Title : Coexisting rifampicin-resistant peritoneal tuberculosis and ventriculoperitoneal shunt–related CSF pseudocyst presenting as a pelvic mass: A complex diagnostic intersection
Abstract:
Background: Ventriculoperitoneal (VP) shunts are a well-established treatment for hydrocephalus; however, distal shunt complications such as peritoneal cerebrospinal fluid (CSF) pseudocysts are uncommon and may present with misleading extracranial features. In tuberculosis (TB)–endemic settings, identification of peritoneal TB may anchor diagnostic reasoning toward infection as the primary etiology, potentially obscuring underlying shunt-related pathology.
Case Presentation: We report a diagnostically complex case of a 22-year-old woman with childhood-onset obstructive hydrocephalus treated with a VP shunt 10 years prior to presentation. She had concurrent peritoneal tuberculosis and was receiving first-line antitubercular (AKT; isoniazid, rifampicin, pyrazinamide, and ethambutol [HRZE]), who developed progressive abdominal distension, ascites, pelvic pain, nausea and vomiting. Initial ultrasonogram and MRI pelvis revealed a cystic right adnexal (ovarian) mass with elevated CA-125, raising concern for ovarian neoplasm in the setting of infection. Ascitic fluid analysis and molecular testing identified Mycobacterium tuberculosis, which was initially presumed to account for the patient’s abdominal findings and guided early management. Despite antitubercular therapy and close follow up, the lesion continued to enlarge, prompting further evaluation. Definitive diagnosis was established only after exploratory laparotomy six months after initial presentation which revealed a large peritoneal CSF pseudocyst encasing the distal VP shunt catheter. Although cytology demonstrated a non-malignant inflammatory process, molecular testing revealed trace Mycobacterium tuberculosis DNA in both omental and pseudocyst wall tissue, with inconclusive rifampicin resistance profiling due to very low bacterial burden. Neurologic evaluation showed frontal intermittent rhythmic delta activity on EEG and chronic hydrocephalus on brain MRI, consistent with altered CSF dynamics.
Discussion: This case illustrates how peritoneal tuberculosis may dominate early diagnostic reasoning and delay recognition of VP shunt–related distal complications. The presence of TB, ascites, and elevated tumor markers reinforced an infectious or gynecologic framework, while the underlying shunt-related CSF pseudocyst remained unrecognized until surgical exploration. Management and follow-up in this case were further complicated by evolving antimicrobial considerations and shunt-related factors. The later identification of rifampicin resistance raised concern for inadequate initial mycobacterial control and necessitated reassessment of antitubercular therapy. Ongoing peritoneal inflammation poses a continued risk for impaired CSF absorption and pseudocyst recurrence, complicating interpretation of follow-up imaging. As a result, longitudinal management requires coordinated multidisciplinary follow-up, with vigilance for overlapping clinical signals rather than reliance on a single explanatory framework.
Conclusion: In TB-endemic settings, clinicians should remain vigilant for VP shunt–related complications even when peritoneal tuberculosis is identified. Peritoneal CSF pseudocysts should be considered in the differential diagnosis of pelvic masses and ascites in shunted patients, particularly when neurologic symptoms worsen despite appropriate antimicrobial therapy.
