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==Introduction==

==Description==

Transudates are a type of [[:Category:Effusions|effusion]] that has a low cellularity and a low protein content.  Transudates occur due to imbalances in the [[Blood Pressure Physiology#Capillary Fluid Shift Mechanism |'''Starling forces''']], of which the two principal examples are hydrostatic pressure and plasma oncotic pressure (or colloid osmotic pressure).  The following causes of transudate effusions are therefore recognised:

Transudates are a type of [[:Category:Effusions|effusion]] that has a low cellularity and a low protein content.  Transudates occur due to imbalances in the [[Control of Blood Pressure & Blood Flow - Anatomy & Physiology#Capillary Fluid Shift Mechanism |'''Starling forces''']], of which the two principal examples are hydrostatic pressure and plasma oncotic pressure (or colloid osmotic pressure).  The following causes of transudate effusions are therefore recognised:

*'''Reduced plasma oncotic pressure''' may occur if plasma proteins are lost.  Albumin contributes 75% of the total oncotic pressure so [[Hypoalbuminaemia|'''hypoalbuminaemia''']] is the major cause of transudate effusions.

*'''Reduced plasma oncotic pressure''' may occur if plasma proteins are lost.  Albumin contributes 75% of the total oncotic pressure so [[Hypoalbuminaemia|'''hypoalbuminaemia''']] is the major cause of transudate effusions.

*'''Increased hydrostatic pressure''' may occur with inappropriate activation of the renin-angiotensin-aldosterone system (RAAS), as in congestive heart failure and portal hypertension.  Both diseases commonly result in high-volume ascites, although this is more often composed of a [[Modified Transudate|modified transudate]].

*'''Increased hydrostatic pressure''' may occur with inappropriate activation of the renin-angiotensin-aldosterone system (RAAS), as in congestive heart failure and portal hypertension.  Both diseases commonly result in high-volume ascites, although this is more often composed of a [[Modified Transudate|modified transudate]].

In general, it is not advisable to drain effusions unless they are causing clinical signs as the procedures are invasive and drainage of large volumes of fluid will further deplete body protein reserves.  Neverthless, pleural and pericardial effusions should be drained to stabilise an animal with dyspnoea or signs of heart failure.

In general, it is not advisable to drain effusions unless they are causing clinical signs as the procedures are invasive and drainage of large volumes of fluid will further deplete body protein reserves.  Neverthless, pleural and pericardial effusions should be drained to stabilise an animal with dyspnoea or signs of heart failure.

The management of hypoalbuminaemia is discussed [[Hypoalbuminaemia|here]].

The [[Hypoalbuminaemia|management of hypoalbuminaemia is discussed here]].

Inappropriate activation of the RAAS is best treated with the diuretic spironolactone (a potassium sparing diuretic) because this prevents aldosterone from acting on Na/K pumps in the distal convoluted tubules and collecting ducts of the renal nephrons.  Frusemide (a loop diuretic) may be used later if aldosterone does not produce satisfactory results.  The underlying cause of the increased hydrostatic pressure should also be addressed.       

Inappropriate activation of the RAAS is best treated with the diuretic spironolactone (a potassium sparing diuretic) because this prevents aldosterone from acting on Na/K pumps in the distal convoluted tubules and collecting ducts of the renal nephrons.  Frusemide (a loop diuretic) may be used later if aldosterone does not produce satisfactory results.  The underlying cause of the increased hydrostatic pressure should also be addressed.       

[[Category:Effusions]]

[[Category:Effusions]]

[[Category:Expert_Review]]

[[Category:Expert_Review]]