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Generalised oedema
Causes
Congestive heart failure
Nephrotic syndrome
Hepatic cirrhosis
Acute glomerulonephritis
Hypothyroidism
Acute renal failure
Chronic renal failure
Pregnancy
Protein losing enteropathy
Severe malnutrition
Drugs—Oestrogens, NSAIDs, corticosteroids, vasodilators, calcium channel blockers (amlodipine)
Note: Amlodipine generally produces pedal oedema.
Pathogenesis
Oedema occurs when there is imbalance between forces causing filtration of fluid and those causing absorption of fluid resulting in net filtration.
It may be due to an elevation in capillary hydraulic pressure, an increase in capillary permeability or an increase in interstitial oncotic pressure, or due to a reduction in plasma oncotic pressure.
Kidneys have a central role in maintaining body fluid homeostasis. They control extracellular fluid volume by adjusting sodium and water excretion.
Antidiuretic hormone (ADH), which is secreted in response to stimuli such as changes in blood volume, tonicity and blood pressure, is the primary regulator of body water.
Effective arterial blood volume (EABV) correlates with extracellular fluid volume. It is sensed by volume homeostatic mechanisms which change renal sodium reabsorption.
In healthy persons, sodium loading increases extracellular fluid volume and EABV, resulting in prompt natriuresis and restoration of normal volumes.
In persons who are volume depleted, EABV and extracellular fluid volume are reduced which activate renin-angiotensin–aldosterone system resulting in renal sodium retention and restoration of normal blood volume.
In oedematous states, there is reduction in EABV which activates sympathetic nervous system, renin–angiotensin¬aldosterone axis and ADH secretion. Because of these compensatory mechanisms, oedema persists.
Pathogenesis of oedema in the commonly encountered clinical conditions like congestive heart failure, nephrotic syndrome and hepatic cirrhosis are discussed.
Clinical features
Cardiac oedema accumulates over dependent parts. In ambulant patients, it occurs symmetrically in the legs, particularly in the pretibial region and around the ankles. It is less in the morning and more towards the evening. Oedema is sacral in bedridden patients.
Oedema of renal origin is classically identified by puffiness of the face, particularly around the periorbital region. 4 In oedema of hepatic origin, the accumulation of fluid is predominantly manifested as ascites.
Management
Treatment may be divided into primary and secondary.
Primary treatment is directed at eliminating the cause of the problem—e.g. improvement of cardiac function, correction of hypoalbuminaemia.
Secondary treatment is mainly concerned with correcting the salt and water overload. They include the following measures:
Restriction in sodium intake—dietary sodium should be restricted to about 50-100 mmol/day. A 'no added salt diet', allowing salt only in cooking, with no addition of salt at table, and avoidance of salty food is generally satisfactory.
Modest restriction of water intake to about 1000 mL/day should be advocated.
Diuretics should be given to increase rate of urinary excretion of sodium and water. Thiazide diuretics (e.g. hydrochlorothiazide 50-100 mg/day) may be used. More powerful loop diuretics (e.g. furosemide 40-120 mg/ day) may be used in severe oedema. In severe renal failure or life-threatening pulmonary congestion, intravenous furosemide may be used.
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