Chronic Venous Insufficiency

ANATOMY AND PHYSIOLOGY
Chronic Venous Insufficiency (CVI) arises due to incompetence of vascular walls as
well as valves of the veins. This disorder leads reduction in blood flow to the heart resulting in
pooling of blood or stasis in the extremities especially the lower limbs. Patients with CVI usually
complain of pain and swelling in the limbs. Conversely, deep venous thrombosis (DVT) arises
when clotting occurs in the deep veins in the lower limbs (Patel & Brenner, 2013). Patients
suffering from DVT usually complain of pain as welling as swelling just as those with CVI. The
presentation of these conditions is almost similar. It is for this reason that health care providers
take extra caution when diagnosis CVI and DVT.

The Pathophysiological Presentation of DVT and CVI

The key pathophysiological difference between CVI and DVT is that DVT occurs in deep
veins whereas CVI occurs majorly in superficial veins. CVI affects popliteal, femoral, and
peroneal veins while DVT mail affects the soleal vein. Chronic Venous Insufficiency arises as a
result of damage of the endothelial walls and valves in the veins (Eberhardt & Raffetto, 2014).
Some of the common causes of CVI include pelvic tumors, DVI, and vascular malformations.
The valves of patients suffering from CVI are incompetent in that they cannot hold blood back
against the force of gravity. Consequently, blood pools in the lower extremities leading to
swelling especially in the ankles and the legs. Moreover, individuals with CVI present with
venous stasis ulcers, varicose veins, pain the feet, and itching and flaking of the skin. On the
other hand, DVT develops due to clotting in the veins. Severe clinical complications occur when
the formed clots lyse and get into the general circulation. Blood from deep veins usually flows
into the lungs. Therefore, when this blood carries clots with it, it may lodge them in the lungs
causing pulmonary embolism, one of the most severe result of DVT (Goldhaber & Bounameaux,
2012). Often CVI presents with dermatitis and ulceration due to the structural difference between

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ANATOMY AND PHYSIOLOGY
the deep veins and superficial veins. That is, the superficial veins have an adipose layer and a
connective tissue whereas the deep veins have a fascia and muscles. This gives deep veins more
protection and structural support.
Venous and arterial thrombosis have a number of similarities although they differ in
terms of their pathophysiology, clinical interventions, and epidemiology. Venous thrombosis
occurs in undamaged parts of venous walls and in areas that have low sheer pressure. This
disorder leads to formation of red thrombi. Conversely, arterial thrombosis occurs in parts that
have high sheer stress and are rich in plaques. Unlike, venous thrombosis, arterial thrombosis
forms white thrombi.
Patient Behavior
The predisposition and pathophysiological advancement of DVT and CVI relies heavily
on the lifestyle of an individual. The pathophysiology of DVT and CVI is enhanced when a
person engages in activities that enhance the metabolic syndrome. Some of the most notable
practices that have been cited to predispose individuals to CVI and DVT include lack of physical
exercises, smoking, intake of meals rich in cholesterol, and psychosocial behavior (Csordas &
Bernhard, 2013). Smoking affects the circulation of blood and enhances blood clotting. On the
other hand, inactivity such as sitting for long periods causes calf muscles to contract hence
inhibiting proper circulation of blood. Lack of activity may also result in increase of weight
which then increases pressure in veins especially in the legs and the pelvis.
When diagnosing of CVI and DVT based on behavior, a physician should enquire the
social history of the patient. For instance, s/he can ask the patient whether s/he smokes or has
ever smoked. If the patient smokes, he should enquire when the patient started smoking and how

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ANATOMY AND PHYSIOLOGY
many sticks he smokes in a day. Questions on whether the patient engages in physical exercises
such as jogging or long distance travelling are also essential in finding a differential diagnosis.
Clinical interventions for these patients involves the use of pharmacological as well as
non-pharmacological approaches. If the patient smokes, a physician should assess the
willingness of the patient to quit smoking. If s/he is willing to make a quit attempt, a brief
counselling session should be introduced, medications such as bupropion will be offered as well
as self-help resources. Follow-up visits should also be scheduled. The patient should also be
advised to engage in physical exercises such as jogging. The patient should also limit his/her
intake of cholesterol, leading factor in DVT development.

Mind Maps

5

ANATOMY AND PHYSIOLOGY

Pathophysiology
Formation of blood clots
in deep veins, which may
then be transported by
blood to the lungs or the
heart.

Clinical presentation
Pain and swelling in
the lower
extremities
especially the ankles

Diagnosis
Patient History
Ultrasound
Venography
MRI and CT

Treatment
Blood Thinners
Clotbustors
Compression Stockings
Recommendation of physical activity an

proper diet

Causes about 1 out of
1000 deaths annually
with Europeans and
North American
populations being
highly affect.

DVT

6

ANATOMY AND PHYSIOLOGY

Pathophysiology
Damage to endothelial
walls in veins and valves,
resulting in pooling of
blood leading to swelling,
pain, and varicose veins

Diagnosis
Physical examination
Ultrasound
Venography

Clinical Presentation
Swelling of legs
Redding of skin around ankles
Varicose veins
Leg UlcersCalf tightness

Diuretics
Anticoagulant
Pentoxifyline
Surgery

Epidemiology
Varies from 1% to 40% in
women and 1% to 17% in men.
Prevalent in developed countries.
CVI

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ANATOMY AND PHYSIOLOGY

References

Berkman, L. F., Kawachi, I., & Glymour, M. M. (Eds.). (2014). Social epidemiology. Oxford
University Press.
Csordas, A., & Bernhard, D. (2013). The biology behind the atherothrombotic effects of cigarette
smoke. Nature Reviews Cardiology, 10(4), 219-230.
Eberhardt, R. T., & Raffetto, J. D. (2014). Chronic venous insufficiency.Circulation, 130(4),
333-346.
Goldhaber, S. Z., & Bounameaux, H. (2012). Pulmonary embolism and deep vein
thrombosis. The Lancet, 379(9828), 1835-1846.
Patel, K., & Brenner, B. (2013). Deep venous thrombosis. Medscape

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