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Leg edema assessment and management.

The significance of leg edema as a symptom of multiple anomalies, from benign manifestations to underlying Graves' disease, is described. Accurate assessment, history taking, and supportive diagnostic tests will assist nurses to manage their patients' with competence. A comprehensive discussion about different types of edema, etiology, pathophysiology, management, and patient education is aimed to equip nurses in independent and collaborative management of lower-extremity edema in their patients.

Edema in lower extremities, unilateral or bilateral, is called leg edema. An expansion of interstitial fluid volume may not be detected readily, but an excess of several liters causes visible and palpable swelling. Edema is defined as a palpable swelling produced by the expansion of the interstitial volume (Stems, 2013) or an increase in extra-cellular volume. Pitting edema gives way on palpation, leaving persistent impressions in the skin; brawny edema offers resistance but leaves no impressions (Goroll & Mulley, 2009; Stems, 2013).

Leg edema could be an initial symptom of a serious underlying problem, or an uncomfortable manifestation without any pathological causes (Goroll & Mulley, 2009). The serious problems involve cardiac, vascular, respiratory, renal, hepatic, or hematologic systems. On the other hand, leg edema could be a benign inconvenience with unknown etiology. Unilateral or bilateral leg edema is a frequent presenting complaint that demands astute diagnostic and referral strategies (Seller & Symons, 2011).

The purpose of this article is to guide clinicians in accurate assessment of leg edema, including understanding the process, connecting with history, differentiating types of leg edema, analyzing causative factors such as systemic vs. local causes, choosing appropriate diagnostic measures, and planning independent and collaborative management. Time and type at referral based on the primary findings as well as prevention and patient and family education are elaborated. Pharmacologic interventions with rationale also are included.

Pathophysiology of Edema

A clear understanding about the pathophysiology is essential to manage the problem effectively. According to Stems (2013), two primary steps occur in edema formation: (a) movement of the fluid from the vascular compartment to the interstitial compartment as a result of altered dynamics, and (b) retention of sodium and water by the kidneys. Fluid exiting the vascular compartment reduces effective circulating volume and eventually renal perfusion. Reduced renal perfusion activates the renin-angiotensin-aldosterone system, resulting in water and sodium retention by the kidneys and returning plasma volume toward normal. This compensatory mechanism helps to re-establish plasma volume in the intravascular compartment. The result is the marked expansion of extracellular fluid volume and a near normal plasma volume.

Fluid movement between the vascular compartment and the interstitial space is regulated by two forces: hydrostastic or hydraulic pressure of the vessel, and oncotic pressure (see Figure 1). The hydrostatic pressure pushes fluid out of the vessels, and the oncotic pressure pulls fluid into the vessels. The resulting difference in pressure gradient varies in capillaries from skeletal muscles to organs and alveolar capillaries. However, the filtered fluid in the interstitial compartment is returned to the vascular compartment by the lymphatic system (Goroll & Mulley, 2009; Stems, 2013).

Consequently, edema formation results from an alteration in any of the above-mentioned mechanisms. Edema does not become clinically apparent until fluid has increased by at least 2.5 liters. These pathophysiological changes are triggered by various clinical conditions and diseases. For example, impaired pumping ability of the heart increases hydrostatic or hydraulic pressure in the extremities caused by poor circulation, and venous pooling will result in capillary leak and interstitial fluid accumulation in the dependent areas such as lower extremities. Leg edema due to increased interstitial volume resulting from low colloid oncotic pressure is seen in protein-losing enteropathy, liver cirrhosis, renal failure, and protein-calorie malnutrition, which may coexist with chronic illnesses. The colloid oncotic pressure of the plasma that keeps fluid in the intravascular compartment is maintained normally by the concentration of electrolytes, glucose, urea, and proteins. In these conditions, however, oncotic pressure drops due to lack of these electrolytes and subsequently alters the flow of fluid between the intravascular and interstitial spaces (Stems, 2013). The altered physiological mechanisms and clinical conditions are summarized in Table 1.

Etiology of Leg Edema

Underlying problems causing leg edema can range from local inflammation to sleep apnea and other pulmonary conditions. Even achalasia has resulted in bilateral leg edema (Baird & Usatine, 2009). The etiology of leg edema can be related to traumatic, infectious, vascular, renal, hepatic, or endocrine pathology. Traumatic causes could include muscle strain, ankle sprain, fracture, and contusion.

