创伤性多发颅内血肿６９例诊治分析

1995～ 1999年 ,我院手术治疗创伤性多发颅内血肿 69例 ,占同期创伤性颅内血肿总数的 17 6%。现分析如下。1　临床资料1 1　一般情况　男 51例 ,女 18例 ;年龄 19～ 69岁 ,平均 4 1 1岁。致伤原因 :交通事故伤 38例 ,钝器打击伤 18例 ,坠落伤 12例 ,其他 1例。均在伤后3ｄ内手术。伤后急诊格拉斯哥昏迷指数 (ＧＣＳ评分 ) 3～ 5分 17例 ,6～ 8分 4 2例 ,9～ 12分 7例 ,13～ 15分 3例。1 2　颅内血肿类型　以硬膜下血肿 脑内血肿为主 ,硬膜外血肿 硬膜下血肿 脑内血肿次之 (附表 )。附表　创伤性多发颅内血肿 6 9例类型与类型分布血　肿　…     

创伤性硬膜下积液转化为慢性硬膜下血肿11例临床诊治体会

目的总结创伤性硬膜下积液转化为慢性硬膜下血肿的临床诊治体会。方法在111例创伤性硬膜下积液转变为慢性硬膜下血肿患者的诊疗过程中,行CT／MRI动态检查,诊断明确后均采取手术治疗。结果创伤性硬膜下积液转化成慢性硬膜下血肿多见于老年人,动态CT和／或MRI检查有助于发现TSE向CSDH的早期转变,手术治疗效果良好。结论创伤性硬膜下积液转化成慢性硬膜下血肿多见于老年患者,其动态转化的时间不确定,动态CT和／或MRI检查有助于早期发现慢性硬膜下血肿形成。手术治疗（包括钻孔引流和开颅血肿清除血肿外膜剥离手术）效果良好。     

急性大脑镰和小脑幕硬膜下血肿的CT及磁共振成像诊断

目的探讨急性大脑镰和小脑幕硬膜下血肿的CT及磁共振成像特征。方法回顾性分析17例急性大脑镰和小脑幕硬膜下血肿的CT及磁共振成像表现。结果 17例急性大脑镰和小脑幕硬膜下血肿中,大脑镰硬膜下血肿5例,小脑幕硬膜下血肿7例,大脑镰并小脑幕硬膜下血肿5例,6例伴有颅盖骨(大脑凸面)部位的硬膜下血肿或脑实质挫裂伤。结论急性大脑镰和小脑幕硬膜下血肿较少见,易误诊为蛛网膜下腔出血、大脑镰钙化,CT和磁共振成像征象具特征性,有助于鉴别。     

改良大骨瓣开颅个体化外减压术治疗重型颅脑损伤伴急性硬膜下血肿

目的 分析改良大骨瓣开颅个体化减压术对重型颅脑损伤伴急性硬膜下血肿治疗效果和手术方法. 方法 回顾性分析2007年7月-2010年6月采用改良大骨瓣开颅个体化减压术治疗重型颅脑损伤伴急性硬膜下血肿患者81例(治疗组)与2004年7月-2007年6月采用标准外伤大骨瓣减压治疗同样的患者65例(对照组)的治疗效果. 结果 伤后6个月GOS评估法判定其疗效:治疗组良好(5分)21例,中残(4分)19例,重残(3分)24例,植物生存(2分)5例,死亡(1分)12例(P＜0.01),预后较好(良好/中残)占49%(P＜0.05),预后较差或差(重残/植物生存/死亡)占51%;对照组良好(5分)12例,中残(4分)9例,重残(3分)22例,植物生存(2分)3例,死亡(1分)19例,预后较好占32%,预后较差占68%.治疗组并发术后颅内血肿、硬膜下积液明显少于对照组(P＜0.05).结论 改良大骨瓣开颅个体化减压术治疗重型颅脑损伤伴急性硬膜下血肿有较好疗效,能有效降低大骨瓣减压术后并发症的发生.     

重型颅脑损伤预后分析

重型颅脑损伤是神经外科的常见病 ,至今病死率仍较高。笔者对我院1987～ 1997年收治的 36 0例重型颅脑损伤的预后分析报告如下。临　床　资　料一般资料 :男 30 5例 ,女 5 5例 ;年龄8个月～ 78岁 ,平均 32 .8岁。致伤原因 :交通伤 2 5 5例 (70 .8% ) ,打击伤 42例(11.7% ) ,摔伤 37例 (10 .3 % ) ,坠落伤2 0例 (5 .6 % ) ,砍伤 6例 (1.7% )。损伤类型 :本组 36 0例中 ,闭合伤 32 0例 ,开放伤 40例 ,单纯硬膜外血肿 5 1例 ,硬膜外血肿伴硬膜下血肿及脑挫裂伤 30例 ,单纯硬膜下血肿 37例 ,硬膜下血肿伴脑挫裂伤 43例 ,急性硬膜下积液 8例 ,原…     

