Tuberculous otitis media: two case reports and literature review.

Abstract

Tuberculous otitis media can be difficult to diagnose because it can easily be confused with other acute or chronic middle ear conditions. Compounding this problem is the fact that physicians are generally unfamiliar with the typical features of tuberculous otitis media. Finally, the final diagnosis can be difficult because it requires special culture and pathologic studies. To increase awareness of this condition, we describe two cases of tuberculous otitis media and we review the literature.

Introduction

Because tuberculous otitis media can easily be confused with other acute or chronic middle ear conditions, its diagnosis is often delayed. The clinical signs and symptoms of tuberculous otitis media were first documented in 1853, and the tuberculous bacillus was first isolated in otic discharge in 1883. (1) Since then, many so-called characteristic clinical features have been described in the literature, including a profuse purulent discharge, profound hearing loss, multiple perforations of the eardrum, and facial paralysis. (2)

The incidence of tuberculosis in the middle ear is very low; tuberculosis accounts for only 0.04% of all cases of chronic suppurative otitis media. (3) When it does occur, it is associated with substantial morbidity, and a delay in initiating therapy can lead to serious complications. These complications include early destruction of the middle ear conductive mechanism, facial paralysis, cochlear involvement with labyrinthitis and sensorineural hearing loss, and intracranial dissemination of infection. (4)

In this article, we describe two cases of tuberculous otitis media and we review the literature in an attempt to increase physician awareness of this disease and to emphasize the need for prompt recognition and treatment.

Case reports

Patient 1. A 40-year-old woman was referred to our department with a 1-year history of a discharge from the right ear and associated hearing loss. The patient had initially been admitted to our hospital 2 years earlier, and she was diagnosed with a pyogenic cerebral abscess. She was discharged after appropriate management, and she had no further complaints.

Twelve months later, she began to notice a gradual hearing loss in her right ear. Soon afterward, the right ear began to emit a purulent, foul-smelling discharge. She also began to experience severe frontal headaches and a low-grade fever with chills. She denied symptoms of cough, weight loss, or hemoptysis. She was treated with antibiotics, but did not respond.

Upon referral to our unit, examination revealed a large subtotal perforation in the right ear in addition to the purulent discharge. Audiometry indicated a 30-dB conductive hearing loss. Chest x-rays detected multiple irregular densities in both lung fields that were consistent with slowly resolving foci of tuberculosis.

Surgical exploration of the right mastoid revealed that a large amount of granulation tissue had involved the malleus and the incus. We performed a modified radical mastoidectomy. Histopathologic analysis of the excised tissue identified chronic inflammatory cells and a number of epithelioid cells and Langhans' giant cells. A large area of caseous necrosis was surrounded by a histiocytic mantle. No acid-fast bacilli could be seen on special staining.

The patient was started on a 9-month course of empiric four-drug antituberculosis treatment with oral rifampin, isoniazid, ethambutol, and pyrazinamide, and she was monitored during regular follow-up visits to the outpatient clinic. After completing her course of treatment, the patient was symptom-free and her antituberculosis treatment was discontinued.

Patient 2. A 19-year-old man came to our outpatient otolaryngology clinic with a complaint of a profuse discharge from his right ear that had persisted for 4 months. The purulent and foul-smelling otorrhea had begun following an episode of trauma to the right eardrum that had been inflicted by a sharp pin. The amount of discharge had progressively increased since its onset. The patient also reported an associated progressive hearing loss in the same ear. He had no history of fever or weight loss, but he did have a history of occasional episodes of hemoptysis that had lasted for 3 months.

Examination revealed the presence of a heavy, yellow, mucoid discharge in the right ear that emanated from a small posteroinferior perforation in the tympanic membrane. Audiometry reflected a conductive hearing loss of 20 to 25 dB. Findings on systemic examination were unremarkable. A chest x-ray detected fibrotic changes in the left mid-lung zone; these changes were suggestive of previously healed pulmonary tuberculosis.

