慢性硬膜下血肿42例改进术式治疗体会

目的 传统的钻孔引流术常导致颅内积气、蛛网膜损伤后硬膜下积液、严重脑损伤继发血肿的并发症，本文将探讨新术式在减少并发症和提高疗效方面的效果。方法 42例慢性硬膜下血肿患者均采用局麻下钻孔，具体钻孔点依血肿最大层面而定，钻开骨孔约1cm大小，于骨孔最高及最底处分别切开硬膜孔约引流管直径大小，留置2根引流管然后缝合头皮，从上管持续9．0％NS冲洗，从下管引流清亮后停止冲洗，注入尿激酶，闭管，结束手术。结果 手术后症状缓解100％，手术后3天复查头颅CT血肿消失40例（95．2％），2例（4．8％）少量残余自行吸收；仅2例颅内少量积气（4．8％）系操作不当导致空气逸入颅腔；1例蛛网膜破裂导致硬膜下积液；1例因引流管刺激脑皮层诱发癫痫，拔除引流管后缓解；无一例继发血肿及脑损伤或其他神经系统功能障碍；无一例复发。结论 本手术方式可明显减少传统手术方式的并发症，缩短了住院周期，值得临床推广。     

钻孔引流治疗慢性硬膜下血肿48例疗效分析

目的探讨钻孔引流治疗慢性硬膜下血肿的方法和疗效。方法经CT引导定位钻孔冲洗引流治疗慢性硬膜下血肿。结果 48例患者血肿清除42例,硬膜下残留低密度少量积液者6例,术后3～6个月未见血肿复发病例。结论钻孔引流术是治疗慢性硬膜下血肿的理想方法。     

慢性硬膜下血肿手术治疗

目的探讨手术治疗慢性硬膜下血肿的近期疗效。方法对确诊慢性硬膜下血肿患者106例,采取单孔钻孔引流91例,采取双孔钻孔引流15例。结果术后血肿引流80%以上,脑组织复张31例;留置引流管3天血肿引流彻底,脑组织复张96例;留置引流管3天血肿无明显减少者3例;血肿引流彻底,脑组织复张欠佳,遗留硬膜下积液3例,引流管移位入脑组织未引起临床症状2例;血肿下脑挫伤及血肿1例,保守治疗,无遗留神经功能障碍;钻孔部位硬膜外血肿1例,保守治疗,治愈出院;术后并发精神障碍1例,予抗精神症状药物,3日后症状消失。结论钻孔引流是慢性硬膜下血肿的有效治疗方式。     

慢性硬膜下血肿66例临床分析

目的探讨慢性硬膜下血肿的诊断和治疗。方法回顾性分析66例慢性硬膜下血肿患者的临床特点、手术方式和预后情况。45例均匀一致低密度影的慢性硬膜下血肿，采用单孔钻颅方法，血肿腔不予冲洗；21例混杂密度影的慢性硬膜下血肿，采用双孔钻颅万珐，仅5例引流欠通畅而予血肿腔冲洗，其余病例血肿腔亦不予以冲洗。结果本组全部治愈。有13例患者有少量硬膜下积液，平均随访3．5个月，4例积液消失，9例减少或无增加。结论单孔或双孔血肿引流是治疗慢性硬膜下血肿的有效方法，根据cT影像学特征，选择不同的手术方式。     

创伤急性硬膜下血肿不同术式效果观察

目的 分析颅脑外伤所致急性硬膜下血肿患者接受急诊实施标准开颅血肿清除加去骨瓣减压术治疗的临床效果。方法 以2021年1月1日至2021年12月31日期间在本院接受急诊治疗的颅脑外伤所致急性硬膜下血肿患者72例为研究对象，将其凭借随机数字表法进行分组。观察组患者接受标准开颅血肿清除加去骨瓣减压术治疗，对照组患者接受血肿清除骨瓣回纳术治疗。对比术后颅内压减弱情况、手术安全性以及治疗效果。结果 术后1天、3天、1周的颅内压对比，观察组均低于对照组（P<0.05）；术后并发症发生率对比，为观察组更低（P<0.05）；术后治疗效果对比，为观察组更高（P<0.05）。结论 颅脑外伤所致急性硬膜下血肿患者接受急诊实施标准开颅血肿清除加去骨瓣减压术治疗取得了明显的治疗效果，患者颅内压明显降低，术后不良反应发生率较低，患者预后更佳。     

