婴儿晚发型维生素K缺乏症颅脑CT表现

目的 探讨婴儿晚发型维生素K缺乏症颅脑CT表现特征，提高定性诊断水平。方法 本文回顾性分析35例维生素K缺乏症颅脑CT表现，并对临床表现和CT所见进行整理分析。结果 (1)以硬膜下血肿和蛛网膜下腔出血较多，而脑实质和脑室出血较少，多部位出血占68．6％，硬膜下血肿多累及枕部，内缘不光滑；(2)一例或两侧大脑半球明显水肿(71．4％)而基底节正常；(3)多部位出血，明显脑水肿和伴有脑疝者预后不良。结论 作者认为累及枕部的硬膜下血肿和蛛网膜下腔出血伴大脑半球广泛水肿，而基底节正常的CT表现是本病颅内出血特征性表现，有一定的定性诊断价值。     

急性硬脑膜下弥散性血肿治疗体会

目的探讨外伤性急性硬膜下弥散性血肿的形成机制和治疗方法。方法回顾性分析了22例颅脑损伤后发生硬膜下弥散性血肿患者的受伤部位、临床表现、头颅CT表现、治疗措施的选择和治疗效果。结果急性硬脑膜下弥散性血肿患者均为减速性损伤所致，术中见到蛛网膜破裂并有脑脊液外漏及蛛网膜下腔出血，血肿呈糊状，弥散均匀分布于一侧大脑半球硬脑膜下、蛛网膜外，选择骨瓣开颅清除血肿并硬膜下引流及保守治疗后，15例患者恢复良好，4例轻残，1例中度残疾，2例死亡。结论外伤性硬膜下弥散性血肿的形成是以脑挫伤为基础，同时蛛网膜破裂，脑脊液外溢至硬膜下腔，与出血混合形成不凝血．在颅内高压的作用下弥散分布于硬膜下腔；硬膜下腔的出血渗入蛛网膜下腔，形成局限性蛛网膜下腔出血。选择骨瓣开颅清除血肿并硬膜下引流，结合脑挫伤程度，行去骨瓣减压，疗效满意。     

急性颅脑创伤后进展性颅内出血的CT表现

目的：探讨急性颅脑创伤后进展性颅内出血（PIH）发生的CT表现与临床价值。方法回顾性分析我院2009-02-2013-09收治的626例急性颅脑创伤患者的临床资料,分析PIH患者与非 PIH患者的CT 表现差异以及PIH发生的危险因素。结果单因素回归分析发现,PIH组与非 PIH组首次CT 表现中颅骨骨折、蛛网膜下腔出血、脑挫裂伤、硬膜外血肿、硬膜下血肿差异有统计学意义（P＜0·05）。多因素回归分析发现,颅骨骨折、蛛网膜下腔出血、脑挫裂伤、硬膜外血肿是影响急性颅脑创伤后进展性颅内出血的独立危险因素（P＜0·05）,蛛网膜下腔出血是最强因素。结论急性颅脑创伤后应尽快进行头颅CT检查,以便尽快确诊PIH及时进行治疗。     

误诊为慢性硬膜下血肿的后交通动脉瘤1例

颅内动脉瘤破裂多表现为蛛网膜下腔出血,头颅CT表现为脑底诸池和脑沟内高密度阴影,有的沿着大脑镰和小脑幕扩展,前交通动脉瘤可表现为额叶内血肿,大脑中动脉瘤可表现为颞叶内血肿,颈内动脉瘤破裂后血液多聚集于同侧脑底池、外侧裂,并可破入基底节、额叶或颞叶内血肿,但动脉瘤破裂在头颅CT上单纯表现为一侧硬膜下血肿的非常罕见,容易引起误诊,现报道如下。     

