CHAPTER 139 Chronic Otitis Media, Mastoiditis, and Petrositis
Otitis media is the most common disease of childhood after viral upper respiratory infections. The acute bacterial infection occurs in 80% of children 1 to 6 years old, and it is the disease most frequently managed with antibiotics in the United States. The infectious and noninfectious complications of otitis media in childhood may result in serious morbidity. Later in life, the infectious complications, including acute and chronic mastoiditis, petrositis, and intracranial infection, still occur despite the widespread use of antibiotics for this disease. The noninfectious sequelae, including chronic perforation of the tympanic membrane, ossicular erosion, labyrinthine erosion, and tympanosclerosis, are major causes of hearing loss throughout the world.
Some cases of acute otitis media (AOM) result in persistent otitis media with effusion (OME), which is recognized as the leading cause of childhood hearing loss. The exact cause of OME is unclear; however, more recent data suggest that reflux of gastric contents may be associated with OME in children.1–4 Although eustachian tube dysfunction alone may lead to effusion of the middle ear, there is mounting evidence that most cases of OME occur as a sequelae of AOM, or at least share the same etiologic factors. Specific causes can be identified in many cases of adult-onset otitis media, such as paranasal sinus disease, nasopharyngeal carcinomas and tumors, and postradiation sequelae.
In most children, AOM and OME subside spontaneously or after medical intervention. It is unknown how many children with OME eventually have complications. The sequelae of otitis media can be considered in two broad categories: (1) direct destructive effects of the localized process, and (2) the effects of auditory deprivation during early childhood. Otitis media may be complicated by acute or chronic perforation of the tympanic membrane, acute mastoiditis, middle ear atelectasis, adhesive otitis media, tympanosclerosis, ossicular erosion or fixation, petrous apicitis, cholesteatoma, chronic otomastoiditis, labyrinthitis, facial paralysis, and intracranial infection. There is evidence that sensorineural hearing loss may result from chronic otitis media with or without cholesteatoma. There is also evidence that the auditory deprivation associated with childhood otitis media may lead to indirect sequelae, such as language and speech delays.
Effects on Mastoid Pneumatization
It has been observed that patients with a history of chronic OME have more sclerotic mastoids with decreased pneumatization compared with healthy subjects. There are two theories to explain this observation: (1) the hereditary theory, which states that children with hypoaeration of the mastoid are prone to OME, and (2) the environmental theory, which states that chronic OME results in hypopneumatization of the mastoid.5 Although measurable correlations between mastoid hypocellularity and OME,6,7 and between the length of the mastoid process or the degree of pneumatization and an abnormal eardrum8 have been proven, a cause-and-effect relationship is unclear. Available evidence generally supports the concept that chronic inflammation in early childhood may lead to new bone formation within the middle ear and mastoid and, subsequently, decreased size of mastoid air cells. Shatz and Sadé9 measured the distance from the lateral sinus to the external auditory canal and found it to be significantly smaller in patients with sclerotic mastoids; they believed that this finding supported the hereditary theory because it was unlikely that otitis would change the position of the lateral sinus. A chronically inflamed mastoid in a young child may not develop normally, however.
Hasebe and colleagues10 carried out a study to establish which type of cholesteatoma is controllable by conservative treatment from the viewpoint of mastoid ventilation. Their clinical observations suggest that progressiveness of cholesteatoma is related to the ventilatory conditions in the mastoid, rather than eustachian tube function, and that conservative treatment may be effective if ears with cholesteatoma have aeration in the mastoid.
Middle Ear Atelectasis and Adhesive Otitis Media
Middle ear atelectasis (Fig. 139-1) is thought to result mainly from long-standing eustachian tube dysfunction. One of the main functions of the eustachian tube is ventilation of the middle ear and mastoid. Opening of the eustachian tube allows exchanging of gases and equalization between the environment and middle ear. The middle ear gases also are exchanged with the middle ear mucosa. Bilateral diffusion between the middle ear cavity and the blood may be an important factor in middle ear atelectasis because the gas composition of the middle ear basically resembles that of venous blood.11
If the atelectasis develops, the tympanic membrane becomes retracted onto the promontory and the ossicles of the middle ear. In atelectatic ears, the middle ear space is partially or completely obliterated, but the tympanic membrane is not adherent to the medial wall of the middle ear, and the mucosal lining of the middle ear is intact. In contrast, adhesive otitis media exists when the middle ear space is totally obliterated, and the tympanic membrane is adherent to the ossicles and promontory; mucosal surfaces are not present. Retraction of the tympanic membrane may lead to erosion of the long process of the incus and the stapes suprastructure (Fig. 139-2).
