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Table of Contents
CASE REPORT
Year : 2020  |  Volume : 8  |  Issue : 4  |  Page : 203-205

When you never thought it would be me


Department of General Medicine, Bangalore Medical College and Research Institute, Bengaluru, Karnataka, India

Date of Submission11-Sep-2019
Date of Decision15-Nov-2019
Date of Acceptance05-Jan-2020
Date of Web Publication23-Oct-2020

Correspondence Address:
Dr. Shivakumar Hrishikesh
Department of General Medicine, Bangalore Medical College and Research Institute, Bengaluru, Karnataka
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/AJIM.AJIM_53_19

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  Abstract 


Tuberculosis, both pulmonary and extrapulmonary, is a procoagulant state, which can lead to deep-vein thrombosis and thromboembolism. Rifampicin, the antitubercular drug by itself, can cause a procoagulant state. Here, we describe the case of a patient diagnosed with pulmonary tuberculosis, on antitubercular treatment for 25 days, who developed pulmonary thromboembolism.

Keywords: Deep-vein thrombosis, procoagulant state, pulmonary thromboembolism, rifampicin, tuberculosis


How to cite this article:
Raveendra K R, Sivaranjani H, Hrishikesh S. When you never thought it would be me. APIK J Int Med 2020;8:203-5

How to cite this URL:
Raveendra K R, Sivaranjani H, Hrishikesh S. When you never thought it would be me. APIK J Int Med [serial online] 2020 [cited 2020 Nov 24];8:203-5. Available from: https://www.ajim.in/text.asp?2020/8/4/203/298937




  Introduction Top


Tuberculosis (TB) is a disease caused by Mycobacterium tuberculosis . Pulmonary TB most commonly affects the upper lobes of the lungs.[1] Both pulmonary and extrapulmonary TB are independent risk factors for pulmonary embolism.[1] The following case describes a patient who developed acute pulmonary thromboembolism as a complication of TB.


  Case Report Top


A 45-year-old female, with a history of cough for 5 months, was diagnosed with sputum-positive TB and started on antitubercular treatment (ATT) for 25 days. The patient now presented with complaints of breathlessness for 1 day, which was sudden in onset, was nonprogressive, was present even at rest, with no aggravating or relieving factors, and was not associated with chest pain or palpitations. The patient did not have any history of preexisting cardiac disease.

On examination, she was found to have pallor; blood pressure was 110/70 mmHg, pulse rate was 90 beats/min, respiratory rate was 25 cycles/min, temperature was 98.8° F, and saturation was 85% at room air and 95% with 4 L oxygen. Respiratory system examination showed tracheal deviation to the right. The right infraclavicular area also had decreased movements, increased vocal fremitus and vocal resonance, dull note on percussion, and fine inspiratory crepitations.

Her investigations were as follows:

  • Complete blood count


    • Hemoglobin – 9.6 g/dl
    • Platelet – 1,81,400 cells/mm3
    • Total count – 9914 cells/mm3
    .

  • Liver function test – Normal
  • Renal function test – Normal
  • Serum electrolytes – Normal
  • Random blood sugar – 89
  • Urine routine –Normal
  • Chest X-ray – Nonhomogenous opacity in the right upper lobe [Figure 1]
  • Arterial blood gas showed respiratory alkalosis
  • Electrocardiography showed right ventricular strain pattern [Figure 2].
Figure 1: Chest X-ray posteroanterior view showing fibrosis of the right upper zone

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Figure 2: Electrocardiography showing T wave inversion in leads v1, v2, and v3 suggestive of right ventricular strain pattern

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In view of the above findings, pulmonary thromboembolism was suspected, and the patient was evaluated in those lines.

D-dimer was found to be >1000.

A computed tomography (CT) pulmonary angiogram (CTPA) was done, which showed a hypodense lesion in the pulmonary artery just distal to the bifurcation of the main pulmonary artery suggestive of acute thrombus. Her coagulation profile was normal: prothrombin time –13.8 s and international normalized ratio –1.20 [Figure 3]
Figure 3: Computed tomography pulmonary angiogram showing hypodense lesion in the pulmonary artery

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Her serum homocysteine levels were also normal. The protein C, protein S, antithrombin III, and factor V Leiden levels were normal. Antinuclear antibody, antiphospholipid antibody (APLA), and anticardiolipin antibody were negative.