Vascular problems are the most common causes of leg swelling. Chronic venous insufficiency (CVI) is the most frequently occurring disorder. It may be congenital, primary (undetermined cause), or secondary. Previous incidence of deep venous thrombosis (DVT) also can lead to venous insufficiency. The incidence of DVT in the presence of incompetent valves and veins may lead to ambulatory venous hypertension. Increased pressure in the veins can cause damage to both the endothelium and the extracellular matrix, and eventually the venous wall (Georgescu et al., 2009). Pressure-related injury to the epithelial cells also can lead to leukocyte migration and a generalized inflammatory response. Consequently, prolonged venous hypertension can induce circulatory changes that may result in hyperpigmentation, lipodermatosclerosis, and even ulceration.

In general, the leg edema associated with DVT will be characterized by achy pain in the legs, erythema, warmth in the affected area, distended collateral veins, and a palpable cord. Other signs and symptoms may include telangiectasia (spider veins), hyperpigmentation of skin of the ankle, atrophie blanche (white scar tissue), and lipodermatosclerosis (induration caused by fibrosis of the subcutaneous fat). A difference is noted in the manifestation of acute and chronic DVT. Acute DVT usually presents with painful leg edema. A severe complication of acute DVT is phlegmasia cerula dolens, commonly known as venous gangrene. Clinical features include severe pain, tissue necrosis, bullae formation, and skin discoloration (Seller & Symons, 2011).

Chronic venous insufficiency increases venous pressures, resulting in extravasation of macromolecules and red blood cells to the dermis. This leads to inflammation and ulceration; the pathologic process will be complicated if there is lymphedema present along with CVI (Silva, Filipe, Cardoso, & Andriessen, 2012). Manifestations of CVI may range from no visible or palpable signs of venous disease to active ulceration.

Other conditions that increase venous pressure in the legs are cardiac diseases, such as biventricular or right-sided heart failure, pulmonary hypertension, and valvular heart disease. However, cardiac dysfunction is the most common cause of bilateral edema seen in older adults. Patients with edema due to heart failure usually have other symptoms, such as dyspnea on exertion, orthopnea, and paroxysmal nocturnal dyspnea. Leg edema, along with fatigue and insomnia, may be early manifestations of congestive heart failure in older patients. Crackles, ventricular gallop, distended neck veins, and cardiomegaly may be present on assessment. Valvular heart disease and pulmonary hypertension also can be detected during physical examination and further confirmed with echocardiography. Obstructive sleep apnea elevates pulmonary artery pressure, resulting in pulmonary hypertension, increased venous pressure, and bilateral leg edema (McCabe & Hardinge, 2011). Pulmonary hypertension due to obstructive sleep apnea (OSA) may manifest as a bilateral edema in patients who are obese. On the other hand, bilateral leg edema may be an important clinical marker for underlying OSA (Shostak & Sarwar, 2009).

Low fluid oncotic pressure in renal dysfunction such as nephrotic syndrome with proteinuria (>1 g daily) also leads to leg edema. Leg edema related to nephrotic syndrome can be confirmed by the presence of proteinuria, hypercholesterolemia, and hypoalbuminemia, and the underlying cause can be established by renal biopsy. Liver dysfunction such as cirrhosis also causes leg edema due to the inability of the liver to synthesize protein, thus lowering fluid oncotic pressure. A history of jaundice, liver disease, or abdominal swelling can be clues to cirrhosis as a cause of leg edema (Seller & Symons, 2011).

Endocrine dysfunction, such as Cushing's disease and Graves' disease also can cause leg edema. In Graves' disease, edema is characterized by a rubbery texture of the skin. This dermopathy of Graves' disease usually occurs over the dorsum of the legs or feet and is termed localized or pretibial myxedema. In this case, symptoms may be nonspecific and include fatigue, cold intolerance, headache, and dry skin. The diagnosis is confirmed by elevated thyroid-stimulating hormone if Graves' disease is in the hypothyroid state (Goroll & Mulley, 2009).

Increased venous pressure due to intrinsic venous obstruction or extrinsic compression from pelvic tumors such as ovarian tumors, prostate carcinoma, and retroperitoneal fibrosis can cause leg edema. Benign prostatic enlargement with bladder distention compressing on the iliac veins has been reported to cause chronic leg edema. Similarly, advanced prostatic carcinoma could present with bilateral leg edema due to lymphatic obstruction. Uterine fibromas (Daylami et al., 2010; Malkan, Singh-Braich, Panait, & Dudrick, 2009) or any other gynecologic cancers can cause leg edema in women. Therefore all women above 40 should be investigated for cancers when presenting with painless unilateral edema. Kaposi's sarcoma in persons with HIV also can cause leg edema (Seller & Symons, 2011).