Not all patients with chronic OME develop atelectasis; in most patients with OME, retraction of the tympanic membrane is limited. In patients with bilateral OME, 1.5% of untreated ears and 2% of ears treated with tubes developed severe atelectasis.12 It may be that repeated bouts of AOM lead to weakening and thinning of the membrane, which allows atelectasis. Sadé and Berco13 showed destruction of the collagen-containing fibrous layer of the tympanic membrane in some ears with recurrent infection. Collagen destruction within the tympanic membrane may lead to another complication of OME—tympanosclerosis. Sadé and Berco13 and Tos and Poulsen14 described four stages of tympanic membrane retraction: stage I, retracted tympanic membrane; stage II, retraction with contact onto the incus; stage III, middle ear atelectasis; and stage IV, adhesive otitis media (Fig. 139-3).
Figure 139-3. Four stages of middle ear atelectasis.
(Adapted from Sadé J, Berco E. Atelectasis and secretory otitis media. Ann Otol Rhinol Laryngol. 1976;85(Suppl 25):66.)
Middle ear atelectasis may be reversible with ventilating tubes. Sadé15 showed that ventilating tubes improved the state of atelectatic ears. Graham and Knight16 reported three cases in which atelectatic tympanic membranes were restored to their normal position by administration of nitrous oxide during anesthesia and insertion of a ventilating tube.
Atelectasis and adhesive otitis media usually coexist with OME, although OME may resolve in these ears, allowing aeration of the attic and mastoid, but leaving a collapsed middle ear. In extreme cases, when hearing loss or ossicular erosion occurs, a myringoplasty for the reinforcement of atelectatic tympanic membrane may be indicated.6,17 Cholesteatomas may originate from deep retraction pockets in which desquamated keratin debris would not be cleared into the ear canal.18,19 These retraction pockets may occur in the pars tensa or pars flaccida of atelectatic ears, and should be considered precursors to cholesteatomas (see discussion of cholesteatoma). Nonpneumatized mastoids may have a limited ability to buffer pressure changes and can manifest as an atelectasis, a retraction pocket, or a cholesteatoma.20
Chronic Otitis Media with Cholesteatoma
Aural cholesteatomas are epidermal inclusion cysts of the middle ear or mastoid (in the case of a retraction pocket cholesteatoma, the “cyst” opens into the external auditory canal). They contain the desquamated debris (principally keratin) from their keratinizing, squamous epithelial lining. Cruveilhier21 first described aural cholesteatoma as a “pearly tumor” of the temporal bone. The term cholesteatoma, coined by the German physiologist Müller22 in 1838, is a misnomer because this entity does not contain cholesterol; the white-yellow keratin flakes found within cholesteatomas grossly resemble cholesterol crystals. Cholesteatomas of the temporal bone may be congenital or acquired. Acquired cholesteatomas are the consequence of OME, AOM, or both. An understanding of the pathogenesis and pathophysiology of aural cholesteatoma is particularly important because the destructive nature of this entity is responsible for much of the morbidity associated with chronic otitis media. The propensity of cholesteatomas to erode bone and the lack of effective, nonsurgical management add importance to the understanding of this disease.
