certified that can be safely used TREATMENT
veterinary pharmacologist in patient?§
or internist with infectious Consult specialists
disease expertise (eg, internal medicine
specialist with infectious
NO disease expertise, veterinary
clinical microbiologist,
veterinary pharmacologist) to
address drug selections and
comorbidities

References
1. Weese JS, Blondeau JM, Boothe D, et al. Antimicrobial use *Enterococci are inherently resistant to penicillin, trimethoprim-sulfa, clindamycin, and


guidelines for treatment of urinary tract disease in dogs and low levels of aminoglycosides. Cephalosporins have limited activity in vivo.2 Most laboratories
cats: Antimicrobial guidelines working group of the International do not report results for these drugs.
Society for Companion Animal Infectious Diseases. Vet Med Int. †Consider ampicillin or gentamicin for isolates that do not have high-level gentamicin resistance.2

2011;2011:263768. ‡Amoxicillin and ampicillin are drugs of choice when the isolate is susceptible.
2. Performance Standards for Antimicrobial Disk and Dilution §Consult an infectious disease specialist and veterinary pharmacologist before considering drugs

(eg, vancomycin, linezolid) to confirm that no as-effective, less costly, and/or safer alternatives are

Susceptibility Tests for Bacteria Isolated From Animals; Approved
Standard, 4th ed—Wayne, PA: Clinical and Laboratory Standards available.
Institute. CLSI Document VET01-A4. 33(7):1-72, 2013.
DIAGNOSTIC/MANAGEMENT TREE h INFECTIOUS DISEASE h PEER REVIEWED

 
 
 
 
ISOLATION OF METHICILLIN-RESISTANT STAPHYLOCOCCUS
Daniel O. Morris, DVM, MPH, DACVD
University of Pennsylvania

Karen A. Moriello, DVM, DACVD

University of Wisconsin–Madison

TRUE PATHOGEN?
YES MAYBE

INVESTIGATION
Coagulase-negative
INVESTIGATION INVESTIGATION Staphylococcus spp other than
Isolates are coagulase positive Isolates are coagulase negative S schleiferi or S lugdunensis
h Staphylococcus pseudintermedius h S schleiferi subsp schleiferi


h S hyicus h S lugdunensis


h S schleiferi subsp coagulans

h S aureus

INVESTIGATION
Isolate from a body cavity
or fluid that is normally sterile

DIAGNOSIS
True pathogen YES NO

Isolate only methicillin resistant? INVESTIGATION

Patient systemically ill
or have life-threatening urgency?

YES NO
YES NO

TREATMENT DIAGNOSIS
Systemic therapy Multidrug-resistant
h R egardless of culture results, isolate INVESTIGATION INVESTIGATION
β-lactam antibiotics are never Repeat culture to Perform cytology,
useful clinical options for confirm absence of gram staining; repeat
methicillin-resistant bacteria other co-pathogens culture to identify true
h Avoid fluoroquinolones unless pathogen

there are no other options TREATMENT
h Avoid clindamycin if isolate is
If systemic therapy

resistant to erythromycin is not an option due
h Adjuvant topical therapy
to drug toxicity or

patient limitations,
topical antiseptic
therapy alone may
be considered
TREATMENT
Topical therapy
h S hampoo or rinse therapy
q24h with chlorhexidine, Suggested Reading
benzoyl peroxide, or TREATMENT Hillier A, Lloyd DH, Weese JS, et al. Guidelines for the diagnosis and
accelerated H 2O 2 Topical antiseptics
h Focal therapy q12-24h with
antimicrobial therapy of canine superficial bacterial folliculitis
as monotherapy (Antimicrobial guidelines working group of the international

mupirocin ointment or fusidic
society for companion animal infectious diseases). Vet Dermatol.
acid cream applied to lesions
25:163-175, e41-e43, 2014.
Papich MG. Antibiotic treatment of resistant infections in small
animals. Vet Clin North Am Small Anim Pract. 43:1091-1107, 2013.
MACROCYCLIC LACTONE-RESISTANT HEARTWORM DISEASE
Andy Moorhead, DVM, MS, PhD
Ray M. Kaplan, DVM, PhD, DEVPC, DACVM (Parasitology)
University of Georgia

INITIAL HEARTWORM ANTIGEN TEST PERFORMED

Antigen positive

INVESTIGATION INVESTIGATION
Evidence of poor Gaps present in testing
compliance or lack and/or product purchase history?
of prophylaxis YES NO

DIAGNOSIS INVESTIGATION INVESTIGATION

Very low suspicion Heartworm antigen test not performed >6 months Heartworm antigen test
of resistance after initiation of compliant prophylaxis performed ≥6 months after initiation
h Test necessary to ensure dog was negative at of compliant prophylaxis
prophylaxis initiation

TREATMENT
MF observed?
Proceed with
AHS-recommended DIAGNOSIS
treatment protocol 1 Low suspicion of resistance

YES

INVESTIGATION
Perform MF suppression test 2,*
h Perform Knott’s test for

quantitation of MF
h Administer ivermectin at 50 µg/kg

PO3 or milbemycin oxime at 1 mg/kg
PO 4
AUTHOR INSIGHT1 • Use a product containing only

milbemycin oxime (ie, no
combination products)
Resistance to ML preventives in canine heartworm cases has been proven, though there are • An adverse reaction is unlikely if

prophylaxis has been compliant,
few documented cases. To the authors’ best knowledge, clinical patterns to date suggest as previous treatments by the
that most proven cases of ML resistance in heartworms have been diagnosed in dogs owner would have been made
while the dog was microfilaremic;
residing in or translocated from the Mississippi Delta region and that cases of resistance are however, because compliance can
rare outside this region. However, it is possible that resistance is more widespread than never be assured, these drugs
should be administered at the
currently recognized. No tests for resistance are available to determine the prevalence and veterinary hospital and the dog
distribution of resistance in heartworms,5 making definitive diagnosis impossible. observed for 6-8 hours
postadministration of
microfilaricide
h Perform a second Knott’s test 7

days after microfilaricide
AHS = American Heartworm Society administration
MF = microfilariae
ML = macrocyclic lactone
 DIAGNOSTIC/MANAGEMENT TREE h INFECTIOUS DISEASE h PEER REVIEWED

 
 
 
 
References
DIAGNOSIS TREATMENT 1. Current Canine Guidelines for the

h R esistance can be neither confirmed nor disproven† h N o special resistance Prevention, Diagnosis, and Management
NO h Even if resistance is present, further transmission management required of Heartworm Infection in Dogs. American

of resistant worms is not possible because MF must h P roceed with Heartworm Society. https://www.
be ingested by mosquitoes for parasite AHS-recommended heartwormsociety.org/images/pdf/2014-
transmission to occur treatment protocol 1 AHS-Canine-Guidelines.pdf. Accessed
September 2015.
2. Geary TG, Bourguinat C, Prichard

RK. Evidence for macrocyclic lactone
anthelmintic resistance in Dirofilaria
immitis. Top Companion Anim Med.
2011;26(4):186-192.
3. Jackson RF, Seymour WG, Beckett

RS. Routine use of 0.05 mg/kg of
ivermectin as a microfilaricide. In: Otto
GF, ed. Proceedings of the Heartworm
Symposium, 1986; Washington, DC: 37-39.
>75% decrease in number of MF?
4. Sasaki Y, Kitagawa H. Effects of

milbemycin D on microfilarial number and
reproduction of Dirofilaria immitis in dogs.
YES NO J Vet Med Sci. 1993;55(5):763-769.
5. Bourguinat C, Lee AC, Lizundia R, et

al. Macrocyclic lactone resistance in
Dirofilaria immitis: failure of heartworm
preventives and investigation of genetic
DIAGNOSIS DIAGNOSIS markers for resistance. Vet Parasitol.
Low suspicion of resistance; if no High suspicion of resistance
2015;210(3-4):167-178.
MF, resistance is highly unlikely
*Performance of the MF suppression test

is recommended by the authors solely to
identify resistant heartworm cases and is
TREATMENT not a normal standard of care procedure for
TREATMENT h I mmediately initiate doxycycline at 10 mg/kg twice treating heartworm cases.
Proceed with AHS-recommended daily for 30 days1 †To the authors’ knowledge, all proven cases
treatment protocol 1 h P roceed with AHS-recommended treatment

of resistance as of time of original publication
protocol 1 (November 2015) have been microfilaremic.
h C onsider a topical product that repels mosquitoes Lack of MF suggests that the case does not
to minimize possibility of transmission involve resistance, the dog has no female
worms, or infections are still immature and
have not yet become patent.
TICK-BORNE INFECTIOUS DISEASE IN U.S. DOGS
Craig Datz, DVM, MS, DABVP (Canine & Feline Practice)*
University of Missouri

TICK-BORNE DISEASE SUSPECTED IN A DOG (EG, FEVER, LETHARGY,

LYMPHADENOPATHY, HISTORY OF TICK EXPOSURE)

Geographic location Clinical signs

Northeast, Eastern Midwest, Southeast, Epistaxis, petechiae, Coughing, Edema, vasculitis of

Seaboard, Southwest ecchymoses respiratory distress extremities (eg, lips,
Midwest, West (most RMS cases pinnae, scrotum)
diagnosed in NC,
OK, AR, TN, MO)

DIAGNOSIS DIAGNOSIS DIAGNOSIS DIAGNOSIS DIAGNOSIS

EHR, ANA, BOR, BAB EHR, RMS, BAB EHR, ANA, RMS ANA, RMS RMS

West, Southwest Southeast Lameness Mucous membrane

color

DIAGNOSIS DIAGNOSIS Effusive (swollen) Joint pain, Pale

EHR, BAB EHR, RMS, BAB joint(s) noneffusive

DIAGNOSIS DIAGNOSIS DIAGNOSIS

BOR EHR, ANA, RMS EHR, ANA, BAB
ANA = anaplasmosis (Anaplasma phagocytophilum)
BAB = babesiosis (Babesia canis, B gibsoni)
BOR = borreliosis (Lyme disease; Borrelia burgdorferi)
EHR = ehrlichiosis (Ehrlichia canis, E ewingii) *Byline reflects author information on original publication. On publication of this collection,
RMS = Rocky Mountain spotted fever (Rickettsia rickettsii) the author’s current credentials and affiliation are Craig Datz, DVM, DABVP (Canine & Feline
Practice), DACVN, at Royal Canin USA, Columbia, Missouri.
 DIAGNOSTIC TREE  h  INFECTIOUS DISEASE  h  PEER REVIEWED

CBC

Normal Thrombocytopenia Anemia Severe, hemolytic

(mild to moderate)

DIAGNOSIS DIAGNOSIS DIAGNOSIS DIAGNOSIS

BOR EHR, ANA, RMS, BAB EHR, ANA, RMS, BAB BAB

Icteric Red blood cell inclusions White blood cell

(organisms) inclusions (morulae)
present in blood smear present in blood smear

DIAGNOSIS Large, piriform Small, round, Granulocytes Monocytes

BAB, RMS (teardrop) oval, ring shaped

DIAGNOSIS DIAGNOSIS DIAGNOSIS DIAGNOSIS

BAB (B canis) BAB (B gibsoni) EHR (E ewingii), EHR (E canis)
ANA
ANEMIA
Caroline M. Kiss, DVM*
Bess J. Pierce, DVM, DABVP, DACVIM†
Virginia-Maryland Regional College of Veterinary Medicine

ANEMIA

INVESTIGATION
h Aggregate reticulocyte count >60 000/mcL (cats) or >8 0 000/mcL (dogs)?
NO


h Evidence of increased MCV, MCHC, or RDW?

YES

DIAGNOSIS
Regenerative anemia

History and physical examination identify a cause of blood loss?

Low to low–normal total solids

YES NO or albumin and globulin?
NO

INVESTIGATION
h Blood loss (2-3 days post acute or chronic without iron deficiency) YES INVESTIGATION

h Rule out GI parasites or ulceration, coagulopathy, thrombocytopenia, Blood smear evaluation

neoplasia, or trauma

Spherocytes or Heinz bodies or Blood parasites Unremarkable Significant acanthocytes,

autoagglutination eccentrocytes RBC morphology schistocytes

DIAGNOSIS DIAGNOSIS Rule out Mycoplasma spp, Rule out occult hemorrhage, DIAGNOSIS
Primary or secondary Anemia/oxidative damage Babesia spp, or IMHA, enzymopathies, Microangiopathic anemia ‡
IMHA h Rule out onions, garlic, Ehrlichia spp hereditary anemias, h Rule out hemangio-


h Rule out underlying zinc, § acetaminophen, hemophagocytic syndromes, sarcoma, DIC, vasculitis,

infectious, neoplastic, and propylene glycol and hypophosphatemia splenic torsion, heat
drug, or toxic process stroke, and dirofilariasis

*Byline reflects author information on original publication. On publication of this

DIC = disseminated intravascular coagulation MCV = mean cell volume

collection, the author’s current credentials are Caroline M. Kiss, DVM, DABVP, with no
IMHA = immune-mediated hemolytic anemia NRBC = nucleated red blood cell current affiliation.
†Byline reflects author information on original publication. On publication of this

MCHC = mean corpuscular hemoglobin concentration RDW = red cell distribution width collection, the author’s current affiliation is Lincoln Memorial University, Harrogate,
Tennessee.
‡Microangiopathic anemia occasionally presents as nonregenerative anemia.

§Spherocyte-like RBC morphology may be noted in zinc toxicity; however, Heinz

bodies are usually more prevalent.
 DIAGNOSTIC TREE h INTERNAL MEDICINE h PEER REVIEWED

 
 
 
 
DIAGNOSIS
Nonregenerative anemia

Is animal presenting with acute clinical signs of anemia (eg, weakness, pallor, tachypnea, tachycardia)?

YES NO

DIAGNOSIS DIAGNOSIS
Preregenerative anemia True nonregenerative anemia
h Low to low–normal total solids h Do history, physical examination, and diagnostic tests


or albumin and globulin levels? indicate that another disease process is occurring?

NO
YES NO YES YES

INVESTIGATION
Presence of microcytosis or hypochromasia?
DIAGNOSIS DIAGNOSIS DIAGNOSIS DIAGNOSIS
Acute blood loss Acute hemolytic Depression by disease 1 Infectious cause
h Rule out disease h Anemia of inflammatory disease h Ehrlichia spp



neoplasia, h Rule out primary h Cancer-associated anemia h Anaplasma spp



trauma, or secondary h Chronic liver and kidney disease h Parvovirus


coagulopathy, IMHA, blood h Critical illness h FeLV
YES NO


thrombocyto- parasites, Heinz h Hypothyroidism h FIV


penia, or GI body anemia, h Hypoadrenocorticism

ulceration microangiopathic
anemia

INVESTIGATION INVESTIGATION
Presence of NRBCs with or without basophilic stippling? Bone marrow aspirate
or core biopsy

Reference
1. Mitchell K, Kruth S. Immune-mediated

hemolytic anemia and other regenerative
anemias. In: Ettinger SJ, Feldman EC, eds. DIAGNOSIS
Textbook of Veterinary Internal Medicine. 7th ed.
YES NO h Bone marrow

St. Louis, MO: Saunders; 2010:761-772. neoplasia
h Aplastic anemia

h Pure red cell aplasia
Suggested Reading

h Myelonecrosis
DIAGNOSIS INVESTIGATION

Abrams-Ogg A. Nonregenerative anemia. In:
h Myelophthisis

Lead poisoning Low to low–normal total serum iron and h Myelodysplastic
Ettinger SJ, Feldman EC, eds. Textbook of

high to high-normal transferrin levels? syndrome
Veterinary Internal Medicine. 7th ed. St. Louis,
MO: Saunders; 2010:788-797.
Giger U. Regenerative anemias caused by blood
loss or hemolyis. In: Ettinger SJ, Feldman EC,
eds. Textbook of Veterinary Internal Medicine. DIAGNOSIS INVESTIGATION
6th ed. St. Louis, MO: Saunders; 2005:1886-1907. Iron deficiency anemia Rule out anemia due to inflammatory
Weiss DJ. Nonregenerative anemias. In: Bonagura JD, h Rule out blood YES NO disease, chronic liver disease,

Twedt DC, eds. Kirk's Current Veterinary Therapy loss chronic or folate or cobalamin deficiency
XIV. St. Louis, MO: Saunders; 2009:272-276.
ANOREXIA IN THE RABBIT
Angela M. Lennox, DVM, DABVP (Avian)
Avian & Exotic Animal Clinic
Indianapolis, Indiana

INVESTIGATION INVESTIGATION
Medical history Complete physical examination
h Signalment
Abdominal Ears/Ear Canal/Eyes Oral Cavity

h Presenting clinical signs
h Pain upon palpation h Palpate base of ears h Examine incisors

h Progression, systems



h Presence of masses, excessive h Evaluate lens/anterior chamber h Perform cursory otoscopic

affected



h Date when last normal
fluid, food, and/or gas* h Note evidence of exophthalmia or examination of oral cavity


epiphora h Palpate jaw

h Medical and surgical

Cardiovascular

history h Murmur, arrhythmia, rate
h Response to any previous
Mentation Respiratory

h General activity level h Increased rate of effort

therapy?


Dermatologic h Interest in environment* h Auscultation



h Hair loss, generalized or under h Evidence of nasal discharge*
Environmental history


h Complete dietary history,
eyes or chin, suggesting epiphora Musculoskeletal
or ptyalism h Reluctance to move Urogenital

including recent changes

h Evidence of ectoparasites h Lameness or discomfort h Pain upon palpation of the
h Potential toxin exposure



h Pododermatitis h Swelling bladder

h Exposure to other pets or


h Character of urine

illness in companions


h History of social structure,
Gastrointestinal Neurologic
h Willingness to eat h Central and/or peripheral nerve

especially recent changes


h Amount and character of stool* deficit
h Changes in environment


(eg, bedding, toys, * Repeat these examinations every 3 to 4 hours while anorexia persists in the hospitalized patient
visitors, disruptions)

Evidence of disease in a specific body system or suggestion of environmental stress as a potential cause of anorexia?

YES NO

INVESTIGATION INVESTIGATION
Diagnostic tests specific to body system: Initial diagnostic tests:
h Oral cavity: complete evaluation of h CBC with blood smear


oral cavity in anesthetized patient h Serum chemistry profile

h Abdominal: radiography h Abdominal radiography


h Musculoskeletal: radiography of spine h Complete evaluation of oral


and limbs cavity in anesthetized patient
h Eyes (exophthalmos): radiography h Urinalysis


Evidence of specific disease?

YES NO

h Initiate treatment for disease If environmental stress is suspected,


or send patient home, have owner hand-feed,
h Conduct further diagnostic testing specific to body system and allow 48 hours for adjustment

 DIAGNOSTIC/MANAGEMENT TREE h INTERNAL MEDICINE h PEER REVIEWED

 
 
 
 
Repeat physical examination

Evidence of disease in a specific body system?

YES NO

Conduct tests specific INVESTIGATION

to body system Consider additional diagnostic tests:
h Infectious disease titers (Encephalitozoon cuniculi)

h Echocardiography (eg, murmur, arrhythmia)

Evidence of disease in a specific body system?

YES NO

Conduct tests specific Repeat physical examination

to body system and review patient history

Evidence of disease in a
specific body system?

YES NO

Conduct tests specific TREATMENT

to body system Therapy options:
h Consider therapeutic trial

h Begin hand-feeding high-fiber liquid diet

h Administer IV fluids to dehydrated patients

h Administer SC fluids to nonclinically dehydrated patients to help

rehydrate GI tract
h Send noncritically ill patients home with instructions on how to hand-feed
Suggested Reading

h Consider analgesia if there is indication of discomfort (eg, ileus)

Lichtenberger M, Lennox AM. Updates and advanced therapies for gastrointestinal h Consider motility-enhancing drugs

stasis in rabbits. Vet Clin N Am Exotic Pet Prac. 2010;13(3):525-543.
CHRONIC DIARRHEA IN CATS
Jörg M.Steiner, MedVet, DrMedVet, PhD, DACVIM, DECVIM-CA*
Texas A&M University

CHRONIC DIARRHEA

INVESTIGATION Negative
Obtain history and physical examination

TREATMENT
Findings suggestive of specific Treat with broad-spectrum anthelmintic agent
disease (eg,abdominal
fluid, neurologic signs)?
YES NO
INVESTIGATION
CBC, serum chemistry profile, urinalysis, thyroxine (T4)‡
Pursue specific disease Fecal smear
and flotation†

Positive Findings suggestive

of specific disease
(eg, hepatic disease,
YES renal failure)? NO
TREATMENT
Treat with specific anthelmintic agent
Pursue specific disease Characterize diarrhea

No response Mostly large bowel Mostly small bowel

Younger cat Older cat

INVESTIGATION INVESTIGATION
Tritrichomonas foetus PCR test Conduct further diagnostics

Positive Negative

TREATMENT INVESTIGATION
Treat with ronidazole Retest for Giardia spp, or test
for other enteropathogens

EPI = exocrine pancreatic insufficiency

Positive Negative
fPLI = feline pancreatic lipase immunoreactivity
fTLI = feline trypsin-like immunoreactivity
PCR = polymerase chain reaction
T4 = total thyroxine TREATMENT
Treat as appropriate
 MANAGEMENT TREE h INTERNAL MEDICINE h PEER REVIEWED

 
 
 
 
INVESTIGATION
Serum cobalamin, folate, fTLI, and fPLI concentrations

YES fTLI <8 µg/L NO

DIAGNOSIS YES fPLI >5.7 µg/L NO

EPI

DIAGNOSIS YES Cobalamin <400 ng/L NO

Treat with enzyme Feline pancreatitis
supplementation

DIAGNOSIS YES Folate <9.7 µg/L NO

Evaluate for risk Distal small intestinal disease
factors and
concurrent
diseases
DIAGNOSIS Dietary trial¶
Proximal small h Primary choice: novel protein diet, hydrolyzed
DIAGNOSIS intestinal disease 
protein diet, or easily digestible diet
Cobalamin deficiency h Secondary choice: high-fiber diet or low-carb

diet
TREATMENT
Low-fat diet, pain
medications,
antiemetics, and TREATMENT TREATMENT
possibly steroids Cobalamin Folate supplementation ||
No response Response
supplementation §

YES Consider biopsies NO

*Byline reflects author’s information on original publication. On


publication of this collection, the author’s current credentials are
Jörg M. Steiner, MedVet, DrMedVet, PhD, DACVIM, DECVIM-CA,
AGAF.
Response Antibiotic trial # No response
†Zinc sulfate flotation for diagnosis of various parasitic ova and

Giardia spp; some clinicians prefer enzyme-linked immunosor-
bent assays for the diagnosis of Giardia spp infections.
‡In cats older than 6 to 7 years of age.
TREATMENT

§Cobalamin supplementation: use cyanocobalamin (vitamin B12)
YES NO

at 250 µg/dose SC once a week for 6 weeks, every other week for Treat according to Consider biopsies
6 weeks, 1 more dose a month after that, and recheck serum histopathologic diagnosis
cobalamin concentration one month after the last dose, or cya-
nocobalamin at 250 µg PO daily for 120 days, and recheck serum
cobalamin concentration two weeks later.
‖Folate should only be supplemented if serum concentrations are Response Treatment trial with an No response

very low (<4 µg/L). immunosuppressive
¶Dietary trial: can use low-antigen diets or easily digestible diets; agent Δ

some response should be seen after 2 weeks, but complete
response could take up to 6 weeks.
#The author prefers tylosin at 25 mg/kg PO q12h for 6 weeks. Consider biopsies

ΔPrednisone with a starting dosage of 2 mg/kg PO q12h, cyclospo-

rine at 5 mg/kg q24h, or budesonide at 1 mg PO q24h.
DIAGNOSING CONSTIPATION,
OBSTIPATION, & MEGACOLON IN CATS
Glenn A. Olah, DVM, PhD, DABVP (Feline)
Winn Feline Foundation
Albuquerque Cat Clinic
Albuquerque, New Mexico

TENESMUS & DYSCHEZIA EVIDENT

INVESTIGATION
Obtain signalment and history, and conduct physical examination, including:
h Urination and defecation habits, including potential decrease in stool or urine output

h History of dysuria, stranguria, hematuria, or periuria

h History of vomiting

h Abdominal palpation (hard stool in colon, urinary bladder size and turgidity)

h Painful bladder

h Protrusion of tissue at the rectum

h Rectal or penile discharge

h Penile tip discoloration (eg, dark red) and/or small crystalline grain present

Urogenital disease suspected First episode of constipation suspected Recurrent episode of constipation suspected

Diagnostics pursued to determine cause?

YES NO

INVESTIGATION Make diagnosis based on TREATMENT

Obtain minimum database, including: diagnostic test results h Rehydration (SC or IV) to

h CBC correct deficit and provide

h Serum chemistry profile maintenance

h Total thyroxine (in patients older than h ± enema


7 years) • Avoid sodium phosphate

h FeLV/FIV status enemas due to potential

h Urinalysis ± urine culture
DIAGNOSIS DIAGNOSIS life-threatening electrolyte

h Abdominal ± pelvic diagnostic imaging imbalance
Urogenital disease Constipation, with

h ± rectal examination (under sedation) h Feline idiopathic • Warm water (5-10 mL/kg)
potential progression



h ± orthopedic examination with lubricant gel (5-10
cystitis to obstipation and

h ± neurologic examination h Urogenital neoplasia mL/cat), DSS (5-10 mL/cat),
megacolon


h Urethral obstruction or lactulose (5-10 mL/cat)

h UTI is recommended

h Urolithiasis h ± polyethylene glycol 3350


h Prostatic disease (rare) solution

• Trickle via NE tube (6-10

mL/kg/hr)
• Defecation usually occurs in

6-12 hours (median, ≈8 hr)
TREATMENT h ± removal of impaction

Treat appropriately for concurrent h ± treatment of any other

diseases and/or urogenital disease concurrent diseases

DSS = dioctyl sodium sulfosuccinate

NE = nasoesophageal
 DIAGNOSTIC/MANAGEMENT TREE h INTERNAL MEDICINE h PEER REVIEWED

 
 
 
 
Bowel movement within 24 hours of treatment?

YES NO

TREATMENT
Repeat therapy
h Rehydration

h Enema

• Avoid sodium phosphate enemas due to potential life-

threatening electrolyte imbalance
• Warm water (5-10 mL/kg) with lubricant gel (5-10 mL/cat), DSS

(5-10 mL/cat), or lactulose (5-10 mL/cat) is recommended
h Manual deobstipation under anesthesia

h Treatment of any other concurrent diseases

TREATMENT
Long-term management

h Maintain hydration

h Adjust diet to canned foods with water or low-residue or psyllium-enriched diets

h Preventive laxative (psyllium, wheat bran, pumpkin, polyethylene glycol 3350, lactulose)

h ± prokinetic agents (eg, cisapride, mosapride, tegaserod, prucalopride)

Patient refractory to medical or dietary management?

YES NO

INVESTIGATION TREATMENT
Repeat or conduct physical Continue medical
examination and minimum database management
as needed

DIAGNOSIS
See Constipation, with potential progression
to obstipation and megacolon, next page

Continues h
 DIAGNOSIS
Constipation, with potential
progression to obstipation
and megacolon*

Determine etiology based on previously performed diagnostic test results

ETIOLOGY ETIOLOGY ETIOLOGY

Behavioral/environmental Neuromuscular dysfunction Inflammation/infection
factors h Spinal disease h Perianal bite wounds


h Environmental change • Intervertebral disk disease and/or abscess


(eg, new home, new • Lumbosacral stenosis/cauda equina syndrome h Anal sacculitis and/or



routine, seasonality) • Sacrocaudal dysgenesis (eg, in Manx cats) abscess

h Inactivity • Infection (eg, FIP, FeLV/FIV) or fungal disease h Arthritis



h Intercat conflict • Neoplasia h Proctitis



h Soiled litter box h Hypogastric or pelvic nerve disease h Perineal fistula and/or



h Stress and/or anxiety • Neoplasia rectal diverticulum


(eg, hospitalization) • Trauma injury
h Submucosal or myenteric plexus neuropathy

• Aging
• Dysautonomia
• Infection (eg, FIP, FeLV/FIV) or fungal disease TREATMENT
TREATMENT • Neoplasia h Abscess treatment

h Address environmental h Colonic smooth muscle dysfunction (ie, megacolon) h Antibiotics



needs (see Suggested h Foreign body removal

Reading, page 96) h Anti-inflammatory drugs

h Address intercat social (eg, NSAIDs, tacrolimus,

structure cyclosporine,
h Address litter box issues TREATMENT corticosteroids)

h 
P rovide stress and/or h Treat or manage underlying cause h Anal gland expression


anxiety management h Further diagnostics may be required and/or removal

*Megacolon is suggestive of neuromuscular dysfunction.

CKD = chronic kidney disease

DM = diabetes mellitus
IBD = inflammatory bowel disease
 DIAGNOSTIC/MANAGEMENT TREE h INTERNAL MEDICINE h PEER REVIEWED

 
 
 
 
ETIOLOGY ETIOLOGY ETIOLOGY
Adverse drug effects Metabolic/endocrine Mechanical obstruction
h Opiates h Metabolic h Intraluminal



h Anticholinergics • Obesity • Colonic foreign body

h Diuretics • Dehydration (due to CKD, hyperthyroidism, or DM) • Anorectal foreign body or


h Antianxiety or • Hypercalcemia (due to CKD or idiopathic hypercalcemia) fecolith

psychotropic drugs h Endocrine • Rectal diverticulum

h Phenothiazines • Hypothyroidism (iatrogenic or acquired) • Perineal hernia

h Barium sulfate • Nutritional or renal secondary hyperparathyroidism • Anorectal stricture/stenosis


h Intramural

• Neoplasia
• IBD
h Extraluminal

• Pelvic fractures and/or


malunions, with secondary
obstipation or megacolon
• Pseudocoprostasis

(eg, in longhair cats)
• Neoplasia

TREATMENT TREATMENT TREATMENT

h Discontinue medication Treat underlying cause (eg, CKD, hyperthyroidism, h Treat or manage underlying

h Change medication DM, idiopathic hypercalcemia) cause

h For pelvic fractures and/or
malunions, perform surgical pelvic
canal widening if obstipation or
megalon is present for <6 months or
subtotal colectomy if obstipation or
megacolon present for >6 months

DIAGNOSIS DIAGNOSIS
Recurrent constipation or Long-standing obstipation
obstipation, with or without or megacolon
reversibly dilated colon for
<6 months

TREATMENT TREATMENT
Go to First/recurrent Perform subtotal colectomy if patient has
episode constipation obstipation for >6 months or if dilated
treatment, page 92 colon (ie, megalon) present for >6 months Continues h
DIAGNOSTIC/MANAGEMENT TREE h INTERNAL MEDICINE h PEER REVIEWED

 
 
 
 
References
Atkins CE, Tyler R, Greenlee P. Clinical, biochemical, acid-base, and Meeson RL, Geddes AT. Management and long-term outcome of
electrolyte abnormalities in cats after hypertonic sodium phosphate pelvic fractures: a retrospective study of 43 cats. J Feline Med Surg.
enema administration. Am J Vet Res. 1985;46(4):980-988. 2017;19(1):36-41.
 
  
Baral RM. Constipation and megacolon. In: Little SE, ed. The Cat: Clinical Rondeau MP, Meltzer K, Michel KE, McManus CM, Washabau RJ. Short
Medicine and Management. St. Louis, MO: Elsevier Saunders; 2012: chain fatty acids stimulate feline colonic smooth muscle contraction.
484-490. J Feline Med Surg. 2003;5(3):167-173.
Bertoy RW. Megacolon in the cat. Vet Clin North Am Small Anim Pract. Rosin E, Walshaw R, Mehlhaff C, Matthiesen D, Orsher R, Kusba J. Subtotal
2002;32(4):901-915. colectomy for treatment of chronic constipation associated with
Byers CG, Leasure C, Sanders N. Feline idiopathic megacolon. Compend idiopathic megacolon in cats: 38 cases (1979-1985). J Am Vet Med Assoc.
Contin Educ Vet. 2006;28(9):658-665. 1988;193(7):850-853.
Carr AP, Gaunt MC. Constipation resolution with administration of polyeth- Scherk M. All bunged up: uclogging the constipation cat. DVM360.
ylene glycol solution in cats (abstract). J Vet Intern Med. 2010;24:753-754. DVM360 website. http://veterinarymedicine.dvm360.com/all-bunged-
unclogging-constipated-cat. Published March 11, 2015. Accessed July
Chandler M. Focus on nutrition: dietary management of gastrointestinal
30, 2018.
disease. Compend Contin Educ Vet. 2013;35(6):E1-E3.
Tam FM, Carr AP, Myers SL. Safety and palatability of polyethylene glycol
Elliott JW, Blackwood L. Treatment and outcome of four cats with
3350 as an oral laxative in cats. J Feline Med Surg. 2011;13(10):694-697.
apocrine gland carcinoma of the anal sac and review of the literature.
J Feline Med Surg. 2011;13(10):712-717. Tomsa K, Steffen F, Glaus T. Life-threatening metabolic disorders after
application of a sodium phosphate containing enema in the dog and
Foley P. Constipation, tenesmus, dyschezia, and fecal incontinence. In:
cat. Schweiz Arch Tierheilkd. 2001;143(5):257-261.
Ettinger SJ, Feldman EC, Côté E, eds. Textbook of Veterinary Internal
Medicine. 8th ed. St. Louis, MO: Elsevier; 2017:171-174. Trevail T, Gunn-Moore D, Carrera I, Courcier E, Sullivan M. Radiographic
diameter of the colon in normal and constipated cats and in cats with
Freiche V, Houston D, Weese H, et al. Uncontrolled study assessing the
megacolon. Vet Radiol Ultrasound. 2011;52(5):516-520.
impact of a psyllium-enriched extruded dry diet on fecal consistency in
cats with constipation. J Feline Med Surg. 2011;13(12):903-911. Washabau RJ. Constipation. In: Washabau RJ, Day MJ, eds. Canine and
Feline Gastroenterology. St. Louis, MO: Elsevier; 2013:93-98.
Gaschen F. Disorders of esophageal, gastric, and intestinal motility in cats.
In: Little SE, ed. August’s Consultations in Feline Internal Medicine, vol. 7. Washabau RJ. Gastrointestinal motility disorders and gastrointestinal
St. Louis, MO: Elsevier; 2016:117-128. prokinetic therapy. Vet Clin North Am Small Anim Pract. 2003;33(5):1007-
1028.
German AC, Cunliffe NA, Morgan KL. Faecal consistency and risk factors
for diarrhoea and constipation in cats in UK rehoming shelters. J Feline Washabau RJ, Hall JA. Diagnosis and management of gastrointestinal
Med Surg. 2017;19(1):57-65. motility disorders in dogs and cats. Compend Contin Educ Vet.
1997;19(6);721-737.
Gregory CR, Guilford WG, Berry CR, Olsen J, Pederson NC. Enteric function
in cats after subtotal colectomy for treatment of megacolon. Vet Surg. Washabau RJ, Holt D. Pathogenesis, diagnosis, and therapy of feline
1990;19(3):216-220. idiopathic megacolon. Vet Clin North Am Small Anim Pract.
1999;29(2):589-603.
Hall EJ. Disease of the large intestine. In: Ettinger SJ, Feldman EC, Côté
E, eds. Textbook of Veterinary Internal Medicine. 8th ed. St. Louis, MO: Washabau RJ, Stalis IH. Alterations in colonic smooth muscle function in
Elsevier; 2017:1565-1592. cats with idiopathic megacolon. Am J Vet Res. 1996;57(4):580-587.
   
Hall JA, Washabau RJ. Diagnosis and treatment of gastric motility White RN. Surgical management of constipation. J Feline Med Surg.
disorders. Vet Clin North Am Small Anim Pract. 1999;29(2):377-395. 2002;4(3):129-138.
Hasler AH, Washabau RJ. Cisapride stimulates contraction of idiopathic
megacolonic smooth muscle in cats. J Vet Intern Med. 1997;11(6):313-318. Suggested Reading
Little S. How I treat … constipation in cats. Paper presented at: Southern Buffington CAT. Household resource checklist. Clinician’s Brief.
European Veterinary 2016 Conference; October 20-22, 2016; Grenada, 2011;9(11):58.
Spain.
 DIAGNOSTIC/MANAGEMENT TREE h INTERNAL MEDICINE h PEER REVIEWED

 
 
 
 
COUGH IN CATS
Janice Dye, DVM, MS, PhD, DACVIM (SAIM)
Raleigh, North Carolina

SNEEZING OR NASAL DISCHARGE? NOISY (STERTOROUS)

YES NO
BREATHING? RETCHING OR GAGGING? ALTERED VOCALIZATION?

