Introduction

• Plasma glucose less than 3.0 mmol/L (55 mg/dL) is significant.
• In animals which have chronically low blood glucose, concentrations may have to drop very low (less than 2.0 mmol/L (35 mg/dL) before clinical signs are exhibited.
• Signs: ataxia, weakness, disorientation, seizures.
• Diagnosis: blood or plasma glucose concentrations. 
• Treatment: feeding and/or glucose (oral or intravenous) and correct underlying cause.

Pathogenesis

Etiology

• Functional islet cell tumor (insulinoma Pancreas: neoplasia: insulinoma ).
• Excessive insulin dosage in diabetics.
•  Xylitol toxicity Xylitol toxicity due to consumption of sugar-free candies and other foods.
• Starvation/malnourishment of neonates.
• Liver disease, particularly large hepatomas Liver: neoplasia.
• Other intra-abdominal tumors, especially hepatocellular carcinoma Liver: hepatocellular carcinoma, splenic tumors Spleen: neoplasia and leiomyosarcomas Leiomyoma/leiomyosarcoma.
• Sepsis Shock: septic.
• Adrenocortical insufficiency Hypoadrenocorticism.
• Glycogen storage diseases Storage disease.
• Severe polycythemia Polycythemia: secondary.

Predisposing factors

• Neonatal/juvenile animals have immature mechanisms for regulating blood glucose.
• Over-activity, cold, other stresses tend to reduce blood glucose.
• Insulin treatment of diabetic dogs.
• Hard work - appears as functional disorder.

Pathophysiology

• Decrease of blood glucose towards the lower end of the physiological range stimulates secretion of counter-regulatory hormones (glucagon, adrenaline, noradrenaline, cortisol, and growth hormone), which increase glycogenolysis and gluconeogenesis and so increase blood glucose concentration.
• Hypoglycemia results from failure of these mechanisms due to excess insulin, deficiency of counter-regulatory hormones, and/or inadequate glucose production.
• Hypoglycemia also → and increased appetitie (might even result in pica Pica).
• If these protective counter-regulatory mechanisms are overwhelmed, hypoglycemia → reduced glucose availability to central and peripheral nervous system → lethargy, weakness, ataxia, disorientation, seizures.
• Prolonged, severe hypoglycemia → reversible or irreversible brain damage, and rarely → death.

Specific

• Neonatal hypoglycemia - gluconeogenesis limited in neonate and limited glycogen stores rapidly deplete - relies upon regular feeding - may develop hypoglycemia after only 12 hour fast.
• Starvaion - severe malnutrition → decreased hepatic glycogen, decreased fat stores → decreased gluconeogenesis → hypoglycemia.
• Glycogen storage diseases Storage disease - genetic abnormality → deficiency in enzymes/defective enzymes involved in glycogen degradation → hypoglycemia. 
• Exogenous agents: direct drug action → hypoglycemia.
• Bacterial shock → depletion of glycogen stores, increased peripheral use of glucose, decreased gluconeogenesis + ?circulatory factors → hypoglycemia.
• Extra-pancreatic tumors:
  • Secretion of insulin/insulin-like/insulin precursor.
  • Accelerated glucose utilization.
  • Inhibited glucose release from liver → hypoglycemia.
• Functional islet cell tumor  → insulin secretion → hypoglycemia.
• Insulin overdose, inappetence/starvation, concurrent illness and/or sudden increase in exercise/stress levels during treatment with insulin may → hypoglycemia.

Diagnosis

Treatment

Outcomes