Coma and GCS assessment

The comatose patient is one of the most challenging presentations in the emergency department, requiring the simultaneous resuscitation, the diagnosis, and the treatment. The Fellowship candidate must know the structured approach (the ABCDE, the rapid glucose, the reversible causes), the Glasgow Coma Scale and its limitations, the differential (the toxic-metabolic vs the structural), and the specific antidotes (the naloxone, the flumazenil, the thiamine), because the comatose patient is the patient in whom the seconds matter — the delayed reversal of the hypoglycaemia, the opioid, or the thiamine deficiency causes the irreversible brain injury.[1][2]

Definition

The coma is the state of unarousable unresponsiveness in which the patient does not open the eyes, does not follow commands, and does not utter comprehensible words. It is distinguished from the stupor (the patient can be briefly aroused with the vigorous stimulation), the confusion (the patient is awake but disoriented), the delirium (the acute fluctuating disturbance of the attention and the cognition), and the vegetative state (the wakefulness without the awareness). The coma is the medical emergency that demands the immediate structured approach. [1]

The structured approach — the ABCDE and the rapid glucose

The comatose patient is approached in parallel: the resuscitation and the diagnosis happen simultaneously. [1]

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The glucose is checked immediately — the hypoglycaemia is the commonest reversible cause of the coma, and the prolonged hypoglycaemia causes the irreversible brain injury. If the glucose is low (below 3 mmol/L), give glucose 25 g IV (50 mL of 50 per cent dextrose) immediately, repeated as needed. In the alcoholic patient, give thiamine 100 mg IV before or with the glucose to prevent the Wernicke encephalopathy (the glucose may precipitate the acute thiamine deficiency). [1]

The Glasgow Coma Scale

The GCS is the most widely used tool for the assessment of the conscious level, and it has three components: the eye opening (E, scored 1 to 4), the verbal response (V, scored 1 to 5), and the motor response (M, scored 1 to 6). The total ranges from 3 (the deepest coma) to 15 (the fully alert). The motor response is the most sensitive component — it is the last to deteriorate in the rising intracranial pressure and the first to improve in the recovery. The best motor response is recorded (the patient is tested in all four limbs and the best response in any limb is scored). [1]

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The GCS has limitations: it is poor at the moderate range (the score of 12 may mean the drunk patient or the patient with the expanding intracranial haematoma), the intubated patient scores V1 (tube), and the best motor response obscures the asymmetric deficit. The AVPU (Alert, responds to Voice, responds to Pain, Unresponsive) is the faster alternative for the triage and the serial assessment, and it correlates roughly with the GCS (A = 15, V = 13, P = 8, U = 3). [1]

GCS scoring in detail — the components, the maximum, the minimum

The GCS is recorded as the three components and the total — E4V5M6 = 15 (the maximum, the fully alert patient) and E1V1M1 = 3 (the minimum, the deepest coma). The minimum is 3, not zero — there is no score of 0 in any component; a patient with no eye opening, no verbalisation, and no motor response scores 3. The Fellowship candidate must record the components separately (the total alone is opaque — a score of 7 may be E2V1M4 or E1V1M5, with very different implications) and add the modifier "T" for the intubated patient (E1VTM5 = the verbal component is untestable because of the tube).[3][4]

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The AVPU — the rapid triage alternative

The AVPU (Alert, responds to Voice, responds to Pain, Unresponsive) is the faster, simpler alternative for the triage, the paramedic handover, and the serial ward assessment. It does not require the detailed testing and it correlates roughly with the GCS — A = GCS 15, V = GCS 13, P = GCS 8, U = GCS 3. The P (responds to Pain) is the threshold for the airway threat — the patient who responds only to pain has the GCS of around 8, and the airway should be reassessed and the intubation considered.[3]

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The FOUR score — the alternative that captures the brainstem

The FOUR (Full Outline of UnResponsiveness) score was developed by Wijdicks to address the limitations of the GCS — the loss of the verbal component in the intubated patient and the absence of the brainstem assessment. It has four components, each scored 0 to 4, with the maximum of 16 and the minimum of 0: the eye response, the motor response, the brainstem reflexes, and the respiration. The FOUR score can be performed in the intubated patient (it has no verbal component), it captures the brainstem function (the GCS does not), and it distinguishes the locked-in syndrome (the normal FOUR with the absent verbal) from the true coma.[5]

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The causes of the coma — AEIOU TIPS

The differential of the coma is vast, but the Fellowship mnemonic AEIOU TIPS organises the causes into the eight rapid-reversibility categories. The mnemonic is the bedside checklist — every comatose patient is screened for each, because the missed reversible cause is the missed preventable death. [1]

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The differential by the speed of the onset