Laryngopharyngeal cough INVESTIGATION

Perform thoracic examination and auscultation, tracheal palpation, thoracic radiography, MDB

INVESTIGATION Adventitial lung sounds Normal or reduced bronchovesicular sounds

Perform MDB, cranial and oral
examination, skull or neck radiography
or CT, rhinoscopy or laryngoscopy

Tracheobronchial cough Nonspecific cough

DIFFERENTIALS
h R hinitis/sinusitis
• Infections Radiographic evidence of bronchial, mixed INVESTIGATION
• Inflammatory (idiopathic) bronchointerstitial, or bronchoalveolar pattern Serology, fecal examinations, BAL
• Atopy-related* or fine-needle lung aspiration
• Neoplasia (cytology/culture), thoracic CT
h L
 aryngitis
• Infectious
• Inflammatory INVESTIGATION
• Postnasal drip* Bronchoscopy and/or airway sampling (cytology/
• Injury (prior intubation) culture), heartworm antigen and antibody DIFFERENTIALS
• Irritant exposure (eg, noxious fumes/ h P neumonia/pneumonitis

gases, particles or dust, smoke • Viral (eg, FHV-1, FCV)
inhalation, ETS, litter) • Parasitic (eg, Dirofilaria spp, other)
h L  aryngeal or nasopharyngeal mass, • Mycotic
polyp, stenosis, or foreign material (eg, DIFFERENTIALS • Bacterial: primary (eg, Bordetella
h Tracheitis/bronchitis • Foreign material

hair, food, medication) spp) or secondary (eg, dental
h C  omorbid conditions (rule-outs similar to • Postnasal drip* disease)
• Megaesophagus laryngitis) h Airway obstruction • Protozoal (Toxoplasma spp)

• Infectious (viral) h Airway mucus, debris


• Laryngeal paralysis • Atopy-related*

• Inflammatory (eg, feline h Airway fluid or hemorrhage


h P leuritis or pleural space disease (eg,



asthma) h Airway collapse FIP, pleural effusions)

• Atopy/allergy-related h Airway compression h I nterstitial lung disease (eg, IPF, other


• HARD h Comorbid conditions subtypes)

• Idiopathic • Megaesophagus h N eoplasia
• Irritant exposure • Laryngeal paralysis h P ulmonary edema—if severe, CHF,
fluid overload
h E xtrapulmonary chronic inflammatory
conditions (rhinitis, otitis, GERD)
AUTHOR INSIGHT
h Cats have a well-developed cough reflex. Coughing dispels mucus and inhaled substances from the BAL = bronchoalveolar lavage

lower airways. CHF = congestive heart failure
h Coughing is not pathognomonic for a specific diagnosis. It often occurs intermittently, with or with- ETS = environmental tobacco smoke

out wheezing or respiratory distress. Alternatively, it can occur with sneezing/nasal discharge, noisy FCV = feline coronavirus
or stertorous breathing, retching/gagging, or even vomiting. FHV-1 = feline herpervirus type 1
h Chronic cough is frequently related to development of airway inflammation, airway obstruction, GERD = gastrointestinal reflux disease

and mucous hypersecretory states.
HARD = heartworm-associated
h In cats, cough is commonly observed with bronchial or asthma-like disease; it is variable in paren- respiratory disease

chymal or pleural space disorders; and is uncommon in cardiac disease alone. However, concurrent IPF = idiopathic pulmonary fibrosis
pulmonary and cardiac disease may occur. MDB = minimum database
h Posttussive vomiting may be a result of air-induced distension of the stomach.
*analogous to human condition

ELEVATIONS IN TOTAL SERUM CALCIUM
Timothy M. Fan, DVM, PhD, DACVIM (SAIM, Oncology)
University of Illinois

ELEVATIONS IN TOTAL SERUM CALCIUM

Signalment INVESTIGATION
h Young,
growing giant breed dog Serum sample integrity
h N onfasting sample with lipemia
h Hemoconcentration with hyperproteinemia

Reevaluate after skeletal maturity

INVESTIGATION
Repeat total serum calcium measurement:
h I n fasted, nonlipemic sample
h Following rehydration of patient

Persistent elevations in Normalization of

total serum calcium serum calcium

DIAGNOSIS
Transient causes
DIFFERENTIAL INVESTIGATION for hypercalcemia
Potential toxin exposure Physical examination
h Plant calcitriol glycosides

h Cholecalciferol rodenticide

h Antipsoriasis creams containing

calcipotriol or calcipotriene

Caudal displacement Pain or disuse of axial or Mass effect involving: Generalized

of heart sounds appendicular skeletal sites h Anal gland peripheral

INVESTIGATION h Mammary gland lymphadenopathy

Supportive diagnostic for h Thyroid gland

vitamin D toxin exposure. Submit h Salivary gland

serum sample evaluating:
h Ionized calcium
INVESTIGATION

h 25-hydroxyvitamin D
Radiography of anatomic sites

h 1,25-dihydroxyvitamin D h Assessment of lung parenchyma


h Assessment of mediastinum INVESTIGATION

h Assessment for bony changes Minimum database

h CBC

h Serum chemistry profile

h Urinalysis

iCa = ionized calcium
PTH = parathyroid hormone
PTH-rp = parathyroid-hormone–related peptide
tCa = total calcium
 DIAGNOSTIC/MANAGEMENT TREE h INTERNAL MEDICINE h PEER REVIEWED

 
 
 
 
INVESTIGATION
Hypercalcemia database
h iCa

h PTH levels

h PTH-rp assessment

h Elevated iCa h Elevated iCa h Elevated iCa h Elevated tCa




h Elevated PTH h Low or normal PTH h Low PTH h Normal iCa




h Undetectable PTH-rp h Undetectable PTH-rp h Elevated PTH-rp h Normal to elevated PTH




h Undetectable PTH-rp

h Elevated creatinine/BUN


INVESTIGATION INVESTIGATION INVESTIGATION INVESTIGATION DIAGNOSIS
Ventral cervical Consider granuloma- Consider neoplastic, Consider humoral Chronic renal disease
ultrasonography tous diseases osteolytic, or hypercalcemia of
h Identification of h Identification of calcitriol-mediated malignancy


parathyroid nodule organism hypercalcemia
h Support with

elevations in
1,25-dihydroxy-
cholecalciferol INVESTIGATION
DIAGNOSIS Cytology or
h Primary histopathology

hyperparathyroidism h Enlarged lymph

h Adenoma nodes

h Adenocarcinoma h Involved soft tissue


h Hyperplasia h Mediastinal masses


h Bone marrow

TREATMENT
Surgical exploratory
with mass removal
DIAGNOSIS No underlying
Neoplasia pathology identified
h Lymphoma or

thymoma
h Leukemia

h Carcinoma or other

h Bone sarcoma DIAGNOSIS

Consider idiopathic
hypercalcemia (cats)
EXERCISE INTOLERANCE
Daniel L. Chan, DVM, MRCVS, DACVECC, DACVN*
Royal Veterinary College
University of London

EXERCISE INTOLERANCE

INVESTIGATION
h Clarify nature of clinical signs

h Determine whether clinical signs are associated with physical activity

Clinical signs suggestive of cardiovascular, No obvious involvement of cardiovascular,
respiratory, or neurologic dysfunction respiratory, or neurologic systems
h Cough

h Dyspnea

h Unconsciousness

h Collapse

h Cyanosis
Observe patient after short course of exercise;

confirm presence of exercise intolerance

INVESTIGATION
Investigate system suggested INVESTIGATION
by nature of clinical signs Physical examination

Assess BCS Cardiovascular abnormality

h Arrhythmias

h Pulse deficits

h Prolonged capillary refill time

BCS ≤6/9; exercise intolerance not BCS ≥7/9; no other abnormality
related to obesity detected DIAGNOSIS
h Investigate for metabolic causes h Investigate for metabolic causes Exercise intolerance not


h CBC h CBC related to obesity; pursue


h Serum chemistry profile h Serum chemistry profile further diagnostic workup for


abnormal system

DIAGNOSIS DIAGNOSIS
Metabolic abnormality No metabolic abnormality;
obesity-related exercise
intolerance

*Byline reflects author information on original DIAGNOSIS


publication. On publication of this collection, the Exercise intolerance not related to
author’s current credentials are Daniel L. Chan, obesity; pursue further diagnostic
DVM, MRCVS, DACVECC, DECVECC, DACVN, FHEA. workup for abnormal system
 DIAGNOSTIC TREE h INTERNAL MEDICINE h PEER REVIEWED

 
 
 
 
Respiratory abnormality Neurologic abnormality Neuromuscular abnormality Orthopedic abnormality
h Cyanosis h Altered mentation h Muscle wasting h Localized pain




h Abnormal lung sounds h Abnormal reflexes h Poor body condition h Reduced range of motion




h Abnormal upper airway sounds h Abnormal gait h Crepitus on joint manipulation



h Dyspnea h Neurologic deficits


DIAGNOSIS DIAGNOSIS DIAGNOSIS DIAGNOSIS
Exercise intolerance not Exercise intolerance not Exercise intolerance not Exercise intolerance not
related to obesity; pursue related to obesity; pursue related to obesity; pursue related to obesity; pursue
further diagnostic workup for further diagnostic workup for further diagnostic workup for further diagnostic workup for
abnormal system abnormal system abnormal system abnormal system
FELINE WEIGHT LOSS
Margie Scherk, DVM, DABVP (Feline Practice)
catsINK
Vancouver, British Columbia

INVESTIGATION INVESTIGATION
WEIGHT LOSS IN CATS
Obtain complete history: Perform physical examination:
h D
 uration of weight loss h B
 ody weight
h O
 ther clinical signs (eg, vomiting or regurgitation, diarrhea) h %
 weight change* and BCS
h T
 ime when patient last appeared or acted normal h M
 uscle condition (eg, normal or
h C
 hanges in diet or eating behavior wasted), see Suggested Reading
h C
 hanges in environment (eg, change of humans or animals h B
 lood pressure evaluation
present in household, routines, placement of food bowls) h C
 oat condition
h D
 ropping of food or difficulty in prehend ing or chewing h F
 unduscopic examination

­
h E
 vidence of orofacial pain h O
 ral examination
h T
 ravel history h A
 bdominal palpation
h C
 hanges in water intake, urine volume or frequency h P
 ulse quality
h C
 hanges in attitude, energy, activity, or mobility  hyroid palpation †
h T
h C
 hanges in litter box use (eg, volume, frequency, character, h T
 horacic auscultation
color of feces) h L
 ymph node palpation

Good appetite Unable to eat Poor appetite

DIFFERENTIALS DIFFERENTIALS DIFFERENTIALS

h Inadequate intake h O ral neoplasia h  rug therapy (eg, antibiotics,
D
• Poor quality or insufficient quantity h O rofacial or dental fracture chemotherapeutic agents)

of food h D ental disease h F eLV/FIV
h M  aldigestion or malabsorption h D ental pain h C hronic kidney disease
• IBD h N europathy h A cute kidney injury
• Lymphoma h Retrobulbar neoplasia or abscess h C holangitis or hepatitis, hepatic
• EPI h O ral, pharyngeal, esophageal lipidosis
• Systemic fungal infection (if disease h P ancreatitis

regionally likely or if travel history h B iliary tree disease
indicates risk) h N eoplasia
• Age-related sarcopenia h IBD

h E  xcessive nutrient loss h S ystemic fungal infection
• Diabetes mellitus h C NS disease

• Hyperthyroidism h B ored with diet ‡
• Parasitism h D istress (eg, environmental, social) §
• Cachexia (eg, cardiac or neoplastic) h N asal disease
• Protein-losing nephropathy h F oreign body

• Protein-losing enteropathy h A bscess
h O  verutilization h F ever
• Pregnancy or lactation h P ain (arthritis, other)

• Strenuous workload
• Temperature extremes
h Inability to access food (stress,

environment, decreased mobility)

* Percentage of weight change = (previous weight – current weight)/previous weight × 100

†Presence or absence of mass does not rule in or out hyperthyroidism

‡Offer a variety of diets; recheck weight in 10-14 days: if no weight gain, perform MDB; if weight gain, continue with new

diet and recheck weight in 14 days
§If history reveals stress, enrich environment with opportunities to hide and perch, move feeding station to quiet and safe

place, add feeding stations (easy access). See Suggested Reading for environmental needs resources.
 DIAGNOSTIC TREE h INTERNAL MEDICINE h PEER REVIEWED

 
 
 
 
Body system suggested?

YES NO

INVESTIGATION TREATMENT
Perform MDB and additional diagnostics Offer variety of diets‡
appropriate for body system:
h O rofacial: stabilize for thorough dental/oral
assessment with dental ± skull imaging under
anesthesia; biopsy if mass is present
h A bdominal: imaging, cobalamin/folate levels, INVESTIGATION
fTLI (if EPI suspected), fPLI in conjunction with Perform MDB and diagnostics:
abdominal imaging (if pancreatitis suspected) h C BC with differential and cell morph ology, serum chemistry profile, retro viral
­
­
h T horacic: imaging serology, total T4 (older cats), urinalysis, fecal testing (numerous types)
h U rogenital: UP/C if persistent protein uria with h A bdominal imaging
­
inactive urine sediment h T horacic imaging
h C obalamin or folate levels

Assess results

Suggested Reading
Normal Abnormal Ellis SL, Roda I, Carney HC, et al. AAFP and ISFM
feline environmental needs guidelines. J Feline
Med Surg. 2013;15(3):219-230.
WSAVA Global Nutrition Committee. Muscle
condition score. World Small Animal Veterinary
INVESTIGATION DIFFERENTIALS Science website. wsava.org/sites/default/files/
Perform biopsies h C hronic kidney disease Muscle%20condition%20score%20chart-Cats.
h G
 I (eg, surgical, endoscopic) h FeLV/FIV pdf. Published 2014. Accessed September 2019.
h S
 tomach, intestine, pancreas, liver, h H epatopathy Your cat's environmental needs: practical tips for
N eoplasia pet owners. American Association of Feline
mesenteric lymph node, spleen h
Practitioners website. catvets.com/public/
h H yperthyroidism
PDFs/ClientBrochures/Environmental%20
h Parasitic infection
GuidelinesEViewFinal.pdf. Published 2013.
h C ardiomyopathy Accessed September 2019.

Normal Abnormal
EPI = exocrine pancreatic insufficiency
fPLI = feline pancreatic lipse immunoreactivity
fTLI = feline trypsinogen-like immunoreactivity
DIAGNOSIS DIFFERENTIALS IBD = inflammatory bowel disease
Consider CNS disease h IBD
h N  eoplasia MDB = minimum database
h F  ungal disease
T4 = thyroxine
UP/C = urine protein:creatinine ratio
HAIRBALLS
Margie Scherk, DVM, DABVP (Feline Practice)
catsINK
Vancouver, British Columbia

HAIRBALL

INVESTIGATION
Investigate history and clinical signs

Dysmotility Stress, compulsive/stereotypic behavior* Skin disease

INVESTIGATION INVESTIGATION INVESTIGATION

h C ontrast radiography Evaluate social interaction/ h V isual examination
h Ultrasonography environment via history, video h Comb, scrape cytology


h Fluoroscopy h Skin biopsy


h Histopathology

DIAGNOSIS
DIAGNOSIS h S ocialinteraction
h E sophagitis • Cat–cat DIAGNOSIS
h Megaesophagus • Cat–human h E ctoparasites

h Hiatal hernia • Cat–dog h Dermatophytosis


h Diaphragmatic hernia h E nvironment h Allergy


h I ntussusception • Boredom
h G I foreign body • Frustration
h I leus
h N eoplasia
h P arasites

AUTHOR INSIGHT
h Clients may use the term hairballs (ie, tubular wads of ingested hair) to describe loose

strands of hair in vomitus or regurgitated/vomited food; it is important to clarify what
they are defining before determining a diagnostic and therapeutic approach.
h The extreme hairball is a trichobezoar—a hard concretion of hair lodged in the stomach

that is too large to vomit or pass through the pylorus and intestines.
h Cats normally ingest small amounts of hair that pass in feces; increased hair ingestion

(eg, skin/coat problems) or abnormal passage of hair (ie, changes in GI motility) may
*Stress can result in overgrooming, especially when a result in hairballs.

cat has compulsive tendencies and is unable to stop
the behavior once initiated.1 h Hairballs signify disease and, although common, are not normal.

 DIAGNOSTIC TREE h INTERNAL MEDICINE h PEER REVIEWED

 
 
 
 
Abdominal pain Urinary tract pain Musculoskeletal pain

INVESTIGATION INVESTIGATION INVESTIGATION

h L aboratory evaluation h U rinalysis
with sediment Radiography
• Serum chemistry profile examination
• CBC h I maging
• Urinalysis • Radiography ± contrast
• Fecal examination • Ultrasonography
• ± T4 DIAGNOSIS
h Ultrasonography Degenerative joint disease

h ± fPLI/fTLI/cobalamin, folate test h A ppendicular

h Biopsy with histopathology h A xial

DIAGNOSIS h S pinal
h Cystitis
• Idiopathic
• Bacterial
DIAGNOSIS h U rolithiasis
h E ndoparasites h U reteral nephrolithiasis
h I BD h P yelonephritis
h P ancreatitis
h B iliary
tree diseases
• Cholangitis
• Cholelithiasis
• Cholecystitis

Reference
1. Mege C. Skin conditions associated with

behavioural disorders. In: Guaguere E, Prelaud P,
eds. A Practical Guide to Feline Dermatology. Iselin,
NJ: Merial; 1999:17.1-17.11.

fPLI = feline pancreatic lipase immunoreactivity

fTLI = feline trypsin-like immunoreactivity
IBD = inflammatory bowel disease
T4 = thyroxine
DIAGNOSTIC/MANAGEMENT TREE h INTERNAL MEDICINE h PEER REVIEWED

 
 
 
 
HYPONATREMIA
Cristina Perez Vera, DVM*
Sally Bissett, BVSc, MVSc, DACVIM†
North Carolina State University

HYPONATREMIA
h Na + <140 mEq/L in dogs

h Na + <150 mEq/L in cats

INVESTIGATION
Plasma osmolality

High (>310 mOsm/kg) Low (<290 mOsm/kg) Normal (290-310 mOsm/kg)

DIAGNOSIS INVESTIGATION DIAGNOSIS

h Hyperglycemia Urine osmolality h Hyperlipemia


h Mannitol infusion h Hyperproteinemia


<100 mOsm/kg >100 mOsm/kg

DIAGNOSIS DIAGNOSIS
Translocational h Pseudohyponatremia

hyponatremia
DIAGNOSIS DIAGNOSIS
Normal water excretion Impaired water excretion

DIAGNOSIS INVESTIGATION
Primary polydipsia Urine sodium level

<20 mmol/L >20 mmol/L

DIAGNOSIS DIAGNOSIS DIAGNOSIS

Hypovolemia Hypervolemia h A ddison’s disease
h V olume depletion h S evere liver disease h Diuretic drug effect

h GI loss h C ongestive heart h SIADH


h Myxedema coma failure h Renal failure


h Third-space loss h N ephrotic syndrome

h Pancreatitis h A dvanced renal

h Peritonitis failure

*Byline reflects author information on original publication. On publication of this collection, the author’s current credentials
Na+ = sodium

and affiliation are Cristina Perez Vera, DVM, PhD, DACVIM, DECVIM, at Tierklinik Aarau West, Oberentfelden, Switzerland.
SIADH = syndrome of inappropriate †Byline reflects author information on original publication. On publication of this collection, Sally Bissett’s current affiliation

secretion of antidiuretic hormone is Regional Veterinary Emergency and Specialty Center, Turnersville, New Jersey.
 DIAGNOSTIC/MANAGEMENT TREE h INTERNAL MEDICINE h PEER REVIEWED

 
 
 
 
ICTERUS IN DOGS
Peter S. Chapman, BVetMed, DECVIM-CA, DACVIM, MRCVS
Veterinary Specialty & Emergency Center
Levittown, Pennsylvania

ICTERUS OBSERVED

Evaluate PCV and/or HCT

Patient anemic?

YES NO

Evaluate reticulocyte count Conduct serum chemistry profile

Regenerative anemia? Elevated liver enzymes?

YES NO YES NO

Recheck PCV and HCT in 1-2 days See Liver enzymes Perform urinalysis
elevated, page 85

LOCALIZATION Anemia progressive? Bilirubinuria

Prehepatic icterus present?

Anemia significant? YES NO

YES NO

Recheck reticulocyte
YES NO count in 2 days Recheck PCV and/
or HCT to rule out
True icterus
unlikely
developing
anemia

Conduct further diagnostic investigation of anemia

Return to Patient anemic?

See Immune-mediated disease See Conduct serum HCT = hematocrit

suspected, next page chemistry profile PCV = packed cell volume Continues h
 IMMUNE-MEDIATED
DISEASE SUSPECTED

Evidence of immune-mediated disease (eg, autoagglutination,

spherocytes, positive Coombs test result)?

YES NO

DIAGNOSIS Possible nonimmune-mediated causes of hemolytic

IMHA anemia (eg, toxins, infectious disease, enzymopathies)?

Evidence of underlying disease?

YES NO

h Consider recent vaccinations,

infectious disease, neoplasia

Conduct further diagnostic


investigation:
h Abdominal radiography to rule
YES NO

out zinc foreign body
h Infectious disease testing,

particularly serologic or PCR
testing for babesiosis
h Genetic testing for congenital
DIAGNOSIS DIAGNOSIS

Secondary IMHA Primary enzymopathies (eg, pyruvate
(idiopathic) IMHA kinase deficiency, phosphofruc-
tokinase deficiency)

TREATMENT TREATMENT
Treatment and/or management h Immunosuppressive therapy

of underlying disease h Other supportive medications

ALP = alkaline phosphatase
ALT = alanine aminotransferase
GGT = gamma-glutamyl transpeptidase
IMHA = immune-mediated hemolytic anemia
 DIAGNOSTIC/MANAGEMENT TREE h INTERNAL MEDICINE h PEER REVIEWED

 
 
 
 
LIVER ENZYMES ELEVATED

Serum chemistry indicators of liver failure (eg, hypoalbuminemia,

hypoglycemia, hypocholesterolemia, low BUN)?

YES NO

DIAGNOSIS Other serum chemistry indicators of cholestasis†

Suspected hepatocellular failure (eg, hypocholesterolemia, elevated GGT)?

LOCALIZATION YES NO
Suspected intrahepatic cause of icterus

LOCALIZATION ALP >2 times ALT value?

Evaluate blood ammonia level* Suspected extrahepatic
cause of icterus

Elevated Normal Conduct further diagnostic YES NO


investigation for extrahepatic
cholestasis:
h Ultrasonography

h Biliary aspiration
Perform abdominal

DIAGNOSIS h Surgical exploration to
ultrasonography

Suspected concurrent evaluate hepatobiliary
hepatic encephalopathy tract
h Liver biopsy

Evidence of extrahepatic biliary
Perform disease (eg, mucocele,
TREATMENT coagulation cholelithiasis, bile duct dilation,
h Antibiotics profile gall bladder wall changes)?

h Lactulose

YES NO
Abnormal Normal

Perform liver biopsy (ultrasound-guided,

TREATMENT h Consider toxin exposure laparoscopic, or laparotomy)

Administration of plasma and/or infectious disease
h Check leptospirosis titers

Proceed as determined by gross and
histopathologic findings

*Clinicians should reference their laboratory’s reference range


when determining whether a value may be elevated, as reference
ranges can vary between laboratories.
†Hypercholesterolemia should only be considered significant if the

patient has been fasted for 8 hours prior to sample collection.
INCREASED LIVER ENZYMES IN DOGS: ALP
Julie Allen, BVMS, MS, MRCVS, DACVIM (SAIM)*
North Carolina State University

INCREASED ALKALINE
PHOSPHATASE†

NO INVESTIGATION YES
Clinical abnormalities?

INVESTIGATION
Check for administration of steroids (including
topical forms), phenobarbital; discontinue INVESTIGATION INVESTIGATION
Weight loss, vomiting, diarrhea, Polyuria, polydipsia, hair coat
decreased appetite changes, polyphagia, panting

INVESTIGATION INVESTIGATION
<1 year of age Recheck ALP in
4-6 weeks INVESTIGATION
CBC, serum chemistry panel,
urinalysis, total T4 analysis

DIAGNOSIS Persistent or
Bone-related progressive ALP
isoenzyme (especially increase INVESTIGATION
in Siberian huskies) Supportive of HAC?

DIFFERENTIAL Breeds with INVESTIGATION NO YES

Bone disease increased incidence h Abdominal ultrasound

(eg, osteosarcoma) of hepatic disease‡ h Fasting and 2-hour

should have postprandial bile acids
elevated liver values INVESTIGATION
pursued h Low-dose dexamethasone
aggressively.

suppression test
h Abdominal ultrasound

h Urine cortisol:creatinine

ratio
h ACTH stimulation test

*Byline reflects author information on original publication. On publication of this

collection, the author’s current credentials and affiliation are Julie Allen, BVMS,
MS, MRCVS, DACVIM (SAIM), DACVP, at Veterinary Information Network.
†Any increased ALP should be rechecked at least once to rule out a spurious

result or laboratory error, particularly in a nonclinical patient.
‡More aggressive evaluation should be considered in breeds predisposed to Normal DIAGNOSIS
HAC

hepatic disease: Bedlington terriers, West Highland white terriers, Labrador
retrievers, standard poodles, cocker spaniels, English springer spaniels,
Doberman pinschers, dalmatians, Scottish terriers, and Skye terriers. Early
diagnosis may improve treatment success and prognosis.
 DIAGNOSTIC TREE h INTERNAL MEDICINE h PEER REVIEWED

 
 
 
 
INVESTIGATION
h Fine-needle aspiration

h Liver biopsy for histopathology, special stains

(eg, rhodanine, Masson trichrome)
h Bile culture

h ± heavy metal quantification if indicated

DIFFERENTIAL DIFFERENTIAL DIFFERENTIAL DIFFERENTIAL DIFFERENTIAL
Nodular hyperplasia Regenerative hyperplasia Hepatic neoplasia Chronic hepatitis Cholangiohepatitis

DIFFERENTIAL DIFFERENTIAL DIFFERENTIAL DIFFERENTIAL

Reactive hepatopathy Idiopathic vacuolar Portosystemic shunt, Biliary disease
hepatopathy portal vein hypoplasia (eg, mucocele)

INVESTIGATION
Other disease (eg, inflammatory
bowel disease, pancreatitis)

Suggested Reading
Bain PJ. Liver. In: Latimer KS, ed. Duncan & Prasse’s Veterinary Laboratory
Medicine: Clinical Pathology. 5th ed. Ames, IA: Wiley Blackwell; 2011:211-230.
Brovida C, Rothuizen J. Liver and pancreatic diseases. In: Ettinger SJ, Feldman ACTH = adrenocorticotropic hormone
EC, eds. Textbook of Veterinary Internal Medicine. 7th ed. St. Louis, MO:
Saunders Elsevier; 2010:1609-1994. ALP = alkaline phosphatase
Twedt DC. Abnormal liver enzymes. A clinical approach. In: American Board of HAC = hyperadrenocorticism
Veterinary Practitioners Proceedings, 2014, Nashville, TN.
INCREASED LIVER ENZYMES IN DOGS: ALT
Julie Allen, BVMS, MS, MRCVS, DACVIM (SAIM)*
North Carolina State University

INCREASED ALANINE
AMINOTRANSFERASE†

INVESTIGATION INVESTIGATION
Rule out hepatotoxin or drug ‡ Clinical abnormalities?
YES

NO
INVESTIGATION INVESTIGATION
Weight loss, vomiting, Signs of muscle disease
diarrhea, decreased
Discontinu e; treat for TREATMENT appetite
hepatotoxicity h Antioxidant trial

h ± empirical antibiotics

(controversial)
INVESTIGATION
h Check AST and creatine


kinase
h Electromyogram


INVESTIGATION h Toxoplasma spp,

Recheck ALT in 4-6 weeks Neospora spp titers

h Pyruvate and lactate

levels
h Muscle biopsy

Normal INVESTIGATION
Persistent or progressive ALT increase

INVESTIGATION
CBC, serum chemistry panel, urinalysis

INVESTIGATION
Evaluate for extrahepatic causes, if suggested by routine diagnostics

h Endocrine disease (eg, hypothyroidism No evidence of extrahepatic disease


diabetes mellitus, HAC)
G I disease (eg, inflammatory bowel disease,
h 
*Byline reflects author information on original publication. On publication of this collection, the author’s current
pancreatitis)

credentials and affiliation are Julie Allen, BVMS, MS, MRCVS, DACVIM (SAIM), DACVP, at Veterinary Information Network.
h Systemic infection (eg, fungal disease such †Any increase in ALT should be rechecked at least once to rule out a spurious result or laboratory error, particularly if the
as histoplasmosis, leptospirosis, sepsis)

patient is subclinical. More aggressive evaluation should be considered in breeds predisposed to hepatic disease:
h Metabolic disease (eg, hyperlipidemia) Bedlington terriers, West Highland white terriers, Labrador retrievers, standard poodles, cocker spaniels, English

h  H ypoxia (eg, congestive heart failure) springer spaniels, Doberman pinschers, dalmatians, and Skye terriers.
‡Acetaminophen, azathioprine, hepatotoxic mushrooms, lomustine, blue-green algae, xylitol, cycad palm, and aflatoxin.

 DIAGNOSTIC TREE h INTERNAL MEDICINE h PEER REVIEWED

 
 
 
 
DIFFERENTIAL INVESTIGATION
h Parasitic migration h Recheck after 1 year of age



h Hepatic growth h Administer empiric dewormer;


recheck after 4-6 weeks

<1 year of age

Normal SBA
INVESTIGATION INVESTIGATION
h Abdominal >1 year of age Recheck ALT in 4-6 weeks Normal

ultrasound
h Fasting and

2-hour post-
prandial bile INVESTIGATION
acids h Fine-needle aspiration Persistent or
Abnormal SBA

h Liver biopsy for histopathology and progressive ALT

special stains (eg, rhodanine, increase
Masson trichrome)
h Bile culture

h ± heavy metal quantification if

indicated

DIFFERENTIAL DIFFERENTIAL DIFFERENTIAL DIFFERENTIAL DIFFERENTIAL

Regenerative hyperplasia Reactive hepatopathy Hepatic neoplasia Chronic hepatitis Cholangiohepatitis

DIFFERENTIAL DIFFERENTIAL DIFFERENTIAL DIFFERENTIAL

Other disease (eg, inflammatory Idiopathic vacuolar Portosystemic shunt, Biliary disease
bowel disease, pancreatitis) hepatopathy portal vein hypoplasia (ALP > ALT; eg, mucocele)

Suggested Reading ALP = alkaline phosphatase

Bain PJ. Liver. In: Latimer KS, ed. Duncan & Prasse’s Veterinary Laboratory Medicine:
Clinical Pathology. 5th ed. Ames, IA: Wiley Blackwell; 2011:211-230. ALT = alanine aminotransferase
Brovida C, Rothuizen J. Liver and pancreatic diseases. In: Ettinger SJ, Feldman EC, AST = aspartate transaminase
eds. Textbook of Veterinary Internal Medicine. 7th ed. St. Louis, MO: Saunders
Elsevier; 2010:1609-1994. HAC = hyperadrenocorticism
Twedt DC. Abnormal liver enzymes. A clinical approach. In: American Board of SBA = serum bile acids
Veterinary Practitioners Proceedings, 2014, Nashville, TN.
LYMPHADENOPATHY IN DOGS
Michelle G. Ritt, DVM, DACVIM
Claire Cannon, BVSc (Hons), DACVIM (Oncology)
Jaime F. Modiano, VMD, PhD
University of Minnesota

LYMPHADENOPATHY

Single or regional enlarged lymph node(s) Multiple enlarged lymph nodes

INVESTIGATION
Perform physical examination

Clinically well; no other abnormalities Abnormality in anatomic location drained by Clinically unwell or other abnormalities
the affected lymph node (eg, periodontal (eg, fever, organomegaly)
disease, focal dermatitis or infection, wounds)

INVESTIGATION INVESTIGATION
Fine-needle aspiration and cytology h Thoracic/abdominal imaging

h 
Testing for tick-borne disease
h CBC, serum chemistry profile, urinalysis

h Ancillary testing for geographic setting/

travel history

DIFFERENTIAL DIFFERENTIAL DIFFERENTIAL

Cytologically normal Nonmalignant lymphadenopathy Malignant
lymphoid tissue h Lymphoid hyperplasia lymphadenopathy

h Reactive lymphadenopathy h Metastatic neoplasia


h Lymphadenitis h Stage I lymphoma
No other regional Thoracic/


lymph nodes abdominal lymph
enlarged, node
no abdominal enlargement;
organomegaly abdominal
TREATMENT DIFFERENTIAL 1 TREATMENT organomegaly
h Observation h Skin infections Biopsy ± diagnostic tests (spleen


h Reassess in h Foreign bodies to identify primary and/or liver)


7-10 days h Rarely, fungal infections tumor and implement

h Treat underlying h Periodontal disease therapy ± referral


condition

Lymphadenopathy persists
References
1. Ruiz de Gopegui R, Peñalba B, Espada Y. Causes of lymphadenopa- 5. Flood-Knapik KE, Durham AC, Gregor TP, Sánchez MD, Durney


thy in the dog and cat. Vet Rec. 2004;155(1):23-24. ME, Sorenmo KU. Clinical, histopathological and immunohis-
2. Rao S, Lana S, Eickhoff J, et al. Class II major histocompatibility tochemical characterization of canine indolent lymphoma.
INVESTIGATION Vet Comp Oncol. 2013;11(4):272-286.

complex expression and cell size independently predict survival in
h Biopsy and histopathology canine B-cell lymphoma. J Vet Intern Med. 2011;25(5):1097-1105. 6. Avery PR, Burton J, Bromberek JL, et al. Flow cytometric char-


h Immunohistochemistry 3. Frantz AM, Sarver AL, Ito D, et al. Molecular profiling reveals prog- acterization and clinical outcome of CD4+ T-cell lymphoma in
dogs: 67 cases. J Vet Intern Med. 2014;28(2):538-546.


h PARR nostically significant subtypes of canine lymphoma. Vet Pathol.
2013;50(4):693-703.

h ± flow cytometry 7. Seelig DM, Avery P, Webb T, et al. Canine T-zone lymphoma:

unique immunophenotypic features, outcome, and popula-

4. Valli VE, Kass PH, San Myint M, Scott F. Canine lymphomas: associ-
tion characteristics. J Vet Intern Med. 2014;28(3):878-886.

ation of classification type, disease stage, tumor subtype, mitotic
rate, and treatment with survival. Vet Pathol. 2013;50(5):738-748.
 DIAGNOSTIC TREE h INTERNAL MEDICINE h PEER REVIEWED

 
 
 
 
INVESTIGATION
Perform physical examination

Clinically unwell or other abnormalities Chronic dermatitis Clinically well, no

(eg, fever, organomegaly) other abnormalities

INVESTIGATION INVESTIGATION
h Thoracic and abdominal imaging INVESTIGATION Fine-needle aspiration

h Testing for tick-borne disease plus cytology
h Fine-needle aspiration plus cytology of >2 representative

CBC, serum chemistry profile, of >2 representative

h
lymph nodes

urinalysis lymph nodes
h Fine-needle aspiration of abnormal organs (enlarged,
Ancillary testing for geographic

h
abnormal echogenicity, masses/nodules) if coagulation

setting/travel history (eg, fungal, times and platelet count are normal
plague, tularemia)

DIFFERENTIAL DIFFERENTIAL Results DIFFERENTIAL

Thoracic/ No thoracic/ inconclusiv e
Nonmalignant h Stage II-V lymphoid Regional
abdominal abdominal

lymphadenopathy neoplasia lymphadenopathy
lymph node lymph nodes h Lymphoid hyperplasia h Lymphoid leukemia with metastatic
enlargement, enlarged,


h Reactive h Nonlymphoid solid neoplasia
abdominal abdominal


lymphadenopathy leukemia
organomegaly organomegaly h Lymphadenitis
(spleen and/or (spleen and/or

liver) liver)

DIFFERENTIAL 1 INVESTIGATION TREATMENT

h Viral, bacterial, rickettsial, h Biopsy, histopathology, immuno- Biopsy ± diagnostic


fungal, or protozoal infections histochemistry for subtyping tests to identify
h Autoimmune diseases (eg, according to WHO classification primary tumor and
INVESTIGATION

systemic lupus erythemato- h ± PARR, flow cytometry, molecular implement therapy

Test based on clinical sus, juvenile cellulitis) diagnostics for treatment and ± referral
suspicion and history h Idiosyncratic drug reactions prognosis

(eg, to cyclosporine) Staging is important for prognosis
and monitoring for remission/relapse

h Heterogeneous h Homogeneous population, including flow cytometry results



population/ and antigen receptor rearrangements by PARR
polyclonal antigen h Diagnosis of lymphoid/nonlymphoid hematologic malignancy

receptor h Testing to confirm diagnosis and subtype of malignancy

rearrangements
h Diagnosis of

PARR = PCR for antigen receptor rearrangement nonmalignant
PCR = polymerase chain reaction lymphadenopathy
TREATMENT
WHO = World Health Organization Implement appropriate treatment based
on subtype of lymphoma/leukemia ± refer to specialist 2-7
MAMMARY GLAND ENLARGEMENT IN FEMALE DOGS
Valeria M. Tanco, DVM, MSc, PhD, DACT
Charleston Veterinary Referral Center
Charleston, South Carolina

ENLARGED MAMMARY GLAND(S) OBSERVED

Intact

INVESTIGATION
Obtain history; conduct physical examination:
h Reproductive history/mammary gland palpation

h Mammary gland discharge evaluation/cytology

h Measure total T4, cTSH levels

h Nursing or recently weaned h Estrus cycle within past 3 months h Older patient



h Purulent/bloody discharge h Potential mating h Asymmetric, nonpainful



h Warm, painful mammary gland h Milky discharge mammary gland masses


DIAGNOSIS INVESTIGATION
Mastitis Check for pregnancy

TREATMENT INVESTIGATION
h Warm packing, massage h Before 25-30 days: perform


h If dam systemically ill, ultrasonography

multiple glands involved, or h After 25-30 days: relaxin testing Pregnant DIAGNOSIS

gangrene present, wean or h After 45 days: perform radiography Galactosis

remove and hand-raise pups; h Check for normal progression of

E-collar to prevent grooming. pregnancy
h Pups should be gradually

weaned, as milk production
exacerbates condition
h Avoid “stripping” milk from Not pregnant

teats
h Antibiotics based on culture

and susceptibility results of
mammary gland discharge. TREATMENT
• Clavulanic acid/amoxicillin, DIAGNOSIS h Avoid “stripping” milk from teats



cephalexin safe for neonates Pseudopregnancy h E-collar to prevent excessive grooming

h Pain management h If not resolving, consider dopamine


• Tramadol safe for neonates antagonist (eg, cabergoline, domperidone)

h IV fluids/supportive care as

needed
 DIAGNOSTIC TREE h INTERNAL MEDICINE h PEER REVIEWED

 
 
 
 
Spayed

INVESTIGATION INVESTIGATION
Obtain history and perform physical examination to check for: Examine patient for clinical signs:
h Thorough examination of mammary gland chain for masses h Polyuria/polydipsia


h Exposure to exogenous hormones (eg, human estrogen h Recurrent skin infections/UTIs


cream or spray) h Alopecia (nonpruritic, bilateral,


h Unclear OVH history (potential ovarian remnant) symmetrical)

h Previous signs of estrus: bleeding, marking, vulvar swelling, h Panting


flagging, attraction of males h Temporal muscle atrophy


h Signs of pseudopregnancy: weight gain, nesting/ h Polyphagia


suggestive behavioral change, appetite change
(see Pseudopregnancy)

INVESTIGATION
Perform diagnostic testing:
h CBC, serum chemistry profile,

urinalysis
DIAGNOSIS INVESTIGATION h Abdominal ultrasonography
Low LH levels

Mammary gland masses h
h ACTH stimulation test/low-dose

• 2 consecutive tests >48 hours

dexamethasone suppression test/


apart urine cortisol:creatinine ratio
h Progesterone >1 ng/mL after (home-caught sample)

HCG/GnRH stimulation or h Measure total T4, cTSH levels
INVESTIGATION diestrual cytology

h Thorough examination of mammary gland h Weight gain, pseudopregnancy

chain for masses

behavior (eg, nesting), appetite
h Exposure to exogenous hormones (eg, human
change

estrogen cream or spray) DIFFERENTIAL
h Positive AMH test
Identify number of affected mammary glands

h
Endocrinopathy

h Thoracic radiography, ultrasonography, CBC/ h Hyperadrenocorticism


serum chemistry profile/urinalysis h Hypothyroidism (less likely)

h Perform FNA mass cytology/ biopsy (usually • If spayed after several estrus cycles

not diagnostic) DIAGNOSIS
Ovarian remnant syndrome
ACTH = adrenocorticotropic hormone
AMH = anti-Müllerian hormone
TREATMENT
h Lumpectomy TREATMENT cTSH = canine thyroid stimulating hormone

h Submit excised mass for definitive diagnosis Exploratory surgery/remnant removal FNA = fine-needle aspirate

h Chain removal if malignant and more than one
GnRH = gonadotropin-releasing hormone

mammary gland affected or local lymph
nodes involved HCG = human chorionic gonadotropin
LH = luteinizing hormone
OVH = ovariohysterectomy
T4 = thyroxine
MAMMARY GLAND ENLARGEMENT IN MALE DOGS
Valeria M. Tanco, DVM, MSc, PhD, DACT
Charleston Veterinary Referral Center
Charleston, South Carolina

