Your activity: 8 p.v.

Chronic otitis media, cholesteatoma, and mastoiditis in adults

Chronic otitis media, cholesteatoma, and mastoiditis in adults
Authors:
Lawrence R Lustig, MD
Charles J Limb, MD
Section Editor:
Daniel G Deschler, MD, FACS
Deputy Editors:
Jane Givens, MD, MSCE
Milana Bogorodskaya, MD
Literature review current through: Dec 2022. | This topic last updated: Jan 15, 2021.

INTRODUCTION — Chronic otitis media (COM) is a recurrent infection of the middle ear and/or mastoid air cells in the presence of a tympanic membrane perforation. Symptoms commonly associated with chronic ear disease include hearing loss, otorrhea, aural fullness, otalgia, and occasionally true vertigo.

Cholesteatoma, a keratinized mass in the middle ear or mastoid, may occur either as a primary lesion or secondary to tympanic membrane perforation. Mastoiditis may occur as a complication of acute otitis media (AOM) or COM.

AOM, an acute illness marked by the presence of middle ear fluid and inflammation of the mucosa that lines the middle ear space, is discussed separately. (See "Acute otitis media in adults".)

Similar to AOM, COM occurs far more commonly in children. These conditions in children are discussed separately. (See "Acute otitis media in children: Clinical manifestations and diagnosis" and "Acute otitis media in children: Treatment" and "Evaluation of otorrhea (ear discharge) in children", section on 'Chronic suppurative otitis media' and "Otitis media with effusion (serous otitis media) in children: Management".)

CLASSIFICATION — A variety of terms are used to categorize chronic infectious or inflammatory conditions of the middle ear, according to the underlying disease process and location.

Chronic otitis media — COM is defined as an ear with a tympanic membrane perforation in the setting of recurrent or chronic ear infections (picture 1).

Benign (or inactive) COM is characterized by a dry tympanic membrane perforation, without active infection.

COM with effusion (formerly known as chronic serous otitis media) is characterized by continuous serous drainage (typically straw-colored).

Chronic suppurative otitis media is diagnosed when there is persistent purulent drainage through a perforated tympanic membrane.

The World Health Organization (WHO) defines chronic suppurative otitis media (CSOM) as "a chronic inflammation of the middle ear and mastoid cavity, which presents with recurrent ear discharges or otorrhea through a tympanic perforation" [1]. The WHO definition requires that otorrhea be present for only two weeks, but the focus of the WHO is primarily on worldwide disease prevention in children. Practically, most otolaryngologists consider the diagnosis of CSOM to be established when discharge persists, despite treatment, for periods varying from six weeks [2] to up to three months [3].

Cholesteatoma — Cholesteatoma is a keratinized, desquamated epithelial collection in the middle ear or mastoid and may occur secondary to tympanic membrane perforation but also may occur as a primary lesion. (See 'Cholesteatoma' below.)

Some otologists also classify COM based on the presence of either a chronic tympanic membrane perforation ("COM mucosal disease") or cholesteatoma ("COM benign squamous disease"). The term "active" is also used if there is otorrhea, and "inactive" if it remains dry.

PATHOGENESIS

Chronic otitis media — In children, chronic ear disease often follows episodes of acute otitis media (AOM). Chronic suppurative otitis media (CSOM) is more common in lower socioeconomic areas and may be related to delay in treatment for AOM, poorer hygienic conditions, increased smoking, or poorer nutrition [1]. The point in time when AOM becomes CSOM is controversial, with definitions ranging from two weeks to three months [1-3].

CSOM in adults occurs in patients with perforation of the tympanic membrane that will not heal. Typically, there is a history of recurrent ear infections in childhood, with longstanding (months or years) otorrhea and hearing loss made worse by water exposure.

Chronic ear disease occurs as a result of Eustachian tube dysfunction, typically related to obstruction (usually due to upper respiratory infection or seasonal allergic rhinitis) [4,5]. By contrast, abnormal patency of the Eustachian tube, termed patulous Eustachian tube, does not cause infection but results in such symptoms as autophony (hearing one's own voice) and ear fullness [4,6]. Rarely, COM with effusion is caused by obstruction of the Eustachian tube orifice in the nasopharynx by a mass or cancer such as nasopharyngeal carcinoma or as a result of radiation treatment for nasopharyngeal malignancy.

Eustachian tube dysfunction results in chronic negative middle ear pressure exerted on the tympanic membrane, the most compliant boundary of the middle ear. Negative pressure pulls the tympanic membrane medially, and retraction pockets can occur with prolonged exposure, usually within the pars flaccida of the tympanic membrane (figure 1) [7,8]. This segment of the tympanic membrane accounts for the upper one-sixth of the surface area of the tympanic membrane and lies superior to the anterior and posterior malleolar folds of the tympanic membrane.

When a patient has AOM, a serous, mucoid, or purulent effusion builds up behind the tympanic membrane. Tympanic membrane rupture and otorrhea may occur if the positive pressure exerted by this effusion exceeds the tensile strength of the tympanic membrane and Eustachian tube dysfunction prevents pressure equilibration. Spontaneous perforations produced under these conditions are part of the compensatory mechanism of the ear and provide a conduit for aeration similar to that produced by myringotomy tubes. In some cases where there are multiple episodes of acute infection, the perforation may become chronic (nonclosing). In such instances, the outer epithelial layer of the tympanic membrane grows over the perforation edges, covering the middle fibrous and inner mucosal layers, and prevents the perforation from closing.

Perforations of the tympanic membrane are classified as central when the annulus (the ligamentous ring surrounding the tympanic membrane) is preserved and marginal when a portion of the annulus or the entire annulus is involved [9,10]. The annulus serves as a protective barrier against squamous epithelial migration into the middle ear. Marginal perforations are more frequently associated with cholesteatoma [9,10].

Cholesteatoma — The term cholesteatoma refers to a keratinized, desquamated epithelial collection in the middle ear or mastoid [11]. The nomenclature of cholesteatoma is misleading, with keratoma perhaps being a better term [12]. Cholesteatomas contain no cholesterol or lipids and are not neoplastic. Cholesteatomas may occur as primary lesions or may be secondary to tympanic membrane perforation or surgery. Congenital cholesteatomas are discussed separately. (See "Cholesteatoma in children", section on 'Congenital cholesteatomas'.)

