Dan D Hershko and Michael M Krausz

Department of Surgery A, Rambam Medical Center, Haifa, Israel

The extracellular fluid volume is maintained within narrow limits in normal human subjects, despite day-to-day variations in the dietary intake of salt and water. Plasma volume, in turn, is determined by the total extracellular fluid volume, and the partitioning of this volume between the extravascular fluid and the intravascular compartments also remains remarkably constant. The relationship of extracellular volume and, in particular, the volume of the plasma compartment to overall vascular capacitance determine to a large extent the fundamental indices of cardiovascular performance such as mean arterial blood pressure and left ventricular filling volume.

Edema is the clinicopathological term used to describe an excessive accumulation of fluids in the extravascular (interstitial) component of the extracellular fluid volume. Depending on the etiology and mechanism leading to its formation, edema may occur locally at specific tissue and organs or it may have a more generalized distribution. Local edema may be the result of a site-specific hemodynamic derangement or it may be formed secondary to an inflammatory reaction to injury and sepsis. Generalized edema, the clinical hallmark of extracellular fluid volume expansion, usually represents the accumulation of excessive volumes of fluid in the interstitial compartment secondary to renal sodium retention, the result of activation of various compensatory mechanisms [1]. Nevertheless, recent studies have suggested that other contributory mechanisms may also have a significant role in the pathophysiology of edema formation.

In clinical practice, when edema is severe and involves all body tissues and organs, it is commonly termed anasarca. Accumulation of edema fluids in the peritoneal cavity is known as ascites and in the pleural cavity as hydrothorax. The composition of the edema is of impor tance, as it too depends on the etiology and mechanism leading to its formation. Noninflammatory edema fluid, such as accumulates in heart failure, cirrhosis of the liver, and various renal diseases, is protein-poor in nature and is termed a transudate. In contrast, the inflammatory edema fluid, which is termed an exudate, is protein- and leukocyte-rich and is associated with increased endothelial permeability. Thus, when characterizing the pathophysiology of edema formation, it is convenient to differentiate between the inflammatory and noninflammatory (hemodynamic) derangements that lead to edema formation.

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