Pediatric Emergencies — Part 4: Neurologic, Metabolic & Fluid Emergencies

Febrile seizure evaluation, status epilepticus protocol with stepwise treatment, clinical dehydration assessment, WHO dehydration classification, ORT protocol, IV fluid calculation with Holliday-Segar rule, hyponatremia correction, and pediatric diabetic ketoacidosis management including 2-bag system and cerebral edema monitoring.

guidelinesMar 2026guidelines

1. Febrile Seizures

Febrile seizures are the most common seizure type in childhood, affecting 2-5% of children between 6 months and 5 years of age. They are defined as seizures occurring in the setting of fever (temperature ≥38°C / 100.4°F) in a child aged 6 months to 5 years, without evidence of central nervous system infection, metabolic disturbance, or a history of afebrile seizures. Despite their frightening presentation, febrile seizures are generally benign with an excellent prognosis.1 2

1.1 Simple vs Complex Febrile Seizures

FeatureSimple Febrile SeizureComplex Febrile Seizure
Duration<15 minutes≥15 minutes
TypeGeneralized (tonic-clonic)Focal features (lateralizing movements, asymmetric posturing)
OccurrenceSingle seizure in 24-hour periodMultiple seizures within 24 hours
Post-ictal periodBrief (returns to baseline within 1 hour)Prolonged or incomplete recovery
Frequency~70-75% of all febrile seizures~25-30% of all febrile seizures
Recurrence risk~30% (1 recurrence); ~10% (≥3 recurrences)~50% recurrence
Epilepsy risk1-2% (similar to general population)4-6%

1.2 Evaluation of Simple Febrile Seizures

The following workup is specifically guided by clinical practice guidelines for simple febrile seizures.1

InvestigationRecommendationRationale
Lumbar punctureNot routinely recommended if the child is well-appearing and fully recovered; consider in infants 6-12 months who are unvaccinated or incompletely vaccinated against Hib and S. pneumoniae; strongly consider if the child received antibiotics (may mask meningitis signs)Risk of bacterial meningitis is very low in a child who has returned to baseline neurologic function
Electroencephalography (EEG)NOT recommended after a simple febrile seizureDoes not predict recurrence or subsequent epilepsy; may show nonspecific abnormalities that lead to unnecessary treatment
Neuroimaging (CT/MRI)NOT recommended after a simple febrile seizureYield is extremely low in simple febrile seizures; CT exposes the child to ionizing radiation without benefit
Blood testsNOT routinely recommendedElectrolytes, glucose, CBC are guided by clinical assessment, not by the seizure itself; may obtain directed labs to evaluate the source of fever
Identify fever sourceYes — evaluate and treat the source of feverThe seizure is triggered by the fever; identify and manage the underlying febrile illness

1.3 Parent/Caregiver Education

TopicKey Messages
PrognosisSimple febrile seizures do not cause brain damage, intellectual disability, or death; they are not epilepsy
Recurrence~30% chance of another febrile seizure, highest in the first year after initial episode; risk factors for recurrence include younger age at onset, lower temperature at time of seizure, shorter duration of fever before seizure, family history of febrile seizures
What to do during a seizurePlace child on side (recovery position); clear area of hard/sharp objects; do NOT put anything in the mouth; do NOT restrain; time the seizure; call emergency services if seizure lasts >5 minutes
Antipyretic prophylaxisAntipyretics (acetaminophen, ibuprofen) treat discomfort from fever but do NOT prevent febrile seizures; routine prophylactic use is not recommended for seizure prevention
Anticonvulsant prophylaxisNOT recommended for simple febrile seizures; potential side effects of daily anticonvulsant medications outweigh the risks of recurrence

1.4 Management of Complex Febrile Seizures

Complex febrile seizures warrant more thorough evaluation:

  • Lumbar puncture: lower threshold, especially if prolonged postictal state, focal features, or age <12 months
  • Neuroimaging: consider emergent CT if focal seizure, prolonged postictal deficit (Todd paralysis >1 hour), or concern for structural lesion
  • EEG: consider outpatient EEG if focal features or multiple complex febrile seizures
  • Observation: longer period of observation in ED or hospital admission
  • Neurology referral: recommended for recurrent complex febrile seizures