GYNECOMASTIA OBSERVED

Neutered Intact

INVESTIGATION INVESTIGATION
Obtain history and perform physical examination to Examine for other signs of feminization:
check for: h Alopecia (hyperpigmented, bilateral, nonpruritic)

h Polyuria/polydipsia h Pendulous prepuce


h Recurrent skin infections/UTIs h Decreased penile size


h Alopecia (nonpruritic, bilateral, symmetrical) h Attraction to male dogs


h Panting h Female positioning for urination


h Temporal muscle atrophy h Potential cryptorchid


h Polyphagia h Abdominomegaly


h Abdominomegaly

h History of exposure to exogenous hormones

(eg, human estrogen cream or spray)†
INVESTIGATION
Perform testicular/diagnostic examination:
h CBC, serum chemistry profile, urinalysis

h Abdominal ultrasonography
INVESTIGATION

h ACTH stimulation test/low-dose dexamethasone
Perform diagnostic testing:

h CBC, serum chemistry profile, urinalysis suppression test/urine cortisol:creatinine ratio

h Abdominal ultrasonography (home-caught urine sample)

h A CTH stimulation test/low-dose dexamethasone h Measure total T4, cTSH levels

h Palpation
suppression test/urine cortisol:creatinine ratio

h Ultrasonography (testes, abdomen, inguinal area)*
(home-caught urine sample)

h M easure total T4, cTSH levels h P reputial cytology for functional testicular neoplasia

(intact, cryptorchid)
h Biopsy of mass/castration of testicle/histopathology

h FNA/cytology of testicles, inguinal lymph nodes

DIFFERENTIAL
Endocrinopathy
h Hyperadrenocorticism
DIFFERENTIAL

h Hypothyroidism (less likely)
Endocrinopathy

h Hyperadrenocorticism

h Hypothyroidism (less likely)

Normal Abnormal testicular cytology/biopsy
*Tumor type cannot be differentiated on ultrasound.
†
Patient contact with humans who use such preparations should
be explored, as it can be causative.
INVESTIGATION
Check for patient history of exposure to exogenous
hormones (eg, human estrogen cream/spray)†
 DIAGNOSTIC TREE h INTERNAL MEDICINE h PEER REVIEWED

 
 
 
 
INVESTIGATION INVESTIGATION
Mass is solitary, white to pale yellow, and firm Multiple tan, soft, small, round masses
h ± medullary aplasia h ± medullary aplasia


h ± prostatic perianal hyperplasia

INVESTIGATION INVESTIGATION
Measure plasma hormone concentrations for: Measure plasma hormone concentrations for:
h ± elevated estradiol h ± elevated estradiol


h Normal testosterone h Elevated testosteron e


INVESTIGATION INVESTIGATION
Check for clinical signs of feminization: Check for clinical signs of feminization:
h Pendulous prepuce h Pendulous prepuce


h Gynecomastia h Gynecomastia


h Symmetrical alopecia h Symmetrical alopeci a


h Hyperpigmentation h Hyperpigmentation


h Preputial keratinization h Preputial keratinization


h Attraction to male dogs h Attraction to male dogs


DIAGNOSIS DIAGNOSIS
Sertoli cell tumor Leydig cell tumor

INVESTIGATION
Confirm via histopathology

TREATMENT
h (Hemi) castration ACTH = adrenocorticotropic hormone

h Blood or platelet transfusion as needed for anemia
cTSH = canine thyroid stimulating hormone

h Preoperative CBC with platelet count to diagnose

medullary aplasia FNA = fine-needle aspiration
T4 = thyroxine
MANAGING ANOREXIA
Lisa P. Weeth, DVM, DACVN*
Red Bank Veterinary Hospital
Tinton Falls, New Jersey

ANOREXIA

Determine energy requirement

h R ER = 70 × BW kg 0.75
h B ased on current body weight

INVESTIGATION
Select feeding method based on:
h Physical examination

h BCS

h Lean muscle mass

h Expected delay in voluntary intake

h Concurrent disease state(s)

DIAGNOSIS DIAGNOSIS
Anorexia Expected anorexia/hyporexia <7 days
h Stable clinical disease h Poor anesthetic candidate


h No evidence of concurrent GI disease h Normal nasopharynx


h Normal mentation

INVESTIGATION
Assess feeding and extraneous factors TREATMENT
h U nfamiliar diet type, flavor, aroma Nasoesophageal or nasogastric tube
h N oisy feeding location h 5 - to 8-Fr
h Frequent treatments h L iquid solution
h F ood near litter box (cats)

TREATMENT
Offer food for voluntary intake
h Familiar, highly palatable foods

h Minimize environmental stressors

h Consider appetite stimulants

*Byline reflects author information on original publication. On publication of this collection, the
BW = body weight


author’s current credentials and affiliation are Lisa P. Weeth, DVM, MRCVS, DACVN, at Weeth Nutrition
RER = resting energy requirement Services, Los Angeles, California.
 MANAGEMENT TREE h INTERNAL MEDICINE h PEER REVIEWED

 
 
 
 
DIAGNOSIS DIAGNOSIS
Expected anorexia or Protracted vomiting or diarrhea,
hyporexia ≥7 days ileus; poor anesthetic candidate

Normal esophagus Esophageal disease Severe pancreatitis TREATMENT

Parenteral nutrition

TREATMENT TREATMENT TREATMENT

Esophagostomy tube Gastrostomy tube Jejunostomy tube
h 1 2- to 18-Fr h 1 8- to 24-Fr h 5 - to 8-Fr
h B  lended canned food h B lended canned food h M onomeric liquid solutions

Monitor and adjust method as needed

h B odyweight (check daily)
h C hange in lean muscle mass
h Biochemical or electrolyte abnormalities
 MANAGEMENT TREE h INTERNAL MEDICINE h PEER REVIEWED

 
 
 
 
OBESITY IN CATS
Deborah E. Linder, DVM, MS, DACVN
Cummings School of Veterinary Medicine at Tufts University

OBESITY DIAGNOSED*

Conduct nutrition assessment, including diet and environment 1-3

Obtain dietary history1-3:

h Current diet (ie, brand, amount, frequency, flavor, dry vs wet)

h Treats, chews
h Table scraps

h Access to wildlife (eg, birds, mice)

h Medication administration

h Supplements

Conduct environmental assessment 1-3:
h Owner description of meal time

h Number of family members

h Number of pets

h Possible access to other pets’ food

h Amount of physical activity

h Enrichment (indoor, outdoor) 4

Evaluate patient’s relationship with owner 5 and owner’s
willingness and readiness to change 6:
h No interest

h Contemplation

h Preparation

h Action

h Maintenance

Conduct physical assessment 1-3:
h BCS 7

• Overweight score: 6/9-7/9
• Obese score: 8/9-9/9
h MCS 8

h Complete physical examination

h Diagnostics (ie, CBC, serum chemistry profile, urinalysis,
MCS = muscle condition score

diagnostic imaging) to determine comorbidities
h Quality-of-life assessment 9

*The AAHA Weight Management

Guidelines define obesity as a
BCS 8/9 or above,1 although the
guidelines, as well as this algorithm,
may be helpful for any pet that is Go to Treatment, next page
above ideal body weight. Continues h
 TREATMENT

Design a weight-loss program that includes1:

h IBW


h Calorie restriction


h Diet selection

h Treat allowance

h Feeding strategies

h Activity plans

h Behavior strategies

h Monitoring and follow-up

Determine target weight with owner1:
h Check medical record for previous IBW and/or BCS

• Consider that each whole BCS change above 5 (on a 9-point scale)

or half of a BCS change above 3 (on a 5-point scale) equals ≈10%
overweight
h Use IBW or alternate goal as target weight based on medical history

(eg, comorbidities) and owner expectations/readiness to change

Set initial caloric restriction1

Caloric intake known Caloric intake unknown

Feed 80% of current caloric intake Feed 80% of RER based on target weight
0.8 × 70 (target weight kg ) 0.75

Select a diet 1,10

h Consider veterinary therapeutic diet if:

• Patient has >20% body weight to lose

• Comorbidities are present

• Patient requires <80% RER to lose weight

h Nutrient profile considerations 11-13 :

• Appropriate calorie density (dry food, <3250 kcal/kg; wet food, <900 kcal/kg)

• Protein levels (>5 g/kg of body weight or ≥8.9 g per 100 kcal of diet)

• I ncreased fiber for satiety if patient is tolerant
h Canned diet if preferred

Create treat allowance plan with owner1:
h ≤10% of daily calories

h Include medication administration

h Include non-negotiables

h Consider compromises if adherence is a concern

 MANAGEMENT TREE h INTERNAL MEDICINE h PEER REVIEWED

 
 
 
 
References
Encourage active lifestyle1,4: 1. Brooks D, Churchill J, Fein K, et al. 2014 AAHA
Kibble hidden around the house

h
weight management guidelines for dogs and

h Food-dispensing toys cats. J Am Anim Hosp Assoc. 2014;50(1):1-11.

h Laser pointers, strings
2. Baldwin K, Bartges J, Buffington T, et al. AAHA

h Kibble tossed around room

nutritional assessment guidelines for dogs and

h Motorized mice/toys cats. J Am Anim Hosp Assoc. 2010;46(4):285-296.

3. Freeman L, Becvarova I, Cave N, et al. WSAVA

nutritional assessment guidelines. Compend
Contin Educ Vet. 2011;33(8):E1-E9.
4. Ellis SL, Rodan I, Carney HC, et al. AAFP and ISFM

feline environmental needs guidelines. J Feline
FOLLOW-UP Med Surg. 2013;15(3):219-230.
5. Linder D, Mueller M. Pet obesity management:

beyond nutrition. Vet Clin North Am Small Anim
Pract. 2014;44(4):789-806.
6. Churchill J. Increase the success of weight

Develop monitoring plan with owner1: loss programs by creating an environment for
h Weigh-in every 2-4 weeks change. Compend Contin Educ Vet. 2010;32(12):E1.

h Determine adherence 7. Laflamme DP. Development and validation of a


• Revisit diet history body condition score system for cats: a clinical
h Record body weight, BCS, MCS tool. Feline Pract. 1997;25(5):13-17.

h Calculate rate of weight loss 8. Michel KE, Anderson W, Cupp C, Laflamme DP.


• Aim for 0.5%-2% of body weight per week Correlation of a feline muscle mass score with

h Slow rate of weight loss if: body composition determined by dual-energy
X-ray absorptiometry. Br J Nutr. 2011;106(Suppl

• Rate >2% per week 1):S57-S59.
• Comorbid condition
9. German AJ, Holden SL, Wiseman-Orr ML, et
• MCS decreases at all (ie, there should be no

al. Quality of life is reduced in obese dogs but

palpable muscle wasting) improves after successful weight loss. Vet J.
h Reduce caloric intake by 10% if:
2012;192(3):428-434.

• Owner is adherent and rate is <0.5% per week 10. Linder DE, Parker VJ. Dietary aspects of weight

management in cats and dogs. Vet Clin North Am
Small Anim Pract. 2016;46(5):869-882.
11. Association of American Feed Control Officials.

Model regulations for pet food and specialty
Troubleshoot with owner in cases of 1,5: pet food under the model bill. In: Association of
h Begging behavior American Feed Control Officials, ed. AAFCO 2017

• Try autofeeders Official Publication. 2017:136-149. http://www.
• Try increased fiber for satiety aafco.org/publications. Accessed March 1, 2017.
h Multipet households 12. Linder DE, Freeman LM, Morris P, et al. Theoret-


• Separate pets with baby gate or by room ical evaluation of risk for nutritional deficiency
• Try microchip reader feeders (ie, devices that with caloric restriction in dogs. Vet Q. 2012;32(3-
4):123-129.

only allow access to pets by scanning microchip)
h Weight-loss plateau 13. Linder DE, Freeman LM, Holden SL, Biourge V,


• Increase physical activity German AJ. Status of selected nutrients in obese
dogs undergoing caloric restriction. BMC Vet
• Consider food with lower calorie density
Res. 2013;9:219.
h Owner guilt or emotional concerns 5

• Discuss concerns with open-ended questions
• Brainstorm treatment strategies with owner
• Consider all members of household IBW = ideal body weight
• Discuss alternatives to food is love method of

care (eg, walking, grooming, interactive play) MCS = muscle condition score
RER = resting energy requirement
OBESITY IN DOGS
Deborah E. Linder, DVM, MS, DACVN
Cummings School of Veterinary Medicine at Tufts University

OBESITY DIAGNOSED*

Conduct nutrition assessment, including diet and environment 1-3

Obtain dietary history1-3:

h Current diet (ie, brand, amount, frequency, flavor, dry vs wet)

h Treats, chews
h Table scraps

h Bones, rawhides

h Medication administration

h Supplements

Conduct environmental assessment 1-3:
h Owner description of meal time

h Number of family members

h Number of pets

h Possible access to other pets’ food

h Amount of physical activity 4

Evaluate patient’s relationship with owner 5 and owner’s
willingness and readiness to change 6:
h No interest

h Contemplation

h Preparation

h Action

h Maintenance

Conduct physical assessment 1-3:
h BCS 7

• Overweight score: 6/9-7/9
• Obese score: 8/9-9/9
h MCS 8

h Complete physical examination, including orthopedic

examination
h Diagnostics (ie, CBC, serum chemistry profile, urinalysis,

diagnostic imaging) to determine comorbidities
h Quality-of-life assessment 9

*The AAHA Weight Management

Guidelines define obesity as having
a BCS 8/9 or above,1 although the IBW = ideal body weight
guidelines, as well as this algorithm, MCS = muscle condition score
may be helpful for any pet that is Go to Treatment, next page
above ideal body weight. RER = resting energy requirement
 MANAGEMENT TREE h INTERNAL MEDICINE h PEER REVIEWED

 
 
 
 
TREATMENT

Design a weight-loss program that includes1:

h IBW

h Calorie restriction

h Diet selection

h Treat allowance

h Feeding strategies

h Activity plans

h Behavior strategies

h Monitoring and follow-up

Determine target weight with owner1:
h Check medical record for previous IBW and/or BCS

• Consider that each whole BCS change above 5 (on a 9-point scale) or half of a

BCS change above 3 (on a 5-point scale) equals ≈10% overweight
h Use IBW or alternate goal as target weight based on medical history (eg,

comorbidities) and owner expectations/readiness to change

Set initial caloric restriction1

Caloric intake known Caloric intake unknown

Feed 80% of current caloric intake Feed 80% of RER based on target weight 0.8 × 70 (target weight kg ) 0.75

Select a diet 1,10

h Consider veterinary therapeutic diet if:

• Patient has >20% body weight to lose
• Comorbidities are present

• Patient requires <80% RER to lose weight
h Nutrient profile considerations 11-13 :

• Appropriate calorie density (dry food, <3100 kcal/kg; wet food, <950 kcal/kg)
• Protein levels (>2.5 g/kg of body weight, or ≥6 g per 100 kcal of diet if restriction is 80% RER)
• Increased fiber for satiety, if patient is tolerant and owner can provide frequent walks
h Canned diet, if greater satiety from increased moisture is desired and if cost is not a client consideration

Create treat allowance plan with owner1:
h ≤10% of daily caloric intake
See Encourage active

h Include medication administration
lifestyle, next page.

h Include nonnegotiables Continues h

h Consider compromises if adherence is a concern

MANAGEMENT TREE h INTERNAL MEDICINE h PEER REVIEWED

 
 
 
 
References
Encourage active lifestyle1,4: 1. Brooks D, Churchill J, Fein K, et al. 2014 AAHA
h Walks

weight management guidelines for dogs and

h Food-dispensing toys cats. J Am Anim Hosp Assoc. 2014;50(1):1-11.

h Chase balls or treats
2. Baldwin K, Bartges J, Buffington T, et al. AAHA

h Underwater treadmill

nutritional assessment guidelines for dogs and

h Agility course cats. J Am Anim Hosp Assoc. 2010;46(4):285-296.

h Active play or walking 3. Freeman L, Becvarova I, Cave N, et al. WSAVA


h Obedience classes nutritional assessment guidelines. Compend

Contin Educ Vet. 2011;33(8):E1-E9.
4. Ellis SL, Rodan I, Carney HC, et al. AAFP and

ISFM feline environmental needs guidelines.
J Feline Med Surg. 2013;15(3):219-230.
5. Linder D, Mueller M. Pet obesity management:
FOLLOW-UP

beyond nutrition. Vet Clin North Am Small Anim
Pract. 2014;44(4):789-806.
6. Churchill J. Increase the success of weight

loss programs by creating an environment
for change. Compend Contin Educ Vet.
Develop monitoring plan with owner1: 2010;32(12):E1.
h Weigh-in every 2-4 weeks 7. Laflamme DP. Development and validation of a


h Determine adherence body condition score system for cats: a clinical

• Revisit diet history tool. Feline Pract. 1997;25(5):13-17.

h Record body weight, BCS, MCS 8. Michel KE, Anderson W, Cupp C, Laflamme DP.


h Calculate rate of weight loss Correlation of a feline muscle mass score with
body composition determined by dual-energy

• Aim for 1%-2% of body weight per week X-ray absorptiometry. Br J Nutr. 2011;106(Suppl

h Slow rate of weight loss if:
1):S57-S59.

• Rate >2% per week 9. German AJ, Holden SL, Wiseman-Orr ML, et

• Comorbid condition

al. Quality of life is reduced in obese dogs but

• MCS decreases at all (ie, there should be no improves after successful weight loss. Vet J.

palpable muscle wasting) 2012;192(3):428-434.
h Reduce caloric intake by 10% if:
10. Linder DE, Parker VJ. Dietary aspects of weight

• Owner is adherent and rate is <1% per week

management in cats and dogs. Vet Clin North

Am Small Anim Pract. 2016;46(5):869-882.
11. Association of American Feed Control Officials.

Model regulations for pet food and specialty
pet food under the model bill. In: Association
Troubleshoot with owner in cases of 1,5: of American Feed Control Officials, ed. AAFCO
h Begging behavior 2017 Official Publication. 2017:136-149. http://

• Try autofeeders www.aafco.org/publications. Accessed on

• Try increased fiber for satiety March 1, 2017.

h Multipet households 12. Linder DE, Freeman LM, Morris P, et al.


• Separate pets with baby gate or by room Theoretical evaluation of risk for nutritional
deficiency with caloric restriction in dogs. Vet Q.

• Try microchip reader feeders (ie, devices that
2012;32(3-4):123-129.

only allow access to pets by scanning
13. Linder DE, Freeman LM, Holden SL, Biourge
microchip)

V, German AJ. Status of selected nutrients in
h Weight-loss plateau
obese dogs undergoing caloric restriction.

• Increase physical activity BMC Vet Res. 2013;9:219.

• Consider food with lower calorie density

h Owner guilt or emotional concerns 5

• Discuss concerns with open-ended

questions
• Brainstorm treatment strategies with owner

• Consider all members of household

• Discuss alternatives to food is love method of

care (eg, walking, grooming, interactive play) MCS = muscle condition score
PANTING
Julie Allen, BVMS, MS, MRCVS, DACVIM (SAIM)*
North Carolina State University

PANTING†

INVESTIGATION
True panting:
h Extremely rapid rate INVESTIGATION

h Lips pulled back throughout inspiration; May be normal:

nares quivering during expiration h W ith exertion, stress,
h Moves freely, no positional restrictions heat, excitement

h Minimal rib cage excursions

h Tongue often protruded

DIFFERENTIAL DIFFERENTIAL DIFFERENTIAL DIFFERENTIAL DIFFERENTIAL
Increased body temperature Obese, overweight Pain CNS disease Behavioral issue
(eg, anxiety)

Normal Increased TREATMENT INVESTIGATION h  C NS disease TREATMENT

environmental environmental affecting
h Institute Further diagnostics h Institute
temperature temperature


weight-loss (eg, imaging) for respiratory behavioral
program source of pain center modification
h Avoid excess h Post ictal h Anxiolytic



exertion, heat therapy
Fever TREATMENT
Institute cooling TREATMENT
Analgesic trial INVESTIGATION
h Routine database
DIFFERENTIAL

INVESTIGATION
h Neurologic examination

Endocrine disease h MRI/CT
Routine database

h
h CSF tap

Infectious

h

disease screening
h Imaging

h Further tests

pending initial DIFFERENTIAL DIFFERENTIAL DIFFERENTIAL
results Hyperadrenocorticism Hyperthyroidism Pheochromocytoma

*Byline reflects author information on


original publication. On publication of
INVESTIGATION INVESTIGATION INVESTIGATION this collection, the author’s current
h Compatible clinical h Compatible h Compatible signs credentials and affiliation are Julie Allen,



signs clinical signs h Routine database BVMS, MS, MRCVS, DACVIM (SAIM),

h Routine database h Routine database h Abdominal DACVP, at Veterinary Information



h UCCR, LDDS, ACTH h T4, fT4, TSH ultrasonography/CT Network.
†Differentials here are more relevant to


stimulation h Urine metanephrine

dogs, but information pertinent to cats

h Abdominal testing (eg, young cat cardiorespiratory,

ultrasonography h Inhibin level hyperthyroid) is relevant where necessary.

h Blood pressure ‡If a young cat is presented with panting,


measurement cardiorespiratory disease must be ruled
out.
 DIAGNOSTIC TREE h INTERNAL MEDICINE h PEER REVIEWED

 
 
 
 
INVESTIGATION
Open-mouth breathing caused by respiratory
distress:
h Flaring of nostrils and/or drawing back of lip


commissures during inspiration
h Extension of neck

h Abduction of elbows

h Comfortable only when standing or in sternal


recumbency

DIFFERENTIAL DIFFERENTIAL DIFFERENTIAL

Medications Hypertension Acidosis DIFFERENTIAL DIFFERENTIAL
Respiratory disease Cardiac disease‡
(eg, laryngeal (eg, congestive heart
paralysis, infiltrative failure, pulmonary
pulmonary disease) hypertension)
INVESTIGATION INVESTIGATION INVESTIGATION
h Steroids h Blood pressure h Blood gas



h Excessive thyroid measurement h Routine


supplementation h Investigate for database

h Diazepam underlying

h Opioids (eg, disease (eg, renal

hydromorphone) disease)

DIFFERENTIAL
h Renal failure

h Diabetic

TREATMENT ketoacidosis
Institute h Ethylene glycol

antihypertensive or salicylate
therapy (eg, toxicity
amlodipine)

ACTH = adrenocorticotropic hormone

fT4 = free thyroxine
LDDS = low-dose dexamethasone suppression
T4 = total thyroxine
TSH = thyroid stimulating hormone
Reference UCCR = urine cortisol: creatinine ratio
1. Kittleson M, Rishniw M. Panting and tachypnea. Veterinary Information Network. http://www.vin.com.
PERITONEAL EFFUSION
Gretchen Statz, DVM, DACVECC*
Internal Medicine Consultant
Antech Diagnostics

PERITONEAL EFFUSION Abdominocentesis and characterization of fluid

Pure transudate Modified transudate Chylous effusion (very rare)

h Clear, colorless h Clear, straw colored h White/opaque



h TP <2.5 g/dL h TP >2.5 g/dL h TP >2 g/dL



h <1000 cells/µL h 1000-7000 cells/µL h Variable cell count



h Mononuclear cells predominate h Mononuclear cells, increasing numbers h Predominantly small lymphocytes



of neutrophils, lymphocytes h Effusion triglycerides > serum triglycerides

Low albumin (<1.5-1.8 g/dL)?
INVESTIGATION
FAST, chest radiography

DIFFERENTIAL
Portal hypertension
h Liver disease
YES NO

h Right-sided heart failure (auscultation, Trauma or thoracic duct rupture?

echocardiography, chest radiography)

DIFFERENTIALS TREATMENT
h Liver failure/disease h Treat as necessary

NO YES

h Addison’s disease h Surgery if indicated


h Protein-losing nephropathy h Monitor


h Protein-losing enteropathy

INVESTIGATION
h Abdominal

ultrasonography Abdominal ultrasonography normal? h Effusion creatinine

h Bile acids >2× serum creatinine

h Resting cortisol levels h Effusion potassium


h Urinalysis (UP:C if >1.4× serum potassium

indicated)
h Vitamin B12/folate

NO YES
DIAGNOSIS
Uroabdomen (transudate/
modified transudate)

DIFFERENTIALS
h Vasculitis (rare)

DIFFERENTIAL DIFFERENTIAL DIFFERENTIAL DIFFERENTIAL h Rickettsial disease

Pancreatitis Hepatic disease Splenic/intestinal torsion Neoplasia h Immune-mediated
TREATMENT

disease
Surgery may be indicated

*Byline reflects author information on original publication. On

TREATMENT TREATMENT TREATMENT TREATMENT

publication of this collection, the author’s current affiliation is
Supportive treatment Biopsy and bile acids Surgery Chemotherapy Antech Diagnostics and Veterinary Specialty and Emergency
Care, Indianapolis, Indiana.
 DIAGNOSTIC TREE h INTERNAL MEDICINE h PEER REVIEWED

 
 
 
 
Suggested Reading
Aronsohn MG, Dubiel B, Roberts B, Powers BE. Prognosis for acute nontraumatic man ED, eds. Textbook of Veterinary Internal Medicine. 7th ed. St. Louis, MO:
hemoperitoneum in the dog: a retreospective analysis of 60 cases (2003- Saunders; 2010:144-147.
2006). J Am Anim Hosp Assoc. 2009;45:72-77. Mandell DC, Drobatz K. Feline hemoperitoneum: 16 cases (1986-1993). J Vet Emerg
Bonczynski JJ, Ludwig LL, Barton LJ, et al. Comparison of peritoneal fluid and Crit Care. 1995;5:93-97.
peripheral blood pH, bicarbonate, glucose, and lactate concentration as a diag- Schmiedt C, Tobias KM, Otto CM. Evaluation of abdominal fluid: peripheral blood
nostic tool for septic peritonitis in dogs and cats. Vet Surg. 2003;32:161-166. creatinine and potassium ratios for diagnosis of uroperitoneum in dogs. J Vet
Chambers G. Abdominal distension, ascites and peritonitis. In: Ettinger SJ, Feld- Emerg Crit Care. 2001;11:275-280.

Exudate Hemorrhagic effusion Malignant effusion

h Turbid, hemorrhagic to purulent h PCV >10% h Light-yellow, clear to cloudy



h TP >2.5 g/dL (often >3 g/dL) h TP >2.5 g/dL h TP >2.5 g/dL



h >5000 cells/µL h Variable cell count h Variable cell count



h Neutrophils predominate h Similar to peripheral blood, does not clot h Neoplastic cells identified



INVESTIGATION INVESTIGATION DIAGNOSIS
h Intracellular bacteria present? FAST, chest radiography Neoplasia

h Peripheral blood glucose >20 mg/dL higher than glucose

in abdominal fluid (also seen in neoplastic effusions)?
h Positive culture (needs treatment before results)?

INVESTIGATION INVESTIGATION
Trauma? Abdominal ultrasonography,
chest radiography, CT

NO YES

TREATMENT
NO YES Surgery ± chemotherapy
Nonseptic effusion Septic effusion

Severely elevated PT/PTT? TREATMENT

h Treat as necessary
TREATMENT

h Abdominal pressure wrap

Emergency h Surgery if indicated

Effusion FIP PCR- surgery ± h Monitor

bilirubin > positive abdominal
serum bilirubin effusion ultrasonography
NO YES

DIAGNOSIS DIAGNOSIS Ruptured or damaged vascular neoplasia/organ

Bile peritonitis FIP

DIFFERENTIAL DIFFERENTIAL
Coagulopathy Ingestion of anti-
coagulant rodenticide
TREATMENT TREATMENT
Surgery Treat as
necessary DIFFERENTIALS DIFFERENTIALS
Cats: Dogs: TREATMENT
h Neoplasia h Neoplasia
Plasma and TREATMENT


h Hepatic diseases (hemangiosarcoma) vitamin K Decontamination ±

FAST = focused assessment with sonography for h Hemorrhagic cyst h Splenic hematoma
emesis ± vitamin K


trauma h Ruptured bladder h Splenic torsion


PT = prothrombin time
PTT = partial thromboplastin time
TP = total protein
TREATMENT
UP:C = urine protein:creatinine ratio Treat as necessary (eg, surgery ± imaging)
PETECHIAE & ECCHYMOSES*
T. Mark Neer, DVM, DACVIM†

PETECHIAE/ECCHYMOSES CBC

TP only (most common cause) TP, anemia

Enzootic region for rickettsial Reticulocyte count

or other tick-borne disease?

>60 000/µL <60 000/µL >60 000/µL

YES NO with blood loss with hemolysis

INVESTIGATION INVESTIGATION INVESTIGATION

Perform serology for: Coagulation screen
h BM cytology


h Ehrlichia spp (PT, PTT, FDP, ATIII)
h Splenic ultrasonography

Thoracic/abdominal

h
h RMSF 
radiography

h Bartonella vinsonii subsp berkhoffii (dogs)
Estrogen levels (dog)

h

h FeLV/FIV (cat)

h Ehrlichia spp serology

Normal Abnormal

DIAGNOSIS DIAGNOSIS Negative

Positive for Positive for
Ehrlichia spp or RMSF Bartonella spp
Negative Positive or
DIAGNOSIS DIAGNOSIS Abnormal
IMT DIC

TREATMENT INVESTIGATION
Doxycycline Perform blood PCR,
(10 mg/kg/day for Search for underlying disease
DIAGNOSIS DIAGNOSIS
culture for ITP TP
21 days) Bartonella vinsonii associated with
underlying
disease
TREATMENT
h Enrofloxacin (10-15 mg/kg/day)
Positive

h Doxycycline (10-20 mg/kg/day)

h Rifampin (10 mg/kg/day)

ANA = antinuclear antibodies FDP = fibrin degradation product PTT = partial thromboplastin time TP = thrombocytopenia
ATIII = antithrombin III IMT = immune-mediated thrombocytopenia RF = rheumatoid factor vWD = von Willebrand’s disease
BM = bone marrow ITP = idiopathic thrombocytopenia RMSF = Rocky Mountain spotted fever vWF = von Willebrand’s factor
DIC = disseminated intravascular coagulation PT = prothrombin time SLE = systemic Iupus erythematosus
 DIAGNOSTIC/MANAGEMENT TREE h INTERNAL MEDICINE h PEER REVIEWED

 
 
 
 
TP, anemia, leukopenia Normal (consider vasculitis, vasculopathy, or thrombopathies)

INVESTIGATION DIAGNOSIS
Normal Buccal mucosal bleeding time Prolonged
BM aspirate cytology

Definitive diagnosis Hypocellular BM INVESTIGATION

vWF assay
Problem Insufficient
resolved assay
(local Normal Low
DIFFERENTIALS INVESTIGATION disease)
h Systemic fungal disease h Ehrlichia spp


(eg, histoplasmosis) serology
h Myeloproliferative neoplasia h Drug history
INVESTIGATION DIAGNOSIS


h Ehrlichia spp morulae
vWD

h Myelophthisis h Clot retraction test


h Platelet aggregation

Abnormal Normal

Positive Negative
TREATMENT
Treat specific disease
DIAGNOSIS DIAGNOSIS
Thrombopathies (rare) Vasculitis or
INVESTIGATION vasculopathy
h BM core biopsy Primary Secondary
INVESTIGATION

h Estrogen levels

h Blood smear for spherocytes INVESTIGATION

h Direct Coomb’s test
Special platelet studies

h ANA test
INVESTIGATION INVESTIGATION

h Heartworm serology

h Babesia spp serology DIAGNOSIS Skin biopsy h RMSF serology


h Aplastic anemia
h Ehrlichia spp

serology

h Myelofibrosis Abnormal
ANA test

h

h RF test
DIAGNOSIS

h Blood culture

Negative Positive Polyarteritis h Cold agglutinin test

h Leukocytoclastic
DIAGNOSIS

Breed-related vasculitis
h Drug-induced
thrombopathies

h American cocker spaniel granulomatous
DIAGNOSIS

h Great Pyrenees
Search for DIFFERENTIALS RMSF

h
h Grey collie
underlying

h Evan’s syndrome Ehrlichiosis

h
h Spitz

disease

h SLE SLE

h
h Basset hound


h Heartworm disease Rheumatoid disease

h
h Otter hound


h Babesiosis Sepsis

h
h Chediak-Higashi—cat



*Article originally published as “Petechiation/Ecchymoses”
†Byline reflects author information on original publication. On publication of this

collection, T. Mark Neer is retired after a successful tenure at Oklahoma State University.
PTYALISM & PSEUDOPTYALISM
Julie Allen, BVMS, MS, DACVIM (SAIM)*
Antech Diagnostics

DROOLING†

Ptyalism‡ (ie, excessive saliva production) Pseudoptyalism‡ (ie, inability to swallow normal saliva production; drooling)

INVESTIGATION
History and examination:
h Complete physical examination, evaluating salivary gland size and symmetry

h Full neurologic examination

h Breed: giant breeds (eg, St. Bernard) or Yorkshire and Maltese terriers (increased PSS incidence)

h Age: young animals likely to ingest toxins/FBs or have congenital issues; neoplasia likely in older animals

h History of vaccination (eg, rabies, calicivirus) or trauma (eg, electric cord injury)

h Exposure to toxins, medications, topical products

h Duration: acute (eg, FB) vs chronic (eg, neoplasm)

h Discoloration of saliva (eg, blood, purulent discharge) suggestive of oral problem

h Halitosis may indicate oral, esophageal, or gastric disease

h Pawing at face or mouth may indicate orofacial pain, hypocalcemia

h Change in eating behavior: dropping food, chewing on one side of the mouth, pseudoanorexia or hyporexia

h Diet (eg, high-protein) can cause drooling because of precipitation of HE in patients with liver dysfunction

h Other GI (ie, retching, regurgitation, vomiting, weight loss) or neurologic (ie, seizures, gagging, dysphagia) signs

Known toxin Known medication exposure Oral cavity abnormal

DIFFERENTIAL DIFFERENTIAL DIFFERENTIAL

Toxicity Medication reaction h Periodontal disease

h Household cleaners h Medications or topical products given h Stomatitis (eg, calicivirus, FeLV/FIV, caustic



h Plants or trees (eg, Kentucky coffee tree, poinsettia) topically or PO (eg, selamectin, moxidectin– agent)

h Insecticide or pesticide (eg, boric acid, aldicarb) imidacloprid) h Immune-mediated disease (eg, pemphigus)


h Rodenticide (eg, zinc phosphide) h Cholinergic drugs (eg, bethanechol), h Tongue lesion (eg, linear FB), glossitis (eg,



h Illicit drugs (eg, cocaine, amphetamines) anticholinesterase drugs (eg, pyridostigmine), uremia, caustic agent), tumor

h Animal venoms (eg, black widow spider, scorpion, cholinesterase inhibitors (eg, OP) h Oropharyngeal disease (eg, tonsillar SCC)


toads [Bufo spp], coral snake, sea hare [Aplysia spp]) h Pyrethrins or pyrethroids h Lip fold abnormalities


h Human sleep aids (eg, zolpidem) h Ivermectin h Faucitis



h Mushrooms (eg, Amanita muscaria) h Bitter drugs


h Metaldehyde

h Human tricyclic antidepressants (eg, clozapine)

h 5-hydroxytryptophan (ie, Griffonia seed extract)

TREATMENT
TREATMENT h Depends on underlying disease

h Discontinue medication h Dental cleaning or extractions


h Supportive care h Anti-inflammatory or immunomodulatory therapy


TREATMENT h Surgical resection or correction

h Depends on toxin exposure

h Dilution if caustic agent *Byline reflects author information on original publication. On publication of this collection, the author’s current

Decontamination (eg, activated charcoal)

h
credentials and affiliation are Julie Allen, BVMS, MS, MRCVS, DACVIM (SAIM), DACVP, at Veterinary Information Network.

h Supportive care †Rabies should always be considered in patients presenting with drooling.

Specific antidote (if available)

h
‡Distinction between ptyalism and pseudoptyalism is not absolute; oropharyngeal and CNS diseases can result in increased


salivary production and inability to swallow.
§HE management includes low-protein diet, enemas, oral antibiotics, lactulose, zinc supplementation, and supportive care.
 DIAGNOSTIC TREE h INTERNAL MEDICINE h PEER REVIEWED

 
 
 
 
Oral cavity normal

Neurologic, GI signs, or abnormal salivary glands No other findings

INVESTIGATION DIAGNOSIS
Minimum database (CBC, chemistry panel, T4, UA) Physiologic
h Response to feeding

h Hyperthermia

h Excitement

h Purring

INVESTIGATION
Additional diagnostics based on findings:
h Bile acids (if HE suspected)

h FeLV/FIV testing

h AChR Ab test (if myasthenia gravis possible)

h FNA/biopsy of lesions (mucocutaneous, oropharyngeal, lingual)

h FNA/biopsy of salivary glands

h Radiography (oral cavity, neck, thorax, abdomen)

h Abdominal ultrasonography

h Portal scintigraphy

h Fluoroscopic evaluation of swallowing

GI disease Neurologic disease Abnormal salivary glands No other findings

DIFFERENTIAL DIFFERENTIAL DIFFERENTIAL DIAGNOSIS

h Any disease resulting in nausea h Seizures h Sialadenitis, necrotizing sialometaplasia Idiopathic or nonresponsive



h Esophageal disease h Infectious disease (eg, rabies, (ie, inflammation of salivary glands)


h Gastric dilatation–volvulus pseudorabies, tetanus, h Sialadenosis–idiopathic non-


h Gastric ulceration botulism) inflammatory salivary gland enlargement

h Renal failure h Myasthenia gravis (may be form of limbic epilepsy)


h Hepatic failure (HE, particularly h Idiopathic trigeminal neuritis h Salivary gland neoplasia TREATMENT



in cats) h Lesions of cranial nerves IX, X, XII h Salivary mucocele h Atropine or glycopyrrolate



to decrease salivary flow
h Preventive measures for

moist dermatitis
h Fluid support (if dehydrated)

TREATMENT TREATMENT TREATMENT h Salivary gland removal

h Treat underlying disease h Anticonvulsants h Sialadenitis: If immune mediated, treat



h Antiemetics, antacids for nausea h Other therapies, depending on with immunosuppressive dose of


h HE management § diagnosis corticosteroids ± phenobarbital

h Sialadenosis: phenobarbital, sclerotherapy

h Mucocele/neoplasia: surgical management

AChR Ab = acetylcholine receptor antibody OP = organophosphates
FB = foreign body PSS = portosystemic shunt
FNA = fine-needle aspiration SCC = squamous cell carcinoma
HE = hepatic encephalopathy T4 = thyroxine
REFRACTORY CANINE
IMMUNE-MEDIATED HEMOLYTIC ANEMIA
Michael J. Day, BSc, BVMS (Hons), PhD, DSc, Dr(hc), DiplECVP, FASM, FRCPath, FRCVS*
University of Bristol

Barbara Kohn, Dr med vet, PD, Prof, DECVIM

Freie Universität Berlin

PRIMARY IMHA
CONFIRMED

INVESTIGATION
h ( Acute-onset) hemolytic anemia
h PCV <35%

h Positive direct Coombs test, spherocytosis, autoagglutination

h No other identifiable causes of anemia

h No underlying causes of secondary IMHA (eg, cancer, infection, inflammation, drugs, vaccination)

TREATMENT
Primary treatment (7-10 days):
h Glucocorticoid therapy

• Prednisolone (2-3 mg/kg/day, given once daily or divided into two doses) or dexamethasone

(0.2-0.4 mg/kg/day IV)
h Packed RBC or whole blood transfusion (or, if available, blood substitute) if PCV is

approximately <14%-16%, depending on overall patient condition
h Crystalloid infusion (to treat or prevent dehydration and DIC)

h Fresh-frozen plasma (to treat DIC, common with IMHA)

h Antibiotics (eg, doxycycline) if tick-borne disease or cryptic infection suspected

h Gastroprotectants omeprazole, sucralfate (simultaneously)

h Consider thromboprophylaxis (eg, heparin, aspirin, clopidogrel)

TREATMENT
Primary treatment for severe disease (eg, IV hemolysis,
autoagglutination) or if no response to steroids:
h Consider adjunct immunomodulatory drug 1

• Mycophenolate mofetil (8-10 mg/kg PO q12h)
• Cyclosporine (5 mg/kg PO q12h)
• Leflunomide (2 mg/kg PO q24h)
• Azathioprine (2 mg/kg or 50 mg/m 2 PO q24h [relatively

slow-acting])
• IV human immunoglobulin (0.5-1 g/kg over >6 hours)

Evaluate after 1 week of initial therapy

*Byline reflects author information on original publication. On publication of this collection, the author’s current
DIC = disseminated intravascular coagulation

affiliation is the School of Veterinary and Life Sciences, Murdoch University, Murdoch, Western Australia.
IMHA = immune-mediated hemolytic anemia
PCV = packed cell volume
 MANAGEMENT TREE h INTERNAL MEDICINE h PEER REVIEWED

 
 
 
 
Clinical response or rise in PCV?

