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Coma: Assessment and Management for MCCQE1

Introduction

Coma is a state of unarousable unresponsiveness in which the patient lies with eyes closed and shows no meaningful response to environmental stimuli. For the MCCQE1, understanding the systematic approach to a comatose patient is a high-yield topic falling under the CanMEDS Medical Expert role. You must be able to differentiate between structural and metabolic causes, perform a targeted neurological exam, and initiate life-saving management.

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Canadian Context: In Canada, the determination of coma and subsequent prognosis often involves multidisciplinary teams. Familiarity with the Neurological Determination of Death (NDD) guidelines published by the Canadian Critical Care Society is essential for advanced management questions.


Pathophysiology and Anatomy

Consciousness requires two intact components:

  1. Arousal (Wakefulness): Dependent on the Ascending Reticular Activating System (ARAS) in the brainstem.
  2. Awareness (Content): Dependent on the cerebral cortex (bilateral hemispheres).

Coma results from:

  • Bilateral hemispheric dysfunction OR
  • Brainstem (ARAS) dysfunction.

Etiology: Structural vs. Metabolic

Distinguishing between structural and metabolic causes is the first diagnostic pivot point.

Characteristics:

  • Usually no focal signs (symmetric exam).
  • Pupils often reactive (resistant to metabolic insult).
  • Mental status changes often precede coma.
  • Etiology: Hypoglycemia, Hypoxia, Drug overdose (Opioids, Benzos), Uremia, Hepatic encephalopathy.

The “AEIOU TIPS” Mnemonic

A useful mnemonic for MCCQE1 preparation to recall causes of altered level of consciousness:

  • Alcohol / Acidosis
  • Epilepsy / Endocrine / Electrolytes
  • Insulin (Hypoglycemia)
  • Opiates / Oxygen (Hypoxia)
  • Uremia
  • Trauma / Temperature (Hypothermia)
  • Infection (Meningitis/Encephalitis)
  • Psychogenic / Poisoning
  • Stroke / Seizure / Shock

Clinical Assessment: The Canadian Approach

Time is brain. The assessment must be rapid and concurrent with stabilization.

Step 1: Stabilization (ABCs)

  • Airway: Assess patency. GCS < 8 = Intubate (General rule).
  • Breathing: Oxygenation and ventilation.
  • Circulation: IV access, fluids, vasopressors if needed.
  • C-Spine: Assume trauma until proven otherwise; apply C-collar.

Step 2: The “Coma Cocktail” (Empiric Therapy)

While obtaining history and labs, consider reversible causes immediately.

  • Thiamine: 100 mg IV (Give before glucose to prevent Wernicke’s Encephalopathy).
  • Dextrose: D50W (1 ampule) if hypoglycemia is suspected or confirmed.
  • Naloxone: If opioid overdose suspected (respiratory depression, pinpoint pupils).

Step 3: Focused History

Obtain collateral history (EMS, family, bystanders).

  • Onset: Abrupt (vascular/seizure) vs. Gradual (metabolic/tumor).
  • Recent complaints: Headache, fever, depression.
  • PMHx: Diabetes, liver disease, substance use.

Step 4: Neurological Examination

Focus on localizing the lesion.

  1. Level of Consciousness: Glasgow Coma Scale (GCS).
  2. Pupils: Size, symmetry, reactivity.
  3. Brainstem Reflexes: Corneal, Oculocephalic (Doll’s eyes), Oculovestibular (Cold calorics).
  4. Motor Response: Posturing (Decorticate vs. Decerebrate).

Glasgow Coma Scale (GCS)

Memorize this table for the MCCQE1.

ComponentResponseScore
Eye OpeningSpontaneous4
To verbal command3
To pain2
None1
Verbal ResponseOriented5
Confused4
Inappropriate words3
Incomprehensible sounds2
None1
Motor ResponseObeys commands6
Localizes pain5
Withdraws from pain4
Flexion to pain (Decorticate)3
Extension to pain (Decerebrate)2
None1
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MCCQE1 Tip: Decorticate posturing (Flexion) implies a lesion above the red nucleus (midbrain). Decerebrate posturing (Extension) implies a lesion below the red nucleus (brainstem). Decerebrate is worse.


Herniation Syndromes

Understanding herniation is critical for identifying surgical emergencies.

🚨 Uncal Herniation (Transtentorial)

The uncus of the temporal lobe herniates through the tentorial notch, compressing the midbrain.

  • Ipsilateral “Blown” Pupil: CN III compression (dilated, fixed).
  • Contralateral Hemiparesis: Compression of cerebral peduncle.
  • Coma: Compression of ARAS.

Diagnostic Investigations

Laboratory

  • Bedside: Glucose (Fingerstick).
  • Blood: CBC, Electrolytes (Na, Ca, Mg), BUN/Cr, LFTs, INR/PTT, ABG, Ammonia, Osmolality.
  • Toxicology: Serum ethanol, acetaminophen, salicylates; Urine drug screen.