Primary acquired – Primary acquired cholesteatomas occur most commonly as a result of Eustachian tube dysfunction (picture 2) [13-15]. Prolonged exposure to negative middle ear pressure causes the tympanic membrane to retract medially. A retraction pocket may eventually become trapped behind the tympanic membrane, inducing inflammatory changes [16,17]. This epithelium-lined pocket accumulates keratinized squamous debris, which forms a cholesteatoma (picture 3) [11,15]. Poor middle ear ventilation results in delayed resolution of infection, persistence of effusion, and ultimately a retracted or perforated tympanic membrane. With growth and proliferation of squamous epithelium, the cholesteatoma grows in size, often eroding the scutum (the sharp edge of the tympanic ring adjacent to the head of the malleus). Further infection with inflammatory changes can lead to aural polyps and granulation tissue throughout the middle ear and mastoid air cell tracts.

Secondary acquired – Tympanic membrane perforation may lead to a secondary acquired cholesteatoma in a small percentage of cases. Squamous epithelium can migrate through the tympanic membrane defect into the middle ear space, and accumulations of squamous debris result in the cholesteatoma [11,13,17]. An iatrogenic form of secondary acquired cholesteatoma may develop if squamous epithelium is implanted in the middle ear space during surgery such as tympanoplasty [18].

Cholesteatomas may result in erosion of the ossicles in the middle ear and consequent hearing loss. In rare cases, they can erode directly into the inner ear. An earlier theory attributed bony erosion to pressure necrosis from the expanding cholesteatoma itself [19]. Several other mechanisms are now recognized as the cause of bone destruction: enzymatic breakdown of collagen by collagenase, acid phosphatase, and acid protease produced by the cholesteatoma; osteoclastic bone resorption; and pyogenic osteitis [20]. Bacterial overgrowth in the area of the cholesteatoma further contributes to the potential for bone destruction.

MICROBIOLOGY — In chronic suppurative otitis media (CSOM), typical pathogens reach the middle ear through two routes of spread [2,21]:

Insufflation of respiratory pathogens through the Eustachian tube from the nasopharynx into the middle ear

Spread from the external ear canal inward through a nonintact tympanic membrane

Studies of CSOM differ in regard to patient age, geography, and the presence of complications such as cholesteatoma, and these inconsistencies likely impact some of the variation in reported pathogens [21-24]. Differences in sampling and processing techniques may also account for some of the variability observed in microbiologic diagnoses. Studies reported in the literature most often sample aural discharge through a sterilized otoscope [23-27]. Swabs of the external ear canal are not adequate for sampling, as they are often contaminated by ear canal flora and provide misleading information [22,28].

Aerobes, anaerobes, and fungi are all potential pathogens in CSOM. Knowledge of the true frequency of polymicrobial infection, particularly the extent of anaerobe involvement, is limited [29,30].

Pseudomonas aeruginosa and Staphylococcus aureus are the most commonly isolated aerobic bacteria in several large case series [21,23-26,31]. The ability of these organisms to form biofilm may contribute to their frequency in CSOM [2]. The prevalence of methicillin-resistant S. aureus (MRSA) varies by region and importantly also predicts differences in susceptibility to commonly used topical therapies (quinolones and aminoglycosides) [25,26]. Antibiotic susceptibility to Pseudomonas can vary widely, making it important to perform susceptibility testing to guide therapy when Pseudomonas infection is suspected or patients fail to respond to an initial empiric course of therapy [31,32].

Less-frequently isolated organisms include enteric gram-negative rods such as Klebsiella, Proteus, and Escherichia coli [21,23,24,32]. Enteric gram-negative rods may be more common in areas at higher risk of infection due to poor hygiene conditions [33].

The role of anaerobes in CSOM has been variably reported, with frequencies of anaerobic isolates ranging from 8 to 59 percent [30]. The lack of standardized technique for sample collection and culture protocol likely accounts for demonstrated large part of the wide range of incidence.

There have also been reports of mycobacteria causing COM, particularly in regions where Mycobacterium tuberculosis is endemic [34,35]. Nontuberculous mycobacterial cases have also been reported [36].

Fungi, particularly Aspergillus spp and Candida spp, although rare, are reported as pathogens as well [23,25].

The expected antimicrobial resistance profile in CSOM will vary based on several factors including geography, prior health care contact, and previous receipt of antibiotics. Cultures for definitive microbiologic diagnosis and susceptibility testing should be pursued if resistant organisms are suspected [22,28]. Cultures should be obtained by microscopy and aspiration; swabs of the ear canal are more likely to be contaminated. Otolaryngology referral for otoscopy is often indicated, as it is necessary to remove any obstructing wax, debris, or drainage to visualize the ear drum and middle ear if a perforation is present.

Cholesteatoma can be associated with a polymicrobial infection [27]; however, the most commonly isolated pathogens remain S. aureus and P. aeruginosa [24,25,27]. The development of eroded ossicles may be more common with Proteus spp, and failure to control infection is more common when Pseudomonas spp are isolated [24].

CLINICAL FEATURES AND PHYSICAL EXAM FINDINGS

Chronic suppurative otitis media — The most common symptom of CSOM is the presence of recurrent or persistent purulent ear drainage. CSOM is most often painless, and patients usually present without fever or other systemic signs of infection. The drainage may be foul smelling.

Patients typically also report hearing loss. The degree of hearing loss is related to the location and size of the tympanic membrane perforation, the status of the ossicles, and to the duration of chronic damage [37].

Physical examination is notable for otorrhea in the presence of a perforated tympanic membrane.

Cholesteatoma — Presenting features of cholesteatoma may vary. Some patients may be totally asymptomatic. Others may present with some combination of hearing loss, dizziness, and/or otorrhea. Cholesteatomas associated with tympanic membrane perforation are typically detected earlier than primary acquired cholesteatomas as the inferior portion of the ear drum is easier to inspect, and hearing loss occurs early [38].

Hearing loss occurs late in the course of primary cholesteatomas since the pars flaccida is the nonvibratory portion of the tympanic membrane. Late conductive hearing loss is also due to erosion of the ossicles, typically the distal portion of the incus. Hearing loss can occur earlier when cholesteatomas are associated with tympanic membrane perforation (eg, secondary cholesteatomas) due to involvement of the vibratory surface area of the tympanic membrane (pars tensa).

The otoscopic findings in cholesteatoma depend on the type of cholesteatoma (primary or secondary).

Primary cholesteatoma - Primary acquired cholesteatomas are typically found in the posterosuperior quadrant of the tympanic membrane, in the pars flaccida (picture 2). The surface of the cholesteatoma is often obscured by crusting or desquamated debris on its lateral surface. Retractions of the pars flaccida lead to attic cholesteatomas that can be particularly difficult to visualize.

Secondary cholesteatoma - When a cholesteatoma is associated with a perforation (secondary acquired cholesteatoma), a pearly mass is usually evident behind the tympanic membrane. These cholesteatomas may appear as skin that has replaced the mucosa of the middle ear.

