9/4/2016

Peripheraloedema(Assessmentof)DiagnosisApproachBestPracticeespaol

Assessment
of peripheral
oedema
Step-by-step
diagnostic
approach

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Peripheral oedema is
a physical
examination nding.
As such, the only
diagnostic test to
ltima actualizacin: Oct 19, 2015
establish the presence of oedema is examination and palpation of
the extremities. Diagnosing the underlying cause of the oedema is the goal of the investigative
evaluation.

History
Elements of the history will help to guide the evaluation. Patients report swelling and a tense
sensation in the extremities, usually worse the longer the extremity remains dependent. They may
describe feeling as though clothing or jewellery no longer t, or may indicate changes in total weight.
If uid retention is systemic, body weight may increase by as much as 10% before pitting oedema is
evident. [1] The speed at which the peripheral oedema developed will determine whether it is acute
or chronic. Abrupt-onset oedema is more likely to represent an important systemic disease and
requires more urgent evaluation. Recent history is important, especially a history of trauma, surgery,
or prolonged immobility, which would increase the likelihood of venous thrombosis. Close temporal
association of the onset of edema with the initiation of medications such as non-steroidal antiinammatory drugs, calcium-channel blockers, thiazolidinediones, corticosteroids, gabapentin,
pregabalin, or oral contraceptives containing oestrogen would support a medicine-induced
aetiology. [20] In addition, a cyclic pattern of oedema may indicate premenstrual oedema. In taking
the history, it is important to elicit associated symptoms of systemic cardiac, pulmonary, hepatic,
renal, or endocrinological disease to guide further testing. Examples of characteristic symptoms
include SOB and/or chest pain from cardiopulmonary disease, changes in urine output from renal
aetiologies, or abdominal discomfort and bloating from hepatic congestion/ascites. Presence of
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Peripheraloedema(Assessmentof)DiagnosisApproachBestPracticeespaol

back pain or weight loss can indicate possible presence of pelvic malignancy causing lower extremity
venous congestion. Changes in sodium intake may also be important in explaining increases in
oedema. However, in the absence of a systemic disorder, changes in dietary salt or water intake
alone do not typically cause oedema, as the healthy kidney has the ability to preserve salt and water
balance. [21]

Physical examination
Comprehensive physical examination is crucial, with focus on the cardiac and pulmonary systems.
The degree of oedema is commonly described on a subjective 0 to 4+ scale in order of increasing
severity. [1] Absence of clinical oedema scores 0, slight pitting (2 mm) scores 1, deeper pitting (4 mm)
scores 2, deep pitting (6 mm) with visible dependent swelling scores 3, and very deep pitting (8 mm)
along with gross distortion of leg contour from swelling scores 4. [22] Describing the level that
oedema extends to proximally on the limbs is also useful in communicating severity of peripheral
oedema. However, these descriptions are inexact and may uctuate depending on the patient's
positioning. Ankle circumference is a simple quantitative test for clinical practice with good interrater reliability. [22] Asymmetry of oedema, tenderness, skin discoloration, elevated jugular venous
pressure, and pulmonary rales may be clues to aetiology. [1] A key discriminating factor in narrowing
aetiologies is whether the oedema is limited to a single extremity or is generalised. Unilateral
oedema, palpable cords, or lymphadenopathy suggests a proximal obstruction of venous ow or
lymphatic drainage. Presence of brosis, ulcers, or skin changes (such as haemosiderin staining and
venous stasis dermatitis) suggests a chronic process. Varicose veins imply venous insuciency.
Examination should focus on evidence of systemic disease of the cardiac, pulmonary, hepatic, or
renal systems. Increased jugular venous pressure is generally a sign of heart failure or systemic
volume overload from severe renal failure.

Diagnostic testing
The underlying aetiology of oedema can be suggested by basic screening tests. [3] [21] Serum
chemistry, hepatic function panel, serum protein, albumin, and urinalysis are indicated. TSH levels,
ECG, and a CXR may be useful when some features of history or physical examination suggest
endocrine or cardiopulmonary disease. Extensive and expensive diagnostic testing for peripheral
oedema is rarely necessary.

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Approach to the patient with peripheral oedemaCreated by Ethan Cumbler, MD

Asymmetrical oedema
For patients with asymmetrical peripheral oedema and no apparent cause (such as radiation or
surgical lymph node dissection), testing should focus on proximal venous or lymphatic obstruction. A
Doppler venous ultrasound can identify venous insuciency, venous thrombosis, or focal venous
compression (e.g., May-Thurner syndrome: compression of the left common iliac vein by the
overlying right common iliac artery). Pelvic ultrasound may also reveal presence of a mass causing
preferential compression of venous ow from one lower extremity.

Bilateral oedema
For patients with diffuse or bilateral oedema, the diagnostic focus is on determining which organ
system is in dysfunction. The rst screening tests are to identify possible reduction in serum oncotic
pressure from severe hypoproteinaemia. Serum protein and albumin can screen for the aetiologies
that cause hypoproteinaemia, such as nephrotic syndrome, protein-losing enteropathies, or
profound malnutrition. Low protein is also a feature of cirrhosis. If low serum albumin is detected,
urinalysis, serum creatinine, and LFTs are ordered to determine if the cause is renal protein wasting,
while the LFTs assess hepatic synthetic dysfunction. Normal urine and hepatic testing suggests
malnutrition or protein-losing enteropathy as the cause of hypoproteinaemia. The history should
distinguish between these 2 clinical entities.
If severe hypoproteinaemia is not present, screening serum chemistries should be ordered to
evaluate for uid retention from renal failure. A hepatic panel evaluates for evidence of cirrhosis,
which causes lower-extremity oedema via a multi-factor process. TSH hormone levels may be
indicated as part of an initial screen, especially if other features of the history and physical
examination suggest hypothyroidism. ECG and CXR are advisable to evaluate for evidence of cardiac
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congestion, especially when the physical examination demonstrates elevated jugular venous
pressure or abnormal cardiopulmonary examination ndings. If cardiopulmonary symptoms are
present, physical examination frequently reveals murmurs, rales, or increased jugular venous
distension. If abnormalities are found on ECG and CXR, then echo is indicated. Echo can establish
right or left heart dysfunction as a cause of congestive features or can suggest pulmonary
hypertension as a result of pulmonary disease or sleep-disordered breathing. Follow-up testing can
then evaluate the underlying reason for the cardiac or pulmonary dysfunction.
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