Edema is a common clinical presentation in any type of medical practice. Patients may complain of swelling or may have vague and subtle symptoms of stiffness, achiness, heaviness, or a feeling of tightness of the shoes. One must first realize that edema itself should not be considered a diagnosis; rather, it should be considered a sign of an underlying disorder, which is not necessarily vascular. It may pose a diagnostic and treatment dilemma because of an exhaustive list of potential causes and its risk of resulting in significant morbidity with ulcer formation. In most cases, however, the dilemma it causes can be solved with a directed, systematic history and physical examination. This chapter focuses on guiding clinicians on the causes of edema and their distinguishing features.
Knowledge of the factors that contribute to edema formation is important in helping clinicians understand and manage patients with edema. There are many physiologic concepts involved in the formation of edema, including salt and water balance and effective blood volume, that are not discussed in this chapter. The factors affecting edema formation in an extremity that are discussed here are hydrostatic pressure, oncotic pressure, capillary permeability, and the lymphatic system.
The extracellular fluid (ECF) is divided into two compartments, plasma and interstitial fluid.1 An increase in the interstitial fluid compartment caused by any one or more of the factors above results in edema and does not necessarily indicate fluid excess.2 The interstitial fluid compartment is able to accommodate several liters of fluid before edema is evident.2
The arterial blood pressure drives filtration from the plasma to the interstitium. Blood pressure diminishes as it enters the venous end, resulting in a pressure gradient, which favors reabsorption back to plasma. There is always a homeostatic balance between filtration and reabsorption. An increase in blood pressure may increase filtration and increased fluid in the interstitium; however, local autoregulation by smooth muscle sphincters on the arterial side protect the capillary bed from increases in systemic arterial pressure. This is why not every patient with hypertension has edema.2,3
The capillary hydrostatic pressure increases in the lower parts of the body because the column of blood increases the hydrostatic pressure to as high as 100 mm Hg in the lower arteries and veins. This is accentuated when an individual stands for a very prolonged period of time.4 Venous flow can be directed centrally against this by way of one way valves which also prevent back flow and an efficient and functional extremity muscle pump system. These decrease the pressure to as low as 20 mm Hg in the veins.3,4 Obstruction caused by intrinsic compression from venous thrombosis or extrinsic compression by a mass, however, can increase the venous pressure.