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 Table of Contents  
CASE REPORT
Year : 2017  |  Volume : 6  |  Issue : 2  |  Page : 184-186

pulmonary tuberculosis: A neglected risk factor for deep venous thrombosis


Department of Respiratory Medicine, J L N Medical College, Ajmer, Rajasthan, India

Date of Web Publication19-May-2017

Correspondence Address:
Ramakant Dixit
Department of Respiratory Medicine, J L N Medical College, Ajmer, Rajasthan
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijmy.ijmy_49_17

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  Abstract 

A case of deep venous thrombosis (DVT) of the lower limb in the absence of known common risk factors and its link with underlying pulmonary tuberculosis is described in a young female patient. Possible underlying mechanisms and awareness regarding tuberculosis as a risk factor for DVT is also emphasized.

Keywords: Deep vein thrombosis, lower limb, pulmonary tuberculosis


How to cite this article:
Gupta A, Dixit R. pulmonary tuberculosis: A neglected risk factor for deep venous thrombosis. Int J Mycobacteriol 2017;6:184-6

How to cite this URL:
Gupta A, Dixit R. pulmonary tuberculosis: A neglected risk factor for deep venous thrombosis. Int J Mycobacteriol [serial online] 2017 [cited 2019 Aug 19];6:184-6. Available from: http://www.ijmyco.org/text.asp?2017/6/2/184/206608




  Introduction Top


Deep vein thrombosis (DVT) is a common preventable and treatable cause of death worldwide. This is predominantly a disease of the elderly with an incidence that rises markedly with age.[1] There are other several factors also that are associated with increased risk of DVT such as major surgeries, prolonged bed rest, oral contraceptive pills, smoking, malignancy, presence of central venous lines, and inherited hypercoagulable states [2],[3]

Tuberculosis is largely neglected as a risk factor for DVT. However, several studies have shown an association between infection by Mycobacterium tuberculosis and vascular complications.[4],[5] Therefore, it is essential to identify such tuberculosis patients who are at risk of developing DVT so as to manage them in time and avoid life-threatening consequences. This report describes a case of DVT in a patient secondary to extensive pulmonary tuberculosis.


  Case Report Top


A 23-year-old female was admitted to our department with complaints of painful swelling of the left lower limb for the last 15 days. She also had dry cough and low-grade fever from the last 2 months. She denied any investigation or specific treatment in the past. She had not undergone any major surgeries in recent past and was not taking any oral contraceptive pills. There was no history of abortions or immobilization also.

General physical examination revealed a poorly built, malnourished female. Her left leg was swollen, shiny, and it was tender to touch with positive Homan's sign [Figure 1]a. Her pulse and blood pressure were normal. Cardiovascular and abdominal examination was unremarkable. Respiratory system examination revealed bilateral crepitations and bronchial breath sounds at the right infraclavicular region. Routine investigations revealed anemia (hemoglobin 10.5 g/dl), leukocytosis (white blood cell 13.8 G/L), and a normal platelet count (235.000/mm 3). Biochemical investigations were within normal limits.
Figure 1: Patient's left lower limb before (a) and after treatment (b).

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Chest X-ray demonstrated bilateral inhomogeneous infiltrates with cavitation at the right upper zone [Figure 2]. Sputum examination showed acid-fast bacilli on routine smear microscopic examination. Due to swelling and tenderness at calf, the possibility of DVT was considered. Ultrasound Doppler study of the left lower limb was performed that revealed DVT at the left pelvic vein, deep femoral vein, external iliac vein, and common iliac vein [Figure 3]. Ultrasound abdomen and connective tissue profile did not show any abnormality. Other investigations such as measurement of prothrombin level, antithrombin III, and antiphospholipid antibodies could not be done due to financial and infrastructure constraints.
Figure 2: X-ray chest of patient showing far advanced pulmonary tuberculosis.

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Figure 3: Doppler ultrasound of limb showing venous thrombosis.

