Update in Otolaryngology I
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Chronic Otitis Media: Diagnosis and Treatment
Anthony F. jaJm, MD*
Chronic otitis media is an indolent inflammation of the middle ear cleft. Two distinct forms of chronic otitis media should be recognized by the clinician. Chronic suppurative otitis media (CSOM) is a recurrent or persistent bacterial infection of the ear. It is distinguished by hearing loss, mucopurulent otorrhea, and a chronic perforation of the tympanic membrane. Chronic otitis media with effusion (COME) is an unresolving inflammation of the middle ear cleft with no otorrhea. It presents with persistent hearing loss and a middle ear filled with thick mucus. The tympanic membrane is intact but markedly retracted. This condition may progress to chronic adhesive otitis media, with complete collapse of the tympanic membrane and atelectasis of the middle ear. Although the definitive treatment of chronic otitis media is best carried out bv the otologist, the initial treating physician has a key role in diagnosis, evalu~tion, and therapy. Before discussing chronic otitis media, the salient anatomic and physiologic features of the middle ear should be reviewed. These structures are diagrammatically shown in Figure l. The middle ear is an air-filled pocket that lies between the ear drum laterally and the inner ear medially. It is connected to the nasopharynx by the eustachian tube. The eustachian tube is closed at rest but opens frequently to equalize air pressure between the middle ear and the outside environment. The opening and closing occurs naturally with swallowing and yawning and can also be brought on by "popping the ears" (modified Valsalva maneuver) and other methods. The middle ear is continuous posteriorly with the mastoid. The part of the middle ear directly medial to the drum is the mesotympanum. The parts below and ahove this level are the hypotympanum and attic, respectively. As the attic continues posteriorly, it narrows to a small passage (aditus ad antrum), which widens again to become the antrum of the mastoid. The hypotympanum and attic cannot be normally seen with an otoscope unless there is a massive perforation of *Professor and Chief, Section of Otolaryngology-Head and I\'eck Surgery, UMDNJ-New Jersey Medical School, l\iewark, New Jersey
Medical Clinics of North America-Vo!' 75, No. 6, November 1991
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Figure 1. Diagram illustrating the clinical anatomy of the middle ear and mastoid. Note eustachian tube (ET), mesotympanum (MT), hypotympanum (HT), and attic (A). The aditus ad antrum connects the middle ear to the mastoid antrum (MA) posteriorly. The ossicles (0) and the course of the facial nerve (FN) are shown.
the drum. The attic is near Shrapnell's membrane (pars flaccida), the upper part of the ear drum, and, therefore, is critical to consider in retractions of the drum such as that seen with chronic otitis media. It is separated from the deep external canal by a thin bony partition (scutum). With attic retraction-type cholesteatoma, this scutum may be eroded as the cholesteatoma enlarges and extends medially. The middle ear is bridged by a chain of three tiny bones. These ossicles are the smallest bones in the body and consist of the hammer (malleus), anvil (incus), and stapes (stirrup). The malleus is partly incorporated into the drum membrane laterally, the stapes footplate occupies the oval window opening of the labyrinth, and the incus links the two. The ossicles are fragile, their blood supply delicate, and their mechanical support tenuous. They are easily damaged by chronic otitis but may also be accidentally dislocated by cleaning, manipulation, or lavage of the ear. The incus is most frequently damaged. The main trunk of the facial nerve criss-crosses the middle ear and mastoid extensively. It enters via the internal auditory canal and curves back at the geniculate ganglion to traverse horizontally along the medial wall of the middle ear, just above the oval window. It then takes a second turn at the mastoid antrum to travel vertically down in the partition between the middle ear and the mastoid. It exits behind the angle of the jaw, where it turns once again to enter the parotid gland and the facial muscles. In the ear, the facial nerve is mostly covered by a bony shell (the facial canal), but there are frequent dehiscences in this covering. At times, the nerve may be exposed, particularly in the region of the oval window. The facial canal may become pathologically eroded by cholesteatoma, such as that seen in chronic otitis media. Particular care must be taken in manipulating the middle ear to avoid damage to this nerve. Even in the best of hands, facial paralysis is the most common serious complication of surgery for chronic otitis media.
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The two types of chronic otitis media differ greatly in presentation, sequelae, and treatment. Their distinguishing features form the substance of this article. There are, however, several features common to both, a review of which follows. It should first be recognized that "chronic otitis media" refers to an inflammation of the entire tubotympanic cavity, from the pharyngeal end of the eustachian tube to the air cells in the mastoid tip. The tubotympanic cavity (or middle ear cleft) develops as an evagination of the embryonic pharynx. Its mucosal lining is topologically a single surface that is continuous with the mucosa of the throat. The mucosal changes that result in a chronic mucoid effusion in COME, or in a mucopurulent drainage in CSOM, therefore affect the entire epithelial surface lining the cavity. Even in the presence of a large perforation, most of this diseased mucosa is not visible with the otoscope. Treatment of chronic otitis media must nonetheless address the entire middle ear cleft. The basic problem underlying all forms of chronic otitis media is the dysfunctional eustachian tube. The eustachian tube normally opens several times a minute. It functions to ventilate the middle ear and to drain mucus and other debris into the pharynx. The tube may fail for various reasons, including a complete physical obstruction, neuromuscular failure to open, or a relative failure, such as when tubal mucosa is overwhelmed by thickened mucus. Whatever the cause (and often several coexist), eustachian tube failure is the single most important factor underlying most forms of middle ear disease. Tube failure can initiate middle ear inflammation, contribute to its persistence, and, in turn, be itself perpetuated by the chronic otitis that results. Effective treatment of both types of chronic otitis must therefore deal with the eustachian tube. Although the specific pathology differs between CSOM and COME, there are also some similarities in the pathologic presentation seen in all forms of chronic otitis media. The mucosa in both CSOM and COME may include increased numbers of goblet cells in an apparent attempt by the ear to produce more mucus to rid itself of the inflammation.! Mucosal metaplasia to a lining of lush tall columnar ciliated cells, in turn, seems to be an attempt to cope with the excess mucus produced. Although the inflammatory infiltrate in the submucosa differs in CSOM and COME, the submucosal layer is markedly thickened in both conditions. The initial edema is later replaced by compaction and fibrosis. 8 The subepithelial thickening and scarring constitute a barrier to the penetration of systemic antibiotics. Therapy must therefore take into account the difficulty of reaching adequate tissue concentrations with oral or parenteral agents. Devascularization is also common to both conditions. Persistent inflammation with resultant scarring decreases the blood supply. Frank infection may lead to thrombosis of smaller vessels. The long-standing negative pressure seen in COME may lead to decreased circulation in the middle ear. The common result in both CSOM and COME is resorption of ossicular parts with precarious circulation. 5 These typically are the handle of the malleus in CSOM and the long process of the incus in COME. Treatment of chronic otitis media must therefore deal not only with eliminating the cause of inflammation but also with repairing the damage produced over time.
