急性颅脑损伤术后继发对侧迟发性血肿诊治分析

目的探讨急性外伤性颅内血肿清除术后继发对侧迟发性血肿的诊治，以提高疗效。方法对36例外伤性颅内血肿清除术中及术后并发对侧迟发性血肿病人的临床资料进行回顾性分析。结果36例对侧迟发性血肿均行手术治疗，其中恢复良好16例，中残6例，重残3例，死亡11例。结论在清除急性外伤性颅内血肿后，若术中发生急性脑肿胀或术后病情恶化．应考虑对侧迟发性血肿形成的可能，及时钻颅探查或复查头颅CT，及早治疗可改善预后。     

迟发性颅内血肿的早期发现及治疗

目的：颅内损伤后，在治疗急性损伤的基础上，及时发现迟发性血肿，并采取正确的治疗措施，可以提高疗效。方法：在入院首次ＣＴ检查未见血肿，病情恶化时要复查ＣＴ；在术中发生急性脑膨出时，应在对侧钻颅探查或术后病人病情恶化时行ＣＴ检查；术后病人行持续颅内压（ＩＣＰ）监测。对短时间内颅内压急剧升高，应及时行ＣＴ检查，及早发现迟发性颅内血肿。结果：本组３３例迟发性颅内血肿患者，预后良好７例，中残５例，重残６例，植物存活０例，死亡１５例，死亡率４５． ５％。结论；在清除急性外伤性颅内血肿时发生急性脑膨出，或病人在病情稳定后出现病情恶化，或颅内压在原基础上突然短时间内急剧升高，应考虑迟发性血肿形成可能，宜尽早钻颅探查或复查ＣＴ，早期发现及时治疗可以改善预后。     

迟发性颅内血肿的早期发现及治疗

目的：颅内损伤后,在治疗急性损伤的基础上,及时发现迟发性血肿,并采取正确的治疗措施,可以提高疗效。方法：在入院首次CT检查未见血肿,病情恶化时要复查CT;在术中发生急性脑膨出时,应在对侧钻颅探查或术后病人病情恶化时行CT检查;术后病人行持续颅内压（ICP）监测。对短时间内颅内压急剧升高,应及时行CT检查,及 早发现迟发性颅内血肿。结果：本组33例迟发性颅内血肿患者,预后良好7例,中残5例,重残6例,植物存活0例,死亡15例,死亡率45.5%。结论：在清除急性外伤性颅内血肿时发生急性脑膨出,或病人在病情稳定后出现病情恶化,或颅内压在原基础上突然短时间内急剧升高,应考虑迟发性血肿形成可能,宜尽早钻颅探查或复查CT,早期发现及时治疗可以改善预后。     

急性颅内血肿清除后继发对侧部位迟发血肿的早期判断

目的 急性外伤性颅内血肿清除的术中及术后，如何发现对侧部位的迟发血肿从而及时治疗来提高疗效。方法在术中发现与术侧不相符合的颅内压增高或发现病人出现新的神经系统体征或生命体征不稳定时，应及时钻颅探查或行CT检查。结果术前手术对侧部位有骨折线，有脑挫裂伤和／或有少量脑出血；对侧硬膜外或硬膜下已有小血肿是引起术后出现对侧迟发血肿的重要原因。结论在清除急性颅内血肿时发生与术侧不相符的颅内压增高或病人出现新的神经系统体征或生命体征不稳定时，应高度怀疑对侧出现迟发血肿，应及时钻颅探查或行CT检查，早诊早治可提高治疗效果。     

急性颅内血肿术后继发非手术区迟发性血肿21例

目的探讨急性颅内血肿清除术后继发非手术区迟发性血肿的发病机制、临床特征,并及时发现提高疗效。方法总结21例病人的临床资料。结果本组病人死亡8例,病死率为38.1%,重残2例,中残4例,良好7例。结论对有可能出现术后迟发性血肿的病人应高度警惕,尤其是术中出现脑肿胀或术后病情恶化及出现新的定位体征者,应考虑迟发性血肿形成可能,宜尽早钻颅探查或复查CT,早期发现及时治疗可改善预后。     

急性颅内血肿术后继发非手术区迟发性血肿21例

目的探讨急性颅内血肿清除术后继发非手术区迟发性血肿的发病机制、临床特征，并及时发现提高疗效。方法总结21例病人的临床资料。结果本组病人死亡8例，病死率为38．1％，重残2例，中残4例，良好7例。结论对有可能出现术后迟发性血肿的病人应高度警惕，尤其是术中出现脑肿胀或术后病情恶化及出现新的定位体征者，应考虑迟发性血肿形成可能，宜尽早钻颅探查或复查CT，早期发现及时治疗可改善预后。     

外伤性迟发性颅内血肿

外伤性迟发性颅内血肿陈建良陈锦伦吴耀晨一般认为，脑外伤后术中脑膨出是急性脑肿胀引起。迟发性颅内血肿的概念提出后，我们加强了对脑外伤开颅术中急性脑膨出原因的观察，发现这种急性脑膨出，一部分是由远隔部位的迟发性硬膜外血肿引起。本文报告近５年来开颅血肿清除...     

