From WikiVet English
Revision as of 20:41, 13 August 2009 by A.allison (talk | contribs) (New page: {{review}} {{toplink |linkpage =General Pathology |linktext =General Pathology |maplink = General Pathology (Content Map) |pagetype =Pathology |sublink1=Circulatory Disorders - Pathology ...)

(diff) ← Older revision | Approved revision (diff) | Latest revision (diff) | Newer revision → (diff)

Jump to navigation Jump to search

WikiPathWikiPath Banner.png


  • Oedema is NOT a disease.
    • Is the sign of a disease state.
  • Oedema is defined as :

"The swelling of tissues resulting from accumulation of excess fluid in the intercellular tissue spaces and serous cavities."

  • Small amounts of fluid are normally present to lubricate cavities and viscera - this is not oedema.
  • Excess fluid may accumulate in:
    • Subcutaneous tissue and between muscle.
    • Serous cavities.
      • Depending on the cavity, this has different terms.
        • Thorax - hydrothorax.
        • Pericardium - hydropericardium
        • Abdomen - hydroperitoneum (ascites).
      • Anasarca is when there is generalised body cavity accumulation plus subcutaneous involvement.
    • Lungs.

Local oedema

  • Local oedema is the local accumulation of excess interstitial fluid.
  • Caused by disturbance of the balance betwen fluid extravasation and resorption at the level of the capillaries.
    • Outwards Forces - arteriolar
      • Vasuclar hydrostatic pressure - 35 mmHg
      • Interstitial osmotic pressure - 3 mmHg
    • Inwards forces - venular
      • Plasma protein osmotic pressure - 25 mmHg
      • Interstitial hydrostatic pressure - 4 mmHg
  • May be of inflammatory or non-inflammatory origin.

Types of Local Oedema

Inflammatory oedema

  • Generated by one or more of the following:
    1. Increased vascular permeability
    2. Increased arteriolar blood pressure
    3. Breakdown of tissue protein or transfer of plasma proteins into ECF.
      • Results in raised osmotic pressure of tissue fluid.
    4. Obstruction to lymphatic drainage.
      • Usually by fibrin.

Lymphatic oedema

  • Results in accumulation of high protein fluid.
  • May provoke a granulation or fibrous tissue response.
  • Due to:
    1. Lymphangitis/ lymphadenitis
      • Acute inflammation of lymphatics/ lymph nodes. R
      • Caused by stasis in lymphatics and/or bacterial infection.
      • E.g. “Monday Morning leg” in horses.
    2. Chronic inflammation caused by persistent or granuloma-producing bacterial infection.
    3. Tumour spread.
      • Metastasis of tumour cell plugs lymphatics and nodes
      • e.g. mammary carcinoma.
    4. Parasitic migration
      • Larvae may be following their normal pathway (e.g. Schistosomiasis), or may be aberrant.

Local venous obstruction

  • Obstruction to venous drainage may be mechanical or inflammatory-mediated.
    • Causes raised hydrostatic pressure.
    • Endothelial permeability increases due to hypoxia.
    • There may be inflammatory damage.
  • Mechanical obstruction, e.g.
  • Venous inflammation (phlebitis)
    • May be associated with thrombosis (thrombophlebitis).

"Allergic" oedema

  • Results from immediate (Type I ) or delayed (Type IV) hypersensitivity.
  • Vasular permeability is increased due to release of histamine and vaso-dilating substances.
  • E.g.
    • Insect stings (immmediate).
    • Vaccination (delayed).
    • Food reaction (delayed).

Pulmonary oedema

  • In the normal state, pulmonary alveoli are kept dry by three mechanisms:
    1. Normal "push-pull" mechanism at capillary level.
    2. Efficient lymphatic drainage by rhythmic pumping action near airways.
    3. Integrity of the alveolar epithelial basement membrane is relatively impermeable.
      • Unlike the capillary basement membrane, which is relatively permeable.
  1. The pumping efficiency of the lymphatics is exceeded.
  2. Fluid accumulates in connective tissue adjacent to airways.
  3. The alveolar walls fill with fluid.
  4. The alveoli abruptly and severely fill with fluid.
    • Associated with the disintegration of alveolar epithelial junctional complexes.

Haemodynamic type
  • Fluid leaks into alveoli via junctional complexes BUT the alveolar basement membrane remains intact.
    • I.e. is due to elevated pulmonary venous pressure.
  • Potentially reversible.
  • Causes:
    1. Cardiogenic
      • Usually left ventricular failure.
      • Also occurs with cardiac overload due to valvular disease.
    2. Mechanical
      • Large primary pulmonary tumours.
      • Severe metastatic disease.
      • Granulomatous infections may raise pulmonary venous pressure.
    3. Neurogenic
      • Seizures or CNS disorder.
      • Rare in domestic species.
Permeability type
  • Fluid fills the alveoli following damage to cells or junctional complexes, or permanent ionic alteration of the alveolar basement membrane.
  • Irreversible.
  • Causes:
    1. Toxins
    2. Aspiration/inhalation
      • Gastric contents (low pH)
      • Smoke.
      • Excess ozone.
      • Oxygen.
  • There may be a combination of haemodynamic and permeability types in electrocution syndromes and "shock" lung.
    • E.g. in Adult Respiratory Distress Syndrome (ARDS).

General oedema

  • 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".

Composition of oedema fluid

  • Inflammatory oedema which produces an exudate.
    • This is a protein rich fluid containing many inflammatory cells.
  • Non inflammatory oedema which produces a transudate.
    • This fluid is low in protein and cells.
  • Transudates and exudates are distinguished by the following criteria:
Criteria Transudate Exudate
Appearance Clear/ pale yellow ("straw coloured") Dark yellow, red or brown. Often cloudy or opaque.
Consistency Thin, serous Viscous
Protein content 0.05 - 0.5%, mainly albumin Usually 2 - 4%
Coagulability No fibrinogen, no coagulation Contains fibrinogen, coagulates
Specific gravity Low (< 1.012) High (1.012 - 1.020) +
Cell content Very low. mesothelial cells, some macropahges and lymphocytes/monocytes. High. Often macrophages, neutrophils, lymphocyes etc. Depends on cause and chronicity

  • Examples of transudates:
    • Ascites
      • Excessive fluid in abdominal cavity.
    • Hydrothorax
      • Excessive fluid in the thorax.
    • Hydropericardium
      • Excessive fluid in the pericardium.
    • Anasarca
      • Generalised tissue oedema most noticeable in subcutaneous tissues.
    • Ventral subcutaneous oedema
  • Seen in heart failure in horses and cattle.