Coma

Published on 01/03/2015 by admin

Last modified 22/04/2025

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Coma

The comatose patient presents a number of problems to the physician, some in relation to initial diagnosis and some later during treatment.

The depth of coma can be defined following clinical examination using a scale such as that in Figure 63.1. This allows clinical staff to establish the severity of the coma and to monitor changes. Obtaining the correct diagnosis is paramount. To this end the most valuable information is usually obtained from the clinical history, but frequently a reliable history is not available.

Fig 63.1 The Glasgow Coma Scale.

Patency of airway, blood pressure, temperature, pupillary reflex and blood glucose concentration need to be monitored repeatedly and a search should be made for evidence of trauma or needlemarks at the time of admission. A careful history and physical examination will give the correct diagnosis in over 90% of cases. Other biochemical tests can help in diagnosis or for the continued monitoring of comatose patients.

Differential diagnosis of coma

A helpful mnemonic in the diagnosis of the unconscious patient is given in Figure 63.2. However, within each of these categories described there are many possible causes. The first priorities in treating an unconscious patient are to ensure that airways are clear and that breathing and circulation are satisfactory.

Fig 63.2 Differential diagnosis of a coma patient.

Drugs and poisons

A wide variety of drugs and poisons can give rise to coma if taken in sufficient dose. In very few cases are there specific clinical signs. Exceptions are the pinpoint pupils of opiate poisoning for which the specific antagonist naloxone is effective in restoring consciousness, and the divergent strabismus (Fig 63.4) associated with tricyclic antidepressant overdose. In most cases of drug or poison-induced coma, conservative therapy is all that is required to maintain vital functions until the substance is eliminated by metabolism and excretion. The best specimen to analyse for diagnosis is urine. Where drugs such as phenytoin or theophylline are suspected, plasma levels should be measured on admission and thereafter until they fall to therapeutic levels (see pp. 118–119).

Fig 63.4 Divergent strabismus.

Alcohol

Alcohol is a common cause of coma in all age ranges. Coma depth and length is associated with the amount of alcohol ingested, and this shows wide interpatient variation. Alcoholic coma can be associated with head injuries, hypothermia and the presence of other drugs with which its action may be additive. In most cases, coma caused by alcohol will resolve relatively rapidly, the exception being when there is hepatic insufficiency. In cases where the blood alcohol level exceeds 80 mmol/L (approximately 5 times the legal driving limit), haemodialysis may be required. The fact that alcohol can be detected on the breath is not sufficient for diagnosis, and a full clinical examination should be made in all cases of alcoholic coma. If acidosis is present, methanol or ethylene glycol poisoning should also be suspected.

Carbon monoxide poisoning

Carbon monoxide poisoning accounts for a large number of deaths in the UK each year. Coma can occur with a carboxyhaemoglobin concentration above 30% of haemoglobin. Carbon monoxide poisoning may be insidious due to a faulty heater or poor ventilation and may be presaged by headaches and confusion. Treatment with oxygen restores oxyhaemoglobin. This is a dangerous form of poisoning that requires careful aftercare.

Hepatic coma

Acute or chronic hepatic failure may result in coma. This is believed to be due to the failing liver’s inability to remove neurotoxins such as ammonia from the blood.

Case history 52

A 20-year-old insulin-dependent diabetic was found unconscious beside his bicycle. An hour or so earlier he had left a party where he had been drinking. He was brought to the Accident and Emergency department.

• What investigations and interventions would be appropriate in this case?

Comment on page 169

Brain death

The diagnosis of brain death is made using criteria outlined in Table 63.1, which includes arterial blood gas analysis. Where measurable sedative drugs have been used (for example in ITU) there must be biochemical confirmation that these drugs are no longer present.

Table 63.1

Criteria for confirming brain death

ALL BRAIN-STEM REFLEXES ARE ABSENT

The pupils are fixed and unreactive to light

The corneal reflexes are absent

The vestibulo-ocular reflexes are absent – there is no eye movement following the injection of 20 mL of ice-cold water into each external auditory meatus in turn

There are no motor responses to adequate stimulation within the cranial nerve distribution

There is no gag reflex and no reflex response to a suction catheter in the trachea

No respiratory movement occurs when the patient is disconnected from the ventilator long enough to allow the carbon dioxide tension to rise above the threshold for stimulating respiration (PCO₂ must reach 6.7 kPa)

The diagnosis of brain death should be made by two experienced doctors, one of whom should be a consultant and the other a consultant or specialist registrar. The tests are usually repeated after an interval of 6–24 hours, depending on the clinical circumstances, before brain death is finally confirmed.

Clinical note