急性外伤性颅内血肿清除术后对侧血肿再次手术的临床研究

急性外伤性一侧颅内血肿清除术后继发对侧迟发性血肿或原对侧血肿增大可以发生在手术过程中或术后较短时间内。此类病人易漏诊或误诊，耽误再次手术时机，死亡率及致残率较高。我院神经外科于2000年10月～2005年7月收治此类病人22例，现就其发生机制及诊治作一探讨。     

清除硬膜下血肿时出现迟发性对侧硬膜外血肿引起的急性脑肿胀附两例报道

外伤性颅内血肿清除术中的急性脑肿胀是脑外科中最严重的并发症之一。其原因可能为脑水肿、充血和迟发性颅内血肿。清除硬膜下血肿时出现对侧迟发性硬膜外血肿,尚未见有报道,本文报道2例。例1,男22岁,车祸致伤一小时入院。病人昏迷,对痛刺激有反应,上肢屈曲。瞳孔等大,光反应迟钝。     

血肿清除术后并发迟发性颅内血肿的临床分析

目的：探讨外伤性颅内血肿清除术后并发迟发性颅内血肿（DPIH）的原因、发病机制及防治措施。方法：790例急性外伤性颅内血肿清除术后，45例出现术后迟发性颅内血肿，将DPIH与未出现术后血肿（WRIH）者在某些临床特征方面进行比较。结果：两组比较，在术前出现脑疝征象、血肿的类型、凝血功能异常、手术方式、术中低血压及治疗结果等方面均存在显著性差异。结论：DPIH的发生与颅脑损伤的程度、类型、治疗方式及全身因素密切相关，其预后很差。血肿清除术后症状不能改善或病情恶化时应行动态CT检查，可尽早发现DPIH。一些预防措施可有助于减少DPIH的发生。     

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。     

自发性脑出血发生血肿扩大的影响因素分析

目的探讨自发性脑出血患者发生血肿扩大的影响因素。方法回顾性分析2018年9月至2019年9月苏州大学附属第一医院神经外科收治的224例自发性脑出血患者的临床资料。所有患者入院时行首次头颅CT平扫(发病时间≤8 h),并于24 h后复查头颅CT,将复查时血肿量增加≥33%或增加≥12.5 ml定义为血肿扩大,并分为血肿扩大组(n=70)与血肿未扩大组(n=154)。收集两组年龄、性别、糖尿病史、初始血肿量、入院时收缩压、入院时格拉斯哥昏迷评分(GCS)以及是否有凝血功能异常等临床资料。判读首次头颅CT平扫时是否存在血肿边缘不规则混合密度征、黑洞征、漩涡征、分叶征、混杂征。采用单因素分析和多因素logistic回归分析法判断影响血肿扩大的因素。结果224例患者中,CT显示血肿边缘不规则混合密度征71例,黑洞征56例,漩涡征51例,分叶征53例,混杂征58例。血肿未扩大组与血肿扩大组患者的年龄、性别以及初始血肿量的差异均无统计学意义(均P>0.05)。与血肿未扩大组比较,血肿扩大组有糖尿病史者和凝血功能异常者占比均高,入院时GCS低、收缩压高以及头颅CT显示有血肿边缘不规则混合密度征、黑洞征、漩涡征、分叶征、混杂征者占比均高(均P<0.05)。多因素logistic回归分析结果显示,有糖尿病史、入院时GCS低、入院时收缩压高、凝血功能异常以及头颅CT显示有血肿边缘不规则混合密度征、黑洞征、漩涡征、分叶征、混杂征均为脑出血患者发生血肿扩大的危险因素(均P<0.05)。结论既往有糖尿病史、入院时GCS低、收缩压高、凝血功能异常以及有CT影像学特征性表现的自发性脑出血患者发生血肿扩大的风险高。     

急性外伤性颅内血肿开颅血肿清除术后迟发血肿相关因素分析

目的 分析颅内血肿开颅血肿清除术患者的临床特征及术后出现迟发血肿的危险因素.方法 以我院2009-03-2013-03收治的68例急性外伤性颅内血肿开颅手术治疗患者为研究对象,根据是否发生迟发血肿进行分组,采用Logistic回归模型分析术后迟发血肿危险因素.结果 多因素Logistic回归分析结果显示血浆凝血酶时间、手术时机、颅骨骨折为发生迟发血肿的危险因素.结论 急性外伤性颅内血肿患者多伴有重型颅脑损伤和颅内占位,术后迟发血肿一般发生于术后12 h内,以脑内血肿、硬膜外血肿、硬膜下血肿为常见,血浆凝血酶时间延长、手术时机短、合并颅骨骨折为高危因素,应引起高度关注.     

