PATHOGENESIS OF OEDEMA:
1. Decreased plasma oncotic pressure.
2. Increased capillary hydrostatic pressure.
3. Lymphatic obstruction.
4. Tissue factors (Increased oncotic pressure of interstitial fluid and
decreased tissue tension)
5. Increased capillary permeability.
6. Sodium and water retention.
1. Decreased Plasma oncotic pressure:
The plasma oncotic pressure exerted by the total amount of plasma
proteins tends to draw fluid into the vessels normally. A fall in the total plasma
protein level (hypoproteinemia less than 5 gm/dl), results in lowering of plasma
oncotic pressure in a way that it can no longer counteract the effect of
hydrostatic pressure of blood. This results in increased outward movement of
fluid from the capillary wall and decreased inward movement of fluid from the
interstitial space, causing oedema.
Hypoproteinemia usually produces generalised edema out of various
plasma proteins, albumin has four times higher plasma oncotic pressure than
globulin, so that it is hypoalbuminemia (albumin below 2.5gm/dl), that results
in oedema more often.
2. Increased capillary hydrostatic pressure:
The hydrostatic pressure of the capillary is the force that normally tends
to drive fluid through the capillary wall into the interstitial space by
counteracting the force of plasma oncotic pressure. A rise in the hydrostatic
pressure at the venular end of the capillary, which is normally low (average
12mm Hg) to a level more than the plasma oncotic pressure, results in minimal
or no reabsorption of fluid at the venular end, consequently leading to ledema.
3. Lymphatic obstruction:
Normally the interstitial fluid in the tissue spaces escapes by way of
lymphatics, so that obstruction to outflow of these channels causes localised
oedema, known as lymphedema.
4. Tissue factors:
The forces acting in the interstitial space – oncotic pressure of the
interstitial space and tissue tension are normally quite small and insignificant to
counteract the effects of plasma oncotic pressure and capillary hydrostatic
pressure respectively. However, in some situations, the tissue factors in
combination with other mechanisms play a role in causation of oedema.
5. Increased capillary Permeability:
An intact capillary endothelium is a semi permeable membrane which
permits the free flow of water and crystalloids, but allows minimal passage of
plasma proteins normally. However, when the capillary endothelium is injured
by “Capillary Poisons” such as toxins and their products, histamine, anoxia,
venoms, certain drugs and chemicals the capillary permeability to plasma
proteins is enhanced due to development of gaps between the endothelial cells.
This, in turn, causes reduced plasma oncotic pressure and elevated
oncotic pressure of interstitial fluid which consequently produces oedema.
6. Sodium and Water retention:
Normally about 80% of sodium is reabsorbed by the proximal
convoluted tubules under the influence of intrinsic renal mechanism. Excessive
retention of sodium and water and their decreased renal excretion occur in
response to hypovolaemia and lowered concentration of sodium in the renal
tubules by stimulation of intrinsic renal and extra – renal mechanisms as well
as via release of ADH.