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A diagnosis of microbiologically confirmed new case of Pulmonary tuberculosis with DVT of the left lower limb was made, and a standard antituberculosis treatment regimen (Category I) was initiated according to body weight as per Revised National Tuberculosis Control Program of India. The patient was given enoxaparin subcutaneously (60 mg twice daily) for 7 days and subsequently warfarin (5 mg/day) with close monitoring of prothrombin time and INR. With this treatment, her general condition improved rapidly; swelling and tenderness of the limb also decreased [Figure 1]b. The latter disappeared completely after 3 weeks. As no other significant risk factor for DVT was evident in our case apart from pulmonary tuberculosis and rapid response was observed with antituberculosis treatment along with anticoagulant therapy, DVT was strongly considered as secondary to the underlying pulmonary tuberculosis.


  Discussion Top


Active pulmonary tuberculosis can be complicated by DVT, associated with a hypercoagulable state secondary to the underlying inflammation. In about 1.5%–3.4% of tuberculosis infection, there is an association between vascular complications and infection by M. tuberculosis.[4],[5] DVT is known to complicate severe pulmonary tuberculosis and may occur at the time of presentation of pulmonary disease as seen in our case or may be seen later in the course of disease or even during treatment.[6]

DVT is most commonly seen in postoperative patients and in patients who are ambulatory for a long time. It is rarely suspected due to underlying tuberculosis in day-to-day clinical practice, and very few publications are there in literature, mostly as case reports.[7] Increased awareness along with availability of noninvasive tests such as color Doppler ultrasonography may result in detection of more cases of tuberculosis associated with DVT in future and likely to reduce the so-called unexpected sudden deaths in few of them if managed properly. Peripheral limb edema in patients of tuberculosis is largely attributed to the hypoproteinemia. However, there are certain signs such as pain and increased surface temperature of the affected limb that are helpful for the diagnosis of DVT in such cases. High probability of suspicion with no delay in diagnosis and management of DVT in such patients should be emphasized.

The exact mechanisms responsible for the development of DVT in tuberculosis patients are not clear. All the three components of Virchow's triad, i.e., hypercoagulability, venous stasis, and endothelial dysfunction, can play a role in the pathogenesis of the DVT associated with tuberculosis. There are several mechanisms in tuberculosis that can produce a hypercoagulable state due to which thromboembolic complications can occur. There are several studies that have shown increased level of plasma fibrinogen, impaired fibrinolysis along with reduction in antithrombin III, protein C, and reactive thrombocytosis resulting in a hypercoagulable state due to which DVT can occur in pulmonary tuberculosis.[4],[6],[8]

Some reports in literature also mention increase in antiphospholipid antibodies in tuberculosis patients, and there is some relationship between these and protein S. Although studies on the activity of prothrombin in tuberculosis are not numerous, it seems that hypoprothrombinemia rather than hyperactivity of prothrombin exists in appreciable number of cases. Some studies indicate that there is prothrombin deficiency in approximately one-third of tuberculosis patients.[4],[9],[10]

Cytokines which are proinflammatory in character can activate the vascular intima and make endothelium thrombogenic. Hepatic synthesis of coagulation proteins can also be stimulated.[11] Increased hypercoagulability state because of the immobility and bed rest due to the morbidity caused by the disease may be potential risk factors in such patient. Thrombosis caused by venous compression from lymph nodes may be another mechanism to cause DVT in such patients.[12]

Literature also states a possible association between the use of rifampicin and DVT with a relative risk of 4.74 in patients treated with rifampicin-containing regimen.[13] It has been suggested that antituberculosis therapy should be immediately started and supplemented with anticoagulant therapy as hemostatic changes improve during the 1st month of treatment.[10] Anticoagulant therapy should be cautiously used in these patients due to the interaction of rifampicin with warfarin analogs, as rifampicin-mediated enzyme induction may reduce the efficacy of warfarin. The newer Xa inhibitors have several advantages over traditional therapy with parenteral anticoagulant, i.e., faster onset of action and lesser bleeding events as compared with the standard therapy.[14]


