Tuberculosis is caused by an infection with the bacterium Mycobacterium tuberculae. In 2004, 14,517 cases of tuberculosis were reported in the United States (17). The infection is spread via respiratory droplets. Pulmonary symptoms predominate, but any organ system can be affected. Spread to the ear can be via direct extension through the nasopharynx, from hematogenous spread, or on rare occasions, via direct implantation through a preexisting tympanic perforation. Tubercular otitis media occurs in 1% of all tuberculosis cases and currently accounts for roughly 0.1% of all cases of otitis media (18-20). Presentation of tubercular otitis is variable but classically is a painless, copious otorrhea with multiple or total tympanic membrane perforations and granulation tissue. Tubercular otitis media has a higher incidence of postauricular fistulae, preauricular lymphadenopathy, and facial nerve involvement when compared to other bacterial causes of otitis media. It is important to note that only 42% of patients with tubercular otitis media have evidence of pulmonary tuberculosis (19).
Facial paralysis is sometimes present in tuberculosis infections and has been estimated at 40% in patients with tubercular otitis (21). The incidence of facial nerve involvement in tuberculosis otitis media seems to be decreasing, with a 30% incidence before 1953 versus a 16% incidence after 1953 (19). The incidence of facial nerve involvement is increased in pediatric patients, with the highest elevation in children less than 10 years of age. Although infections are often bilateral, facial nerve involvement is almost always unilateral (22). In fact, clinicians should have a high index of suspicion for tuberculosis in any child with facial paralysis and otorrhea (21). Damage to the facial nerve is from direct involvement with the mycobacterium on the nerve itself or through nerve impingement from a sequestrum or subperiosteal abscess.
Diagnosis can be made through cell culture, but mycobacterium is difficult to isolate and often takes a prolonged incubation before identification can be made. The purified protein derivative (PPD) test, a skin test for tuberculosis, can be used as a screening tool and often identifies patients with previous exposure to tuberculosis. Chest X rays along with sputum cultures are used to identify patients with active pulmonary disease. Histopathology demonstrates the classic finding of caseating granulomas and acid fast bacilli. The treatment of tuberculosis entails multiple concurrent antibiotics over extended periods. Isonazid, rifampin, pyrazinamide, ethambutol, and streptomycin all have activity against the mycobacterium.
The treatment of facial palsy in active tubercular otitis media or mastoiditis is controversial. Singh published a review of 43 patients to assess the role of surgery in tuberculous mastoiditis. Of the patients, 17 had facial paralysis in this study. He found that 92% of patients treated with antituberculosis medical therapy without surgery had recovery of the facial nerve, with only 80% of patients undergoing surgery (cortical mastoidectomy and removal of sequestrum) obtaining recovery. In the surgical patients, facial nerve decompression was not performed as a part of the operation. These results may reflect more severe cases being selected into the surgical group. The authors concluded that the only role for surgery is incision and drainage of a postauricular abscess or removal of sequestrum, if present; and chemotherapeutic management is the treatment of choice for tubercular mastoiditis (22). Harbert in 1964 had a similar conclusion and felt that surgical intervention was contraindicated as a treatment for facial paralysis in tuberculosis infections (23). However, many other investigators have advocated strongly for decompressive surgery. These investigators cite complete facial nerve recovery, without hearing loss or other complications, as the expected outcome of decompressive surgery (20,24-26).
The prognosis of facial nerve recovery depends heavily on early diagnosis and treatment with antitubercular drugs. In a review by Singh, when treatment was initiated within five days of developing facial palsy, nearly all patients had complete nerve recovery. When therapy was delayed more than two months after developing facial palsy, patients rarely demonstrated a favorable outcome (22). See Chapter 12 for further discussion of tuberculosis.
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