Surgery of Ventilation and Mucosal Disease

Acute otitis media without effusion

Acute otitis media (AOM) without effusion is characterized by an inflamed ME mucosa and tympanic membrane in the absence of ME effusion. This can be seen in the early stages of AOM with effusion or during its resolution. The tympanic membrane appears dull, erythematous, hypervascular, and inflamed; normal landmarks are often lost. In infants and children, AOM without effusion is usually caused by the same organisms that are isolated from acute OME. The treatment principles are the same and are discussed later.

Acute otitis media with effusion (acute OME)

Acute OME occurs most frequently in infants. Redness with or without bulging of the tympanic membrane, fever, irritability, and pain are hallmark signs and symptoms. The older child with acute OME has a red tympanic membrane and ME effusion but may not have pain or fever. ME effusion is generally purulent. Casselbrant and associates reported a 43% cumulative incidence of acute OME in a study of 198 newborns followed monthly until the age of 2 years. In the Greater Boston Otitis Media Study Group, infants had an average of 1.2 episodes per year, with 46% of children having had three or more episodes by the age of 3 years.

Recurrent AOM refers to frequent bouts of AOM. The child most likely had an intercurrent, persistent (chronic) OME (COME); the effusion became infected, and the child developed an AOM. Recurrent AOM is an indication for surgical intervention (see later), so documentation of the number and duration of episodes is important.

Otitis media with effusion

OME simply refers to fluid in the ME without signs or symptoms of ear infection. Asymptomatic OME can be classified as acute (<3 weeks), subacute (3 weeks to 3 months), or chronic (>3 months). Note that “acute” and “chronic” refer to the temporal course of the disease, not to severity. OME synonyms include secretory otitis media, nonsuppurative otitis media, or serous otitis media; the most commonly used is OME. As noted above, the fluid can be serous, purulent, or mucoid.

Chronic suppurative otitis media

Chronic suppurative otitis media (CSOM) is a chronic (>6 weeks in this disease categorization) infection of the ME and mastoid, in which a central perforation of the tympanic membrane (or a patent tympanostomy tube) and discharge (otorrhea) are present. The infection involves both the mastoid and ME and usually drains through a central perforation. Chronic otorrhea through a nonintact tympanic membrane (perforation or ventilation tube) may or may not be caused by cholesteatoma; cholesteatoma may or may not cause CSOM. CSOM should not be confused with COME; in the latter, no perforation (and therefore no otorrhea) is present.

Idiopathic hemotympanum

The clinical hallmark of idiopathic hemotympanum (IH) is the dark blue–appearing tympanic membrane or ME space. There is usually no antecedent history of trauma, but trauma can induce this condition. IH represents a tissue response of the temporal bone mucosa to the presence of a foreign body: cholesterol crystals. Three etiologic factors are thought to be responsible: poor mastoid drainage, hemorrhage, and obstruction of ventilation. COME is the principal precursor, and cholesterol granuloma is the histopathological correlate.

These cholesterol cysts can take an aggressive course and cause bone erosion and osteitis. The treatment is generally surgical drainage (see later).

Microbiology

Bluestone et al. obtained aspirates of ME effusions by tympanocentesis in infants and children with AOM or OME. Thirty-five percent of aspirates from ears with AOM grew Streptococcus pneumoniae , 23% grew Haemophilus influenzae , and 14% grew Moraxella catarrhalis . Introduction of the pneumococcal vaccine significantly reduced the incidence of pneumococcal diseases, including otitis media.

The asymptomatic ME effusion (OME) was previously thought to be sterile. Newer, more sensitive cultures, and the introduction of polymerase chain reaction (PCR) testing, have shown bacteria and bacterial DNA in asymptomatic ME effusions. These investigators found that 77% of ME effusions had PCR evidence of the three major organisms (with or without being culture positive), whereas only 28% were culture positive; the most common bacteria were H. influenzae (54.5%), M. catarrhalis (46.4%), and S. pneumoniae (29.9%). Other isolated bacteria included Staphylococcus aureus and gram-negative enteric bacilli; in infants younger than 6 weeks of age, gram-negative bacilli cause about 20% of AOM episodes.

