Most patients who have suffered severe but lesser degrees of hypoxia will have stabilized their breathing and cardiac activity by the time they are first examined; yet they are comatose, with the eyes slightly divergent and motionless but with reactive pupils, the limbs inert and flaccid or intensely rigid, and the tendon reflexes diminished. Within a few minutes after cardiac action and breathing have been restored, generalized convulsions and isolated or grouped myoclonic twitches may occur. Either of these phenomena are poor prognostic signs. With severe degrees of injury, the cerebral and cerebellar cortices and parts of the thalami are partly or completely destroyed but the brainstem-spinal structures survive. Tragically, the individual may survive for an indefinite period in a state that is variously referred to as cortical death, irreversible coma, or persistent vegetative state (see discussion of these subjects in Chap. 16). Some patients remain mute, unresponsive, and unaware of their environment for weeks, months, or years. Long survival is usually attended by some degree of improvement but the patient appears to know nothing of his present situation and to have lost all past memories, cognitive function, and capacity for meaningful social interaction and independent existence (a minimally conscious state, actually a severe dementia; see Chap. 16). One has only to observe such patients and their families to appreciate the gravity of the problem, the family’s anguish, and the tremendous expense of medical care. The only person who does not appear to suffer is the patient.
With lesser degrees of anoxic-ischemic injury, the patient improves after a period of coma lasting hours or less. Some of these patients quickly pass through this acute post-hypoxic phase and proceed to make a full recovery; others are left with varying degrees of permanent disability.
The findings on imaging studies vary. The most common early change in cases of severe injury is a loss of the distinction between the cerebral gray and white matter (Fig. 39-1); patients with this finding are invariably comatose and few awaken with a good neurologic outcome. With less severe and predominantly hypotensive-ischemic events such as cardiac arrest, arterial borderzone (watershed) infarctions become evident in the border zones between the anterior, middle, and posterior cerebral arteries (Fig. 39-2). The clinical syndromes associated with borderzone infarction are discussed below. Yet another pattern of brain destruction, seen at times also in CO poisoning, consists of striatal damage that is evident more by imaging than by clinical features (Fig. 39-3).
Brain Death From Hypoxia-Ischemia (See Chap. 16 for a Full Discussion)
This represents the most severe degree of hypoxia, usually caused by circulatory arrest; it is manifest by a state of complete unawareness and unresponsiveness with abolition of all brainstem reflexes. Natural respiration cannot be sustained; only cardiac action and blood pressure are maintained. No electrical activity is seen in the EEG (it is isoelectric). At autopsy one finds that most, if not all, the gray matter of cerebral, cerebellar, and brainstem structures—and in some instances, even the upper cervical spinal cord—has been severely damaged.
One must always exercise caution in concluding that a patient has this form of irreversible brain damage, because anesthesia, intoxication with certain drugs, and hypothermia may also cause deep coma and an isoelectric EEG but permit recovery. Therefore it is often advisable to repeat the clinical and laboratory tests after an interval of a day or so, during which time the results of toxic screening also become available. The authors’ experience corroborates the general notion that the vital functions of patients with the brain death syndrome usually cannot be sustained for more than several days without external intervention. In exceptional cases, however, the provision of adequate fluid, vasopressors, and respiratory support allows preservation of the body in a comatose state for longer periods. These issues are discussed extensively in Chap. 16.