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Educational draft · awaiting clinical reviewUse Rapid for revision, not patient-care decisions. Check current national and local guidance and the BNF or BNFC before acting.

Coma, reduced consciousness and brain death testing

Neurology · UK scope · Sources checked 27 Aug 2026 · Clinical review pending

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Escalate

Any unexplained reduction in consciousness is an emergency: protect the airway, support breathing and circulation, check glucose immediately, treat seizures and rapidly reversible causes, assess trauma and obtain senior anaesthetic, emergency, neurological or neurosurgical help. Neurological criteria for death are never assessed until prerequisites and exclusions in the current UK Code of Practice are met by appropriately qualified clinicians.

Synopsis

Stabilise and investigate reduced consciousness systematically, distinguish reversible depression from catastrophic brain injury and understand the tightly governed UK process for diagnosing death using neurological criteria.

  • Use ABCDE before neurological taxonomy. Hypoxia, hypercapnia, hypotension and hypoglycaemia can cause or worsen brain injury and must be corrected while history and examination proceed.
  • Record the best eye, verbal and motor responses that make up GCS, not only the total. Note intubation, language, hearing, sedation, paralysis, facial injury and baseline disability that limit components.
  • Establish exact onset and trajectory from witnesses, ambulance records and digital or medication evidence; ask about trauma, headache, seizure, fever, toxins, diabetes, pregnancy, organ failure and psychiatric risk.
  • Inspect pupils, gaze, eye position, motor asymmetry, tone, reflexes, plantar responses, breathing pattern, meningism, rash, temperature and signs of trauma while avoiding repeated painful stimulation.
  • Pinpoint pupils and respiratory depression suggest opioid effect but are not diagnostic; unequal or newly fixed pupils may indicate herniation, ocular trauma, drug exposure or pre-existing disease.
  • Postictal states usually improve. Persistent failure to recover, subtle twitching, gaze deviation, recurrent episodes or unexplained coma raises non-convulsive status and the need for urgent EEG advice.
  • A normal initial CT does not exclude early ischaemia, meningitis, encephalitis, toxic-metabolic disease, non-convulsive seizure or all diffuse axonal injuries.
  • Brainstem reflex examination used during resuscitation is not equivalent to formal neurological determination of death; sedatives, neuromuscular blockade and metabolic or temperature confounders must be resolved.
  • The 2025 UK Code of Practice is the controlling reference for neurological criteria for death. Testing follows a documented plan, prescribed prerequisites, specified brainstem and apnoea components, and required examiner standards.
  • Spinally mediated movement can occur after death has been confirmed using neurological criteria; clinicians should anticipate and explain this possibility without improvising interpretation.
  • Communication with family should be staged, clear and separate diagnosis of death from possible donation discussions, using the terminology and support set out in national and local policy.

Key red flags

Impending herniation pattern

Falling consciousness with a newly dilated or unreactive pupil, progressive motor asymmetry, abnormal posturing, irregular respiration or Cushing-type physiology raises critical intracranial mass effect and requires immediate airway, neurosurgical and imaging action.

Toxic opioid pattern

Reduced respiratory rate and tidal volume, impaired consciousness and small pupils with a compatible exposure suggests opioid toxicity. Hypoxia, mixed overdose and intracranial disease must still be considered, and response to naloxone does not end observation.

Meningoencephalitic pattern

Fever, headache, photophobia, neck stiffness, rash, seizures, focal findings or behavioural change may indicate meningitis or encephalitis. Classic meningism can be absent in older, immunocompromised or deeply obtunded patients.

Non-convulsive seizure pattern

Unexplained persistent unresponsiveness, fluctuating cognition, subtle facial or limb twitching, eyelid myoclonia or eye deviation after a seizure or brain injury can represent ongoing electrical seizure and requires urgent EEG-supported assessment.

Diffuse metabolic encephalopathy

Symmetric motor findings, asterixis, multifocal myoclonus and fluctuating arousal with organ failure or biochemical disturbance suggests metabolic dysfunction, but new focal signs still mandate structural assessment.

Locked-in mimic of coma

A patient with ventral pontine injury may be conscious but quadriplegic and anarthric, retaining vertical eye movement or blinking. Deliberately test command-following through eye movements before concluding awareness is absent.

Investigation priorities

01
Immediate glucose, blood gas and ECGFirst step

Identify rapidly reversible hypoglycaemia, ventilatory failure, acid-base disturbance and cardiotoxic or electrolyte effects.

Management branches

Undifferentiated comaResuscitate and diagnose in parallel

A patient is unresponsive or substantially below their documented baseline without an established immediately reversible explanation.

  1. Call for senior and airway help, use cervical-spine precautions when indicated, support oxygenation, ventilation and circulation, check glucose, gain IV access and treat active convulsive seizure.
  2. Obtain collateral history and examine GCS components, pupils, gaze, limbs, breathing, temperature, rash and trauma; send focused blood tests, ECG and toxicology samples without delaying urgent CT.
  3. Treat suspected infection, poisoning, metabolic crisis or intracranial catastrophe through the relevant protocol and repeat neurological findings after each intervention or deterioration.

Key medicines

Intravenous glucose for severe hypoglycaemiaGive 150–200 mL glucose 10% or 75–100 mL glucose 20% intravenously, then recheck promptly and repeat or infuse according to response and local emergency policy.Ensure IV patency because hypertonic glucose extravasation injures tissue; investigate the cause, monitor for recurrence and do not delay glucose while arranging thiamine in a malnourished patient.
Naloxone for suspected opioid toxicityTitrate intravenous naloxone in locally approved increments to restore adequate ventilation rather than full alertness; use the current emergency or toxicology protocol and repeat dosing or infusion when long-acting opioids outlast it.Abrupt high-dose reversal can precipitate severe withdrawal, agitation, vomiting and sympathetic stress; its duration may be shorter than the opioid, and non-response does not exclude another emergency.
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Sources and review status4 sources · checked 27 Aug 2026 · clinical review pending+
Sources

Sources and review status

National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.

  • AoMRC 2025 diagnosis and confirmation of death CodeCurrent authoritative UK criteria, professional process and communication standards for diagnosing death.
  • NICE NG232 head injury recommendationsEmergency assessment, imaging and serial observation standards for trauma-related reduced consciousness.
  • Resuscitation Council UK adult advanced life supportABCDE resuscitation, reversible-cause and post-resuscitation principles for the critically unresponsive adult.
  • NICE NG217 epilepsy recommendationsAssessment and treatment standards for convulsive and non-convulsive seizure-related impaired consciousness.

Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem · Content changes

Authoring stateRapid draftClinical stateAwaiting reviewJurisdictionUnited Kingdom