外伤性大脑纵裂出血的诊断体会

<正> 临床资料 本组24例,男20例,女4例;年龄16～68岁,平均46.8岁。致伤原因:交通事故16例,高处坠落伤4例;打击伤4例。额部着力3例,颞部着力11例,顶部着力8例,枕部着力2例。受伤至入院均在36小时之内。所有病人头部CT显示均可见大脑纵裂池高密度影。诊断为轻性闭合性颅脑损伤15例,中型闭合性颅脑损伤9例。其中大脑纵裂蛛网膜下腔出血12例,大脑纵裂硬膜下血肿5例,大脑纵裂蛛网膜下腔出血合并大脑纵裂硬膜下血肿2例,大脑镰钙化3例,大脑镰动静脉畸形2例。均经降颅压、止血、营养脑神经及对症治疗后治愈出院。     

颅脑损伤首次CT检查阴性的原因分析

目的分析颅脑损伤首次CT检查而复查CT、MRI阳性的表现及原因。方法对我科收治的78例颅脑损伤首次CT检查阴性，但复查CT、MRI发现迟发性颅内病变病人的临床资料进行回顾性分析。结果首次CT检查阴性但复查CT、MRI的阳性表现为迟发性血肿，脑干血肿，横窦沟硬膜外血肿，脑挫裂伤，蛛网膜下腔出血，硬膜下腔积液，弥漫性脑肿胀，弥漫性轴索损伤。首次CT检查阴性与检查时间，病变发展，受伤部位等因素有关。结论对首次头部CT检查阴性结果者,应仔细行神经系统的常规检查，密切观察患者的病情，及时复查CT、MRI以指导治疗，改善预后。     

急性颅脑损伤后颅内进展性出血的早期CT征象及复查时机

目的探讨急性颅脑损伤后颅内进展性出血(PH)患者的早期CT征象及CT复查时机。方法回顾性分析2006年6月至2009年1月收治的630例颅脑损伤患者的临床资料,比较患者连续头颅CT扫描的表现,确定是否发生PH。分析PH与非PH患者在受伤到首次CT检查时间及伤后早期CT征象等方面的差异,并采用Logistic回归分析PH发生的影响因素。结果本组189例(30.0%)发生PH,其中有155例在伤后2h内行CT扫描(82.0%)。受伤到首次CT扫描时间越短以及伤后首次CT表现为颅骨骨折、蛛网膜下腔出血、挫裂伤、脑肿胀、中线移位、硬膜外血肿、硬膜下血肿、颅内多发血肿患者越容易发现PH(P<0.01)。Logistic回归分析显示,PH组与非PH组在伤后早期CT表现为颅骨骨折、蛛网膜下腔出血、脑挫裂伤以及初发血肿类型为硬膜外血肿是预测PH发生的最佳因素(P<0.01)。结论对于颅脑损伤后早期(2h内)即行首次头颅CT检查的患者,如果CT表现为颅骨骨折、蛛网膜下腔出血、脑挫裂伤、硬膜外血肿者,应进行更早的连续CT扫描以期能早期发现PH,进行早期治疗。     

颅脑外伤后发生嗅觉障碍的相关危险因素分析

目的探讨颅脑外伤后发生嗅觉障碍的相关危险因素分析。方法本研究纳入了2014年1月至2016年12月长征医院神经外科收治的以颅脑外伤为主要诊断的患者共80例,分为嗅觉损伤组和嗅觉正常组。通过分析患者基本信息、受伤原因、入院格拉斯哥昏迷评分(GCS)、受力部位,是否存在脑挫裂伤、血肿、水肿,蛛网膜下腔出血等情况,是否存在颅底骨折、鼻骨等面颅骨折,评估颅脑外伤后发生嗅觉障碍的危险因素。结果颅脑外伤后嗅觉障碍共17例,约占颅脑外伤患者的21%,单因素分析显示患者嗅觉障碍与颅底骨折,额叶的挫伤、血肿或水肿存在明显相关性,而与手术、受力部位、蛛网膜下腔出血、颞枕顶部脑挫裂伤、血肿或水肿无相关性。结论额叶的挫裂伤、血肿和水肿以及颅底骨折是外伤后嗅觉障碍的相关危险因素,患者入院GCS评分等因素与嗅觉障碍的发生未显示出明显相关性。     

