高血压脑出血术后并发下消化道大出血1例治疗体会

2009年3月我科收治高血压脑出血开颅术后并发下消化道出血患者1例,经积极治疗,痊愈出院。     

微创治疗高血压脑出血术后相关并发症的原因及处理

目的探讨微创治疗高血压脑出血术后相关并发症的原因及相应处理措施。方法2009-11-2011-11我院诊治60微创治疗高血压脑出血术后并发症患者,对其术后相关并发症进行分析和处理。结果60例中并发消化道出血10例,并发肺炎13例,并发急性肾损伤14例,再出血11例,水电解质平衡紊乱12例。治疗后痊愈56例,死亡4例,其中死于多脏器功能障碍综合征1例,呼吸衰减2例,急性肾功能衰竭1例。结论微创治疗高血压脑出血手术时,要注意其高危因素,严密观察患者的病情变化,并积极预防并发症。     

小骨窗开颅治疗高血压脑出血40例临床分析

目的分析高血压脑出血患者小骨窗开颅的治疗效果。方法对我院收治的40例高血压脑出血患者进行小骨窗开颅术血肿清除治疗,手术完成后4周对所有患者进行Glasgow预后评估,统计分析患者恢复和并发症情况。结果所有患者均成功进行手术,无术中死亡病例,术后17例持续高血压,11例发生消化道出血,9例发生肺部感染或泌尿系统感染,2例复发脑出血后死亡。结论小骨窗开颅术治疗高血压脑出血多数患者预后较好,但应注意围手术期的抗感染治疗。     

高血压脑出血并发消化道出血高危因素分析

目的探讨影响高血压脑出血并发消化道出血的因素并提出预防措施。方法总结１９９１年５月至１９９６年５月间我院收治的２４０例高血压脑出血病人的有关资料，其中发生消化道出血者４１例。采用Ｌｏｇｉｓｔｉｃ回归模型分析各种可能因素对促使高血压脑出血并发消化道出血的作用。结果单因素分析显示：１出血部位，２意识状态，３血肿量，４出血破入脑室，５使用激素这５个因素显示统计学意义。但进入Ｌｏｇｉｓｔｉｃ多变量回归模型的因素只有出血破入脑室。结论出血破入脑室可能是导致消化道出血最危险的因素，尽早减压应是预防消化道出血的重要措施。     

高血压脑出血术后并发消化道出血32例分析

我院从1990年1月至1999年12月间,共手术治疗高血压脑出血患者77例,术后并发消化道出血者32例。1 临床资料1.1 一般资料 本组77例中男46例,女31例,年龄48～72岁,平均64岁;54例为壳核出血,15例为丘脑出血,5例血肿破入脑室,3例小脑出血,所有病例均行骨窗开颅行血肿清除 去骨瓣减压术。 32例并发消化道出血的患者中25例解柏油样稀便,4例单纯呕血,3例两者兼有。从发生时间看,最早者距离脑出血26h,最晚15d,其中26h～4d者17例,4～7d者7例,7～15d者8例。本病的主要诊断依据为术后出现呕血或肉眼可见的柏油样便,潜血阳性,本组已排除原有溃疡病史者。     

影响高血压脑出血立体定向排空术预后的相关因素分析

目的分析影响立体定向排空术治疗高血压脑出血患者预后的因素。方法总结2002年2月～2007年12月收治的76例高血压脑出血患者采用立体定向排空术的临床资料,结合随访资料进行分析,确定影响预后的主要因素。结果术后再出血9例,其中丘脑5例(3例破入脑室),基底节区4例,有脑疝形成4例,均为发病12h内手术,再出血死亡计7例;颅内感染3例;肺部感染10例,2例死亡;应急性消化道溃疡出血5例,1例死亡。超早期手术、血肿部位、血肿破入脑室是术后再出血的主要危险因素。术后出院前共死亡10例,占13.2%,其中有脑疝形成者术后共计死亡7例(包括随访病例),占死亡人数的46.7%,脑疝、再出血、血肿部位、坠入性肺部感染、应急性消化道溃疡出血是患者术后死亡的主要影响因素。结论立体定向排空术治疗高血压脑出血,应正确选择手术时机,防止再出血、坠入性肺部感染和应急性消化道溃疡出血,以改善高血压脑出血患者的预后。     