Imaging

  • CT Head (Non-contrast): The gold standard initial imaging to rule out hemorrhage, mass effect, or hydrocephalus.
  • CTA (CT Angiography): If basilar artery thrombosis is suspected.
  • MRI Brain: Superior for posterior fossa lesions, diffuse axonal injury, or early ischemia (DWI sequences).

Other

  • Lumbar Puncture: ONLY after CT excludes mass effect. Indicated for suspected meningitis or subarachnoid hemorrhage (if CT negative).
  • EEG: To rule out non-convulsive status epilepticus.

Canadian Guidelines: Neurological Determination of Death (NDD)

In Canada, “Brain Death” is legally defined as the irreversible loss of the capacity for consciousness combined with the irreversible loss of all brainstem functions, including the capacity to breathe.

Key Criteria (Summary):

  1. Etiology: Established cause capable of causing NDD.
  2. Deep Coma: No motor response to pain (excluding spinal reflexes).
  3. Absent Brainstem Reflexes:
    • Fixed pupils.
    • Absent corneal reflex.
    • Absent oculocephalic/oculovestibular reflexes.
    • Absent gag/cough reflex.
  4. Apnea Test: No respiratory effort despite PaCO2 ≥ 60 mmHg (and ≥ 20 mmHg above baseline).

Key Points to Remember for MCCQE1

  • Glucose first: Always check capillary glucose in any patient with altered mental status.
  • Thiamine before Glucose: In suspected malnutrition/alcohol use disorder, give thiamine before glucose to prevent precipitating Wernicke’s encephalopathy.
  • Pupils: In metabolic coma, pupils are usually small but reactive. In structural coma, pupils are often asymmetric or unreactive.
  • Basilar Thrombosis: A “locked-in” patient may look comatose but has intact awareness. Look for vertical eye movements (often the only preserved motor function).
  • Naloxone: Has a short half-life. Patients may require repeated doses or an infusion.

Sample Question

Clinical Scenario

A 68-year-old male with a history of hypertension and atrial fibrillation is brought to the Emergency Department after collapsing at home. On arrival, he is comatose. His blood pressure is 190/110 mmHg, heart rate is 90 bpm, and respiration is irregular.

On neurological examination:

  • GCS is 4 (E1, V1, M2).
  • The right pupil is 7 mm and fixed; the left pupil is 3 mm and reactive.
  • There is decerebrate posturing on the left side.
  • Doll’s eye reflex is absent.

Which of the following is the most likely diagnosis?

Options

  • A. Pontine hemorrhage
  • B. Right-sided Uncal herniation
  • C. Opioid overdose
  • D. Metabolic encephalopathy
  • E. Left-sided Subdural hematoma

Explanation

The correct answer is:

  • B. Right-sided Uncal herniation

Detailed Explanation: This clinical presentation is classic for Uncal Herniation.

  • Ipsilateral Blown Pupil: The right pupil is dilated (7 mm) and fixed. This is caused by the herniating uncus (temporal lobe) compressing the ipsilateral Oculomotor nerve (CN III) and its parasympathetic fibers.
  • Contralateral Motor Deficit: The compression of the ipsilateral cerebral peduncle (specifically the corticospinal tract) results in contralateral hemiparesis or posturing (in this case, left-sided decerebrate posturing).
  • Coma: Compression of the midbrain reticular activating system leads to a low GCS.
  • History: The history of HTN and Afib suggests a catastrophic intracranial event (hemorrhage or massive embolic stroke) leading to increased ICP.

Why other options are incorrect:

  • A. Pontine hemorrhage: Typically presents with pinpoint pupils (damage to descending sympathetic fibers), not a unilateral blown pupil.
  • C. Opioid overdose: typically presents with bilateral pinpoint pupils and respiratory depression, not asymmetric pupils and posturing.
  • D. Metabolic encephalopathy: Usually presents with symmetric deficits and reactive pupils.
  • E. Left-sided Subdural hematoma: A left-sided lesion would typically cause a left blown pupil (ipsilateral) and right-sided motor symptoms.

References

  1. Medical Council of Canada. (n.d.). Objectives for the Qualifying Examination Part I. Retrieved from mcc.ca.
  2. Shemie, S. D., et al. (2006). Severe brain injury to neurological determination of death: Canadian forum recommendations. CMAJ, 174(6), S1-S13.
  3. Toronto Notes. (2023). Neurology: Coma and Impaired Consciousness. Toronto Notes for Medical Students, Inc.
  4. Young, G. B. (2023). Stupor and coma in adults. In: UpToDate, Post, T.W. (Ed.), UpToDate, Waltham, MA.

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