ISSN:
1432-055X
Keywords:
Schlüsselwörter Aneurysmatische Subarachnoidalblutung
;
Zerebraler Vasospasmus
;
Kalziumantagonisten
;
Hypervolämische Hämodilution
;
Induzierte arterielle Hypertension
;
Key words Aneurysmal subarachnoid haemorrhage
;
Cerebral vasospasm
;
Calcium antagonists
;
Hypervolaemic haemodilution
;
Induced arterial hypertension
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Description / Table of Contents:
Abstract Only 53%–58% of patients with a subarachnoid haemorrhage (SAB) following the rupture of a cerebral aneurysm survive without neurological damage. Morbidity and mortality are closely related to the delayed ischaemic neurological deficit due to cerebral vasospasm. The following review gives an account of pathophysiological mechanisms; the importance of treatment with calcium antagonists, hypervolaemic haemodilution, and induced arterial hypertension is discussed in light of the current literature. Pathophysiology. In addition to other vasoactive substances in the blood, haemoglobin, which is released from lysed erythrocytes on the 2nd to 4th day after the haemorrhage, plays an important role in inducing vasospasm. An inflammatory angiopathy ensues, with complete resolution after 6–12 weeks. The cerebral blood flow (CBF) is reduced depending on the extent of vasospasm. Irreversible infarction may follow the decrease of CBF below a critical value. Severe vasospasm causes autoregulatory disturbances and reduced responsiveness of cerebral vessels to CO2. Calcium antagonists. The calcium blocker nimodipine causes dilatation of small pial vessels with increased CBF. However, systemic vasodilation with the subsequent fall in blood pressure may limit the increase in CBF. Furthermore, it is known that nimodipine decreases intracellular calcium concentrations resulting in some protection against ischaemic cellular injury. Seven placebo-controlled clinical studies have shown that nimodipine improves the outcome of patients with severe neurological damage due to cerebral vasospasm. Hypervolaemic haemodilution. Volume expansion and haemodilution to a hematocrit of 30%–33% is suggested to improve cerebral perfusion during vasospasm. The central venous and pulmonary capillary wedge pressures should be 10–12 mm Hg and 15–18 mm Hg, respectively. But there is no evidendence of improved outcome with this measure, and pulmonary edema is a frequent side effect. However, impairment of cerebral perfusion and increased neurological damage can be demonstrated with hypovolaemia and haemoconcentration. Induced arterial hypertension. In the presence of cerebral vasospasm and resulting autoregulatory disturbances, cerebral perfusion can be increased by raising systemic arterial pressure. This measure, too, fails to improve neurological outcome. Conclusion. Treatment of cerebral vasospasm following a SAB aims to avoide any impairment of cerebral perfusion. Hypovolaemia and haemoconcentration have to be corrected. Normoventilation should be established to avoid hypocapnic vasoconstriction. Nimodipine should be administered continuously after a SAB. In view of the autoregulatory disturbances, systemic hypotension with its danger of decreased CBF must be prevented. The importance of hypervolaemic haemodilution and/or induced arterial hypertension is not clear. Despite therapeutic efforts, the number of patients who have survived a SAB without a substantial neurological deficit has not increased.
Notes:
Nach wie vor überleben lediglich 53–58% der Patienten mit einer Subarachnoidalblutung (SAB) durch Ruptur eines zerebralen Aneurysmas ohne neurologische Defizite. Eine der wichtigsten Determinanten der Morbidität und Mortalität ist die protrahiert auftretende neurologische Verschlechterung, delayed ischemic neurologic deficit (DIND), durch Vasospasmus der zerebralen Gefäße. In dieser Übersichtsarbeit werden die Pathophysiologie dargestellt und der Stellenwert der Therapie mit Kalziumantagonisten, hypervolämischer Hämodilution und induzierter arterieller Hypertonie anhand der akuten Literatur beurteilt. Dem Hämoglobin, das durch Lyse der Erythrozyten am 2.–4. Tag nach der Blutung freigesetzt wird, kommt eine besondere Bedeutung in der Pathogenese des Vasospasmus zu. In Abhängigkeit von der Ausprägung des Vasospasmus kommt es zur Reduktion des zerebralen Blutflusses (CBF). Kalziumantagonisten vom Dihydropyridintyp können die Überlebensqualität von Patienten mit schwerem neurologischen Defizit durch Vasospasmus verbessern. Ob eine induzierte Hypervolämie und eine Hämodilution bis zu einem Hämatokrit von 30–33% die zerebrale Mikrozirkulation günstig beeinflussen können, ist nicht geklärt. Aufgrund der gestörten Autoregulation der zerebralen Gefäße bei Vasospasmus kann durch Induktion einer arteriellen Hypertension die zerebrale Perfusion gesteigert werden. Eine erhoffte Verbesserung des neurologischen Folgezustands durch Erhöhen des zerebralen Perfusionsdrucks ist allerdings bis heute nicht nachgewiesen.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/s001010050148
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