Key Clinical Questions
How can the history and physical examination findings direct the evaluation of lower extremity edema?
What diagnostic or laboratory studies will help better delineate the differential diagnosis?
What therapeutic options may be beneficial in the management of edema?
A 42 year old woman with a medical history of vascular disease presented to the emergency department with difficulty walking from painful leg and foot wounds present for 4 weeks. Her medical history included traditional vascular risk factors (hypertension, diabetes, hyperlipidemia), coronary artery disease (four myocardial infarctions, s/p stent placement, ischemic cardiomyopathy with ejection fraction of 25% of left apical thrombus), venous thromboembolism (deep venous thromboembolism, pulmonary embolism, s/p inferior vena caval filter placement), warfarin associated gastrointestinal bleeding, and status post partial amputation of her right foot due to osteomyelitis. She had not been taking her medications for two weeks. She complained of acute blisters of unknown etiology on her feet. The left was more involved than the right. She had previously been evaluated at an outside hospital for similar findings and a biopsy was done without defining an underlying etiology. On examination vital signs included temperature 99.4 (F); heart rate 116; blood pressure 133/93, respiratory rate 20, with a room air pulse oximetry at 100%. Her neck veins were distended and elevated to 14 cm. She was tachycardic with a regular rate with a 3/6 systolic murmur at the apex. No gallop was noted. Her lungs were clear without wheezes or crackles. Her abdomen was soft. No abdominal bruits were noted. She was tender to palpation in the right upper quadrant. Lower extremity edema extended from the feet to the proximal hips and lower abdominal wall bilaterally. There were multiple punched-out fibrous-based wounds as well as intact fluid-filled blisters over the thighs and posterior knees. The left foot was completely involved with a partially hemorrhagic bulla. Pulses were not palpable. Initial laboratory examination revealed a hemoglobin of 7.7 g/dl; hematocrit 26.1%. Albumin was 1.8 g/dl, prealbumin 5.0 mg/dl, and total protein was 6.5 g/dl. BUN and creatinine were 21 and 1.14 respectively. Glucose was elevated at 401 mg/dl. Urinalysis demonstrated 3+ protein, 2+ blood, and 1000 mg/dl glucose. Further workup during the admission was directed at identifying the etiology of the volume overload, managing the edema, and local wound care. |
Introduction
Edema or lower extremity swelling is a common clinical complaint of both hospitalized and ambulatory patients. The differential diagnosis for lower extremity swelling is quite extensive. Despite the clinical frequency of the complaint, few clinical series address the etiology, evaluation, or diagnostic approach to lower extremity swelling. Clinically, edema and lymphedema are often mistakenly used interchangeably to refer to soft tissue fluid accumulation. However, these conditions are very different with respect to their pathophysiology and clinical implications.
All swelling results from an increase in interstitial or tissue fluid, which is mostly water. The transcapillary tissue fluid may be predominantly water (edema), the result of abnormal intravascular hydrostatic pressure or oncotic pressure, or may be due to the failure of the lymphatics to clear residual tissue fluid and proteinaceous material from the tissue space (lymphedema). Venous return is responsible for approximately 80% of tissue fluid drainage and transportation from the interstitial space. The lymphatic system accommodates the return of protein, cellular debris, and the remaining 20% of interstitial fluid. Therefore, lymphedema has a distinct pathophysiology resulting in regional increases in protein-rich fluid due to either decreased uptake or transport of tissue fluid. This will be discussed in more detail at the end of the chapter.
Pathophysiology
Intravascular and extravascular fluid homeostasis requires stable capillary filtration supported by normal venous and lymphatic return to the systemic circulation. If the capillary fluid filtration rate exceeds the tissue drainage or transportation rate, fluid will accumulate within the extravascular space. Capillary filtration depends upon a normal, intact vascular endothelium and adequate serum oncotic pressure or protein/albumin content as well as equal ion distribution between the intravascular and extravascular compartments. In the most basic terms, if capillary filtration is adequately offset by vascular reabsorption, normal tissue fluid balance is maintained.
Maintaining endothelial integrity is the initial step in controlling edema. Vascular integrity is tightly regulated. As part of normal fluid homeostasis approximately 30% of post-capillary venule endothelial junctions are open and permeable. When regulation is disrupted, increased permeability may result in edema. This mechanism typically underlies the edema associated with inflammation, infection, trauma, or medications. Most stimuli that affect vascular integrity are reversible and do not cause permanent endothelial impairment.
