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Addison’s Disease in the Dog - Part 2

Catharine Scott-Moncrieff MA, Vet MB, MS, DACVIM, DSAM, DECVIM

How I treat a dog with suspected Addison’s disease and confirm the diagnosis?

Rapid treatment of dogs with suspected Addison’s disease is vital, especially if profound electrolyte abnormalities are present. Hyperkalaemia in particular can be life-threatening if not treated expeditiously. It is very important to also confirm the diagnosis of Addison’s disease whilst starting initial therapy, because once replacement therapy with glucocorticoids has been initiated it is very difficult to retrospectively confirm the diagnosis. Although longterm treatment of hypoadrenocorticism requires provision of exogenous glucocorticoids and usually mineralocorticoids, in the short-term aggressive fluid therapy is the mainstay of treatment and will temporarily correct most life-threatening electrolyte abnormalities.

An example of the acute management of a dog with suspected Addison’s disease is shown in case study 1. The goal should be to treat the disease manifestations (e.g. hypovolaemic shock, hypoglycaemia, and azotaemia) while also confirming the diagnosis. Treatment with hypertonic saline for fluid resuscitation should be avoided in patients with severe hyponatraemia because rapid increases in serum sodium can result in cerebral myelinosis. If immediate glucocorticoid supplementation is considered necessary prior to completion of the ACTH stimulation test, dexamethasone (0.25-2.0 mg/kg) is the drug of choice. If glucocorticoid treatment can be delayed until after the ACTH stimulation test is completed, other treatment options include hydrocortisone hemisuccinate or hydrocortisone phosphate (2-4 mg/kg IV), or methylprednisolone sodium succinate (1-2 mg/kg IV). If the clinical suspicion of hypoadrenocorticism is high, administration of one dose of an injectable mineralocorticoid should be considered, depending upon the initial response of the patient to fluid therapy and the anticipated time for results of cortisol testing to be available. Emergency therapy for severe hyperkalaemia (if potassium >6.5 mmol/L) may be required. Other adjunctive treatments required may include IV dextrose for hypoglycaemia, blood transfusion for haemorrhagic anaemia, colloidal support, and correction of severe metabolic acidosis (if serum bicarbonate <12 mmol/L). In dogs with less severe signs of illness that do not require immediate fluid therapy, measurement of baseline cortisol may be the initial diagnostic test. If the cortisol concentration is >56 nmol/L, a diagnosis of hypoadrenocorticism can be ruled out. ACTH stimulation testing can then be performed on dogs with low basal cortisol concentrations.

What is the best approach for long-term management of the disease?

Dogs with classic Addison’s disease require lifelong treatment with both glucocorticoids (e.g. prednisone) and mineralocorticoids (e.g. fludrocortisone or desoxycorticosterone pivalate (DOCP)).

Glucocorticoid: Maintenance treatment with oral glucocorticoids should be initiated once systemic signs of illness have responded to parenteral treatment. Prednisone is the supplement of choice in dogs: starting at 0.1 to 0.22 mg/kg, the dose is gradually tapered to the lowest level that controls the clinical signs. Excessive dosage may cause clinical signs of hypercortisolism. The dose of prednisone necessary for maintenance treatment ranges from <0.05-0.4 mg/kg (19,20). Prednisone can be completely discontinued in as many as 50% of dogs being treated with fludrocortisone because of the intrinsic glucocorticoid activity of this drug. However most dogs treated with DOCP require treatment with a low dose of prednisone at least every other day as DOCP lacks glucocorticoid activity.
Mineralocorticoid: Dogs with hyperkalaemia and/or hyponatraemia must also be treated with a mineralocorticoid. Desoxycorticosterone pivalate (DOCP) is a long-acting compound that is administered initially at 2.2 mg/kg IM or SC q 25 days (19,20). The final maintenance dose required for good clinical control ranges from 0.8-3.4 mg/kg/dose at intervals ranging from 14-35 days. Most dogs can be managed with monthly injections and few dogs require a dose >2.2 mg/kg. To control costs the dose of DOCP may be tapered by 10% a month while monitoring the sodium and potassium concentrations until the minimum dose that maintains normal electrolyte concentrations is identified. Fludrocortisone acetate is an alternative option for mineralocorticoid supplementation if daily oral therapy is preferred. The starting dose is 0.02 mg/kg PO, either as a single dose or divided twice a day. The dose of fludrocortisone required to control clinical signs ranges from 0.01-0.08 mg/ kg/day and the required dose usually increases over time (19). Some dogs treated with fludrocortisone develop clinical signs of hypercortisolism such as PU/PD even when additional supplementation is withdrawn, presumably due to the intrinsic glucocorticoid activity of fludrocortisones (20). In these dogs, consideration should be given to switching to DOCP. Note that hydrocortisone is a poor choice for long-term management of hypoadrenocorticism because the ratio of glucocorticoid to mineralocorticoid activity is 1:1 and an excessive glucocorticoid dose must be administered in order to achieve an adequate mineralocorticoid effect.
Glucocorticoid-deficient Addison’s disease: Dogs without electrolyte abnormalities (secondary hypoadrenocorticism or atypical primary hypoadrenocorticism) do not require mineralocorticoid supplementation initially; however dogs with primary atypical hypoadrenocorticism (see case study 2) should be monitored carefully because of risk of progression to complete adrenal failure. Electrolyte concentrations should be monitored every 1-3 months for at least the first year after glucorticoid diagnosis and the owners should be educated to monitor for clinical signs of mineralocorticoid deficiency.

