eMedicine Specialties > Otolaryngology and Facial Plastic Surgery > Middle Ear & Mastoid

Middle Ear, Chronic Suppurative Otitis, Medical Treatment

Author: David Parry, MD, Staff Physician, Department of Otolaryngology-Head and Neck Surgery, ENT Associates of Children's Hospital, Boston
Coauthor(s): Peter S Roland, MD, Professor, Department of Neurological Surgery, Professor and Chairman, Department of Otolaryngology-Head and Neck Surgery, Director of Clinical Center for Auditory, Vestibular and Facial Nerve Disorders, Chief of Pediatric Otology, University of Texas Southwestern Medical Center; Adjunct Professor of Communicative Disorders, University of Texas School of Human Development
Contributor Information and Disclosures

Updated: Jul 7, 2009

Introduction

Background

Chronic suppurative otitis media (CSOM) is a disease well known to otolaryngologists. This disease differs from chronic serous otitis media. Chronic serous otitis media may be defined as a middle ear effusion, without perforation, which is reported to persist more than 1-3 months, depending on the author. CSOM is a perforated tympanic membrane with persistent drainage from the middle ear. The chronically draining ear can be difficult to treat for a variety of reasons. This article presents the pathophysiology of the disease, treatment alternatives, and complications.¹

The ancient Egyptians recognized CSOM as a disease of the ear and treated it with fluids of duck grease, borax, and cow milk. Traditional healers in India recommended both medicinal and behavioral treatments. They advised drinking butter, maintaining silence, and avoiding fatigue to cure CSOM. Hippocrates understood the recurrent nature of CSOM and placed patients on different medical and behavioral therapies, depending on the time course of their suppuration. Initially, he prescribed hot water, human milk, and sweet wine, along with avoiding the sun, strong wind, and smoky rooms. For recurrent cases, he added a topical powder consisting of lead oxide and lead carbonate.

CSOM is defined as chronic otorrhea (ie, >6-12 wk) through a perforated tympanic membrane (TM).^2,3 Chronic suppuration can occur with or without cholesteatoma, and the clinical history of both conditions can be very similar. The treatment plan for cholesteatoma always includes tympanomastoid surgery with medical treatment as an adjunct. Cholesteatoma and its management are not considered in this article.

Pathophysiology

CSOM is initiated by an episode of acute infection. The pathophysiology of CSOM begins with irritation and subsequent inflammation of the middle ear mucosa. The inflammatory response creates mucosal edema. Ongoing inflammation eventually leads to mucosal ulceration and consequent breakdown of the epithelial lining. The host's attempt at resolving the infection or inflammatory insult manifests as granulation tissue, which can develop into polyps within the middle ear space. The cycle of inflammation, ulceration, infection, and granulation tissue formation may continue, destroying surrounding bony margins and ultimately leading to the various complications of CSOM.

Pseudomonas aeruginosa, Staphylococcus aureus, Proteus species, Klebsiella pneumoniae, and diphtheroids are the most common bacteria cultured from chronically draining ears. Anaerobes and fungi may grow concurrently with the aerobes in a symbiotic relationship. The clinical significance of this relationship, although unproven, is theorized to be an increased virulence of the infection. Understanding the microbiology of this disease enables the clinician to create a treatment plan with the greatest efficacy and least morbidity.

Microbiology

P aeruginosa is the most commonly recovered organism from the chronically draining ear. Various researchers over the past few decades have recovered pseudomonads from 48-98% of patients with CSOM.

P aeruginosa uses pili to attach to necrotic or diseased epithelium of the middle ear. Once attached, the organism produces proteases, lipopolysaccharide, and other enzymes to prevent normal immunologic defense mechanisms from fighting the infection. The ensuing damage from bacterial and inflammatory enzymes creates further damage, necrosis, and, eventually, bony erosion leading to some of the complications of CSOM. Fortunately, in the immunocompetent individual, the infection rarely causes serious complications or disseminated disease. Pseudomonal infections commonly resist macrolides, extended-spectrum penicillins, and first- and second-generation cephalosporins. This can complicate treatment plans, especially in children.

S aureus is the second most common organism isolated from chronically diseased middle ears. Reported data estimate infection rates from 15-30% of culture positive draining ears. The remainder of infections is caused by a large variety of gram-negative organisms. Klebsiella (10-21%) and Proteus (10-15%) species are slightly more common than other gram-negative organisms.

