YL-1型针微创穿刺引流治疗急性硬膜外血肿的临床分析

目的探讨YL-1型针微创穿刺引流治疗急性硬膜外血肿的临床疗效。方法急性硬膜外血肿19例,采用CT引导定位,以血肿中心为靶点,YL-1型颅内血肿粉碎穿刺针经头皮穿刺冲洗、粉碎、引流血肿,并联合尿激酶(1×104~2×104U/次)溶解血肿。结果本组19例全部治愈,术后持续引流时间平均3.6(3~5)d,无一例需要输血,未出现术中大出血或术后血肿复发。无一例死亡,亦未发生颅内感染、张力性气颅等并发症。拔针前复查CT证实血肿清除90%~100%,占位效应消失或明显减轻。住院时间平均9.6(6~15)d。出院时日常生活量表(activity of daily living,ADL)分级:Ⅰ级17例,Ⅱ级2例。13例随访3~6月,平均(4.5±1.5)月,GOS分级均为Ⅰ级。结论 YL-1型针微创穿刺引流术治疗急性硬膜外血肿,疗效确切、微创、节省医疗费用,手术时准确选择适应证、把握手术时机非常重要。     

外伤性硬膜外血肿穿刺治疗76例分析

硬膜外血肿是基层医院常见的颅脑损伤疾病，约占外伤性颅内血肿的30％左右，其中绝大多数(86．2％)属于急性血肿：急性外伤性硬膜外血肿的传统治疗观念以骨瓣开窗血肿清除为主2000年6月～2004年2月，我院选择性应用特制一次性使用颅内血肿穿刺针穿刺清除治疗外伤性急性硬膜外血肿76例，效果满意，现报告如下。     

急性外伤性硬膜外血肿的微创穿刺治疗

目的探讨微创穿刺引流术治疗急性外伤性硬膜外血肿的疗效。方法2009年6月-2012年6月采用YL-1型一次性颅内血肿穿刺针行微创穿刺引流术治疗外伤性硬膜外血肿68例。根据CT定位确定穿刺点、穿刺方向及穿刺针长度,以电钻将YL-1型一次性颅内血肿穿刺针送人血肿靶点,抽吸血肿后,血肿腔内分次注入尿激酶（一般用生理盐水2—5ml溶人20000～50000U尿激酶）溶解引流出残存血肿,术后复查CT,血肿基本清除、中线结构移位恢复后拔针。结果68例均穿刺成功。经CT确诊2d完全清除32例,3d22例,5d10例;2例并发新鲜出血中转开颅手术;2例并发脑疝术前采用此方法急救后改骨瓣开颅手术治愈。头痛立即缓解18例,肢体麻木无力立即消失3例,其他病例临床症状3～5d逐渐好转。术后住院7～15d,平均12d。68例随访3—6个月：完全失语1例,智力轻度减退4例（合并脑挫裂伤）,无死亡病例。结论微创穿刺引流术治疗急性外伤性硬膜外血肿操作简便、快捷、创伤小、疗效好。     

穿刺引流治疗外伤性硬膜下积液30例

报道穿刺引流治疗外伤性硬膜下积液30例,术前CT定位,在局麻下使用YL-1型颅内血肿粉碎穿刺针进行穿刺引流.全组均治愈,无一例死亡.术后硬膜外血肿1例,气颅3例,均治愈,随访6个月～1年6个月,平均9个月,未复发.     

