Ch. 38 PVD, DVT – Flashcards

The leading cause of PAD is atherosclerosis, a gradual thickening of the intima (the innermost layer of the arterial wall) and media (middle layer of the arterial wall). This results from the deposit of cholesterol and lipids within the vessel walls and leads to progressive narrowing of the artery. Although the exact cause(s) of atherosclerosis are unknown, inflammation and endothelial injury play a major role (see Chapter 34). Significant risk factors for PAD include tobacco use, diabetes, hyperlipidemia, elevated C-reactive protein, and uncontrolled hypertension, with the most important being tobacco use. Nicotine is a vasoconstrictor, and tobacco smoke impairs transport and cellular use of oxygen, and increases blood viscosity and homocysteine levels. Other risk factors include family history, hypertriglyceridemia, increasing age, hyperho mocysteinemia, hyperuricemia, obesity, sedentary lifestyle, and stress.4,7 Women with low lifetime recreational activity are at greater risk for PAD than similar men.8 Atherosclerosis more commonly affects certain segments of the arterial tree. These include the coronary (see Chapter 34), carotid (see Chapter 58), and lower extremity arteries. Clinical symptoms occur when vessels are 60% to 75% blocked.

PAD of the lower extremities affects the aortoiliac, PAD of the lower extremites affect the femoral, popliteal, tibial, or peroneal arteries. The severity of clinical manifestations depends on the site and extent of blockage and the amount of collateral circulation. The classic symptom of PAD of the lower extremities is intermittent claudication. Other symptoms include paresthesia, numbness or tingling in the toes or feet, rest pain, and the loss of both pressure and deep pain sensations. Physical findings include thin, shiny, and taut skin with loss of hair on the lower legs; diminished or absent pedal, popliteal, or femoral pulses; elevation pallor; and reactive hyperemia when the limb is in a dependent position. Complications of PAD include nonhealing ulcers over bony prominences on the toes, feet, and lower leg, and gangrene. Amputation may be required if blood flow is not restored. Various tests are used to diagnose PAD, including Doppler ultrasound with segmental blood pressures, calculating the ankle-brachial index (ABI), and angiography. The overall goals for the patient with lower-extremity PAD include adequate tissue perfusion, relief of pain, increased exercise tolerance, and intact, healthy skin on extremities. The first treatment goal for patients with PAD is to aggressively modify all cardiovascular risk factors. All tobacco use must be stopped. Drug therapy includes statins, antiplatelet agents, and angiotensin-converting enzyme (ACE) inhibitors. Two drugs approved to treat intermittent claudication are cilostazol (Pletal) and pentoxifylline (Trental). The primary nondrug treatment for claudication is tobacco cessation and a formal exercise-training program, with walking being the most effective exercise. Interventional radiologic procedures for PAD include percutaneous transluminal balloon angioplasty with stenting or atherectomy The most common surgical procedure for PAD is a peripheral arterial bypass operation with autogenous vein or synthetic graft material to bypass or carry blood around the lesion. All patients with PAD should be taught the importance of meticulous foot care. Critical limb ischemia is a chronic condition characterized by ischemic rest pain, arterial leg ulcers, and/or gangrene of the leg caused by advanced PAD.

Acute arterial ischemia is a sudden interruption in the arterial blood supply to a tissue, organ, or extremity that, if untreated, results in tissue death. Common causes include embolism, thrombosis, or trauma. Specific manifestations depend on the area affected of the body. Signs and symptoms of an acute arterial ischemia usually have an abrupt onset and include the "six Ps": pain, pallor, pulselessness, paresthesia, paralysis, and poikilothermia. Treatment options include anticoagulation, thrombolysis, embolectomy, surgical revascularization, or amputation.

Past health history: Tobacco use, diabetes mellitus, hypertension, hyperlipidemia, hypertriglyceridemia, hyperuricemia, impaired renal function, obesity; ↑ high-sensitivity C-reactive protein, homocysteine, or lipoprotein (a) [Lp(a)] levels; positive family history, sedentary lifestyle, stress Health perception-health management: Family history of cardiovascular disease; tobacco use, including exposure to environmental smoke Nutritional-metabolic: High sodium, saturated fat, and cholesterol intake; elevated Hb A1C Activity-exercise: Exercise intolerance Cognitive-perceptual: Buttock, thigh, or calf pain that is precipitated by exercise and that subsides with rest (intermittent claudication) or progresses to pain at rest; burning pain in forefeet and toes at rest; numbness, tingling, sensation of cold in legs or feet; progressive loss of sensation and deep pain in extremities Sexuality-reproductive: Erectile dysfunction Plan appopriate nursing care for the patient with acute arterial ischemic disorders of the lowers extremities. Nursing Diagnosis: •Ineffective peripheral tissue perfusion related to deficient knowledge of contributing factors•Activity intolerance related to imbalance between oxygen supply and demand•Ineffective self-health management related to lack of knowledge of disease and self-care measures Planning: The overall goals for the patient who has lower extremity PAD include (1) adequate tissue perfusion; (2) relief of pain; (3) increased exercise tolerance; and (4) intact, healthy skin on the extremities.

