OEDEMA

OEDEMA

  Oedema may be defined as abnormal and excessive accumulation of free fluid in interstitial tissue space and serous cavities.

1. Free fluid in tissue cavity or body cavity:-

     Depending upon the body cavity in which the fluid accumulates, it is corresponding known as ascites, hydrothorax and hydropericardium.

2. 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.

 In the case of oedema in the subcutaneous oedema is divided into two parts-

a. Pitting oedema:-

      In case of oedema in the subcutaneous tissue, momentry pressure of finger produces a depression known as pitting oedema.

b. Non-pitting oedema or solid oedema:-

  In which no pitting is produce on pressure. Ex- elephanticis, myxoedema.

The oedema may be of two main type-

1. Localized

2. Generalized 

1. Localized:-

     When limited to an organ or limb. Ex: lymphatic oedema, inflammatory oedema, allergic oedema.

2. Generalized oedema:-

     When it is systemic in distribution particularly noticible in the subcuteneous tissue. Ex: renal oedema, cardiac oedema, nutritional oedema.

      Besides, there are few special forms of oedema. Ex- pulmonary oedema, cerebral oedema.

Depending upon fluid composition oedema fluid may be -

1. Transudate

2. Exudate

1. Transudate:-

      Which is more often the case (low protein content and few cells are present) such as in oedema of cardiac and renal disease.

2. Exudate:-

    Such as in inflammatory oedema (High protein content and presence of WBC and RBC cells).

Pathogenesis of oedema:-

     Oedema is caused by mechanism that interfere with normal fluid balance plasma, interstitial fluid and lymph fluid.

Note:-

Normal fluid exchange:-

     At the arterioler end  of the capillaries the balance between the hydrostatic pressure 32mm Hg and plasma oncotic pressure 25mmHg is the hydrostatic pressure of 7mmHg. Which is the outward riding force so that the small quantity of fluid and solute leave the vessel to enter the interstitial space.

  At the venular end of the capilary the balance between the hydrostatic pressure 12 mmHg and plasma oncotic pressure 25mmHg is the osmotic pressure of 13mmHg which is the inward force. so that the fluid and solute re-enters the plasma.

  Tissue tension is the hydrostatic protein of interstitial fluid and is lower then the hydrostatic pressure in the capilary at the end.

  Effective hydrostatic hydrostatic pressure. That drives fluid through the capilary wall into to interstitial space.

Pathogenesis of oedema:-

1. Decreased plasma oncotic pressure:-

       The plasma oncotic pressure exerted by the total amount of plasma protein tends to draw fluid into the vessels normaly.

  A fall in the total plasma protein level (Hypoproteimnia) of less than 5gm per dl) result in lowering plasma oncotic pressure in a way that it can no longer counter act effect of hydrostatic pressure of blood. This result in increase outward movement of fluid from the capilary wall and decreased invert movement of fluid from the interstitial space causing oedema. 

 Hypoproteinmia usually produces generalized oedema. Eg- Oedema of renal diseased -- nephrotic syndrome, acute glominulo nephritis, ascitis of liver disease- (cirosis).

2. Increased capillary hydrostatic pressure:-

        The hydrostatic pressure of the capillary is the force that normally tends to dry fluid from the capillary wall into the interstitial space by counter acting the force of plasma oncotic pressure.

    A rise in the hydrostatic pressure at the venular end of the capillary which is normally low to a level more than the plasma, oncotic pressure results in minimal or no reabsorption of fluid at eh vennular end. Consequently leading to oedema.

Eg:-  Oedema of the cardiac disease--  congestive cardiac failure, constructive pericarditis,

Postular oedema-- transient oedema of feet and ankles due to increased venous pressure seen in individual who remain erect for long time.

3. Lymphatic obstruction:-

       Nonmally the interstitial fluid in the tissue spaces escapes by way to lymphatic. obstruction to outflow of these channel causes localized oedema, also known as lymphoedema.

Eg-= filaria

4. Tissue factor:-

      In some situation the tissue factor in combination with other mechanism play a role causation of oedema.

 Eg:- Elevation of oncotic pressure of interstitial fluid due to incresed vascular permeability and inadequate removal of protein by lymphatics.

5. Increase capillary permeability:-

      An intact capillary endothelium is semi permeable membrane which permits the free flow of water and crystalloids but allow minimum passage of plasma protein.

However when the capillary endothelium is injured such as toxin and there products, capillary permeability to plasma protein is inhenced due to development of gaps between the endothelium cells leading to leakage of plasma protein into interstitial space which may lead to oedema.

6. Sodium and water retention:-

        Normally about 80% of sodium is reabsorbed by PCT while retentionof water is affected by release of Anti-diuretic harmone. 

Intrinsic renal mechanism :-

    It is activated in response to sudden reduction in effective arterial blood volume Hypovolemia. As a result of this renal ischemia occur which causes reduction in glomerular filtration rate, decreased excretion of sodium in the urine and consequent retention of sodium which can lead to oedema.

Anti- diuretic harmone mechanism:-

      Retention of sodium leads to retention of water secondarily under the influence of ADH or vaso pression.