The diagnosis of aural cholesteatoma is made on otoscopic examination, including endoscopic and microscopic evaluation or surgical exploration. Special imaging procedures, such as high-resolution computed tomography (CT) and magnetic resonance imaging (MRI), may suggest the presence of cholesteatomas within the temporal bone, and may be used to complement the clinical examination. High-resolution CT is useful for operative planning and is recommended for all revision mastoid operations. The symptoms of cholesteatoma vary; some cholesteatomas are asymptomatic, whereas others become infected and rapidly cause bone destruction. Some patients seen by the physician show slowly progressive conductive hearing loss, and frequently patients with cholesteatomas consult a physician because of chronic otitis with purulent otorrhea. The otorrhea from an infected cholesteatoma often is malodorous because of the frequent infection with anaerobic bacteria.23
Patients with infected cholesteatoma occasionally are misdiagnosed as having external otitis. Careful follow-up evaluation and thorough canal débridement of a patient with otorrhea are mandatory because the cholesteatoma may not be evident during an acute flare-up. Some patients have signs and symptoms of the complications of a cholesteatoma: vertigo and hearing loss caused by a labyrinthine fistula, facial nerve paralysis, or intracranial infection.
The otoscopic appearance of an aural cholesteatoma also varies. A typical attic retraction cholesteatoma (Fig. 139-4) appears as a defect of variable size adjacent to the posterosuperior portion of the tympanic membrane. The center of the defect contains keratin debris (primary acquired cholesteatoma). In other patients, keratinizing epithelium has migrated through a perforation into the middle ear (secondary acquired cholesteatoma) (Fig. 139-5). Cholesteatomas sometimes appear behind or within an intact tympanic membrane—so-called congenital cholesteatoma (Fig. 139-6). These cholesteatomas have been considered to be congenital, but more recent experimental evidence raises the possibility that they may originate during an inflammatory process.24 An infected cholesteatoma sometimes manifests as an “aural polyp.” These “polyps” actually are granulation tissue at the junction between an eroding cholesteatoma and bone. The presence of an aural polyp in a chronically infected ear should be considered to be a cholesteatoma until proved otherwise. Occasionally, a cholesteatoma cannot be seen otoscopically, but is discovered during tympanomastoid surgery.
Figure 139-4. Primary acquired cholesteatoma in the region of the pars flaccida with scutum erosion.
Figure 139-5. Cholesteatoma developing at the margin of perforation (secondary acquired cholesteatoma) with secondary infection.
The exact prevalence of cholesteatoma is unknown. In 1978, there were 4.2 hospital discharges per 100,000 population with cholesteatoma.25 In addition, there were 13.8 hospital discharges per 100,000 population with chronic otitis media without cholesteatoma. Studies by Harker23 documented an annual incidence of 6 cholesteatomas per 100,000 population. Tos26 found an annual incidence of 3 cholesteatomas in children and 12.6 cholesteatomas in adults per 100,000 population. In the human temporal bones with chronic otitis media, cholesteatoma was observed in 36% of ears with perforations and in 4% of ears without the perforated tympanic membranes.27
Congenital cholesteatomas, by definition, originate from areas of keratinizing epithelium within the middle ear cleft. Michaels28 showed that a small area in the anterior tympanum in the developing fetus often contains a small area of keratinizing epithelium. He found epidermoid formation in 37 of 68 temporal bones of fetuses at 10 to 33 weeks’ gestation. Congenital cholesteatomas may originate in this region. Although congenital cholesteatomas generally are seen as pearl-like masses behind an intact membrane, Koltai and coworkers29 presented a convincing case that some congenital cholesteatomas advance to perforate and become chronically infected, taking on the appearance of an acquired cholesteatoma. Potsic and colleagues,30 in a review of 172 series of congenital cholesteatomas, developed a useful staging system: stage I, limited to one quadrant; stage II, involving multiple quadrants without ossicular involvement; stage III, ossicular involvement without mastoid extension; and stage IV, mastoid involvement. They showed a correlation between stage and risk of residual disease; stage IV carries a 67% risk of residual cholesteatoma.
The pathogenesis of acquired cholesteatoma has been debated for more than a century. There are four basic theories of the pathogenesis of acquired aural cholesteatoma: (1) invagination of the tympanic membrane (retraction pocket cholesteatoma), (2) basal cell hyperplasia, (3) epithelial ingrowth through a perforation (the migration theory), and (4) squamous metaplasia of middle ear epithelium (Fig. 139-7). Additionally, Sudhoff and Tos19 proposed a combination of the invagination and basal cell theories as an explanation for retraction pocket cholesteatoma formation.