A gradual and progressive onset over several weeks to months suggests lymphedema, chronic venous insufficiency, some systemic process, or exposure to particular medications. Lymphedema and chronic venous insufficiency account for a considerable percentage of chronic regional leg edema, and lymphedema may be a clue to malignant disease in the pelvis, abdomen, or retroperitoneal space. Leg edema observed in women could be benign, as in cyclic edema seen during childbearing years or pregnancy. Idiopathic edema without any causes is sometimes found in young women under age 40; it also can be associated with the use of nonsteroidal anti-inflammatory drugs (NSMDs). The upright position exacerbates idiopathic edema, and swelling seen in the last half of the menstrual cycle indicates a premenstrual syndrome. Conversely, unilateral leg edema in women over age 40 can be a manifestation of a cancerous growth (Goroll & Mulley, 2009).

Apart from malignancy, mechanical causes such as tight jeans, pantyhose, or garters also can promote leg edema. Rapid accumulation over several days is typical of acute glomerulonephritis, and a gradual accumulation over weeks or months may be related to systemic illness. If the fluid accumulation is observed during the day and subsides during the night, it suggests the physiologic disturbance is mild, whereas the presence of swelling that persists day and night suggests the underlying cause is more complicated. Edema localized in a single extremity denotes local obstruction to venous or lymphatic drainage, whereas generalized edema (anasarca) is typical of glomerulonephritis, the nephrotic syndrome, and congestive heart failure. If dyspnea appeared before edema, it may be due to left ventricular failure, whereas edema precedes dyspnea in acute glomerulonephritis and the nephrotic syndrome. Ascites may be seen in cirrhosis or constructive pericarditis and right heart failure; however, in right heart failure, ascites follows edema and in other situations ascites is seen before generalized edema. Chronic edema is a progression of acute edema, with swelling lasting longer than 3 months. If the legs are normal size when a person rises in the morning and swell later, the person is experiencing acute edema; chronic edema is marked by swelling even after the person remains in bed for 8 hours. For example, benign prostatic enlargement with bladder distention compressing on the iliac veins has been reported to cause chronic leg edema (Hampton, 2010).

Infectious Causes

Cellulitis is the most common cause of leg edema related to infection. Stasis dermatitis in patients with venous insufficiency often results in breakdown of the skin and ulceration that may resemble cellulitis. However, stasis dermatitis arises as a result of venous insufficiency, so it is likely to be accompanied by pitting edema. This type of venous edema responds to leg raising and to the use of elastic compression stockings; such interventions are ineffective in cellulitis. In addition, cellulitis tends to be unilateral, while stasis dermatitis is bilateral in most cases. Other infectious causes that result in leg edema are deep tissue abscess and osteomyelitis. The differentiating features of cellulitis and stasis dermatitis are highlighted in Table 2.

Pharmacological Causes

Drug-related edema is not infrequent. Certain drugs, hormones, and antihypertensive agents may precipitate a soft, pitting leg edema. Some drugs can cause edema by enhancing renal sodium reabsorption through an unknown mechanism (Stems, 2013). The edema seen in direct vasodilators is related to this cause, and thiazolidinediones and estrogen may do the same. On the other hand, calcium channel blockers, especially dihydropyridines, cause edema by capillary leakage resulting from the dilation of the precapillary sphincter. NSMDs inhibit renal prostaglandin synthesis and can exacerbate edema. Many antipsychotic or antineoplastic medications, ibuprofen, and opioids can precipitate syndrome of inappropriate antidiuretic hormone. This type of fluid retention results either from an altered response to antidiuretic hormone (ADH) or increased production of ADH in response to the medication (Simon, 2010). The amount of time from the administration of a new drug to the onset of leg edema often suggests a cause-and-effect relationship. Discontinuation of the salt-retaining and vasodilating drugs (e.g., diazoxide) will alleviate leg swelling if the edema is related to medications. Drug-related edema usually develops gradually, occurs bilaterally, and subsides upon withdrawal of the offending agent. Any patient with edema should be asked about medications that could cause or aggravate fluid retention. Some medications that cause leg edema are listed in Table 3 (Seller & Symons, 2011).

