#fluid overload

Fluid overload is defined by an increase in total body water, accompanied by an increase in total body Na+.

This condition has an association with edema, an accumulation of fluid in the interstitial tissues.

Major causes of inappropriate ECF expansion:

1. Disturbed Starling forces (reduced effective circulating volume [ECV], edema)

Systemic venous pressure increase (right-heart failure, constrictive pericarditis)

Local venous pressure increase (left-heart failure, vena cava obstruction)

Portal vein obstruction

Reduced oncotic pressure (nephrotic syndrome)

Combined disorders (cirrhosis)

Derangement of Starling forces leads to an expansion of the interstitial compartment, at the expense of ECF volume.

2. Primary hormone excess (increased effective circulating volume)

Primary hyperaldosteronism

Cushing's syndrome

Syndrome of inappropriate ADH secretion (SIADH)

3. Primary renal sodium retention (increased effective circulating volume)

Acute glomerulonephritis

Volume excess disorders are associated with decreased capillary oncotic pressure and/or increased capillary hydrostatic pressure. This causes either movement of capillary fluid to the interstitial compartment or the inability of the capillary to re-uptake interstitial fluid.

In all cases, edema results.

Causes of edema:

Increased venous hydrostatic pressure

Heart failure

Venous obstruction/deep vein thrombosis

Failure of venous valves (venous HTN/varicose veins)

Failure of venous pumps (immobility, paralysis)

Mechanism: congestive pooling increases hydrostatic pressure, leading to pushing of fluid into the interstitial compartment in affected areas

Excess renal retention of sodium/H2O (mineralcorticoid excess, Conns syndrome)

Mechanism: direct expansion of ECF volume increases hydrostatic pressure, leading to movement of fluid into the interstitial compartment

Decreased plasma proteins 

burns, wounds = loss of plasma proteins.

chronic liver disease = can't make new protein

protein malnutrition = not consuming enough protein

Mechanism: loss of plasma proteins lowers oncotic pressure, enabling movement of fluid into interstitial compartment due to hydrostatic pressure overcoming lowered oncotic pressure

Blockage of lymphatic return

Mechanism: thin lymphatic vessels continue to pull from interstitium but are unable to drain, expanding endlessly

Treatment of inappropriate ECF fluid expansion:

1. Diuretics

Predominantly a pharm topic. In brief:

Carbonic anhydrase inhibitors like acetazolamide act on the proximal tubule, and are among the least potent in terms of diuretic effect.

Loop diuretics like furosemide act at the loop of Henle, and are very potent diuretics.

Thiazide diuretics like chlorothiazide act at the distal tubule, and are moderately potent diuretics.

Potassium-sparing diuretics like spironolactone operate on the collecting duct, and are not terribly potent diuretics. But they reduce K+ loss.

2. Fluid restriction/reduced intake

3. Fluid removal by hemodialysis/removal directly from blood

4. Fluid removal from body cavities

Thoracentesis (thoracic cavity)

Paracentesis (abdominal cavity)

5. Lymphatic decongestion therapy