The Fellowship candidate must also frame the differential by the speed of the onset — the sudden onset (the vascular — the stroke, the subarachnoid, the intracerebral haemorrhage; the cardiac — the post-arrest, the arrhythmia), the rapid onset over minutes to hours (the metabolic — the hypoglycaemia, the hyponatraemia; the toxic — the overdose, the CO; the infectious — the meningitis), and the gradual onset over hours to days (the tumour, the abscess, the chronic subdural, the hepatic, the uraemic). The history from the family, the paramedic, and the nursing home is the key — the speed of the onset narrows the differential before any test. [1]

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Differential diagnosis — the toxic-metabolic vs the structural

The coma is divided into the toxic-metabolic (the bilateral cerebral dysfunction from the systemic disturbance) and the structural (the focal brainstem or the hemispheric lesion). [1]

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The specific antidotes and the rapid reversibility

The comatose patient is given the specific antidotes empirically if the cause is suspected, because the diagnosis may be unclear at the presentation and the delay to the antidote may be the irreversible injury: [1]

• Naloxone 400 mcg IV (or 800 mcg IM) for the suspected opioid overdose (the pin-point pupils, the reduced respiratory rate, the needle marks). Titrate to the respiratory rate, not the full reversal — the rapid reversal causes the acute withdrawal and the agitation.
• Flumazenil 200 mcg IV for the suspected benzodiazepine overdose. Use cautiously — it may precipitate the seizures in the chronic user or the mixed overdose.
• Glucose 25 g IV for the hypoglycaemia (the finger-prick glucose below 3 mmol/L).
• Thiamine 100 mg IV for the suspected Wernicke encephalopathy (the alcoholic, the malnourished).
• Naloxone and the glucose are given to every comatose patient of unknown cause — the "coma cocktail." [1]

The investigations

The finger-prick glucose is the first test. The venous blood gas (the pH, the lactate, the electrolytes, the glucose, the carboxyhaemoglobin if the CO poisoning is suspected). The full blood count, the U&E, the LFTs, the troponin, the coagulation. The drug screen (the paracetamol level, the salicylate level, the ethanol level, the toxicology screen if the overdose is suspected). The urinalysis (the ketones for the DKA, the drug screen). The non-contrast CT of the brain if the structural cause is suspected or the toxic-metabolic screen is unrevealing. The lumbar puncture if the meningitis or the encephalitis is suspected (after the CT). The EEG if the non-convulsive status epilepticus is suspected (the patient who does not wake up after the seizure).[1]

The neurological examination

The comatose patient is examined for the clues to the cause: the pupils (the pin-point of the opioid or the pontine haemorrhage; the dilated of the atropine or the post-anoxic; the asymmetric of the third-nerve palsy or the uncal herniation), the eye movements (the doll's-eye reflex and the caloric testing — the intact brainstem moves the eyes conjugately), the corneal reflex (the intact facial nerve and the trigeminal nerve), the gag reflex (the intact glossopharyngeal and the vagus), the motor response (the purposeful movement vs the posturing — the decorticate flexion suggests the cortical lesion, the decerebrate extension suggests the brainstem lesion), the reflexes and the plantar responses (the Babinski sign in the upper-motor-neurone lesion), and the meningism (the neck stiffness of the meningitis or the subarachnoid haemorrhage). [1]

The pupils — the window to the brainstem

The pupils are the single most informative bedside sign in the comatose patient, because the pupillary light reflex is robust — it is the last reflex to be lost in the toxic-metabolic coma (the barbiturate, the ethanol) and it is the first reflex to be lost in the structural brainstem lesion. The Fellowship candidate must record the size, the symmetry, and the reactivity of both pupils, and the lesion is inferred from the pattern.[8]

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The brainstem reflexes — the systematic assessment

The brainstem reflexes are assessed to localise the level of the lesion (the diencephalon, the midbrain, the pons, the medulla) and to detect the progression of the herniation. There are four reflexes that the Fellowship candidate must elicit in every comatose patient: the pupillary, the corneal, the gag (and the cough), and the oculomotor (the doll's-eye and the cold-caloric). [1]

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The motor response — the posturing and the level

The motor response to the pain localises the lesion: the purposeful movement (the localisation above the clavicle) indicates the intact cortex; the decorticate posturing (the M3 — the slow flexion, the adduction of the arm, the extension of the leg) indicates the hemispheric or the thalamic lesion with the intact brainstem; the decerebrate posturing (the M2 — the extension, the adduction, the internal rotation of the arm, the extension of the leg) indicates the midbrain or the upper-pons lesion. The flaccidity with no response (the M1) indicates the lower-pons or the medullary lesion — the deep brainstem involvement and the poor prognosis. [1]

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Intubation criteria — when to secure the airway

The comatose patient is intubated when the airway is threatened, the protective reflexes are lost, or the ventilation is inadequate. The Fellowship criteria are: [1]

