脑出血后迟发性脑水肿二例临床分析并文献复习

发布时间：2018-03-26 16:31

  本文选题：脑出血　切入点：迟发性脑水肿　出处：《浙江大学》2017年硕士论文

【摘要】：目的探讨脑出血后迟发性脑水肿形成的病因、病理生理机制及其相关危险因素和治疗方法。方法回顾性分析了 2例脑出血后迟发性脑水肿患者的病史、临床表现、实验室及影像学检查、治疗经过及预后。结果病例1是25岁的年轻女性,该患者主要特点是妊高症病史,顺产后急性起病,血肿吸收近1月后出现迟发性脑水肿。患者增强MRI显示血肿周围有一环形强化,考虑炎症反应改变包膜形成可能性最大。该患者还有年轻、出血量大于30ml、血压较高、纤维蛋白原高等迟发性脑水肿危险因素。该患者内科联合脱水治疗效果差,后因水肿进展,中线移位行去骨瓣减压术,术后恢复可。病例2,中年男性,为急性起病的高血压患者,有高血压病史,未曾服药,偶有抽烟饮酒,起病后三联降压药也没有见到明显的降压效果,为难控制高血压。ICH后3周出现迟发性脑水肿。考虑该患者因长期高血压未控制,脑内大小血管条件差,易发生水肿,一旦发生较难控制,且出血量大,受损范围广,血糖和纤维蛋白原也较高,NIHSS评分为15分,这些都是该患者发生迟发性脑水肿的相关危险因素。该患者联合脱水并积极控制血压,后期血压逐渐稳定,水肿逐渐吸收。结论脑水肿是脑出血后常见的并发症,有神经功能恶化甚至是脑疝的风险,严重时危及生命,并与临床预后息息相关。迟发性脑水肿往往出现在脑出血2周后,确切的病理生理机制目前观点不一,尚未有定论,但普遍观点是和占位效应、缺血再灌注损伤、血肿成分如红细胞、血红蛋白、铁离子等、白细胞和血小板、凝血酶、血压调节受损、补体、甘露醇使用不当相关,年龄、性别、高血压、出血量、纤维蛋白原升高、高血糖、高NIHSS评分、MMPs、脑利钠肽、吸烟、包膜形成等可能是ICH后迟发性脑水肿的危险因素,在临床上需警惕。
[Abstract]:Objective to investigate the etiology, pathophysiological mechanism, risk factors and treatment of delayed cerebral edema after intracerebral hemorrhage. Methods the history and clinical manifestations of 2 patients with delayed cerebral edema after intracerebral hemorrhage were analyzed retrospectively. Results case 1 was a 25-year-old young woman with a history of pregnancy-induced hypertension (PIH) and an acute onset after birth. Delayed cerebral edema occurred after hematoma absorption for nearly one month. Enhanced MRI showed a ring enhancement around the hematoma, and the possibility of capsule formation was most likely to be changed by considering the inflammatory reaction. The patient was also young, with blood loss greater than 30 ml and high blood pressure. Risk factors of advanced delayed cerebral edema with fibrinogen. This patient was treated by internal medicine combined with dehydration, but later because of the progress of edema, the midline transposition underwent decompression of bone flap, and recovered after operation. Case 2, middle age male, For patients with acute onset of hypertension, they have a history of hypertension, have not taken medicine, occasionally smoke and drink alcohol, and the triple antihypertensive drug has not seen any obvious effect of lowering blood pressure after the onset of the disease. Delayed cerebral edema occurred 3 weeks after the difficult control of hypertension. ICH. Considering that the patient has poor blood vessel condition and easy edema due to long-term hypertension, once it is difficult to control, the amount of blood loss is large, and the range of damage is wide. Blood glucose and fibrinogen were also higher and NIHSS scores were 15, which were the risk factors for delayed brain edema. The patient was dehydrated and actively controlled blood pressure, and later blood pressure gradually stabilized. Conclusion Cerebral edema is a common complication after intracerebral hemorrhage. It has the risk of nerve function deterioration or even cerebral hernia, which is life-threatening and closely related to clinical prognosis. Delayed cerebral edema often occurs 2 weeks after intracerebral hemorrhage. The exact pathophysiological mechanism has not yet been concluded, but the general view is that it is associated with space-occupying effects, ischemia-reperfusion injury, hematoma components such as red blood cells, hemoglobin, iron ions, white blood cells and platelets, thrombin, etc. Impaired blood pressure regulation, improper use of complement, mannitol, age, sex, hypertension, blood loss, increased fibrinogen, hyperglycemia, high NIHSS scores, brain natriuretic peptide, smoking, The formation of capsule may be the risk factor of delayed cerebral edema after ICH.
【学位授予单位】：浙江大学
【学位级别】：硕士
【学位授予年份】：2017
【分类号】：R743.34
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本文编号：1668652