Case Report
Inferior Vena Cava Thrombosis Complicating Tuberculosis
R Abid*, I Oueslati, N Bousetta, S Saihi, N Ben Abdelhafidh, R Battikh and B Louzir
Department of Internal Medicine, Military Hospital of Tunis, Tunisia
*Corresponding author: Rym Abid, Internal Medicine Department. Military Hospital of Tunis, Tunisia, 1008 Montfleury, Tunis, Tunisia
Published: 15 Jul, 2018
Cite this article as: Rym Abid, Internal Medicine
Department. Military Hospital of Tunis,
Tunisia, 1008 Montfleury, Tunis, Tunisia
Abstract
Tuberculosis (TB) remains a major global health problem in developing countries with a myriad of
presentations and complications. Deep Venous thrombosis is a rare complication of this disease. We
report an unusual case of Inferior vena cava thrombosis complicating isolated lymphadenopathy
tuberculosis. A 23 year-old male presented with a three months history of moderate abdominal pain
associated with anorexia, asthenia, weight loss, fever and night sweats. The patient’s abdominal and
chest Computed Tomography (CT) revealed cervical, axillary and abdominal lymph nodes associated
with a floating thrombus in the inferior vena cava. Mycobacterium tuberculosis (MT) infection was
confirmed by the bacteriological and histopathology examination of the axillary lymph node biopsy
specimen. He was treated with low-molecular-weight heparin, acenocoumarol and antituberculous
drugs. His general state improved and he responded well to anticoagulation therapy.
Keywords: Tuberculosis; Venous thrombosis; Prognosis
Introduction
Tuberculosis (TB) remains a major global health problem in developing countries. Clinical
presentations depend on localizations and with a myriad of presentations and complications.
Tuberculosis infection can be of pulmonary or extrapulmonary type [1]. Like other infectious
diseases, TB can cause thrombosis by various mechanisms such as local invasion, venous
compression or by producing a transitory hypercoagulable state. Although deep venous thrombosis
is considered a rare event and because it can be fatal, it is crucial to suspect it to perform an early
diagnosis and initiate prompt treatment [2].
We report an unusual case of Inferior vena cava thrombosis as a complication of isolated
tuberculous abdominal lymphadenopathy in a young man.
Case Presentation
A twenty-three-year-old Tunisian male soldier presented with a three months history of
abdominal pain. He was an active smoker of one pack per day for the past of six years, a moderate
alcohol consumer and had sexual risk behaviors. There was no history of past illness and no family
history of chronic disease. The patient had received BCG vaccination at birth and had never
contacted a patient with TB. The patient denied recent trauma, surgery, immobilization, or family
history of thrombotic disorder.
The abdominal pain was insidious in onset, slowly progressive, moderate, generalized and was
associated with anorexia, asthenia, weight loss and fever. The fever was low-grade and not associated
with chills or rigors, but was associated with night sweats.
On examination he was afebrile and had multiple cervical, supra clavicular, axillary and inguinal
lymph nodes. Abdominal examination was normal including per rectal examination. Clinical
examination of other systems was clinically normal.
Laboratory findings on admission revealed a normal WBC count (6100 G/mm3) normochromic
normocytic aplastic anaemia (haemoglobin 10 g/dl), lymphopenia (lymphocyte count =700/mm3),
normal platelet count (293000/mm3) with high Erythrocyte sedimentation rate (ESR =90 mm in
the first hour) and elevated C-reactive protein (27 mg/l). His renal and liver functions were normal.
Coombs’ test was positive. A chest X-ray film was normal.
Ultrasound examination of abdomen showed multiple lymph nodes. The patient’s abdominal
and chest computed tomography revealed cast of adenomegaly to axillary left supra clavicular
necrotic center and lower left jugulo carotidienne, cast of the hepatic hilum adenomegaly coelio
mesenteric, aortic lateral inter aortico cellar and retro cave. The scan also showed a floating thrombus
in the inferior vena cava in renal stretched to the common and internal right iliac vein (Figure 1).
A Mantoux test showed pronounced erythema with in duration
of 13 mm.
Histopathology examination of the left axillary lymph node
biopsy specimen revealed the presence of granulomas in the lymph
node tissues with marked epithelioid cell changes as well as giant
cells formation associated to caseation and necrosis. Another biopsy
specimen was found to contain acid-fast bacilli. Mycobacterium
tuberculosis (MT) infection was confirmed by culture on Lowenstein-
Jensen agar and MT organisms were found to be sensitive to all
first-line antituberculosis drugs. Serologic tests for HIV, HBV and
HCV were negative. Because of the unusual location of the patient’s
thrombosis, an evaluation was performed for hematologic disorders.
Laboratory assessment of protein C and S activity, cardiolipin
antibodies and antithrombin III activity was unrevealing. Malignancy
was ruled out with physical exam, imaging and histopathology
examination of the lymph node biopsy. The patient was put on
low-molecular-weight heparin (Innohep 0.5 ml/day) and 15 days
later, acenocoumarol (1 mg/day) was started after biopsy. The target
International Normalized Ratio (INR) of 2.0-3.0 was achieved, 35
days later, with a daily acenocoumarol 10 mg dose (5 mg twice/day).
