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Lower Extremity Edema

To Maintain a Balance, Treat the Underlying Disease

Vol. 6 • Issue 8 • Page 16

Edema of the lower extremities is a common complaint in the primary care setting. While most patients who present with lower-extremity edema are elderly, the problem can present in patients of any age group. The etiologies range from life-threatening disorders, such as congestive heart failure or malignancies, to drug-induced or idiopathic causes. Managing lower-extremity edema requires you to diagnose and treat the underlying disorder. A thorough history and physical examination will direct you to the necessary ancillary studies and tests to establish the diagnosis.

The extracellular space in the body consists of the plasma volume and the interstitial space. The movement of body fluid within the extracellular space is controlled by hydrostatic pressure and colloid oncotic pressure, often referred to as the Starling forces.1Any alteration in either one of these forces causes a fluid movement from one space to another, and edema may occur.

Lower-extremity edema, a condition in which body tissues of the lower extremity contain excess fluid, is a common presenting complaint in the primary care setting. The axiom "treat the underlying disease" should guide your approach to this condition.

A good differential diagnosis is important to guide the evaluation and separate life-threatening conditions from more benign etiologies (Table 1). Initial evaluation should determine onset, distribution and associated symptoms such as dyspnea or recent weight changes. Questions about past medical history should specifically address cardiac disease, alcohol use, medication use and recent trauma or increased physical activity. Physical exam should, at a minimum, consist of cardiovascular, respiratory, abdominal, musculoskeletal and integumentary system examination.

Unilateral Lower-Extremity Edema

Deep-vein thrombosis. Venous stasis, endothelial injury and hypercoaguability (Virchow's triad) are the main factors associated with deep-vein thrombosis (DVT). A patient with a DVT will frequently complain of pain, heat and swelling of the affected region. The pain may occur at rest or only during exercise. Important questions include history of trauma, prolonged periods of immobility or a history of deep-vein thrombosis. DVT rarely occurs in people without underlying factors but may be an indicator of a more serious problem.

The affected limb should first be visualized for any skin growth or hair growth changes and measured to compare with the unaffected limb. A difference greater than 1.4 cm in a man or greater than 1.2 cm in a woman is highly suspicious of underlying pathology.2The foot should be dorsiflexed to elicit calf pain, which is a positive Homan's sign. A useful physical exam tool is the presence of pain with inflation of a blood pressure cuff around the calf. Most patients should be able to tolerate pressures up to 160 to 180 mm Hg. Laboratory studies should consist of complete blood count and prothrombin and partial thromboplastin times.

Ascending contrast venography is the gold standard of diagnostic testing, although there is significant morbidity associated with venograms. Impedance plethysmography (IPG) is a noninvasive technique that is highly sensitive in detecting above-knee thrombosis, but it fails to detect many below-knee thrombi.

Doppler ultrasound ("duplex") studies are more widely used, with a sensitivity of 93% and specificity of 98% in symptomatic patients.3In asymptomatic patients the sensitivity drops to 59%, while the specificity remains at 98%; therefore, serial studies may be necessary.

Occult malignancy. Edema affecting only one limb should raise the suspicion of occult malignancy, especially in men older than 40 or anyone with a known primary cancer. Onset is usually gradual, occasionally with lower abdominal or limb pain. Questions should cover unusual weight loss, fever, changes in bowel or bladder habits and hematuria or hematochezia. The physical exam is usually unremarkable. Homan's sign will be negative, and guaiac-positive stools may be found. Computed tomography (CT) with contrast or magnetic resonance imaging (MRI) of the abdomen may reveal a tumor compressing the iliac vein.

Lymphedema is another common cause of unilateral edema. Primary lymphedema, either congenital or hereditary, affects women more frequently than men. Secondary lymphedema results from damage or obstruction to the lymphatic channels (Table 2). The most common cause of lymphedema worldwide is filariasis.

Patients will usually complain of a dull, heavy sensation in the leg, usually without pain. The majority of complaints are usually about the appearance of the leg. In early stages the limb is soft and pits easily, later it assumes a woody texture as the tissues become indurated and fibrotic. In the chronic stage, the shape of the limb changes and the toes may become square; at this point, the edema is no longer pitting. Ultrasound or CT of the abdomen and pelvis can be used to detect obstructing lesions.

