01OverviewDefinition, clinical context and the essential points that orientate the chapter.
Consciousness depends on functioning cerebral hemispheres and the brainstem arousal system. A focal lesion can impair awareness through mass effect or brainstem involvement, whereas glucose deprivation, hypoxia, carbon dioxide retention and toxins can impair distributed neuronal function. This distinction helps organise the differential, but mixed causes are common: an intoxicated person may also have fallen, aspirated and developed hypoglycaemia.
The examination has two simultaneous aims: identifying immediate physiological threats and finding evidence of the cause. Obtain the last known normal time and collateral information from witnesses, carers, ambulance staff and medication records. Establish baseline cognition, communication and mobility. An apparent low verbal score may reflect aphasia or a language barrier, while a newly falling motor response can signal genuine deterioration requiring immediate escalation.
Key points
- A glucose measurement belongs in the initial assessment of every unexplained reduction in consciousness.
- Record eye, verbal and motor Glasgow Coma Scale components, pupils and their trend; the total alone loses useful information.
- Alcohol on the breath or an apparent overdose does not exclude head injury, haemorrhage, infection or hypoglycaemia.
- Protect ventilation before moving an unstable patient to CT; oxygen saturation can remain normal during hypoventilation on oxygen.
- New focal weakness, unequal pupils or deteriorating motor response needs urgent investigation for structural intracranial disease.
- Persistent failure to recover after a seizure requires reconsideration of the diagnosis, including non-convulsive status and an underlying brain lesion.
02AetiologyUnderlying causes, associations and risk factors, with why each one matters.
Structural disease
Haemorrhage, traumatic lesions, large infarction and hydrocephalus can impair consciousness through disrupted arousal pathways or pressure effects. Focal findings and the time course help prioritise imaging and specialist referral.
Systemic or toxic causes
Hypoglycaemia, hypoxia, hypercapnia, infection and sedating drugs impair neuronal function without requiring a focal brain lesion. Several mechanisms may coexist and require treatment in parallel.
03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.
- 1Energy failure
Neurons depend on continuous delivery of oxygen and glucose. Inadequate supply impairs function rapidly and can cause seizures or lasting injury if the physiological problem persists.
- 2Pressure and brainstem dysfunction
An expanding intracranial lesion can distort brainstem structures and compromise cerebral perfusion. Deteriorating conscious level with pupil asymmetry therefore demands urgent assessment rather than prolonged observation alone.
- 3Drug-related hypoventilation
Depressed respiratory drive raises arterial carbon dioxide, which can further impair awareness. Supplemental oxygen may correct hypoxaemia while leaving this mechanism untreated, making respiratory examination essential.
04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.
Listen for obstructive noise and inspect respiratory depth as well as rate. Bradypnoea suggests drug effect or central respiratory failure; deep rapid breathing can accompany metabolic acidosis. Neither pattern establishes a diagnosis without further assessment.
Compare pupils, limb movement and response to commands. Lateralising signs, a recent severe headache, head trauma or anticoagulant use raise concern for intracranial pathology even when an alternative metabolic abnormality is also present.
Look for fever, hypothermia, shock, purpura, dehydration and abnormal glucose. Cerebral dysfunction may be the first conspicuous sign of sepsis or endocrine failure, particularly in an older adult with little physiological reserve.
Small pupils with depressed ventilation support opioid toxicity. A witnessed convulsion, tongue injury or transient confusion supports a seizure, but continuing rhythmic twitching or unexplained failure to wake should prompt specialist assessment for ongoing seizure activity.
05InvestigationsWhat to request, why it matters and how to interpret it.
Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.
- 01
Bedside glucose and blood gasFirst step - Why
- Identify a rapidly reversible substrate problem and assess ventilation or acidaemia.
- Interpretation and limitations
- Treat a low glucose immediately rather than awaiting central laboratory confirmation. A raised carbon dioxide tension may explain drowsiness but still requires assessment of airway protection and the cause of ventilatory failure.