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The most common serious complication of chronic otitis media is cholesteatoma. This is a skin-lined keratin cyst that invades the middle ear and that can grow and erode into structures adjacent to the temporal bone. 6 Cholesteatoma may arise as a complication of both CSOM and chronic mucoid otitis media. Although the mechanism of development differs, the end result may be similar. Treatment of both types of chronic otitis media must thus take into account not only the disease but also its potential complications. In the introductory paragraphs of this article we emphasized the features common to both forms of chronic otitis media. Although it is conceptually important to understand these similarities, CSOM and COME are, in fact, very different diseases. The rest of this article discusses separately the diagnostic features that distinguish them, as well as current approaches to the treatment of these conditions and their complications. CHRONIC SUPPURATIVE OTITIS MEDIA Diagnosis Chronic purulent infection of the middle ear usually begins in childhood. There is often a history of frequent childhood upper respiratory tract infections. 2 Recurrent acute otitis media may predispose to CSOM, although this is not seen in every case. CS OM is more frequent among patients who live in crowded conditions and who lack access to good medical care. In the United States, CSOM is often a disease of recent immigrants or inner city dwellers. The symptoms of CSOM are hearing loss and otorrhea. Pain is not a feature, although irritation of the ear canal may cause itching, discomfort, or even a secondary otitis externa. The hearing loss is primarily conductive and usually moderate, although it may be as much as 60 decibels when ossicular resorption is present. In some long-standing cases, there is also a degree of nerve deafness, which may be the result of toxins absorbed into the labyrinth via the round window. Because of the lack of pain and the intermittent nature of the otorrhea, patients often present months after the onset of CSOM. The initial evaluation of patients with CSOM should include a visual examination, bacterial culture, and radiographic examination. Visual examination with the otoscope is available to every internist but permits only a partial assessment of the ear. The ear with chronic otitis media with perforation is best examined with a microscope. This permits the clinician to distinguish a true perforation from a gossamer-thin drum segment that has collapsed. It also permits some manipulation, such as suctioning, which clears the area of debris. It must be stressed that manipulation through an otoscope is dangerous and is best left to the trained specialist with access to a microscope. The clinician has no depth perception with a monocular otoscope, and the potential for damage to the ossicles and facial nerve is significant. The visible features of CSOM are a nonhealing perforation of the ear
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drum, with intermittent or recurrent drainage. s The perforation may be pinpoint in size or may be subtotal, involving most of the tympanic membrane. The perforation may be central or marginal. Central perforations involve the pars tensa and are surrounded by a rim of drum remnant. Marginal perforations are peripheral and have the edge of the bony canal (annulus) as one of their margins. The perforation in CSOM is usually central. The rim of the perforation is thickened, and the remaining tympanic membrane is often damaged. It may be collapsed, thinned, or infiltrated with tympanosclerosis. The perforation in CSOM offers a window that permits direct examination of the middle ear. Although the visible area is only a small part of the entire cleft, the clinician can draw some inferences regarding the rest of the middle ear and mastoid. Some of the middle ear mucosa is usually visible through the perforation. Its appearance is highly variable. Some ears may exhibit a flat, thin, whitish lining representing squamous metaplasia and subepithelial tympanosclerosis. In other instances, there is a lush glairy mucosa matted with thick mucopus. Frank granulation tissue is uncommon in long-standing uncomplicated CSOM. Depending on the size and location of the perforation, the ossicles may also be visible. The umbo, representing the insertion of the tip of the malleus handle, is often resorbed in CSOM. The handle is shortened and pulled medially by scar contracture of the middle ear ligaments. The tip of the handle may actually be in contact with the promontory forming the medial wall. If the incudo-stapedial joint is visible through the perforation, it may also show resorption. The tip (lenticular process) of the incus at the joint may undergo fibrous degeneration or total resorption (Fig. 2). The drainage is usually mucopurulent, greenish, and fetid (Fig. 3). It arises from chronically infected and oversecreting middle ear mucosa. If there is granulation tissue in the middle ear, the discharge may be blood tinged, although this is uncommon. The drainage may be highly intermit-
Figure 2. Subtotal perforation. Chronic recurrent infection has destroyed most of the tympanic membrane. The handle of the malleus is touching the promontory. The membrane remnant lies directly on the head of the stapes posteriorly. The bony septations of the hypo- . tympanum are clearly visible. (Photograph courtesy of Michael Hawke, MD.)
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Figure 3. Chronic suppurative otitis media. Note the thickened tympanic membrane and the chronic central perforation with viscous mucopurulent otorrhea. (Photograph courtesy of Michael Hawke, MD.)
tent, with the ear often dry for months. It recurs typically with upper respiratory tract infections. Inadvertent soiling of the middle ear by water after swimming or bathing can also lead to otorrhea. Bacteriologic studies usually reveal a mixed infection of gram-negative and anaerobic organisms. Pseudomonas aeruginosa usually predominates. 12 Treatment based on this assumption can be started at the initial visit. Nonetheless, it is useful to obtain a culture of the ear canal before treatment. Some ears may resist treatment because of unexpected and unusual pathologic flora. In chronic cases, ears that have been treated with intermittent drops may harbor Pseudomonas strains that are resistant to the usual first-line medications. Radiologic evaluation is useful for two reasons. If extensive or complicated chronic otitis media is suspected, visualization of the mastoid and adjacent structures can be helpful. If surgical therapy is contemplated, the otologist can also use the anatomic information in planning the procedure. Of the various imaging modalities available, CT gives the most information in chronic otitis media. 10 Plane mastoid views (such as Stenvers and Townes) are inadequate for detailed examination. Routine head CT scans are not diagnostic for CSOM. The cuts are too wide (usually 5 mm) and are usually not carried down low enough to include all of the mastoid. A noncontrast CT scan in the axial plane should be ordered. Magnified views of the temporal bone are helpful, both of bone and soft tissue windows. The sections should be thin, no more than 2 mm in width. Overlapping 2mm cuts give even more information. Sagittal or coronal reconstructions can also be requested for better visualization of the attic or hypotympanum; usually this is not necessary. MRI studies do not give a clear picture of bony contours, although they may be useful in visualizing soft tissue structures. In the patient with suspected intracranial extension of an otogenic infection, MRI is the better modality. The usual CT findings in CSOM include a bony anatomy that is
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relatively intact. The mastoid process may be underdeveloped. There may be mucosal swelling in the middle ear and mastoid. Swelling of the mucosa covering the mastoid septae will blur the air/tissue contrast and may give the false impression of demineralization or bony resorption. CT cannot distinguish between loculated inspissated fluid, polypoid mucosa, or a soft tissue mass. Pockets of fluid collection may therefore be overinterpreted as a soft tissue mass or cholesteatoma. The diagnosis of cholesteatoma can only be made with certainty if an apparent soft tissue mass is also accompanied by definite bony resorption. Although early cholesteatomas will initially occupy the available space without bone resorption, these cannot be distinguished radiologically from the other soft tissue masses mentioned previously. A common misconception regarding CT scans should be clarified. In both CSOM and COME, radiologists commonly use the term mastoiditis. Radiologic mastoiditis refers to any inflammatory change in the mastoid area, whether fluid build-up, mucosal edema, or bony change. Because the middle ear and mastoid are parts of the same cavity, it stands to reason that radiologic changes in the middle ear will be mirrored in the mastoid. The clinician's historic concept of mastoiditis, an acute abscess of the mastoid with potentially lethal intracranial proclivities, is a rare and very different condition. We should not be misled by radiologists' use of this word. Its meaning and implications are very different. Treatment Treatment of CSOM involves two phases: the eradication of infection and the reconstruction of the damaged middle ear. Treatment of infection involves topical toilet, antibiotic therapy, and, at times, surgery. Reconstruction involves surgical repair of the middle ear and its conductive mechanism. The initial treatment of CSOM is medical. Although this is not always successful, it can at times obviate the need for surgery in the presence of active suppuration. Even if surgery is needed as part of initial treatment, the ear should be cleaned up as much as possible before operation to minimize the risk of bleeding, injury to middle ear structures, and postoperative reinfection. Medical treatment of CSOM involves topical debridement of the infected mucosal surfaces, followed by topical and systemic antibiotics. 7 The ear should initially be debrided as much as possible. This helps to visualize the anatomy and to prepare the surface for further treatment. The ear canal can be debrided safely by swabbing it with cotton-tipped applicators. Such cleaning should be done under direct vision only and never blindly. Great care must be taken not to enter the middle ear. If the middle ear is filled with infected discharge or tissue, the patient should be referred to an otologist. If the ear is only slightly infected and the mucosa only mildly irritated, drops can be used effectively. This is particularly true in an ear with a large perforation and, thus, ready access to the middle ear. However, there is no point in using ear drops in an ear in which the mucosa is awash with mucopus and the ear canal caked with infected debris. The use of drops is also less effective in an ear with profuse drainage but only a small perforation.
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If the mucosa is covered with discharge, it should be debrided. This is done most safely by an otologist, because too brisk an irrigation may result in ossicular damage, and use of a solution that is too cool or too warm may create a caloric stimulus and resultant vertigo. A variety of topical drops are available. The physician can choose between single drugs and compounds, solutions or suspensions, and otic and ophthalrnologic· preparations. The usual initial choice is an otic compound that includes several antibiotics and steroids in an acidified viscous medium. These drops usually contain polymyxin, neomycin, and other drugs that are systemically toxic but topically useful. Although this form of "shotgun therapy" is usually effective, there may be reasons for choosing another type of drop. When a large infected mucosal surface is exposed, a suspension may give more prolonged contact than a solution. If the discharge is predominantly purulent, the clinician may wish to avoid topical steroids and instead choose a pure antibiotic preparation. If culture shows organisms that have become resistant to topical antibiotics, acetate drops, such as Domboro solution or Vosol can be used. Dilute acetic acid is cidal to Pseudomonas Sp.9 These agents are also a good choice when the patient has a contact allergy to neomycin. 12 Ophthalmic drops are aqueous and buffered to a neutral pH. They are useful when a small perforation or a narrowed ear canal prevents adequate penetration of the more viscous otic drops. Children who find acidic ear drops irritating will often accept ophthalmic drops in the ear. The drops are instilled by retracting the pinna to open the ear canal. After the drops enter the ear canal, repeated pressure on the tragus creates a plunger effect that displaces the air and forces the liquid into the middle ear. The patient should keep the affected ear upright for 3 or 4 minutes and then allow the excess liquid to run out. Occlusion of the canal with cotton creates an anaerobic environment and prolongs the infection. The most common cause of the failure of topical drops is the prescription of an inadequate amount. Keeping in mind that the infected surface includes the entire middle ear and mastoid, it is recommended that the ear canal be filled with drops (approximately 10) and that the medication be forced into the middle ear by tragal pressure three times a day for at least 10 days. The patient will use several bottles of drops in the course of therapy. If this treatment fails, the ear can be cultured and specific antimicrobial therapy started. Otologists often use powder insufflation in the treatment of chronic otitis media. 13 Powders are useful when there is good access to the middle ear through the ear canal, such as with subtotal perforations or after mastoidectomy. Systemic antibiotics may be given orally or parenterally. Although the initial treatment of CSOM is topical, oral medications may be added, especially when cultures reveal an organism that is susceptible. Betalactamase resistant penicillin analogues are a good adjunct to topical drops. Ciprofloxacin is particularly useful, because it is the first oral antibiotic with consistent anti-Pseudomonas activity. To prevent the emergence of resistant strains, it should be given judiciously and for at least 10 days. Ciprofloxacin is expensive and cannot be given to children under the age of 17 years.
