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Chest Infections |

Bilateral Pulmonary Embolism in a Patient With Active Cavitary Pulmonary Tuberculosis: A Rare Association FREE TO VIEW

Ram K Chopra, MD; Aditi Takale, MBBS; Vaibhav Pandharkar, MD
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Ruby hall, Pune, India


Chest. 2015;148(4_MeetingAbstracts):174A. doi:10.1378/chest.2228524
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Abstract

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: Infections are risk factors for venous thromboembolism (VTE), especially if severe and acute. Several small case series have found an association between VTE and active tuberculosis. Although VTE is a rare complication of pulmonary tuberculosis, it may be a potentially life threatening event. Actually VTE can be a presenting feature of TB, occur a few days after the diagnosis or late in the course of disease, even in patients on anti tuberculous treatment (ATT). Like other infectious diseases, TB can cause thrombosis by various mechanisms such as local invasion, venous compression or by producing a transitory hypercoagulable state. These changes can normalize with an adequate ATT. Because VTE can be fatal, it is crucial to suspect it to perform an early diagnosis and initiate prompt treatment. Our case highlights the occurrence of DVT with bilateral pulmonary embolism in a patient of active pulmonary tuberculosis on anti tubercular treatment, a significant but rare association. According to retrospective data from South African hospital in mid 1980s, White et al. stated that DVT rate was 3.4% within 2 weeks after initiation of therapy.[3]

CASE PRESENTATION: 40 years old male ambulatory patient, on treatment for sputum positive pulmonary tuberculosis for last 4 weeks, presented with painful swelling of right leg of 8 days and acute onset dyspnoea of 24 hrs duration. Family history was non significant. He was tachypnoeic , normotensive, pulse 140/minute and raised JVP. His right leg was swollen and tender. Chest auscultation revealed bronchial breathing with crepitations on right upper chest. Cardiovascular and abdomen examination was normal.ABG showed hypoxemia with p02 of 66 mm Hg.ECG showed sinus tachycardia and echocardiography revealed dilated right atrium and right ventricle, moderate tricuspid regurgitation and pulmonary artery hypertension suggestive of pulmonary embolism. Venous Doppler showed large thrombus in right ileo femoral vein. Chest X-ray showed thick walled cavity in right upper zone surrounded by infiltrates. CT thorax showed giant cavity with surrounding infiltrations in right upper lobe. CT pulmonary angiography revealed bilateral thrombi in main pulmonary arteries. (radiology images will be put up during poster presentation.) CRP levels were high(5.30 mg/dl).Serum fibrinogen levels were elevated with thrombocytosis (platelet count of 635000/mm3) and no deficiency of anti thrombin 3, protein C or S. Anti phospholipid antibodies were negative. He was put on heparin and nasal oxygen and later oral anticoagulant. Of course also put on 4 drugs anti tubercular treatment as per standard protocol. 4 weeks later repeat echocardiography showed reduction of RA, RV dilatation and pulmonary artery pressure with improvement of breathlessness.

DISCUSSION: Our patient shows that VTE may complicate severe pulmonary tuberculosis and these events occur at presentation or later in the course of disease. The first report of an association between active tuberculosis and pulmonary embolism was in 1950, in which PE was found 27 times in 111 autopsy subjects of active tuberculosis (24.3%) [1]. The prevalence of VTE among patients with active tuberculosis, in one large multi variate analysis model was 2.07%, more common in black men than women [2]. The presence of hypercoagulability state among TB patients was postulated as a consequence of elevated fibrinogen with reactive thrombocytosis, the direct endothelial damage promoted by the tubercle bacillus, and the use of Rifampicin. However, this complication of tuberculosis is very rare and the thrombogenic potential of tuberculosis is infrequently reported in literature. Elevation of fibrinogen levels, thrombocytosis with increased platelet aggregation seems to induce hypercoagulability state in active tuberculosis and improves with treatment like in our patient.

CONCLUSIONS: This case report and several other clinical reports emphasize that patients with severe pulmonary tuberculosis are at risk for VTE and should be included in VTE risk evaluation similar to any acute and severe infection. Adequate prophylaxis and prompt management of pulmonary embolism can play a vital role in the survival of this subset of patients.

Reference #1: Thomas J.Moran: Autopsy Incidence of Pulmonary Embolism in Tuberculosis, Diseases of the Chest 09/1950;18(2):171-3.

Reference #2: Active Tuberculosis and Venous Thromboembolism, Dentan C etal, Clin Infect Dis,2014 Feb;58(4):495-501

Reference #3: White et al, Venous thrombosis and Rifampicin. Lancet. 1989;2:434-435[Pub Med]

DISCLOSURE: The following authors have nothing to disclose: Ram K Chopra, Aditi Takale, Vaibhav Pandharkar

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