The invagination theory5 of the genesis of cholesteatoma generally is regarded as one of the primary mechanisms of the formation of attic cholesteatomas. Retraction pockets of the pars flaccida deepen because of negative middle ear pressure and possibly repeated inflammation (see Fig. 139-2). As the retraction pocket deepens, desquamated keratin cannot be cleared from the recess, and a cholesteatoma results. The origin of such retraction pocket cholesteatomas is thought to be eustachian tube dysfunction (or OME) with resultant negative middle ear pressure (ex vacuo theory). Usually, the pars flaccida, being less fibrous and less resistant to displacement, is the source of the cholesteatoma.
The result of this type of cholesteatoma (so-called primary acquired cholesteatoma) is an apparent defect in the posterosuperior quadrant of the tympanic membrane and erosion of the adjacent canal wall.31 Although these defects have the appearance of a marginal perforation, it is not a perforation, but rather an invagination. Sadé20 showed that epithelial migration patterns within attic retraction pockets are altered. This failure of epithelial migration may allow the accumulation of keratin within a retraction pocket, with subsequent enlargement merely from the accumulation of keratin within a relatively closed space. This theory has been supported by the experimental creation of retraction pockets by use of the eustachian tube obstruction,32 and external auditory canal ligation.33
Ruah and colleagues31 suggested that inflammation of middle ear and persistent mesenchyme lead to a greater inflammatory reaction in pars flaccida and posterosuperior quadrant of the tympanic membrane of the human temporal bones with serous and purulent otitis media in children. These findings support this theory of primary acquired cholesteatoma in children. Retraction pockets are considered as precursors to cholesteatoma. Bacteria can infect the keratin matrix, forming biofilms leading to chronic persistent infection. The presence of bacterial biofilms in the cholesteatoma matrix may lead to epithelial proliferation and invasion of the cholesteatoma.34,35
Basal Cell Hyperplasia Theory
Another possible mechanism for the histogenesis of cholesteatoma was suggested by Lange in the 1920s.49 In this theory, he proposed that epithelial cells (prickle cells) of the pars flaccida could invade the subepithelial tissue by means of proliferating columns of epithelial cells. Nearly 40 years later, Ruedi50 supported this hypothesis with clinical and experimental evidence. For epithelium to invade into the lamina propria, the basal lamina (basement membrane) should be altered. Basal lamina disruptions now have been documented in human51,52 and animal53 cholesteatomas.
Huang and colleagues54 and Masaki and coworkers55 provided experimental support of this theory by showing that epithelial ingrowth from the tympanic membrane can be induced by instillation of propylene glycol into the middle ear of chinchillas. These basal lamina breaks allow the invasion of epithelial cones into the subepithelial connective tissue and the formation of microcholesteatomas. This mechanism may explain some types of human cholesteatomas, even those occurring behind an intact tympanic membrane.56 According to this theory, microcholesteatomas may enlarge and then perforate secondarily through the tympanic membrane, leaving the typical appearance of an attic cholesteatoma. This sequence of events has not been documented, although the alternations in the differentiation of keratinocytes and basal cell layer of cholesteatoma matrix have been observed in several studies.
Abnormal distribution of epidermal differentiation markers, such as filaggrin and involucrin,57 c-jun and p53 proteins,58 and increased epidermal growth factor receptor,59,60 has been shown in middle ear cholesteatoma matrix. Increased levels of proteins cytokeratin 13 and cytokeratin 16, which are markers for differentiation and hyperproliferation, were also found.61 Kim and Chole39 showed the increased expression of cytokeratin 13 and cytokeratin 16 in the area of the peripheral area of the pars tensa of induced cholesteatoma by ear canal ligation and in the peripheral and central area of pars tensa of induced cholesteatoma by eustachian tube obstruction. Sakamoto and associates62 found ErbB-2 protein to be overexpressed, and cell proliferation and apoptosis of keratinocytes accelerated. Caspases play a key role in apoptosis; Miyao and coworkers63 suggested that caspase-8, which is activated by the induction of tumor necrosis factor-α, leads to activation of caspase-3, which activates apoptotic nucleases in cholesteatoma tissue.