When the patient did not respond to a 7-day course of antibiotics, he was advised to undergo surgical exploration of the mastoid. Surgery revealed that large amounts of granulation tissue were present in the middle ear, in the mastoid, over the facial ridge, and in the area of the facial recess. The stapes was also involved, and a perilymph leakage from the oval window was observed. Histopathologic analysis of the granulation tissue identified multiple discrete epithelioid granulomas that were characterized by aggregates of epithelioid cells, Langhans' giant cells, and a few areas of necrosis. The patient was diagnosed with a chronic granulomatous inflammation that was consistent with tuberculosis.

The patient was prescribed the same four-drug antituberculosis regimen for 6 months and was followed closely by both the otolaryngology and pulmonology departments. During follow-up, his mastoid cavity remained dry and he experienced no further symptoms. He was advised to continue drug treatment for a total of 9 months.

Discussion

Tuberculous otitis media is generally considered a disease of children and young adults, as patients <15 years of age account for 84% of all cases. (5) In the West, the annual incidence of tuberculous otitis media has decreased during the past 60 years from 5.5 cases per 100,000 population before 1953 to 2.3 cases after 1953. (3, 6-8) This decrease has been attributed to the declining incidence of tuberculosis itself. However, in areas where tuberculosis is endemic, data have shown that there has been a steady increase in its incidence (2,000 to 3,000 new cases per year) and that there was a subsequent increase in the total number of diagnosed cases of tuberculous otitis media (from 31 in 1984 and 1985 to 43 cases from 1985 through 1990) (8, 9) These figures are probably representative of the situation in our country (Pakistan), although we do not have any significant data of our own.

The pathogenesis of tuberculous otitis media involves one of three major mechanisms: (1) aspiration of mucus through the eustachian tube, (2) blood-borne dissemination from other tuberculous foci, or (3) in rare cases, direct implantation through the external auditory canal and a tympanic membrane perforation. (4)

The clinical manifestations of tuberculous otitis media vary greatly, but the most common feature is an aural discharge of insidious onset. Most patients also experience an associated acute-onset hearing loss that is disproportionate to the extent of their disease. (4) The hearing loss can be either conductive (90% of patients), sensorineural (~8%), or mixed (~2%). (10) Characteristically, there is little or no otalgia. (3, 6-10)

Examination of the affected ear will usually reveal pale-yellow granulation tissue on a thickened and hyperemic tympanic membrane. Perforations usually occur in the area of the granulation early in the disease as a result of the coalescence of the granulomas. (4) The consistency of the discharge ranges from thick and mucoid to thin and watery. The granulomatous process often produces a visible destruction of the ossicles, which can be seen through the tympanic membrane perforation. (1, 4, 6) As the disease progresses, the amount of granulation tissue can become profuse and lead to an attic-antral blockage. A direct extension of the mucosal disease can lead to mastoiditis or tuberculous osteomyelitis of the temporal bone. Associated facial nerve paralysis is seen in approximately 16% of adult cases and 35% of pediatric cases. (9, 10) Another reported complication is a severe intracranial spread of the infection that results in extradural abscess formation or tuberculous meningitis; these latter manifestations can be the initial signs of tuberculous otitis media. (5) Labyrinthitis and petrositis have also been reported in association with the mastoid disease. (1)

The differential diagnosis is broad and includes such disorders as histoplasmosis, North American blastomycosis, South American blastomycosis, syphilis, midline granuloma, Wegener's granulomatosis, histiocytosis X, nocardiosis, necrotizing external otitis, lymphoma, bacterial otitis media, and cholesteatoma. (11) These diagnoses can be ruled out clinically by the presence of pain and the type and consistency of the discharge.

In diagnosing tuberculous otitis media, it is important to consider it as a differential diagnosis of chronic suppurative otitis media. The diagnosis of tuberculous otitis media is often missed in the early stages or is made only after surgical treatment for otitis media, (3, 4, 7-9, 12-14) as happened in the two cases we report in this article. Patients who have known or suspected active extra-aural tuberculosis and chronic suppurative otitis media should also be evaluated for tuberculous otitis media. (5) The assessment should include a thorough examination of the ear, a chest x-ray, and skin testing.(4) The prevalence of active or inactive pulmonary tuberculosis in patients with tuberculous otitis media ranges from 14 to 93%,(3,6-9,14-17) and 40 to 50% of patients with tuberculous otitis media have no evidence of tuberculosis elsewhere. (6,7,10,13) External ear canal cultures have been reported to be positive for tuberculosis in 5 to 35% of cases, and smears are positive in approximately 2O%.(17) However, confirming the diagnosis can be difficult because the high rate of secondary bacterial infection of the tuberculous middle ear (79%) can prevent the identification of Mycobacterium tuberculosis on either staining or culture. (8,12,16)

