Canine, Maltese, 2 years old, male, neutered, 8.4 lbs.
The dog has been shaking for three days and currently is being treated with amoxicillin. The dog is anorexic and lethargic
and is walking acceptably.
Johnny Hoskins, DVM, Ph.D., Dipl. ACVIM
The findings include rectal temperature 101.2° F, heart rate 165/min, respiratory rate 20/min, pink mucous membranes, normal
capillary refill time, and normal heart and lung sounds. The dog has a non-painful abdomen but constipated stool palpated.
The neurological examination is normal.
A complete blood count, serum chemistry profile and urinalysis were performed and are outlined in Table 1.
Table : Results of laboratory tests
Thorough abdominal ultrasonography was performed with the dog positioned in dorsal recumbency.
The liver shows an inhomogeneous texture in its parenchyma. No masses noted within the liver parenchyma. The gall bladder
is mildly distended, and its walls are not thickened or hyperechoic. The gall bladder does contain some sludge material. The
common bile duct is slightly dilated. The spleen shows a homogeneous to inhomogeneous texture in its parenchyma - no masses
Image 1 and 2.
The left and right kidneys are similar in size, shape and echotexture. Each kidney shows an inhomogeneous texture in the renal
cortex. The renal pelvis is slightly dilated in the right kidney. No masses or calculi were noted in either kidney. The urinary
bladder is distended with urine and contains some urine sediment material. No masses or calculi noted. The left and right
adrenal glands are similar in size and shape. The stomach, small intestines and colon are normal. The pancreas shows an inhomogeneous
texture in its parenchyma.
In this case, most likely hypoadrenocorticism is present. There was no obvious evidence of cancer noted during this abdominal
ultrasound study. At this point, an ACTH stimulation test is warranted now, and then therapy for hypoadrenocorticism is started
with fluids and prednisone. After the results of the ACTH stimulation test are known, then Florinef or injectable mineralocorticoid
is started. The following information may be helpful.
Review on hypoadrenocorticism
Primary hypoadrenocorticism is most often diagnosed in young dogs. Secondary hypoadrenocorticism resulting from ACTH deficiency
is relatively common in dogs afflicted with deficiencies of the pituitary gland.
The clinical signs of hypoadrenocorticism are intermittent vomiting, diarrhea, weight loss, lethargy, anorexia and weakness.
These signs often resolve with fluid therapy and/or corticosteroid treatment. Physical examination of dogs in an acute hypoadrenal
crisis shows weak pulse, bradycardia, prolonged capillary refill time, depression and severe muscle weakness. Clinical findings
of hypoadrenocorticism that heighten the index of suspicion include a normal or slow heart rate in the face of circulatory
shock and the waxing and waning course of disease prior to collapse.
Image 3, 4, and 5.
Severe hyponatremia and hypochloremia associated with hyperkalemia are the hallmarks of hypoadrenocorticism. Although a serum
Na:K ratio of less than 27:1 is considered suggestive of hypoadrenocorticism, it is never pathognomonic. Gastrointestinal
disease, acute renal failure, and postrenal azotemia may also cause a low Na:K ratio. Some dogs with hypoadrenocorticism,
especially those dogs with only a glucocorticoid deficiency, will not show the typical electrolyte disturbances. Azotemia
and hyperphosphatemia are also associated with primary hypoadrenocorticism and make it difficult to differentiate from the
azotemia of acute renal failure. The hematologic abnormalities are eosinophilia and lymphocytosis or normal eosinophil and
lymphocyte counts in the face of any metabolic stress. The anemia of hypoadrenocorticism usually results from ongoing hemorrhagic
gastroenteritis and not caused by the endocrine problem itself. Although hypoglycemia is more commonly associated with secondary
or atypical hypoadrenocorticism, it is infrequently seen with primary hypoadrenocorticism. Urine specific gravity is frequently
low and is attributed to an inadequate medullary gradient due to sodium depletion and decreased medullary blood flow. Dilute
urine along with azotemia and hyperkalemia may easily be mistaken for acute renal failure.