16.1 Diabetes Mellitus & Diabetic Ketoacidosis

Type 1 vs. Type 2 Diabetes Mellitus in Children

Diabetes mellitus in children is dominated by type 1 diabetes mellitus (T1DM), an autoimmune disease in which cytotoxic T cells destroy pancreatic beta cells, producing absolute insulin deficiency. T1DM has two incidence peaks — ages 4-6 years and 10-14 years — and classically presents with the triad of polyuria, polydipsia, and polyphagia plus unintentional weight loss over days to weeks. Because young children often cannot recognize or verbalize these symptoms, roughly 27-40% of children with new-onset T1DM present already in DKA (higher still in children under age 5), including in regional cohorts such as a Jeddah, Saudi Arabia emergency-department series. This is a critical exam pearl: DKA at first presentation is common, not exceptional, so any unexplained vomiting, dehydration, or altered mental status in a child should prompt a bedside glucose check.

Type 2 diabetes mellitus (T2DM) is increasingly diagnosed in children as childhood obesity rises, and Arab Board candidates should expect it to be tested alongside T1DM. T2DM results from insulin resistance with a relative, not absolute, insulin deficiency.

Diagnostic Criteria for Diabetes

Any one of the following confirms diabetes (per American Diabetes Association criteria), and should be repeated on a separate day unless the patient has unequivocal hyperglycemia with classic symptoms:

• Fasting plasma glucose ≥126 mg/dL (7.0 mmol/L) — no caloric intake for at least 8 hours
• 2-hour plasma glucose ≥200 mg/dL (11.1 mmol/L) during an oral glucose tolerance test (OGTT)
• Hemoglobin A1c (HbA1c) ≥6.5%
• Random plasma glucose ≥200 mg/dL (11.1 mmol/L) in a patient with classic hyperglycemic symptoms or a hyperglycemic crisis

Diabetic Ketoacidosis: Diagnostic Criteria

Diabetic ketoacidosis (DKA) occurs when absolute or severe relative insulin deficiency triggers unrestrained lipolysis, hepatic ketogenesis, and gluconeogenesis. The diagnosis requires all three of the following together:

1. Hyperglycemia: blood glucose >200 mg/dL (11 mmol/L)
2. Acidosis: venous pH <7.3 or serum bicarbonate <15 mEq/L
3. Ketosis: ketonemia (beta-hydroxybutyrate) and/or ketonuria

Severity is graded by the degree of acidosis:

Fluid and Insulin Management Principles

The overriding management goal is to correct dehydration, hyperglycemia, and ketoacidosis gradually. The single most heavily tested principle: rapid correction is dangerous, because it is the strongest recognized risk factor for cerebral edema.

• Fluids: give an initial bolus only if the child is in shock (10-20 mL/kg isotonic saline over 1-2 hours); replace the remaining deficit (typically 5-10% of body weight) evenly over 24-48 hours, not rapidly, and avoid hypotonic fluids early in treatment.
• Insulin: start an IV regular insulin infusion at 0.05-0.1 unit/kg/hour, beginning about 1-2 hours after fluid resuscitation starts. Never give an insulin bolus — a bolus provides no benefit and increases cerebral edema risk.
• Potassium: total-body potassium is depleted even when the initial serum level looks normal or high, because acidosis shifts potassium out of cells. Add potassium to IV fluids once the level is known and urine output is confirmed — insulin therapy will otherwise drive serum potassium down rapidly and dangerously.
• Glucose: once blood glucose falls to about 250-300 mg/dL (14-17 mmol/L), add dextrose to the IV fluids while continuing the insulin infusion until the ketoacidosis itself resolves (pH normalizes, anion gap closes) — insulin should never be stopped just because glucose has normalized.
• Bicarbonate: avoid except in life-threatening acidosis with hemodynamic compromise; bicarbonate use is an independent risk factor for cerebral edema.
• Monitoring: hourly glucose and neurologic checks; electrolytes and blood gas every 2-4 hours.

Cerebral Edema: The Key Exam Trap

Cerebral edema is the most feared complication of pediatric DKA and the leading cause of DKA-related death and long-term neurologic morbidity in children. Clinically significant cerebral edema complicates well under 1% of DKA episodes, but carries a disproportionate share of DKA mortality, typically emerging 4-12 hours after treatment begins — not at presentation.

Risk factors include: new-onset diabetes, young age (under 5 years), longer duration of symptoms before presentation, severe acidosis or high initial blood urea nitrogen (BUN), rapid IV fluid administration, use of hypotonic fluids, bicarbonate administration, giving insulin within the first hour of fluid therapy, and a corrected serum sodium that fails to rise (or falls) as glucose corrects — sodium should rise as glucose falls, and a flat or falling corrected sodium during treatment is a red flag.

Warning signs, often abrupt: headache, altered mental status or new irritability, recurrent vomiting after initial clinical improvement, bradycardia with hypertension (Cushing triad), falling oxygen saturation, and papilledema.

Management if cerebral edema is suspected: treat immediately, before imaging — give mannitol 0.5-1 g/kg IV over 10-15 minutes (or hypertonic 3% saline 5-10 mL/kg as an alternative), elevate the head of the bed to 30 degrees, reduce the IV fluid rate by about one-third, and prepare for intubation if the airway is compromised. On the exam, the correct answer is always to treat first — waiting for a CT scan to confirm the diagnosis costs time the brain does not have.