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. Because detectable generalized edema in the adult reflects a gain of ≥3 L, renal retention of salt and water is necessary. Distribution of edema can be an important guide to cause.
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 also may 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, and abdominal mass. Ascites (fluid in peritoneal cavity) and hydrothorax (in pleural space) also may present as isolated localized edema, due to inflammation or neoplasm.
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, nephrotic syndrome, or CHF.
In CHF, diminished cardiac output and arterial underfilling result in both decreased renal perfusion and increased venous pressure with resultant renal Na retention due to renal vasoconstriction, intrarenal blood flow redistribution, direct Na-retentive effects of norepinephrine and angiotensin II, and secondary hyperaldosteronism leading to distal tubular Na retention.
In cirrhosis, arteriovenous shunts and peripheral vasodilation are the proximate causes of Na retention. Ascites accumulates when increased intrahepatic vascular resistance produces portal hypertension. As in heart failure, the effects of excess intrarenal and circulating norepinephrine, angiotensin II, and aldosterone lead to renal Na retention and worsening edema. Reduced serum albumin and increased abdominal pressure also promote lower-extremity edema.
In acute or chronic renal failure, edema occurs if Na intake exceeds kidneys’ 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., nephrotic syndrome, nutritional deficiency, chronic liver disease) may lower plasma oncotic pressure, promoting fluid transudation into interstitium; lowering of effective blood volume stimulates renal Na retention and causes edema. In nephrotic syndrome, loss of protein into the urine also leads to primary Na retention, through effects on tubular Na transport.
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 (Table 38-1).