Approach to the unconscious patient and coma

• An unconscious patient is a time-critical emergency: airway, breathing and circulation first, then diagnosis and specific treatment in parallel.
• Coma means a patient is completely unaware and unresponsive even to vigorous stimulation, despite eye opening to pain at best.
• The Glasgow Coma Scale (GCS) scores eye, verbal and motor responses from 3 to 15; a score under 8 marks coma in this framework. ^[3]
• The main reversible causes are metabolic and toxic (especially hypoglycaemia, opioid overdose, alcohol), followed by structural brain disease and infection.
• Do not wait for a diagnosis before treating: check glucose immediately and give intravenous glucose, naloxone for suspected opioid toxicity and thiamine when Wernicke's encephalopathy is possible.
• Brain death is permanent coma with absent brainstem reflexes and apnoea; it is diagnosed only after catastrophic brain injury, correction of confounders, and exclusion of reversible causes.

By the end of this page you should be able to:

1. Define coma and the two mechanisms that produce it.
2. Calculate and interpret a Glasgow Coma Scale score, including its component and total ranges.
3. Use a systematic ABCDE approach to identify reversible causes early.
4. Recognise the brainstem reflexes and the pupillary and breathing patterns that localise lesions.
5. Recognise the common herniation syndromes and their red-flag signs.
6. Explain the immediate management of suspected opioid, hypoglycaemic and Wernicke's causes.
7. Outline how brain death (death by neurologic criteria) is diagnosed, and quote the temperature, blood pressure and blood gas thresholds used.
8. Compare the United States AAN consensus guideline with current United Kingdom national guidance.

Consciousness has two parts: arousal (being awake) and awareness (of self and surroundings). Coma reflects failure of both. Impaired consciousness is best described by what the patient actually does, avoiding vague labels such as "drowsy" or "mildly unconscious".^[1]

There are two main mechanisms. The first is a diffuse insult to both cerebral hemispheres (for example hypoxia, hypoglycaemia, drugs or toxins). The second is disruption of the ascending reticular activating system in the midbrain and pons, whose signals travel to the thalamus and cortex; the thalamus plays a central role in maintaining arousal and can be damaged directly or through brainstem problems.^[1] A focal lesion outside these systems, such as a small cortical stroke, does not itself cause coma.

Unconscious patients are commonly seen by physicians and are challenging to manage; the situation is time-sensitive, so a systematic team approach is required.^[1] Mortality in non-traumatic coma is high and variable; one systematic review reports a range of 25 to 87 percent.^[1] In a Swedish cohort of coma patients presenting to an emergency department, initial inpatient mortality was 27 percent, rising to 39 percent at one year.^[1] Patients with a GCS of 3 to 5 at presentation have significantly higher mortality than those with a GCS of 7 to 10.^[1]

Because many causes are reversible, early physiological stability and diagnosis are what improve outcome.^[1]

The brain is enclosed in a rigid skull. The Monro-Kellie doctrine holds that any rise in intracranial pressure is initially buffered by displacement of cerebrospinal fluid and changes in cerebral blood volume. Once those buffers are exhausted, brain tissue is driven across rigid dural folds or through skull openings, producing herniation syndromes.^[4] Brain herniation is life-threatening and needs urgent attention.^[4]

Low or absent brainstem reflexes are the clinical signature of brainstem failure. The ascending reticular activating system and the cranial nerve nuclei that mediate pupillary, corneal, oculocephalic, gag and cough reflexes sit in the midbrain, pons and medulla. Damage here, or transtentorial herniation compressing these structures, produces the coma and reflex loss that characterise the most severe cases.

Cooksley and colleagues organise the causes of non-traumatic coma into four groups (neurological, metabolic, diffuse physiological brain dysfunction, and psychiatric/functional).^[1] The table is a deliberate starting point: in a real patient the groups overlap, and trauma must be considered even when none is reported, particularly in older people and those on anticoagulants.^[1]

A clinically useful bedside mnemonic is AEIOU-TIPS: Alcohol, Epilepsy/Encephalopathy/Endocrine, Insulin (hypoglycaemia), Opiates, Uraemia, Trauma, Infection, Psychiatric, Stroke/Seizure/Syncope. It is a memory aid only; the table above is the safer working list. A very common public-domain mnemonic is included here because it helps recall; mnemonics from a copyrighted source are not copied.

