A 25-year-old, gravidity 3, parity 1, spontaneous abortion 1, and medical abortion with suction curettage 1, woman referred to our clinic with diffuse abdominal pain of 2-week duration, massive ascites, and prolonged intermittent fever rising up to 40.0 C. She had suffered from a spontaneous abortion of 20-week gestation in another hospital nine days ago. She reported a lack of appetite, dizziness, sweating, and raised temperature persisting for at least 3 weeks. She denied cough or weight loss. On physical examination, she had an abdominal distension that suggested a fluid collection, diffuse tenderness especially in lower abdomen, and unremarkable uterine cervix with positive motion tenderness test. No signs of portal hypertension were present. Transvaginal ultrasound confirmed the presence of ascites and bilateral hydrosalpinx (Figure 1). Her hemoglobin, thrombocyte, C-reactive protein, and white blood count were 7.9 gr/dL, 112000 /mm3, 21.6 mg/L, and 8010 mu/L with low lymphocyte number, respectively. HIV test, serologies for hepatitis, and cultures of blood and urine were negative. Renal function tests and hepatic transaminase levels were in normal range. Serum carcinogenic antigen (Ca)-125 level was 669 Units/mL. Chest radiography revealed small pleural effusions bilaterally. The diagnostic paracentesis yielded inflammation with lymphocyte predominance and reactive mesothelial cells. Cytological analysis for atypical cells was negative. No acid-fast bacilli were seen by microscopy. Results of TB polymerase chain reaction (PCR) and culture of the ascitic fluid were negative. The patient was initially treated with intravenous broad-spectrum antibiotics, but medical treatment failed to improve her clinical condition, and she was further admitted to intensive care unit. Based on history and laboratory review, thoracic and abdominal computed tomography (CT) scans were obtained to further workup the etiology of the ascites. These studies demonstrated bilateral pleural effusion, atelectasis, pulmonary parenchymal frosted glass aspect, massive ascites, hepatomegaly, hepatosteatosis, and a pattern of peritoneal carcinomatosis with formation of an omental cake without definite adnexial tumoral mass. Upper gastrointestinal tract endoscopy revealed no pathologic findings. About 7 days after admission, the patient subsequently underwent diagnostic laparoscopy, which revealed massive ascites, extensive adhesions between viscera, and numerous tiny nodular implants on the peritoneal surfaces, liver, stomach, ovaries, intestine, omentum, and mesentery. Because of the presence of suspicion for malignancy, laparoscopy converted to exploratory laparotomy. Adhesiolysis was performed. The uterus was 6-8 weeks in size with nodular serosal surface. Bilateral fallopian tubes were grossly distended and were tortuous with unrecognizable fimbria. Multiple targeted biopsies were taken from the suspicious implants. Tissue samples from the fimbria, peritoneum, and omentum were sent for frozen section analysis and were found to be consistent with granulomatous inflammation. Some tissue samples and ascitic fluid were sent for the microbiologic examination.
Postoperatively, antimycobacterial therapy with isoniazid, rifampin, pyrazinamide, and ethambutol was planned and started empirically. She was hypotensive and required vasopressors. Her blood gasses and control chest radiography which revealed diffuse pulmonary infiltrates were compatible with ARDS. The patient was sedated, and lung protective mechanical ventilation strategies were used. At fifth day of the antituberculous treatment multiorgan failure occurred in terms of pulmonary, hepatic, and renal insufficiency. She developed refractory metabolic acidosis with coagulopathy and pancytopenia, and she died of ARDS, septic shock, and multiorgan failure on her twelfth day of hospitalization. Final histopathological examination of the biopsy specimens showed chronic caseating granulomas with central necrosis (Figure 2), and the tissue culture grew Mycobacterium tuberculosis.