2. Status Epilepticus

Status epilepticus (SE) is defined as a seizure lasting ≥5 minutes or two or more seizures without return to baseline neurologic function between seizures. This represents a time-sensitive neurologic emergency. Mortality is 3-7% in children, and morbidity (including cognitive sequelae) increases with seizure duration. The likelihood of spontaneous termination decreases with each passing minute, making rapid, protocolized benzodiazepine administration the single most important intervention.3 4

2.1 Status Epilepticus Protocol: Stepwise Treatment

Phase 1: Stabilization and First-Line Therapy (0-5 minutes)

TimeAction
0–2 minABCs: position airway, suction if needed, supplemental oxygen, pulse oximetry, place on monitor; check glucose (treat hypoglycemia immediately: D10W 5 mL/kg IV for neonates, D25W 2-4 mL/kg for infants)
0–5 minBENZODIAZEPINE (first-line) — administer one of the following:
DrugRouteDoseMax DoseNotes
MidazolamIM0.2 mg/kg10 mgPreferred if no IV access (fastest to administer)
MidazolamIN (intranasal)0.2 mg/kg10 mgUse concentrated formulation (5 mg/mL); split between nares
MidazolamBuccal0.2 mg/kg10 mgPlace between cheek and gum
MidazolamIV0.1-0.2 mg/kg10 mgIf IV access already established
LorazepamIV0.1 mg/kg4 mgLonger anticonvulsant duration (~12-24 hours) than midazolam
DiazepamIV0.2 mg/kg10 mg (child); 20 mg (adolescent)Rapid onset but short anticonvulsant duration (~20 min); redistribution
DiazepamPR (rectal)0.5 mg/kg20 mgFor home/prehospital use; gel formulation available

Phase 2: Established Status Epilepticus (5-20 minutes)

TimeAction
5–10 minIf seizure continues: give second dose of benzodiazepine (same drug and route, or alternative route/drug if first was not IV and IV is now available)
5–20 minEstablish IV/IO access if not already obtained
5–20 minOrder labs: BMP (glucose, sodium, calcium, magnesium), CBC, VBG, lactate, anticonvulsant levels (if applicable), toxicology screen
10–20 minIf seizure persists after 2 doses of benzodiazepine: proceed to second-line therapy

Phase 3: Second-Line Therapy (20-40 minutes)

Choose ONE of the following. The ESETT trial in 2019 demonstrated non-inferiority among these three agents for benzodiazepine-refractory status epilepticus.4

DrugDoseAdministrationProsCons
Levetiracetam40-60 mg/kg IV (max 4,500 mg)Over 10-15 minutesMinimal sedation; no cardiovascular depression; no drug interactions; safe in hepatic dysfunctionMay be slightly less effective than fosphenytoin in some subgroups; IV formulation required
Fosphenytoin20 mg PE/kg IV (max 1,500 mg PE)Over 10-20 minutes (max rate: 3 mg PE/kg/min in children, 150 mg PE/min in adults)Long track record; effectiveHypotension, arrhythmia (requires cardiac monitoring); contraindicated in known cardiac conduction defects; drug interactions
Phenobarbital20 mg/kg IV (max 1,000 mg)Over 15-20 minutes (max rate: 1 mg/kg/min)Effective especially in neonates; long duration of actionSignificant respiratory depression and sedation; hypotension; may obscure neurologic exam
Valproic acid20-40 mg/kg IV (max 3,000 mg)Over 5-10 minutesBroad spectrum; minimal hemodynamic effectsHepatotoxicity (avoid in age <2 years, mitochondrial disease); pancreatitis; teratogenic

Phase 4: Refractory Status Epilepticus (>40 minutes)

If seizures persist despite adequate doses of benzodiazepine AND one second-line agent:

InterventionDetails
Try a second second-line agentIf levetiracetam was used first, try fosphenytoin or phenobarbital (or vice versa)
Prepare for RSI and continuous infusionIf seizure continues, intubate for airway protection and begin one of the following:
Midazolam infusionLoad: 0.2 mg/kg IV bolus; Infusion: 0.05-2 mg/kg/hr; titrate to burst suppression on continuous EEG
Pentobarbital infusionLoad: 5-15 mg/kg IV over 30-60 min; Infusion: 0.5-5 mg/kg/hr; significant hemodynamic depression — requires vasopressor support
Propofol infusionLoad: 1-2 mg/kg IV; Infusion: 1-5 mg/kg/hr; CAUTION: propofol infusion syndrome risk in children (metabolic acidosis, rhabdomyolysis, cardiac failure); limit duration and dose; generally avoid in young children
Ketamine infusionLoad: 1-2 mg/kg IV; Infusion: 0.5-5 mg/kg/hr; NMDA antagonist; may be neuroprotective; less hemodynamic depression; increasing use in pediatric RSE