手术方法对高血压脑出血术后生存状况及并发症影响

目的 探讨不同手术方法对高血压脑出血术后生存状况及并发症的影响.方法 对我科收治的80例高血压脑出血且血肿量大于30ml的临床资料按照手术方法不同分为2组:立体定向组和开颅组,对术后30d内生存状况及并发症进行对照研究.结果 40例立体定向组术后30d内存活35例(87.5%),GCS评分为11.6±4.0分,肺部感染9例(22.5%),消化道出血5例(12.5%),再出血2例(5%).40例开颅组术后30d内存活27例(67.5%),GCS评分为8.2±4.4分,肺部感染19例(47.5%),消化道出血13例(32.5%),再出血8例(20%).对两组术后GCS评分、生存率及并发症发生率进行统计学分析显示立体定向组疗效优于开颅组(均为P＜0.05),差异有显著性.结论 立体定向血肿穿刺抽吸术治疗高血压脑出血手术简单,创伤小,术后并发症少、生存率和生存质量较高,是治疗高血压脑出血较为理想的手术方法.     

急性脑血管病与消化道出血

急性脑血管病合并消化道出血是严重并发症,也是引起致命的危险因素。本科从1975年至1982年收治的急性脑血管病(包括脑出血与脑梗塞)的住院病人中经过筛选,资料比较完整的165例中统计,合并消化道出血为34例,其中脑出血55例并发出血19例,脑梗塞110例并发出血15例。本文就消化道出血发病率、死亡率,与高血压,意识障碍程度及出血时间,方式,予后等进行小     

奥美拉唑治疗脑出血并发应激性溃疡的临床观察

目的 比较西米替丁和奥美拉唑预防高血压性脑出血并发应激性溃疡出血的效果.方法 100例高血压性脑出血患者随机分成西米替丁对照组 (62例)和奥美拉唑治疗组 (63例),观察住院期间消化道出血情况及病死率.结果 西米替丁组和奥美拉唑组并发应激性溃疡出血的发生率分别为19.3%和6.3%,西米替丁组病死率为11.2%,明显...     

高血压脑出血并消化道出血危险因素分析

本文回顾分析 12 0例高血压脑出血患者 ,其中并发消化道出血 2 3例 ,现将其临床资料进行总结 ,探讨可能引起高血压脑出血患者并发消化道出血的危险因素。1　临床资料1 1　一般资料　本组 12 0例高血压脑出血病人均经临床及CT证实 ,排除并发消化道其他疾病及资料不全者。消化道出血以呕吐咖啡样胃内容物或胃管抽出血性胃内容物 ,排黑便或大便潜血试验 ( +++)以上为诊断标准。脑出血量采用多田公式( 1981年 )计算 ,血肿量 (ml) =(最大出血层面 )长轴×短轴×层面数×π/6。 12 0例中男 72例 ,女 48例 ,男∶女为 1 5∶1。年龄 42～ 76岁 ,平均…     

颅脑损伤术后迟发性颅内血肿的形成机制

目的 探讨颅脑损伤术后非手术区迟发性颅内血肿的临床特征及形成机制。方法 回顾性分析29例颅脑损伤术后经CT扫描或再次开颅探查证实为飞黄腾达这发性血肿的发生部位，发生时间，及其与脑挫裂伤，颅骨骨折等原发伤的关系。结果 血肿发生部位与手术部位关系；邻近型8例，远隔型12例，对侧型9例；发生在脑内9例，硬膜外12例，硬膜下7例。脑室内1例；12例术后硬膜外血肿中有9例可见颅骨骨折；9例术后脑内血肿中有7例可见脑挫裂伤。结论 颅脑损伤术后迟发性颅内血肿中，硬膜外，硬膜下与脑内血肿形成机制不尽相同，颅骨骨折，脑挫裂伤，脑膜或皮质血管破裂，桥静脉断裂等局部损伤影响不同类型血肿的形成，脑血管麻痹，低氧血症等是非手术区迟发性血肿形成的病理基础。     

