Types of oedema pathology
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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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