# Diabetic Ketoacidosis: Pediatric Protocols vs. Adult Protocols

## Introduction

Diabetic ketoacidosis (DKA) is an acute, life-threatening complication of diabetes mellitus characterized by **hyperglycemia, metabolic acidosis, and ketonemia**. While the biochemical derangement is similar across ages, management protocols differ substantially between pediatric and adult patients, particularly regarding fluid resuscitation rates and the risk of **cerebral edema** in children.

## Definition and Diagnostic Criteria

### DKA Criteria
**Blood glucose** >200 mg/dL (often >300 mg/dL in adults; may be lower in pediatric patients on insulin) **Venous pH** <7.3 or serum bicarbonate <18 mEq/L. **Ketonemia** (beta-hydroxybutyrate >3 mmol/L) or ketonuria.

### Severity Classification

| Severity | Mild | Moderate | Severe |
|---|---|---|---|
| pH | 7.2-7.3 | 7.1-7.2 | <7.1 |
| Bicarbonate | 15-18 | 10-15 | <10 |
| Mental status | Alert | Drowsy | Obtunded/coma |

## Pathophysiology

**Insulin deficiency** (absolute in Type 1; relative in Type 2) combined with counter-regulatory hormone excess. Unopposed glucagon, cortisol, catecholamines, and growth hormone drive: Hepatic gluconeogenesis and glycogenolysis (hyperglycemia) Lipolysis and ketogenesis (ketonemia and acidosis) Osmotic diuresis (dehydration and electrolyte losses) Total body potassium is depleted despite initially normal or elevated serum potassium.

![Diagram of DKA pathophysiology showing insulin deficiency cascade](images/dka-pathophysiology.jpg)

## Epidemiology and Precipitants

### Pediatric
DKA is the presenting diagnosis in **30-40% of new-onset Type 1 diabetes** in children. Precipitants: New diagnosis, insulin omission (especially in adolescents), illness, pump failure. Younger children (<5 years) are at highest risk for misdiagnosis and severe DKA.

### Adult
More commonly occurs in known diabetics. Precipitants: Infection (most common), medication non-adherence, new-onset diabetes, myocardial infarction, substance use. **Euglycemic DKA**: Increasingly recognized with SGLT2 inhibitor use (glucose may be <250 mg/dL)

## Pediatric DKA Management (ISPAD/AAP Guidelines)

### Fluid Resuscitation
**Initial bolus**: 10-20 mL/kg 0.9% NaCl over 1-2 hours (only if hemodynamically compromised) **Maintenance + deficit replacement**: Correct estimated deficit (typically 5-10%) evenly over **24-48 hours**. Use isotonic fluids initially; transition to 0.45-0.9% NaCl with dextrose once glucose <300 mg/dL. **Avoid rapid fluid administration** due to cerebral edema risk.

### Insulin
**Continuous IV insulin infusion**: 0.05-0.1 units/kg/hour (no initial bolus) Do not start insulin until potassium is confirmed 3.5 mEq/L or above. Target glucose decline of 50-100 mg/dL per hour. Add dextrose to fluids when glucose approaches 300 mg/dL to allow continued insulin infusion.

### Potassium Replacement
Begin potassium replacement with initial fluids if serum K+ <5.5 mEq/L. 20-40 mEq/L in maintenance fluids (KCl and KPO4 combination) Monitor serum potassium every 1-2 hours initially.

### Bicarbonate
**Generally NOT recommended** in pediatric DKA. Consider only if pH <6.9 with hemodynamic compromise.

## Adult DKA Management (ADA Guidelines)

### Fluid Resuscitation
**Initial bolus**: 1-1.5 L (15-20 mL/kg) 0.9% NaCl in the first hour. Subsequent fluids: 250-500 mL/hour of 0.45% or 0.9% NaCl depending on sodium. More aggressive fluid resuscitation than pediatric protocols. Add D5 to fluids when glucose <200 mg/dL.

