OEDEMA

Definition

 Abnormal accumulation of fluid in the intercellular tissue spaces or body cavities

 Localized : Due to obstruction of venous outflow – leg
 Generalized : Chronic venous Congestion or heart failure
Terms used to describe oedema

 Anasarca: Generalized subcutaneous oedema

 Ascites: Fluid in peritoneal cavity
 Hydrothorax; Edematous fluid in thorax
 Hydropericardium: Edematous fluid in pericardium
Oedema is of two types

1. Inflammatory oedema
2. Non-inflammatory odema
Mechanism of oedema formation

Two forces called “STARLING’S FORCES “

 Filtration force: Expels fluid from the vessel

 Absorption force: Draws fluid into the vessel
Physiology of fluid balance

 At the arterial end of capillary hydrostatic pressure is 45mm of Hg and osmotic pressure of blood is 30mm of Hg
(due to albumin / globulin). Therefore, fluid expelled into the intercellular space (filtration force) is 15mm Hg.
 At te venous end, hydrostatic pressure of blood falls to 15mm of Hg and osmotic pressure of blood is 30mm of Hg.
Therefore, absorption force is 15mm of Hg

CAUSES OF OEDEMA

 Decreased plasma osmotic pressure

 Increased hydrostatic pressure
 Increased permeability of vascular endothelium
 Lymphatic obstruction
 Sodium retention
Decreased plasma osmotic pressure - Hypoproteinemia (Albuminemia)

 Decreased protein synthesis

 Excessive loss from blood - Low osmotic pressure in the blood - More fluid flows into intercellular space
Hydrostatic pressure at arterial end is 45mm Hg and osmotic pressure at arterial end is 20mm Hg. So, the rate of fluid
flow into tissues is 25mm Hg. Osmotic pressure at venous end is 20mm Hg and hydrostatic pressure is 15mm Hg.
Thereby, the rate of fluid flow in to vein is 5mm Hg. Because of the pressure diffeences ( Hydrostatic and osmotic
pressure) at the arterial and venous end, the rate of fluid accumulation in tissues is 20mm Hg

Decreased plasma osmotic pressure mostly results in generalised and severe oedema

 Malnutrition
 In advanced hepatic disease (Cirrhosis), protein synthesis will be affected leading to nutritional or cachetic
oedema
 Loss of protein through intestine and stomach - stomach worms → Parasitic oedema
 Kidney or renal amyloidosis – blood lost in urine - Renal odema
Increased hydrostatic pressure

 General or passive hyperaemia → venous stasis

 Central lesion in heart or lungs or local obstruction in a vein
Hydrostatic pressure at arterial end is 45mm Hg, whereas osmotic pressure is 30mm Hg. So the rate of fluid flow into
tissues is 15mm Hg. At the venous end, osmotic pressure is 30mm Hg and hydrostatic pressure is 25mm Hg. The rate of
fluid flow into vein is 10mm Hg. So the rate of fluid accumulating in tissues is 5mm Hg.

 This type of oedema is mild. Mainly the cause is in the heart. Hence called cardiac oedema.
Increased permeability of capillary endothelium

 Due to venous stasis → increased hydrostatic pressure

 Inflammation
Lymphatic obstruction

Causes

 Tumours, cyst, abscess, bandages, thrombi

 Parasites (Demodex canis, mites)
 Filariasis – Wucheria bancrofti - humans
 Inflammatory conditions – farcy; ulcerative lymphangitis
In lymphatic obstruction, fluid and protein in intercellular space will not be drained leading to oedema
(LYMPHOEDEMA)

Sodium retention

Causes

 Congestive heart failure

 Nephrosis/Nephritis
 Acute renal failure
Due to failure of excretion sodium in urine, water will be retained leading to generalized oedema

Differences between transudate and exudate

S. Characters Transudate Exudate

No.

1 Colour Clear, water like pale yellow Cloudy, white, yellow-red

2 Consistency Thin, watery no tissue Thick, creamy, contains tissue

fragments fragments

3 Odour None Have odour

4 Ph Alkaline Acidic

5 Specific 1.015 or less 1.018 or higher

gravity

6 Protein Low, < 3% High > 4%

7 Cell count Low High, RBCs, WBCs

8 Enzyme count Low High

9 Bacteria None Present

10 Inflammation None Present

Macroscopical appearance

 Swollen, increase in weight

 Cold due to decrease blood, flow and increase heat dissipation
 Less color
 No pain
 Incision results in flow of fluid from cut surface
 Pits on pressure
 Fibrosis
Microscopical appearance

