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Peripheral oedema

Starling’s principles:

Distribution of ECF depends on:

Venous tone (which determines the capacitance of the blood compartment and thus hydrostatic pressure)
Capillary permeability
Oncotic pressure (mainly dependent on serum albumin)
Lymphatic drainage

Depending on these factors, fluid accumulation may result in expansion of interstitial volume, blood volume or both

Clinical features:

Peripheral oedema is caused by expansion of the ECF volume by at least 2L (15%)

Ankles are normally the first to be affected
Oedema may be noticed in the face (particularly in the morning)
In bed-bound patients, oedema may accumulate in the sacral area
Expansion of the interstitial volume also causes:

Pulmonary oedema
Pleural effusion
Pericardial effusion
Ascites

Expansion of the blood volume causes:

A raised JVP
Cardiomegaly
Added heart sounds
Raised arterial BP

Causes:

Heart failure
Hypoalbuminaemia
Hepatic cirrhosis (owing largely to peripheral vasodilatation)
Sodium retention

Treatment:

Treat the underlying cause where possible
The mainstay of therapy is diuretics

Loop diuretics:

E.g. Frusemide
Potent
Stimulate excretion of both NaCl and water
Also increase venous capacitance (resulting in rapid clinical improvement in patients with LVF)

Side-effects include:

Hyperuricaemia (resulting in gout)
Hypokalaemia
Hypomagnesaemia
Decreased glucose tolerance
Ototoxicity (due to an action on sodium pump activity in the inner ear)

Thiazide diuretics:

E.g. bendrofluazide
Less potent than loop diuretics
Reduce peripheral vascular resistance by an unknown mechanism
Reduce calcium excretion
Cause relatively more hyperuricaemia, glucose intolerance and hypokalaemia than loop diuretics

Potassium-sparing diuretics:

Relatively weak diuretics
Most commonly used in combination with loop or thiazide diuretics to prevent hypokalaemia
Two types:

Spironolactone (aldosterone antagonist, therefore reduces Na⁺ absorption
Amiloride (inhibits sodium uptake in the collecting duct and reduces renal potassium excretion)


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	Peripheral oedema Starling’s principles: Distribution of ECF depends on: Venous tone (which determines the capacitance of the blood compartment and thus hydrostatic pressure) Capillary permeability Oncotic pressure (mainly dependent on serum albumin) Lymphatic drainage Depending on these factors, fluid accumulation may result in expansion of interstitial volume, blood volume or both Clinical features: Peripheral oedema is caused by expansion of the ECF volume by at least 2L (15%) Ankles are normally the first to be affected Oedema may be noticed in the face (particularly in the morning) In bed-bound patients, oedema may accumulate in the sacral area Expansion of the interstitial volume also causes: Pulmonary oedema Pleural effusion Pericardial effusion Ascites Expansion of the blood volume causes: A raised JVP Cardiomegaly Added heart sounds Raised arterial BP Causes: Heart failure Hypoalbuminaemia Hepatic cirrhosis (owing largely to peripheral vasodilatation) Sodium retention Treatment: Treat the underlying cause where possible The mainstay of therapy is diuretics Loop diuretics: E.g. Frusemide Potent Stimulate excretion of both NaCl and water Also increase venous capacitance (resulting in rapid clinical improvement in patients with LVF) Side-effects include: Hyperuricaemia (resulting in gout) Hypokalaemia Hypomagnesaemia Decreased glucose tolerance Ototoxicity (due to an action on sodium pump activity in the inner ear) Thiazide diuretics: E.g. bendrofluazide Less potent than loop diuretics Reduce peripheral vascular resistance by an unknown mechanism Reduce calcium excretion Cause relatively more hyperuricaemia, glucose intolerance and hypokalaemia than loop diuretics Potassium-sparing diuretics: Relatively weak diuretics Most commonly used in combination with loop or thiazide diuretics to prevent hypokalaemia Two types: Spironolactone (aldosterone antagonist, therefore reduces Na⁺ absorption Amiloride (inhibits sodium uptake in the collecting duct and reduces renal potassium excretion)
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