Hypoadrenocorticism

• What is primary hypoadrenocorticism?

  Addison’s disease:

  • Deficiency of glucocorticoids (cortisol) and deficiency of mineralcorticoids (aldosterone).
  • Occurs with the loss of 85-90% of the adrenal cortex.
• What causes hypoadrenocorticism in the dog?

  Idiopathic atrophy

  • Probably immune mediated destruction.

  Iartogenic

  • Drugs: mitoctane, trilostane.
  • Surgery: bilateral adrenalectomy
• What is secondary hypoadrenocorticism?

  Rare deficiency of ACTH.

  Cause deficiency if glucorticoids but not (life threatening) deficiency of mineralcorticoids.
• What is the pathophysiology of hypoadrenocorticism?

  Aldosterone deficiency:

  • Loss of Na+, Cl, H2O
  • Retention of K+, H+
  • Pre-renal azotaemia (apparent renal failure)

  Glucocorticoid deficiency:

  • Decreased stress intolerance, gastrointestinal signs, weakness, appetite loss, anaemia, impaired gluconeogenesis.
• What are the history and clinical signs of hypoadrenocorticism?

  Chronic:

  • Waxing waning form with non-specific signs.

  Acute:

  • Addison ‘crisis’ form with marked hypovolaemia and azotaemia.
• What is the signalment for hypoadrenocorticism?

  Breeds:

  • Standard poodles
  • Bearded collies.
  • Great Dane’s
  • Portuguese water dogs
  • Rottweilers
  • WHW terrier
  • Soft-coated Wheaten terriers.

  Young to middle age

  • 3 months to 14 years
  • Median 4-6 years
• What are the general clinical signs of hypoadrenocorticism?

  Collapsed, weak, hypothermic.

  Depression

  Thin

  Dehydration

  Bradycardia

  Melena/haematochezia (uncommon)

  • Abdominal pain with melena is sometimes a feature and the disease can resemble pancreatitis clinically.
• What are the clinical signs of chronic hypoadrenocorticism?

  Vague and non-specific.

  Waxing and waning

  Intermittent collapse/ weakness

  Anorexia

  Diarrhoea

  Vomiting

  Weight loss

  Lethargy

  Depression
• What are the haematology of hypoadrenocorticism?

  Lack of stress leucogram (34-71%)

  Anaemia (34-17%)

  • Decreased erythrocytosis due to lack of cortisol
  • GI blood loss.

  Eosinophilia (10%)

  • Due to lack of cortisol.

  Lymphocytosis (13%)

  • Due to lack of cortisol.

  Relative neutropenia

  • Less inhibition of vascular margination.
• Overview of primary hypoadrenocorticism

  Loss of both gluocorticoid and mineralcorticoid output.

  Clinical signs and lab results attributable to deficiency of glucocorticoids and mineralcorticoids.

  Often Na:K changes (reduced Na:K ration, elevated K and/or low Na)
• Overview of atypical hypoadrenocorticism

  This is primary hypoadrenocorticism (same adrenal cortex pathology) bit with normal electrolytes.

  Clinical signs and lab results attribute to deficiency of glucocorticoids.
• Overview of secondary hypoadrenocorticism

  Loss of glucocorticoids only (GDH - glucocorticoid deficients hypoadrenocorticism).

  Clinical signs and lab results attribute to deficiency of glucorticoids.
• What are the lab results for classic primary hypoadrenocorticism?

  Unexpected lack of stress leukogram

  Azotaemia (Urea, Creatinine, Phosphate)

  Hyonatraemia

  Hyperkalaemia

  Na:K

  Acidosis

  Hypochloremia

  Hypercalcaemia

  Hypoalbuminaemia

  Hypocholesterolaemia
• What are the lab results for secondary and atypical primary hypoadrenocorticism?

  Unexpected lack of stress leukogram.

  Hypoglycaemia

  Hypoalbuminaemia

  Hypocholesterolaemia.
• Why measure aldosterone?

  Differentiate primary from secondary hypoadrenocorticism.

  Diagnose primary hypoadrenocorticism despite having started glucocorticoids.

  Diagnose primary hypoadrenocorticism despite normal electrolytes.
• How do you treat acute hypoadrenocorticism?

  Resuscitate intravascular volume - IV fluids (NaCl).

  Check correction of Na:K ratio.

  Glucocorticoids (fluids first)

  • Hydrocortisone 5-10mg/kg IV every 6 hours
  • Dexamethasone 0.5-2.0mg/kg IV
  • Methyl prednisolone sodium 1-2 mg/kg IV.
• Restoration of intravascular volume

  Place IV catheter.

  Begin 0.9% saline or Hartmann’s solution at 20-90 ml/kg/hr.

  Assess effectiveness frequently.

  Once volume restores, reduce rate to maintenance (2ml/kg/hr)

  Continue fluids until hydration status, urine output, serum electrolytes and azotaemia are corrected.
• Fluid reversal of hypokalaemia

  FLUID THERAPY!!!!!
• Longterm management - primary hypoadrenocorticism

  Desoxycortone pivalate:

  • Licensed
  • Mineralcorticoid replacement only, so need to supplement with prednisolone.
  • Given by injection approx q20-30 days, dose interval adjusted by Na:K monitoring.

  Fludrocortisone:

  • Not licensed
  • Mineralcorticoid and glucocorticoid replacement.
  • Oral medication BID
• Long term management - glucocorticoids

  Prednisolone 0.2mg/kg

  Required as adjunct for Zycortal therapy.

  Not required for Fludrocortisone except during stress and illness.

  Required for secondary hypoadrenocorticism (GDH).