颅脑损伤去骨瓣减压术后硬膜下积液的危险因素分析

目的探讨影响颅脑损伤去骨瓣减压术后硬膜下积液发生的独立危险因素。方法回顾性分析2012年2月至2014年2月149例颅脑损伤去骨瓣减压术患者的临床资料,其中术后发生硬膜下积液47例（积液组）,未发生硬膜下积液102例（非积液组）。对其危险因素进行单因素分析和多因素Logistic回顾分析。结果两组患者入院时GCS评分、手术时机、血肿位置、血肿量、基底池受压、中线结构位移≥10 mm、蛛网膜下腔出血及脑积水发生率差异有统计学意义（P〈0.05）;多因素Logistic回归分析结果显示,入院时GCS评分≤5分、血肿量〉40 ml、中线结构位移≥10 mm、蛛网膜下腔出血、脑积水、基底池受压是颅脑损伤去骨瓣减压术后硬膜外积液的独立危险因素。结论损伤严重、血肿量大、CT表现为基底池受压和中线结构位移≥10 mm、并发蛛网膜下腔出血及脑积水的颅脑损伤患者在去骨瓣减压术后发生硬膜下积液的风险较高,应给予重视。     

CT定位微创颅内血肿清除术治疗颅内血肿120例临床分析

目的探讨CT定位微创血肿清除术治疗颅内血肿的临床效果。方法对16例硬膜外血肿、24例慢性硬膜下血肿、80例各种脑内血肿行CT定位微创血肿清除术治疗,并进行随访研究。结果患者均按日常生活能力分级(ADL)评定预后。所有硬膜外及硬膜下血肿效果良好,血肿清除率为90%～100%,随访结果均为ADLⅠ级。动脉瘤致自发性蛛网膜下腔出血破入脑室者、新生儿维生素K缺乏迟发性脑出血及高血压性脑叶出血共13例,效果亦较好,随访良好率100%。高血压基底节、丘脑出血及出血破入脑室者65例中ADLⅠ级10例,Ⅱ级17例,Ⅲ级11例,Ⅳ级9例,Ⅴ级3例,死亡15例。结论微创颅内血肿清除术创伤小、疗效确切,值得临床推广。     

婴儿期维生素K缺乏症颅内出血的CT分析

目的：为进一步提高对婴儿期维生素Ｋ缺乏症所致颅内出血ＣＴ征象的认识,方法：回顾性分析经临床证实有各种颅内出血的ＣＴ改变共９７例,结果：按颅内出血的部位及并发症分为单纯性,混合性,其ＣＴ改变主要以急性和亚急性出血为主,以蛛网膜下腔出血,硬膜下出血,混合性脑出血多见,常合并有大面积脑水肿。     

A case of intracranial hemorrhage in a young infant due to vitamin K deficiency: comparison of MRI and CT findings

We reported a case of intracranial hemorrhage due to vitamin K deficiency in a 43-day-old male infant whose MRI findings were compared with CT findings. The infant was vacuum delivered at the 40th gestational week and Apgar score was 9 at 5 min after birth. He weighed 2,750 g at birth and was breast-fed. His growth was normal after birth, but forty-one days after birth, the infant became febrile and vomited three times. Forty-two days after birth, right hemiconvulsions occurred and the infant vomited again. He was brought to our clinic forty-three days after birth, because cranial CT showed multiple intracranial hemorrhages. On admission, skin color was pale, and the patient was somnolent. The anterior fontanel was bulging and tense. Neurological examination revealed right hemiparesis. Since laboratory data indicated that intracranial hemorrhage resulted from vitamin K deficiency, administration of vitamin K and blood transfusion were carried out. MRI examination was made three days after admission, and demonstrated a posterior fossa subdural hematoma as well as a left frontal subdural hematoma associated with intracerebral hemorrhage. Five days after admission, left frontal subdural hematoma was removed by left frontal craniotomy, and twenty-six days after the operation he was discharged without any neurological deficits.(ABSTRACT TRUNCATED AT 250 WORDS)     

