Glucose

Blood glucose concentration represents an equilibrium among dietary intake, hormonal interactions (insulin, glucagon, glucocorticoids, catecholamines, and growth hormone), and biochemical pathways (glycogenolysis, gluconeogenesis, and glycolysis).

Hypoglycemia

Hypoglycemia is either the result of poor sample handling, pathologic states, or fasting. Delayed separation of serum from the blood cells may allow time for these cells to consume glucose, thus causing false low glucose levels. Fasting usually does not result in hypoglycemia except in neonatal animals (Box 22.19). Newborns have limited energy reserves, and any disease (mainly septicemia and diarrhea), injury, congenital defect, maternal rejection, agalactia, or management error that limits energy intake can result in marked hypoglycemia associ­ated with profound depression, even coma. In calves with acute severe diarrhea, blood glucose may fall below 40 mg/dL (2.2 mmol/L) in 30% to 50% of cases.⁶⁴ One study has shown that 34% of critically ill foals are hypoglycemic.⁶⁵ Hypoglycemia may also be seen in animals with acute toxic enteritis, coliform mastitis, septicemia, and colic associated with strangulated bowel, as well as in the later stages of endotoxemia and in some horses with exhaustion after prolonged exercise, hepatic insufficiency, islet B cell neoplasia, hepatocellular carcinoma, and surreptitious injections of insulin. Hypoglycemia is a reasonably consistent feature with primary ketosis and fat cow syndrome in cattle, with pregnancy toxemia in sheep and goats, and in hyperlipemia syndrome, which is seen primarily in pregnant or lactating ponies. Rapid, semiquantitative field tests for blood glucose (Dextrostix, Boehringer Mannheim Diag­nostics, Inc., Indianapolis, Ind.) or handheld human glucometers provide a practical means of early recognition of this problem.

Hyperglycemia

Hyperglycemia may be seen with excitement, transportation, or stress and probably is mediated by increases in catecholamine and glucocorticoid hormones (Box 22.20). The stress and pain of acute severe colic in horses frequently results in hypergly­cemia occurring in approximately 50% of the colic cases, and

■ BOX 22.19

Causes of Hypoglycemia

Common Causes

Inappetence in newborns

Sepsis

Pregnancy toxemia

Endotoxic shock (late stages)

Hepatic failure

Uncommon Causes

In vitro glycolysis by red blood cells

In vitro glycolysis by eperythrozoonosis

■ BOX 22.20

Causes of Hyperglycemia

Common Causes

Acute severe colic in horses

Stress and excitement

Cushing syndrome Glucocorticoid administration

Xylazine administration

Uncommon Causes

Overly rapid administration of dextrose Diabetes mellitus elevations of blood glucose above 250 mg∕dL(14 mmol/L) are associated with a poor prognosis in such cases. In one study all the animals with colic that did not survive had a mean glucose level of 234 mg/dL (13 mmol/L).⁶⁷ Endotoxemia initially results in a transient hyperglycemia that may be followed by marked hypoglycemia in the terminal stages of toxemia. The later stages of Cushing syndrome in horses are generally associated with a non-insulin-responsive hyperglycemia and glycosuria. Similar changes can be induced transiently when exogenous glucocorticoid hormones are administered at a high dose rate. Insulin-responsive diabetes mellitus rarely occurs in large animals but has been reported in association with destructive pancreatic lesions. Hyperglycemia in large animals has also been associated with iatrogenic hyperadrenocorticism, pheochromocytomas, after strenuous exercise, after prolonged halothane anesthesia, administration of xylazine or detomidine, during administration of glucose, endotoxemia, proximal duodenal obstruction in cattle, and pituitary pars intermedia dysfunction in horses. Hyperglycemia is rarely encountered in equine metabolic syndrome (EMS).