Management of Patients with Peripheral Vascular Disease PDF

MANAGEMENT OF PATIENT WITH ALTERATION IN PERIPHERAL PERFUSION PRESENTED BY: JED KEONI UY JOLO, RN REVIEW OF ANATOMY, PHYSIOLOGY AND FUNCTION OF PERIPHERAL SYSTEM THE BLOOD VESSELS: THE VASCULAR SYSTEM Taking blood to the tissues and back 1. Arteries- a critical part of your cardiovascular system, are blood vessels that distribute oxygen- rich blood to your entire body. 2. Arterioles- -small blood vessels that carry blood away from your heart, are connectors between your arteries and capillaries. -They control your blood pressure and blood flow throughout your body, using their muscles to change their diameter. They also link to capillaries to exchange oxygen, nutrients and waste. 3. Capillaries- the smallest and most numerous of the blood vessels, form the connection between the vessels that carry blood away from the heart (arteries) and the vessels that return blood to the heart (veins). 4. Venules- the smallest and most numerous of the blood vessels, form the connection between the vessels that carry blood away from the heart (arteries) and the vessels that return blood to the heart (veins). 5. Veins- blood vessels located throughout your body that collect oxygen-poor blood and return it to your heart. BLOOD VESSELS: ANATOMY The walls of the arteries and arterioles are composed of three layers (Tunics) 1. Tunica Intima- inner endothelial cell layer (Endothelium) 2. Tunica Media- middle layer of smooth muscle and elastic tissue ; Controlled by sympathetic nervous system 3. Tunica Externa- Mostly Fibrous connective tissue REVIEW OF THE CNS It is divided into two parts: Brain and Spinal Cord There 2 sets of antagonistic nerves in the Autonomic Nervous System which is the SNS and PNS When talking about Sympathomimetic, meaning it mimics the Sympathetic Nervous System effects by releasing a neurotransmitter Norepinephrine which: Increase all, except GI and GU (The ﬂight and ﬁght response). -Eyes: Dilates pupils -Lungs: Dilate Bronchioles -Heart: Increases Heart rate -Blood vessels: Constriction -Gastrointestinal: Relaxes smooth muscles of gastrointestinal tract -Bladder: Relaxes bladder muscle Parasympathomimetic on the other hand, mimics the Parasympathetic Nervous System effects by releasing a neurotransmitter called Acetylcholine which: Decreases all, except GI and GU (Rest and Digest) -Constricts pupils -Constricts bronchioles and increases secretions -Decrease heart rate -Dilates blood vessels -Increase peristalsis -Constricts bladder DIFFERENCES BETWEEN BLOOD VESSEL TYPES Walls of the arteries are the thickest Lumens of veins are the larger Skeletal muscle “milks” blood in veins toward the heart Walls of capillaries are only one cell layer thick to allow for exchanges between blood and tissue ASSESSMENT OF THE VASCULAR SYSTEM The nurse should perform a focused health history and physical assessment to establish a patient’s baseline and identify alterations in the vascular system ASSSESSMENT 1. HEALTH HISTORY TAKING 2. PHYSICAL ASSESSMENT 3. PALPATION OF PULSES DIAGNOSTIC EVALUATION The nurse should educate the patient on the purpose of the diagnostic studies, what to expect, and any possible side effects related to these examinations. DOPPLER ULTRASOUND FLOW STUDIES When pulses cannot be reliably palpated, a handheld continuous wave (cw) doppler ultrasound device may be used to detect blood ﬂow This handheld device emits a continuous signal through the patient’s tissues. the signals are reﬂected by the moving blood cells and received by the device. Continuous wave doppler ultrasound detects blood ﬂow in peripheral vessels. combined with computation of ankle or arm pressures. This diagnostic technique helps health care providers characterized the nature of peripheral vascular disease NURSING IMPLICATIONS FOR ANKLE BRACHIAL PRESSURE INDEX Nurses should perform a baseline ABI on any patient with decreased pulses or any patient 65 years or older, especially patients with a history of diabetes or nicotine use ARTERIAL DISORDERS ARTERIOSCLEROSIS – stiffening/ decreased elasticity of the blood vessel ATHEROSCLEROSIS- accumulation of lipids, calcium, blood components, carbohydrates and ﬁbrous tissue on the intimal layer of the artery that cause atheromas or plaque formation