Page 911 - Small Animal Internal Medicine, 6th Edition
P. 911
CHAPTER 50 Disorders of the Adrenal Gland 883
results of the ACTH stimulation test, UCCR, and serum important to avoid an addisonian crisis in cats undergoing
electrolyte concentrations, initially performed 4 weeks after bilateral adrenomegaly.
VetBooks.ir initiation of trilostane treatment—earlier if clinical signs HYPOADRENOCORTICISM
suggestive of hypoadrenocorticism or clinical signs sugges-
tive of hypoglycemia in cats with insulin-resistant diabetes
develop. The dosing schedule should be continued if
improvement in clinical signs and test results are noted by 4 Etiology
weeks, even if the goals of therapy have not yet been attained. Hypoadrenocorticism is a deficiency of mineralocorticoids
The dosing schedule should be changed if no improvement (i.e., aldosterone), glucocorticoids (i.e., cortisol), or both.
or worsening of clinical signs and test results are observed at Primary adrenocortical insufficiency (Addison’s disease)
4 weeks. In general, twice-daily dosing provides better with a deficiency of mineralocorticoid and glucocorticoid
control than once-daily dosing and should be the initial secretion is the most common. Primary hypoadrenocorti-
adjustment in cats that remain symptomatic at the starting cism is usually classified as idiopathic because the cause
dose given once daily. Subsequent adjustments in the dose of the disease is not obvious, and necropsies are usually
of trilostane should be based on findings at the 4-week done years after the diagnosis is established, at which time
rechecks. A decrease in insulin requirements will usually idiopathic atrophy of all layers of the adrenal cortex is the
occur as control of PDH is attained. Mellett et al. (2013) most frequent histopathologic finding. Immune-mediated
reported a median survival of 617 days in 15 cats treated with destruction of the adrenal cortices is believed to occur in
trilostane. most dogs with idiopathic adrenal insufficiency; lympho-
Adrenalectomy is the treatment of choice for ADH; bilat- plasmacytic inflammation and fibrosis are common findings
eral adrenalectomy is also an effective treatment for PDH. in animals that undergo necropsy near the time of diagno-
Medical treatment with trilostane is usually necessary for sis. Bilateral destruction of the adrenal cortex by neopla-
4 to 6 weeks before adrenalectomy to reverse the catabolic sia (e.g., lymphoma), granulomatous disease, hemorrhagic
state of the cat, improve skin fragility and wound healing, infarction, arterial thrombosis, or drugs such as mitotane
and decrease the potential for perioperative complications. and trilostane can also cause primary adrenocortical insuf-
The surgical approach and medical management during and ficiency. For clinical signs to develop, it is believed that at
after surgery are similar to those used in dogs (see p. 875). least 90% of the adrenal cortices must be destroyed. The
Treatment for hypoadrenocorticism should begin immedi- zones of the adrenal cortices are usually damaged at about
ately after bilateral adrenalectomy and should include inject- the same rate, with aldosterone and cortisol deficiencies typi-
able DOCP (2.2 mg/kg administered subcutaneously every cally occurring in tandem. Destruction is progressive, ulti-
25 days initially; Percoten-V) or fludrocortisone acetate mately leading to complete loss of adrenocortical function.
(0.05 mg/cat administered orally q12h initially; Florinef), Dogs and cats typically have complete loss of adrenocorti-
as well as prednisolone (1-2.5 mg once daily). Subsequent cal function at the time hypoadrenocorticism is diagnosed.
adjustments in the dose of DOCP or fludrocortisone acetate A partial deficiency syndrome characterized by inadequate
should be based on periodic measurement of serum elec- adrenal reserve may occur initially, with clinical signs mani-
trolyte concentrations (see p. 888). Insulin therapy can be fested only during times of stress such as boarding, travel,
discontinued in approximately 50% of cats once hyperadre- and surgery. As destruction of the adrenal cortex progresses,
nocorticism is eliminated, and diabetes is easier to control hormone secretion becomes inadequate even under non-
with the use of less insulin in the remaining cats. stressful conditions, and a true metabolic crisis occurs with
no obvious inciting event.
Prognosis Mineralocorticoids (i.e., aldosterone) control sodium,
The prognosis is guarded to poor. Untreated hyperadrenal potassium, and water homeostasis. In the setting of primary
cats die within months after the diagnosis has been estab- adrenocortical insufficiency, loss of aldosterone secretion
lished because of the deleterious effects of chronic hypercor- results in impaired renal conservation of sodium and chlo-
tisolism and insulin-resistant diabetes mellitus on skin ride and excretion of potassium, leading to the development
integrity and immune function, and as a result of progressive of hyponatremia, hypochloremia, and hyperkalemia. The
weight loss leading to severe cachexia. The effectiveness of inability to retain sodium and chloride reduces extracellular
trilostane remains to be evaluated in a large group of hyper- fluid volume, leading to progressive development of hypovo-
adrenal cats. Unilateral (ADH) or bilateral (PDH) adrenal- lemia, hypotension, reduced cardiac output, and decreased
ectomy has the potential for excellent success; however, perfusion of the kidneys and other tissues. Hyperkalemia has
success depends, in part, on correction of the debilitated a deleterious effect on cardiac function, causing decreased
state and skin fragility with medical treatment before surgery, myocardial excitability, an increased myocardial refractory
involvement of a surgeon with expertise in adrenal surgery, period, and slowed conduction. A concurrent glucocorticoid
avoidance of perioperative complications, and the client’s deficiency typically results in gastrointestinal tract signs
commitment to managing iatrogenic adrenal insufficiency (e.g., anorexia, vomiting, diarrhea, weight loss) and changes
after bilateral adrenalectomy. Periodic evaluation of serum in mental status (e.g., lethargy). One of the hallmark signs
electrolytes and review of the treatment protocol are of hypocortisolism is impaired tolerance to stress, and