Several models were developed before the era of current therapies to predict the outcome of hypoxic-ischemic coma. All of them incorporate simple clinical features involving loss of motor, verbal, and pupillary functions in various combinations. The most often cited study of the prognostic aspects of coma following cardiac arrest in the past had been by Levy and colleagues of 210 patients, which provided the following guidelines: 13 percent of patients attained a state of independent function within 1 year; at the time of the initial evaluation, approximately 25 percent of patients had absent pupillary light reflexes, none of whom regained independent function; by contrast, the presence on admission of reactive pupils, eye movements, and any motor response, a configuration displayed in approximately 10 percent, was associated with a better prognosis in almost 50 percent of cases. The absence of neurologic function in any of these spheres at 1 day after cardiac arrest, unsurprisingly, was associated with an even poorer outcome. Similarly, Booth and colleagues analyzed previously published studies and determined that 5 clinical signs at 1 day after cardiac arrest predicted a poor neurologic outcome or death: (1) absent corneal responses, (2) absent pupillary reactivity, (3) no withdrawal to pain, and (4) the absence of any motor response. In the era of colling therapy, some of these clinical signs cannot be observed. In any case, concurrent intoxication must be excluded. The use of somatosensory evoked potentials in the prognostication of coma is discussed in Chaps. 2 and 16.
The question of what to do with patients in such states of protracted coma is a societal as much as a medical problem. The neurologist can reasonably be expected to state the level and degree of brain damage, its cause, and the prognosis based on their own and published experience. One prudently avoids heroic, lifesaving therapeutic measures once the nature of this state has been determined with certainty. However, some patients who show clinical and EEG cerebral reactivity to verbal commands will make a degree of recovery, most often to a disabled state.
Treatment of Hypoxic-Ischemic Encephalopathy
Treatment is directed initially to the prevention of further hypoxic injury. A clear airway is secured, cardiopulmonary resuscitation is initiated, and every second counts in their prompt utilization. Supplemental oxygen may be of value during the first hours but is probably of little use after the blood becomes well oxygenated. Once cardiac and pulmonary function are restored, there is experimental and clinical evidence that reducing cerebral metabolic requirements by inducing hypothermia has a beneficial effect on outcome and may prevent the delayed worsening referred to above. The use of high-dose barbiturates has not met with the same success.