DEFINITION • Oedema may be defined as abnormal and excessive accumulation of “free fluid” in the interstitial tissue spaces and serous cavities. • Free fluid in body cavities: Depending upon the body cavity in which the fluid accumulates, it is correspondingly known as ascites (if in the peritoneal cavity), hydrothorax or pleural effusion (if in the pleural cavity), and hydropericardium or pericardial effusion (if in the pericardial cavity). • Free fluid in interstitial space: The oedema fluid lies free in the interstitial space between the cells and can be displaced from one place to another • The oedema may be of 2 main types: 1. Localised when limited to an organ or limb e.g. lymphatic oedema, inflammatory oedema, allergic oedema. 2. Generalised (anasarca or dropsy) when it is systemic in distribution, particularly noticeable in the subcutaneous tissues e.g. renal oedema, cardiac oedema, nutritional oedema. Depending upon fluid composition, oedema fluid may be: transudate which is more often the case, such as in oedema of cardiac and renal disease; or exudate such as in inflammatory oedema. PATHOGENESIS OF OEDEMA The following mechanisms may be operating singly or in combination to produce 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 A fall in the total plasma protein level (hypoproteinaemia of less than 5 g/dl), results in lowering of plasma oncoticpressure 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. The examples of oedema by this mechanism are seen in the following conditions: i) Oedema of renal disease e.g. in nephrotic syndrome, acute glomerulonephritis. ii) Ascites of liver disease e.g. in cirrhosis of the liver. iii) Oedema due to other causes of hypoproteinaemia e.g. in protein-losing enteropathy. 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 12 mmHg) to a level more than the plasma oncotic pressure results in minimal or no reabsorption of fluid at the venular end, consequently leading to oedema The examples of oedema by this mechanism are seen in the following disorders: i) Oedema of cardiac disease e.g. in congestive cardiac failure, constrictive pericarditis. ii) Ascites of liver disease e.g. in cirrhosis of the liver. iii) Passive congestion e.g. in mechanical obstruction due to thrombosis of veins of the lower legs, varicosities, pressure by pregnant uterus, tumours etc. iv) Postural oedema e.g. transient oedema of feet and ankles due to increased venous pressure seen in individuals who remain standing erect for longtime such as traffic constables 3. LYMPHATIC OBSTRUCTION. Normally, the interstitial fluid in the tissue spaces escapes by way of lymphatics. Obstruction to outflow of these channels causes localized oedema, known as lymphoedema The examples of lymphoedema include the following: i) Removal of axillary lymph nodes in radical mastectomy for carcinoma of the breast produces lymphoedema of the affected arm. ii) Pressure from outside on the main abdominal or thoracic duct such as due to tumours, effusions in serous cavities etc may produce lymphoedema. iii) Inflammation of the lymphatics as seen in filariasis (infection with Wuchereria bancrofti) results in chronic lymphoedema of scrotum and legs known as elephantiasis. iv) Occlusion of lymphatic channels by malignant cells may result in lymphoedema. 4. TISSUE FACTORS The two 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. These are as under: i) Elevation of oncotic pressure of interstitial fluid as occurs due to increased vascular permeability and inadequate removal of proteins by lymphatics. ii) Lowered tissue tension as seen in loose subcutaneous tissues of eyelids and external genitalia. 5. INCREASED CAPILLARY PERMEABILITY An intact capillary endothelium is a semipermeable 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 various ‘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, leading to leakage of plasma proteins into interstitial fluid. This, in turn, causes reduced plasma oncotic pressure and elevated oncotic pressure of interstitial fluid which consequently produces oedema • The examples of oedema due to increased vascular permeability are seen in the following conditions: i) Generalised oedema occurring in systemic infections, poisonings, certain drugs and chemicals, anaphylactic reactions and anoxia. 6. SODIUM AND WATER RETENTION • The possible factors responsible for causation of oedema by excessive retention of sodium and water in the extravascular compartment via stimulation of intrinsic renal and extra-renal mechanisms as well as via release of ADH are as under: i) Reduced glomerular filtration rate in response to hypovolaemia. ii) Enhanced tubular reabsorption of sodium and consequently its decreased renal excretion. iii) Increased filtration factor i.e. increased filtration of plasma from the glomerulus. iv) Decreased capillary hydrostatic pressure associated with increased renal vascular resistance The examples of oedema by these mechanims are as under: i) Oedema of cardiac disease e.g. in congestive cardiac failure. ii) Ascites of liver disease e.g. in cirrhosis of liver. iii) Oedema of renal disease e.g. in nephrotic syndrome, acute glomerulonephritis.