老年重症慢性硬膜下血肿的微创治疗

目的 探讨微创手术方法在老年重症慢性硬膜下血肿的应用价值。方法 1997年2月-2001年2月对34例老年重症慢性硬膜下血肿(Chronic subdural hematoma，CSDH)采用经皮颅内血肿前(上)部穿刺、浅置管、注入尿激酶液化血肿、辅以促进受压脑组织复位等措施进行回顾性分析。结果 术前血肿量平均97ml；术后血肿清除或基本清除。受压脑组织复位时间24h-96h，平均42h。均痊愈出院。29例术后随访3月-48月，平均19月，Barthel指数评分正常22例，生活自理7例；CT随访21例，正常14例，脑萎缩5例，轻度局限性硬膜下积液2例。结论 微创血肿清除术尤其适合老年CSDH的治疗，疗效满意,复发率低。     

双钻孔冲洗与持续导管引流治疗老年人慢性硬膜下血肿21例

目的 探讨老年人慢性硬膜下血肿的手术方式。方法 分析21例经双钻孔冲洗与持续导管引流的老年人慢性硬膜下血肿患者的临床资料。结果 21例老年人慢性硬膜下血肿均行双钻孔冲洗与持续导管引流术，术后10天头颅CT检查，5例血肿完全消失，16例血肿腔内有少许低密度硬膜下积液；无再出血及气颅等并发症。结论 应用双钻孔冲洗与持续导管引流术治疗老年人慢性硬膜下血肿，术后并发症少，效果良好。     

慢性硬膜下血肿的临床诊治分析

目的探讨慢性硬膜下血肿的形成机制及双孔引流、单孔引流或骨瓣开颅血肿清除及包膜切除等诊治方法的分析。方法回顾性分析本院收治的慢性硬膜下血肿患者73例,分别根据病情给予双孔引流、单孔引流或骨瓣开颅血肿清除及包膜切除术、保守治疗,分析其临床资料。结果术后各组患者的临床症状均有不同程度的好转,感觉异常除3例恢复不明显外其余均明显恢复,各组病例2周后复查气颅及残余积液均消失,2个月后随访亦无复发迹象。结论慢性硬膜下血肿发病机制复杂,根据病情给予双孔引流、单孔引流或骨瓣开颅血肿清除及包膜切除术或保守治疗,均能获得较好的预后。     

慢性硬膜下积液与慢性硬膜下血肿的关系

我院自1996．5-2000．10收治外伤性慢性硬膜下积液共65例，其中演变为慢性硬膜下血肿10例，经钻孔引流手术治疗，预后良好，报告如下。     

慢性硬膜下血肿钻单孔双管引流手术治疗体会

【摘要】〓目的〓探讨慢性硬膜下血肿钻单孔置双管外引流术的疗效。方法〓回顾性分析我院2011年6月~2014年3月收治69例慢性硬膜下血肿患者行钻单孔置双管引流手术治疗后的情况。结果〓58例临床症状体征消失,11例改善,无症状加重及死亡病例。经术后1~7天复查CT提示,69例血肿均大部份减少或基本消失,10例并发颅内血肿腔少量积气、积液,随访3个月全部恢复,无复发病例。结论〓慢性硬膜下血肿选择钻单孔置双管外引流效果良好,并发症较少。     

