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出血性扁桃体炎

Hemorrhagic tonsillitis.

作者信息

Levy S, Brodsky L, Stanievich J

机构信息

Department of Otolaryngology, State University of New York, Buffalo.

出版信息

Laryngoscope. 1989 Jan;99(1):15-8. doi: 10.1288/00005537-198901000-00004.

Abstract

Eleven patients with acute and/or chronic tonsillitis, who presented with a spontaneous tonsillar hemorrhage are reported and discussed. Two patterns of hemorrhage were noted: 1. diffuse, parenchymal bleeding and 2. localized bleeding from dilated surface vessels. Pharyngeal culture for group A beta-hemolytic Streptococcus was positive in six patients (55%). Monospot, heterophile antibodies, complete blood cell count, prothombin time, partial thromboplastin time, and viral studies did not consistently demonstrate any abnormality. Two patients, however, did have an elevation in liver enzymes. In five patients, the bleeding stopped spontaneously; in five patients the bleeding was controlled with local chemical cautery. In two patients, Avitene was used for hemostasis. One other patient's bleeding was controlled by electrocautery while the patient was under anesthesia for endoscopic evaluation of hemoptysis. Two patients required blood transfusions; one of these patients had a history of factor IX deficiency. Four case histories are discussed in detail to illustrate the varied clinical presentation and some pitfalls in diagnosing and managing this rarely reported complication of tonsillitis. Possible mechanisms for the pathophysiology include increased tonsillar blood flow, necrosis of tonsillar surface cells, and trauma to dilated surface vessels. No common bacterial or viral etiology could be determined in this rare, but potentially serious, complication of tonsillitis.

摘要

本文报告并讨论了11例患有急性和/或慢性扁桃体炎且出现自发性扁桃体出血的患者。观察到两种出血模式:1. 弥漫性实质出血;2. 扩张表面血管的局部出血。6例患者(55%)A组β溶血性链球菌咽培养呈阳性。嗜异性凝集试验、嗜异性抗体、全血细胞计数、凝血酶原时间、部分凝血活酶时间及病毒学检查均未持续显示任何异常。然而,有2例患者肝酶升高。5例患者出血自行停止;5例患者通过局部化学烧灼控制出血。2例患者使用明胶海绵止血。另有1例患者在接受咯血内镜评估的麻醉过程中,通过电灼控制出血。2例患者需要输血;其中1例患者有IX因子缺乏病史。详细讨论了4个病例史,以说明这种扁桃体炎罕见并发症的多样临床表现以及诊断和处理中的一些陷阱。病理生理学的可能机制包括扁桃体血流量增加、扁桃体表面细胞坏死以及扩张表面血管的创伤。在这种罕见但可能严重的扁桃体炎并发症中,无法确定常见的细菌或病毒病因。

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