2.2 Key Principles

  • Time is brain: every minute of ongoing seizure increases neuronal injury and decreases the probability of seizure termination
  • Do not under-dose benzodiazepines: a common error is giving subtherapeutic doses; use full weight-based dosing
  • IM midazolam for no IV access: the RAMPART trial demonstrated that IM midazolam was at least as effective as IV lorazepam when IV access was not pre-existing, primarily because of faster time to drug administration
  • Monitor for respiratory depression: all anticonvulsants can cause hypoventilation; have bag-mask ventilation equipment immediately available
  • Continuous EEG monitoring is essential during treatment of refractory status epilepticus to detect ongoing electrographic seizures after clinical motor manifestations have ceased (electroclinical dissociation)3 4

3. Dehydration Assessment and Fluid Management

Dehydration is the most common fluid and electrolyte disturbance in pediatric emergency medicine, most frequently caused by acute gastroenteritis. Accurate assessment of dehydration severity guides the urgency and route of rehydration. Oral rehydration therapy is the preferred method for mild-moderate dehydration and is underutilized in many emergency departments.5 6

3.1 Clinical Dehydration Scale (CDS)

The Clinical Dehydration Scale is a validated 4-item scoring tool for children 1 month to 5 years with suspected dehydration due to gastroenteritis.5

Feature0 Points1 Point2 Points
General appearanceNormalThirsty, restless, or lethargic but irritable when touchedDrowsy, limp, cold, sweaty; ± comatose
EyesNormalSlightly sunkenVery sunken
Mucous membranes/tongueMoistStickyDry
TearsPresentDecreasedAbsent
Total ScoreDehydration SeverityEstimated Deficit
0No dehydration<3%
1–4Some (mild-moderate) dehydration3-6%
5–8Moderate-severe dehydration6-9%

3.2 WHO Dehydration Classification

The World Health Organization uses a simplified classification system widely applied in resource-limited settings and endorsed for global use.6

ClassificationClinical SignsEstimated DeficitTreatment
No dehydrationNo signs of dehydration; child drinks normally; all clinical signs negative<5% (50 mL/kg)Plan A: Home management; continue oral fluids and feeding; educate caregiver on danger signs
Some dehydration (≥2 of the following signs)Restless/irritable; sunken eyes; drinks eagerly/thirsty; skin pinch goes back slowly (1-2 seconds)5-10% (50-100 mL/kg)Plan B: ORS 75 mL/kg over 4 hours in supervised setting; reassess after 4 hours
Severe dehydration (≥2 of the following signs)Lethargic/unconscious; sunken eyes; unable to drink or drinks poorly; skin pinch goes back very slowly (>2 seconds)>10% (>100 mL/kg)Plan C: IV fluids immediately: 30 mL/kg LR (or NS) in 30 min (infant) or 1 hr (child >1 yr), then 70 mL/kg over 5 hrs (infant) or 2.5 hrs (child); reassess frequently

3.3 Traditional Clinical Assessment

SignMild (3-5%)Moderate (6-9%)Severe (≥10%)
Mental statusAlert, normalIrritable, restlessLethargic, obtunded
ThirstSlightly increasedModerately increasedDrinks poorly; too lethargic to drink
Heart rateNormalMildly increasedMarkedly increased
Blood pressureNormalNormal (compensated)Hypotension (decompensated)
Respiratory rateNormalIncreasedDeep (Kussmaul if acidotic)
EyesNormalSunkenDeeply sunken
TearsPresentDecreasedAbsent
Mucous membranesMoistDryParched
Skin turgorNormalDecreased (tenting 1-2 sec)Markedly decreased (tenting >2 sec)
Capillary refill<2 seconds2-3 seconds>3 seconds
Urine outputNormal to slightly decreasedDecreased (oliguria)Minimal or anuria
Fontanelle (if open)FlatSunkenMarkedly sunken

3.4 Oral Rehydration Therapy (ORT) Protocol

ORT is the first-line treatment for mild-to-moderate dehydration and is as effective as IV rehydration for gastroenteritis-related dehydration. It is recommended by the international health and pediatric professional societies as the preferred rehydration method.5 6

