Veterinary Medicine - June 2008 - (Page 328)

Canine hypoadrenocorticism PEER-REVIEWED Relative hypoadrenocorticism: An emerging concern When the body is stressed from severe illness, trauma, or surgery, glucocorticoid production is stimulated. Glucocorticoids promote vasoactive responses to catecholamines and help regulate vascular permeability, thus contributing to the maintenance of blood pressure and intravascular volume.1 The role of glucocorticoids in critical illness has been well-studied in people. Most critically ill people have higher basal and ACTH-stimulated plasma cortisol concentrations than healthy individuals do. However, in 38% of people with severe sepsis, relative adrenal insufﬁciency (RAI) has been recognized.2 In RAI, the basal cortisol concentration is variable, and an inadequate response after ACTH stimulation is noted. This blunted cortisol response has been linked to an increased mortality in people with severe sepsis and septic shock.2 Low-dose corticosteroid treatment has signiﬁcantly improved survival in people with sepsis-induced RAI.3 The exact pathogenesis of RAI is unknown. It has been speculated that certain inﬂammatory mediators may suppress the hypothalamic-pituitary-adrenal axis, or disseminated intravascular coagulation may cause adrenal infarction or hemorrhage.4 RAI has been investigated in dogs with various critical illnesses, including sepsis.1,4 In dogs with naturally developing sepsis, a blunted blood cortisol response to ACTH (difference between pre-ACTH and post-ACTH stimulation plasma cortisol concentrations ≤ 3 µg/dl) was signiﬁcantly associated with hypotension and mortality.4 However, in a different study of dogs with a variety of critical illnesses, no signiﬁcant difference was noted between basal and post-ACTH stimulation plasma cortisol concentrations between dogs in the survivor and nonsurvivor groups.1 RAI is evaluated in dogs by performing a standard ACTH stimulation test using the full 0.25-mg/dog ACTH dose given intravenously.1,4 Lower doses of ACTH may be more appropriate for evaluating RAI, but no evidence supports this hypothesis in veterinary medicine at this time. It is unknown whether glucocorticoid administration is beneﬁcial in dogs with RAI.4 REFERENCES 1. Prittie JE, Barton LJ, Peterson ME, et al. Pituitary ACTH and adrenocortical secretion in critically ill dogs. J Am Vet Med Assoc 2002;220(5):615-619. 2. Yang Y, Liu L, Zhao B, et al. Relationship between adrenal function and prognosis in patients with severe sepsis. Chin Med J 2007;120(18):1578-1582. 3. de Jong MF, Beishuizen A, Spijkstra JJ, et al. Relative adrenal insuf ciency as a predictor of disease severity, mortality, and bene cial effects of corticosteroid treatment in septic shock. Crit Care Med 2007;35(8):1896-1903. 4. Burkitt JM, Haskins SC, Nelson RW, et al. Relative adrenal insuf ciency in dogs with sepsis. J Vet Intern Med 2007;21(2):226-231. phate, prednisolone sodium succinate, or hydrocortisone phosphate when hypoadrenocorticism is suspected in a critically ill dog (Table 4).13 Continue injectable glucocorticoids until maintenance therapy is instituted. ACTH stimulation test timing. Ideally, an ACTH stimulation test should be performed before you administer glucocorticoids. However, glucocorticoids should not be withheld pending the results of the test. If an ACTH stimulation test cannot be performed immediately, administer glucocorticoids until hypoadrenocorticism is con rmed. Dexamethasone is an ideal glucocorticoid in this situation since it is rapid-acting and, unlike other glucocorticoids, will not directly interfere with the cortisol assay.9,13 A single intravenous injection of dexamethasone at ≤ 1 mg/kg does not signi cantly decrease post-ACTH stimulation plasma cortisol concentrations 24 hours after dexamethasone administration in dogs.27 Although 5 mg/kg dexamethasone administered intravenously signi cantly decreases post-ACTH stimulation plasma cortisol concentrations 24 hours after the dexamethasone administration (control dogs’ cortisol concentrations 15.1 ± 3.1 µg/100 ml; dexamethasonetreated dogs’ cortisol concentrations 10.6 ± 1.7 µg/100 ml), this degree of suppression would be unlikely to result in an inappropriate diagnosis of hypoadrenocorticism.27 However, it is important to consider that long-term glucocorticoid administration will eventually lead to adrenal cortical atrophy and a lack of cortisol production post-ACTH stimulation. For this reason, ACTH stimulation testing should be performed as soon as possible in any dog suspected of having hypoadrenocorticism, and the results should be interpreted in light of previous exogenous glucocorticoid administration. Treat hyperkalemia Any patient with hyperkalemia-induced clinical signs or electrocardiographic signs of cardiotoxicity should receive immediate therapy with intravenous 10% calcium gluconate (Table 4). Calcium gluconate affects the transmembrane potential of myocardial cells, protecting the heart from potassium’s toxic effects.2,9 The protective effect will last 30 to 60 minutes, which should allow enough time for other potassium-lowering therapies to start working.9 All patients with hyperkalemia should be given intravenous uid therapy. Fluid diuresis lowers serum potassium concentrations through dilution and by promoting renal potassium excretion. For patients with mild hyperkalemia and no signs of cardiotoxicity, intravenous uid therapy alone may correct hyperkalemia.3 For patients with moderate to severe hyperkalemia or signs of cardiotoxicity, additional treatments such as dextrose with or without insulin or sodium bicarbonate 328 June 2008 VETERINARY MEDICINE

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Veterinary Medicine - June 2008 Contents Leading Off Clinical Exposures Idea Exchange A Challenging Case: Conjunctival Lymphoma in a Cat Updates on Canine Hypoadrenocorticism Product Preview CE Form Advertiser Index Marketplace/Classifieds Mind Over Miller Clinical Edge - June 2008 Table of Contents Managing Diabetes Mellitus in Cats: What Makes it Work? Porcine Insulin Zinc Suspension in the Management of Feline Diabetes Mellitus Monitoring Diabetes Mellitus in Diabetic Cats Feline Diabetes Mellitus: Important Client Communication Points

Veterinary Medicine - June 2008

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