Hydrocephalus following aneurysmal SAH.
An aneurysm-induced hydrocephalus was observed in two series of patients who were treated antifibrinolytically in different ways: A = 3 g/day of AMCA + 3 - 400,000 KIU/day of aprotinins, B = 6 g/day of AMCA. Group A showed significantly less formation of hydrocephalus and ischaemic complications. In the survey, various factors (neurological condition, number of haemorrhages, localisation of the aneurysm) play a part in the formation of the hydrocephalus following subarachnoid haemorrhage (SAH). The same is true of the high correlation with preceding severe ischaemic complications after SAH (p less than 0.005). The administration of antihypertensives leads to a significantly higher rate of ischaemic complications but does not exert an influence on the formation of hydrocephalus. It is assumed that the close relationship is the essential cause of cerebral ischaemia and development of hydrocephalus after SAH, that is, erythrocyte decomposition products which explain the observed relations between the two. The results obtained do not support the thesis of periventricular ischaemia as the cause of the development of a clinically significant hydrocephalus after SAH.
D001059:Apoproteins / Q000627:therapeutic use; D004359:Drug Therapy, Combination; D006801:Humans; D006849:Hydrocephalus / Q000188:drug therapy / Q000209:etiology*; D002532:Intracranial Aneurysm / Q000150:complications*; D007427:Intracranial Pressure / Q000187:drug effects; D012422:Rupture, Spontaneous; D013345:Subarachnoid Hemorrhage / Q000150:complications*; D014148:Tranexamic Acid / Q000627:therapeutic use
D001059:Apoproteins; D014148:Tranexamic Acid