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Update on the medical and surgical treatment of chronic suppurative otitis media without cholesteatoma.

A diagnosis of chronic suppurative otitis media (CSOM) without cholesteatoma requires the presence of four conditions:

* The otorrhea must emanate from the middle ear via a tympanic membrane perforation or a tympanostomy tube.

* The middle ear must be free of keratin debris.

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

* The otorrhea must persist beyond 6 weeks despite medical therapy, including debridement and administration of oral and topical preparations, or the patient must experience recurrences of shorter duration. (1,2)

Microbiology

Conventional culture and speciation techniques tell us that the organisms typically associated with CSOM are Pseudomonas aeruginosa, Staphylococcus aureus, Staphylococcus epidermidis, Staphylococcus saprophyticus, Enterobacteriaceae spp., diphtheroids, streptococci, anaerobes, yeast, and fungi. (3,4) But these standard identification techniques are not as sensitive as the newer molecular speciation technology, which may revolutionize our understanding of what we think we know. Other pathogens may be in play. Over the course of the next few years, our understanding of the microbiology of CSOM may change radically.

Etiology

No consensus exists regarding the specific etiology of CSOM. We believe that it might represent a microbial infection, but it might also represent simple colonization and overgrowth in an ear that remains moist because of tubotympanic pathology. Such problems may include a tympanic membrane defect or eustachian tube dysfunction. Damage caused by acute otitis media (AOM) has been implicated, and immunologic deficiency is a problem in some patients. In most cases, the cause of CSOM is likely multifactorial. (5-7)

Tympanic membrane defect. While much is said about the role of a tympanic membrane defect, the actual evidence to support its role as a causative factor is not as strong as we would like. By definition, CSOM requires the presence of a tympanic membrane defect, be it a perforation or a tympanostomy tube. We know that we can often cure CSOM by performing a tympanoplasty. This raises the question as to whether tubotympanic reflux is involved. Some patients with tympanic membrane perforations or tympanostomy tubes, particularly adults and older children, will express mucus from the ear every time they swallow. (6)

Several facts argue against tympanic membrane defects as a primary cause of CSOM. For one, traumatic perforations rarely lead to CSOM. Second, infections with CSOM pathogens, such as P aeruginosa, can occur with an intact tympanic membrane. The literature on AOM dismisses the role of Paeruginosa and staphylococci as contaminants. A study of tympanoplasty procedures in Finland many years ago showed that the likelihood of a tympanic membrane reperforation was greater in patients who had P aeruginosa infections preoperatively. (8) So in fact, a tympanic membrane defect may be the result of CSOM or infection with certain pathogens rather than an inciting event.

Eustachian tube dysfunction. Animal experiments have shown that eustachian tube obstruction significantly increases the likelihood of developing P aeruginosa otitis media, which may subsequently perforate the tympanic membrane and progress into a polymicrobial infection similar to what we typically see in humans. (9,10) This suggests that eustachian tube dysfunction may be a contributing factor in CSOM. This represents a real change in our thinking, where we no longer believe that a perforation must already be present before the P aeruginosa can infiltrate the middle ear. We also know that pathologically patent eustachian tubes may predispose certain patients (e.g., Eskimos and aboriginal North Americans) to CSOM, as well. However, although upper respiratory tract infections are common and often cause eustachian tube obstruction, we very rarely see CSOM as a result. (6,11)

Damage from AOM. Another popular belief is that CSOM is a sequela of inadequately treated recurrent AOM. Studies from the aboriginal populations of Australia suggest that the aggressive treatment of AOM may be associated with a lower incidence of CSOM. (12,13) Conversely, CSOM is more common in developing countries where access to AOM treatment is limited. In the West, most CSOM patients have a history of recurrent AOM, but we don't know much more about this relationship. We do know that AOM causes mucosal sloughing, impairs ciliary clearance, exposes microbial binding sites, induces scarring, and may lead to localized blockage such as antral block. But again, AOM rarely leads to CSOM.

