Mild degrees of hypoxia without loss of consciousness induce only inattentiveness, poor judgment, and incoordination; in our experience, there have been no or minimal lasting clinical effects in such cases, although Hornbein and colleagues found a slight decline in visual and verbal long-term memory and mild aphasic errors in Himalayan mountaineers who had earlier ascended to altitudes of 18,000 to 29,000 ft. These observations make the point that profound anoxia may be well tolerated if arrived at gradually. For example, we have seen several patients with advanced pulmonary disease who were fully awake when their arterial oxygen pressure was in the range of 30 mm Hg. This level, if it occurs abruptly, causes coma. An important derivative observation is that degrees of hypoxia that at no time abolish consciousness rarely, if ever, cause permanent damage to the nervous system.
In the circumstances of severe global ischemia with prolonged loss of consciousness, the clinical effects can be quite variable. Following cardiac arrest, for example, consciousness is lost within seconds but recovery can be complete if breathing, oxygenation, and cardiac action are restored within 3 to 5 min. Beyond 5 min there is usually permanent injury. Clinically, however, it is often difficult to judge the precise degree and duration of ischemia, because slight heart action or an imperceptible blood pressure may have served to maintain the circulation to some extent. Hence some individuals have made an excellent recovery after cerebral ischemia that apparently lasted 8 to 10 min or longer. Subnormal body temperatures, as might occur when the body is immersed in ice-cold water, greatly prolong the tolerable period of hypoxia. This has led to the successful application of moderate cooling after cardiac arrest as a technique to limit cerebral damage (see further on in Treatment of Hypoxic-Ischemic Encephalopathy section).
Generally speaking, anoxic patients who demonstrate intact brainstem function as indicated by normal pupillary light and ciliospinal responses, reflexive eye movements induced by passive head turning (doll’s eye movements), and other vestibulo-ocular reflexes have a more favorable outlook for recovery of consciousness and perhaps of all mental faculties. Conversely, the absence of these brainstem reflexes even after circulation and oxygenation have been restored, particularly pupils that fail to react to light, implies a grave outlook as elaborated further on. If the damage is almost total, coma persists, decerebrate postures may be present spontaneously or in response to painful stimuli, and bilateral Babinski signs can be evoked. In the first 24 to 48 h, death may terminate this state in a setting of rising temperature, deepening coma, and circulatory collapse, or the syndrome of brain death intervenes, as discussed below.