CHEMISTRY PROFILE INTERPRETATION









  Serum glucose is moderately to markedly elevated. Common considerations for hyperglycemia in the dog include:
 
PERSISTENT
  • diabetes mellitus
  • acute pancreatitis
  • hyperadrenocorticism
TRANSIENT
  • 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 appropriate history.

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.

 

 

Faculty Advisor: Dr. McManus
Student: Jeremy Wentz, Mechelle Regester
Pictures also provided by Dr. Dez Hughes
Information and help also provided by Dr. Saunders, Dr. Habecker, Dr. Walton, Dr. King, Dr. Sweeney, Dr. Wilkins, and Dr. Ward, Dr. Wadell, Dr. Callan
Copyright 2000 University of Pennsylvania School of Veterinary Medicine