YES NO

TREATMENT INVESTIGATION
h 
C ontinue immunosuppressive dose for 1-2 weeks, then taper PCV fails to increase or anemia is nonregenerative:
drug over several months (pending patient response) h If nonregenerative anemia, consider nonregenerative IMHA

• After 6 months, prednisolone (and any adjunct or pure red cell aplasia

immunomodulatory drug, 1 at a time) might be withdrawn • Evaluate bone marrow
h 
M onitor closely for adverse effects 1 h Consider adjunct immunomodulatory agent

h Consider further evaluation for disease-causing secondary

IMHA
h Avoid increasing prednisolone dose

TREATMENT
h 
M onitor for adverse effects or signs of relapse after each
dose reduction
h 
M onitor lifelong for signs of relapse or other immune- Clinical response?
mediated disease

TREATMENT YES NO
Relapse:
h Consider repeating diagnostic workup

• Reevaluate for disease that could cause secondary IMHA
h Start or increase prednisolone and consider adjunct

immunomodulatory therapy Evaluate for
h Low-dose maintenance immunosuppressive treatment may
underlying disease

be necessary
h Monitor for adverse effects 1

Reference
1. Swann JW, Garden OA, Fellman CL, et al. ACVIM consensus statement on the

treatment of immune-mediated hemolytic anemia in dogs. J Vet Intern Med.
2019;33(3):1141-1172.

Suggested Reading
Garden OA, Kidd L, Mexas AM, et al. ACVIM consensus statement on the diagnosis

of immune-mediated hemolytic anemia in dogs and cats. J Vet Intern Med.
2019;33(2):313-334.
HORNER SYNDROME
Mark Troxel, DVM, DACVIM (Neurology)
Massachusetts Veterinary Referral Hospital
Woburn, Massachusetts

HORNER SYNDROME

INVESTIGATION
Look for:
h Miosis

h Enophthalmos
h Ptosis
h Elevated nictitans

INVESTIGATION
Obtain history:
h R ecent ear infection
h O titis media signs (eg, head shaking, ear scratching)
h Trauma
h O ther signs of neurologic disease:
• CNS signs (eg, mental dullness, cranial nerve deficits, weakness, circling, vestibular signs)

• Cervical hyperpathia

• Cranial mediastinal signs (eg, coughing, dyspnea, decreased thoracic compressibility)

MRI, CT, and phenylephrine INVESTIGATION
tests not pursued Phenylephrine test:
h I nstill 1 drop of 10% phenylephrine into
each eye
h M onitor time to resolution of signs*

INVESTIGATION
No history or evidence of
otitis media, radiographic
abnormalities, or intracranial/
cervical signs
Resolves <20 min Resolves 20-45 min Resolves >45 min or no resolution

DIAGNOSIS
Idiopathic Horner syndrome DIFFERENTIAL DIFFERENTIAL DIFFERENTIAL
Postganglionic lesion Preganglionic lesion Upper motor neuron lesion
h Otitis media (most h Idiopathic Horner h Neoplasia



common) syndrome h Encephalitis/myelitis (eg, GME,

h Cavernous sinus h Brachial plexus infectious disease)


INVESTIGATION or orbital disease injury/avulsion h Infarction

Wait 4-8 weeks to confirm (uncommon–rare) h Neoplasia (eg, h Intervertebral disk disease


whether signs resolve nerve sheath tumor, h Fibrocartilaginous embolism

lymphoma, thoracic h Trauma

neoplasia)
 DIAGNOSTIC TREE h NEUROLOGY h PEER REVIEWED

 
 
 
 
INVESTIGATION
h  hysical examination
P
h P alpation for cervical lesion
h C BC
h S erum chemistry panel
h T hyroid hormone testing
h O toscopy
h C ervical, thoracic radiography

History or evidence of otitis media Abnormalities on radiographs or

intracranial/cervical signs present:
h Mental dullness

h Circling

h Paresis
TREATMENT

h Central vestibular signs

Systemic antibiotics, ideally based on middle ear culture, h Neck pain

for 4-8 weeks, but empirical therapy (eg, cephalexin, h Postural reaction deficits

amoxicillin-clavulanic acid) can be attempted.

No improvement; other signs develop

INVESTIGATION
Brain and neck MRI

No obvious cause identified TREATMENT

Treat underlying disease *In many cases, time to resolution is determined by

visible improvement of enophthalmos, ptosis, and
elevated nictitans. Miosis may not resolve.
DIAGNOSIS
Idiopathic Horner GME = granulomatous meningoencephalitis
syndrome
 DIAGNOSTIC/MANAGEMENT TREE h NEUROLOGY h PEER REVIEWED

 
 
 
 
INTRACRANIAL VS EXTRACRANIAL SEIZURES
Natasha Olby, VetMB, PhD, DACVIM (Neurology)
North Carolina State University

SEIZURES

INVESTIGATION INVESTIGATION INVESTIGATION

History: Minimum database: Toxin exposure:
h R ecently whelped h CBC, serum chemistry profile, UA h Lead: measure blood levels


h R ecent thyroid/parathyroid surgery h BP h Organophosphate: measure


h T hyroid mass h Pre- and postprandial serum bile cholinesterase activity

h E thylene glycol toxicosis acid tests h Ethylene glycol: check


ethylene glycol test

h Measure calcium

h Correct for hypoalbuminemia

Abnormal Normal minimum
minimum database database

Total Ca <1.5 mmol/L (6 mg/dL)

Go to Extracranial Go to Intracranial
Disease, next page Disease, page 137

DIAGNOSIS
Hypocalcemia

TREATMENT
Treat with 0.5-1.5 mL/kg 10% Ca gluconate
by slow IV injection. Monitor ECG. If
seizing, consider treating without waiting
for Ca levels in view of compatible history.

BP = blood pressure
Ca = calcium
UA = urinalysis

*Byline reflects author information on original publication.


On publication of this collection, the author’s current credentials Continues h
are Natasha Olby, VetMB, PhD, MRCVS, DACVIM (Neurology).
 EXTRACRANIAL DISEASE

Glucose <60 mg/dL, rest of Fasting Hyperlipidemia: Systolic BP (repeatable)

blood analysis normal triglycerides cholesterol; >180 mm Hg
consider: ± retinal lesions
h Hypothyroidism

h Hyperadrenocorticism

h Pancreatitis

TREATMENT h Diabetes mellitus

Treat with glucose if seizing or
h Hepatic disease
DIAGNOSIS

h Nephrotic syndrome
abnormal mentation: Hypertension

h K aro syrup
h I V dextrose 200 mg/kg
(dilute 50% dextrose to 10%)

DIAGNOSIS Consider:
Hypothyroidism h Renal disease

(ie, low total T4, high TSH) h Hyperadrenocorticism

h Pheochromocytoma
Check insulin level on

hypoglycemic blood sample

DIAGNOSIS
Idiopathic hyperlipidemia
DIAGNOSIS (other causes ruled out)
Insulinoma
(ie, amended insulin glucose ratio >30)

DIAGNOSIS
Elevated pre- and postprandial Hyponatremia/hypernatremia
serum bile acid tests

Consider:
h Adipsia: thalamic disease
Abdominal US, rectal scintigraphy

h Restricted access to water

h Increased water loss (eg,

diabetes insipidus)
h Increased water intake

h Increased salt intake

h Increased salt loss (eg,

DIAGNOSIS Normal blood flow: whipworm infestation)
consider liver biopsy h Diuretics
Portosystemic shunt

(ie, abnormal blood flow)
 DIAGNOSTIC/MANAGEMENT TREE h NEUROLOGY h PEER REVIEWED

 
 
 
 
INTRACRANIAL DISEASE

No neurologic deficits between seizures Neurologic deficits between seizures

INVESTIGATION
Image brain: CT or MRI
Dogs 1-5 years Dogs <1 year Consider US in young toy breed
of age or >5 years of age with persistent fontanelle

DIAGNOSIS
Primary epilepsy likely;
offer full workup or Normal Abnormal
continued monitoring for
additional neurologic signs

CSF analysis
DIAGNOSIS DIAGNOSIS DIAGNOSIS
Edema Mass Congenital
h Inflammation anomaly

h Vascular event

INVESTIGATION
Brain tumor vs
Normal Normal cell count; elevated protein Elevated cell count; abscess or granuloma
elevated protein h Thoracic

radiography/
abdominal US
(metastasis check)
DIFFERENTIALS h Consider biopsy or
DIAGNOSIS

Consider: surgical removal
h Vascular event Encephalitis

h Neurodegenerative process

h Neoplasia

h Sequela to recent seizures

INVESTIGATION
Check titers for infectious
diseases (eg, CDV infection,
ehrlichiosis, RMSF, BP = blood pressure
cryptococcosis, CDV = canine distemper virus
toxoplasmosis, neosporosis)
GME = granulomatous meningoencephalitis
RMSF = Rocky Mountain spotted fever
T4 = thyroxine
DIAGNOSIS TSH = thyroid-stimulating hormone
GME or necrotizing encephalitis
(ie, titers negative) US = ultrasonography
DIAGNOSTIC/MANAGEMENT TREE h NEUROLOGY h PEER REVIEWED

 
 
 
 
PARESIS OR PARALYSIS IN CATS*
Mark Rishniw, BVSc, MS, DACVIM (Cardiology & Internal Medicine)†
Cornell University

PARESIS OR PARALYSIS IN CATS

Evidence of trauma (eg, torn claws, abrasions, open wounds)?

YES NO

Dyspnea or tachypnea?

Evidence of limb Evidence of spinal

fracture or injury misalignment
on palpation,
flaccid tail
YES NO

INVESTIGATION INVESTIGATION
Limb radiography Spinal radiography Evident pain or vocalizing Cervical
(myelography) ventroflexion,
pupillary
dilatation, cat
obtunded?
Pelvic limbs painful, swollen; muscle hard; footpads pale
or cyanotic; no flow on blood pressure Doppler probe

Blood analysis

Murmur/gallop/arrhythmia?

YES NO

DIAGNOSIS DIAGNOSIS DIAGNOSIS DIAGNOSIS

Hyperthyroidism Thiamine deficiency Organophosphate Hypokalemia
Pleurocentesis positive? Creatine kinase elevated toxicity

DIAGNOSIS
Feline aortic
YES NO thromboembolism

TREATMENT
Drain thoracic cavity
DIAGNOSIS
Cardiomyopathy

*Article originally published with the title “Paresis/Paralysis”

INVESTIGATION †Byline reflects author information on original publication. On publication

Radiography (lateral, quick) or echocardiography (minimal) of this collection, the author’s current credentials are Mark Rishniw, BVSc,
MS, PhD, DACVIM (Cardiology & Internal Medicine).
REFRACTORY SEIZURES
Hillary Haydon Greatting, DVM, MS, DACVIM
Tom Jukier, DVM
Washington State University

CONFIRMED SEIZURES

Perform interictal neurologic examination

ABNORMAL NORMAL

INVESTIGATION Idiopathic epilepsy possible*

Perform CBC, serum chemistry profile,
bile acid assay, thyroid panel,
and serum ammonia level tests to
rule out reactive seizures
INVESTIGATION
Assess seizure frequency

DIAGNOSIS
Structural epilepsy suspected

<2 seizures in 6 months ≥2 seizures in 6 months

INVESTIGATION
Consider MRI and CSF analysis

TREATMENT TREATMENT
No therapy recommended Begin single AED, with goal of monotherapy:
h Phenobarbital 1 (2.5-3.5 mg/kg PO q12h)

TREATMENT h Potassium bromide (20-30 mg/kg q24h)

Treat underlying disease

INVESTIGATION
Reassess seizure frequency
AED = antiepileptic drug

*Idiopathic epilepsy can be subclassified into genetic epilepsy (identified genetic


background), suspected genetic epilepsy (breed prevalence >2%), or epilepsy
of unknown cause (nature unknown with no structural disease).5 Diagnosis of <1 seizure in 3-6 months >1 seizure in 3-6 months
idiopathic epilepsy can be suggested if there is a history of ≥2 unprovoked epileptic
seizures occurring ≥24 hours apart, the patient’s age at epileptic seizure onset is
between 6 months and 6 years, interictal physical and neurologic examinations are
unremarkable (except for antiepileptic-drug–induced neurologic abnormalities and INVESTIGATION
postictal neurologic deficits), and no clinically significant abnormalities are found Adequate control:
on minimum database blood tests and urinalysis.6 However, diagnosis is ideally h Monitor blood (ie, serum AED) levels
made on exclusion (ie, normal brain MRI and CSF analysis) or further supported by

h Perform appropriate blood work (ie, CBC,
electroencephalography.5

serum chemistry profile) if applicable
 DIAGNOSTIC/MANAGEMENT TREE h NEUROLOGY h PEER REVIEWED

 
 
 
 
INVESTIGATION
Inadequate control: AUTHOR INSIGHT
h Check serum blood levels of AED
h Ensure sufficient length of time for therapeutic trial (ie, h A definition of refractory epilepsy is not established for dogs, but it


steady-state drug level has been reached) is generally agreed that an animal with frequent or severe seizures
h Reevaluate diagnosis; repeat neurologic examination
or intolerable side effects despite appropriate antiepileptic drug

(AED) therapy is considered refractory to treatment.3
h Levetiracetam and zonisamide are increasingly the drugs of choice

Therapeutic levels reached (phenobarbital 15-35 µg/mL for monotherapy by some neurologists. A recent study found no
or potassium bromide 1-3 mg/mL)? reduction in monthly seizure frequency when levetiracetam was
used as a sole agent.4 However, little additional information is
available in the veterinary literature on the efficacy of these medi-
cations as sole agents.
YES NO h Some AEDs (eg, levetiracetam, zonisamide) have a reported “hon-

eymoon effect,” with dogs developing tolerance over time.
h Gabapentin and pregabalin are not known efficacious AEDs but

anecdotally may help with seizure control in patients tolerant to
DIAGNOSIS Maximize current AED;
other medications.
Refractory epilepsy ensure owner compliance

References
1. Podell M, Volk HA, Berendt M, et al. 2015 ACVIM small animal consensus statement

on seizure management in dogs. J Vet Intern Med. 2016;30(2):477-490.
TREATMENT 2. Muñana KR, Nettifee-Osborne JA, Papich MG. Effect of chronic administration of
Initiate second anticonvulsant:

phenobarbital, or bromide, on pharmacokinetics of levetiracetam in dogs with
h Phenobarbital
epilepsy. J Vet Intern Med. 2015;29(2):614-619.
h Potassium bromide
3. Muñana KR. Management of refractory epilepsy. Top Companion Anim Med.
h Levetiracetam 20 mg/kg PO q8h (extended release, 30 mg/kg PO

2013;28(2):67-71.

q12h); dose may need to be increased when used with phenobarbital 2 4. FredsØ N, Sabers A, Toft N, MØller A, Berendt M. A single-blinded phenobarbital-
h Zonisamide 5-10 mg/kg PO q12h (for dogs already receiving
controlled trial of levetiracetam as monotherapy in dogs with newly diagnosed

phenobarbital, 10 mg/kg PO q12h) epilepsy. Vet J. 2016;208:44-49.
5. Berendt M, Farquhar RG, Mandigers PJJ, et al. International veterinary epilepsy task

force consensus report on epilepsy definition, classification and terminology in
companion animals. BMC Vet Res. 2015;11:182.
6. De Risio L, Bhatti S, Muñana K, et al. International veterinary epilepsy task force

consensus proposal: diagnostic approach to epilepsy in dogs. BMC Vet Res.
2015;11:148.
INVESTIGATION INVESTIGATION
Adequate control: Inadequate seizure control:
h Continue current h ≈30% of dogs are not controlled with AEDs 3 Suggested Reading


therapy Farnbach GC. Serum concentrations and efficacy of phenytoin, phenobarbital, and
primidone in canine epilepsy. J Am Vet Med Assoc. 1984;184(9):1117-1120.
Holliday TA. Seizure disorders. Vet Clin North Am Small Anim Pract. 1980;10(1):3-29.
Knowles K. Idiopathic epilepsy. Clin Tech Small Anim Pract. 1998;13(3):144-151.
Kwan P, Schachter SC, Brodie MJ. Drug-resistant epilepsy. N Engl J Med. 2011;365(10):919-
926.
Consider tolerance TREATMENT TREATMENT
to AED Lane SB, Bunch SE. Medical management of recurrent seizures in dogs and cats. J Vet
Consider adding Change seizure
Intern Med. 1990;4(1):26-39.
AEDs: control goals:
h Topiramate (2-10 h Increase
Podell M, Fenner WR. Bromide therapy in refractory canine idiopathic epilepsy. J Vet
Intern Med. 1993;7(5):318-327.


mg/kg PO q12h) interictal periods
h Gabapentin (10-20 h Decrease seizure
Schwartz-Porsche D, Löscher W, Frey HH. Therapeutic efficacy of phenobarbital and
TREATMENT primidone in canine epilepsy: a comparison. J Vet Pharmacol Ther. 1985: 8(2):113-119.


mg/kg PO q6-8h) duration
Change to newer AED h Pregabalin (3-4
Thomas WB. Idiopathic epilepsy in dogs and cats. Vet Clin North Am Small Anim Pract.
(eg, levetiracetam to 2010;40(1):161-179.

mg/kg PO q8h)
zonisamide) von Klopmann, Rambeck B, Tipold A. Prospective study of zonisamide therapy for
refractory idiopathic epilepsy in dogs. J Small Anim Pract. 2007;48(3):134-138.
SPINAL PAIN
Mark Troxel, DVM, DACVIM (Neurology)
Massachusetts Veterinary Referral Hospital
Woburn, Massachusetts

SPINAL PAIN

INVESTIGATION
General history:
h S ignalment
h P resenting signs
h Vaccination status
h C urrent medications
h Travel
h Toxin exposure
h S ystemic signs (eg, vomiting, diarrhea,
coughing, change in appetite)
h O ther sick animals in household

INVESTIGATION
History specific to spinal pain:
h O nset: acute or insidious
h D uration of signs
h P rogressive or nonprogressive
h R esponse to treatment(s)
h H istory of trauma
h P revious spinal pain
h P ain worse after rest or exercise
INVESTIGATION h D oes pain lessen with activity?
INVESTIGATION
Physical, orthopedic, and neurologic examinations: h I ncontinence
Minimum databas e:
h S pinal pain in back or neck h C BC
h L imping/lameness
h Fever h S erum chemistry profile
h L ocation of spinal pain noted by owner

h Heart murmur h Urinalysis


h Pain at LS region, on digital rectal examination, h P oint-of-care tick-borne

or elevation of tail (suggests LS disease) pathogen testing or tick serology
h Joint effusion or pain

Evidence of systemic disease that could TREATMENT
explain clinical signs? If positive for tick-borne
pathogen, administer doxycycline

YES NO
Response to treatment?

INVESTIGATION INVESTIGATION
C&S = culture & sensitivity testing
Additional diagnostics as Spinal radiography YES
indicated: (best performed under
h Thoracic/abdominal sedation)
CSF = cerebrospinal fluid

radiography
FNA = fine-needle aspiration h Abdominal ultrasonography

h Echocardiography
IgA = immunoglobulin A DIAGNOSIS

h Arthrocentesis with fluid
Tick-borne disease

LS = lumbosacral analysis/C&S
h Infectious disease serology

 DIAGNOSTIC TREE h NEUROLOGY h PEER REVIEWED

 
 
 
 
Cause identified?

NO YES

Patient younger than 2-3 years? INVESTIGATION

Radiographic abnormalities detected:
h Vertebral endplate lysis = discospondylitis
• Perform urine and blood C&S; Brucella canis serology


• Empirical antibiotics (eg, cephalexin [22 mg/kg PO q12h])
–Consider Aspergillus spp infection if German shepherd dog
– Consider disk aspiration with bacterial/fungal C&S if poor
NO YES

response to antibiotics
h Fracture/luxation; bone lysis (ie, neoplasia, osteomyelitis);
mineralized disk material in spinal canal (advanced imaging
recommended)
h N arrowed/collapsed disk space
INVESTIGATION • Consider advanced imaging after assessing duration/severity

Assess duration/severity of pain of pain (see left)
h Degenerative joint disease or spondylosis deformans

(may be incidental finding)

Acute (<1 month) or mild to moderate pain Chronic (>1 month) or severe pain TREATMENT
Advanced diagnostics/treatment as indicated:
h A dvanced imaging: MRI, CT, myelography
h C SF analysis
h S urgery: spinal cord decompression, excision/biopsy of lesion
h F NA or biopsy of lesion(s)
TREATMENT h C SF C&S if CSF analysis shows neutrophilic pleocytosis
Medical management:
h I nfectious disease testing
h Strict activity restriction × 2-4 weeks
h J oint fluid analysis/C&S if joint effusion/pain
• Crate or small-room confinement at
h S erum IgA level if suspected steroid-responsive meningitis

all times unless patient sitting quietly
h I f suspected multiple myeloma, serum protein electrophoresis,
in owner’s lap
• Carry outside to eliminate; short, urine Bence Jones protein, bone marrow aspiration
h U rine and/or blood C&S if bacterial infection suspected

controlled leash walks (just long
enough to allow elimination)
• No running, jumping, or stairs Clinical signs resolved?

h Consider NSAID trial
h Pain medication (eg, gabapentin) in
painful patients TREATMENT
h For patients with neck pain: Treatment based on final diagnosis:
• Use harness for life h S urgery

• Elevate food and water bowls h C orticosteroids or NSAIDs
YES NO

h P ain medication
h A ntibiotics
h P hysical therapy
h A cupuncture

Clinical signs
progress to paresis, TREATMENT *Patients younger than 2-3 years of age
ataxia or paraplegia Gradual return to normal

are more likely to have meningitis than
activity level over 2-4 weeks intervertebral disk disease, so early
intervention is recommended.

Clinical signs recur? YES

VESTIBULAR DISEASE
Simon R. Platt, BVMS, MRCVS, DACVIM (Neurology), DECVN*
University of Georgia

HEAD TILT, SPONTANEOUS

NYSTAGMUS, ROLLING/FALLING/
LEANING, OR ATAXIA

INVESTIGATION
Investigate for CVD

INVESTIGATION
History:
h Signalment

h Indoor/outdoor (feline)
INVESTIGATION

h Presenting signs
Physical examination:

h Date of onset h Ears/nose/throat: evidence of otitis externa, abnormal


h Progression
tympanum, nasal lesion, or discharge

h Preventives used h Eyes: fundic abnorm alities, uveitis


h Medical and surgical history h Cardiovascular: murmur, arrhythmia, heart rate, pulse quality


h Toxin or pharmaceutical exposure h Respiratory: crackles, wheezes


h Travel history h Abdomen: pain, organomegaly


h Littermates affected h Integumentary: lesions compatible with trauma/bite or


penetrating wounds, especially over head
h Lymph nodes: lymphadenopathy

h Rectal: prostatic enlargement and/or pain, anal sac abnormalities

h Musculoskeletal: joint swelling/pain, lameness, or muscle atrophy

INVESTIGATION
History of trauma, toxin exposure, similar illness in associated animals?

Systemic disease suggested?

YES NO

NO YES
TREATMENT INVESTIGATION
Investigate and treat Neurologic examination
as appropriate
INVESTIGATIO N INVESTIGATION
h MDB for anesthesia h CBC, serum biochemistry, UA


h Thoracic radiography if h Thoracic 3-view radiography


h Gait: evidence of paresis? >6 years of age for h Abdominal imaging: radiography


h Postural reactions: evidence of anesthesia ± ultrasonography

deficits? h Systemic BP assessment h Lymph node aspiration


h Neck pain? h Advanced imaging h ECG ± echocardiography if cardiac abnormality



h Vertical nystagmus, cranial nerves (eg, CT, MRI) h Infectious disease ± blood cultures


h II-VI/IX-XII dysfunction? h CSF analysis h Bone marrow aspiration/biopsy if CBC



h ± infectious disease titers suggests abnormal bone marrow function

h ± storage disease testing

NO YES Normal Abnormal

TREATMENT
Treat as appropriate
 DIAGNOSTIC TREE h NEUROLOGY h PEER REVIEWED

 
 
 
 
Horner syndrome?

NO YES

Reconsider mentatio n Investigate for PVD

INVESTIGATION
Examination:
Abnormal Normal h Consider age (geriatric)

h Ears/nose/throat:

evidence of otitis externa,
abnormal tympanum,
pharyngeal mass
h Lymph nodes:

lymphadenopathy
h Bulla palpation: pain

Abnormal

NO YES

*Byline reflects author information on


INVESTIGATION INVESTIGATION original publication. On publication of
Thyroid profile: h MDB and thoracic radiographs this collection, the author’s current
credentials are Simon R. Platt, BVMS,

h Consider congenital based on for anesthesia if >6 years of age
MRCVS, DACVIM (Neurology), DECVN,

age and breed h Skull radiographs, CT, MRI of
FRCVS.

h Confirm no local or systemic middle or inner ear

toxic medications administered h ± myringotomy

h ± hearing testing BP = blood pressure

CVD = central vestibular disease
MDB = minimum database
PVD = peripheral vestibular disease
DIFFERENTIAL Progresses
UA = urinalysis
If acute, consider idiopathic
 DIAGNOSTIC TREE h ONCOLOGY h PEER REVIEWED

 
 
 
 
INTERPRETING NEUTROPHIL COUNT
AFTER CHEMOTHERAPY
Antony S. Moore, BVSc, MVSc, DACVIM (Oncology)
Angela E. Frimberger, VMD, DACVIM (Oncology)
Veterinary Oncology Consultants
Wauchope, New South Wales, Australia

INTERPRETING NEUTROPHIL COUNT

AFTER CHEMOTHERAPY

INVESTIGATION
CBC

INVESTIGATION
Assess absolute neutrophil count (cells/mcL)

Values at expected nadir; no Myelosuppressive chemotherapy due

myelosuppressive chemotherapy due

Neutrophils Neutrophils
Neutrophils Neutrophils ≤3000 cells/mcL >3000 cells/mcL
>1000 cells/mcL <1000 cells/mcL

TREATMENT TREATMENT
TREATMENT Delay scheduled h

No change in
No change Patient afebrile, Patient febrile, lethargic myelosuppressive treatment
in treatment normal energy and or inappetent, or treatment until h Continue protocol

appetite, no GI signs GI signs present neutrophils >3000
cells/mcL (recheck
CBC in 3-7 days)

TREATMENT TREATMENT
h Prophylactic Emergency

antibiotics h Hospitalize and treat

h Monitor at home for sepsis

h R educe future dose of h Aggressive IV fluids

responsible drug by and antibiotics
25% h Other supportive

h Recheck neutrophil measures (eg, plasma

count at expected transfusion) as
nadir after dose clinically indicated
adjustment
MANAGEMENT OF CUTANEOUS MELANOMA
Heather M. Wilson-Robles, DVM, DACVIM (Oncology)
Texas A&M University

CUTANEOUS MELANOMA CONFIRMED

Excision complete?

YES

Low, moderate, or high MI?

h Low MI (<3) h Moderate MI (3-5) h High MI (>5)

h Well-differentiated h Mild-to-moderate atypia h Moderate-to-severe atypia



histologically (ie, cells look
like normal melanocytes)

Conduct prognostic tests to

determine melanoma grade
TREATMENT
Benign; no further therapy
indicated

Low grade High grade

TREATMENT h Complete full staging


No further therapy indicated (eg, chest radiography,
regional lymph node
aspiration, CBC, serum
chemistry profile,
urinalysis)
h Consider adjuvant

therapy

TREATMENT
h Chemotherapy

h Immunotherapy

h Monitoring for

metastasis and
recurrence
 MANAGEMENT TREE h ONCOLOGY h PEER REVIEWED

 
 
 
 
NO

Low, moderate, or high MI?

h Low MI (<3) h Moderate MI (3-5) h High MI (>5)

h Well differentiated h Mild-to-moderate atypia h Moderate-to-severe atypia



(ie, cells look like normal
melanocytes)

TREATMENT Complete full staging (eg, chest radiography,

h Re-excision regional lymph node aspiration, CBC, serum

TREATMENT h Radiation therapy chemistry profile, urinalysis)

h Re-excision

h Radiation therapy

Re-excision possible? Metastatic lesions?

YES NO NO YES

Complete margins (ie, >2 mm clean tissue surrounding sample) postsurgery?

TREATMENT
h Radiation therapy

h ± chemotherapy

h ± immunotherapy

h Monitoring

YES NO

TREATMENT TREATMENT
h Chemotherapy or h Radiation therapy MI = mitotic index


immunotherapy h ± chemotherapy

h Monitoring h ± immunotherapy


h Monitoring

ANISOCORIA
Caryn E. Plummer, DVM, DACVO
University of Florida

ONE PUPIL SMALLER OR LARGER THAN THE OTHER—WHICH IS AFFECTED?

DIFFERENTIAL DIFFERENTIAL
Affected pupil is smaller (miosis) Affected pupil is larger (mydriasis)

h Scleral injection, corneal edema, Scleral injection or corneal edema?


aqueous flare, hypopyon,
hyphema, hypotony?
h Corneal ulceration/trauma/defect?

YES N0

YES NO
IOP elevated?

DIAGNOSIS INVESTIGATION
h Anterior uveitis h Elevated nictitans?


h Corneal ulceration/ h Enophthalmos?


trauma h Ptosis?
YES NO

h Other intraocular

disease
h Synechiae

DIAGNOSIS DIAGNOSIS
YES NO Glaucoma h Pharmacologically induced

INVESTIGATION mydriasis (secondary to
h Apply fluorescein stain drugs used for uveitis or
ocular surface disease [eg,

h Tick/fungal titers,
inflammation, corneal ulcer])

serum chemistry
profile, CBC, DIAGNOSIS h Afferent lesion with anterior

radiography Horner syndrome segment inflammation
h Thorough ocular INVESTIGATION INVESTIGATION

diagnostics and IOP Investigate for history Investigate for
measurement of head trauma, signs exposure to
of CNS disease miotic agents
INVESTIGATION (eg, prostaglandin
Confirm with topical analogs, β-blockers,
10% phenylephrine pilocarpine)
(postganglionic
lesions will show sign
resolution in <10 min)

CN III = third cranial nerve (ie, oculomotor nerve)

IOP = intraocular pressure
 DIAGNOSTIC TREE h OPHTHALMOLOGY h PEER REVIEWED

 
 
 
 
Exposure to mydriatics (eg, atropine, tropicamide, epinephrine, phenylephrine, anticholinergic agents, certain plant toxins)?

YES NO PUPILLARY TESTING:

DETERMINING WHICH
PUPIL IS AFFECTED
TREATMENT Anisocoria (ie, asymmetric pupils at
Treat as necessary
INVESTIGATION INVESTIGATION rest, potentially caused by ocular or
Investigate for history of head trauma, signs of CNS disease Is the eye visual?
neurologic disorders or pharmacologic
intervention) may not be apparent at
outset. Pupil response to light and
dark stimulation should be checked:
YES NO
h In ambient lighting, use a dim light

source held at least arm’s distance
from the patient to visualize the
DIFFERENTIALS DIFFERENTIAL
Efferent lesion or mechanical inhibition Afferent lesion tapetal reflection, which will
delineate pupil size.
h Darken the room and using the light

Exposure to mydriatics? source to visualize the tapetal
reflection, evaluate the degree of
Congenital Acquired
dilation in each pupil: both pupils
should dilate in darkened condi-
tions; one pupil failing to dilate indi-
DIFFERENTIALS DIFFERENTIALS cates the affected eye.
h Retinal dysplasia (severe) h Retinal


h Retinal detachment detachment/ h Stimulate each eye separately with

YES NO

h Optic nerve hypoplasia degeneration
a bright light: both pupils should

h Optic nerve coloboma h Chorioretinitis


h Optic neuritis constrict in response to bright light;

h Optic nerve atrophy
one pupil failing to constrict fully

h Glaucoma

TREATMENT h Retrobulbar lesion indicates the affected eye.

Treat as necessary
h Optic tract lesion

Acquired Congenital
Suggested Reading
Martin CL. Problem-based management of
DIFFERENTIALS ocular emergencies. In: Martin CL, ed.
h Iris hypoplasia Ophthalmic Disease in Veterinary Medicine.

h Iris coloboma London: Manson Publishing; 2010: 93-104.

DIFFERENTIAL Ventrolateral strabismus? DIFFERENTIAL Ollivier FJ, Plummer CE, Barrie KP. Opthalmic
Iris atrophy Posterior synechiae examination and diagnostics. In:
(ie, scalloped pupil (adhesions of iris to Gelatt KN, ed. Essentials of Veterinary
margin, holes in anterior lens capsule; Ophthalmology. Ames, IA: Wiley-Blackwell;
stroma) usually following 2008:3-34.
YES anterior uveitis) Shamir MH, Ofri R. Comparative neuro-
ophthalmology. In: Gelatt KN, ed.
Veterinary Ophthalmology. 4th ed. Ames,
IA: Blackwell Publishing; 2007:1406-1469.
DIAGNOSIS
Oculomotor nerve (CN III) palsy
ANTERIOR UVEITIS
Alison Clode, DVM, DACVO*
North Carolina State University

CLOUDY, RED, PAINFUL, OR BLIND EYE

INVESTIGATION
Complete ophthalmic examination to determine if AU is causing signs

INVESTIGATION
AU active or chronic?

INVESTIGATION INVESTIGATION
Signs of active AU: Signs of chronic AU:
h Flare/hyphema/hypopyon h Permanent anterior or posterior


h Fibrin in anterior chamber synechiae

h Miosis h Keratic precipitates, associated


h Iridal hyperemia endothelial scars

h Ocular hypotony h Iridal hyperpigmentation


h Anterior or posterior synechiae h Resistance to pharmacologic


h Keratic precipitates mydriasis

h Corneal edema h Cataract


h Episcleral injection/congestion

AU primary condition or secondary to systemic disease?

INVESTIGATION INVESTIGATION
Systemic conditions causing AU: Ocular conditions causing AU:
h Immune-mediated (uveodermatologic h Ulcerative corneal disease


syndrome) h Scleral disease (necrotizing scleritis)

h Infectious (fungal, algal, bacterial, viral, h Cataract


rickettsial, parasitic, protozoal) h Blunt or penetrating trauma

h Metastatic/generalized neoplasia (lymphoma) h Intraocular neoplasia


h Hyperlipidemic syndromes h Immune-mediated


h Hyperviscosity syndromes h Idiopathic


INVESTIGATION INVESTIGATION
Diagnostic confirmation of systemic conditions: Diagnostic confirmation of ocular conditions:
h Complete physical examination h Ulcerative corneal disease: fluorescein dye application; visual inspection for infection signs


h Multiple additional diagnostic tests based on (eg, cellular infiltrate, stromal loss)

concurrent signs (eg, CBC, serum chemistry profile, h Scleral disease (necrotizing scleritis): visual evaluation for scleral vascularization, mass effect

urinalysis, urine culture, lymph node aspirate, thoracic/ h Cataract: visual evaluation for lenticular opacity; ocular ultrasound

abdominal radiography, abdominal ultrasonography) h Blunt or penetrating trauma: visual evaluation for penetrating wound; ocular ultrasound

h Serology (eg, tick titers, fungal) h Intraocular neoplasia: visual evaluation for pigmented or nonpigmented iridal or ciliary body


mass effect; ocular ultrasound
h Immune-mediated: diagnosed by exclusion

 DIAGNOSTIC TREE h OPHTHALMOLOGY h PEER REVIEWED

 
 
 
 
Corneal ulceration/infection or penetrating wound present?

YES NO

TREATMENT TREATMENT
h Topical prophylactic antibiotic if not infected (ie, h Topical corticosteroid (prednisolone acetate, dexamethasone)



neomycin/polymyxin B/bacitracin) q6-8h q6-8h
h Topical therapeutic antibiotic if infected or penetrating h Topical atropine q12-72h, depending upon degree of mydriasis



wound present (fluoroquinolone q4-6h) h Systemic analgesia (NSAID, opioid, corticosteroid) depending


h Topical atropine q12-72h, depending on degree of mydriasis on disease/condition

h Topical lubricating drops q6-8h h Treatment of underlying cause (cataract removal, systemic


h Systemic analgesia/opioid antimicrobials, chemotherapy)

h Systemic NSAID for inflammation

Resolution occurs with nonspecific
If AU is secondary to corneal TREATMENT topical anti-inflammatory therapy
disease, resolution occurs with If AU is secondary to systemic disease, treat ulcerative disease and and medical or surgical therapy
corneal disease resolution consider additional topical NSAID (flurbiprofen, diclofenac) q12h of underlying cause

IOP >20 mm Hg?

YES NO

TREATMENT TREATMENT
h Topical carbonic anhydrase No additional treatment

inhibitor q8-12h
h Topical β-blocker q12h

Complete posterior synechiae present?

