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This is perhaps one of the oldest entities of ENT 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.
CSOM is initiated by an episode of acute infection. It 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 body’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.
The larger the TM perforation, the more likely the patient is to 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.In Britain, 0.9% of children and 0.5% of adults have CSOM. In Israel, only 0.039% of children are affected.
Much of the problem of CSOM comes from the associated conductive hearing loss and the social stigma of pus coming out of the affected ear. The serious complications of CSOM arises from associated intracranial complications. CSOM itself is not a fatal disease. Another compication is development of sensorineural hearing loss. In these cases hearing loss becomes very severe and at this stage even operating these ears is not likely to correct them.
Certain population subsets are at increased risk for developing CSOM. The American Indian , Eskimo and Indians 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.
Prevalence of CSOM appears to be distributed equally between males and females.
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.
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.
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.
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 CSOM increases with the following circumstances.
