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

Hydrostatic Pressure

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.

Oncotic Pressure

Proteins, mainly albumin, are responsible for the plasma oncotic pressure. The concentration of proteins in the plasma is greater than the concentration of proteins in the interstitial fluid. This concentration gradient causes fluid to shift toward the compartment with the higher oncotic pressure, which is normally plasma.

Capillary Permeability

The capillary membrane is semipermeable. Changes in the capillary wall permeability may be mediated by cytokines as well as endothelial-derived circulating vasodilatory prostaglandins and nitrous oxide.² An increase in the capillary permeability allows plasma proteins to exit into the interstitial space, thus increasing the oncotic pressure of the interstitial space relative to the plasma, resulting in an increase in interstitial fluid accumulation.

The Lymphatic System

The lymphatic system is a direct outflow system for the interstitial fluid. In this system, excess fluid made up of waste products and proteins is filtered from the general circulation because of the pressure gradient, local arterial pulsation, one-way valves, and an efficient and functional extremity muscle pump system.

Acute Edema

The first step in determining the cause of edema is to determine the acuity of onset. Edema that has occurred suddenly over hours or days should alert one to the possibilities of a deep venous thrombosis (DVT), a ruptured Baker’s cyst, a ruptured gastrocnemius muscle, compartment syndrome, gout, or cellulitis. These are usually unilateral and associated with pain. Associated symptoms or activities that precede the development of edema may give a clue to the diagnosis.

A patient who has recently been immobilized, had surgery or a recent hospitalization, had recent trauma, or has an underlying malignancy would alert one to suspect DVT. Edema after a period of heavy exertion and associated with ecchymosis around the ankle would likely be secondary to a ruptured gastrocnemius muscle. Edema associated with fevers, chills, or erythema is likely secondary to cellulitis. A patient with osteoarthritis of the knees who presents with new-onset edema is likely to have a ruptured Baker’s cyst, although the immobility from osteoarthritis may also result in DVT.

Duplex ultrasonography can readily detect thrombosis and should be performed as soon as possible to expedite appropriate treatment. It can also determine if there is a ruptured Baker cyst or a ruptured gastrocnemius muscle.

Chronic Edema

Edema that has a gradual and progressive onset over weeks to months is most likely secondary to chronic venous insufficiency (CVI), lymphedema, or congestive heart failure (CHF) with or without pulmonary hypertension; however, the list is extensive (Table 43-1), and some of the acute causes such as DVT can also present this way. Systemic causes should also be sought out. In contrast to acute edema, chronic edema is usually painless and can be unilateral or bilateral.

Chronic Venous Insufficiency

A history of DVT, varicose veins (personal history or family history), or surgery on the affected extremity strongly suggests CVI. Patients with CVI may also have a history of relief of symptoms with elevation of the limb. They may complain of itching, scaling, or redness of the legs. CVI can be primary or secondary. Primary CVI is usually caused by congenitally absent or abnormal venous valves, which would result in an increased hydrostatic pressure. Secondary CVI may be caused by previous thrombosis that has damaged the venous valves; direct trauma to a vein; or external compression by another structure such as an adjacent aneurysm, artery, or mass. All of these result in edema because of an elevation in the hydrostatic pressure.