DIAGNOSIS — A careful ear examination can establish the diagnosis, with attention aimed to determine if there is a cholesteatoma. This may require otomicroscopy with suctioning, necessitating referral to an otolaryngologist. For routine serous otitis media, the drum is typically intact with a yellowish hue or there may be visible air bubbles behind the tympanic membrane. In cases of chronic suppurative otitis media, there is typically a perforation that may be partial or complete, often with associated purulent otorrhea and inflamed middle ear mucosa. In the case of a primary cholesteatoma, the otoscopic examination will reveal a retracted area of the tympanic membrane, usually of the pars flaccida but also occasionally of the pars tensa, that contains squamous debris or inflammatory tissue. Alternatively, there may be an obstructive polyp. Pictures of primary cholesteatomas are shown (picture 4 and picture 5 and picture 6). In secondary cholesteatomas, the tympanic membrane may be completely intact (after a perforation has healed, for example), but a white mass may be visible behind the tympanic membrane.

Gram stains and cultures, to assist in guiding therapy, are usually reserved for cases that fail standard topical therapy. Specimens for culture should be acquired through aspiration using a sterile otomicroscope, as specimens obtained by direct ear swabs are typically contaminated with flora from the outer ear canal.

If there is no response to medical therapy, persistent granulation tissue should be biopsied to rule out a neoplastic or granulomatous process [39].

Hearing loss is often reported, and formal audiometry should be considered in all patients who report hearing loss or present with ongoing otorrhea to establish the type and degree of hearing loss.

Accurate diagnosis of primary cholesteatoma mandates a careful cleaning of the canal and drum in order to fully inspect for retractions under microscopy. While standard otoscopy may be sufficient, cholesteatoma is better visualized with otomicroscopy or otoendoscopy.

Obstruction of the Eustachian tube orifice in the nasopharynx by a mass or cancer such as nasopharyngeal carcinoma or as a result of radiation treatment for nasopharyngeal malignancy is a rare cause of chronic serous otitis media. Fiberoptic nasopharyngoscopy should be performed to rule out nasopharyngeal pathology in patients with recurrent unilateral serous otitis media. There are limited data regarding the yield of nasopharyngoscopy in the workup of isolated otitis media with effusion, but it should be borne in mind that individuals from China, Southeast Asia, and Northern Africa are at increased risk for nasopharyngeal carcinoma [40]. (See "Epidemiology, etiology, and diagnosis of nasopharyngeal carcinoma", section on 'Geographic and ethnic distribution'.)

Imaging — For all patients with cholesteatoma, we obtain computed tomography (CT) of the temporal bone. These images can help to define the extent of disease, whether there is erosion, fistula formation, or intracranial or labyrinthine involvement [4,41,42]. Patients with extensive, active disease are often systemically ill and will have localizing signs of infection.

Magnetic resonance imaging (MRI) is more sensitive and should be ordered (without and with gadolinium) when intracranial complications (eg, direct extension or meningocele or encephalocele) are suspected. MRI provides excellent soft tissue detail but lacks the bony detail needed for operative planning and thus is complementary to CT [43]. In addition, MRI is useful for following possible disease recurrence [44].

DIFFERENTIAL DIAGNOSIS — The differential diagnosis for chronic suppurative otitis media includes external otitis, granulomatous disease (eg, granulomatosis with polyangiitis, histiocytosis X), mycobacterial infection, and malignancy such as nasopharyngeal carcinoma. Many of these conditions may present with mucopurulent otorrhea, visible inflammation or granulation tissue, and/or thickening of the ear canal skin. The presence of pain or failure to respond to medical therapy should lead to further evaluation with imaging, culture and/ or biopsy, to establish a definitive diagnosis. (See "External otitis: Pathogenesis, clinical features, and diagnosis" and "Granulomatosis with polyangiitis and microscopic polyangiitis: Clinical manifestations and diagnosis" and "Clinical manifestations, pathologic features, and diagnosis of Langerhans cell histiocytosis", section on 'Clinical manifestations' and "Epidemiology, etiology, and diagnosis of nasopharyngeal carcinoma".)

COMPLICATIONS

Mastoiditis — A spectrum of disease is associated with mastoiditis. Mastoid effusion is often seen on computed tomography (CT) scan in patients with both acute otitis media (AOM) and chronic suppurative otitis media (CSOM) and is not usually clinically significant. Symptomatic coalescent mastoiditis is a rare complication of both AOM and chronic otitis media but can be serious due to proximity of the mastoid to the posterior cranial fossa, lateral sinuses, facial nerve canal, semicircular canals, and the petrous tip of the temporal bone. Mastoiditis complicating CSOM can result in bony erosion and temporal lobe abscess or can cause septic thrombosis of the lateral sinus.

Acute mastoiditis occurs more commonly in children than adults, and its incidence has declined dramatically in the antibiotic era with routine use of antibiotics for the treatment of otitis media. It is a rare occurrence in adults but can complicate CSOM with or without cholesteatoma. One study that reviewed almost 3000 cases of CSOM in a nine-year period in Turkey reported 25 cases of mastoid abscess [45].

Clinical mastoiditis may present with fever, posterior ear pain and/or local erythema over the mastoid bone, edema of the pinna, or a posteriorly and downward displaced auricle. In coalescent mastoiditis, CT demonstrates characteristic loss of the trabecular bone [46].

CT scan should always be performed when mastoiditis is suspected. If there is a concern for an intracranial process (ie, sigmoid sinus thrombosis, intracranial abscess), then a magnetic resonance imaging (MRI) scan should also be considered. Patients with acute mastoiditis should be admitted to the hospital and intravenous (IV) antibiotics should be started.

Antibiotics for the treatment of mastoiditis presenting as a complication of chronic otitis should include coverage for S. aureus, Pseudomonas, and enteric gram-negative rods, as well as Streptococcus pneumoniae and Haemophilus influenza. If patients do not respond to conservative therapy with IV antibiotics, further intervention is warranted. This involves mastoidectomy for debridement of necrotic bone. Myringotomy is an adjunct to mastoidectomy for the treatment of acute mastoiditis. When cholesteatoma is present, a tympanomastoidectomy is performed to remove both the necrotic bone in the mastoid and cholesteatoma. (See 'Surgical treatment' below.)

Facial nerve palsy — CSOM with or without cholesteatoma can be complicated by facial nerve palsy. This can occur through involvement of the dehiscent facial nerve or through direct bony erosion [46,47]. The onset is usually gradual. In one case series of 70 patients with complicated CSOM, 14 percent of the patients had accompanying facial palsy [48]. Treatment of facial paralysis in the setting of CSOM, with or without cholesteatoma, requires surgical intervention [46].