Human toll-like receptors are crucial in the induction and activation of innate immunity in the course of an infection. Expression of toll-like receptor–3 on the epithelium and some cells within the perimatrix and the presence of T cells may suggest that apart from innate immune responses, mechanisms of adaptive immunity also operate in cholesteatoma.64 Data from Parisier and colleagues65 suggested that fibroblasts in the subepithelium of cholesteatomas showed an invasive phenotype, whereas fibroblasts from postauricular and ear canal skin appeared either weakly invasive or not invasive. In a similar study, Chole and colleagues66 found that normal fibroblasts and fibroblasts from induced cholesteatomas did not exhibit the invasive phenotype characteristics of true neoplastic cells.
Other lines of evidence support the basal cell hyperplasia/migration theory. Increased expression of human intercellular adhesion molecule-1 and intercellular adhesion molecule-2 has been shown, suggesting a role in cell migration into tissue.40 The presence of heat shock proteins 60 and 70 suggested proliferation and active differentiation of basal keratinocytes in cholesteatomas.58 There are some reports that immune response is involved in the hyperproliferative state of cholesteatoma epithelium.52,67,68 Langerhans cells may initiate immune reaction and promote proliferation of keratinizing epithelium via an interleukin (IL)-1α and transforming growth factor (TGF)-β mechanism.42,67,69
Epithelial Invasion Theory
The epithelial invasion theory36 states that keratinizing squamous epithelium from the surface of the tympanic membrane invades or migrates into the middle ear from a perforation in the tympanic membrane. This theory is supported by clinical observation and experimental evidence. Weiss37 showed that epithelial cells could migrate along a surface by a process that he called contact guidance, and that, when they encounter another epithelial surface, they stop migrating, for which he used the term contact inhibition. van Blitterswijk and Grote38 reported that cytokeratin 10, which was seen in the meatal epidermis and migrating epithelium, was preferentially expressed in the cholesteatoma matrix, rather than in the middle ear mucosa. This finding suggests an epidermal origin of cholesteatoma. Kim and Chole39 showed increased cytokeratin 10 expression in the peripheral area of the pars tensa of induced cholesteatoma by ear canal ligation and in the peripheral and the central area of the pars tensa of induced cholesteatoma by eustachian tube obstruction. The findings of this study also support the basal cell hyperplasia hypotheses for the pathogenesis of aural cholesteatoma, with regard to hyperproliferation, migration, and an altered differentiation of keratinocytes.39 High levels of fibronectin and tenascin and focal disruptions of the basement membrane, were reported in the middle ear cholesteatoma, supporting the concept of the invasion theory.40–43
This theory also is supported by investigations in animal cholesteatoma models and human temporal bones. Jackson and Lim44 gave histologic and ultrastructural evidence that keratinizing epithelium can migrate into the cat bulla by contact guidance. It is likely that in some tympanic membrane perforations, inflammation damages the inner mucosal lining of the tympanic membrane, allowing the outer keratinizing epithelium to migrate inward and generate a cholesteatoma. Hueb and associates45 showed similar evidence in chinchillas. Palva and colleagues46 showed histologic evidence for this theory in human temporal bones. Cholesteatomas originating after temporal bone fractures may result from this mechanism; fractures within the ear canal may allow ingrowth of keratinizing epithelium by contact guidance.47 7,12-Dimethylbenz[a]anthracene, a chemical carcinogen, could induce the advancing of the keratinizing squamous epithelium into or under the mucosal layer, and ingrowth and spreading over the middle ear cavity and eustachian tube in the rat ear.48
Squamous Metaplasia Theory
Wendt70 theorized that the simple squamous or cuboidal epithelium of the middle ear cleft could undergo a metaplastic transformation into keratinizing epithelium. Sadé15,71 supported this theory, noting that epithelial cells are pluripotent and can be stimulated by inflammation to become keratinizing. According to this theory, an area of keratinizing epithelium within the middle ear would enlarge because of accumulated debris and contact with the tympanic membrane. With intercurrent infection and inflammation, the cholesteatoma would lead to lysis of the tympanic membrane and perforation, resulting in the typical appearance of an attic cholesteatoma. This theory is supported by the demonstration that biopsy specimens from the middle ear of children with OME sometimes contain islands of keratinizing epithelium.15
Some experimental evidence supports the contention that middle ear mucosa can become metaplastic and keratinize. Chole and Frush72 showed that extreme vitamin A deficiency leads to the formation of keratinizing epithelium within the middle ear and eustachian tube of rats. None of their experimental animals had developed cholesteatomas. Consequently, there is no direct evidence that cholesteatomas arise by squamous metaplasia of the middle ear mucosa.
