TB peritonitis in VPS child with no CNS TB

Abstract

An 8-year-old female child for whom a ventriculoperitoneal (VP) shunt was inserted for congenital hydrocephalus (HCP) at the age of 1month presented with abdominal distention, constipation and low-grade fever of 10 days duration. The family reported patient had decreased appetite with associated unquantified weight loss for the past 1 month. There was no history of headache, vomiting, abnormal body movement, blurring of vision, or loss of consciousness. She had history of close contact with close relative living with the family who was on anti-TB therapy for pulmonary TB. Otherwise she has no history of known chronic illness and was not on any medication. Past medical history revealed patient underwent VP shunt insertion for congenital HCP at the age of 1 month after she presented with progressive increase in head size, right-sided body weakness and repeated episodes of jerky type of abnormal body movement with loss of consciousness. At that time treatment for seizure disorder was started with an unspecified antiepileptic drug (AED) with excellent seizure control. The medication was discontinued at the age 6 years and patient has been seizure free ever since. Physical examination showed an alert but chronically sick looking malnourished child with a weight of 18 kg and height of 121 cm (body mass index [BMI] < 3SD). Vital signs evaluation revealed a fever of 38.1^oC and tachycardia (pulse rate: 130 – 142). The VP shunt valve was easily compressible and refilled immediately. There was no skin erythema along shunt tract site. The chest was clear with good air entry bilaterally and no added sounds. The abdomen was distended and tender to palpation. Digital rectal examination demonstrated impacted stool but no blood on examining finger. Neurologic exam was unremarkable except for right side hemiparesis (motor power of 4/5) which was apparent since infancy.  Initial laboratory results, including complete blood count (CBC), serum electrolytes, renal function test (RFT), and liver function test (LFT), were normal except for elevated erythrocyte sedimentation rate (ESR) at 26 mm/hr and C-reactive protein (CRP) at 116 mg/L. Abdominal ultrasound indicated moderate ascites, peritoneal thickening, ileocecal bowel thickening with dilated small bowels, and a VP shunt distal catheter. Brain CT scan showed dilated ventricles and widening of frontal and temporal sulci, primarily on the left. Chest ultrasound and X-ray were unremarkable. A presumptive diagnosis of spontaneous bacterial peritonitis with potential distal shunt failure was made, leading to an emergency shunt exteriorization. Approximately 2 liters of xanthochromic ascitic fluid and 10cc of clear cerebrospinal fluid (CSF) were aspirated. CSF analysis was unremarkable, and cultures were negative; however, the peritoneal collection tested positive for rifampicin non-resistant Mycobacterium tuberculosis (MTB). Anti-TB therapy was initiated, but eight days later, it was discontinued due to drug-induced hepatitis. After treatment for hepatitis and normalization of liver function tests, the exteriorized shunt was removed, and a ventriculopleural (VPL) shunt was inserted. Anti-TB drugs were reinitiated without complications, and the patient was discharged improved. At her latest follow-up, she completed six months of anti-TB therapy and reported resolution of previous complaints, with the VPL shunt well tolerated and no respiratory issues. In conclusion, TBP is a rare cause of VP shunt malfunction that requires a high index of clinical suspicion to diagnose. Delays in diagnosis are common and can lead to poor outcomes. With timely and appropriate management utilizing alternative CSF diversionary techniques and ant-TB therapy, satisfactory outcome should be achievable.