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急性中耳炎的内耳及面神经并发症,重点关注细菌学和病毒学

Inner ear and facial nerve complications of acute otitis media with focus on bacteriology and virology.

作者信息

Hydén Dag, Akerlind Britt, Peebo Markus

机构信息

Department of Otolaryngology, Linköping University Hospital, Linköping, Sweden.

出版信息

Acta Otolaryngol. 2006 May;126(5):460-6. doi: 10.1080/00016480500401043.

Abstract

CONCLUSION

Among 20 patients with inner ear complications and/or peripheral facial palsy secondary to acute otitis media (AOM) a proven or probable bacteriological cause was found in 13 (65%). In seven patients (35%), a proven or probable viral cause was found. Only two of the patients (10%), with a proven bacterial AOM and a clinical picture of a purulent labyrinthitis in both, together with a facial palsy in one, had a substantial degree of dysfunction. Although the number of patients in this study is relatively low our findings show that inner ear complications and facial palsy due to AOM can be of both bacterial and viral origin. Severe sequelae were found only where a bacterial origin was proven.

OBJECTIVES

Inner ear complications and/or peripheral facial palsy secondary to AOM are rare. The general understanding is that they are due to bacterial infections. However, in some of these patients there are no clinical or laboratory signs of bacterial infections and they have negative bacterial cultures. During recent years different viruses have been isolated from the middle ear or serologically proven in AOM patients and are thought to play a pathogenetic role. We suggest that in some cases of AOM complications from the inner ear and the facial nerve can be caused by viruses. The purpose of our study was to analyze infectious agents present in patients with inner ear complications and/or facial palsy arising from AOM.

PATIENTS AND METHODS

The medical records of 20 patients who had inner ear complications and/or facial palsy following AOM ( unilateral in 18, bilateral in 2) between January 1989 and March 2003 were evaluated. Bacterial cultures were carried out for all patients. Sera from 12 of the patients were stored and tested for a battery of specific viral antibodies. In three patients, investigated between November 2002 and March 2003, viral cultures were also performed on samples from the middle ear and nasopharynx.

RESULTS

Nineteen patients had inner ear symptoms. Eight of them had a unilateral sensorineural hearing loss and vertigo, three had vertigo as an isolated symptom and one, with bilateral AOM, had bilateral sensorineural hearing loss. Seven patients had a combination of facial palsy and inner ear symptoms (unilateral sensorineural hearing loss in three, unilateral sensorineural hearing loss and vertigo in two, bilateral sensorineural hearing loss and vertigo in one, with bilateral AOM, and vertigo alone in one). One patient had an isolated facial palsy. Healing was complete in 11 of the 20 patients. In seven patients a minor defect remained at follow-up (a sensorineural hearing loss at higher frequencies in all). Only two patients had obvious defects (a pronounced hearing loss in combination with a moderate to severe facial palsy (House-Brackman grade 4) in one, distinct vestibular symptoms and a total caloric loss in combination with a high-frequency loss in the other. Eight patients had positive bacteriological cultures from middle ear contents: Streptococcus pneumoniae in two, beta-hemolytic Streptococcus group A in two, beta-hemolytic Streptococcus group A together with Staphylococcus aureus in one, Staph. aureus alone in one and coagulase-negative staphylococci (interpreted as pathogens) in two. In the 12 patients with negative cultures, there was a probable bacteriological cause due to the outcome in SR/CRP and leukocyte count in five. In four patients serological testing showed a concomitant viral infection that was interpreted to be the cause (varicella zoster virus in two, herpes simplex virus in one and adenovirus in one.) In three there was a probable viral cause despite negative viral antibody test due to normal outcome in SR/CRP, normal leukocyte count, serous fluid at myringotomy and a relatively short pre-complication antibiotic treatment period.

摘要

结论

在20例继发于急性中耳炎(AOM)的内耳并发症和/或周围性面瘫患者中,13例(65%)发现了已证实或可能的细菌学病因。7例(35%)患者发现了已证实或可能的病毒学病因。仅2例(10%)患者,经证实为细菌性AOM且二者均有化脓性迷路炎的临床表现,其中1例伴有面瘫,存在严重功能障碍。尽管本研究中的患者数量相对较少,但我们的研究结果表明,AOM所致的内耳并发症和面瘫可能源于细菌和病毒。仅在证实为细菌感染源的病例中发现了严重后遗症。

目的

继发于AOM的内耳并发症和/或周围性面瘫较为罕见。一般认为它们是由细菌感染引起的。然而,在其中一些患者中,没有细菌感染的临床或实验室迹象,且细菌培养结果为阴性。近年来,已从AOM患者的中耳中分离出不同病毒或通过血清学证实,并且认为这些病毒起到了致病作用。我们认为,在某些AOM引起内耳和面神经并发症的病例中,可能是由病毒引起的。我们研究的目的是分析AOM引起的内耳并发症和/或面瘫患者体内存在的感染因子。

患者和方法

对1989年1月至2003年3月期间20例AOM后出现内耳并发症和/或面瘫的患者(18例单侧,2例双侧)的病历进行评估。对所有患者进行细菌培养。保存了12例患者的血清,并检测了一系列特异性病毒抗体。在2002年11月至2003年3月期间调查的3例患者中,还对中耳和鼻咽部样本进行了病毒培养。

结果

19例患者有内耳症状。其中8例有单侧感音神经性听力损失和眩晕,3例以眩晕为唯一症状,1例双侧AOM患者有双侧感音神经性听力损失。7例患者同时有面瘫和内耳症状(3例单侧感音神经性听力损失,2例单侧感音神经性听力损失和眩晕,1例双侧感音神经性听力损失和眩晕且为双侧AOM,1例仅眩晕)。1例患者仅有面瘫。20例患者中有11例完全康复。7例患者在随访时有轻微缺陷(均为高频感音神经性听力损失)。仅2例患者有明显缺陷(1例为明显听力损失合并中度至重度面瘫(House-Brackman 4级),另1例为明显的前庭症状、冷热试验完全消失合并高频听力损失)。8例患者中耳内容物细菌培养呈阳性:2例为肺炎链球菌,2例为A组β溶血性链球菌,1例为A组β溶血性链球菌合并金黄色葡萄球菌,1例为单纯金黄色葡萄球菌,2例凝固酶阴性葡萄球菌(判定为病原菌)。在12例培养结果为阴性的患者中,5例根据血沉/CRP及白细胞计数结果推断可能存在细菌学病因。4例患者血清学检测显示存在合并的病毒感染,被判定为病因(2例为水痘带状疱疹病毒,1例为单纯疱疹病毒,1例为腺病毒)。3例患者尽管病毒抗体检测为阴性,但根据血沉/CRP结果正常、白细胞计数正常、鼓膜切开术时有浆液性积液以及并发症前抗生素治疗时间相对较短,推断可能存在病毒学病因。

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