Deep Venous Thrombosis (DVT) and Chronic Venous Insufficiency (CVI).

Posted: December 24th, 2022

Deep Venous Thrombosis (DVT) and Chronic Venous Insufficiency (CVI).

Review the section “Diseases of the Veins” (pp. 598-599) in Chapter 23 of the Huether and McCance text. Identify the pathophysiology of chronic venous insufficiency and deep venous thrombosis. Consider the similarities and differences between these disorders.
Select a patient factor different from the one you selected in this week’s Discussion: genetics, gender, ethnicity, age, or behavior. Think about how the factor you selected might impact the pathophysiology of CVI and DVT.Deep Venous Thrombosis (DVT) and Chronic Venous Insufficiency (CVI). Reflect on how you would diagnose and prescribe treatment of these disorders for a patient based on the factor you selected.

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Review the “Mind Maps—Dementia, Endocarditis, and Gastro-oesophageal Reflux Disease (GERD)” media in the Week 2 Learning Resources. Use the examples in the media as a guide to constructing two mind maps—one for chronic venous insufficiency and one for venous thrombosis. Consider the epidemiology and clinical presentDeep Venous Thrombosis (DVT) and Chronic Venous Insufficiency (CVI).ation of both chronic venous insufficiency and deep venous thrombosis.

To Complete:
>>>Write a 2- to 3-page paper that addresses the following:
Compare the pathophysiology of chronic venous insufficiency and deep venous thrombosis. Describe how venous thrombosis is different from arterial thrombosis.
Explain how the patient factor you selected might impact the pathophysiology of CVI and DVT. Describe how you would diagnose and prescribe the treatment of these disorders for a patient based on the factor you selected.
Construct two mind maps—one for chronic venous insufficiency and one for deep venous thrombosis. Include the epidemiology, pathophysiology, and clinical presentation, as well as the diagnosis and treatment you explained in your paper.Deep Venous Thrombosis (DVT) and Chronic Venous Insufficiency (CVI).

Deep Venous Thrombosis (DVT) and Chronic Venous Insufficiency (CVI): Epidemiology, Pathophysiology, Clinical Presentation, Diagnosis, and Management
Deep venous thrombosis (DVT) and chronic venous insufficiency (CVI) are two vascular conditions that are related. CVI causes stasis of blood in the deep veins of the extremities. This stasis thereafter may lead to formation of a clot hence thrombosis in the deep vein. This clot from the DVT may then dislodge and cause pulmonary embolism, a life-threatening medical emergency.Deep Venous Thrombosis (DVT) and Chronic Venous Insufficiency (CVI).
Pathophysiology
Since the two are related as indicated above, their pathophysiology is also tied to one another. In CVI, valvular incompetence, venous hypertension (due to the pooling of blood), and vessel wall inflammation interact to produce symptoms of venous insufficiency. In immobile patients and those with cardiac disease, the process above is speeded up by improper functioning of the muscle pump and the heart (vascular pump) respectively. The pooling of blood on the deep veins result in venous hypertension. Coupled with the hemodynamic changes that ensue, the release of various vasoactive chemicals is initiated. Subsequently, chemokines, adhesion molecules, and other mediators of inflammation are produced. The end result endothelial injury (Huether & McCance, 2017; Santler & Goerge, 2017; Hammer & McPhee, 2014).
As for DVT, the pathophysiology is tied to impaired venous return (venous stasis) and malfunctioning of either or both the muscle pump and the vascular pump (the heart). As stated above, stasis can occur due to CVI hence the relationship between the two. As such, injury to the vascular endothelium of the deep veins in the extremities results in inflammation. At times, this injury may be the result of invasive medical procedures such as insertion of a central venous catheter. Coupled with hypercoagulability of the blood, the result is development of thrombi in the deep leg, arm, or pelvic veins. This is DVT (Huether & McCance, 2017; Santler & Goerge, 2017; Hammer & McPhee, 2014).Deep Venous Thrombosis (DVT) and Chronic Venous Insufficiency (CVI).
Venous Thrombosis vs Arterial Thrombosis
Venous thrombosis occurs in the nlood vessels that return blood to the heart. Basically, a clot forms in one of the deep veins usually due to hypercoagulability and injury to the venous endothelium. The thromboembolism from this usually leads to pulmonary embolism. Arterial thrombosis on the other hand involves clot formation in the vessels carrying oxygenated blood from the heart. Unlike in venous thrombosis, the cause here is usually the formation of an atheromatous or fatty plaque in the arterial wall. This progressively narrows the arterial lumen increasing the velocity of blood passing at that particular point. The increased friction causes damage to the arterial endothelium and a clot begons to form. This may finally dislodge and cause a myocardial infarction or heart attack (if it is on the coronary arteries), or a stroke (if it is in the brain) (Huether & McCance, 2017; Santler & Goerge, 2017; Hammer & McPhee, 2014).Deep Venous Thrombosis (DVT) and Chronic Venous Insufficiency (CVI).
The Obesity Factor
Obesity as a patient predisposing factor plays a very important role in the pathophysiology of both CVI and DVT. For a start, it has been explained above that immobile or physically inactive persons are at greater risk of developing CVI and DVT. This is because the action of the muscle pump in aiding venous return will be absent. It is a fact that persons who are obese loathe walking or just engaging in any phusical activity. The other reason is that the heart of an obese person is overburdened. Its efficiency as a vascular pump is significantly reduced due to the increased body mass and lack of exercise. This encourages venous stasis (Huether & McCance, 2017; Hammer & McPhee, 2014).
Epidemiology, Clinical Presentation, Diagnosis, and Treatment
The average prevalence of CVI has been put at 1 in 4 people in the general population. There is however considerable variability in the figures for males and for females. Age, obesity, and a family history are significant risk factors. For DVT, about 200,000 persons develop the condition annually, with the incidence standing at 80 diagnoses per 100,000 (Huether & McCance, 2017; Hammer & McPhee, 2014). The clinical presentation of CVI includes night leg cramps, itchiness of the legs, edema and a feeling of heaviness in the legs. Untreated, huge varicose veins greater than 3mm in diameter become visible to the naked eye. As for DVT, symptoms include calf tenderness, edema, and swelling of the whole extremity (Huether & McCance, 2017)..Deep Venous Thrombosis (DVT) and Chronic Venous Insufficiency (CVI).
Diagnosis of CVI is basically done based not only on imaging tests, but also on the history and clinical presentation. The imaging studies include duplex ultrasonography and phlebography (contrast-enhanced X-ray of the affected veins). For DVT, the rule of thumb is to use doppler ultrasonography for diagnosis (Huether & McCance, 2017; Hammer & McPhee, 2014). Treatment of both CVI and DVT can be either conservative or invasive, depending on the stage and the severity of symptoms. For uncomplicated CVI, physical therapy in addition to manual compression therapy is the standard. If severe, surgery to remove the incompetent vein or isolate the source of stasis is the last option. For DVT, treatment is by anticoagulants. Surgery may however be the next option in the case of recalcitrant thrombi (Huether & McCance, 2017; Santler & Goerge, 2017).Deep Venous Thrombosis (DVT) and Chronic Venous Insufficiency (CVI).