Thromboangiitis obliterans (Buerger's disease) is a rare nonatherosclerotic, segmental, recurrent inflammatory disorder of the small and medium-sized arteries, veins, and nerves of the upper and lower extremities. Patients may have intermittent claudication of the feet, hands, or arms. As the disease progresses, rest pain and ischemic ulcerations develop. There are no laboratory or diagnostic tests specific to Buerger's disease. Treatment includes complete cessation of tobacco use in every form. Conservative management includes the use of antibiotics to treat any infected ulcers and analgesics to manage the ischemic pain. Surgical options include revascularization, implantation of a spinal cord stimulator, and sympathectomy.

Raynaud's phenomenon is an episodic vasospastic disorder of small cutaneous arteries, most frequently involving the fingers and toes. The exact etiology is unknown. Clinical symptoms include vasospasm-induced color changes of the fingers, toes, ears, and nose (white, blue, and red). An episode usually lasts only minutes but in severe cases may persist for several hours. Symptoms usually are precipitated by exposure to cold, emotional upsets, caffeine, and tobacco use. Diagnosis is based on persistent symptoms for at least 2 years. There is no diagnostic test. Patient teaching should be directed toward prevention of recurrent episodes. Temperature extremes and all tobacco products should be avoided. Calcium channel blockers are the first-line drug therapy.

Risk factors for SVT: increased age, pregnancy, obesity, malignancy, thrombophilia, estrogen therapy; recent sclerotherapy (treat. for varicose veins); long-distance travel, history of CVI, SVT, or VTE, endothelial alterations (Buerger's disease), SVT may be unprovoked.

Persistent leg symptoms 1 month after VTE, VTE located near the iliofemoral junction, extensive VTE, recurrent VTE, obesity, older age, and female gender.

Pt may have a palpable, firm, subcutaneous cordlike vein. Surrounding area may be itchy, tender or painful to the touch, reddened, and warm. Mild temp. elevation and leukocytosis may be present. Extremity edema may or may not occur. Lower extremity SVT often involves one or more varicose veins

Pt w/ lower extremity VTE may or may not have unilateral leg edema, pain, tenderness w/ palpation, dilated superficial veins, a sense of fullness in the thigh or the calf, paresthesias, warm skin, erythema, or a systemic temp > 100.4 F (38 C). If inferior vena cava is involved, both legs may be edematous and cyanotic. If superior vena cava is involved similar symptoms may occur in the arms, neck, back and face.

Collaborative care for SVT: duplex ultrasound is used to confirm dx (clot 5 cm or larger) and to find clot extension into a deep vein. For pts with lower leg SVT treatment is (LMWH aka Lovenox) for 45 days or phorphylactic dose of fondaparinux (Arixtra). If SVT is in short vein segment < 5cm and is not near saphenofemoral junction anticoagulants are not necessary and NSAIDS can ease symptoms. Elastic compression stockings, topical NSAIDs and mild excercise (walking) will also help pt.

VTE prophylaxis for hospitalized patients depends on individual patient risk and may involve early ambulation, elastic compression stockings, sequential compression devices, and anticoagulation. The goals in the treatment of VTE are to prevent propagation of the clot, development of any new thrombi, and embolization. Anticoagulation therapy is routinely used. Three major classes of anticoagulants are available: (1) vitamin K antagonists, (2) thrombin inhibitors (direct and indirect), and (3) factor Xa inhibitors, such as fondaparinux. Warfarin, a vitamin K antagonist, inhibits activation of the vitamin K-dependent coagulation factors. Indirect thrombin inhibitors include unfractionated heparin (UH) and low-molecular-weight heparin (LMWH). Direct thrombin inhibitors include lepirudin (Refludan) and bivalirudin (Angiomax) and are administered by continuous IV infusion. Some VTE patients require surgical therapy, including thrombectomy and placement of vena cava interruption devices, such as the Greenfield filter. Nursing diagnoses and collaborative problems for the patient with VTE revolve around the problems of acute pain, ineffective health maintenance, risk for impaired skin integrity, and the potential complications of bleeding related to anticoagulant therapy and pulmonary embolism. The overall goals for the patient with VTE include pain relief, decreased edema, no skin ulceration, no bleeding complications, and no evidence of pulmonary emboli. Discharge teaching should focus on elimination of modifiable risk factors for VTE, the importance of elastic compression stockings and monitoring of laboratory values, medication instructions, and guidelines for follow-up.

