Coma is a sleep-like state with no purposeful response to the environment and from which the patient cannot be aroused. The eyes are closed and do not open spontaneously. The patient does not speak, and there is no purposeful movement of the face or limbs. Verbal stimulation produces no response. Painful stimulation may produce no response or nonpurposeful reflex movements mediated through spinal cord or brainstem pathways. Coma results from a disturbance in the function of either the brainstem reticular activating system above the mid pons or of both cerebral hemispheres (Figure 3-1).
Anatomic basis of coma. Consciousness is maintained by the normal functioning of the brainstem reticular activating system above the mid pons and its bilateral projections to the thalamus and cerebral hemispheres. Coma results from lesions that affect either the reticular activating system or both hemispheres.
The approach to diagnosis of the comatose patient consists first of emergency measures to stabilize the patient and treat presumptively certain life-threatening disorders, followed by efforts to establish an etiologic diagnosis.
F. Plum and Posner’s Diagnosis of Stupor and Coma. 4th ed. Oxford, UK: Oxford University Press; 2007.
Ensure patency of the airway and adequacy of ventilation and circulation (Table 3-1). Adequacy of ventilation can be established by the absence of cyanosis, a respiratory rate greater than 8/min, the presence of breath sounds on auscultation of the chest, and the results of arterial blood gas studies. If any of these suggest inadequate ventilation, the patient should be ventilated mechanically. Measurement of the pulse and blood pressure provides a rapid assessment of the status of the circulation. Circulatory embarrassment should be treated with intravenous fluid replacement, pressors, and antiarrhythmic drugs, as indicated.
Insert an intravenous catheter and withdraw blood for determination of serum glucose and electrolytes, hepatic and renal function tests, prothrombin time, partial thromboplastin time, complete blood count, and drug screen.
Begin an intravenous infusion and administer dextrose, thiamine, and naloxone. Every comatose patient should be given 25 g of dextrose intravenously, typically as 50 mL of a 50% dextrose solution, to treat possible hypoglycemic coma. Because administration of dextrose alone may precipitate or worsen Wernicke encephalopathy (see Chapter 4, Confusional States) in thiamine-deficient patients, all comatose patients should also receive 100 mg of thiamine by the intravenous route. To treat possible opiate overdose, the opiate antagonist naloxone, 0.4 to 1.2 mg intravenously, should also be administered routinely to comatose patients. The benzodiazepine antagonist flumazenil, 1 to 10 mg intravenously, may be useful when benzodiazepine overdose contributes to coma. However, it should not be used in patients with a history of seizures, chronic benzodiazepine abuse, or suspected co-ingestion ...