The body’s fluid system operates under a delicate balance that if upset, precipitates a condition known as edema. According to Scallan and Huxley (2010), edema is a condition in which an inordinate quantity of fluid gathers in body tissue. The fluid can accumulate either inside cells (cellular edema) or inside the collagen-mucopolysaccharide matrix, which exists in the interstitial spaces (interstitial edema). In either case, the fluid causes swelling. As such, in simple terms, edema is a medical terminology used to denote swelling. The condition can affect any part of the body, but it mostly affects the legs. It results from a variety of factors such as pregnancy, underlying diseases such as heart failure or liver cirrhosis, medication, physical inactivity, burns, genes, and sitting or standing for long. These factors act in different ways to cause edema. One of the well-known ways through which they act is the elevation of capillary pressure. This essay investigates how the elevation of capillary pressure results in edema.
One of the typologies of edema, which results from increased capillary pressure, is known as hydrostatic edema (Scallan & Huxley, 2010). It occurs when excess fluid accumulates in the interstitial spaces, due to elevated hydrostatic capillary pressure. The idea here is that since the fluid that flows into the interstitial space comes from the capillaries, an increase in capillary pressure will tend to force more fluid into the interstitium. Hydrostatic edema differs from permeability edema in the sense that although both occur as a result of increased capillary pressure, the latter results from interference with the normal operation of pores in the vascular membrane. Normally, the body’s fluids flow between the intra-vascular and the extra-vascular compartments of the body. This flow takes place via pores in the vascular membrane. As such, when the physical structure of the pores is altered, it also alters the pattern of flow of the body fluids (Grossman, 2013). The consequence of this change is that it reduces the rate of filtration, which should conventionally be higher than the rate of re-absorption. It, therefore, leads to the flow of a lower than normal quantity of fluid from the capillaries into the interstitium, translating to higher pressure in the capillaries. The third typology of edema, which also results from increased capillary pressure, is known as Lymphedema. In this type of edema, increased pressure in the capillaries leads to higher than normal filtration such that the lymphatic system cannot pump away enough fluid to restore balance in the interstitium. As a result, the interstitium swells with excess fluid.
Each of the above-described examples of edema development results from some pathophysiological change in the body. Hydrostatic edema, for example, occurs when venous pressure rises above normal levels. Capillary hydrostatic pressure is an aggregate of arterial and venous pressures (Grossman, 2013). Thus, an increase in either can lead to an increase in capillary hydrostatic pressure. However, changes in venous pressure are more likely to cause a change in capillary hydrostatic pressure compared to changes in arterial pressure. Thus, hydrostatic edema almost exclusively results from increased venous pressure (Grossman, 2013). The case of permeability edema is slightly different. The pathophysiological change that occurs, in this case, is the disruption of the physical form of the pores in the vascular membrane. This interference impairs the functionality of the pores or the membrane as a whole, altering the flow of fluids between the intra-vascular and extra-vascular compartments. This change is almost similar to the change that takes place with the incidence of Lymphedema. In this form of edema, the ability of the lymphatic system to function normally is also impaired limiting its ability to pump fluids away from the interstitium. Thus, like in the case of permeability edema, there is interference with the functionality of a particular body system. They, however, differ based on the affected body systems.
In conclusion, it is worth noting that the three examples discussed above only differ insofar as their etiology is concerned. However, all of them affect the interstitium. As such, they could fundamentally be the same kind of edema, but the processes through which they come into being are different.
Grossman, S. (2013). Porth’s pathophysiology: Concepts of altered health states. New York, NY: Lippincott Williams & Wilkins.
Scallan, J., & Huxley, V. (2010). Capillary fluid exchange: Regulation, functions, and pathology. San Rafael, CA: Morgan & Claypool Life Sciences.