慢性硬膜下血肿钙化伴脑积水1例

2018-11-15 孙峰 宁同波 崔皓 大连医科大学学报

患者,男,49岁,因“左眼视力下降伴头痛1月余”于2015年10月2日来威海市中心医院眼科就诊,行鞍区MRI检查示:右侧颞顶部颅板下梭形异常信号,硬膜外血肿?幕上脑室积水、扩张。遂以“右侧颞顶部硬膜外血肿、脑积水”收入威海市中心医院神经外科。

1.临床资料
 
患者,男,49岁,因“左眼视力下降伴头痛1月余”于2015年10月2日来威海市中心医院眼科就诊,行鞍区MRI检查示:右侧颞顶部颅板下梭形异常信号,硬膜外血肿?幕上脑室积水、扩张。遂以“右侧颞顶部硬膜外血肿、脑积水”收入威海市中心医院神经外科。
 
追问病史,自诉20余年前头部外伤,当时无特别不适,未处置。无高血压糖尿病、肝炎结核病史。查体:除双眼视力下降外未见阳性体征。完善检查:头CT示:右侧颞顶部颅板下梭形密度影,符合硬膜外血肿钙化,侧脑室积水扩张(图1)。

图1 右颞顶混杂密度影。侧脑室扩大
 
全麻下行“开颅血肿清除术”,术中见颅骨内板反应性增生,硬膜下一骨化性肿物与硬脑膜粘连紧密,十字切开硬膜予以剥离,见肿物外壁似龟甲状,分块切除,见肿物内容物呈“绿豆沙”样(图2),分块挖出,内见混有钙化块。肿物内侧壁钙化与蛛网膜无粘连,分块切除。脑组织受压明显,萎缩较重,搏动尚可。术中病理示坏死组织。术中诊断硬膜下血肿钙化。术后病理回报陈旧性血肿伴钙化(图3)。

图2 内容物呈烂泥样改变。A:术中切开肿物;B:取出的肿物内容物
 
图3术后病理——陈旧血肿伴钙化。A:坏死出血组织(×100);B:钙化组织(×100)
 
术后患者自觉双眼视力较前稍有改善,未再头痛,但出现癫痫大发作1次,给予苯巴比妥、地西泮对症治疗,后康复出院。随访2周、1个月、3个月、6个月、1年无癫痫发作及其他头部不适。
 
2.讨论
 
慢性硬膜下血肿(chronic subdural hematoma,CSDH)是神经外科常见疾病,好发于小儿及老年人,占颅内血肿的10%,占硬膜下血肿的25%,但钙化型的CSDH少见,约占慢性硬膜下血肿的0.3%~2.7%。钙化型CSDH往往病史较长,症状出现较晚,呈进行性加重。此需要相应的代偿机制缓解颅内压不断增高,如老年人脑萎缩使颅腔容积相对增大,分析本例患者,双侧脑室扩张是其代偿因素。
 
该患者颅脑CT双侧脑室扩张,非脑积水及脑萎缩表现,且患者无颅高压症状,综合考虑为患者自然生理表现,大的脑室为血肿占位提供了缓冲空间。钙化型CSDH的CT可表现为颅骨内板下新月形、半月形或梭形低或等或高密度影,部分内有环形分隔或条状高密度影,中线结构不同移位,侧脑室受压变形,大部分内膜呈高密度影。本例首诊医师根据既往经验,认为典型硬膜外血肿表现为“凸透镜形”,硬膜下血肿表现为“新月形”,导致未能准确诊断。因此,临床工作中应注意病例的复杂性,对于形状不规则,密度不均匀的硬膜下血肿应结合患者的发病原因及CT增强扫描或磁共振检查以明确。钙化型CSDH首选骨瓣开颅血肿清除术,单纯钻孔引流术几乎无效,已机化的血肿粘连重,引流术术后易出现血肿残留、出血、癫痫、复发等,需清除分隔和切除血肿包膜。本例患者误诊选择开颅手术,未影响治疗效果。术后出现癫痫并发症,可能与血肿清除脑组织移位有关。
 
原始出处:

孙峰,宁同波,崔皓.慢性硬膜下血肿钙化伴脑积水1例[J].大连医科大学学报,2018,40(01):95-96.

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慢性硬膜下血肿(chronic subdural hematoma,CSDH)发病机制目前尚未明确,血肿常不断进展,很难自愈,需要临床干预;病程常在3个月内,超过1年者少见,有文献报道长达34年。本文报道1例病程超过50年稳定型盔甲样CSDH。

Heart:特发性慢性大面积心包积液的结局分析

由此可见,“特发性”慢性大面积心包积液的演变通常是良性的,大多数病例的积液量有所减少,约40%的病例积液消退。心脏压塞的风险为2.2%/年,并且在没有干预的情况下保守治疗患者的无复发/并发症存活期更好。

再生障碍性贫血并发慢性硬膜下血肿1例报告

患者,21岁,男性。因头部外伤史2月余,突发头痛伴恶心、呕吐3天入院。入院查体:体温36.5°C,脉搏70次/min,血压130/85mmHg,呼吸18次/min。神清语利,查体合作,双侧瞳孔直径20mm光反射灵敏,颈软,无抵抗,四肢肌力V级,双侧巴氏征(+)。余查体未见明显异常。既往史:再生障碍性贫血18年,平日输注悬浮红细胞(2U、1次/3~4周)治疗,再生障碍相关贫血性心脏病史2年余。

多次根除幽门螺杆菌失败,慢性胃炎反复发作

患者女,57岁,多次胃镜示:慢性糜烂性胃炎,幽门螺杆菌阳性,半年前呼气试验3000+。