Hypoadrenocorticism Diagnosis and Management in Dogs PDF

FEATURES PEER REVIEWED shutterstock.com/schubbel  PEER REVIEWED FEATURES ISSUES IN ENDOCRINOLOGY Diagnosis and Management of Hypoadrenocorticism in Dogs Pamela Galati, BVetMed, MRCVS Pa...

FEATURES PEER REVIEWED shutterstock.com/schubbel  PEER REVIEWED FEATURES ISSUES IN ENDOCRINOLOGY Diagnosis and Management of Hypoadrenocorticism in Dogs Pamela Galati, BVetMed, MRCVS Patty Lathan, VMD, MS, DACVIM (SAIM) Mississippi State University College of Veterinary Medicine, Starkville, Miss. Primary hypoadrenocorticism, also known as hypoadrenocorticism is classified as idiopathic. Addison’s disease, is a syndrome caused by However, it can also occur secondary to other bilateral dysfunction of the adrenal cortices. The disorders that result in bilateral adrenal gland adrenal glands are located in the abdomen destruction (e.g., amyloidosis, hemorrhage, and medial to the kidneys and are composed of the neoplasia).4 A recent report described cortex (outer portion) and medulla (inner hypoadrenocorticism secondary to intravascular portion). Within the adrenal cortex are 3 distinct lymphoma in a 2-year-old German shepherd.8 layers, which are responsible for production of different hormones. From the outermost to the Most cases of hypoadrenocorticism represent a innermost, these layers are the zona glomerulosa, deficiency of glucocorticoids (primarily cortisol) zona fasciculata, and zona reticularis. Cells in and mineralocorticoids (primarily aldosterone), these layers produce aldosterone, cortisol, and but other manifestations can occur. Atypical adrenal androgens, respectively. Addison’s disease causes signs of isolated glucocorticoid deficiency. Some affected dogs are Hypoadrenocorticism is primarily a disease of in very poor condition and considered to be dogs and occurs only rarely in cats. This experiencing an addisonian crisis. In addition to condition is heritable and most commonly the more commonly reported gastrointestinal affects dogs of 4 breeds: standard poodles,1 signs that may be evident from a thorough Portuguese water dogs,2 Nova Scotia duck tolling history, dogs experiencing an addisonian crisis retrievers,3 and bearded collies. Other commonly are in hypovolemic shock and may have affected breeds include West Highland white collapsed. In this article, we describe the terriers,4,5 Great Pyrenees,6 and wheaten diagnosis and management of these terriers.4,5 Although the most common cause is manifestations of hypoadrenocorticism. thought to be immune-mediated adrenalitis,7 in the absence of a definitive diagnosis, most THE GREAT PRETENDER Because hypoadrenocorticism in the dog has the ability to mimic other common diseases, it can be challenging to make the proper diagnosis. todaysveterinarypractice.com JULY/AUGUST 2019 47  FEATURES PEER REVIEWED PRESENTATION The clinical signs of hypoadrenocorticism can vary along a continuum of severity and chronicity (BOX 1). Because glucocorticoids help counteract the effects of stress and maintain normal gastrointestinal mucosal integrity and function, many dogs with glucocorticoid deficiency initially display waxing and waning nonspecific signs such as episodic vomiting, diarrhea, melena (FIGURE 1), lethargy, and dehydration. These dogs may respond well to supportive care;9 thus, underlying hypoadrenocorticism can initially go undiagnosed. However, when mineralocorticoid deficiency FIGURE 1. Melena is common in dogs with accompanies glucocorticoid deficiency, clinical signs hypoadrenocorticism, although because of ileus, it may not can become more severe. Aldosterone stimulates be obvious until after the dog has been hospitalized for 2 to 3 days. It is often present when packed cell volume drops sodium, chloride, and water retention along with precipitously after an addisonian crisis but no other cause potassium excretion in the distal renal tubules; for the drop can be found. therefore, lack of aldosterone results in hypochloremia, hypovolemia, acidosis, and hyperkalemia.10 In patients with atypical Addison’s disease, clinical signs Serum Chemistry result from cortisol deficiency alone. In a dog with compatible history and clinical signs, a sodium:potassium ratio of less than 27 should prompt Among patients experiencing addisonian crisis, some definitive testing. Be aware that low sodium:potassium have previously received treatment for