Diabetic Emergencies in Children

Quick Reference Card

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Definition and Overview

Diabetic Ketoacidosis (DKA)

Diabetic ketoacidosis represents the most serious acute metabolic complication of type 1 diabetes mellitus in children and remains the leading cause of diabetes-related mortality in pediatric patients. [1,2] DKA is characterized by the biochemical triad of hyperglycemia, ketonemia/ketonuria, and metabolic acidosis resulting from absolute or relative insulin deficiency combined with counter-regulatory hormone excess.

The International Society for Pediatric and Adolescent Diabetes (ISPAD) 2022 consensus guidelines define DKA by the presence of: blood glucose >200 mg/dL (11.1 mmol/L), venous pH less than 7.3 or serum bicarbonate less than 18 mEq/L, and ketonemia (blood beta-hydroxybutyrate >3 mmol/L) or moderate-to-large ketonuria. [1]

Hypoglycemia

Hypoglycemia in children with diabetes represents a common and potentially life-threatening complication of insulin therapy. The International Hypoglycemia Study Group defines clinically significant hypoglycemia as blood glucose less than 54 mg/dL (3.0 mmol/L), a level associated with impaired cognitive function and increased risk of severe hypoglycemia. [3]

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Epidemiology

DKA Epidemiology

The epidemiology of pediatric DKA demonstrates significant geographic and demographic variation, with important implications for prevention strategies.

Risk Factors for DKA at Diagnosis: [4,5]

• Younger age (less than 5 years) - 3-fold increased risk
• Lower socioeconomic status
• Lack of access to healthcare
• Delayed diagnosis of T1DM
• Ethnic minorities in some regions
• Countries with low T1DM incidence (reduced awareness)

Risk Factors for Recurrent DKA: [1,7]

• Poor metabolic control (elevated HbA1c)
• Previous DKA episodes
• Adolescent females
• Psychiatric comorbidity (depression, eating disorders)
• Insulin omission (intentional or unintentional)
• Lack of health insurance
• Insulin pump failure

Hypoglycemia Epidemiology

Hypoglycemia is the most common acute complication in children with T1DM receiving insulin therapy. [3,8]

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Pathophysiology

DKA Pathophysiology

The development of DKA results from the interplay between absolute or relative insulin deficiency and counter-regulatory hormone excess, creating a catabolic state that affects carbohydrate, lipid, and protein metabolism. [1,10]

Insulin Deficiency and Counter-Regulatory Hormone Excess

Exam Detail: Hormonal Changes in DKA:

Key Pathway: Insulin deficiency leads to unrestrained lipolysis, releasing free fatty acids (FFAs) from adipose tissue. Hepatic beta-oxidation of FFAs generates acetyl-CoA, which is converted to ketone bodies (beta-hydroxybutyrate and acetoacetate) rather than entering the Krebs cycle due to glucagon-mediated stimulation of carnitine palmitoyltransferase-1 (CPT-1). [10]

Metabolic Consequences

1. Hyperglycemia:

   • Decreased peripheral glucose uptake (muscle, adipose)
   • Increased hepatic gluconeogenesis (from amino acids, glycerol)
   • Increased hepatic glycogenolysis
   • Results in osmotic diuresis and dehydration

2. Ketogenesis:

   • Lipolysis releases FFAs → hepatic ketogenesis
   • Ketone bodies (beta-hydroxybutyrate:acetoacetate ratio 10:1 in severe DKA)
   • Ketoacids dissociate → H+ ions → metabolic acidosis
   • Anion gap elevation

3. Fluid and Electrolyte Derangements:

Cerebral Edema Pathophysiology

Cerebral edema represents the most devastating complication of pediatric DKA, accounting for 60-90% of DKA-related deaths. [6,11] The pathophysiology remains incompletely understood but involves multiple mechanisms.