外侧裂区急性硬膜下血肿的临床分析

目的 探讨外侧裂区急性硬膜下血肿的治疗方法。方法 对46例患者进行回顾性分析,全部病例入院后即行头颅CT检查,其中44例行手术治疗。结果 本组外侧裂区急性硬膜下血肿主要是因脑挫裂伤,皮层血管破裂出血所致,手术是其主要治疗手段。本组死亡15例,重残3例,轻残8例。结论 外侧裂区急性硬膜下血肿死亡率较高,应尽快明确诊断,及时手术,手术宜采取大骨瓣开颅。术后可给予活血药物以改善脑缺血缺氧。     

经皮穿刺结合开颅手术救治创伤性特急性颅内血肿

目的 总结经皮穿刺结合开颅手术救治创伤性特急性颅内血肿的经验.方法 采用经皮穿刺结合开颅减压手术对12例创伤性特急性颅内血肿的患者进行救治,其中硬膜下血肿7例,硬膜外血肿3例,硬膜外合并硬膜下血肿2例;术前双侧瞳孔散大6例,单侧瞳孔散大6例,呼吸改变8例.入院GCS 3分4例,4分6例,7分2例.结果 穿刺后9例患者瞳孔有不同程度回缩,7例患者自主呼吸转平稳.手术后24 h内死亡2例,24 h后死亡4例,生存6例.随访6个月～2年.GOS评分良好4例,植物生存2例,死亡6例.结论 经皮穿刺结合开颅手术是救治特急性颅内血肿的一种行之有效的方法.     

小儿颅脑外伤280例CT诊断分析

目的：分析小儿颅脑外伤的临床及CT表现特点。方法：本组男206例，女74例，年龄8个月～14岁，平均6岁。280例均有完整的CT资料，其中35例检查2次，12例检查3次，4例行MRI检查。结果：颅骨骨折52例，占18．6％；硬膜外血肿50例，占18．0％；硬膜下血肿58例，占20．7％；蛛网膜下腔出血19例，占6．8％；脑室出血4例，占1．5％；脑内血肿45例，占16．0％；脑挫裂伤50例，占18．0％；弥漫性轴索损伤6例，占2．1％；脑疝2例，占0．7％；创伤性脑梗塞7例，占2．5％。85．0％的病例有2种以上CT表现。结论：(1)小儿颅脑外伤与成人相比有其相对特殊的临床特点；(2)CT检查快速、准确，是小儿颅脑外伤首选影像检查方法。     

自发性硬膜下血肿的临床及CT分析

目的:分析自发性硬膜下血肿的临床和CT表现特点,提高本病的认识。方法:回顾分析16例自发性硬膜下血肿的CT和临床资料。结果:CT表现:血肿多位于大脑突面,多累及2~3个部位。急性期4例,亚急性期6例,慢性期6例,均表现为颅内板下弧形,“3”字形,新月状不同密度影,最大血肿厚度大于10mm有8例,不同程度的脑中线移位。临床表现:除1例快速进入昏迷外,其余早期表现为头痛、头晕,恶心、呕吐,易疲劳,智力衰退、模糊,继而出现偏瘫,意识障碍,昏迷等,11例经内科保守治疗和4例外科手术治疗患者症状明显好转和痊愈。结论:自发性硬膜下血肿多见于老年人,CT表现以亚急性期和慢性期多见,且出血量大而范围广,脑中线移位明显。临床起病隐袭,早期临床表现无特异性,症状加重时往往出血量大,早期易延误诊断,及时治疗临床效果好。     

天幕切开早期辅助高压氧治疗创伤性脑疝疗效观察

目的探讨高压氧对提高创伤性脑疝天幕切开患者病残率和病死率的影响。方法将74例创伤性脑疝分为两组,治疗组46例,对照组8例。治疗组除在开颅血肿清除骨窗减压及天幕切开术的基础上早期行高压氧治疗外,其他治疗方法相同。结果天幕切开高压氧治疗组GCS评分3~5分18例,6~8分28例,恢复良好19例(41·3%),中残11例(23·9%),重残6例(13·0%),植物生存6例(13·0%),死亡4例(8·7%)。与对照组相比,差异均非常显著(P<0.01)。结论积极开展早期高压氧治疗能进一步降低开颅血肿清除骨窗减压及天幕裂孔切开术治疗创伤性脑疝的病残率和病死率。     