that may obstruct the normal ﬂow of the blood. OBSTRUCTION OF THE BLOOD FLOW= INCREASE CARDIAC OUTPUT TO PROVIDE MORE BLOOD TO THE TISSUES AND ORGAN. SIGNS AND SYMPTOMS: 1. Ischemia- blood ﬂow is restricted or reduced in the tissue or organ, especially the heart (when the heart is hypoxic, it causes imbalance between oxygen supply and oxygen demand) 2. Hypoxia- a state in which oxygen is not available in suﬃcient amounts at the tissue level to maintain adequate homeostasis; 3. Hypoxemia- decreased oxygenation in the blood 4. Tachycardia- compensatory mechanism to promote blood ﬂow REFER CAD MATERIALS AS REVIEW FOR THE CLINICAL MANAGEMENT, NURSING MANAGEMENT, AND OTHER NURSING INTERVENTIONS PERIPHERAL ARTERIAL OCCLUSIVE DISEASE BUERGER’S DISEASE (THROMBOANGITIS OBLITERANS) Cause: 1. Blockage/ Obstruction in the peripheral arteries/ arteries secondary to blood clot. 2. Leads to tissue ischemia 3. There will be pain/ inﬂammation complications: tissue necrosis / cell death Common in males (20-40 yrs. Old) Idiopathic (unknown cause) Autoimmune problem that attacks arteries/ veins, that causes occlusion, decreased in circulation, decreased in oxygenation. Signs and symptoms or clinical manifestations (Buerger’s) 5 P’s 1. Pain- increased when walking - decreased when resting it is called- Intermittent Claudication 2. Pulseless 3. Pallor 4. Paresthesia- Tingling sensation, Prickling “Pins & Needles”, Numbness 5. Poikilothermia- Thickening of the toe nails upon dependency: Rubor RISK FACTORS -Smoking – nicotine -Viscous Blood (DM, Dehyrated/ Dehydration, increased LDL, Increased RBC ) -Sedentary Lifestyle -prolonged presence (longer than 48 hours) of an IV catheter in the same site, the use of contaminated IV equipment, -trauma -Virchow’s Triad – Stasis H-Hypercoagulation E- Hereditary/ Endothelial Injury Stasis occurs when the valves are dysfunctional or the muscles of the extremities are inactive more frequently in people who are obese, -have congestive heart failure, -have been on long trips without regular exercise, -have a prolonged surgical procedure, or are immobile for long periods (e.g., with spinal cord injuries or fractured hips). Also at risk are pregnant women and women in the postpartum period Patient with atrial ﬁbrillation is also at high risk because of stagnation of blood in the atria and the eddying in blood ﬂow caused by irregular ventricular contractions in response to the atrial ﬁbrillation. Some medications (e.g., corticosteroids, quinine) predispose a patient to DVT formation. ENDOTHELIAL DAMAGE Damage to the endothelial surface of the vein may be caused by trauma or external pressure and occurs any time a venipuncture is performed. Damaged endothelium has decreased ﬁbrinolytic properties, predisposing to thrombus development. HYPERCOAGULABILIT Y OF BLOOD Hypercoagulability of blood occurs in many hematologic disorders, particularly polycythemia, severe anemias, various malignancies (especially cancers of the breast, brain, pancreas, and gastrointestinal tract), antithrombin III deﬁciency, protein C deﬁciency, protein S deﬁciency, antiphospholipid, antibodies, elevated homocysteine levels, and factor V Leiden mutation A patient with sepsis is predisposed to hypercoagulable state in response to endotoxins that are released. Women of childbearing age who take estrogen- based oral contraceptives or postmenopausal women who use hormone replacement therapy (HRT) are at increased risk for venous thromboembolism disease. Women who use oral contraceptives and smoke double their risk because of the constricting effect of nicotine on the blood vessel wall. Smoking may also cause hypercoagulability. PATHOPHYSIOLOGY Red blood cells (RBCs), white blood cells (WBCs), platelets, and ﬁbrin adhere to form a thrombus. A frequent site of thrombus formation is the valve cusps of veins, where venous stasis allows accumulation of blood products. As the thrombus enlarges, increased numbers of blood cells and ﬁbrin collect behind it, producing a larger clot with a “tail” that eventually occludes the lumen of the vein. If a thrombus only partially occludes the vein, If the thrombus does not become detached, it undergoes lysis or becomes ﬁrmly organized and adherent within 5 to 7 days. The organized thrombi may detach and result in