nonspecific signs; ratios can occur in dogs with other conditions (e.g., others have not because they displayed no clinical signs. renal failure,11 trichuriasis,12 pregnancy,13 and body cavity effusions11) (BOX 2). DIAGNOSTICS Additional abnormalities on serum biochemistry panels For any dog suspected to have hypoadrenocorticism, an can include azotemia, hypoalbuminemia, excellent screening test is resting cortisol levels. This hypocholesteremia, hypoglycemia, hypercalcemia, and test is sensitive in that if the resting cortisol level is elevated liver enzyme levels (BOX 3). Most patients do greater than 2.0 mcg/dL, for almost all dogs you can not have all of these abnormalities but instead may rule out hypoadrenocorticism. However, a low resting have a few that are severe (e.g., hypoglycemia and/or cortisol level alone can be normal for some dogs and azotemia). Most dogs with hypoadrenocorticism show thus a definitive diagnosis requires further testing. Classic bloodwork abnormalities associated with hypoadrenocorticism are hyperkalemia, hyponatremia, and lack of a stress leukogram.4 BOX 2 Differential Diagnoses Other Than Hypoadrenocorticism for Low Sodium:Potassium Ratio BOX 1 Classic and Potential Clinical Digestive system Signs of Hypoadrenocorticism Acute kidney injury (anuria or oliguria) Decreased appetite Trichuriasis Vomiting, hematemesis Cavitary effusions (e.g., chylothorax) Diarrhea, melena Pregnancy and periparturient illness Lethargy or decreased willingness to Receipt of angiotensin-converting exercise enzyme drug 48 JULY/AUGUST 2019 todaysveterinarypractice.com  PEER REVIEWED FEATURES vague symptoms that can prompt investigation of other body systems, including the gastrointestinal tract and kidneys. The laboratory findings for dogs with BOX 4 Procedure for Performing ACTH Stimulation Test18 hypoadrenocorticism are similar to those of acute kidney injury (e.g., azotemia, electrolyte changes, and 1. Collect a blood sample into a red top tube. isosthenuria); thus, hypoadrenocorticism should always be a major differential diagnosis for dogs with these 2. Administer 5 mcg/kg of synthetic ACTH IV (up to a maximum of 250 mcg/dog). laboratory findings. Avoid use of compounded formulations. 3. After 60 minutes, collect a second blood In dogs with atypical Addison’s disease, electrolyte sample. derangements are absent; hence, we rely on the signs of 4. Submit both serum samples for cortisol hypocortisolism (e.g., vomiting, diarrhea, melena, measurement. lethargy) to raise suspicion and prompt testing. One study suggested that aldosterone levels in patients with atypical Addison’s disease are low;14 it is unclear as to why patients with atypical Addison’s disease do not have electrolyte abnormalities. than 750 lymphocytes/mcL (and no previous receipt of glucocorticoids), hypoadrenocorticism is unlikely.15 Complete Blood Count In addition to not showing a stress leukogram, dogs Along with clues from the serum biochemistry, a with hypoadrenocorticism can be mildly to severely normal lymphocyte count may further raise suspicion anemic. Severe anemia is often accompanied by melena for hypoadrenocorticism because a dog ill from another and/or hematochezia, caused by gastrointestinal cause should have lymphopenia secondary to cortisol bleeding resulting from increased vascular permeability release (stress leukogram).4 One study found that for all in the absence of cortisol. The packed cell volume dogs with hypoadrenocorticism, lymphocyte counts (PCV) in patients in addisonian crisis may initially be were greater than 750/mcL; thus, for dogs with fewer within reference range or mildly decreased but 1 to 2 days later severely decreased after rehydration and further blood loss. Because of ileus, which is common in dogs with hypoadrenocorticism, melena may not be apparent for 2 to 3 days. BOX 3 Common Clinicopathologic Abnormalities in Dogs With Hypoadrenocorticism Imaging Hyperkalemia Diagnostic imaging is not typically required for the diagnosis of hypoadrenocorticism. However, because of Hyponatremia the nonspecific signs of this disease, thoracic and Hypochloremia abdominal imaging are often included in the diagnostic Acidosis workup of these patients. Some ultrasonographic and Azotemia radiographic signs can be helpful. As you might expect, Hypoglycemia ultrasonography has shown that the adrenal glands are Increased alanine and aspartate