PhaseVolumeMethodDuration
Rehydration phase50 mL/kg (mild) or 100 mL/kg (moderate)ORS solution (e.g., standard WHO-ORS: Na 75 mEq/L, glucose 75 mmol/L, osmolality 245 mOsm/L); give small frequent sips (5-10 mL every 1-2 minutes via syringe, cup, or spoon)4 hours
Maintenance phaseReplace ongoing losses: 10 mL/kg for each watery stool; 2 mL/kg for each vomitContinue ORS + resume age-appropriate diet (BRAT diet not specifically recommended; early refeeding encouraged)Until diarrhea resolves

ORT Failure (indication for IV fluids):

  • Persistent vomiting despite small frequent sips (give ondansetron 0.15 mg/kg IV/PO, max 4 mg, to reduce emesis and improve ORT success)
  • Severe dehydration with hemodynamic instability
  • Altered mental status
  • Ileus / abdominal distension
  • Inability to keep pace with ongoing losses

3.5 IV Fluid Calculation: Deficit Replacement + Maintenance

Step 1: Calculate Deficit Volume

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

Example: 10 kg child with 7% dehydration → 0.07 × 10 × 1000 = 700 mL deficit

Step 2: Calculate Maintenance Fluids (Holliday-Segar 4-2-1 Rule)

Body WeightHourly RateDaily Rate
First 10 kg4 mL/kg/hr100 mL/kg/day
Next 10 kg (11–20 kg)2 mL/kg/hr50 mL/kg/day
Each additional kg (>20 kg)1 mL/kg/hr20 mL/kg/day

Examples:

Child WeightHourly Maintenance RateDaily Maintenance Volume
8 kg4 × 8 = 32 mL/hr100 × 8 = 800 mL/day
15 kg(4 × 10) + (2 × 5) = 50 mL/hr1,000 + 250 = 1,250 mL/day
25 kg(4 × 10) + (2 × 10) + (1 × 5) = 65 mL/hr1,000 + 500 + 100 = 1,600 mL/day
40 kg(4 × 10) + (2 × 10) + (1 × 20) = 80 mL/hr1,000 + 500 + 400 = 1,900 mL/day
70 kg(4 × 10) + (2 × 10) + (1 × 50) = 110 mL/hrMaximum typically capped at ~2,400 mL/day

Step 3: Total Fluid Plan

  • Subtract any boluses already given from the deficit volume
  • Replace deficit over 24 hours (give half in first 8 hours, remainder over next 16 hours) for isotonic dehydration
  • Add maintenance to deficit replacement
  • Replace ongoing losses mL for mL

Step 4: Fluid Type

  • Maintenance IV fluid: isotonic crystalloid (NS or LR) is now recommended for pediatric maintenance fluids to reduce risk of hospital-acquired hyponatremia; hypotonic fluids (0.45% NS, D5 0.2% NS) are no longer recommended as routine maintenance due to risk of hyponatremia
  • Add dextrose: D5NS or D5LR for maintenance once serum glucose is normal
  • Add potassium: 20 mEq/L KCl to maintenance fluid once urine output is established and potassium level is confirmed normal or low5 7

4. Hyponatremia

Hyponatremia (serum sodium <135 mEq/L) in children can be life-threatening, particularly when acute or severe, due to the risk of cerebral edema. Conversely, overly rapid correction carries the risk of osmotic demyelination syndrome (ODS), though ODS is less common in children than adults.7

4.1 Classification

SeveritySerum NaSymptoms
Mild130-134 mEq/LOften asymptomatic; may have nausea, headache
Moderate125-129 mEq/LNausea, headache, lethargy, muscle cramps
Severe<125 mEq/LAltered mental status, seizures, coma, respiratory arrest

4.2 Symptomatic Hyponatremia Emergency Treatment

IndicationTreatmentGoal
Seizures or altered mental status from acute hyponatremia3% hypertonic saline (513 mEq/L): 2-5 mL/kg IV over 10-20 minutes; may repeat once if symptoms persistRaise serum Na by 4-6 mEq/L to stop seizures; this small increase is usually sufficient to resolve acute symptoms
After acute symptoms controlledSlow correction with NS or fluid restrictionMaximum correction rate: 8-10 mEq/L in 24 hours (some guidelines recommend ≤8 mEq/L/24h); faster rates risk osmotic demyelination
Chronic hyponatremia (>48 hours or unknown duration)Even more cautious correction: 6-8 mEq/L in 24 hoursHigher risk of ODS with rapid correction of chronic hyponatremia