钻孔引流治疗外伤性硬膜外血肿68例临床分析

目的探讨钻孔引流治疗外伤性硬膜外血肿的适应证及手术时机。方法回顾性分析钻孔引流治疗的68例外伤性硬膜外血肿患者的临床资料。结果术后临床症状完消失58例(85.3%),好转7例(10.3%),中转骨瓣开颅血肿清除术3例(4.4%)。结论钻孔引流治疗外伤性硬膜外血肿操作简单、创伤小、费用低,可作为部分外伤性硬膜外血肿的首选治疗方法。     

急性外伤性颅内血肿术后再出血的原因及防范

目的:探讨急性外伤性颅内血肿术后再出血的原因及防治措施。方法:对18例急性外伤性颅内血肿术后再出血病人的临床特点,放射资料,治疗过程进行回顾性分析。结果:本组硬膜外血肿10例,脑内血肿6例,硬膜下血肿2例。血肿位于脑挫伤及颅骨骨折处12例,手术止血不仔细4例,术中出现低血压12例,术中出现急性脑膨出4例,术后血压不稳躁动8例。本组手术16例,死亡7例。结论:手术减压引起颅压下降为外伤性急性颅内血肿再出血的主要原因,以硬膜外及脑内血肿多见。脑挫伤及骨折的存在是再出血的潜在危险,术中急性脑膨出是再出血的表现形式,手术操作不规范,术中低血压及术后躁动构成了再出血的其它因素。全面彻底准确的手术操作,维持术中术后稳定的血压是防止再出血的关键。     

微创穿刺引流术治疗急性硬膜外血肿86例

目的探讨微创穿刺引流术治疗硬膜外血肿的疗效。方法采用CT引导定位,血肿中心为靶点,YL-1型颅内血肿粉碎穿刺针经头皮穿刺冲洗粉碎引流联合尿激酶(2万~6万U)溶解血肿治疗硬膜外血肿86例。结果大血肿组(血肿量30~100 m l)44例,无效10例(22.7%,10/44),改行开颅血肿清除术后痊愈;余34例中术后3~5 d血肿引流干净25例,血肿少量残留(≤5 m l)9例。小血肿组(血肿量<30 m l)42例,术后1~3 d内均引流干净。出院时ADL分级:Ⅰ级72例,Ⅱ级14例。76例随访3~12个月,(5.3±3.7)月,按GOS分级均恢复良好。结论微创穿刺引流术治疗硬膜外血肿疗效确切、微创,准确选择适应证、把握手术时机至关重要。     

锥颅置管引流治疗硬膜外血肿32例分析

目的探讨锥颅置管注人尿激酶引流治疗硬脑膜外血肿的临床疗效。方法在CT定位下锥颅穿刺血肿置引流管注入尿激酶使血肿液化后引流清除血肿。结果32例手术均成功,临床症状均明显好转或消失,复查CT示血肿消失或基本消失,无并发症。结论锥颅置管引流治疗硬膜外血肿方法安全、微创、简便、临床效果满意。     

微创术治疗高血压脑出血40例

目的 观察颅内血肿微创清除术治疗高血压性脑出血的疗效.方法 对40例高血压性脑出血患者,采用YL-1型一次性颅内血肿粉碎穿刺针经皮穿颅清除血肿.结果 经过治疗,40例高血压性脑出血患者血肿清除率为80%～100%,存活率为92.5%.结论 利用YL-1型一次性颅内血肿粉碎穿刺针微创清除术治疗高血压性脑出血效果显著,值得...     

急性颅内血肿清除后继发对侧迟发性血肿

目的 探讨急性外伤性颅内血肿清除的术中及术后，及时发现对侧迟发性血肿并治疗的意义。方法 在术中发生急性脑肿胀时应在对侧钻颅探查或术后病人恶化时行CT检查。结果 治疗15例对侧迟发血肿病人其中2例死亡，手术死亡率为6％。结论 在清除急性外伤性颅内血肿时发生急性脑肿胀，或术后病情恶化，应想到对侧可能是迟发性血肿形成，宜尽早复查CT及钻颅探查，早诊早治可改善预后。     

Diffuse axonal injury and early intracranial sequelae in severe head injury.