shorter and thinner in affected dogs than in those of aminotransferase levels their unaffected counterparts.16 Radiographs may Hypercalcemia indicate hypovolemia (e.g., small heart and liver and Hypoalbuminemia decreased diameter of the cranial lobar pulmonary artery and caudal vena cava).17 Hypocholesterolemia Anemia Eosinophilia Definitive Diagnosis Lack of stress leukogram To confirm hypoadrenocorticism, an adrenocorticotropic hormone (ACTH) stimulation test (BOX 4) must be performed. This test is performed by todaysveterinarypractice.com JULY/AUGUST 2019 49  FEATURES PEER REVIEWED measuring serum cortisol concentrations before and 1 more difficult to titrate the drug to an acceptable hour after administration of synthetic ACTH. Use of dosage. For example, an increase in fludrocortisone synthetic cosyntropin at 5 mcg/kg, compared with the dose may be necessary to keep sodium and potassium previously used dose of 250 mcg/dog, helps reduce the within normal parameters, but this increased dose may costs associated with testing.18 In addition, result in a higher than necessary glucocorticoid effect reconstituted cosyntropin can be stored in plastic (not and precipitate undesirable consequences of glass) syringes and frozen for up to 6 months without hypercortisolemia. affecting efficacy,19 making it more cost-effective for practitioners who would otherwise not use an entire DOCP: Because DOCP has only mineralocorticoid vial before effectiveness is affected. A definitive activity, concurrent glucocorticoid (e.g., prednisone) diagnosis of hypoadrenocorticism can be made when supplementation is always necessary. However, post-ACTH cortisol levels are less than or equal to 2 many clinicians prefer DOCP because of its mcg/dL. A recent study evaluated dogs that were efficacy and the ability to adjust glucocorticoid suspected of having hypoadrenocorticism but had supplementation independently. In addition, DOCP higher cortisol concentrations (up to 10 mcg/dL) after is more likely than fludrocortisone to normalize ACTH stimulation testing.20 For these dogs, renin activity, suggesting that DOCP is a more hypoadrenocorticism was ruled out for the following effective mineralocorticoid supplement for dogs reasons: another disease (inflammatory bowel disease) with hypoadrenocorticism.16 Two formulations of was diagnosed, they did not respond to glucocorticoid DOCP are available: Percorten-V (Elanco, elanco. administration, or signs of hypoadrenocorticism did com) and Zycortal (Dechra Pharmaceuticals, dechra. not return after discontinuation of glucocorticoids. In com). The U.S. Food and Drug Administration– our experience, rare patients with confirmed approved label for each formulation recommends hypoadrenocorticism may have post-ACTH an initial dose of 2.2 mg/kg22,23 every 25 days. stimulation cortisol results of 2 to 3 mcg/dL. However, 1 publication documents using lower doses,24 and we often begin treatment with a dose of 1.5 mg/kg. Zycortal is labeled for SC administration; TREATMENT Percorten-V is labeled for IM administration Some patients exhibit chronic clinical signs only; only but can also be given SC25 off-label. others, however, experience a life-threatening addisonian crisis, requiring acute stabilization and After the initial dose of DOCP is given, electrolytes intensive therapy. The rest of the patients lie should be checked at 14 days to assess the dosage and somewhere in between; although their condition is not at 25 days to assess the dosing interval. At 14 days, if immediately life-threatening, they may require fluid hyponatremia or hyperkalemia is present, increase the therapy and other supportive care in addition to steroid next dose (at 25 to 28 days) by 10% to 15%; if supplementation. hypernatremia or hypokalemia is present, decrease the next dose by 10% to 15%. At 25 days, if hyponatremia or hyperkalemia is present, decrease the dosing interval Chronic Disease by 1 to 2 days. If electrolytes are within reference range, For most hypoadrenocorticism patients who are to make the dosing interval more convenient for the clinically stable, treatment consists of supplementation client we often extend the dosing interval to 28 days, at with a mineralocorticoid and a glucocorticoid. which time we confirm that the electrolytes are within reference range. One study demonstrated that the dosing interval can be extended as long as 