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Parenteral antibiotics should be considered in patients who have failed to respond to other measures. Patients with profuse and unrelenting otorrhea, those with threatening complications, or patients who cannot comply with other measures can be considered for intravenous therapy. Intravenous administration not only provides more consistent blood levels but permits the use of aminoglyeosides and other antibiotics that cannot be given by mouth. If intravenous therapy is started, it should be continued for 2 to 6 weeks. The decision to treat with intravenous drugs is usually made by the otologist after all other measures have failed. This therapy is carried out in consultation with an infectious disease specialist, and peak and trough levels are followed to avoid toxicity. Intravenous therapy may be given either in hospital or in the home, using an indwelling heparin lock. Surgical treatment of CSOM is performed for two reasons: the eradication of infection and the subsequent reconstruction of the middle ear. Although the description of these techniques 15 is beyond the scope of this article, a few general principles should be considered. Because the main reservoir of infection in CSOM is the mastoid, some form of mastoidectomv is usually part of the treatment when the infection is unremitting. This operation involves an incision over the mastoid process followed by the removal of the mastoid cortex and its air cells. Mastoidectomv removes a large portion of the infected and oversecreting mucosa. In thi~ way, it can reduce or even eliminate the otorrhea. By converting the dozens of tiny air compartments of the mastoid into a single diverticulum, recurrent infection is more easily visualized and treated. If the mucosa is completely removed and the mastoid bowl is opened into the ear canal, it can become lined by skin. Skin is more resistant to infection and can even become selfcleansing. Skin is either permitted to grow in from the ear canal or is placed surgically as pedicled or free grafts. In some instances, the surgeon may choose to obliterate the mastoid cavity with muscle or fat. This further reduces the surface at risk for recurrent infection. It is impossible to remove all of the diseased mucosal lining the tubotympanic cavity. For this reason, the surgeon can only hope to tip the balance in favor of healing; he or she cannot convert the infected ear to a sterile field by means of surgery. Reconstruetive surgery involves rebuilding the tympanic membrane and ossicular chain. This group of operations, collectively called tympanoplasty, can be carried out only when the infection has been treated adequately. Closing the middle ear by grafting the tympanic membrane can only succeed if the middle ear is clean and there is adequate eustachian tube function to permit membrane vibration. If eustachian tube function is compromised, reconstruction must include ventilating the middle ear, using a long-term vent tube. This enhances the take rate fo-r tympanic membrane grafts, because it prevents negative pressure in the middle ear with consequent graft loss. A variety of materials are used in tympanoplasty. These include fascia and perichondrium to repair the ear drum and homograft or synthetic ossicles to rebuild the conductive chain. The fascia is obtained from the temporalis muscle via a small postauricular incision, whereas perichondrium can be harvested from the tragus of the ear.
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The ossicular chain is rebuilt using either the patient's own tissues or synthetic devices. Partial or total ossicular replacement prostheses (PORPs and TORPs) are available in a variety of polymeric and ceramic materials. The newest of these prostheses is made of hydroxylapatite, a mineral normally found in bone. Hydroxylapatite prostheses are very biocompatible and do not exhibit the problems of infection and extrusion seen with the older plastic devices. Complete reconstruction of a scarred middle ear cannot always be carried out in one step and may have to be staged. When appropriate staging, ventilation, and ossicular prostheses are used, most middle ears can be reconstructed to achieve a significant improvement in hearing.
CHRONIC OTITIS MEDIA WITH EFFUSION The middle ear may be chronically inflamed without suppuration. COME usually begins with eustachian tube obstruction. In the abscence of other factors, a mechanical obstruction of the tube results in negative middle ear pressure followed by the transudation of thin tissue fluid. This condition, commonly seen following airplane flights, is serous otitis media. It is usually an acute or subacute condition. Chronic mucoid otitis media (Fig. 4) results when the effects of eustachian tube obstruction are compounded by an inflammation of the middle ear mucosa. The cause of this inflammation is not always clear. Allergy may have a role,2 as well as a subacute bacterial infection. 13 The presence of bacteria evokes an inflammatory response but does not proceed to suppuration. 4 For this reason, the tympanic membrane does not perforate, and no otorrhea is seen. The lining of the middle ear becomes hyperplastic and produces a thick mucous exudate. 5 Eustachian tube patency, which may have been marginally present initially, is compromised in the face of this large quantity of viscid mucus, and a functional obstruction may develop.
Figure 4. Chronic mucoid otitis media. The membrane is dark pink and injected. There is moderate retraction, most readily seen over the pars flaccida. (Photograph courtesy of Michael Hawke, MD.)
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It is important to realize that the hallmark of this condition is not negative pressure in the middle ear but the accumulation of excessive mucus. In fact, in the early stages, this exudate is often under positive pressure, and at myringotomy, it extrudes through the incision of its own accord. It is further important to consider that the mucus formed is potentially harmful to the middle ear. It is acidic and contains cellular debris, dead bacteria, as well as inflammatory by-products. Ifleft untreated, the exudate can organize by forming mucin and fibrin. As the material grows more concentrated, the middle ear space gradually collapses and becomes atelectatic. The tympanic membrane adheres to the promontory and the ossicles, the epithelial surfaces disintegrate, and fibrocystic degeneration results in an end-stage middle ear (Fig. 5). The only clinical symptom of COME is hearing loss. The degree of hearing loss may vary but is usually in the 25 to 45 decibel range. Otoscopic examination reveals an intact tympanic membrane. The membrane appears thickened and opaque. Its color may be pink or amber but is always different from its normal greyish pink translucent appearance. If the drum has begun to retract, this is most easily seen over the pars flaccida (Shrapnell's membrane). Later, the main portion of the drum (pars tensa) also begins to collapse. The handle of the malleus appears chalky white in contrast to the darker drum. Its short process and, later, the handle stick out in contrast, similar to a tentpole as a tent is collapsed. As the malleus is pulled medially at the umbo, its handle appears to be foreshortened. As the retraction continues, the drum may drape over the incus and the head of the stapes. These dramatic changes are absent in early COME. The altered color and texture of the membrane are the most consistent findings. On pneumatic otoscopy, the drum does not move. Tuning fork tests confirm a conductive hearing loss in the ear. It is important to realize that COME is a chronic process, with the
Figure 5. Severe atelectasis of the middle ear. The tympanic membrane is collapsed. The malleus, incus, and head of stapes are clearly seen. Note the partial resorption of the lenticular process of the incus. The small residual middle ear space near the eustachian' tube (below) shows fluid and air bubbles. (Photograph courtesy of Michael Hawke, MD.)