In order to rule out embolism from other sites, venous Doppler of the lower limb and two-dimensional (2D) echocardiogram (echo) were done, and the presence of thrombus was ruled out.

Based on the above evidence, a diagnosis of pulmonary thromboembolism was made.

According to the algorithm for the management of pulmonary thromboembolism, our patient was normotensive, and 2D echo showed a normal left ventricular function. Hence, our patient could be managed with anticoagulation alone. She was initiated on heparin, and oxygen was supplemented. Her condition improved significantly, and she was discharged with the oral anticoagulant dabigatran 150 mg BD. She was followed up after 3 months, and her thromboembolism had resolved (which was confirmed by repeat CTPA).


  Discussion Top


Out of the 9.6 million cases of TB occurring worldwide every year, India contributes 23% of the cases. Although deep-vein thrombosis (DVT) is rare, it is associated with TB in 1.5%–3.4% of the cases. It is necessary to identify TB patients who are at risk of developing DVT and venous thromboembolism. Studies have shown that approximately 1.5%–3.4% of patients on antitubercular therapy develop DVT.[1] Approximately one-third of these patients with symptomatic DVT manifest with pulmonary embolism.[1]

Pathogenesis

  • One-third of patients with TB have anemia leading to reactive thrombocytosis, which, in turn, leads to a hypercoagulable state causing DVT[1]
  • Pro-inflammatory cytokines make the vascular endothelium thrombogenic by activating the vascular intima, causing changes on the endothelial cell surface protein and also the presence of type 1 plasminogen activator inhibitor and tissue factor antigen in pulmonary arterial endothelial cells of patients infected with TB[2],[3]
  • TB leads to the production of cytokines which act on the liver, leading to increased synthesis of coagulation proteins such as factor 8 and fibrinogen. Elevated plasma fibrinogen and decreased antithrombin 3 levels were found in patients with disseminated TB, contributing to DVT[4],[5]
  • APLAs were detected in patients with TB, which causes a procoagulant state[6]
  • These hematological parameters worsen during the first 2 weeks of therapy in many cases, but they normalize after a month of ATT. The return of these hematological parameters to a normal level is a good indicator of disease control[7]
  • Thrombosis can also occur when the retroperitoneal lymphadenopathy associated with the TB compresses on the inferior vena cava, resulting in inferior vena caval thrombosis[1]
  • Rifampicin, the antitubercular drug, causes increased production of procoagulant proteins by the liver, thereby disrupting the procoagulant and anticoagulant balance, leading to DVT[8]
  • Patients with severe TB can be nonambulatory, which also leads to DVT.[1]


Venous thromboembolism can also be the presenting feature of TB.[9]

DVT can occur within the first 2 months of starting antitubercular therapy. It also has a recurrence rate of 7% at 6 months.[10]


  Conclusion Top


In patients who have been started on antitubercular therapy, presenting with acute-onset breathlessness, a differential diagnosis of acute pulmonary thromboembolism should be considered.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Gupta A, Mrigpuri P, Faye A, Bandyopadhyay D, Singla R. Pulmonary tuberculosis – An emerging risk factor for venous thromboembolism: A case series and review of literature. Lung India 2017;34:65-9.  Back to cited text no. 1
[PUBMED]  [Full text]  
2.
Andus T, Bauer J, Gerok W. Effects of cytokines on the liver. Hepatology 1991;13:364-75.  Back to cited text no. 2
    
3.
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. 3
    
4.
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. 4
    
5.
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. 5
    
6.
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. 6
    
7.
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. 7
    
8.
White NW. Venous thrombosis and rifampicin. Lancet 1989;2:434-5.  Back to cited text no. 8
    
9.
Gogna A, Pradhan GR, Sinha RS, Gupta B. Tuberculosis presenting as deep venous thrombosis. British medical journal 1999;75:104-5.  Back to cited text no. 9
    
10.
Prandoni P, Lensing AW, Cogo A, Cuppini S, Villalta S, Carta M, et al . The long-term clinical course of acute deep venous thrombosis. Ann Intern Med 1996;125:1-7.  Back to cited text no. 10
    


    Figures

  [Figure 1], [Figure 2], [Figure 3]



 

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