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Edema is defined as a clinically apparent increase in interstitial fluid volume, which may expand by several liters before the abnormality is evident.(1) Depending on its cause, edema may be localized or have a generalized distribution. Anasarca refers to gross, generalized edema and is recognized by puffiness in the face. It is particularly noticeable in the periorbital areas, and by the generalized pitting of the skin following pressure. Common signs noted by patients include rings that fit more snugly on fingers, or shoes that become uncomfortably tight, particularly towards evening. These are all clues that edema may be present. Ascites is the term used to describe edema in the peritoneal cavity, and hydrothorax describes accumulation of fluid in the pleural cavity.
To have a better understanding of causes of edema, it is necessary to review the body's fluid dynamics. Approximately one-third of the body water is confined to extracellular space. Of that, about 25 percent is plasma volume, with the remainder being interstitial fluid. The exchange of fluid between these two extracellular compartments is usually balanced, so that a steady state exists between the sizes of the two compartments. The pressure forces that control the exchange between the vascular system and the interstitial fluid are known as Starling forces. The hydrostatic pressure within the vasculature and the colloid oncotic pressure within the interstitial fluid tend to move fluid out of the vasculature and into the interstitial space. Conversely, the hydrostatic pressure of the interstitial fluid, also known as tissue tension, and the colloid oncotic pressure of the vascular system, tend to move fluid in the opposite direction, back into the vessels. The movement of fluid from one compartment to the other takes place at the capillaries, with exchange from the vasculature and into the interstitial fluid being made at the arteriolar end of the capillaries, and fluid being moved back into the vasculature from interstitial fluid at the venous end of the capillaries and lymphatics. Therefore, though a large exchange of fluid takes place, a balance exists as long as there is not a significant alteration in the hydrostatic or oncotic pressures in either of the compartments. The development of edema occurs as a result of an alteration in pressures that cause a net movement of fluid from the vascular space and into the interstitium or a body cavity.
Edema may also be caused by damage to the capillary endothelium. The most frequent experiences of this type of localized edema would be from such causes as thermal burns or mechanical trauma. The bumps and bruises that cause swelling are as a result of damage to the capillary endothelium. This damage increases capillary permeability and allows proteins to transfer into the interstitial space. Capillary permeability may be altered by chemical or bacterial sources as well as thermal or mechanical injuries. It is this type of damage to capillary endothelium and resultant increase in capillary permeability that is thought to be responsible for inflammatory edema. It is generally localized, non-pitting, and accompanied by other signs of inflammation such as heat, redness, and tenderness.
To formulate a hypothesis about the pathophysiology of an edematous state, it is important to discriminate between primary events, such as venous or lymphatic obstruction; reduction of cardiac output; hypoalbuminemia; trapping of fluid in spaces such as the peritoneal cavity; or an increase in capillary permeability, and the predictable secondary consequences, which include renal retention of salt and water in an attempt to restore plasma volume. Both the primary event and the secondary consequences may contribute to the formation of edema.(1)
Many forms of edema are caused by a reduction in effective arterial blood volume. This means that
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