Rare Causes

Other rare clinical situations, ranging from very common problems such as long flights to unusual cancers, also can result in leg edema. For example, adrenocortical carcinoma involving the inferior vena cava and extended into the right atrium manifests as bilateral leg edema resulting from high right atrial pressure. Elevated central venous pressure caused by cardiovascular obstruction and dyspnea from multiple pulmonary emboli due to the large atrial myxoma also can manifest as leg edema. Pulmonary cryptococcosis causes leg edema as well. Intravenous leiomyomatosis produces leg edema, as does ruptured sinus of Valsalva aneurysm of the heart (the sinuses of Valsalva are dilatations in the aortic wall superior to the attachments of the three aortic valve cusps) (Tingler, Hulse, Failinger, & Warden, 2009). Urinary obstruction can cause pressure on the inferior vena cava, resulting in leg edema. May-Thurner syndrome and bladder distention in a post-stroke patient were reported by Im and colleagues (2009). May-Thurner syndrome, DVT of the iliofemoral vein, is caused by compression of the left common iliac vein by the overlying right common iliac artery. Ruptured Baker's cyst and ruptured gastrocnemius muscle in runners are also possible causes of leg edema. However, these conditions are associated with activity and sudden onset of edema (Seller & Symons, 2011).

Types of Leg Edema

Leg edema can be of different types: venous edema, lymphedema, or lipedema. As discussed previously, venous edema results from the extravasation of interstitial fluid into the interstitial space due to increased capillary filtration pressure or low fluid oncotic pressure. On the other hand, primary lymphedema is caused by obstruction of the lymphatic flow and accumulation of protein-rich interstitial fluid. The result is increased hydrostatic pressure and congestion of the extremities. Painless swelling starts in the foot and ankle and progresses proximally, subsiding in the morning on awakening and worsening by the end of the day. Eventually, the swelling becomes permanent, secondary to fibrosis of the skin and subcutaneous tissues. Lymphedema involves the dorsum of the toes and feet and pits with difficulty. The skin color and texture are normal until the later stages, when the skin becomes thickened and darkened, and develops multiple papillomatous projections called lymphostatic verrucosis (mossy foot). Lipedema, an accumulation of fatty tissue in the lower extremities, is seen with obesity. It spares the dorsum of the feet, stops at the ankle, and presents in overweight women. Leg edema also is seen in older patients with painful ischemic feet. Swelling in this case is due to the accumulation of fluid when the legs are kept in a dependent position in an attempt to relieve ischemic pain. Important aspects of edema that give clinical clues to leg edema are discussed below. Lymphedema and lipedema are differentiated in Table 4.

Edema Assessment

A thorough inspection of the legs is important to differentiate among infection, thrombosis, chronic venous insufficiency, chronic arterial insufficiency, and acute arterial occlusion. For example, thick, taut, fibrotic skin indicates a chronic problem, and redness and lymphangitic streaks are found in cellulitis. The presence of echymoses on the ankle seen with midcalf pain suggests gastrocnemius muscle mpture. Chronic venous insufficiency may present with statis dermatitis (Hazin, Abuzetun, & Khatri, 2009) and/or varicose veins (Raju & Neglen, 2009). Changes in the color may involve brown pigmentation, erythema, pallor, and/or bluish discoloration. Skin changes with a warty texture indicate lymphedema, and the presence of hemosiderin deposits suggests venous insufficiency. Hemosiderin deposits are caused by red blood cells leaving the blood vessel with high hydrostatic pressure; the cells die and the hemoglobin is released into the extracellular space. Another change observed is dermal mucinosis; cutaneous focal mucinosis is characterized by asymptomatic flesh-colored papules or nodules occurring on extremities. The cause is a dysfunction of fibroblasts in a localized area of the skin which secretes excessive mucin (Pugashetti, Zedek, Seiverling, Rajendran, & Berger, 2010). An increase of I cm in circumference may indicate an accumulation of 3,600 ml of fluid in the body. In a leg edema associated with chronic venous insufficiency or a peripheral vascular disease situation, hair distribution will be decreased. In cellulitis-related leg edema, the presence of cuts, scrapes, or fissures may signal the port of entry for infection. Along with systemic signs of inflammation, these signs support the diagnosis of cellulitis (Raju & Neglen, 2009).

