Sugiura M, Yozawa Y, Kubo O, Kitamura K, Kimata S, Hagiwara H, Joshita H
No To Shinkei. 1985 Dec;37(12):1155-61.
A case of subarachnoid hemorrhage complicated by neurogenic pulmonary edema and neurogenic myocardial damage is reported. A 50-year-old woman was admitted following the sudden onset of headache and disturbance of consciousness due to a ruptured internal carotid posterior communicating artery aneurysm on the right side. She showed respiratory failure due to pulmonary edema, which subsequently improved with the mechanical ventilation. After that, she manifested chest distress and hypotensive episode then occurred. An ECG showed QS wave and ST elevation which suggested the presence of inferolateral myocardial damage. Subsequent rises in serum GOT, GPT, LDH and CPK were noticed. CPK-MB and LDH I and V isozyme levels rose. An echo cardiogram showed hypokinesis of the apical half of the left ventricular septum. The patient died on 5th hospital day due to rerupture of the cerebral aneurysm. Autopsy revealed diffuse myocytolysis with coagulation necrosis of the heart muscle without occlusion of coronary arteries. A small hemorrhagic lesion was found in the hypothalamus. We suggested that a hypothalamic lesion due to subarachnoid hemorrhage stimulated the sympathetic nervous system which in turn discharged endogenic catecholamine. This was probably accompanied by vasospasm of the coronary arteries and systemic peripheral arterioles. Furthermore, myocardial oxygen consumption could have been increased by the increase in catecholamine. Finally, it gave rise to neurogenic pulmonary edema and extensive diffuse myocytolysis of the heart occurred.
报告了一例蛛网膜下腔出血并发神经源性肺水肿和神经源性心肌损伤的病例。一名50岁女性因右侧颈内动脉后交通动脉瘤破裂,突发头痛和意识障碍入院。她因肺水肿出现呼吸衰竭,随后通过机械通气得以改善。此后,她出现胸部不适,继而发生低血压发作。心电图显示QS波和ST段抬高,提示存在下壁心肌损伤。随后血清谷草转氨酶、谷丙转氨酶、乳酸脱氢酶和肌酸磷酸激酶升高。肌酸磷酸激酶同工酶MB以及乳酸脱氢酶I和V同工酶水平升高。超声心动图显示左心室间隔心尖半部运动减弱。患者于住院第5天因脑动脉瘤再次破裂死亡。尸检发现心肌弥漫性肌细胞溶解伴凝固性坏死,冠状动脉无阻塞。下丘脑发现一个小出血性病变。我们认为,蛛网膜下腔出血导致的下丘脑病变刺激了交感神经系统,进而释放内源性儿茶酚胺。这可能伴有冠状动脉和全身外周小动脉的血管痉挛。此外,儿茶酚胺增加可能导致心肌耗氧量增加。最终,引发了神经源性肺水肿,并出现了心脏广泛弥漫性肌细胞溶解。