What is the prognosis for Addison’s disease?

The prognosis for dogs with Addison’s disease is usually excellent, although the expense of mineralocorticoid supplementation (especially in large dogs) may cause some owners to opt for euthanasia. In a study of 205 dogs treated for hypoadrenocorticism the median survival time was 4.7 years (range 7 days - 11.8 years) (19).

What should I do if my patient does not respond well to treatment?

Occasionally dogs with Addison’s disease do not respond well to treatment or have adverse effects associated with therapy. The most important cause of poor response to treatment is an inadequate mineralocorticoid dose. Other causes include the presence of an undiagnosed concurrent illness such as hypothyroidism. The presence of megaoesophagus or severe gastrointestinal haemorrhage can also complicate response to treatment. The most common adverse effect of therapy is PU/PD which is usually due to excessive glucocorticoid supplementation or the intrinsic glucocorticoid activity of fludrocortisone. In dogs with PU/PD the glucocorticoid dose should first be tapered or discontinued. If the problem persists, consideration should be given to switching to an alternative mineralocorticoid treatment (20).

Conclusion

Hypoadrenocorticism is a complex illness that has been rightly labelled “the Great Pretender”. Dysfunction of the adrenal gland should be considered as a potential differential diagnosis in any dog presenting with acute or chronic systemic illness. A diagnosis of Addison’s disease should never be excluded based on normal electrolyte concentrations. Appreciation of the myriad ways that patients with hypoadrenocorticism may present should increase the index of suspicion for this disease and decrease the likelihood of missing the diagnosis.

 

 

 

This article was kindly provided by Royal Canin, makers of a range of veterinary diets for dogs and cats.  For the full range please visit www.RoyalCanin.co.uk or speak to your Veterinary Business Manager:

References

1. Famula TR, Belanger JM, Oberbauer AM. Heritability and complex segregation analysis of hypoadrenocorticism in the standard poodle. J Small Anim Pract 2003; 44: 8-12.

2. Oberbauer A, Bell JS, Belanger JM, et al. Genetic evaluation of Addison’s disease in the Portuguese water dog, BMC Vet Res 2006; 2: 15-21.

3. Hughes AM, Nelson RW, Famula TR, et al. Clinical features and heritability of hypoadrenocorticism in Nova Scotia duck tolling retrievers: 25 cases (1994- 2006). J Am Vet Med Assoc 2007; 231: 407-412.

4. Oberbauer A, Benemann KS, Belanger JM, et al. Inheritance of hypoadrenocorticism in bearded collies. Am J Vet Res 2002; 63: 643-647.

5. Kelch WJ, Smith CA, Lynn RC, et al. Canine hypoadrenocorticism (Addison’s disease). Comp Contin Educ 1998; 20: 921-935.

6. Peterson ME, Kintzer PP, Kass PH. Pretreatment clinical and laboratory findings in dogs with hypoadrenocorticism: 225 cases. J Am Vet Med Assoc 1996; 208: 85-91.

7. Medinger TL, Williams DA, Bruyette DS. Severe gastrointestinal tract hemorrhage in three dogs with hypoadrenocorticism. J Am Vet Med Assoc 1993; 202: 1869-1872.

8. Saito M, Olby NJ, Obledo L, et al. Muscle cramps in two standard poodles with hypoadrenocorticism. J Am Anim Hosp Assoc 2002; 38: 437-443.

9. Langlais-Burgess L, Lumsden JH, Mackin A. Concurrent hypoadrenocorticism and hypoalbuminemia in dogs: A retrospective study. J Am Anim Hosp Assoc 1995; 31: 307-311.

10. Adamantos S, Boag A. Total and ionized calcium concentrations in dogs with hypoadrenocorticism. Vet Rec 2008; 163: 25-26.

11. Thompson AL, Scott-Moncrieff JC, Anderson JD, et al. Comparison of classic hypoadrenocorticism with glucocorticoid-deficient hypoadrenocorticism in dogs: 46 cases (1985-2005). J Am Vet Med Assoc 2007; 230: 1190-1194.

12. Lifton SJ, King LG, Zerbe CA: Glucocorticoid Deficient Hypoadrenocorticism in Dogs: 18 Cases (1986-1995). J Am Vet Med Assoc 1996; 209: 2076-2081.

13. Adler JA, Drobatz KJ, Hess RS, et al. Abnormalities of serum electrolyte concentrations in dogs with hypoadrencorticism. J Vet Intern Med 2007; 21: 1168-1173.

14. Melián C, Stefanacci J, Peterson ME, et al. Radiographic findings in dogs with naturally-occurring primary hypoadrenocorticism. J Am Anim Hosp Assoc 1999; 35: 208-212.

15. Hoerauf A, Reusch C. Ultrasonographic evaluation of the adrenal glands in six dogs with hypoadrenocorticism. J Am Anim Hosp Assoc 1999; 35: 214-218.

16. Lennon EM, Boyle TE, Hutchins RG, et al. Use of basal serum or plasma cortisol concentrations to rule out a diagnosis of hypoadrenocorticism in dogs: 123 cases (2000-2005). J Am Vet Med Assoc 2007; 231: 413-416.

 

This article was previously published on VetGrad.co.uk in 2011.


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