Oedem
a
Introductio
• It may be ndefined as abnormal and
excessive accumulation of “free fluid” in
the interstitial tissue spaces and serous
cavities.
• Free fluid in body cavities
– Ascites: peritoneal cavity
– Hydrothorax or pleural effusion: pleural cavity
– Hydropericardium or pericardial effusion:
pericardial cavity
• Free fluid in interstitial space: space between
the cells
Oedema:
Types
• The oedema may be of 2 main
types:
• Localised
– Lymphatic oedema,
– Inflammatory oedema
– allergic oedema
• Generalised (anasarca or dropsy)
– Renal oedema,
– Cardiac oedema,
– Nutritional oedema.
• Reduced Plasma Osmotic
Oedema: Pressure
(Hypoproteinemia)
– Protein-losing
glomerulopathies (nephrotic
• Causes
Increased Hydrostatic Pressure
– Impaired venous return
syndrome)
– Liver cirrhosis (ascites)
– Congestive heart failure – Malnutrition Protein-losing
– Constrictive pericarditis Gastroenteropathy
– Ascites (liver cirrhosis) • Lymphatic Obstruction
– Venous obstruction or
– Inflammatory
– Neoplastic
compression
• Thrombosis,
– Postsurgical
– Postirradiation
• External pressure
• Sodium Retention
(e.g., – Excessive salt intake with
mass), renal insufficiency
• Lower extremity inactivity – Increased tubular
with prolonged reabsorption of sodium
dependency • Inflammation
– Arteriolar dilation – Acute inflammation
– Chronic inflammation
• Heat,
– Angiogenesis
• Neurohumora
l
PATHOGENESIS OF
• OEDEMA
Its caused by mechanisms that interfere with
normal fluid balance of plasma, interstitial fluid
and lymph flow.
– Decreased plasma oncotic pressure
– Increased capillary hydrostatic pressure
– Lymphatic obstruction
– Tissue factors (increased oncotic pressure of
interstitial fluid, and decreased tissue tension)
– Increased capillary permeability
– Sodium and water retention
• Intrinsic renal mechanism
• Renin angiotensin-aldosterone system
• ADH mechanism
Tissue factors
• Elevation of oncotic pressure of the interstitial fluid –
due to increased vascular permeability
inadequate removal of proteins by lymphatics
• Lowered tissue tension
Increased capillary permeability
• Semipermeable membrane
• Capillary endothelium injured by poisons, toxins, venoms
• Gaps between endothelial cells- increased oncotic pressure of
interstitial fluid
- reduced plasma oncotic pressure
Eg :
• Generalised oedema in infection, poisoning, anaphylaxis
• Localised oedema
- inflammatory oedema
- angioneurotic oedema – neurogenic or allergic in origin
Renal
Oedema
• Generalised oedema occurs in certain
diseases of renal origin.
– Nephrotic syndrome,
– Some types of glomerulonephritis –
Nephritic Syndrome
– Renal failure due to acute tubular injury.
Nephrotic
• syndrome
Chracterised by persistent and heavy
proteinuria (albuminuria) – causing
hypoalbuminaemia
• These causes decreased plasma oncotic
pressure
resulting in severe generalised oedema.
• Also there is activation of renin-angiotensin-
aldosterone mechanism which results in
retention of sodium and water.
• These vicious cycle which persists till
the albuminuria continues.
• Classically more severe in the subcutaneous
tissues as well as in the visceral organs.
Nephritic
•
Syndrome
Conditions such as in acute diffuse
glomerulonephritis and rapidly
progressive glomerulonephritis (nephritic
oedema).
• There is excessive reabsorption of sodium
and water in the renal tubules via renin-
angiotensin- aldosterone mechanism.
• Mild as compared to nephrotic oedema.
• Begins in the loose tissues such as on the
face around eyes, ankles and genitalia.
ACUTE TUBULAR
INJURY
• Acute tubular injury following shock or
toxic chemicals.
• damaged tubules lose their capacity for
selective reabsorption and concentration
of the glomerular filtrate
• Resulting in increased reabsorption
and oliguria.
