General Oedema

Introduction

• General oedema involves subcutaneous and tissue spaces/body cavities.
• Indicative of severe upset of overall body fluid balance.
  • Usually one or more vital organ system is abnormal.
• Requires one or more of the following conditions:
  1. General increase in arteriolar hydrostatic pressure.
  2. Decrease in osmotic pressure of blood.
  3. Increase in tissue fluid osmotic pressure.
     • E.g. sodium retention in renal disease.
  4. Increased capillary permeability.
     • E.g. due to hypoxic damage.

Types of General Oedema

Cardiac oedema

• Seen in heart failure.
  • Shows that cardiac output fails to meet the demands of the tissues throughout the body.
  • Left-side failure gives pulmonary congestion.
    • Leads to pulmonary oedema.
  • Right-side failure gives systemic congestion.
    • Leads to generalised oedema.
• Chronic venous congestion develops when cardiac output fails to keep pace with venous return to the heart.
• Fluid balance is further complicated by secondary renal impairment.
  • Sodium is retained, triggering the renin-aldosterone loop with further sodium retention.

Renal oedema

• Kidney malfunction induces oedema as a consequence of deranged sodium and water handling.
  • There is often secondary cardiac involvement.
    • Due to via renin effect on heart and myocardial depressant factor.
• Causes:
  1. Acute glomerulonephritis
     • Reduction in glomerular filtration rate results in systemic hypertension and retention of excess sodium and water.
  2. Nephrotic syndrome
     • A glomerular filtration defect gives selective heavy loss of plasma proteins (especially albumin)
       • Reduction of plasma osmotic potential results in oedema.
  3. Acute renal tubular necrosis
     • Tubules can no longer selectively reabsorb sodium and other electrolytes.
       • Water retention with the sodium and urea produces oedema.
  4. Fibrosing glomerulonephritis
     • Causes systemic hypertension and secondary cardiac failure with oedema.

Protein-losing enteropathies

• Mucosal damage leads to loss of ability to absorb and retain proteins.
  • Plasma proteins, especially albumin are lost.
    • Circulating plasma proteins area therefore reduced, leading to oedema.
• E.g.
  • Johne's disease in cattle and sheep.
  • Ulcerative colitis or regional enteritis in dogs.
• For more on protein-losing enteropathies, see Protein-Losing Diseases.

Hepatic oedema

• Associated with severe liver damage.
  • Liver damage may be:
    • Actue
      • E.g. due to acute fascioliasis or canine viral hepatitis.
      • Lymphatics and blood vessels of the liver and peritoneal caivity are damaged.
        • Results in "overflow" of fluid into the peritoneal cavity.
      • Additionally, hepatocyte damage may result in inadequate inactivation of aldosterone.
        • Increases sodium retention giving further water accumulation in the abdomen
    • Chronic
      • E.g. metastatic neoplasia or fibrosing hepatopathy (cirrhosis).
      • Failure to produce plasma proteins leads to osmotic imbalance in the peripheral circulation.
      • This is seen as subcutaneous oedema.
        • E.g. "bottle jaw".