4.3 3% Saline Quick Reference

  • Concentration: 513 mEq Na/L
  • Expected Na rise: 1 mEq/L per 1 mL/kg of 3% saline administered
  • Practical dosing: 2 mL/kg bolus of 3% saline raises Na by approximately 2 mEq/L
  • Monitor: serum Na every 1-2 hours during active correction; every 4-6 hours during slower correction
  • If overcorrection occurs: consider administering desmopressin (DDAVP) 0.25-1 mcg IV and/or D5W to re-lower sodium

5. Pediatric Diabetic Ketoacidosis (DKA)

DKA is the most common life-threatening endocrine emergency in children. It occurs in approximately 30% of children at initial diabetes diagnosis and 1-10% of known diabetics per year. Cerebral edema is the most feared complication, occurring in 0.5-1% of DKA episodes and accounting for 60-90% of DKA-related deaths in children. Unlike adult DKA protocols, pediatric DKA management emphasizes cautious fluid replacement and avoidance of rapid osmolality shifts.8 9

5.1 DKA Diagnostic Criteria

ParameterDKA Criteria
Blood glucose>200 mg/dL (>11 mmol/L); or known diabetes with glucose >250 mg/dL
Venous pH<7.30
Serum bicarbonate<15 mEq/L
Ketonemia/ketonuriaPositive serum beta-hydroxybutyrate (>3 mmol/L) or moderate-large urine ketones
Anion gapElevated (>12)

DKA Severity:

SeverityVenous pHBicarbonateClinical
Mild7.20-7.3010-15 mEq/LAlert; mild dehydration
Moderate7.10-7.195-9 mEq/LLethargic; Kussmaul respirations; moderate dehydration
Severe<7.10<5 mEq/LObtunded/comatose; Kussmaul or respiratory depression; severe dehydration; possible hemodynamic instability

5.2 Initial Resuscitation

PriorityInterventionDetails
1Volume resuscitation10 mL/kg NS bolus over 30-60 min (NOT 20 mL/kg); may repeat × 1 if hemodynamically unstable; total initial bolus should not exceed 20 mL/kg
2Laboratory studiesBMP (glucose, Na, K, Cl, CO2, BUN, Cr), VBG, beta-hydroxybutyrate, phosphorus, magnesium, calcium, CBC, HbA1c, UA
3Correct electrolytesIf K <3.5: add 40 mEq/L KCl to IV fluids and HOLD insulin until K ≥3.5; if K 3.5-5.5: add 20-40 mEq/L potassium to IV fluids; if K >5.5: hold potassium but recheck q1-2h (K will fall with insulin and hydration)
4Establish monitoringContinuous telemetry; hourly vitals; strict I&O; neuro checks q1h; POC glucose q1h

5.3 Fluid Replacement: 2-Bag System

The 2-bag system allows rapid adjustment of dextrose concentration without interrupting fluid delivery or requiring new bag preparation. This is the preferred method in many pediatric centers.8 9

Principle: Two bags of identical electrolyte composition run simultaneously through a Y-connector; one bag contains dextrose (D10NS + KCl), the other does not (NS + KCl). The relative rates of the two bags are adjusted to achieve the desired dextrose concentration.

Step 1: Calculate total fluid rate

  • Estimated dehydration: assume 5-7% for moderate DKA, 7-10% for severe
  • Deficit = % dehydration × weight (kg) × 1,000 (mL)
  • Subtract any bolus already given from the deficit
  • Replace remaining deficit evenly over 24-48 hours (most protocols use 48 hours)
  • Add maintenance (Holliday-Segar) to deficit replacement rate
  • Do NOT exceed 1.5-2× maintenance rate (excessive fluid rates are associated with increased cerebral edema risk)

Step 2: Prepare 2 bags

BagComposition
Bag A (no dextrose)NS (0.9% NaCl) + 20 mEq/L KCl + 20 mEq/L KPhos (or 40 mEq/L KCl)
Bag B (with dextrose)D10NS (10% dextrose in 0.9% NaCl) + 20 mEq/L KCl + 20 mEq/L KPhos

