oedema

OedemaDr. Deepak K. Gupta

Introduction

• It may be defined 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

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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.


Oedema: Causes• Increased Hydrostatic Pressure

– Impaired venous return – Congestive heart failure – Constrictive pericarditis– Ascites (liver cirrhosis) – Venous obstruction or

compression• Thrombosis, • External pressure (e.g.,

mass), • Lower extremity inactivity

with prolonged dependency– Arteriolar dilation

• Heat,• Neurohumoral

dysregulation,

• Reduced Plasma Osmotic Pressure (Hypoproteinemia)– Protein-losing

glomerulopathies (nephroticsyndrome)

– Liver cirrhosis (ascites) – Malnutrition Protein-losing

Gastroenteropathy

• Lymphatic Obstruction– Inflammatory – Neoplastic– Postsurgical – Postirradiation

• Sodium Retention– Excessive salt intake with renal

insufficiency– Increased tubular reabsorption

of sodium

• Inflammation– Acute inflammation – Chronic inflammation – Angiogenesis


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


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 andwater 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 forselective reabsorption and concentration of the glomerular filtrate

• Resulting in increased reabsorption and oliguria.

• Excessive retention of water and electrolytesand rise in blood urea


Cardiac Oedema• Generalised edema caused due to right-sided and congestive cardiac

failure.• 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 Oedema• Most important form of local oedema• it causes serious functional impairment• 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 oncoticpressure.

• 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 interstitialoedema.

• Alveolar lining cells break and the alveolar airspaces are flooded with fluid

• Driving the air out of alveolus - seriously hampering the lung function.

• Ex: left heart failure, mitral stenosis, pulmonary veinobstruction, thyrotoxicosis, cardiac surgery, nephroticsyndrome and obstruction to the lymphatic outflow bytumour or inflammation


Increased vascular permeability

• 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 extrapulmonaryinfections, 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


References

• Robbinson's basic pathology 8 ed

• Harsh Mohan - Textbook of Pathology 6th Ed.

• Color atlas of pathology


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oedema

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