With such uncertainty, we must reexamine our traditional model of CSOM. We should look at the ear as an ecosystem in which there are many different ways to change the growth of various organisms.

Evaluation

There is no point in performing an evaluation of a patient with CSOM if the findings are not likely to change the treatment plan. Evaluation methods include endoscopic, microbiologic, hematologic, immunologic, and radiologic investigations. I do not perform all of these evaluations routinely, but I do perform all of them at one time or another.

Endoscopic evaluation. I routinely perform nasopharyngoscopy in adults with unilateral ear disease. The only time I perform nasopharyngoscopy in children is when I have a specific suspicion that it will detect something in the nasopharynx, such as adenoid pathology. I think that our improved understanding of eustachian tube physiology will lead to an increase in the use of tubal endoscopy. In some cases, tubal endoscopy will be more or less just an extension of nasopharyngoscopy, but other times it will involve actually passing the scope up the eustachian tube in a search for polyps. I do not routinely perform an endoscopic evaluation of the ear except for patients who are undergoing a second-look operation and for those who have unique pathology that requires visualization of narrow recesses, such as the protympanum-proximal eustachian tube.

Microbiologic evaluation. Opinions vary greatly among clinicians as to when a culture becomes necessary. I do not culture until routine treatment measures have failed and when pathology that can only be treated with surgery, such as cholesteatoma, has been ruled out. All the antibiotics in the world are not going to eliminate a cholesteatoma. In most chronically draining perforations, tympanoplasty will be preferable to heroic medical efforts with culture-directed intravenous antibiotics. In unusual circumstances where conventional medical treatment has failed and tympanoplasty is contraindicated, cultures may help direct therapy. One must always be cautious when interpreting culture results in CSOM because the presence of a microorganism could represent simple colonization rather than an indication of a causal role in the infection.

Hematologic evaluation. Blood evaluations, such as measurement of white blood cell counts, are necessary only in cases of pending complications.

Immunologic evaluation. I've treated a number of patients over the course of my career who turned out to have deficiencies that required immunoglobulin therapy. But obviously, immunologic evaluation is not something that is done routinely. I evaluate for such conditions only in children who have demonstrated more of a generalized predisposition to infections and in patients who have failed repeated courses of both medical and surgical interventions. Far more often, atopic disease may contribute to the ongoing tubotympanic dysfunction in CSOM.

Radiologic evaluation. I do not routinely obtain computed tomography (CT) for every patient with a chronically draining ear because CSOM is generally benign and usually follows a predictable course. It usually does not change my plan of care. I limit my use of imaging to cases in which atypical presentations make me concerned about more serious pathology (e.g., a tumor) or possible complications (e.g., a semicircular canal fistula). For example, I would obtain CT on a patient who had vertigo or pain in association with CSOM. Primary care physicians and general otolaryngologists might find CT more useful to rule out serious pathology and to determine whether referral to an otologist is indicated.

Locally directed medical management

We all recognize the need to clean the ear, whether by debridement, suctioning, or dry mopping. Unfortunately, most primary care physicians do not have an operating head on their otoscope, much less an operating microscope and a suction, so most are not equipped to thoroughly debride an ear.

Many clinicians advocate dry-ear precautions for patients with a perforation or tympanostomy tube. I don't routinely restrict water exposure unless the patient has demonstrated problems with water exposure. A good deal of literature suggests that swimming has little if any impact on the rate of otorrhea in children with tympanostomy tubes. (14)

Topical rinses with dilute vinegar and/or isopropyl alcohol may (mechanically) clean and (chemically) disinfect the ear. Exposure to such agents should be limited (i.e., the ear should not remain soaked with these solutions) because ototoxicity may occur. After the ear is rinsed, it should be dried with a hair dryer set on a low heat or air only. In some cases, insufflation of boric acid, with or without antimicrobial agents, may further eliminate otorrhea.

