Edema is defined as a clinically apparent increase in the interstitial fluid volume, which may expand by several liters before the abnormality is evident. Therefore, a weight gain of several kilograms usually precedes overt manifestations of edema, and a similar weight loss from diuresis can be induced in a slightly edematous patient before “dry weight” is achieved. Anasarca refers to gross, generalized edema. Ascites (Chap. 43) and hydrothorax refer to accumulation of excess fluid in the peritoneal and pleural cavities, respectively, and are considered special forms of edema.
Depending on its cause and mechanism, edema may be localized or have a generalized distribution. Edema is recognized in its generalized form by puffiness of the face, which is most readily apparent in the periorbital areas, and by the persistence of an indentation of the skin after pressure; this is known as “pitting” edema. In its more subtle form, edema may be detected by noting that after the stethoscope is removed from the chest wall, the rim of the bell leaves an indentation on the skin of the chest for a few minutes. When the ring on a finger fits more snugly than in the past or when a patient complains of difficulty putting on shoes, particularly in the evening, edema may be present.
About one-third of total-body water is confined to the extracellular space. Approximately 75% of the latter is interstitial fluid, and the remainder is in the plasma compartment.
The forces that regulate the disposition of fluid between these two components of the extracellular compartment frequently are referred to as the Starling forces. The hydrostatic pressure within the vascular system and the colloid oncotic pressure in the interstitial fluid tend to promote movement of fluid from the vascular to the extravascular space. By contrast, the colloid oncotic pressure contributed by plasma proteins and the hydrostatic pressure within the interstitial fluid promote the movement of fluid into the vascular compartment.
As a consequence of these forces, there is movement of water and diffusible solutes from the vascular space at the arteriolar end of the capillaries. Fluid is returned from the interstitial space into the vascular system at the venous end of the capillaries and by way of the lymphatics. Unless these channels are obstructed, lymph flow rises with increases in net movement of fluid from the vascular compartment to the interstitium. These flows are usually balanced so that there is a steady state in the sizes of the intravascular and interstitial compartments, yet a large exchange between them occurs. However, if either the hydrostatic or the oncotic pressure gradient is altered significantly, a further net movement of fluid between the two components of the extracellular space will take place. The development of edema then depends on one or more alterations in the Starling forces so that there is increased flow of fluid from the vascular system into the interstitium or into a body cavity.
Edema due to an increase in capillary pressure may result from an elevation of venous pressure caused by obstruction to venous and/or lymphatic drainage. An increase in capillary pressure may be generalized, as occurs in congestive heart failure (see below). The Starling forces also may be imbalanced when the colloid oncotic pressure of the plasma is reduced owing to any factor that may induce hypoalbuminemia, such as severe malnutrition, liver disease, loss of protein into the urine or into the gastrointestinal tract, or a severe catabolic state. Edema may be localized to one extremity when venous pressure is elevated due to unilateral thrombophlebitis (see below).
Edema may also result from damage to the capillary endothelium, which increases its permeability and permits the transfer of proteins into the interstitial compartment. Injury to the capillary wall can result from drugs, viral or bacterial agents, and thermal or mechanical trauma. Increased capillary permeability also may be a consequence of a hypersensitivity reaction and is characteristic of immune injury. Damage to the capillary endothelium is presumably responsible for inflammatory edema, which is usually nonpitting, localized, and accompanied by other signs of inflammation—i.e., erythema, heat, and tenderness.
Reduction of Effective Arterial Volume
In many forms of edema, the effective arterial blood volume, a parameter that represents the filling of the arterial tree, is reduced. Underfilling of the arterial tree may be caused by a reduction of cardiac output and/or systemic vascular resistance. As a consequence of 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 retention of salt and, therefore, of water, ultimately leading to edema.
Renal Factors and the Renin-Angiotensin-Aldosterone (Raa) System
(See also Chap. 342) In the final analysis, renal retention of Na+ is central to the development of generalized edema (Fig. 36-1). 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 cells surrounding the afferent arteriole) into a signal for increased renin release. Renin is an enzyme with a molecular mass of about 40,000 Da that acts on its substrate, angiotensinogen, an α2-globulin synthesized by the liver, to release angiotensin I, a decapeptide, which in turn is converted to angiotensin II (AII), an octapeptide. AII has generalized vasoconstrictor properties; it is especially active on the renal efferent arterioles. This action reduces the hydrostatic pressure in the peritubular capillaries, whereas the increased filtration fraction raises the colloid osmotic pressure in these vessels, thereby enhancing salt and water reabsorption in the proximal tubule as well as in the ascending limb of the loop of Henle.
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