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| Journal of the New Zealand Medical Association,
27-October-2006, Vol 119 No 1244
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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.
Case reportA 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.
DiscussionTuberculosis 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: drmithunraj@gmail.com
References:
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