Difference between revisions of "General Oedema"

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[[Category:Circulatory Disorders - Pathology]]
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[[Category:Circulatory Disorders - Pathology]][[Category:Chris Palgrave reviewing]]

Revision as of 11:01, 21 July 2011

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.
        • 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".