COMA and OVERDOSE

Coma: state without meaningful response to environmental stimuli from which the patient cannot be aroused
Approach to scenario
Stupor: unresponsiveness from which the patient can be aroused 1. Ensure pt stable / ABC’s
Lethargy: state of decreased awareness and mental status (patient may appear wakeful) 2. History / Physical
Clinical Manifestations - onset, toxidrome
ABCs (First and Foremost) - Pupils, stem reflexes
Historical features - focused (from family, friends, police, paramedics, old chart, medic-alert) 3. Investigations
 Previous/recent head injury (hematoma), - CT head, drugs
 Onset - Sudden (ICH, SAH, Cardiac), Gradual (mass, metabolic, bugs or drugs) 4. Management
 Limb twitching, incontinence, tongue biting (post-ictal state) - ABCs
 Confusional/delirious state (toxic/metabolic cause), DM (hypo- or hyperglycemia) - ICU, antidote
 Depression: drug overdose (medications, alcohol, or drugs- Call Poison Control Centre)
o What toxin/How much/When did it happen (have EMS/family bring in Pill Bottles)
o Note: asymptomatic after 4-6h suggests toxicity is unlikely except in the case
of slow/extended release formulations or clonidine Differential Diagnosis (DIMS)
 PMHx (Obtain corroborative history from friends/family, EMS, old charts), Meds, Drugs
Allergies, EtOH, Substance abuse  EtOH, Barbiturates, benzos, narcotics
 Heavy metals (Arsenic, Lead, Mercury)
Physical Examination  Solvents (Acetone)
 ABC’s, vital signs, monitoring (IV, O2, BP, telemetry) Infection
o Glucometer, Coma Cocktail (D50, Narcan 0.4-2mg IV, Thiamine 100 mg IV)  Encephalitis, meningitis, cerebral abscess
o Hypothermia: Drugs (Cools - CO, Opiates, Oral hypoglycemic, Liquor,  Sepsis, pneumonia, UTI, HIV/AIDS
Sedative Hypnotics) Metabolic
o Hyperthermia: Infection, Drugs (NASA - NMS, Antihistamines, Serotonin  Uraemia, liver failure, electrolyte
syndrome, Sympathomimetics, Anticholinergics) imbalance (Na+, Ca2+)
 Hypoxia: Anemia, Respiratory Failure,
o Hypertension and Bradycardia (Cushing reflex): raised ICP
HF, Acute Heart Block, PE, CO poisoning
o Hypotension and Bradycardia: Antiarrhythmics (1a, 1c, 3), Clonidine,  Endocrine: Hyper/hypothyroid,
Digoxin, -blockers, CCBs, Organophosphates/Carbamates, Opiates, Sedatives Hyper/hypoglycaemia,
 Management - dysrhythmias (ACLS, HCO3 – Na-channel block Cushing’s/Addisonian crisis
induced WC tachycardia)  Nutritional: thiamine, vitamin B12, folate
 IVF , Pressors (Dopamine 1st choice - may need high doses Structural (Asymmetric/absent pupil reaction,
with multiple agents) EOM, motor findings)
o Tachycardia: infection/drug overdose/withdrawal  Bilateral Cerebral Hemispheres
 Diffuse lesion/trauma/ischemia
o Respiratory Rate  Brainstem infarct/hemorrhage
 > 20: acidosis, pulmonary edema, pneumonia, PE, ARDS, salicylates  Brainstem compression (posterior
 < 8: opiates, ACh inhibitors fossa/supratentorial mass, SDH, Epidural
o Respiratory Pattern hematoma, cerebellar bleed, neoplasm,
 Cheyne-Stokes - Cortical, brainstem or toxic/metabolic abscess, inflammation, hydrocephalus)
 Kussmaul’s: rapid, deep breathing – Pons, metabolic acidosis
 Ataxic breathing (Biot's): chaotic pattern – Medullary (preterminal)
 Agonal gasps - Bilateral lower brainstem damage
 General
o Signs of trauma (battle sign, raccoon eyes, hemotympanum, nasal CSF leak)
o Posture
 Decorticate posture – better prognosis (UE flexion - damage to hemispheres or diencephalon above the midbrain)
 Decerebrate posture – worse prognosis (UE extension - damage to midbrain or upper pons)
 Peripheral
o Needle marks, i.e. IV drug abuse
 HEENT
o Neck stiffness
o Pupils
 Pinpoint (< 1mm) – bilateral pontine/narcotics
 Pinpoint with lacrimation – cholinergic toxicity
 Reactive and small – metabolic, deep bilateral hemispheral lesions
 Unilateral fixed dilated (CN3) – ipsilateral midbrain, uncal herniation or compression
 Bilateral dilated and unreactive – midbrain, anticholinergic
o Fundi – Papilledema
o EOM – look for CN3, 4 and 6 palsies and gaze palsies
 Deconjugate gaze - suggests brain stem lesion
 Conjugate tonic gaze - toward a frontal deficit (i.e. infarct) lesion (FEF), away from a pontine deficit lesion
o Brainstem Reflexes –
 Corneal - pontine pathways for CN V and VII
 Oculocephalic reflex (Doll's Eyes) – when head is moved in one direction the eyes should move in opposite direction
 In a conscious person this reflex is suppressed by the cortex
 If present, signifies intact brainstem (pons and midbrain)
 Oculovestibular reflex (Cold water calorics) – irrigation with cold ice water
 Intact brainstem (comatose pt): tonic deviation of both eyes to the side of cold, with no nystagmus away