*Byline reflects author information on original

AU = anterior uveitis

publication. On publication of this collection,
TREATMENT the author’s current affiliation is Port City IOP = intraocular pressure
Topical atropine or tropicamide q12-24h Veterinary Referral Hospital, Portsmouth,
New Hampshire.
BLINDNESS
Alison Clode, DVM, DACVO*
North Carolina State University

BLINDNESS

INVESTIGATION INVESTIGATION INVESTIGATION

Thorough history: Visual examination: Thorough ophthalmic examination
h D uration h Ability to navigate

h O nset (acute vs progressive) in light and dark
h I ndependent of lightness/darkness h Globe/orbital

h A ssociated with: asymmetry
• Ocular pain/discharge h Signs of ocular pain

• Change in eye appearance h Ocular redness

• Change in environment h Ocular cloudiness

• Signs of systemic illness h Clarity of visual axis

• Signs of neurologic disease INVESTIGATION INVESTIGATION
h Toxin exposure
Response and reflex Intraocular pressure measurement
h Other animals affected
examination (normal 10-25 mm Hg)

INVESTIGATION INVESTIGATION INVESTIGATION >25 mm Hg <10 mm Hg
Menace response Dazzle reflex (ie, blink Direct + consensual
response to extremely PLR
bright light)

DIAGNOSIS DIAGNOSIS
DIFFERENTIALS Glaucoma†: Anterior uveitis†:
Absence indicates DIFFERENTIALS h Scleral injection + h Miosis + aqueous flare +


intraocular, retinal, DIFFERENTIALS Absence indicates corneal edema + hypopyon
optic nerve, optic Absence indicates retinal, optic nerve, mydriasis h May have negative

chiasm, or cortical retinal, optic nerve, optic chiasm, or h Variable dazzle menace, direct and

disease optic chiasm, or brainstem disease reflex in acute consensual PLR if
brainstem disease glaucoma posterior uveitis also
h Dazzle reflex, direct present

and consensual
negative in chronic
glaucoma

DIFFERENTIALS
h Systemic infection (viral,

bacterial, rickettsial,
DIFFERENTIALS mycotic, algal, parasitic,
h Primary breed-related protozoal)

glaucoma h Noninfectious

h Secondary glaucoma: inflammatory

• Anterior uveitis (uveodermatologic
• Lens luxation syndrome, lens induced,
PLR = pupillary light reflex • Intraocular tumor trauma, ulcerative
corneal disease)
SARD = sudden acquired retinal degeneration h Neoplastic (primary

intraocular melanoma,
ciliary body adenoma) or
metastatic (lymphoma,
*Byline reflects author information on original publication. On publication of this collection, the adenocarcinoma)

author’s current affiliation is Port City Veterinary Referral Hospital, Portsmouth, New Hampshire. h Systemic hypertension
†
Associated with acute blindness

‡
h Systemic hyperlipidemia
Not associated with acute blindness

 DIAGNOSTIC/MANAGEMENT TREE h OPHTHALMOLOGY h PEER REVIEWED

 
 
 
 
INVESTIGATION INVESTIGATION INVESTIGATION
Funduscopic examination: Schirmer tear test: Fluorescein dye application
h Tropicamide 1% for dilation h Normal >15 mm wetting/min


h Evaluate retinal vasculature, optic h Reduction may induce opacification


nerve head, tapetal reflectivity, of cornea (pigmentation,
nontapetal pigmentation vascularization, fibrosis)
DIAGNOSIS
Uptake at corneal
ulcer:
h Associated with


corneal
opacification
DIAGNOSIS DIAGNOSIS DIAGNOSIS DIAGNOSIS DIFFERENTIALS (edema,
Chorioretinitis†: Optic neuritis†: Retinal detachment †: Retinal degeneration‡: Normal funduscopic vascularization,
h Indistinct retinal h Optic nerve h Anterior h Vascular examination: cellular infiltration)




vasculature + hyperemia + displacement of attenuation + h SARD may be likely h Associated with


multifocal lesions swelling + retina (± associated tapetal h Perform mild to severe

of tapetal hypo- peripapillary retinal vessels) with hyperreflectivity + electroretinogram reflex anterior
reflectivity (cellular detachment subretinal optic nerve atrophy to confirm uveitis (miosis,
exudate or fluid h Negative dazzle accumulation of h Negative dazzle diagnosis flare, hypopyon)


transudate) reflex and PLR fluid or cells reflex and PLR at h May be associated

h Negative dazzle (bullous retinal end stage with acute

reflex and PLR detachment) blindness, but less
h Veil-like likely (unilateral

appearance to disease)
retina with lack of
retinal vessels over
DIFFERENTIALS tapetum =
h Systemic infection (viral, bacterial, rickettsial, rhegmatogenous

mycotic, algal, parasitic, protozoal) detachment
h Negative dazzle
h Noninfectious inflammatory


(uveodermatologic syndrome, granulomatous reflex and PLR
meningoencephalitis)
h Neoplastic (primary [astrocytoma] melanoma)

or metastatic (lymphoma, adenocarcinoma)
h Systemic hypertension
DIFFERENTIALS

h Exudative detachment associated with

advanced chorioretinitis
h Steroid-responsive (no identifiable systemic

disease condition)
h Rhegmatogenous retinal detachment:

• Postoperative (eg, lens surgery)
• Breed related (Shih-tzu, collie, Labrador

retriever)
CATARACTS IN CATS: DIAGNOSIS
Mary Rebecca Telle, DVM*
Diane Hendrix, DVM, DACVO
University of Tennessee

CATARACT SUSPECTED

INVESTIGATION
Assess patient breed and age for signalment

Young and/or purebred Himalayan, Young (<2 years) and not purebred Himalayan, Middle-aged (ie, 2-5 years)
Birman, Persian, or British shorthair Birman, Persian, or British shorthair

Suspect congenital and/ Likely secondary cataract Likely primary (Birman cats 2)
or inherited cataract 1-3 or seconda ry cataract

INVESTIGATION
Gather patient history:
h Pertinent ocular history

h Trauma

Menace response h Cloudiness Fundic examination (direct vs indirect)

h Absent: mature cataract, chronic uveitis, h Haziness h May not be able to assess fundus,



or retinal detachment h Decreased or absent vision depending on cataract maturity or

h Present: immature cataract or nuclear anterior chamber debris

sclerosis h May be normal

h May have other lesions if systemic disease

(eg, fungal, protozoal) is present
INVESTIGATION
Perform ophthalmic
examination
Pupillary light reflexes IOP
h Normal: primary cataract h Decreased: anterior uveitis may be present


h Miosis and/or difficulty assessing suggests h Increased: primary or secondary glaucoma


uveitis may be present or cause of cataract may
INVESTIGATION have resolved (ie, transient uveitis)
Evaluate lens for
opacity
h Dilate with

Fluorescein stain tropicamide unless Anterior chamber assessment
h Positive if trauma to cornea has occurred elevated IOP or lens h Normal: could denote primary cataract


luxation h Abnormal: anterior uveitis is present (eg,

flare, hypopyon, hyphema, keratic
precipitates on corneal endothelium)

Opacity found

DIAGNOSIS
Nuclear sclerosis Cloudiness, bluish discoloration (evenly White and opaque
h h Classify


distributed), and rounded (dependent on maturity) cataract by
h Center of lens h Vision possibly affected DIAGNOSIS stage of


h Functional vision not affected h Tapetal reflection and Cataract progression,
TREATMENT


h Bilateral and symmetrical fundus partially or location, or

No treatment h Tapetal reflection and fundus still visible completely obscured cause

needed
*Byline reflects author information on original publication. On publication of this collection, the

author’s current affiliation is University of Wisconsin-Madison. IOP = intraocular pressure
 DIAGNOSTIC TREE h OPHTHALMOLOGY h PEER REVIEWED

 
 
 
 
Stage of progression INVESTIGATION YES
Vision present?

Hypermature cataract Present Present

h Advanced and decreased and unchanged
NO


h Shimmering areas


h Wrinkled anterior lens capsule


h Reduced lens size
Mature cataract 
h Tapetal reflection may or may
Entire lens volume Incipient cataract

h
Immature cataract not be present

h Loss of vision and h <10%-15% lens
15%-99% lens volume

h


menace volume

Location

Early
immature cataract

Subcapsular Capsular Cortical Nuclear Equatorial

Primary See Congenital Toxic and metabolic

and primary
breeds and
signalment
Cause
Nutritional secondary Primary Arginine deficiency from
hyperparathyroidism; hypoparathyroidism milk replacer
leads to (ie, hypercalcemia, h No longer an


Secondary (most common) hypercalcemia 4 hyperphosphatemia)5 important cause
because of
commercial products
h May diminish with age

h Diffuse anterior and

Uveitic (most common) Lens luxation Glaucoma posterior lens
h May see posterior synechiae, rubeosis iridis, aqueous h In cats, usually h Primary
opacification and



flare, fibrin, keratic precipitates, miosis, low IOP secondary to h Secondary (more common
vacuolations

h IOP will be elevated if secondary glaucoma develops uveitis in cats): uveitis, neoplasia

Inflammatory Infectious Neoplastic Idiopathic
h Immune-mediated

h Diagnosis of exclusion

h Mostly affects middle-age to older cats
Bacterial Fungal

h Affects one or both eyes
h Septic lens implantation h Blastomyces dermatitidis

h Iris nodules, keratic precipitate, fibrin,


syndrome 6 h Coccidioides immitis

cataract, glaucoma

h Histoplasma capsulatum
h Usually not painful

h Cryptococcus neoformans

h May result in enucleation if long-term

h Encephalitozoon cuniculi 7

therapy fails

Viral
h FIV Protozoal Metastatic Primary

h FeLV h Toxoplasma gondii
h Lymphoma h Diffuse iridal melanoma


h Feline infectious


h Hemangiosarcoma h Trauma-associated sarcoma

peritonitis References & Suggested


h Adenocarcinoma (highly malignant) Reading on page 160

DIAGNOSTIC TREE h OPHTHALMOLOGY h CONTINUED FROM PAGE 157

 
 
 
 
CATARACTS IN CATS: DIAGNOSIS
REFERENCES & SUGGESTED READING
References
1. Rubin LF. Hereditary cataract in Himalayan cats. Feline Pract. 1986;16:14-15.

2. Schwink K. Posterior nucleus cataracts in two Birman kittens. Feline Pract. 1986;16:31-33.

3. Narfström K. 1999 Hereditary and congenital ocular disease in the cat. J Feline Med Surg.

1999;1(3):135-141.
4. Bassett JR. Hypocalcemia and hyperphosphatemia due to primary hypoparathyroidism in

a six-month-old kitten. J Am Anim Hosp Assoc. 1998;34(6):503-507.
5. Stiles J. Cataracts in a kitten with nutritional secondary hyperparathyroidism. Prog Vet

Comp Ophthalmol. 1991;4:296-298.
6. Bell CM, Pot SA, Dubielzig RR. Septic implantation syndrome in dogs and cats: a distinct

pattern of endophthalmitis with lenticular abscess. Vet Ophthalmol. 2013;16(3):180-185.
7. Benz P, Maass G, Csokai J, et al. Detection of Encephalitozoon cuniculi in the feline

cataractous lens. Vet Ophthalmol. 2011;14(Suppl 1):37-47.

Suggested Reading
Peiffer RL JR, Belkin PV. Keratolenticular dysgenesis in a kitten. J Am Vet Med Assoc.
1983;182(11):1242-1243.
Peiffer RL, Gelatt KN. Cataracts in the cat. Feline Pract. 1974;4:34-38.
Lim CC, Reilly CM, Thomasy SM, Kass PH, Maggs DJ. Effects of feline herpesvirus type 1 on
tear film break-up time, Schirmer tear test results, and conjunctival goblet cell density in
experimentally infected cats. Am J Vet Res. 2009;70(3):394-403.
Richter M, Guscetti F, Spiess B. Aldose reductase activity and glucose-related opacities in
incubated lenses from dogs and cats. Am J Vet Res. 2002;63(11):1591-1597.
Shukla AK, Pinard CL. Feline uveitis. Compend Contin Educ Vet. 2012;34(9):E1.
Stiles J. Feline Ophthalmology. In: Gelatt KN, Gilger BC, Kern TJ, eds. Veterinary
Ophthalmology. 5th ed. Ames, IA: Wiley-Blackwell; 2013:1519-1520.
Williams DL, Heath MF. Prevalence of feline cataract: results of a cross-sectional study of
2000 normal animals, 50 cats with diabetes and one hundred cats following dehydrational
crises. Vet Ophthalmol. 2006;9(5):341-349.
Zhan GL, Miranda OC, Bito LZ. Steroid glaucoma: corticosteroid-induced ocular hypertension
in cats. Curr Eye Res. 1992;54(2):211-218.
CATARACTS IN CATS: TREATMENT
Mary Rebecca Telle, DVM*
Diane Hendrix, DVM, DACVO
University of Tennessee

CATARACT IDENTIFIED

INVESTIGATION
NO
Uveitis present?

YES

TREATMENT
Pursue therapeutic
management and
monitoring to:
Steroidal (eg, Nonsteroidal (eg, h Stabilize blood- Prednisolone Robenacoxib

prednisolone flurbiprofen, ketorolac, aqueous barrier, h 1-2 mg/kg once a or meloxicam

acetate) diclofenac) decrease day (extra-label)
h May negatively h Not as effective as inflammation to h Taper to lowest h Efficacy is




affect corneal steroids, but may be preserve vision possible dose as questionable, but
health used when steroids are h Treat ocular pain uveitis resolves drug may be useful

h Avoid if corneal contraindicated h Prevent and/or h Use if topical when steroids are



ulceration is h May be used as minimize sequelae medications are contraindicated

present, as these adjunctive therapy h Treat clinical signs not effective and (while looking for

drugs may delay h Use caution with h Treat underlying infectious disease neoplastic or


healing topical NSAIDs, which condition is ruled out fungal cause)
can affect glomerular
filtration rate1

Administer topical anti-inflammatory Administer systemic anti-inflammatories

drugs (steroidal and/or nonsteroidal) (NSAIDs or corticosteroids)
1-4 times a day

Administer mydriatic to treat cycloplegia Treat clinical signs as necessary and monitor
and prevent synechiae formation

Atropine, tropicamide
h Every 8-24 hours or every other day, depending on severity Small, nonprogressive Dense, progressive cataract;

h Tropicamide duration is shorter and strength is less potent cataract; vision not affected vision significantly affected

than atropine, so dosing may need to be more frequent
h Atropine ophthalmic ointment is recommended in cats, as

atropine solution is bitter
Monitor every 3-6 months for 1 year Treat underlying cause or
*Byline reflects author information on original publication. On publication of this
for cataract progression and/or diagnose as primary
inflammation; then monitor yearly cataract

collection, the author’s current affiliation is University of Wisconsin-Madison.
or if clinical signs progress
 MANAGEMENT TREE h OPHTHALMOLOGY h PEER REVIEWED

 
 
 
 
INVESTIGATION
Perform preoperative screening
h Minimum database (CBC, serum chemistry

profile, urinalysis)
h Electroretinography to evaluate retinal function

h Ocular ultrasonography to rule out retinal

detachment

TREATMENT TREATMENT
Pursue medical management Pursue surgical management
h Phacoemulsification

h Enucleation

h Intracapsular lens extraction

Phacoemulsification (best Enucleation Intracapsular lens extraction
option for primary cataract) h Traumatic cataract with h Lens luxation


severe phacoclastic uveitis h Prognosis depends on duration

and underlying cause

Consider if: Not recommended if:

h Primary or h Chronic uveitis present


congenital cataract h Secondary cataract

h Underlying disease h Glaucoma present


treatable and under h Retinal dysfunction or

control detachment present
h Neurologic signs present

and suggestive of lesions
in visual cortex

Reference
1. Lanuza R, Rankin AJ, KuKanich B,

Meekins JM. Evaluation of systemic
absorption and renal effects of topical
ophthalmic flurbiprofen and diclofenac
in healthy cats. Vet Ophthalmol.
2015;19(Suppl 1):24-29.
 DIAGNOSTIC/MANAGEMENT TREE h OPHTHALMOLOGY h PEER REVIEWED

 
 
 
 
DECREASED TEAR PRODUCTION IN DOGS
Ian Herring, DVM, MS, DACVO
Virginia–Maryland College of Veterinary Medicine

STT <15 MM/MIN

h   echeck in 24-72 hours

R
Has the patient had immediate or recent sedation,
h  Effects of topical atropine YES general anesthesia (<24 hours), topical anesthetic application
may last several days to
(<30 min), or topical atropine administration?
weeks after discontinuation

NO

INVESTIGATION
Look for history of risk factors, including local radiation therapy, lacrimotoxic drug
administration (eg, sulfonamides), prior nictitans gland prolapse (especially if excised)

Early or subclinical KCS Mild-to-moderate KCS Severe KCS

(STT 11-14 mm/min) (STT 5-10 mm/min) (STT <5 mm/min)

Bilateral Unilateral Unilateral Bilateral

Ocular clinical signs of KCS (eg,

blepharospasm, conjunctival
hyperemia, mucoid/mucopurulent
Ipsilateral dry nose, concurrent neurologic deficits Juvenile onset,
ocular discharge, keratitis)?
(eg, ipsilateral facial/trigeminal dysfunction)? Yorkshire terrier

NO YES NO YES h  C ongenital alacrima

likely
h Fluorescein stain

Risk factors in history? cornea to evaluate
Recheck in 2-4 weeks for ulceration
h See Table 3,

page 165
NO YES
h  I f STT still decreased, h N eurogenic KCS
consider treating (see likely
Table 1, next page) See Table 2, next page h F luorescein stain
h Some patients can h Idiopathic or immune- cornea to evaluate


have a slightly mediated KCS likely for ulceration
subnormal STT that is h Fluorescein stain cornea h See Table 4,

clinically benign

to evaluate for ulceration Recheck STT in 2-4 page 165
h See Table 1, next page weeks; adjust therapy

as appropriate
KCS = keratoconjunctivitis sicca
STT = Schirmer tear test Continues h
 TABLE 1

TREATMENT FOR IDIOPATHIC/IMMUNE-MEDIATED KCS

Treatment Application

Topical ophthalmic cyclosporine (1%-2% solution, Apply to affected eye(s) q12h; lifelong
0.2% ointment), tacrolimus (0.03%) therapy required

Topical lacrimomimetic PRN (ie, artificial tears; products Apply until signs resolve (usually
containing sodium hyaluronate may be particularly beneficial) unnecessary when STT >8 mm/min)

Topical ophthalmic broad-spectrum antibiotic Apply to affected eye(s) q8h for 10-14 days
(eg, neomycin, polymyxin B, gramicidin solution) or until corneal ulceration (if present) is
healed

Topical mucolytic medication (2.5%-5% N-acetylcysteine) Apply q6-8h if copious mucopurulent

discharge is present

Warm compress to eyelids, periocular hair trimming, facial Apply as warranted

cleaning

TABLE 2

TREATMENT FOR KCS SECONDARY TO RISK FACTORS

Treatment Application

Discontinue lacrimotoxic medication if suspected in KCS N/A

pathogenesis

Topical ophthalmic cyclosporine or tacrolimus can be attempted Apply to affected eye(s) q12h
(see Table 1) but is generally ineffective in these cases

Topical lacrimomimetic PRN (ie, artificial tears; products Apply until signs resolve (usually
containing sodium hyaluronate may be particularly beneficial) unnecessary when STT >8 mm/min)

Topical ophthalmic broad-spectrum antibiotic Apply to affected eye(s) q8h for 10-14 days
(eg, neomycin, polymyxin B, gramicidin solution) or until corneal ulceration (if present) is
healed

Topical mucolytic medication (2.5%-5% N-acetylcysteine) Apply q6-8h if copious mucopurulent

discharge is present

Warm compress to eyelids, periocular hair trimming, facial Apply as warranted

cleaning
 DIAGNOSTIC/MANAGEMENT TREE h OPHTHALMOLOGY h PEER REVIEWED

 
 
 
 
TABLE 3

TREATMENT FOR CONGENITAL ALACRIMA

Treatment Application

Topical lacrimomimetic PRN (ie, artificial tears; Apply until signs resolve (usually necessary when
products containing sodium hyaluronate may be STT >8 mm/min)
particularly beneficial)

Topical ophthalmic broad-spectrum antibiotic (eg, Apply to affected eye(s) q8h for 10-14 days or
neomycin, polymyxin B, gramicidin solution) until corneal ulceration (if present) is healed

Topical mucolytic medication (2.5%-5% Apply q6-8h if copious mucopurulent discharge

N-acetylcysteine) is present

Warm compress to eyelids, periocular hair trimming, Apply as warranted

facial cleaning

TABLE 4

TREATMENT FOR NEUROGENIC KCS Suggested Reading

Guiliano EA. Diseases and surgery of the
canine lacrimal secretory system.
In: Gelatt KN, Gilger BC, Kern TJ,
Treatment Application eds. Veterinary Ophthalmology. 5th
ed. Oxford, UK: John Wiley & Sons;
2013:912-944.
Topical ophthalmic 0.2% pilocarpine q6-8h or 2% Initial oral dose, 2 drops/20 pounds (10 kg) Matheis FL, Walser-Reinhardt L,
oral pilocarpine body weight q12h; increase 1 drop at a time to Spiess BM. Canine neurogenic
effect or until systemic toxicity (eg, salivation, keratoconjuctivitis sicca: 11 cases
(2006-2010). Vet Ophthalmol.
vomiting, diarrhea) is evident 2012;15(4):288-290.
Miller PE. Lacrimal system. In: Maggs
Topical lacrimomimetic PRN (ie, artificial tears; Apply until signs resolve (usually unnecessary DJ, Miller PE, Ofri R, eds. Slatter’s
products containing sodium hyaluronate may be when STT >8 mm/min) Fundamentals of Veterinary
Ophthalmology. 5th ed. St. Louis,
particularly beneficial) MO: Elsevier Saunders; 2013:165-
183.
Topical ophthalmic broad-spectrum antibiotic Apply to affected eye(s) q8h for 10-14 days or Westermeyer HD, Ward DA, Abrams K.
(eg, neomycin, polymyxin B, gramicidin solution) until corneal ulceration (if present) is healed Breed predisposition to congenital
alacrima in dogs. Vet Ophthalmol.
Topical mucolytic medication (2.5%-5% Apply q6-8h if copious mucopurulent discharge 2009;12(1):1-5.

N-acetylcysteine) is present

Monitor for blepharospasm N/A KCS = keratoconjunctivitis sicca

STT = Schirmer tear test
*Spontaneous resolution may occur; therapy can be discontinued after resolution.
EPIPHORA IN DOGS
Christina Korb, DVM
DJ Haeussler Jr, DVM, MS, DACVO
The Animal Eye Institute
Cincinnati, Ohio

EPIPHORA (IE, OVERFLOW OF TEARS) OBSERVED

Perform STT*

STT >25 mm/min STT 15-25 mm/min

Blepharospasm present? Eyelid malformation or deformity observed?

YES NO YES NO

DIAGNOSIS DIAGNOSIS DIAGNOSIS h Confirm presence and patency of lacrimal puncta


Overproduction of Overproduction of Inappropriate drainage; h Examine for foreign bodies

aqueous tears aqueous tears tears draining onto face h For dogs in which diagnostic investigation cannot be pursued

from ocular from iatrogenic in-clinic, cleaning the drainage with warm water and a tissue
surface due to administration of is acceptable.
irritation or pain lacrimostimulants
(ie, stimulated (eg, cyclosporine,
lacrimation) tacrolimus)
DIFFERENTIALS
h M edial canthal or
ventromedial entropion
• Obstruction of puncta Nonpatent or absent Patent and visible

secondary to lacrimal puncta lacrimal puncta
DIFFERENTIALS TREATMENT conformation
h Distichiasis Discontinue or (brachycephalic dogs)

h Ectopic cilia reduce h Medial canthal trichiasis


h Allergic conjunctivitis frequency of h Facial nerve paralysis


h Blepharitis medication DIAGNOSIS h Perform Jones test or


h Eyelid masses Blockage of lacrimal puncta fluorescein dye

h Keratitis passage test to

h Corneal ulcer confirm duct patency

h Anterior uveitis Conduct nasolacrimal
TREATMENT h


h Acute glaucoma duct irrigation
Surgical correction (eg,

h Anterior lens luxation h Perform MRI, CT, or
modified Hotz-Celsus, DIFFERENTIALS


h Keratoconjunctivitis skull radiography with
medial canthoplasty) of

h Medial canthal h Punctal atresia (ie, congenital dacryocystorhinogra-

eyelid defect; lubrication if

trichiasis absence of puncta) phy to localize lesion
facial nerve paralysis is h Micropuncta

diagnosed h Imperforate puncta

h Fibrosis from chronic

inflammation or traumatic
laceration resulting in
TREATMENT stenosis or occlusion
Treat primary disorder h Neoplasia of surrounding

tissue resulting in invasion or
occlusion
h Cyst

h Symblepharon

*Normal STT values: ≥15 mm/min
TREATMENT
Perform surgical correction, if possible

26 cliniciansbrief.com April 2020

 
 
 DIAGNOSTIC TREE h OPHTHALMOLOGY h PEER REVIEWED

 
 
 
 
DIAGNOSIS
Obstruction of nasolacrimal apparatus
(eg, nasolacrimal canaliculi, nasolacrimal duct,
nasal punctum)

DIFFERENTIALS DIFFERENTIALS
Congenital Acquired
h E ctopic nasolacrimal h S evere rhinitis or sinusitis swelling resulting
openings in occlusion Suggested Reading
h N asolacrimal atresia (ie, h Trauma or fracture of maxillary or lacrimal Gelatt KN. Canine nasolacrimal duct and

absence of all or portion of bone lacrimal secretory systems: diseases
nasolacrimal apparatus) h Fibrosis from chronic inflammation or and surgery. In: Gelatt KN. Essentials of

traumatic laceration resulting in stenosis or Veterinary Ophthalmology. 3rd ed. Ames,
occlusion IA: Wiley-Blackwell; 2014:186-199.
h Severe periodontal disease and tooth root
Giuliano EA. Diseases and surgery of the

abscesses canine lacrimal secretory system.
h Foreign body (eg, fox tails, grass awns)
TREATMENT In: Gelatt KN, Gilger BC, Kern TJ, eds.

h R emove cause, if possible obstruction Veterinary Ophthalmology. 5th ed. Ames,
h Dacryocystitis (ie, swelling of nasolacrimal
h I rrigate
to attempt to IA: Wiley-Blackwell; 2013:912-944.

re-establish patency apparatus) resulting in occlusion
h Aneurysmal dilation of duct
Grahn BH, Sandemeyer LS. Diseases and
h L avage with appropriate surgery of the canine nasolacrimal

h Neoplasia of apparatus or surrounding
antibiotics and corticosteroids system. In: Gelatt KN, Gilger BC, Kern TJ,

h P erform nasolacrimal duct tissues resulting in invasion or occlusion
eds. Veterinary Ophthalmology. 5th ed.
stenting Ames, IA: Wiley-Blackwell; 2013:894-911.
h P erform surgery (eg,
Lim CC. The third eyelid, nasolacrimal
dacryocystorhinostomy, system, and precorneal tear film. In:
dacryocystobuccostomy, Lim CC. Small Animal Ophthalmic Atlas
dacryocystomaxillosinusotomy) and Guide. Ames, IA: Wiley-Blackwell;
to reposition puncta or 2015:83-90.
reconstruct apparatus

April 2020 cliniciansbrief.com 27

 
 
EXOPHTHALMOS
Paul E. Miller, DVM, DACVO
University of Wisconsin–Madison

EXOPHTHALMOS

h M ass effect posterior to globe equator

h D ifficultyretropulsing globe into orbit
h L agophthalmos
h E xposure keratitis
h T hird eyelid protrusion
h C hemosis
h O cular discharge

“Apparent” exophthalmos
(retrobulbar lesion is not present)

DIAGNOSIS DIAGNOSIS DIAGNOSIS DIAGNOSIS DIAGNOSIS DIAGNOSIS

Shallow orbit Facial palsy Macropalpebral Episcleritis Proptosis Buphthalmos
h B rachycephalic h N o blink reflex fissure h N odular or h L ids trapped h E nlarged globe
breeds h A bnormally large diffuse scleral behind globe due to chronic
h I OP is normal eyelid opening thickening h History of glaucoma

h G lobe normal h M ay mimic trauma h Usually elevated


buphthalmos IOP
h S cleral h Corneal diameter


thickening larger than
visible normal
TREATMENT h I nflamed globe
TREATMENT h Blindness

h N ormal corneal h R eplace h Usually painful
If extreme globe exposure or pigmentary keratitis globe if
is present, perform a medial and/or lateral canthal diameter possible
closure to limit corneal exposure. h E nucleate if
irreparable
damage
TREATMENT
Consider
h E nucleation
h E visceration and
prosthesis
h G lobe salvage
procedures

IOP = intraocular pressure

US = ultrasound
 DIAGNOSTIC TREE h OPHTHALMOLOGY h PEER REVIEWED

 
 
 
 
True exophthalmos
(retrobulbar lesion is present)

Bilateral Unilateral

INVESTIGATION
Further clinical examination
DIAGNOSIS DIAGNOSIS h D etermine direction of globe deviation:

Masticatory muscle myositis Extraocular muscle myositis • Purely anterior displacement—intraconal mass, optic nerve, extraocular muscle

h M asticatory muscles h M asticatory muscles normal disease
swollen h G lobe deviated along orbital axis • Anterior deviation plus deviation in a second direction—tissues posterior to globe

h Muscle biopsy h Young dogs that may create the second deviation form differential list (eg, frontal sinus,

h ± eosinophilia h ± imaging (eg, US, CT, MRI) zygomatic mucocele, etc)

h P ain on opening mouth:
• Yes—abscess or inflammatory disease
• No—neoplasia
h Oral examination: penetrating wounds or mass posterior to last molar

TREATMENT
h O ral prednisone
h ± azathioprine

INVESTIGATION
Further diagnostics
h O rbital US
h S kull radiography
h C T/MRI
h F ine-needle aspiration
h Cytology
h B iopsy
h ± surgical exploration

DIAGNOSIS DIAGNOSIS DIAGNOSIS DIAGNOSIS DIAGNOSIS DIAGNOSIS

Abscess/Cellulitis Orbital foreign body Orbital Arteriovenous fistula Neoplasia Zygomatic mucocele
h P ainful h ± history of trauma hemorrhage/air h R are h U sually nonpainful h ± pain depending
h M ay complicate h U sually h C an
see or feel h Many types on inflammation

abscess traumatic pulsations reported h S aliva-like fluid
h Rule out clotting h Usually primary on aspiration


abnormalities and malignant
TREATMENT h Usually resolves

h A ttempt to drain under spontaneously
anesthesia (often via TREATMENT TREATMENT
mouth) h S urgical
removal if h S urgical ligation to TREATMENT
h D rain not successful: inflammation is repair TREATMENT h M ay
require
cellulitis present h C onsult
with surgical excision
h Cytology, culture/ oncologist
sensitivity
h C onsider antibiotics with
anaerobic spectrum (eg,
amoxicillin/clavulanic
acid or metronidazole)
h I f recurrent, consider
foreign body
INCREASED & DECREASED INTRAOCULAR PRESSURE
Alison Clode, DVM, DACVO
Port City Veterinary Referral Hospital
Portsmouth, New Hampshire

PATIENT PRESENTED WITH BLIND, PAINFUL, CLOUDY, AND/OR RED EYE

Perform ophthalmic examination:


h Menace response

h Reflexes (eg, dazzle, direct and consensual PLR, palpebral)

h Schirmer tear test

h Fluorescein stain

h Anterior segment examination

h Posterior segment examination

h Tonometry

Determine IOP

Increased IOP (>20 mm Hg) Normal IOP (10-20 mm Hg) Decreased IOP (<10 mm Hg)

Confirm increased IOP Cause of observed ophthalmic Confirm decreased IOP




h Calibrate tonometer changes is other ocular (or h False-low readings are rare


h Check collar/harness tightness CNS) condition, not glaucoma h Calibrate tonometer


h Minimize manual restraint (eg, pressure or uveitis h Minimize manual restraint


on neck and around eyes) h Consider age (mild IOP reduction [generally

no more than 1-3 mm Hg] may be
considered normal in older dogs and cats)

Increased Not increased

Decreased Not decreased

DIAGNOSIS Go to Normal IOP (10-20 mm


Glaucoma Hg) or Decreased IOP (<10
mm Hg), based on IOP DIAGNOSIS Cause of observed

Uveitis ophthalmic changes is
see page 170 other ocular (or CNS)
condition, not glaucoma
Determine whether glaucoma is acute or chronic based on or uveitis

clinical signs
h Acute: pain, diffuse corneal edema, episcleral injection,

blindness (negative menace response, negative dazzle,
negative PLRs)
h Chronic: buphthalmos, Haab’s striae (Descemet’s membrane

tears), cataract, lens subluxation, optic nerve atrophy,
retinal vascular attenuation, tapetal hyperreflectivity,
blindness (negative menace response, negative dazzle,
negative PLRs), any clinical signs noted for acute patients,
although signs of pain may not be present
 DIAGNOSTIC/MANAGEMENT TREE h OPHTHALMOLOGY h PEER REVIEWED

 
 
 
 
Determine primary vs secondary

Primary: anatomic abnormality in the aqueous humor Secondary: acquired obstruction to outflow of


drainage pathway aqueous humor, leading to build-up of aqueous
h Predisposed breed (eg, American cocker spaniel, humor in the eye and increased IOP

basset hound, chow chow, Siberian husky; see h Clinical signs:

Suggested Reading, page 171, for more breeds) • Uveitis or intraocular hemorrhage
h Predisposed age (ie, early- to middle-a ge) –Flare, hypopyon, hyphema

h Clinical signs: –Miosis or dyscoria (eg, posterior synechiae)

• Mydriasis –Iridal hyperemia
• Absence of significant uveitis, anterior lens –History of low IOP


luxation, intraocular tumor • Intraocular tumor
–Visible intraocular mass
–Corresponding anterior uveitis
–Buphthalmos
• Anterior lens luxation
Conduct diagnostic procedures for primary glaucoma –Lens visible in the anterior chamber

h Genetic testing –Dyscoria with altered pupil mobility

• Available for some breeds (eg, beagle, Norwegian • Cataract formation

elkhound, shar-pei) –Visible cataract
• May indicate genetic predisposition –Shallow anterior chamber due to lens

• Useful for breeding programs enlargement
h Gonioscopy (referral procedure) –Deep anterior chamber due to lens resorption

• Perform on unaffected eye to allow visualization

of a portion of drainage angle, which suggests
predisposition to primary glaucoma in the
affected eye
h Electroretinography (referral procedu re) Conduct diagnostic procedures for secondary


• Evaluate retinal electrical activity glaucoma
• Provides prognostic information for vision h Ocular ultrasonography

• Evaluate structural changes to globe
• Check for presence of intraocular mass, lens

luxation, buphthalmos
h Electroretinography (referral procedure)

Go to Treatment of Primary • Evaluate retinal electrical activity
Glaucoma, page 171 • Prognostic information for vision
h Systemic evaluation for uveitis, neoplasia

• CBC, serum chemistry profile, urinalysis
• Infectious disease titers
• Chest radiography
• Abdominal ultrasonography
• Lymph node aspiration
• Blood pressure
• Others based on systemic signs (eg, joint taps for

lameness; skin biopsy for skin lesions)

IOP = intraocular pressure Go to Treatment of Secondary

PLR = pupillary light reflex Glaucoma, page 171

Continues h
 DIAGNOSIS
Uveitis

Confirm presence of uveitis


h Miosis

h Flare, hypopyon, and/or hyphema

h Posterior synechiae

h Iridal hyperemia

h Intraocular pigment dispersion

NO YES

Geriatric animals may experience slight Determine underlying cause of uveitis

reduction (1-3 mm Hg) in IOP, without uveitis

Ocular Nonocular


h Trauma (blunt or penetrating) h Systemic infection


h Corneal ulcer h Systemic neoplasia


h Lens-induced h Immune-mediated/idiopathic


h Intraocular tumor

Conduct further diagnostic investigation

h Ocular ultrasonography

• Evaluate structural changes to globe

• Check for presence of intraocular mass,
TREATMENT TREATMENT

lens luxation
Treat specific underlying cause: Nonspecific anterior uveitis therapy: h Systemic evaluation for uveitis, neoplasia
h Facilitation of corneal ulcer h Specific medications and frequencies

• CBC, serum chemistry profile, urinalysis


healing based on severity of uveitis

• Infectious disease titers
h Lensectomy h Topical corticosteroid (eg,

• Chest radiography


h Intraocular tumor removal dexamethasone, prednisolone acetate)*

• Abdominal ultrasonography

h Topical mydriatic cycloplegic (eg,

• Others based on systemic signs (eg,

atropine)

joint taps for lameness; skin biopsy for
h Topical NSAID (eg, diclofenac, ketorolac,
skin lesions)

bromfenac)
h Systemic anti-inflammatory medications

(eg, NSAIDs or corticosteroids based on
underlying cause)
TREATMENT
Based on diagnostic results
h Systemic antimicrobials

h Systemic chemotherapy
PROGNOSIS

h Systemic immunosuppression
Based on:

h Severity of inflammation

h Response to therapy

• Slow tapering of medications is essential

h Ability to identify and treat underlying cause

 DIAGNOSTIC/MANAGEMENT TREE h OPHTHALMOLOGY h PEER REVIEWED

 
 
 
 
TREATMENT OF PRIMARY GLAUCOMA TREATMENT OF SECONDARY GLAUCOMA
h IOP-lowering medication h IOP-lowering medication


• Specific medications and frequencies vary with • Specific medications and frequencies vary with acute


acute vs chronic and primary vs secondary vs chronic and primary vs secondary glaucoma
glaucoma • Carbonic anhydrase inhibitors (eg, dorzolamide,


• Carbonic anhydrase inhibitors (eg, dorzolamide, brinzolamide)

brinzolamide) • β blockers (eg, timolol)


• Prostaglandin analogues (eg, latanoprost, h Treatment of underlying cause


travoprost) • Topical anti-inflammatory medications


• β blockers (eg, timolol) • Systemic anti-inflammatory medications


• Parasympathomimetic medications (eg, • Other medications, as indicated for cause of uveitis†


demecarium bromide, pilocarpine) • Lensectomy (referral procedure)


h Glaucoma-specific surgical intervention • Intraocular tumor removal (referral procedure)


• Laser cycloablation (referral procedure) h Glaucoma-specific surgical intervention

• Gonioimplantation (referral procedure) • Laser cycloablation (referral procedure)


• Gonioimplantation (referral procedure)


PROGNOSIS
Prognosis depends on underlying cause and response to treatment. If
signs of pain continue, definitive treatment may require:
h Enucleation

h Evisceration

h Ciliary body chemical ablation (eg, intravitreal gentamicin injection)

*Provided no corneal ulcer is present
IOP = intraocular pressure †In patients with secondary glaucoma due to posterior synechiae and iris bombe, atropine

may be indicated to break open the pupil and restore aqueous humor flow.

Suggested Reading
Bergstrom BE, Stiles J, Townsend WM. Canine panuveitis: a retrospective evaluation of 55 cases (2000- 2015). Vet
Ophthalmol. 2017;20(5):390-397.
Plummer CE, Regnier A, Gelatt KN. The canine glaucomas. In: Gelatt KN, Gilger BC, Kern TJ, eds. Veterinary Ophthalmology.
5th ed. Ames, IA: Wiley-Blackwell; 2013:1050-1145.
Tofflemire KL, Wang C, Jens JK, Ellinwood NM, Whitley RD, Ben-Shlomo G. Evaluation of three hand-held tonometers in
normal canine eyes. Vet J. 2017;224:7-10.
RED EYE
Caryn E. Plummer, DVM, DACVO
University of Florida

RED EYE

Blepharospasm present? Pupil size

YES NO Miotic Midrange Mydriatic

Discharge present?
DIAGNOSIS DIAGNOSIS
h Corneal ulcer h Chronic keratitis DIAGNOSIS DIAGNOSIS DIAGNOSIS
h Anterior h KCS/ h Subacute or


h Anterior uveitis h Chronic glaucoma



uveitis (alone conjunctivitis chronic


h Acute glaucoma h Posterior segment
or as reflex h Keratitis glaucoma


h Acute lens luxation hemorrhage/


reaction to h Corneal ulcer h Posterior

h Acute KCS disease (in absence



corneal ulcer) without segment
YES NO

of anterior uveitis)
accompanying disease (retina,
h Episcleritis
anterior uveitis optic nerve)

h Episcleritis h Iris atrophy


h Anterior uveitis

with secondary
DIAGNOSIS glaucoma
h Chronic glaucoma h Acute

Serous Mucoid h Posterior segment

congestive

hemorrhage/
glaucoma
disease (in absence
of anterior uveitis)

DIAGNOSIS DIAGNOSIS
h Acute conjunctivitis h KCS


h Corneal ulcer h Chronic


h Anterior uveitis conjunctivitis

h Acute glaucoma h Chronic keratitis


CHECKLIST: EXAMINING THE RED EYE
) Observe eye to determine what part(s) are affected, what appears ) Perform ocular surface staining:


normal or abnormal, whether eye is painful, and presence of • Fluorescein staining to assess corneal epithelium defects, NLD


discharge. patency, and tear film breakup time and stability
• Seidel test to identify leakage of aqueous humor through cornea
) Develop list of diagnostic differentials based on ocular changes and

• Rose bengal staining to measure precorneal tear film quality and

conduct diagnostic testing.

integrity
) Determine whether eye is visual.
) Perform tonometry to estimate IOP: elevation consistent with


) Assess pupil size and light reflexes. glaucoma, decrease consistent with intraocular inflammation.

