Hansen D, Hannemann L, Specht M, Schaffartzik W
Klinik für Anaesthesiologie und Operative Intensivmedizin, Klinikum Benjamin Franklin, FU, Berlin.
Anaesthesist. 1995 Apr;44(4):219-29. doi: 10.1007/s001010050148.
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 evidence 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 avoid 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.
脑动脉瘤破裂后发生蛛网膜下腔出血（SAB）的患者中，只有53%-58%能存活且无神经功能损害。发病率和死亡率与脑血管痉挛导致的迟发性缺血性神经功能缺损密切相关。以下综述阐述了病理生理机制；根据当前文献讨论了钙拮抗剂、高容量血液稀释和诱导性动脉高血压治疗的重要性。病理生理学。除血液中的其他血管活性物质外，出血后第2至4天从裂解红细胞中释放的血红蛋白在诱导血管痉挛中起重要作用。随之发生炎症性血管病，6-12周后完全消退。脑血流量（CBF）根据血管痉挛的程度而降低。CBF降至临界值以下可能导致不可逆梗死。严重血管痉挛会导致自动调节紊乱和脑血管对二氧化碳的反应性降低。钙拮抗剂。钙阻滞剂尼莫地平可使软脑膜小血管扩张，CBF增加。然而，全身血管扩张及随后的血压下降可能会限制CBF的增加。此外，已知尼莫地平可降低细胞内钙浓度，从而对缺血性细胞损伤有一定保护作用。七项安慰剂对照临床研究表明，尼莫地平可改善因脑血管痉挛导致严重神经功能损害患者的预后。高容量血液稀释。建议扩容并将血细胞比容稀释至30%-33%，以改善血管痉挛期间的脑灌注。中心静脉压和肺毛细血管楔压应分别为10-12 mmHg和15-18 mmHg。但尚无证据表明该措施能改善预后，且肺水肿是常见的副作用。然而，低血容量和血液浓缩可导致脑灌注受损和神经损伤加重。诱导性动脉高血压。在存在脑血管痉挛及由此导致的自动调节紊乱的情况下，可通过提高体循环动脉压来增加脑灌注。该措施也未能改善神经功能结局。结论。SAB后脑血管痉挛的治疗旨在避免脑灌注受损。必须纠正低血容量和血液浓缩。应建立正常通气以避免低碳酸血症性血管收缩。SAB后应持续给予尼莫地平。鉴于自动调节紊乱，必须预防全身低血压及其导致CBF降低的风险。高容量血液稀释和/或诱导性动脉高血压的重要性尚不清楚。尽管进行了治疗，但SAB后存活且无严重神经功能缺损的患者数量并未增加。