Cautery can be extremely helpful for treating granulation tissue, especially when an ototopical preparation has failed. Trichloroacetic acid can be used to promote healing of persistent tympanic membrane perforations. This isn't all that common a practice, but it can be very effective. I anesthetize with tetracaine on a cotton pledget applied for 30 minutes. I use a microswab dipped in 85% trichloroacetic acid to cauterize the edges of the perforation until the margin of the perforation turns white. Most cases require repeat procedures, so I have the patient return every week or two until the hole is closed. With this technique, I have also been able to salvage many eardrums that had not healed with tympanoplasty.

Insult avoidance is certainly important. Patients need to avoid products such as hair spray and other substances that can infiltrate the ear canal and cause problems. One substance that commonly causes middle ear inflammation is topical neomycin, to which roughly 1 in 6 patients will demonstrate skin sensitivity.

I am a big advocate of topical antimicrobials in conjunction with other modalities. The literature on antibiotic treatment of CSOM is limited, but some studies do indicate that ototopical antibiotics for CSOM are more efficacious than antiseptics alone and more efficacious than oral antibiotics. The data also suggest that their efficacy may be enhanced by the addition of a steroid. The Cochrane Database published a systematic review of 9 randomized controlled trials in which systemic antibiotics were compared with topical antibiotics or antiseptics for the treatment of chronically discharging ears with underlying eardrum perforations in more than 800 patients of all ages. (15) The analysts found that quinolone antibiotic drops were better than oral or injected antibiotics, including systemic quinolones, for drying the ear. The advantage of nonquinolone topical antibiotics (without steroids) or antiseptics over systemic treatment was less clear. No benefit was seen when systemic antibiotic treatment was added to topical antibiotic treatment, although the evidence was limited.

Systemic medical management

Systemic treatment of CSOM has traditionally relied on parenteral antibiotics aimed at P aeruginosa. At least short-term control can be achieved in upwards 0f 90% of patients with culture-directed parenteral therapy. (16-19) I tend not to use such treatment in most of my patients because of the lasting success of surgical management in the vast majority of cases. If there is evidence of allergy, immunodeficiency, or gastroesophageal reflux, adjunctive therapy should be directed at controlling these conditions.

Surgical management

A number of conditions can present as CSOM that are not benign or easily treated with medical management: cholesteatomas, foreign bodies, unusual pathogens (e.g., mycobacteria), immunologic deficiencies, congenital anomalies, cerebrospinal fluid leaks, and neoplasms.

Cholesteatomas are not always obvious. I recently saw a child with a normal-appearing, intact eardrum and conductive hearing loss. The CT image was almost pristine. The only anomaly was a minute bit of soft tissue on the promontory that turned out to be a cholesteatoma. Herein lies one advantage of surgery over medical management: It is much easier to discern surgical pathology with direct visualization than it is with radiographic imaging.

Foreign bodies include tympanostomy tubes, extruding ossicular prostheses, glove powder, Silastic sheeting, hearing aid molding material, and many other substances. Their presence can lead to the formation of granulation tissue and require surgical intervention because current medical therapies are ineffective at controlling most foreign-body reactions.

Biofilms have become a popular topic of late--perhaps too popular. It is possible that the biofilm concept is being overused in an attempt to explain complex host-pathogen interactions. Nevertheless, we do understand enough about biofilms that we should consider what their role might be in disease states such as CSOM. Biofilm formation can lead to increased resistance to antibiotics, absolute resistance to immunoglobulins, collateral damage by defense systems and, ultimately, to persistent disease. This could explain why many cases of CSOM respond more favorably to surgery than to medical treatment. (20-22)

Surgical procedures that have been performed in patients with CSOM include adenoidectomy, tympanoplasty, mastoidectomy, sinus surgery, tympanostomy tube removal, and eustachian tuboplasty. Infected adenoids can contain a reservoir of pus and contribute to CSOM. Although the results of small studies have been mixed, an adenoidectomy in such a patient at the time of a tympanoplasty or mastoidectomy can eliminate that reservoir and hasten recovery. (23)