The bacteriology of CSOM, with or without cholesteatoma, is different. The most frequently isolated bacteria include Pseudomonas aeruginosa (most common), S. aureus , Corynebacterium , Klebsiella pneumoniae , and anaerobes. Given better culture techniques, anaerobes have been increasingly isolated from chronically suppurating ears; these organisms include Bacteroides spp., Peptococcus spp., Peptostreptococcus spp., and Propionibacterium acnes .

Acute otitis media

Retrograde reflux of material from the nasopharynx through the eustachian tube (ET) is thought to account for the introduction of microorganisms into the ME. Bacteria colonize the nasopharynx and infect the host as a result of a breakdown in the barrier or protective factors in the nasopharynx, ET, and ME. AOM is principally a sequela of viral upper respiratory tract infections (URIs). URI impairs ciliary motility and breaks down mucosal barriers that prevent bacterial adherence and growth. Poor clearance of secretions results in stasis and allows bacteria to infect the host. Pathogenic bacteria that appear in the nasopharynx following a URI are the same as those cultured from ME effusions ( S. pneumoniae and H. influenzae ). The adenoid is a likely source of infecting bacteria in ME disease; Pillsbury and associates demonstrated higher bacterial colony counts in the adenoids of children with recurrent otitis media than in those undergoing adenoidectomies for adenoid hypertrophy without otitis media.

During a URI, sneezing, blowing the nose, and swallowing in the presence of a nasal obstruction may create a pressure differential between the nasopharynx and ME, introducing bacteria into the ME through the ET.

Finally, ET dysfunction (ETD) also accounts for OME. The ET has three functions: (1) clearance of secretions from the ME into the nasopharynx, (2) protection of the ME from nasopharyngeal pathogens, and (3) equalization of pressure between the atmospheric pressure (in the nose and ear canal) and ME pressure. The ME is an aerated “sinus.” It too must be ventilated and cleared of secretions, and the ET serves this capacity.

In children, the ET is short, horizontal, and relatively flaccid. As a result, the protective function of the tube is compromised, and retrograde reflux of secretions from the nose into the ME may occur. During an acute infection, ciliary function is also compromised, leading to the stasis of secretions and persistent effusion.

Chronic otitis media with effusion

Two theories have been proposed to account for the persistence of ME effusions in the absence of acute infection. As demonstrated by the Boston Collaborative Group, persistent effusion is a natural sequela of acute ME infection: ME effusion persists for 1 month in 40% of children after an episode of AOM, 2 months in 20%, and 3 or more months in 10%. Because pathogenic bacteria and bacterial DNA have been recovered from “nonacutely infected” fluid in the ME, ^, the ET obstruction and retained secretions in these cases appear to be the result of the acute infection rather than the cause.

Meanwhile, ETD may be a primary disorder that causes acute and chronic OME. Primary ETD results in poor ventilation of the ME space. This leads to negative pressure in the ME, and the resultant transudation of fluid. Negative ME pressure also causes hypoxia and hypercapnia of the ME mucosa, resulting in goblet cell hyperplasia and hypersecretion. The result is a sterile fluid that becomes secondarily infected. The fluid accumulation resolves only after adequate ventilation is restored, either by the return of ET function or by placement of alternative ventilation, such as a ventilation tube.

According to Gates, the available evidence lends support to the theory that the secretory changes in the ME that exist in COME are histological sequelae of a chronic infection rather than a separate pathological disorder. The majority of COME cases begin as acute infections of the ME; postinflammatory alterations in the mucosa of the ME and ET lead to persistent effusion. Obstruction of the ET is, therefore, secondary to infection and not the cause of it. ET obstruction then prevents clearance of secretions, impedes ventilation and drainage, and perpetuates the inflammatory process.

Allergic rhinitis has been recognized as a risk factor in the development of COME. The actual prevalence of “allergic” COME has been reported in the literature, with a very broad range of 10% to 90%.