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entire cavity of the middle ear and mastoid filled by sticky mucus. Air bubbles or an air/fluid meniscus are never seen in this condition. This finding is seen in resolving serous otitis media and indicates the return of eustachian tube function. The diagnosis of COME necessitates that the clinician maintain a degree of suspicion. Chronic hearing loss, especially when it is gradual in onset or unilateral, is often ignored by the patient for a period of time. Once diagnosed, however, the condition should be treated promptly to minimize permanent damage to the ear. The issue in COME is not merely the accumulation of fluid in the middle ear. If the fluid, which is acidic and may be noxious to the structures of the middle ear, is untreated, it may lead to permanent changes. These include scarring, loss of ossicular tissue, and a complete and irreversible obliteration of the middle ear space. 5 Treatment Chronic mucoid otitis media requires drainage. This procedure, myringotomy, involves a small incision in the tympanic membrane. A ventilation tube is often inserted at the same time to maintain the patency of the incision. A limited trial of antibiotics may be given, particularly when there is a past history of recurrent otitis media with resolution. Antihistamines are usually not effective, because they dry the mucosal surfaces and further impair the mucociliary clearing mechanism. Decongestants, oral or topical, may be tried. The role of inhalant and food allergies in COME is controversial. Nonetheless, in children with chronic mucoid effusion, an allergic history should be sought and medically addressed. If there is a history of allergy and in the absence of infection, oral or nasal steroids may be effective early in the disease process. l l The effect of drainage in COME is two-fold. It relieves the abnormal pressure within the middle ear by opening the tympanic membrane and evacuates the mucus that has accumulated. It also permits the marginally functional eustachian tube to recover and function as a natural vent and drain. The effect is analogous to a juice can. One hole does not permit the juice to pour, but a second opening permits a free flow. Different methods of ventilation can be used. In chronic mucoid otitis media, the surgeon usually selects a tube that remains in place for a longer time. When fluid accumulates in the middle ear, the clinician should always weigh the possibility of an obstructing mass in the nasopharynx. Enlarged adenoids are often found in conjunction with COME in children, and adenoidectomy may facilitate management of the ear.2 In adults, nasopharyngeal carcinoma usually causes a serous, not mucoid, effusion, which is classically unilateral. Nasal and sinus problems often have a role in eustachian tube insufficiency. A posterior nasal septal deviation may cause functional obstruction near the pharyngeal opening of the eustachian tube. Decreased air flow may result in an inspissation of mucus posteriorly. This is experienced by the patient as a persistent postnasal drip and may make the ipsilateral eustachian tube opening prone to obstruction. Frank obstruction of the nasal passages by nasal polyps or enlarged allergic turbinates also interferes with aeration and proper mucus flow around the eustachian tube orifice. Mucus drainage from the sinuses is normally carried posteriorly in two
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streams that surround the eustachian tube cushion. Increased or infected drainage seen with chronic sinusitis may result in eustachian tube obstruction. CHOLESTEATOMA
When keratinizing epithelium lodges within the middle ear, its continued growth and desquamation leads to the build up of keratin. A keratincontaining cyst, called a cholesteatoma, develops.6 Over time, the keratin flakes continue to accumulate, and the cholesteatoma enlarges. Due to a combination of pressure and enzymatic action, the enlarging cholesteatoma destroys adjacent bony structures. An untreated cholesteatoma may thus destroy the ossicles and, eventually, the bony labyrinth and facial nerve canal. Over time, the cholesteatoma will outgrow the boundaries of the middle ear and mastoid and invade the intracranial cavity. Cholesteatomas are usually accompanied by infection. There are two reasons for this. Either the skin ingrowth is the result of an attempted healing of a granulating surface in the middle ear or the moist keratin debris becomes colonized and serves as a nidus for pathogenic bacteria. Keratin is perceived by the body as a foreign protein, and as keratinproducing epithelium undermines middle ear mucosa, the inflammation is exacerbated. Cholesteatomas may develop with both forms of chronic otitis media. In CSOM, the inflamed middle ear lining seems to invite the ingrowth of squamous epithelium from the deep external ear canal (Fig. 6). This occurs classically by way of a marginal perforation. With more central perforations, the remaining rim of tympanic membrane acts as a mechanical barrier that hinders the ingrowth of skin. In COME, the long-standing and extreme collapse of the ear drum
Figure 6. Cholesteatoma associated with CSOM. There is a subtotal perforation of the membrane. Cholesteatoma is invading the middle ear. Note the white ' keratin debris enveloping the malleus. (Photograph courtesy of Michael Hawke, MD.)
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produces segmental pockets of retraction. As these pockets deepen, it becomes more difficult for keratin to clear the neck of the invagination. An accumulation of keratin develops (Fig. 7). As the keratin mass enlarges, the fundus of the pocket deepens and broadens, and its neck grows more attenuated. 14 The bolus of keratin is hygroscopic, and moisture in the ear canal makes the retraction cholesteatoma swell. As the keratin absorbs moisture, it becomes macerated and forms a good bacterial nutrient. 3 Retraction cholesteatomas develop most commonly in Shrapnell's membrane (attic retraction) or in the posterior pars tensa (mesotympanic retraction). It is important for the clinician to identify cholesteatomas promptly, because this condition usually requires surgical treatment. Early cholesteatomas may be mistaken for ear wax or debris, and even in the presence of otorrhea the diagnosis may be missed. This is unfortunate, because expanding cholesteatomas may damage the ossicular chain, facial nerve, and even the labyrinth with resultant facial paralysis, hearing loss, and vertigo. The earlier a cholesteatoma is diagnosed and treated, the less likely these complications will ensue. Otoscopic examination is usually diagnostic. In CSOM, white debris may be seen in the middle ear. Because cholesteatomas in CSOM are usually infected, the debris is partially covered by mucopus. A fringe of granulation tissue represents the foreign body reaction evinced by the keratin. In COME, a deep attic retraction pocket may be filled by keratin. A small attic perforation, particularly if it is discharging, may represent the neck of a long and deep attic retraction cholesteatoma. A granulation tissue polyp may appear to guard the entrance to an attic retraction cholesteatoma. Patients with cholesteatoma often complain of a discharge that is particularly fetid. It may be blood tinged due to friable granulations. In complicated cholesteatomas, the patient may complain of dizziness, particularly when pressing on the ear. This is the result of a labyrinthine fistula
Figure 7. Cholesteatoma associated with COME. The tympanic membrane is thickened, dark, and retracted, with a mucoid middle ear effusion. Shrapnel!' s membrane has invaginated into the attic, forming an attic retraction cholesteatoma. (Photograph courtesy of Michael Hawke, MD).
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due to bony erosion. Long-neglected cholesteatomas can lead to facial paralysis, brain abscess, or sigmoid sinus thrombosis. These conditions are fortunately rare but emphasize the fact that chronic otitis media, whether suppurating or mucoid, is not always an innocuous disease. Both forms of chronic otitis media require accurate diagnosis and appropriate treatment. CONCLUSION
The primary care physician should recognize two forms of chronic otitis media. Chronic suppurative otitis media presents with otorrhea, hearing loss, and a perforated tympanic membrane. Chronic otitis media with effusion causes hearing loss only and is associated with a collapsed intact ear drum. The initial evaluation of both conditions rests with the primary clinician. Definitive treatment requires surgery and is important to avoid permanent hearing loss and possible cholesteatoma formation. REFERENCES 1. Bernstein J: Middle ear mucosa: Histological, histochemical, immunochemical and immunological aspects. In Jahn AF, Santos-Sacchi J (eds): Physiology of the Ear. New York, Raven Press, 1988, pp 59-80 2. Bluestone CD: Management and therapy of otitis media. In Alberti PW, Ruben RJ (eds): Otologic Medicine and Surgery. New York, Churchill Livingstone, 1988, pp 1173-1201 3. Brook I: Aerobic and anaerobic bacteriology of cholesteatoma. Laryngoscope 91:250, 1981 4. Brook I, Finegold SM: Bacteriology of chronic otitis media. JAMA 241:487-488, 1979 5. Hawke M, Jahn AF: Diseases of the ear-clinical and pathologic aspects. New York, Cower Medical Publishers (Lea & Febiger), 1987 6. Jahn AF: Cholesteatoma: What is it, how did it get there, and how do we get rid of it? Otolaryngol Clin North Am 22:847-857, 1989 7. Jahn AF, Abramson M: Medical management of chronic otitis media. Otolaryngol Clin North Am 17:673-677, 1984 8. Jahn AF, Farkashidy J: Newer perspectives on the pathology of chronic otitis media. Can J Otolaryngol 9: 131-142, 1980 9. Jones EH: External Otitis: Diagnosis and Treatment. Springfield, Ill, Charles C Thomas, 1965 10. Liu DCP, Bergeron RT: Contemporary radiologic imaging in the evaluation of middle ear-attic-antral complex cholesteatomas. Otolaryngol Clin North Am 22:897-909, 1989 11. Macknin J, Jones R: Oral dexamethasone for treatment of persistent middle ear effusion. Pediatrics 75:329, 1985 12. Mawson S, Ludman H: Diseases of the Ear, ed 4. London, Edward Arnold Publishers, 1979 13. Riding KH, Bluestone CD, Michaels RH, et al: Microbiology of recurrent and chronic otitis media with effusion. J Pediatrics 93:739-743, 1978 14. Sade J: Pathogenesis of attic cholesteatomas. J R Soc Med 71:716-732, 1978 15. Tos M: Tympanomastoiditis: Management and treatment. In Alberti PW, Ruben RJ (eds): Otologic Medicine and Surgery. New York, Churchill Livingstone, pp. 1203-1239, 1988
Address reprint requests to Anthony F. Jahn, MD 556 Eagle Rock Avenue Roseland, NJ 07068
0025--7125/91 $0.00 + .20
Chronic Otitis Media: Diagnosis and Treatment
Anthony F. jaJm, MD*
Chronic otitis media is an indolent inflammation of the middle ear cleft. Two distinct forms of chronic otitis media should be recognized by the clinician. Chronic suppurative otitis media (CSOM) is a recurrent or persistent bacterial infection of the ear. It is distinguished by hearing loss, mucopurulent otorrhea, and a chronic perforation of the tympanic membrane. Chronic otitis media with effusion (COME) is an unresolving inflammation of the middle ear cleft with no otorrhea. It presents with persistent hearing loss and a middle ear filled with thick mucus. The tympanic membrane is intact but markedly retracted. This condition may progress to chronic adhesive otitis media, with complete collapse of the tympanic membrane and atelectasis of the middle ear. Although the definitive treatment of chronic otitis media is best carried out bv the otologist, the initial treating physician has a key role in diagnosis, evalu~tion, and therapy. Before discussing chronic otitis media, the salient anatomic and physiologic features of the middle ear should be reviewed. These structures are diagrammatically shown in Figure l. The middle ear is an air-filled pocket that lies between the ear drum laterally and the inner ear medially. It is connected to the nasopharynx by the eustachian tube. The eustachian tube is closed at rest but opens frequently to equalize air pressure between the middle ear and the outside environment. The opening and closing occurs naturally with swallowing and yawning and can also be brought on by "popping the ears" (modified Valsalva maneuver) and other methods. The middle ear is continuous posteriorly with the mastoid. The part of the middle ear directly medial to the drum is the mesotympanum. The parts below and ahove this level are the hypotympanum and attic, respectively. As the attic continues posteriorly, it narrows to a small passage (aditus ad antrum), which widens again to become the antrum of the mastoid. The hypotympanum and attic cannot be normally seen with an otoscope unless there is a massive perforation of *Professor and Chief, Section of Otolaryngology-Head and I\'eck Surgery, UMDNJ-New Jersey Medical School, l\iewark, New Jersey
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Figure 1. Diagram illustrating the clinical anatomy of the middle ear and mastoid. Note eustachian tube (ET), mesotympanum (MT), hypotympanum (HT), and attic (A). The aditus ad antrum connects the middle ear to the mastoid antrum (MA) posteriorly. The ossicles (0) and the course of the facial nerve (FN) are shown.