Intracranial complications — Intracranial complications of CSOM are potentially life-threatening and require immediate intervention. They include suppurative thrombophlebitis of the lateral and/or cavernous sinuses, meningitis, and intracranial abscesses [45]. These complications are rare in the era of effective antibiotics, with one large review estimating an overall rate of 0.1 to 2.0 percent. In a retrospective chart review involving 33 patients over a 15-year period in Brazil, meningitis and intracranial abscess were the most common serious problems [49].

Signs of intracranial involvement are severe earache, seizures, fever, constant and persistent headache, nausea and vomiting, or focal neurological symptoms. Patients who present with these complications should be evaluated and treated promptly. Empiric intravenous therapy should be started to cover the typical pathogens including methicillin-resistant S. aureus and Pseudomonas. (See 'Systemic antibiotics' below.)

MEDICAL MANAGEMENT — The goals of the treatment of chronic suppurative otitis media (CSOM) are to stop otorrhea, heal the tympanic membrane, eradicate current infection, prevent complications, and prevent recurrence. The optimal treatment strategy remains to be determined but involves a combination of adherence to the principles of aural hygiene and the appropriate utilization of antibiotic therapy and surgical intervention involving the tympanic membrane, middle ear, and mastoid. Intranasal glucocorticoids, decongestants, and antihistamines are not indicated in the treatment of CSOM.

Antibiotics

Topical antibiotics — Topical antibiotics remain the first-line treatment for otorrhea in chronic otitis media [22,28,50,51]. However, in a 2020 Cochrane review, there was low-certainty evidence to support the efficacy of topical antibiotics [52]. In theory, topical antibiotic therapy may be more effective than systemic medications in resolving otorrhea due to the difficulty of systemic drug penetration through the devascularized mucosa of the middle ear and mastoid. Additionally, initial use of topical therapy may be preferable to systemic antibiotics because increased concentration of topical agents in the middle ear may decrease the rate of resistance as well as limit systemic absorption [22,28,53,54]. However, there are reports of increasing quinolone resistance in CSOM with the use of topical therapy [31].

While the literature for medical therapy for CSOM is not robust, there is some evidence for the efficacy of topical fluoroquinolones [52]. Due to their acceptable safety profile, topical fluoroquinolones are preferred to other agents [28,50,55-59] and are the only ototopical agents approved in the United States for use in an ear with a tympanic membrane perforation.

A systematic review of nine randomized trials (833 participants) found that trials were generally of poor methodologic quality with short follow-up but that topical quinolone antibiotics were better than systemic antibiotics at clearing discharge at two weeks (relative risk [RR] 3.21, 95% CI 1.88-5.49) [50]. The evidence was not clear comparing other topical antibiotics with systemic antibiotics.

In a systematic review of five randomized trials, there was not statistical difference found between quinolone and nonquinolone antibiotics; a positive trend toward quinolones was not seen after accounting for trial heterogeneity [60].

In a randomized trial of 155 adults with CSOM treated with topical ciprofloxacin (0.2 percent) compared with 138 patients treated with polymyxin B, neomycin, and hydrocortisone therapy, there was no significant difference in the rate of absence of otorrhea or culture negative drainage at 6 to 12 days [61].

Several studies suggest that fluoroquinolone drops may be superior to topical aminoglycoside agents, but data are limited by small sample sizes [21,50,58,62,63].

Topical quinolone antibiotics were significantly better than topical antiseptics at one to four weeks in seven randomized trials, while results were more mixed when comparing nonquinolone topical drops with antiseptics [60].

No benefit was seen for the addition of systemic antibiotics to topical therapy in a review of three randomized trials [50].

The standard quinolone therapy consists of ciprofloxacin or ofloxacin drops used twice daily for a two-week course, although up to four weeks may provide benefit in some cases without increasing complication rates [58,61,64]. Many sources recommend warming the otic solutions in the hands for a few minutes, as instillation of cold drops may cause dizziness. The patient should lie on their side with the affected ear up during and for several minutes after instillation. Some sources recommend pushing on the tragus several times to facilitate movement of the drops into the middle ear.

Due to the concern for ototoxicity with aminoglycoside containing agents, the 2004 American Academy of Otolaryngology-Head and Neck Surgery (AAO-HNS) consensus panel recommended that "when possible, topical antibiotic preparations free of potential ototoxicity are preferred over ototopical agents that have the potential for injury if the middle ear and mastoid are open" [55,56].

There is a lack of evidence to evaluate the benefit of the addition of a topical corticosteroid to topical antibiotic therapy, but the AAO-HNS consensus panel supported its consideration if granulation tissue is present [28].

Systemic antibiotics — Systemic antibiotics should be considered in patients at risk for complicated or invasive ear infections or in those who have received several courses of empiric topical therapy and are at higher risk for resistant organisms. In these circumstances, cultures should be obtained for microbiologic diagnosis and susceptibility data to guide selection of antimicrobial agents [22,26,28,31,50]. Empiric treatment while waiting for culture data should be based on the individual's previous cultures and prior antibiotic exposure, as well as local antibiotic resistance profiles.

Previous antibiotic exposure is a concern for potential failure of topical therapy with quinolones due to bacterial resistance to this class of drugs [31]. In one study of 231 outpatients, 88 had otorrhea that failed to resolve after two to three weeks of ciprofloxacin drops. Ciprofloxacin-resistant P. aeruginosa was isolated in all 88 patients. In this study, imipenem was the antimicrobial agent with the most reliable sensitivity [31].

CSOM secondary to S. aureus should also be guided by culture data with empiric therapy based on systemic symptoms and risk factors for antibiotic resistance [26].

Aural toilet — Although there are no randomized controlled trials evaluating its use, aural irrigation can be of benefit in treating COM when used as a supplement to antibiotic therapy [22,28,65]. The rationale is that aural irrigation serves the dual purpose of cleaning the ear of mucoid discharge, temporarily reducing the quantity of infected material from the middle ear and facilitating middle ear penetration of topical antibiotics [22,28,66]. A variety of irrigation solutions have been tried, including 1:1 dilutions of vinegar, saline, or povidone iodine with water, though some of these solutions can occasionally cause discomfort when used (ie, vinegar), while high concentrations of iodine have been shown to be ototoxic in animal models [67]. If self-irrigation is performed, it should be under the supervision and direction of an otolaryngologist who can monitor progress with serial otomicroscopy.

Irrigation solutions should be warmed to near body temperature to prevent vertigo. They can be instilled into the ear with a rubber bulb or a dropper and removed by suctioning using the same instrument, or the ear can be mopped dry after fluid instillation. Aural irrigation is typically performed two to three times daily until discharge disappears [22].