Incidence and causes of intracranial hemorrhage in infancy: a prospective surveillance study after vitamin K prophylaxis

In order to evaluate the effect of vitamin K prophylaxis on the incidence of intracranial hemorrhage (ICH) in infants aged from 1 week to 12 months, a prospective surveillance study, from 1974 to 1988, was performed on the well-defined population of Nagasaki Prefecture, Japan. The incidence of ICH in infancy markedly decreased, from 34.3/100,000 to 10.1/100,000 live births, with the oral administration of vitamin K2 at both birth and 1 week, or with additional supplementation at 1 month of age. The diminished incidence was attributed to the decreased occurrence of acute ICH due to late hemorrhagic disease (LHD), a late onset form of vitamin K deficiency, and chronic subdural hematoma. On comparing the possible etiological factors, and clinical and laboratory findings between these 2 groups, it became apparent that chronic subdural hematoma shared some etiological factors (such as breast-feeding, liver dysfunction and no supplementation of vitamin K) with LHD. Furthermore, chronic subdural hematoma developed in some patients who had previously had acute ICH due to LHD. These findings suggest that coagulopathy due to vitamin K deficiency, including LHD, is causally related in the majority of, if not all, cases of chronic subdural hematoma without any history of trauma or central nervous system infections.     

Abusive Head Trauma in Infants and Children in Japan

Subdural hematoma in infants can be caused by abuse, and is thought to be more likely if subdural hematoma is associated with retinal hemorrhage and cerebral edema. In Japan, few doctors disagree that cases of subdural hematoma with retinal hemorrhage and cerebral edema with multiple findings on the body are more likely to have been caused by abuse rather than by household accident. On the other hand, in cases where there are no other significant physical findings, only subdural hematoma and retinal hemorrhage, there is a difference of opinion as to whether the injury was caused by an accident or abuse. The reason for this is that neurosurgeons in Japan promoted the concept that infants can develop subdural hematomas and retinal hemorrages due to minor trauma at home before the concept of abusive head trauma became known. In addition, the age distribution of subdural hematomas in Japan differs from that in other countries, with peaks at around 8 months, and the reason for this remains unclear. Therefore, the etiology of infant subdural hematoma in Japan needs to be investigated in greater detail.     

Intracranial hemorrhage in infancy due to vitamin K deficiency: report of a case with multiple intracerebral hematomas with ring-like high density figures

It is well known that vitamin K deficiency is an important cause of the spontaneous intracranial hemorrhage in infancy. A 60-day-old male infant with spontaneous intracerebral hematomas due to vitamin K deficiency was presented. He was breast-fed. He had been medicated oral antibiotic agent for diarrhea and fever. Three days later he developed petechien, vomiting and twitching, and became drowsy. The blood studies showed anemia, and advance of ESR. He was administered of vitamin K immediately. CT scan was showed four intracerebral hematomas with niveau, which were surrounded by high-density rings. The ring-like figures were unique for this case. The reason may be next, we think. Under the states in which blood can separate easily with advance of ESR, blood clot would adhere to the wall of the hematomas. So these hematomas showed ring-like figures and had niveau in them. CT scan of this case was also interesting because there was little deviation in spite of the big hematomas. The reason of this may be that the brain of infancy is incomplete in myelination and contains much water, and that the possibility of bleeding due to vitamin K occurs slowly. We examined 84 cases of intracranial hemorrhage due to vitamin K deficiency from literatures, and they were all identified for the hemorrhage sites by CT scan. Subarachnoidal hemorrhage was in 72 cases (85.7%), subdural hemorrhage was in 41 cases (48.8%), intracerebral hematomas was in 36 cases (42.9%) and intraventricular hemorrhage was in 9 cases (10.7%). In 52 cases the CT findings were described.(ABSTRACT TRUNCATED AT 250 WORDS)     

Intracranial hemorrhage in an infant due to vitamin K deficiency --successful management of spontaneous intracerebral and subjural hematoma]