 Space between adjacent cells widened

 During life space filled with fluid
 H&E stain - fine granular material - stains faintly pink - ↑ pink if ↑ protein
 Atrophy of parenchymatous cells
 Fibrosis - chronic cases
Significance and result

 Disappears if cause is removed

 Oedema in lung & brain are fatal
 Subcutaneous oedema impairs wound healing

TYPES OF OEDEMA

1. Inflammatory oedema
2. Cardiac oedema
3. Renal oedema
4. Hunger/Famine/War oedema
5. Pulmonary oedema
6. Cachetic oedema
7. Myxoedema
8. Parasitic oedema
9. Angioneurotic oedema
10. Brisket disease
1. Inflammtory oedma

 Toxins damage blood vessels - Increased permeability of endothelium - Fluid rich in protein pass out -
“INFLAMMATORY EXUDATE”
2. Cardiac oedema

 Congestive heart failure leads to CVC which results in insufficient renal circulation ischaemia leading to oliguria
with diminished chloride excetion. This results in sodium retention which raises tissue osmotic pressure
aggrevating oedema
 Oedema - Abdominal cavity - Ascites

 Causes for cardiac oedema

 Increased hydrostatic pressure of blood
 Increased vascular permeability
 Sodium retention
 Symptoms
 Oedema of dependant parts
 Traumatic pericarditis in bovines
Cardiac oedema may develop in horses with chronic vesicular emphysema.

3. Renal oedema

 In acute glomerulonephritis (in man), oedema in face and eyelids are usually seen.
 Causes of acute glomerulonephritis are
 Decreased osmotic pressure of blood
 Toxins damage glomerular capillaries resulting in albuminuria and hypoproteinaemia.
 Increased osmotic pressure of ECF
 In acute nephritis, oliguria / Anuria results in sodium retention
 Increased capillary permeability
 Increased hydrostatic pressure in capillaries in venous side
 Toxins damage kidney and heart causing cardiac failure and its outcome is CVC
 Subacue nephritis and nephrosis
 Decreased colloidal osmotic pressure of blood
 Increased sodium retention
 Hypoalbuminaemia stimulates adrenal cortex to secrete increased amount of aldosterone which helps in
reabsorption of sodium chloride. This retained salt increases osmotic pressure and cause oedema.
 Chronic glomerulonephrtis
 Hypertension for long period throws great strain on heart resulting in heart failure and thereby
causing CVC which increases blood pressure in capillaries. As a resut of this, oedema occurs.
4. Hunger / Famine / war oedema

 Hypoproteinaemia → Decreased plasma osmotic pressure

 War / famine → Decreased protein availability
5. Pulmonary oedema

 Causes
 Cardiac failure - hypertension; valvular disease - pericarditis
 Renal lesions
 Pressure on pulmonary veins by neoplasm
 Injury to brain
  Rapid removal of effusion from pleural / peritoneal cavity
 Poisons
 Infections

Oedema - Lung - Rib markings

6. Cachetic oedema

 Anaemia
 Wasting diseases
 Malnutrition
 Cardiac illness
7. Myxoedma

 This occurs in chronic thyroid deficiency. In this condition there will be increased protein accumulation in tissue
fluid which raises pressure of fluid locally and water is drawn into the site.
8. Parasitic oedema

 This type of oedema is most commonly seen in animals suffering with stomach worms, liver flukes, amphistomes.
During migratory life of cercaria, haemorrhage & necrosis occurs in liver. Adult flukes inhabitats bileduct causing
chronic irritation of lining mucosa of the duct resulting in cirrhosis. Affected liver cannot synthesis protein leading
to oedema formation.
 Due to hypoproteinemia, there will be an accumulation of fluid in lower jaw called as “BOTTLE JAW” which is a
characteristic feature of parasitic oedema.
9. Angioneurotic oedema

 In man, allergens like snake venom produces hypersensitivity reaction which increases capillary permeability
resulting in oedema in lips, glottis, thorax
 In animals (cattle, horses), endogenous / exogenous allergens (plant, protein; fish meal) cause release of
histamine which damage blood vessels and oedema results.
10. Brisket disease

 Cattle moved to high altitude 9000ft above sea level develop oedema in abdomen, brisket, neck and jowl.
 At high altitudes, partial pressure of oxygen is decreased. The resulting hypoxia develops polycythemia (Increased
viscosity of blood) and polypnoea (Increased heart beat). Cardiac muscle becomes degenerated as it works in
hypoxic condition and hence hypertrophied heart slowly dilates and which draws valves downwards resulting in
valvuar incompetency and gives rise to chronic venous congestion.
 Reason for development of oedema in high altitude
 Hypoxia
 Chronic venous congestion - Develops due to increased capillary blood pressure and hypoxia