Approach to Oedema and Generalised Swelling
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Direct answer
Oedema is excess interstitial fluid producing visible swelling, and its cause is found by asking which Starling force has failed. Cardiac failure, nephrotic syndrome and cirrhosis account for most generalised oedema, and each has a distinctive pattern, plasma protein and biochemical clue. Serum albumin, urine protein and natriuretic peptide levels separate the common causes quickly.
What you must remember
- Cardiac oedema: dependent swelling that worsens through the day, raised jugular venous pressure, raised natriuretic peptide and usually normal albumin.
- Renal oedema: periorbital swelling on waking, proteinuria above 3.5 g per day, serum albumin below 30 g/L and hyperlipidaemia in nephrotic syndrome.
- Hepatic oedema: ascites with a serum-ascites albumin gradient of 1.1 g/dL or above, low albumin and raised INR from synthetic failure.
- Nutritional oedema: low albumin from protein-energy malnutrition, classically seen in kwashiorkor, and treated with cautious refeeding.
- Lymphatic oedema: brawny swelling of the legs in lymphatic filariasis, pitting early but non-pitting when chronic, progressing to elephantiasis in chronic disease.
- Drug oedema: dihydropyridine calcium channel blockers cause ankle oedema by dilating precapillary arterioles, while NSAIDs and corticosteroids cause sodium retention.
- Non-pitting myxoedema: puffy, non-pitting swelling with raised TSH and low free thyroxine.
Reading the common causes side by side
A 60-year-old woman presents with ankle swelling for a month, and the first task is to identify which Starling force has failed. The comparison below covers the three commonest causes of generalised oedema.
| Clue | Cardiac failure | Nephrotic syndrome | Cirrhosis |
|---|---|---|---|
| Distribution | Dependent, worse by evening | Periorbital on waking, then generalised | Ascites first, legs later |
| Typical cause | Ischaemic or valvular heart disease | Minimal change or membranous disease | Alcohol or viral hepatitis |
| Jugular venous pressure | Raised | Normal | Normal |
| Serum albumin | Usually normal | Below 30 g/L | Low |
| Urine protein | Negligible | Above 3.5 g per day | Negligible |
| Key sign | Crackles and an S3 gallop | Frothy urine and lipiduria | Spider naevi and jaundice |
| Ascites | Uncommon | Uncommon | Prominent |
| Confirmatory test | Echocardiography | Quantified urine protein | Ascitic fluid analysis |
Albumin and urine protein separate the renal and hepatic causes, while venous pressure and echocardiography point to the heart. The ascitic fluid gradient is the key discriminator in the liver group, because a value of 1.1 g/dL or above confirms portal hypertension as the mechanism of fluid leak.
Where the exam tries to catch you
Most wrong answers attribute every swollen ankle to the heart.
- Trap: blaming heart failure for all pedal oedema Correct: amlodipine and other dihydropyridines cause ankle oedema with normal venous pressure, so drug history comes first.
- Trap: calling non-pitting, brawny swelling simple oedema Correct: non-pitting swelling suggests lymphatic obstruction from filariasis, and myxoedema is also non-pitting.
- Trap: assuming a low albumin always means nephrotic syndrome Correct: liver synthetic failure and malnutrition also lower albumin, so urine protein is measured before naming the cause.
Frequently asked questions
How is cardiac oedema distinguished from nephrotic oedema?
Cardiac oedema is accompanied by raised jugular venous pressure and a raised natriuretic peptide, with albumin usually normal. Nephrotic oedema shows periorbital swelling, proteinuria above 3.5 g per day and serum albumin below 30 g/L. Quantifying urine protein is usually the most decisive single test.
What does a serum-ascites albumin gradient tell you about ascites?
A serum-ascites albumin gradient of 1.1 g/dL or above suggests portal hypertension, as in cirrhosis or cardiac ascites. A lower gradient points to peritoneal causes such as tuberculous peritonitis or peritoneal carcinomatosis. The gradient is calculated from paired serum and ascitic fluid albumin values.
Why is lymphatic filariasis oedema described as non-pitting?
Lymphatic oedema is non-pitting because chronic lymphatic obstruction causes fibrosis and protein-rich fluid that does not indent easily. Lymphatic filariasis typically produces brawny swelling of the legs or arms, progressing to elephantiasis in advanced disease. Pressing the skin does not leave a lasting dent.
Which drugs commonly cause peripheral oedema?
Dihydropyridine calcium channel blockers such as amlodipine commonly cause ankle oedema by dilating precapillary arterioles. NSAIDs and corticosteroids cause sodium and water retention, and thiazolidinediones such as pioglitazone also cause fluid retention. Drug causes should be considered before cardiac or renal disease is assumed.