Abstract
The pathophysiological features of severely ill patients with a subarachnoid hemorrhage (SAH) due to a rupture of an intracranial aneurysm are described, with special reference to treatment strategy during the acute stage. Although global ischemia must be the predominant damage to the brain, a therapeutic assessment of low grade cases should be made carefully. Patients should be observed for changes in clinical symptoms, which could consist of complex mixtures of cerebral damage such as ischemia, intracerebral hemorrhage, intraventricular hemorrhage, edema and (or) hydrocephalus. A line should be placed between Grade IV and V cases with a Glasgow Coma Scale (GCS) score of 6 and 5, because the outcome of GCS Group 6 is significantly better (p<0.01) than GCS Group 5, and is the same as those of GCS Group 7. There are many patients however with an initial score of GCS score of 5, 4 and 3, who can achieve a favorable outcome if proper treatment is provided. A systemic sympathetic hyperdischarge is another problem during the acute stage. This may often cause serious cardio-pulmonary disorders such as myocardial ischemia, arrhythmias, pulmonary edema or even apnea. This transient, stormy, sympathotonia can be quantitatively assessed by a rapid elevation of both epinephrine and nor-epinephrine in blood serum after SAH. The author has confirmed that the value obtained by dividing the blood glucose level (mg dL^<-1>) by the serum potassium level (mEq L^<-1>) correlates well with changes of serum catecholamine levels. By defining this value as a stress index (SI), and calculating it from the blood glucose and potassium level, one can evaluate the sympathetic tone, and therefore the probability of occurrence of serious systemic complications during an acute stage after SAH.