emboli. Turbulence of blood ﬂow is a major factor contributing to detachment of the thrombus from the vein wall. The thrombus can become an embolus that generally ﬂows through the venous circulation to the heart and lodges in the pulmonary circulation. Thus it becomes a pulmonary embolus. DIAGNOSTIC TEST D-DIMER Protein C&S Arteriogram- Dye- Result: Dye stops (+) for occlusion Nursing Mgt. check for allergies (Dye) NURSING MANAGEMENT 1. Assess Circulation -Capillary reﬁll test- best -Pulse – distal: Dorsalis pedis -U/O -if (-) pulse: Doppler UTZ 2. Promote Circulation -walking -X constrictions -ROM 3.Health Education - stop smoking - foot care : avoid walking barefoot/ avoid cavass shoes- leads to decreased perspiration and causes irritation 4. shoes: Well ﬁtted 5. Cut toenail 6. Apply Lanolin UPPER EXTREMITY ARTERIAL DISEASE Arterial stenosis and occlusions occur less frequently in the upper extremities (arms) than in the legs, and cause less severe symptoms because the collateral circulation is signiﬁcantly better in the arms. The arms also have less muscle mass and are not subjected to the workload of the legs. ANEURYSM Localized, irreversible dilatation of an artery due to an alteration in the integrity of its walls. Fusiform Aneurysm Localized, irreversible dilatation of an artery due to an alteration in the integrity of its walls. Saccular Aneurysm Projects from only one side of the vessel One side of the arterial wall is dilated Bulbous protrusion of one side of the arterial wall Saccular Aneurysm Projects from only one side of the vessel One side of the arterial wall is dilated Bulbous protrusion of one side of the arterial wall Aortic Dissection Occasionally, in an aorta diseased by arteriosclerosis, a tear develops in the intima or the media degenerates, resulting in a dissection There is separation between the tunica media and tunica intima. Usually is a hematoma that splits the layers of the arterial wall. Thoracic Aortic Aneurysm Approximately 70% of all cases of thoracic aortic aneurysm are caused by atherosclerosis. Occurs most frequently in men between the ages of 50 and 70 years old, and are estimated to affect 10 of every 100,000 older adults. Clinical Manifestations Symptoms vary and depend on how rapidly the aneurysm dilates and how the pulsating mass affects surrounding intra-thoracic structures. Some patients are asymptomatic. In most cases, pain is the most prominent symptom. Dyspnea- the result of pressure of the aneurysm sac against the trachea, a main bronchus, or the lung itself. Cough, frequently paroxysmal (sudden, uncontrollable outburst) and with a brassy quality. Hoarseness Stridor Vocal weakness or aphonia (complete loss of the voice), resulting from pressure against the laryngeal nerve. Dysphagia (diﬃculty in swallowing)- due to impingement on the esophagus by the aneurysm Diagnostic Findings Chest X-ray Computed Tomography Angiography (CTA) MRA (Magnetic Resonance Angiogram) Transesophageal echocardiography (TEE)  CTAs are typically performed because they are widely available, can be completed rapidly, and can remove cardiac motion artifacts, enhancing their accuracy Medical Management Treatment is based on whether the patient is symptomatic and whether the aneurysm is expanding in size, caused by an iatrogenic injury. General measures such as controlling blood pressures and correcting risk factors are helpful Beta blockers (Mainstay of medical treatment for aortic aneurysms). Ex. Metoprolol, atenolol, carvedilol ARBs (Angiotensin Receptor Blockers) ‘tans’ Losartans, valsartan, irbesartan Hydralazine Abdominal Aortic Aneurysm  The most common cause of abdominal aortic aneurysm is atherosclerosis.  Affects men two to six times more often than women  Two to three times more common in White versus Black men  Most prevalent in patients older than 65 years of age  Most of these aneurysms occur below the renal arteries (infrarenal aneurysms). -Untreated, the eventual outcome may be rupture and death. Pathophysiology All aneurysms involve a damaged media layer of the vessel. May be caused by congenital weakness, trauma, or disease. After an aneurysm develops, it tends to enlarge. Risk Factors Genetic predisposition Nicotine use Hypertension; more than half of the patients with aneurysms have hypertension. Clinical Manifestations Pulsatile mass over the abdomen. Low back pain, lower abdominal pain, and ﬂank pain. This is due to compression of structures and nerve endings in the area by the dilated artery Collapse and shock due to hemorrhage. Facts  The most common cause of aneurysm is hypertension  The most dangerous complications of aneurysm is rupture  Collaborative management -Antihypertensive drugs -Surgery Raynaud’s Disease Common in females (20-40 years old) Cause: 1. Vasospasm of the arteries/ arterioles 2. Tissue ischemia, but no tissue necrosis. 