Combined mastoidectomy and tympanoplasty has been considered the gold standard for the treatment of chronically draining ears. Tympanoplasty alone is usually sufficient. Obviously, there are benefits to performing a mastoidectomy. For example, you can't identify a cholesteatoma in the mastoid unless you open the mastoid, and it takes only a few minutes to perform. But it's just not necessary to do so routinely in uncomplicated CSOM. (24,25)

Management algorithms

Pediatric CSOM. I always start with debridement and an ototopical medication, even if the patient has already been taking a drop. Many patients have debris that impairs the efficacy of an ototopical preparation, so this needs to be cleared. It's important to teach parents the proper way to administer the drops so that the antibiotic actually has a chance to work. The fact that a patient has already been taking drops prescribed by a pediatrician or family practitioner doesn't mean that the patient has taken them correctly or that the drops are getting into the middle ear or that the patient has received an adequate amount.

Treating a comorbidity such as an allergy obviously is important. Removing or replacing a tympanostomy tube has its advantages and disadvantages. For instance, in a patient with bilateral tympanostomy tubes and unilateral CSOM, I am concerned that something, such as cotton or paper from the drapes, might have gotten trapped around the tube at the time of tube placement. We may need to treat inflammation around a foreign body, such as a tympanostomy tube, more aggressively, whether the underlying mechanism is a biofilm, extraneous debris, sensitivity to the tube, or something else. This will often involve removal of the foreign body if more conservative measures prove to be ineffective. I would consider performing an adenoidectomy at the time of tube replacement to minimize the nasopharyngeal reservoir of pathogens.

If CSOM occurs in the absence of a tube, the next step is tympanic membrane cautery, which was discussed earlier. The next option is tympanoplasty, with or without adenoidectomy. Adenoidectomy is more likely to be beneficial in children younger than 7 or 8 years than in children aged 16 years or older. Mastoidectomy may be more effective in ears with more chronic infection. If the ear is still draining through a residual perforation after tympanoplasty, I will repeat tympanic membrane cautery. This will salvage most residual perforations. The next step is an immunologic evaluation to look for an IgG subclass deficiency; Ig[G.sub.2] deficiency is one of the more common findings in patients with recurrent AOM. If a revision tympanoplasty becomes necessary, I'll be more aggressive. If I haven't done so yet, I will perform a simultaneous adenoidectomy or mastoidectomy. My last resort is parenteral antibiotics.

Adult CSOM. The adult algorithm is quite similar to the pediatric plan. I am more aggressive in pursuing rhinosinusitis in adults. I tend to favor a canal-wall-up mastoidectomy when the ear is continually or repeatedly wet. Canal-wall-down procedures are rarely necessary, nor is culture-directed parental antibiotic therapy.

References

(1.) Paparella MM, Bluestone CD, Arnold W, et al. Definition and classification. Ann Otol Rhinol Laryngol 1985;94(suppl 116):8-9.

(2.) Klein JO, Tos M, Hussl B, et al. Recent advances in otitis media. Definition and classification. Ann Otol Rhinol Laryngol 1989;98(suppl 139):10.

(3.) Kenna MA, Bluestone CD. Microbiology of chronic suppurative otitis media in children. Pediatr Infect Dis 1986;5:223-5.

(4.) Papastavros T, Giamarellou H, Varlejides S. Role of aerobic and anaerobic microorganisms in chronic suppurative otitis media. Laryngoscope 1986;96:438-42.

(5.) Kenna MA. Etiology and pathogenesis of chronic suppurative otitis media. Ann Otol Rhinol Laryngol 1988;97(suppl 131): 16-17.

(6.) Bluestone CD, Klein JO. Intratemporal complications and sequelae of otitis media. In: Bluestone CD, Stool SE, eds. Pediatric Otolaryngology. Vol. 1. Philadelphia: W.B. Saunders; 1990:487-536.