- 02
Urgent CT head when indicated - Why
- Identify haemorrhage, traumatic injury, hydrocephalus or another structural cause.
- Interpretation and limitations
- After head injury in an adult, a focal neurological deficit, post-traumatic seizure or initial GCS of 12 or less is a NICE indication for CT within one hour. Stabilise airway and circulation during preparation.
- 03
Electrolytes, renal and liver tests - Why
- Investigate metabolic encephalopathy and guide treatment safety.
- Interpretation and limitations
- Sodium, calcium and renal abnormalities may be causal or contributory. Interpret the size and rate of change; a longstanding modest abnormality should not prematurely close the investigation of sudden coma.
- 04
ECG, selected toxicology and EEG - Why
- Detect poisoning complications and investigate persistent unexplained impaired awareness.
- Interpretation and limitations
- An ECG can reveal conduction toxicity before a drug is identified. Request specific drug concentrations when they change management; urgent EEG needs neurological coordination when non-convulsive status is suspected.
06Differential diagnosisRealistic alternatives and the features that help distinguish them.
Postictal state
Confusion and sleepiness may follow a seizure, but the expected direction is recovery. Persistent or worsening impairment requires reconsideration of ongoing seizure activity, injury, infection or a metabolic trigger.
Metabolic encephalopathy
Glucose, sodium, calcium, renal or hepatic disturbances can produce diffuse dysfunction. The clinical picture and change from baseline determine whether the laboratory finding adequately explains the presentation.
Intracranial emergency
Trauma, sudden headache, focal weakness or unequal pupils increase concern for structural disease. A concurrent low glucose or positive drug history does not safely exclude a second diagnosis.
07ManagementImmediate care, first-line treatment, alternatives and escalation.
01Worked caseGlucose correction with an unresolved neurological deficitFirst stepAn insulin-treated adult becomes unconscious after a fall. Glucose is 2.1 mmol/L; IV access is present, breathing is adequate with airway support, and the left arm moves less than the right.+
- 1Protect the airway, maintain cervical precautions appropriate to the fall, summon senior help and administer IV glucose immediately while another clinician records neurological findings.
- 2Give 200 mL of 10% glucose over 15 minutes, checking the prescribed volume so that a larger bag is not inadvertently infused. Recheck glucose ten minutes after treatment.
- 3The repeat glucose is 5.4 mmol/L and the patient begins speaking, but left arm weakness persists. The biochemical response has corrected one problem; it does not explain away the focal deficit.
- 4Arrange CT head within one hour under the adult head-injury pathway, with continuing observations and an explicit airway plan for transfer. Communicate the fall, original glucose, treatment and residual deficit.
- 5After imaging and acute assessment, identify the insulin dose and missed food contributing to the episode. Plan repeat glucose checks and medication review; do not reflexively stop all basal insulin in type 1 diabetes.
02Seizure branchA convulsion continues beyond five minutesGeneralised convulsions persist despite immediate airway support and correction of hypoglycaemia, with IV access and resuscitation equipment available.+
- 1First lineFollow an immediately available individual emergency plan; otherwise give IV lorazepam as first-line treatment and record all prehospital benzodiazepine doses.
- 2Second lineIf seizure activity continues, obtain expert help and give a second benzodiazepine dose after five to ten minutes. Prepare second-line IV antiseizure treatment after two doses rather than repeatedly stacking benzodiazepines.
- 3Verify both seizure termination and adequate breathing. Persistent unconsciousness may reflect medication, the underlying disease or continuing non-convulsive seizure activity and requires an active assessment plan.
03Toxic branchDepressed breathing after a suspected opioidAn adult has a pulse but breathes five times per minute, with small pupils and evidence of recent opioid exposure.+
- 1Support the airway and ventilate with a bag-mask device while help and monitoring are obtained; do not wait for toxicology tests or an antidote response before providing ventilation.
- 2Use titrated naloxone appropriate to the severity and context, seeking recovery of effective spontaneous breathing and airway reflexes rather than forcing complete arousal.
