Journal of the New Zealand Medical Association, 27-October-2006, Vol 119 No 1244
Inferior vena cava thrombosis complicating tuberculosis
Mithun Raj, Aparna Agrawal
Thrombosis of the inferior vena cava (IVC) is one of the rarest manifestations of tuberculosis with only two cases reported in the literature. We describe the case of a 32-year-old male with disseminated tuberculosis and IVC thrombosis causing a diagnostic dilemma.
A 32-year-old male labourer presented with a history of fever, productive cough, and weight loss of 6 months duration and abdominal distension lasting 1 month. There was no past history of deep vein thrombosis (DVT), recent long journey, surgery, or prolonged immobilisation. Furthermore, there was no history suggestive of any connective tissue disorder.
Examination revealed a poorly built, malnourished male with stable vitals. He was febrile with a temperature of 101°F. Respiratory examination was notable for the presence of diminished breath sounds over the right lung base with stony dullness on percussion. There were coarse crepitations heard over the right infraclavicular area. The abdomen was distended with shifting dullness and there were dilated tortuous veins visible over the lateral abdominal wall with cephalad flow (Figure 1).
Figure 1. Dilated, tortuous abdominal wall veins
Investigations revealed a haemoglobin level of 10 g/dL, total leukocyte count 18,000/mm3, differential—polymorphs 40%, lymphocytes 60%, platelets 320,000/mm3. Peripheral blood smear was normal. Renal and liver function tests were normal.
Chest X-ray showed massive right-sided pleural effusion with fluffy infiltrates over the right upper zone. Sputum examination revealed numerous acid fast bacilli (AFB) in three consecutive early morning samples.
Pleural fluid analysis showed an exudate with protein 4.6 g/dL and sugar 54 mg/dL with 80% lymphocytes on microscopy. Pleural fluid adenosine deaminase (ADA) was positive at 80 U/L.
Ultrasound of the abdomen showed mild hepatomegaly, paraaortic lymphadenopathy, and free fluid, which on testing was an exudate with predominance of lymphocytes and positive ADA. HIV serology was negative.
A diagnosis of disseminated tuberculosis was made and the patient was started on antitubercular treatment (ATT) with four drugs: isoniazid, rifampicin, pyrazinamide, and ethambutol. On ATT, he became afebrile with improvement in constitutional symptoms, dyspnoea, and cough but his abdominal distension progressively worsened over the next week.
In view of dilated veins over the abdomen and worsening abdominal symptoms, a Doppler ultrasonogram (Duplex Scan) was performed which showed IVC obstruction with thrombus in the intra- and retrohepatic portion of IVC extending to just above the renal vein.
A computed tomogram later confirmed the findings. His rheumatoid factor, serum C-reactive protein, anti-nuclear antibody (ANA), and anticardiolipin antibody tests were negative.
Serum homocysteine was within normal limits. The patient was started on unfractionated heparin (12,500 U – subcutaneous) twice a day along with warfarin 5 mg once daily, and the INR was adjusted to 2.4.
He improved on ATT with significant weight gain and regression of ascites. Right pleural effusion cleared completely and repeat chest films were normal. He was subsequently discharged with advice regarding continuation of ATT and long-term anticoagulation but was later lost to follow-up due to non-attendance.
Tuberculosis is a disorder of protean manifestations and is considered to cause a hypercoagulable state. Severe pulmonary tuberculosis (PTB) is sometimes complicated by DVT and there are isolated reports of thrombosis occurring in unusual sites like portal veins and cerebral venous sinuses.1,2
Hypercoagulablity in tuberculosis can be attributed to several factors like decreased antithrombin 3 and protein C, elevated plasma fibrinogen levels, and increased platelet aggregation.3,4 In addition, the systemic inflammatory state prevalent in tuberculosis causes endothelial cell damage predisposing to local thrombosis.
Thrombosis of the inferior vena cava is a rare manifestation of tuberculosis with only two cases reported in the literature.5 The diagnostic implications of IVC thrombosis in tuberculosis is well summarised in our case. The fact that the patient’s ascites worsened, despite ATT, made us search for alternative causes, and Doppler ultrasound subsequently proved IVC obstruction.
Additional tests for primary thrombophilic states could not be obtained in the case presented as the patient was commenced on anticoagulation prior to testing. The hypercoagulable state seen in tuberculosis has therapeutic implications as well. In a case of tuberculosis there is a strong case for prophylactic anticoagulation with heparin and avoiding central venous catheters.6 Anticoagulant therapy in tuberculosis is also problematic as the main antitubercular drugs (INH and rifampicin) are strong enzyme inducers and can interfere with warfarin levels.
In conclusion, DVT may be one of the atypical presentations of tuberculosis and the possibility of IVC obstruction should be considered in a tuberculous ascites resistant to ATT.
Author information: Mithun Raj, Resident; Aparna Agrawal, Professor; Department of Internal Medicine, JIPMER (Jawaharlal Institute of Postgraduate Medical Education and Research), Pondicherry, India
Correspondence: Dr Mithun Raj, Department of Internal Medicine, JIPMER (Jawaharlal Institute of Postgraduate Medical Education and Research), Pondicherry 605 006, India. Phone: +91 (0)413 9894087833; email: email@example.com
issue | Search journal |
Archived issues | Classifieds
| Hotline (free ads)
Subscribe | Contribute | Advertise | Contact Us | Copyright | Other Journals