3. Idiopathic (unknown) CAUSES Stress Smoking SLE (Systemic Lupus Erymathosus) - Autoimmune R.A - Rheumatoid Arthritis –Autoimmune Autoimmune- Attacks connective tissues causing vasculitis that causes spasm Common site: ﬁnger, toes CLINICAL MANIFESTATIONS Ischemic pain Poor blood circulation Poor wound healing Risk for infection Pulse deﬁcit Bilateral/ symmetrical Altered sensation (pain/ numbness) Cold extremities during white/ blue phase Warm extremities during Red Phase Watch out for: OHP- orthostatic hypotention (postural) – Risk for injury (RED phase) CARDINAL MANIFESTATIONS Progressive color shifting of ﬁngers and toes White – Blue – Red contrict - constrict – Dilate- Raynaud’s Phenomenon (Sudden/ Explained vasodilation) DIAGNOSTIC TEST 1. Arteriogram 2. Doppler 3. Ice water test- soak pt. hand DRUG THERAPY Calcium channel blockers are the ﬁrst- line drug therapy. Calcium channel blockers such as nifedipine (Procardia) and diltiazem (Cardizem) relax smooth muscles of the arterioles by blocking the inﬂux of calcium into the cells, thus reducing the number of vasospastic attacks. ADVERSE EFFECTS calcium channel blockers include tachycardia, headache, ﬂushing, dizziness, and peripheral edema. Sympathectomy is considered only in advanced cases. Patients with Raynaud’s phenomenon should also receive routine follow-up to monitor possible connective tissue or autoimmune disease. MANAGEMENT V- Vasodilators- Alpha cholinergic blockers A- Avoid Stress W- Warm clothing A- avoid injury C- Caution (safety) S- Stop smoking= treat underlying ause VENOUS DISORDERS Venous Thromboembolism Deep vein thrombosis (DVT) and pulmonary embolism (PE) collectively make up the condition called venous thromboembolism (VTE). DEEP VEIN THROMBOSIS Due to blood clot Location: Deep vein/ Larger veins both w/ inﬂammation: non-visible Cardinal sign: Homan Sign (Calf pain at dorsiﬂexion of the foot) Also has similar symptoms to varicose veins RISK FACTOR Virchow’s Triad – Refer previous slides for SHE (Stasis, Hypercoagulation, and Endothelial Damage). CAUSE Increased pooling of blood, causing thrombus formation or clot in deep vein (calf). If thrombus is dislodged, it becomes an embolus “travelling clot” Travels to pulmonary artery Complications: Pulmonary embolism S&S of Pulmonary Embolism  Air hunger – increased RR  Blood tinged sputum  Chest pain  Elevated temperature  Diﬃculty of breathing S AND S OF DVT Fever (low-grade) Inﬂammation + pain = sudden onset Swelling Redness Warmth Pain Edema- unilateral (one side) – increase calf measurement Sign: Homan’s- pain upon dorsiﬂexion of the foot DIAGNOSTIC TESTS 1. UTZ -venous duplex -Result: shows clot/ thrombus 2. Venography -conﬁrms -Result: dye- stops (+) for occlusion or clot DRUGS 1. Anticoagulants -heparin -Warfarin = prevents blood clot 2. Thrombolytics Dissolves blood clot VARICOSE VEIN - Distended vein d/t damaged or incompetent valves *valve – gatewate prob: 2 way valve -Retention of blood Common: Lower extremities *Minor case- retention of blood - no retention - spider veins Complication:-Deep Vein Thrombosis -Thrombophlebitis PULMONARY EMBOLISM is the blockage of pulmonary arteries by thrombus, fat or air emboli, and tumor tissue. Other sites of origin include the right side of the heart (especially with atrial ﬁbrillation), upper extremities (rare), and the pelvic veins (especially after surgery or childbirth). Lethal PEs most commonly originate in the femoral or iliac veins. Emboli are mobile clots that generally do not stop moving until they lodge at a narrowed part of the circulatory system. Thrombi in the deep veins can dislodge spontaneously. However, a more common mechanism is jarring of the thrombus by mechanical forces, such as sudden standing, and