Edema

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[edit] Edema

Geoffrey A. Modest

Edema typically results from either an increase in fluid pressure (e.g., from obstruction, congestive heart failure), decrease in oncotic pressure (e.g., from nephrotic syndrome, chronic hepatic insufficiency), or increased capillary permeability (from medications such as calcium channel blockers or idiopathic cyclic edema). In an average-sized person, edema is clinically detectable after 5 to 10 lbs of excess fluid. The algorithm for edema is divided into patients presenting with generalized, typically symmetric edema vs. those with regional, asymmetric edema (e.g., edema of one arm or leg).

[edit] Generalized/Symmetric

[edit] History.

There are several clues in the pattern of edema that might suggest different etiologies: monthly edema in menstruating women suggests idiopathic cyclic edema (probably estrogen-mediated), the development of ascites before peripheral edema suggests cirrhosis as the etiology, the development of edema prior to ascites suggests cardiac or renal etiologies, and the association with emotional stress or allergens suggests angioedema. Edema preferentially of the face or eyes suggests a renal etiology (acute glomerulonephritis, nephrotic syndrome), angioedema, myxedema, or protein malnutrition. Nonpitting edema suggests either chronic lymphedema, lipedema (lipodystrophy of the lower legs, typically sparing the feet), chronic venous stasis edema, myxedema (typically pretibial, either diffuse or in well-circumscribed areas, and associated with Graves' disease), and angioedema. See the algorithm for generalized pitting edema.

[edit] Physical Examination.

It is important to check the jugular venous pressure (JVP), preferably using the right side of the neck, since the right innominate and jugular veins form a straight line. Isolated clinical examination findings are, however, of limited utility.^[1] Increases in JVP can occur without cardiorespiratory etiology, and JVP can be normal even in patients with severe systolic dysfunction.

[edit] Medications.

Medications can be associated with edema; some may be mediated through worsening congestive heart failure (e.g., β-blockers) and others perhaps by direct vascular effects (e.g., dihydropyridine calcium channel blockers such as nifedipine have associated edema up to 10% of the time). Steroids and estrogen are also associated with edema.

[edit] Laboratory.

A chest x-ray may be helpful at this point. However, if the history and physical examination are highly suggestive of a heart failure (see E), the chest x-ray may not be necessary because the sensitivity (51%) and specificity (79%) for an ejection fraction of less than 40% are not sufficiently informative in most clinic situations, especially as an isolated finding.^[1]

[edit] Cardiac or Pulmonary.

Cardiac or pulmonary etiologies are likely if there is a known history of cardiac or pulmonary disease, or if specific symptoms or signs are present that are related to decreased ejection fraction (e.g., systolic dysfunction) and/or increased filling pressure (e.g., diastolic dysfunction, valvular or pericardial disease, or pulmonary disease). The clinical predictors^[1] for increased filling pressure are radiographic vascular redistribution, JVP elevation, dyspnea, orthopnea, tachycardia, decreased systolic or pulse pressure, S₃, rales, and abdominal-jugular reflux; the clinical predictors for decreased ejection fraction are radiographic cardiomegaly or vascular redistribution, anterior Q waves on electrocardiogram (ECG), left bundle branch block, sustained apical impulse, pulse greater than 90, systolic blood pressure less than 90, S₃, rales, dyspnea, prior myocardial infarction (MI), or high creatine kinase (CK) elevation in post-MI patients. More than three of the above predictors are usually present if edema is due to a cardiac/pulmonary etiology (high probability). If a chest

x-ray had not been done previously (and it may not be useful in patients with a high probability of heart disease based on clinical grounds solely), it may provide useful information in the group of patients with an intermediate probability (i.e., between one and three of the above clinical predictors).

[edit] Cardiac Tamponade and Constrictive Pericarditis.