For prognosis, the aetiology matters: non-traumatic coma presenting with stroke carries the highest mortality, while coma due to epilepsy or poisoning carries the best prognosis.^[1]

The four core elements of care, history, examination, investigation and treatment, should run in parallel rather than in series.^[1] A systematic ABCDE approach (airway, breathing, circulation, disability, exposure) should be used by the team.^[1]

Practical points from the same review:^[1]

• A collateral history from relatives, bystanders and paramedics is vital; paramedics are skilled at surveying the scene for clues such as drug packets or a suicide note.
• In older people, especially those on anticoagulants, intracranial bleeding remains a strong possibility even without a history of falls or external injury.
• Generalised tremor or myoclonus points toward a metabolic cause.
• Hepatic encephalopathy may produce a musty breath; organophosphate poisoning a garlic breath.
• Kussmaul breathing suggests severe metabolic acidosis (often diabetic ketoacidosis); ataxic (Biot's) breathing suggests a lower pontine lesion; central neurogenic hyperventilation (at least 25 breaths per minute) suggests a pontine or midbrain lesion; opioid overdose causes shallow breathing with a depressed rate. ^[1]
• Cheyne-Stokes breathing is seen with many pathologies and is not helpful for pinpointing a diagnosis.

If there is any doubt, immobilise the cervical spine. Death comes soonest when airway and breathing fail, so intubation should be considered in patients with a GCS of 8 or less, or in those who cannot protect their airway.^[1]

The GCS offers an objective way to describe impaired consciousness. It evaluates three aspects of responsiveness: eye opening, verbal response and motor response, each scored and reported separately as well as summed.^[3] It was formulated by Teasdale and Jennett in Glasgow in 1974; in 1977 the total score was increased from 14 to 15 points to include the withdrawal response, and zero scores for any component were excluded to avoid confusion from missing data.^[3]

Coma is defined clinically as a GCS under 8, or U on the AVPU (Alert, responsive to Voice, responsive to Pain, Unresponsive) scale.^[1]

Interpretation:^[1][3]

• The three components should be recorded separately (for example "E2 V2 M4 = GCS 8") as well as summed, because a total hides important differences.
• Motor response runs 1 to 6, verbal 1 to 5 and eye opening 1 to 4.
• A GCS of 3 to 5 carries significantly higher mortality than a GCS of 7 to 10.^[1]
• The GCS is not a diagnosis. It is a description of the level of consciousness, used in scores from trauma and critical illness and in the NIH Common Data Elements for head injury studies.
• Eye movements are hard to assess fully in an unconscious patient; where there is no concern about neck injury, the doll's eyes (oculocephalic) reflex can be tested.

StatPearls notes that the scale is used in over 75 countries.^[3]

After the ABC, perform a focused neurological examination and measure the level of consciousness formally with the GCS.^[1] Motor responses may be purposeful (the patient pulling at an airway adjunct) or reflexive (withdrawal, flexion, extension); stimuli should be applied in a graded way: verbal, then tactile, then noxious.^[1]

Pupils help localise:^[1]

• Small pupils (under 2 mm): opioid toxicity or a pontine lesion. ^[1]
• Mid-size pupils (4 to 6 mm) unresponsive to light: midbrain lesion. ^[1]
• Maximally dilated pupils (over 8 mm): drug toxicity such as anticholinergic overdose. ^[1]
• A mixed, dilated pupil: third (oculomotor) nerve compression from uncal herniation.

Eye movement examination can add localising value. Tarnutzer and colleagues remind us that assessing eye movements in a comatose patient provides information about the integrity of the brainstem and its connections to higher brain regions, and can unmask occult seizures.^[7] The doll's eyes reflex and cold caloric (oculovestibular) testing examine the same brainstem pathways; loss of conjugate movement away from the direction of head turn suggests brainstem dysfunction.^[1] Fundoscopy matters too: papilloedema in posterior reversible encephalopathy, or subhyaloid haemorrhage in subarachnoid haemorrhage.^[1]

Breathing patterns also localise (see above).

