Introduction
According to Huether (2012), venous insufficiency is a medical condition characterized by the inability of the veins of the lower extremities to effectively push blood back to the inferior vena cava. The venous blood evades its normal antegrade flow path and refluxes down the veins in the lower segments resulting to lower limb venous congestion. Syndromes in this condition are mostly due to valvular incompetence common in the low pressure superficial venous system, although they may also be due to incompetence of the valves in the deep venous systems.
Pathophysiology of CVI
The failure of the valves of superficial veins is attributed to various mechanisms; the most common mechanisms include congenitally weak walls of veins, which dilate under normal pressure ending up with secondary valvular failure. Additionally, normal valve walls become excessively distensible as a side effect of hormones in some conditions such as pregnancy.
Valvular incompetency plays a major role in the Pathophysiology of CVI, where the venous blood in the lower extremities flows back. Some of the risk factors include aging, long sitting or standing hours that eliminate the effect of the muscle pump in aiding venous flow. Reduced mobility is also a major factor that plays a role in stasis.
Venous hypertension also plays a role in the pathophysiology of chronic venous insufficiency in a number of ways. First, there is increase in the venous pressure that transcends the venules and the capillaries; hence, impeding the flow. Secondly, static states in the capillaries contribute to the trapping of leucocytes, which later release proteolytic enzymes and free radicals that end up damaging the capillary basement membrane. A fibrin Cuff is then formed and edema is resultant leading to decreased oxygen delivery and eventually hypoxia, inflammation and loss of tissue. Creation of primary high pressure leakage points between the superficial and the deep systems. The failure of the key valves in the communication between the deep and the superficial systems is the reason for high pressure in the venous system. The causes of the high pressure in the deep system that result to leakage include failure of the junction valves and failure of the perforator valves.
Deep Venous Thrombosis
Deep venous thrombosis is the development of blood clots in the deep veins commonly in the lower extremities that drain into the inferior vena cava and results to pain and swelling. The most dangerous effect is when the clot dislodges and embolize in the lungs. The signs and symptoms are both specific and nonspecific for DVT: redness, leg swelling, discoloration of the region and a palpable cord in the leg vein. Non specific signs and symptoms include warm skin, slight fever, visible surface veins and pain (Huether, 2012).
Epidemiology
Medical studies indicate that most of the DVT cases are occult and may resolve spontaneously, pulmonary embolism is the major cause of more than 300,000 deaths yearly in the United States. Research indicates that about 80 out of 100,000 cases are diagnosed annually. Additionally, about 1 out of 20 persons develop DVT in their lifetime (Madara & Denino, 2008). The incidences increase with age and immobilization. DVT s common in individuals more than 40 years of age in both sexes. The male to female ration is 1.2:1, which indicates that males are at a higher risk in comparison to females. Additionally, the whites and the blacks are at higher risk than the Hispanics and the Asian populations.
Pathophysiology
Virchow’s triad includes venous stasis, Hypercoagulability of the blood and damage to the venous endothelial. Venous stasis leads to slowed transit time of the blood in the venous system due to slowed of obstruction to flow.
Deep venous thrombosis is different from arterial thrombosis in a number of ways. First, arterial thrombosis is the formation one or more clots or a plague in an artery. It forms an embolism when it reaches an area where the plague cannot pass through; hence, occluding oxygenated blood from reaching organs distal to the emboli. It ends up causing ischemia and hypoxia and leads to tissue and organ death termed as necrosis. Common sites include legs and feet to cause gangrene. In the brain, arterial emboli cause stroke and in the heart, it results to myocardial infarction.
Madara and Denino (2008) further explain that common risk factors that predispose to arterial embolism include arterial fibrillation, injury to the arterial walls and thrombophillic conditions. Mitral stenosis predisposes to cerebral embolism and endorcaditis. Additionally, arterial emboli commonly result from areas of atherosclerosis especially in the aorta and other large arteries. The clots mostly embolize in the legs and cause gangrene of the extremities. As opposed to warmth in DVT as a clinical manifestation, arterial embolism will manifest with coldness of the areas occluded, pulselessness, muscle pain and spasms. The affected area appears pale and numb due to impaired blood flow and innervations.
Diagnosis
The diagnosis of chronic venous insufficiency and deep venous thrombosis is clinical through history and clinical examination. In order to diagnose deep venous thrombosis, imaging devices such as ultrasound are important. Clinical assessment predicts the likelihood of DVT implores the use of D-dimer test. D-dimers are fibrin degradation products with increased levels when thrombus is being dissolved by plasmin. Clinical assessment implores the Wells score in assessing the probability and prediction of the disease. The possible score is ranged from -2 to 9 and uses several evaluations. Interpretation can be likely or unlikely, ternary (high, moderate or low probability). In a binary interpretation, a score of 2 and above is categorized as likely while one 1 and below is categorized as unlikely.
Treatment
Definitive treatment include the use of anticoagulants that prevent further coagulation, although they do not act on the existing clots and after five days, the patient should receive vitamin K antagonist after cessation of heparin.
Compression stockings are used to apply high pressure at the ankles are recommended to symptomatic patients and the use should be as soon as possible after anticoagulant therapy for at least 2 years. Other options include inferior vena cava filters due to the presumption of their ability to reduce the risk of pulmonary embolism (preserved for those with contraindications to anticoagulation therapy).
Thrombolysis is catheter directed and can be systemic depending on the medical capabilities of the physician. Thrombectomy is a mechanical procedure that involves the surgical removal of the thrombus. However, it is considered in ileofemoral DVT that is symptomatic for less than 7 days, good functional status of the patient with a life expectancy of more than one year.
Mind maps
References
Huether, S. (2012). Understanding Pathophysiology (5th ed., p. 1159). St. Louis, Mo: Elsevier.
Madara, B., & Denino, V. (2008). Cardiovascular System 267. In Quick Look Nursing: Pathophysiology (2nd ed., p. 612). Sudbury, Mass.: Jones and Bartlett.
Porth, C., & Porth, C. (2011). Disorders of Blood Flow 405. In Essentials of pathophysiology: Concepts of altered health states (3rd ed., p. 1256). Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins.
