Harrison’s Manual of Medicine
Soft tissue swelling due to abnormal expansion of interstitial fluid volume. Edema fluid is a plasma transudate that accumulates when movement of fluid from vascular to interstitial space is favored. Since detectable generalized edema in the adult reflects a gain of ³3 L, renal retention of salt and water is necessary for edema to occur. Distribution of edema can be an important guide to cause.
LOCALIZED EDEMA Limited to a particular organ or vascular bed; easily distinguished from generalized edema. Unilateral extremity edema is usually due to venous or lymphatic obstruction (e.g., deep venous thrombosis, tumor obstruction, primary lymphedema). Stasis edema of a paralyzed lower extremity may also occur. Allergic reactions (“angioedema”) and superior vena caval obstruction are causes of localized facial edema. Bilateral lower extremity edema may have localized causes: e.g., inferior vena caval obstruction, compression due to ascites, abdominal mass. Ascites (fluid in peritoneal cavity) and hydrothorax (in pleural space) may also present as isolated localized edema, due to inflammation or neoplasm.
GENERALIZED EDEMA (See Fig. 17-1) Soft tissue swelling of most or all regions of the body. Bilateral lower extremity swelling, more pronounced after standing for several hours, and pulmonary edema are usually cardiac in origin. Periorbital edema noted on awakening often results from renal disease and impaired Na excretion. Ascites and edema of lower extremities and scrotum are frequent in cirrhosis or CHF. In CHF, diminished cardiac output and effective arterial blood volume result in both decreased renal perfusion and increased venous pressure with resultant renal Na retention due to renal vasoconstriction, intrarenal blood flow redistribution, and secondary hyperaldosteronism.
FIGURE 17-1. Diagnostic approach to edema. JVD, jugular venous distention; CO, cardiac output.
In cirrhosis, arteriovenous shunts lower effective renal perfusion, resulting in Na retention. Ascites accumulates when increased intrahepatic vascular resistance produces portal hypertension. Reduced serum albumin and increased abdominal pressure promote lower extremity edema.
In nephrotic syndrome, massive renal loss of albumin lowers plasma oncotic pressure, promoting fluid transudation into interstitium; lowering of effective blood volume stimulates renal Na retention.
In acute or chronic renal failure, edema occurs if Na intake exceeds kidney’s ability to excrete Na secondary to marked reductions in glomerular filtration. Severe hypoalbuminemia [<25 g/L (2.5 g/dL)] of any cause (e.g., nephrosis, nutritional deficiency states, chronic liver disease) may lower plasma oncotic pressure sufficiently to cause edema.
Less common causes of generalized edema: idiopathic edema, a syndrome of recurrent rapid weight gain and edema in women of reproductive age; hypothyroidism, in which myxedema is typically located in the pretibial region; drugs such as steroids, estrogens, and vasodilators; pregnancy; refeeding after starvation.
Primary management is to identify and treat the underlying cause of edema (Fig. 17-1).
Dietary Na restriction (<500 mg/d) may prevent further edema formation. Bed rest enhances response to salt restriction in CHF and cirrhosis. Supportive stockings and elevation of edematous lower extremities will help mobilize interstitial fluid. If severe hyponatremia (<132 mmol/L) is present, water intake should also be reduced (<1500 mL/d). Diuretics (Table 17-1) are indicated for marked peripheral edema, pulmonary edema, CHF, inadequate dietary salt restriction. Complications are listed in Table 17-2. Weight loss by diuretics should be limited to 1–1.5 kg/d. Metolazone may be added to loop diuretics for enhanced effect. Note that intestinal edema may impair absorption of oral diuretics and reduce effectiveness. When desired weight is achieved, diuretic doses should be reduced.
Table 17-1 Diuretics for Edema (See also Table 17-2)
Table 17-2 Complications of Diuretics
In CHF (Chap. 116), avoid overdiuresis because it may bring a fall in cardiac output and prerenal azotemia. Avoid diuretic-induced hypokalemia, which predisposes to digitalis toxicity.
In cirrhosis, spironolactone is the diuretic of choice but may produce acidosis and hyperkalemia. Thiazides or small doses of loop diuretics may also be added. However, renal failure may result from volume depletion. Overdiuresis may result in hyponatremia and alkalosis, which may worsen hepatic encephalopathy (Chap. 155).
In nephrotic syndrome, albumin infusion should be limited to very severe cases (pts with associated hypotension), since rapid renal excretion prevents any sustained rise in serum albumin.
For a more detailed discussion, see Braunwald E: Edema, Chap. 37, p. 217, in HPIM-15.