From a clinical perspective, it seems that each of these pathogenic mechanisms accounts for a proportion of acquired cholesteatomas. Regardless of the pathogenesis of aural cholesteatomas, they all share certain properties. Cholesteatomas are prone to recurrent infection, and they characteristically erode the bone of the ossicles and the otic capsule. Aural cholesteatomas originating from the vicinity of the tympanic membrane exhibit typical growth patterns into the temporal bone. Because most acquired cholesteatomas originate by invagination of the pars flaccida, their growth is limited by the mucosal folds and suspensory ligaments of the ossicles. The pars flaccida may invaginate into the lateralmost portion of the epitympanum (Prussak’s space) and then into the recesses of the epitympanum posteriorly, lateral to the body of the incus, inferiorly into the middle ear by way of the pouch of von Tröltsch (Fig. 139-8), or anteriorly into the protympanum (Fig. 139-9).73–75
Figure 139-8. Posterior mesotympanic cholesteatoma. This sac forms because of retraction of the posterior portion of the pars tensa, and frequently invades the sinus tympani and facial recess. Extension to the mastoid occurs medial to ossicle heads (arrows).
(From Jackler RK. The surgical anatomy of cholesteatoma. Otolaryngol Clin North Am. 1989;22:883.)
Figure 139-9. Anterior epitympanic cholesteatoma. Invagination of the epitympanum anterior to the malleus head and neck creates a cholesteatoma sac that threatens the horizontal facial nerve and geniculate ganglion. Forward extension into the supratubal recess is common (arrows).
(From Jackler RK. The surgical anatomy of cholesteatoma. Otolaryngol Clin North Am. 1989;22:883.)
The expansion of cholesteatoma may result in bone erosion of the ossicles, otic capsule, fallopian canal, tegmen tympani, and tegmen mastoideum. These complications may cause intracranial complications (Box 139-1). The erosion of ossicles, most commonly in the incus, may result in conductive hearing loss. The severity of hearing loss is related to the status of the ossicles and the position of the cholesteatoma sac. Erosion of the otic capsule occurs most commonly in the lateral semicircular canal and rarely in the cochlea. A labyrinthine fistula has been reported in 10% of cholesteatomas in adults and children,76 which may result in sensorineural hearing loss and vertigo. Sensorineural hearing loss may result from the secondary suppurative labyrinthitis or from the cochlear hair cell loss adjacent to cholesteatoma.66 Facial nerve paralysis may occur acutely as a result of infection or slowly as a result of expansion of the cholesteatoma. Erosion of the tegmen tympani or the tegmen mastoideum may lead to development of a brain hernia or cerebrospinal fluid leakage.77
Box 139-1 Complications and Emergency States of Chronic Otitis Media with Cholesteatoma
Because cholesteatomas contain keratin debris enclosed in a tissue space, they are subject to recurrent infection. The bacteria found in infected cholesteatomas differ from bacteria found in AOM or OME. Significant anaerobic bacteria are present. The most common aerobic bacterium is Pseudomonas aeruginosa, and the most common anaerobic microorganism is Bacteroides sp (Table 139-1).78
|Bacteria||No. of Cases|
|Klebsiella, Enterobacter, Serratia||4|
|CBC group F|
Modified from Harker LA, Koontz FP. The bacteriology of cholesteatomas. In: McCabe BF, Sadé J, Abramson M, eds. Cholesteatoma: First International Conference. New York: Aesculapius Publishers; 1977.