Exam Detail: Proposed Mechanisms of Cerebral Edema: [6,11,12]

1. Vasogenic Edema:

   • Blood-brain barrier disruption from ketone bodies and inflammatory mediators
   • Increased cerebral blood flow during treatment
   • Na+/K+-ATPase dysfunction

2. Cytotoxic Edema:

   • Intracellular osmolyte accumulation during chronic hyperosmolarity
   • Rapid osmotic shifts during treatment
   • Cerebral ischemia-reperfusion injury

3. Interstitial Edema:

   • Disrupted CSF dynamics
   • Increased cerebral venous pressure

Risk Factors for Cerebral Edema: [6,11,12]

PECARN FLUID Trial Findings: [13] The landmark PECARN FLUID trial (2018) randomized 1,389 children with DKA to receive either 0.45% or 0.9% saline at fast or slow rehydration rates. Key findings:

• No significant difference in acute brain injury outcomes across fluid groups
• Glasgow Coma Scale score decline occurred in similar proportions (11.9-12.6%)
• Clinically apparent brain injury rare (0.9%)
• Supports that cerebral edema risk is primarily related to disease severity at presentation rather than treatment factors

Hypoglycemia Pathophysiology

Hypoglycemia results from an imbalance between insulin action and glucose availability. [3,8]

Counter-Regulatory Response:

Hypoglycemia Unawareness: [9]

• Develops with recurrent hypoglycemia
• Impaired autonomic warning symptoms
• Counter-regulatory hormone thresholds shift lower
• Reversible with hypoglycemia avoidance (2-3 weeks)

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Clinical Presentation

DKA Presentation

Symptoms

Physical Examination Findings

⚠️ Red Flag: Cerebral Edema Warning Signs - Treat Immediately: [6,11]

Treatment: DO NOT wait for imaging - treat empirically if suspected

Hypoglycemia Presentation

Age-Specific Presentations: [3,8]

• Infants/Toddlers: Irritability, pallor, poor feeding, seizures
• School-age: Difficulty concentrating, behavioral changes, tremor
• Adolescents: Classic autonomic and neuroglycopenic symptoms

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Differential Diagnosis

DKA Differential

Exam Detail: Key Differentiating Features - DKA vs HHS:

Hypoglycemia Differential (in non-diabetics)

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Diagnostic Approach

Initial Assessment for DKA

Algorithm

Clinical Pathway

Step 1: Confirm DKA Diagnosis

• Point-of-care blood glucose
• Venous blood gas (pH, pCO2, HCO3)
• Blood ketones (beta-hydroxybutyrate) or urine ketones

Step 2: Assess Severity

• Calculate dehydration (clinical assessment - often overestimated)
• Categorize DKA severity (mild/moderate/severe)
• Assess neurological status (GCS)

Step 3: Baseline Investigations

Calculated Parameters

Anion Gap: [1]

Anion Gap = Na+ - (Cl- + HCO3-)
Normal: 12 ± 2 mEq/L
DKA: Typically 20-30 mEq/L (high anion gap metabolic acidosis)

Corrected Sodium: [1,14]

Corrected Na+ = Measured Na+ + 2 × [(Glucose mg/dL - 100) / 100]
OR
Corrected Na+ = Measured Na+ + 2.4 × [(Glucose mmol/L - 5.5) / 5.5]

Expected Corrected Sodium Change: During treatment, corrected Na+ should rise as glucose falls. Failure of Na+ to rise or a fall in Na+ during treatment is a risk factor for cerebral edema. [11,12]

Effective Osmolality:

Effective Osm = 2 × Na+ (mEq/L) + Glucose (mg/dL)/18
Normal: 275-295 mOsm/kg

Monitoring During Treatment

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Management

DKA Management Principles

Phase 1: Initial Stabilization (0-1 hour)

Airway/Breathing:

• Assess airway, provide oxygen if needed
• Avoid intubation if possible (loss of respiratory compensation)
• If intubation required, maintain pre-intubation minute ventilation

Circulation - Initial Fluid Resuscitation: [1,13]

Key Point: The PECARN FLUID trial supports that fluid rate and tonicity do not significantly impact cerebral edema risk. However, judicious resuscitation avoiding excessive fluid remains prudent. [13]

Do NOT give insulin bolus: Associated with increased cerebral edema risk. [1,11]

Phase 2: Rehydration and Insulin (1-24+ hours)

Fluid Replacement [1,2]

Calculate Fluid Requirements:

Total Deficit = Estimated % dehydration × body weight (kg) × 10
Maintenance = Standard maintenance requirements
Replacement = Total deficit + Maintenance - Initial bolus volume
Give replacement over 24-48 hours

