Pathophysiology of CVI and DVT

Chronic Venous Insufficiency (CVI) is a fault in the venous system culminating into swell up of the legs and feet (Raffetto, 2018). The occurrence is as a result of weak valves unable to close up entirely leading to the building up of pressure in the feet and legs. The faults in the venous system include reflux, whereby, the normal flow of blood in the legs and feet is reversed due to standing for long hours. Blood clots, in a severe case, damage the veins leading to chronic failure in the venous system. Signs of CVI include severe feet and leg swelling, discolored skin, and varicose veins. Whereas, Deep Venous Thrombosis (DVT) is said to occur when there is the formation of blood clots in the veins located deep in the body, more often in the legs (Stouffer & Shealhan, 2001). The occurrence can be painless or painful, and discoloration of the skin. The cause of DVT has been associated with medical conditions that have an impact in blood clotting mechanism. The clots can be life-threatening when they get lodged into the lungs and the heart.

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Arterial and venous thrombosis can be viewed to be different pathophysiological occurrences because of differences in anatomy and how they are presented clinically. Arterial thrombosis is associated with clotting, whereby, blood flowing under high pressure and rich in platelets form around ruptured endothelium. However, venous thrombosis is associated with the clotting system, such that, the blood is flowing under low pressure but platelets form around endothelium walls which is intact (PRANDONI, 2007).

Age factor in CVI and DVT

Age is considered to be the greatest risk factor in the development of thrombosis in the vein and artery. The explanation is based on reduced mobility by old people, reduction in venous compliance around the calf region among other factors (Vangevelde, & Sramek, 2010). Moreover, muscle fibers present in vessel walls are characterized with reduced functions as the age progresses. Consequently, the vessel valves thicken with collagen increase. Therefore, aging leads to loss of valve functionality leading to reflux and the possibility of DVT development (Stouffer & Shealhan, 2001).

Diagnosis can be made through the use of compression ultrasonography. The test determines the compressibility of a segment in the venous system. Doppler may be added to make the identification of vessels more effective, or when the initial diagnosis is not precise. Treatment of venous thrombosis can be done by using rivaroxaban, LMWH, or other unfractionated heparin. Old age people are discouraged against treatment by exclusive use of Vitamin K antagonists. LMWH is administered daily for about five to 10 days, after that, treatment by Vitamin K antagonists can ensue. Excretion of LMWH is exclusively renal; hence unfractionated heparin is the preferred therapeutic agent in cases of renal dysfunction in old patients.

Mind Maps

3552825395605Pathophysiology

Blood clots and weak valves leading to swelling of legs, discoloration, varicose veins.

00Pathophysiology

Blood clots and weak valves leading to swelling of legs, discoloration, varicose veins.

104775394970Epidemiology

17% in males, 40% in females.

Popular in Western countries.

00Epidemiology

17% in males, 40% in females.

Popular in Western countries.

Chronic Venous Insufficiency

36861752476501790700247650

4133850247650Diagnosis

Compression Ultrasonography

00Diagnosis

Compression Ultrasonography

1971675200025Chronic Venous Insufficiency

In

00Chronic Venous Insufficiency

In

3686175109220

1447800660402781300660400151765Clinical Presentation

Numerous clotting

00Clinical Presentation

Numerous clotting

197167593980Treatment

rivaroxaban, LMWH, unfractionated heparin

00Treatment

rivaroxaban, LMWH, unfractionated heparin

4267200229235Pathophysiology

Clots in deep veins inside the body

Painless or painful

Discoloration

00Pathophysiology

Clots in deep veins inside the body

Painless or painful

Discoloration

Deep Venous Thrombosis

-952524130Epidemiology

Occurrence 1 per 1000 people

Prevalent in men than women

00Epidemiology

Occurrence 1 per 1000 people

Prevalent in men than women

365760040640

1971675216535

243840024765Deep Venous Thrombosis

00Deep Venous Thrombosis

-114300281940Clinical Presentation

Fault in clotting system

Platelets lodge on intact endothelium walls

00Clinical Presentation

Fault in clotting system

Platelets lodge on intact endothelium walls

3657600203203057525203201857375203204314825100330Diagnosis

Compression Ultrasonography

00Diagnosis

Compression Ultrasonography

2124075123825Treatment

rivaroxaban, LMWH, unfractionated heparin

00Treatment

rivaroxaban, LMWH, unfractionated heparin

References

PRANDONI, P. (2007). Venous thromboembolism and atherosclerosis: is there a link?. Journal Of Thrombosis And Haemostasis, 5, 270-275. doi: 10.1111/j.1538-7836.2007.02467.x

Raffetto, J. (2018). Pathophysiology of Chronic Venous Disease and Venous Ulcers. Surgical Clinics Of North America, 98(2), 337-347. doi: 10.1016/j.suc.2017.11.002

Stouffer, G., & Shealhan, R. (2001). Deep Venous Thrombosis: A Review of the Pathophysiology, Clinical Features, and Diagnostic Modalities. https://www.amjmedsci.org/article/S0002-9629(15)34544-4/pdf

Vangevelde, K., & Sramek, A. (2010). The Effect of Aging on Venous Valves | Arteriosclerosis, Thrombosis, and Vascular Biology. https://www.ahajournals.org/doi/10.1161/ATVBAHA.110.209049