Definition

Venous thromboembolism (VTE) can manifest as Deep Vein Thrombosis (DVT), Ischemic Stroke, and
Pulmonary Embolism (PE) that they are coming from the same pathological entity (Wong and Chaudhry,
2013, Koupenova et al., 2016, A. Caprini, 2005). Thromboembolism might stem from the words
Thrombus and Embolus. Embolus can be defined as an intravascular material that moves from its origin
which allows occlusion in a more distal part of the blood vessel. Although embolus generally can be
blood clot, fat, water, amniotic fluid or tumor, PE is often caused by thrombus originating from the deep
veins of the legs (Wong and Chaudhry, 2013).

Etiology

The etiology of VTE can be explained by Virchow's triad theorem which explains the predisposition of
thrombus, namely Hypercoagulability, Stasis, and endothelial damage (Wong and Chaudhry, 2013).

Firstly, this hypercoagulability can be either hereditary or acquired. Hereditary hypercoagulability can be
as factor V leiden (mutations that cause factor Va to be resistantly inactivated, prothrombin G20210A
(mutations that cause increased prothrombin production), and difficiency antithrombin, protein S and C,
and plasminogen. Meanwhile, acquired hypercoagulability can be caused by cancer chemotheraphy,
oral contraceptives and hormone replacement therapy, pregnancy and postpartum period, central
obesity, and heparin-induced thrombocytopenia (Wong and Chaudhry, 2013).

Secondly, VTE can also be caused by stasis which can cause endothelial injury directly by reducing
natural fibrinolysis. Decreased mobility, polycythemia, and congestive heart failure can cause stasis to
occur (Wong and Chaudhry, 2013).

Thirdly, VTE can be caused by endothelial damage and dysfunction. Endothelial dysfunction can lead to
decreased synthesis of NO and prostacyclin and increased endothelin-1. Meanwhile, endothelial
damage can cause exposure to subendothelial tissue and collagen with platelets (Wong and Chaudhry,
2013). Both of them can lead to blood clotting formation.

Pathophysiology of Deep vein thrombosis (Wong and Chaudhry, 2013

Deep venous thrombosis is used as a common cause of extremity, which is commonly from calf veins,
specifically in the soleus sinusoids and cusps of the valves. Venous valve is avascular so that the
decrease of oxygenated blood flow causes exposure to endothelial conditions with hypoxemia.

The endothelium responds by exposing the adhesion molecule that invites leukocytes. This cell moves
tissue factor to the endothelium, which can be complex with VIIa to begin the coagulation cascade via
extrinsic pathway. The main components of this venous thrombi are over fibrin and trapped in the clot.
Platelets also contribute, but only slightly (Wong and Chaudhry, 2013).

Meanwhile, skeletal muscle pumps the venous to prevent DVT so that activated clotting factors spread
and cause new thrombus formation. When the clot doesn’t resolve, it will spread proximally and can
colonize the condition of the blood vessels that are suitable (Wong and Chaudhry, 2013).

Pathophysiology of Pulmonary embolism (Swaroop and Tarbox, 2013)

PE is a condition in which DVT releases and embolizes the pulmonary circulation resulting in occlusion
and disrupting gas exchange and circulation. Pulmonary artery obstruction results in dead space
ventilation because capillary ventilation exceeds capillary blood flow. this causes ventilation-perfusion
mismatch and induces the release of serotonin and thromboxane from activated platelets. As a result,
vasoconstriction is very likely to occur in the unaffected areas of lung and cause increased pulmonary
pressure resulting in the occurrence of right heart failure. This can result in impaired left ventricular
filling and can cause hypoxemia and tissue hypoxia.

A. Caprini, J. (2005). Update on Risk Factors for Venous Thromboembolism. The American Journal
of Medicine. [online] Available at:
https://www.venousdisease.com/Publications/Update%20on%20risk%20factors-caprini.pdf
[Accessed 3 Jan. 2018].
B. Koupenova, M., Kehrel, B., Corkrey, H. and Freedman, J. (2016). Thrombosis and platelets: an
update. European Heart Journal, [online] 38(11). Available at:
https://www.researchgate.net/publication/311986292_Thrombosis_and_platelets_An_update
[Accessed 3 Jan. 2019].
C. Swaroop, M. and Tarbox, A. (2013). Pulmonary embolism. International Journal of Critical Illness
and Injury Science, [online] 3(1), p.69. Available at:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3665123/ [Accessed 3 Jan. 2019].
D. Wong, E. and Chaudhry, S. (2003). Venous thromboembolism (VTE) | McMaster
Pathophysiology Review. [online] Pathophys.org. Available at: http://www.pathophys.org/vte/
[Accessed 3 Jan. 2019].