Primary malignant mesothelioma of the pericardium.

Primary malignant mesothelioma of the pericardium.
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原发性心包恶性间皮瘤。

DOI:
10.1016/0002-8703(92)90950-z
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发表时间:
1992
影响因子:
4.8
通讯作者:
L. Tiszlavicz
L. Tiszlavicz
中科院分区:
医学2区
文献类型:
--
作者:
T. Fazekas;I. Ungi;L. Tiszlavicz

文献摘要

被引文献

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男,41岁,因突发性左偏瘫及昏睡而入院。尽管严重脱水,他的病情在几小时内恶化;出现偏瘫和昏迷。心律不规则,二尖瓣区有不典型收缩期杂音。双侧颈动脉均可见搏动,颈动脉上方未见杂音。实验室检查正常,除了中度贫血(血细胞比容,37 ";血红蛋白,11.8%;红细胞沉降,123毫米/小时)。脑脊液蛋白含量正常;红细胞含量为700万/L。心电图(ECG)显示二度房室传导阻滞伴文克巴赫传导(图1)或完全性房室传导阻滞发作。由于深度无意识伴枕骨僵硬和斜视,紧急诊断程序集中在中枢神经系统(CNS)。彩色多普勒超声显示右侧颈内动脉完全闭塞,就在分叉上方。颅脑计算机断层扫描(CT)显示右半球广泛的脑梗死。神经外科人员不建议干预。病人的病情迅速恶化;他出现了脑干症状死于心肺骤停病程提示颈动脉闭塞是由血栓栓塞引起的;不考虑恶性肿瘤。尸检发现心脏周围有450毫升轻度出血性液体(重380克),其下在增厚的心包上可见透镜状肿瘤灶。肿瘤组织侵入心肌,冠状动脉嵌埋于其中。肿瘤浸润左、右心房、房室交界区、纤维环、室间隔、右心室,突破心内膜,即跨壁生长,突入心腔(图2)。心房增大,左侧心房腔内肿物被纤维蛋白覆盖。右脑半球肿胀,切面呈新鲜的部分出血性白色软化。右颈内动脉颅内部分充满肿瘤栓塞(图3,A)。大面积脑水肿是导致死亡的原因
A 41-year-old man was admitted because of sudden left hemiparesis and a soporific state. In spite of massive dehydration, his condition worsened within hours; hemiplegia and coma developed. The heart rhythm was irregular with an atypical systolic murmur in the mitral area. Pulsation of the carotid arteries was palpable on both sides and no murmur could be heard above them. Laboratory tests were normal, apart from moderate anemia (hematocrit, 37”;: hemogloblin, 11.8%; and erythrocyte sedimentation rate, 123 mm/hr). The protein content of the cerebrospinal fluid was normal; erythrocytes were found in it (7 million/L). The electrocardiogram(ECG) revealed a second-degree atrioventricular(AV) block with Wenckebach conduction (Fig. 1) or episodes of complete AV block. Since the profound unconsciousness was accompanied by occipital stiffness and anisocoria, the urgent diagnostic procedures were focused on the central nervous system (CNS). Colorcoded Doppler ultrasonography demonstrated a complete occlusion of the right internal carotid artery immediately above the bifurcation. Cranial computed tomography (CT) scanning disclosed an extensive cerebral infarct in the right hemisphere. Neurosurgery personnel did not recommend intervention. The patient’s condition rapidly deteriorated; brainstem symptoms appeared and he died of cardiorespiratory arrest. The course of the disease suggested that the carotid occlusion was caused by thromboembolism; malignancy was not considered.Autopsy revealed 450 ml of slightly hemorrhagic fluid around the heart (which weighed 380 gm), under which lentiform tumorous foci were seen on the thickened pericardium. The myocardium was invaded by tumor tissue, and the coronary vessels were embedded in this. The neoplasm infiltrating both left and right atrium, the AV junctional region, the anulus fibrosus, the interventricular septum, and the right ventricle broke through the endocardium,-ie, grew transmurally and protruded into the cavities of the heart (Fig. 2). The atria were enlarged, and the left atria1 intracavitary tumor mass was covered by fibrin. There was a right cerebral hemisphere swelling and its cut surface exhibited a picture of fresh, partly hemorrhagic white softening. The intracranial part of the right internal carotid artery was filled with tumor embolism (Fig. 3, A). The extensive cerebral edema was responsible for death.