) Perform STT for quantitative assessment of tear production. ) Complete examination and systemic diagnostic testing as indicated.


 DIAGNOSTIC TREE h OPHTHALMOLOGY h PEER REVIEWED

 
 
 
 
What part of the eye is red?

Anterior chamber Cornea† Fundus (reflection) Conjunctiva Iris Sclera/episclera

DIAGNOSIS DIAGNOSIS DIAGNOSIS DIAGNOSIS DIAGNOSIS DIAGNOSIS

h Hyphema h Uveitis h Variation of normal h Conjunctivitis h Anterior uveitis h Glaucoma






h Anterior uveitis h Glaucoma (atapetal or (allergic, bacterial, (iridal hyperemia h Anterior uveitis



h Trauma h KCS (quantitative hypopigmented) viral) or intrastromal h Lens luxation



h Retinal and qualitative) h Posterior segment h KCS (quantitative homorrhage) h Corneal ulcer




detachment h Keratitis hemorrhage and qualitative) h Intraocular h Episcleritis



h Systemic h Corneal ulcer • Retinal h Excitement neoplasia (primary h Excitement





hypertension detachment or metastatic) (scleral injection)
h Intraocular • Chorioretinitis h Bleeding disorder h Scleral



neoplasia (primary • Systemic hemorrhage

or metastatic) hypertension (trauma)
h Bleeding disorder INVESTIGATION • Bleeding disorder INVESTIGATION


h STT • Intraocular h STT



h Rose bengal neoplasia h Rose bengal INVESTIGATION


staining (primary or staining h Ultrasonography

h Cytology metastatic) h Cytology h Systemic workup* INVESTIGATION



INVESTIGATION h Fluorescein staining h Fluorescein staining h Fluorescein staining h Fluorescein staining




h Ultrasonography h Pupil size h Pupil size



h Systemic workup* h IOP h IOP



h Fluorescein staining

h Pupil size INVESTIGATION

h IOP h Ultrasonography


h Systemic workup*

h Fluorescein staining

h Pupil size

h IOP

CONJUNCTIVAL CONGESTION
OR EPISCLERAL INJECTION?
h Conjunctival vessels are movable over

sclera.
h Episcleral vessels are fixed and typically

larger. *Systemic workup = minimum database, systemic blood pressure,
IOP = intraocular pressure

coagulation parameters, infectious disease titers, thoracic or
h Conjunctival vessels will blanch more abdominal imaging KCS = keratoconjunctivitis sicca

†Cornea is rarely red unless vascularization is present; blood may
rapidly following application of a vaso-

also be present within the stroma or behind the cornea, within NLD = nasolacrimal duct
constricting agent (ie, phenylephrine, the anterior chamber, giving the impression of a red cornea
STT = Schirmer tear test
epinephrine).
 DIAGNOSTIC TREE h OPHTHALMOLOGY h PEER REVIEWED

 
 
 
 
CLINICAL SIGNS OF SELECTED OPHTHALMIC DISEASES
Kenneth L. Abrams, DVM, DACVO*
Veterinary Ophthalmology Services, Inc
Warwick, Rhode Island

ADNEXAL DISEASES

Ocular Corneal Intraocular Specific

Discharge Opacity Pressure Findings &
Comments

Mucous Serous Squinting Conjunctival Vessels Pigment Edema Increased Decreased Aqueous Decreased
redness flare/cells vision

Distichiasis – 1–2 ± ± – – – – – – – 2nd row of cilia

Ectopic cilia – 3–4 4 3 – – ± – – – – • Cilium


protrudes
through
palpebral
conjunctiva
• Can cause


corneal ulcers

Entropion ± 2–4 2–4 1–3 – – – – – – – • Rolled-in eyelid


• Can cause


corneal ulcers

Prolapsed ± ± – ± – – – – – – – Observation of
nictitans prolapsed gland
(cherry eye)

Everted – – – ± – – – – – – – Scrolled
cartilage cartilage

Blocked ± 2–3 ± – – – – – – – – Negative

nasolacrimal fluorescein
duct passage test

Follicular – 1–2 – ± – – – – – – – Prominent third

hyperplasia eyelid follicles

— = not present; ± = variable; 1 = mild; 2-3 = moderate; 4 = severe; ERG = electroretinogram

*Byline reflects author information on original publication. On publication of this collection, Continues h
the author is retired after a successful tenure with Veterinary Ophthalmology Services, Inc.
DIAGNOSTIC TREE h OPHTHALMOLOGY h PEER REVIEWED

 
 
 
 
CORNEAL DISEASES

Ocular Corneal Intraocular Specific Findings

Discharge Opacity Pressure & Comments

Mucous Serous Squinting Conjunctival Vessels Pigment Edema Increased Decreased Aqueous Decreased
redness flare/cells vision

Corneal ulcer, ± 2–4 2–4 1–4 1–4 – 1–3 – – – – Fluorescein stain + can
uninfected cause uveitis

Kerato- 2–4 – 1–3 2–4 1–4 1–4 ± – – – – Schirmer tear test <15
conjunctivitis mm/min
sicca

Pannus – 0–2 – 1–3 2–4 2–4 ± – – – 1–4 Usually starts as infero-

temporal disease

Pigmentary ± ± – 1–2 1–2 3–4 – – – – 1–4 Usually nasal areas first

keratitis

Endothelial – – – 1–3 – – 1–4 – – – ± Generalized edema—

dystrophy older patient

— = not present; ± = variable; 1 = mild; 2-3 = moderate; 4 = severe; ERG = electroretinogram

INTRAOCULAR DISEASES

Ocular Corneal Intraocular Specific Findings

Discharge Opacity Pressure & Comments

Mucous Serous Squinting Conjunctival Vessels Pigment Edema Increased Decreased Aqueous Decreased
redness flare/cells vision

Cataract – – – – – – – – – – 1–4 Lens opacification

Acute ± ± ± 2–4 – – – 4 – ± 4 Lethargy is prominent

glaucoma

Uveitis ± ± 1–4 1–3 – – – – 3–4 2–4 1–4 Light sensitive

Anterior lens ± ± 3–4 1–4 – – ± 1–4 – – 2–4 Observation of lens in

luxation anterior chamber

Retinal – – – – – – – – – – 2–4 Various focal points of

detachment fundic structures

Retinal – – – – – – – – – – 3–4 Fundus: vascular

degeneration attenuation, tapetal
hyperreflectivity; ERG
diminished

Optic neuritis – – – – – – – – – – 4 Papilledema? Pupil

reflexes absent; ERG
present

— = not present; ± = variable; 1 = mild; 2-3 = moderate; 4 = severe; ERG = electroretinogram

FORELIMB LAMENESS & ELBOW PAIN
Laura E. Peycke, DVM, MS, DACVS*
Texas A&M University

FORELIMB LAMENESS AND ELBOW PAIN

INVESTIGATION
Orthopedic examination (nonsedated)

INVESTIGATION
Pain associated with any of the following?
h 
Hyperextension
h 
Hyperflexion
h 
Caudal compartment palpation
YES h 
Internal or external rotation of the NO
antebrachium

INVESTIGATION INVESTIGATION
Orthopedic examination (sedated) Consider:
h 
More in-depth limb examination, including neurologic examination
h 
Bone scan (soft tissue and bone phases)

Trauma?

YES NO

INVESTIGATION INVESTIGATION
Are any of the following present? h Crepitus
h 
Crepitus h Effusion of caudal joint

h  h Soft tissue thickening/swelling

YES Effusion NO
h 
Medial/lateral instability

INVESTIGATION INVESTIGATION INVESTIGATION

Radiography: Consider: Radiography:

h Mediolateral view h 
Radiography
 (mediolateral and h Mediolateral view


h Craniocaudal view craniocaudal views) h Craniocaudal view

 stressed view

h ± h 
More
 in-depth examination of limb h Flexed lateral

h 
Conservative
 management with
monitoring
h 
If
 pain persists, pursue bone scan, CT
DIAGNOSIS DIAGNOSIS
Fracture Subluxation/luxation Normal

TREATMENT TREATMENT DIAGNOSIS TREATMENT INVESTIGATION

Surgical intervention Closed reduction Ligament damage Closed reduction with spica More in-depth examination,
(rigid internal fixation) with spica splint splint or surgical management with consideration given
for 4 weeks (open reduction) to radiography, bone scan,
and CT
 DIAGNOSTIC/MANAGEMENT TREE h ORTHOPEDICS h PEER REVIEWED

 
 
 
 
Abnormal

Lysis/proliferative Incongruency Degenerative changes Effusion

lesion, soft tissue ± radiographic changes ± effusion ± radiographic changes
swelling

INVESTIGATION
DIAGNOSIS DIAGNOSIS DIAGNOSIS Arthrocentesis
Neoplasia/ Asynchronous Trochlear notch
osteomyelitis growth of dysplasia
radius and ulna

DIAGNOSIS
INVESTIGATION Premature Nonsuppurative Mononuclear cells Suppurative
Biopsy and INVESTIGATION closure of distal (<10% vacuolated
bacterial/fungal CT (changes radius or ulnar MN cells indicate
culture & sensitivity secondary to elbow growth plates normal joint fluid)
dysplasia?)
DIAGNOSIS
Degenerative
joint disease
>10% vacuolated
TREATMENT MN cells
Ulnar osteotomy
or angular
limb deformity
correction
INVESTIGATION INVESTIGATION
Bacteria No bacteria
visualized visualized
(infectious) (noninfectious)
DIAGNOSIS DIAGNOSIS DIAGNOSIS
United anconeal Osteochondritis Fragmented medial
process dissecans coronoid process
DIAGNOSIS DIAGNOSIS
Septic arthritis Immune-mediated

TREATMENT INVESTIGATION
Surgical removal CT (even with no radiographic changes)
*Byline reflects author information
or reattachment TREATMENT INVESTIGATION
of process (ulnar Joint flush Bacterial/fungal

on original publication. On publica-
tion of this collection, the author’s osteotomy if culture & sensitivity
current credentials are Laura E. incongruency
Peycke, DVM, MS, DACVS, CCRP. exists) TREATMENT
Arthroscopy or
arthrotomy INVESTIGATION
CT = computed tomography with debridement Bacterial/fungal culture &
(ulnar osteotomy if sensitivity, synovial biopsy
MN = mononuclear cells
incongruency exists)
LAMENESS IN DOGS
James L. Cook, DVM, PhD, DACVS, DACVSMR*
University of Missouri

LAMENESS INVESTIGATION INVESTIGATION

Evaluate history and h Stance and posture


client observations h Stride length and duration


h L imb tracking
h S ymmetry
h Head bob

Thoracic limb lameness Combination thoracic limb

and pelvic limb lameness

INVESTIGATION
Complete thoracic limb orthopedic examination: INVESTIGATION
h Localize apparent pain (flexion elicits Complete further diagnostics:

pain more readily in thoracic limb joints) h N eurologic examination†
h Assess for long bone pain h C BC, serum chemistry profile, urinalysis,

h Localize crepitus arthrocentesis and synovial

h Examine ROM for pain/mechanical limitations fluid analysis of joints with effusion

h T ick titers

DIFFERENTIALS
Check for muscle atrophy ‡:
h S pinatus suggests shoulder problem
h B rachial suggests elbow problem
h A ntebrachial suggests carpal problem
h Diffuse suggests neurologic problem

INVESTIGATION
Examine for joint effusion (elbow, carpus)

INVESTIGATION
INVESTIGATION Perform further diagnostics:
h S edate with analgesia
Evaluate stability: h P alpate ROM and conduct stability tests again to differentiate
h S houlder: abduction angle, craniocaudal,
painful response from mechanical causes
mediolateral, internal/external rotation h R adiograph affected area(s) ± stress/special views (eg, biceps
h E lbow: varus, valgus
h C arpus: varus, valgus, flexion, extension
groove, oblique, pronated, supinated) when indicated

Consider arthrocentesis if no definitive diagnosis

*Byline reflects author information on original


publication. On publication of this collection, the
author’s current credentials are James L. Cook, DVM, Consider advanced imaging ± arthroscopy if no definitive diagnosis
PhD, DACVS, DACVSMR, OTSC.
 DIAGNOSTIC TREE h ORTHOPEDICS h PEER REVIEWED

 
 
 
 
Pelvic limb lameness
ORTHOPEDIC EXAMINATION:
TECHNIQUES & SIGNS
INVESTIGATION h Stance & posture: Look for externally rotated
Complete pelvic limb orthopedic examination: limb, shifting weight off ≥1 limbs, sitting with ≥1
h Localize apparent pain (extension elicits pain
pelvic limbs extended (ie, sit test), elbows

more readily in pelvic limb joints)
h Assess for long bone pain
abducted, and pelvic limb adducted.

h Localize crepitus

h Examine ROM for pain/mechanical limitations
h Stride length & duration: Evaluate walk and trot


for stride length symmetry and duration of stance;
shortened stride, decreased stance time, and
DIFFERENTIALS stilted gait indicate lameness and can help localize
Check for muscle atrophy ‡: if asymmetric.
h G luteal suggests hip problem
h Q uadriceps suggests stifle problem
h C rural suggests hock problem
h Limb tracking: Look for limb crossing the center

h Diffuse suggests neurologic problem line during straight line walk or trot, circumduction
of limb, wide-based in thoracic and pelvic limbs,
and asymmetry of limb tracking.

INVESTIGATION h Symmetry: Examine for above signs plus loading

Examine for joint effusion (stifle, hock) (ie, pad flare), joint angles, swing phase duration
and distance, pelvic excursion (ie, hip hike), turning
(eg, circles, figure-8 patterns), and ascents and
INVESTIGATION descents.
Evaluate stability:
h H ip: Barden, Barlow, and Ortolani tests
h Head bob: Check whether head is lifted when

h S tifle: cranial drawer, tibial thrust, internal affected thoracic limb is in stance phase (ie, up on
rotation, patellar luxation, varus, valgus
h H ock: varus, valgus lame, down on sound).

†
Nerve root signature is a common cause of lameness.

‡
When localizing a problem, evaluating apparent pain may be less effective

than identifying muscle atrophy, as it is difficult to flex one joint without
ROM = range of motion affecting others, either by movement or engagement of muscles that
cross multiple muscles (eg, biceps during elbow extension).
MUSCULAR WEAKNESS
Laura V. Lane, DVM*
Theresa E. Rizzi, DVM, DACVP
Oklahoma State University

INVESTIGATION
MUSCULAR WEAKNESS h Signalment and history

h Physical and neurologic examination

h Minimum database (CBC, serum chemistry profile, urinalysis)

Cardiovascular/ Electrolyte abnormalities Metabolic disturbances
respiratory h Polyuria/polydipsia

h Abnormal rate/ h Organ dysfunction


rhythm h Neoplasia

h Murmur

h Cough

DIFFERENTIALS
DIFFERENTIALS DIFFERENTIALS DIFFERENTIALS Anemia
Sodium Potassium Calcium h Low packed cell volume
If increased, consider: If increased, consider: If increased, consider:


h Low hemoglobin concentration
INVESTIGATION h Free water loss h Renal retention h Lymphoma





Cardiac workup: h Salt poisoning h Urinary tract h Primary



h Electrocardiography h Hyperaldosteronism obstruction hyperparathyroidism


h Echocardiography h Hypoadrenocorticism DIFFERENTIALS


h Radiography
If decreased, consider: h Metabolic acidosis If decreased, consider: Acid–base abnormalities


h Blood pressure h GI loss h Renal disease If metabolic acidosis, consider:



measurement h Hypoadrenocorticism If decreased, consider: h Hypoparathyroidism h Diarrhea


h Pulse oximetry

h Congestive heart h GI/urinary loss h Eclampsia h Ethylene glycol toxicity




h Heartworm test


failure h Diuretic use h Ethylene glycol

If metabolic alkalosis, consider:


h Hepatic disease h Fluid diuresis toxicity h Vomiting


h Aldosterone-

h GI obstruction

secreting tumor 
If respiratory acidosis, consider:
DIFFERENTIALS h Pulmonary disease

Consider: If respiratory alkalosis, consider:
h Cardiomyopathies h Hypoxemia

h Arrhythmias/


conduction failure DIFFERENTIALS DIFFERENTIALS
h Pericardial disease Magnesium Phosphorus

h Heartworm disease If increased, consider: If increased, consider: DIFFERENTIALS

h Hypotension/ h Increased intake h GI/renal loss Cholesterol abnormalities



hypertension h Diabetic ketoacidosis If increased, consider:

h Drug effects If decreased, consider: h Hypercalcemia of h Hypothyroidism



h Pneumonia h Decreased intake malignancy h Hyperadrenocorticism



h Pulmonary h GI/renal loss h Hyperadrenocorticism h Diabetes mellitus




thromboembolism h Primary
If decreased, consider:

h Chronic hyperparathyroidism h Hypoadrenocorticism

inflammatory

disease

DIFFERENTIAL
Inadequate nutrition

DIFFERENTIALS
Glucose abnormalities
If increased, consider:
h Diabetes mellitus

h Hyperadrenocorticism

If decreased, consider:
*Byline reflects author information on original publication. On publication h Hypoadrenocorticism


IVD = intervertebral disk disease of this collection, the author’s current credentials and affiliation are h Insulinoma

Laura V. Lane, DVM, DACVP, at IDEXX Laboratories, Irvine, California. h Hepatic disease

h Paraneoplastic disease

 DIAGNOSTIC/MANAGEMENT TREE h ORTHOPEDICS h PEER REVIEWED

 
 
 
 
Endocrine disease Infectious disease Neurologic abnormalities
h Polyuria/polydipsia h Endemic area h Ataxia



h Travel history h Circling



h Seizures

h Paresis

h Cervical ventroflexion

INVESTIGATION h Plantigrade stance

Endocrine workup INVESTIGATION
h Hormonal tests Infectious disease workup

h Imaging h Serologic testing


h Demonstration of organism

h Polymerase chain reaction INVESTIGATION

h Culture Neurologic workup

h Imaging

h CSF evaluation

h Muscle biopsy

h Electromyography
DIFFERENTIALS See Electrolyte DIFFERENTIALS

Adrenal abnormalities Thyroid DIFFERENTIALS
Consider: Consider: Consider:
h Hypoadrenocorticism h Hypothyroidism h Bacterial/viral



h Hyperadrenocorticism h Hyperthyroidism h Rickettsial



h Mitotane toxicity h Heartworm


h Trilostane adverse h Protozoal/fungal


h Tick paralysis
effect

h Pheochromocytoma

DIFFERENTIALS DIFFERENTIALS DIFFERENTIALS DIFFERENTIALS
Brain Neuromuscular Spinal cord Polyneuropathy
Consider: Consider: Consider: Consider:
h Encephalitis h Polymyositis h IVD h Polyradiculoneuritis




h Vestibular disorder h FeLV h Cauda equina h Endocrine disease




h Epilepsy h Muscular syndrome h Drugs (eg, vincristine,



h Drug effects dystrophies h Space-occupying chloramphenicol)


h Thiamine deficiency h Protozoal myositis lesion h Toxins (lead)



h Space-occupying h Dermatomyositis h Fibrocartilaginous h Tick paralysis




lesion h Myasthenia gravis embolism h Botulism


h Metabolic storage h Systemic lupus h Degenerative h Feline acromegaly




disease h Dysautonomia myelopathy h Diabetic neuropathy


h Feline hypokalemic h Wobbler syndrome


polymyopathy h Meningitis

h Breed-specific h Pain


myopathies (ie,
Labrador retreiver,
Great Dane)
SHOULDER PAIN/LAMENESS
Derek B. Fox, DVM, PhD, DACVS
University of Missouri-Columbia

SHOULDER PAIN/LAMENESS

INVESTIGATION
Abnormal Neurologic examination Normal

INVESTIGATION INVESTIGATION
Consider: Orthopedic examination (awake) INVESTIGATION
h T horacic radiography h P ain on biceps test Palpation: remainder
h C BC, serum chemistry profile, h P ain on hyperextension
urinalysis
YES h P ain on hyperflexion
NO of limb/cervical and
thoracic spine
h C T/MRI of axilla/thoracic spine h P ain on rotation (abnormalities
h M yelography and pain)

INVESTIGATION TREATMENT INVESTIGATION

Palpation Sedation Radiography (medial–lateral, cranial–caudal, skyline)

INVESTIGATION
Normal Shoulder abduction test Excessive
Lytic/proliferative Degenerative joint disease DIAGNOSIS
lesion Osteochondritis
dissecans
(flattening of
See Medial shoulder instability suspected caudal-medial
See Effusion humeral head)
DIAGNOSIS
Neoplasia/
severe
osteomyelitis Calcification of
INVESTIGATION
Palpation for bicep
(bacterial/ supraspinatus TREATMENT
fungal) Surgical removal
Negative inflammation Positive
of cartilage
flap with
debridement of
See subchondral bed
Proliferation and mineralization Multidirectional
in biceps groove instability
INVESTIGATION suspected
Cranial —caudal shoulder TREATMENT
­
Negative drawer test Positive
Surgical removal
of calcification, if
Biceps tenosynovitis suspected no other source
Medial shoulder
instability of pain detected
See Scapular excursion with
suspected and lamenes
internal shoulder rotation
persists after
conservative
See Ultrasound evaluation management
of biceps to confirm Multidirectional
instability
suspected

See
Conservative treatment
 DIAGNOSTIC/MANAGEMENT TREE h ORTHOPEDICS h PEER REVIEWED

 
 
 
 
INVESTIGATION
Scapular excursion with internal
shoulder rotation

YES NO

DIAGNOSIS Effusion
Contracture of infraspinatus tendon

INVESTIGATION
TREATMENT Arthrocentesis
Surgical release of the infraspinatus

Suppurative DIAGNOSIS
Degenerative
joint disease
(Nonsuppurative)
Infectious Noninfectious

Immune-mediated DIAGNOSIS
DIAGNOSIS Hemarthrosis
Septic tick-borne (Nonimmune-
mediated)
Erosive Nonerosive

DIAGNOSIS DIAGNOSIS
Rheumatoid- Idiopathic
like arthritis

INVESTIGATION INVESTIGATION
Arthroscopy or arthrotomy for joint exploration to confirm Ultrasound evaluation of biceps to confirm

TREATMENT TREATMENT
Surgical Conservative treatment
management (cage rest and NSAID
therapy) followed by
physical rehabilitation
DYSTOCIA IN THE BITCH
Cheryl Lopate, DVM, MS, DACT
Reproductive Revolutions
Aurora, Oregon
Wilsonville Veterinary Clinic
Wilsonville, Oregon

DYSTOCIA

INVESTIGATION
History:
h O vulation timing (progesterone, LH, vaginal cytology,
vaginoscopy) performed to determine gestation length
h B reeding dates
h P rior history of dystocia or health issues
h P regnancy at term

INVESTIGATION
Confirm pregnancy with imaging before proceeding

CRT = capillary refill time

INVESTIGATION
FHR = fetal heart rate Physical examination:
h A ttitude, Hydration, TPR, MM/CRT
LH = luteinizing hormone h C ardiovascular status
MM = mucous membranes h A bdominal palpation
h D igital examination (stricture/septum/tag) and response to feathering
TPR = temperature/pulse/ h F etus/membranes palpable in canal
respiration

Signs of labor INVESTIGATION

h S tage 1: panting, trembling, nesting, drop in temperature, uterine Radiography:
contractions (via tocodynamometry), progesterone <2 ng/mL h C onfirm
pregnancy and number of fetuses
h S tage 2: water breaking, visible abdominal or uterine contractions h Signs of fetal obstruction or death

via tocodynamometry, visible allantoic/amniotic sac or fetal parts h Pelvic abnormality preventing delivery

h V ulvar discharge (clear, bloody, green/black, light green) h Feto–pelvic disparity

h Fetal malposition, malposture, malpresentation

INVESTIGATION
Ultrasonographic Signs of dystocia Ultrasonography:
signs of fetal stress h S tillbirth/difficult
resuscitation h C onfirm pregnancy
h F HR <190 bpm h G estation length >66 days from LH surge h Fetal heart rates

h P lacental or >72 days from last breeding h Placental integrity

detachment h > 4 hours from rupture of first h Fetal fluids

h I ncreased density chorioallantois (if detected) h Fetal maturation assessment (intestinal and renal development, peristalsis evident)

of fetal fluids h >2 hours between births
h F etal death h >30 minutes of hard straining without
h I ntrauterine delivery of first puppy
hemorrhage, h H eavy green/black discharge before
uterine edema delivery of puppy
h L arge amounts of bright red blood/
INVESTIGATION
Blood work:
hemorrhage h B lood loss/anemia detected? Do not confuse with normal pregnancy anemia
h Abdominal pain, collapse, or distracted
h R /O hypoglycemic (glucose <70 mg/dL)

mothering h R /O hypocalcemia (ionized calcium <1.30 mmol/L or corrected total serum calcium
<9 mg/dL)
h Corrected calcium (mg/dL) = 3.5 – albumin (g/dL) + serum calcium (mg/dL)

182 cliniciansbrief.com
 
 
 DIAGNOSTIC/MANAGEMENT TREE h REPRODUCTION h PEER REVIEWED

 
 
 
 
DIAGNOSIS
Dystocia confirmed?

YES NO

TREATMENT
h M onitor for normal labor progression
INVESTIGATION INVESTIGATION h I f signs of distress/dystocia appear,

Check for the following: Look for signs of: begin dystocia management
h F HR >190 on all fetuses h F etal distress (bradycardia)
h < 4 fetuses remain h Exhaustion

h F etal size and position consistent with vaginal delivery h >4 fetuses remain

FAST FACTS

h P hysical condition stable with adequate energy to
complete vaginal delivery

h Feathering = repeated strokes with firm

TREATMENT pressure on dorsal vestibulovaginal wall;
Cesarean section
TREATMENT should elicit strong abdominal contraction.
Medical management
h Calcium may increase the strength of con-

tractions. If given first, then oxytocin may
not be necessary.
Response to feathering/uterine contractions? • Calcium gluconate 10% does not need to be

diluted and can be dosed at 0.5 mL/10 lb
(4.5 kg) SC.
• Calcium gluconate 23% should be diluted

Strong contractions Weak/no contractions
at least 1:3 to prevent severe tissue reaction
or irritation; anecdotal evidence has shown
a 1:4 dilution with sterile water may be
dosed at 1 mL/10 lb (4.5 kg) SC.
TREATMENT TREATMENT
h Calcium SC, may further increase contraction strength; can be h 10% calcium gluconate at 0.22 mL/kg SC h Calcium may be repeated q4-6h to maintain



given at the same time as oxytocin. h Wait 30-60 minutes before giving oxytocin
stronger uterine contractions.

h Oxytocin at 0.25-2 IU/bitch IM or SC; repeat up to 3× per puppy if no puppy delivered with calcium alone.

h Oxytocin can result in decreased placental

blood flow or premature placental separa-
Puppy delivered? Puppy delivered? tion, leading to fetal hypoxia, bradycardia, or
death. Repeated doses against fetal obstruc-
NO YES YES NO tion can result in uterine rupture. Calcium is
safer if there is concern about obstruction.

TREATMENT TREATMENT TREATMENT

Cesarean section h Wait 30 minutes Oxytocin at 0.25-2 IU/ If progression ceases

h If next puppy not delivered, give oxytocin at 0.25-2 IU/bitch bitch IM or SC; repeat

IM or SC; repeat up to 3× per puppy up to 3× per puppy
h Repeat calcium if inertia develops (more than 2 hours

between puppies) or if strength of contractions decreases.
Can be repeated up to every 4-6 hours

cliniciansbrief.com 183
 
PENILE DISCHARGE IN DOGS
Cheryl Lopate, DVM, MS, DACT*
Reproductive Revolutions
Aurora, Oregon

PENILE OR PREPUTIAL DISCHARGE

INVESTIGATION
Presenting signs:
h P reputial or penile discharge (eg, bloody, purulent, mucoid)
h E xcessive licking or signs of genital pain/discomfort
h S tranguria, hematuria, dysuria, pollakiuria
h C onstipation, ribbon-like stool, tenesmus

INVESTIGATION
Clinical considerations:
h I nability to extend penis from prepuce
h Lymphoid follicles or vesicular lesions on penis or prepuce
h P enile, urethral, or prostatic mass (smooth, irregular)
h I rregular mucosal surface on penis or prepuce
h P etechiae or ecchymoses on mucosal surfaces or skin
h E nlarged scrotum, scrotal contents
h E nlarged prostate on digital rectal examination

DIFFERENTIALS DIFFERENTIALS DIFFERENTIALS

Clear or mucoid discharge Hemorrhagic discharge Purulent discharge
h P ersistent penile frenulum h Trauma (penile, preputial) h P ersistent penile frenulum
h H ypospadias h F oreign body h Hypospadias

h Traumatic penile adhesions h H erpesvirus infection1,2 h Trauma, hair impaction

h P himosis h B rucella canis infection h Foreign body

h H erpesvirus infection1,2 h B alanoposthitis or prostatitis from aerobic h Phimosis

h N eoplasia (penile, preputial) bacteria, Mycoplasma spp, Ureaplasma spp, fungi h B canis infection

h H ormonal imbalance with puberty, h B enign prostatic hyperplasia h Balanoposthitis, prostatitis, orchitis,

exogenous steroids, enodgenous h N eoplasia of prostate, urethra, bladder, penis, or epididymitis from aerobic bacteria,
estrogen (Sertoli cell tumor) prepuce or squamous metaplasia of the prostate Mycoplasma spp, Ureaplasma spp, fungi
h U TI or incontinence h E xogenous steroids or endogenous estrogen h Neoplasia—urethral, penile, preputial,

h P oor hygiene (Sertoli cell tumor, estrogen creams or patches) 3 prostatic
h C alicivirus infection h U TI or urolith h UTI or urolith

h C oagulopathy h Poor hygiene

h P oor hygiene
h S nake or insect bite

See Perform diagnostics

References
1. Hill H, Maré CJ. Genital disease in dogs caused by canine herpesvirus. Am J Vet Res. 1974;35:669-672.

2. Anvik JO. Clinical considerations of canine herpesvirus infection. Vet Med. 1974;86:394-403.

3. Doig PA, Ruhnke HL, Bosu WT. The genital Mycoplasma and Ureaplasma flora of healthy and diseased dogs. Can J Comp Med. 1981;45:233-238.

4. Rosendal S. Canine mycoplasmas: Their ecologic niche and role in disease. J Am Vet Med Assoc. 1982;180:1212-1214.

AGID = agar gel immunodiffusion
*Byline reflects author information on original publication. On publication of this collection, UA = urinalysis

the author is also at Wilsonville Veterinary Clinic, Wilsonville, Oregon.
 DIAGNOSTIC/MANAGEMENT TREE h REPRODUCTION h PEER REVIEWED

 
 
 
 
INVESTIGATION
Perform diagnostics

INVESTIGATION INVESTIGATION INVESTIGATION

General procedures: Prostate/bladder disease: Penile/preputial disease: AUTHOR INSIGHT
h C
 BC, serum chemistry h U ltrasound
of prostate, bladder, urethra h E xtrusion of entire penis past
panel h Cytology of prostatic secretion, bulbus glandis h To differentiate UTI from prostatic


h U  rinalysis and urine sediment or aspirates or urine sediment h Cytology of penile or preputial
culture h Cystocentesis for UA or urine culture surface lesions infection, compare culture and

h C  oagulation panel, h Cytology or histopathology of prostatic h P reputial cytology to look for cytology of a cystocentesis or

buccal mucosal wash, aspirate, or biopsy evidence of hyperestrogenism
bleeding time for h Culture of third fraction of ejaculate, (cornification) catheter-obtained sample with a

platelet function prostatic wash fluid, or aspirate/biopsy h E ndoscopic examination of the prostatic fluid wash or prostatic
h T  est for hemospermia h Preputial mucosal cytology to look for prepuce
aspirate sample.

h B  canis screening test; evidence of hyperestrogenism h R adiography to assess os penis
if positive for B canis, (cornification) h U rethral catheterization to assess
AGID h Abdominal radiography for partial obstruction from mass h All bacteria that can cause


h Contrast urethrography in urethra or at seminal colliculus pathology can also be normal flora.

High numbers of a single organism
along with signs of infection or
TREATMENT inflammation suggest the organism
h T
 reatment of underlying condition is pathologic. Mixed populations
h G
 entle cleansing with saline or a very dilute (weak tea-colored) povidone-iodine solution for balanoposthitis
h P  robiotics for balanoposthitis or if patient is treated with long-term antibiotics to help maintain normal GI flora indicate normal flora; antibiotics
h A  ntibiotics based on culture and susceptibility testing results for prostatitis or cystitis are not required. Mycoplasma spp is
h F  oreign body removal
h S  urgical removal of masses or correction of anatomic defects a common co-isolate when
h T  reat benign prostatic hyperplasia with neutering, antiandrogens, or gonadotropin agonists infection is present, but it may not
h B  enign neglect for hormonal imbalance of peripubertal individuals
h D  iscourage licking indicate pathologic infection.4
h R  ecurrent infections—investigate prostate or urinary tract for primary source of infection Common normal floras include
h R  estrict exposure to exogenous hormones
h C  ontact state veterinarian if B canis confirmed Escherichia coli, Pseudomonas spp,
Staphylococcus spp, Streptococcus
spp, Pasteurella spp, Klebsiella spp,
and Mycoplasma spp.
HOW TO PERFORM PROSTATIC WASH
h Some yellowish-white to slight light-
h Allow the patient to urinate

greenish-tinged preputial discharge

h Sedate the patient is normal. Intact and brachycephalic

dogs tend to have increased normal
h Empty the dog’s bladder via catheter and flush with 5-10 mL of saline, save sample for urine
discharge. The amount of normal

cytology and culture
discharge tends to increase with
h Pass a polypropylene or red rubber catheter over the pelvis rim, with a digit in the rectum, age, as self-grooming diminishes

position the tip of the catheter just caudal to the prostate with aging.
h Vigorously massage the prostate per rectum with the inserted digit h Infection may be secondary to


inappropriate or prolonged
h Occlude the urethral opening and inject 5-10 mL sterile saline
antibiotic therapy and bacterial

h Advance the catheter forward a few centimeters while aspirating as much sample as possible overgrowth of pathologic

organisms.
h Perform cytology and culture on the recovered sample and compare to urine sample

PREGNANCY IN DOGS
Bruce W. Christensen, DVM, MS, DACT
Kokopelli Assisted Reproductive Services
Woodland, California

BREEDING OCCURS

Breeding purposeful or accidental?

Purposeful (see Purposeful Accidental

Breeding Options)

INVESTIGATION
Perform early pregnancy (30 days Observed Suspected
gestation) diagnostics:
h Palpation: may be challenging

until fetal skeletons ossify,
starting at 45 days
h Serum relaxin: hormone in
INVESTIGATION

dogs made exclusively by the Perform vaginal cytology* for
placenta; reliable at 30 days presence of sperm. Presence of
h Ultrasonography: reliable at 30
sperm confirms mating, although

days absence of sperm does not
h Radiography not useful for
definitively rule out mating

pregnancy diagnosis at this
stage of gestation

Terminate potential pregnancy or wait to confirm pregnancy

Perform late pregnancy (55-60
days gestation) diagnostics:
h Ultrasonography to assess fetal

viability and estimate
gestational age
h Radiography to count fetuses

Terminate Wait for diagnosis

Pursue immediate treatment After 30 days, perform early

options: pregnancy diagnostics:
h Spay (best option if no planned h Palpation: may be challenging


breeding future) until fetal skeletons ossify,
or starting at 45 days
h Medical treatment/resorption h Serum relaxin: hormone in


via estradiol cypionate or dogs made exclusively by the
estradiol benzoate† placenta; reliable at 30 days
h Ultrasonography: reliable at 30

days
h Radiography not useful for

pregnancy diagnosis at this
stage of gestation
AI = artificial insemination
TCI = transcervical insemination
 DIAGNOSTIC/MANAGEMENT TREE h REPRODUCTION h PEER REVIEWED

 
 
 
 
Pregnancy confirmed?

YES NO

Discuss responsible
PURPOSEFUL
breeding options or BREEDING OPTIONS
Termination via Termination via future spay with owner
ovariohysterectomy medical treatment/ Breeding should be timed and managed
(best option if no resporption:
planned breeding h Glucocorticoids using vaginal cytology, vaginoscopy,

future) h Prostaglandins (eg,
and progesterone to determine

cloprostenol)
h Dopamine agonists luteinizing hormone surge, ovulation

(eg, cabergoline) date, fertile period, and estimated
h Prostaglandin +
whelping date. Insemination options

dopamine agonist
h Aglepristone (not
include:

available in North
America)
h Fresh semen (natural mating,
vaginal AI, TCI)
h Chilled/shipped semen (vaginal AI, TCI)
Perform follow-up:
h Recheck serum
h Frozen semen (TCI, surgical AI)

progesterone 4
days after starting
mismating
treatment; should
be baseline
h Recheck
Reference

ultrasonography
4-8 days after 1. Whitacre MD, Yates DJ, VanCamp SD, Meuten

starting mismating DJ. Detection of intravaginal spermatozoa after
treatment to natural mating in the bitch. Vet Clin Pathol.
document 1992;21(3):85-87.
termination of
pregnancy

*Although negative predictive value of vaginal cytology within the first 24 hours of mating has been reported

to be as great as the positive predictive value,1 the possibility of a false negative still warrants confirming
pregnancy later. Therefore, the value of performing vaginal cytology is questionable.
†
Must administer within 1-2 days of mating. Use caution with timing and dose. Adverse effects include

aplastic anemia and pyometra.
VULVAR HEMORRHAGIC DISCHARGE
John P. Verstegen III, DVM, MSc, PhD, DECAR*
Karine J. Onclin, DVM, PhD, DECAR*
University of Florida

VULVAR HEMORRHAGIC DISCHARGE

INVESTIGATION
External examination

Abnormal Normal

DIAGNOSIS DIAGNOSIS INVESTIGATION

h Recessed vulva h Ulcerations Vaginal examination:



h Hypoplastic h Trauma h Vaginal cytology



vulva h Vulvitis h Vaginoscopy


h Microbiologic testing (eg, CHV, Brucella

spp, bacterial culture/quantification†)

TREATMENT TREATMENT
Vulvoplasty Local and causal
treatments Normal

Intact Spayed

DIAGNOSIS INVESTIGATION
h Estrus LH/AMH levels

h Bleeding from urinary

tract or uterus

Normal Abnormal
*Byline reflects author information
AI = artificial insemination

on original publication. On publication
AMH = anti-Müllerian hormone of this collection, the authors’ current
affiliation is with TherioExpert, Liège,
CHV = canine herpesvirus Belgium, and University of Nottingham, DIAGNOSIS DIAGNOSIS
United Kingdom. Bleeding of h Remnant ovary

LH = luteinizing hormone †Bacterial culture results should be other origin: h Stump pyometra

h Bladder

OHE = ovariohysterectomy interpreted with caution; most

h Coagulopathy
commonly cultured bacteria are part of

TVT = transmissible venereal tumors normal vaginal flora.