The importance of diffuse axonal injury (DAI) and early intracranial sequelae was studied in 107 patients with diffuse and focal brain injuries. Comprehensive neuropathological study was also undertaken in 24 fatal patients. The mortality rate was clearly the highest in traumatic subarachnoid hemorrhage, followed by acute subdural hematoma, cerebral contusion with delayed hematoma formation, traumatic intracerebral hematoma, diffuse cerebral swelling, DAI with classical features, and finally nearly normal on computed tomographic scans. The mean flow velocities in the middle cerebral artery recorded by transcranial Doppler ultrasound were variable in diffuse brain injury, but commonly decreased on the hematoma side depending on increased intracranial pressure and decreased cerebral perfusion pressure in focal brain injury. Deep-seated hemorrhagic lesions did not expand in diffuse brain injury, but sizable hematoma developed within 24 hours in focal brain injury. The platelet count was significantly lower in patients with poor outcomes in focal brain injury. Histological evidence of classical DAI was found in eight (50%) of 16 cases with focal brain injury. DAI of varying severity is the common subjacent lesion in patients with severe head injury, but the final outcome varies greatly with different lesion types.     

Clivus epidural hematoma: a case report

An acute traumatic epidural hematoma extending from the odontoid process to the dorsum sella is described. The mechanism for the formation of an extradural hematoma in this unusual location seems to be related to age and a severe hyperflexion injury.     

Traumatic false aneurysms of the middle meningeal artery

The authors report a rare case of traumatic false aneurysm of the middle meningeal artery associated with a delayed contralateral extradural hematoma. The extradural hematoma was evacuated, and the pseudoaneurysm was removed to avoid delayed rupture. The literature on traumatic aneurysms is reviewed.     

The incidence of delayed traumatic intracerebral hematoma with extradural hemorrhages

After introduction of computerized tomography (CT), we experienced 22 patients with traumatic extradural and intracerebral combined hematomas, of whom 15 underwent sequential CT scans. In 14 of the 22 patients or 13 of the 15 patients whose initial CT scans were performed early, within 6 hours after injury, intracerebral hematomas developed more slowly than extradural hematomas. In ten of the 13 patients, development of intracerebral hematomas was demonstrated only after removal of extradural hematomas, and in four patients acute brain swelling was observed during surgery. Therefore it is emphasized that the incidence of post-surgical intracerebral hematoma with extradural hemorrhages is high and that acute brain swelling during surgery for extradural hematomas is largely caused by the delayed intracerebral hematomas.     

Differences of acute and chronic epidural hematoma]

Standard neurosurgical management demands prompt evacuation of all extradural hematomas to obtain a low incidence of mortality and morbidity. In selected cases some authors have suggested that moderate hematomas can be managed conservatively without risk to the patient and with a normal outcome. The goal of this study was to analyze the differences in preoperative clinical parameters between a group of acute and a group of chronic extradural hematomas (chronic extradural hematoma was defined as a delay of more than 72 h from the accident to diagnosis). One hundred fifteen (115) patients with extradural hematomas underwent a standard evaluation, documentation and neurosurgical management (prompt evacuation of all extradural hematomas through a craniotomy). Ninety-five patients (83%) had an acute extradural hematoma. Twenty patients (17%) had a chronic extradural hematoma. We analyzed the following parameters: age, cause of accident, clinical findings, Glasgow Coma Score, morphology of hematoma, location of hematoma, cause of bleeding and clinical outcome. The mean age (chronic 30/acute 32) and age distribution were not significantly different between groups. There were no differences in the cause of accident. All patients in both groups had skull fractures. There was no difference between groups regarding hematoma location, most of there being located in the temporal fossa. In the group of acute extradural hematomas, 62% of patients had a Glasgow Coma Score of less than 8 and 47% had pupillary dilation. In the group of chronic extradural hematomas, moderate clinical symptoms were found, with headache and discrete psychological changes most common. Eighty percent (80%) of the patients had a Glasgow Coma Score of greater than 13 and no patients had pupillary dilation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Development of a traumatic intracranial hematoma after a "minor" head injury