SURGICAL TREATMENT — Surgery is indicated for patients who develop complications of chronic otitis, to remove infected tissue in the middle ear or mastoid, and to repair ear damage that results in hearing loss. Surgical therapy is guided by the following principles:

Eradication of irreversible disease – Abnormal squamous epithelium (cholesteatoma), polypoid disease, and infected bone must be removed in order to create a dry, safe ear that is free of infection [11].

Preservation of anatomic contour – It is important to preserve the acoustic characteristics of the ear, when possible, though some patients with intractable disease will require a more aggressive approach that may impact conductive hearing. (See 'Mastoidectomy' below.)

Reconstruction of the sound transformer mechanism – Ossicular prostheses are available for reconstruction. The presence of healthy, nondiseased mucosa is critically important to achieve success [11,68]. (See 'Ossicular chain reconstruction' below.)

Restoration of tympanic and mastoid aeration – Aeration is required for both maintenance of a disease-free state and for maximal auditory function [69,70].

Long-term monitoring is essential to rule out recurrent disease in the middle ear or mastoid and to maximize cavity hygiene [71].

Cholesteatoma — Cholesteatoma removal is typically performed in conjunction with tympanoplasty and, if the lesion extends superiorly or posteriorly, mastoidectomy [72]. While concurrent treatment of allergic disease, chronic sinusitis, and adenotonsillar hypertrophy is helpful in conjunction with cholesteatoma removal, none of these measures will prevent the need for eventual surgical excision.

Surgical approaches to cholesteatoma are determined by three principal considerations:

The extent of the disease

The size and pattern of mastoid pneumatization

Eustachian tube dysfunction

The surgical techniques that are employed for cholesteatoma are classified as tympanoplasty with or without mastoidectomy and with or without ossicular reconstruction.

Tympanoplasty — In common practice, tympanoplasty refers to reconstructive surgery of the ear drum and ossicular chain. More formally, tympanoplasty is a procedure to eradicate disease in the middle ear and reconstruct the ossicular chain, which may or may not involve tympanic membrane grafting or mastoid surgery. The decision of whether to proceed with tympanoplasty rests upon a number of principles, including the desire to improve hearing and/or the need to close off the middle ear to avoid infection when water enters the canal.

Tympanoplasty is generally performed after infection has been eradicated for a minimum of three months.

Tympanoplasty is typically carried out through either an endaural incision for smaller cholesteatomas or a postauricular incision for larger ones [73].

The two main types of tympanoplasty are medial graft and lateral graft tympanoplasty. The medial graft technique is useful for most central perforations. Although a more surgically demanding procedure, the lateral graft technique affords better visualization of the anterior tympanic membrane and is useful for difficult marginal or large perforations.

Mastoidectomy — Mastoidectomy is a crucial component of surgical treatment when cholesteatoma extends beyond the middle ear space, when mastoid cells become chronically infected with buildup of granulation tissue that prevents proper aeration of the mastoid, or when there is a subperiosteal abscess over the surface of the mastoid cortex.

Mastoidectomy involves opening the mastoid air cells, with preservation of the tegmen tympani, sigmoid sinus, facial nerve, vestibular labyrinth, and ossicles. The goal of surgery is eradication of disease and improved aeration of the mastoid-middle ear system.

Intact canal wall versus canal wall down approaches differ in the exposure they offer, technical difficulty, prospects for postoperative hearing, and needs for postoperative care. In canal wall intact mastoidectomy, the air cells of the mastoid are removed while the posterior bony external auditory canal wall is kept intact. Intact canal wall procedures provide greater convenience of postoperative care and often promote a better level of conductive hearing. Maintaining the bony canal obviates the need to take precautions against exposure to water and typically provides a better fit for a hearing aid if one is needed postoperatively. However, canal wall intact mastoidectomy procedures can be technically more challenging and have a higher rate of recurrent cholesteatoma than canal wall down procedures [74].

In many cases, the extent of disease or the need for greater exposure in cholesteatoma removal mandates removal of the posterior bony external auditory canal (canal wall down mastoidectomy). This exteriorizes the entire mastoid cavity, promoting maximal mastoid aeration and allowing long-term monitoring for recurrence of cholesteatoma. Open-cavity techniques typically lead to a decrease in hearing [75]. There is a risk of recurrent discharge from bacterial or fungal overgrowth on retained debris within the open cavity. This underscores the need for postoperative vigilance over years and maintenance of a clean, safe cavity with regular cleaning by an otolaryngologist (picture 7). It is crucial that a wide meatoplasty be performed to enable inspection of the complete extent of the mastoid cavity.

No controlled prospective studies are available that compare intact canal versus canal wall down procedures. Outcomes reported from case series comparing the two techniques likely involve selection bias, as intact canal wall mastoidectomies tend to be reserved for more limited disease while more aggressive cholesteatomas will often be treated with canal wall down mastoidectomies. A 2014 systematic review of studies of cholesteatoma treated with mastoidectomy was unable to come to conclusions about best practices; individual studies reported different outcome measures and could not be compared [76].

Recurrent cholesteatomas are more common in intact canal wall procedures due to the formation of retraction pockets in the grafted drum into the middle ear, epitympanum, or facial recess [71,74]. An intact canal wall procedure for cholesteatoma usually requires re-exploration within one year to rule out residual or recurrent disease; residual or recurrent cholesteatoma is found in re-exploration of canal wall intact procedures in approximately one-third of cases [71,74]. Re-exploration enables the detection of lesions that are typically less than 5 mm in greatest diameter and enables complete removal with minimal dissection. Multiple recurrences of cholesteatomas are not uncommon. In some cases, a very active recurrent cholesteatoma found during the second stage procedure may warrant a more radical procedure in which the canal wall is removed.

Mastoid cavities are occasionally obliterated using homograft or allograft materials. Advantages of obliteration include less cold sensitivity, improved hearing, and decreased drainage [77]. However, such reconstructions may be susceptible to recurrent infection either due to primary infection of the graft material or blockage of adjacent air cell tracts and susceptible to recurrent disease if the primary cholesteatoma matrix was not completely eradicated [78].

Ossicular chain reconstruction — Cholesteatoma and chronic otitis media have the propensity to erode bone. In many cases, the small ossicular chain bones (malleus, incus, and stapes) are either partially or totally destroyed secondary to cholesteatoma and chronic infection. The long process of the incus, due to its relatively scant vascular supply, appears especially vulnerable to bony destruction [79].

When chronic ear disease results in significant hearing loss due to ossicular involvement, an important component of surgical therapy is reconstruction of the ossicular chain. Ossicular chain reconstruction employs a partial or total prosthesis to provide a medium for sound conduction where ossicular discontinuity is present.

Hearing rehabilitation surgery is frequently performed as part of a second-stage procedure after tympanomastoidectomy [79,80]. With improvements in prosthesis material selection and design, combined with a better understanding of indications for ossicular reconstruction, hearing rehabilitation is often successfully achieved in the treatment of chronic ear disorders. Closure of the air-bone gap to within 20 dB has been reported in 80 percent of patients [81].