changes in the rate of blood ﬂow, such as those that occur with Valsalva maneuver. In addition to dislodged thrombi, less common causes of PE include fat emboli (from fractured long bones), air emboli (from improperly administered IV therapy), bacterial vegetations, amniotic ﬂuid, and tumors. In Tumor emboli may originate from primary or metastatic malignancies. CLINICAL MANIFESTATION anxiety and the sudden onset of unexplained dyspnea, tachypnea, or tachycardia. cough, pleuritic chest pain, hemoptysis, crackles, fever, accentuation of the pulmonic heart sound, and sudden change in mental status as a result of hypoxemia. Massive emboli may produce sudden collapse of the patient with shock, pallor, severe dyspnea, and crushing chest pain. However, some patients with massive PE do not have pain. The pulse is rapid and weak, the BP is low, and an ECG indicates right ventricular strain. Medium-sized emboli often cause pleuritic chest pain, dyspnea, slight fever, and a productive cough with blood-streaked sputum. A physical examination may reveal tachycardia and a pleural friction rub. An ECG and chest x-ray may indicate right ventricular hypertrophy secondary to pulmonary hypertension. COMPLICATIONS Pulmonary infarction (death of lung tissue) is most likely when the following factors are present: (1) occlusion of a large or medium-sized pulmonary vessel (greater than 2 mm in diameter), (2) insuﬃcient collateral blood ﬂow from the bronchial circulation, (3) preexisting lung disease. Pulmonary hypertension also results from hypoxemia. Pulmonary hypertension eventually results in dilation and hypertrophy of the right ventricle. DIAGNOSTIC TESTING Lung Scan PE D-dimer testing If the lung scan is inconclusive, pulmonary V angiography is recommended. Pulmonary angiography is an invasive procedure that involves the insertion of a catheter through the antecubital or femoral vein, advancement to the pulmonary artery, and injection of contrast media A spiral (or helical) computed tomography (CT) scan ABG analysis COLLABORATIVE CARE The objectives of treatment are to (1) prevent further growth or multiplication of thrombi in the lower extremities, (2) prevent embolization from the upper or lower extremities to the pulmonary vascular system, and (3) Provide cardiopulmonary support DRUG THERAPY Heparin and warfarin (Coumadin) Anticoagulant agent – warfarin, etc. Thrombolytic agents, such as drugs that ends with a suﬃx “kinase” Streptokinase, Alteplase, Reteplase, Etc. SURGICAL THERAPY Pulmonary Embolectomy Preoperative pulmonary angiography NURSING MANAGEMENT Nursing Implementation Health Promotion Nursing measures aimed at prevention of pulmonary embolism parallel those for prophylaxis of deep vein thrombosis ACUTE INTERVENTION The patient should be kept on bed rest in a semi-Fowler position to facilitate breathing. An IV line should be maintained for medications and ﬂuid therapy. The nurse should know the side effects of medications and observe for them. Oxygen therapy should be administered as ordered. Careful monitoring of vital signs, ECG, ABGs, and lung sounds is critical to assess the patient’s status. The patient is usually anxious because of pain, sense of doom, inability to breathe, and fear of death. EVALUATION The expected outcomes are that the patient who has a pulmonary embolism will have adequate tissue perfusion and respiratory function adequate cardiac output increased level of comfort no recurrence of PE RISK FACTORS -Adult= high risk -congenital -obesity/ Pregnancy -Smoking -alcohol -DM -HPN -Trauma CLINICAL MANIFESTATIONS Warm skin Tender to touch Increased Pelvic Venous Pain Increased leg size d/t peripheral edema Decreased Pulse Quality N: +4 Decreased Pulse Grading N:+2 PULSE QUALITY – VIA PALPATION 0= absent +1= impairment +2= moderate impairment (weaker) +3= slight impairment +4= normal PULSE GRADING 0= Absent +1= diminished +2= normal +3= increased pulsation- Boundary MANAGEMENT Position- Legs above level of the heart -worsens w/ dependent position NSG. MGT. 1. Relieve pain - bed rest= 5-7 days - warm moist heat - X ambulation - analgesics: acetaminophen (Tylenol) 2. Promote Venous Return - elevate legs - elastic stockings (antiembolic) - X hip ﬂexion - Decrease Vit. K THROMBOPHLEBITIS -D/t blood clot Location: Smaller