Brain herniation is pathological displacement of brain tissue across dural folds or through skull openings, driven by pressure gradients between compartments; it is life-threatening.^[4] The common clinically described types are:^[4]

1. Subfalcine (cingulate) herniation - the cingulate gyrus is pushed under the falx cerebri. ^[4]
2. Uncal herniation - the medial temporal lobe is pushed under and across the tentorium; this compresses the third (oculomotor) nerve, giving the mixed dilated pupil that heralds rising intracranial pressure. ^[4]
3. Central (descending transtentorial) herniation - downward displacement of the diencephalon and midbrain through the tentorial notch, usually from diffuse cerebral oedema or bilateral mass effect. ^[4]
4. Tonsillar herniation - the cerebellar tonsils are forced through the foramen magnum; this is immediately dangerous to the medulla and its vital centres. ^[4]
5. Upward (ascending transtentorial) herniation - a posterior fossa mass drives cerebellar structures up through the tentorial notch, distorting the midbrain and obstructing CSF pathways and venous drainage. ^[4]

Raised intracranial pressure also produces the pupillary changes described above and changes in posture (abnormal flexion or extension). Suspected raised pressure is managed in a 30 degree head-up tilt position, with neurosurgical or neurology input.^[1]

Specific treatment depends on the underlying aetiology; "coma cocktails" should be avoided.^[1] The following three are highlighted because they are time-critical and reversible, and should not wait for a full diagnosis.

Glucose. Before any other investigation, a bedside capillary blood glucose must be performed to exclude hypoglycaemia.^[1] If glucose is low (or the test is unavailable), intravenous glucose is the immediate treatment of choice: glucagon can take up to 15 minutes to act and is ineffective in patients with liver disease, depleted glycogen stores or malnutrition.^[1] Intravenous glucose should be used at a dose appropriate to the patient and formulation available; check your local formulary.

Naloxone. In cases of clinical suspicion of toxicity, specific antidotes should be used; intravenous naloxone is the antidote for opioid toxicity.^[1] Opioid overdose typically produces small (under 2 mm) pupils and shallow, slow breathing.^[1] Naloxone reverses respiratory depression; beware of renarcotisation with long-acting opioids, so observe and repeat or infuse as needed per local protocol.

Thiamine. In hypoglycaemic patients at risk of Wernicke's encephalopathy, such as those with a history of alcohol excess, intravenous thiamine should be co-administered with glucose.^[1] Thiamine is given before or with glucose in this situation to avoid precipitating or worsening Wernicke's. Dosing follows local guidance.

Other points. If benzodiazepine overdose is suspected, flumazenil can be considered, but it is contraindicated in patients with a history of seizures and can provoke seizures with concomitant tricyclic overdose.^[1] Antibiotics for suspected sepsis should be commenced early with blood cultures taken first where possible.^[1]

After the bedside glucose, the aim is to find a structural cause or an infection. Typical immediate investigations include full blood count, glucose (even if capillary glucose was normal), urea and electrolytes, calcium, liver function, clotting, toxicology (including paracetamol, salicylate and blood alcohol), ECG, chest X-ray, arterial blood gas (including carbon monoxide), and microbiology when fever or sepsis is suspected.^[1]

Urgent brain CT is important; structural pathology should always be considered if the cause is not obvious from the initial assessment. CT of the brain is the investigation of choice to exclude intracranial blood, stroke or space-occupying lesions; MRI is used if CT is normal but diagnosis remains unclear.^[1] Lumbar puncture should be considered if the cause remains unclear or a central nervous system infection is suspected, provided there is no contraindication. EEG is used when non-convulsive status epilepticus is suspected.^[1]

Brain death is the irreversible (permanent) loss of function of the brain as a whole. The AAN consensus guideline states the concept as permanent coma and loss of all brainstem function, with inability to breathe in the setting of an adequate stimulus (hypercarbia and acidosis), in a patient with a known cause of catastrophic brain injury.^[5] The clinical diagnosis rests on three things: coma, brainstem areflexia and apnoea.^[5]