90 days, but Mineralocorticoids this study used a dose of 2.2 mg/kg and initially Mineralocorticoid supplementation is available in 2 required up to weekly electrolyte assessments to forms: daily oral (fludrocortisone) and monthly determine the optimal dosing interval.26 We prefer to injection (desoxycorticosterone pivalate [DOCP]). adjust the dose rather than extend the dosing interval beyond 28 to 30 days, and we do not recommend Fludrocortisone: Fludrocortisone acetate (0.01 mg/kg adjusting both dose and dosing interval. After the PO q12h) possesses both glucocorticoid and optimal dose and interval are determined, most clients mineralocorticoid activity.21 Although the dual can be taught to give DOCP at home. functions may seem like a benefit, they can make it 50 JULY/AUGUST 2019 todaysveterinarypractice.com  PEER REVIEWED FEATURES Glucocorticoids Addisonian Crisis All patients receiving DOCP must receive supplemental Dogs experiencing addisonian crisis may have glucocorticoids. Some patients receiving arrhythmias and/or bradycardia as a result of fludrocortisone do not require additional prednisone hyperkalemia and require treatment specifically targeted long-term, but these patients seem to stabilize more at correcting the hyperkalemia. Hypoglycemia has been quickly when additional glucocorticoid is given initially reported in up to 38% of dogs with hypoadrenocorticism,9 and then tapered after stabilization.27 so insulin therapy for treatment of hyperkalemia should be withheld until normal blood glucose levels are For glucocorticoid replacement, oral prednisone at a confirmed. If severe enough, hypoglycemia may lead to starting dose of 0.5 to 1.0 mg/kg/day is usually seizures.2 Dogs experiencing addisonian crisis often recommended. This dose should be gradually lowered have moderate to severe prerenal azotemia. (over several weeks) to an optimal dose that controls signs of hypoadrenocorticism and avoids side effects Prompt recognition or suspicion of an addisonian (e.g., polyuria, polydipsia, polyphagia, panting). Larger crisis and subsequent treatment (BOX 5) are dogs seem to be more sensitive to the side effects of paramount to a successful outcome. Fluid resuscitation glucocorticoids. Although published maintenance doses (FIGURE 2) is of utmost importance and will address are usually 0.1 to 0.22 mg/kg/day,4 we have managed a hypovolemia, hypotension, metabolic acidosis, and number of patients with lower doses (as low as 0.03 hyperkalemia.31 The latest recommendation is to give mg/kg/day). Dosage adjustments should be based on a balanced crystalloid solution (e.g., Plasmalyte 148, clinical signs only; for dogs with confirmed naturally lactated Ringer’s, or Normosol-R).32 The previous occurring hypoadrenocorticism, an ACTH stimulation recommendation was to give 0.9% sodium chloride. test should not be repeated for monitoring purposes. However, neurologic signs in dogs receiving treatment for addisonian crises are thought to be the result of myelinolysis secondary to rapid correction of Atypical Addison’s Disease hyponatremia;33,34 this concern, however, is valid only Because dogs with atypical Addison’s disease have signs if the hyponatremia is chronic. When the patient’s of glucocorticoid deficiency only, they require sodium concentration is less than 120 mEq/L, we glucocorticoid supplementation only, administered monitor sodium concentrations more often and may according to the guidelines described above. For some use a fluid with a lower sodium concentration than of these dogs, electrolyte abnormalities may eventually lactated Ringer’s solution. Sodium concentration develop and require mineralocorticoid should not be increased by more than 12 mEq/L supplementation. Rechecking electrolytes is every 24 hours.34 In addition, balanced crystalloids recommended 2 weeks after diagnosis, then every are more alkalinizing than sodium chloride. Fluid month for 3 months, then every 3 months for 1 year. resuscitation should be performed with boluses of 20 to 30 mL/kg over 15 to 20 minutes; after administration of each bolus, vital signs (heart rate, pulse quality, and blood pressure) should be reassessed. Fluid resuscitation is considered complete when vital signs have returned to reference range. Lactate levels can also be used as an objective measure. After the patient has received appropriate fluid resuscitation, IV dexamethasone can