veins/ superﬁcial - both w/ inﬂammation: Visible *Same nursing management and medical management with DVT CLINICAL MANIFESTATION The most common cause of superﬁcial thrombophlebitis in the upper extremities is trauma to the vein caused by IV therapy. Superﬁcial thrombophlebitis in the lower extremities is usually related to trauma to the varicose veins. This type of superﬁcial thrombophlebitis is more common in older patients with long-standing venous insuﬃciency and in women during pregnancy. Superﬁcial thrombophlebitis is typically diagnosed on the basis of physical examination alone COLLABORATIVE CARE elevation of the affected extremity to promote venous return and decrease the edema and the application of warm, moist heat. If the superﬁcial thrombophlebitis is associated with an IV catheter or solution, the IV catheter should be removed immediately. If the superﬁcial thrombophlebitis has occurred in the lower extremity, elastic compression stockings are recommended once the acute thrombophlebitis has resolved. Mild oral analgesics such as aspirin or acetaminophen with codeine Nonsteroidal anti-inﬂammatory drugs (NSAIDs) such as ibuprofen (Motrin, Advil) Anticoagulant therapy Antibiotics and/or corticosteroids NURSING INTERVENTIONS TO PREVENT BLEEDING COMPLICATIONS IN PATIENTS RECEIVING ANTICOAGULANTS ASSESSMENT Monitor vital signs as indicated. Examine appropriate laboratory coagulation tests for achieved therapeutic levels. Inspect skin frequently, especially under splinting devices. Perform assessments frequently to observe for signs and symptoms of bleeding and/or clotting. Evaluate lower extremity for ecchymosis/hematoma development if sequential compression hose used. Test urine and stool for occult blood as indicated. Notify the health care provider of any abnormalities in assessments, vital signs, or laboratory values. INJECTIONS Minimize venipunctures. Do not give IM injections. Use small-gauge needles for venipunctures unless replacement therapy requires a larger gauge. Apply manual pressure for at least 10 minutes (or longer if needed) on venipuncture sites. PATIENT Avoid restrictive clothing. Reposition the patient carefully at regular intervals. Use support pads, mattresses, bed cradles and therapeutic beds as indicated. Avoid removing/disrupting established clots. Instruct patient not to forcefully blow nose. Administer stool softeners to avoid hard stools and constipation. Limit application—use paper tape as appropriate. Perform care in a gentle manner. Use soft toothbrushes or foam swabs for oral care. Apply moisturizing lotion to skin. Do not use lemon-glycerin swabs. Humidify O2 source. Utilize electric razors, not straight razors. Lubricate tubes adequately prior to insertion. Apply antiembolism stockings(e.g.,TED hose)as ordered SURGICAL THERAPY include venous thrombectomy (rarely performed) and inferior vena cava interruption Vena cava interruption devices, such as the Greenﬁeld or Simon-Nitinol ﬁlters, can be inserted percutaneously through superﬁcial femoral or internal jugular veins COMPLICATIONS air embolism, improper placement, and migration of the ﬁlter more distally into the venous system. Venous congestion Pulmonary Embolism NURSING DIAGNOSIS Acute pain related to venous congestion, impaired venous return, and inﬂammation Ineffective health maintenance related tolack of knowledge about disorder and its treatment Risk for impaired skin integrity related to altered peripheral tissue perfusion Potential complication: bleeding related to anticoagulant therapy Potential complication: pulmonary embolism related to embolization of thrombus, dehydration, and immobility PLANNING The overall goals are that the patient with venous thrombosis (1) relief of pain, (2) decreased edema (3) no skin ulceration, (4) no complications from anticoagulant therapy, and (5) no evidence of pulmonary emboli. NURSING IMPLEMENTATION Observe for any indication of bleeding, including epistaxis and bleeding gingivae. Urine should be assessed for gross or microscopic hematuria. A smoky appearance to the urine is sometimes noted if blood is present. A specimen should be checked daily for hematuria. Particular attention should be paid to the protection of skin areas that may be traumatized. Surgical incisions should be closely observed