- Definition
- Pathophysiology
- Systems Affected
- Genetics
- Incidence/Prevalence
- Geographic Distribution
- Signalment
- Signs
- Causes
- Risk Factors
BASICS
The glucose concentration is greater than the laboratory reference interval.
- Serum glucose concentration depends on a variety of factors, including intestinal absorption, hepatic production, hormonal regulation, and tissue utilization
- Hyperglycemia may result from insulin-dependent diabetes mellitus (type 1) due to lack of insulin production
- Hyperglycemia may result from insulin resistance due to EMS or PPID (formerly referred to as equine Cushing's disease). Sometimes the 2 syndromes may coexist
- EMS is characterized by insulin resistance/dysregulation, which can lead to hyperglycemia
- PPID is due to functional adenomas or adenomatous hypertrophy and hyperplasia of the pars intermedia of the pituitary gland. Decreased release of dopamine from the hypothalamus is thought to result from oxidative damage; decreased dopaminergic inhibition of the pars intermedia leads to increased secretion of POMC by melanotropes. POMC is cleaved into ACTH, α-melanocyte-stimulating hormone, β-endorphin, and corticotropin-like intermediate lobe peptide. ACTH causes increased cortisol release from the adrenal glands, which can lead to hyperglycemia through increased hepatic gluconeogenesis
- Epinephrine causes hyperglycemia by inhibiting insulin secretion and stimulating glucagon secretion in the pancreas. Epinephrine also stimulates glycogenolysis and gluconeogenesis in the liver. Therefore, the “fight or flight” response and, rarely, pheochromocytomas, can cause hyperglycemia
- Physiologic, transient, postprandial hyperglycemia may occur
- Hyperglycemia may be associated with SIRS (e.g. sepsis [colitis, pleuropneumonia, metritis] trauma, acidosis, burns) owing to dysregulation of glucose homeostasis
- Early in septic or hypovolemic shock, increased catecholamines, glucagon, and glucocorticoids can increase hepatic gluconeogenesis, leading to hyperglycemia
- Endocrine/metabolic—hormonal regulation of gluconeogenesis and glycogenolysis
- Renal/urologic—PU/PD caused by glucosuria, resulting in osmotic diuresis
- Nervous—may result in CNS dysfunction due to increased osmolality
Ponies, Miniature horses, and some horse breeds (e.g. Warmbloods, Morgans, and Saddlebreds) may be predisposed to EMS.
- EMS—obesity, regional adiposity (e.g. cresty neck, tail-head fat), infertility, and laminitis
- PPID—generalized hypertrichosis (hirsutism), abnormal fat distribution, weight loss, muscle wasting, pendulous abdomen, PU/PD, recurrent infections (e.g. sinusitis, hoof abscess, dental disease, dermatitis), or laminitis. Horses with early PPID may be subclinical
- Anxiety—tachycardia, tachypnea, sweating
- Absolute insulin deficiency (i.e. hypoinsulinemia)/type 1 diabetes mellitus—uncommon in horses; may be secondary to destruction of pancreatic islets from chronic pancreatitis or immune-mediated polyendocrinopathy (rare)
- EMS—genetic predisposition to insulin dysregulation/insulin resistance with resulting hyperglycemia; there is possible overproduction of cortisol from adipose tissue
- PPID—excessive ACTH leads to overproduction of cortisol, which stimulates hepatic gluconeogenesis, decreases peripheral glucose utilization, and causes insulin resistance, all of which lead to hyperglycemia
- Pheochromocytoma—excessive catecholamine release
- Physiologic hyperglycemia can occur postprandially due to epinephrine-mediated excitement or cortisol-mediated stress responses
- SIRS—insulin resistance with reduced glucose utilization and increased gluconeogenesis from release of epinephrine and cortisol
- Iatrogenic hyperglycemia can result from administration of dextrose-containing fluids, parenteral nutrition, corticosteroids, α2-agonists (xylazine or detomidine)
DIAGNOSIS
TREATMENT
MEDICATIONS
FOLLOW-UP
MISCELLANEOUS