Palpation of the legs answers various questions. Is the edema bilateral or unilateral? Are pulses decreased distal to the site? Are they equal bilaterally? Is the temperature the same from one side to the other? Is there any tenderness? If there is tenderness, what is its location, intensity, and depth? Is the consistency of the tissue soft, firm, or hard? Is sensation intact? Is there leg pain associated with palpation? Is there a palpable cord of thrombosed vein? Is there a Homan's sign (pain on dorsiflexion)? A positive Homan's sign may suggest the presence of a DVT; however, a negative Homan's sign does not exclude a diagnosis of DVT. A palpable popliteal cyst and/or calf muscle tenderness along with a history of reactive arthritis may suggest pseudophlebitis syndrome. The symptoms of pseudothrombophlebitis include pain, swelling, erythema, and tenderness. Pseudothrombophlebitis is caused by rupture of a popliteal cyst, causing synovial fluid leakage and inflammatory irritation to the gastrocnemius muscle. Palpation assesses the distribution of the edema. In the case of lipidema, the dorsum is spared, while the dorsum is involved in lymphedema. Lymphedema is nontender, and a positive KaposiStemmer sign (the inability to pinch a fold of skin on the dorsum at the base of the second toe) can confirm lymphedema. Pitting edema is seen in DVT and venous insufficiency; increased jugular venous distention, along with crackles and ascites, indicates systemic problems. Edema measurement has various methods: pitting depth, pit time, circumference, weight increase, ankle circumference, and water displacement. Ankle circumference and water displacement show excellent reliability, but ankle circumference is a practical, easy method of edema measurement (Brodovicz et al., 2009). Edema assessment includes measuring calf circumference. A difference of 3 cm or more at three anatomical locations (the lower calf at 7 cm proximal to the midpoint of the medial malleolus, behind the medial malleolus, and the dorsum of the foot) indicates edema.

Laboratory Diagnosis

A liver function test or hepatic panel can suggest liver problems that lead to edema. Serum albumin below 2 g/dL often leads to edema, most commonly in liver diseases. An elevated brain-type natriuretic peptide (BNP) above 100 mcg/dL may suggest heart failure; if the BNP is below 100 mcg/dL, heart failure is less likely. An elevated D-dimer suggests DVT as a possible cause. Normal D-dimer can exclude a diagnosis of DVT. It is elevated in pregnancy, but generally returns to normal in 15 days (Collins, 2009).

Sleep study and echocardiogram can exclude pulmonary hypertension or associated right atrial pressure elevation. Lymphoscintigraphy (the direct visualization of lymphatic vessels) helps to diagnose any lymph obstruction. Leg edema due to DVT and the hypercoagulable stage can be excluded by a D-dimer test or confirmed by venous ultrasound (Collins, 2009).

Diagnostic Steps

The diagnosis of CVI requires a careful combination of patient history, physical examination, and findings on noninvasive duplex Doppler ultrasound. Edema developed over 1 day to a few days suggests the cause is deep venous occlusion or cellulitis, especially if the edema is accompanied by pain. Magnetic resonance imaging, computed tomography (CT), and spiral CT venography are used to determine the distribution of edema. Cross-sectional areas of muscle tissue will be increased in venous obstruction; obesity and lipedema will exhibit as increased subcutaneous fat; lymphedema will be shown as an increase in interstitial space with a honeycomb pattern. Lymphangiography is used occasionally to directly visualize the lymphatic vessels. Venography is the gold standard for the diagnosis of DVT. Rabe, St(icker, and Ottillinger (2010) introduced volumetry as a method of evaluating venous edema and the effect of therapy to reduce edema. Venous volumetry measures edema by the volume of water displaced by the leg when placed in equipment filled with water. However, even though the measurement could be very accurate, the procedure can lead to performance errors. Therefore, conventional methods and imaging are the current practice. Three steps are needed to evaluate leg edema: discontinue all potentially causative medications; obtain an echocardiography for patients over age 45; and if the echocardiogram is positive for pulmonary hypertension, obtain a sleep study.

Management of Edema

Conservative management and compression are recommended for patients in the early stages of venous disease. Initiation of conservative care focuses on weight loss as appropriate to reduce pressure on the veins. Graduated compression stockings, stretching, and calisthenics may be helpful for prolonged standing. Compression stockings should be changed every 6 months. Patient education and use of compression bandages also can prevent ulcer recurrence (Kelechi & Johnson, 2012).

Compression therapy is vital but using compression bandages or hosiery is based on patient cooperation. Even though compression therapy is very effective in reducing edema, patient cooperation can be a concern. Most common complaints affecting adherence to therapy are pain and tightness. Providing analgesics, correctly measuring the calf circumference, encouraging the patient to ambulate with new hosiery, and elevating the legs rather than removing the hosiery are strategies to promote adherence. If pain occurs, detecting any arterial disease is important. Hosiery should be applied before the patient gets out of bed. Limb measurement should be done every 3 months (Brown, 2011). Patients should avoid sleeping in a chair.