  Conclusion Top


Our case emphasizes on the importance of keeping a high index of suspicion of DVT in patients with pulmonary tuberculosis. Early initiation of antituberculosis treatment along with anticoagulant therapy can prevent the potentially fatal complication of the disease. Low molecular weight heparins are safer and require minimal monitoring. The overall morbidity and mortality may also be decreased if the condition is timely diagnosed and managed properly.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Silverstein MD, Heit JA, Mohr DN, Petterson TM, O'Fallon WM, Melton LJ 3rd. Trends in the incidence of deep vein thrombosis and pulmonary embolism: A 25-year population-based study. Arch Intern Med 1998;158:585-93.  Back to cited text no. 1
    
2.
Anderson FA Jr., Spencer FA. Risk factors for venous thromboembolism. Circulation 2003;107 23 Suppl 1:19-6.  Back to cited text no. 2
    
3.
Moheimani F, Jackson DE. Venous thromboembolism: Classification, risk factors, diagnosis, and management. ISRN Hematol 2011;2011:124610.  Back to cited text no. 3
    
4.
Lang IM, Mackman N, Kriett JM, Moser KM, Schleef RR. Prothrombotic activation of pulmonary arterial endothelial cells in a patient with tuberculosis. Hum Pathol 1996;27:423-7.  Back to cited text no. 4
    
5.
El Fekih L, Oueslati I, Hassene H, Fenniche S, Belhabib D, Megdiche ML. Association deep veinous thrombosis with pulmonary tuberculosis. Tunis Med 2009;87:328-9.  Back to cited text no. 5
    
6.
Robson SC, White NW, Aronson I, Woollgar R, Goodman H, Jacobs P. Acute-phase response and the hypercoagulable state in pulmonary tuberculosis. Br J Haematol 1996;93:943-9.  Back to cited text no. 6
    
7.
Mark PL, Ashok PP, Deshpande RB, Mahashur AA. A patient with hypercoagulable state due to tuberculosis. Indian J Chest Dis Allied Sci 2009;51:49-51.  Back to cited text no. 7
    
8.
Zahn DW, Peirce CT. Venous thrombosis and pulmonary embolism in tuberculosis. Am J Med 1948;5:716-28.  Back to cited text no. 8
    
9.
Suárez Ortega S, Artiles Vizcaíno J, Balda Aguirre I, Melado Sánchez P, Arkuch Saade ME, Ayala Galán E, et al. Tuberculosis as risk factor for venous thrombosis. An Med Interna 1993;10:398-400.  Back to cited text no. 9
    
10.
Turken O, Kunter E, Sezer M, Solmazgul E, Cerrahoglu K, Bozkanat E, et al. Hemostatic changes in active pulmonary tuberculosis. Int J Tuberc Lung Dis 2002;6:927-32.  Back to cited text no. 10
    
11.
Tilg H, Wilmer A, Vogel W, Herold M, Nölchen B, Judmaier G, et al. Serum levels of cytokines in chronic liver diseases. Gastroenterology 1992;103:264-74.  Back to cited text no. 11
    
12.
Gogna A, Pradhan GR, Sinha RS, Gupta B. Tuberculosis presenting as deep vein thrombosis. Postgrad Med J 1999;75:104-5.  Back to cited text no. 12
    
13.
White NW. Venous thrombosis and rifampicin. Lancet 1989;2:434-5.  Back to cited text no. 13
    
14.
Agnelli G, Gallus A, Goldhaber SZ, Haas S, Huisman MV, Hull RD, et al. Treatment of proximal deep-vein thrombosis with the oral direct factor Xa inhibitor rivaroxaban (BAY 59-7939): The ODIXa-DVT (Oral Direct Factor Xa Inhibitor BAY 59-7939 in Patients With Acute Symptomatic Deep-Vein Thrombosis) study. Circulation 2007;116:180-7.  Back to cited text no. 14
    


    Figures

  [Figure 1], [Figure 2], [Figure 3]


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