• Excessive retention of water and
electrolytes and rise in blood urea
Cardiac
• Generalised edema
cardiac failure.
Oedema
caused due to right-sided and congestive
• Influenced by gravity - dependent oedema
• Reduced cardiac output
– causes hypovolaemia which in turn activates
– intrinsic-renal and extra-renal hormonal (reninangiotensin-
aldosterone) mechanisms.
– as well as ADH secretion resulting in sodium and water retention
• Back Pressure Hypothesis
– Right sided heart failure - elevated central venous pressure
– transmitted backward to the venous end of the capillaries,
– raising the capillary hydrostatic pressure and consequent
transudation;
• Forward Pressure Hypothesis
– Chronic hypoxia - injure the capillary wall
– Causing increased capillary permeability and result in oedema
– This theory lacks support since the oedema by this mechanism is
exudate whereas the cardiac oedema is typically transudate
Cardiac
Oedema
Pulmonary
• Most important form of local oedema as it causes serious
functional Oedema
impairment
• Fluid accumulation in tissue space as well as alveoli
• ETIOPATHOGENESIS.
– Elevation of pulmonary hydrostatic pressure
– Increased capillary permeability
Elevation in pulmonary
hydrostatic pressure
• In heart failure, there is increase in the pressure in
pulmonary veins which is transmitted to
pulmonary capillaries.
• These causes imbalances between pulmonary
hydrostatic pressure and the plasma oncotic pressure.
• Excessive fluid moves out of pulmonary capillaries into
the interstitium of the lungs.
• These are cleared by the lymphatics present around
the bronchioles and veins.
• As the capacity of the lymphatics to drain the fluid is
exceeded (about ten-fold increase in fluid), the excess
fluid starts accumulating in the interstitium
Elevation in pulmonary
hydrostatic pressure
• Prolonged elevation of hydrostatic pressure and due
to high pressure of interstitial oedema.
• Alveolar lining cells break and the alveolar
air spaces are flooded with fluid
• Driving the air out of alveolus - seriously
hampering the lung function.
• Ex: left heart failure, mitral stenosis, pulmonary vein
obstruction, thyrotoxicosis, cardiac surgery, nephrotic
syndrome and obstruction to the lymphatic outflow
by tumour or inflammation
Increased vascular permeability
(Irritant Oedema)
• Damage in vascular endothelium as well as the
alveolar epithelial cells (alveolo-capillary membrane).
• Increased vascular permeability.
• Excessive fluid and plasma proteins leak out -
initially into the interstitium and subsequently into
the alveoli
• Examples: fulminant pulmonary and
extrapulmonary infections, inhalation of toxic
substances, aspiration, shock, radiation injury,
hypersensitivity to drugs or antisera, uraemia and
acute respiratory distress syndrome (ARDS)
Acute high altitude
• oedema
Individuals climbing to high altitude suddenly without halts
and without waiting for acclimatisation
• Suffers from serious circulatory and respiratory ill-effects.
• Particularly at heights of 2500 metres.
• These changes include
– Pulmonary edema,
– Congestion
– widespread minute haemorrhages.
• These changes can cause death within a few days.
• The underlying mechanism appears to be anoxic damage to
the pulmonary vessels.
• However, if acclimatisation to high altitude is allowed to take place
• the individual develops polycythaemia,
• raised pulmonary arterial pressure,
• Increased pulmonary ventilation
• a rise in heart rate and increased cardiac output
PATHOLOGICAL CHANGES
• Fluid accumulation in basal region of lungs
• Thinkened interlobar septa and dilated
lymphatics
• Chest x ray- Linear lines perpendicular to pleura-
Kerly ‘s line
• GROSS- heavy,moist,crepitant.
• Cut surface- exudes frothy fluid
• Microscopically-interstial and alveolar oedema.
Eosinoplilic,granular, pink proteinaceous
material admixed with RBCs.
THANKS…
…
[Link]/notesdent
al
Reference
s
• Robbinson's basic pathology 8 ed
• Harsh Mohan - Textbook of Pathology 6th
Ed.
• Color atlas of pathology
