Coma

The clinical assessment of coma is outlined in Box 1. Coma is usually readily recognizable. Potential differential diagnoses include:

‘Locked in syndrome’: This results from a high midbrain lesion or a severe generalized neuropathy, which prevent the patient from all movement despite having a normal consciousness.

Catatonia: This is a psychiatric state of unresponsiveness.

Vegetative state: In patients with diffuse bihemispheric disease but normal brain stem function, this may lead to a vegetative state. This is not usually relevant to the acute diagnosis of coma.

The next issue is to determine the cause so as to direct future management of the coma (Box 1). This can be broadly divided into the following categories:

Coma with neck stiffness. This can arise from meningitis, subarachnoid haemorrhage and, rarely, as a result of foramen magnum herniation.

Coma with focal signs. It is especially important to detect signs of herniation. Other causes include supratentorial and infratentorial lesions.

Coma without focal signs, relating to diffuse cerebral lesions.

Management of coma

Coma is a medical emergency requiring resuscitation. There are two main strands of treatment: (i) supportive treatment applicable to all patients with coma, and (ii) specific treatment of the underlying cause.

Supportive

Supportive treatment is aimed at avoiding the complications of unconsciousness. Key elements include:

protecting airways

maintaining blood pressure – intravenous fluids or inotropes as needed

emptying the stomach contents using a nasogastric tube

avoidance of deep venous thrombosis using thromboembolic deterrent (TED) stockings

maintaining homeostasis, particularly the blood gases and electrolytes

urinary catheterization

nursing with regular turning or use of an air mattress to avoid pressure sores.

Identification and treatment of specific underlying causes

This is in large part going to be dictated by the clinical situation.

Coma with neck stiffness

With fever

Give broad-spectrum antibiotics to cover likely meningitic organisms. Undertake a brain scan followed by lumbar puncture, if there is no contraindication on scanning. Further treatment would depend on CSF findings (p. 38).

Without fever

Arrange a CT brain scan. If diagnostic of subarachnoid haemorrhage, management is as described on page 72. If no blood is seen or the scan is not diagnostic, proceed to lumbar puncture.

Coma with focal signs

This requires cerebral imaging to determine the underlying cause. Frequently this can be anticipated on the basis of the history. These patients may require manoeuvres to reduce their intracranial pressure, which include:

mannitol infusion

dexamethasone

intubation and hyperventilation to reduce intracranial pressure.

Further management would depend on the underlying diagnosis.

Coma without signs or neck stiffness

The history is likely to be the most useful aspect in establishing the underlying cause. This may be sufficiently clear cut, for example overdose, alcohol excess or post-ictal state. However, there are situations where other investigations are essential.

Investigations include glucose, urea and electrolytes. Blood gases and a toxicology screen may be important. In some circumstances liver function tests, ammonia, group and even red cell transketolase screening (for low vitamin B1) can be useful. If these do not yield useful information, cerebral imaging needs to be undertaken. Lumbar puncture should be considered as encephalitis can often be difficult to diagnose. An EEG can be helpful in this and in the diagnosis of epilepsy and encephalitis.

Treatment will depend on the underlying cause. For example, a metabolic disturbance should be corrected. N.B. A low sodium should be corrected slowly to avoid complications such as central pontine myelinolysis. Antiviral agents can be used in encephalitis.

Specific treatments

These include:

hypoglycaemia – glucose

opiate overdose – naloxone

benzodiazepine overdose – flumazenil

Wernicke’s encephalopathy – thiamine (rare)

Addisonian crisis – steroids (rare).

Prognosis in coma

This depends on the underlying cause. The outcome from traumatic coma is considered on page 79. Prognosis depends on the cause and duration of coma. Patients with focal signs, especially pupillary signs, do particularly badly.

Criteria for brain stem death are used to determine when ventilatory and other support can be discontinued (Box 2).

Box 2 Diagnosis of brain stem death in the UK

The diagnosis of brain death relies on three elements:

1. The cause of failure of brain function is known to be irreversible.

2. The absence of cerebral function and the patient is unresponsive and unreceptive.

3. There is an absence of brain stem function.

Before testing, metabolic abnormalities should be corrected and time allowed for sedative medications to clear.

Brain stem tests

Tests for brain stem function are undertaken by two senior physicians on two occasions. No response must be found to any of the following:

pupillary responses

doll’s head eye movements

eye movements on caloric testing

corneal responses

gag responses

response to painful stimuli

respiratory response to hypercapnoea after preoxygenation giving a high oxygen flow, and then turning the ventilator off to allow the pCO₂ to rise to 8 kPa.

An EEG is not required to make the diagnosis.

Coma due to drug overdosage usually has a good outcome. A hypoglycaemic coma, if short-lived, usually leaves no sequelae.

Other causes of medical coma have a worse prognosis, with an overall recovery rate of only 15%.

Coma and alteration of consciousness

Coma is a medical emergency.

Coma arises from lesions directly affecting the reticular activation system in the brain stem or a generalized process affecting the whole cortex.

The commonest causes of coma are drug overdose and head trauma.

Hypoglycaemia needs to be considered early and treated quickly.

Management involves a systematic assessment and investigation running in parallel with resuscitation.