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  Intact cerebral hemispheres (awake pt): rapid corrective conjugate movement away from the side of tonic
deviation
 Gag (in brain death  absent cough with suctioning, sucking, and rooting reflexes)

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  Full Neuro (Sensory, motor, reflexes, rectal)
o Look for lateralizing signs i.e. asymmetry
o Look for spontaneous motor response
o Response to painful stimulation - Withdrawal, Decorticate, Decerebrate, Flaccid response - medullary lesion
o Reflexes + Babinski - Hyperreflexia (unilateral - structural UMN lesion); Hyporeflexia (metabolic or drugs)
 Full Cardiovascular (JVP, pulses, precordial IPA), Respiratory (IPPA), Abdominal (IPPA) Examination
Investigations
 Bloodwork
o CBC, lytes, Urea, Cr, glucose, Serum OSM, Anion gap, Ca, Mg, PO4, lactate, liver enzymes, albumin, CK, ABG, Urine R&M
o Drug tox screen
 General - Alcohols (not ethylene glycol), Acetaminophen, ASA, Sedatives/hypnotics, Barbiturates
 Specific - Methanol, ethylene glycol, carboxy/methemoglobin, Fe, Li, digoxin, theophylline, phenobarbital
 CXR plus/minus AXR - “CHIPS”: Chloral hydrate, CCl4, Ca, Heavy metals, Fe, K, ASA, foreign bodies
 ECG - Assess QRS, QT and for blocks
 CT Head - Rule out structural lesion TOXIDROMES
 LP - If fever, neck stiffness or lack of explanation Sedatives, Hypnotics and Alcohol Toxidrome
 Clinical Presentation
 EEG - Diffuse slow waves suggest metabolic; focal spikes may suggest structural o Sedation or coma
Treatment o Mild ↓ in temperature, HR, BP, RR
o Ataxia, slurred speech + pupil changes
ABC’s Opiates
 Oxygen, IV access, Monitors  Clinical Presentation
 Admit the patient to the ICU or CCU o Sedation or coma
Treat the Underlying Cause o Mild ↓ in temperature, HR, BP
Toxin Antidote/Treatment o Significant ↓↓ RR (important differentiator)
Acetaminophen N-acetylcysteine (Mucomyst) o Constricted pupils
Anticholinergics (not TCA) Physostigmine Sympathomimetics
Benzodiazepines flumazenil (Anexate)  Clinical Presentation
-blockers glucagons, atropine, isoproterenol o ↑ Temp, HR, BP (>Ach toxidrome):
Calcium Channel blockers calcium gluconate, glucagons o Dilated pupils plus diaphoresis (important
Carbon Monoxide 100% oxygen, hyperbaric O2 differentiator from Ach)
Cyanide Lilly kit (amyl nitrite, then sodium nitrite): Na thiosulfate o CNS (restlessness, tremor, seizure)
Digoxin stop digoxin, use FAB fragments (Digibind), restore K+ o Psych (agitation, euphoria, psychosis)
Heparin protamine sulfate o GI (nausea and vomiting)
Heavy Metals desferroxime, penicillamine  Drugs – Cocaine, amphetamines, caffeine,
Insulin glucose/glucagons o Decongestants, LSD, PCP, Theophylline
Iron desferroxime o Thyroid hormone
Isoniazid (INH) pyridoxine  Mimics: ASA toxicity, Sed-hypnotic withdrawal
Methanol/Ethylene glycol ethanol or fomepizole Anticholinergics
MetHb/Nitrites methylene blue  Clinical Presentation
Opioids naloxone (Narcan) o Hot as a Hare (Hyperthermia)