Assessments: Monitor vital signs as indicated. Examine urine and stool for overt and occult signs of blood. Inspect skin frequently, especially under any splinting devices. Evaluate platelet count for signs of heparin-induced thrombocytopenia. Evaluate appropriate laboratory coagulation tests for target therapeutic levels. Evaluate lower extremity for ecchymosis or hematoma development if sequential compression device used. Perform assessments frequently to observe for signs and symptoms of bleeding (e.g., hypotension, tachycardia) or clotting. Notify the health care provider of any abnormalities in assessments, vital signs, or laboratory values. Avoid intramuscular injections. Minimize venipunctures. Use small-gauge needles for venipunctures unless ordered therapy requires a larger gauge. Apply manual pressure for at least 10 min (or longer if needed) on venipuncture sites Avoid restrictive clothing. Apply moisturizing lotion to skin. Use electric razors, not straight razors. Perform physical care in a gentle manner. Instruct patient not to forcefully blow nose. Avoid removing or disrupting established clots. Humidify O2 source if supplemental O2 is ordered. Use soft toothbrushes or foam swabs for oral care. Reposition the patient carefully at regular intervals. Limit tape application. Use paper tape as appropriate. Administer stool softeners to avoid hard stools and straining. Lubricate tubes (e.g., suction catheter) adequately before insertion. Avoid restraints if possible. Use only soft, padded restraints if needed. Use support pads, mattresses, bed cradles, and therapeutic beds as indicated. Apply elastic compression stockings or sequential compression devices as ordered and with attention to proper size, application, and use. Perform risk for fall and skin breakdown assessments per agency policy and implement safety measures as needed.

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patho: Superficial veins in lower extremities become dilated and tortuous in response to increased venous pressure. Vein valve leaflets are stretched and become incompetent (don't fit together), and incompetent veins then allow backward blood flow, esp. when pt is standing which results further venous pressure and distention. Collab care and review: Varicose veins, or varicosities, are dilated, tortuous subcutaneous veins most frequently found in the saphenous system. The etiology of varicose veins is unknown, and risk factors include congenital weakness of the vein structure, female gender, use of hormones (oral contraceptives or HT), increasing age, obesity, pregnancy, venous obstruction resulting from thrombosis or extrinsic pressure by tumors, or occupations that require prolonged standing. The most common symptom is an ache or pain after prolonged standing, which is relieved by walking or by elevating the limb. Nocturnal leg cramps in the calf may occur. Collaborative care involves rest with the affected limb elevated, compression stockings, and exercise, such as walking. A number of treatment options exist, including sclerotherapy, laser therapy, high-intensity pulsed-light therapy, and surgical procedures, such as phlebectomy and vein ligation. Treatment is optional if varicose veins are only a cosmetic problem. Prevention is a key factor related to varicose veins. Teach the patient measures to promote venous circulation.

Patho and etiology: Long-standing primary varicose veins and PTS can progress to CVI. As a result of ambulatory venous hypertension RBCs leak from the capillaries and venules into the tissue which produce edema and chronic inflammatory changes. Enzymes in the tissue break down RBCs causing the release of hemosiderin, which causes a brownish skin discoloration. Over time, the skin and subcutaneous tissue around the ankle are replaced by fibrous tissue, resulting in thick hardened contracted skin. Although the causes of CVI are known the exact patho of venous leg ulcers is unknown. Collab care and review: Chronic venous insufficiency (CVI), a common medical problem in women and older adults, results in increased ambulatory venous hypertension. CVI can result from long-standing varicose veins or post-thrombotic syndrome and can lead to venous leg ulcers. Clinical manifestations include the skin of the lower leg appearing leathery, with a characteristic brownish or "brawny" appearance, edema and eczema, and pruritus. Venous ulcers classically are located above the medial malleolus. The wound margins are irregularly shaped, and the tissue is typically a ruddy color. Ulcer drainage may be extensive. Pain is present and may be worse when the leg is in a dependent position. Compression is essential to the management of CVI, venous ulcer healing, and prevention of ulcer recurrence. Compression options include elastic wraps, custom-fitted elastic compression stockings, elastic tubular support bandages, a Velcro wrap, sequential compression devices, a paste bandage with an elastic wrap, and multilayer (three or four) bandage systems. Moist environment dressings are the basis of wound care and include transparent film dressings, hydrocolloids, hydrogels, foams, impregnated gauze, and combination dressings. Assess nutritional status. Monitor wounds for signs of infection. The usual treatment for infection is debridement, wound excision, and systemic antibiotics. Alternative treatments may include coverage with a split-thickness skin graft, cultured epithelial autograft, allograft, or bioengineered skin. Long-term management of venous leg ulcers should focus on teaching the patient about self-care measures because the incidence of recurrence is high. Proper foot and leg care is essential to avoid additional trauma to the skin. The patient with CVI should avoid standing or sitting with the feet dependent for long periods. Teach patients with venous ulcers to elevate their legs above the level of the heart to reduce edema. Once an ulcer is healed, encourage a daily walking program. Prescription elastic compression stockings should be worn daily and replaced every 4 to 6 months to reduce the occurrence of CVI.