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Presentation

Little Bear

Little Bear is a 7 1/2 year old, male neutered, mixed breed dog. On November 8, 20**, he presented to Animal Kind Veterinary Hospital for decreased activity and dramatically decreased appetite of one week’s duration. His family also reported that he seemed to be drinking more water than usual, had an episode of vomiting three days prior, and was passing less stool than usual. There was no history of travel, dietary indiscretion, or known toxin exposure.

On physical exam, Little Bear was recognized to be significantly dehydrated and somewhat underweight at 42.5 pounds. His veterinarian recommended he be admitted to Animal Kind for diagnostic testing and inpatient care. Intravenous fluid therapy was initiated while initial screening lab tests were being run and we began to look for a specific diagnosis to explain these vague signs. Click on the images to view the test results.

iStat venous blood gas 11/8

Little Bear's blood chemistry panel.

Initial Testing

Little Bear’s test results confirmed our clinical impression of significant dehydration (elevated blood urea nitrogen/BUN, increased hematocrit/HCT). His blood pH was low, a condition known as acidosis.  Acidosis is a serious condition which causes patients to have poor blood perfusion, decreases the body’s ability to deliver glucose to cells, and can even lead to cardiac arrhythmias. Another important finding was the presence of multiple electrolyte abnormalities (sodium, potassium, and chloride).  The veterinary clinician felt that the increased blood potassium level, or hyperkalemia might be the most specific clue to Little Bear’s illness.  The presence of a decreased blood sodium level, or hyponatremia, was also unusual because dehydrated patients generally have an increased level of sodium in the blood. The very slight increase in the liver enzyme alanine aminotransferase (ALT) was suspected to be a secondary finding related to rather than causing his gastrointestinal signs.

Treatment and Secondary Testing

Based on these initial findings, Animal Kind veterinarians and staff continued intravenous electrolyte fluid therapy adding dextrose as well to assist glucose delivery to Little Bear’s body. Also, adrenal function testing was performed and a dose of the corticosteroid dexamethasone was administered. The additional test was an adrenocorticotropic hormone (ACTH) stimulation test. In this test, samples of the patient’s blood are obtained before and two hours after administration of ACTH.  ACTH, a messenger normally secreted by the pituitary gland, signals the adrenal gland to produce the hormone cortisol. The ACTH stimulation test enables veterinary clinicians to assess adrenal gland function.

Progress and Testing Results

Reference laboratory CBC and urinalysis

 

 

Additional screening test results from the Antech reference laboratory were reported the following day. Aside from some mild changes consistent with dehydration in the parameters of the complete blood count (CBC), the specific gravity of Little Bear’s urine was less concentrated than expected for a dehydrated patient.

 

 

 

 

iStat venous blood gas 11/9

After a night of intravenous fluids and nursing care with our overnight veterinary technician, Little Bear was brighter and began to eat. Repeat measurement of his blood electrolytes (image on the right) showed significant improvement and his acidosis had resolved. He was able to come off intravenous fluid therapy and transition to oral corticosteroid supplementation with prednisone in the place of the injectable dexamethasone of the day before. He was able to go home with his family that evening.

 

 

ACTH stimulation test

On November 10, we obtained the results of the ACTH stimulation test and his diagnosis. It demonstrated that Little Bear had significantly decreased adrenal hormone secretion. This condition is known as Addison’s disease or hypoadrenocorticism.  Hypoadrenocorticism, though not common, occurs in many species. The disease is characterized by loss of functional tissue of the adrenal glands resulting in deficiency of hormones essential to regulation of multiple metabolic pathways. Many organs are affected by the absence of these hormones including the kidneys, the gastrointestinal tract, and the cardiovascular system. For this reason, hypoadrenocorticism is associated with a wide variety of symptoms. In fact it has been nicknamed “the great imitator” in medical circles.  Overt signs of illness rarely occur until the adrenal glands are hardly functioning at all. Only at that point are patients likely to have abnormalities on screening lab tests. Even then multiple other conditions are capable of causing similar signs and many similar laboratory findings. This diagnosis cannot be obtained without specific testing of the adrenal gland. Veterinarians rely on information obtained by physical examination, response to treatment of clinical problems such as dehydration, and patterns of abnormalities on screening tests to recognize the need for such testing. The hyperkalemia, hyponatremia, elevated blood urea nitrogen, and lack of urine concentration exhibited by Little Bear were not enough to be sure of the diagnosis, but as a group did alert the veterinarian to pursue more specific testing.

Conclusion

Fortunately for Little Bear, hypoadrenocorticism has a good prognosis with treatment. Now on long-term hormone replacement therapy administered regularly by his family and monitored by periodic visits to Animal Kind, he has his appetite back, has gained weight, and is doing very well.