Office Management of Tympanic Membrane Perforation and the Draining Ear

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Chapter 8 Office Management of Tympanic Membrane Perforation and the Draining Ear

Peter S. Roland, Brandon B. Isaacson, Joe W. Kutz

Otorrhea can arise from many causes: acute and chronic external otitis, acute and chronic otitis media, chronic myringitis, and secondary to a cerebrospinal fluid (CSF) fistula.

OTORRHEA FROM CEREBROSPINAL FLUID FISTULA

CSF is a rare cause of persistent or intermittent otorrhea. CSF otorrhea may be classified as spontaneous or acquired. Temporal bone trauma is the most common cause of acquired CSF otorrhea, but it may also arise secondary to neoplasms, infections, and iatrogenic causes.

Brodie and Thompson ¹ observed that CSF otorrhea resulting from temporal bone fractures resolved within 1 week of onset in 95 of 122 subjects (77.8%). They also showed that leaks persisting beyond 7 days had a much higher incidence of meningitis (23% versus 3%). Iatrogenic CSF otorrhea may occur immediately after surgery or may be delayed for days or years.

Spontaneous CSF otorrhea may result from congenital temporal bone abnormalities, or can arise in the setting of normal temporal bone morphology as a consequence of arachnoid granulations, or increased intracranial pressure.^2,³ More recent studies have shown that subjects with spontaneous CSF otorrhea are often morbidly obese and often have empty or partially empty sella on radiographic examination.^3,⁴

Patients who are eventually diagnosed with CSF otorrhea are often initially identified during an evaluation of persistent unilateral middle ear effusion. The diagnosis is often confirmed when persistent watery drainage follows myringotomy. A careful history may elicit symptoms of intermittent positional nasal drainage. The diagnosis is usually established by history and physical examination, but may be confirmed with β₂-transferrin if enough fluid can be collected. High-resolution temporal bone computed tomography (CT) and magnetic resonance imaging (MRI) with cisternogram, FIESTA, or CISS images are complementary studies often obtained in evaluating patients with CSF otorrhea.

Traumatic CSF otorrhea is often managed conservatively with stool softeners, head of bed elevation, serial lumbar punctures, or lumbar drainage. Occasionally, patients require operative management if conservative measures fail. The surgical approach is dictated by the fracture location, and hearing status in patients with temporal bone trauma. Patients with little or no residual hearing can be managed with a transmastoid or translabyrinthine approach, whereas patients with residual hearing can be managed with a middle fossa approach.

Spontaneous CSF otorrhea requires surgical repair of cases caused by fistula between the subarachnoid space and temporal bone air cell system. The middle fossa approach is often used because these patients commonly have multiple tegmen defects. A transmastoid approach may be used if the defect is solitary and is sufficiently lateral in the temporal bone, or if the patient has significant medical comorbidities. CSF otorrhea resulting from congenital inner ear anomalies may be managed via a transcanal or transmastoid approach. Autologous (e.g., bone, cartilage, fascia) and nonautologous (e.g., acellular dermal matrix [AlloDerm], bone cement) materials have been used to repair these defects. Bone defects with communication into the posterior fossa are usually repaired with a transmastoid approach.

CHRONIC SUPPURATIVE OTITIS MEDIA

Definition

There is no widely agreed on definition of chronic suppurative otitis media (CSOM). Nonetheless, most practicing otologists would agree that the following elements should be present:

1. The drainage must be purulent, mucoid, or mucopurulent.

2. The otorrhea must arise from the middle ear space through a tympanic membrane perforation or tympanostomy tube.

3. Drainage must persist beyond 3 weeks despite appropriate medical management.^5,⁶

Although some otologists refer to an infected cholesteatoma as a form of CSOM, others prefer to limit the term only to ears without cholesteatoma. Although many of the management principles discussed in this chapter may be applicable to individuals with an infected cholesteatoma, surgery, and not office management, is the mainstay of treatment when cholesteatoma is present. Consequently, ears with cholesteatomas are not a focus in this discussion.

