吸毒人群颅脑损伤33例临床特点

目的探讨吸毒人群颅脑损伤的临床特点。方法对杭州市中医院及温州医科大学附属第三医院近10年来共收治33例吸毒并颅脑损伤患者的临床资料进行回顾性分析。总结临床特点及治疗。结果所有患者均出现呕吐,多伴复合伤。均行头颅CT检查。硬膜外血肿3例,硬膜下血肿2例,单处脑挫裂伤8例,多处脑挫裂伤15例,脑挫裂伤伴有硬膜下血肿3例,脑挫裂伤伴有脑室内出血2例。按照GOS预后评分,恢复良好23例,中度残疾7例,严重残疾2例,长期植物生存状态1例。结论吸毒人群颅脑损伤临床表现重,病情恢复慢。脑挫裂伤在其中较为多见,神经功能损害重。并发症多,预后差。     

去骨瓣减压术33例临床应用体会

随着交通事故、建筑意外等造成外伤增多,颅脑外伤病人也增加,重型颅脑损伤约占颅脑损伤20%,死亡率很高。我院自2003年1月至2008年5月收治了33例重型颅脑损伤开颅手术患者的临床资料,均行去骨瓣减压术,现将救治及预后情况总结报告如下。1资料与方法1.1一般资料:本组患者33例,男26例,女7例,年龄15~54岁,平均为30岁。致伤原因:车祸27例(81.8%),坠伤3例(9%),钝物击伤2例(6%),锐器伤1例(3%)。1.2临床表现:①术前意识状态处于不同程度昏迷者30例,病人术前GCS评分3~5分9例,6~8分21例,9~12分3例。②瞳孔变化:一侧瞳孔散大光反应消失6例,双侧瞳孔散大光反应消失2例。③合并伤:颜面部损伤14例,四肢骨折5例,血气胸2例。④有颅底骨折征象(脊液耳鼻漏)15例。1.3 CT检查结果:患者入院时均行头颅CT检查,显示硬膜外血肿8例(24.2%);硬膜下血肿15例(45.4%);混合型血肿7例(21.2%);单纯广泛脑挫裂伤、弥漫性脑肿胀3例(9.0%)。颅内血肿≥30 ml,中线移位>5 mm并有脑室受压。1.4治疗:本组33例患者均行开颅手术,具体方法:根据颅内血种或脑挫裂...     

重型颅脑损伤术后大面积脑梗塞分析

本院自１９９５年１月至２００１年１２月，对重型颅脑损伤患者进行手术治疗后，出现大面积脑梗塞３０例，占同期颅脑损伤６２８６例的０．４８％。现总结分析如下。１临床资料１．１一般资料：本组男性２１例，女性９例；年龄１８～７１岁，平均４２岁；车祸伤２３例，跌坠伤６例，打击伤１例。１．２临床表现：入院时GCS评分３～８分，一侧瞳孔散大１２例，两侧瞳孔散大６例。入院时均经CT检查，脑挫裂伤伴硬膜下血肿１４例，脑挫裂伤伴脑内血肿１０例，硬膜外血肿２例，脑肿胀４例。除脑挫裂伤灶与血肿外，在脑实质内未见大片低CT值区…     

严重对冲性额颞底部脑损伤96例手术治疗体会

后枕部着力致颅脑损伤时，常引起额颞底部对冲伤，对应的单或双侧额颞底部脑挫裂伤或（和）颅内血肿形成，若处理不当或不及时，则死亡率与伤残率高。本院自2001年4月～2006年6月经手术治疗严重对冲性额颞底部脑损伤96例，现报告如下。     

重型颅脑损伤一侧去骨瓣减压术后对侧迟发颅内血肿临床分析和预防

目的分析重型颅脑损伤一侧去骨瓣减压术后对侧迟发型颅内血肿发生的原因并提出预防和处理的方法。方法回顾性分析本院经治的12例出现重型颅脑损伤一侧去骨瓣减压术后对侧迟发型颅内血肿患者的病例特点、治疗经过和预后情况,并结合文献对该手术并发症进行分析。结果 12例患者均行再次开颅手术清除对侧迟发性颅内血肿术。术前CT提示对侧合并颅骨骨折6例,术中出现术侧急性脑膨出并证实对侧迟发性血肿8例。术后3月随访,患者预后良好1例,中残3例,重残5例,死亡4例。结论重型颅脑损伤一侧去骨瓣减压术后对侧迟发型颅内血肿多发生在首次术后24小时内,对于术前CT提示存在对侧颅骨骨折、术中出现急性脑膨出等情况的患者,应当高度警惕该并发症的发生。及时的发现并手术治疗是争取良好预后的关键。     

