What are the possible causes of lower‑leg edema?

Causes of Lower Leg Edema

Lower leg edema results from five primary mechanisms: venous insufficiency, lymphatic obstruction, systemic volume overload (cardiac/renal/hepatic disease), decreased oncotic pressure, and increased capillary permeability—with the distribution pattern (bilateral vs. unilateral) being the most critical distinguishing feature. 1

Systemic Causes (Typically Bilateral)

Cardiac Disease

• Heart failure is the most common systemic cause, producing bilateral pitting edema through increased central venous hypertension, increased capillary permeability, and plasma volume expansion 1, 2
• Both biventricular failure and heart failure with preserved ejection fraction can cause edema 1
• Associated symptoms include dyspnea, orthopnea, paroxysmal nocturnal dyspnea, jugular venous distention, S3 gallop, and pulmonary rales—though absence of rales does not exclude heart failure 1, 3
• BNP/NT-proBNP testing helps confirm or exclude heart failure 1, 2

Renal Disease

• Kidney disorders cause edema through increased protein loss (decreased plasma oncotic pressure) and sodium/water retention 1, 2
• Check serum albumin and urinalysis with protein quantification 1

Hepatic Disease

• Liver cirrhosis decreases protein synthesis, leading to decreased plasma oncotic pressure and increased systemic venous hypertension 1, 2

Medication-Induced Edema

• Calcium channel blockers (especially dihydropyridines) are a common cause of bilateral ankle edema 1, 2
• Other culprits include NSAIDs, hormones, vasodilators, and thiazolidinediones 2
• Thiazolidinediones can precipitate heart failure and require cardiac screening before initiation 3

Other Systemic Causes

• Obstructive sleep apnea can cause bilateral leg edema even without pulmonary hypertension 3, 4
• Hypoproteinemia from any cause reduces oncotic pressure 5
• Idiopathic cyclic edema 5

Localized Causes (Typically Unilateral or Asymmetric)

Chronic Venous Insufficiency

• Most common localized cause in older patients, characterized by peripheral edema with hyperpigmentation, lipodermatosclerosis, and skin changes 1, 2
• Results from primary valvular incompetence, prior deep venous thrombosis, or extrinsic venous obstruction 6
• Edema typically worsens with prolonged standing and improves with elevation 1
• Affects 25% of adults (C2-C3 disease) and 5% have advanced disease (C4-C6) 6
• Duplex ultrasound shows venous reflux >500 ms 3

Deep Vein Thrombosis (DVT)

• Causes acute unilateral edema that may become chronic (post-thrombotic syndrome) 1, 2
• Must be excluded first even in bilateral presentations before attributing edema to benign causes 1
• Use Wells score for pretest probability; if <2, high-sensitivity D-dimer can exclude DVT 1
• If Wells score ≥2, perform complete duplex ultrasound 1

Lymphedema

• Characterized by brawny, nonpitting edema 4
• Can be primary or secondary to tumor, trauma, pelvic surgery, inguinal lymphadenectomy, or radiation therapy 4
• May present unilaterally or bilaterally 2

Cellulitis/Erysipelas

• Rapidly spreading areas of edema, redness, and heat with possible lymphangitis 6
• Predisposing factors include obesity, previous cutaneous damage, edema from venous insufficiency, lymphatic obstruction, and disrupted skin barriers 6
• Most commonly affects lower legs 6
• Streptococci (groups A, B, C, or G) are the most common pathogens, often originating from macerated interdigital toe spaces 6

Immobility-Related Edema

• Venous stasis from immobility itself (not anatomical problems) can cause edema in patients with severe gait disturbance 7
• Gravity significantly influences severity 7

Nonthrombotic Iliac Vein Lesions (NIVL)

• Can cause significant edema extending to the thigh 3
• May require iliac vein stent placement 3

Key Distinguishing Features

Distribution Pattern

• Bilateral symmetric edema → systemic causes (cardiac, renal, hepatic, medications) 1, 2
• Unilateral or asymmetric edema → localized pathology (DVT, venous insufficiency, lymphedema, compression) 1, 2

Timing

• Worsening in evening → venous insufficiency 1, 2
• Worsening in morning → other causes 1, 2

Skin Changes

• Hyperpigmentation, lipodermatosclerosis, or ulceration → chronic venous insufficiency 1
• Peau d'orange appearance → cellulitis/erysipelas 6
• Brawny, nonpitting skin → lymphedema 4

Essential Diagnostic Evaluation

Physical Examination

• Assess for pitting vs. non-pitting edema 1, 2
• Check jugular venous distention, pulmonary rales, S3 gallop, hepatojugular reflux 1, 2
• Palpate all pulses (dorsalis pedis, posterior tibial, femoral, popliteal) 1, 3
• Inspect feet for color, temperature, skin integrity, ulcerations, hair loss, trophic changes 1, 3
• Look for signs of liver or renal disease 1

Laboratory Testing

• BNP/NT-proBNP for heart failure evaluation 1, 2
• Complete metabolic panel including creatinine and electrolytes 1
• Serum albumin and urinalysis with protein quantification 1
• Liver function tests 2

Vascular Assessment

• Ankle-brachial index (ABI) to evaluate for peripheral arterial disease—mandatory before compression therapy 3, 2
• Duplex ultrasound for venous insufficiency or DVT 3, 2

Critical Pitfalls to Avoid

• Never attribute bilateral edema to venous disease alone—bilateral venous insufficiency is uncommon; investigate systemic causes first 1
• Never use compression therapy without checking ABI first in patients with PAD risk factors (age >50 with atherosclerosis risk factors, age >70, smoking, diabetes) 3
• Do not exclude DVT based on bilateral presentation—always calculate Wells score and proceed accordingly 1
• Do not assume absence of pulmonary rales rules out heart failure 3
• Review medication list thoroughly, as drug-induced edema is frequently overlooked 2