Coma Assessment
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Direct answer
Coma — a state of eyes-closed unarousable unresponsiveness — is approached in one fixed order: secure the airway (intubate at GCS 8 or below), check glucose and give thiamine before glucose in the malnourished or alcoholic patient, and only then localise the cause into structural (needs urgent CT) versus metabolic-toxic (needs laboratories, antidotes and often EEG). The pupils, motor responses and pattern of brainstem reflexes do the localising at the bedside, and every unexplained coma with subtle fluctuation deserves an EEG to unmask non-convulsive status epilepticus.
What you must remember
- Definitions that separate the look-alikes: coma (eyes closed, unarousable, no understandable response), vegetative state/unresponsive wakefulness syndrome (eyes open, no awareness), minimally conscious state (intermittent, inconsistent awareness), locked-in syndrome (aware and quadriparetic, vertical eye movements preserved — de-efferented pons, classically basilar thrombosis).
- Glasgow Coma Scale: eye (4), verbal (5), motor (6); score the best response; a total of 8 or below is the airway threshold; always report components, and record the trauma modification (verbal untestable).
- The FOUR score (Full Outline of UnResponsiveness: eye, motor, brainstem, respiration) captures brainstem function and breathing pattern, and works in intubated patients.
- Immediate bloods: glucose (the cheapest coma reversal), sodium, calcium, renal and liver function including ammonia, thyroid function, blood gas, and toxicology screen; blood cultures and LP when infection is plausible.
- Pupils localise: one fixed dilated pupil — uncal herniation compressing the third nerve; both mid-position and fixed — brainstem death or severe brainstem injury; pinpoint — opioids or pontine lesion; small reactive — metabolic or diencephalic.
- Motor asymmetry or focal seizures point structural — CT now; a symmetric, flaccid, pupils-reactive picture with asterixis or myoclonus points metabolic.
- Herniation syndromes: uncal (ipsilateral dilated pupil, contralateral hemiparesis; occasionally ipsilateral hemiparesis from Kernohan's notch — a false-localising sign), central (small pupils, Cheyne-Stokes, decortate then decerebrate).
- Non-convulsive status epilepticus underlies a surprising fraction of unexplained comas — order EEG; treatable causes such as autoimmune encephalitis, HSV encephalitis and Wernicke encephalopathy are found only when looked for.
- Prognostic caution: sedation, hypothermia and early timing confound early predictors in metabolic coma — serial examination decides.
The first thirty minutes
A 47-year-old man is found unresponsive at home, breathing, afebrile, no trauma signs. Minute one to five: airway and positioning, oxygen, access; glucose 38 mg/dL, and a whiff of alcohol on the breath. The reflex that must not fire here is "push 50 per cent dextrose alone": in the alcoholic or malnourished patient, intravenous thiamine (commonly 200 mg or more, per local protocol) is given before or with the glucose, because glucose metabolism consumes thiamine and can precipitate Wernicke encephalopathy in a deficient brain. Glucose follows; if the coma resolves, the work has just begun — the whys of the hypoglycaemia (sulfonylurea? insulin? liver failure?) are the real diagnosis. If he does not awaken: next ten minutes run in parallel — naloxone and flumazenil considered only with the matching toxidrome (flumazenil used sparingly for seizure risk in chronic benzodiazepine users), pupils examined (4 mm, symmetric, reactive — arguing against a blown third nerve), motor response to pain (withdraws symmetrically), and the decision tree: any asymmetry, seizures, fever with neck stiffness, or unarousable state warrants CT before LP. Laboratories drawn with the first cannula return: sodium 118 mmol/L — severe hyponatraemia as the co-driver, corrected carefully to avoid osmotic demyelination. Had the pupils been unequal and the right side flaccid, the same thirty minutes ends in the CT scanner, not the laboratory — and had he been unresponsive with twitching eyelids and no metabolic answer at all, the day's last order would be an urgent EEG for non-convulsive status.
Where students slip
The order of the first two drugs is the most-tested single fact: thiamine before (or with) glucose in the alcoholic — reversed by the unwary in every option set. The second slip is quoting a total GCS without components, or intubating before scoring when scoring is still possible; the component record is what communicates. Third is the false-localising Kernohan sign — the hemiparesis on the same side as a subdural or uncal mass, from compression of the contralateral cerebral peduncle against the tentorium. And the locked-in patient, written off as comatose, is the ethical trap: instruct "ask him to look up" before declaring unresponsiveness.
Frequently asked questions
Why is thiamine given before glucose in suspected alcoholic coma?
Glucose loading accelerates thiamine consumption in a deficient patient and can precipitate or worsen Wernicke encephalopathy — give thiamine before or with the dextrose.
Which pupillary findings suggest a structural lesion?
A single fixed dilated pupil (third nerve compression by uncal herniation), or bilateral mid-position fixed pupils (brainstem injury); pinpoint pupils suggest opioids or a pontine lesion; small reactive pupils favour a metabolic cause.
What is the Kernohan notch phenomenon?
False localising ipsilateral hemiparesis: a supratentorial mass herniates and compresses the contralateral cerebral peduncle against the tentorium, weakening the side of the lesion.
Why order an EEG in unexplained coma?
Non-convulsive status epilepticus is a treatable cause of unexplained coma and subtle fluctuating states, and only EEG (with searches for HSV, autoimmune and metabolic causes) exposes it.