the drum. The attic is near Shrapnell's membrane (pars flaccida), the upper part of the ear drum, and, therefore, is critical to consider in retractions of the drum such as that seen with chronic otitis media. It is separated from the deep external canal by a thin bony partition (scutum). With attic retraction-type cholesteatoma, this scutum may be eroded as the cholesteatoma enlarges and extends medially. The middle ear is bridged by a chain of three tiny bones. These ossicles are the smallest bones in the body and consist of the hammer (malleus), anvil (incus), and stapes (stirrup). The malleus is partly incorporated into the drum membrane laterally, the stapes footplate occupies the oval window opening of the labyrinth, and the incus links the two. The ossicles are fragile, their blood supply delicate, and their mechanical support tenuous. They are easily damaged by chronic otitis but may also be accidentally dislocated by cleaning, manipulation, or lavage of the ear. The incus is most frequently damaged. The main trunk of the facial nerve criss-crosses the middle ear and mastoid extensively. It enters via the internal auditory canal and curves back at the geniculate ganglion to traverse horizontally along the medial wall of the middle ear, just above the oval window. It then takes a second turn at the mastoid antrum to travel vertically down in the partition between the middle ear and the mastoid. It exits behind the angle of the jaw, where it turns once again to enter the parotid gland and the facial muscles. In the ear, the facial nerve is mostly covered by a bony shell (the facial canal), but there are frequent dehiscences in this covering. At times, the nerve may be exposed, particularly in the region of the oval window. The facial canal may become pathologically eroded by cholesteatoma, such as that seen in chronic otitis media. Particular care must be taken in manipulating the middle ear to avoid damage to this nerve. Even in the best of hands, facial paralysis is the most common serious complication of surgery for chronic otitis media.
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The two types of chronic otitis media differ greatly in presentation, sequelae, and treatment. Their distinguishing features form the substance of this article. There are, however, several features common to both, a review of which follows. It should first be recognized that "chronic otitis media" refers to an inflammation of the entire tubotympanic cavity, from the pharyngeal end of the eustachian tube to the air cells in the mastoid tip. The tubotympanic cavity (or middle ear cleft) develops as an evagination of the embryonic pharynx. Its mucosal lining is topologically a single surface that is continuous with the mucosa of the throat. The mucosal changes that result in a chronic mucoid effusion in COME, or in a mucopurulent drainage in CSOM, therefore affect the entire epithelial surface lining the cavity. Even in the presence of a large perforation, most of this diseased mucosa is not visible with the otoscope. Treatment of chronic otitis media must nonetheless address the entire middle ear cleft. The basic problem underlying all forms of chronic otitis media is the dysfunctional eustachian tube. The eustachian tube normally opens several times a minute. It functions to ventilate the middle ear and to drain mucus and other debris into the pharynx. The tube may fail for various reasons, including a complete physical obstruction, neuromuscular failure to open, or a relative failure, such as when tubal mucosa is overwhelmed by thickened mucus. Whatever the cause (and often several coexist), eustachian tube failure is the single most important factor underlying most forms of middle ear disease. Tube failure can initiate middle ear inflammation, contribute to its persistence, and, in turn, be itself perpetuated by the chronic otitis that results. Effective treatment of both types of chronic otitis must therefore deal with the eustachian tube. Although the specific pathology differs between CSOM and COME, there are also some similarities in the pathologic presentation seen in all forms of chronic otitis media. The mucosa in both CSOM and COME may include increased numbers of goblet cells in an apparent attempt by the ear to produce more mucus to rid itself of the inflammation.! Mucosal metaplasia to a lining of lush tall columnar ciliated cells, in turn, seems to be an attempt to cope with the excess mucus produced. Although the inflammatory infiltrate in the submucosa differs in CSOM and COME, the submucosal layer is markedly thickened in both conditions. The initial edema is later replaced by compaction and fibrosis. 8 The subepithelial thickening and scarring constitute a barrier to the penetration of systemic antibiotics. Therapy must therefore take into account the difficulty of reaching adequate tissue concentrations with oral or parenteral agents. Devascularization is also common to both conditions. Persistent inflammation with resultant scarring decreases the blood supply. Frank infection may lead to thrombosis of smaller vessels. The long-standing negative pressure seen in COME may lead to decreased circulation in the middle ear. The common result in both CSOM and COME is resorption of ossicular parts with precarious circulation. 5 These typically are the handle of the malleus in CSOM and the long process of the incus in COME. Treatment of chronic otitis media must therefore deal not only with eliminating the cause of inflammation but also with repairing the damage produced over time.