be administered. Dexamethasone does not interfere with results of a subsequent ACTH stimulation test because it is not detected by the cortisol assay, whereas prednisone, prednisolone, and methylprednisolone are. The patient should remain hospitalized and receiving IV fluids until electrolyte abnormalities are stabilized and any clinical FIGURE 2. Administration of IV fluids is imperative for a dog experiencing an addisonian crisis. ECG and abnormalities are controlled with oral medications. blood pressure are monitored to look for indications of Among these oral medications will be prednisone. In hyperkalemia and to determine response to therapy. the acute phase immediately after recovery from crisis, todaysveterinarypractice.com JULY/AUGUST 2019 51  FEATURES PEER REVIEWED BOX 5 Treatment of Addisonian Crisis Correct the following: Hypovolemia and hypotension Alpha-2 agonists (e.g., inhaled albuterol or IV Balanced crystalloids, 20 to 30 mL/kg; reassess terbutaline at 0.01 mg/kg29) and repeat if necessary. Hypoglycemia Acidosis 1 mL/kg 50% dextrose, diluted 1:2 with balanced IV fluid therapy is almost always adequate. crystalloid Hyperkalemia Severe anemia from gastrointestinal blood loss Fluids are usually adequate unless severe (>8.5 to Packed red blood cell transfusion 9.0 mEq/L) or ECG derangements (bradycardia, Glucocorticoid deficiency spiked T waves, flattened to absent P wave, Dexamethasone, 0.2 mg/kg IV initially, then 0.1 widened QRS complexes) are present. mg/kg q12h until oral prednisone is tolerated. ECG derangements/severe hyperkalemia CAN be given before obtaining samples for Calcium gluconate, 10% solution: 0.5 to 1.5 mL/kg ACTH stimulation test over 10 to 15 minutes. Watch ECG for worsening OR bradycardia as a side effect. Will stabilize the heart but does not treat hyperkalemia directly. Hydrocortisone sodium succinate, 0.5 to 0.625 Dextrose, 1 mL/kg 50% dextrose, diluted 1:3 with mg/kg/hr. 30 CANNOT be given before obtaining balanced crystalloids28 samples for ACTH stimulation test. R insulin, 0.2 U/kg, followed by a bolus of 1 to 2 Supportive therapy g dextrose/unit of insulin, then dextrose added Warming measures if patient is hypothermic to balanced crystalloids to make a 2.5% to 5.0% Anti-emetics solution of dextrose Dogs with life-threatening arrhythmias should Gastroprotectants receive insulin. Dextrose alone will help decrease Pain management the potassium concentration by causing Nutrition (patients are usually eating within endogenous insulin release, but this takes 24 hours) more time. we usually give 0.5 to 1.0 mg/kg/day. As the dog transitions to at-home care, the dose should be gradually lowered over a few weeks. Mineralocorticoid supplementation with DOCP or fludrocortisone is usually postponed until the diagnosis of hypoadrenocorticism is confirmed. Future dosing will need to be based on laboratory results, particularly electrolyte concentrations, and clinical signs. PROGNOSIS For dogs with properly diagnosed hypoadrenocorticism, the prognosis and quality of life are good (FIGURE 3); most of these dogs die of something unrelated to hypoadrenocorticism. One study encompassing 205 dogs revealed a median survival time of 4.7 years with no significant effect resulting from factors such as age, FIGURE 3. This golden retriever exhibited nonspecific breed, sex, or weight.35 However, clients must be well lethargy and gastrointestinal signs after a new (human) aware of subtle signs of illness and committed to daily baby joined the household. He was 2 years old at the time of diagnosis and is thriving 8 years later. He receives 1.3 mg/ medication and regular rechecks for the rest of the dog’s kg of DOCP q30d and 0.03 mg/kg prednisone/day. Dogs life. With proper treatment and regular veterinary with hypoadrenocorticism typically have a great quality of follow-up, dogs with hypoadrenocorticism can lead a life as long as the clients are diligent about maintaining an appropriate medication and monitoring schedule. long and healthy life. 52 JULY/AUGUST 2019 todaysveterinarypractice.com  PEER REVIEWED FEATURES References 1. Famula TR, Belanger JM, Oberbauer AM. Heritability and complex 25. McCabe MD, Feldman EC, Lynn RC, Kass PH. 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Hydrocortisone in the management of disease in the dog. JAAHA 1986;22:789-794. acute hypoadrenocorticism in dogs: a retrospective series of 30 cases. 