Some Causes of Edema

Cause	Suggestive Findings	Diagnostic Approach*
Increased hydrostatic pressure, fluid overload
Right heart failure (primary or secondary to left-sided disease or to constrictive pericarditis or pericardial effusion) directly increasing venous pressure	Symmetric, dependent, painless, pitting edema; often with left-sided heart failure, with dyspnea during exertion, orthopnea, and paroxysmal nocturnal dyspnea Commonly, lung crackles, S3 or S4 gallop or both (due to left heart failure); jugular venous distention, hepatojugular reflux, and Kussmaul sign With constrictive pericarditis or pericardial effusion, in addition to jugular venous distention, hepatojugular reflux, and Kussmaul sign, may note distant or weak heart sounds.	Chest radiography and ECG Usually echocardiography
Pregnancy and premenstrual state	Symmetric, dependent, painless, usually mild pitting edema Apparent by history	Clinical evaluation
	Symmetric, dependent, painless, usually mild pitting edema	Clinical evaluation
Iatrogenic (eg, excessive intravenous fluids)	Symmetric, dependent, painless, usually mild pitting edema Apparent by history and medical record	Clinical evaluation
Increased hydrostatic pressure, venous obstruction
DVT	Acute, pitting edema in a single, usually lower extremity, usually with pain; sometimes Homans sign (pain in the calf when the foot is dorsiflexed) Redness, warmth, and tenderness; possibly less marked than in soft-tissue infection Sometimes a predisposing factor (eg, recent surgery, trauma, immobilization, hormone replacement, cancer)	Ultrasound D-dimer testing
Chronic venous insufficiency	Chronic edema in one or both lower extremities, with brownish discoloration, discomfort but not marked pain, and sometimes skin ulcers Often associated with varicose veins	Clinical evaluation
Extrinsic venous compression (eg, by tumor, a gravid uterus, or marked abdominal obesity)	Nonpainful, slowly developing edema If tumor compresses the superior vena cava, usually facial plethora, distended neck veins, and absent venous pulse waves above the obstruction	Clinical evaluation Ultrasound or CT if tumor is suspected
Prolonged absence of skeletal muscle pumping activity on extremity veins	Prolonged immobility (eg, being bedbound or on a long airline flight) Painless, symmetric, dependent edema	Clinical evaluation
Decreased plasma oncotic pressure†
Nephrotic syndrome	Diffuse edema, often significant ascites, and sometimes periorbital edema	24-hour urine collection to check for protein loss Serum albumin level
Protein-losing enteropathy	Significant diarrhea	Testing for cause Sometimes endoscopy Sometimes serum and 24-hour stool testing for alpha-1-antitrypsin
Reduced albumin synthesis (eg, in liver disorders or undernutrition)	Often with significant ascites Causes often apparent by history If cause is a chronic liver disorder, often jaundice, spider angiomas, gynecomastia, palmar erythema, and testicular atrophy	Serum albumin, liver tests, PT/PTT
Increased capillary permeability
Angioedema (allergic, idiopathic, hereditary)	Sudden, focal, asymmetric, nondependent subcutaneous or submucosal edema, more often involving the face, lips, oral mucosa, extremities, or genitals	Clinical evaluation
Injury (eg, burns, chemicals, toxins, blunt trauma)	Focal edema, sometimes erythematous; causes apparent by history	Clinical evaluation
Severe sepsis (causing vascular endothelial leakage)	Obvious sepsis syndrome with fever, tachycardia, focal infection Painless, symmetrical edema	Cultures Imaging studies as needed
Soft-tissue infection (eg, cellulitis, necrotizing myofasciitis)	If due to cellulitis, usually redder (or darker on dark skin) and more painful and tender than that due to angioedema and more circumscribed than that due to DVT With necrotizing infections, severe pain, constitutional symptoms	Clinical evaluation Cultures Sometimes ultrasound to rule out DVT
Lymphatic obstruction
Iatrogenic (eg, after lymph node dissection in cancer surgery or after radiation therapy)	Etiology usually apparent by history Initially pitting edema, with fibrosis developing later	Clinical evaluation
Congenital (rare)	Often onset in childhood, but for some types, only later onset May be familial	Sometimes lymphoscintigraphy
Lymphatic filariasis	History of being in an endemic area Usually focal edema, sometimes involving the genitals	Microscopic examination of blood smear
* Most patients with generalized edema require complete blood count (CBC), electrolytes, blood urea nitrogen (BUN), creatinine, liver tests, serum protein measurement, and urinalysis (to check for proteinuria).
† Decreased plasma oncotic pressure often triggers secondary sodium and water retention, leading to fluid overload.
DVT = deep venous thrombosis; NSAIDs = nonsteroidal anti-inflammatory drugs; PT = prothrombin time; PTT = partial thromboplastin time; S3 = third heart sound; S4 = fourth heart sound.