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The most common serious complication of chronic otitis media is cholesteatoma. This is a skin-lined keratin cyst that invades the middle ear and that can grow and erode into structures adjacent to the temporal bone. 6 Cholesteatoma may arise as a complication of both CSOM and chronic mucoid otitis media. Although the mechanism of development differs, the end result may be similar. Treatment of both types of chronic otitis media must thus take into account not only the disease but also its potential complications. In the introductory paragraphs of this article we emphasized the features common to both forms of chronic otitis media. Although it is conceptually important to understand these similarities, CSOM and COME are, in fact, very different diseases. The rest of this article discusses separately the diagnostic features that distinguish them, as well as current approaches to the treatment of these conditions and their complications. CHRONIC SUPPURATIVE OTITIS MEDIA Diagnosis Chronic purulent infection of the middle ear usually begins in childhood. There is often a history of frequent childhood upper respiratory tract infections. 2 Recurrent acute otitis media may predispose to CSOM, although this is not seen in every case. CS OM is more frequent among patients who live in crowded conditions and who lack access to good medical care. In the United States, CSOM is often a disease of recent immigrants or inner city dwellers. The symptoms of CSOM are hearing loss and otorrhea. Pain is not a feature, although irritation of the ear canal may cause itching, discomfort, or even a secondary otitis externa. The hearing loss is primarily conductive and usually moderate, although it may be as much as 60 decibels when ossicular resorption is present. In some long-standing cases, there is also a degree of nerve deafness, which may be the result of toxins absorbed into the labyrinth via the round window. Because of the lack of pain and the intermittent nature of the otorrhea, patients often present months after the onset of CSOM. The initial evaluation of patients with CSOM should include a visual examination, bacterial culture, and radiographic examination. Visual examination with the otoscope is available to every internist but permits only a partial assessment of the ear. The ear with chronic otitis media with perforation is best examined with a microscope. This permits the clinician to distinguish a true perforation from a gossamer-thin drum segment that has collapsed. It also permits some manipulation, such as suctioning, which clears the area of debris. It must be stressed that manipulation through an otoscope is dangerous and is best left to the trained specialist with access to a microscope. The clinician has no depth perception with a monocular otoscope, and the potential for damage to the ossicles and facial nerve is significant. The visible features of CSOM are a nonhealing perforation of the ear
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drum, with intermittent or recurrent drainage. s The perforation may be pinpoint in size or may be subtotal, involving most of the tympanic membrane. The perforation may be central or marginal. Central perforations involve the pars tensa and are surrounded by a rim of drum remnant. Marginal perforations are peripheral and have the edge of the bony canal (annulus) as one of their margins. The perforation in CSOM is usually central. The rim of the perforation is thickened, and the remaining tympanic membrane is often damaged. It may be collapsed, thinned, or infiltrated with tympanosclerosis. The perforation in CSOM offers a window that permits direct examination of the middle ear. Although the visible area is only a small part of the entire cleft, the clinician can draw some inferences regarding the rest of the middle ear and mastoid. Some of the middle ear mucosa is usually visible through the perforation. Its appearance is highly variable. Some ears may exhibit a flat, thin, whitish lining representing squamous metaplasia and subepithelial tympanosclerosis. In other instances, there is a lush glairy mucosa matted with thick mucopus. Frank granulation tissue is uncommon in long-standing uncomplicated CSOM. Depending on the size and location of the perforation, the ossicles may also be visible. The umbo, representing the insertion of the tip of the malleus handle, is often resorbed in CSOM. The handle is shortened and pulled medially by scar contracture of the middle ear ligaments. The tip of the handle may actually be in contact with the promontory forming the medial wall. If the incudo-stapedial joint is visible through the perforation, it may also show resorption. The tip (lenticular process) of the incus at the joint may undergo fibrous degeneration or total resorption (Fig. 2). The drainage is usually mucopurulent, greenish, and fetid (Fig. 3). It arises from chronically infected and oversecreting middle ear mucosa. If there is granulation tissue in the middle ear, the discharge may be blood tinged, although this is uncommon. The drainage may be highly intermit-
Figure 2. Subtotal perforation. Chronic recurrent infection has destroyed most of the tympanic membrane. The handle of the malleus is touching the promontory. The membrane remnant lies directly on the head of the stapes posteriorly. The bony septations of the hypo- . tympanum are clearly visible. (Photograph courtesy of Michael Hawke, MD.)
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Figure 3. Chronic suppurative otitis media. Note the thickened tympanic membrane and the chronic central perforation with viscous mucopurulent otorrhea. (Photograph courtesy of Michael Hawke, MD.)
tent, with the ear often dry for months. It recurs typically with upper respiratory tract infections. Inadvertent soiling of the middle ear by water after swimming or bathing can also lead to otorrhea. Bacteriologic studies usually reveal a mixed infection of gram-negative and anaerobic organisms. Pseudomonas aeruginosa usually predominates. 12 Treatment based on this assumption can be started at the initial visit. Nonetheless, it is useful to obtain a culture of the ear canal before treatment. Some ears may resist treatment because of unexpected and unusual pathologic flora. In chronic cases, ears that have been treated with intermittent drops may harbor Pseudomonas strains that are resistant to the usual first-line medications. Radiologic evaluation is useful for two reasons. If extensive or complicated chronic otitis media is suspected, visualization of the mastoid and adjacent structures can be helpful. If surgical therapy is contemplated, the otologist can also use the anatomic information in planning the procedure. Of the various imaging modalities available, CT gives the most information in chronic otitis media. 10 Plane mastoid views (such as Stenvers and Townes) are inadequate for detailed examination. Routine head CT scans are not diagnostic for CSOM. The cuts are too wide (usually 5 mm) and are usually not carried down low enough to include all of the mastoid. A noncontrast CT scan in the axial plane should be ordered. Magnified views of the temporal bone are helpful, both of bone and soft tissue windows. The sections should be thin, no more than 2 mm in width. Overlapping 2mm cuts give even more information. Sagittal or coronal reconstructions can also be requested for better visualization of the attic or hypotympanum; usually this is not necessary. MRI studies do not give a clear picture of bony contours, although they may be useful in visualizing soft tissue structures. In the patient with suspected intracranial extension of an otogenic infection, MRI is the better modality. The usual CT findings in CSOM include a bony anatomy that is
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relatively intact. The mastoid process may be underdeveloped. There may be mucosal swelling in the middle ear and mastoid. Swelling of the mucosa covering the mastoid septae will blur the air/tissue contrast and may give the false impression of demineralization or bony resorption. CT cannot distinguish between loculated inspissated fluid, polypoid mucosa, or a soft tissue mass. Pockets of fluid collection may therefore be overinterpreted as a soft tissue mass or cholesteatoma. The diagnosis of cholesteatoma can only be made with certainty if an apparent soft tissue mass is also accompanied by definite bony resorption. Although early cholesteatomas will initially occupy the available space without bone resorption, these cannot be distinguished radiologically from the other soft tissue masses mentioned previously. A common misconception regarding CT scans should be clarified. In both CSOM and COME, radiologists commonly use the term mastoiditis. Radiologic mastoiditis refers to any inflammatory change in the mastoid area, whether fluid build-up, mucosal edema, or bony change. Because the middle ear and mastoid are parts of the same cavity, it stands to reason that radiologic changes in the middle ear will be mirrored in the mastoid. The clinician's historic concept of mastoiditis, an acute abscess of the mastoid with potentially lethal intracranial proclivities, is a rare and very different condition. We should not be misled by radiologists' use of this word. Its meaning and implications are very different. Treatment Treatment of CSOM involves two phases: the eradication of infection and the reconstruction of the damaged middle ear. Treatment of infection involves topical toilet, antibiotic therapy, and, at times, surgery. Reconstruction involves surgical repair of the middle ear and its conductive mechanism. The initial treatment of CSOM is medical. Although this is not always successful, it can at times obviate the need for surgery in the presence of active suppuration. Even if surgery is needed as part of initial treatment, the ear should be cleaned up as much as possible before operation to minimize the risk of bleeding, injury to middle ear structures, and postoperative reinfection. Medical treatment of CSOM involves topical debridement of the infected mucosal surfaces, followed by topical and systemic antibiotics. 7 The ear should initially be debrided as much as possible. This helps to visualize the anatomy and to prepare the surface for further treatment. The ear canal can be debrided safely by swabbing it with cotton-tipped applicators. Such cleaning should be done under direct vision only and never blindly. Great care must be taken not to enter the middle ear. If the middle ear is filled with infected discharge or tissue, the patient should be referred to an otologist. If the ear is only slightly infected and the mucosa only mildly irritated, drops can be used effectively. This is particularly true in an ear with a large perforation and, thus, ready access to the middle ear. However, there is no point in using ear drops in an ear in which the mucosa is awash with mucopus and the ear canal caked with infected debris. The use of drops is also less effective in an ear with profuse drainage but only a small perforation.
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If the mucosa is covered with discharge, it should be debrided. This is done most safely by an otologist, because too brisk an irrigation may result in ossicular damage, and use of a solution that is too cool or too warm may create a caloric stimulus and resultant vertigo. A variety of topical drops are available. The physician can choose between single drugs and compounds, solutions or suspensions, and otic and ophthalrnologic· preparations. The usual initial choice is an otic compound that includes several antibiotics and steroids in an acidified viscous medium. These drops usually contain polymyxin, neomycin, and other drugs that are systemically toxic but topically useful. Although this form of "shotgun therapy" is usually effective, there may be reasons for choosing another type of drop. When a large infected mucosal surface is exposed, a suspension may give more prolonged contact than a solution. If the discharge is predominantly purulent, the clinician may wish to avoid topical steroids and instead choose a pure antibiotic preparation. If culture shows organisms that have become resistant to topical antibiotics, acetate drops, such as Domboro solution or Vosol can be used. Dilute acetic acid is cidal to Pseudomonas Sp.9 These agents are also a good choice when the patient has a contact allergy to neomycin. 12 Ophthalmic drops are aqueous and buffered to a neutral pH. They are useful when a small perforation or a narrowed ear canal prevents adequate penetration of the more viscous otic drops. Children who find acidic ear drops irritating will often accept ophthalmic drops in the ear. The drops are instilled by retracting the pinna to open the ear canal. After the drops enter the ear canal, repeated pressure on the tragus creates a plunger effect that displaces the air and forces the liquid into the middle ear. The patient should keep the affected ear upright for 3 or 4 minutes and then allow the excess liquid to run out. Occlusion of the canal with cotton creates an anaerobic environment and prolongs the infection. The most common cause of the failure of topical drops is the prescription of an inadequate amount. Keeping in mind that the infected surface includes the entire middle ear and mastoid, it is recommended that the ear canal be filled with drops (approximately 10) and that the medication be forced into the middle ear by tragal pressure three times a day for at least 10 days. The patient will use several bottles of drops in the course of therapy. If this treatment fails, the ear can be cultured and specific antimicrobial therapy started. Otologists often use powder insufflation in the treatment of chronic otitis media. 13 Powders are useful when there is good access to the middle ear through the ear canal, such as with subtotal perforations or after mastoidectomy. Systemic antibiotics may be given orally or parenterally. Although the initial treatment of CSOM is topical, oral medications may be added, especially when cultures reveal an organism that is susceptible. Betalactamase resistant penicillin analogues are a good adjunct to topical drops. Ciprofloxacin is particularly useful, because it is the first oral antibiotic with consistent anti-Pseudomonas activity. To prevent the emergence of resistant strains, it should be given judiciously and for at least 10 days. Ciprofloxacin is expensive and cannot be given to children under the age of 17 years.