He received also anti-tuberculosis treatment: HRZE 4 tablets/
day (isoniazid (200 mg/day), rifampin (480 mg/day), pyrazinamide
(1200 mg/day) and ethambutol (800 mg/day) for 2 months and then
isoniazid (200 mg/day) and rifampin (480 mg/day) for 8 months.
No adverse effects were seen. His general state improved and he
responded well to anticoagulation therapy.
Figure 1
Figure 1
MRI: floating thrombus in the inferior vena cava in renal stretched
to the common and internal right iliac vein.
Discussion
Tuberculosis is a major killer worldwide mainly affecting people
of developing countries. There were an estimated 8 million new cases
of TB, resulting in 1.9 million deaths, with the greatest burden of
disease in developing nations. Actually, tuberculosis is a disease with
a wide variety of clinical presentations and recently, there is a relative
increase in the incidence of extrapulmonary involvement. Lymph
node is the most common extrapulmonary site of tuberculosis [1].
Vascular complications associated with mycobacterium
tuberculosis infection had been reported in the literature and occurred
in 1.5% to 3.4% of tuberculosis infection. Venous thromboembolism
is a rare complication of tuberculosis and can be the presenting
feature of TB, occur a few days after the diagnosis or late in the course
of the disease, even in patients on ATT [2].
The factors commonly associated with the pathogenesis of
thrombosis are: alteration in the wall of the vein, alteration in the
blood constituents and slowing of the stream [2,3].
Tuberculosis has several mechanisms that induce a
hypercoagulable state and can lead thromboembolic complications.
The association between inflammation, haemostatic changes and
hypercoagulable state has been established in tuberculosis recently.
Hypercoagulability in tuberculosis is attributed to decreased
antithrombin 3 and protein C, elevated plasma fibrinogen level,
increased platelet aggregation and reactive thrombocytosis. Apart
from high frequency of antiphospholipid antibody levels in a patient
with tuberculosis, deficiency of protein S has been mentioned [3,4].
But, in our patient all these were normal.
Cytokines by their pro-inflammatory character will activate the
vascular intima and make thrombogenic endothelium. They will also
lead to a stimulation of hepatic synthesis of coagulation proteins
[5,6]. These risks of hypercoagulability are increased by immobility
and bed rest because of the morbidity caused by the disease. However,
thrombosis can also result from venous compression by lymph nodes
in ganglionar forms of TB, as retroperitoneal adenopathies may cause
inferior vena cava thrombosis in the absence of any haemostatic
abnormalities [7,8].
Many reports demonstrate that thrombotic phenomena in
patients occurs in several sites including hepatic veins, the vena porta,
jugular vein, iliac vein, inferior vena cava. Retroperitoneal para-aortic
lymphadenopathy is commonly seen in tuberculosis and have been
reported to cause mechanical venous obstruction in few patients in
literature [3,9].Tubercular lymph nodes may cause IVC thrombosis
either by a large collective matted mass or due to minor obstruction
in the presence of an underlying predisposed heredity thrombophilic
state. In our case, protein C, S, antithrombin 3 levels and activated
partial thromboplastin time (for lupus anticoagulant) were normal,
thus eliminating a predisposed thrombophilic state. Hence, large
matted tubercular lymph node masses are the probable explanation
for the IVC and iliofemoral thrombosis in our patient.
Regardless of the cause, prompt recognition of IVC thrombosis
is important because of the potential acute complications. IT carries
a higher risk of pulmonary embolism than lower extremity deep
venous thrombosis with 33% reported. There is also risk associated
with clot propagation including extension to the renal veins and
extension to the hepatic veins. Though rarely reported, critical
limb ischemia secondary to phlegmasia cerulean dolens is another
potential complication [10]. Physical exam findings and symptoms
are variable and dependent on the degree and location of occlusion.
Once suspected, the diagnosis of IVC thrombosis is established
through imaging. Computed tomography with contrast and
Magnetic Resonance Imaging (MRI) has been shown to be equally
sensitive. The gold standard imaging modality is venography, though
this is invasive and time consuming, but it is the preferred method if
surgical intervention is planned [6,7,10]. In our case, CT identified
the presence of caval thrombosis.
Frequently, a higher dose of acenocoumarol is necessary to
achieve therapeutic INR levels, because of rifampicin effects on
cytochrome P450. Additionally, this drug may also contribute to
the hypercoagulable state by decreasing production and increasing
clearance of anticoagulant hepatic proteins [4,10].
Conclusion
Thromboembolic disease is to search systematically at the TB view of the risk of occurrence of this complication particularly in extensive and severe forms. Prophylactic anticoagulation finds its indications in these forms. Inferior vena cava thrombosis may be one of the atypical presentations of tuberculosis and the possibility of retroperitoneal tubercular lymphadenitis should be considered in cases of unexplained thrombosis.
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