6110 Creston Avenue
Des Moines, Iowa 50321
Phone(515) 280-3100

ISU Student Experience

Atypical Addison's in Adult Mix Breed

Written by: Melissa W. • 2016 Scholar


A 5 year old, spayed female Pomeranian Mix named Tiffany presented at Iowa Veterinary Specialties with vomiting and diarrhea for 5 days duration.

She was laterally recumbent and unresponsive upon arrival to the hospital. Her temperature was low at 97.7 degrees Fahrenheit. Some blood was present on the thermometer. Her heart rate was 80 and she had a respiratory rate of 16. Her gums were bright pink and tacky. She had a capillary refill time of less than 1 second with a systolic blood pressure of 110 mmHg.
Differential diagnoses included hemorrhagic gastroenteritis, pancreatitis, foreign body ingestion, gastroenteritis, and Addisonian crisis.

Diagnostic Tests

Abdominal radiographs- Fluid filled intestines. No obstruction or foreign body noted.

Abnormal findings on the blood work included the following:
Hyoglycemia GLU: 10 mg/dL- range 74-143
Hypoproteinemia TP 4.2 mg/dL-range 5.2-8.2
Hypoalbuminemia ALB 1.6 g/dL- range 2.3-4.0
Mild anemia HCT 36%- range 37.3-61.7

We then did an ACTH Stimulation Test by testing a baseline cortisol level and then giving 25mcg Cortrosyn (synthetic ACTH) to try and stimulate her adrenal glands.  Both levels were low
baseline cortisol <0.5 mg/dL
1 hr post cortisol <0.5 mg/dL

Discussion points to consider: Tiffany’s blood sugar was very low (10 mg/dl), her proteins were mildly low (total protein and albumin) and her differential(looking at the percentages of different types of white blood cells) was normal.


Atypical Addison’s Disease or hypoadrenocorticism. The clinical signs pointing to this diagnosis were vomiting and diarrhea. On the bloodwork the lack of changes in the types of white blood cells points to this diagnosis as well. The final deciding factor was that we could not stimulate the cortisol to increase after administration of the adrenocorticotropin hormone analogue cosyntropin and that the baseline was low. Cortisol helps the body address various stresses placed upon an individual – there is a normal level found in the blood stream.  When the body is distressed, this level goes up in normal individuals causing changes in the percentages of various white blood cells and increases blood sugar levels.  This is a case of atypical Addison’s since the electrolyte values are normal; the adrenal glands produce hormones other than cortisol which regulate electrolyte levels.


Oxygen therapy was administered upon arrival. Intravenous catheter was placed and a 25% dextrose 10 mL bolus of fluids was administered since her blood glucose was very low. Intravenous famotidine 10 mg/mL 0.18mL, cerenia 10 mg/mL 0.3 mL, and sucralfate ¼ of a 1 gram tablet to treat the vomiting. Metronidazole 5mg/mL 17mL was given intravenously to treat the diarrhea. Dexamethasone SP 4 mg/mL 0.6mL IV  was given to be a supplement what little cortisol she had. She was hospitalized for two days on supplemental fluids with Normosol R and dextrose with routine blood glucose checks and then a final pack cell volume, total protein, and lactate. On day 2 Tiffany was switched over to oral prednisolone 3 mg/mL 0.6mL, ¼ tablet of 1 gram sucralfate, and 0.5mL of metronidazole 100 mg/mL orally. She went home on a tapering dose of prednisolone from 0.6mL to 0.3mL to be on for life. During times of stress such as boarding etc. As well as sucralfate and metronidazole. Tiffany’s owners are to increase the dose to 0.6mL once a day for 3 days before the event and then 3 days after the event to mimic the body’s normal stress response.


Hypoadrenocorticism is defined as low mineralocorticoids, glucocorticoids, or both. The adrenal glands specifically the outer cortex makes the mineralocorticoids and glucocorticoids. Mineralocorticoids are necessary to maintain proper salt (sodium and potassium) and water content in the body. Glucocorticoids decrease inflammation and increase free glucose in the bloodstream. Both of these are hormones released from the adrenal glands when the pituitary gland stimulates them to be released. Adrenal gland destruction can lead to addison’s disease. This can be from neoplasms, drugs such as mitotane and trilostane, blood clots, or infection. For there to be clinical signs there has to be 90% destruction of the cortex. Typically both sections of the cortex that make the mineralocorticoids and glucocorticoids are destroyed at the same rate. So typically Addison’s presents like the above patient but also with Na and K disturbances. It is atypical to not have the electrolyte disturbances and therefore it is at times harder to diagnose that the adrenal gland is damaged. But when properly diagnosed the prognosis is excellent. So don’t forget to have routine check-ups with your primary care veterinarian!

Nelson, R. W., Couto, C. G. (2009). Small animal internal medicine. St. Louis, MO: Mosby/Elsevier.

View All Scholars

"All the Vet techs and receptionists were nothing but phenomenal and soooo understanding!"

read more testimonials >