1. GCS 8 or below — the airway reflexes are unreliable below this threshold; the risk of the aspiration and the hypoventilation mandates the definitive airway.
2. The loss of the gag or the cough reflex — the unprotected airway, regardless of the GCS.
3. The hypoventilation — the respiratory rate below 8, the rising CO₂, the falling oxygen.
4. The inability to maintain or protect the airway — the pooling of the secretions, the noisy breathing, the absent swallow.
5. The predicted deterioration — the rising intracranial pressure, the expanding haematoma, the impending herniation. [1]

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Herniation syndromes — the time-critical structural coma

The herniation is the displacement of the brain across the dural folds, and it is the final common pathway of the expanding intracranial mass — the minutes matter. There are four syndromes that the Fellowship candidate must recognise:[8]

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The Cushing reflex — the late sign of the rising intracranial pressure

The Cushing reflex (the hypertension, the bradycardia, the irregular respiration) is the brainstem response to the rising intracranial pressure — the hypertension to maintain the cerebral perfusion, the bradycardia from the baroreceptor reflex, the irregular breathing from the brainstem distortion. It is a late sign — by the time it appears, the herniation is imminent. The hypertension with the bradycardia in the comatose patient is the raised intracranial pressure until proven otherwise — the head elevation 30 degrees, the hyperventilation, the mannitol or the hypertonic saline, the urgent CT and the neurosurgery. [1]

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Prognosis — the post-anoxic coma and the predictors

The prognosis of the coma depends on the cause, but the post-anoxic coma (after the cardiac arrest) is the one for which the evidence is strongest, because the systematic prognostication is the standard of care. The Fellowship candidate must know the ERC-ESICM stepwise algorithm and the predictors of the poor outcome.[6][7]

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The locked-in syndrome and the cognitive-motor dissociation

The locked-in syndrome (the de-efferented state — the quadriplegia and the anarthria with the preserved consciousness) is caused by the pontine lesion (the basilar-artery occlusion) that spares the cortex. The patient is awake and aware but can move only the vertical eyes and the eyelids — the command-following eye movement is the diagnostic sign. The Fellowship candidate must test the eye tracking in every comatose patient, because the misdiagnosis of the locked-in as the vegetative is the catastrophic error — the patient hears the conversation about the withdrawal of the care. The modern fMRI and the EEG reveal the cognitive-motor dissociation (the patient who is behaviourally unconscious but who can follow commands on the neuroimaging) in up to 25 per cent of the patients with the disorders of the consciousness — the implications for the prognostication and the end-of-life decisions are profound.[9]

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Management — the airway and the disposition

The airway is the priority — the comatose patient with the GCS of 8 or below, the loss of the protective reflexes, or the hypoventilation is intubated. The rapid sequence intubation with etomidate 0.3 mg/kg IV and rocuronium 1.2 mg/kg IV is used to protect the C-spine and to prevent the aspiration. The specific antidotes are given before the intubation if the rapidly reversible cause is suspected: naloxone 400 mcg IV for the opioid, glucose 25 g IV for the hypoglycaemia, flumazenil 200 mcg IV for the benzodiazepine. The comatose patient with the suspected meningitis is given ceftriaxone 2 g IV, vancomycin 1.5 g IV, dexamethasone 10 mg IV, and aciclovir 10 mg/kg IV before the LP. The comatose patient is admitted to the HDU or the ICU; the patient with the rapidly reversible cause (the hypoglycaemia, the opioid) who recovers fully may be discharged after the observation and the cause investigation. The raised intracranial pressure is treated with the head elevation 30 degrees, the mannitol 0.5 g/kg IV or the hypertonic saline 3 per cent 250 mL IV, and the urgent neurosurgical referral for the definitive decompression.[2]

Complications and prognosis

The complications are the aspiration pneumonia (the reduced consciousness and the loss of the protective reflexes — the commonest pulmonary complication, treated with the ceftriaxone 2 g IV), the pressure sores (the regular turning and the pressure-area care), the venous thromboembolism (the prophylactic enoxaparin 40 mg subcutaneously daily and the compression stockings), the rhabdomyolysis (from the prolonged immobility — check the creatine kinase, treat with the aggressive IV fluid to maintain the urine output), the corneal abrasion (from the incomplete eye closure — the eye taping and the lubricant), the seizures (the prophylactic levetiracetam), and the death. The prognosis depends on the cause and the depth of the coma: the toxic-metabolic coma is often fully reversible with the specific antidote; the structural coma (the intracerebral haemorrhage, the traumatic brain injury) has a variable prognosis depending on the lesion size and the GCS at the presentation; the post-anoxic coma (after the cardiac arrest) has the worst prognosis, particularly if the pupil reflexes are absent at 24 hours or the somatosensory evoked potentials are absent at 72 hours. [1]

