Fig. 4.2 Factorsinfluencingfluidmovementacrosscapillarywalls.Capillaryhydrostaticandosmoticforcesarenormallybalancedsothereislittlenetmovementoffluidintotheinterstitium.However,increasedhydrostaticpressureordiminishedplasmaosmoticpressureleadstoextravascularfluidaccumulation(edema).Tissuelymphaticsdrainmuchoftheexcessfluidbacktothecirculationbywayofthethoracicduct;however,ifthecapacityforlymphaticdrainageisexceeded,tissueedemaresults.
colloid typically is a protein-poor transudate; by contrast, because of increased vascular permeability, inflammatory edema fluid is a protein-rich exudate with a high specific gravity. The usual cutoffs for specific gravity (<1.012 for transudates and >1.020 for exudates) illustrate the point but are not clinically useful. We will now discuss the various causes of edema.
Increases in hydrostatic pressure are mainly caused by disorders that impair venous return. Local increases in intravascular pressure caused, for example, by deep venous thrombosis in the lower extremity can cause edema restricted to the distal portion of the affected leg. Generalized increases in venous pressure, with resultant systemic edema, occur most commonly in congestive heart failure (Chapter 11).
Fig. 4.3 illustrates the interlocking mechanisms that underlie generalized edema resulting from cardiac, renal, and hepatic failure. Several factors increase venous hydrostatic pressure in patients with congestive heart failure (
Fig. 4.3 ). The reduced cardiac output leads to systemic venous congestion and resultant increase in capillary hydrostatic pressure. At the same time reduction in cardiac output results in hypoperfusion of the kidneys, triggering the renin-angiotensin-aldosterone axis and inducing sodium and water retention (secondary hyperaldosteronism). In patients with normal heart function, this adaptation increases cardiac filling and cardiac output, thereby improving renal perfusion. However, the failing heart often cannot increase its cardiac output in response to the compensatory increases in blood volume. Instead, a vicious cycle of fluid retention, increased venous hydrostatic pressures, and worsening edema ensues. Unless cardiac output is restored or renal water retention is reduced (e.g., by salt restriction or treatment with diuretics or aldosterone antagonists), this downward spiral continues. Because secondary hyperaldosteronism is a common feature of generalized edema, salt restriction, diuretics, and aldosterone antagonists also are of value in the management of generalized edema resulting from non-cardiac causes.
Reduction of plasma albumin concentrations leads to decreased colloid osmotic pressure of the blood and loss of fluid from the circulation. Under normal circumstances, albumin accounts for almost half of the total plasma protein. Therefore, conditions in which albumin is either lost from the circulation or synthesized in inadequate amounts are common causes of reduced plasma osmotic pressure. Nephrotic syndrome is the most important cause of albumin loss from the blood. In diseases that are characterized by nephrotic syndrome (Chapter 14), the glomerular capillaries become leaky, leading to the loss of albumin (and other plasma proteins) in the urine and the development of generalized edema. Reduced albumin synthesis occurs in the setting of severe liver disease (e.g., cirrhosis) (Chapter 16) and protein malnutrition (Chapter 8). Regardless of cause, low albumin levels lead in a stepwise fashion to edema, reduced intravascular volume, renal hypo-perfusion, and secondary hyperaldosteronism. Unfortunately, increased salt and water retention by the kidney not only fails to correct the plasma volume deficit but also exacerbates the edema, because the primary defect—low serum protein—persists.
Edema may result from lymphatic obstruction that compromises resorption of fluid from interstitial spaces.