TREATMENT
Perform surgery
 DIAGNOSTIC/MANAGEMENT TREE h REPRODUCTION h PEER REVIEWED

 
 
 
 
Abnormal

Anatomic abnormalities Masses Infection

DIAGNOSIS
h Stricture

h Double vagina DIAGNOSIS DIAGNOSIS DIAGNOSIS DIAGNOSIS DIAGNOSIS

h Fibrous band Tumor TVT Hyperplasia/ Herpesvirus Brucella spp

h Ectopic urethra prolapse

DIAGNOSIS DIAGNOSIS
TREATMENT Nonspecific vaginitis: Other bacterial
TREATMENT h Radiotherapy
h Prepubertal infection (rule

h Adult out UTI)

Surgical correction h Chemotherapy


Nonbreeding Breeding
Intact Spayed animal animal

DIAGNOSIS DIAGNOSIS
h Often benign and localized h Often invasive


h Often leiomyoma/fibroma and malignant No ulceration Ulceration No ulceration Ulceration

h Often

leiomyosarcoma
h Other type of

tumor (eg,
TREATMENT transitional cell TREATMENT TREATMENT TREATMENT TREATMENT
Surgical correction + OHE if carcinoma) OHE + OHE + prolapse h Purse-string h Removal +


not intended for reproduction purse-string removal suture + AI purse-string
suture • If pregnant, suture + AI

remove at • If pregnant,

50-55 days remove at
50-55 days

TREATMENT TREATMENT
Surgical Surgical
correction; correction
address causes including total
if secondary vaginal ablation
 DIAGNOSTIC/MANAGEMENT TREE h RESPIRATORY MEDICINE h PEER REVIEWED

 
 
 
 
ABNORMAL RESPIRATORY SOUNDS
Leah A. Cohn, DVM, PhD, DACVIM (SAIM)
University of Missouri

THORACIC AUSCULTATION*

Decreased bronchovesicular Adventitial sounds Increased bronchovesicular

sounds sounds

DIAGNOSIS DIAGNOSIS
Rule out: Wheeze/rhonchus (ie, Crackles/rales (ie, discontinuous Pleural friction rub (ie, Rule out:
h Shallow inspiration continuous “musical” sounds) “Velcro” like sounds) cyclic “grating” sounds) h Pulmonary edema


h Obesity h Pneumonia


h Atelectasis h Increased turbulence


h Pleural effusion of airflow

h Pneumothorax h Hyperpnea


h Thoracic mass h Referred upper
DIAGNOSIS INVESTIGATION DIAGNOSIS


Rule out: Radiographic imaging Rule out: airway noise
h Airway obstruction Alveolar pattern? h Pleuritis


h Airway secretions

h Asthma

h Severe bronchitis

TIPS & TACTICS
YES NO h Several abnormal respiratory sounds are heard

without a stethoscope (eg, stertor, stridor), but
others are heard only on thoracic auscultation.
DIAGNOSIS Thoracic auscultation requires intense attention
Rule out: to detail. Auscultation should be done in a quiet
Cranioventral Perihilar Caudodorsal/ h Pulmonary
environment.

distribution distribution diffuse fibrosis
h Early pulmonary
Growling, purring, and panting make accurate

edema h

h Early aspiration
auscultation impossible.

pneumonia
DIAGNOSIS DIAGNOSIS DIAGNOSIS h Deep breaths facilitate auscultation; holding the
Rule out: Rule out: Rule out:

h Bacterial h Congestive h Noncardiogenic nostrils closed for a few moments will encourage



pneumonia heart failure pulmonary 1 or 2 deep breaths afterward.
h Aspiration edema (eg,

pneumonia electrocution,
h Hemorrhage postseizure)
h Normal lung sounds are described as bronchove-


h Acquired sicular, but bronchovesicular sounds can indicate

respiratory
distress disease when they are increased or decreased in
syndrome intensity or heard in an abnormal location.
h Fungal
Adventitial sounds are always abnormal.

pneumonia
h Protozoal
Adventitial sounds or altered bronchovesicular

pneumonia h

h Rickettsial
*Abnormal sounds on auscultation can occur sounds can occur alone or in combination.

pneumonitis

alone or in combination; they may also be heard h Hemorrhage
throughout the thorax or only in some areas. h Crackles are usually best heard on inspiration;


inducing a cough may facilitate auscultation
when the cough subsides.
 NASAL DISCHARGE IN CATS
Douglas Palma, DVM, DACVIM (SAIM)
The Animal Medical Center
New York, New York

Acute signs (<3 weeks) CHRONIC OR ACUTE SIGNS

OF NASAL DISCHARGE

Epistaxis No additional INVESTIGATION Abnormal results

clinical Physical examination
abnormalities

DIAGNOSIS Green/yellow mucoid/ Peracute nature; Facial pain Oral/lingual Deviation of soft
h Structural disease mucopurulent unilateral ulceration; palate; palpable

(eg, neoplasia, ocular signs nasopharyngeal lesion
mycotic or dental
disease)
h Less likely:
DIAGNOSIS

systemic disease, DIAGNOSIS DIAGNOSIS h Dental disease
coagulopathy, DIAGNOSIS <1 year of age

h Infectious h Foreign body h Less likely (acute

hypertension


rhinitis h Infectious nature): destructive h Viral rhinitis


(bacterial, viral) rhinitis rhinitis (mycotic, (FHV-1, feline
h Secondary chronic viral, calicivirus)

infection immune-mediated)
h Neoplasia h Neoplasia DIAGNOSIS
INVESTIGATION


h Less likely: h Nasopharynge al


h S ystemic workup foreign body INVESTIGATION polyps
(eg, blood h S aline TREATMENT h Nasopharynge al


pressure, CBC, hydropulsion h I nfectious stenosis
serum chemistry h A dvanced disease testing h Fungal
INVESTIGATION


profile, coagulation imaging/ (PCR) granuloma
h D entistry
profile) TREATMENT diagnostics h Supportive
h A dvanced imaging/ (localized pain to

h S upportive h ± antibiotics, care (eg,
diagnostics teeth)
care if infectious h C ryptococcal LCAT hydration,
h ± empirical h R adiography antipyretics)
antibiotics (dental, nasal)
h Antiviral INVESTIGATION

h N asal flushing
h A dvanced therapy (eg, h S edated
h ± nasal culture
imaging/ famciclovir, nasopharyngeal
diagnostics polyprenyl examination
immuno- h R adiography
stimulant, (open-mouth,
DIAGNOSIS intranasal lateral)
h Viral rhinitis (FHV-1,
vaccine) h A dvanced

feline calicivirus)
Serous/ Postanesthesia; imaging/
h Allergic/
diagnostics

inflammatory/ serohemorrhagic postemesis
h C ryptococcal
bacterial rhinitis
LCAT
(B bronchiseptica,
C felis)

DIAGNOSIS DIAGNOSIS
h Nasopharyngitis h <1 year:
Ear infection; Neurologic >1 year


h Nasopharyngeal stenosis nasopharyngeal
ear mass signs of age

TREATMENT h Nasal/nasopharyngeal polyp

h V iral PCR testing foreign body h >5 years:

(FHV-1, feline neoplasia
calicivirus)
h Supportive care (eg,
INVESTIGATION DIAGNOSIS

hydration,
antipyretics, appetite h C ryptococcal
h Neoplasia
TREATMENT

stimulants) LCAT
h Mycotic disease
INVESTIGATION

h S edated nasopharyngeal
h Antiviral therapy h A dvanced
exam h S edated

(eg, famciclovir, h S aline
imaging/
hydropulsion nasopharyngeal
polyprenyl h ± antibiotics
diagnostics
examination FHV-1 = feline herpesvirus-1
immunostimulant, h A dvanced imaging/
intranasal vaccine) diagnostics FNA = fine-needle aspiration
h Antihistamine trials

LCAT = latex cryptococcal
agglutination test
LSA = lymphosarcoma
PCR = polymerase chain reaction
 DIAGNOSTIC/MANAGEMENT TREE h RESPIRATORY MEDICINE h PEER REVIEWED

 
 
 
 
Chronic signs (>3 weeks)

Chronic, Predominantly Chronic, Chronic,

intermittent; normal hemorrhagic nonprogressive progressive, or
between episodes (intermittent or >5 years of age
isolated)

Abnormal retropulsion; Soft-tissue

exophthalmos; pain on swelling/mass >1 year duration;
opening mouth Responsive to antibiotics? >2 years of age DIAGNOSIS
DIAGNOSIS at onset h Neoplasia


h Structural h Chronic



disease (eg, rhinitis (viral
neoplasia, recrudescence,
DIAGNOSIS YES mycotic or
DIAGNOSIS h Viral disease / recurrent
dental disease) DIAGNOSIS bacterial

h Retrobulbar inflammatio n h Less likely: h Chronic idiopathic infection)

abscess/cellulitis (periocular swelling, 

systemic rhinitis h Fungal rhinitis
h Dental disease/ severe conjunctivitis)


disease h Allergic rhinitis

abscessation h Fungal granuloma

DIAGNOSIS h Less likely: foreign

h Infiltrative disease h Neoplasia


h Bacterial disease body, neoplasia,


(eg, LSA,

(primary [rare], viral disease
Cryptococcus spp,
secondary) INVESTIGATION
Aspergillus spp) h Dental disease (eg, INVESTIGATION h I nfectious disease

fistula, abscess) h R ecommend
testing (PCR, ±
INVESTIGATION systemic workup
h I nfectious disease bacterial culture,
exposure history
(eg, blood TREATMENT FeLV/FIV testing)
pressure, CBC, h A ntihistamine h Cryptococcal
INVESTIGATION h Viral PCR testing


serum chemistry trials LCAT

h D ental radiography (FHV-1, felin e TREATMENT profile, FeLV/ h A nti-inflammatory
h C ryptococcal calicivirus)
h Advanced
LCAT


h A ntibioticsas needed FIV testing, trials
h O h Empirical treatment imaging/
 cular h ± nasal flushing/ coagulation h I mmuno- diagnostics

ultrasonography of clinical signs culture profile) modulatory trials
h A dvanced imaging/ h FNA and/or biopsy h D ental radiography h A dvanced h ± advanced

diagnostics (soft-tissue mass) h E xtraction/cleaning imaging/ imaging/
h Cryptococcal LCAT h ± advanced diagnostics diagnostics

h Advanced imaging/ imaging/diagnostics

diagnostics
Severe stertor;
open-mouth breathing

Strong suspicion NO
of dental disease (serous,
concurrent ocular) <1 year of age at onset

DIAGNOSIS
h Viral rhinitis (FHV-1, feline calicivirus)

h Bacterial rhinitis (secondary)
DIAGNOSIS INVESTIGATION

h Young animals: nasopharyngeal stenosis, DIAGNOSIS DIAGNOSIS

polyps h Dental disease h Viral rhinitis (FHV-1, h Nasopharyngeal h S edated nasopharyngeal



h Allergic or inflammatory rhinitis feline calcivirus) stenosis examination

h Less likely (acute nature): neoplasia, h Nasopharyngeal h N asal radiography
h Allergic rhinitis



fungal rhinitis, primary bacterial rhinitis polyp h A dvanced imaging/
h Cleft palate diagnostics

TREATMENT
h D ental
radiography
INVESTIGATION h Tooth

h V iralPCR testing (FHV-1, feline calicivirus) extraction/
h N asal cleaning
TREATMENT
flushing/culture (aerobic, h Viral PCR testing (FHV-1, feline calicivirus)
mycoplasma)

h FeLV/FIV testing
h S edated nasopharyngeal examination

h Supportive care (eg, hydration, antipyretics, appetite
h S kull radiography (open-mouth, lateral)

stimulants)
h C ryptococcal LCAT
h Antiviral therapy (eg, famciclovir, polyprenyl
h A dvanced imaging/diagnostics

immunostimulant, intranasal vaccine)
h Antihistamine trials

NASAL DISCHARGE IN DOGS
Douglas Palma, DVM, DACVIM (SAIM)
The Animal Medical Center
New York City, New York

CHRONIC OR ACUTE SIGNS OF NASAL DISCHARGE

Acute (≤3 Weeks) Chronic (>3 weeks), see page 194

INVESTIGATION
Obtain exposure history (eg, shelters, dog parks, Peracute onset; severe and/or unilateral signs?
daycare) and vaccination status

Recent exposure history?

YES NO

Recent history of
anesthesia or vomiting?
YES NO

YES NO
Systemic signs Localized signs

DIAGNOSIS DIAGNOSIS
h Nasopharyngitis h Foreign body
DIAGNOSIS


h Nasopharyngeal h Allergic or infectious
h CPIV


stenosis rhinitis

Respiratory signs Nonrespiratory signs h Bordetella bronchiseptica h P neumonyssoides

h P neumonyssoides caninum
caninum (ie, nasal mites)
(ie, nasal mites) h Neoplasia
h Microsporum canis


DIAGNOSIS DIAGNOSIS INVESTIGATION
h N asopharyngeal
h CIV h CDV


h CPIV h Pantropic CCoV examination
INVESTIGATION


h N asal saline flush
h CRCoV TREATMENT

or saline h A dvanced diagnostics
h Streptococcus h S upportive care ±

zooepidemicus hydropulsion (eg, rhinoscopy)
hospitalization h A dvanced imaging/ h A dditional diagnostics
h Bordetella h I solation from

diagnostics (eg, CT (eg, antihistamines,
bronchiseptica TREATMENT other dogs
scan, rhinoscopy) antibiotics, anthelmint-
h ± Mycoplasma cynos, h Supportive care ± h ± antibiotics to

h ± antibiotics ics, infectious disease

CBoV, or CnPnV hospitalization treat secondary
testing)
h Isolation from infections

other dogs h ± anthelmintics or
h 
A ntibiotics to treat antifungal therapy
primary or as indicated
secondary
bacterial infections
 DIAGNOSTIC/MANAGEMENT TREE h RESPIRATORY MEDICINE h PEER REVIEWED

 
 
 
 
Concurrent signs Epistaxis

Conduct systemic workup (eg,

CBC, serum chemistry profile)
Weight loss; anorexia Ocular displacement; Coughing; pyrexia; Neurologic signs and infectious disease and
protrusion dyspnea coagulation testing

DIAGNOSIS DIAGNOSIS DIAGNOSIS DIAGNOSIS

h Systemic disease h Neoplasia h CRDC h Nasal neoplasia




(eg, disseminated, h Dental disease h Community-acquired h Fungal rhinitis Systemic No systemic



neoplastic, h Infection pneumonia h CDV disease found disease found


infectious) h Abscess (bacterial, viral) h Pantropic CCoV


h Lower respiratory h Viral rhinitis


infection h Aspiration, fungal,

h Pyrexia or eosinophilic

h Vasculitis pneumonia DIAGNOSIS

INVESTIGATION h 
Nasal
h A dvanced imaging/ neoplasia
diagnostics (primary or
h D ental imaging metastatic)
INVESTIGATION INVESTIGATION h Fungal

h M etabolic workup h A dvanced imaging/diagnostics rhinitis
(eg, CBC, serum h I nfectious disease testing; PCR h Foreign

chemistry profile, h ± antibiotics body
urinalysis) h Dental

h I maging (eg, disease
radiography)
h I nfectious disease
testing

TREATMENT
CBoV = canine bocavirus h S upportive
care and treatment
as indicated
CDV = canine distemper virus
CIV = canine influenza virus
CnPnV = canine pneumovirus
CPIV = canine parainfluenza virus
CRCoV = canine respiratory coronavirus
CRDC = canine respiratory disease complex
Pantropic CCoV = pantropic variant of canine coronavirus Continues h
DIAGNOSTIC/MANAGEMENT TREE h RESPIRATORY MEDICINE h PEER REVIEWED

 
 
 
 
Chronic (>3 weeks)

Mucoid (eg, green, yellow) See Epistaxis, previous page Serous

Static; nonprogressive Chronic; progressive Static; mild Chronic;

progressive

DIAGNOSIS
Bilateral Unilateral Bilateral Unilateral h Allergic or chronic inflammatory


rhinitis
h P neumonyssoides caninum (ie,
nasal mites)
h Neoplasia

DIAGNOSIS DIAGNOSIS DIAGNOSIS DIAGNOSIS
h Allergic or chronic h Dental disease h Chronic inflammatory h Fungal rhinitis





inflammatory rhinitis h Fungal rhinitis rhinitis h Neoplasia


h Nasopharyngeal h Neoplasia h Neoplasia h Dental disease
TREATMENT




stenosis h Foreign body h Fungal rhinitis h Foreign body



h Dental disease h E mpiric rhinitis therapy

h A ntihistamines
h A nthelmintics
h A dvanced diagnostics (eg, CT,
TREATMENT Conduct airflow MRI, rhinoscopy, biopsy/
h Antihistamines INVESTIGATION examination histopathology)

h Anthelmintics h Dental imaging


h Cautious h Advanced diagnostics (eg, CT, MRI, rhinoscopy,


consideration to biopsy/histopathology)
anti-inflammatory
drugs (eg, prednisone,
piroxicam)
h Advanced diagnostics Obstructed airflow Nonobstructed airflow

(eg, CT, MRI,
rhinoscopy, biopsy/
histopathology)

DIAGNOSIS DIAGNOSIS
h Neoplasia h Fungal rhinitis


h Foreign body h Dental disease


h Bacterial rhinitis h Foreign body


h Neoplasia

INVESTIGATION
h Dental imaging

h Advanced diagnostics (eg, CT, MRI,

rhinoscopy, biopsy/histopathology)
ACUTE RENAL FAILURE
Vanessa E. Von Hendy-Willson, DVM*
Larry G. Adams, DVM, PhD, DACVIM (SAIM)
Purdue University

ACUTE RENAL FAILURE

INVESTIGATION INVESTIGATION INVESTIGATION Azotemia,

History and clinical signs: Physical examination: Initial diagnostics: hyperphosphatemia,
h Signalment h Hydration status h CBC metabolic acidosis,



h Duration of signs h BCS h Serum chemistry profile hypocalcemia,



h Medications h Oral examination (halitosis, h Urinalysis hypo- or hyperkalemia,



h Toxin exposure ulcers) h Blood pressure isosthenuria,


h Travel h Abdominal palpation (pain, h Abdominal radiography/ultrasonography proteinuria, glucosuria†


h Tick exposure renal enlargement)

h Concurrent illness h Auscultation (bradycardia)

h Recent anesthesia h Other systemic signs


h Anorexia

h PU/PD

h Lethargy, weakness

h Nausea

h Vomiting

h CNS signs
DIAGNOSIS DIAGNOSIS

h Diarrhea

h Oliguria/anuria Intrinsic renal azotemia Prerenal azotemia
 

h Isosthenuria h Concentrated USG

h Fractional excretion of Na >1% 
h Fractional excretion of Na <1%

h Increased anion gap

Evidence of Hypotension
UP/C >1‡ Nephrotoxi cant Ischemic Exogenous blood loss
toxin or
­
drug exposure event
infectious
agent
History of
DIAGNOSIS Absolute dehydration,
decrease prior
Consider acute
in effective anesthesia?
glomerulonephritis
DIAGNOSIS INVESTIGATION INVESTIGATION blood volume
­
Consider acute Drug levels h Ethylene glycol

interstitial nephritis test
h Leptospiro sis titers Relative

INVESTIGATION
­
h Tick-borne disease decrease in

Investigate underlying titers effective blood
inflammatory or DIAGNOSIS volume
Consider acute tubular necrosis
­
infectious diseases

*Byline reflects author information on original publication. On


publication of this collection, the author’s current credentials and
INVESTIGATION affiliation are Vanessa E. Von Hendy-Willson, DVM, MS, DACVIM,
Additional diagnostics: Upstate Vet Emergency and Specialty Care, Greenville, South Carolina.
h Determine urine output (if oliguria/anuria, also consider postrenal azotemia) †
Not all findings must be present to continue.

h Abdominal ultrasonography ‡
No history of nephrotoxicant drug exposure, ischemic event, toxin, or


h Urine culture infectious agent

h Consider renal biopsy if unresponsive to treatment

 DIAGNOSTIC TREE h UROLOGY/NEPHROLOGY h PEER REVIEWED

 
 
 
 
DIAGNOSIS
Postrenal azotemia
h Hyperkalemia
h Abdominal effusion
h Radiographic evidence of obstruction or oliguria/anuria

INVESTIGATION
Hyperkalemia h Abdominal ultrasonography (if upper tract obstruction or rupture suspected)
and hyponatremia

h Contrast urethrogram (if lower tract obstruction or rupture suspected)
without oliguria

DIAGNOSIS
Consider DIAGNOSIS Obstruction not confirmed; DIAGNOSIS INVESTIGATION
hypoadrenocorticism Confirmed urethral or suspect ureteral obstruction Bladder or Ascites noted:
­
(Addison’s disease) ureteral obstruction urethral tear abdominocentesis
for fluid creatinine
concentration
INVESTIGATION
EU or antegrade pyelogram
(if serum creatinine <5 mg/dL; no EU if ≥5 mg/dL)
Uroabdomen

EU = excretory urogram
DIAGNOSIS Not INVESTIGATION
Diagnostic Consider CT with
Na = sodium
Ureteral obstruction diagnostic
contrast or antegrade PU/PD = polyuria/polydipsia
pyelogram if CT UP/C = urine protein:creatinine ratio
not available USG = urine specific gravity
AZOTEMIA & ACUTE KIDNEY INJURY
Gregory F. Grauer, DVM, MS, DACVIM (SAIM)
Sarah Guess, DVM, MS*
Kansas State University

FIRST-TIME DIAGNOSIS OF AZOTEMIA OR ACUTE-ONSET AZOTEMIA

INVESTIGATION
Assess USG

Hypersthenuria present (dogs, ≥1.030; cats, ≥1.035)?

YES NO

Rule out postrenal azotemia (from obstruction or leakage) with Probable renal azotemia
ultrasonography and positive contrast imaging, if necessary

INVESTIGATION
TREATMENT
Rule out CKD and acute-on-chronic
If prerenal dehydration/azotemia confirmed (eg, skin tenting, tacky
kidney disease (Table, page 200)
mucous membranes, elevated serum albumin concentration),
initiate fluid therapy to rehydrate patient (Table 2, page 200)

TREATMENT
Azotemia resolves? Initiate fluid therapy (if not already started)
to rehydrate patient (Table 2, page 200)

Azotemia resolves?
YES NO
AKI = acute kidney injury
BP = blood pressure
CKD = chronic kidney
disease
Volume-responsive TREATMENT
azotemia Reassess adequacy of YES NO
KCl = potassium volume replacement after
chloride 24 hours and 48 hours;
NaCl = sodium chloride continue fluid therapy
PCR = polymerase chain DIAGNOSIS Go to
reaction Prerenal azotemia AKI suspected
superimposed on inability
UP:C = urine protein:
creatinine ratio to concentrate urine (eg,
*Byline reflects author information on original publication. diabetes mellitus,

USG = urine specific gravity On publication of this collection, Sarah Guess’s current
affiliation is Washington State University.
hypoadrenocorticism,
hypercalcemia, pyometra)
 MANAGEMENT TREE h UROLOGY/NEPHROLOGY h PEER REVIEWED

 
 
 
 
AKI SUSPECTED

INVESTIGATION
Perform complete minimum database (ie, CBC, serum chemistry profile with electrolytes, urinalysis with sediment examination, BP)

DIAGNOSTICS INVESTIGATION
h L eptospirosis serum titers and urine Rule out CKD via imaging, history, and physical examination (Table 1, next page)
leptospirosis PCR
h Urine culture, UP:C

h Abdominal ultrasonography to find obstruction

caused by nephrolithiasis, evidence of
pyelonephritis, or abdominal effusion AKI confirmed
h Acutely elevated serum creatinine with isosthenuria (USG 1.008-1.012)

or minimally concentrated urine (USG 1.013-1.030/1.035)

TREATMENT
Initiate fluid therapy and diagnostics for
nonspecific AKI. Other therapy may be considered: NO Cause known? YES TREATMENT
h A ntihypertensive therapy (eg, amlodipine) Treat underlying condition
h A ntibiotics if pyelonephritis or leptospirosis is (eg, toxicity,
suspected; avoid aminoglycosides and other thromboembolism)
nephrotoxic antibiotics TREATMENT
h P ain medications; avoid NSAIDs Fluid therapy
h N utritional therapy (eg, nasoesophageal tube,
esophagostomy tube, total parenteral nutrition) if
patient not vomiting
h Treatment for uremic ulcers, if present
h A ntiemetics (eg, ondansetron, dolasetron)
STEP 1 STEP 6
Choose replacement fluids (eg, lactated h M onitor for signs of over-
Ringer’s solution, 0.9% NaCl [if hyperkalemic]) hydration (eg, increased
bronchovesicular sounds,
Anuria tachycardia, serous nasal
h U rine output 0 mL/kg/hr, despite adequate
discharge, chemosis,
rehydration weight gain, increased
h C autious use of volume expansion and/or diuretics STEP 2
central venous pressure)
because of no proven benefit Estimate dehydration % (eg, skin tenting, h R echeck creatinine and
h R eassess capillary refill time, central venous pressure);
electrolytes every 6-24
h P rognosis is poor, especially if no response to determine timeline for correction (eg, 4-6
hours
therapy and worsening azotemia hours; Table 2, next page)

Oliguria
h U rine output <0.5 mL/kg/hr after rehydration STEP 5
h C autious use of volume expansion and/or diuretics
STEP 3 Reassess
because of no proven benefit Determine if electrolyte supplementation is h I f weight loss occurs,

h R eassess
needed (eg, KCl ≤0.5 mEq/kg/hr) calculate kg lost × 1000 and
h P rognosis is guarded, unless converted to polyuria, add to current fluid rate;
for which prognosis improves with response to recheck weight in 4-6 hours
h B
 ase fluid therapy volume
rehydration
STEP 4 on urine output
Initiate fluid therapy
Polyuria h M easure body weight every 4-6 hours
h U rine output >1 mL/kg/hr h Q uantify urine output if possible
h B ase fluid rate on output and body weight gain or (Table 3, next page) Continues h
loss
h P rognosis is fair-to-good, especially with resolving

azotemia
MANAGEMENT TREE h UROLOGY/NEPHROLOGY h PEER REVIEWED

 
 
 
 
TABLE 1 TABLE 2

HISTORY, EXAMINATION, EXAMPLE OF FLUID VOLUME

& LABORATORY FINDINGS REQUIREMENTS FOR A 20-KG DOG
OF CKD & AKI WITH 8% DEHYDRATION & AKI

Findings CKD AKI Deficit needs (8% × 20 kg) = 1600 mL

over 6 hours (replace over 4-6 hours)
Weight loss, poor coat condition, + -
poor body condition Maintenance (60 mL/kg/day) = 1200 mL/day

Small, irregular kidneys (on radiography + - Continuing losses (dog vomits = 400 mL/day
or palpation) 4 times at 100 mL/episode)

Nonregenerative anemia + - Total = 3200 mL/day


(deficit replaced over 4-6
Acidosis/hyperkalemia - + hours if possible)

Oliguria/anuria - +
TABLE 3
Small, irregular kidneys with + -
hyperechoic cortices with or without HYPOTHETICAL COMPARISON
loss of corticomedullary junction (on OF TOTAL FLUID NEEDS IN NORMAL,
ultrasonography) OLIGURIC, & POLYURIC DOGS
Chronic history of polyuria/polydipsia or + -
stage 1 CKD
Normal Oliguric Polyuric
Urine sediment changes compatible with - +
tubular cell damage (eg, granular casts, Insensible 20 mL/kg/day 20 mL/kg/day 20 mL/kg/day
renal tubular epithelial cells) fluid needs

Relatively severe signs for magnitude of - + Sensible fluid 40 mL/kg/day 6 mL/kg/day 165 mL/kg/day
azotemia needs (urine
+ = presence more likely; - = presence less likely output)

Total 60 mL/kg/day 26 mL/kg/day 185 mL/kg/day

Suggested Reading
Cowgill LD, Langston C. Acute kidney insufficiency. In: Bartges J, Polzin D, eds. Nephrology and Urology of Small Animals. West Sussex, United Kingdom: Wiley-Blackwell;
2011:472-523.
Harison E, Langston C, Palma D, Lamb K. Acute azotemia as a predictor of mortality in dogs and cats. J Vet Intern Med. 2012;26(5):1093-1098.
Langston C. Acute uremia. In: Ettinger SJ, Feldman EC, eds. Textbook of Veterinary Internal Medicine. 7th ed. St. Louis, MO: Saunders Elsevier; 2010:1969-1985.
Ross L. Acute renal failure. In: Bonagura JD, Twedt DC, eds. Kirk’s Current Veterinary Therapy XIV. St. Louis, MO: Saunders Elsevier; 2009:879-882.
CANINE URINARY INCONTINENCE
India F. Lane, DVM, MS, EdD, DACVIM
University of Tennessee

INVOLUNTARY URINE LEAKAGE

Normal (ie, small, empty) bladder, low residual volume

INVESTIGATION INVESTIGATION
Abnormal physical or Normal physical and
neurologic examination neurologic examination

Juvenile dog Adult dog

DIFFERENTIALS
h Central CNS disease

h Canine cognitive

dysfunction syndrome INVESTIGATION Abnormal urinalysis Rule out Normal urinalysis
Full diagnostic prostatic
evaluation and imaging (eg,
neoplasia),
urethral
INVESTIGATION disease INVESTIGATION
DIFFERENTIAL DIFFERENTIAL Diagnostic workup; treat (male) Intermittent urine
Ectopic ureter or Congenital urethral PU/PD disorder or UTI first leakage while resting
other anomaly incompetence

TREATMENT Resolved Not resolved

Surgical or endourologic intervention

TREATMENT
Trial drug treatment with α1 sympathomimetic (male or female) or estrogenic agents (eg, estriol [female])

Resolved Incompletely resolved

INVESTIGATION
Good response Poor or no response Reassess dose, compliance;
consider imaging of abdom en

TREATMENT
Endoscopic bulking agent * DIAGNOSIS
Urethral incompetence Poor response
confirmed and resolved

Poor response
TREATMENT
Combination drug treatment with α1 sympathomimetic and estrogenic agents (female);
testosterone or combination sympathomimetic and testosterone agents (male)
TREATMENT
Artificial urethral sphincter placement

*Collagen products are not available in all markets; polydimethylsiloxane and dextranomer/hyaluronic acid are similarly effective agents. Poor response

 DIAGNOSTIC/MANAGEMENT TREE h UROLOGY/NEPHROLOGY h PEER REVIEWED

 
 
 
 
Urine leakage while active or after voiding Distended bladder, high residual volume (overflow incontinence)

Bladder overactivity Urine pooling (female)

INVESTIGATION INVESTIGATION
Normal neurologic Abnormal neurologic
examination examination

TREATMENT
Episioplasty
DIFFERENTIAL DIFFERENTIAL
Organic bladder Idiopathic INVESTIGATION DIAGNOSIS
disease (UTI, Identify or rule out partial Spinal or autonomic
uroliths, neoplasia) urinary obstruction disease

TREATMENT
Antimuscarinic trial

DIFFERENTIALS DIFFERENTIALS
Partial obstruction: Functional urine
h Prostatic disease retention:

(especially neoplasia) h Bladder atony
Poor or no response Resolved

h Urolith h Functional obstruction


h Urethral neoplasia h Detrusor-urethral


h Trauma or blood clot dyssynergia (DUD)

INVESTIGATION DIAGNOSIS
Reassess diagnosis Bladder overactivity confirmed
TREATMENT TREATMENT
Alleviate obstruction Catheterize or manually express
and reassess bladder to keep bladder small;
initiate pharmacologic treatment
TREATMENT and address underlying issues
Address bladder
disease or new
diagnosis

DIAGNOSTIC PLAN
h Signalment h Urinalysis and culture h Trial treatment



h History and/or observation h Confirmation of diagnosis h Assessment of response



Poor or no response Resolved h Pattern of incontinence h Management of refractory cases h Management of



h Physical and neurologic • Advanced diagnostics for juvenile concurrent disorders


DUD = detrusor-urethral dyssynergia
assessment or refractory cases (eg, imaging,
PU/PD = polyuria/polydipsia cystoscopy)
h Bladder palpation

 MANAGEMENT TREE h UROLOGY/NEPHROLOGY h PEER REVIEWED

 
 
 
 
FELINE CALCIUM OXALATE UROLITHIASIS
Sally C. Perea, DVM, MS, DACVN*
Davis Veterinary Medical Consulting
Davis, California

UROLITH REMOVAL/PASSAGE

INVESTIGATION
YES Calcium oxalate diagnosis confirmed by stone analysis? NO

YES Urinary tract infection present? NO Submit stone for analysis

TREATMENT NO Hypercalcemia present? YES

Perform urine culture and treat
with appropriate antibiotics

Underlying cause
NO of hypercalcemia YES
NO Renal function normal? YES identified?

TREATMENT TREATMENT
TREATMENT TREATMENT Implement dietary treatment Institute medical
Implement dietary treatment with Implement dietary treatment with for idiopathic hypercalcemia treatment to
therapeutic renal diet. Select a canned a therapeutic diet for prevention (diet change ± high fiber ± low address underlying
food and recommend adding water to diet of calcium oxalate uroliths calcium and low to moderate cause of
vitamin D); select a canned food hypercalcemia
± water added to the diet

INVESTIGATION INVESTIGATION
Recheck CBC, serum chemistry profile, Recheck urinalysis in 3-4 weeks to
and urinalysis in 3-4 weeks to monitor monitor appropriate response to INVESTIGATION
appropriate response to diet; continue diet; continue monitoring every Recheck serum calcium and urinalysis in 4-6 weeks to
monitoring every 3-4 months 3-4 months monitor appropriate response to treatment or diet;
continue monitoring every 3-4 months

Crystalluria or high urine

NO specific gravity (>1.025) YES Persistent
identified on recheck? hypercalcemia
NO and/or
YES
crystalluria?

TREATMENT TREATMENT
Continue with treatment plan Add additional water to food
(≈2 cups per 1 cup dry food or TREATMENT TREATMENT
≈1/4 cup per 1 cup canned food) Continue with Consider
treatment plan transition to
therapeutic diet
for the
prevention of
calcium oxalate
TREATMENT uroliths
*Byline reflects author information on original Consider adding potassium citrate or

publication. On publication of this collection, thiazide diuretic to treatment protocol
the author’s affiliation is with Royal Canin.
FLUOROQUINOLONE-RESISTANT ESCHERICHIA COLI
Patricia M. Dowling, DVM, MSc, DACVIM (Large Animal), DACVCP
University of Saskatchewan

FQ-RESISTANT ESCHERICHIA COLI

Isolated

h F Q-resistantisolates are frequently multidrug resistant

h S uggested alternative antimicrobials should be used only with favorable susceptibility test results
h T herapeutic concentrations may not be achievable with intracellular or deep tissue infections or in the
presence of biofilms

INVESTIGATION
Identify infection

DIAGNOSIS DIAGNOSIS DIAGNOSIS

UTI Systemic infection Dermal or wound infection

INVESTIGATION INVESTIGATION INVESTIGATION

Identify type Identify type Identify type

DIAGNOSIS
h P neumonia

DIAGNOSIS DIAGNOSIS h S epticemia DIAGNOSIS DIAGNOSIS

Cystitis h P yelonephritis Deep pyoderma Superficial bacterial
h Prostatitis or wound folliculitis or wound

TREATMENT
Oral TREATMENT TREATMENT
h N itrofurantoin Oral or parenteral Topical
• Human drug h P radofloxacin PO h S hampoo q24h with chlorhexidine, povidone–
h P radofloxacin • Extra-label in dogs iodine, acetic acid/boric acid, or benzoyl
• Extra-label in dogs h A mikacin IV, IM, SC peroxide
h Trimethoprim– • Unlikely to achieve therapeutic concentrations in h Local therapy with medical-grade honey,


sulfamethoxazole sequestered or deep tissue infections neomycin–bacitracin–polymyxin B, or silver
h C hloramphenicol • Because of nephrotoxicity, therapy limited to 5-7 days sulfadiazine

h F osfomycin • High-protein diet can reduce risk for renal damage 1 h Nano silver-impregnated dressing


• Human drug h F osfomycin PO
• Human drug
h M eropenem IV, SC
• Human drug
h C efoxitin or cefotetan IV, IM, SC
• Human drug
h A mpicillin–sulbactam IV
• Human drug FQ = fluoroquinolone
 DIAGNOSTIC/MANAGEMENT TREE h UROLOGY/NEPHROLOGY h PEER REVIEWED

 
 
 
 
AUTHOR INSIGHT
h Some FQ-resistant isolates are susceptible to

third-generation FQ pradofloxacin.
h Most are susceptible to nitrofurantoin, amikacin,

fosfomycin, and meropenem.

Reference
1. Grauer GF, Greco DS, Behrend EN, et al. Effects of dietary protein

conditioning on gentamicin-induced nephrotoxicosis in healthy
male dogs. Am J Vet Res. 1994;55(1):90-97.