Etiology

Many, perhaps most, cases of CSOM arise from acute infections that have not resolved. Whether or not all cases of CSOM have an infectious etiology is unclear. Antonelli and colleagues ^5,⁶ have suggested that some cases may be due simply to “bacterial colonization and overgrowth in an ear that remains moist because of tubal pathology.” Many authors believe that allergy alone can result in chronic drainage through tympanic membrane perforation, at least occasionally.

Although tympanic membrane perforations are invariably present (by definition), the etiologic role of membrane perforations in the development of CSOM is also unclear. Sometimes the tympanic membrane perforation is simply a result of the initial middle ear infection that never resolves. Alternatively, there are some cases in which a long-standing, dry perforation becomes infected, and the infection persists either because of lack of treatment or inadequate or inappropriate treatment. Most tympanic membrane perforations do not result in infected middle ears, however, and, when they do, most such infections, during the acute phase, respond briskly to appropriate treatment.

As noted by Bluestone and others,^7,⁸ a nonintact tympanic membrane (perforation or tympanostomy tube or both) eliminates the “middle ear cushion” and facilitates eustachian tube reflux. By eliminating the middle ear cushion, a tympanostomy tube or tympanic membrane perforation allows air to escape from the middle ear space, which eases the retrograde reflux of nasopharyngeal secretions into the middle ear. Eustachian tube reflux may be an especially important etiologic factor in populations who are otherwise prone to it (e.g., aboriginal North Americans).

Many cases of CSOM arise from inadequately or incompletely treated cases of acute otitis media (AOM). Gibney and coworkers ⁹ showed that aggressive treatment of AOM in aboriginal children in Australia reduces the incidence of CSOM. It is usually unclear why an acute infection fails to resolve and becomes chronic. We do know that AOM causes mucosal sloughing, causes impairment of ciliary clearance, and exposes microbial binding sites.^5.6 Even so, only a few episodes of AOM evolve into CSOM.

The onset of CSOM is characterized initially by increased vascularity of the mucosa and submucosa. As CSOM persists, the proportion of chronic inflammatory cells increases. This increase in cells leads to osteitis and mucosal edema with ulceration, and two important pathophysiologic events follow: (1) capillary proliferation, which results in formation of granulation tissue and polyps, and (2) a rarifying osteitis, which ultimately produces new bone formation and fibrosis. Osteitis is present in virtually 100% of CSOM patients, a finding that distinguishes CSOM from more transient pathologic alterations in the middle ear cleft.¹⁰

Bacteriology

CSOM is predominantly a gram-negative infection, although staphylococcal species occur with sufficient frequency that they must be taken into consideration when any microbial therapy is considered. Pseudomonas aeruginosa is generally the most common gram-negative organism, but other gram-negative organisms are commonly encountered, especially species of Enterobacteriaceae.¹¹ The extent to which anaerobic organisms or fungi or both are pathogenically involved is controversial. Anaerobic organisms are often present, but whether or not they are cultured depends on how rigorously they are sought.^12,¹³ The contributions of anaerobes to pathophysiology remain unclear. Fungi are commonly recovered, but the extent to which they are pathogens as opposed to saprophytes is unresolved, and probably variable.

Pathophysiology

Granulation tissue is almost an invariant accompaniment of CSOM. It can develop quickly in a draining ear, and is already present in many infections of less than 6 weeks’ duration. The presence of granulation tissue, especially when it is abundant, may be a factor that contributes to treatment failure of acute infections, and the evolution of AOM into CSOM. The formation of granulation tissue in the middle ear begins with a break in the basement membrane of the surface epithelial cells. Inflammatory cells in the underlying lamina propria traverse through the broken basement membrane and enter the lumen of the middle ear space. The rupture of the basement membrane and epithelial lining cell is caused by bacterial toxins, inflammatory mediators produced by ruptured liposomes, and the accumulation of subepithelial fluid and vacuoles, all of which exert pressure on the surface epithelium.¹⁴

