Diabetic Ketoacidosis

STICKY SITUATION:

By Christian Franco Ruiz
PGY-3 Pediatrics, Saint Peter's University Hospital

A CASE OF HYPERGLYCEMIA

CASE PRESENTATION

3 yo 9 mo M with Type 1 Diabetes Mellitus who presented to OSH due to multiple episodes of nonbloody and nonbilious vomiting

CASE PRESENTATION

Based on this statement alone — a toddler with T1DM and vomiting — what else would you want to know from me to decide how to proceed with management?

Current illness

• 1 day prior --> abdominal pain, increased frequency of urination, and dryness of the mouth

• On the day of admission, beginning at 2am --> 5 episodes of nonbloody, nonbilious vomiting

• No recent illness (fever, URI symptoms). No sick contacts. Not in day care

Current illness

• Decreased PO intake

• Mom unsure when was last urine output

Diabetes history

• Diagnosed in July 2025 when he presented in severe diabetic ketoacidosis

• Currently regimen:

  • Insulin glargine 9 units daily (given 8am, last given day prior to admit)

  • Regular insulin as follows:

    • Carb correction: 1 u per 30 g carb before breakfast and dinner, 1 u per 40 g carb before lunch

    • Insulin sensitivity: 1 u per 175mg/dl over the target of 175 mg/dl

Diabetes history

• Wears a Dexcom 7

  • GMI: 9.2% , 14-day avg BG: 245 ± 98 mg/dL

  • COV: 40% (goal <36%)

  • TIR (70–180 mg/dL): 28% (goal >70%)

    • Very High (>250 mg/dL): 50%

    • High (181–250 mg/dL): 21%

    • Low (<70 mg/dL): 1%

    • Very Low (<54 mg/dL): <1%

Diabetes history

• GMI 9.2% / Avg BG 245 → chronic hyperglycemia, poor control.

• Coefficient of Variation (COV) 40% → significant variability, ↑ risk for both highs and lows.

• Time in Range (TIR) 28% → way below target (ADA goal: >70% in pediatrics).

• Very High 50% → spending half the time dangerously hyperglycemic.

• Lows <1% → hypoglycemia is rare (so the issue isn’t overtreatment, it’s undertreatment / insulin insufficiency).

OSH COURSE

NS bolus 20ml/kg x1
Labs show: pH 7.11, HCO₃ 10.3, BE -18, glucose 700
Patient was then transferred.

PHYSICAL EXAMINATION

• Vital signs

• Hydration status: dry mucous membranes, poor skin turgor, sunken eyes

• Respiratory findings: Kussmaul respirations (deep, rapid breathing due to acidosis)

• Abdominal exam: diffuse abdominal tenderness

• Neurological exam: mental status, focal neurologic deficits (ex. CN palsies, abn pupillary responses)

DIABETIC KETOACIDOSIS

BIOCHEMICAL CRITERIA
1. Hyperglycemia: glucose > 200 mg/dL (>11.1 mmol/L)
2. Metabolic acidosis: venous pH < 7.3, serum bicarbonate level < 15 mEq/L (<15 mmol/L)
3. Ketonemia (blood beta-hydroxybutyrate > 3 mmol/L) or moderate to severe ketonuria

MOST COMMON CAUSES OF DKA

• New onset DM (30% of T1DM or 10% of T2DM)

• Infection / intercurrent illness

• Inadequate insulin administration

• Medications: high-dose corticosteroids, atypical antipsychotic agents, diazoxide, and immunosuppressive medications

RISK FACTORS FOR DKA

Insulin omission
Previous DKA episodes
Inadequate insulin dose
Infection

KNOWN T1DM

Younger age (<2 years)
Delayed diagnosis
Low socioeconomic status

NEW DIAGNOSIS

Recurrent DKA --> psychological considerations (stress of chronic disease, rebellion against authority, fear of weight gain, and eating

disorders

DKA SEVERITY

• Mild: pH <7.3, CO2 <15

• Moderate: pH <7.2, CO2 <10

• Mild: pH <7.1, CO2 <5

new onset labs

• Kids with new-onset T1DM are at higher risk of other autoimmune diseases (thyroid disease, celiac, less commonly Addison’s).

• These tests do not change acute DKA management — but they are crucial to:

  • Confirm diagnosis (autoimmune vs other diabetes).

  • Screen for coexisting autoimmune conditions.

  • Establish a baseline for monitoring long-term complications.

dka management

• Stabilize – airway, breathing, circulation.

• Fluids first – cautious rehydration over 24–48 hrs.

• Insulin after fluids – 0.05–0.1 U/kg/hr.

• Potassium replacement – once urine output present.

• Avoid bicarbonate – unless pH ≤6.9 with poor perfusion.

• Monitor hourly – glucose, neuro checks, frequent electrolytes.

HYDRATION

• Hypovolemic shock - NS bolus 20ml/kg should be rapidly infused with reassessment after each bolus

• Dehydration without shock - NS bolus 10ml/kg over 30 to 60 minutes.

• Patients with DKA are typically 5-10% dehydrated

INSULIN THERAPY

• Start 0.05–0.1 U/kg/hr IV infusion

• Monitor:

  • Glucose hourly

  • Blood gases q1–2 hrs

• Continue until DKA resolves (not just until glucose normalizes)

• Expected glucose drop: 36–90 mg/dL/hr (2–5 mmol/L/hr)

• If drop is too rapid, add dextrose:

  • Glucose <200 → D5NS

  • Glucose <150 → D10NS

potassium replacement

• 💧 Replace once urine output confirmed and not hyperkalemic

• 🧪 Initial K⁺ may be normal/high → but total body deficit always present

  • Shifts out of cells (acidosis)

  • Losses from vomiting + osmotic diuresis

• 💉 Insulin drives K⁺ into cells → risk of hypokalemia

• 📌 If K⁺ <5.5 → add 20 mEq/L KCl to IV fluids

BICARBONATE SUPPLEMENTATION?

