Venous hospitalisation for acute illness, nursing home confinement,

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Venous thromboembolism
(VTE) is characterised by clot formation within a vein resulting in reduced
blood flow, which in turn can lead to necrosis of localised tissue and organs (Yau, Teoh, & Verma, 2015). Any venous
circulation can be affected by thrombosis, and in VTE deep vein thrombosis
(DVT) and pulmonary embolism (PE) is included. The incidence in Europe ranges
from 104-183 per 100.000 person-years (Heit, 2015). In the United states
there is a yearly occurrence of 200.000 new cases (Kroegel &
Reissig, 2003).
There are several known risk factors for VTE including age, active cancer,
major surgery, neurological disease with leg paresis, hospitalisation for acute
illness, nursing home confinement, trauma or fracture, pregnancy, oral
contraception, non-contraceptive oestrogen plus progestin, oestrogen,
progestin, BMI, urinary tract infection and prior superficial vein thrombosis (Heit, 2015). VTE is further
associated with a high rate of recurrence and reduced survival (Heit, 2015).

Development of venous
thrombosis is characterised by three key features (according to Virchow’s
triad): venous stasis, hypercoagulable states and vascular endothelium injury.
Venous stasis occurs when there is a hemodynamic imbalance which occurs in
regions with slow blood flow, the pooled blood will activate the coagulation
system resulting in a local hypercoagulability. This can lead to endothelial
damage which in turn leads to further activation of the homeostasis system.
Hypercoagulable states occur when the balance between pro- and anticoagulant is
in favour of procoagulant. Injury to the vascular endothelium causes changes in
the clotting system which contributes to the hypercoagulability (Kroegel & Reissig, 2003).

The endothelium
separates the blood from the surrounding tissue and serves many functions,
amongst them is to regulate the vascular tone and it is also involved in
cellular adhesion, vessel wall inflammation and smooth muscle cell
proliferation. Under normal conditions, the endothelial surface prevents platelets
from attaching and thereby prevents thrombosis. This is done by production of
nitric oxide and prostaglandin I2. Occurrence of vascular injury causes
endothelial dysfunction whereby cellular and protein material can gather at the
site of injury, creating a blood clot (Yau, Teoh, & Verma, 2015). Once the
endothelium becomes inflamed, a two-step process of activation is initiated. In
the type I activation (stimulation) leads to elevated levels of Ca2+
which leads to increased blood flow and recruitment of leukocytes. Type II
activation is mediated by tumour-necrosis factor (TNF) and interleukin-1 (IL-1)
which in turn leads to an increase in blood flow, vascular leakage of plasma
proteins and recruitment of leukocytes. Thrombus formation is important in
inflammation since it by separating the infected tissue from healthy tissue,
prevents the microbes from spreading. (Pober & Sessa, 2007) The regulation of
blood coagulation is therefore important in development of VTE (Yau, Teoh, & Verma, 2015).

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