A Dog with Hypothermia leads to the discovery of Addisons Disease.
VETERINARIAN SPECIALTY CASE STUDY
Bonita presented to us in shock with a low heart rate, low temperature, weak pulses and a history of bloody diarrhea. She was immediately treated with intravenous fluids and glucose that quickly helped stabilize her from a near comatose state…
Bonita is a 2.5 year old female intact Chihuahua. She was referred to Animal Specialty Group by Ambassador Dog and Cat Hospital for hypothermia. Bonita had been having severe hematochezia for the past two days. The owner stated that Bonita had recurrent bouts of diarrhea every month.
Bonita presented in shock with weak distal pulses, delayed capillary refill time, and bradycardia. She was obtunded and opisthotonic. Her pupils were miotic and non-responsive to light. Her temperature was too low to register on a thermometer, and a Doppler blood pressure could not be obtained (presumably due to hypotension).
An intravenous catheter was immediately placed in her cephalic vein, blood was obtained to ascertain her acid/base/electrolyte status, and a bolus of warm isotonic crystalloid fluids was started. The bloodwork showed that she was severely hypoglycemic, hypoproteinemic, and had a severe lactic acidosis. She was bolused 50% dextrose diluted 1:1 and started on 5% dextrose supplementation. After the dextrose and fluid boluses, Bonita became alert and her neurologic status improved. Her blood pressure, physical examination, blood glucose, and blood gas were monitored on a periodic basis.
Given Bonita’s history of waxing and waning diarrhea, we were suspicious of atypical Addison’s disease (hypoadrenocorticism). We performed an in-house cortisol test which showed that her cortisol level was <0.6 µg/dL (normal range: 2.5-30 µg/dL). To confirm the diagnosis, an ACTH stimulation test was performed, and both pre and post ACTH cortisol levels were <0.7µg/dL (normal ranges pre: 1-5 µg/d; post: 8-17 µg/dL).
During resuscitation efforts Bonita was given an injection of Dexamethasone SP for her suspected Addisons disease. She was placed on intravenous crystalloid fluids with dextrose, and started on a hetastarch constant rate infusion for colloidal support. Bonita was given parenteral ampicillin-sulbactam and enrofloxacin for possible sepsis/GI translocation from her severe hematochezia and famotidine was started for stress erosion prophylaxis.
With hypoadrenocorticism, the adrenal cortex is destroyed and the patient may become deficient in mineralocorticoids, glucocorticoids or both occur. The adrenal gland is made up of two regions, the cortex and the medulla. The medulla secretes catecholamines and does not play a part in Addisons disease. The adrenal cortex has three layers that produce different types of hormones. One type of hormone produced is cortisol, a glucocorticoid. Glucocorticoids are hormones that regulate the stress response and are important for metabolic activity, gastrointestinal function, glucose regulation, as well as maintaining vascular tone and reactivity to catecholamines. Mineralocorticoids, a second type of hormone produced by the adrenal cortex, control electrolytes (sodium reabsorption and potassium excretion) and water regulation. These hormones maintain blood volume by the retention of sodium and water. Lastly, the adrenal cortex produces sex hormones. The stimulation to release these hormones from the adrenal cortex comes from the pituitary gland in the form of adrenocorticotropic hormone (ACTH).
The most commonly affected patients are female middle aged dogs (4-6 years). This disease is rare in cats. Breeds that are reported to be predisposed to developing hypoadrenocorticism include the standard poodle, Portuguese water dog, bearded collie, Great Dane, Rottweiler, Nova Scotia duck tolling retriever and soft-coated wheaten terrier.
For clinical signs to develop about 90% of the adrenal cortex must be damaged. Typical Addisons disease is characterized by a deficiency in both glucocorticoids and mineralocorticoids. Atypical Addisons disease is characterized by a deficiency in only glucocorticoids. Patients can present in different ways and it is often a difficult disease to diagnose. Some patients are very sick, like Bonita, presenting in an Addisonian crisis. Other patients may present only mildly ill or with chronic clinical signs, such as vomiting, diarrhea, and polyuria/polydipsia. Often the history we obtain from the owner documents multiple bouts of diarrhea and/or vomiting over long period of time. Changes in mental status and lethargy can occur. Due to cortisol deficiency, dogs with hypoadrenocorticism show clinical signs during times of stress.
To diagnose Addisons disease we use the history in conjunction with diagnostic testing. Complete bloodwork and ACTH stimulation tests help diagnose the disease. An ACTH stimulation test allows us to see the body’s cortisol response to synthetic ACTH. If there is no response then the diagnosis is made. Bloodwork may show the characteristic electrolyte imbalance of hyperkalemia and hyponatremia (typically a Na:K ratio < 27:1).
The in-house cortisol snap test measures basal cortisol levels. A basal cortisol level <2mcg/dL is suggestive but not confirmatory of Addisons disease. The in-house cortisol snap test proved useful in Bonita’s case, as it helped determine that she was in an Addisonian crisis which prompted us to give her a 4 times physiologic dose of corticosteroids. Dexamethasone (0.1 mg/kg intravenously) was chosen as immediate treatment for Bonita, as it will not interfere with the confirmatory ACTH stimulation test.
After resuscitation a full blood chemistry panel was performed. At that time Bonita’s electrolytes had become abnormal and characteristic of typical hypoadrenocorticism. She was therefore supplemented with desoxycorticosterone pivalate (DOCP), a synthetic mineralocorticoid. Often Addisonian patients that are critically ill will develop the characteristic electrolyte abnormalities in the days to week after being resuscitated.
After a short time in the ICU, with intensive monitoring and supportive care, Bonita made a full recovery. She will need lifelong treatment with prednisone (tapered to the lowest effective dose) and DOCP.
It is important to periodically check bloodwork and electrolytes as well as monitor how our patients are responding at home to be able to taper therapy appropriately. It may be helpful to give these patients increased doses of glucocorticoids during times of anticipated stress. We also recommend that Addisonian patients be spayed or neutered as being intact and going through heat cycles puts additional stress on the body.
With proper medical management, our Addisonian patients can live relatively normal lives.
REFERENCES:  Nelson RW, and Couto CG. Hypoadrenocorticism. Small Animal Internal Medicine. 4th ed. Mosby Elsevier, St Louis Missouri 2009; 836-841;  Klein SC, and Peterson ME. Review article: Canine Hypoadrenocorticism: Part I. Can Vet J 2010; 51:63–69;  Catharine J, and Scott-Moncrieff R. Veterinary Internal Medicine. 7th ed. Saunders Elsevier, St Louis Missouri 2010; 1847-1857.
Besides his professional interest in surgery and emergency medicine, Dr. Andreas Andreou also has a passion for avian and exotic medicine. In 2004, he was honored with the Pamela Slack Award, which is presented to the third-year veterinary student who has demonstrated the most outstanding competence and motivation in avian medicine.