Anasarca is a severe global oedema caused by the accumulation of fluid in the interstitial space.
It have varied aetiologies and can arise through several mechanisms that ultimately lead to a change in the Starling forces: the equation really only providing for alteration of the oncotic or hydrostatic gradients. The permeability coefficient could also change but this is not likely to be the problem.
The classical Starling principle has been mostly abandoned in favour of a modernised and far more complicated one. It is now understood that there is a supraendothelial glycocalyx that is very involved in regulating transvascular fluid movement. It is also apparent that most interstitial fluid is carried away by the lymphatic system rather than being reabsorbed by the venules.
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Hydrostatic pressure changes
Increased hydrostatic pressure is basically secondary to hypertension. As the capillary hydrostatic pressure increases the rate of movement of fluid out of the vasculature increases and there is net fluid exchange into the interstitium.
Heart failure
Failure of the bodies great pump ultimately leads to oedema as fluid is deposited in the interstitium more rapidly than it can be collected and removed from the body.
Kidney failure
If the kidneys fail to excrete adequate volumes the consequent fluid overload expands the intravascular volume. This usually increases the blood pressure. Regardless, with the circulating volume expanded by a solution that is permitted easily between compartments the resulting hydrostatic gradient is equalised by interstitial fluid shift.
Medications
As with most conditions, the doctors potions may cause anasarca. Some suspects are:
- Corticosteroids
- Calcium-channel blockers
- NSAIDs
Oncotic pressure changes
If the colloid osmotic-pressure gradient changes it will also produce a net fluid shift. The principle cause of this is hypoalbuminaemia, arising either from decreased synthesis or protein wasting. Any physiological or pathological state that leads to reduced plasma albumin concentrations would alter the oncotic gradient.
Liver failure
The liver maintains the plasma albumin content, thus, failure of synthetic function leads to depletion of the primary component that maintains the oncotic pressure.
Kidney failure
Significant protein wasting renal pathology such as nephrotic syndrome can produce hypoalbuminaemia as well as significant hypogammaglobulinaemia. The latter has very little to do with anasarca but it does effectively obliterate the humoral immune system.
Malnutrition
Significant reduction in dietary protein impedes the body’s ability to maintain the albumin concentration.