Coma and alteration of consciousness

Published on 10/04/2015 by admin

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Coma and alteration of consciousness

Coma is a common and important medical emergency, accounting for 3% of acute hospital admissions. This section discusses the terminology used in this field, which is often confusing, then considers the aetiology and pathogenesis of coma, then outlines a pragmatic approach to these patients.

Terminology

There are many different terms used to describe different types of altered consciousness, for example coma, stupor, confusion or obtundation. Unfortunately these mean different things to different people and so are of limited use. This in part reflects the complicated nature of consciousness, making it unsurprising that this cannot be summed up in a single word. It therefore is more useful to try and quantify consciousness individually using specific descriptions or scales (see below). Altered consciousness and coma are a spectrum. The differential diagnosis and management vary according to the level of consciousness. Within that spectrum, however, coma can be recognized as being very much at one end. Coma can be practically defined as unrousable unconsciousness and is discussed in this section.

Aetiology and pathogenesis

Consciousness depends on the intact functioning of the reticular activating system in the brain stem and the cerebral cortex. Coma and altered consciousness arise from disturbance of these elements (Table 1). This can arise from:

image infratentorial lesions that disrupt the reticular activating system directly
image supratentorial lesions – large enough to cause herniation (p. 48) or large enough to disrupt the cortex
image diffuse cerebral insult that affects the function of the cortex and reticular activation system.

Table 1 Some causes of coma

Site of disease Causes
Infratentorial
Infarct
Haemorrhage
Tumour
Inflammatory lesion

Supratentorial
Subarachnoid haemorrhage
Extradural or subdural haematoma
Intracranial haemorrhage
Tumour
Infarct

Diffuse
Metabolic:

hypoglycaemia, hyperglycaemia, hyponatraemia, hypernatraemia, hypoxia, acidosis, hypothyroidism, hepatic failure

Toxic
Drugs
Alcohol
Epilepsy
Multiple sedative drugs, in particular benzodiazepines and other sedative drugs
Hypothermia
Infections
Meningitis, encephalitis

Coma

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

image ‘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.
image Catatonia: This is a psychiatric state of unresponsiveness.
image 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:

image Coma with neck stiffness. This can arise from meningitis, subarachnoid haemorrhage and, rarely, as a result of foramen magnum herniation.
image Coma with focal signs. It is especially important to detect signs of herniation. Other causes include supratentorial and infratentorial lesions.
image Coma without focal signs, relating to diffuse cerebral lesions.

Box 1 Assessment of patients with coma

1. History. It is important that this be obtained from anyone that may help – ambulance personnel, passers-by. Silent witnesses, such as a wallet or bracelet, are often very informative.
2. Examination.

• General – vital signs – pulse, blood pressure, temperature, respiration and blood glucose.
• External signs of trauma, including Battle’s signs (as on p. 79), evidence of injections, bitten tongue or neck stiffness.
• Neurological examination:

– Glasgow Coma Scale (p. 129)
– pupillary examination (Table 2)
– doll’s head eye movements
– fundoscopy
– signs of any other neurological abnormality
– look for facial asymmetry and asymmetry of limbs
– tone, posture or response to pain
– asymmetry of reflexes or plantar responses may be useful.

Table 2 Pupillary responses in coma

image

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:

image protecting airways
image maintaining blood pressure – intravenous fluids or inotropes as needed
image emptying the stomach contents using a nasogastric tube
image avoidance of deep venous thrombosis using thromboembolic deterrent (TED) stockings
image maintaining homeostasis, particularly the blood gases and electrolytes
image urinary catheterization
image 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:

image mannitol infusion
image dexamethasone
image 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:

image hypoglycaemia – glucose
image opiate overdose – naloxone
image benzodiazepine overdose – flumazenil
image Wernicke’s encephalopathy – thiamine (rare)
image 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:

image pupillary responses
image doll’s head eye movements
image eye movements on caloric testing
image corneal responses
image gag responses
image response to painful stimuli
image 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

image Coma is a medical emergency.
image Coma arises from lesions directly affecting the reticular activation system in the brain stem or a generalized process affecting the whole cortex.
image The commonest causes of coma are drug overdose and head trauma.
image Hypoglycaemia needs to be considered early and treated quickly.
image Management involves a systematic assessment and investigation running in parallel with resuscitation.

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