Signs of Oedema

Signs

Oedema

Oedema is defined as an abnormal accumulation of fluid within the interstitial spaces. A number of mechanisms are thought to be involved in the development of oedema. Normally tissue fluid is formed by a balance of hydrostatic and osmotic pressure.

Hydrostatic pressure is the pressure within the blood vessel (high in arteries, low in veins). Oncotic pressure is produced by the large molecules within the blood (albumin, haemoglobin) and draws water osmotically back into the vessel. The hydrostatic pressure is high at the arterial end of a capillary bed hence fluid is forced out of the vasculature (see Fig. 2.1).

The colloid osmotic pressure then draws fluid back in at the venous end of the capillary bed as the hydrostatic pressure of the venules is low. Any remaining interstitial fluid is then returned to the circulation via the lymphatic system.

Mechanisms of cardiovascular oedema include the following:

·        Raised venous pressure raising the hydrostatic pressure at the venous end of the capillary bed (right ventricular failure, pericardial constriction, vena caval obstruction).

·        Salt and water retention occurring in heart failure, which increases the circulating blood volume with pooling on the venous side again raising the hydrostatic pressure.

·        The liver congestion that occurs in right-sided heart failure may reduce hepatic function, including albumin production. Albumin is the major factor responsible for the generation of the colloid osmotic pressure that returns the tissue fluid to the vasculature. A drop in albumin therefore results in an accumulation of oedema.

Oedema is described as pitting (an indentation or pit is left after pressing with a thumb for several seconds) or nonpitting. Cardiac oedema is pitting unless long standing when secondary changes in the lymphatics may cause a nonpitting oedema. Distribution is dependent on the patient. Patients who are confined to bed develop oedema around the sacral area rather than the classical ankle and lower leg distribution. Pleural effusions and ascites may develop in severe failure.