Congenital and acquired cholesteatomas can be eradicated from the temporal bone only by surgical resection. The goals of surgery are to eradicate disease and manage complications and, secondarily, to reconstruct the middle ear. The decision whether to perform surgery depends on the nature and extent of disease, the existence of complications, mastoid pneumatization, eustachian tube function, hearing status of both ears, the reliability of the patient, and the experience and skill of the surgeon.77,79 Surgical approaches include atticotomy, simple mastoidectomy, canal wall-up or canal wall-down procedures, radical mastoidectomy, modified radical mastoidectomy, and Bondy procedure.
The open (canal wall-down) and the closed (intact canal with facial recess) procedures have advantages and disadvantages (Table 139-2). The reported results of both procedures vary. Residual disease and recurrent disease occur in 11% to 27% and 5% to 13% of patients undergoing the closed procedure, whereas residual or recurrent disease occurs in 2% to 10% of patients undergoing the open procedure.80 In the cases of labyrinthine fistula, facial nerve paralysis, and intracranial complications, surgery should be performed as soon as possible.
|Physiologic position of tympanic membrane||Residual and recurrent cholesteatoma may occur|
|Enough middle ear space||Incomplete exteriorization of facial recess|
|No mastoid cavity problem||Second-stage operation often required|
|Residual cholesteatoma easily found on follow-up evaluation||Mastoid cavity problem often|
|Recurrent cholesteatoma rare||Middle ear shallow and difficult to reconstruct|
|Total exteriorization of facial recess||Position of pinna may be altered; second-stage operation sometimes required|
Modified from Harker LA, Koontz FP. The bacteriology of cholesteatomas. In: McCabe BF, Sadé J, Abramson M, eds. Cholesteatoma: First International Conference. New York: Aesculapius Publishers; 1977.
In some patients, a cholesteatoma can be débrided of entrapped keratin by direct removal or by irrigation. In some cases, surgical intervention is impossible or not advisable; the patient may not be medically able to withstand surgery, or the risks of surgery may not outweigh the benefits in some patients with only-hearing ears. Irrigation with 1 :1 : 1 distilled white vinegar, distilled water, and 70% isopropyl alcohol may keep some cholesteatomas stable if their opening into the ear canal is sufficiently large (Box 139-2). If surgery is required for a cholesteatoma in an only-hearing ear, careful preoperative evaluation and operative planning, perioperative use of antibiotics and steroids, ossicular reconstruction, and postoperative care should be considered.81
Box 139-2 Management of Chronic Otitis Media with Cholesteatoma
Factors for Determination of Treatment
Chronic Otitis Media without Cholesteatoma
Acute or recurrent infection of the middle ear may result in a permanent perforation of the tympanic membrane. Ears with chronic perforations without cholesteatoma may be chronically or intermittently infected. Three times as many operations were performed in the United States for this disease as were performed for cholesteatomas.25 Paparella and Kim81a reported that of 375 primary tympanomastoid operations for chronic mastoiditis, two thirds were performed in ears with granulation tissue and without cholesteatoma.
Tympanic membrane perforation (Fig. 139-10) may result from AOM, chronic otitis media, or trauma (injury or surgery). In some instances, a dry, simple perforation results from a single episode of AOM (i.e., necrotizing otitis media). Perforation of the tympanic membrane, especially involving the tympanic anulus, may allow ingrowth of the keratinizing epithelium of the ear canal or tympanic membrane, leading to cholesteatoma. An ear with a simple perforation may become infected because of contamination from the ear canal or because of a smoldering infection in the mastoid. A simple perforation commonly is seen as a low-frequency conductive hearing loss clinically. This finding is supported by experimental perforation in rats.82 The tympanic membrane velocity was found to be decreased in the low frequency in a small perforation and in the high and low frequencies in a large perforation.83
Chronic otomastoiditis without cholesteatoma is marked by the presence of irreversible inflammatory changes within the middle ear and mastoid. The factors that allow acute infections within the middle ear and mastoid to develop into chronic infections are unclear. da Costa and colleagues27 found granulation tissue in 96%, ossicular changes in 96%, tympanosclerosis in 43%, cholesteatoma in 36%, and cholesterol granuloma in 21% of the human temporal bones of patients with chronic otitis media with a perforated tympanic membrane (Table 139-3