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Addison’s disease: why do we miss it?
LONDON, ON − Hypoadrenocorticism is known for being an often overlooked and difficult to diagnose disease. It has been called the “great pretender” and it is reportedly uncommon in dogs and rare in cats. However, if there is awareness of what to look for and which patients are at greatest risk, it can be neither difficult to recognize nor diagnose. Also, it is not as uncommon as one may think, explained Ann Wortinger BIS, LVT, VTS (ECC, SAIM), presenting at the Ontario Association of Veterinary Technicians Conference. A veterinary nurse plays a vital role in the monitoring, care, and diagnosis of these patients.
Pathophysiology
Addison’s disease is generally the result of bilateral adrenal atrophy with fibrosis that is thought to be idiopathic in most cases. Inadequate secretion of glucocorticoids and mineralocorticoids by the adrenal cortex are responsible for its signs and symptoms. The primary mineralocorticoid secreted by the adrenal cortex is aldosterone, which promotes renal resorption of sodium and water and excretion of potassium and hydrogen ions. The primary adrenocortical glucocorticoids are cortisol and corticosterone, which are responsible for stimulating appetite, maintaining blood glucose and blood pressure, promoting free water loss through the kidneys, protecting against shock, and helping to respond to stress. Ninety percent of adrenal function must be compromised before clinical signs become evident.
Signalment and clinical signs
Hypoadrenocorticism most often develops in young to middle age female dogs. Breeds that seem to have a higher risk are Standard Poodles, Portuguese Water dogs, Great Danes, Labrador Retrievers, Rottweilers, West Highland Terriers, and Wheaten Terriers. Ms. Wortinger explained that the presentation of this disease can vary widely, from intermittent to chronic or nonspecific signs. Signs of Addison’s disease can vary widely and may include all or only one of the following signs: lethargy, anorexia, vomiting, diarrhea, weight loss, weakness, trembling, polyuria, and polydipsia. Animals may also present with acute collapse accompanied by hypovolemic shock known as an Addisonian crisis. These patients will have pale mucous membranes, a slow or increased capillary refill time (CRT), and profound weakness.
Laboratory abnormalities
A complete blood count including manual differential, chemistry panel, electrolyte analysis, acid/base assessment, and ACTH stimulation test are all necessary for any patient suspected of having Addison’s disease. Classic abnormalities associated with hypoadrenocorticism are hyponatremia, hyperkalemia, azotemia, with a mild to moderate to normal anion gap and metabolic acidosis. Azotemia (BUN up to or over 200 mg/dl) associated with Addison’s is generally pre-renal in nature, despite a low urine specific gravity (<1.030) due to increased sodium losses. White blood cell counts are generally normal.
Radiographic and ECG abnormalities
Thoracic radiographs may reveal the presence of microcardia due to hypovolemia. Megaesophagus may also be noted, which resolves with therapy. ECG will have profound changes if hyperkalemia is present. Bradycardia with tall peaked T waves, a widening and flattening of the QRS complex, prolonged PR interval with a decreased P wave amplitude, and increase in duration of the P wave may occur.
ACTH stimulation
ACTH stimulation testing assesses the adrenal reserve capacity of the patient. Ms. Wortinger said that this is the only way to confirm the presence or absence of Addison’s disease. This test should be run as soon as Addison’s is suspected. Cortisol levels are stable in plasma or serum for as long as five days at room temperature. Post stimulation values are consistently less than 5.0 µg/ml in dogs with hypoadrenocorticism.
Treatment
Treatment of an Addisonian crisis involves treating the hypotension and hypovolemia, as well as concurrent electrolyte and acid/base abnormalities, and providing glucocorticoid replacement. Intravenous fluid therapy is first-line treatment in these patients. 0.9% NaCl is generally the initial fluid of choice due to hyperkalemia and hyponatremia. A typical shock fluid bolus (60-90 ml/kg over 1 hour) may be required. If a steroid is needed before completion of an ACTH stimulation test, dexamethasone is the drug of choice as it will not interfere with the test results. If the patient is stable until completion of ACTH-stimulation test, then hydrocortisone hemisuccinate or hydrocortisone phosphate are the glucocorticoids of choice. These have both gluco and mineralocorticoid activity. Prednisolone sodium succinate is an alternate choice as a rapid-acting glucocorticoid.
The effect of dilution from IV fluid therapy is often sufficient to adequately manage hyperkalemia. If the hyperkalemia is so severe that it is causing life-threatening alterations to heart function as seen on the ECG, or remains persistently high in the plasma, then additional treatments may be required. The metabolic acidosis present in these patients is usually mild, and is treated adequately by addressing the underlying problems of hypotension and dehydration (i.e. fluid therapy).
Maintenance therapy
Initially hypoadrenal patients should be managed with both glucocorticoids and mineralocorticoid supplementation. Oral prednisone or prednisolone (initially 0.2-0.5 mg/lb/day divided into two doses 12 hours apart) should be continued for 3-4 weeks. Dosages should be tapered by 50% per week until discontinued, or until the lowest effective dose to prevent signs of glucocorticoid deficiency. Ms. Wortinger stressed that this is a physiologic dose of glucocorticoids, not a therapeutic dose, and will be much lower than what technicians are used to using. Initially IV fluid therapy normalizes mineral values, but control of signs is dependent on administration of mineralocorticoids. There are two options for mineralocorticoid replacement: fludrocortisone acetate (Florinef-0.02 mg/kg/d PO) or desoxycorticosterone pivalate (DOCP-2.2 mg/kg IM or SQ q. 25-30 days). Florinef has both mineral and glucocorticoid action. She added that for owners not prohibited by its cost or the commitment to daily medication, it can be an effective long-term treatment. Initially Florinef is often used, with the patient transitioning to DOCP for long-term maintenance. Maintenance prednisone dosing may be required in some patients receiving DOCP. Owners should be given a supply of prednisone to keep on hand, to use during stressful situations with either medication choice. Patients should be monitored closely. Electrolyte levels should be checked every 4-7 days for the first 1-2 weeks of therapy, then every 3-4 months through the first year, so medication dosages can be adjusted accordingly. The minimum effective dose for any medication should be used.
Ms. Wortinger concluded by saying that the prognosis for Addisonian patients is
excellent when they are well-controlled. The owners need to be educated to the
life-long commitment necessary to treat these patients and the follow up exams and
bloodwork that will be needed on a regular basis. The owners also need to be aware
of their pet’s increased glucocorticoid needs during stressful situations, and
supplement accordingly.
