The Patient with Reduced Consciousness

Introduction

Reduced consciousness is a presentation, not a diagnosis. It ranges from mild drowsiness to deep coma, and the underlying cause can be anything from an easily reversible metabolic derangement to a catastrophic intracranial event - which is why the assessment has to be systematic rather than led by a guess at the diagnosis.

The physiological basis is either diffuse dysfunction of both cerebral hemispheres (most metabolic, toxic and infective causes) or dysfunction of the reticular activating system in the brainstem (structural lesions, particularly those causing brainstem compression). This distinction is why a normal brainstem examination in a globally unresponsive patient points towards a metabolic or toxic cause, while asymmetric findings point towards a structural one.

In UK emergency departments, the commonest identifiable causes are broadly metabolic and toxic - alcohol, prescribed and illicit drugs, and hypoglycaemia account for a large share of presentations - followed by post-ictal states, stroke, and infection. Holding all of these in mind at once, rather than anchoring early on the most memorable diagnosis, is what the structured approach below is designed to achieve.

The single most important habit is to treat reduced consciousness as a medical emergency requiring an ABCDE assessment first, and a differential diagnosis second.¹ A GCS calculated before the airway is secured is meaningless if the patient goes on to aspirate.

Immediate assessment

Follow the ABCDE structure, with disability given particular weight in this presentation.

• Airway - check patency and protective reflexes; a GCS of 8 or below is assumed to mean the airway is unprotected
• Breathing - respiratory rate and pattern (Cheyne-Stokes breathing suggests bilateral hemispheric or diencephalic dysfunction), oxygen saturation, and an arterial blood gas to assess for hypoxia and hypercapnia
• Circulation - blood pressure (both severe hypotension and malignant hypertension can impair consciousness), pulse, and signs of sepsis or shock
• Disability - AVPU or GCS, pupils, blood glucose, focal neurology, temperature (see below for grading)
• Exposure - look for a medical alert bracelet, needle marks, signs of trauma, rashes (non-blanching purpura suggests meningococcal sepsis), and fetor (ketotic, hepatic, uraemic, alcoholic)

Grading the conscious level

AVPU (Alert, responds to Voice, responds to Pain, Unresponsive) is a fast screening tool suitable for the initial ABCDE pass. The Glasgow Coma Scale gives a more granular, reproducible score out of 15 that can be trended over time, which matters more than any single reading.

A useful rule of thumb: roughly, AVPU 'V' correlates with a GCS around 12-13, 'P' with a GCS around 8, though this is only approximate and should not replace a formal score when precision matters, such as after head injury.

Brainstem examination

In deeper unresponsiveness, brainstem reflexes help localise the problem and distinguish a structural brainstem lesion from a metabolic or toxic cause, which typically preserves them until very late.

• Pupillary light reflex - preserved in most metabolic and toxic causes (opioids being a notable exception, causing pinpoint but reactive pupils); absent or asymmetric suggests a structural lesion
• Corneal reflex - absent bilaterally suggests deep coma or brainstem dysfunction
• Oculocephalic reflex (doll's eye) - only tested once cervical spine injury has been excluded; preserved reflex eye movement (eyes stay fixed on a point as the head is turned) suggests an intact brainstem
• Gag and cough reflex - relevant to airway protection as much as localisation; their absence is itself an indication to secure the airway
• Respiratory pattern - Cheyne-Stokes breathing (cyclical waxing and waning) suggests bilateral hemispheric or diencephalic dysfunction; ataxic, irregular breathing suggests a lower brainstem lesion and predicts imminent respiratory arrest

Immediately reversible causes

Three causes should be actively sought and treated in every patient with reduced consciousness of unclear cause, because doing so is fast, safe and potentially transformative.

Differential diagnosis

Once immediate threats are excluded, work through a structured differential. A useful way to organise it is by mechanism: structural, metabolic/toxic, infective, and post-ictal/functional.

