Case study: Baby Triplett
Baby is a spayed female Dachshund cross of undetermined age. She was transferred to VRHOH emergency services, where she was evaluated by Dr. Heather Rubi. Dr. Rubi referred Baby to Dr. Scott Helms.
Baby had a history of pancreatitis and recently had a decreased appetite. She was also reported to have had trouble with her bowel movements. Her primary care veterinarian had previously prescribed prednisone for suspected inflammatory gastrointestinal disease. She is reported to have responded well to prednisone with resolution of her gastrointestinal signs. Her last dose of prednisone was administered approximately six weeks before Baby came to Veterinary Referral Hospital of Hickory.
On presentation to VRHOH, she was normothermic, BAR, and nonpainful. She had a heartrate of 114 and a respiratory rate of 36. Her abdomen was tense on palpation, but no other abnormalities were detected on physical exam.
Radiographs were taken, and while there was some gas present, there was no radiographic evidence of a functional or mechanical obstruction.
Treatment was initiated with fluid therapy using a balanced electrolyte solution, pantoprazole, and ondansetron. Her bloodwork showed an azotemia, with a BUN of 99.3 and a creatinine of 2.8. Baby also had elevated phosphorus (6.5) and total calcium (15.3). Her liver values, glucose, chloride, and CBC were normal. However, her sodium was low, at 129, and potassium high at 6.3. A mild metabolic acidosis was also noted along with an elevated ionized calcium. Her in-house basal cortisol was 1.2.
|Chemistry (DRI-CHEM)||CBC||Blood Gas|
|Test||Value||Reference Range||Test||Value||Reference Range||Test||Value||Reference Range|
|BUN||99.3||9.0-29.0 mg/dl||WBC||10.77||6.0-17.0 103/uL||pO2||40.2||24.0-54.0 mmHg|
|Creatinine||2.8 H||0.4-1.4 mg/dl||NEU||8.22||3.62-12.30 103/uL||cSO2||73.4||40.0-90.0%|
|BUN/Creat Ratio||35.5||LYM||1.82||0.83-4.91 103/uL||PCO2||32.1||30.0-47.0 mmHg|
|Phosphorus||6.5 H||1.9-5.0 mg/dl||MONO||0.42||0.14-1.97 103/uL||Bicarbonate||17.7||16.0-28.0 mmol/L|
|Calcium||>15.3||9.0-12.2 mg/dl||EOS||0.30||0.04-1.62 103/uL||cTCO2||18.7||18.0-28.0 mmol/L|
|Corrected Ca||—||9.0-12.2 mg/dl||BAS||0.01||0.00-0.12 130/uL||pH||7.351 L||7.360-7.460|
|Total Protein||9.0 H||5.5-7.6 g/dl||NEU %||76.4||52.0-81.0%||BE, ECF||-7.9 L||-5.0-5.0 mmol/L|
|Albumin||4.3 H||2.5-4.0 g/dl||LYM %||16.8||12.0-33.0%||Sodium||129 L||140-151 mmol/L|
|Globulin||4.7 H||2.0-3.6 g/dl||MONO %||3.9||2.0-13.0%||Potassium||6.3 H||3.5-5.0 mmol/L|
|Alb/Glob Ratio||0.9||EOS %||2.8||0.5-10.0%||Chloride||106||106-127 mmol/L|
|Glucose||123||75-125 mg/dl||BAS %||0.1||0.0-1.3%||Calcium, ionized||1.55 H||1.13-1.42 mmol/L|
|Cholesterol||185||120-310 mg/dl||RBC||7.97||5.10-8.50 106/uL||Anion gap||12||5-22 mmol/L|
|ALT (GPT)||47||0-120 U/l||HGB||17.5||11.0-19.0 g/dL||Lactate||2.29||0.60-3.00 mmol/L|
|ALP||27||0-140 U/l||HCT||47.1||33.0-56.0%||Glucose||116||63-124 mg/dL|
|GGT||<10||0-14 U/l||MCV||59.1 L||60.0-76.0 fL||HCT||58 H||36-55%|
|Total Bilirubin||<0.1||0.0-0.5 mg/dl||MCH||22.0||20.0-27.0 pg|
Baby’s clinical picture, including her history and the laboratory testing completed by emergency services, was suggestive of possible hypoadrenocorticism (Addison’s disease).