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Parenteral antibiotics should be considered in patients who have failed to respond to other measures. Patients with profuse and unrelenting otorrhea, those with threatening complications, or patients who cannot comply with other measures can be considered for intravenous therapy. Intravenous administration not only provides more consistent blood levels but permits the use of aminoglyeosides and other antibiotics that cannot be given by mouth. If intravenous therapy is started, it should be continued for 2 to 6 weeks. The decision to treat with intravenous drugs is usually made by the otologist after all other measures have failed. This therapy is carried out in consultation with an infectious disease specialist, and peak and trough levels are followed to avoid toxicity. Intravenous therapy may be given either in hospital or in the home, using an indwelling heparin lock. Surgical treatment of CSOM is performed for two reasons: the eradication of infection and the subsequent reconstruction of the middle ear. Although the description of these techniques 15 is beyond the scope of this article, a few general principles should be considered. Because the main reservoir of infection in CSOM is the mastoid, some form of mastoidectomv is usually part of the treatment when the infection is unremitting. This operation involves an incision over the mastoid process followed by the removal of the mastoid cortex and its air cells. Mastoidectomv removes a large portion of the infected and oversecreting mucosa. In thi~ way, it can reduce or even eliminate the otorrhea. By converting the dozens of tiny air compartments of the mastoid into a single diverticulum, recurrent infection is more easily visualized and treated. If the mucosa is completely removed and the mastoid bowl is opened into the ear canal, it can become lined by skin. Skin is more resistant to infection and can even become selfcleansing. Skin is either permitted to grow in from the ear canal or is placed surgically as pedicled or free grafts. In some instances, the surgeon may choose to obliterate the mastoid cavity with muscle or fat. This further reduces the surface at risk for recurrent infection. It is impossible to remove all of the diseased mucosal lining the tubotympanic cavity. For this reason, the surgeon can only hope to tip the balance in favor of healing; he or she cannot convert the infected ear to a sterile field by means of surgery. Reconstruetive surgery involves rebuilding the tympanic membrane and ossicular chain. This group of operations, collectively called tympanoplasty, can be carried out only when the infection has been treated adequately. Closing the middle ear by grafting the tympanic membrane can only succeed if the middle ear is clean and there is adequate eustachian tube function to permit membrane vibration. If eustachian tube function is compromised, reconstruction must include ventilating the middle ear, using a long-term vent tube. This enhances the take rate fo-r tympanic membrane grafts, because it prevents negative pressure in the middle ear with consequent graft loss. A variety of materials are used in tympanoplasty. These include fascia and perichondrium to repair the ear drum and homograft or synthetic ossicles to rebuild the conductive chain. The fascia is obtained from the temporalis muscle via a small postauricular incision, whereas perichondrium can be harvested from the tragus of the ear.
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The ossicular chain is rebuilt using either the patient's own tissues or synthetic devices. Partial or total ossicular replacement prostheses (PORPs and TORPs) are available in a variety of polymeric and ceramic materials. The newest of these prostheses is made of hydroxylapatite, a mineral normally found in bone. Hydroxylapatite prostheses are very biocompatible and do not exhibit the problems of infection and extrusion seen with the older plastic devices. Complete reconstruction of a scarred middle ear cannot always be carried out in one step and may have to be staged. When appropriate staging, ventilation, and ossicular prostheses are used, most middle ears can be reconstructed to achieve a significant improvement in hearing.
CHRONIC OTITIS MEDIA WITH EFFUSION The middle ear may be chronically inflamed without suppuration. COME usually begins with eustachian tube obstruction. In the abscence of other factors, a mechanical obstruction of the tube results in negative middle ear pressure followed by the transudation of thin tissue fluid. This condition, commonly seen following airplane flights, is serous otitis media. It is usually an acute or subacute condition. Chronic mucoid otitis media (Fig. 4) results when the effects of eustachian tube obstruction are compounded by an inflammation of the middle ear mucosa. The cause of this inflammation is not always clear. Allergy may have a role,2 as well as a subacute bacterial infection. 13 The presence of bacteria evokes an inflammatory response but does not proceed to suppuration. 4 For this reason, the tympanic membrane does not perforate, and no otorrhea is seen. The lining of the middle ear becomes hyperplastic and produces a thick mucous exudate. 5 Eustachian tube patency, which may have been marginally present initially, is compromised in the face of this large quantity of viscid mucus, and a functional obstruction may develop.
Figure 4. Chronic mucoid otitis media. The membrane is dark pink and injected. There is moderate retraction, most readily seen over the pars flaccida. (Photograph courtesy of Michael Hawke, MD.)
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It is important to realize that the hallmark of this condition is not negative pressure in the middle ear but the accumulation of excessive mucus. In fact, in the early stages, this exudate is often under positive pressure, and at myringotomy, it extrudes through the incision of its own accord. It is further important to consider that the mucus formed is potentially harmful to the middle ear. It is acidic and contains cellular debris, dead bacteria, as well as inflammatory by-products. Ifleft untreated, the exudate can organize by forming mucin and fibrin. As the material grows more concentrated, the middle ear space gradually collapses and becomes atelectatic. The tympanic membrane adheres to the promontory and the ossicles, the epithelial surfaces disintegrate, and fibrocystic degeneration results in an end-stage middle ear (Fig. 5). The only clinical symptom of COME is hearing loss. The degree of hearing loss may vary but is usually in the 25 to 45 decibel range. Otoscopic examination reveals an intact tympanic membrane. The membrane appears thickened and opaque. Its color may be pink or amber but is always different from its normal greyish pink translucent appearance. If the drum has begun to retract, this is most easily seen over the pars flaccida (Shrapnell's membrane). Later, the main portion of the drum (pars tensa) also begins to collapse. The handle of the malleus appears chalky white in contrast to the darker drum. Its short process and, later, the handle stick out in contrast, similar to a tentpole as a tent is collapsed. As the malleus is pulled medially at the umbo, its handle appears to be foreshortened. As the retraction continues, the drum may drape over the incus and the head of the stapes. These dramatic changes are absent in early COME. The altered color and texture of the membrane are the most consistent findings. On pneumatic otoscopy, the drum does not move. Tuning fork tests confirm a conductive hearing loss in the ear. It is important to realize that COME is a chronic process, with the
Figure 5. Severe atelectasis of the middle ear. The tympanic membrane is collapsed. The malleus, incus, and head of stapes are clearly seen. Note the partial resorption of the lenticular process of the incus. The small residual middle ear space near the eustachian' tube (below) shows fluid and air bubbles. (Photograph courtesy of Michael Hawke, MD.)