Fluid Rate Guidelines:

• Do not exceed 1.5-2× maintenance rate
• Typical rate: 3-4 mL/kg/hr (or calculated replacement)
• Duration: 24-48 hours for complete rehydration

Fluid Composition:

Insulin Infusion [1,2]

Adjusting Insulin:

• If glucose falling >100 mg/dL/hr: Consider reducing insulin rate
• If glucose falling less than 50 mg/dL/hr: Check insulin delivery, may increase rate
• When glucose less than 300 mg/dL: Add dextrose to fluids, continue insulin until ketones clear

Exam Detail: Why Continue Insulin When Glucose is Controlled?

Insulin is required to:

1. Suppress ketogenesis (primary goal)
2. Clear ketone bodies
3. Reverse acidosis

Glucose normalizes before acidosis resolves. Continue insulin at reduced rates with dextrose infusion until:

• pH >7.3
• Bicarbonate >18 mEq/L
• Blood ketones less than 0.6 mmol/L
• Anion gap normalized

Potassium Replacement [1,2]

Critical Points:

• Total body K+ is always depleted despite initial serum levels
• K+ falls rapidly with insulin (drives K+ intracellularly)
• ECG monitoring if K+ less than 3 or >6 mEq/L
• Use KCl or mixture of KCl/K2PO4 (40:60)

Bicarbonate Therapy [1,2]

⚠️ Red Flag: Bicarbonate is NOT routinely recommended in pediatric DKA

• No proven benefit on outcomes
• May paradoxically worsen intracellular/CSF acidosis
• Associated with increased cerebral edema risk (controversial)
• May cause hypokalemia
• Delays ketone clearance

Consider ONLY if:

• pH less than 6.9 with hemodynamic compromise
• Life-threatening hyperkalemia
• Severe cardiac dysfunction

Cerebral Edema Management [6,11,12]

Recognition:

• Usually occurs 4-12 hours after treatment initiation (but can be earlier or later)
• Subtle warning signs may precede clinical deterioration

Immediate Treatment (Do NOT delay for imaging):

Repeat hyperosmolar therapy: May repeat if no response in 30 minutes. May alternate mannitol and hypertonic saline.

Hypoglycemia Management [3,8]

Mild Hypoglycemia (Conscious, Able to Swallow)

Treatment:

• 15-20 grams fast-acting carbohydrate (glucose tablets, juice, regular soda)
• Recheck blood glucose in 15 minutes
• Repeat if still less than 70 mg/dL
• Follow with complex carbohydrate once >70 mg/dL

Severe Hypoglycemia (Altered Consciousness/Unable to Swallow)

D10W vs D50W in Children: [8]

• D10W preferred in children to avoid extravasation injury and rebound hyperglycemia
• D50W (50% dextrose) should be diluted or avoided in young children

Post-Treatment:

• Monitor glucose every 15-30 minutes
• Once conscious: oral complex carbohydrate
• Identify precipitating cause
• Adjust insulin regimen if needed

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Disposition

ICU Admission Criteria [1,2]

Ward/Floor Admission

• Mild-moderate DKA in known diabetic
• Stable, responding to treatment
• No neurological concerns
• Adequate monitoring capability

Transition to Subcutaneous Insulin [1,2]

Criteria for Transition:

• Tolerating oral intake
• pH >7.3, bicarbonate >18 mEq/L
• Blood ketones less than 0.6 mmol/L (or urine ketones negative/trace)
• Anion gap normalized

Transition Protocol:

• Give SC rapid-acting insulin 15-30 minutes BEFORE stopping IV insulin
• Overlap prevents recurrence of ketosis
• Use known insulin regimen or calculate new doses
• New-onset: ~0.5-1.0 units/kg/day total (lower in honeymoon phase)

Discharge Criteria (Hypoglycemia)

• Resolved hypoglycemia with treatment
• Cause identified and addressed
• Able to tolerate oral intake
• Safe home environment with supervision
• Education on hypoglycemia recognition and treatment
• Follow-up arranged

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Special Populations

Infants and Young Children (less than 5 years) [1,4]

Adolescents [7]

Insulin Pump Users [1,15]

New-Onset Diabetes [4,5]

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Complications

DKA Complications

Hypoglycemia Complications

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Prevention and Education

DKA Prevention [1,7,16]

Sick Day Rules:

1. Never stop insulin - May need to increase doses during illness
2. Monitor blood glucose frequently - Every 2-4 hours
3. Check ketones - If glucose >250 mg/dL or during illness
4. Maintain hydration - Small, frequent sips of fluids
5. Seek help early - Contact diabetes team if ketones moderate/large

When to Seek Emergency Care:

• Persistent vomiting (unable to keep fluids down)
• Moderate-large ketones not clearing
• Blood glucose persistently >300 mg/dL
• Altered mental status
• Rapid/deep breathing
• Abdominal pain

Hypoglycemia Prevention [3,8]

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Key Guidelines

Major Society Guidelines

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Exam-Focused Content

Common Exam Questions

MRCPCH/Pediatric Board Questions:

1. "A 4-year-old presents with polyuria, polydipsia, and vomiting. Blood glucose is 450 mg/dL, pH 7.15. Describe your management."
2. "What are the risk factors for cerebral edema in pediatric DKA?"
3. "How would you manage an 8-year-old found unconscious by parents who has known Type 1 DM?"
4. "Describe the pathophysiology of DKA."
5. "What are the criteria for transitioning from IV to SC insulin?"

Viva Points

Viva Point: Opening Statement: "Diabetic ketoacidosis is an acute, life-threatening complication of type 1 diabetes characterized by hyperglycemia greater than 200 mg/dL, metabolic acidosis with pH below 7.3 or bicarbonate below 18 mEq/L, and ketonemia with blood beta-hydroxybutyrate above 3 mmol/L."

Key Facts to Quote:

• "20-40% of children with new-onset T1DM present in DKA" [4]
• "Cerebral edema occurs in 0.5-0.9% of DKA episodes and accounts for 60-90% of DKA mortality" [6]
• "The PECARN FLUID trial showed no significant difference in brain injury rates across different fluid protocols" [13]
• "Insulin infusion at 0.05-0.1 units/kg/hr without bolus is the standard of care" [1]

Common Mistakes to Avoid

Model Answer

Q: "A 6-year-old with known Type 1 diabetes presents with vomiting, abdominal pain, and drowsiness. pH 7.08, glucose 520 mg/dL, ketones 5.2 mmol/L. Describe your management."

A: "This child has severe diabetic ketoacidosis based on pH below 7.10 and significant ketonemia. My immediate priorities are:

Initial stabilization: I would ensure IV access with two large-bore cannulae, obtain blood samples for VBG, electrolytes, ketones, and begin fluid resuscitation with 10 mL/kg of 0.9% normal saline over 30-60 minutes. Given the drowsiness, I would assess GCS and perform hourly neurological observations.

Ongoing management: After initial fluid bolus, I would calculate fluid replacement to be given over 24-48 hours, not exceeding 1.5 times maintenance. I would start insulin infusion at 0.05-0.1 units/kg/hour ONE to TWO hours after fluids, importantly without a bolus dose. Potassium replacement would commence once serum K+ is below 5.5 mEq/L and urine output is confirmed.

Monitoring: Hourly blood glucose and neurological observations, 2-4 hourly electrolytes and VBG. I would watch for cerebral edema, which occurs in 0.5-0.9% of cases and is the leading cause of DKA mortality.

If cerebral edema suspected: I would immediately elevate the head of bed, reduce IV fluids by one-third, and give mannitol 0.5-1 g/kg or 3% saline 2.5-5 mL/kg without waiting for imaging.

Precipitant: I would investigate for infection or missed insulin doses as precipitants.

This management approach follows ISPAD 2022 consensus guidelines."

