Page 946 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition

Endocrine system 921

VetBooks.ir Aetiology/pathophysiology for sepsis or other life-threatening disease. Clinical
signs in horses with adrenal insufficiency are often
The adrenal gland is made up of the adrenal cor-
tex and the adrenal medulla. The outermost zone
weight loss, diarrhoea and polyuria and polydipsia
of the adrenal cortex is the zona glomerulosa, vague and include poor appetite, muscle weakness,
which secretes mineralocorticoids (aldosterone); with dilute urine.
the middle zone is the zona fasciculata, which
secretes glucocorticoids (cortisol); and the inner- Differential diagnosis
most zone is the zona reticularis, which secretes Differential diagnosis for foals with adrenal insuf-
adrenal androgens. The adrenal medulla secretes ficiency includes sepsis, ruptured bladder and enteri-
catecholamines (primarily adrenaline [epineph- tis. Differential diagnosis in adult horses includes
rine]). The hypothalamic– pituitary adrenal (HPA) sepsis or an internal abscess, poor diet, parasitism,
axis develops immediately prior to birth and does colitis and renal disease.
not mature until several weeks after birth, which
may predispose foals to developing adrenal insuf- Diagnosis
ficiency. High ACTH concentrations in the face of Hyponatraemia and hypochloraemia with hyper-
normal or low cortisol concentrations in premature kalaemia is the hallmark of adrenal insufficiency.
or septic foals point to an inability of the adrenal In instances of glucocorticoid insufficiency with-
gland to respond to stimuli appropriately. The rea- out mineralocorticoid involvement, the classic
sons why CIRCI develops are poorly understood- electrolyte distribution may not be present, and
but are thought to be related to direct effects of the the absence of hyperkalaemia does not rule out
inciting pathological process on the adrenal gland, adrenal insufficiency. The ACTH response test
exhaustion of synthetic capacity and decreased sen- can produce a definitive diagnosis. Several proto-
sitivity of target tissues to the effects of cortisol. cols have been published (see Table 6.12), but in
Horses with sepsis are also prone to developing all of them one is determining whether the adre-
infarcts of the adrenal glands, which may further nal glands can respond to exogenous ACTH by
inhibit their function. secreting cortisol.
Adrenal insufficiency in animals without a predis-
posing disease is rare in horses. In many instances, Management
the horse has received prolonged anabolic or cor- Treatment with corticosteroids rapidly reverses the
ticosteroid administration suggesting that down- clinical signs. In acute situations, parenteral dexa-
regulation of their endogenous axis is an important methasone at a dose of 25 mg/450 kg/day is indicated.
component in equine patients. Cortisol replacement therapy in CIRCI consists
of 1–4 mg/kg/day hydrocortisone i/v. Long-term
Clinical presentation replacement in horses and foals can be accomplished
The clinical presentation of a foal or horse with with oral prednisolone at a dose of 0.25–1.0 mg/kg
RAI is one that is responding poorly to treatment p/o q24 h.

Table 6.12 Protocol for ACTH stimulation testing
1 Take a control serum sample
®
2 Administer 0.1 µg/kg consyntropin (Cortrosyn )i/v
3 Take additional serum sample 30 minutes after
4 Submit samples for cortisol determination
5 30-minute sample should be double the baseline value of cortisol