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entire cavity of the middle ear and mastoid filled by sticky mucus. Air bubbles or an air/fluid meniscus are never seen in this condition. This finding is seen in resolving serous otitis media and indicates the return of eustachian tube function. The diagnosis of COME necessitates that the clinician maintain a degree of suspicion. Chronic hearing loss, especially when it is gradual in onset or unilateral, is often ignored by the patient for a period of time. Once diagnosed, however, the condition should be treated promptly to minimize permanent damage to the ear. The issue in COME is not merely the accumulation of fluid in the middle ear. If the fluid, which is acidic and may be noxious to the structures of the middle ear, is untreated, it may lead to permanent changes. These include scarring, loss of ossicular tissue, and a complete and irreversible obliteration of the middle ear space. 5 Treatment Chronic mucoid otitis media requires drainage. This procedure, myringotomy, involves a small incision in the tympanic membrane. A ventilation tube is often inserted at the same time to maintain the patency of the incision. A limited trial of antibiotics may be given, particularly when there is a past history of recurrent otitis media with resolution. Antihistamines are usually not effective, because they dry the mucosal surfaces and further impair the mucociliary clearing mechanism. Decongestants, oral or topical, may be tried. The role of inhalant and food allergies in COME is controversial. Nonetheless, in children with chronic mucoid effusion, an allergic history should be sought and medically addressed. If there is a history of allergy and in the absence of infection, oral or nasal steroids may be effective early in the disease process. l l The effect of drainage in COME is two-fold. It relieves the abnormal pressure within the middle ear by opening the tympanic membrane and evacuates the mucus that has accumulated. It also permits the marginally functional eustachian tube to recover and function as a natural vent and drain. The effect is analogous to a juice can. One hole does not permit the juice to pour, but a second opening permits a free flow. Different methods of ventilation can be used. In chronic mucoid otitis media, the surgeon usually selects a tube that remains in place for a longer time. When fluid accumulates in the middle ear, the clinician should always weigh the possibility of an obstructing mass in the nasopharynx. Enlarged adenoids are often found in conjunction with COME in children, and adenoidectomy may facilitate management of the ear.2 In adults, nasopharyngeal carcinoma usually causes a serous, not mucoid, effusion, which is classically unilateral. Nasal and sinus problems often have a role in eustachian tube insufficiency. A posterior nasal septal deviation may cause functional obstruction near the pharyngeal opening of the eustachian tube. Decreased air flow may result in an inspissation of mucus posteriorly. This is experienced by the patient as a persistent postnasal drip and may make the ipsilateral eustachian tube opening prone to obstruction. Frank obstruction of the nasal passages by nasal polyps or enlarged allergic turbinates also interferes with aeration and proper mucus flow around the eustachian tube orifice. Mucus drainage from the sinuses is normally carried posteriorly in two
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streams that surround the eustachian tube cushion. Increased or infected drainage seen with chronic sinusitis may result in eustachian tube obstruction. CHOLESTEATOMA
When keratinizing epithelium lodges within the middle ear, its continued growth and desquamation leads to the build up of keratin. A keratincontaining cyst, called a cholesteatoma, develops.6 Over time, the keratin flakes continue to accumulate, and the cholesteatoma enlarges. Due to a combination of pressure and enzymatic action, the enlarging cholesteatoma destroys adjacent bony structures. An untreated cholesteatoma may thus destroy the ossicles and, eventually, the bony labyrinth and facial nerve canal. Over time, the cholesteatoma will outgrow the boundaries of the middle ear and mastoid and invade the intracranial cavity. Cholesteatomas are usually accompanied by infection. There are two reasons for this. Either the skin ingrowth is the result of an attempted healing of a granulating surface in the middle ear or the moist keratin debris becomes colonized and serves as a nidus for pathogenic bacteria. Keratin is perceived by the body as a foreign protein, and as keratinproducing epithelium undermines middle ear mucosa, the inflammation is exacerbated. Cholesteatomas may develop with both forms of chronic otitis media. In CSOM, the inflamed middle ear lining seems to invite the ingrowth of squamous epithelium from the deep external ear canal (Fig. 6). This occurs classically by way of a marginal perforation. With more central perforations, the remaining rim of tympanic membrane acts as a mechanical barrier that hinders the ingrowth of skin. In COME, the long-standing and extreme collapse of the ear drum
Figure 6. Cholesteatoma associated with CSOM. There is a subtotal perforation of the membrane. Cholesteatoma is invading the middle ear. Note the white ' keratin debris enveloping the malleus. (Photograph courtesy of Michael Hawke, MD.)
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produces segmental pockets of retraction. As these pockets deepen, it becomes more difficult for keratin to clear the neck of the invagination. An accumulation of keratin develops (Fig. 7). As the keratin mass enlarges, the fundus of the pocket deepens and broadens, and its neck grows more attenuated. 14 The bolus of keratin is hygroscopic, and moisture in the ear canal makes the retraction cholesteatoma swell. As the keratin absorbs moisture, it becomes macerated and forms a good bacterial nutrient. 3 Retraction cholesteatomas develop most commonly in Shrapnell's membrane (attic retraction) or in the posterior pars tensa (mesotympanic retraction). It is important for the clinician to identify cholesteatomas promptly, because this condition usually requires surgical treatment. Early cholesteatomas may be mistaken for ear wax or debris, and even in the presence of otorrhea the diagnosis may be missed. This is unfortunate, because expanding cholesteatomas may damage the ossicular chain, facial nerve, and even the labyrinth with resultant facial paralysis, hearing loss, and vertigo. The earlier a cholesteatoma is diagnosed and treated, the less likely these complications will ensue. Otoscopic examination is usually diagnostic. In CSOM, white debris may be seen in the middle ear. Because cholesteatomas in CSOM are usually infected, the debris is partially covered by mucopus. A fringe of granulation tissue represents the foreign body reaction evinced by the keratin. In COME, a deep attic retraction pocket may be filled by keratin. A small attic perforation, particularly if it is discharging, may represent the neck of a long and deep attic retraction cholesteatoma. A granulation tissue polyp may appear to guard the entrance to an attic retraction cholesteatoma. Patients with cholesteatoma often complain of a discharge that is particularly fetid. It may be blood tinged due to friable granulations. In complicated cholesteatomas, the patient may complain of dizziness, particularly when pressing on the ear. This is the result of a labyrinthine fistula
Figure 7. Cholesteatoma associated with COME. The tympanic membrane is thickened, dark, and retracted, with a mucoid middle ear effusion. Shrapnel!' s membrane has invaginated into the attic, forming an attic retraction cholesteatoma. (Photograph courtesy of Michael Hawke, MD).
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due to bony erosion. Long-neglected cholesteatomas can lead to facial paralysis, brain abscess, or sigmoid sinus thrombosis. These conditions are fortunately rare but emphasize the fact that chronic otitis media, whether suppurating or mucoid, is not always an innocuous disease. Both forms of chronic otitis media require accurate diagnosis and appropriate treatment. CONCLUSION
The primary care physician should recognize two forms of chronic otitis media. Chronic suppurative otitis media presents with otorrhea, hearing loss, and a perforated tympanic membrane. Chronic otitis media with effusion causes hearing loss only and is associated with a collapsed intact ear drum. The initial evaluation of both conditions rests with the primary clinician. Definitive treatment requires surgery and is important to avoid permanent hearing loss and possible cholesteatoma formation. REFERENCES 1. Bernstein J: Middle ear mucosa: Histological, histochemical, immunochemical and immunological aspects. In Jahn AF, Santos-Sacchi J (eds): Physiology of the Ear. New York, Raven Press, 1988, pp 59-80 2. Bluestone CD: Management and therapy of otitis media. In Alberti PW, Ruben RJ (eds): Otologic Medicine and Surgery. New York, Churchill Livingstone, 1988, pp 1173-1201 3. Brook I: Aerobic and anaerobic bacteriology of cholesteatoma. Laryngoscope 91:250, 1981 4. Brook I, Finegold SM: Bacteriology of chronic otitis media. JAMA 241:487-488, 1979 5. Hawke M, Jahn AF: Diseases of the ear-clinical and pathologic aspects. New York, Cower Medical Publishers (Lea & Febiger), 1987 6. Jahn AF: Cholesteatoma: What is it, how did it get there, and how do we get rid of it? Otolaryngol Clin North Am 22:847-857, 1989 7. Jahn AF, Abramson M: Medical management of chronic otitis media. Otolaryngol Clin North Am 17:673-677, 1984 8. Jahn AF, Farkashidy J: Newer perspectives on the pathology of chronic otitis media. Can J Otolaryngol 9: 131-142, 1980 9. Jones EH: External Otitis: Diagnosis and Treatment. Springfield, Ill, Charles C Thomas, 1965 10. Liu DCP, Bergeron RT: Contemporary radiologic imaging in the evaluation of middle ear-attic-antral complex cholesteatomas. Otolaryngol Clin North Am 22:897-909, 1989 11. Macknin J, Jones R: Oral dexamethasone for treatment of persistent middle ear effusion. Pediatrics 75:329, 1985 12. Mawson S, Ludman H: Diseases of the Ear, ed 4. London, Edward Arnold Publishers, 1979 13. Riding KH, Bluestone CD, Michaels RH, et al: Microbiology of recurrent and chronic otitis media with effusion. J Pediatrics 93:739-743, 1978 14. Sade J: Pathogenesis of attic cholesteatomas. J R Soc Med 71:716-732, 1978 15. Tos M: Tympanomastoiditis: Management and treatment. In Alberti PW, Ruben RJ (eds): Otologic Medicine and Surgery. New York, Churchill Livingstone, pp. 1203-1239, 1988
Address reprint requests to Anthony F. Jahn, MD 556 Eagle Rock Avenue Roseland, NJ 07068