不同手术方式治疗高血压性脑出血的疗效比较及术后再出血影响因素分析

目的探讨神经导航辅助微创穿刺血肿引流术（NAMIEH）、小骨窗开颅血肿清除术（SWCEH）与大骨瓣开颅血肿清除术（LBFEH）治疗高血压性脑出血的疗效及术后再出血影响因素Logistic回归分析。 方法回顾性分析自2016年9月至2019年3月解放军联勤保障部队第九一医院神经外科收治的134例高血压性脑出血患者的临床资料,根据手术治疗方式的不同将其分为NAMIEH组38例、SWCEH组45例与LBFEH组51例。记录2组患者术前及术后7、14 d出血量、GCS评分、NIHSS评分、Barthel指数以及治疗后临床疗效并进行比较,并将高血压性脑出血患者术后再出血影响因素采用Logistic回归分析。 结果3组患者术前出血量、GCS评分、NIHSS评分及Barthel指数比较,差异无统计学意义（P>0.05）;3组患者术后7、14 d出血量、GCS评分、NIHSS评分及Barthel指数比较,差异均有统计学意义（P<0.05）;3组患者术前及术后7、14 d出血量及NIHSS评分均依次明显降低,GCS评分及Barthel指数均依次明显升高,且组内任意两时间点比较差异均有统计学意义（P<0.05）。NAMIEH组、SWCEH组再出血、血肿残留及并发症发生率均分别明显低于LBFEH组,NAMIEH组再出血发生率（10.53%）、血肿残留发生率（5.26%）及术后并发症发生率（15.79%）均明显低于SWCEH组（P<0.05）。以高血压性脑出血患者术后再出血为因变量,对单因素分析中的可能术后再出血影响因素进行Logistic回归分析,结果显示合并糖尿病、术前收缩压、发病至手术时间、血肿形状、破入脑室、术前出血量、术前GCS评分、术前NIHSS评分、术前Barthel指数、凝血功能异常、术后并发症及总住院时间为高血压性脑出血患者术后再出血的独立影响因素（均P<0.05）。 结论NAMIEH治疗高血压性脑出血的临床效果明显优于SWCEH及LBFEH,可有效促进神经功能的恢复,明显降低再出血及术后并发症的发生率,且合并糖尿病、术前收缩压、发病至手术时间等为高血压性脑出血患者术后再出血的独立影响因素。     

Infrequent Hemorrhagic Complications Following Surgical Drainage of Chronic Subdural Hematomas

Chronic subdural hematomas mainly occur amongst elderly people and usually develop after minor head injuries. In younger patients, subdural collections may be related to hypertension, coagulopathies, vascular abnormalities, and substance abuse. Different techniques can be used for the surgical treatment of symptomatic chronic subdural hematomas : single or double burr-hole evacuation, with or without subdural drainage, twist-drill craniostomies and classical craniotomies. Failure of the brain to re-expand, pneumocephalus, incomplete evacuation, and recurrence of the fluid collection are common complications following these procedures. Acute subdural hematomas may also occur. Rarely reported hemorrhagic complications include subarachnoid, intracerebral, intraventricular, and remote cerebellar hemorrhages. The causes of such uncommon complications are difficult to explain and remain poorly understood. Overdrainage and intracranial hypotension, rapid brain decompression and shift of the intracranial contents, cerebrospinal fluid loss, vascular dysregulation and impairment of venous outflow are the main mechanisms discussed in the literature. In this article we report three cases of different post-operative intracranial bleeding and review the related literature.     