Lymphoscintigraphy and lymphangiography can be used to distinguish between primary and secondary lymphedema.

Miscellaneous causes. Other etiologies to consider are cellulitis, gout or septic arthritis. The patient should be questioned about onset of symptoms, injury to the site and history of diabetes mellitus. Physical examination may demonstrate pain, redness and warmth at the site. An elevated body temperature indicates possible systemic involvement. Erythrocyte sedimentation rate, complete blood count, radiographs and joint fluid aspiration and analysis will aid in these diagnoses.

Bilateral Edema

Congestive heart failure. Weight gain and bilateral lower extremity edema may be the initial signs of congestive heart failure. Patients may complain of dyspnea with exertion, orthopnea or fatigue. The patient may also complain of nocturia; this is caused by increased venous return while lying down that results in increased urine output.4Physical examination may reveal pitting lower extremity edema, S3 gallop, jugular venous distention or basilar rales. Chest X-ray may reveal cardiomegaly. Complete blood count may reveal an anemia of high output heart failure.5Echocardiogram may demonstrate a pericardial effusion indicative of chronic heart failure.

Hepatic insufficiency. Chronic hepatic insufficiency is a common cause of impaired albumin synthesis with a resulting edema. A history of alcoholism or hepatitis may be an indicator of cirrhosis. Patients often experience anorexia, nausea and vomiting, malaise and weight loss. Fever may be present, as high as 39.4°C (103°F) in up to half of cases. The physical examination usually demonstrates jaundice, arterial "spider" angiomas, tender hepatomegaly and splenomegaly in approximately one-third of patients. Severe cases may include ascites, bleeding and encephalopathy. Appropriate laboratory studies include a complete blood count to detect anemia or leukocytosis, a liver function test, a chemistry panel to assess renal function and urinalysis for proteinuria. The serum albumin level is usually depressed, and the prothrombin time is frequently prolonged.

Nephrotic syndrome. Nephrotic syndrome is defined as proteinuria in excess of 3 g to 3.5 g daily accompanied by edema, hypoalbuminemia and hyperlipidemia. Presenting signs and symptoms may include hypertension, anorexia, oliguria and retinal sheen.6The skin will have a notable pallor that is accentuated by the edema, and striae will often appear on the extremities as the skin is stretched. Ascites and hydrothorax are common findings in these patients. In addition to the large amounts of protein found in the urine, the sediment contains casts, renal tubular cells that may contain fatty droplets (oval fat bodies), and a number of erythrocytes.7The complete blood count may show a mild normochromic anemia, but the anemia becomes more severe as the amount of renal damage increases. Nitrogen retention also reflects the amount of renal damage present, and the serum cholesterol level is greatly increased. A renal biopsy can confirm the diagnosis and may indicate the overall disease prognosis.

Medication side effects. Edema is a frequent side effect of many commonly prescribed drugs, the most commonly these being nonsteroidal anti-inflammatory medications (Table 3). Symptoms usually resolve on discontinuing the causative agent.

Thyroid disorders. Hypothyroidism, presenting with pretibial edema and periorbital swelling, may indicate myxedema or Grave's disease. In myxedema, the thyroid is usually not palpable and the skin is thick and dry with minimal hair present. Cold intolerance is a frequent complaint. The patient's voice often becomes hoarse and deep, while auditory acuity may decrease. In Grave's disease, patients complain of heat intolerance, excessive sweating and frequent bowel movements. The patient usually appears anxious and restless, and the skin is warm and moist. Cardiovascular examination may reveal a wide pulse pressure and sinus tachycardia. The single most useful measurement is the serum thyroid-stimulating hormone (TSH), although occasionally in mild thyrotoxicosis an ultrasensitive TSH or the thyrotropin-releasing hormone (TRH) stimulation test may be necessary.

Stress fracture. Stress fractures resulting from unusual stress on the weight-bearing bones may result in edema, either unilateral or bilateral in some cases. These injuries result from physical stress in people unaccustomed to such activities ("weekend warriors"), or people in training who change their level of activity at a pace beyond the capability of their bones. Radiographs 2 to 3 weeks after the onset of injury may indicate change in the cortical margins or the callus of a healing fracture. Bone scan may be indicated when plain radiographs are normal, but the patient continues to experience pain.