for evidence of bleeding. Stools should be tested to determine the presence of occult blood from the gastrointestinal tract. Mental status changes, especially in the older patient, should be assessed as a possible indication of cerebral bleeding. Intramuscular injections should not be given. The nurse should review with the patient any medications currently being taken that may interfere with anticoagulant therapy The nurse should ask if the patient is taking any herbal products. Herbs can interfere with anticoagulant The nurse should monitor PTT, INR, hemoglobin, hematocrit, and platelet levels when a patient is receiving anticoagulant drugs. Platelet counts are monitored to assess for heparin-induced thrombocytopenia. Medication doses are titrated according to EVALUATION -The expected outcomes are that the patient with venous thrombosis will have minimal to no pain -Intact skin -no signs of respiratory distress -no signs of hemorrhage or occult bleeding COMPLEMENTARY ALTERNATIVE THERAPIES garlic, ginger, ginkgo, ginseng, goldenseal, feverfew, chamomile, angelica, bilberry, and evening primrose. Effects Can interfere with clotting in various ways. One common mechanism is to inhibit platelet aggregation. NURSING IMPLICATIONS herbs should be used with caution or not at all in patients with bleeding or clotting disorders or those taking anticoagulant and antiplatelet drugs (e.g, warfarin [Coumadin], heparin, low- molecular-weight heparin, aspirin, ticlopidine Ticlid, clopidogrel. These herbs should be discontinued at least 2 to 3 weeks before surgery to avoid potential complications. CHRONIC VENOUS INSUFFICIENCY AND VENOUS LEG ULCERS Chronic venous insuﬃciency (CVI) is a common problem in the elderly. CVI, which often occurs as a result of previous episodes of DVT, can lead to venous leg ulcers (formerly called venous stasis ulcers or varicose ulcers). ETIOLOGY The causes of CVI include vein incompetence, deep vein obstruction, congenital venous malformation, arteriovenous ﬁstula, and calf muscle failure. The basic dysfunction is incompetent valves of the deep veins. PATHOPHYSIOLOGY As a result, hydrostatic pressure in the veins increases and serous ﬂuid and red blood cells (RBCs) leak from the capillaries and venules into the tissue, resulting in edema. Enzymes in the tissue eventually 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 pathophysiology of venous ulcers remains unknown. It is known that decreased ﬁbrinolysis, pericapillary ﬁbrin cuffs, and WBC trapping CLINICAL MANIFESTATIONS AND COMPLICATIONS In individuals with CVI, the skin of the lower leg is leathery, with a characteristic brownish or “brawny” appearance from the hemosiderin deposition. Edema has usually been persistent for a prolonged period. Eczema, or “stasis dermatitis,” is often present, and pruritus is a common complaint. Venous ulcers classically are located above the medial malleolus. Venous ulcers are typically partial thick wounds that extend through the epidermis and portions of the dermis. Ulcer drainage may be extensive, especially when the leg is edematous. The ulcer is often quite painful, particularly when edema or infection is present. Pain may be worse when the leg is in a dependent position. Ulcer pain adversely affects the patient’s quality of life. If the venous ulcer is untreated, the lesion becomes more extensive, eroding wider and deeper. Recurrent episodes of cellulitis may lead to destruction of the superﬁcial lymphatics, causing a secondary lymphedema to develop. On very rare occasions, severe CVI with long- standing non-healing venous ulceration may result in the patient’s need to have an amputation. COLLABORATIVE CARE Compression is essential to the management of CVI, venous ulcer healing, and prevention of ulcer recurrence. A variety of options are available to achieve compression including elastic wraps, custom-ﬁtted compression stockings, elasticated tubular support bandages, a Velcro wrap (Circaid), sequential pneumatic compression devices, paste banda (Unna’s boot) with an elastic wrap, and multilayer (three o four) bandage regimens. Moist environment dressings are the mainstay of wound care. A variety of dressings are available that provide a moist environment and include transparent ﬁlm dressings, hydrocolloids, hydrogels, foams, calcium