• F H Vermeij, D Hasan, M Vermeulen, H L Tanghe, and J van Gijn.
• Department of Neurology, University Hospital Rotterdam Dijkzigt, The Netherlands.
• Neurology. 1994 Oct 1; 44 (10): 1851-5.

AbstractWe studied the predictive factors for deterioration from hydrocephalus that developed during the first 28 days after admission in 660 patients following aneurysmal subarachnoid hemorrhage (SAH). Deterioration from hydrocephalus was defined as deterioration of consciousness with no detectable cause other than hydrocephalus confirmed by a repeat CT with a bicaudate index exceeding the 95th percentile for age. Deterioration from hydrocephalus occurred in 143 (22%) of the 660 patients. The variables included in the analysis were sex, age, loss of consciousness at ictus, sum score on the Glasgow Coma Scale on admission, sum score of cisternal blood and presence of ventricular blood on initial CT, hydrocephalus on initial CT, confirmed aneurysm, rebleeding, delayed cerebral ischemia, and treatment with tranexamic acid for 4 (short-term treatment) or 28 (long-term treatment) days. In a multivariate analysis with the Cox proportional hazards model incorporating fixed and time-dependent covariates, sum score of cisternal blood on initial CT (hazard ratio 3.15, p < 0.000001), presence of ventricular blood on initial CT (hazard ratio 1.66, p = 0.004), hydrocephalus on initial CT (hazard ratio 3.37, p < 0.000001), and long-term treatment with tranexamic acid (hazard ratio 2.40, p < 0.000001) were significantly related with the development of hydrocephalus. We conclude that a high amount of blood after SAH and delay of the resorption of cisternal and ventricular blood caused by long-term treatment with tranexamic acid increases the risk of deterioration from hydrocephalus after SAH.

29 keywords...

hide…