We have analyzed features of patients who had what appeared initially to be a minor head injury but who developed an acute traumatic intracranial hematoma. Over a 10-year period, 183 patients who were able to open their eyes spontaneously, were oriented to person, place, and time, and who obeyed commands when they were first seen at a hospital subsequently underwent operation for an acute intracranial hematoma. The hematoma was extradural in 54% of these patients. A history of altered consciousness or symptoms of headache and vomiting were present in 61% of the patients; 33% had a focal neurological deficit, and 43% had either focal deficit or signs of a basal skull fracture. A skull fracture was shown radiologically in 60% of patients, including 52% of those not clinically suspected of having an intracranial lesion. Six months after injury, 77% of the patients had made a moderate or good recovery. The possibility that a patient who has recently sustained a head injury might develop an acute intracranial hematoma can never be completely discounted, even when there are no abnormal clinical signs, and a skull x-ray retains a useful place in the investigation of selected patients with a minor head injury.     

Serial changes in acute extradural hematoma size and associated changes in level of consciousness and intracranial pressure

The authors report the cases of 37 patients encountered during the past 4 years who exhibited acute extradural hematoma but were initially treated conservatively because no or only small hematomas were observed on admission. The frequency of hematoma enlargement, hematoma size, and changes in the level of consciousness and intracranial pressure (ICP) were examined in these patients. The hematomas enlarged in 24 (64.9%) of the 37 patients, and attained a maximum thickness of 25 mm or greater in 19 patients (51.3%). The level of consciousness could be closely observed during enlargement of the hematomas in 13 patients: the level remained unchanged in eight, deteriorated in two, and improved in three, indicating relative stability in the state of consciousness despite the marked changes in hematoma size. The patients whose hematoma enlarged after the initial examination included three who underwent initial CT examination 5 hours after the injury. In five patients enlargement of extradural hematomas was observed unexpectedly during conservative treatment under ICP monitoring. The ICP also remained stable in three patients until the follow-up examination, but showed a rapid increase in two after a period of stability. However, there was no difference in the final size of the hematomas between the patients showing an increase in ICP and those who did not. These findings suggest that extradural hematomas enlarge progressively at rates varying with the condition of the source of hemorrhage. Moreover, a period of stability in the level of consciousness, such as the lucid interval seen in patients with extradural hematoma, is considered to be a period during which compensatory mechanisms can maintain the stability of the intracranial condition during progressive enlargement of the hematoma.     

Delayed onset of traumatic extradural hematoma

During a 4 1/2-year period, seven patients with delayed onset of an extradural hematoma were seen among 80 consecutively treated cases of extradural hematoma for a frequency of 8.75%. The hematomas were insignificant or not present on initial computerized tomography (CT) scanning. Repeat CT scans within 24 hours of admission showed sizeable hemorrhages. Six hematomas were evacuated, and one was reabsorbed spontaneously. In only one patient did neurological deterioration herald the onset of the extradural hematoma, four patients remained unchanged, and two improved before diagnosis. Intracranial pressure (ICP) was monitored in five patients, four of whom showed intermittent rise in pressure despite preventive treatment. Intracranial hypotension and rapid recovery from peripheral vascular collapse seemed to be contributory factors in the delayed onset of an extradural hematoma. Awareness of this entity, a high degree of vigilance, ICP monitoring, and repeat CT scanning within 24 hours of injury are strongly recommended in these cases, especially after decompression by either surgical or medical means, recovery from shock, or whenever there is evidence of even minimal bleeding under a skull fracture on the initial CT scan.     

Rapid spontaneous disappearance of an acute extradural hematoma: case report

The authors report the case of a patient presenting with an acute extradural hematoma and diffuse axonal injury. Control CT scan performed 4 hours later showed the complete resolution of the extradural collection together with increased evidence of shearing injuries. The mechanism of the hematoma resolution may probably be related to the concomitant acute brain swelling.     

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.