Cause

Suggestive Findings

Diagnostic Approach*

Increased hydrostatic pressure, fluid overload

Right heart failure (primary or secondary to left-sided disease or to constrictive pericarditis or pericardial effusion) directly increasing venous pressure

Symmetric, dependent, painless, pitting edema; often with left-sided heart failure, with dyspnea during exertion, orthopnea, and paroxysmal nocturnal dyspnea

Commonly, lung crackles, S3 or S4 gallop or both (due to left heart failure); jugular venous distention, hepatojugular reflux, and Kussmaul sign

With constrictive pericarditis or pericardial effusion, in addition to jugular venous distention, hepatojugular reflux, and Kussmaul sign, may note distant or weak heart sounds.

Chest radiography and ECG

Usually echocardiography

Pregnancy and premenstrual state

Symmetric, dependent, painless, usually mild pitting edema

Apparent by history

Clinical evaluation

Symmetric, dependent, painless, usually mild pitting edema

Clinical evaluation

Iatrogenic (eg, excessive intravenous fluids)

Symmetric, dependent, painless, usually mild pitting edema

Apparent by history and medical record

Clinical evaluation

Increased hydrostatic pressure, venous obstruction

DVT

Acute, pitting edema in a single, usually lower extremity, usually with pain; sometimes Homans sign (pain in the calf when the foot is dorsiflexed)

Redness, warmth, and tenderness; possibly less marked than in soft-tissue infection

Sometimes a predisposing factor (eg, recent surgery, trauma, immobilization, hormone replacement, cancer)

Ultrasound

D-dimer testing

Chronic venous insufficiency

Chronic edema in one or both lower extremities, with brownish discoloration, discomfort but not marked pain, and sometimes skin ulcers

Often associated with varicose veins

Clinical evaluation

Extrinsic venous compression (eg, by tumor, a gravid uterus, or marked abdominal obesity)

Nonpainful, slowly developing edema

If tumor compresses the superior vena cava, usually facial plethora, distended neck veins, and absent venous pulse waves above the obstruction

Clinical evaluation

Ultrasound or CT if tumor is suspected

Prolonged absence of skeletal muscle pumping activity on extremity veins

Prolonged immobility (eg, being bedbound or on a long airline flight)

Painless, symmetric, dependent edema

Clinical evaluation

Decreased plasma oncotic pressure†

Nephrotic syndrome

Diffuse edema, often significant ascites, and sometimes periorbital edema

24-hour urine collection to check for protein loss

Serum albumin level

Protein-losing enteropathy

Significant diarrhea

Testing for cause

Sometimes endoscopy

Sometimes serum and 24-hour stool testing for alpha-1-antitrypsin

Reduced albumin synthesis (eg, in liver disorders or undernutrition)

Often with significant ascites

Causes often apparent by history

If cause is a chronic liver disorder, often jaundice, spider angiomas, gynecomastia, palmar erythema, and testicular atrophy

Serum albumin, liver tests, PT/PTT

Increased capillary permeability

Angioedema (allergic, idiopathic, hereditary)

Sudden, focal, asymmetric, nondependent subcutaneous or submucosal edema, more often involving the face, lips, oral mucosa, extremities, or genitals

Clinical evaluation

Injury (eg, burns, chemicals, toxins, blunt trauma)

Focal edema, sometimes erythematous; causes apparent by history

Clinical evaluation

Severe sepsis (causing vascular endothelial leakage)

Obvious sepsis syndrome with fever, tachycardia, focal infection

Painless, symmetrical edema

Cultures

Imaging studies as needed

Soft-tissue infection (eg, cellulitis, necrotizing myofasciitis)

If due to cellulitis, usually redder (or darker on dark skin) and more painful and tender than that due to angioedema and more circumscribed than that due to DVT

With necrotizing infections, severe pain, constitutional symptoms

Clinical evaluation

Cultures

Sometimes ultrasound to rule out DVT

Lymphatic obstruction

Iatrogenic (eg, after lymph node dissection in cancer surgery or after radiation therapy)

Etiology usually apparent by history

Initially pitting edema, with fibrosis developing later

Clinical evaluation

Congenital (rare)

Often onset in childhood, but for some types, only later onset

May be familial

Sometimes lymphoscintigraphy

Lymphatic filariasis

History of being in an endemic area

Usually focal edema, sometimes involving the genitals

Microscopic examination of blood smear

* Most patients with generalized edema require complete blood count (CBC), electrolytes, blood urea nitrogen (BUN), creatinine, liver tests, serum protein measurement, and urinalysis (to check for proteinuria).

† Decreased plasma oncotic pressure often triggers secondary sodium and water retention, leading to fluid overload.

DVT = deep venous thrombosis; NSAIDs = nonsteroidal anti-inflammatory drugs; PT = prothrombin time; PTT = partial thromboplastin time; S3 = third heart sound; S4 = fourth heart sound.

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Edema