Pathophysiology
Spontaneous hypoadrenocorticism (Addison's disease)
is caused by failure of adrenal gland secretion of glucocorticoids and mineralocorticoids.
The underlying pathology is usually immune mediated destruction of the adrenal
cortices. Spontaneous central (pituitary mediated) hypoadrenocorticism
occurs much less commonly and results from inadequate pituitary ACTH secretion.
"Central hypoadrenocorticism" is most commonly iatrogenic.
Signalment and Clinical Signs
Various breeds are predisposed including standard poodles, West Highland
white terriers, Great Danes and bearded collies. Young-middle aged dogs
(males and females) are typically affected (average age 4 years).
The history is frequently vague, with intermittent clinical signs and variable
response to symptomatic therapies. Anorexia, vomiting, diarrhoea, weakness,
exercise intolerance, polydipsia and polyuria are usual. Gastrointestinal
haemorrhage is not uncommon. Clinical signs may be precipitated by a stressful
event such as kennelling, veterinary attention or domestic changes.
Diagnostic Tests
Hyperkalaemia, hyponatraemia, hypochloraemia, hypercalcaemia, azotemia,
metabolic acidosis, hypoglycaemia, lymphocytosis and eosinophilia are typical.
A mild normocytic normochromic anaemia may occur and there may be evidence
of anaemia secondary to GI blood loss. A useful clue can be the presence
of an inappropriately "normal" or increased lymphocyte
count in a clinically ill dog due to reduced circulating glucocorticoids.
Radiographic findings relate to hypovolaemia. Urinalysis generally demonstrates
inappropriately dilute urine.
This can lead to a misdiagnosis of primary renal dysfunction. ECG abnormalities
generally reflect the electrolyte disturbances. Confirmation requires an
ACTH stimulation test which demonstrates inadequate adrenocortical reserve
capacity. Aldosterone measurement can be used to retrospectively confirm
Addison's disease in dogs that have already been started on therapy with
glucocorticoids. Endogenoues circulating ACTH concentrations are increased
in primary Addison's disease but not so in central Hypoadrenocorticism.
Treatment
Treatment of the acute hypoadrenal crisis is a true medical emergency. Therapy
should be primarily directed at restoring circulating blood volume, correcting
electrolyte and acid-base status, and glucocorticoid supplementation. Life-threatening
hyperkalaemia can be treated with iv glucose solution, sodium bicarbonate
administration, soluble insulin therapy or calcium gluconate administration.
These therapies must be very carefully controlled: doses and protocols are
reported elsewhere. Please contact the lab for specific advice if required.
Chronic therapy of the stable Addisonian dog consists of permanent mineralocorticoid
therapy (fludorcortisone acetate, starting dose 0.015mg/kg/day).
Dogs may or may not also require concurrent glucocorticoid therapy. Initially
dogs should be medicated with 0.5 mg/kg prednisolone, on a tapering regime.
In some cases glucocorticoid therapy can be stopped, but others require
a low dose (approx 0.2 mg/kg/day) for life. |