SESSION TITLE: Tuberculosis Global Case Reports
SESSION TYPE: Global Case Report Poster
PRESENTED ON: Tuesday, October 27, 2015 at 01:30 PM - 02:30 PM
INTRODUCTION: Tuberculosis (TB) is one of the most devastating curable infectious diseases in the world. Venous thrombo-embolism (VTE) has been seen to occur in patients with active tuberculosis. The co-entity seems to be more common than suspected.
CASE PRESENTATION: 40 year old male presented with complaints of shortness of breath and right sided chest pain for 1 day. The patient had history of irregular anti- tubercular treatment (ATT) one year back. He had no history of other co morbid illness, prolonged surgery or bed ridden status. On examination, the patient was tachypneic and hemodynamically stable. He had bilateral pitting pedal oedema and on chest auscultation had crackles on left side. ECG was suggestive of P-pulmonale in all leads. Chest x-ray revealed bilateral fibrocavitory lesion and his ABG was suggestive of type I respiratory failure. Sputum smear was positive for AFB but line probe assay did not reveal rifampicin resistance. Bilateral lower limb doppler revealed partial thrombosis of bilateral femoral and popliteal veins. CT pulmonary angiography was suggestive of thrombus in middle lobar branch of right pulmonary artery. ANA , beta 2 glycoprotein and anti cardiolipin antibody were negative. He was treated with ATT (isoniazid, rifampicin, pyrazinamide, ethmabutol, streptomycin) along with anticoagulant therapy. His INR was maintained in the range of 2- 3. Patient showed marked clinic improvement and was discharged in hemodynamically stable condition.
DISCUSSION: VTE with TB is usually missed, as presentation with pedal oedema is usually taken as a consequence of malnutrition, amyloidosis or cor-pulmonale and worsening dyspnea is considered as worsening of disease itself. Prevalence of 3-4% deep vein thrombosis in patients with pulmonary tuberculosis has been reported. The pathophysiological process that may explain the relation between tuberculosis and VTE include: increase in plasma fibrinogen and factor VIII, reactive thrombocytosis, local compression of veins by the enlarged reactive lymph nodes, injury to endothelium and alteration in the normal blood flow. However, the exact mechanism is still unknown. In a study it has been shown that the patients with VTE and TB have higher mortality than TB and VTE alone. Considering the potential seriousness VTE should be suspected early in the course of TB.
CONCLUSIONS: With a causative link, patients with TB are at risk of developing VTE. It is important to sensitise all clinicians to this complication of TB by reporting a case observed in our institution. Further research is required to evaluate factors that may increase the chances of VTE in PTB and also to develop a protocol for timely diagnosis of VTE in TB patients.
Reference #1: Turken O, Kunter E, Sezer M, et al. Hemostatic changes in active pulmonary tuberculosis. Int J Tuberc Lung Dis 2002;6:927-32.
Reference #2: Robson et al. Acute-phase response and the hypercoagulable state in pulmonary tuberculosis. Br J Hematol 1996 Jun;93(4):943-9
Reference #3: Dentan et al. Active Tuberculosis and Venous Thromboembolism: Association According to International Classification of Diseases, Ninth Revision Hospital Discharge Diagnosis Codes. Clinical Infectious Diseases 2014;58(4):495-501
DISCLOSURE: The following authors have nothing to disclose: Robin Gupta, Ashok Janmeja, Deepak Aggarwal
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