Pathophysiology of Lower Limb DVT and Testis Epididymitis/Hydrocele

Pathophysiology 1
PATHOPHYSIOLOGY
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Pathophysiology 2
Lower Limb DVT (Deep Venous Thrombosis)
Pathophysiology
Deep venous thrombosis is caused by blood clots in the veins, specifically those found in
the legs. When blood clots are dislodged from a vein, they move through blood and eventually
find their way to the lungs, causing a condition known as a pulmonary embolism (Thompson
2015). Deep vein thromboses together with pulmonary embolisms make up a condition referred
to as venous thrombo-embolism (VTE) (Stone et al. 2017). The main function of clotting is to
minimize blood clots through a process known as coagulation. When something goes wrong
during the coagulation process, there is a potential for clot build up which leads to thrombosis
(Blann 2015). Blood clots or thrombosis are caused by poor blood circulation, varicose veins,
congestive heart failure, pregnancy, an injury to the vein, hormone therapy or susceptibility to
blood clots (Thompson 2015).
The pathophysiology of deep vein thrombosis can trace its background to the work of a
German doctor known as Rudolf Virchow. He identified three factors, known as Virchow’s triad,
which caused blood clots to develop within the deep veins and these factors were venous stasis,
injury/trauma and hypercoagulability (Rumbaut & Thiagarajan 2010). Venous stasis is seen to
play the biggest role in the formation of blood clots within veins especially in post-surgical
patients and those who have experienced vascular trauma (Behravesh et al. 2017). While stasis
can lead to the development of blood clots, research is still unclear on whether stasis alone can
cause enough blood clot formation (Rumbaut & Thiagarajan 2010).
Endothelial injuries have been proposed by researchers to cause thrombosis if they are
occur in the deep vein valve pockets. The endothelial injuries trigger an increase in P-selectin

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production which in turn increases production of platelet-endothelial and platelet-leukocyte-
endothelial cells that create blood clots (Rumbaut & Thiagarajan 2010). Endothelial P-selectin
contributes to inflammatory mechanisms that are localized and various inflammatory stimuli
which lead to deep vein thrombosis. Hypercoagulability refers to conditions that exist in a
procoagulant state because of hemostatic imbalances within the body that lead to thrombosis.
Coagulation factors play an important role in venous thrombosis when they are activated because
they concentrate in areas that have a reduce blood flow like the valve pockets found in the lower
limbs (Rumbaut & Thiagarajan 2010).
Defects in the mechanisms that promote anticoagulation such as antithrombin deficiency
or fibrin deposits play a significant role in causing deep vein thrombosis (Rumbaut &
Thiagarajan 2010). In addition, the initiation of a coagulation cascade caused by the release of
tissue factor due to tumors or tissue damage increases the risk of a person developing DVT
(Behravesh et al. 2017). Thrombosis mostly occurs in the deep vein valve pockets of the lower
legs in areas that have decreased blood flow.
These valves usually help to promote blood flow but they also have a potential to be sites
for venous stasis and hypoxia (Stone et al. 2017). Blood clots are caused by tissue factor which
leads to the conversion of prothrombin to thrombin and this process is later followed by fibrin
deposition. Prothrombin, produced in the liver, is a protein essential in blood clotting while
thrombin converts fibrinogen into fibrin during blood coagulation (Blann 2015).
Sonographic Appearance
A venous duplex ultrasound of the lower limbs makes use of two components to detect
deep vein thrombosis and these are a Doppler imaging of the leg using spectral waveform

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analysis and color-flow imaging or compression techniques using a transducer that makes use of
B-mode or gray-scale images. The main criterion for diagnosing deep vein thrombosis is the
inability to compress the vein. The secondary criteria for diagnosing the condition is the presence
of a thrombus in the vein, distention within the veins, the lack of a Doppler spectral signal and no
response to valsalva maneuvers (Karande et al. 2016). The Venous duplex ultrasound can also
detect whether the thrombus is acute or chronic. For an acute diagnosis, there is venous
distention with partial or no compression of the vein while for a chronic diagnosis, there is no
compression and the vein has an irregular shape with blood clots present on the walls (Karande
et al. 2016).
The American College of Radiology (ACR) has developed guidelines that can be used to
diagnose deep vein thrombosis through the use of ultrasound. These guidelines are compression
should be done in the lower extremity when using the ultrasound, the color and spectral Doppler
should show there is adequate blood flow in the vein and also phasicity (Karande et al. 2016).
The images below show acute DVT. Image A and B are gray-scale or B-mode ultrasound images
of the left femoral vein with the arrow pointing to an enlarged vein that has no compression.
Image C is a color image generated by a spectral Doppler showing a lack of flow within the vein
(Karande et al. 2016).