颅脑对冲伤与冲击伤再手术病例诊治探讨

目的探讨颅脑对冲伤与冲击伤患者需再次手术的原因与处理方法。方法回顾性分析2010-01—2014-01受伤机制为对冲伤与冲击伤的需再次开颅手术的24例患者的病例资料。结果本组再次开颅病例术后随访3~6个月,按格拉斯哥预后评分(GOS)判定预后,恢复良好12例(50%),重残2例,植物生存2例,死亡8例(33%)。结论颅脑创伤需手术患者术前应仔细研究患者的受伤机制,分析影像学资料,及时诊断并处理对侧迟发性颅内血肿和扩大的脑挫裂伤灶,能提高其治愈率,减少死残率,改善患者预后。     

小脑挫裂伤临床特点分析

目的探讨创伤后小脑挫裂伤的艋床特点及救治策略。方法对小脑挫裂伤19例患者的临床资料进行分析,根据小脑挫裂伤严重程度,采取保守治疗或手术治疗。结果19例患者中,手术治疗12例,保守治疗7例,恢复良好7例,中残3例,死亡9例。结论小脑挫裂伤多为中重型颅脑外伤,患者年龄偏大,损伤机制以枕部减速伤为主,常合并幕上对冲部位挫裂伤,小脑挫裂伤合并的血肿及时手术清除及枕下减压、脑室外引流,可挽救生命,改善患者的预后。     

迟发性外伤性颅内血肿30例分析

目的总结迟发性外伤性颅内血肿(DTICH)的诊治经验。方法患者均头部CT检查,首次检查于伤后1～3 h。正常8例,脑挫裂伤伴血肿9例,硬膜下血肿6例,硬膜外血肿7例,颅内积气5例。复查头部CT发现血肿时间22例于伤后3～6 h,4例于伤后3～7 d,4例伤后7d以后发现。其中脑内血肿22例(额叶10例、颞叶12例),硬膜下血肿6例,硬膜外血肿2例。血肿与受力点关系,直接着力12例,对冲部位18例。迟发性颅内血肿指首次检查(CT扫描)未发现,经过一定时间后复查发现的血肿,或手术、尸检在原无血肿部位发现血肿。其产生的机理尚不清楚。结果 30例中14例有颅骨骨折及硬脑膜中动脉破裂,5例原发血肿,11例迟发性血肿发生在颅骨骨折部位。可能与血肿清除后填塞现象解除及骨折线渗血加速有关。结论对有颅骨骨折的颅内血肿患者,如血肿不在骨折线附近,或骨折线较长,原发血肿位于骨折线的一端,血肿清除后,颅内压仍高或脑膨出者,首先应排除远隔部位骨折线附近迟发血肿的可能。     

颅脑损伤并发霉菌感染的原因分析和护理对策

目的:分析急性颅脑损伤并发霉菌感染的原因。方法:对20例急性颅脑损伤并发霉菌感染的原因进行分析。结果:20例急性颅脑损伤患者并无呼吸道感染史及抗生素应用史,其中脑内血肿伴脑挫裂伤4例,硬膜下血肿9例,硬膜外血肿伴蛛网膜下腔出血7例,发生时间为7～11天。结论:颅脑病变严重程度,抗生素、糖皮质激素的长期应用,患者年龄大, 机体抗力差,是导致霉菌感染的最常见原因。根据易发原因,提出相应护理对策。     

保守治疗外伤性颅内血肿160例

我院2000年10月至2003年6月对入院时无明显手术指征的160例外伤性颅内血肿患者首选非手术治疗,结果6例死亡,现报道如下。临床资料1.一般资料:160例患者中男112例,女48例,年龄2~71岁,平均32岁。均有明确外伤史。急性血肿127例,亚急性血肿33例。入院时意识呈浅昏迷33例,嗜睡或烦躁76例,其余均清醒。头痛150例,呕吐82例,外伤性癫痫发作9例,除8例原发性动眼神经损伤者外其余患者瞳孔均正常。颅脑CT示:小脑幕上血肿140例,幕下血肿20例。幕上血肿位于硬膜外39例,硬膜下53例,脑内25例,多发23例;小脑幕下血肿硬膜外14例,硬膜下4例,小脑内2例。血肿…     

