A 20-year-old woman presented to the medicine outpatient department with complaints of chronic cough with sputum of a two-month duration and with a history of significant weight loss of 6 kilogram over 6 months. She also had low grade fever of the same duration. Pain in the left hypochondrium was present for 15 days which was also accompanied by abdominal distension. There was a positive family history of pulmonary tuberculosis in the mother who had been adequately treated 4 years earlier. On physical examination the patient appeared pale and her weight was below the 3rd percentile on the CDC growth chart. A chest examination revealed dullness on percussion and decreased vocal fremitus over the infra-scapular region on both sides and lower lateral chest wall with a diminished air entry on the left side. The abdomen was tender on palpation in the left hypochondrium with mild splenomegaly. The routine blood investigations revealed anaemia, haemoglobin of 8.5 gm/dl (normal range 13-18 gm/dl). The total white blood cell (WBC) counts were within normal limits with a relative lymphocytosis (WBC-5800/mm3 with 52% neutrophils and 48% lymphocytes). The platelet count was 250x103/micro-litre (150x103 to 450x103 per micro-litre of blood) and ESR was elevated to 86 mm in the first hour (normal range is 0-22 mm/hr for men and 0-29 mm/hr for women). The liver function tests were mildly elevated. The total bilirubin was 2 mumol/L (normal level 0.2-0.8 mumol/L) with indirect bilirubin of 1.2 mumol/L and direct bilirubin of 0.8 mumol/L. The serum aspartate amino transferase (AST) was 150 units/L and the alanine amino transferase (ALT) level was 84 units/litre (normal range of AST is 10-40 units/L and of ALT is 10-55units/L). Her chest radiograph demonstrated miliary opacities with a left pleural effusion. The sputum examination was positive for acid fast bacilli confirming pulmonary tuberculosis. The patient was started on anti-tubercular (ATT) treatment. The drugs that were given during the intensive phase of 2 months were isoniazid, rifampicin, ethambutol and pyrazinamide in a standard dose regimen, with a possible subsequent continuation of ATT depending on the patient's response.
An abdominal ultrasound (USG) was performed because of the abdominal complaints and it revealed hepato-splenomegaly with multiple small hypoechoic nodules that were scattered throughout the liver and spleen as well as a left-sided pleural effusion. Ascites was noticed in the Morison's pouch, pelvis and the inter-bowel region. The splenic vein had an increased calibre of 1.2cm with a vague hyperechogenicity within it, and demonstrated turbulent flow suggestive of splenic vein thrombosis. The portal vein was normal in calibre (1.2 cm) and showed a monophasic hepatopetal flow.
CECT of the thorax and the abdomen was performed to assess the burden of the disease in the chest and also to evaluate the splenic vein. Eighty ml of 350 mg% Omnipaque was used to perform the CECT examination after a delay of 35 seconds, from the root of the neck down to the iliac crest. CECT revealed a left pleural effusion with miliary nodules scattered throughout both lungs along with necrotic mediastinal lymph nodes (Figure 1A, 1B)
CT confirmed hepato-splenomegaly with multiple non-enhancing hypodense lesions suggestive of granulomas, as shown in Figure 2. In addition, a 1x1 cm wedge-shaped area was seen with the base abutting the lateral border of the spleen, suggestive of a small infarct, as shown in Figure 3.
A partial linear filling defect was seen in the splenic vein which confirmed the presence of a partial thrombus, as shown in Figure 4A, 4B.
There was no thrombus in the portal vein or in any of the porto-systemic collaterals. There were sub-centimetre lymph nodes in the omentum, porto-caval region and mesentery. The presence of partial splenic vein thrombosis warranted a work-up for a hypercoagulable state in the patient. The fibrinogen level was elevated to 17.64 mumol/L (normal 4.41-13.23 mumol/L). Prothrombin time was prolonged to 20 seconds (normal range 11-13.5 seconds), the INR was 1.7 (normal range is 0.8-1.1in people who are not on anticoagulant therapy). The levels of protein C, protein S, anti-phospholipid antibodies, anti-thrombin III, factor V Leiden mutation were all normal. Low Molecular Weight Heparin (LMWH) was instituted and the patient was kept under close ultrasound and Doppler follow-up. The thrombus was seen to resolve in 5 weeks.