Cardiac tamponade most typically occurs in the setting of uremia, neoplastic disease, and idiopathic pericarditis. In diagnosing cardiac tamponade, a study of 56 patients^[2] found the frequency of specific signs was increased cardiac silhouette on chest x-ray in 95%, respiratory rate >20/min in 80%, tachycardia in 77%, paradoxical pulse in 77%, systolic blood pressure >100 mm Hg in 64%, hepatomegaly in 55%, and decreased heart sounds in 34%. A normal echocardiogram effectively rules out this diagnosis. Constrictive pericarditis typically occurs in the setting of a preexisting disorder (e.g., tuberculosis [TB], amyloid, uremia, cardiac surgery, acute pericarditis, rheumatoid arthritis, lupus). The examination often is similar to hepatic cirrhosis with hepatomegaly and development of ascites disproportionate to peripheral edema, but with the additional findings of increased JVP, which may be associated with Kussmaul's sign (failure of neck veins to decline during inspiration), and paradoxical pulse (in 30%). Restrictive cardiomyopathies (e.g., secondary to amyloid, sarcoid, hemochromatosis) present similarly. The echocardiogram may not be abnormal in these settings, and in patients with a high likelihood of either constrictive pericarditis or restrictive cardiomyopathy further testing may be required.

[edit] Cor Pulmonale.

Cor pulmonale typically presents as dyspnea not relieved by sitting upright and tachypnea. A pronounced right ventricular heave and loud pulmonary component of the second heart sound may be appreciated. Cor pulmonale may be associated with pulmonary vascular disease (chronic pulmonary emboli, primary pulmonary hypertension), parenchymal pulmonary disease (chronic obstructive pulmonary disease [COPD], interstitial lung disease), or obstructive sleep apnea. The echocardiogram is a very sensitive test in the setting of cor pulmonale associated with peripheral edema.

[edit] Severe Anemia.

Severe anemia can be associated with high-output heart failure. The echocardiogram may not be sensitive enough to rule out this diagnosis. Even moderate degrees of anemia (hemoglobin below 7.5 gm/dl) may cause heart failure in a patient with reduced myocardial reserve.

[edit] Severe Hypoalbuminemia.

Severe hypoalbuminemia, with serum albumin less that 2 gm/dl, is typically necessary to cause edema. This low level of albumin is usually secondary to nephrotic syndrome (with marked proteinuria on urinalysis), advanced cirrhosis (although typically disproportionately more ascites to edema from portal hypertension), protein-losing enteropathy, or severe malnutrition.

[edit] Acute Glomerulonephritis.

In acute glomerulonephritis, edema is predominantly in the periorbital areas, although it may exist elsewhere (dependent edema, ascites). The urinalysis is abnormal, with red cells and protein (usually nonnephrotic range). Red cell casts (frequently diagnostic) may be intermittent.

[edit] Malnutrition.

Malnutrition from severe protein-energy restriction may be accompanied by loss of subcutaneous fat and muscle mass, serum transferrin level <1 gm/L, lymphocyte counts <800, and impaired delayed hypersensitivity.

[edit] Idiopathic Edema.

Idiopathic edema is a diagnosis of exclusion, typically in women of childbearing age, associated with several pound changes in weight over the course of the day and followed by fluid mobilization upon recumbency and diuresis. These patients when given a water load will excrete the excess water when recumbent and not when upright.

[edit] Preeclampsia and Cushing's Syndrome.

Preeclampsia should be considered in a pregnant woman with edema, especially with proteinuria and hypertension. Also, 62% of patients with Cushing's syndrome have edema, although the typical body habitus, hypertension, hirsutism, and purple striae suggest the diagnosis (see Chapter 98 ).

[edit] Regional/Asymmetric

[edit] History and Physical Examination.

There are several items in the history and physical examination that help guide the workup and diagnosis of regional edema. The time course of the edema is useful. Sudden onset of regional edema would suggest a traumatic origin, a ruptured Baker's cyst, or acute thrombophlebitis. Edema after leg trauma or after prolonged sitting, especially on a hard bench, suggests deep venous thrombosis (DVT). Erythema and warmth suggest an inflammatory etiology (e.g., cellulitis, gout, DVT), and accompanying tender nodularity suggests erythema nodosum. Enlarged adenopathy suggests an infectious etiology (cat-scratch, filariasis). Varicose veins can be associated with mild edema. Chronic venous insufficiency from incompetent venous valves and/or DVT can result in a dull aching in the legs and edema, especially after prolonged standing, which resolve on leg elevation. Brown discoloration of the skin often accompanies long-term chronic venous insufficiency. Of note, bilateral, apparently generalized leg edema can be associated with either bilateral regional causes (e.g., bilateral DVTs or venous insufficiency) or a more proximal regional cause (e.g., DVT obstruction in the inferior vena cava).

[edit] Trauma.

Trauma can be associated with a variety of conditions leading to regional edema, including a ruptured muscle or tendon (e.g., gastrocnemius tear), local hematoma, and compartment syndrome.