Structural

• Ischaemic or haemorrhagic stroke, particularly brainstem or large territory infarcts
• Traumatic brain injury - extradural, subdural or intracerebral haemorrhage
• Subarachnoid haemorrhage
• Space-occupying lesion - tumour, abscess, with or without herniation
• Hydrocephalus

Metabolic and toxic

• Hypoglycaemia or, less acutely, severe hyperglycaemia (DKA, HHS)
• Hyponatraemia or other severe electrolyte disturbance
• Hepatic encephalopathy - raised ammonia, liver disease, precipitants such as GI bleed, infection or constipation
• Uraemic encephalopathy
• Hypercapnia (CO2 narcosis) in decompensated respiratory failure
• Myxoedema coma - hypothyroidism, hypothermia, bradycardia
• Alcohol intoxication or withdrawal
• Drug toxicity - opioids, benzodiazepines, tricyclic antidepressants, carbon monoxide
• Hypothermia or hyperthermia

Infective

• Meningitis or encephalitis
• Sepsis of any source, particularly in the elderly where confusion may be the only presenting sign
• Cerebral abscess

Other

• Post-ictal state following a seizure, witnessed or not
• Non-convulsive status epilepticus - can present as unexplained reduced consciousness without visible convulsions
• Psychogenic unresponsiveness - a diagnosis of exclusion, sometimes suggested by resistance to eye opening or normal reflex responses inconsistent with organic coma

History and examination

The patient often cannot give a history, so collateral information becomes central: paramedics, family, carers, GP records and the scene itself (empty tablet packets, alcohol, a suicide note, evidence of a fall) can be more informative than the examination.

• Onset - sudden (suggests vascular or seizure) versus gradual (suggests metabolic, infective or a slowly expanding mass)
• Preceding symptoms - headache, fever, trauma, seizure activity, chest pain, breathlessness
• Past medical history - diabetes, epilepsy, liver or renal disease, psychiatric illness
• Drug history and access to drugs - prescribed medication, illicit drugs, alcohol, and what is missing from a counted supply
• Pupils - pinpoint (opioids, pontine lesion), fixed and dilated unilaterally (third nerve palsy from uncal herniation - a neurosurgical emergency), fixed and dilated bilaterally (severe hypoxic-ischaemic injury, some drug toxicity)
• Focal neurology - asymmetric limb tone, reflexes or plantar responses suggest a structural lesion
• Signs of trauma - scalp lacerations, Battle's sign, panda eyes, CSF rhinorrhoea/otorrhoea suggest a base of skull fracture
• Neck stiffness and rash - suspect meningitis; a non-blanching purpuric rash suggests meningococcal sepsis

Investigations

• Capillary and laboratory glucose
• FBC, U&E, LFTs, calcium, magnesium, phosphate - a full metabolic screen
• Venous or arterial blood gas - hypoxia, hypercapnia, acid-base status, and lactate
• Ammonia if hepatic encephalopathy is suspected
• TFTs if myxoedema coma is a possibility
• Blood cultures and inflammatory markers if sepsis or CNS infection is suspected
• Paracetamol and salicylate levels, and a wider toxicology screen where the history suggests overdose
• ECG - arrhythmia as a cause of syncope or hypoperfusion, or QT prolongation from drug toxicity
• CT head - urgently for trauma, focal neurology, suspected raised intracranial pressure, or any unexplained reduced conscious level without a clear metabolic cause²
• Lumbar puncture - after CT has excluded a contraindication, if CNS infection or subarachnoid haemorrhage remains suspected
• EEG if non-convulsive status epilepticus is suspected

Management principles

Management runs on two tracks simultaneously: supporting physiology that is failing right now, and treating the specific cause once it becomes apparent. Neither should wait for the other - a patient with a low GCS from a large intracerebral haemorrhage still needs their airway protected while imaging and neurosurgical referral are arranged in parallel.

• Secure the airway if GCS is 8 or below, or protective reflexes are otherwise inadequate
• Treat the identified cause - glucose, naloxone, antibiotics for suspected CNS infection (do not delay for imaging or LP if bacterial meningitis is suspected),³ thrombolysis pathway for ischaemic stroke within the window, surgical evacuation for an expanding haematoma
• Manage suspected raised intracranial pressure while awaiting definitive treatment - head-up tilt to 30°, maintain normocapnia and adequate blood pressure, and involve neurosurgery early
• Regular neurological observations, including GCS trended over time - a falling GCS is more informative than a single value
• Involve critical care early if airway, breathing or circulatory support is needed, or the conscious level is fluctuating rapidly

Red flags

Prognosis

Prognosis depends entirely on the underlying cause and how quickly it is identified and treated - reversible causes such as hypoglycaemia or opioid toxicity carry an excellent prognosis if treated promptly, while a large intracranial catastrophe or prolonged hypoxic-ischaemic injury carries a poor one regardless of subsequent care. This range is exactly why the systematic, reversible-causes-first approach matters more than the eventual label attached to the presentation.