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Author: Simon Rinaldi

A reduced conscious level is characterized by impaired awareness and decreased responsiveness to external stimuli. Akinetic mutism, functional unresponsiveness, severe neuromuscular impairment and the locked-in syndrome can sometimes be mistaken for a reduced conscious level.

In patients aged <40, poisoning is the commonest cause of a reduced conscious level not due to trauma, and in those >60, stroke. However, the differential diagnosis is broad (Table 3.1). Stabilization of the patient, with rapid identification and treatment of reversible causes, is required to achieve a good outcome. Management is summarized in Figure 3.1.

Priorities

  1. Stabilize the airway, breathing and circulation

    For detailed guidance, see Chapters 1, 59, 112 (airway management), 11 and 113 (management of respiratory failure) and 2 (management of hypotension and shock).

  2. Exclude and correct hypoglycaemia
    • If blood glucose is <4.0 mmol/L, give 100 mL of 20% glucose or 200 mL of 10% glucose over 15–30 min IV, or glucagon 1 mg IV/IM/SC.
    • Recheck blood glucose after 10 min, if still below 4.0 mmol/L, repeat the above IV glucose treatment.
    • In patients with malnourishment or alcohol-use disorder, there is a remote risk of precipitating Wernicke's encephalopathy by a glucose load: prevent this by giving thiamine 100 mg IV before or shortly after glucose administration. See Chapter 81 for further management of hypoglycaemia.
  3. Treat prolonged or recurrent major seizures
    • Take into account prehospital treatment. Give lorazepam (which is less likely to cause respiratory suppression) 0.1 mg/kg (typically 4–8 mg) IV over 5–10 min (Table 16.2), midazolam 10 mg buccally (NICE-recommended, but only licensed in patients <18 years), or diazepam 10–20 mg IV at a rate of <2.5 mg/min (faster injection rates carry the risk of sudden apnoea).
    • If the seizure does not terminate, give a second dose, to a maximum total dose of lorazepam 8 mg or diazepam 40 mg.
    • See Chapter 16 for further management of seizures/status epilepticus.
  4. Give naloxone, if opioid poisoning is possible or must be excluded
    • If the respiratory rate is <12/min, or the pupils are pinpoint, or there is other reason to suspect opioid poisoning, give naloxone 800μgm IV every 2–3 min up to a total dose of 3200μgm or until the respiratory rate is >15/min.
    • If there is a response to bolus naloxone, start an IV infusion: add naloxone 2000μgm to 500 mL glucose 5% or normal saline (4μgm/mL) and titrate against the respiratory rate and conscious level. The plasma half-life of naloxone is 1h, shorter than that of most opioids.
    • In patients who have taken partial opioid agonists such as buprenorphine, methadone and tramadol, repeated large (1200μgm) doses of naloxone may be required to achieve a satisfactory response.
    • If there is no response to naloxone, opioid poisoning is excluded.
  5. Give flumazenil, if coma is a complication of the therapeutic use of benzodiazepine in hospital

    Give flumazenil 200μgm IV over 15s; if needed, further doses of 100μgm can be given at 1-min intervals up to a total dose of 2 mg.

  6. Once the patient is stabilized, make a full clinical assessment (Table 3.2) and arrange urgent investigation (Table 3.3)
    • Document the level of consciousness in objective terms, using the Glasgow Coma Scale (see Figure 3.2).
    • Examine for signs of head injury (e.g. scalp laceration, bruising, bleeding from an external auditory meatus or from the nose). If there are signs of head injury, assume additional cervical spine injury until proved otherwise: the neck must be immobilized in a collar and X-rayed before you check for neck stiffness and the oculocephalic response.
    • Check for neck stiffness.
    • Record the size of pupils and their response to bright light (Figure 3.3). Examine the fundi.
    • Check the oculocephalic response. This is a simple but important test of an intact brainstem. Rotate the head to left and right. In an unconscious patient with an intact brainstem, both eyes rotate in the opposite direction from movement of the head.
    • Examine the limbs: tone, response to a painful stimulus (nailbed pressure), tendon reflexes and plantar responses.
  7. Make a diagnosis

    The differential diagnosis for reduced consciousness can be split into three groups on the basis of the presence or absence of focal signs and meningism (Table 3.1).

    • If bacterial meningitis or viral meningo-encephalitis are possible (because of fever and meningism), empirical anti-microbial therapy (with cefotaxime (plus ampicillin in patients over 55 or at increased risk of listeria infection) and aciclovir) should be started immediately, after taking blood for culture. See Chapters 68 and 69.
    • If acute adrenal insufficiency is possible (Chapter 90) give hydrocortisone 200 mg IV. Fludrocortisone is not required in addition as this dose of hydrocortisone has sufficient mineralocorticoid action.
    • If CT shows a mass lesion or hydrocephalus, seek urgent advice from a neurosurgeon

Further Management

  • Further management is directed by the working diagnosis, based on the clinical signs, CT findings and laboratory results (Table 3.1).
  • Patients with a reduced conscious level should be nursed in a high-dependency or intensive-care unit.
  • In all patients, regular reassessment of the depth of coma, eye signs and neurology is required to establish any progression or resolution. Complications arising from coma, such as pressure injury of skin and muscle, deep vein thrombosis, respiratory infection/aspiration and contractures need to be considered and pre-empted where possible. Some patients, for example those with a malignant MCA territory infarct, may require close monitoring and repeat neuroimaging if neurosurgical intervention/decompressive craniectomy is being considered.
  • Induced hypothermia can improve the neurological prognosis for coma after cardiac arrest.
  • In some patients no cause is apparent for their reduced conscious level. Early in the presentation, it is reasonable to give glucose, thiamine, naloxone and corticosteroid empirically, before laboratory results are available, if hypoglycaemia, Wernicke's encephalopathy, opioid toxicity or acute adrenal insufficiency are possible.
  • For those remaining in cryptogenic coma there are a number of considerations:
    • Could this be a coma mimic, such as functional unresponsiveness?
    • Has non-convulsive status epilepticus been excluded?
    • Could this be an autoimmune/paraneoplastic encephalopathy (for which serological diagnostic support may be delayed or inconclusive)? Should empirical immunosuppression be trialled?
    • Has existing brain pathology (or extreme age) resulted in more prolonged or deeper coma than otherwise expected – for example following a brief seizure or lesser degrees of metabolic derangement – or produced misleading localizing signs despite the acute process being non-focal?
  • It is also important to remember that the history and toxicology may not disclose the ingestion of all relevant drugs, that hepatic encephalopathy can occur with normal liver function tests, and that CSF PCR does not detect all cases of viral encephalitis.

Further Reading

Edlow JA, Rabinstein A, Traub SJ, Wijdicks EF. (2014) Diagnosis of reversible causes of coma. Lancet 384, 20642076.

Royal College of Physicians (2013) Prolonged disorders of consciousness: National clinical guidelines. London, RCP, https://www.rcplondon.ac.uk/guidelines-policy/prolonged-disorders-consciousness-national-clinical-guidelines.

Traub SJ, Wijdicks EF. (2016) Initial diagnosis and management of coma. Emerg Med Clin North Am 34, 777793.