The next step in the formulation of granulation tissue occurs when a small piece of the herniated lamina propria extrudes through the ruptured area between epithelial cells. Initially, the extruded lamina propria pushes into the middle ear without any epithelial covering. Angiogenic growth factors incite capillary budding, vascular hyperpermeability, and fibroblast recruitment—that is, granulation tissues form. If the growth of granulation tissue is vigorous and aggressive, polyps develop.¹⁵ Meyerhoff and colleagues¹⁰ evaluated temporal bone from subjects with CSOM and reported that granulation tissue develops in 90% of all CSOM, and in 100% of cases of CSOM that develop intracranial complications.

ACUTE OTITIS MEDIA WITH AN OPEN TYMPANIC MEMBRANE

Inadequately treated AOM with a nonintact tympanic membrane is a frequently cited cause of CSOM.¹⁶ Acute infections in an ear with a nonintact tympanic membrane are frequently inadequately or inappropriately treated (especially in children) because it is not universally recognized that in many ways an acute infection occurring in an open middle ear cavity is significantly different from classic AOM. Most importantly, the microbiology is significantly different. Although some cases of acute infection in an open middle ear arise from the typical AOM pathogens—Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis—most, especially in patients older than 2 years, are caused by species of Staphylococcus, Pseudomonas, or other gram-negative organisms.¹⁷ Yeasts (Candida spp.) are occasionally encountered when the eardrum is not intact, but rarely when the middle ear space is closed.¹⁷ The oral antibiotics usually prescribed for AOM are poorly active against Staphylococcus and completely inactive against gram-negative organisms. Individuals treated with these systemic antibiotics consequently are often treated inappropriately or inadequately. Aggressive, appropriate treatment of acute middle ear infections in individuals with a nonintact tympanic membrane is an important way of preventing the development of CSOM.

Another meaningful difference between AOM with an intact tympanic membrane and AOM in an open middle ear is that the natural history of these two infections seem to be different. It is well established that 80% or more of untreated children with AOM and intact eardrums recover spontaneously, and that suppurative complications are unlikely. Ruohola and associates ^18,¹⁹ found that AOM in children with tympanostomy tubes is significantly different in this respect: at the end of their study, 60% of nontreated children still had infection and drainage.

MANAGEMENT OF OTORRHEA

There are three principal components to effective management of the draining ear:

1. Effective aural toilet

2. Use of an appropriate antimicrobial agent

3. Management of granulation tissue

Aural Toilet

Effective aural toilet mechanically decreases the bacterial burden, eliminates debris that nurtures bacterial growth, and removes obstacles to the effective delivery of antimicrobial agents. The most effective aural toilet is achieved using an operating microscope and microinstrumentation. When microscopic débridement cannot be performed, the use of irrigation solutions to remove debris and mucopurulent exudate is a reasonable alternative. Irrigation of the external auditory canal can be performed at home using a small bulb syringe. When used in combination with antimicrobial drops, irrigation should precede the instillation of drops by 20 to 30 minutes, allowing time for the instilled irrigation solution to drain out of the ear completely.

Various solutions have been advocated for this purpose, including 3% hydrogen peroxide, vinegar, and isopropyl alcohol. Many otologists dilute these solutions 50:50 with sterile water. Water alone should not be used. The use of water alone increases the ambient humidity; may alkalize the ear canal or middle ear space or both; and, if not sterile, can introduce pathogenic organisms. Isopropyl alcohol is not recommended because it can be painful on instillation and is potentially ototoxic.

“Dry mopping” refers to the use of twisted pieces of cotton or tissue pushed into the external auditory canal to “mop up” and remove any secretions within the canal. Its effectiveness is unknown, but it may be better than nothing, especially if the principal component to be removed is liquid and not desquamated epithelial debris or inspissated mucopus.

