[Evaluation of the dopamine induced hypertension therapy for vasospasm (author's transl)]

The purpose of this study is to clarify the usefulness and the limitations of the dopamine induced hypertension therapy (DIH) in the treatment of symptomatic vasospasm secondary to aneurysmal rupture. Twelve patients suffering from ischemic complications of vasospasm were treated with DIH and large quantities of intravascular fluids. All underwent cerebral angiography and CT scan in order to ascertain if their neurological deteriorations were due to vasospasm. In 9 cases, the levels of consciousness and neurological state were improved within a few hours after DIH started. It suggests that their ischemic symptoms were dependent on their systemic blood pressure. In one case, whose vasospasm was extensive and diffuse, DIH was life-saving, however the patient remained bedridden. In 2 cases, vasospasm was too intense for DIH to prevent continued neurological deteriorations. There seems to be a correlation between the effect of DIH and the angiographic grade of vasospasm (Table 1). The ultimate results of these 12 cases were compared with those of 46 cases which suffered from symptomatic vasospasm but were not treated with DIH (Table 3). There was no significant difference between the two groups. One died of severe brain edema, which may have been aggravated by DIH. In such a case where diffuse brain edema and breakdown of blood-brain barrier are observed on CT scan, DIH can be hazardous. However, in a case where CT scan before or during the therapy shows a localized low density area of infarction, DIH can be beneficial by preventing the progression of cerebral ischemia, in spite of a possible risk of bringing about hemorrhagic infarction. Our conclusions are as follows: 1) DIH is useful in many cases involving significant vasospasm. 2) DIH is less useful in such a case whose angiogram shows extensive vasospasm throughout the internal carotid and vertebro-basilar systems, and should be performed carefully in coordination with measures to reduce intracranial pressure. DIH is expected to protect the brain tissue from ischemia by increasing blood flow through the arteries of vasospasm and collateral circulation, but should not dilate the histologically changed arteries. Further clinical studies including cerebral blood flow measurements are necessary to define precisely the effectiveness, the indication and contraindication, and the mechanism of action of DIH.