Types of Oedema - Pathology

(Robbins & Kumar Basic Pathology, Chapter 3)

What is Oedema?

Oedema is an accumulation of interstitial fluid within tissues. About 60% of lean body weight is water; most of the extravascular fraction is interstitial fluid. When fluid collects in body cavities rather than tissue it is called an effusion:

Cavity	Term
Pleural cavity	Hydrothorax
Pericardial cavity	Hydropericardium
Peritoneal cavity	Hydroperitoneum / Ascites
Generalised + body cavities	Anasarca

Underlying Mechanisms (Starling Forces)

Fluid movement between the vascular and interstitial spaces is governed by two opposing forces:

Vascular hydrostatic pressure - pushes fluid out of capillaries
Colloid osmotic pressure (produced by plasma proteins, mainly albumin) - pulls fluid back in

The small net outflow of fluid is normally drained by lymphatics back to the bloodstream. Oedema results when this balance is disrupted.

Classification by Mechanism / Types

1. Increased Hydrostatic Pressure (Non-inflammatory)

Mechanism: Impaired venous return raises capillary pressure, forcing fluid into the interstitium.

Causes:

Congestive heart failure - most important systemic cause. Reduced cardiac output causes venous pooling + renal hypoperfusion → renin-angiotensin-aldosterone activation → sodium and water retention (secondary hyperaldosteronism) → worsening oedema (vicious cycle)
Deep venous thrombosis (localised leg oedema)
Constrictive pericarditis
Liver cirrhosis (portal hypertension)
External compression by a mass
Lower extremity dependency/inactivity
Arteriolar dilation (heat, neurohumoral dysregulation)

Fluid type: Protein-poor transudate

2. Reduced Plasma Osmotic Pressure (Hypoproteinaemia)

Mechanism: Low plasma albumin reduces the force pulling fluid back into vessels.

Causes of low albumin:

Nephrotic syndrome - glomerular damage allows albumin to leak into urine (proteinuria)
Liver cirrhosis / severe liver disease - reduced albumin synthesis
Protein malnutrition (kwashiorkor)

Secondary hyperaldosteronism again develops, but the salt/water retention worsens oedema because the primary defect (low albumin) persists.

Fluid type: Protein-poor transudate

3. Lymphatic Obstruction (Lymphoedema)

Mechanism: Blocked lymphatics prevent resorption of interstitial fluid.

Causes:

Filariasis (parasitic infection) - massive oedema of lower extremities ("elephantiasis")
Inflammatory conditions (recurrent cellulitis)
Neoplastic infiltration of lymph nodes
Post-surgical/post-radiation scarring (e.g., arm oedema after axillary lymph node dissection in breast cancer)

Fluid type: Protein-rich (lymph stasis causes protein accumulation)

4. Sodium Retention (Renal causes)

Mechanism: Increased sodium retention leads to obligatory water retention, expanding intravascular volume and raising hydrostatic pressure.

Causes:

Renal failure (acute or chronic) - reduced GFR
Post-streptococcal glomerulonephritis

Fluid type: Transudate

5. Inflammatory Oedema

Mechanism: Release of vasoactive mediators (histamine, bradykinin, leukotrienes, cytokines) increases vascular permeability, allowing protein-rich fluid to leak out.

Causes: Any inflammation - infection, immune reaction, trauma, burns

Fluid type: Protein-rich exudate (key distinction from non-inflammatory types)

Summary: Transudate vs Exudate

Feature	Transudate	Exudate
Protein content	Low	High
Mechanism	Hydrostatic/osmotic imbalance	Increased vascular permeability
Causes	Heart failure, nephrotic syndrome, cirrhosis, renal failure	Inflammation, infection
Appearance	Clear, watery	Turbid, may be purulent

Morphology (Gross & Microscopic)

Subcutaneous oedema:

Follows gravity - legs when standing, sacrum when recumbent = dependent oedema
Finger pressure leaves a temporary pit = pitting oedema
Renal/nephrotic syndrome often presents as periorbital oedema (loose connective tissue of eyelids affected first)

Pulmonary oedema:

Lungs 2-3x normal weight
Cut surface exudes frothy, sometimes blood-tinged fluid
Most common cause: left ventricular failure
Also: renal failure, acute lung injury, infections

Cerebral oedema:

Can be localised (abscess, tumour) or generalised (trauma, metabolic)
Sulci narrow as gyri swell and flatten against skull
Life threatening - herniation through foramen magnum, compression of brainstem → death

Clinical Significance

Location	Key Concern
Subcutaneous	Signals cardiac or renal disease; impairs wound healing
Pulmonary	Impairs ventilation; creates environment for infection
Cerebral	Life threatening - brain herniation, brainstem compression

Source: Robbins & Kumar Basic Pathology, Chapter 3 (Haemodynamic Disorders)

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