2. Definition
• Edema is defined as a palpable swelling produced
by expansion of the interstitial fluid volume
UpToDate
3. PATHOPHYSIOLOGY OF EDEMA
FORMATION
There are two basic steps involved in edema formation:
● An alteration in capillary hemodynamics that favors the
movement of fluid from the vascular space into the
interstitium
● The retention of dietary or intravenously administered
sodium and water by the kidneys
Uptodate
4.
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8. Clinical assessment
• Dependent areas, such as the ankles and lower legs,
are typically affected first but oedema can be
restricted to the sacrum in bed-bound patients
• Pitting oedema tends to accumulate in the ankles
during the day and improves overnight as the
interstitial fluid is reabsorbed
• Conversely, facial oedema on waking is common
Davidson’s
9. • Ascites is common and often an earlier feature in
children or young adults, and in liver disease
• Raised JVP and pulmonary oedema are common in
the context of increased total extracellular fluid such
as in cardiac and renal failure
• Features of intravascular volume depletion
(tachycardia, postural hypotension) may occur when
oedema is due to decreased oncotic pressure or
increased capillary permeability
Davidson’s
10. • If oedema is localised – for example, to one
ankle but not the other – then local inflammation,
venous thrombosis or lymphatic disease should
be suspected
• Non-pitting oedema is typically due to lymphatic
obstruction , hypothyroidism , systemic sclerosis
Davinson’s
11. Investigations
• S. creatinine and s. electrolytes
• liver function and serum albumin, and the urine tested
for protein
• Further imaging of the liver, heart or kidneys may be
indicated, based on history and clinical examination
• Where ascites or pleural effusions measurement of
protein, glucose and LDH, and microscopy for cells in
the aspirate will usually differentiate a transudate from
an exudate
Davidson’s
12. GENERAL PRINCIPLES OF THERAPY
• Treatment of edema consists of reversal of the
underlying disorder, dietary sodium restriction (
restriction of sodium intake to 100 mmol/24 hrs)
• Restriction of water intake to 1.0–1.5 L/24 hrs is rarely
needed unless the plasma sodium falls below 125
mmol/L. In most patients, diuretic therapy
• Mild oedema usually responds to elevation of the legs,
compression stockings, or a thiazide or a low dose of
a loop diuretic
Davidson’s
13. • In nephrotic syndrome, renal failure and severe
cardiac failure, very large doses of diuretics,
sometimes in combination, may be required
• Diuretics are not helpful in the treatment of oedema
caused by increased capillary permeability or by
venous or lymphatic obstruction
Davidson’s
14. • During management of ascites, the patient should be
weighed regularly. Diuretics should be titrated to
remove no more than 1 L of fluid (or 1 kg body weight)
daily to avoid excessive fluid depletion
Davidson’s
15. USE OF DIURETICS
• Diuretic therapy in generalized edematous states is
generally begun with a loop diuretic, such as
furosemide (40–160 mg/day).In addition to monitoring
the degree of diuresis, hypokalemia, metabolic
alkalosis and hyponatremia
• For patients with cirrhosis, spironolactone (100–400
mg/day) and a loop diuretic is the preferred initial
regimen
• For patients with nephrotic syndrome, higher-than-
usual doses of a loop diuretic may be required
Davidson’s
Editor's Notes
High protein ascites (‘exudate’; protein concentration > 25 g/L (2.5 g/
dL) or a SAAG of < 11 g/L (1.1 g/dL). low protein concentration (‘transudate’; protein concentration < 25 g/L
(2.5 g/dL)) and A gradient of > 11 g/L (1.1 g/dL)
Titrated: Slowly increasing the doses of a medicine by very small amounts over days, week, months to find the right dose that s effective for patient