• ❌ Not recommended in routine DKA

• ⚠️ No benefit in resolution; historically linked to worse outcomes

• 🚫 Risk: paradoxical CNS acidosis

• ✅ Only use if:

  • Severe hyperkalemia OR

  • Severe acidosis (pH ≤6.9) with impaired cardiac contractility

CEREBRAL EDEMA

• 🧠 Most feared complication of pediatric DKA

• Occurs in 0.5–0.9%, but causes most DKA deaths

• Typically develops 4–12 hrs into treatment

• Risk factors:

  • Young age, new-onset DM

  • Severe acidosis (pH <7.1, HCO₃ very low)

  • High BUN (dehydration)

  • Rapid fluid resuscitation/tonicity shifts

CEREBRAL EDEMA

• Early warning signs

  • Headache, irritability, behavior change

  • Vomiting, incontinence

  • Bradycardia + hypertension (Cushing triad evolving)

• Progressive signs

  • Drowsiness, confusion, declining mental status

  • Cranial nerve palsies, abnormal pupils

• Late signs

  • Seizures, coma, hypoventilation, respiratory arrest

👉 Hourly neuro checks are mandatory in all DKA patients

CEREBRAL EDEMA

• 🚨 Treat immediately if suspected — do NOT wait for CT

• Supportive measures

  • Elevate HOB 30°

  • Avoid hypotension, hypoxia, excess fluids

• Hyperosmolar therapy

  • Mannitol 0.5–1 g/kg IV over 10–15 min

  • OR 3% hypertonic saline 2.5–5 mL/kg IV over 10–15 min

  • Both acceptable; no proven superiority

hyperosmolar hyperglycemic state

• Onset more insidious.

• Glucose >600, Osm >320, HCO3 >15, absent/trace ketones

• Dehydration more profound.

• Mortality ~10x higher than DKA.

• Complications: thrombosis, rhabdo, stroke, pancreatitis.

• Management:

  • Aggressive isotonic fluids first (deficit ~12–15% body weight).

  • Transition to hypotonic for hypernatremia.

  • Delay insulin until after fluids.

  • PICU monitoring.

INPATIENT MANAGEMENT OF HYPERGLYCEMIA

• Insulin regimen

  • Basal–bolus for stable patients

  • calculate TDD ~0.5–1.0 U/kg/day prepubertal, 1–1.5 pubertal

  • 50% - basal (long-acting insulin), 50% - bolus (regular insulin)

  • Regular insulin dose based on:

    • Carb correction: 500/TDD

    • Insulin sensitivity factor: 1800/TDD

INPATIENT MANAGEMENT OF HYPERGLYCEMIA

• Monitoring: before meals and at bedtime, 12am, 3am

• Glycemic targets:

  • Critically ill: 140–180.

  • Non-critically ill: 100–180.

• Hypoglycemia:

  • <70 = treat.

  • <54 = urgent.

  • <40/AMS = severe → glucose/glucagon.

  • 15–20 g rapid carbs if awake; glucagon if unable to take PO.

Multiple Choice

A 15-year-old with DKA develops sudden bradycardia, hypertension, and vomiting 6 hours into treatment. What is the immediate best next step?

• Order a stat CT scan of the brain.

• Stop IV fluids.

• Give IV mannitol or hypertonic saline.

• Increase insulin infusion.

• Administer IV bicarbonate.

Multiple Choice

A 7-year-old in DKA has a sodium of 128 mmol/L with glucose 540 mg/dL. What is the corrected sodium, and what is its significance?

• 128; significant hyponatremia needing hypertonic saline

• 132; consistent with dilutional hyponatremia

• 138; sodium is actually normal after correction

• 142; concerning for hypernatremia

• 146; increased risk of cerebral edema

Multiple Choice

A 10-year-old girl with DKA is improving, but her bicarbonate is still 11 mmol/L even though her anion gap has closed. Which explanation best fits?

• Persistent ketoacidosis

• Renal tubular acidosis

• Ongoing sepsis

• Hyperchloremic metabolic acidosis

• Lactic acidosis

Multiple Choice

A 14-year-old in severe DKA is on an insulin infusion. Glucose falls from 450 to 200 mg/dL in 2 hours, but pH remains 7.10, HCO₃ 9. What is the next best step?

• Stop insulin infusion.

• Add D5 to fluids and continue insulin.

• Increase insulin dose.

• Give IV bicarbonate.

• Switch to SC insulin.

Multiple Choice

A 4-year-old boy is in DKA. His initial potassium is 2.8 mmol/L. What is the best management approach?

• Start insulin immediately and replace K afterwards.

• Replace potassium first and delay insulin until K normalizes.

• Give IV bicarbonate to correct hypokalemia.

• Start IV calcium gluconate.

• Restrict fluids to prevent worsening hypokalemia.

Multiple Choice

In children with DKA, which parameter best indicates resolution of DKA?

• Blood glucose <200 mg/dL.

• pH >7.30.

• HCO₃ >18 with closed anion gap.

• Normal urine ketones.

• Corrected Na >135 mmol/L.

Multiple Choice

A 9-year-old boy is recovering from DKA. Labs show glucose 160, pH 7.32, HCO₃ 19, AG 12. What is the most appropriate next step?

• Stop IV insulin and transition to SC regimen with overlap.

• Continue IV insulin until glucose <150.
  

• Start IV bicarbonate.

• Give IV dextrose and continue insulin.

• Repeat blood gas in 1 hour before changing therapy