alginates, impregnated gauze, gauze moistened with saline, and combination dressings. Nutritional status and intake should be evaluated in a patient with a venous leg ulcer. A balanced diet with adequate protein, calories, and micronutrients is essential for healing. Nutrients most important for healing include protein, vitamins A and C, and zinc. Foods high in protein (e.g., meat, beans, cheese, tofu),vitamin A (green leafy vegetables), vitamin C (citrus fruits, tomatoes, cantaloupe), and zinc (meat, seafood) must be provided. For patients with coexistent diabetes mellitus, maintaining normal blood glucose levels facilitates the healing process. For overweight individuals with CVI and no active venous ulcer, a weight-reduction diet may be prescribed. CLINICAL SIGNS OF INFECTION Change in quantity, color, or odor of the drainage; presence of pus; erythema of the wound edges; change in sensation around the wound; warmth around the wound; increased local pain, edema, or both; dark-colored granulation tissue; induration around the wound delayed healing; and Cellulitis NURSING MANAGEMENT Long-term management of venous leg ulcers should focus on teaching the patient about self-care measures because the incidence of recurrence is high. DISORDERS OF THE LYMPHATIC SYSTEM The lymphatic system consists of a set of vessels that spread throughout most of the body The ﬂuid drained from the interstitial space by the lymphatic system is called lymph The ﬂow of lymph depends on the intrinsic contractions of the lymph vessels, the contraction of muscles, respiratory movements, and gravity LYMPHANGITIS AND LYMPHADENITIS Lymphangitis is an acute inﬂammation of the lymphatic channels It arises most commonly from a focus of infection in an extremity The infectious organism is a hemolytic streptococcus The lymph nodes located along the course of the lymphatic channels also become enlarged, red, and tender (acute lymphadenitis). They can also become necrotic and form an abscess (suppurative lymphadenitis) The nodes involved most often are those in the groin, axilla, or cervical region. LYMPHEDEMA AND ELEPHANTIASIS Lymphedema may be primary (congenital malformations) or secondary (acquired obstructions). Tissue swelling occurs in the extremities because of an increased quantity of lymph that results from obstruction of lymphatic vessels lymphedema praecox which is caused by hypoplasia of the lymphatic system of the lower extremity is congenital seen in the arm after an axillary node dissection (e.g., for breast cancer) and in the leg in association with varicose veins or chronic thrombophlebitis Lymphatic obstruction caused by a parasite (ﬁlaria) Elephantiasis lead by chronic ﬁbrosis, thickening of the subcutaneous tissues, and hypertrophy of the skin The goal of therapy is to reduce and control the edema and prevent infection CELLULITIS most common infectious cause of limb swelling can occur as a single isolated event or a series of recurrent events sometimes misdiagnosed as recurrent thrombophlebitis or chronic venous insuﬃciency occurs when an entry point through normal skin barriers allows bacteria to enter and release their toxins in the CELLULITIS acute onset of swelling, localized redness, warmth, and pain frequently associated with systemic signs of fever, chills, and sweating redness may not be uniform and often skips areas and eventually develops a pitting “orange peel” appearance Regional lymph nodes may also be tender and enlarged MEDICAL MANAGEMENT Oral antibiotic therapy Severe, patient is treated with IV antibiotics Key to preventing recurrent episodes of cellulitis lies in adequate antibiotic therapy for the initial event and in identifying the site of bacterial entry NURSING MANAGEMENT elevate the affected area 3 to 6 in above heart level apply cool, moist packs to the site every 2 to 4 hours until the inﬂammation has resolved then transition to warm moist packs caution when applying warm packs because burns may occur Education should focus on preventing a recurrent episode patient with peripheral vascular disease or diabetes should receive education or reinforcement about skin and foot care THANK YOU!!!!

Management of Patients with Peripheral Vascular Disease PDF

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