Hope you guys are familiar with the name pathology. Oedema is one of the most important concepts in pathology. This word has its origin from the Greek word “oidema” which means swelling. Oedema is nothing but fluid accumulation and it is a common derangements of body fluid. It is defined as abnormal and excessive accumulation of “free fluid” in the interstitial tissue spaces and serous cavities.
Fluid accumulates in different body cavities and depending upon the body cavity in which the fluid accumulates it gets a different name.
- If the fluid accumulates in the peritoneal cavity, it is known as ascites
- If it gets accumulates in the pleural cavity it is called hydrothorax/pleural effusion
- If the fluid accumulates in the pericardial cavity, then it is called hydropericardium/pericardial effusion.
The oedema fluid lies free in the interstitial space where it can be displaced from one place to another. Momentary pressure of finger produces a depression called pitting oedema and the other one is called non-pitting oedema where no pitting is produced on pressure.
Oedema is classified into two main types: Localised and Generalised. Localized oedema is limited to an organ or limb whereas the generalized oedema is systematic in distribution mostly noticeable in subcutaneous tissues. Depending upon the fluid composition, oedema fluid may be transudate or exudate.
Coming to the most important concept that is nothing but the pathogenesis of oedema.
PATHOGENESIS OF OEDEMA:
Oedema is caused by mechanisms that interfere with the normal fluid balance of plasma, interstitial fluid, and lymph flow. Oedema is produced by the given below mechanisms that may be operating singly or in combination.
- Decreased plasma oncotic pressure
- Increased capillary hydrostatic pressure
- Lymphatic obstruction
- Tissue factors
- Increased capillary permeability
- Sodium and water retention
DECREASED PLASMA ONCOTIC PRESSURE:
The result of increased outward movement of the fluid from the capillary wall and decreased inward movement of the fluid from the interstitial space is due to the lowering of the plasma oncotic pressure. This lowering of plasma oncotic pressure is again due to the fall in the plasma protein level that is called hypoproteinaemia. Hypoproteinaemia commonly produces generalised oedema. Here the hydrostatic pressure remains normal.
INCREASED CAPILLARY HYDROSTATIC PRESSURE:
The increased hydrostatic pressure at the capillary which is low results in the minimal/no reabsorption of the fluid which consequently leads to oedema. Here the tissue tension and oncotic pressure remain normal whereas the hydrostatic pressure is increased
LYMPHATIC OBSTRUCTION:
Lymphatic obstruction also called lymphoedema is defined as the obstruction to the lymphatic outflow. But the tissue tension, hydrostatic pressure, and the oncotic pressure remain normal in this case.
TISSUE FACTOR:
The forces acting in interstitial spaces are oncotic pressure and tissue tension. Changes in these tissue factors such as elevation of oncotic pressure and decreased tissue tension would remain as the causative for oedema.
INCREASED CAPILLARY PERMEABILITY:
Capillary endothelium is a semipermeable membrane where it can be injured by various agents such as capillary poisons, venoms, anoxia and chemicals etc., The injury to capillary endothelium leads to increased permeability. This, in turn, leads to the leakage of the plasma proteins. This results in reduced plasma oncotic pressure and increased oncotic pressure in the interstitial fluid. This consequently leads to oedema.
SODIUM AND WATER RETENTION:
The arterial baroreceptors are stimulated by Hypovolaemia which is present in the carotid sinus and aortic arch. This causes renal ischaemia which causes a reduction in the excretion of sodium in the urine and this is the intrinsic renal mechanism. The extrarenal mechanism describes the involvement of aldosterone which is considered as a sodium retaining hormone.
Aldosterone increases the sodium content by reabsorbing it in the renal tubules. A large amount of ADH (Anti-diuretic hormone) also called vasopressin increases the retention of water and produces highly concentrated urine.
DIAGNOSIS AND TREATMENT
The physicians would diagnose oedema by performing a physical exam and verifying the doubts by asking questions related to the injury.
Mild oedema generally goes away on its own while severe oedema needs treatment guided by the physician who normally suggests drugs that expel the excess fluid.
Hope you guys now know one of the main concepts of pathology.
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