对冲性硬膜下血肿大骨瓣开颅减压预防急性脑膨出的效果

 目的 探讨对冲性硬膜下血肿行标准外伤大骨瓣开颅减压术预防急性脑膨出的效果。方法 回顾性分析2010-05至2015-05本院神经外科收治的86例对冲性颅脑外伤患者,按手术方式分为大骨瓣开颅减压组和常规组,每组各43例,常规组患者实施常规骨瓣开颅减压术,大骨瓣开颅减压组行标准外伤大骨瓣开颅减压术,比较两组治疗效果。结果 大骨瓣开颅减压组患者的术中脑膨出率39.53%、术后切口疝发生率11.63%均显著地低于常规组的67.44%、34.88%(P<0.05),大骨瓣开颅减压组患者术后脑中线恢复率72.09%显著地高于常规组的46.51%(P<0.05);两组患者迟发性血肿发生率、术中病死率差异无统计学意义。术后第1、3、7天大骨瓣开颅减压组患者的格拉斯哥昏迷评分(GCS)值显著地高于常规组患者(P<0.05)。根据格拉斯哥预后评分(GOS)评价标准,大骨瓣开颅减压组患者术后6个月的预后效果优于常规组(P<0.05)。结论 对冲性硬膜下血肿颅脑外伤患者行标准外伤大骨瓣开颅减压术对于防治术中急性脑膨出具有显著地效果,同时有利于改善患者的近期预后。     

手术治疗慢性硬脑膜下血肿318例

目的　探讨慢性硬脑膜下血肿的手术治疗方法。　方法　回顾性分析 318例慢性硬脑膜下血肿 (CSDH)病人的临床特点、神经影像学资料、手术方法和结果。　结果　 318例病人首次手术均采用颅骨钻孔冲洗并闭式引流术 ,仅 37例血肿复发后需再次手术处理 ,其中 33例接受骨瓣开颅血肿及包膜清除术或内窥镜手术后痊愈 ,另 4例老年脑萎缩病人在再次手术前死于伴随疾病。　结论　颅骨钻孔冲洗并闭式引流术是治疗CSDH的首选方法 ,即使对术前发现血肿包膜增厚者亦适用。骨瓣开颅血肿及包膜清除术适用于血肿壁坚厚、脑萎缩致脑膨起困难者及分隔型血肿等情况。对分隔型血肿 ,内窥镜手术可替代常规开颅术。     

小儿急性颅内血肿(附105例分析)

1958～1985年我院收治小儿急性颅内血肿105例。男78例,女27例。年龄自5个月至5岁。头部外伤占93.3％,脑血管畸形及肿瘤卒中占3.8％。硬膜外或硬膜下血肿85例(80.9％),余20例(19.1％)系多发或脑内血肿。多有颅压增高与脑受压征象,癫痫的发生率占25.7％。103例采取钻孔或骨瓣开颅清除血肿,2例经前囟穿刺抽出积血。手术结果,痊愈90例(85.7％),死亡11例(10.5％)。作者认为,对本病应早期诊治,并预防手术中发生休克与衰竭。     

Acute subdural hematomas: atypical CT findings

Seventy-one patients with acute subdural hematomas were examined by CT within 72 hr of a documented head injury. Lesions often did not have the classical appearance of a homogeneous, high-density extracerebral collection of blood in a crescentic configuration. Specifically, 28 patients (39%) had mixed-density subdural hematomas (MDSDH) with various degrees of low-density blood within the subdural space. In 10 of these 28 patients, the hematoma had a relatively localized mass effect with a convex inner margin, occasionally mimicking the appearance of an epidural hematoma. The MDSDH group differed from the typical homogeneous high-density subdural hematomas in that they were larger (average maximal thickness was 18.1 mm versus 8.0 mm), had more midline shift, and had a higher mortality rate (50% versus 26%). Four patients with MDSDH demonstrated an unusual pattern of ventricular compression with trapping of cerebrospinal fluid in the body of the ipsilateral ventricle and compression of the body of the contralateral ventricle. This pattern has to our knowledge not been previously described. Possible causes of the low-density regions within the hematomas include unclotted blood in an early stage of hematoma development, serum extruded during the early phase of clot retraction, or cerebrospinal fluid within the subdural space due to an arachnoid tear.     

CT在颅内血肿微创治疗前后的应用价值(附32例报告)

目的探讨CT在颅内血肿微创治疗前后的临床应用价值. 资料与方法对32例颅内血肿患者于微创术前做CT定位和术后CT复查评价.32例中,外伤性硬膜外血肿12例,外伤性硬膜下血肿5例,高血压脑出血12例,其他原因致颅内血肿3例. 结果外伤性颅内血肿17例(硬膜外12例,硬膜下5例)微创治疗满意,无后遗症,尤其是硬膜外血肿效果更佳.高血压及其他原因所致颅内血肿15例中,微创治疗成功12例,死亡2例,1例因术后有活动性出血且出血量大而行手术开颅清除血肿.成功的12例中5例有后遗症. 结论术前CT定位和选择最佳适应证是微创治疗成功的术后CT复查是评价微创治疗效果的有效方法.     

