7.1 Diabetes Mellitus & DKA

Pediatric diabetes and why DKA looks different in children

Diabetic ketoacidosis (DKA) remains one of the most tested endocrine emergencies on the CCRN Pediatric exam because it blends metabolic, neurologic, and fluid-electrolyte nursing priorities. In children, DKA most often occurs in new-onset type 1 diabetes mellitus or in established diabetes when insulin is omitted, pumps fail, or an intercurrent illness (especially gastroenteritis or infection) increases insulin demand. Type 2 diabetes can also present with DKA in adolescents, but absolute insulin deficiency with ketogenesis is still the core pathophysiology.

Without adequate insulin, peripheral tissues cannot use glucose. Counter-regulatory hormones (glucagon, catecholamines, cortisol, growth hormone) drive hepatic glucose production and lipolysis. Free fatty acids are converted to ketone bodies (primarily beta-hydroxybutyrate and acetoacetate), producing a high anion gap metabolic acidosis. Osmotic diuresis from hyperglycemia causes profound dehydration, electrolyte losses, and hypovolemia—yet total-body potassium is depleted even when the measured serum potassium looks normal or high.

Diagnostic criteria and clinical presentation

Pediatric DKA is generally defined by:

• Hyperglycemia — typically plasma glucose >200 mg/dL (euglycemic DKA is uncommon but possible with SGLT2 exposure or limited carbohydrate intake)
• Acidosis — venous pH <7.3 and/or bicarbonate <15–18 mEq/L (severity often stratified by pH: mild ~7.2–7.3, moderate ~7.1–7.2, severe <7.1)
• Ketosis — positive serum or urine ketones; beta-hydroxybutyrate is the preferred bedside marker
• Elevated anion gap — Na − (Cl + HCO3), typically >12 mEq/L

Classic bedside findings include polyuria, polydipsia, weight loss, fruity acetone breath, Kussmaul respirations, abdominal pain that can mimic an acute abdomen, tachycardia, delayed capillary refill, and progressive lethargy. Young children may present with nonspecific irritability, vomiting, or “failure to thrive” rather than a clear diabetes history. Always search for a precipitant: infection, missed insulin, pump site failure, trauma, or (in adolescents) intentional omission.

Fluid and insulin priorities — order matters

The treatment sequence the exam expects is volume restoration first, then continuous insulin, with potassium managed continuously. Cerebral edema risk makes pediatric fluid strategy more cautious than many adult protocols.

1. Airway, breathing, circulation. Protect the airway if consciousness is depressed. Give oxygen as needed. Obtain vascular access and send glucose, blood gas, electrolytes, BUN/creatinine, beta-hydroxybutyrate, and CBC.
2. Isotonic fluid resuscitation. If the child is in shock (poor perfusion, hypotension), give 10–20 mL/kg of 0.9% sodium chloride and reassess. Additional cautious boluses may be needed for persistent shock, but avoid large, rapid volume dumping once perfusion improves. After resuscitation, calculate remaining fluid deficit and replace it evenly over 24–48 hours with isotonic (or near-isotonic) fluid plus maintenance, adding glucose when blood glucose falls into the target range (commonly near 200–250 mg/dL). Many PICUs use a two-bag system (one bag without dextrose, one with dextrose) so insulin can continue while glucose is stabilized.
3. Insulin infusion — no bolus. After approximately the first hour of fluids, start regular insulin at 0.05–0.1 units/kg/hr by continuous IV infusion. An insulin bolus is not recommended in children because abrupt osmotic shifts may contribute to cerebral edema. Target a gradual glucose decline of roughly 50–100 mg/dL per hour. Continue insulin until the anion gap closes and ketosis resolves—not merely until glucose normalizes.
4. Potassium replacement. Correct hypokalemia before starting insulin if serum K+ is low (commonly hold insulin until K+ is at least ~3.3 mEq/L). Once insulin begins, expect serum K+ to fall; add potassium to IV fluids unless the child is anuric or hyperkalemic with ECG changes.

Cerebral edema — the pediatric DKA killer

Clinically apparent cerebral edema occurs in roughly 0.5–1% of pediatric DKA episodes but accounts for most DKA-related deaths. Risk is highest in younger children, new-onset diabetes, severe acidosis/hypocapnia, and rapid osmolar changes. It usually appears within the first 4–12 hours of treatment, often after the child seemed to be improving.

Warning signs every CCRN Pediatric nurse must escalate immediately:

• Headache, recurrent vomiting after initial improvement
• Slowing heart rate with rising blood pressure (Cushing-type pattern) or unexpected hypertension
• Irritability, confusion, decreased responsiveness, incontinence
• Cranial nerve findings, unequal or sluggish pupils, posturing
• Desaturation or respiratory irregularity suggesting rising intracranial pressure

Immediate management (do not wait for CT to start therapy if the child is deteriorating):

• Call for help; secure airway if GCS is falling
• Elevate the head of bed ~30 degrees; keep head midline
• Give mannitol 0.5–1 g/kg IV over ~15–20 minutes or 3% hypertonic saline (commonly 5–10 mL/kg) per protocol
• Reduce fluid rate; continue careful metabolic correction
• Arrange neuroimaging after airway and osmotherapy are addressed

Nursing documentation should capture serial neurologic exams, exact fluid volumes, insulin rate changes, and the glucose trajectory—these details drive both bedside safety and exam vignettes.