Office Management of Tympanic Membrane Perforation and the Draining Ear

Definition

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

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

• Otorrhea must arise from the middle ear space through a tympanic membrane perforation or tympanostomy tube.

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

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

Etiology

Most cases of CSOM arise from acute infections that have not been resolved. Whether all cases of CSOM have an infectious etiology is unclear. Antonelli et al. ^, have suggested that some cases may be due simply to “bacterial colonization and overgrowth in an ear that remains moist because of tubal pathology.” Allergies may be the only predisposing factor that results in chronic drainage through the tympanic membrane perforation.

Although tympanic membrane perforations are invariably present (by definition), the role of membrane perforations in the development of CSOM is unclear. Occasionally, tympanic membrane perforation is a result of an initial middle ear infection that never resolves. Alternatively, in some cases in which a long-standing, dry perforation becomes infected, the infection persists because of either inadequate or inappropriate treatment. Infection in the setting of a tympanic membrane perforation is uncommon; however, most cases respond rapidly once the appropriate treatment is initiated.

As noted by Bluestone et al., ^, a nonintact tympanic membrane (perforation or tympanostomy tube) 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 susceptible populations (e.g., Indigenous North Americans).

Many cases of CSOM arise from inadequately or incompletely treated cases of acute otitis media (AOM). Gibney et al. 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. AOM results in mucosal sloughing, impaired ciliary clearance, and exposes microbial binding sites. ^, Even so, few episodes of AOM evolve into CSOM.

The onset of CSOM is initially characterized by increased vascularity of the mucosa and submucosa. The proportion of chronic inflammatory cells increases over time in untreated or refractory CSOM. This increase in chronic inflammatory cells leads to osteitis and mucosal edema with ulceration, and two important pathophysiological events follow: (1) capillary proliferation, which results in the 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 pathological alterations in the middle ear cleft.

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. The extent to which anaerobic organisms, fungi, or both are pathogenically involved is controversial. Anaerobic organisms are often present, but whether they are identified depends on how rigorously they are sought. ^, The contribution of anaerobes to the pathophysiology remains unclear. Fungi are commonly recovered, but the extent to which they are pathogens, as opposed to saprophytes, remains unresolved and is probably variable.

Pathophysiology

Granulation tissue is an invariable component 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 abundant, may contribute to treatment failure in 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. Inflammation in the underlying lamina propria traverses through the broken basement membrane and enters the lumen of the middle ear space. The rupture of the basement membrane and epithelial lining cells 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.

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 exposed lamina propria is pushed into the middle ear without any epithelial covering. Granulation tissue forms secondary to the secretion of angiogenic growth factors that incite capillary budding, vascular hyperpermeability, and fibroblast recruitment. Accelerated granulation tissue formation may result in the formation of a polyp. Meyerhoff et al. evaluated temporal bones 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.