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
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