Five to 10% of infections are polymicrobial in etiology, often demonstrating a combination of gram-negative organisms and S aureus. The anaerobes (Bacteroides, Peptostreptococcus, Peptococcus) and fungi (Aspergillus, Candida) complete the spectrum of colonizing organisms in this disease. The anaerobes make up 20-50% of the isolates in CSOM and tend to be associated with cholesteatoma. Fungi have been reported in up to 25% of cases, but their pathogenic contribution to this disease is unclear.

Frequency

United States

The larger the TM perforation, the more likely the patient is to develop CSOM. The risk of developing otorrhea (but not necessarily CSOM) through a ventilation tube is reportedly 21-50%. Annually, more than a million tubes are placed to treat recurrent otitis media and otitis media with effusion. Studies report that 1-3% of patients with ventilation tubes develop CSOM.

Some studies estimate the yearly incidence of CSOM to be 39 cases per 100,000 persons in children and adolescents aged 15 years and younger.

International

In Britain, 0.9% of children and 0.5% of adults have CSOM. In Israel, only 0.039% of children are affected.

Mortality/Morbidity

Much of the morbidity of CSOM comes from the associated conductive hearing loss and the social stigma of an often fetid fluid draining from the affected ear. The mortality of CSOM arises from associated intracranial complications. CSOM itself is not a fatal disease. Although some studies report sensorineural hearing loss as a morbid complication of CSOM, other evidence conflicts with this claim.

Race

Certain population subsets are at increased risk for developing CSOM. The American Indian and Eskimo demonstrate an increased risk of infection. Eight percent of American Indians and up to 12% of Eskimos are affected by CSOM. The anatomy and function of the eustachian tube play a significant role in this increased risk. The eustachian tube is wider and more open in these populations than in others, thus placing them at increased risk for nasal reflux of bacteria common to AOM and recurrent AOM and leading to more frequent development of CSOM. Other populations at increased risk include children from Guam, Hong Kong, South Africa, and the Solomon Islands.

Sex

Prevalence of CSOM appears to be distributed equally between males and females.

Age

Exact prevalence in different age groups is unknown, though some studies estimate the yearly incidence of CSOM to be 39 cases per 100,000 individuals in children and adolescents aged 15 years and younger.⁴

Clinical

History

Patients with CSOM present with a draining ear of some duration and a premorbid history of recurrent AOM, traumatic perforation, or placement of ventilation tubes. Typically, they deny pain or discomfort.

• A common presenting symptom is hearing loss in the affected ear.
• Reports of fever, vertigo, and pain should raise concern about intratemporal or intracranial complications.
• A history of persistent CSOM after appropriate medical treatment should alert the physician to consider cholesteatoma.

Physical

• The external auditory canal may or may not be edematous and is typically not tender.
• The discharge varies from fetid, purulent, and cheeselike to clear and serous.
• Granulation tissue is often seen in the medial canal or middle ear space.
• The middle ear mucosa visualized through the perforation may be edematous or even polypoid, pale, or erythematous.

Causes

The diagnosis of CSOM requires a perforated TM. These perforations may arise traumatically, iatrogenically with tube placement, or after an episode of AOM, which decompresses through a tympanic perforation.¹

The mechanism of infection of the middle ear cleft is postulated to be translocation of bacteria from the external auditory canal through a perforation into the middle ear. Some authors suggest that the pathogenic organisms may enter through reflux of the eustachian tube. The data supporting this theory are inconclusive. Most of the pathogenic bacteria are those common to the external auditory canal.

The risk of developing otorrhea (but not necessarily CSOM) through a ventilation tube is reportedly 21-50%. Annually, more than a million tubes are placed in the United States for recurrent otitis media and otitis media with effusion. Studies have reported that 1-3% of patients with ventilation tubes develop this disease.

The risk of developing CSOM increases with the following circumstances⁴ :

• A history of multiple episodes of AOM
• Living in crowded conditions
• Daycare facility attendance
• Being a member of a large family

Studies trying to correlate the frequency of the disease with parental education, passive smoke, breastfeeding, socioeconomic status, and the annual number of upper respiratory tract infections are inconclusive.

Patients with craniofacial anomalies are special populations at risk for CSOM. Cleft palate, Down syndrome, cri du chat syndrome, choanal atresia, cleft lip, and microcephaly are other diagnoses that increase the risk of CSOM, presumably from altered eustachian tube anatomy and function.

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