Bilateral Tuberculous Otitis Media with Cerebellar Abscess in an Immunocompromised Child

DISCUSSION

Extrapulmonary tuberculosis is a common disease in India and other developing nations. In a cross-sectional study by Stani et al., the incidence of extrapulmonary tuberculosis was 6.1% which was much lower compared to reported incidences from the western world which was 15–40%.¹ TBOM accounts for 0.1% of all cases and 1.7% of extrapulmonary tuberculosis in India.¹ TBOM is often diagnosed late because of the rarity of occurrence and difficulty in diagnosis.^2,3 The duration of illness in our present report was 3 years. In endemic countries, tuberculous otitis media is an important differential diagnosis of chronic otorrhea that is unresponsive to conventional antibacterial therapy. Rarely, if these cases are operated suspecting chronic active otitis media, otorrhea may recur and healing maybe slow and incomplete. Cough, fever, and night sweats maybe present.⁴ Classically, painless otorrhea and multiple perforations of the tympanic membrane were described as findings suspicious of TBOM.⁵ However, in a series of 13 cases published by Yaniv et al., patients with severe conductive hearing loss, abundant pale granulations, and an eroded malleus handle were more commonly diagnosed with TBOM.⁶ Presence of facial nerve palsy is highly suggestive of TBOM.³ Chronic ear discharge from both ears in an immunocompromised child, such as in our report should be highly suspicious of tuberculous otitis media.

The bacilli can gain entry into the middle ear through (1) Eustachian tube, (2) Blood stream, (3) Contiguously from intracranial and extracranial sites⁷, and (4) Genital tract of the mother with genital tuberculosis during birth (rare).⁸

Our patient was found to have Acid-fast bacilli (AFB) in ear discharge on ZN staining. Ordinarily, TBOM is a difficult case to diagnose. Positive culture for tubercle bacilli yields the most definitive evidence. However, AFB are found in ear discharge only in 5–35% of the cases of TBOM.^2,3 For diagnosing TBOM, chest radiograph, purified protein derivative skin testing, and ZN staining of ear secretions for AFB are necessary. Surgical biopsy demonstrates chronic caseous necrosis and granuloma formation. Middle ear mucosal biopsy and aural polypectomy yielded diagnosis in only 30 and 35% of the cases, respectively.⁹

Most common intracranial complications of TBOM include tuberculoma, otitic hydrocephalus, and tuberculous meningitis¹⁰. Differential diagnoses of a brain abscess on radiology include pyogenic abscess, fungal abscess and tuberculoma. Tuberculous abscess can be diagnosed with MRI. Tubercular abscesses can be single or multiple, often being multiloculated. These abscesses have smooth walls with regular thickness and show ring enhancement on contrast. On Diffusion Weighted Imaging (DWI), low apparent diffusion coefficient has been found in fungal, tubercular abscesses, and pyogenic abscesses. Tuberculous brain abscesses exhibit significantly lower magnetization transfer ratios compared with those of pyogenic abscesses, with no evidence of amino acids on MR specroscopy – a spectral hallmark of the pyogenic abscess.¹¹

Only one case of tuberculous cerebellar abscess as a complication of TBOM has been reported in literature.¹² Patient was a 14-year-old girl from Thailand diagnosed to have right TBOM with right cerebellar abscess on CT scan. Presence of hydrocephalus is not commented upon. Patient was managed with right radical mastoidectomy and aspiration of the abscess along with continuation of ATT.

Our patient had hydrocephalus which was initially managed with Ventricolo Peritonial (VP) shunt followed by aspiration of the abscess and ATT. However, the abscess recurred and patient underwent suboccipital craniectomy and excision of the abscess. TBOM was managed with ATT.

Kirsch et al. reported that most of the cases with TBOM resolve with ATT and do not require surgery.³ The case reported by Peninnah Oberdorfer had a small well-defined abscess without distortion of the fourth ventricle and percutaneous aspiration was plausible.

Conversely, the abscess in our case was large with perilesional edema causing distortion of the fourth ventricle with resultant hydrocephalus. Percutaneous aspiration in this scenario must have been undertreatment and hence excision of the abscess by craniotomy was considered as a better alternative. The initial non-responsiveness of the treatment could also be related to the CD4 counts, nutrition, or other factors which cannot be conclusively proved to be responsible.

A series of tubercular cerebellar abscesses have been reported by Chakraborti et al.¹³ from National Institute of Mental Health and Neuro Sciences in which 10 cases of cerebellar tuberculosis were reported. Two among them had previous history of CSOM, three had pulmonary tuberculosis, two had disseminated disease, one had Pott’s spine and rest had no significant past history. Therefore, it can also be concluded that in a case of tuberculous cerebellar abscess, CSOM or pulmonary infection must be actively sought.

Despite the fact that cerebellar abscess in a case of CSOM points to the presence of pyogenic organisms, it is prudent to test for presence of AFB, especially in endemic countries. Patients with tuberculous cerebellar abscess have good outcome when recognized early and managed both medically as well as surgically. On the other hand, TBOM can be managed with ATT alone in most of the cases.²