[edit] Venous Stasis Disease.

Venous stasis disease typically presents with chronic edema and brown skin discoloration, related to the breakdown of red blood cells. Sometimes there can be stasis dermatitis, where this background pigment can have a superimposed erythema and warmth, occasionally difficult to differentiate from cellulitis.

[edit] Acute Inflammation.

Acute inflammation may cause edema, commonly associated with gout, cellulitis (which may be associated with an underlying osteomyelitis), or stasis dermatitis. It is frequently difficult to distinguish these entities, since gout may be associated with significant periarticular erythema and edema (and appear as cellulitis), and stasis dermatitis (with its underlying brown discoloration and superimposed erythema) may be associated with a cellulitis.

[edit] Acute Venous Thrombosis.

Acute venous thrombosis, either superficial or deep, typically presents with unilateral edema, calf pain, and erythema. The clinical predictors of DVT^[3] include active cancer, paralysis or recent plaster immobilization, recently bedridden more than 3 days and/or major surgery, localized tenderness along the deep venous system distribution, swelling of the entire leg, calf swelling more than 3 cm when compared to the opposite leg, collateral superficial vein dilation (excluding varices), and the lack of other likely alternative diagnoses. There is high probability of DVT when three or more of these criteria are present. Other predisposing factors include hypercoagulable states, recent pregnancy, and lupus. Although contrast venography is the gold standard for diagnosis, serial compression ultrasonography (days 1, 2, and 8) has a positive predictive value of 94%.^[4] Recent studies suggest a role for magnetic resonance imaging as a sensitive test for proximal DVT, with the additional benefit of providing excellent resolution of the inferior vena cava, pelvic veins, and pulmonary emboli.^[5]

[edit] Reflex Sympathetic Dystrophy.

In reflex sympathetic dystrophy (RSD) edema can be a prominent feature, along with pain (typically burning or aching, and increased with dependency of extremity), in early RSD. Later, RSD can be associated with autonomic dysfunction, increased reflexes, spasm, and trophic changes. Precipitating events are found in two thirds of cases: assess history of trauma (most common etiology), MI (now less than 1%), cerebrovascular accident (CVA), tendinitis/bursitis, and certain medications (antituberculous medications, barbiturates, cyclosporin A).

[edit] Lymphedema.

Lymphedema can be bilateral/symmetric or regional. Initially, there is soft, pitting edema, which becomes nonpitting and “woody” after years, as tissues become indurated and fibrotic. Lymphedema is rarely primary; however, when lymphedema is primary, it often appears before age 20, with a “tarda” form beginning after age 35. Usually, lymphedema is secondary to infection (thrombosis and fibrosis after recurrent bacterial lymphangitis), tumor (most often prostate in men and lymphoma in women), filariasis, trauma, rheumatoid arthritis, and chronic contact dermatitis. Lymphedema should be differentiated from lipedema, where there is lipodystrophy with accumulation of fatty tissue, typically sparing the feet.

[edit] Obstruction.

Obstruction can cause bilateral peripheral edema if obstruction of venous return is above the legs, including use of a tight girdle, retroperitoneal fibrosis, proximal DVT (i.e., pelvic or higher), fibroids or ovarian pathology in women, or prostate cancer in men.

[edit] Upper Extremity Edema.

Upper extremity edema is unusual, but it is often associated with superior vena cava syndrome or trauma (including postsurgical, intravenous catheter).

[edit] Superior Vena Cava Syndrome.

Superior vena cava (SVC) syndrome typically presents as rapid progression of facial and upper body edema. SVC syndrome may be associated with dyspnea and stridor, especially when the patient is supine, as the syndrome becomes more severe. SVC syndrome is typically associated with an increased JVP. There may be prominent cutaneous veins of upper chest and abdomen. The vast majority of cases are associated with cancer, typically lung cancer or lymphoma.

[edit] Noninvasive Studies.

Noninvasive studies are reliable in detecting obstruction at the point that the obstruction is complete enough to cause distal edema.

[edit] REFERENCES

[edit] ADDITIONAL READINGS

• DW Alexander, RC Schlant, V Fuster: Hurst's the heart ed 9. New York: McGraw-Hill; 1998:
• KJ Isselbacher,et al.: Harrison's principles of internal medicine ed 13. New York: McGraw-Hill; 1994: