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Diabetic Emergencies in Children

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Overview

Diabetic Emergencies in Children

Quick Reference

Critical Alerts

  • Cerebral edema is the major DKA complication in children: Monitor closely
  • Fluid resuscitation: Slower than adults: 10-20 mL/kg bolus, then gradual
  • Insulin infusion: 0.05-0.1 units/kg/hr: Do NOT bolus
  • Potassium replacement: Start early: Once K <5.5 and urine output confirmed
  • Hypoglycemia can kill quickly: Treat immediately with glucose
  • New-onset DKA: Consider type 1 diabetes debut

Key Diagnostics (DKA)

ParameterValue
Blood glucose>00 mg/dL (11 mmol/L)
Venous pH<7.3
Serum bicarbonate<15 mEq/L
KetonesPositive (blood β-hydroxybutyrate > mmol/L)

DKA Severity

SeveritypHBicarbonate
Mild7.25-7.3015-18 mEq/L
Moderate7.10-7.2410-14 mEq/L
Severe<7.10<10 mEq/L

Emergency Treatments

ConditionTreatmentDetails
DKA (initial)NS 10-20 mL/kg over 1-2 hoursDo not exceed 40 mL/kg in first 4 hours
DKA (insulin)0.05-0.1 units/kg/hr IV infusionStart after initial fluid bolus
HypoglycemiaDextrose 0.5-1 g/kg IVD10W or D25W
Cerebral edemaMannitol 0.5-1 g/kg or 3% saline 2.5-5 mL/kgEmergent

Definition

Overview

Diabetic emergencies in children primarily include diabetic ketoacidosis (DKA) and hypoglycemia. DKA is the most common cause of death in children with type 1 diabetes, primarily due to cerebral edema. Early recognition and careful management are essential. Hypoglycemia can occur in diabetic children on insulin and requires immediate treatment.

Classification

Diabetic Ketoacidosis (DKA):

CriterionValue
Hyperglycemia>00 mg/dL (11 mmol/L)
AcidosisVenous pH <7.3 or bicarbonate <15 mEq/L
KetosisBlood ketones > mmol/L or urine ketones moderate/large

Hypoglycemia:

SeverityBlood Glucose
Mild54-70 mg/dL (3-3.9 mmol/L)
Moderate40-54 mg/dL (2.2-3 mmol/L)
Severe<40 mg/dL (2.2 mmol/L) or symptomatic requiring assistance

Epidemiology

  • DKA at diagnosis: 20-40% of children with new-onset T1DM present in DKA
  • DKA in known diabetics: 1-10% per year
  • Cerebral edema incidence: 0.5-1% of pediatric DKA
  • Cerebral edema mortality: 21-24%
  • Hypoglycemia: Common in insulin-treated diabetes

Etiology

DKA Precipitants:

CauseNotes
New-onset T1DMMost common cause in children
Missed insulin dosesAdolescents, noncompliance
Insulin pump failureRapid DKA onset
Infection/illnessIncreased insulin requirements
Trauma, surgeryStress hyperglycemia

Hypoglycemia Causes:

CauseNotes
Insulin excessDosing error, missed meal
ExerciseIncreased glucose utilization
Sulfonylurea use (rare in peds)Prolonged hypoglycemia
Alcohol (adolescents)Inhibits gluconeogenesis

Pathophysiology

DKA Mechanism

  1. Insulin deficiency + counter-regulatory hormone excess:
    • Glucagon, cortisol, catecholamines, GH increase
  2. Hyperglycemia:
    • Decreased glucose uptake, increased gluconeogenesis
    • Osmotic diuresis → Dehydration
  3. Ketogenesis:
    • Lipolysis → Free fatty acids → Ketone bodies (β-hydroxybutyrate, acetoacetate)
    • Anion gap metabolic acidosis
  4. Electrolyte derangements:
    • Total body potassium depletion (despite normal/high serum K)
    • Phosphate depletion
    • Sodium losses

Cerebral Edema in Pediatric DKA

Risk Factors:

  • Younger age (<5 years)
  • New-onset diabetes
  • Severe DKA (low pH, low bicarb)
  • Elevated BUN at presentation
  • Rapid fluid administration (controversial)
  • Failure of Na to rise with treatment
  • Bicarbonate administration (controversial)

Mechanism:

  • Not fully understood
  • May involve osmotic shifts, vasogenic edema, cellular injury

Hypoglycemia Mechanism

  • Insulin excess → Excessive glucose uptake
  • Symptoms from neuroglycopenia (brain glucose deprivation)
  • Counter-regulatory response (catecholamines) causes autonomic symptoms

Clinical Presentation

DKA Symptoms

CategorySymptoms
HyperglycemiaPolyuria, polydipsia, weight loss
DehydrationDry mouth, decreased urine output, tachycardia
AcidosisKussmaul respirations (deep, rapid), fruity breath
GINausea, vomiting, abdominal pain
NeurologicLethargy, confusion (concerning for cerebral edema)

Hypoglycemia Symptoms

CategorySymptoms
AutonomicSweating, tremor, palpitations, hunger, pallor, anxiety
NeuroglycopenicConfusion, irritability, drowsiness, slurred speech, seizures, coma

History

DKA Key Questions:

Hypoglycemia Key Questions:

Physical Examination

DKA:

FindingSignificance
DehydrationTachycardia, dry mucous membranes, decreased skin turgor
Kussmaul respirationsAcidosis compensation
Fruity/acetone breathKetosis
Abdominal tendernessDKA-associated, rule out surgical abdomen
Altered mental statusSevere DKA, impending cerebral edema

Hypoglycemia:

FindingSignificance
DiaphoresisAutonomic response
Tremor, tachycardiaCatecholamine surge
Altered LOC, confusionNeuroglycopenia
SeizureSevere hypoglycemia

Known diabetic? Insulin type, pump?
Common presentation.
Recent illness or infection?
Common presentation.
Missed insulin doses?
Common presentation.
Timeline of polyuria, polydipsia, weight loss
Common presentation.
Nausea, vomiting, abdominal pain
Common presentation.
Altered mental status
Common presentation.
Red Flags

Cerebral Edema Warning Signs (DKA)

FindingAction
Headache, altered mental statusConsider cerebral edema
Bradycardia, hypertension (Cushing response)Emergent treatment
Pupillary changesHerniation imminent
PosturingHerniation
Rising serum sodium that fails to rise with treatmentRisk factor
Rapid neurological deteriorationTreat immediately

Treat empirically for cerebral edema if suspected—do NOT wait for imaging

DKA Red Flags

FindingConcern
pH <7.1Severe DKA
Altered consciousnessCerebral edema or severe acidosis
Shock (hypotension, poor perfusion)Requires aggressive resuscitation
Age <2 yearsHigher risk of cerebral edema
New-onset diabetesHigher risk of cerebral edema

Differential Diagnosis

DKA-Like Presentations

DiagnosisFeatures
Hyperosmolar hyperglycemic state (HHS)Very high glucose (>00), minimal ketosis, altered LOC
Salicylate poisoningAnion gap acidosis, tinnitus, history
SepsisFever, source of infection
GastroenteritisVomiting, diarrhea, less acidosis
Inborn errors of metabolismYounger age, recurrent acidosis
Starvation ketosisMild ketosis, no hyperglycemia

Hypoglycemia Differential

DiagnosisFeatures
Insulin overdoseKnown diabetic, insulin use
InsulinomaRecurrent fasting hypoglycemia, non-diabetic
Adrenal insufficiencyHypotension, electrolyte abnormalities
SepsisHypoglycemia in severely ill
Ingestion (sulfonylurea)History of access

Diagnostic Approach

Initial Labs (DKA)

TestPurpose
Blood glucoseHyperglycemia confirmation
Venous blood gaspH, pCO2
BMPElectrolytes, BUN, creatinine, anion gap
Serum ketones (β-hydroxybutyrate)Ketosis confirmation
UrinalysisGlucose, ketones
CBCLeukocytosis common (even without infection)
HbA1cChronic glycemic control

Anion Gap Calculation

  • Anion gap = Na – (Cl + HCO3)
  • Normal: 8-12 mEq/L
  • Elevated in DKA due to ketoacids

Corrected Sodium

  • Corrected Na = Measured Na + 1.6 × [(glucose - 100) / 100]
  • Important for assessing true dehydration and cerebral edema risk

Monitoring

ParameterFrequency
Blood glucoseHourly
Electrolytes, VBGEvery 2-4 hours
Neurological statusEvery hour initially
Fluid input/outputContinuous

Treatment

DKA Management Principles

  1. Fluid resuscitation: Restore intravascular volume, avoid rapid correction
  2. Insulin infusion: Inhibit ketogenesis, lower glucose
  3. Electrolyte replacement: Especially potassium
  4. Monitor for cerebral edema: Most important complication
  5. Identify/treat precipitant: Infection, missed insulin

Phase 1: Initial Resuscitation (First 1-2 Hours)

Fluid Bolus:

WhatHow
NS (0.9% saline)10-20 mL/kg over 1-2 hours
Repeat if neededUp to 40 mL/kg in first 4 hours
GoalRestore perfusion, NOT rapid rehydration

Do NOT give insulin bolus: Start infusion after initial fluid

Phase 2: Rehydration and Insulin

Maintenance Fluids:

  • Calculate deficit + maintenance over 24-48 hours
  • Use NS initially, then 0.45-0.9% saline with potassium
  • Avoid >1.5-2× maintenance rate

Insulin Infusion:

DoseNotes
0.05-0.1 units/kg/hrStart 1-2 hours after fluids
Do NOT bolusIncreases cerebral edema risk
Goal glucose drop50-100 mg/dL/hr

Add Dextrose When Glucose <300 mg/dL:

  • Switch to D5 0.45% NS or D10 0.45% NS
  • Continue insulin to clear ketones (NOT just normalize glucose)

Potassium Replacement

Serum KAction
>.5 mEq/LHold potassium until K <5.5
4-5.5 mEq/LAdd 20-40 mEq/L to fluids
3.5-4 mEq/LAdd 40-60 mEq/L to fluids
<3.5 mEq/LHold insulin until K repleted; higher replacement

Beware: Serum K falls rapidly with insulin—replace early

Bicarbonate: NOT Routinely Recommended

  • No proven benefit in pediatric DKA
  • May increase cerebral edema risk
  • Consider ONLY if pH <6.9 with hemodynamic compromise

Cerebral Edema Treatment

Signs: Headache, altered LOC, bradycardia, hypertension, posturing

Treatment:

AgentDose
Mannitol0.5-1 g/kg IV over 20 minutes
OR Hypertonic saline (3%)2.5-5 mL/kg IV over 10-15 minutes
  • Elevate head of bed to 30°
  • Reduce IV fluid rate by 1/3
  • Intubation if needed (avoid hyperventilation)
  • Urgent neurosurgery consult
  • CT head (but do NOT delay treatment)

Hypoglycemia Treatment

Mild (Able to Swallow):

  • 15-20 g fast-acting carbohydrate (juice, glucose tabs)
  • Recheck glucose in 15 minutes

Severe (Unable to Swallow/LOC Impaired):

RouteTreatment
IV Dextrose0.5-1 g/kg (D10W: 5-10 mL/kg; D25W: 2-4 mL/kg)
IM Glucagon (if no IV)0.5 mg (<25 kg) or 1 mg (>5 kg)

Follow with complex carbs: Once awake, give snack to prevent recurrence


Disposition

ICU Admission (DKA)

  • Severe DKA (pH <7.1, HCO3 <5)
  • Altered mental status
  • Cerebral edema or high risk
  • Hemodynamic instability
  • Age <2 years
  • New-onset diabetes

Floor Admission (DKA)

  • Mild-moderate DKA, stable
  • Responding to treatment
  • No cerebral edema signs

Discharge (Hypoglycemia)

  • Resolves with treatment
  • Cause identified and corrected
  • Diabetes education provided
  • Safe to go home with supervision

Follow-Up

SituationFollow-Up
DKA resolvedEndocrinology within 1 week; diabetes education
New-onset diabetesInpatient diabetes education before discharge
Recurrent hypoglycemiaEndocrinology; adjust insulin regimen

Patient Education

DKA Prevention (For Families)

  • Never stop insulin, even when sick
  • Check blood glucose and ketones when ill
  • Sick day rules: Extra fluids, adjust insulin, seek care early
  • Recognize DKA warning signs: Vomiting, abdominal pain, rapid breathing

Hypoglycemia Prevention

  • Eat regular meals and snacks
  • Carry fast-acting glucose at all times
  • Recognize early symptoms (hunger, shakiness)
  • Treat immediately—don't wait

When to Seek Emergency Care

  • Persistent vomiting, unable to keep fluids down
  • Moderate-large ketones
  • Altered mental status, confusion
  • Rapid breathing
  • Blood glucose very high or very low not responding to treatment

Special Populations

Infants and Toddlers (<5 Years)

  • Higher risk of cerebral edema
  • Symptoms may be non-specific
  • More cautious fluid management

Adolescents

  • Insulin omission (intentional) common
  • Eating disorders (diabulimia)
  • Psychosocial support essential

Insulin Pump Users

  • DKA can develop rapidly (no long-acting depot)
  • Remove pump; start IV insulin
  • Evaluate for pump malfunction

New-Onset Diabetes

  • Higher risk of severe DKA and cerebral edema
  • Requires comprehensive diabetes education before discharge
  • Endocrinology referral essential

Quality Metrics

Performance Indicators

MetricTargetRationale
Hourly neuro checks during DKA100%Cerebral edema detection
Insulin infusion started within 2 hours>5%After initial fluids
Potassium monitored every 2-4 hours100%Prevent hypokalemia
Avoid bicarbonate unless pH <6.9>5%Reduces complications
Diabetes education before discharge100%Prevent recurrence

Documentation Requirements

  • DKA severity (mild/moderate/severe)
  • Fluid rates and composition
  • Insulin infusion rate
  • Hourly glucose and neuro checks
  • Potassium levels and replacement
  • Cerebral edema assessment

Key Clinical Pearls

DKA Pearls

  • Cerebral edema is the killer: Monitor neuro status religiously
  • Slow fluid resuscitation: Avoid rapid correction
  • Insulin infusion, NO bolus: Reduces cerebral edema risk
  • Potassium drops fast: Replace early once K <5.5
  • Don't stop insulin when glucose normalizes: Continue until ketones clear
  • Bicarbonate is rarely indicated: May worsen outcomes

Hypoglycemia Pearls

  • Treat immediately: Brain damage occurs quickly
  • D10W safer than D50W in children: Less hyperglycemia; less extravasation injury
  • Glucagon for no IV access: Effective IM/SC
  • Find the cause: Missed meal, excess insulin, exercise
  • Follow with complex carbs: Prevent recurrence

Disposition Pearls

  • Low threshold for ICU in pediatric DKA: Especially severe or young
  • New-onset diabetes = education before discharge: Essential
  • Endocrine follow-up for all: Optimize long-term management

References
  1. Wolfsdorf JI, et al. ISPAD Clinical Practice Consensus Guidelines 2018: Diabetic ketoacidosis and the hyperglycemic hyperosmolar state. Pediatr Diabetes. 2018;19(Suppl 27):155-177.
  2. Glaser N, et al. Risk factors for cerebral edema in children with diabetic ketoacidosis. N Engl J Med. 2001;344(4):264-269.
  3. Kuppermann N, et al. Clinical Trial of Fluid Infusion Rates for Pediatric Diabetic Ketoacidosis (PECARN FLUID Trial). N Engl J Med. 2018;378(24):2275-2287.
  4. American Diabetes Association. Standards of Medical Care in Diabetes—2024. Diabetes Care. 2024;47(Suppl 1).
  5. Rewers A, et al. Presence of diabetic ketoacidosis at diagnosis of diabetes mellitus in youth: SEARCH for Diabetes in Youth. Pediatrics. 2008;121(5):e1258-e1266.
  6. Koves IH, et al. The accuracy of clinical assessment of dehydration during diabetic ketoacidosis in childhood. Diabetes Care. 2004;27(10):2485-2487.
  7. Edge JA, et al. The risk and outcome of cerebral oedema developing during diabetic ketoacidosis. Arch Dis Child. 2001;85(1):16-22.
  8. UpToDate. Diabetic ketoacidosis in children: Treatment. 2024.

At a Glance

EvidenceStandard
Last UpdatedRecently

Guidelines

  • NICE Guidelines
  • BTS Guidelines
  • RCUK Guidelines