Even when there is no disruption in vascular permeability, edema may be caused by increased capillary filtration with the shift of intravascular fluid from the vessels into the extravascular space. This is usually due to physiological changes in oncotic pressure, changes in hydrostatic pressure, or changes in intravascular fluid volume (Table 84-1). In this case, normal homeostasis and fluid balance between the intravascular and extravascular space is determined by pressure and oncotic gradients.
Capillary filtration
Changes in venous pressure
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Intravascular oncotic pressure is influenced by protein and albumin content. If oncotic pressure within the vessels is decreased by nutritional depletion of albumin or protein, decreased synthesis as in cirrhosis, or by a loss of protein through the kidneys or the gastrointestinal tract, water will move from the vessels into the interstitium to maintain a constant oncotic pressure between the intravascular and extravascular compartments. Similarly, if the intravascular oncotic pressure is decreased due to intravascular fluid or volume accumulation this will also promote fluid shifts into the tissues and cause edema.
The calf muscle pump is required to propel the column of venous blood back to the heart against a high pressure gradient along with competent venous valves to maintain normal venous return. Anything that disrupts or impairs the calf muscle pump may be associated with edema. Immobility, an impaired or shuffling gait frequently seen in the elderly or those with neurologic disorders, and paresis are common conditions that cause loss of the calf muscle pump. |
A second important pressure gradient (hydrostatic pressure) occurs within the venous system. There is a static pressure within the veins that depends on the height of the column of blood. Any condition that raises the resting right heart pressures or intravenous pressure may cause edema (Table 84-1). Normal systemic venous return relies upon a normal cardiac pump, an intact calf muscle pump, intact venous valves to support antegrade venous return, and a pressure gradient between the ankle and the right heart. Chronic venous hypertension may result when any of these primary components are abnormal.
Venous valvular insufficiency due to loss of valve integrity or damage will frequently result in increased venous pressures, so-called venous hypertension. The loss of valve integrity may be primary, related to varicose veins and valve degeneration, or secondary, from trauma or injury to the valves usually associated with venous thrombosis. Regardless, loss of valve integrity may result in increased venous pressure due to the static column of blood within the vein and secondary increased capillary filtration along the pressure gradient.
The importance of the calf muscle pump, in conjunction with competent venous valves, must not be overlooked for normal venous return. Venous pressure at the ankle may be as high as 100 mm Hg in the standing position. The calf muscle pump is required to propel the column of venous blood back to the heart against this pressure gradient. Anything that disrupts or impairs the calf muscle pump may be associated with edema. Immobility, an impaired or shuffling gait frequently seen in the elderly or those with neurologic disorders, and paresis are common conditions that cause loss of the calf muscle pump.
A common cause of edema in hospitalized patients is an increase in plasma volume. Increased plasma volume caused by sodium and water retention results in secondary changes in both intravascular pressure as well as lowered oncotic forces. Plasma volume is maintained through intact renal excretion of ions followed by passive water excretion. Heart failure, renal disease, liver disease, medications, pregnancy, or any other condition that augments the neurohormonal reabsorption of sodium and water through activation of vasopressin or the renin-angiotensin-aldosterone system may result in secondary edema due to sodium and water retention. In reality, most edema is multifactorial and many variables and pathophysiologic mechanisms may be contributing. Clinical clues and historical elements may help focus your evaluation of the patient. A thorough evaluation of edema should focus on evaluating for underlying cardiopulmonary, kidney disease, liver disease, contributing medications, and venous disorders.
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The approach to lower extremity edema of an unclear etiology should focus on the most common clinical contributors. Testing should be used to evaluate the clinical conditions with the most significant impact. Edema is frequently considered cosmetic, but the underlying clinical contributors may indeed be life threatening. The most important clinical questions that may help evaluate edema are the following:
Is the swelling unilateral or bilateral?
What is the age of the patient?
Are there associated clinical symptoms of pain, erythema, fever, or systemic illness?
What are the onset, duration, and progression of the symptoms?
Are there associated clinical examination findings?
What exacerbates or relieves the edema?
Is there known coexisting medical illness, predisposing factors, or medications known to cause edema?
Evaluation
The differential diagnosis of unilateral edema can be extensive (Table 84-2
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