Addison’s disease is caused by a lower-than-normal production of glucocorticoids and mineralocortioids. Occasionally atypical hypoadrenocorticism is seen, manifesting as only a deficiency of glucocorticoids. Adrenal hormones control salt, sugar, and water balance in the body. The disease most commonly affects young to middle-aged female dogs. Signs of hypoadrenocorticism include weakness, depression, lack of appetite, vomiting, diarrhea, and occasionally increased thirst and urine production. If a patient with suspected hypoadrenocorticism has a basal cortisol below 2, an ACTH stimulation must be completed for confirmation of disease. In patients with basal cortisol levels above 2, hypoadrenocorticism is very unlikely.
As Baby’s basal cortisol was below 2, an ACTH stimulation test was completed by collecting a pre-sample, injecting 37.5 mg of consyntropin IV, and collecting a one-hour post sample. Both samples were submitted to an outside lab for cortisol analysis. An abdominal ultrasound was then completed to assess for other potential abdominal disease. No significant abnormalities were noted other than mild bilateral pyelectasia with a mild increase in renal resistive indexes. A urine sample was collected by cystocentesis and sent to the reference lab for a urinalysis and culture.
The next day, Baby was resting comfortably and was more normally vocal. She was eating and drinking normally with no vomiting. She developed a large bowel diarrhea and was started on metronidazole. Her ACTH stimulation test results came back consistent with hypoadrenocorticism. Her results were as follows:
PRE-ACTH CORTISOL <0.2 ug/dL
POST ACTH CORTISOL (1) <0.2 ug/dL
Labwork completed on day two showed:
|BE,ECF||-0.1||-5.0 – 5.0 mmol/L|
|Sodium||138 L||140-151 mmol/L|
|Potassium||5.5 H||3.5-5.0 mmol/L|
|Calcium, ionized||1.52 H||1.13-1.42 mmol/L|
|Anion gap||7||5-2 mmol/L|
|Lactate||3.46 H||0.60-3.00 mmol/L|
Note the BUN decrease from 99.3 on day one to 28.9 on day two. Her creatinine decreased from 2.8 to 1.3 in the same period. Baby was given an injection of desoxycorticosterone pivalate and started on oral prednisone.
On the third day, Baby was continuing to do well with a normal appetite and water intake. Baby’s urinalysis results were as follows:
|Epi Cell||Rare (0-1)|
Baby’s final diagnosis was hypoadrenocorticism. There was no ultrasonographic evidence of pancreatic disease. Her ionized calcium, potassium, and renal values normalized, and her most recent sodium was near normal. Baby was started on desoxycorticosterone pivalate injections at an initial frequency of q 25 days and oral prednisone at an initial dose of 2.5 mg PO q 24 h in 7 days. Baby was schedule to have her electrolytes rechecked in 2 weeks or sooner if she was not eating and drinking normally or had recurrent vomiting or diarrhea.
Addison’s disease is often first diagnosed when a dog is stressed. Dogs normally produce increased cortisol levels in response to stress. For many dogs, precipitating stress can be as simple as a change in day-to-day routine, such as being boarded or having house guests. Recurrent gastrointestinal signs are common due to cortisol deficiency. Most patients with hypoadrenocorticism will have polyuria and polydipsia with a low urine specific gravity. In fact, 60% of Addisonian patients will have a low urine specific gravity. 92% of patients will have a lack of a stress leukogram, 95% hyperkalemia, and 81% hyponatremia. Severe hyperkalemia can cause life threatening arrhythmias.
Treatment of hypoadrenocorticism usually requires lifelong administration of both a mineralocorticoid and a glucocorticoid. Patients with Addison’s Disease may need occasional increases in their glucocorticoid during stressful events. Prognosis with appropriate therapy and monitoring is good.