Compression therapy is contraindicated in arterial insufficiency and heart failure. Ankle-brachial index (ABI) measurement with Doppler ultrasonography is recommended to exclude serious arterial disease (ABI < 0.7) before initiating compression therapy. Use of Comprilan[R] short, stretchable bandages helps to reduce leg edema in older adults by limiting the usage of diuretics and improving well-being (Midttun, Ahmadzay, & Henriksen, 2010). Investigation of blood pressure changes in the lower extremities found no pressure difference during Comprilan use, eliminating doubt that bandages may compromise peripheral circulation. Suprasorb[R] dressing, short stretchable bandages with biosynthetic cellulose dressing used as a compression bandage, has proved to be very effective for ulcers. This dressing reduces bacterial load and supports wound cleansing (Silva et al., 2012). Medicated compression bandages (Unna boots, Unna-Flex) are special roll bandages impregnated with zinc oxide, calamine lotion, glycerine, and gelatin to treat ulcers due to CVI. Three-layered and four-layered bandages also are used for complicated CVI with ulcers. Elevation of the affected leg will improve venous return and reduce edema (the increased gravity will help to drain fluid back to the systemic circulation through the porous vessel walls, through incompetent venous valves back to the systemic circulation). However, in patients with heart failure, leg elevation should be delayed until oxygen saturation measurement is acceptable after diuretic therapy (Cooper, 2011; Mercadante, Villari, Ferrera, David, & Intravaia, 2009).

Enhancing Vasomotion

Exercise and walking propel lower-extremity circulation upward and reduce venous congestion. Compression hose or compression stockings (20-30 mm Hg for moderate disease, 30-40 mm Hg for more severe disease) have greatest pressure in the ankle area and less pressure toward the midthigh. This pressure difference will assist in squeezing the lower-extremity fluid compartment to translocate fluid toward the upper parts of the body and reduce venous congestion. This in turn prevents venostasis, increased pressure, and edema in the presence of cellulitis or ulcer. Heising, Haase, Sippel, Riedel, and Junger (2009) found compression therapy over a period of 4 weeks had a significant influence on myogenic vessel activity. A compression pump is avoided in the presence of any pain or numbness, arteriosclerosis, massive edema caused by heart failure, deformity of the limbs, and any skin condition, such as gangrene, dermatitis, wounds, recent skin grafts, venous thrombosis, or phlebitis. Among patients with lymphedema, leg-raising exercises, pressure-gradient stockings, and the use of intermittent-pressure devices at night are helpful.

Proper shoe wear, care and lubrication of the skin, and early treatment of any small trauma are important aspects of therapy to prevent more serious complications, such as venous stasis ulcers, cellulitis, or osteomyelitis. Other nonsurgical interventions include the use of a sequential compression device and calf muscle stimulation. Calf muscle stimulation can have a very positive effect in lowering lymphedema in patients with congestive heart failure (Pierce & McLeod, 2009).

Diuretic Therapy

Candidates for diuretic therapy include patients with bilateral leg edema secondary to a systemic cause, such as congestive heart failure, renal insufficiency, or cirrhosis. Some patients with edema due to venous insufficiency also may respond well to diuretics as initial drug therapy following leg elevation exercises and the use of graduated compression stockings.

Diuretics should be used with caution, especially in older patients receiving other medications or with multiple coexisting diseases. Possible adverse effects include electrolyte imbalance, metabolic abnormalities, and potential dehydration. Highdose furosemide (Lasix[R]) in small-volume hypertonic saline is an effective treatment option for peripheral edema treatment in patients with CVI (Mercadante et al., 2009). For example, 100 mg furosemide dissolved in 50 ml hypertonic saline infused over 1 hour will reduce edema and improve the patient's mobility.

Endothelium Protectant Agents

Epithelial dysfunction can be reverted by endothelium protectant agents, such as captopril (Capoten[R]), losartan (Cozaar[R]), troglitazone (Rezulin[R]), pravastatin (Pravachol[R]), or simvastatin (Zocol[R]) (Carrasco, Ranero, Hong, & Vidrio, 2009). Relaxation is enhanced by the endothelium-protecting agents, troglitazone being the least and simvastatin the most effective. These cardiovascular protecting agents can play a role in the treatment of CVI.

Adjuvant Therapy

Wound care guidelines recommend additional medications such as pentoxifylline (Trental[R]) 400 mg three times a day as an adjunct to compression therapy. Peri-ulcer injection of granulocyte-macrophage colony-stimulating factor can improve wound healing. Horse chestnut seed extract may be useful in reducing pain and swelling (Kelechi & Johnson, 2012).

