The most reliable index for assessing the level of consciousness at any moment is the patient’s response to external stimuli. (How quick and how accurate are the patient’s responses to questions, to touch, to pain, etc?) Brain stem reflexes also allow an accurate estimate of the level of consciousness—pupillary responses to light, corneal reflexes, oculocephalic and caloric responses, cough and gag reflexes, pattern of breathing, etc. Motor activity of the extremities, either spontaneous or induced by the examiner’s stimulus, provides assessment of the entire neuraxis. Does the patient move the extremities purposefully, equally, and briskly, or is there failure to move at all? Which extremities do not move? Nonpurposeful or reflex movement of the arms and legs may also establish the level of neuraxis function, though less reliably (eg, decorticate or decerebrate posturing).
Depressed consciousness may occur abruptly (eg, cerebral concussion) or gradually (eg, barbiturate overdose), often with fluctuations in the level of consciousness (eg, waxing-waning consciousness associated with subdural hematoma). Accurate and repeated examinations will establish not only the level of consciousness but also its changing course. The urgency of diagnosis depends largely upon the rate of change in the patient’s course as determined by repeated examinations.
Central nervous system infections (eg, encephalitis, meningitis) are usually accompanied by systemic signs of infection and a progressively worsening course. Cerebral abscess, on the other hand, behaves more like an expanding neoplasm than a fulminating infection.
Vascular occlusions (emboli, thrombosis) usually cause abrupt neurologic deficits without grossly impaired consciousness, whereas cerebral hemorrhage typically causes abrupt coma with profound neurologic deficits. Conversely, subarachnoid hemorrhage may occur without any alteration of wakefulness. Degenerative diseases are usually slowly progressive, dementing illnesses that dull consciousness but characteristically do not produce coma.
Laboratory and radiographic tests help to establish the clinical diagnosis. Routine examinations should include a complete blood count, urinalysis, plasma glucose, blood urea nitrogen, and serum electrolytes.
Urine and blood for toxicologic study are essential if poisoning is a possibility. Head CT and spinal x-rays or CT scans as well as chest x-ray are obvious aids after trauma. Cerebrospinal fluid analysis is an essential step toward diagnosis of meningitis or subarachnoid hemorrhage. Lumbar puncture is rarely helpful in the assessment of head trauma and probably is contraindicated during the initial workup after injury.
Although most patients are unconscious for a single reason, some may have combined or additive reasons. A severe head injury may have been caused by abrupt coma induced by cerebral hemorrhage in a hypertensive patient, or a diabetic patient with glioblastoma multiforme may be in coma from an insulin overdose and not from the expanding neoplasm. The physician must be aware of these possible—though uncommon—complexities.
The administration of intravenous hypertonic glucose (50%, 50 mL) is occasionally diagnostic but should be done only after blood has been taken for glucose measurement and before an intravenous glucose drip has been started.
Most patients with depressed consciousness should undergo CT scanning or MRI to establish the presence or absence of an intracranial mass lesion. Appropriate therapy depends on the early recognition of the specific intracranial problem.
Protection of the airway and control of shock are fundamental principles of management of patients with depressed consciousness. Most complications of coma can be attributed to failure to follow these basic rules. Responsive patients with good cough reflexes can often protect their own airways. Other patients, usually stuporous or comatose, require endotracheal intubation in order to
reduce the likelihood of aspiration of gastric contents
ensure unrestricted gas exchange (PO2, PCO2).
Adequate tracheal suctioning, frequent changes in position, pulmonary physiotherapy, and intermittent positive pressure breathing help maintain good pulmonary function once the airway is secure.
Shock must be controlled. If it is due to hypovolemia, blood and fluids must be given intravenously. In the absence of trauma, other causes of hypotension must be sought and treated specifically (eg, gram-negative sepsis).
A nasogastric tube (to sample ingested drugs, to remove gastric contents that might be aspirated into the lungs, etc), intravenous cannulas to administer drugs and fluids, and an indwelling bladder catheter to assess fluid balance are necessary steps in the early management of comatose patients.