Hörmann K
ENT-Department, University of Hamburg, West Germany.
Acta Otolaryngol Suppl. 1987;440:1-59.
The intention of this study was to gain insight into the pathogenesis, pathophysiology and course of middle ear effusions by means of an animal experiment. Simultaneously the clinical relevance of an electro-acoustical, non-invasive diagnostic procedure should be evaluated. Furthermore a method which permits prognostic statements had to be established using viscosimetry, in order to plan therapy for this most common childhood disease. The questions asked initially can be answered along the following lines: 1. The pathogenesis of middle ear effusions caused by a tubal dysfunction is submitted to a staged course. The Initial Stage is based on the condition of negative pressure. It presents with the onset of an inflammatory process including the forming of an inflammatory edema in the lamina propria with capillary proliferation, vascular dilatation and infiltrating round cells. An epithelial-mesenchymal interaction induces hyperplasia and differentiation of epithelial cells. An exudate of low viscosity develops inside the tympanum. In the course of the Secretory Stage, between the 30th and 80th day, an actively secreting respiratory epithelium is formed out of metaplasia. The viscosity of the mucus produced thereby increases by an exponential function between the 30th and 80th day, with statistic significance. The pathological process comes to a halt after the 80th day. The Steady State of chronic mucoid otitis media is found. The effusion's viscosity has increased extremely, due to active absorption of the middle ear mucosa. Toxic impairment of the secreting epithelium causes arrest of the mucociliary transport mechanism. A partial recovery with adhesive alterations results. 2. The alterations in the lamina mucosa found in the initial and secretory stage are reversible, once a regular tubal function is restored. 3. The osseous appositions, brought about by each relapse, are only partially reversible and lead to a reduction in pneumatized cavities. 4. Scheduled tympanometry; i.e. measuring impedance, is directly correlated with the acute pathophysiological condition and its course. Thus it permits statements concerning the progress and prognosis of the disorder. 5. The method of viscosimetry developed proved to be successful in determining the stage of the dynamic pathological process of middle ear effusion. 6. Presupposing the transferability of animal experimental findings to human conditions, a clinical conclusion can be drawn from our evaluations. An effusion resisting conservative therapy should be treated surgically by insertion of a ventilation tube after 3 months at the latest.
本研究旨在通过动物实验深入了解中耳积液的发病机制、病理生理学及病程。同时,应评估一种电声非侵入性诊断程序的临床相关性。此外,必须使用粘度测定法建立一种能够进行预后判断的方法,以便为这种最常见的儿童疾病制定治疗方案。最初提出的问题可按以下思路回答:1. 由咽鼓管功能障碍引起的中耳积液的发病机制呈阶段性过程。初始阶段基于负压状态。其表现为炎症过程的开始,包括固有层出现炎症性水肿,伴有毛细血管增生、血管扩张和圆形细胞浸润。上皮 - 间充质相互作用诱导上皮细胞增生和分化。鼓室内形成低粘度渗出液。在分泌阶段,即第30天至第80天期间,化生形成活跃分泌的呼吸上皮。在此期间,由此产生的黏液粘度呈指数函数增加,具有统计学意义。第80天后病理过程停止。出现慢性黏液性中耳炎的稳定状态。由于中耳黏膜的主动吸收,积液粘度极度增加。分泌上皮的毒性损伤导致黏液纤毛转运机制停滞。导致粘连改变的部分恢复。2. 一旦恢复正常的咽鼓管功能,在初始阶段和分泌阶段发现的黏膜层改变是可逆的。3. 每次复发引起的骨质增生仅部分可逆,并导致气化腔减少。4. 定期鼓室导抗测量;即测量阻抗,与急性病理生理状况及其病程直接相关。因此,它可以对疾病的进展和预后做出判断。5. 所开发的粘度测定法被证明在确定中耳积液动态病理过程的阶段方面是成功的。6. 假设动物实验结果可应用于人类情况,我们的评估可得出临床结论。对抗保守治疗的积液应最迟在3个月后通过插入通气管进行手术治疗。