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Clinical Pearls

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Quality Metrics and Documentation

Performance Indicators

Documentation Requirements

Initial Assessment:

• DKA severity classification (mild/moderate/severe)
• GCS score and neurological examination
• Estimated percentage dehydration
• Initial vital signs
• Working diagnosis and precipitating factor

Ongoing Documentation:

• Hourly glucose and neurological status
• Fluid rates and composition
• Insulin infusion rate and adjustments
• Electrolyte results with time stamps
• Any complications or concerns
• Input/output balance

Discharge Documentation:

• Confirmation of DKA resolution criteria met
• Transition to SC insulin timing and doses
• Sick day management education completed
• Hypoglycemia management education completed
• Follow-up arrangements with diabetes team
• Emergency contact information provided

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Monitoring Flowsheet

DKA Monitoring Template

PEDIATRIC DKA MONITORING FLOWSHEET

Patient: _________________ Weight: ______ kg  Date: _________

Hour:        | 0  | 1  | 2  | 3  | 4  | 5  | 6  | 8  | 12 | 24 |
-------------|----|----|----|----|----|----|----|----|----|----|
VITALS:
HR           |    |    |    |    |    |    |    |    |    |    |
RR           |    |    |    |    |    |    |    |    |    |    |
BP           |    |    |    |    |    |    |    |    |    |    |
Temp         |    |    |    |    |    |    |    |    |    |    |
-------------|----|----|----|----|----|----|----|----|----|----|
NEURO:
GCS          |    |    |    |    |    |    |    |    |    |    |
Pupils       |    |    |    |    |    |    |    |    |    |    |
Headache     |    |    |    |    |    |    |    |    |    |    |
-------------|----|----|----|----|----|----|----|----|----|----|
LABS:
Glucose      |    |    |    |    |    |    |    |    |    |    |
pH           |    |    |    |    |    |    |    |    |    |    |
HCO3         |    |    |    |    |    |    |    |    |    |    |
K+           |    |    |    |    |    |    |    |    |    |    |
Na+          |    |    |    |    |    |    |    |    |    |    |
Corr Na+     |    |    |    |    |    |    |    |    |    |    |
BOHB         |    |    |    |    |    |    |    |    |    |    |
Anion Gap    |    |    |    |    |    |    |    |    |    |    |
-------------|----|----|----|----|----|----|----|----|----|----|
FLUIDS:
Type         |    |    |    |    |    |    |    |    |    |    |
Rate mL/hr   |    |    |    |    |    |    |    |    |    |    |
Input mL     |    |    |    |    |    |    |    |    |    |    |
Output mL    |    |    |    |    |    |    |    |    |    |    |
-------------|----|----|----|----|----|----|----|----|----|----|
INSULIN:
Rate U/kg/hr |    |    |    |    |    |    |    |    |    |    |
-------------|----|----|----|----|----|----|----|----|----|----|
K+ GIVEN:
mEq/L in IVF |    |    |    |    |    |    |    |    |    |    |
-------------|----|----|----|----|----|----|----|----|----|----|

CEREBRAL EDEMA WARNING SIGNS - CHECK EACH HOUR:
[ ] Headache (new/worsening)    [ ] GCS decline ≥2 points
[ ] Inappropriate bradycardia   [ ] Incontinence (new)
[ ] Irritability/confusion      [ ] Posturing
[ ] Papilledema                 [ ] Pupillary changes

IF ANY SIGN PRESENT → IMMEDIATE INTERVENTION

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Troubleshooting Common Problems

DKA Treatment Troubleshooting

Hypoglycemia Treatment Troubleshooting

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Emergency Drug Reference

Medications for DKA

Medications for Hypoglycemia

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Calculation Reference

Fluid Calculations

Maintenance Fluid Rate (Holliday-Segar):

0-10 kg:     100 mL/kg/day (4 mL/kg/hr)
10-20 kg:    1000 mL + 50 mL/kg/day over 10 kg (1000 mL + 2 mL/kg/hr)
>20 kg:      1500 mL + 20 mL/kg/day over 20 kg (1500 mL + 1 mL/kg/hr)

Example: 25 kg child:

• Maintenance = 1500 + (20 × 5) = 1600 mL/day = 67 mL/hr

Deficit Calculation:

Deficit (mL) = % dehydration × weight (kg) × 10

Example: 25 kg child with 7% dehydration
Deficit = 7 × 25 × 10 = 1750 mL

Replacement Rate (over 24-48 hours):

Hourly Rate = (Deficit + Maintenance - Bolus already given) / 24-48 hours

Corrected Sodium Calculation

Corrected Na+ = Measured Na+ + 2 × [(Glucose mg/dL - 100) / 100]