Surgical Interventions

Operative procedures for CVI disease include endovenous ablation of the great saphenous vein, or subfascial endoscopic perforator surgery and sclerotherapy. Radio frequency ablation and foam sclerotherapy improve incompetent perforating veins (Buczkowski, Munschauer, & Vasquez, 2009). Surgical correction of pathological venous reflux is possible by saphenofemoral ligation (Casian, Gutsu & Culiuc, 2009).

Radio frequency ablation (RFA) is quite similar to laser ablation in that it uses an endovascularly placed heat source to produce vascular and endothelial damage, thrombosis, and eventual occlusion of the treated vein. According to Schoonover (2009), RFA and endovenous laser treatment are almost the same. In RFA, direct heating (less than that induced in laser treatment) causes contraction of the collagen in the vessel wall and loss of the endothelial lining to occlude the vein. The preoperative preparation and evaluation are similar to that for laser ablation. Similarly, in foam sclerotherapy, foam sclerosants are injected into the larger vessels first, followed by the smaller diameter vessels. The concentration of the sclerosants depends on the diameter of the involved vessel; a higher concentration of agent is injected into a vessel of larger diameter. Postoperative application of a compressive dressing allows the vessel to occlude and eventually form scar tissue. Radio frequency ablation tends to cause less bruising. Subfascial endoscopic perforator vein surgery (SEPS) is used as a part of a treatment regimen for severe CVI (Luebke & Brunkwall, 2009).


Leg edema is managed with diuretic therapy, elevation, exercise, and elastic wrappings in most cases. However, patients with suspected DVT should be referred for further evaluation and management in acute care settings. Unilateral leg edema in females age 40 or older should be investigated for any malignancy. Bilateral edema with symptoms should be referred to a cardiologist, and a case of sleep apnea should be evaluated in a sleep study lab. Patients with marked lymphatic obstruction not relieved by conservative methods need to be seen by a surgeon (Luebke & Brunkwall, 2009; Schnoover, 2009).


Research has found women with active sun exposure habits to be at a significantly lower risk of VTE (Lindqvist, Epstein, & Olsson, 2009). Vitamin D is obtained from sunlight exposure, diet, or dietary supplements. Because most dietary products are low in vitamin D, the major source is ultraviolet B (UVB) radiation, which penetrates the skin and converts 7-dehydrocholesterol to 25-hydroxycholecaldferol vitamin D3 (25-OHVitD) via previtamin D.

Patient and Family Teaching

Most cases of leg edema are chronic, so affected patients need education to manage their condition. Salt restriction is the most important measure, along with diuretic therapy and leg elevation. Avoiding tight-fitting clothing, prolonged standing, and dependent positions help to prevent clot formation. Patient education for skin care in chronic edema includes washing daily with neutral soap and drying carefully, keeping skin folds clean and dry, applying emollients and vegetable-based products rather petrolatum (Flour, 2013). Compression stockings should be applied initially by trained fitters in the early morning and worn throughout the day. Patients need to buy at least two pairs of stockings at the same time and use them alternately to avoid machine washing and drying the stockings.

Foot massage has a positive effect on edema in late pregnancy. Foot massage is different from reflexology. Foot massage is more general because the manipulation of soft tissue moves extravascular fluid without disturbing intravascular fluid. Twenty minutes of foot massage given for 5 days to an experimental group proved effective in reducing leg circumference compared to the control group (Coban & Sirin, 2010).


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Pathophysiology and Etiology of Leg Edema

Pathophysiology                 Etiology

Increased hydrostatic    Excessive fluid retention,
pressure                 impaired venous drainage,
                         prolonged standing, venous
                         valvular incompetence,
                         vasodilating drugs

Increased capillary      Albumin movement into
permeability             interstitium, diminished oncotic
                         pressure, sepsis-induced
                         release of cytokines
                         (interleukin-1 or tumor
                         necrosis factor),

Lymphatic                Hinders the reabsorption of
obstruction              lymphatic fluid.

Hypoalbuminemia          Loss of albumin in the urine or
                         decreased synthesis results in
                         low fluid oncotic pressure.

Hypercoagulability       Inflammation and
                         hypercoagulability increase
                         the risk of DVT.

Refeeding edema          Patients who fast for at least 3
                         days retain sodium after
                         refeeding with carbohydrates.

