Peripheral Oedema

oPatientPlus articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use, so you may find the language more technical than the condition leaflets.

Peripheral oedema results from soft-tissue swelling due to the accumulation of interstitial fluid. Interstitial fluid consists of the extracellular fluid excluding plasma, and includes lymph, cerebrospinal fluid (CSF), eye, synovial fluid, serous fluid, and secretions of the gastrointestinal tract. A 70 kg adult male has 12 litres of interstitial fluid (30% of total body water), and it is generally considered a 15% increase in body weight (2 litres of fluid) is required for clinical oedema.

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  • Pitting dependent oedema (ankle if mobile, sacral when bed-bound):
    • Immobility:
      • Increased fluid pressure from venous stasis.
    • Varicose veins.
    • Obesity:
      • Increased fluid pressure from sodium and water retention; should not to be confused with non-pitting lymphoedema.
    • Cardiac:
      • Increased fluid pressure: right heart failure, constrictive pericarditis.
    • Drugs:
    • Hepatic:
      • Decreased oncotic pressure: cirrhosis causing hypoalbuminaemia.
    • Renal:
    • Gastrointestinal:
    • Pregnancy:
      • Increased fluid pressure both from sodium and water retention and venous stasis from pelvic obstruction.
    • High-altitude illness:
      • Oedema of face, hands and ankles may occur.
    • Idiopathic oedema:
      • Associated with cyclical high lymph volume overload, or dynamic insufficiency: usually in a woman aged 20-40 years.
      • Variable and not related to menstrual periods.
      • Diagnosis is based on the exclusion of other causes of oedema.
    • Post-thrombotic syndrome:
      • Late complication of deep vein thrombosis (DVT) which occurs in up to two-thirds of patients.
      • May present with pain, oedema, hyperpigmentation, and even skin ulceration.
      • May result from remaining venous obstructions, from reflux, or both.
      • Rate of reflux is highest during the 6-12 months after an acute DVT.
      • It may be temporary and self-limiting or not resolve and persist at variable severity.
  • Pitting localised limb oedema:
    • DVT.
    • Compression of large veins by tumour or lymph nodes.
    • Following hip replacement or knee replacement.
    • Local infection, trauma (including burns, which may also cause generalised oedema because of protein loss), animal bites or stings.
  • Non-pitting lower limb oedema:
    • Hypothyroidism (mucopolysaccharide deposition).
    • Lymphoedema:
      • Blocked lymph channels: surgical damage, radiation, malignant infiltration, infectious (eg filariasis), congenital (eg Milroy's disease).
    • Allergy:
  • Duration: swelling due to venous insufficiency is usually a long-standing problem.
  • Distribution of oedema:
    • Dependent oedema in an otherwise well patient suggests a benign cause such as immobility or varicose veins.
    • Pulmonary and ankle oedema are typical of cardiac failure.
    • Hands and face, which is most marked after lying down, occurs in hypoproteinaemia.
    • Ascites in liver failure, nephrotic syndrome, protein malnutrition.
    • Unilateral swelling, particularly of the calf, suggests a deep venous thrombosis.
    • Oedema in angio-oedema is mainly restricted to the face and lips, although any part of the body may be affected.
    • Hydroceles: fluid often accumulates in the scrotal sac, eg in nephrotic syndrome.
  • Associated symptoms: breathlessness of recent onset may be due to cardiac failure, anaemia, lung cancer or pleural effusions (eg from nephrotic syndrome).
  • Past history: ischaemic heart disease, chronic lung disease, DVT (past history could lead to venous insufficiency).
  • Examination is directed towards assessment of the cause of oedema and therefore a full assessment including the cardiovascular system and abdomen is required.
  • Unilateral ankle oedema should raise suspicion of a DVT but oedema may be bilateral in inferior vein obstruction and, in cases of bilateral oedema, one side may be more affected and therefore more obvious than the other.
  • Pitting dependent oedema will become sacral if bed-bound.
  • Urine testing: (a combination of profuse proteinuria and oedema, with hypoalbuminuria confirmed on blood testing is pathognomonic of nephrotic syndrome).
  • Haemoglobin (anaemia may be a cause or aggravating factor of heart failure).
  • Renal function and electrolytes (renal failure).
  • LFTs (liver failure; may show hypoproteinaemia in cirrhosis, nephrotic syndrome, protein-losing enteropathy).
  • Thyroid function tests (for hypothyroidism).
  • Abdominal ultrasound: will reveal, for example, pelvic tumour, ascites, liver metastases.
  • CXR: if heart failure or lung malignancy is suspected.
  • ECG: if heart failure is suspected.
  • Duplex Doppler scan.
  • Lymphoscintigraphy.[2]
  • Treatment is based on the cause.
  • Empirical treatment with diuretics is inappropriate in the absence of a clear diagnosis.


Further reading & references

  1. Lee P, Kinsella J, Borkman M, et al; Bilateral pleural effusions, ascites, and facial and peripheral oedema in a Diabet Med. 2007 Nov;24(11):1282-5.
  2. Brautigam P, Foldi E, Schaiper I, et al; Analysis of lymphatic drainage in various forms of leg edema using two compartment lymphoscintigraphy. Lymphology. 1998 Jun;31(2):43-55.

Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. EMIS has used all reasonable care in compiling the information but make no warranty as to its accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions.

Original Author:
Dr Colin Tidy
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Document ID:
1350 (v22)
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