Example: Na+ 128 mEq/L, Glucose 600 mg/dL
Corrected Na+ = 128 + 2 × [(600-100)/100]
              = 128 + 2 × 5
              = 138 mEq/L

Anion Gap Calculation

Anion Gap = Na+ - (Cl- + HCO3-)
Normal: 12 ± 2 mEq/L

Example: Na+ 140, Cl- 100, HCO3- 10
AG = 140 - (100 + 10) = 30 mEq/L (elevated)

Effective Osmolality

Effective Osm = 2 × Na+ (mEq/L) + Glucose (mg/dL)/18
Normal: 275-295 mOsm/kg

Example: Na+ 135, Glucose 450
Effective Osm = 2(135) + 450/18 = 270 + 25 = 295 mOsm/kg

Insulin Infusion Calculation

Standard concentration: 50 units Regular Insulin in 50 mL NS = 1 unit/mL

Rate calculation:
- At 0.1 units/kg/hr: Rate (mL/hr) = 0.1 × weight (kg)
- At 0.05 units/kg/hr: Rate (mL/hr) = 0.05 × weight (kg)

Example: 30 kg child at 0.1 units/kg/hr
Rate = 0.1 × 30 = 3 mL/hr = 3 units/hr

Glucose Infusion Rate

GIR (mg/kg/min) = [Dextrose concentration (%) × IV rate (mL/hr)] / [6 × weight (kg)]

Example: D10 at 100 mL/hr for 25 kg child
GIR = (10 × 100) / (6 × 25) = 1000/150 = 6.7 mg/kg/min

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Family Education Resources

Sick Day Management Handout

WHEN YOUR CHILD WITH DIABETES IS SICK:

NEVER stop insulin - Even if not eating, body needs insulin when sick

CHECK more often:

• Blood glucose every 2-4 hours
• Blood or urine ketones if glucose >250 mg/dL or feeling unwell
• Temperature

FLUIDS are essential:

• Small, frequent sips
• If glucose high: water, sugar-free drinks
• If glucose low: regular juice, regular soda

SEEK HELP if:

• Vomiting more than twice
• Unable to keep fluids down
• Ketones moderate or large
• Blood glucose stays >300 mg/dL despite extra insulin
• Difficulty breathing or fast breathing
• Confusion or excessive sleepiness
• Abdominal pain that doesn't improve

CONTACT your diabetes team for guidance on insulin adjustments

EMERGENCY: Go to hospital if:

• Cannot keep any fluids down for >4 hours
• Large ketones that won't clear
• Very sleepy or confused
• Fast, deep breathing

Hypoglycemia Action Plan

RECOGNIZE LOW BLOOD SUGAR:

• Shaky, sweaty, hungry
• Pale, irritable, confused
• Trouble concentrating

TREAT IMMEDIATELY (Rule of 15):

1. Give 15 grams fast sugar:

   • 4 glucose tablets
   • 4 oz (1/2 cup) juice
   • 4 oz regular soda
   • 1 tablespoon honey

2. Wait 15 minutes

3. Recheck blood sugar

   • If still less than 70 mg/dL → repeat step 1
   • If >70 mg/dL → give a snack with protein

IF UNCONSCIOUS OR SEIZING:

• Do NOT put anything in mouth
• Give glucagon injection (if trained)
• Call emergency services (911)
• Place on side (recovery position)

ALWAYS carry:

• Fast-acting sugar
• Glucagon kit
• Medical ID

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References

1. Glaser N, Fritsch M, Garg SK, et al. ISPAD Clinical Practice Consensus Guidelines 2022: Diabetic ketoacidosis and hyperglycemic hyperosmolar state. Pediatr Diabetes. 2022;23(7):835-856. doi:10.1111/pedi.13406

2. Wolfsdorf JI, Allgrove J, Craig ME, et al. ISPAD Clinical Practice Consensus Guidelines 2014: Diabetic ketoacidosis and hyperglycemic hyperosmolar state. Pediatr Diabetes. 2014;15(Suppl 20):154-179. doi:10.1111/pedi.12165

3. International Hypoglycaemia Study Group. Glucose Concentrations of Less Than 3.0 mmol/L (54 mg/dL) Should Be Reported in Clinical Trials: A Joint Position Statement. Diabetes Care. 2017;40(1):155-157. doi:10.2337/dc16-2215