Drug induced             Increases sodium retention

Pathophysiology                 Clinical Conditions

Increased hydrostatic    Heart failure, pulmonary
pressure                 hypertension, primary renal sodium
                         retention, refeeding edema,
                         pregnancy, and idiopathic edema

Increased capillary      Burns, trauma, infection, allergic
permeability             reactions, episodic capillary leak
                         syndrome, ARDS, diabetes
                         mellitus, kwashiorkor, idiopathic

Lymphatic                Node enlargement due to
obstruction              malignancy, malignant ascites,
                         radical lymph node dissection,

Hypoalbuminemia          Nephrotic syndrome, protein-losing
                         enteropathy, liver disease,

Hypercoagulability       Hereditary reasons; estrogen and
                         progestin increase the risk of DVT.

Refeeding edema          Fasting, starvation

Drug induced

Pathophysiology                 Additional Comments

Increased hydrostatic    Reduction in vascular tone due to
pressure                 stroke and venous compression
                         by cyst also can increase
                         hydrostatic pressure.

Increased capillary      Malnutrition syndrome or
permeability             kwashiorkor edema was ascribed
                         previously to hypoalbuminemia.

Lymphatic                Myxedema is marked by excess
obstruction              of interstitial albumin and other
                         proteins, indicating obstruction of
                         lymphatics for fluid return in
                         addition to increased capillary

Hypoalbuminemia          Chronic hypoalbuminemia alone
                         does not produce edema.

Hypercoagulability       Clinical symptoms can be very

Refeeding edema

Drug induced             Drug-induced edema is often of
                         uncertain origin.

Cellulitis vs. Stasis Dermatitis

       Cellulitis                           Stasis Dermatitis

Acute                                Chronic

Unilateral                           Bilateral in most incidences

Crusting and scaling are rare.       Crusting and scaling are common.

Associated with symptoms of          Associated with symptoms of
infection                            venous insufficiency

Proximal red streaks may be seen.    Chronic pitting edema is seen.

Proximal lymphadenopathy may be      Ulcers may be present.

Elastic bandage does not help.       Elastic bandage is helpful.

Table 3.

Pathophysiological Mechanism of Drug-Induced Edema

Underlying Physiology                    Medications

Sodium overload         Potent vasodilators like minoxidil and

Sodium overload         Estrogens (alone or in oral contraceptives)

Sodium reabsorption     Hypoglycemics: pioglitazone or rosiglitazone

Renal dysfunction       NSAIDs

Hyperpermeability       Calcium channel blockers
of blood vessel         Interleukin-2 therapy (e.g., GM-CSF, G-CSF)

Uncertain mechanism     Chemotherapeutic agent such as docetaxel,
                        used in the treatment of metastatic breast

Underlying Physiology                    Mechanisms

Sodium overload         Induce edema by enhancing renal sodium
                        reabsorption. The fall in blood pressure both
                        directly and by activating the
                        renin-angiotensin aldosterone and sympathetic
                        nervous systems stimulates sodium retention.

Sodium overload         May promote sodium retention, primarily in
                        patients with impaired estrogen metabolism
                        due to hepatic disease.

Sodium reabsorption     Cause stimulation of sodium reabsorption by
                        the sodium channels in the luminal membrane
                        of collecting tubule cells, which is the same
                        site stimulated by aldosterone.

Renal dysfunction       Inhibit renal prostaglandin synthesis and can
                        exacerbate edema in patients with underlying
                        heart failure or cirrhosis.

Hyperpermeability       Dihydropyridines in particular may cause
of blood vessel         leakage out of the capillary due to
                        dilatation of the precapillary sphincter.

Uncertain mechanism     Produces fluid retention that is cumulative
                        and dose-limiting. The exact mechanism for
                        this is not known.


Lipedema vs. Lymphedema

   Characteristics            Lipedema             Lymphedema

Hereditary factor       Absent                 Present

History of erysipelas   Absent                 Present

Occurrence              Less common            More common

Sex                     Exclusively in         Not sex-related

Distribution            Bilateral and          Unilateral,
                        symmetrical            bilateral, or

Feet                    Minimum involvement,   Dorsum involved
                        dorsum spared

Progression             Involved areas         Distal to proximal

Kaposi-Stemmer sign     Negative               Positive
(inability to pinch
a fold of skin at the
base of second toe)

Pain on digital         Common                 Absent

Cuff sign (sharp        Present                Absent
demarcation between
normal and abnormal

Elevation of the        Minimal effect         Somewhat helpful

Source: Langendeon, Habbema, Nijsten, & Neumann (2009)
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Title Annotation:CNE SERIES; continuing nursing education
Author:Simon, Elizabeth B.
Publication:MedSurg Nursing
Article Type:Report
Geographic Code:1USA
Date:Jan 1, 2014
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