- 3Reassess for recurrent respiratory depression and other causes if the response is incomplete. Arrange continued observation because the opioid effect may outlast the antagonist.
Key medicines and prescribing safety3 treatments · regimens, roles and cautions+
Glucose for severe hypoglycaemia
Give 200 mL of 10% glucose IV over 15 minutes, or 100 mL of 20% glucose over 15 minutes; both provide 20 g. Recheck glucose ten minutes later and repeat if it remains below 4 mmol/L.Check cannula patency and the exact volume. Consider the smaller volume in cardiac or renal failure. Once awake with glucose above 4 mmol/L, provide longer-acting carbohydrate and investigate recurrence risk.
Glucagon when IV access is unavailable
Give 1 mg IM for severe insulin-associated hypoglycaemia while continuing attempts to obtain IV access.Response is less reliable with starvation, alcohol misuse, liver disease or sulfonylurea-associated hypoglycaemia. Recheck glucose and do not let unsuccessful glucagon delay IV glucose.
Lorazepam for convulsive status epilepticus
Usual adult initial dose is 4 mg IV with immediate resuscitation support; dilute Lorazepam Macure injection with an equal volume of a compatible diluent. Repeat a benzodiazepine once after 5–10 minutes if convulsions persist, accounting for earlier doses.Respiratory depression is particularly likely with other sedatives. Frailty and organ impairment require senior dose assessment; use an alternative specialist plan where product contraindications apply. This is not treatment for undifferentiated coma.
08ComplicationsImportant consequences, why they occur and why they matter clinically.
Aspiration and airway loss
Reduced protective reflexes expose the patient to vomiting-related aspiration and upper-airway obstruction. Airway position, suction, ventilation and timely advanced support are central preventive measures.
Secondary brain injury
Sustained hypoxia, hypotension, uncontrolled seizures or severe glucose disturbance can worsen an initial cerebral insult. Repeated physiological assessment limits avoidable additional injury while definitive treatment is organised.
Recurrent deterioration
A short-lived response to glucose or an antidote can be followed by relapse when the causative medicine persists. Observation and a cause-specific prevention plan are necessary after apparent improvement.
09Monitoring and follow-upTreatment response, safety checks and longer-term review.
- Repeat GCS components, pupil size and reactivity, respiratory rate and oxygen requirement after each intervention; document actual times to expose a deteriorating trend.
- Observe breathing continuously after benzodiazepines or opioid reversal, with capnography where appropriate; a recovered saturation does not establish normal ventilation.
- Continue glucose surveillance after initial correction, particularly with renal impairment, sulfonylureas or long-acting insulin, which can cause prolonged recurrence.
- During transfer, provide personnel and equipment capable of managing deterioration; communicate the current airway status, neurological trend and outstanding urgent actions.
10Special situationsVariants, exceptions and circumstances that change the usual approach.
Communication affects scoring
Aphasia, hearing impairment or limited shared language can reduce apparent responsiveness. Describe the observed behaviour and its limitations instead of implying that every low verbal score measures sedation.
Collateral history changes urgency
A reliable last known normal time can determine access to time-sensitive neurological treatment. Seek it early while resuscitation continues, including when the person was found asleep.
Lumbar puncture is a later decision
Suspected central nervous system infection needs urgent treatment and senior assessment. Airway compromise, shock or signs of raised intracranial pressure must be addressed before considering lumbar puncture.
Arousal is not recovery
Brief eye opening after stimulation does not establish sustained airway protection or capacity. Judge spontaneous behaviour, physiological stability and the ability to maintain improvement without repeated prompting.
11Common pitfallsFrequent interpretation and management errors.
- 01
Do not give oral glucose or drinks to someone who cannot protect their airway, even when hypoglycaemia seems obvious.
- 02
Do not label a patient intoxicated without checking glucose, injury history and the trajectory of conscious level.
- 03
Do not regard cessation of visible convulsions as proof that both ventilation and cerebral function have recovered.
- 04
Do not let one corrected abnormality obscure a persistent focal deficit, worsening headache or unexplained failure to return towards baseline.