Cerebral blood flow and oxygen uptake, and cerebrospinal fluid biochemistry in severe coma.

Thirty-eight patients in coma due to head trauma, cerebrovascular accidents, hypoxia, hypoglycaemia, or barbiturate intoxication, and 15 cases of brain death were studied. Cerebral metabolic rate of oxygen (CMRO(2)) was obtained from the arteriovenous oxygen difference and cerebral blood flow (CBF) measured by intra-arterial (133)Xenon method. If hypothermia and CNS depressants were excluded, CMRO(2) below one-third of normal was incompatible with regaining of consciousness, but this was seen in only three comatose patients. Irrespective of the clinical outcome (death, vegetative survival, or recovery), CMRO(2) values of one-third to two-thirds of normal were seen in the majority of coma patients. CMRO(2) measurements were of no practical value to predict the prognosis in coma, even when the effect of temperature and sedatives were considered. In brain death the CBF studies gave indirect evidence of cerebral circulatory arrest. The cerebrospinal fluid (CSF) was obtained for analysis of lactate, pyruvate, and bicarbonate in 29 cases. Increased CSF lactate levels were found in all groups except barbiturate intoxication. The finding of a negative correlation between CSF bicarbonate and log CBF suggests that the CSFpH determines the wide range of CBF in coma.