Conditions That Cause Large Increases in Extracellular Fluid Volume but with Normal Blood Volume
There are several conditions in which extracellular fluid volume becomes markedly increased but blood volume remains normal or even slightly reduced. These condi-tions are usually initiated by leakage of fluid and protein into the interstitium, which tends to decrease the blood volume. The kidneys’ response to these conditions is similar to the response after hemorrhage. That is, the kidneys retain salt and water in an attempt to restore blood volume toward normal. Much of the extra fluid, however, leaks into the interstitium, causing further edema.
The general mechanisms that lead to extracellular edema are reviewed. One of the most important clinical causes of edema is the so-called nephrotic syndrome. In nephrotic syndrome, theglomerular capillaries leak large amounts of protein into the filtrate and the urine because of an increased permeability of the glomerulus. Thirty to 50 grams of plasma protein can be lost in the urine each day, some-times causing the plasma protein concentration to fall to less than one-third normal. As a consequence of the decreased plasma protein concentration, the plasma colloid osmotic pressure falls to low levels. This causes the capillaries all over the body to filter large amounts of fluid into the various tissues, which in turn causes edema and decreases the plasma volume.
Renal sodium retention in nephrotic syndrome occurs through multiple mechanisms activated by leakage of protein and fluid from the plasma into the interstitial fluid, including activation of various sodium-retaining systems such as the renin-angiotensin system, aldosterone, and possibly the sympathetic nervous system. The kidneys continue to retain sodium and water until plasma volume is restored nearly to normal. However, because of the large amount of sodium and water retention, the plasma protein concentration becomes further diluted, causing still more fluid to leak into the tissues of the body. The net result is massive fluid retention by the kidneys until tremendous extra-cellular edema occurs unless treatment is instituted to restore the plasma proteins.
A similar sequence of events occurs in cirrhosis of the liver as in nephrotic syndrome, except that in liver cir-rhosis, the reduction in plasma protein concentration results from destruction of the liver cells, thus reducing the ability of the liver to synthesize enough plasma proteins. Cirrhosis is also associated with large amounts of fibrous tissue in the liver structure, which greatly impedes the flow of portal blood through the liver. This in turn raises capillary pressure throughout the portal vascular bed, which also contributes to the leakage of fluid and proteins into the peritoneal cavity, a condition called ascites. Once fluid and protein are lost from the circulation, the renal responses are similar to those observed in other conditions associated with decreased plasma volume. That is, the kidneys continue to retain salt and water until plasma volume and arte-rial pressure are restored to normal. In some cases, plasma volume may actually increase above normal because of increased vascular capacity in cirrhosis; the high pressures in the portal circulation can greatly distend veins and therefore increase vascular capacity.
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