8. Buckley M, Chapman P, Walsh A. Glucocorticoid-deficient J Small Anim Pract 2016 57:227-233. hypoadrenocorticism secondary to intravascular lymphoma in the 32. Burkitt Creedon JM. Hypoadrenocorticism. In: Silverstein DC, Hopper adrenal glands of a dog. Aust Vet J 2017;95(3):64-67. K, editors. Small Animal Critical Care Medicine. 2nd ed. St. Louis, MO: 9. Willard MD, Schall WD, McCaw DE, Nachreiner RF. Canine Elsevier; 2015:380-383. hypoadrenocorticism: report of 37 cases and review of 39 previously 33. Churcher R, Watson A, Eaton A. Suspected myelinolysis following reported cases. JAVMA 1982;180(1):59-62. rapid correction of hyponatremia in a dog. JAAHA 1999;35(6):493-497. 10. Lanen Van K, Sande A. Canine hypoadrenocorticism: pathogenesis, 34. Brady CA, Vite CH, Drobatz KJ. Severe neurologic sequelae in a dog diagnosis, and treatment. Top Companion Anim Med 2014;29(4):88-95. after treatment of hypoadrenal crisis. JAVMA 1999;215(2):210, 222-225. 11. Bell R, Mellor DJ, Ramsey I, Knottenbelt C. Decreased 35. Kintzer PP, Peterson ME. Treatment and long-term follow-up of 205 sodium:potassium ratios in cats: 49 cases. Vet Clin Pathol dogs with hypoadrenocorticism. J Vet Intern Med 1997;11(2):43-49. 2005;34(2):110-114. 12. Nielsen L, Bell R, Zoia A, et al. Low ratios of sodium to potassium in the serum of 238 dogs. Vet Rec 2008;162(14):431-435. 13. Seth M, Drobatz KJ, Church DB, Hess RS. White blood cell count and the sodium to potassium ratio to screen for hypoadrenocorticism in dogs. J Vet Intern Med 2011;25(6):1351-1356. 14. Baumstark ME, Sieber-Ruckstuhl NS, Muller C, et al. Evaluation of Pamela Galati aldosterone concentrations in dogs with hypoadrenocorticism. J Vet Dr. Galati is an internal medicine resident at Mississippi Intern Med 2014;28:154-159. State University College of Veterinary Medicine. 15. Schaer M, Halling KB, Collins KE, Grant DC. Combined hyponatremia She completed her veterinary degree at the Royal and hyperkalemia mimicking acute hypoadrenocorticism in three Veterinary College in London, followed by a rotating pregnant dogs. JAVMA. 2001;218(6):897-899. and specialty internship at a private practice in 16. Hoerauf A, Reusch C. Ultrasonographic evaluation of the adrenal Long Island, New York. Her clinical interests include glands in six dogs with hypoadrenocorticism. JAAHA 1999;35(3):214-218. endocrinology and hematology. 17. Melian C, Stefanacci J, Peterson M, Kintzer P. Radiographic findings in dogs with naturally-occurring primary hypoadrenocorticism. JAAHA 1999;35(3):208-212. Patty Lathan 18. Lathan P, Moore GE, Zambon S, Scott-Moncrieff JC. Use of a low-dose Dr. Lathan received a BA in chemistry from Texas ACTH stimulation test for diagnosis of hypoadrenocorticism in dogs. J Vet Intern Med 2008;22(4):1070-1073. A&M University and a VMD from the University 19. Frank LA, Oliver JW. Comparison of serum cortisol concentrations of Pennsylvania. She completed an internship at in clinically normal dogs after administration of freshly reconstituted Mississippi State University and a small animal internal versus reconstituted and stored frozen cosyntropin. JAVMA medicine residency at Purdue University in 2007. She is 1998;212(10):1569-1571. an associate professor of small animal internal medicine 20. Wakayama JA, Furrow E, Merkel LK, Armstrong PJ. A retrospective at Mississippi State University. Her primary interest is study of dogs with atypical hypoadrenocorticism: a diagnostic cut-off endocrinology, specifically the management of adrenal or continuum? J Sm Anim Pract 2017;58:365-371. disease and diabetes mellitus. She has published several 21. Plumb’s Veterinary Drug Handbook. 8th ed. plumbsveterinarydrugs. articles and book chapters, given lectures throughout com. Accessed February 2019. the United States and internationally, and is president of 22. Percorten. Assets.ctfassets.net/7dgyj1n4n527/5iMMYVfzugSeYcwAgy SuGs/214cf0e0f5b2efb214c5055bcbae632d/Percorten_Label_8.5x11. the Society for Comparative Endocrinology. pdf. Accessed February 2019. 23. Zycortal. Dechra-us.com/products/details/zycortal®-suspension- (desoxycorticosterone-pivalate-injectable-suspension)-25-mg-ml. Accessed February 2019. 24. Bates JA, Shott S, Schall WD. Lower initial dose desoxycorticosterone pivalate for treatment of canine primary hypoadrenocorticism. Aust Vet J 2013;91:77-82. todaysveterinarypractice.com JULY/AUGUST 2019 53