A one-month-old male infant with spontaneous intracerebral and subdural hematomas due to vitamin K deficiency was described. He was breastfed. Loose stools continued and began to contain blood. He had fever, vomiting and convulsion, and became drowsy. The blood studies showed anemia and hypoprothrombinemia. Left carotid angiograms revealed intracerebral and subdural hematomas. He was treated successfully by immediate operation and administration of vitamin K. 2) Vitamin K deficient hemorrhage beyond the immediate newborn period was discussed with reference in the literature. Three etiologic factors included, decreased vitamin K intake, decreased intestinal absorption of vitamin K and decreased production of vitamin K by colon bacteria. The most important factor of the three seemed to be low vitamin K intake. Intracranial hemorrhage was recognized in about one third of the cases in the literature. It was emphasized that vitamin K deficiency occurring beyond the immediate newborn period was very important as a cause of intracranial hemorrhage in infancy.     

慢性硬膜下血肿合并急性脑梗塞

目的 探讨慢性硬膜下血肿合并急性脑梗塞的病因、预防与诊断治疗。方法 总结慢性硬膜下血肿合并急性脑梗塞22例，结合献分析。结果 慢性硬膜下血肿合并同侧大面积脑梗塞3例，基底节区梗塞11例，其他脑梗塞8例，其中慢性硬膜下血肿术后脑梗塞12例。结论 血容量不足、凝血机制障碍、脑灌注压降低、血管痉挛、脑动脉硬化与心脏疾病是慢性硬膜下血肿合并急性脑梗塞的原因。血肿钻孔引流、纠正血容量、扩容、解痉、脱水、降颅压、神经保护和抗血小板聚集是其有效治疗手段。     

急性幕上性脑出血患者脑水肿体积与高迁移率族蛋白B1的关系

目的 探讨脑出血后高迁移率族蛋白B1(high mobility group protein B1,HMGB1)水平的变化及其与脑出血后继发性脑水肿的关系。方法 收集152例幕上性脑出血患者的入院各基线资料及发病24 h时的HMGB1水平和发病后3或4 d复查头颅CT显示的相对水肿体积。结果 初入院的HMGBl水平要显著高于对照组(P<0.05),且24 h患者HMGBl水平与第3或4 d CT复查显示的相对水肿体积呈正相关(r=0.87,P=0.001)。结论 脑出血后HMGBl水平显著升高,且与脑水肿体积进展程度呈正相关。     

深静脉穿刺管在治疗婴儿硬膜下血肿及积液中的临床应用

目的 探讨深静脉穿刺管在治疗婴儿硬膜下血肿及积液中的应用疗效.方法 使用深静脉穿剌管治疗婴幼儿硬膜下血肿及积液19例,其中急性硬膜下血肿9例,慢性硬膜下血肿6例,硬膜下积液4例,经前囟穿剌置入深静脉穿剌管于硬膜下持续引流治疗硬膜下血肿及积液,持续引流3～7 d,观察疗效.结果 均穿刺置管成功,术后1～7 d复查头颅CT,硬膜下血及硬膜下积液均基本清除,全部病例均存活.结论 深静脉穿剌管治疗婴儿硬膜下血肿及积液中是安全有效的方法.     

迟发性维生素K缺乏并颅内出血临床分析

目的 探讨维生素K缺乏症并颅内出血误诊原因、诊断、手术治疗及其预后。方法 回顾性分析我院自1994年1月至2002年收治的维生素K缺乏症并颅内出血患儿48例。结果 本组48例，临床治愈27例，好转10例，放弃治疗3例，死亡8例；其中18例手术中，15例治愈，2例好转，1例死亡。结论 迟发性维生素K缺乏并颅内出血，见于新生儿和婴儿，发病突然，部分病例有前驱感染和使用抗生素的病史，易于误诊。CT检查、PT检验和维生素K治疗可有效确诊。对有手术指征，手术治疗可以提高治愈率，降低死亡率，改善生存质量。