7.2 Hyperglycemia & Hypoglycemia

Critical-illness hyperglycemia in the PICU

In critically ill children, hyperglycemia is common even without preexisting diabetes. Stress catecholamines, cortisol, glucagon, cytokines, and exogenous catecholamine infusions promote glycogenolysis, gluconeogenesis, and insulin resistance. Glucose values frequently rise above 180–200 mg/dL during sepsis, trauma, burns, postoperative cardiopulmonary bypass, and steroid therapy.

Unlike DKA, stress hyperglycemia usually lacks significant ketoacidosis. Still, marked hyperglycemia worsens osmotic diuresis, dehydrates the intravascular space, impairs leukocyte function, and is associated with worse outcomes in many PICU cohorts. Nursing priorities include accurate point-of-care and laboratory confirmation, avoidance of concentrated dextrose boluses that spike glucose, and titration of a regular insulin infusion when protocol thresholds are crossed—typically aiming for a moderate target range rather than aggressively “tight” adult-style control that increases hypoglycemia risk. Recheck glucose frequently (often hourly on an insulin drip), watch for hypokalemia as insulin drives potassium intracellularly, and never leave an insulin infusion running if nutrition or dextrose-containing fluids are interrupted.

Hyperglycemia also appears when parenteral nutrition or high-dextrose fluids are advanced too quickly, during high-dose glucocorticoids, and with calcineurin inhibitors in transplant patients. The CCRN Pediatric exam expects you to separate stress hyperglycemia (insulin ± reduce dextrose load) from DKA/HHS-spectrum disease (fluids, insulin, ketone/gap management).

Hypoglycemia across the pediatric age spectrum

Hypoglycemia is equally dangerous because the developing brain depends on a continuous glucose supply. Definitions vary slightly by age and guideline, but a practical PICU approach treats glucose <50–60 mg/dL as concerning in many infants and children, and acts even sooner for symptomatic patients. Neonates often have lower operational thresholds in the first hours of life, yet any symptomatic low glucose is an emergency regardless of the number on the meter.

Neonatal through adolescent differentials

Think by age and physiology rather than a single adult algorithm:

Hyperinsulinemic hypoglycemia is especially important in neonates and infants: insulin inappropriately suppresses ketones and free fatty acids, so the brain lacks both glucose and alternative fuels. Critical sample labs drawn at the time of hypoglycemia—glucose, insulin, C-peptide, beta-hydroxybutyrate, free fatty acids, cortisol, growth hormone, lactate, ammonia, and acylcarnitine profile—are gold for diagnosis. Do not delay treatment to obtain labs, but draw them during the low if vascular access allows.

Adrenal insufficiency (congenital adrenal hyperplasia in neonates, or central adrenal failure after steroid withdrawal or pituitary disease) presents with hypoglycemia plus hyponatremia, hyperkalemia (primary adrenal failure), hypotension, and poor stress response. Inborn errors (fatty-acid oxidation defects, glycogen storage disease, gluconeogenic defects) often declare during fasting or illness with hypoketotic or unusual metabolic patterns.

Treatment nursing — act fast, then stabilize

1. Confirm and treat simultaneously. If the child is symptomatic or glucose is critically low, give dextrose immediately. Do not wait for a second lab if the clinical picture is clear and a reliable meter reading is low.
2. Age-appropriate dextrose. Neonates and young infants commonly receive D10W (often 2–5 mL/kg IV). Older children may receive D25 in carefully calculated aliquots; D50 is generally avoided in young children because of osmolarity and sclerosing risk, and if used in adolescents it must be diluted/dosed carefully per policy. A common teaching dose framework is roughly 0.5–1 g/kg of glucose. Recheck glucose in 5–15 minutes and repeat if still low.
3. If no IV access. Give intramuscular or subcutaneous glucagon (dose by weight/protocol) while obtaining access—most effective when glycogen stores exist (less reliable in prolonged starvation or liver failure).
4. Prevent rebound. After the bolus, start a continuous dextrose-containing infusion (often beginning around glucose infusion rates of 4–8 mg/kg/min in neonates/infants and titrating upward). For suspected hyperinsulinism, unusually high glucose infusion rates may be required, and endocrine therapies (e.g., diazoxide, octreotide) are specialist-driven.
5. Safety surveillance. Continuous cardiorespiratory monitoring during severe hypoglycemia, seizure precautions, and documentation of neurologic recovery are mandatory. In children with diabetes, treat the low, then adjust the insulin plan—do not simply “push D50 and resume the same basal rate” without analysis.

Nursing pitfalls the exam loves

• Stopping a dextrose infusion while an insulin drip continues
• Misreading a low capillary glucose in a poorly perfused shock patient without lab confirmation—and conversely, delaying treatment in an obviously symptomatic child
• Attributing neonatal apnea solely to “immaturity” without checking glucose
• Missing toxidromes: oral hypoglycemics in toddlers cause prolonged hypoglycemia requiring extended monitoring
• Ignoring cortisol-dependent patients who become hypoglycemic during sepsis—stress-dose steroids may be required

Stable glycemic control in the PICU is neurologic protection. Whether the problem is stress hyperglycemia or age-specific hypoglycemia, the nursing sequence is the same: recognize early, treat with the right dextrose concentration for the child’s size, recheck promptly, and chase the differential when lows recur.