4. Rewers A, Klingensmith G, Davis C, et al. Presence of diabetic ketoacidosis at diagnosis of diabetes mellitus in youth: The SEARCH for Diabetes in Youth Study. Pediatrics. 2008;121(5):e1258-e1266. doi:10.1542/peds.2007-1105

5. Dabelea D, Rewers A, Stafford JM, et al. Trends in the prevalence of ketoacidosis at diabetes diagnosis: The SEARCH for Diabetes in Youth Study. Pediatrics. 2014;133(4):e938-e945. doi:10.1542/peds.2013-2795

6. 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. doi:10.1056/NEJM200101253440404

7. Randall L, Begovic J, Hudson M, et al. Recurrent diabetic ketoacidosis in inner-city minority patients: Behavioral, socioeconomic, and psychosocial factors. Diabetes Care. 2011;34(9):1891-1896. doi:10.2337/dc11-0701

8. Abraham MB, Jones TW, Naranjo D, et al. ISPAD Clinical Practice Consensus Guidelines 2018: Assessment and management of hypoglycemia in children and adolescents with diabetes. Pediatr Diabetes. 2018;19(Suppl 27):178-192. doi:10.1111/pedi.12698

9. Graveling AJ, Frier BM. Impaired awareness of hypoglycaemia: A review. Diabetes Metab. 2010;36(Suppl 3):S64-S74. doi:10.1016/S1262-3636(10)70470-5

10. Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN. Hyperglycemic crises in adult patients with diabetes. Diabetes Care. 2009;32(7):1335-1343. doi:10.2337/dc09-9032

11. Edge JA, Jakes RW, Roy Y, et al. The UK case-control study of cerebral oedema complicating diabetic ketoacidosis in children. Diabetologia. 2006;49(9):2002-2009. doi:10.1007/s00125-006-0363-8

12. Lawrence SE, Cummings EA, Gaboury I, Bhattacharyya S, Bhattacharyya A. Population-based study of incidence and risk factors for cerebral edema in pediatric diabetic ketoacidosis. J Pediatr. 2005;146(5):688-692. doi:10.1016/j.jpeds.2004.12.041

13. Kuppermann N, Ghetti S, Schunk JE, et al. Clinical Trial of Fluid Infusion Rates for Pediatric Diabetic Ketoacidosis. N Engl J Med. 2018;378(24):2275-2287. doi:10.1056/NEJMoa1716816

14. Hillier TA, Abbott RD, Barrett EJ. Hyponatremia: Evaluating the correction factor for hyperglycemia. Am J Med. 1999;106(4):399-403. doi:10.1016/s0002-9343(99)00055-8

15. Hanas R, Lindgren F, Lindblad B. A 2-yr national population study of pediatric ketoacidosis in Sweden: Predisposing conditions and insulin pump use. Pediatr Diabetes. 2009;10(1):33-37. doi:10.1111/j.1399-5448.2008.00441.x

16. Choleau C, Maitre J, Filipovic Pierucci A, et al. Ketoacidosis at diagnosis of type 1 diabetes in French children and adolescents. Diabetes Metab. 2014;40(2):137-142. doi:10.1016/j.diabet.2013.11.001

17. Muir AB, Quisling RG, Yang MC, Rosenbloom AL. Cerebral edema in childhood diabetic ketoacidosis: Natural history, radiographic findings, and early identification. Diabetes Care. 2004;27(7):1541-1546. doi:10.2337/diacare.27.7.1541

18. Marcin JP, Glaser N, Barnett P, et al. Factors associated with adverse outcomes in children with diabetic ketoacidosis-related cerebral edema. J Pediatr. 2002;141(6):793-797. doi:10.1067/mpd.2002.128888

19. American Diabetes Association. Standards of Medical Care in Diabetes—2024. Diabetes Care. 2024;47(Suppl 1):S1-S291. doi:10.2337/dc24-SINT

20. Tasker RC, Lutman D, Peters MJ. Hyperventilation in severe diabetic ketoacidosis. Pediatr Crit Care Med. 2005;6(4):405-411. doi:10.1097/01.PCC.0000163677.78174.56