MR characteristics of subdural hematomas and hygromas at 1.5 T

MR images of 24 patients with 33 subdural collections were retrospectively reviewed to determine the spectrum of MR findings associated with such lesions. The lesions were dated by history, when available. Hematomas were grouped as follows: acute, four; early subacute, four; late subacute, four; chronic, 13. Six collections were classified as rehemorrhage; and two patients had CSF hygromas. Subdural hematomas evolved in a pattern similar to intracerebral hemorrhage with the exception of chronic subdural hematomas, in which isointensity of hypointensity relative to gray matter was observed on short TR/TE images compared with the persistent very high signal intensity noted in chronic parenchymal hematomas. Hemosiderin was rarely seen in chronic hematomas. These findings are most likely the result of the absence of a blood-brain barrier, which allowed clearance and dilution of blood products. Subdural hematomas with repeat hemorrhage demonstrated multiple phases of bleeding with layering phenomenon and more frequent hemosiderin deposition. It is possible that the clearance of blood products, as observed in chronic subdural hematomas, is impaired or poorly functional when rehemorrhage occurs. The persistence of high signal from methemoglobin in a hematoma that is expected to be in the chronic phase also suggests repeated hemorrhage. Acute CSF subdural hygromas had signal intensities identical to CSF without MR evidence of blood products. At surgery, clear fluid under pressure was found. MR imaging, with its unique ability to delineate the various phases of hemorrhage, is well suited to the evaluation of subdural hemorrhage.     

Subdural hematomas in infants with benign enlargement of the subarachnoid spaces are not pathognomonic for child abuse

BACKGROUND AND PURPOSE: Patients who have benign enlargement of the subarachnoid spaces (BESS) have long been suspected of having an increased propensity for subdural hematomas either spontaneously or as a result of accidental injury. Subdural hematomas in infants are often equated with nonaccidental trauma (NAT). A better understanding of the clinical and imaging characteristics of subdural hematomas that occur either spontaneously or as a result of accidental trauma may help distinguish this group of patients from those who suffer subdural hematomas as a result of NAT. The purpose of this study is to describe the clinical and imaging characteristics of subdural hematomas that occur either spontaneously or as a result of accidental injury in infants with BESS. METHODS: We conducted a retrospective review of all patients with BESS complicated by subdural hematomas evaluated at a single institution from 1998 to 2004. Data concerning the patient's clinical presentation, physical findings, imaging, and management are described. RESULTS: During the study period, 7 patients with BESS complicated by subdural hematoma were identified. Their mean age at identification of the subdural hematoma was 7.4 months of age. In 5 cases, there was no recognized trauma before identification of the subdural hematoma. In 3 cases, baseline CT or MR imaging was available, showing prominent subarachnoid spaces without any evidence of subdural hemorrhage. CONCLUSION: Although suspicious for NAT, subdural hematomas can occur in children either spontaneously or as a result of accidental trauma. Caution must be exercised when investigating for NAT based on the sole presence of subdural hematomas, especially in children who are otherwise well and who have BESS.     

Investigating the possibility and probability of perinatal subdural hematoma progressing to chronic subdural hematoma,with and without complications,in neonates,and its potential relationship to the misdiagnosis of abusive head trauma

The high incidence of subdural hematoma (SDH) from birthing was first identified with MRI by Looney in 2007 and was then more accurately determined by Rooks in 2008. Rooks screened 101 “normal” deliveries and demonstrated that 46% of the babies in her series and by inference, approximately 46% of the 4 million born normally in the US have SDH that formed in the perinatal (birthing) period during labor. Both metabolic strain and physical forces exerted on the head damage the capillaries within the dura (the intradural capillary bed), which is the source of the blood in the SDH that results from labor and delivery or at times from labor alone. While child abuse pediatricians relying on Rooks, maintain that no permanent complications result, her study was limited to 101 subjects and the sole criteria for resolution was the resolution of the SDH as seen on follow-up MRI. In fact, Rooks did have one patient (1%) who had complications that lead to symptoms and findings often associated with abuse. The purpose of this article is to explore if there is a complication rate for perinatal (PSDH) that supports that 1% of complications that are definable by different criteria. Next, if there are complications, how many of the roughly 2,000,000 cases of perinatal acute subdural hematoma every year in the United States will suffer them? Then, what are the clinical manifestations of the complications if they occur? Lastly, do the complications cause or mimic some or all of the findings that are offered by board certified child abuse pediatricians as evidence of child abuse? The article argues that a small percentage, but significant number of neonates, suffer birth related complications and findings secondary to the development of chronic subdural hematoma CSDH) that are often misdiagnosed as abusive head trauma.