Coma

Definition

Coma is a state of reduced alertness and unresponsiveness from which the patient cannot be aroused — an eyes-closed state of unarousability. It is not simply deep sleep; external stimuli (verbal commands, pain) fail to elicit a meaningful response.

Coma is typically self-limited and has several possible outcomes:

Full recovery (e.g., after anaesthesia-induced coma or treated metabolic cause)
Death or progression to brain death (irreversible cessation of all brain function, including brainstem)
Vegetative state (isolated preservation of brainstem function with no cortical awareness)
Minimally conscious state (MCS) — some preserved but limited integrated cerebral function

(Plum and Posner's Diagnosis and Treatment of Stupor and Coma)

Pathophysiology

Consciousness requires the intact function of both cerebral hemispheres and/or the brainstem reticular activating system (RAS). For coma to occur, one of the following must be disrupted:

Diffuse/global brain dysfunction — as in metabolic, toxic, or hypoxic causes; the brain is globally affected with no localizing signs.
Bilateral cortical dysfunction — e.g., bilateral large hemisphere infarcts or severe encephalopathy.
Brainstem lesion — e.g., hemorrhage into the pons or midbrain disrupting the RAS.

A unilateral hemispheric lesion alone (e.g., a single stroke in one hemisphere) should NOT cause coma — both hemispheres or the brainstem must be impaired.

Herniation Syndromes

Uncal herniation: Medial temporal lobe shifts and compresses the upper brainstem → progressive drowsiness → unresponsiveness. The ipsilateral pupil becomes sluggish, then fixed and dilated (CN III compression).
Central herniation: Progressive loss of consciousness, loss of brainstem reflexes, decorticate → decerebrate posturing, and irregular breathing.

(Tintinalli's Emergency Medicine)

Causes

Diffuse/Metabolic (no localizing signs)

Category	Examples
Encephalopathies	Hypoxic, hypertensive, metabolic
Metabolic substrate deficiency	Hypoglycemia, hyperglycemia/hyperosmolar state
Electrolyte abnormalities	Hypo/hypernatremia, hypercalcemia
Organ failure	Hepatic encephalopathy, uremia/renal failure
Endocrine	Addison's disease, hypothyroidism (myxoedema coma)
Respiratory	Hypoxia, CO₂ narcosis
Toxins/Drugs	Opioids, barbiturates, alcohol, sedatives, anticholinergics
Temperature	Hypothermia (<31°C causes coma regardless of cause), hyperthermia/heat stroke
Nutritional deficiency	Wernicke's encephalopathy (thiamine deficiency)

Structural/CNS (localizing signs often present)

Traumatic brain injury
Intracerebral or subarachnoid hemorrhage
Ischemic stroke (bilateral or brainstem)
Cerebral edema
CNS infection (meningitis, encephalitis)
Brain tumor/abscess
Seizures (post-ictal state)

Clinical Assessment

Glasgow Coma Scale (GCS)

The most widely used scoring system. Total score ranges from 3 (deepest coma) to 15 (normal):

Component	Score	Response
Eye Opening	4	Spontaneous
	3	To voice
	2	To pain
	1	None
Verbal	5	Oriented
	4	Confused
	3	Inappropriate words
	2	Incomprehensible sounds
	1	None
Motor	6	Follows commands
	5	Localizes pain
	4	Withdraws
	3	Flexion (decorticate)
	2	Extension (decerebrate)
	1	None

GCS ≤ 8 is the conventional threshold for defining coma.

An alternative is the FOUR Score (Full Outline of Unresponsiveness), which also assesses brainstem reflexes and respiratory patterns — useful in intubated patients where verbal responses can't be obtained.

Neurological Examination

Spontaneous movements: Restlessness suggests near-wakefulness; absence of movement on one side suggests hemiplegia.
Pupils: Fixed, dilated → severe midbrain or CN III compression; pinpoint → opioids or pontine lesion.
Eye movements: Assessed via oculocephalic ("doll's eye") and oculovestibular reflexes to test brainstem integrity.
Motor posturing: Decorticate (flexion) → cortical injury; Decerebrate (extension) → deeper brainstem injury.
Asterixis/myoclonus: Suggests metabolic encephalopathy (uremia, hypoxia, drug intoxication).

Initial Management

Airway, Breathing, Circulation first — intubate if apnea, airway obstruction, or aspiration risk
Correct reversible metabolic causes immediately:
- Hypoglycemia → IV dextrose
- Opioid overdose → IV naloxone
- Suspected Wernicke's → IV thiamine (given before glucose)
- Hypoxia, hypercapnia, hypotension → correct urgently
Treat raised ICP if present
Suspected bacterial meningitis → IV vancomycin + 3rd-generation cephalosporin + dexamethasone without delay
Suspected ischemic stroke/basilar thrombosis → CT to exclude hemorrhage, then consider tPA or mechanical thrombectomy

(Harrison's Principles of Internal Medicine, 22nd Ed.)

Prognosis

Metabolic comas generally carry a far better prognosis than traumatic or anoxic comas.
For anoxic coma, pupillary and motor responses at day 1, day 3, and day 7 have predictive value — but these rules are less reliable in the setting of therapeutic hypothermia.
Young patients may have ominous early signs yet still recover — early prognostication (outside of brain death) should be cautious.
GCS has predictive value in trauma but not reliably in other causes.

Sources: Plum and Posner's Diagnosis and Treatment of Stupor and Coma | Harrison's Principles of Internal Medicine, 22nd Ed. | Tintinalli's Emergency Medicine

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