### Insulin
**Continuous IV insulin infusion**: 0.14 units/kg/hour OR 0.1 units/kg/hour after 0.1 units/kg bolus. Target glucose decline of 50-75 mg/dL per hour. Transition to subcutaneous insulin when: pH >7.3, bicarbonate >15, glucose <200, patient is eating. **Overlap IV and subcutaneous insulin** by 1-2 hours to prevent rebound DKA.

### Potassium Replacement
If K+ <3.3: Hold insulin, replace potassium aggressively (20-40 mEq/hour) If K+ 3.3-5.3: Add 20-30 mEq/L to each liter of IV fluid. If K+ >5.3: Hold potassium, recheck in 2 hours.

### Bicarbonate
Consider if pH <6.9 (100 mmol NaHCO3 in 400 mL water with 20 mEq KCl over 2 hours)

![Side-by-side comparison of pediatric vs adult DKA protocols](images/dka-protocol-comparison.jpg)

## Cerebral Edema

### Epidemiology
Occurs in **0.5-1% of pediatric DKA episodes**; mortality 20-25%. Extremely rare in adult DKA. Risk factors: Younger age, new diagnosis, longer duration of symptoms, higher BUN, lower pCO2.

### Clinical Signs
Headache, vomiting, altered mental status after initial improvement. Cushing triad (hypertension, bradycardia, irregular respirations) Pupillary changes, posturing.

### Management
**Hypertonic saline** (3%) 2.5-5 mL/kg over 10-15 minutes OR **mannitol** 0.5-1 g/kg IV. Reduce IV fluid rate; Elevate head of bed; Emergent neuroimaging once stabilized; Intubation may be necessary but avoid hyperventilation.

## Monitoring

**Hourly**: Blood glucose, vital signs, neurologic checks (pediatric) **Every 2-4 hours**: BMP (Na, K, Cl, HCO3, BUN, Cr), venous blood gas, beta-hydroxybutyrate. **Corrected sodium**: Should rise as glucose falls; failure to rise suggests excess free water. **Anion gap**: Track closure as marker of resolution.

## Transition to Subcutaneous Insulin

Ensure patient is tolerating oral intake. Administer long-acting insulin 1-2 hours before discontinuing insulin drip. In new-onset Type 1 diabetes: Begin insulin education, carbohydrate counting, glucose monitoring. In known diabetics: Identify and address the precipitating factor.

![Monitoring checklist for DKA management](images/dka-monitoring-checklist.jpg)

## Clinical Pearls

Cerebral edema is the leading cause of death in pediatric DKA; cautious fluid resuscitation and avoiding rapid osmolarity shifts are paramount. In adult DKA, fluid resuscitation is more aggressive; cerebral edema is exceedingly rare. Always check potassium before starting insulin; hypokalemia with insulin can be fatal. Euglycemic DKA from SGLT2 inhibitors is a diagnostic pitfall; check ketones even with normal glucose. The med-peds physician should be comfortable with both protocols and recognize the critical differences in fluid management.

## References

1. Wolfsdorf JI, Glaser N, Agus M, et al. ISPAD Clinical Practice Consensus Guidelines 2018: Diabetic ketoacidosis and hyperglycemic hyperosmolar state. *Pediatr Diabetes*. 2018;19(Suppl 27):155-177.
2. Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN. Hyperglycemic crises in adult patients with diabetes. *Diabetes Care*. 2009;32(7):1335-1343.
3. Glaser N, Barnett P, McCaslin I, et al. Risk factors for cerebral edema in children with diabetic ketoacidosis. *N Engl J Med*. 2001;344(4):264-269.
4. Dhatariya KK, Vellanki P. Treatment of diabetic ketoacidosis (DKA)/hyperglycemic hyperosmolar state (HHS): Novel advances in the management of hyperglycemic crises. *Curr Diab Rep*. 2017;17(8):33.