胰腺钝性损伤急诊CT诊断与外科治疗

【摘要】〓目的〓探讨胰腺损伤的诊断及外科治疗。方法〓回顾分析经临床诊疗和手术证实为钝性胰腺损伤(13例)患者CT表现和治疗结果。结果〓13例患者中,胰腺挫伤4例,挫裂伤9例,其中胰腺横断伤1例;均伴有胰周被膜、肾前筋膜增厚,胰腺周围脂肪间隙模糊及积液;2例伴假囊肿形成。合并伤包括脾挫裂伤5例,肝挫裂伤6例,肾挫裂伤3例。12例痊愈,1例死亡,3例术后6月假性囊肿形成。结论〓腹部CT检查对胰腺损伤的早期诊断及治疗具有非常重要的价值。     

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。     

单额开颅治疗双额叶挫裂伤伴血肿

目的总结单额开颅治疗双额叶挫裂伤的经验。方法回顾性分析21例双额叶挫裂伤患者的临床资料,均采用单额开颅治疗。入院时GCS评分:9～11分13例,6～8分6例,3～5分2例。结果术后第1 d所有病例均行头颅CT复查,无一例出现迟发性颅内血肿或残余血肿。对侧挫裂伤及血肿基本清除(>75%)15例,部分清除(50%～75%)6例。术后6个月按GOS分级标准,恢复良好13例,中残4例,重残3例,死亡1例。结论采用单额开颅能有效清除双额叶挫裂伤及血肿,并具有缩短手术时间、减轻手术创伤等优点,具有较好的临床实用价值。     

Acute brain edema in fatal head injury: analysis by dynamic CT scanning

Dynamic computerized tomography (CT) was performed on 42 patients with acute head injury to evaluate the hemodynamics and to elucidate the nature of fatal diffuse brain bulk enlargement. Patients were divided into two groups according to the outcome: Group A included 17 nonfatally injured patients, eight with acute epidural hematomas and nine with acute subdural hematomas; Group B included 25 fatally injured patients, 16 with acute subdural hematomas and nine with bilateral brain bulk enlargement. Remarkable brain bulk enlargement could be seen in all fatally injured patients with acute subdural hematoma. In 29 (69%) of 42 patients, dynamic CT was performed within 2 hours after the impact. In the nonfatally injured patients with brain bulk enlargement, dynamic CT scans suggested a hyperemic state. On the other hand, in 17 (68%) of the 25 fatally injured patients, dynamic CT scans revealed a severely ischemic state. In the fatally injured patients with acute subdural hematoma, CT Hounsfield numbers in the enlarged hemisphere (hematoma side) were significantly lower than those of the opposite side (p less than 0.001). Severe diffuse brain damage confirmed by follow-up CT scans and uncontrollable high intracranial pressure were noted in the fatally injured patients. Brain bulk enlargement following head injury originates from acute brain edema and an increase of cerebral blood volume. In cases of fatal head injury, acute brain edema is the more common cause of brain bulk enlargement and occurs more rapidly than is usually thought.     

Acute spontaneous subdural hematoma of arterial origin

BACKGROUND: Acute subdural hematoma is usually associated with cerebral contusion or laceration of the bridging veins following a head injury. However, several cases of acute subdural hematoma without head injury (acute spontaneous subdural hematoma) have been reported. METHODS: Among 162 cases of acute subdural hematoma admitted to our departments between 1996 and 2003, we repoort eight cases of acute spontaneous subdural hematoma. These cases fulfilled the following criteria. 1) Head injury was either trivial or absent. 2) Neither aneurysm nor arteriovenous malformation was apparent. 3) CT scan revealed neither brain contusion nor traumatic subarachnoid hemorrhage. 4) At operation, laceration of the cortical artery was observed. In this article, we describe the clinical feature (age, sex, Glasgow Coma Scale [GCS] Score on admission, past history, CT appearance, and outcome) associated with this condition. RESULTS: Patients ranged in age from 68 to 85 years (average 74.8 years), and were comprised of 3 males and 5 females. Previous medical history included cerebral infarction in 6 of the 8 patients and myocardial infarction in 1 patient. These seven patients were taking antiplatelet manifestation. GCS on admission ranged from 4 to 13. Five of the 7 patients on antiplatelet medication had secondary insults, such as hypoxia. On CT, hematoma thickness ranged from 13.2mm to 42.5mm (average 22.6mm), and midline shift ranged from 10.0mm to 24.0mm (average 16.5mm). Neurological outcome evaluated using the Glasgow Outcome Scale was as follows, good recovery n = 2, moderate disability n = 2, severe disability n = 3, persistent vegetative state n = 1. CONCLUSION: The mechanism of acute spontaneous subdural hematoma is influenced by the presence of pre-existing cerebrovascular disease and by the use of antiplatelet agents. In such cases, the possibility of cortical arterial bleeding should be taken into account, and craniotomy should be performed.     