Future directions — Balloon dilatation of the Eustachian tube is an evolving technology used for the treatment of Eustachian tube dysfunction. (See "Eustachian tube dysfunction", section on 'Surgical management if symptoms persist despite medical therapy'.)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Acute otitis media, otitis media with effusion, and external otitis".)

SUMMARY AND RECOMMENDATIONS

Chronic otitis media (COM) is a recurrent infection of the middle ear and/or mastoid air cell tract in the presence of a tympanic membrane perforation. Chronic suppurative otitis media (CSOM) is diagnosed when there is persistent purulent drainage through a perforated tympanic membrane. Cholesteatoma refers to a keratinized, desquamated epithelial collection in the middle ear or mastoid and may occur secondary to tympanic membrane perforation but also may occur as a primary lesion. (See 'Classification' above.)

Chronic ear disease occurs as a result of Eustachian tube dysfunction with negative middle ear pressure causing rupture of the tympanic membrane. Cholesteatomas may occur as primary lesions or may be secondary to tympanic membrane perforation or surgery. Cholesteatomas may result in erosion of the ossicles in the middle ear and consequent conductive hearing loss and rarely cause a sensorineural hearing loss due to erosion into the labyrinth. (See 'Pathogenesis' above.)

Pseudomonas aeruginosa and Staphylococcus aureus are the most commonly isolated aerobic bacteria in several large case series of CSOM. The prevalence of methicillin-resistant S. aureus varies by region. Less frequently, gram-negative rods or anaerobes are found and fungi are occasionally reported. Cholesteatoma can be associated with a polymicrobial infection, but the most commonly isolated pathogens remain S. aureus and P. aeruginosa. (See 'Microbiology' above.)

Although definitions vary, most otolaryngologists consider the diagnosis of CSOM when discharge persists through a tympanic membrane perforation for six weeks to three months. CSOM is often painless, though hearing loss is often reported. Cholesteatomas are often asymptomatic or may be associated with hearing loss, dizziness, and/or otorrhea. The presence of cholesteatoma should always be investigated in patients with CSOM and usually requires otomicroscopy. (See 'Clinical features and physical exam findings' above.)

The diagnosis of CSOM can often be made with direct otoscopy, but referral to an otolaryngologist for otomicroscopy with suctioning is indicated if the diagnosis is unclear or inadequate visualization precludes the ability to rule out a cholesteatoma. Cultures obtained by direct ear swabbing are not helpful due to contamination. Imaging with computed tomography (CT) is indicated if extracranial complications are suspected (patients with systemic illness); magnetic resonance imaging (MRI) is indicated if an intracranial complication is suspected and may be an adjunct to CT for evaluation of cholesteatoma for operative planning. (See 'Diagnosis' above.)

While a mastoid effusion and inflammation is commonly seen by CT in patients with acute otitis media (AOM) or COM, symptomatic mastoiditis is a rare and potentially serious complication. Clinical mastoiditis may present with fever, ear pain, edema, and a displaced auricle. Treatment includes aggressive antibiotics to include coverage for S. aureus and enteric gram-negative rods when associated with chronic otitis. Surgery is required if an abscess is present. (See 'Mastoiditis' above.)

Complications of CSOM include facial nerve palsy, suppurative thrombophlebitis of the lateral or cavernous sinuses, meningitis, and intracranial abscesses. (See 'Complications' above.)

We recommend initial treatment for CSOM with a topical quinolone antibiotic (Grade 1B). Due to the potential for ototoxicity in the presence of a ruptured tympanic membrane, we suggest not using topical aminoglycosides when alternative agents are available (Grade 2C). We recommend not using systemic antibiotics as an adjunct to topical drops for initial treatment (Grade 1B). However, systemic antibiotics are indicated for patients with complications of CSOM, for those who fail to respond to topical therapy after two to three weeks, and for those who have been previously treated with several courses of empiric topical therapy and are at risk for resistant organisms. Cultures should be obtained prior to initiating systemic antibiotics. (See 'Medical management' above.)

Although there are no randomized controlled trials evaluating its use, aural irrigation can be of benefit in treating COM when used as a supplement to antibiotic therapy.

Surgery is indicated for patients who develop complications of chronic otitis, to remove infected tissue in the middle ear or mastoid, and to repair ear damage that results in hearing loss. Surgery is also indicated for management of cholesteatoma, as spontaneous resolution is not expected. Surgery may include mastoidectomy, tympanoplasty, and/or ossicular reconstruction. (See 'Surgical treatment' above.)

ACKNOWLEDGMENT — The editorial staff at UpToDate would like to acknowledge Rachel Baden, MD, and Mary LaSalvia, MD, who contributed to an earlier version of this topic review.

