Intensivtherapie nach aneurysmatischer Subarachnoidalblutung

Abstract

Aneurysmal subarachnoid hemorrhage (SAH) is a devastating disease and nearly one third of patients die in the acute phase. Due to the bleeding event, a hyperactive sympathetic nervous system and an uncontrolled inflammatory response have a profound local and systemic impact on other organ functions. Neuroendocrinological disorders and cardiopulmonary morbidity are dominant. Despite a decrease in hospital mortality for high volume centers, a high proportion of survivors suffer from neurological deficits. Knowledge of the pathophysiology of vasospasms in the later stages of the disease has increased. Anti-inflammatory treatment does not improve the outcome. Nimodipine prophylaxis in the first 96 h after SAH seems to be the only intervention which has been proven to be advantageous in studies; however, nearly every second survivor of SAH suffers from some neurological deficits and more than one third of survivors report depressive episodes or symptoms of posttraumatic stress disorder.

An Observational Study on the Effect of Nimodipine on Cerebral Blood Flow Velocity and Oxygenation in Patients with Subarachnoid Haemorrhage

“…As a lipophilic vasodilator, we expected nimodipine to cause cerebrovascular dilation with elevated CBF and rSO 2 . Due to its low bioavailability and in accordance with previous studies 1,2,10) , it is conceivable that the gastric administration of nimodipine failed to attain therapeutic plasma concentrations needed to achieve the desired effect. However, in this clinical study, nimodipine plasma concentrations were not measured and hence a dose-effect relation cannot be analyzed.…”

“…If clinically significant DCI occurs, arterial hypertension is recommended to improve cerebral perfusion 12) . While several studies report increased cerebral blood flow (CBF) due to nimodipine, few show reduced CBF linked to decreased MAP and CPP 5,10,16) . In contrast, one retrospective study even revealed an enhanced risk of CVS with a higher need for vasopressor agents associated with nimodipine administration 10) .…”

“…While several studies report increased cerebral blood flow (CBF) due to nimodipine, few show reduced CBF linked to decreased MAP and CPP 5,10,16) . In contrast, one retrospective study even revealed an enhanced risk of CVS with a higher need for vasopressor agents associated with nimodipine administration 10) . Nimodipine is routinely used to prevent CVS, but its effect on patients with existing CVS might be risky.…”

“…It remains unclear how many patients were indeed affected by CVS in the present study. TCD is widely used to consider CVS if mean BFV in MCA exceeds 120 cm/sec 10) . Overall, mean BFV in our patients remained within a physiological range.…”