外伤性迟发性颅内血肿救治体会

目的探讨外伤性迟发性颅内血肿的发病机制、早期诊断及治疗。方法回顾性分析 60例外伤性迟发性颅内血肿临床资料,通过临床观察并CT复查,确诊外伤性迟发性颅内血肿,手术治疗46例,保守治疗14例。结果恢复良好20例,中残18例,重残8例,植物生存2例,死亡12 例。结论脑挫伤、蛛网膜下腔出血、颅骨骨折、高龄为外伤性迟发性颅内血肿的高危因素,细致观察,早期CT复查可以及时发现,提高治疗效果。     

Mild hypothermia for hemispheric cerebral infarction after evacuation of an acute subdural hematoma in an infant

The use of mild hypothermia to treat hemispheric infarction after evacuation of an acute subdural hematoma in an infant is reported. The patient, a 2-year-old boy, presented with a deteriorating level of consciousness after a fall from a tree. Computed tomography (CT) scan revealed an acute subdural hematoma on the right side with marked midline shift, and emergency evacuation of the hematoma was performed. The postoperative course was uneventful until the patient's intracranial pressure (ICP) rose and his condition deteriorated 3 days after surgery. CT scan revealed a hemispheric infarction on the injured side. Mild hypothermia was induced to control the ICP and protect the brain. While the hypothermia was effective in lowering the elevated ICP, it failed to arrest progression of the infarction. The patient was discharged with mild disability 2 months after the injury. No serious complications occurred during or after the hypothermia. Our experience indicates that hypothermia can be a useful procedure for controlling the ICP in children with severe traumatic brain injury including acute subdural hematoma, although its capability to protect the brain from severe, progressive ischemia appears to be limited.     

A case of infected subdural hematoma following chronic subdural hematoma irrigation]

A 71-year-old female complicating Parkinson disease and diabetes mellitus was admitted to our medical center for urinary tract infection one month after burr hole irrigation and drainage of left chronic subdural hematoma. Klebsiella pneumonia was detected in the bacterial culture of her urine. As antibiotic therapy started, her condition and peripheral white blood cell counts were improved. But consciousness level got worsened and right hemiparesis appeared. A CT scan showed re-accumulation of left subdural fluid so an emergent irrigation was performed. The old hematoma with slightly yellowish, bloody purulent fluid was found and an intracapsular drain was inserted. Klebsiella pneumonia was detected from the bacterial culture of the hematoma. After 10 days, a CT scan showed subdural fluid collection again, so, total hematoma capsule removal was performed. After the operation, her neurological and serological condition improved and she was discharged without any neurological deficits. Klebsiella pneumonia existing urinary tracts rarely infected subdural hematoma cavity via hematogenous dissemination. We must keep in mind this complication may occur when we see compromised host like this case. Total removal of infected hematoma capsule is considered as radical treatment.     

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.     

Hypertensive intracerebral hematoma after aneurysmal subarachnoid hemorrhage

We report a patient with sequential intracerebral hematoma in bilateral basal ganglia after an aneurysmal subarachnoid hemorrhage. A 55-year-old woman presented with sudden loss of consciousness without a past history of hypertension. Subarachnoid hemorrhage secondary to a ruptured anterior communicating artery aneurysm was seen on initial CT and an intracerebral hematoma was observed in both basal ganglia 3 hours later on a follow-up CT scan. We suggest that delayed intracerebral hematoma may occur due to increased intracranial pressure caused by aneurysmal rupture and discuss the possible mechanisms of this occurrence.     

Acute interdural hematoma mimicking epidural hematoma: a case report

Intracranial hematoma rarely presents between two dural layers of pachimeninges. Here, we present a case of an interdural hematoma with similar appearance to an epidural hematoma. A 51-year-old man presented with a left temporal contusion following a motor vehicle accident. After craniotomy and contusion removal, the post-operative CT scan showed a parietal intracranial hematoma located posterior and superior to the bone flap. The CT scan appearance of the new hematoma was similar to the CT scan appearance of an epidural hematoma. Upon operation, we determined that the hematoma was located between two layers of dura mater, i.e., an interdural hematoma. We removed the hematoma and sutured the two layers of dura to each other at multiple sites. Interdural hematoma is a rare entity. Its appearance in a CT scan can be mistaken for an extradural hematoma.