18 Retraction Pockets and Atelectasis

Retraction pockets (RPs) and tympanic membrane (TM) atelectasis are common problems encountered by otolaryngologists. Left untreated, natural progression of this disease spans a predictable continuum of disease from the initial inciting factor to destructive disease with increasing morbidity.1 TM retraction is a dynamic process, often occurring in the setting of poor eustachian tube (ET) function, negative middle ear pressure, and chronic otitis media (COM), with subsequent weakening of focal regions of the collagenous lamina propria of the TM.² Sequellae include destruction of the middle ear space and ossicles resulting in hearing loss and acquired cholesteatoma formation.³

The importance of diagnosis, initial and follow-up medical and surgical management, and prevention of disease progression cannot be further stressed. Although patients present early on to the general internists and otolaryngologists, the more advanced and complicated ears typically are referred to an otologist. This chapter will review information regarding the etiology of TM RPs, identification and diagnosis, medical and surgical management, as well as potential prevention of disease progression.

Etiology and Pathogenesis

The etiology of middle ear pathology and more specifically, TM retraction stems from ET dysfunction and poor ventilation of the middle ear space.^4,5 ET dysfunction can be caused by mucosal edema resulting from esophageal reflux, allergy, and infection. Other etiologies include abnormalities in cartilage, ET musculature such as in those with cleft palate, nasopharyngeal masses including adenoid hypertrophy, and physiologic ET position in children versus adults.⁶ Temporal bone specimens have been studied to further understand the relationship between RPs and middle ear pathology. Yoon investigated 1408 temporal bones, both with otitis media with effusion (OME) and COM, comparing them to normal ears.¹ Ears with middle ear fluid, TM atrophy, and thickening of middle ear mucoperiosteum were more likely to have RPs, and those with RPs were more likely to have precholesteatoma or cholesteatoma matrix, supporting the theory that chronic disease progressively leads to TM histologic changes, to RPs, and ultimately to cholesteatoma formation. Ruah looked at 38 bones from children, including normal ears, ears with serous otitis media (SOM), and ears with purulent otitis media, and concluded that the latter two types of ears were more likely to contain pars flaccida and posterior-superior pars tensa retraction.⁷ These findings support the theory that degradation of the fibrous layer of the TM from middle ear inflammation results in TM retraction and its subsequent sequellae. Additionally, mesenchyme in the lamina propria, which is normally resorbed within the first few months of life, was found to persist for up to 3 years in the ears of children with inflammatory disease, weakening their TM further by not allowing the elastin to fully mature.

The TM is composed of highly organized fibrous framework consisting of both radially and circumferentially oriented lamina propria that is sandwiched between the cuboidal middle ear mucosal cells medially and squamous epithelia laterally. In the pars tensa, vimentin filaments are densely packed to provide tensile strength, and in the pars flaccida, the lamina propria consists of loose connective tissue of collagen and elastin, nerves, blood vessels, and lymphatic vessels. When an area becomes weakened, it becomes thin and inelastic due to loss of fibers, resulting in the overall appearance of TM atrophy. If focal areas become retracted, they are seen as such on physical examination. When diffuse, the entire TM can collapse or adhere onto the promontory. When there is consistent negative middle ear pressure, the entire TM increases in surface area and is thus pulled medially.^4,5 Poor middle ear ventilation exerts negative pressure on the TM, resulting in OME and mucosal disease. This further contributes to TM weakening and atrophy of the lamina propria. The pars flaccida and posterior-superior region of the pars tensa are morphologically weak points on the TM, thereby predisposed to retraction. The pars flaccida lacks fibrocartilaginous annulus, and accounts for 40% of RPs.⁴ The posterior-superior quadrant of the pars tensa is more delicate because of fewer circular fibers and reduced thickness of the fibrocartilaginous ring, accounting for 60% of RPs here.

Diagnosis and Physical Examination

TM retractions can present as incidental findings on physical examination, or may be found on examination of a symptomatic ear. The patient may complain of hearing loss, aural fullness, tinnitus, and otalgia. Some may have overt allergy symptoms including nasal congestion, and some may also have concurrent sinus disease.

RPs can be classified based on the topographic location on the TM and degree of the retraction. In 60% of cases, the RPs are located in the pars tensa; 36% of them in the posterior-superior quadrant, and 16% in the inferior quadrant.⁴ The posterior-superior portion is the most common due to embryologically poor elastin quality in the lamina propria.⁸ They are very frequently wide necked retractions that are self-cleaning, but can develop into a RP filled with cholesteatoma. The remaining 40% of retractions are found in the pars flaccida. The retraction can also be classified as simple, where the external aperture is larger than the internal aperture, or as a pocket, where the external aperture is narrower than the internal aperture.1

Various staging systems have been proposed to associate the appropriate treatment depending on the location or type of TM retraction (Table 18.1). The staging most ubiquitously used and quoted in the literature to describe retractions in the pars tensa was proposed by Sade, ranging from grade I through IV.⁹

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