Cardiopulmonary hemodynamic changes during acute subdural hematoma evacuation

The aim of this study was to clarify the mechanism of hemodynamic changes leading to intraoperative hypotension during evacuation of acute subdural hematoma. To our knowledge, little data is available about the mechanism of hemodynamic changes during surgical interventions to decrease intracranial pressure after severe head injury. The influence of preoperative hypotension on intraoperative hypotension was examined. Hemodynamic studies (pulmonary artery catheterization) were carried out in 15 patients before and after acute subdural hematoma evacuation. All patients were assessed for hemodynamic parameters, evacuated hematoma volume, and intracranial pressure measurements. Comparison between just before and after evacuation of the hematoma showed that the mean arterial pressure, pulmonary arterial pressure, systemic vascular resistance, pulmonary vascular resistance, central venous pressure, and pulmonary capillary wedge pressure all decreased after hematoma evacuation. However, the cardiac index was unchanged after hematoma evacuation. Mean arterial blood pressure is dependent on the cardiac index and vascular resistance, so the decrease in arterial blood pressure during hematoma evacuation was the result of a decline in vascular resistance. The influence of preoperative blood pressure on intraoperative hemodynamic changes was analyzed by dividing the patients into two groups, the preoperative hypotension group and preoperative nonhypotension group. The decrease in mean arterial blood pressure was more marked in the preoperative hypotension group than in the preoperative nonhypotension group. Intraoperative hypotension during evacuation of acute subdural hematoma is caused by a decrease in vascular resistance. Preoperative hypotension is a also risk factor for intraoperative hypotension.     

Clinical study of reaccumulation and persistence of chronic subdural hematoma; setting an Ommaya reservoir

We treated 57 cases of chronic subdural hematoma by aspiration via the Ommaya reservoir following burr hole opening and irrigation of the hematoma in order to reduce the reaccumulation and persistence of the hematoma. An Ommaya reservoir was placed on the following patients: (1) the volume of hematoma was more than 100 ml and/or (2) expansion of the brain after evacuation of the hematoma was poor. However in spite of these techniques there were 6 cases (10.5%) of recurrence and 21 cases (36.8%) with persistence of the hematoma cavity for longer than 2 months after the first operation. The recurrence was due to occlusion of the Ommaya reservoir by massive rebleeding into the hematoma cavity in cases with a large subdural hematoma and/or an immature external membrane. Persistence of the hematoma cavity for longer than 2 months after the first operation was due to minor rebleeding and CSF inflow into the hematoma cavity through the damaged inner membrane in cases of acute onset and/or or coexisting intracranial disease (brain atrophy, cerebral infarction and subdural effusion). The most suitable cases for application of this technique were those with poor expansion of the brain after evacuation of the hematoma, or those with a mature external membrane and a medium-size hematoma.     

Two cases of impending herniation due to multiple traumatic acute subdural hematomas: combination of burr hole evacuation and craniotomy

A contralateral extra-axial hematoma sometimes occurs during an operation on an acute subdural hematoma and may become fatal. Using a combined procedure of burr hole evacuation and craniotomy, we treated 2 cases of multiple traumatic acute subdural hematomas. Our policy for such cases is first to perform a burr hole evacuation for the acute subdural hematoma in the emergency room, while simultaneously preparing the operation room for a possible further operation. Next, we perform computed tomography (CT) of the brain. If the evacuation does not provide enough decompression, we either carry out a craniotomy at the same site, or, we observe the patient without resorting to craniotomy. However, if the patient's condition deteriorates, burr hole evacuation is repeated and/or craniotomy is carried out as soon as possible on the lesion at the already prepared operation room. Both of our patients received craniotomy for another subdural hematoma after the burr hole evacuation. Though his intracranial pressure was well managed during the acute stage, one of the patients died 21 days after the trauma due to an extensive brain infarction caused by vasospasm. The other regained consciousness and was able to walk 5 months after the trauma in spite of cerebral infarction from vasospasm. The possible mechanism of vasospasm in severe head injury is also discussed.     

