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About two-thirds of total body water is intracellular and one-third is extracellular. Approximately one-fourth of the latter is in the plasma and the remainder comprises the interstitial fluid. Edema represents an excess of interstitial fluid that has become evident clinically.

There is constant interchange of fluid between the two compartments of the extracellular fluid. The hydrostatic pressure within the capillaries and the colloid oncotic pressure in the interstitial fluid promote the movement of water and diffusible solutes from plasma to the interstitium. This movement is most prominent at the arterial origin of the capillary and falls progressively with the decline in intracapillary pressure and the rise in oncotic pressure toward the venular end. Fluid is returned from the interstitial space into the vascular system largely through the lymphatic system. These interchanges of fluids are normally balanced so that the volumes of the intravascular and interstitial compartments remain constant. However, a net movement of fluid from the intravascular to the interstitial spaces takes place and may be responsible for the development of edema under the following conditions: (1) an increase in intracapillary hydrostatic pressure; (2) inadequate lymphatic drainage; (3) reductions in the oncotic pressure in the plasma; (4) damage to the capillary endothelial barrier; and (5) increases in the oncotic pressure in the interstitial space.


In many forms of edema, the effective arterial blood volume, a parameter that represents the filling of the arterial tree and that effectively perfuses the tissues, is reduced. Underfilling of the arterial tree may be caused by a reduction of cardiac output and/or systemic vascular resistance, by the pooling of blood in the splanchnic veins (as in cirrhosis), and by hypoalbuminemia (Fig. 37-1A). As a consequence of this underfilling, a series of physiologic responses designed to restore the effective arterial volume to normal are set into motion. A key element of these responses is the renal retention of sodium and, therefore, water, thereby restoring effective arterial volume, but sometimes also leading to the development or intensification of edema.


Clinical conditions in which a decrease in cardiac output (A) and systemic vascular resistance (B) cause arterial underfilling with resulting neurohumoral activation and renal sodium and water retention. In addition to activating the neurohumoral axis, adrenergic stimulation causes renal vasoconstriction and enhances sodium and fluid transport by the proximal tubule epithelium. RAAS, renin-angiotensin aldosterone system; SNS, sympathetic nervous system. (Modified from RW Schrier: Ann Intern Med 113:155, 1990.)


The diminished renal blood flow characteristic of states in which the effective arterial blood volume is reduced is translated by the renal juxtaglomerular cells (specialized myoepithelial ...

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