Expanding traumatic intracerebral contusion/hematoma

BACKGROUND AND AIMS: Delayed traumatic hematomas and expansion of already detected hematomas are not uncommon. Only few studies are available on risk factors of expanding hematomas. A prospective study was aimed to find out risk factors associated with such traumatic lesions. MATERIALS AND METHODS: Present study is based on 262 cases of intracerebral hematomas / contusions out of which 43 (16.4%) hematomas expanded in size. computerized tomography (CT) scan was done in all the patients at the time of admission and within 24 hours of injury. Repeat CT scan was done within 24 hours, 4 days and 7 days. Midline shift if any, prothrombin time, activated partial thromboplastin time, bleeding time, clotting time and platelet counts, Glasgow coma scale at admission and discharge and Glasgow outcome score at 6 months follow up were recorded. RESULTS: Twenty six percent, 11.3 and 0% patients developed expanding hematoma in Glasgow Coma scale (GCS) of 8 and below, 9-12 and 13-15 respectively. The chances of expanding hematomas were higher in patients with other associated hematomas (17.4%) as compared to isolated hematoma (4.8%) (Fisher's exact results P =0.216). All the cases of expanding hematoma had some degree of midline shift and considerably higher proportion had presence of coagulopathy. The results of logistic regression analysis showed GCS, midline shift and coagulopathy as significant predictors for the expanding hematoma. Thirty nine patients (90.7%) of the total expanding hematomas developed within 24 hours of injury. CONCLUSIONS: Enlargement of intracerebral hematomas is quite common and majority of them expand early after the injury. These lesions were common in patients with poor GCS, associated hematomas, associated coagulopathy and midline shift.     

重症高血压性脑出血患者围手术期综合治疗

目的探讨重症高血压性脑出血围手术期综合治疗的临床意义。方法回顾性分析150例重症高血压性脑出血患者围手术期采用的综合治疗,包括开颅手术清除血肿、合理控制血压和降低颅内高压,加强呼吸道的护理,合理应用抗生素以及对高血糖、消化道出血等对症支持治疗。结果 150例重症高血压性脑出血患者,死亡27例,病死率18%;经治疗后3月随访,日常生活能力(activity daily living,ADL)标准判定,Ⅰ～Ⅲ级占80.49%。结论重症高血压性脑出血患者不仅需要早期或超早期的手术治疗,同时也需要围手术期合理的控制血压、降颅内压、良好的呼吸道护理、营养支持、防治并发症等综合治疗,这对危重患者获得较长的生存时间和较好的生存质量至关重要。     

Intracranial hemorrhage in infancy due to vitamin K deficiency: report of a case with multiple intracerebral hematomas with ring-like high density figures

It is well known that vitamin K deficiency is an important cause of the spontaneous intracranial hemorrhage in infancy. A 60-day-old male infant with spontaneous intracerebral hematomas due to vitamin K deficiency was presented. He was breast-fed. He had been medicated oral antibiotic agent for diarrhea and fever. Three days later he developed petechien, vomiting and twitching, and became drowsy. The blood studies showed anemia, and advance of ESR. He was administered of vitamin K immediately. CT scan was showed four intracerebral hematomas with niveau, which were surrounded by high-density rings. The ring-like figures were unique for this case. The reason may be next, we think. Under the states in which blood can separate easily with advance of ESR, blood clot would adhere to the wall of the hematomas. So these hematomas showed ring-like figures and had niveau in them. CT scan of this case was also interesting because there was little deviation in spite of the big hematomas. The reason of this may be that the brain of infancy is incomplete in myelination and contains much water, and that the possibility of bleeding due to vitamin K occurs slowly. We examined 84 cases of intracranial hemorrhage due to vitamin K deficiency from literatures, and they were all identified for the hemorrhage sites by CT scan. Subarachnoidal hemorrhage was in 72 cases (85.7%), subdural hemorrhage was in 41 cases (48.8%), intracerebral hematomas was in 36 cases (42.9%) and intraventricular hemorrhage was in 9 cases (10.7%). In 52 cases the CT findings were described.(ABSTRACT TRUNCATED AT 250 WORDS)     

Age-related spontaneous intracerebral hematoma in a German community

We investigated incidence, age distribution in relation to etiology, and localization of spontaneous intracerebral hematoma in 100 consecutive cases. Incidence in the total population of the Giessen area was estimated to be greater than 11/100,000 inhabitants/yr and increased with age. There was a trend toward higher incidence in males. Overall mortality was 27%, 22% of 58 patients aged less than 70 years and 33% of 42 patients aged greater than or equal to 70 years. Hypertensive putaminal hematoma showed the highest mortality rate (42%, 10 of 24 cases). Chronic alcoholism and anticoagulant medication influenced the mortality rate unfavourably. We found the following localizations and etiologies to have a specific relation with age: 1) lobar hematomas from vascular malformations, group aged less than 40 years; 2) hypertensive putaminal hematomas and hypertensive thalamic hematomas, group aged 40-69 years; and 3) lobar hematomas, group aged greater than or equal to 70 years. Alcoholism was an additional factor in 38% of the 13 middle-aged men with hypertensive putaminal hematomas. Fourteen cases of spontaneous intracerebral hematoma were possibly due to cerebral amyloid angiopathy. Six of these 14 patients had recurrent lobar hematomas, but only three of the six could be histologically investigated. In these three cases, cerebral amyloid angiopathy was proven.     