Significance of consecutive bilateral surgeries for patients with acute subdural hematoma who develop contralateral acute epi- or subdural hematoma

BACKGROUND: Although rare, patients with acute subdural hematoma (ASDH) because of severe head injury can develop contralateral acute epi- or subdural hematoma, requiring consecutive surgical procedures. The choice of treatment strategies for such patients is clinically important. METHODS: Among 88 patients with ASDH who were surgically treated over 13 years, we encountered and studied 5 patients who developed contralateral acute epi- or subdural hematoma (5.7%). RESULTS: All 5 patients were male, ranging in age from 17 to 40. According to the Glasgow Coma Scale on admission, 1 patient was rated 3, 1 was 4, 1 was 5, and 2 were 6. All patients underwent consecutive surgical procedures for ASDH and contralateral ASDH and/or acute epidural hematoma, and were given postoperative supportive therapy with barbiturates and mild hypothermia. Patients' outcomes according to the Glasgow Outcome Scale were as follows: 1 patient, good recovery (20.0%); 1, mild disability (20.0%); 2, severe disability (40.0%), and 1, persistent vegetative state (20.0%). No patients died. Although decompressive craniectomy and evacuation of hematoma may lead to contralateral acute epi- or subdural hematoma in patients with ASDH, this therapy is justified because hematoma irrigation with trephination therapy has a poor outcome for comatose patients. CONCLUSION: Awareness of intraoperative brain swelling is important, as it suggests the development of contralateral hematoma. Immediate computed tomography and a rapid return to the operating room are therefore critical.     

Acute brain swelling during evacuation of subdural hematoma caused by delayed contralateral extradural hematoma: report of two cases

Two patients experienced severe brain swelling during the evacuation of acute subdural hematomas. Postoperative computed tomographic (CT) scans revealed delayed extradural hematomas on the sides opposite the subdural hematomas. Extradural bleeding occurred in the area of the fractured skull. One patient improved neurologically after evacuation of the extradural hematoma, and the other was not operated because he was moribund. Drilling exploratory burr holes in the fractured area may have been a better strategy than awaiting a postoperative CT scan. The reduction of intracranial pressure after the removal of subdural hematoma was postulated to be the most important factor contributing to the formation of the extradural hematoma.     

Acute subdural hematoma in infancy

BACKGROUND: Acute subdural hematoma in infants is distinct from that occurring in older children or adults because of differences in mechanism, injury thresholds, and the frequency with which the question of nonaccidental injury is encountered. The purpose of this study is to analyze the clinical characteristics of acute subdural hematoma in infancy, to discover the common patterns of this trauma, and to outline the management principles within this group. METHODS: Medical records and films of 21 cases of infantile acute subdural hematoma were reviewed retrospectively. Diagnosis was made by computed tomography or magnetic resonance imaging. Medical records were reviewed for comparison of age, gender, cause of injury, clinical presentation, surgical management, and outcome. RESULTS: Twenty-one infants (9 girls and 12 boys) were identified with acute subdural hematoma, with ages ranging from 6 days to 12 months. The most common cause of injury was shaken baby syndrome. The most common clinical presentations were seizure, retinal hemorrhage, and consciousness disturbance. Eight patients with large subdural hematomas underwent craniotomy and evacuation of the blood clot. None of these patients developed chronic subdural hematoma. Thirteen patients with smaller subdural hematomas were treated conservatively. Among these patients, 11 developed chronic subdural hematomas 15 to 80 days (mean = 28 days) after the acute subdural hematomas. All patients with chronic subdural hematomas underwent burr hole and external drainage of the subdural hematoma. At follow-up, 13 (62%) had good recovery, 4 (19%) had moderate disability, 3 (14%) had severe disability, and 1 (5%) died. Based on GCS on admission, one (5%) had mild (GCS 13-15), 12 (57%) had moderate (GCS 9-12), and 8 (38%) had severe (GCS 8 or under) head injury. Good recovery was found in 100% (1/1), 75% (8/12), and 50% (4/8) of the patients with mild, moderate, and severe head injury, respectively. Sixty-three percent (5/8) of those patients undergoing operation for acute subdural hematomas and 62% (8/13) of those patients treated conservatively had good outcomes. CONCLUSIONS: Infantile acute subdural hematoma if treated conservatively or neglected, is an important cause of infantile chronic subdural hematoma. Early recognition and suitable treatment may improve the outcome of this injury. If treatment is delayed or the condition is undiagnosed, acute subdural hematoma may cause severe morbidity or even fatality.     