Before any evaluation, the cause must be a known catastrophic mechanism (traumatic brain injury, vascular event, space-occupying lesion, hypoxic-ischaemic injury, infection, toxin or metabolic cause).^[5] Confounders must be excluded: hypothermia, hypotension, CNS-depressing drugs, neuromuscular blockade, metabolic and endocrine derangement.^[5]

• Core body temperature must be maintained at least 36 degrees Celsius before evaluation.^[5]
• Systolic blood pressure at least 100 mmHg and mean arterial pressure at least 75 mmHg in adults.^[5]
• Alcohol blood level at or under 80 mg/dL if clinically indicated, and drug levels in the therapeutic or subtherapeutic range; if levels are unavailable, allow at least 5 half-lives of CNS-depressing drugs to pass.^[5]
• Exclude pharmacologic paralysis (train-of-four or deep tendon reflexes).^[5]
• In infants and children under 24 months, wait at least 48 hours after the acute brain injury before evaluating.^[5]
• In patients older than 24 months after hypoxic-ischaemic injury, wait at least 24 hours.^[5]
• If core temperature has been under 35.5 degrees Celsius, wait at least 24 hours after rewarming to at least 36 degrees.^[5]

The patient must be comatose and unresponsive to visual, auditory and tactile stimulation, with no motor response other than spinally mediated reflexes after noxious stimulus, and absence of the following brainstem reflexes: pupillary response to bright light, corneal reflex, oculocephalic (doll's eyes) and/or oculovestibular (cold caloric) reflex, facial movement to noxious stimulus, gag reflex, cough reflex and (in infants under 6 months) sucking/rooting reflex.^[5] Spinally mediated reflexes can occur in brain death and do not invalidate the diagnosis.^[5]

Both the 2023 AAN guideline and the UK 2025 Code (see below) allow determination despite preserved neuroendocrine function, since the hypothalamic-hypophyseal axis may remain intact; this is not inconsistent with the whole-brain standard.^[5]

All adult patients need at least one apnoea test after the final neurologic examination.^[5] Pre-oxygenate for at least 10 minutes to achieve a PaO2 above 200 mmHg, ensure normal PaCO2 of 35 to 45 mmHg and pH 7.35 to 7.45 before starting (or the known chronic baseline in chronic hypercapnia), then disconnect and deliver 100 percent oxygen through a catheter at 4 to 6 L/min placed just above the carina.^[5]

The test is consistent with brain death when there are no respirations, the pH is under 7.30 and the PaCO2 is at least 60 mmHg and at least 20 mmHg above the pre-test baseline.^[5] Abort the test for hypotension, hypoxaemia (saturation under 85 percent) or a haemodynamically significant arrhythmia; a spontaneous breath means the criteria are not met.^[5]

Ancillary testing is not routinely required; it is used when a component of the examination or the apnoea test cannot be completed or interpreted.^[5] EEG (plus auditory and somatosensory evoked potentials), CT angiography and MRI/MR angiography should not be used for this purpose in the 2023 guideline.^[5] Acceptable tests include four-vessel catheter angiography, radionuclide perfusion scintigraphy and (in adults) transcranial Doppler.^[5]

The United States AAN consensus guideline (Greer et al, 2023) is the major US source for adults and children, combining adult and paediatric brain death determination into one document and updating the 2010 AAN adult and 2011 paediatric guidelines.^[6]

The United Kingdom national guidance is the Academy of Medical Royal Colleges 2025 Code of Practice for the Diagnosis and Confirmation of Death, an authoritative medical consensus for all contexts and all age groups in the UK; the 2026 review by Scott and Thomas summarises its key changes.^[8] The two guidance sets broadly agree, but with differences worth knowing:

• Age limit: UK guidance makes the transition to adult criteria at 2 years rather than 2 months, closer to US practice.^[8]
• Apnoea test: UK end targets are PaCO2 at least 60 mmHg (8.0 kPa) and pH under 7.30, with a minimum apnoea period of 5 minutes and a rise of at least 20 mmHg from a starting PaCO2 of at least 40 mmHg, aligning with international targets.^[8]
• Temperature: UK guidance requires a minimum core temperature of 36 degrees at testing, with at least 24 hours' observation after correction if it has been under 36 degrees (except transient and temporary reductions).^{[8] [5]}
• Number of tests and apnoea tests: UK practice for brain death diagnosis uses two sets of clinical tests (age-adjusted), whereas the 2023 AAN guideline requires only one examination and one apnoea test in adults.^[5][8]
• Ancillary tests: the 2025 UK Code expects ancillary testing when, for example, the eyes or ears cannot be examined; EEG has been removed from routine UK use, similar to the 2023 AAN position.
• The UK Code's definition is framed as permanent loss of the capacity for consciousness with permanent loss of the capacity to breathe, identified by permanent cessation of brainstem function.^[8]
• Age under 37 weeks corrected gestation: neither UK nor US guidance supports diagnosing brain death at this age.^[5][8]

Prognosis in non-traumatic coma depends on cause, GCS at presentation and comorbidity.^[1] Mortality ranges widely (25 to 87 percent in one systematic review); patients with GCS 3 to 5 fare worse than those with GCS 7 to 10.^[1] Stroke-related coma carries the highest mortality; epilepsy or poisoning the best.^[1] Survival and recovery are best discussed with senior physicians, critical care and (for poor prognosis) the patient's family, including ceilings of care and cardiopulmonary resuscitation decisions.^[1]

• Children. Myths aside, the GCS was developed for adults and adapted for children; in younger children, modified scores are used, but the principles here remain the same. Coma in a child demands the same ABCDE approach, glucose check and senior involvement. Brain death diagnosis in children follows paediatric-specific guidance (age-adjusted observation periods, two examinations).
• Older adults. Even after minor injury, or in the absence of a witnessed fall, intracranial bleeding is common in anticoagulated older patients; image early.^[1]
• Pregnancy. If a catastrophically brain-injured pregnant patient is determined brain dead, organ support may be continued to achieve delivery of a viable infant; this decision requires maternal-fetal medicine, neonatology and neurology input, and is ethically complex.^[5]
• Low-resource settings. The bedside capillary glucose is the one immediate test that must not be missed; without CT, clinical localisation (pupils, breathing patterns, level of consciousness) and the history guide management, and referral for neuroimaging should be arranged urgently where possible. Intubation and airway protection depend on available skills and equipment; escalate early.

Ocular motor and vestibular examination of the comatose patient gives information about brainstem integrity and its rostral connections and can reveal occult seizures.^[7] In modern practice this is now the standard of care rather than an optional refinement.

• Coma is complete unawareness and unresponsiveness; describe what the patient does rather than using vague labels.
• The two mechanisms are diffuse cerebral insult and disruption of the ascending reticular activating system in the midbrain and pons.
• Use an ABCDE approach with history, examination, investigation and treatment running in parallel.
• Always check bedside glucose first; give intravenous glucose, naloxone for opioid toxicity and intravenous thiamine with glucose when Wernicke's is possible; avoid coma cocktails.
• Coma is GCS under 8 (or U on AVPU); record components separately as well as the total.
• GCS motor response 1 to 6, verbal 1 to 5, eye opening 1 to 4; total 3 to 15. ^[1]
• Pupils, eye movements and breathing patterns localise; a dilated pupil suggests uncal herniation.
• Common herniation types are subfalcine, uncal, central, tonsillar and upward; herniation is life-threatening.
• Urgent brain CT excludes blood, stroke and mass; MRI follows if CT is unrevealing.
• Brain death requires permanent coma, brainstem areflexia and apnoea in a patient with a known catastrophic brain injury after confounders are excluded.
• Brain-death testing thresholds include temperature at least 36 degrees, adult blood pressure systolic at least 100 and MAP at least 75 mmHg, apnoea test PaCO2 at least 60 mmHg and pH under 7.30. ^[5]
• EEG, CT angiography and MRI angiography should not be used as ancillary tests in the 2023 AAN guideline.
• UK 2025 national guidance and the US AAN 2023 guideline agree on most thresholds but differ in number of examinations.

Read next: increased intracranial pressure, stroke, hypoglycaemia and diabetic ketoacidosis, opioid overdose and toxidromes, Wernicke encephalopathy, subarachnoid haemorrhage, status epilepticus, airway management and rapid sequence intubation.