The comatose patient in the ICU

What it is

Coma is a state of unarousable unresponsiveness: the eyes stay closed, there is no sleep-wake cycle and no purposeful response to stimuli. It needs either damage to the ascending reticular activating system in the upper brainstem and thalamus or diffuse dysfunction of both cerebral hemispheres; a single hemisphere lesion does not cause coma unless it compresses the brainstem. Causes fall into structural lesions (haemorrhage, stroke, trauma, tumour, abscess, herniation) and diffuse problems (toxic, metabolic, infectious, seizures and hypothermia). Structural causes tend to give asymmetric signs; metabolic and toxic causes give symmetric signs with reactive pupils. The first minutes follow a fixed order: airway, breathing, circulation, cervical spine if trauma is possible, capillary glucose, and treatment of quick reversible causes such as hypoglycaemia or an opioid toxidrome, with thiamine in patients at risk of deficiency. Then the examination grades the depth of coma with the Glasgow Coma Scale (eye opening, verbal response and best motor response, scored and recorded separately) and localises the problem through the pupils, eye movements, brainstem reflexes, breathing pattern and motor responses. Non-contrast CT of the head comes early; blood tests, toxicology, EEG for non-convulsive seizures and lumbar puncture follow according to suspicion. In the ICU, sedatives often confound the examination, so it is repeated off sedation whenever possible.

What to assess

• Level of consciousness with the GCS, using a central painful stimulus for the motor response (best side counts).
• Pupils: size, symmetry and reaction to light.
• Eye movements and brainstem reflexes: oculocephalic (only when the neck is cleared), oculovestibular, corneal, gag and cough.
• Breathing pattern: periodic, hyperventilation, ataxic or apnoeic breathing helps localise brainstem damage.
• Motor responses: localising, withdrawal, abnormal flexion (decorticate), extension (decerebrate) or none; and any asymmetry.
• Signs of the cause: head injury, neck stiffness, fever, rash, needle marks, jaundice, the smell of alcohol or ketones.

How it is done (and why)

1. Secure airway, breathing and circulation; protect the cervical spine if trauma is possible — hypoxia and hypotension worsen brain injury.
2. Check capillary glucose and treat hypoglycaemia, with thiamine if at risk — the most quickly reversible cause.
3. Look for a toxidrome and give an antidote when the picture fits, such as an opioid antagonist — fast diagnosis and treatment.
4. Score the GCS by components and examine pupils, reflexes, breathing and motor responses — localises structural vs diffuse causes.
5. Order a non-contrast head CT early — finds haemorrhage, mass effect and hydrocephalus that need surgery.
6. Send electrolytes, renal and liver tests, ammonia, blood gas and toxicology — metabolic causes are common and treatable.
7. Do an EEG if the cause is unclear or there are subtle twitches — non-convulsive status epilepticus is easily missed.
8. Perform a lumbar puncture when infection is suspected and imaging shows it is safe — meningitis and encephalitis need early treatment.

Findings that change the plan

• A fall of two or more GCS points, or a new unilateral dilated pupil: suspect herniation and call neurosurgery at once.
• Hypertension with bradycardia and irregular breathing (Cushing response) signals raised intracranial pressure.
• Fever with neck stiffness: start empirical treatment for meningitis without waiting for the lumbar puncture.
• Eyes that move vertically on command in an apparently unresponsive patient: think locked-in syndrome, not coma.
• Do not prognosticate early: sedation, hypothermia, organ failure and drugs can depress the examination for days.

Next step

• Record the GCS by components, the pupils and the time, and repeat at the intervals set for the cause.
• Call neurosurgery or neurology at once for a mass lesion, hydrocephalus, falling GCS or pupil changes.
• Hold or lighten sedation regularly to reassess, unless intracranial pressure requires deep sedation.
• If brainstem reflexes are lost with a known irreversible cause, consider formal brain death testing.
• Talk to the family early about what is known and what is not, and revisit goals of care as the picture becomes clear.

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Elsewhere in DurgiPedia

• Level of consciousness and the Glasgow Coma Scale
• Pupils: light reflex and abnormal pupils (Marcus Gunn, Horner, Argyll Robertson)
• Deep tendon reflexes and their grading
• Intracranial hypertension syndrome
• Cerebral blood flow, brain metabolism and intracranial pressure

Connections

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Educational content; it does not replace supervised training, your institution's protocols or the anaesthetist's or intensivist's decision. It contains no doses and no ventilator or infusion settings.

Sources: Coma (StatPearls (NCBI Bookshelf), 2023); Glasgow Coma Scale (StatPearls (NCBI Bookshelf), 2026).

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Representative model, for educational purposes only.