Hyperglycemia and hypoglycemia can cause severe clinical signs requiring emergency treatment.
DKA is a complex, multifactorial, life-threatening disease process resulting in fluid, acid-base, and electrolyte abnormalities. DKA occurs due to a relative or absolute insulin deficiency caused by beta cell failure, loss or inactivity of cellular insulin receptors, inappropriate insulin dose, or insulin resistance. Physical exam findings of DKA include dehydration, acetone breath, mental dullness, thin BCS/muscle wasting, unkempt haircoat, weakness, shock, and neurologic signs. Blood work abnormalities include azotemia, isothenuria, glucosuria, ketonuria, elevated AST/ALT, elevated cholesterol, hyperglycemia, elevated triglycerides, metabolic acidosis, decreased chloride, decreased potassium, decreased magnesium, elevated or decreased sodium, and decreased phosphorus. The four hallmarks of diagnosing DKA include hyperglycemia, glucosuria, ketonuria or ketone presence in serum/plasma, and metabolic acidosis. IV fluids are an important aspect of treating DKA. Fluids help normalize blood pressure, correct electrolyte losses, correct acidosis, correct osmolality, lowers blood glucose and promotes renal excretion of glucose, and decreases concentration of counter-regulatory enzymes. IV fluid rate should be based on maintenance fluids, ongoing losses, and correcting dehydration over 12-24 hours. Fluids should be tailored to patient based on skin turgor, mm, body weight, and urine specific gravity. Electrolytes including phosphorus should be monitored every 6 hours as rapid shifts can occur with insulin therapy. Insulin therapy should be started once the animal is hydrated. Insulin can be given as bolus injections or a constant rate infusion and the amount given is based on serum glucose levels.
An infrequent but well documented complication of diabetes mellitus is Hyperglycemia Hyperosmolar Syndrome (HHS). HHS is defined as diabetes with hyperglycemia greater than 600mg/dL, minimal or absent ketones, and serum osmolality greater than 350mOsm. The pathogenesis of HHS is similar to DKA with a few distinct differences. There is a small amount of insulin and hepatic glucagon resistance inhibits lipolysis thus preventing ketosis. Losses (osmotic diuresis, vomiting) and decreased water consumption lead to hypovolemia and decreased GFR preventing the excretion of glucose. Concurrent disease precipitates the crisis as in DKA however CHF and renal failure predominate due to the detrimental effects on the GFR. Physical exam findings are similar to DKA but there is no acetone breath, weight loss is an inconsistent finding, and neurologic signs predominate including dullness, stupor, coma, ataxia, CN deficits, twitching, and/or seizures. Goal of IV fluids is to replace the fluid deficit and return osmolality to normal range but hypernatremia should not be corrected faster than 0.5 – 1 mEq/hr. Initial fluid of choice is 0.9% NaCl to prevent rapid decrease in osmolality. Insulin therapy is not as critical as in resolution of DKA. Large improvements in hyperglycemia can be seen just in replacing fluid deficit thus restoring GFR. Generally a less aggressive drop in the glucose level is attempted by decreasing the insulin dose by 25-50% that of the DKA protocol. High mortality rate due to the severity of the syndrome and presence of concurrent disease.
Hypoglycemia
Clinical signs of hypoglycemia include neuroglycopenia which is a shortage of glucose in the brain causing altered mentation, weakness, ataxia, blindness, and seizures. Prolonged hypoglycemia can lead to permanent blindness and seizures. Other clinical signs can include pacing, restlessness, vocalization, shaking, trembling, GI signs, polyphagia, tachypnea, bradycardia, and circulatory collapse. Common causes of hypoglycemia includes excess insulin or insulin analogue (exogenous insulin overdose, insulinoma, paraneoplastic, and medications such as sulfonylureas and xylitol), an excess in glucose utilization (sepsis, Babesia, “hunting dog” hypoglycemia, paraneoplastic), and decreased glucose production (decreased hepatic stores in toy breeds and neonates, hepatic dysfunction, Addison’s).
Treatment of hypoglycemia includes an initial dextrose bolus (0.5 – 1ml/kg) of 50% dextrose diluted 1:1 in 0.9%NaCl followed by supplementing dextrose in IV fluids (usually 2.5-5%/L). A central line should be placed if greater than 5% dextrose/ L needs to be given due to hypertonicity and phlebitis. The owners can apply karo or pancake syrup, or honey to mucous membranes at home. Aggressive dextrose therapy should be avoided in animals with hypoglycemia caused by insulinoma as dextrose may exacerbate insulin release resulting in rebound hypoglycemia and clinical signs.
