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.