Ankle edema due to chronic venous insufficiency is a common finding in the elderly population. Patients may complain of a dull ache associated with prolonged standing that is relieved by rest. Examination usually reveals edema, superficial varicose veins with erythema and hyperpigmentation. Skin ulcerations may occur near the medial and lateral malleoli. These patients should avoid prolonged sitting or standing, which raise venous pressure. Fitting these patients with compression stockings to be worn during the day and prescribing frequent leg elevation are important control measures.8Ulcers should be treated with wet-to-dry dressings and occasionally compressive dressings containing antiseptic solutions. Surgical interruption of incompetent communicating veins may be necessary for recurrent ulceration and severe edema.

Miscellaneous causes. Several idiopathic states cause edema, but these are diagnoses of exclusion. Heat edema is characterized by swelling of the feet and ankles after prolonged sitting or standing in hot weather. An increase in aldosterone as the body adapts to heat exposure may result in an accumulation of salt and water with resultant edema.9Idiopathic cyclic edema or premenstrual edema results from sodium and water retention resulting from increased estrogen production. Weight gain of 4 to 5 pounds with significant diurnal variations, headaches and increased thirst are highly suggestive of this condition. Lower-extremity edema associated with arthralgias and painful erythematous nodelike lesions is characteristic of erythema nodosum.10

The Underlying Cause

In evaluating lower-extremity edema, it's important to determine the underlying cause. This prevents potential harm caused by inappropriate therapy. The majority of etiologies for unilateral edema have greater life-threatening potential, and this may necessitate a more aggressive approach in the evaluation of unilateral edema. A thorough history and physical examination are the key in the assessment of lower extremity edema. Selected ancillary studies (Table 4) will further assist in obtaining the definitive diagnosis.

Nelson A. Sawyer is a primary care physician assistant in the U.S. Army and is currently stationed in South Korea.


1. Braunwald E. Edema. In: Isselbacher K, Braunwald E, Wilson JD, Martin JB, Fauci AS, Kasper DL, eds. Harrison's Principles of Internal Medicine. 13th ed. New York, NY: McGraw-Hill; 1994;1:183­-187.

2. Kontos HA. Vascular diseases of the limbs. In: Bennett JC, Plum F, eds. Cecil's Textbook of Medicine. 20th ed. Philadelphia, Pa: WB Saunders Co; 1996;1:354.

3. Powell AA, Armstrong MA. Peripheral edema. Am Fam Physician. 1997;53(5):1721-1735.

4. Rao KV. Emergency renal problems. In: Tintinalli JE, Krome RL, Ruiz R, eds. Emergency Medicine: A Comprehensive Study Guide. 4th ed. New York, NY: McGraw-Hill; 1996:354-357.

5. Olson PR. Edema. In: Mengel MB, Schwiebert LP, eds. Ambulatory Medicine: The Primary Care of Families. 2nd ed. Stamford, Conn: Appleton & Lange; 1996:125-129.

6. Nephrotic syndrome. In: Dambro MR, ed. Griffith's 5 Minute Clinical Consult. Philadelphia, Pa: Williams & Wilkins; 1997:714.

7. Vincenti FG, Amend WJC Jr, Diagnosis of medical renal diseases. In: Tanagho EA, McAninch JW. Smith's General Urology. 14th ed. Norwalk, Conn: Appleton & Lange; 1995:592-603.

8. Tierney LM Jr, Messina LM. Blood vessels and lymphatics. In: Tierney LM Jr, McPhee SJ, Papadakis MA, eds. Current Medical Diagnosis and Treatment. 36th ed. Stamford, Conn: Appleton & Lange; 1997:432-462.

9. Rakel RE. Textbook of Family Practice. 5th ed. Philadelphia, Pa: WB Saunders Co; 1995:880.

10. Fulcher W. Thermal and environmental injuries. In: Habif TE, ed. Clinical Dermatology. 3rd ed. St. Louis, Mo: Mosby; 1996:875-890.


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