Chapter 036. Edema (Part 1) doc

Chapter 036. Edema
(Part 1)

Harrison's Internal Medicine > Chapter 36. Edema
Edema: Introduction
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. 44) and hydrothorax refer to
accumulation of excess fluid in the peritoneal and pleural cavities, respectively,
and are considered to be special forms of edema.
Depending on its cause and mechanism, edema may be localized or have a
generalized distribution; it 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 following 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 in
putting on shoes, particularly in the evening, edema may be present.

Pathogenesis
About one-third of total-body water is confined to the extracellular space.
Approximately 75% of the latter, in turn, is interstitial fluid and the remainder is
the plasma.

Starling Forces
The forces that regulate the disposition of fluid between these two
components of the extracellular compartment are frequently 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. On the other hand, the colloid oncotic
pressure contributed by plasma proteins and the hydrostatic pressure within the
interstitial fluid, referred to as the tissue tension, promote the movement of fluid
into the vascular compartment.
As a consequence of these forces, there is a 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 a steady state exists in the sizes of the intravascular
and interstitial compartments, and, yet, a large exchange between them occurs.
However, should either the hydrostatic or oncotic pressure gradient be
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 due to 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 may also 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).

Capillary Damage
Edema may also result from damage to the capillary endothelium, which
increases its permeability and permits the transfer of protein 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 may also 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—
redness, heat, and tenderness.