轻中型颅脑损伤合并颈椎骨折的临床诊治

目的总结轻中型颅脑损伤合并颈椎骨折的临床诊治经验，提高对颅颈联合伤的认识和重视程度。方法对我科近两年收治的42例轻中型颅脑损伤合并颈椎骨折患者的临床资料进行回顾性分析。结果行颅脑CT检查显示，29例可见不同程度的脑挫裂伤、硬膜外血肿、硬膜下血肿、脑内血肿或混合型血肿；颈椎CT和X线平片显示，单侧关节突骨折脱位14例，棘突骨折8例，单纯椎体楔形压缩性骨折8例，爆裂性骨折3例，齿突骨折7例，枢椎椎弓骨折2例；经CT血管造影或磁共振血管造影证实颈椎骨折合并椎动脉损伤7例。所有患者均未行开颅手术，针对颈椎骨折。采用颈托或颈围固定、枕颌带牵引等非手术治疗20例，另22例接受Crutchfield钳颅骨牵引、颈前路齿突骨折螺丝钉固定术或钢板内固定术治疗。出院时GOS分级5级24例．4级18例。结论颅颈联合伤在临床上并不少见，应高度重视对颅脑损伤患者的颈部检查和保护，早期应进行颈椎CT扫描并预防椎动脉等血管损伤并发症。     

高血压性脑出血血肿清除术后癫痫发作的影响因素分析

目的 探讨高血压性脑出血颅内血肿清除术后并发癫痫发作的影响因素。方法 回顾性分析2011年3月至2018年7月开颅血肿清除术治疗的485例高血压性脑出血的临床资料。采用多因素logistic回归分析检验术后并发癫痫的危险因素。结果 485例中,术后发生癫痫62例（12.9%）。多因素logistic回归分析结果显示,血肿体积≥60 ml、血肿位于小脑、术后再出血、术后电解质紊乱、脑电图异常、术前C反应蛋白（CRP）水平升高、术前肿瘤坏死因子-α（TNF-α）水平升高、术前白细胞介素-6（IL-6）水平升高是术后并发癫痫发作的独立危险因素（P<0.05）。结论 高血压性脑出血开颅血肿清除术后癫痫发作发生率较高,对于血肿较大、血肿位于小脑、术后再出血、术后电解质紊乱、脑电图异常、术前CRP、TNF-α、IL-6水平升高的病人,应采取针对性措施预防术后癫痫发作。     

早期应用尼莫地平治疗脑出血的临床疗效报告

目的 :探讨用尼莫地平降低血压 ,提升颅内压 ,从而控制高血压脑内出血。方法 :将 6 5例脑出血病人随机分为两组 ,治疗组 35例 ,用尼莫地平 10mg静滴 ;对照组 30例 ,用 2 0 %甘露唇 2 5 0ml,每日 2次或 3次 ,两组治疗 7天 ,2周内复查头颅CT。结果 :治疗组的血压平均由 179/ 10 4降至 15 1/ 91mmHg ,对照组由 181/ 10 8降为 180 /10 3mmHg ,两组比较有统计学意义 (P <0 0 1) ,对照组血肿扩大 18例 (6 0 % ) ,治疗组为 3例 (8 5 7% ) ,两组比较有统计学意义 (P <0 0 1)。对照组死亡 7例 ,因脑疝 6例 ,并发症死亡 1例 ;治疗组因肺部感染和消化道出血死亡 1例。结论 :尼莫地平可扩张血管 ,降低血压和提高颅内压 ,使破损血管壁的跨壁压力梯度下降 ,有止血和防止再出血的功能 ,可作为首选抢救药物之一 ,发病早期患者无脑疝或因颅高压引起的昏迷 ,就不要用甘露醇类的降低颅内压的药物 ,以免血肿扩大