Endogenous arterial blood pressure increase after aneurysmal subarachnoid hemorrhage.

Spontaneous blood pressure rise is a frequently observed phenomenon following aneurysmal subarachnoid hemorrhage (SAH). Facing the risk of aneurysmal rebleeding and the occurrence of delayed cerebral ischemia it is unclear how to react to these endogenous-driven blood pressure changes, as their predictive value for clinical course and functional outcome is still unknown. Endogenous blood pressure characteristics within 21 days after SAH were retrospectively analyzed in 93 patients. Any use of vasopressors for active induction of hypertension marked the end of data collection. Mean arterial blood pressure (MAP) was related to the onset of cerebral vasospasm and patient characteristics (Hunt&Hess, age, pre-existing hypertension, antihypertensive therapy, sedation). Predictors for cerebral infarction and functional outcome were calculated using a logistic regression model. A significant MAP increase was observed in all patients from day 3 to day 7. Patients developing cerebral vasospasm had an overall steeper increase of MAP during this period (11.1 ± 11.4 mmHg vs. 6.5 ± 8.9 mmHg, p = 0.04). MAP rise started already 3 days before detection of vasospasm. Lower MAP values were recorded in patients with poor Hunt&Hess grade, under sedation and thus in patients with poor outcome. MAP had no impact on the development of cerebral infarction. In univariate analysis MAP on day 5 (OR 0.95, 95 %-CI: 0.89-0.99), MAP on day 6 (OR 0.95, 95 %-CI: 0.91-1.00), Hunt&Hess grade (OR 1.72, 95 %-CI: 1.14-2.60), sedation (OR 17.04, 95 %-CI: 2.08-139.51) and stroke (OR 5.82, 95 %-CI: 1.63-20.82) were predictors for poor outcome. In multivariable analysis, only sedation (OR 13.72, 95 %-CI: 1.62-115.94) and ischemic stroke (OR 4.48, 95 %-CI: 1.16-17.31) remained significant. Spontaneous MAP increase occured in all patients following SAH. It was highly influenced by clinical parameters, thereby limiting its prognostic value for functional outcome. However, a steep increase of MAP might be an early clinical marker to identify patients at risk for developing cerebral vasospasm.

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