Evidence and regional guidelines

The contemporary framework is the GCS for the serial assessment, the CT for the structural exclusion, the rapid glucose for the hypoglycaemia, and the coma cocktail (the naloxone, the glucose, the thiamine) for the empiric reversal.[1]

Exam practice

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Exam pearls

• The glucose first — the hypoglycaemia is the commonest rapidly reversible cause.
• GCS 8 or below = intubate. The motor response is the most sensitive component.
• AVPU for the rapid triage: A = GCS 15, V = 13, P = 8, U = 3.
• The "coma cocktail": naloxone 400 mcg IV, glucose 25 g IV, thiamine 100 mg IV.
• Thiamine before the glucose in the alcoholic — to prevent the Wernicke encephalopathy.
• The asymmetric pupils or the unilateral weakness = the structural lesion until proven otherwise.
• The non-convulsive status epilepticus is the cause of the unexplained coma — the EEG is diagnostic.
• The doll's-eye reflex and the caloric testing assess the brainstem integrity.
• E4V5M6 = 15 (the max); E1V1M1 = 3 (the min) — there is no score of 0. Record the components separately, not just the total.
• The FOUR score (eye, motor, brainstem, respiration; 0–16) for the intubated patient and the suspected brainstem lesion — it has no verbal component.
• AEIOU TIPS — Alcohol, Epilepsy, Insulin, Overdose, Uraemia, Trauma, Infection, Poisoning, Stroke. The bedside checklist for every comatose patient.
• The pupils: pinpoint = opioids or pontine; small reactive = metabolic or early herniation; mid-position fixed = midbrain; dilated fixed = uncal herniation or post-anoxic.
• The pupillary reflex is the last to be lost in the metabolic coma and the first to be lost in the structural — equal reactive pupils point to the metabolic.
• The cold-caloric (COWS: Cold-Opposite, Warm-Same) for the brainstem if the C-spine is not cleared — never do the Doll's eyes if the C-spine is uncleared.
• Decorticate (M3, flexion) = above the red nucleus (the hemisphere); decerebrate (M2, extension) = at or below the red nucleus (the midbrain).
• The central pain stimulus (the supraorbital, the trapezius) — not the nail-bed, which gives the spinal-reflex withdrawal misread as M4.
• Cushing triad (hypertension, bradycardia, irregular breathing) — a late sign of the rising ICP; the herniation is imminent.
• Always CT before the LP in the comatose patient — the LP herniates the brain (the posterior fossa mass, the obstructive hydrocephalus).
• The locked-in syndrome (the pontine lesion) — the vertical eye movement is preserved; test the eye tracking in every comatose patient.
• The post-anoxic prognosis: the bilaterally absent pupil reflex at ≥72 h or the absent N20 SSEP at ≥24 h — the reliable poor-outcome predictors.
• The empirical antibiotics (the ceftriaxone 2 g, the vancomycin, the aciclovir 10 mg/kg) before the LP — the imaging delay is not the treatment delay.
• The flumazenil is the cautious antidote — it precipitates the seizures in the chronic user and the mixed overdose; reserve for the isolated iatrogenic or the pure benzodiazepine. [1]

Red flags

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References

1. [1]Expert Panel on Neurological Imaging, Ledbetter LS, Shah LM, et al. ACR Appropriateness Criteria® Altered Mental Status, Coma, Delirium, and Psychosis: 2024 Update J Am Coll Radiol, 2024.PMID 39488349
2. [2]Llorens P, Piqueras-Rodriguez F, Herrero P, et al. Prevalence, risk factors, and prognosis of the need for physical and chemical restraint in older patients attending emergency departments. EDEN-50 Am J Emerg Med, 2026.PMID 42000676
3. [3]Teasdale G, Maas A, Lecky F, et al. The Glasgow Coma Scale at 40 years: standing the test of time Lancet Neurol, 2014.PMID 25030516
4. [4]Aguilar-Fuentes V, Orozco-Puga P, Jiménez-Ruiz A The Glasgow Coma Scale: 50-year anniversary Neurol Sci, 2024.PMID 38436790
5. [5]Wijdicks EFM, Bamlet WR, Maramattom BV, et al. Validation of a new coma scale: The FOUR score Ann Neurol, 2005.PMID 16178024
6. [6]Sandroni C, D'Arrigo S, Cacciola S, et al. Prediction of poor neurological outcome in comatose survivors of cardiac arrest: a systematic review Intensive Care Med, 2020.PMID 32915254
7. [7]Scarpino M, Lolli F, Lanzo G, et al. Do changes in SSEP amplitude over time predict the outcome of comatose survivors of cardiac arrest? Resuscitation, 2022.PMID 36375653
8. [8]Hall WA, Munakomi S Uncal Herniation 2026.PMID 30725793
9. [9]Bodien YG, Allanson J, Cardone P, et al. Cognitive Motor Dissociation in Disorders of Consciousness N Engl J Med, 2024.PMID 39141852