Antimicrobial Therapies

Elimination of infection is crucial to the successful management of a draining ear. Consequently, appropriate antimicrobial treatment is pivotal. Infection that is limited to the external auditory canal or an open mastoid cavity can sometimes be managed with the use of antiseptics or acidifying agents, or both, alone. When effective, these agents have several advantages: they are inexpensive, are easy to procure, do not promote bacterial resistance, and are generally effective against bacteria and fungi. The relative merits of one of these preparations versus another is generally unknown, although Tom ²⁰ showed that Cresylate is more effective in vitro than other antiseptics against fungal organisms.

The acidifying agents and antiseptics are unattractive agents when the middle ear is open. Almost all have been shown to be potentially ototoxic. Most of these preparations are acidic (ototoxic in itself) and may be quite painful when they come in contact with the middle ear mucosa, which is of neutral pH.

When antibiotics are used, topical delivery in the form of otic drops is more effective and safer than the use of systemic antibiotics, either orally or parenterally.²¹^–²⁵ ²⁷ By using a topical agent, the physician can deliver a concentration of medication that is several orders of magnitude higher in affected tissues than the concentration that can be achieved by using a systemic agent. A 3 to 5 drop dose of a 0.3% solution of antibiotic contains only 90 to 150 mg of medication, but its concentration is 3000 μg/mL, which exceeds the minimum inhibitory concentration of any known relevant pathogen. In contrast, consider the typical drug levels in middle ear fluid that can be achieved by three systemic antibiotics:

Cefuroxime 1 to 2 μg/mL

Amoxicillin 8 to 10 μg/mL

Ceftriaxone 25 to 30 μg/mL

Because the concentration of medicine delivered to infected tissue is so much higher than can be achieved with systemic antibiotics, antibiotic sensitivities as determined by clinical laboratories are irrelevant. These sensitivity determinations made by clinical laboratories are based on what are believed to be realistically achievable tissue levels after systemic administration of a drug. An organism with a minimal inhibitory concentration (MIC) of 4 to ciprofloxacin would generally be considered to be a “resistant” organism because it is unlikely that a tissue level of 4 μg/mL of ciprofloxacin could be achieved by oral or parenteral administration of ciprofloxacin. If otic drops with a concentration of 3000 μg/mL (a concentration available in commercial preparations) is delivered, however, the organism would succumb. Consequently, sensitivity determinations made in clinical laboratories can be safely ignored when topical therapy is used.

A second important consequence of such high concentrations is that the risk of the emergence of resistant organisms is minimized. Neither resistant clones already present nor newly emerging resistant mutants would survive in such very high concentrations of antibiotic. Despite the very high concentration of antibiotic in topical ear drops, the risk of systemic side effects or adverse reactions is very low because the total dose administered (approximately 1 mg per dose) is low, and systemic absorption is limited.

Skepticism has been voiced that topical drops would not provide sustained levels of antibiotic inside the middle ear space, especially if the perforation is small or delivery is through a tympanostomy tube. Ohyama and associates ²⁶ documented that topical antibiotic drops can be, and often are, effectively delivered into the middle ear space and have long dwell times. These investigators measured the persistence of a single dose of topically applied 0.3% ofloxacin in otorrhea fluid, serum, and middle ear mucosa at various time intervals after administration. They found a very high level of antibiotic in the otorrhea fluid several hours later. Perhaps the most surprising finding was the high concentration of drug in biopsy specimens of middle ear mucosa approximately 1 hour after the administration of ear drops. As expected, drug concentrations in serum were very low or nondetectable.

The superior efficacy of topically applied antibiotics is well documented in the literature. Esposito and colleagues ²⁸ studied 60 subjects with CSOM who were randomly assigned to receive one of three treatment regimens: one group received oral ciprofloxacin twice a day, another received three drops of ciprofloxacin solution twice a day, and a third group received oral and topical ciprofloxacin doses twice a day. The topical group had a clinical response rate of 100% and a bacteriologic cure rate of 95%, and the topical/oral group had response rates of 95% and 85%. By contrast, the group that received oral antibiotics alone had a clinical response rate of 65% and a rate of bacterial eradication of only 40%. These differences were statistically significant.²⁸ Two years later, Esposito and colleagues²⁹

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