  1. Chronic suppurative otitis media: Burden of illness and management options. World Health Organization, Geneva, Switzerland, 2004. http://www.who.int/pbd/deafness/activities/hearing_care/otitis_media.pdf (Accessed on January 13, 2011).
  2. Roland PS. Chronic suppurative otitis media: a clinical overview. Ear Nose Throat J 2002; 81:8.
  3. Goycoolea MV, Hueb MM, Ruah C. Otitis media: the pathogenesis approach. Definitions and terminology. Otolaryngol Clin North Am 1991; 24:757.
  4. Jung TT, Hanson JB. Classification of otitis media and surgical principles. Otolaryngol Clin North Am 1999; 32:369.
  5. Seibert JW, Danner CJ. Eustachian tube function and the middle ear. Otolaryngol Clin North Am 2006; 39:1221.
  6. Poe DS. Diagnosis and management of the patulous eustachian tube. Otol Neurotol 2007; 28:668.
  7. Danner CJ. Middle ear atelectasis: what causes it and how is it corrected? Otolaryngol Clin North Am 2006; 39:1211.
  8. Wiet RJ, Micco A, Bedoya O. Cholesteatoma. In: Therapy in Otolaryngology-Head & Neck Surgery, Gates GA (Ed), Mosby, Baltimore 1998.
  9. da Costa SS, Alves de Souza LC, Ribeiro de Toledo Piza M. The flexible endaural tympanoplasty: pathology-guided, pathogenesis-oriented surgery for the middle ear. Otolaryngol Clin North Am 1999; 32:413.
  10. Oktay MF, Cureoglu S, Schachern PA, et al. Tympanic membrane changes in central tympanic membrane perforations. Am J Otolaryngol 2005; 26:393.
  11. Glasscock M, Haynes D, Storper I, Bohrer P. Surgery for chronic ear disease. In: Clinical Otology, Hughes G, Pensak M (Eds), Thieme, New York 1997. p.215.
  12. Wullstein HL, Wullstein SR. Cholesteatoma. Etiology, nosology and tympanoplasty. ORL J Otorhinolaryngol Relat Spec 1980; 42:313.
  13. Persaud R, Hajioff D, Trinidade A, et al. Evidence-based review of aetiopathogenic theories of congenital and acquired cholesteatoma. J Laryngol Otol 2007; 121:1013.
  14. Semaan MT, Megerian CA. The pathophysiology of cholesteatoma. Otolaryngol Clin North Am 2006; 39:1143.
  15. Ramakrishnan Y, Kotecha A, Bowdler DA. A review of retraction pockets: past, present and future management. J Laryngol Otol 2007; 121:521.
  16. Sudhoff H, Tos M. Pathogenesis of sinus cholesteatoma. Eur Arch Otorhinolaryngol 2007; 264:1137.
  17. Kuo CL. Etiopathogenesis of acquired cholesteatoma: prominent theories and recent advances in biomolecular research. Laryngoscope 2015; 125:234.
  18. Vikram BK, Udayashankar SG, Naseeruddin K, et al. Complications in primary and secondary acquired cholesteatoma: a prospective comparative study of 62 ears. Am J Otolaryngol 2008; 29:1.
  19. WALSH TE, COVELL WP, OGURA JH. The effect of cholesteatosis on bone. Ann Otol Rhinol Laryngol 1951; 60:1100.
  20. Chole RA, Donald PJ. Petrous apicitis. Clinical considerations. Ann Otol Rhinol Laryngol 1983; 92:544.
  21. Verhoeff M, van der Veen EL, Rovers MM, et al. Chronic suppurative otitis media: a review. Int J Pediatr Otorhinolaryngol 2006; 70:1.
  22. Acuin, J. Chronic Suppurative otitis media. Burden of Illness and Management Options. World Health Organization. Geneva, Switzerland, 2004. who.int/pbd/deafness/activities/hearing_care/otitis_media.pdf (Accessed on January 05, 2011).
  23. Yeo SG, Park DC, Hong SM, et al. Bacteriology of chronic suppurative otitis media--a multicenter study. Acta Otolaryngol 2007; 127:1062.
  24. Vartiainen E, Vartiainen J. Effect of aerobic bacteriology on the clinical presentation and treatment results of chronic suppurative otitis media. J Laryngol Otol 1996; 110:315.
  25. Park DC, Lee SK, Cha CI, et al. Antimicrobial resistance of Staphylococcus from otorrhea in chronic suppurative otitis media and comparison with results of all isolated Staphylococci. Eur J Clin Microbiol Infect Dis 2008; 27:571.
  26. MacNeil SD, Westerberg BD, Romney MG. Toward the development of evidence-based guidelines for the management of methicillin-resistant Staphylococcus aureus otitis. J Otolaryngol Head Neck Surg 2009; 38:483.
  27. Ricciardiello F, Cavaliere M, Mesolella M, Iengo M. Notes on the microbiology of cholesteatoma: clinical findings and treatment. Acta Otorhinolaryngol Ital 2009; 29:197.
  28. Hannley MT, Denneny JC 3rd, Holzer SS. Use of ototopical antibiotics in treating 3 common ear diseases. Otolaryngol Head Neck Surg 2000; 122:934.
  29. Brook I, Burke P. The management of acute, serous and chronic otitis media: the role of anaerobic bacteria. J Hosp Infect 1992; 22 Suppl A:75.
  30. Brook I. The role of anaerobic bacteria in otitis media: microbiology, pathogenesis, and implications on therapy. Am J Otolaryngol 1987; 8:109.
  31. Jang CH, Park SY. Emergence of ciprofloxacin-resistant pseudomonas in chronic suppurative otitis media. Clin Otolaryngol Allied Sci 2004; 29:321.
  32. Lee SK, Lee MS, Jung SY, et al. Antimicrobial resistance of Pseudomonas aeruginosa from otorrhea of chronic suppurative otitis media patients. Otolaryngol Head Neck Surg 2010; 143:500.
  33. van Hasselt P, van Kregten E. Treatment of chronic suppurative otitis media with ofloxacin in hydroxypropyl methylcellulose ear drops: a clinical/bacteriological study in a rural area of Malawi. Int J Pediatr Otorhinolaryngol 2002; 63:49.
  34. Brar T, Mrig S, Passey JC, et al. Complicated coexisting pyogenic and tuberculous otitis media affecting the temporozygomatic, infratemporal, and parotid areas: report of a rare entity. Ear Nose Throat J 2013; 92:E10.
  35. Hwang GH, Jung JY, Yum G, Choi J. Tuberculous otitis media with facial paralysis combined with labyrinthitis. Korean J Audiol 2013; 17:27.
  36. Lundman L, Edvardsson H, Ängeby K. Otomastoiditis caused by non-tuberculous mycobacteria: report of 16 cases, 3 with infection intracranially. J Laryngol Otol 2015; 129:644.
  37. Maharjan M, Kafle P, Bista M, et al. Observation of hearing loss in patients with chronic suppurative otitis media tubotympanic type. Kathmandu Univ Med J (KUMJ) 2009; 7:397.
  38. Holt JJ. Cholesteatoma and otosclerosis: two slowly progressive causes of hearing loss treatable through corrective surgery. Clin Med Res 2003; 1:151.
  39. Lee, K. Essential Otolaryngology, McGraw-Hill, New York, NY 2003. Vol 8.
  40. Dang PT, Gubbels SP. Is nasopharyngoscopy necessary in adult-onset otitis media with effusion? Laryngoscope 2013; 123:2081.
  41. Roland PS, Meyerhoff WL. Open-cavity tympanomastoidectomy. Otolaryngol Clin North Am 1999; 32:525.