(7.) Antonelli PJ, Juhn SK, Goycoolea MV, Giebink GS. Middle ear susceptibility to Pseudomonas infection during acute otitis media. Ann Otol Rhinol Laryngol 1993;102:531-6.

(8.) Vartiainen E, Kansanen M. Tympanomastoidectomy for chronic otitis media without cholesteatoma. Otolaryngol Head Neck Surg 1992;106:230-4.

(9.) Antonelli PJ, Juhn SK, Goycoolea MV, Giebink GS. Pseudomonas otitis media after eustachian tube obstruction. Otolaryngol Head Neck Surg 1992;107:511-15.

(10.) Antonelli PJ, Juhn SK, Le CT, Giebink GS. Acute otitis media increases middle ear susceptibility to nasal injection of Pseudomonas aeruginosa. Otolaryngol Head Neck Surg 1994; 110:115-21.

(11.) Daly KA. Epidemiology of otitis media. Otolaryngol Clin North Am 1991;24:775-86.

(12.) Morris PS, Leach AJ, Silberberg P, et al. Otitis media in young Aboriginal children from remote communities in Northern and Central Australia: A cross-sectional survey. BMC Pediatr 2005;5:27.

(13.) Gibney KB, Morris PS, Carapetis JR, et al. The clinical course of acute otitis media in high-risk Australian Aboriginal children: A longitudinal study. BMC Pediatr 2005;5:16.

(14.) Lee D, Youk A, Goldstein NA. A meta-analysis of swimming and water precautions. Laryngoscope 1999;109:536-40.

(15.) Macfadyen CA, Acuin JM, Gamble C. Systemic antibiotics versus topical treatments for chronically discharging ears with underlying eardrum perforations. Cochrane Database Syst Rev 2006;(1): CD005608.

(16.) Brook I. Anaerobic isolates in chronic recurrent suppurative otitis media. Treatment with carbenicillin alone and in combination with gentamicin. Infection 1979;7:247-51.

(17.) Kenna MA, Bluestone CD, Reilly JS, Lusk RP. Medical management of chronic suppurative otitis media without cholesteatoma in children. Laryngoscope 1986;96:146-51.

(18.) Supance JS, Bluestone C. "How I do it"--otology and neurotology. A specific issue and its solution. Medical management of the chronic draining ear. Laryngoscope 1983;93:661-2.

(19.) Fliss DM, Dagan R, Houri Z, Leiberman A. Medical management of chronic suppurative otitis media without cholesteatoma in children. J Pediatr 1990; 116:991-6.

(20.) Buret A, Ward KH, Olson ME, Costerton JW. An in vivo model to study the pathobiology of infectious biofilms on biomaterial surfaces. J Biomed Mater Res 1991 ;25:865-74.

(21.) Hoyle BD, Jass J, Costerton JW. The biofilm glycocalyx as a resistance factor. J Antimicrob Chemother 1990;26:1-5.

(22.) Gilbert P, Collier PJ, Brown MR. Influence of growth rate on susceptibility to antimicrobial agents: Biofilms, cell cycle, dormancy, and stringent response. Antimicrob Agents Chemother 1990;34: 1865-8.

(23.) Gianoli GJ, Worley NK, Guarisco JL. Pediatric tympanoplasty: The role of adenoidectomy. Otolaryngol Head Neck Surg 1995;113: 380-6.

(24.) McGrew BM, Jackson CG, Glasscock ME III. Impact of mastoidectomy on simple tympanic membrane perforation repair. Laryngoscope 2004; 114:506-11.

(25.) Mishiro Y, Sakagami M, Takahashi Y, et al. Tympanoplasty with and without mastoidectomy for non-cholesteatomatous chronic otitis media. Eur Arch Otorhinolaryngol 2001;258:13-15.

Patrick J. Antonelli, MD, MS, FACS
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Author:Antonelli, Patrick J.
Publication:Ear, Nose and Throat Journal
Date:Oct 1, 2006
Words:3249
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