Acute subdural hematoma with swirl signs: clinical analysis of 15 cases

From July 2003 to July 2009, 15 cases of subdural hematoma with swirl signs were treated in our hospital and their clinical data were retrospectively analysed. The mortality was compared between these patients and those with typical acute subdural hematoma who were treated at the same time in our hospital. Among the 15 cases, full recovery was achieved in 4 cases, slight disability in 2, grave disability in 2 and death in 7 （46.7%）. The mortality of these patients was conspicuously higher than that of typical sub- dural hematoma （14/83, 16.9%, P〈0.01）. Subdural hematoma with swirl signs is often suggestive of hazardous pathogenetic condition and early diagnosis and prompt surgical intervention is essential to reduce mortality.     

Chronic subdural hematoma in infancy. Clinical analysis of 30 cases in the CT era

The cases of 30 infants with chronic subdural hematoma treated surgically between 1978 and 1987 (after the introduction of computerized tomography) were reviewed. This series was limited to infants presenting with increased intracranial pressure, neurological deficits, or developmental retardation. Nineteen patients were male and 11 were female, ranging in age from 1 to 14 months (average 6.1 months). The surgical treatment was initiated with percutaneous subdural tapping which was repeated periodically, if indicated, for 2 weeks. If the patients failed to respond to subdural tapping, subdural-peritoneal shunting was installed. The follow-up periods were from 3 months to 9 years 8 months (average 4 years 10 months). Computerized tomography at that time disclosed disappearance or minimal collection of subdural fluid in 28 cases (93%) and a significant collection (greater than 5 mm) in two (7%). Neurological examination revealed that the patients were "normal" in 17 cases (57%), "mildly or moderately disabled" in nine (30%), and "severely disabled" in four (13%). The majority of disabled patients had lesions secondary to infantile acute subdural hematoma, child abuse, or hemorrhagic diathesis. These results indicate that the treatment protocol in the present series is acceptable for the elimination of subdural hematoma. Together, early diagnosis and treatment of the etiological conditions causing the lesion are indispensable for obtaining a satisfactory neurological outcome.     

Acute non-traumatic extensive subdural spinal hematoma

Acute spinal subdural hematoma is a somewhat rare pathology. Its severity comes from the constitution of an acute spinal cord compression. In many cases MRI is useful for the differential diagnosis with the epidural hematoma. A 79-year-old patient was referred for emergency neurosurgery for acute spinal cord compression. The vascular risk in this patient was significant: hypertension, oral anticoagulants. Clinically, acute non-traumatic subdural spinal hematoma was suspected. The spinal cord MRI was in favor of the diagnosis which was confirmed intraoperatively. The surgical procedure revealed an extensive hematoma which infiltrated the spinal cord. The diagnosis of nontraumatic subdural spinal hematoma may be difficult in some cases and correctly established only during the surgical procedure. In comparison with reports in the literature, we discuss the underlying mechanisms of this hematoma. Spinal subdural haematoma must be considered in patients taking anticoagulant therapy or with a coagulation disorder who present signs of acute spinal cord compression. MRI sagittal T1 and T2-weighted images are adequate and reliable for diagnosis of spinal subdural hematoma. Prompt surgical evacuation of this hematoma is crucial.     

Contralateral development of chronic subdural hematoma after evacuation of chronic subdural hematoma. A case report

Contralateral acute complications such as acute epi/subdural hematomas can be encountered after evacuation of a chronic subdural hematoma, though they are rare. We found only one case of chronic subdural hematoma following the surgery for contralateral chronic subdural hematoma, have been published in English language literature. A 73-year-old male admitted to our hospital with a right-sided subdural hematoma. The subdural hematoma was evacuated through a burr-hole. A left-sided subdural higroma appeared after operation and turned into classical subdural hematoma in the course of time. After evacuation of contralateral chronic subdural hematoma, the patient recovered completely. All stages of the development of contralateral chronic subdural hematomas were shown by serial computed tomograms. It was suggested that traumatic chronic subdural hematomas develop from mostly subdural higromas. If contralateral subdural higroma is seen after surgical evacuation of a chronic subdural hematoma, the possibility of development of contralateral chronic subdural hematoma must be kept on mind.