Unilateral edema (Table 4.1) is a common clinical complaint, particularly of the lower extremities, and is routinely seen in the outpatient setting. Most patients with unilateral lower extremity edema should be considered for venous Doppler assessment to screen for the presence of a deep venous thrombosis (DVT), regardless of whether it is associated with pain (Chapter 32). Rectal, pelvic, and regional lymph node examinations should be conducted if a malignancy is suspected (6,7,8).

Besides a DVT, mechanisms for a painful unilateral swelling may include the following. The postphlebitic syndrome commonly follows a DVT (9). A ruptured popliteal (Baker) cyst produces posterior knee tenderness and occasionally petechiae and may clinically resemble a DVT (10). A tear or rupture of the gastrocnemius muscle is often acute and can be confused with a DVT (11). Soft tissue infections (cellulitis and fasciitis) can initially appear with swelling and pain, before the development of erythema or warmth. A psoas muscle hematoma or abscess can also produce unilateral swelling and may be associated with flank or hip pain as well as a painful leg-lift test result (psoas sign).

Bilateral lower extremity or generalized edema (Table 4.2) is the primary result of three mechanisms: an increase in central venous pressure, such as in pulmonary hypertension; renal sodium and water retention, as with a primary renal disease; or a reduction in cardiac output with activation of the sympathetic nervous system and the renin-angiotensin system, as seen with CHF. The distribution of the edema is influenced by the hydrostatic effects of gravity (dependent edema) and by the limitation in venous and lymphatic return, and the edema often accumulates in dependent structures such as the scrotum or the abdominal pannus in obese patients. Generalized edema limited primarily to above the diaphragm can result from infection, dermal irritants, or compression or obstruction of the superior vena cava and mediastinal vasculature, as is seen with chest neoplasms (12).

Chronic right ventricular failure may be the result of left ventricular dysfunction, pulmonary hypertension, or chronic lung disease. It produces marked bilateral edema, often with ascites, as a result of an increase in central venous pressure. Acute right-sided heart failure secondary to a large pulmonary embolism or a myocardial infarction also produces elevated central venous pressures.
A careful review of the history to seek evidence of chest pains consistent with angina or a prior cardiac history (myocardial infarction or angina) should be completed early in the evaluation of generalized edema. CHF resulting from left ventricular systolic or diastolic dysfunction, or both, is one of the most common mechanisms for bilateral edema and is often associated with pleural effusion or ascites. Hepatic cirrhosis is the end point of chronic liver disease (e.g., viral hepatitis, alcoholic liver disease). Edema of hepatic origin is primarily in the lower extremities and abdominal cavity and is proportional to the elevation in portal venous pressure. A history of a change in urinary frequency, hematuria, or foamy urine supports a renal process for the edema. The edema associated with the nephrotic syndrome (urinary protein loss of more than 3.0 g per day) is the result of a marked reduction in serum albumin and occasionally by venous thrombosis that results from the associated hypercoagulable state. Minimal-change disease, membranous glomerulopathies, diabetic renal disease, human immunodeficiency virus infection, glomerulosclerosis, and myeloma kidney are common causes of the nephrotic syndrome (13).