• Hypoglycemia is defined as a serum glucose <70 mg/dL.
• Tight glucose control has been shown to improve outcomes in critically ill patients; however, hypoglycemia is the most common complication of insulin therapy and has more immediate and direct deleterious effects.
• Additionally, severely ill, elderly patients, and neonates have an increased susceptibility to the deleterious effects of hypoglycemia (permanent neurologic damage and death).

• Iatrogenic hypoglycemia
  • Overdose of insulin or other antidiabetic drug ingestion.
  • Decreased exogenous glucose intake (missed meals/snack or after overnight fasting).
• Alcohol ingestion
• Side effect of certain drugs: Haloperidol, pentamidine, quinine, and nonselective beta-blockers.
• Severe illness
• Tumors: Pancreatic islet cell adenoma or carcinoma, hepatoma, and sarcoma
• Adrenal insufficiency
• Autoimmune processes
• Increased sensitivity to insulin following exercise, weight loss, or due to insulin sensitizers.
• Renal failure: Decreased clearance of insulin
• Neonates
  • Preterm delivery
  • Transient hypoglycemia of the newborn
  • IUGR
  • Sepsis
  • Hypothermia
  • Birth asphyxia
  • Inborn errors of metabolism
  • Hepatic enzyme deficiencies
  • Transplacental exposure to maternal hypoglycemic medications
• Elderly: Frail, polypharmacy, and multiple hospital admissions.

• Glucose is a principal energy substrate for the body; for the brain, it is the sole energy substrate.
• Glucose is synthesized from gluconeogenesis (from the metabolism of pyruvate, lactate, glycerol, and glucogenic amino acids) and glycogenolysis that results from the breakdown of glycogen.
• In normal glucose homeostasis, blood glucose levels are tightly regulated by insulin, glucagon, epinephrine, and cortisol. The liver is the principal storage site for glucose in the form of glycogen.
• A decrease in blood glucose level will cause
  • Drops in endogenous insulin production
  • Release of epinephrine, glucagon, growth hormone, and cortisol that act as counterregulatory hormones.
  • An increase in hepatic glucose production
  • A decrease in peripheral utilization of glucose
  • Neurogenic and neuroglycopenic symptoms
• Diabetes
  • Type 1, or insulin-dependent, diabetics have reduced or absent insulin secretion. In addition, they have an impaired release of counterregulatory hormones such as glucagon and epinephrine.
  • In type 2 diabetes, patients are capable of generating and secreting insulin, but peripheral tissues are resistant to its effects. There is a lower risk of hypoglycemia compared to type 1 diabetes, potentially due to the sustained ability to secrete counterregulatory hormones.
  • Exogenous insulin administration and oral antihyperglycemic medications (e.g., sulfonylureas) can cause iatrogenic hypoglycemia.
• Neonatal hypoglycemia can cause seizure and permanent brain damage. The brain utilizes glucose as the sole substrate of energy. In the rapidly growing neonatal brain, cerebral consumption comprises nearly 90% of their total glucose consumption; however, neonates are susceptible to hypoglycemia due to
  • Inadequate hepatic glycogen reserve
  • Immaturity of the liver in synthesizing glucose (hepatic gluconeogenesis).
  • Relative hyperinsulinism in infants of diabetic mother
  • Inherited disorders of metabolism
  • Impaired release of counterregulatory hormones
• Evidence is suggesting that the benefits of tight glucose control may be outweighed by the potential harm of hypoglycemia.
  • The ACCORD trial revealed that intensive glucose control in patients with type 2 diabetes mellitus (HBA1C <6%) is associated with increased mortality and no reduction in adverse cardiovascular events.
  • The NICE SUGAR study revealed that in the ICU patients treated with IIT had increased mortality. IIT was defined as a blood glucose aim of 81–106 g/dL; the conventional group was defined as a blood glucose aim of <180 g/dL.
  • Several studies report that maintaining a stable glucose level is equally important to the absolute glucose values. Fluctuations in glucose control lead to oxidative stress that cause macrovascular complications.
• Cardiac surgical patients, particularly those requiring prolonged intensive care admissions, are an exception; they show a clear benefit from strict glycemic control.

• Diabetics. Preoperative assessment of glucose control, type and dose of medications, frequency of hypoglycemia, and current HBA1C level is needed.
• On the day before surgery
  • Oral medications are usually dosed normally
  • Long or intermediate-acting insulin can be taken in usual doses while on a normal diet. Evening of night doses are normally decreased.
  • If hypoglycemic while NPO, treat with 15–20 gm of glucose. Options include clear liquids, in the form of sugary drinks and fruit juices, sodas, or electrolyte solutions.
  • Blood sugar checks should be done frequently when NPO.
• On the morning of surgery
  • In type 2 diabetics, oral medications and short-acting injectables should be withheld.
  • Insulin pumps should be maintained at a basal rate and short-acting insulin should be withheld.
  • for morning cases, hold intermediate-acting insulin or give a percentage of the dose calculated as below:
    • Fraction = [(dosing interval in hours) – (hours of fast during interval)]/(dosing interval in hours)
  • for cases later in the day, maintain a basal rate for patients on an insulin pump and for patients on intermediate insulin, give a percentage of the dose based on the formula above.
• In the recover room or hospital ward, resume oral hypoglycemic agents and insulin with food.
• Hyperglycemia in the perioperative period. Correction doses of ultra short-acting insulin: 1–4 U IV typically decreases blood sugar by 50 mg/dL.

• Seizure
• Vasovagal attack
• Cardiac arrhythmia
• Panic attack

• Hyperglycemia
• Diabetes Mellitus

251.2 Hypoglycemia, unspecified

E16.2 Hypoglycemia, unspecified

Michael S. Green , DO

Poovendran Saththasivam , MD