  42. Swartz JD. Imaging diagnosis of middle ear lesions. Curr Probl Diagn Radiol 2002; 31:4.
  43. Locketz GD, Li PM, Fischbein NJ, et al. Fusion of Computed Tomography and PROPELLER Diffusion-Weighted Magnetic Resonance Imaging for the Detection and Localization of Middle Ear Cholesteatoma. JAMA Otolaryngol Head Neck Surg 2016; 142:947.
  44. Dubrulle F, Souillard R, Chechin D, et al. Diffusion-weighted MR imaging sequence in the detection of postoperative recurrent cholesteatoma. Radiology 2006; 238:604.
  45. Osma U, Cureoglu S, Hosoglu S. The complications of chronic otitis media: report of 93 cases. J Laryngol Otol 2000; 114:97.
  46. Smith JA, Danner CJ. Complications of chronic otitis media and cholesteatoma. Otolaryngol Clin North Am 2006; 39:1237.
  47. Yetiser S, Tosun F, Kazkayasi M. Facial nerve paralysis due to chronic otitis media. Otol Neurotol 2002; 23:580.
  48. Dubey SP, Larawin V. Complications of chronic suppurative otitis media and their management. Laryngoscope 2007; 117:264.
  49. Penido Nde O, Borin A, Iha LC, et al. Intracranial complications of otitis media: 15 years of experience in 33 patients. Otolaryngol Head Neck Surg 2005; 132:37.
  50. Macfadyen CA, Acuin JM, Gamble C. Systemic antibiotics versus topical treatments for chronically discharging ears with underlying eardrum perforations. Cochrane Database Syst Rev 2006; :CD005608.
  51. Macfadyen CA, Acuin JM, Gamble C. Topical antibiotics without steroids for chronically discharging ears with underlying eardrum perforations. Cochrane Database Syst Rev 2005; :CD004618.
  52. Brennan-Jones CG, Head K, Chong LY, et al. Topical antibiotics for chronic suppurative otitis media. Cochrane Database Syst Rev 2020; 1:CD013051.
  53. Klein JO. Strategies for decreasing multidrug antibiotic resistance: role of ototopical agents for treatment of middle ear infections. Am J Manag Care 2002; 8:S345.
  54. Weber PC, Roland PS, Hannley M, et al. The development of antibiotic resistant organisms with the use of ototopical medications. Otolaryngol Head Neck Surg 2004; 130:S89.
  55. Roland PS, Stewart MG, Hannley M, et al. Consensus panel on role of potentially ototoxic antibiotics for topical middle ear use: Introduction, methodology, and recommendations. Otolaryngol Head Neck Surg 2004; 130:S51.
  56. Matz G, Rybak L, Roland PS, et al. Ototoxicity of ototopical antibiotic drops in humans. Otolaryngol Head Neck Surg 2004; 130:S79.
  57. Haynes DS, Rutka J, Hawke M, Roland PS. Ototoxicity of ototopical drops--an update. Otolaryngol Clin North Am 2007; 40:669.
  58. Tong MC, Woo JK, van Hasselt CA. A double-blind comparative study of ofloxacin otic drops versus neomycin-polymyxin B-hydrocortisone otic drops in the medical treatment of chronic suppurative otitis media. J Laryngol Otol 1996; 110:309.
  59. Deitmer T. Topical and systemic treatment for chronic suppurative otitis media. Ear Nose Throat J 2002; 81:16.
  60. Pick RM. Lasers in dentistry: soft tissue procedures. CDS Rev 1992; 85:20.
  61. Miró N. Controlled multicenter study on chronic suppurative otitis media treated with topical applications of ciprofloxacin 0.2% solution in single-dose containers or combination of polymyxin B, neomycin, and hydrocortisone suspension. Otolaryngol Head Neck Surg 2000; 123:617.
  62. Manolidis S, Friedman R, Hannley M, et al. Comparative efficacy of aminoglycoside versus fluoroquinolone topical antibiotic drops. Otolaryngol Head Neck Surg 2004; 130:S83.
  63. Agro AS, Garner ET, Wright JW 3rd, et al. Clinical trial of ototopical ofloxacin for treatment of chronic suppurative otitis media. Clin Ther 1998; 20:744.
  64. Suzuki K, Nishimura T, Baba S, et al. Topical ofloxacin for chronic suppurative otitis media and acute exacerbation of chronic otitis media: optimum duration of treatment. Otol Neurotol 2003; 24:447.
  65. Browning GG, Gatehouse S, Calder IT. Medical management of active chronic otitis media: a controlled study. J Laryngol Otol 1988; 102:491.
  66. Acuin J. Chronic suppurative otitis media. BMJ Clin Evid 2007; 2007.
  67. Ozkiriş M, Kapusuz Z, Saydam L. Ototoxicity of different concentrations povidone-iodine solution applied to the middle ear cavity of rats. Indian J Otolaryngol Head Neck Surg 2013; 65:168.
  68. Mehta RP, Rosowski JJ, Voss SE, et al. Determinants of hearing loss in perforations of the tympanic membrane. Otol Neurotol 2006; 27:136.
  69. Jackson C. The chronic draining ear. In: Current Therapy in Otolaryngology-Head & Neck Surgery, Gates GA (Ed), Mosby, Baltimore 1998.
  70. Takahashi H, Sato H, Nakamura H, et al. Correlation between middle-ear pressure-regulation functions and outcome of type-I tympanoplasty. Auris Nasus Larynx 2007; 34:173.
  71. Mishiro Y, Sakagami M, Kitahara T, et al. The investigation of the recurrence rate of cholesteatoma using Kaplan-Meier survival analysis. Otol Neurotol 2008; 29:803.
  72. Omran A, De Denato G, Piccirillo E, et al. Petrous bone cholesteatoma: management and outcomes. Laryngoscope 2006; 116:619.
  73. Glasscock ME 3rd, Johnson GD, Poe DS. Surgical management of cholesteatoma in an only hearing ear. Otolaryngol Head Neck Surg 1990; 102:246.
  74. Sheehy JL. Tympanoplasty: outer surface grafting technique. In: Otologic Surgery, Brackmann D, Shelton C, Arriaga M (Eds), WB Saunders, Philadelphia 1994. p.121.
  75. Stankovic MD. Audiologic results of surgery for cholesteatoma: short- and long-term follow-up of influential factors. Otol Neurotol 2008; 29:933.
  76. Mor N, Finkel DA, Hanson MB, Rosenfeld RM. Middle ear cholesteatoma treated with a mastoidectomy: a systematic review of the measures used. Otolaryngol Head Neck Surg 2014; 151:923.
  77. Dornhoffer JL, Smith J, Richter G, Boeckmann J. Impact on quality of life after mastoid obliteration. Laryngoscope 2008; 118:1427.
  78. Lee YH, Lee NJ, Kim JH, Song JJ. CT, MRI and gallium SPECT in the diagnosis and treatment of petrous apicitis presenting as multiple cranial neuropathies. Br J Radiol 2005; 78:948.
  79. Kemink J, Niparko J. Ossicular disorders in chronic otitis media. In: Current Therapy in Otolaryngology: Head & Neck Surgery, Gates GA (Ed), Mosby, Baltimore 1990.
  80. Kim HH, Battista RA, Kumar A, Wiet RJ. Should ossicular reconstruction be staged following tympanomastoidectomy. Laryngoscope 2006; 116:47.
  81. Roth JA, Pandit SR, Soma M, Kertesz TR. Ossicular chain reconstruction with a titanium prosthesis. J Laryngol Otol 2009; 123:1082.
Topic 15312 Version 39.0

References