The nasal mucosa, ME space, nasopharynx, and ET (the ME system) could each potentially serve as the target organ of an allergic reaction, resulting in the production of COME. Not only have allergic effector cells been isolated in each area, but the intimate anatomic relationships also ensure that disruption of the normal functions in one area (i.e., nose) may have an undesirable effect in another (ear).

Idiopathic hemotympanum

Long-standing cases of COME that develop granulomatous deposits in the ME and mastoid can lead to IH. The symptoms of IH are similar to those of OME, namely hearing loss with a plugged or pressure sensation in the ear. IH is more common in adults than in children, and is characterized by a dark blue–appearing tympanic membrane; fluid at myringotomy is dark brown and oily in consistency. Histologically, cholesterol crystals are observed; hence, the pathological term is cholesterol granuloma. A small mucosal hemorrhage, in the absence of adequate ventilation and drainage, is theorized to result in the deposition of hemosiderin, iron, and blood breakdown products into the submucosa. The contents can occupy the ME space or be walled off, resulting in cyst development. The cyst then slowly expands, causing bone thinning and erosion.

Acute otitis media and recurrent acute otitis media

For a single episode of AOM, antimicrobial therapy targets the most common offending pathogens: S. pneumoniae , H. influenzae , and M. catarrhalis . We recommend a 10-day course of amoxicillin as a first-line empiric therapy. Clinical practice guidelines from the American Academy of Pediatrics argue for observation without antibiotic therapy in select patients with AOM ( Table 5.1 ). Studies have shown a rise in β-lactamase-producing organisms ( H. influenzae and M. catarrhalis ); β-Lactamase renders the organism that produces it resistant to penicillin (and ampicillin). Persistent or recurrent AOM may be secondary to a β-lactamase-producing organism and requires a broader-spectrum antibiotic; good choices in this setting include cefuroxime, erythromycin-sulfisoxazole, trimethoprim-sulfamethoxazole, amoxicillin-clavulanate, or cefaclor. Antipyretics, but not aspirin, are also indicated for children with AOM.

A child (or adult) with an infectious complication of otitis media demands more aggressive therapy, including intravenous antibiotics and possible surgical intervention (see Chapter 18 ).

Children with recurrent AOM may exhibit normal ME examinations between episodes or may retain persistent effusions and also fall into the category of COME. The goal of any treatment for a patient with recurrent AOM is the long-term prevention of further episodes of otitis media.

The placement of tympanostomy tubes is an effective treatment for preventing recurrent otitis media. Many authorities accept four episodes of AOM within 6 months as a criterion for tympanostomy tube placement. Gebhart was the first to demonstrate a reduction in the number of new episodes of AOM following the insertion of tympanostomy tubes.

The role of adenoidectomy in the treatment of recurrent AOM is controversial. Although Paradise et al. found significant reductions in the incidence of AOM during the first (28% reduction) and second (35% reduction) years following adenoidectomy. A formal study examining the role of adenoidectomy in the treatment of recurrent AOM has not been conducted. The results of studies on COME and adenoidectomy may or may not be applicable for patients with recurrent AOM. In contrast, adenoidectomy is an appropriate surgical treatment for patients with recurrent AOM and persistent ME effusion (see below).

Chronic otitis media with effusion

As mentioned, 10% of children with AOM have persistent ME effusion 3 or more months after resolution of the acute infection. Because most children clear the effusion within 1 to 2 months, these patients need no further therapy. The minority who retain fluid in the ME for more than 3 months, however, are at risk for other sequelae, including hearing loss, language delay, vertigo or imbalance, tympanic membrane changes (including atelectasis and retraction pockets), further ME pathology (including ossicular problems and adhesive otitis), and discomfort with nighttime wakefulness and irritability.

A number of treatment strategies have been proposed for COME, including antimicrobial therapy, antihistamines and decongestants, corticosteroids, tympanostomy tubes with or without adenoidectomy, and mastoidectomy. Updated clinical practice guidelines from the American Academy of Otolaryngology-Head and Neck Surgery do not recommend antibiotics, antihistamines, decongestants, or corticosteroids for the treatment of COME. These modalities, as well as allergic strategies, will be briefly reviewed.