OEDEMA

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Pathology - oedema

1. Define oedema and explain the pathogenesis of oedema of renal origin.


2. Define edema. Describe the pathogenesis pathology of pulmonary edema
3. Differences between transudate and exudate

Differences between transudate and exudate

Define oedema and explain the pathogenesis of oedema


Definition
Oedema may be defined as abnormal and excessive accumulation of “free fluid” in the
interstitial tissue spaces and serous cavities

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.

PATHOGENESIS
Oedema is caused by mechanisms that interfere with normal fluid balance of plasma, interstitial
fluid and lymph flow. 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


The plasma oncotic pressure exerted by the total amount of plasma proteins tends to draw fluid
into the vessels normally. A fall in the total plasma protein level (hypoproteinaemia of less than 5
g/dl), results in lowering of plasma oncotic pressure. 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

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 (Fig. 15.3,C).
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

3. Lymphatic obstruction
Normally, the interstitial fluid in the tissue spaces escapes by way of lymphatics. Obstruction to
outflow of these channels causes localised 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) Inflammation of the lymphatics as seen in filariasis

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

5. Increased capillary permeability


Normally, intact capillary endothelium acts as a semipermeable membrane, allowing the free
flow of water and crystalloids while restricting the passage of plasma proteins. In the presence
of capillary toxins like histamine, anoxia, venoms, certain drugs, and chemicals, endothelial cell
damage increases capillary permeability to proteins. This leads to gaps between cells, resulting
in plasma protein leakage into interstitial fluid. Consequently, reduced plasma oncotic pressure
and elevated interstitial fluid oncotic pressure cause edema.

6. Sodium and water retention.


Natrium (Na) is the Latin term for sodium. Normally, about 80% of sodium is reabsorbed by the
proximal convoluted tubule under the influence of either intrinsic renal mechanism or extra-renal
mechanism while retention of water is affected by release of antidiuretic hormone.
Mechanisms involved in oedema by sodium and water retention is by Intrinsic renal mechanism,
Extra-renal mechanism or ADH mechanism

Explain the pathogenesis of oedema of renal origin.


Renal Oedema Generalised oedema occurs in certain diseases of renal origin such as in
nephrotic syndrome, some types of glomerulonephritis, and in renal failure due to acute tubular
injury.
1. Oedema in nephrotic syndrome.
Nephrotic syndrome involves persistent and heavy albuminuria, causing hypoalbuminemia and
decreased plasma oncotic pressure, leading to severe generalized edema. This
hypoalbuminemia triggers a cycle involving decreased plasma volume, activation of the
renin-angiotensin-aldosterone mechanism, and retention of sodium and water, perpetuating the
edematous condition. A similar mechanism is observed in protein-losing enteropathy,
emphasizing the role of protein loss in edema development. Nephrotic edema is notably severe,
affecting subcutaneous tissues and visceral organs, resulting in enlarged, heavy organs with
tense capsules.

2. Oedema in nephritic syndrome.


Oedema occurs in conditions with diffuse glomerular disease such as in acute diffuse
glomerulonephritis and rapidly progressive glomerulonephritis. In contrast to nephrotic oedema,
nephritic oedema is not due to hypoproteinaemia but is largely due to excessive reabsorption of
sodium and water in the renal tubules via reninangiotensin-aldosterone mechanism. The
nephritic oedema is usually mild as compared to nephrotic oedema and begins in the loose
tissues such as on the face around eyes, ankles and genitalia.

3. Oedema in acute tubular injury.


Acute tubular injury following shock or toxic chemicals results in gross oedema of the body. The
damaged tubules lose their capacity for selective reabsorption and concentration of the
glomerular filtrate resulting in increased reabsorption and oliguria. Besides, there is excessive
retention of water and electrolytes and rise in blood urea.
Describe the pathogenesis pathology of pulmonary edema
Acute pulmonary oedema is the most important form of local oedema as it causes serious
functional impairment but has special features. It differs from oedema elsewhere in that the fluid
accumulation is not only in the tissue space but also in the pulmonary alveoli.
Pulmonary oedema can result from either the elevation of pulmonary hydrostatic pressure or the
increased capillary permeability

1. Elevation in pulmonary hydrostatic pressure (Haemodynamic oedema). In heart failure, there


is increase in the pressure in pulmonary veins which is transmitted to pulmonary capillaries. This
results in imbalance between pulmonary hydrostatic pressure and the plasma oncotic pressure
so that excessive fluid moves out of pulmonary capillaries into the interstitium of the
lungs.Pulmonary capillary endothelium develops fenestrations, allowing plasma proteins and
fluid passage into interstitium. Lymphatics clear interstitial fluid but are overwhelmed, leading to
interstitial edema in loose tissues around bronchioles, arteries, and lobular septa. Prolonged
elevation of hydrostatic pressure and due to high pressure of interstitial oedema, the alveolar
lining cells break and the alveolar air spaces are flooded with fluid (alveolar oedema) driving the
air out of alveolus, thus seriously hampering the lung function.

2. Increased vascular permeability (Irritant oedema). The vascular endothelium as well as the
alveolar epithelial cells (alveolo-capillary membrane) may be damaged causing increased
vascular permeability so that excessive fluid and plasma proteins leak out, initially into the
interstitium and subsequently into the alveoli.

3. Acute high altitude oedema. Sudden ascent to high altitudes leads to severe circulatory and
respiratory issues. Problems typically start above 2500 meters.These changes include
appearance of oedema fluid in the lungs, congestion and widespread minute haemorrhages.
These changes can cause death within a few days. The underlying mechanism appears to be
anoxic damage to the pulmonary vessels.

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