Discussion:
Tuberculosis is a disease known to the world for ages and primarily affects the respiratory system. It can spread to any organ like the brain, heart, abdomen, bones, etc., leading to grave complications like meningitis, pericarditis, perforation of the intestines, and osteomyelitis, and severe life-threatening sepsis as well [3]. Rarely, it can also complicate to cause PE.
TB has the potential to cause venous thrombois and has been described in a few studies. A retrospective review conducted on 3293 tuberculosis patients showed that 46 had coexisting diagnosed venous thromboembolism (VTE) with a mean age: 53.4 ±19.6 years [4]. None of the 46 reported cases received thromboprophylaxis before the VTE events as they were fully ambulatory until they developed VTE. In 2019 a retrospective analysis of 7,905 patients diagnosed with Tuberculosis, 0.6% exhibited pulmonary thromboembolism (PTE), deep venous thrombosis (DVT), or both at or after the time of diagnosing TB [5]. Another reported case described an unusual left-arm DVT site in an asymptomatic young PTB patient [6].
Tuberculosis, pulmonary, and extra-pulmonary, has been suggested as an independent risk factor for venous thromboembolism (VTE). An underlying mechanism is yet unclear, but it is described as multifactorial in the literature. All three components of Virchow’s triad, i.e., hypercoagulability, venous stasis, and endothelial dysfunction, maybe a possibility to cause VTE in TB [7]. Other factors that also contribute to TB’s thrombogenic state include reactive thrombocytosis, anemia, and release of pro-inflammatory cytokines damaging the vascular endothelium during the disease process [7]. Turken et al. described a hypercoagulable state in active TB due to the imbalance between the pro-coagulant and anticoagulant factors such as increased fibrinogen, factor VIII plasminogen activator inhibitor 1 plasma levels, and depressed anti-thrombin III and protein C levels in the first month of treatment [8].
Early initiation of anti TB medications has been described to decrease the hypercoagulable state in TB patients [5]. In terms of treatment, LMWH is safer and requires minimal monitoring [5]. The overall morbidity and mortality are also decreased. Moreover, oral anticoagulation, especially with warfarin, needs carefully monitored because of hepatic enzyme induction by anti-tuberculosis drugs that increase the hepatic clearance of oral anticoagulant, resulting in higher doses of the drug; therefore, NOACs can also be considered [2,5].
Our patient was young, ambulatory, and did not have any risk factors for thromboembolism like decreased mobility, malignancy, immunocompromised state, or hereditary thrombophilia diseases. He was kept on a prophylactic dose to prevent thromboembolism during his hospital stay, and still, he developed pulmonary embolism. Thus, it signifies the risk of developing PE in TB patients.