Suggested Reading
Hubka P, Boothe DM. In vitro susceptibility of canine and feline
Escherichia coli to fosfomycin. Vet Microbiol. 2011;149(1-2):277-282.
Liu X, Boothe DM, Jin Y, Thungrat K. In vitro potency and efficacy
favor later generation fluoroquinolones for treatment of canine
and feline Escherichia coli uropathogens in the United States.
World J Microbiol Biotechnol. 2013;29(2):347-354.
Maaland M, Guardabassi L. In vitro antimicrobial activity of
nitrofurantoin against Escherichia coli and Staphylococcus
pseudintermedius isolated from dogs and cats. Vet Microbiol.
2011;151(3-4):396-399.
Shaheen BW, Boothe DM, Oyarzabal OA, Smaha T. Antimicrobial
resistance profiles and clonal relatedness of canine and feline
Escherichia coli pathogens expressing multidrug resistance in the
United States. J Vet Intern Med. 2010;24(2):323-330.
HEMATURIA IN DOGS
Gideon Daniel, DVM, DACVIM (SAIM)
Friendship Hospital for Animals
Washington, DC

Mary Anna Labato, DVM, DACVIM (SAIM)

Cummings School of Veterinary Medicine at Tufts University

HEMATURIA SIGNS OBSERVED

Differentiate hematuria vs pigmenturia

Microscopic only* Microscopic and macroscopic*

Rule out iatrogenic Recommend further diagnostic testing, Petechiae,

hematuria secondary particularly if recurrent or clinical signs present ecchymoses, bruising
to cystocentesis (eg, pollakiuria, dysuria, stranguria)

Recheck urinalysis with Lower urinary tract localization (pollakiuria, dysuria, DIAGNOSIS
free-catch voided sample stranguria; timing of hematuria: initial/beginning of voiding †) Primary hemostatic disorder
(normal, <5 RBC/HPF)

Hematuria resolved?
Normal urogenital examination Abnormal urogenital examination

YES NO INVESTIGATION DIAGNOSI S

CBC, serum chemistry profile, urine Prostatic disease, transmissible venereal
culture, abdominal radiography, tumor, estrus, vaginitis, trauma
coagulation panel, ultrasonography

DIAGNOSIS DIAGNOSIS Abnormalities on radiographs or No identifiable cause

Infectious disease Cystourethrolithiasis ultrasounds (eg, prostatomegaly,
(bacterial, fungal, or lymphadenopathy, renomegaly, masses)
parasitic infection)

*Macroscopic hematuria occurs when the quantity of blood


TREATMENT TREATMENT in urine is visible to the naked eye (eg, pink, red, dark brown
in color; may contain blood clots). Microscopic hematuria is
Antibiotics based Cystoscopy, characterized by small numbers of RBCs in urine and is only
on culture and susceptibility cystotomy, voiding visible during microscopic examination of urine sediment.4
results, antifungals or urohydropropulsion, †
The timing of hematuria is not always diagnostically accurate.
antiparasitics based on percutaneous ‡
Renal hematuria is often subclinical. MSM = methylsulfonylmethane
urinalysis results cystolithotomy
 DIAGNOSTIC/MANAGEMENT TREE h UROLOGY/NEPHROLOGY h PEER REVIEWED

 
 
 
 
Upper urinary tract localization (polyuria, polydipsia; timing of
hematuria: end or total [ie, at the end of or throughout urination]†)‡

INVESTIGATION
Abdominal ultrasonography (+CBC, serum chemistry profile, urine culture if not already performed)

No identifiable cause

DIAGNOSIS
Neoplasia Cystoscopy
DIAGNOSIS
Benign renal hematuria

TREATMENT
Surgical resection, TREATMENT
chemotherapy, radiation therapy Sclerotherapy3

DIAGNOSIS
Inflammatory disease (eg, polypoid cystitis)
References
1. Runge JJ, Berent AC, Mayhew PD,
Weisse C. Transvesicular percutaneous
TREATMENT cystolithotomy for the retrieval of cystic
NSAIDs, MSM2 and urethral calculi in dogs and cats: 27
DIAGNOSIS cases (2006-2008). J Am Vet Med Assoc.
Radiolucent stones 2011;239(3):344-349.
2. Martinez I, Mattoon JS, Eaton KA, Chew
DJ, DiBartola SP. Polypoid cystitis in
17 dogs (1978-2001). J Vet Intern Med.
2003;17(4):499-509.
TREATMENT 3. Berent AC, Weisse CW, Branter E, et
Cystoscopy, cystotomy, voiding al. Endoscopic-guided sclerotherapy
urohydropropulsion, percutaneous cystolithotomy1 for renal-sparing treatment of
idiopathic renal hematuria in dogs: 6
DIAGNOSIS cases (2010-2012). J Am Vet Med Assoc.
2013;242(11):1556-1563.
Prostatic disease
4. Forrester SD. Diagnostic approach to
hematuria in dogs and cats. Vet Clin North
Am Small Anim Pract. 2004;34(4):849-866.

Culture, prostatic massage, cytology/biopsy

Suggested Reading
Laflamme DP, Hannah SS. Nutritional
genomics. In: Ettinger SJ, Feldman EC,
eds. Textbook of Veterinary Internal
TREATMENT Medicine; vol 1. 7th ed. St. Louis, MO:
Antibiotics, NSAIDs, castration ± prostatectomy, chemotherapy Saunders Elsevier; 2010:163-166.
ISOLATION OF METHICILLIN-RESISTANT
STAPHYLOCOCCUS SPP IN CANINE URINE CULTURE
J. Scott Weese, DVM, DVSc, DACVIM
University of Guelph

MRS SPP IN URINE CULTURE*

Isolated

INVESTIGATION
Coagulase positive (eg, Staphylococcus aureus, S pseudintermedius, S schleiferi subsp coagulans)

INVESTIGATION
Intact male?

YES NO

INVESTIGATION INVESTIGATION
Investigate potential Clinical signs of lower UTI (eg, dysuria, pollakiuria,
prostatic disease stranguria, hematuria, inappropriate urination)?

YES NO INVESTIGATION
Cytologic evidence of infection (eg, pyuria, hematuria)? †

Teatment indicated
(see Treatment)
YES NO
Suggested Reading
Nicolle LE, Bradley S, Colgan R, Rice JC, Schaeffer A, Hooton TM, Infectious Diseases
Society of America, American Society of Nephrology, American Geriatric Society.
Infectious Diseases Society of America guidelines for the diagnosis and treatment of
INVESTIGATION Likely contaminant
asymptomatic bacteriuria in adults. Clin Infect Dis. 2005;40(5):643-654. Treatment may be indicated (see or subclinical
Treatment) bacteriuria
Weese JS, Blondeau J, Boothe D, et al. Antimicrobial use guidelines for treatment of
h Consider other possible causes of h Treatment not
urinary tract disease in dogs and cats: antimicrobial guidelines working group of the


International Society for Companion Animal Infectious Diseases. Vet Med Int. 2011. pyuria indicated
doi:10.4061/2011/263768. h Consider repeat culture or

Weese JS, van Duijkeren E. Methicillin-resistant Staphylococcus aureus and Staphylococ- clinical monitoring
cus pseudintermedius in veterinary medicine. Vet Microbiol. 2010;140(3-4):418-429.
 MANAGEMENT TREE h UROLOGY/NEPHROLOGY h PEER REVIEWED

 
 
 
 
TREATMENT
MRS spp are inherently resistant to all
β-lactams (eg, penicillins, cephalo-
sporins, carbapenems); response of
MRS spp to fluoroquinolones is
INVESTIGATION unpredictable.
Coagulase negative (eg, S haemolyticus, S epidermidis)
h Possible treatment options include

nitrofurantoin, fosfomycin (dogs
only), doxycycline, minocycline,
INVESTIGATION trimethoprim-sulfonamide,
Intact male? aminoglycosides.
h Consider and address potential

underlying causes (eg, uroliths,
endocrinopathy, anatomical
defects), especially if recurrent
YES NO disease.

Acute, Sporadic UTI

h Treat for 3-7 days.

INVESTIGATION INVESTIGATION
Investigate potential Clinical signs of lower UTI (eg, dysuria, pollakiuria, Recurrent or Relapsing UTI
prostatic disease stranguria, hematuria, inappropriate urination)? h Treat for 3-28 days.

• Shorter durations (eg, 3-5 days)

may be appropriate for acute,
recurring infections.
• Longer durations (eg, 14-28 days)
YES NO

may be indicated for cases in
which elimination of the bacteria
may be difficult (eg, chronic infec-
INVESTIGATION Likely contaminant or tion with significant bladder wall
Cytologic evidence of infection (eg, pyuria, hematuria)? † subclinical bacteriuria invasion, bladder mass, debris in
h Treatment not indicated
bladder).

*Cystocentesis should be used when possible.
YES NO

If culture is from a free-catch sample, repeat
with cystocentesis to rule out contamination.
†This can also occur with noninfectious

etiologies.

INVESTIGATION INVESTIGATION
MRS = methicillin-resistant Staphylococcus
Consider repeat culture Investigate other causes of clinical signs
h Treat if repeat culture is not an option (see Treatment)

POLYURIA & POLYDIPSIA IN DOGS & CATS
Gregory F. Grauer, DVM, MS, DACVIM (SAIM)
Kansas State University

POLYDIPSIA POLYURIA

Increased water intake (>80-100 mL/kg q24h) Increased urine production (>50 mL/kg q24h)

h O smotic factors: increased plasma osmolality

h Nonosmotic factors: hypotension, hyperthermia, hypovolemia, pain, drugs

INVESTIGATION
Assess signalment, history, examination findings, and MDB
(CBC, serum chemistry profile, complete urinalysis, urine culture)

USG <1.025 (dogs) or <1.040 (cats) can suggest

PU/PD (see Urine Concentration Levels)

Abnormalities found?

YES NO
(most common) (least common)

INVESTIGATION Quantitate water

Pursue appropriate diagnostics, including: consumption (if necessary)
h T horacic, abdominal, renal imaging
h T hyroid, adrenal function testing
h B ile acids
h L eptospira titers
h H yperadrenocorticism, Cushing’s disease testing Rule out otherwise silent
Cushing’s disease

DIAGNOSIS Hyperadrenocorticism
TREATMENT Hyperadrenocorticism ruled out
Treat as necessary

Rule out CKD:

Stage 1 or early stage 2

CKD confirmed Evaluate further: renal imaging, UP:C, blood pressure, GFR
 DIAGNOSTIC TREE h UROLOGY/NEPHROLOGY h PEER REVIEWED

 
 
 
 
CKD ruled out

Differentiate primary PU/PD from secondary PU/PD with plasma osmolality

URINE CONCENTRATION LEVELS
Early-morning urine is best to assess
concentrating ability.
Perform gradual water deprivation test cautiously*—cut water consumption by
5%-10% q48h until patient receives 80-90 mL/kg q24h for 10-14 days h Hyposthenuria = <1.008

h Isosthenuria = 1.008-1.012

h Minimally concentrated = 1.012-1.029 (dogs),

Hypersthenuric urine produced?
1.012-1.039 (cats)

YES NO h Hypersthenuria = ≥1.030 (dogs), ≥1.040 (cats)

DIFFERENTIAL DIAGNOSIS
Primary polydipsia Primary polyuria

DIFFERENTIAL INVESTIGATION
Includes: Evaluate response to exogenous ADH while there is a stimulus to concentrate urine
h P sychogenic/
behavioral
polydipsia
h P ortosystemic
shunt/hepatic Hypersthenuric urine produced?
encephalopathy
h H yperthyroidism
h G I tract disease
YES NO

DIAGNOSIS DIFFERENTIAL
Pituitary/central Nephrogenic diabetes insipidus
diabetes insipidus h P rimary (rarely, congenital)
h S econdary (more commonly, acquired)

ADH = antidiuretic hormone

DIFFERENTIAL
AKI = acute kidney injury For older patients, DIFFERENTIAL
consider acquired Secondary or acquired causes include:
CKD = chronic kidney disease disease (eg, neoplasia, h A KI, CKD, pyelonephritis
inflammatory h H yperadrenocorticism
GFR = glomerular filtration rate
or infectious disease, h H ypoadrenocorticism
MDB = minimum database head trauma) h P yometra
h H ypercalcemia, paraneoplastic syndrome
PU/PD = polyuria/polydipsia h H ypokalemia, potassium depletion
UP:C = urine protein:creatinine ratio h Drugs (eg, diuretics, anticonvulsants, corticosteroids)
h Liver disease
USG = urine specific gravity *Test can be harmful, as it must create a stimulus to h Renal medullary solute washout

concentrate urine (ie, mild dehydration) h Diabetes mellitus
h High-salt diet
PROTEINURIA
Jonathan Dear, DVM, DACVIM (SAIM)
University of California, Davis

PROTEINURIA

USG >1.030 or protein ≤25 mg/dL USG <1.030 or protein >25 mg/dL

Likely clinically insignificant Active sediment (WBC, RBC, bacteria)?

NO YES

INVESTIGATION INVESTIGATION
Analyze UP:C Perform bacterial culture and susceptibility testing

Abnormal (≥0.5 dog, ≥0.4 cat) Normal (<0.5 dog, <0.4 cat) Positive Negative

INVESTIGATION Monitor TREATMENT

Perform serum chemistry panel Treat according to
results of culture and
susceptibility testing

Azotemic?

NO YES

INVESTIGATION INVESTIGATION
Recheck in 2 weeks Evaluate systemic BP

Elevated Normal

TREATMENT INVESTIGATION
Control BP (amlodipine, ACE Perform infectious disease testing
inhibitor therapy) and recheck UP:C

TREATMENT Positive Negative

Address infectious disease and recheck UP:C
 DIAGNOSTIC/MANAGEMENT TREE h UROLOGY/NEPHROLOGY h PEER REVIEWED

 
 
 
 
INVESTIGATION
Pursue diagnostic imaging; investigate for chronic
inflammatory or infectious disease or neoplasia

DIFFERENTIAL DIFFERENTIAL DIFFERENTIAL DIFFERENTIAL DIFFERENTIAL

Urinary calculi Genitourinary Bladder polyp and/or Pyelectasis Normal or sonographic evidence
neoplasia sonographic evidence of glomerular disease
of cystitis

TREATMENT TREATMENT
Remove and analyze INVESTIGATION Culture urine TREATMENT
calculi; consider Consider bladder INVESTIGATION (if not already Initiate diet therapy (low protein), omega-3
preventive therapy tumor antigen testing, 1 Perform cystoscopy for done) and treat supplementation, and ACE inhibitor therapy
diagnostic catheter- biopsy and culture according to results
ization, cystoscopic of susceptibility
biopsy, or FNA and testing
cytology
INVESTIGATION
Recheck UP:C (pooled sample; goal,
<0.5 dog, <0.4 cat, or 50% reduction)

Responding to treatment Persistently elevated

INVESTIGATION TREATMENT
Recheck UP:C and kidney Increase ACE inhibitor therapy
panel in 2-4 weeks

INVESTIGATION
Recheck
BP = blood pressure
FNA = fine-needle aspiration Reference
1. Henry CJ, Tyler JW, McEntee MC, et al. Evaluation of
UP:C = urine protein:creatinine ratio

a bladder tumor antigen test as a screening test for
USG = urine specific gravity transitional cell carcinoma of the lower urinary tract in INVESTIGATION
dogs. Am J Vet Res. 2003;64(8):1017-1020. Kidney biopsy; submit to pathology service
RECURRENT URINARY TRACT INFECTION
Gregory F. Grauer, DVM, MS, DACVIM (SAIM)
Kansas State University

CLINICAL SIGNS OF UTI: POLLAKIURIA,

STRANGURIA/DYSURIA, PERIURIA, HEMATURIA

Determine diagnosis on the basis of history and urine sediment

INVESTIGATION
Confirm infection (rule out contamination) by obtaining urine sample via cystocentesis (ideal)
or by quantitatively culturing urine obtained via catheter from a male dog

INVESTIGATION
Rule out predisposing causes (eg, perivulvar dermatitis/excessive licking or urine leakage,
vulval involution, vaginal strictures, urethral thickening, prior urethrostomy, cystic calculi)

First presentation: select either sediment examination or urine culture Repeat presentation

INVESTIGATION INVESTIGATION
Air-dried urine sediment examination via modified Wright’s stain (Diff-Quik) Urine culture: quantitative if voided/catheter sample

Bacteria No bacteria Negative Positive

TREATMENT INVESTIGATION
Antimicrobial treatment based on sediment examination Evaluate patient for sterile causes of urinary
(eg, trimethoprim–sulfamethoxazole for gram-negative rods at 15 mg/kg tract inflammation (eg, neoplasia, polyps),
PO q12h,† amoxicillin for gram-positive cocci at 11-15 mg/kg PO q8h for 7-10 days) evidence of renal hematuria, or behavioral
problems; reculture with fresh urine sample if
culture result is in question

Resolution Recurrence

†Sensitivity of gram-negative rods is known to be unpredictable, as a large proportion of them will be Escherichia coli. If gram-negative

rods are seen on urine sediment, culture and susceptibility testing is advised.
‡No studies have evaluated efficacy and adverse effects of these protocols in dogs. To avoid creating resistant infections, this

administration should be reserved for dogs with reinfections when predisposing causes cannot be corrected. Treatment is initiated after
standard dose of antimicrobial therapy has been successful. Other considerations for antimicrobial selection should include adverse
events and culture and susceptibility test results. Protocols include fluoroquinolones, cephalosporins, or ß-lactam antimicrobials. This
is typically recommended for ≥6 months and urinalysis/culture should be performed every 4-8 weeks. If UTI occurs during treatment,
treat as a complicated UTI. Prophylactic, low-dose therapy can be restarted after reinfection resolves.1
 DIAGNOSTIC/MANAGEMENT TREE h UROLOGY/NEPHROLOGY h PEER REVIEWED

 
 
 
 
TREATMENT
Treatment based on
antimicrobial sensitivity

INVESTIGATION
Examine sediment in 3-5 days to
assess effectiveness of antimicrobial Recurrence
agent; sediment should contain no
(or reduced) WBCs; culture if
sediment examination indicates
continued or worsened inflammation
INVESTIGATION
Rule out predisposing causes via local testing (eg,
imaging of thickened bladder wall, urachal remnants,
polyps, cystic calculi) and/or systemic testing (eg,
INVESTIGATION CBC, serum chemistry profile); causes may include
Examine sediment 3-4 hyperthyroidism, exogenous steroid treatment,
days before discontinuing hyperadrenocorticism, diabetes mellitus, or CKD
treatment

TREATMENT
INVESTIGATION Long-term antimicrobial treatment
Repeat urinalysis and based on antimicrobial sensitivity
culture 10-14 days after
treatment cessation

Resolution Resolution Recurrence

TREATMENT
Treatment to help prevent recurrent UTI Urine culture and antimicrobial
treatment to resolve clinical signs

TREATMENT TREATMENT TREATMENT

Low-dose prophylactic antimicrobial treatment: Cranberry extract § Methenamine
involves one-half to one-third therapeutic daily (urinary antiseptic)||
dose administered immediately after last
nighttime void to inhibit/minimize uropathogenic
growth, decreasing bacterial adhesion, and
colonization of the uroepithelium. ‡ CKD = chronic kidney disease

§Canine studies evaluating efficacy of cranberry extract are limited; however, some in vitro data show promising

results. One study demonstrated that E coli in urine from dogs receiving cranberry extract PO had decreased the
ability to adhere to Madin-Darby canine kidney cells.2 Based on this, PO administration of cranberry extract may
help reduce E coli reinfections in patients with compromised host defense mechanisms. It may be beneficial to use
products evaluated for canine use.
||The most commonly used urinary antiseptics include methenamine, which may be considered in patients with recurrent Continues h

infection or potentially untreatable/unresolved immunity breaches. For this to be effective, urine must be acidic.
DIAGNOSTIC/MANAGEMENT TREE h UROLOGY/NEPHROLOGY h PEER REVIEWED

 
 
 
 
REASONS FOR POOR THERAPEUTIC RESPONSE
h Use of ineffective drugs or insufficient therapy duration: Relapse

h Failure of owner to comply with prescription: Relapse

h GI disease, concurrent intake of food and drug (decreased

absorption), or impaired renal concentrating ability (decreased
antibiotic concentrations in urine): Relapse
h Impaired drug action, either because bacteria are not multiplying or

because they are in an inaccessible area (eg, prostate, neoplasia,
uroliths): Relapse
For penetration into prostatic tissue, antimicrobial agents should be
lipid soluble, not be highly protein-bound, and ionize at the tissue’s pH.
Fluoroquinolones, trimethoprim–sulfamethoxazole, and chloramphenicol
can achieve prostate gland penetration.
h Failure to recognize and eliminate predisposing causes: Reinfection

h Presence of mixed bacterial infection in which antimicrobial therapy

eradicates only one pathogen: Relapse
h Iatrogenic reinfection via catheterization: Reinfection

h Development of drug resistance in bacteria: Relapse

References
1. Seguin MA, Vaden SL, Altier C, et al. Persistent urinary tract infections and reinfections in

100 dogs (1989-1999). J Vet Intern Med. 2003;17:622-631.
2. Smee N, Grauer GF, Schermerhorn T. Investigations into the effect of cranberry extract on

bacterial adhesion to canine uroepithelial cells. J Vet Intern Med. 2011;25:722.
 MANAGEMENT TREE h ANESTHESIA h PEER REVIEWED

 
 
 
 
ANESTHETIC HYPOTENSION
Maria Angeles Jimenez Lozano, DVM, CertVA, DECVAA, MRCVS
North Downs Specialist Referrals
Bletchingley, United Kingdom

ANESTHETIC HYPOTENSION
(MABP ≤60 mm Hg)

DIAGNOSIS
Low SVR (ie, too much vasodilation)

DIFFERENTIAL DIFFERENTIAL
Sympathetic blockade Vasodilation from drug (eg, acepromazine,
(epidural/spinal anesthetics) propofol, alfaxalone, inhalant)

TREATMENT TREATMENT
Reduce inhalants1-5; use vasopressors to treat vasodilation, Reduce anesthetic doses, balance anesthetic technique
give fluids for relative hypovolemia correction

DIFFERENTIAL
Patient-related conditions (eg, sepsis,
SIRS, toxins, histamine release)

TREATMENT
Use vasopressors to treat vasodilation, fluids to treat relative
hypovolemia, antihistaminics or steroids to treat histamine release Continues h

References
6. Short CE, Bufalari A. Propofol anaesthesia. Vet Clin
PERTINENT CALCULATIONS 1. Mutoh T, Nishimura R, Kim H, Matsunaga S, Sasaki N.


Cardiopulmonary effects of sevoflurane, compared North Am Small Anim Pract. 1999;29(3):747-778.
with halothane, enflurane and isoflurane, in dogs. 7. Patrick MR, Blair IJ, Feneck RO, Sebel PS. A compari-
Blood pressure = CO × SVR Am J Vet Res. 1997;58(8):885.

h son of the haemodynamic effects of propofol
2. Hikasa Y, Ohe N, Takase K, Ogasawara S. Cardio- (‘Diprivan’) and thiopentone in patients with coro-

h CO = SV × HR pulmonary effects of sevoflurane in cats: compari- nary artery disease. Postgrad Med J. 1985;61(Suppl
son with isoflurane, halothane, and enflurane. 3):23-27.
Res Vet Sci. 1997;63(3):205. 8. Mulier JP, Wouters PF, Van Aken H, Vermaut G, Van-
CO = cardiac output

3. Hikasa Y, Kanwanabe H, Takase K, Ogasawara S. dermeersch E. Cardiodynamic effects of propofol in

HR = heart rate Comparison of sevoflurane, isoflurane, and halo- comparison with thiopental: assessment with a
thane anesthesia in spontaneously breathing cats. transesophageal echocardiographic approach.
MABP = mean arterial blood pressure Vet Surg. 1996;25(3):234-243. Anaesth Analg. 1991;72(1):28-35.
SIRS = systemic inflammatory response syndrome 4. Ebert TJ, Harkin CP, Muzi M. Cardiovascular 9. Ebert TJ, Muzi M, Berens R, Goff D, Kamppine JP.


responses to sevoflurane: a review. Anaesth Analg. Sympathetic responses to induction of anesthesia in
SV = stroke volume 1995;81(6 Suppl):S11-S22. humans with propofol or etomidate. Anesthesiology.
5. Eger EI 2nd. The pharmacology of isoflurane. 1992;76(5):725-733.
SVR = systemic vascular resistance

Br J Anaesth. 1984;56 (Suppl 1):71S-99S.
 ANESTHETIC HYPOTENSION DIAGNOSIS
(MABP ≤60 mm Hg) Low cardiac output

DIAGNOSIS DIAGNOSIS DIAGNOSIS

Low contractility High afterload Low preload (low venous return,
low end-diastolic volume)

DIFFERENTIAL TREATMENT
Anesthetic drugs, 6-8 inhalants, Reduce vasopressors
injectables (eg, halothane, thiopental, and α 2 agents
α 2 agonists, propofol, ketamine in
catecholamine-depleted patients)

TREATMENT TREATMENT
Use positive inotropes (eg, Avoid strong cardiovascular
ephedrine, dobutamine, suppressant drugs, reduce anesthetic
dopamine, epinephrine) doses, balance anesthetic technique

DIFFERENTIAL DIFFERENTIAL DIFFERENTIAL

Increased intrathoracic Low circulatory volume, relative Patient-related conditions
pressure, IPPV, pneumothorax, hypovolemia with vasodilation, absolute (eg, aorta caval compression)
intrathoracic mass hypovolemia with dehydration, GI losses,
crystalloid, and/or blood loss

DIFFERENTIAL
INVESTIGATION Dorsal recumbency for obese/
Spontaneous breathing, low-tidal TREATMENT pregnant/ascitic/abdominal
volume IPPV, permissive Vasopressors (eg, phenylephrine, mass patients; iatrogenic,
hypercapnia,* no PEEP vasopressin, norepinephrine) to treat surgical manipulation
vasodilation; crystalloids, colloids,
blood products

TREATMENT TREATMENT
Thoracocentesis if fluid Tilt operation table, treat mass/
is present, remove mass pressure, add bolus of
crystalloids

AV = atrioventricular
*Permissive hypercapnia is a
BOAS = brachycephalic obstructive airway syndrome
ventilation strategy in which
IPPV = intermittent positive pressure ventilation oxygenation is prioritized over
expired carbon dioxide. Higher than
MABP = mean arterial blood pressure normal carbon dioxide levels are
PEEP = positive end-expiratory pressure allowed because of low ventilation
that preserves the lungs.
 MANAGEMENT TREE h ANESTHESIA h PEER REVIEWED

 
 
 
 
DIAGNOSIS
Inadequate heart rate and rhythm

DIAGNOSIS DIAGNOSIS DIAGNOSIS

Bradycardia Tachycardia Arrhythmias

INVESTIGATION INVESTIGATION
Inadequate ventricular filling if No synchrony on atrial or
heart rate is too high ventricular contraction

DIFFERENTIAL DIFFERENTIAL DIFFERENTIAL

Anesthetic drugs (eg, Patient-related condition (eg, AV blocks, atrial
ketamine, alfaxalone, hypovolemia, hyperthermia, fibrillation, ventricular
sympathomimetic drugs) hypoxemia, hypercapnia, pain, arrhythmias
cardiac disease)

TREATMENT TREATMENT TREATMENT

Stop/decrease Replace volume; cool patient; administer IPPV Treat arrhythmia
drugs, avoid use and 100% oxygen, analgesia; if all normal but
cardiac disease, use antiarrhythmics

DIFFERENTIAL DIFFERENTIAL DIFFERENTIAL

Increased vagal tone (GI stimulation, Anesthetic drugs (propofol, 6,8,9 Patient-related condition
cervical surgeries, respiratory disease, opioids, α2 agonists) (eg, hypothermia, hyperkalemia
IPPV, oculocardiac reflex, breed end-stage metabolic disease, cardiac
predisposition [eg, BOAS]) disease, extreme hypoxemia)

TREATMENT TREATMENT TREATMENT

Stop vagal stimulus; use Avoid strong cardiovascular suppressant Warm patient, treat
anticholinergics (eg, atropine, drugs, lower doses, or reverse drugs; hyperkalemia, use
glycopyrrolate) use anticholinergics (eg, atropine, anticholinergics,
glycopyrrolate) or sympathomimetics improve oxygenation
if anticholinergics are ineffective
SEPARATION ANXIETY IN DOGS
Debra F. Horwitz, DVM, DACVB
Veterinary Behavior Consultations
St. Louis, Missouri

OWNER-ABSENT PROBLEM BEHAVIOR

Other causes ruled out by investigation and/or video?
(EG, ELIMINATION, VOCALIZATION, DESTRUCTION)

YES NO

Evidence of attachment and Anxiety at departure cues?

following behaviors? NO NO

YES YES

TREATMENT TREATMENT TREATMENT

h P redictable interactions Uncouple cues from departure: Act as if h L eave toy stuffed with delectable food*
h C ue–response relationship to foster departing without doing so; these should last h B e calm: All departures and returns must be
reliable and positive interactions using only 3-5 seconds to avoid creating anxiety. toned down; want to leave a calm dog
food rewards Goal: Dog no longer responds to cues with h Use dog appeasing pheromone diffuser
h S
 it/stay when owner leaves room to anxiety. Dog is calm before beginning h A dd medication after routine blood
decrease following behavior treatment each time. analysis; use branded (vs generic)
h G  ive attention only when dog is calm Increased anxiety is possible in some animals veterinary-labeled medications when
to decrease attention seeking with multiple sessions in the same day. If available (eg, fluoxetine, clomipramine)‡
h T  each dog to settle or relax in safe area noted, owner should consult their veterinarian.

INVESTIGATION NO Reevaluate
Recheck
Diminished following behaviors?
No anxious responses to
departure cues?
BEHAVIOR MODIFICATION TREATMENT PLAN
Begin planned training departures h Depart and remain away only for

YES h Establish safety signal† (eg, music, TV, air predetermined period of time (usually 1-2

freshener, novel location) minutes)
h Determine minimum departure time: h Return, ignore dog except to matter-of-factly


Generally very short (1-3 minutes), perhaps walk for elimination
TREATMENT
Continue behavior only walk to the door h Dog must be calm before repeating. Assess

modification treatment plan h Departure training must simulate real anxiety level of the dog; it is often not practical

departures: If owner always uses a car, train up or helpful to do more than 1-3 training
to use cars for longer departure simulations. departures per 24 hours
h Place dog in safe area h Never use safety signal on regular

h Deploy safety signal† departures with unregulated length
of absences
 DIAGNOSTIC/MANAGEMENT TREE h BEHAVIOR h PEER REVIEWED

 
 
 
 
INVESTIGATION
h Elimination:House-training issues often occur when owner is present If supportive of separation anxiety,
or absent. Verify outdoor elimination and ask about storm or noise return to YES.
phobias/reaction to outside stimuli (eg, deliveries).
h Vocalization: Record audio or video to identify pitch and frequency to
differentiate anxiety from territorial response or noise/storm reaction.
h Destruction: If animal is destructive both alone and with the owner at
home, record a video to determine if anxiety is present and there are Not supportive
any storm/noise phobias or territorial responses. Determine how soon of separation anxiety
after owner departure destruction occurs.

DIAGNOSIS
Other anxiety condition, sensitivity,
or medical condition causing
anxiety or pain

INVESTIGATION TREATMENT
Use medication and behavior modification Begin to wean off medication, commonly
until behavior stablizes and signs 2-3 months of calm behavior decrease 25% a week depending on
of anxiety at departure and during owner when dog is alone and there severity of signs. If anxiety reappears,
absence have diminished or ceased. are no other anxieties remain at lower dose to see if dog
If anxiety has not diminished after 4-6 stabilizes; if not, return to higher dose and
weeks, review treatment and potential maintain for at least 4 weeks. Assess
confounding factors. remaining anxiety via video.

*Must also be provided at other times to avoid toy becoming departure cue.

†A distinctive action owner takes just prior to training departures (eg, putting dog in novel location; out of

confinement), employed to help the dog associate these departures with quick returns and no anxiety.
‡The decision to use drugs should be based on a combination of severity of problem and owner’s tolerance

of behaviors. In some cases, medication should be prescribed on the first visit. Additional medications
(eg, benzodiazepines) prior to departure may be necessary for some animals in addition to daily medication
to help with panic and extreme anxiety associated with departure.

cliniciansbrief.com 11
 
 DIAGNOSTIC/MANAGEMENT TREE  h  FORENSIC MEDICINE   h  PEER REVIEWED

ADDRESSING ANIMAL SEXUAL ABUSE

Nancy Bradley, DVM, MNM*
Arizona Humane Society
Phoenix, Arizona

Karyn Rasile, RN, BSN, MAEd, CFN, SANE-A, AFN-BC

Scottsdale Healthcare
Scottsdale, Arizona

SUSPECTED OR ACTUAL SEXUAL ASSAULT

Veterinarian able and willing to perform

the medical-forensic examination?

NO YES

TREATMENT
Place animal in clean kennel with
removable bedding and INVESTIGATION INVESTIGATION
Elizabethan collar; post NPO <120 hours since injury >120 hours since injury
placard on cage

INVESTIGATION
h 
N otify law enforcement and INVESTIGATION INVESTIGATION
forensic professionals; suggest h 
F or owned animal, obtain client For stray animal,
evidence collection consent for medical and/or forensic obtain law
h 
A lert law enforcement if examination enforcement seizure
perpetrator is known or h 
If the owner does not consent, the police paperwork
suspected may seek to obtain a search warrant
h 
If the examination is being authorized,
document under whose authority

Release animal to law

enforcement or humane society
INVESTIGATION
Check entire body with black light or alternative light source

INVESTIGATION
Swab (wet) any fluorescent areas

INVESTIGATION
Perform head-to-tail examination:
h S wab genitals and oral cavity (do not take
rectal temperature before obtaining swabs)
h M easure and document all injuries
h C ollect blood and urine, and take radiographs
h Document findings

*Byline reflects author information on original publication.

On publication of this collection, Nancy Bradley-Siemens’
current affiliation is Midwestern University in Glendale, Arizona.
Report to law enforcement
EMESIS INDUCTION
Kendon Kuo, DVM, MS, DACVECC
Katherine Gerken, DVM, MS, DACVECC
Auburn University

PATIENT EXHIBITS DIETARY INDISCRETION, OR EVIDENCE OF DIETARY INDISCRETION

(EG, CHEWED PACKAGING, MISSING ITEMS, FOOD COLORING ON FACE) IS FOUND

Hydrocarbon or petroleum distillates (eg, gasoline, kerosene, motor oil, transmission fluid, tiki torch oil) used or suspected?

YES NO

High risk for aspiration; do not induce emesis Does suspected or known ingested substance have sharp edges?

TREATMENT YES NO
h 
C onsider endoscopic or surgical retrieval
h 
C an consider feeding a bulk high-fiber diet

Is substance corrosive or caustic (eg, zinc phosphide)?

TREATMENT
Do
h  not induce emesis, as it may worsen
the caustic effects of these substances
h 
D ilutesubstances orally with water, milk, or
magnesium hydroxide instead of removing YES NO
h 
P rovide support (eg, analgesics,
gastroprotectants) based on clinical signs
h 
B atteries must be removed immediately*
Does the patient have an underlying medical condition (eg, brachycephaly,
upper airway disease, laryngeal paralysis, megaesophagus)?

Emesis induction is high-risk;

consider gastric lavage
YES NO

Has the patient already vomited?

Vomiting may not have removed contents;

consider emesis if stomach contents remain YES NO
as identified via ultrasonography/radiography

Is mentation appropriate, and can patient protect the airway?

*In cases of battery ingestion, some clinicians may recommend radiography to

determine whether alkaline batteries are intact; if so, emesis can be safely induced. YES NO
All lithium/disc or punctured alkaline batteries should be removed via scope or
surgery. Button batteries in the esophagus require immediate removal; if in the
stomach or beyond, consider feeding a bulky diet to promote passage, although
this has risk for complications (eg, ulceration, perforation).
See TREATMENT
Time since Consider gastric lavage
ingestion with airway protection
18  cliniciansbrief.com  January/February 2021
 MANAGEMENT TREE  h  TOXICOLOGY/ EMERGENCY MEDICINE & CRITICAL CARE  h  PEER REVIEWED

Time since ingestion†

<2 hours 2-8 hours >8 hours

TREATMENT INVESTIGATION INVESTIGATION

Induce emesis h 
D elayed gastric h Stomach contents identified on
emptying (eg, after ultrasound images or radiographs?
ingestion of salicylates, h Extended-release formulation of
opioids, medications suspected?
anticholinergics,
tricyclic or
CAT DOG antidepressants)?
h Stomach contents
identified on ultrasound
images or radiographs?
h Large amount of xylitol
YES NO
TREATMENT TREATMENT gum (dogs), grapes or
h 
Xylazine:0.44 mg/kg IM h Apomorphine: 0.03 raisins (dogs), iron
h 
D exmedetomidine: mg/kg IV or IM or 6.25 mg tablets, chewable
7 µg/kg IM or 3.5 µg/kg IV subconjunctivally (flush multivitamins, blood or See E mesis not
h 
H ydromorphone: after emesis and use bone meal? Treatment: indicated;
h  S evere‡ ingestion, high
0.1 mg/kg SC caution with corneal Induce emesis provide
ulceration) risk for adverse effects (gray box) treatment
h Tranexamic acid: related to toxin, and specific to
50 mg/kg IV lack of an antidote? exposure and
h 3% hydrogen peroxide: care based on
1-5 mL/kg up to 50 mL clinical signs as
(avoid if possible, as needed
esophagitis and gastritis
could occur)
YES NO

If emesis is unsuccessful: See Emesis not indicated;

h 
R epeat induction agent once, typically 5-15 minutes after Treatment: provide treatment
first dose but dependent on agent and route Induce emesis specific to exposure and
h  C onsider offering food bolus prior to second induction (gray box) care based on clinical
h  C onsider gastric lavage signs as needed
h  C onsider endoscopic or surgical removal
h  C onsider bulk feeding (through offered food) to promote
passage of toxin
h  Treat supportively for maximum toxic dose
NOT RECOMMENDED
FOR EMESIS
h 
L iquid soap
†Due to the lack of a specific timeline recommendation in veterinary medicine, the h 
I pecac syrup
authors provide these time frames based on time passed since suspected ingestion. h 
S alt
‡Ingestion is considered severe if the amount or type of toxicant ingested leads to higher h 
D igital induction
risk for more serious toxicity. h 
M ustard powder
h 
H ydrogen peroxide (cats)

January/February 2021  cliniciansbrief.com  19

 MANAGEMENT TREE  h  PARASITOLOGY  h  PEER REVIEWED

PERSISTENT HOOKWORM INFECTIONS IN DOGS

Pablo David Jimenez Castro, DVM
Ray M. Kaplan, DVM, PhD, DEVPC, DACVM (Parasitology)
University of Georgia

PERSISTENT INFECTION AFTER ≥1

COURSE OF ANTHELMINTIC THERAPY

Perform FECRT

Treat with the same drug that is suspected of being ineffective

Perform FECs using a quantitative method (eg, McMaster, Mini-FLOTAC) on the day of treatment and again 10-14 days later

<75% FECR 75%-89% FECR 90%-95% FECR >95% FECR

h 
I ndicative of resistance h 
S uggestive of resistance h 
S uspicious of resistance h 
Treatment is effective
h 
Eggs in initial fecal h 
E ggs in initial fecal h 
E ggs in initial fecal h 
E ggsin initial fecal
examination prior to examination prior to examination prior to examination prior to
FECRT unlikely due to LL FECRT could be due to FECRT could be due to FECRT likely due to LL
resistance or LL resistance or LL

Treat* with febantel/ h 

R echeck fecals every
pyrantel/praziquantel + few months, preferably
moxidectin or h 
R esults considered inconclusive using FEC
fenbendazole + pyrantel + h Repeat FECRT at next course of treatment
moxidectin and perform a
second FECRT

<90% FEC reduction?

FEC = fecal egg count

h 
C ontinue with triple-combination treatment until
dog ceases shedding of hookworm eggs FECR = fecal egg count reduction
YES NO h 
Perform FECs at monthly intervals to monitor egg
shedding FECRT = fecal egg count reduction test
h 
I f egg shedding persists, repeat FECRT LL = larval leakage

h 
C onsider treatment with emodepside*
h 
Perform pretreatment FEC and
re-evaluate FEC 10-14 days later
h 
M onthly treatment with emodepside
may be needed for an extended period
*See accompanying article, Persistent or Suspected-Resistant
of time Hookworm Infections, page 61, for dose recommendations and
h 
Perform FECs at monthly intervals to
monitor for egg shedding discussion.

August 2020  cliniciansbrief.com  59