Primary intracranial hypotension associated with chronic subdural hematoma--report of 2 cases

Low spinal fluid pressure syndrome is characterized by orthostatic headache aggravated in upright position. It is classified into two from etiological standpoint i.e. primary and secondary (most often seen after lumbar puncture). On the other hand, low spinal fluid pressure is one of the promoting factors of chronic subdural hematoma. We report 2 cases of primary low spinal fluid pressure syndrome (primary intracranial hypotension) associated with chronic subdural hematoma. Case 1 is a 47-year-old man who was admitted with disorientation following 2 week history of orthostatic headache. Spinal fluid pressure was 7mmH2O in the lateral recumbent position. CT scan revealed bilateral isodense chronic subdural hematoma. The subdural hematoma reaccumulated 17 days after the first operation. Case 2 is a 31-year-old woman who was admitted with 4 week history of progressive orthostatic headache accompanied by nausea and vomiting. Spinal fluid pressure was 0 mmH2O. CT scan and cerebral angiography showed bilateral chronic subdural hematoma. The hematoma reaccumulated 20 days after the first operation. Six cases including our two cases of primary intracranial hypotention associated with chronic subdural hematoma have been reported. When changes of characters of headache, especially mental symptoms and disturbances of consciousness occurred in patients with chronic orthostatic headache, association of chronic subdural hematoma should be suspected. In cases with chronic subdural hematoma associated with low spinal fluid pressure syndrome, the reaccumulation of hematoma tends to occur after burr hole opening and irrigation of hematoma.     

Computerized tomography (CT), EMI scanner, in the diagnosis of acute traumatic intracranial hematomas (author's transl)

Eighteen examinations of acute head trauma have been performed using computerized tomography (CT), EMI scanner, before and after operation in our department since September, 1975. Diagnostic findings in CT before emergency operations of 5 cases including epidural hematoma (1), subdural hematoma (2), intracerebral hematoma (1), and combined hematoma (1) were presented and the diagnostic value of this new method was compared with that of cerebral angiography. CT was proved to be highly valuable in the diagnosis of not only intracranial hematomas but also cerebral edema, cerebral contusion and other abnormalities of the brain structures in head injury.     

Temporal lobe lesions in head injury

Summary In cases of closed head injury temporal lobe lesionse.g. contusion, laceration, pulping, or intracerebral haematoma frequently result in an expanding process. These are frequently associated with an overlying subdural haematoma. Eighty five cases of such lesions from a consecutive series of 1,000 cases of head injury have been analyzed. The lesions are caused by severe injury resulting in loss of concsiousness and skull fracture. Most of them are contre-coup lesions. Clinically they manifest themselves like any other acute or subacute intracranial hematoma. The majority of the patients have contralateral hemiparesis and pupillary abnormalities. Carotid angiography is valuable for diagnosis. These lesions are likely to be missed when exploratory burr holes are made or, are erroneously diagnosed as acute subdural haematoma or brain oedema. Smaller lesions, not showing progressive deterioration, may respond to conservative treatment. However, surgical decompression is essential in most cases. A fronto-temporal osteoplastic craniotomy or a large Scoville trephine hole is essential to deal with these lesions adequately.     

Acute subdural hematoma originating from the lacerated intracranial internal carotid arteries--case report

A 51-year-old male presented with laceration of the bilateral intracranial internal carotid arteries (ICAs) manifesting as acute subdural hematoma (SDH) after a fall of 3 m. Brain computed tomography showed acute SDH appearing as irregular mixed high and low density and causing midline shift. During the operation, massive liquiform hematoma flowed out from the deep portion around the cranial base and systemic blood pressure decreased abruptly. Hemostasis was impossible and he died soon after the operation. Autopsy revealed skull fractures in the bilateral sphenoidal, orbital, temporal, frontal, parietal, and occipital bones, and laceration of the bilateral ICAs in the cavernous sinuses at the fracture sites. Acute SDH can be caused by laceration of the ICA.