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pressure in a way that it can no longer counteract the effect  v) Milroy’s disease or hereditary lymphoedema is due to  97
           of hydrostatic pressure of blood. This results in increased  abnormal development of lymphatic channels. It is seen in
           outward movement of fluid from the capillary wall and  families and the oedema is mainly confined to one or both
           decreased inward movement of fluid from the interstitial  the lower limbs (Chapter 15).
           space causing oedema  (Fig. 5.3,B).  Hypoproteinaemia  4. TISSUE FACTORS. The two forces acting in the inter-
           usually produces generalised oedema (anasarca). Out of the  stitial space—oncotic pressure of the interstitial space and  CHAPTER 5
           various plasma proteins, albumin has four times higher  tissue tension, are normally quite small and insignificant to
           plasma oncotic pressure than globulin; thus it is mainly hypo-  counteract the effects of plasma oncotic pressure and
           albuminaemia (albumin below 2.5 g/dl) that results in  capillary hydrostatic pressure respectively. However, in
           oedema more often.                                  some situations, the tissue factors in combination with other
              The examples of oedema by this mechanism are seen in  mechanisms play a role in causation of oedema (Fig. 5.3,E).
           the following conditions:                           These are as under:
           i) Oedema of renal disease e.g. in nephrotic syndrome, acute  i) Elevation of oncotic pressure of interstitial fluid as occurs due
           glomerulonephritis.                                 to increased vascular permeability and inadequate removal
           ii) Ascites of liver disease e.g. in cirrhosis of the liver.  of proteins by lymphatics.
           iii) Oedema due to other causes of hypoproteinaemia e.g. in  ii) Lowered tissue tension as seen in loose subcutaneous tissues
           protein-losing enteropathy.                         of eyelids and external genitalia.
           2. INCREASED CAPILLARY HYDROSTATIC PRES-            5. INCREASED CAPILLARY PERMEABILITY. An intact
           SURE. The hydrostatic pressure of the capillary is the force  capillary endothelium is a semipermeable membrane which
           that normally tends to drive fluid through the capillary  permits the free flow of water and crystalloids but allows
           wall into the interstitial space by counteracting the force  minimal passage of plasma proteins normally. However,
           of plasma oncotic pressure. A rise in the hydrostatic  when the capillary endothelium is injured by various
           pressure at the venular end of the capillary which is  ‘capillary poisons’ such as toxins and their products,  Derangements of Homeostasis and Haemodynamics
           normally low (average 12 mmHg) to a level more than the  histamine, anoxia, venoms, certain drugs and chemicals, the
           plasma oncotic pressure results in minimal or no    capillary permeability to plasma proteins is enhanced due
           reabsorption of fluid at the venular end, consequently  to development of gaps between the endothelial cells, leading
           leading to oedema (Fig. 5.3,C).                     to leakage of plasma proteins into interstitial fluid. This, in
              The examples of oedema by this mechanism are seen in  turn, causes reduced plasma oncotic pressure and elevated
           the following disorders:                            oncotic pressure of interstitial fluid which consequently
           i) Oedema of cardiac disease e.g. in congestive cardiac failure,  produces oedema (Fig. 5.3,F).
           constrictive pericarditis.                             The  examples of oedema due to increased vascular
           ii) Ascites of liver disease e.g. in cirrhosis of the liver.  permeability are seen in the following conditions:
           iii) Passive congestion e.g. in mechanical obstruction due to  i) Generalised oedema occurring in systemic infections,
           thrombosis of veins of the lower legs, varicosities, pressure  poisonings, certain drugs and chemicals, anaphylactic
           by pregnant uterus, tumours etc.                    reactions and anoxia.
           iv) Postural oedema e.g. transient oedema of feet and ankles  ii) Localised oedema. A few examples are as under:
           due to increased venous pressure seen in individuals who  Inflammatory oedema as seen in infections, allergic
           remain standing erect for longtime such as traffic constables.  reactions, insect-bite, irritant drugs and chemicals. It is
           3. LYMPHATIC OBSTRUCTION.  Normally, the inter-        generally exudate in nature.
           stitial fluid in the tissue spaces escapes by way of lympha-  Angioneurotic oedema is an acute attack of localised
           tics. Obstruction to outflow of these channels causes localised  oedema occurring on the skin of face and trunk and may
           oedema, known as lymphoedema (Fig. 5.3,D).             involve lips, larynx, pharynx and lungs. It is possibly
              The examples of lymphoedema include the following:  neurogenic or allergic in origin.
           i) Removal of axillary lymph nodes in radical mastectomy for  6. SODIUM AND WATER RETENTION. Before descri-
           carcinoma of the breast produces lymphoedema of the  bing the mechanism of oedema by sodium and water
           affected arm.                                       retention in extravascular compartment, it is essential to
           ii) Pressure from outside on the main abdominal or thoracic  recollect the normal regulatory mechanism of sodium and
           duct such as due to tumours, effusions in serous cavities etc  water balance.
           may produce lymphoedema. At times, the main lymphatic  Natrium  (Na) is the Latin term for sodium. Normally,
           channel may rupture and discharge chyle into the pleural  about 80% of sodium is reabsorbed by the proximal
           cavity (chylothorax) or into peritoneal cavity (chylous  convoluted tubule under the influence of either intrinsic renal
           ascites).                                           mechanism or extra-renal mechanism while retention of
           iii) Inflammation of the lymphatics as seen in filariasis (infection  water is affected by release of antidiuretic hormone (Fig. 5.4):
           with Wuchereria bancrofti) results in chronic lymphoedema  Intrinsic renal mechanism is activated in response to
           of scrotum and legs known as elephantiasis.         sudden reduction in the effective arterial blood volume
           iv) Occlusion of lymphatic channels by malignant cells may  (hypovolaemia) e.g. in severe haemorrhage. Hypovolaemia
           result in lymphoedema.                              stimulates the arterial baroreceptors present in the carotid
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