Serum glucose is moderately to markedly elevated. Common considerations
for hyperglycemia in the dog include:
- diabetes mellitus
- acute pancreatitis
- Stress (steroid) effect
- Excitement (epinephrine)
- sepsis (very transiently)
The 4+ glucosuria evident on urinalysis suggests that hyperglycemia
has been persistent, unlike that seen with stress/excitement alone.
Hyperadrenocorticism also typically causes a persistent hyperglycemia,
but generally only of mild to moderate magnitude. Diabetes mellitus or
acute pancreatitis would be the top considerations in this case.
Evaluation of serum amylase, lipase, or trypsin-like immunoreactivity (TLI)
may aid in distinguishing between these 2 considerations.
Slight to mild elevation in hepatic leakage enzymes is present (ALT,
AST) suggesting mild hepatocellular injury. Evaluation of serum CPK
would help to rule out contribution from muscle injury.
Moderate-marked elevation in ALKP with concurrent elevation in GGT
and total bilirubin suggests cholestasis. Other possible causes for
elevation in ALKP could include endogenous hypercortisolemia (stress,
hyperadrenocorticism), or exogenous administration of steroids. Skeletal
growth in young dogs (particularly large breeds) typically causes only
mild elevations in ALKP, and is unlikely in this patient (due to age and
size). Other bone lesions (neoplasia, lytic osteomyelitis,
hyperparathyroidism) could be ruled out by evaluating ALKP isoenzymes,
as well as physical exam findings, radiographic findings, and other
chemistry panel data (lack of hyperphosphatemia, and hypercalcemia).
Drug induction (i.e. – anticonvulsants) would be ruled out with
Mild hypercholesterolemia is present, and in this case is most likely
attributable to cholestasis, pancreatitis, or diabetes mellitus. Other
causes of hypercholesterolemia include endocrine disorders
(hypothyroidism, hyperadrenocorticism), hypoproteinemia/hypoalbuminemia
secondary to protein-losing enteropathy or protein-losing nephropathy/nephrotic
syndrome, or diet.
Electrolyte alterations include mildly decreased bicarbonate, and
slightly increased anion gap (titrational acidosis). Organic acids which
may accumulate, resulting in bicarbonate titration and acidosis include
lactic acid (in cases of anemia or hypoxia), uremic acids (in cases of
azotemia), and ketoacids (in cases of diabetes mellitus, or starvation).
Ketoacidosis is most likely in this patient, and is supported by the 1+
ketonuria evident on urinalysis.
The moderate hypokalemia seen may be secondary to anorexia,
gastrointestinal losses, or renal losses. In the face of acidosis, even
mild hypokalemia is significant, and suggests whole body potassium
depletion. Supplementation of IV fluids would be essential. During
acidosis, movement of potassium from the ICF to the ECF (in exchange for
H+) typically results in mild hyperkalemia. With correction of acidosis
and administration of insulin, potassium moves back into the ICF,
lowering serum concentrations. In an already hypokalemic patient, severe
life-threatening hypokalemia may occur.