Organophosphates atropine, pralidoxime o Blind as a Bat (Dilated pupils)
Salicylates alkalinize urine, restore K+ o Dry as a Bone (Dry skin)
TCAs sodium bicarbonate o Red as a Beet (Vasodilatation)
Warfarin vitamin K; (FFP if necessary) o Mad as a Hatter (Agitation/halluc)
o Seizing like a squirrel
Criteria for Diagnosis of Brain Death (updated 2012) o The bowels and bladder lose their tone while
the heart goes on alone
 The diagnosis of brain death is usually made by neurologic examination, provided certain (Ileus, Urine retention, tachycardia)
prerequisites are met:  Drugs:
o the underlying cause is understood; and o Antidepressants (esp. TCAs), carbamazepin
o confounding from drug intoxication or poisoning, metabolic derangements, and o Antipsychotics, Antiparkinsonians,
o Antispasmodics (Baclofen, Flexeril),
hypothermia have been ruled out.
o Antihistamines (gravol, diphenhydramine)
o Belladonna alkaloids (e.g. atropine,
 The neurologic examination must demonstrate all 3: scopolamine)
1. Coma Cholinergics
2. No cerebral response to external stimuli (ie. absent brain-originating motor  Clinical Presentation (“SLUDGE”)
response, including no response to pain stimulus above the neck or other brain- o Salivation, Lacrimation, Urination
originating movements, eg, seizures, decerebrate or decorticate posturing) o Diaphoresis, GI – Diarrhoea, Emesis
3. Absent brainstem reflexes (including no papillary rxn to light, with pupils midpoint o Plus…↓ BP, ↑↓ HR, Bronchospasm
or dilated).  Seizures/skeletal muscle excitation
 Meiosis Bronchorrhea
 An apnea test is performed in all patients meeting all other brain death criteria who are stable  Drugs - Cholinergics (nicotine, mushrooms)
enough to undergo the test. o Anticholinesterases (physostigmine)
 Pre-oxygenate to avoid hypoxia as test may take 10 minutes o Organophosphates
 Turn off AC vent Extrapyramidal signs and symptoms
 No respiratory effort when PaCO2 > 60mmHg and pH <7.28 (or >  Clinical Presentation
20mmHg above baseline) o Dysphonia, dysphagia, laryngospasm
 May become unstable – 26% cardiac dysrhythmias o Torticollis, rigidity and tremor
o Oculogyric crisis, trismus (deviation of
eyes in all directions)
 Observation period is variable [Old indication - 12 hour period of no cortical or brainstem
functioning must have elapsed, with 2 evaluations separated by time performed by 2 separate
specialists. In Canada, 2001 recommendations said 1 doctor observing over 6 hrs]

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  Ancillary tests are required when clinical criteria cannot be applied and to supplement the clinical examination in young children. Tests of brain blood flow
may be preferred in the setting of hypothermia and metabolic or drug confounders, while electrophysiologic testing may be more reliable in the setting of
hypotension, craniotomies, and other factors that lower intracranial pressure.

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