本文選題：腦出血　切入點：遲發(fā)性腦水腫　出處：《浙江大學》2017年碩士論文

【摘要】：目的探討腦出血后遲發(fā)性腦水腫形成的病因、病理生理機制及其相關(guān)危險因素和治療方法。方法回顧性分析了 2例腦出血后遲發(fā)性腦水腫患者的病史、臨床表現(xiàn)、實驗室及影像學檢查、治療經(jīng)過及預后。結(jié)果病例1是25歲的年輕女性,該患者主要特點是妊高癥病史,順產(chǎn)后急性起病,血腫吸收近1月后出現(xiàn)遲發(fā)性腦水腫。患者增強MRI顯示血腫周圍有一環(huán)形強化,考慮炎癥反應改變包膜形成可能性最大。該患者還有年輕、出血量大于30ml、血壓較高、纖維蛋白原高等遲發(fā)性腦水腫危險因素。該患者內(nèi)科聯(lián)合脫水治療效果差,后因水腫進展,中線移位行去骨瓣減壓術(shù),術(shù)后恢復可。病例2,中年男性,為急性起病的高血壓患者,有高血壓病史,未曾服藥,偶有抽煙飲酒,起病后三聯(lián)降壓藥也沒有見到明顯的降壓效果,為難控制高血壓。ICH后3周出現(xiàn)遲發(fā)性腦水腫�？紤]該患者因長期高血壓未控制,腦內(nèi)大小血管條件差,易發(fā)生水腫,一旦發(fā)生較難控制,且出血量大,受損范圍廣,血糖和纖維蛋白原也較高,NIHSS評分為15分,這些都是該患者發(fā)生遲發(fā)性腦水腫的相關(guān)危險因素。該患者聯(lián)合脫水并積極控制血壓,后期血壓逐漸穩(wěn)定,水腫逐漸吸收。結(jié)論腦水腫是腦出血后常見的并發(fā)癥,有神經(jīng)功能惡化甚至是腦疝的風險,嚴重時危及生命,并與臨床預后息息相關(guān)。遲發(fā)性腦水腫往往出現(xiàn)在腦出血2周后,確切的病理生理機制目前觀點不一,尚未有定論,但普遍觀點是和占位效應、缺血再灌注損傷、血腫成分如紅細胞、血紅蛋白、鐵離子等、白細胞和血小板、凝血酶、血壓調(diào)節(jié)受損、補體、甘露醇使用不當相關(guān),年齡、性別、高血壓、出血量、纖維蛋白原升高、高血糖、高NIHSS評分、MMPs、腦利鈉肽、吸煙、包膜形成等可能是ICH后遲發(fā)性腦水腫的危險因素,在臨床上需警惕。
[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.
【學位授予單位】：浙江大學
【學位級別】：碩士
【學位授予年份】：2017
【分類號】：R743.34
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本文編號：1668652