Even when a thorough preoperative investigation for tuberculosis is performed (including a Mantoux' test, chest x-ray, and staining or culture of otic discharge), tuberculous otitis media might still be detected in only 26% of patients. Mastoid x-rays usually show surprisingly little abnormality except for an increased density of the soft tissues in the antrum.(4) Recent studies have shown that computed tomography (CT) is the best imaging modality available for the diagnosis of tuberculous mastoiditis; CT provides more information than do standard plain films and it is more accurate and useful than polycycloidal tomography and magnetic resonance imaging.(18)

Histopathologic examination of the involved middle ear and mastoid mucosa will show three types of changes: miliary, granulomatous, and caseous.(1) The miliary type is associated with superficial infection, the granulomatous type with superficial bony involvement, and the caseous type with massive necrosis and sequestration.(4)

After proper diagnosis, the initial management of tuberculous otitis media should be medical. Antituberculosis drugs dramatically improve the prognosis in most patients. For complete cure, drug therapy should be taken for at least 6 months. During serial follow-up examinations, the physician should look at otic discharge as the benchmark for defining the response to treatment. (8) Surgical intervention should be added to drug therapy in cases of complications. However, tympanoplasty or mastoidectomy in the absence of appropriate drug therapy will likely be complicated by fistulae, nonhealing of suture lines, and tympanoplasty failure. (1,10) When surgery is required, the techniques and guidelines are the same as those for the surgical treatment of chronic bacterial otitis media, with or without cholesteatoma. (4)

Acknowledgment

The authors are thankful to Shaikh Rahmatullah, secretary in the Division of Otolaryngology-Head and Neck Surgery at the Aga Khan University, for his cooperation and clerical help.

References

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(4.) Windle-Taylor PC, Bailey CM. Tuberculous otitis media: A series of 22 patients. Laryngoscope, 1980;90: 1039-44.

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(9.) Singh B. Role of surgery in tuberculous mastoiditis. J Laryngol Otol 1991;105:907-15.

(10.) Wallner LJ.. Tuberculous otitis media. Laryngoscope 1953;63: 1058-77.

(11.) M'Cart HW. Tuberculous disease of the middle ear. J Laryngol Otol 1925;40:456-66.

(12.) Mathens P. Tuberculosis of middle ear in children. Ann Otol Rhinol Laryngol 1907;16:390-425.

(13.) Munzel MA. Tympanoplasty and tuberculosis of the middle ear. Clin Orolaryngol 1978;3:311-3.

(14.) Mumtaz MA, Schwartz RH, Grundfast KM, Baumgartner RC. Tuberculosis of the middle ear and mastoid. Pediatr Infect Dis 1983;2:234-6.

(15.) Schuknecht HF. Pathology of the Ear. 2nd ed. Philadelphia: Lea and Febiger, 1993:206-8.

(16.) Ramages LJ, Gertler R. Aural tuberculosis: A series of 25 patients. J Laryngol Otol 1985;99:1073-80.

(17.) Odetoyinvo O. Early diagnosis of tuberculous otitis media. J Laryngol Otol 1988;102:133-5.

(18.) Hoshino T, Miyashita H, Asai Y. Computed tomography of the temporal bone in tuberculous otitis media. J Laryngol Otol 1994;108:702-5.

From the Division of Otolaryngology-Head and Neck Surgery, Department of Surgery, Aga Khan University Hospital, Karachi, Pakistan.

Reprint requests: Dr. Mohammad Sohail Awan, Division of Otolaryngology-Head and Neck Surgery, Department of Surgery, Aga Khan University Hospital, Stadium Rd., Karachi 74800, Pakistan. Phone: [phone]; fax: [phone]; e-mail: [e-mail]