Step 3: Adjust rates based on blood glucose

Blood GlucoseBag A RateBag B RateEffective Dextrose
>300 mg/dL100% of total rate0%0% dextrose
250-300 mg/dL75%25%2.5% dextrose
200-250 mg/dL50%50%5% dextrose
150-200 mg/dL25%75%7.5% dextrose
<150 mg/dL0%100%10% dextrose

Goal: maintain blood glucose between 150-300 mg/dL during DKA treatment; glucose should decline by no more than 50-100 mg/dL per hour

5.4 Insulin Therapy

ParameterDetails
When to start1-2 hours AFTER starting IV fluids (NOT at time of presentation); initial fluid resuscitation alone lowers glucose; starting insulin too early accelerates osmolality shifts
PreparationRegular insulin 50 units in 50 mL NS (1 unit/mL) OR 50 units in 500 mL NS (0.1 unit/mL); prime tubing with insulin solution before connecting (insulin adsorbs to IV tubing)
Starting dose0.05-0.1 units/kg/hr continuous infusion; 0.05 units/kg/hr is increasingly preferred to avoid excessively rapid glucose decline
Do NOT give insulin bolusInsulin boluses are contraindicated in pediatric DKA (associated with increased cerebral edema risk)
TitrationTarget glucose decline of 50-100 mg/dL/hr; if glucose falling too fast, increase dextrose concentration (2-bag system) rather than decreasing insulin rate
Minimum insulin rate0.03-0.05 units/kg/hr; do NOT turn off insulin drip — add more dextrose instead (turning off insulin prolongs ketoacidosis)
Transition to subcutaneousWhen ALL of the following are met: venous pH >7.30, bicarbonate >15 mEq/L, anion gap closed (<12), patient tolerating oral intake, beta-hydroxybutyrate <1 mmol/L; overlap IV and SC insulin by 30-60 minutes before discontinuing drip

5.5 Cerebral Edema Monitoring and Management

Cerebral edema is the leading cause of death in children with DKA. Risk factors include younger age (<5 years), new-onset diabetes, severe DKA (pH <7.1), higher initial BUN, failure of Na to rise with treatment, and excessive fluid administration.8 9

Warning Signs (Modified GCS assessment q1h):

Warning SignDescription
HeadacheNew, worsening, or persistent headache during treatment
Altered mental statusDeterioration in GCS; inappropriate irritability or somnolence; failure to improve as expected
Vital sign changesBradycardia, hypertension (Cushing response); irregular respirations
Neurologic signsPosturing (decorticate/decerebrate); pupillary asymmetry; cranial nerve palsies (especially CN III and VI); papilledema
IncontinenceNew onset urinary incontinence in a previously continent child

Emergency Treatment of Cerebral Edema:

PriorityInterventionDetails
1Reduce IV fluid rateReduce to minimum rate immediately
2Elevate head of bed30 degrees; keep head midline
3Mannitol0.5-1 g/kg IV over 15-20 minutes; may repeat in 30 minutes if no response; keep serum osmolality <320 mOsm/kg
4Hypertonic saline (alternative or adjunct)3% NaCl: 2.5-5 mL/kg IV over 10-15 minutes; may be preferred if hypotensive (mannitol causes diuresis)
5IntubationIf GCS ≤8 or respiratory failure; avoid hyperventilation (target PaCO2 35-40 mmHg); mild hyperventilation (PaCO2 30-35) only as temporizing measure for imminent herniation
6CT headOnce patient is stabilized; assess for herniation, hemorrhage, or other structural cause
7Neurosurgery consultationFor consideration of ICP monitoring or decompressive craniectomy in refractory cases

5.6 Monitoring Schedule During DKA Treatment

ParameterFrequency
Point-of-care glucoseEvery 1 hour
Neurologic status (GCS)Every 1 hour
Vital signsEvery 1 hour (continuous telemetry)
BMP (Na, K, Cl, CO2, glucose, BUN, Cr)Every 2-4 hours
VBG (pH, pCO2)Every 2-4 hours
Beta-hydroxybutyrateEvery 2-4 hours
Calcium, magnesium, phosphorusEvery 4-6 hours
Strict intake and outputContinuous

5.7 Corrected Sodium Calculation

Hyperglycemia causes dilutional hyponatremia by drawing water into the intravascular space. Corrected sodium should be calculated and trended during DKA treatment.

Corrected Na = Measured Na + 1.6 × [(glucose - 100) / 100]

  • Corrected sodium should rise as glucose falls during treatment
  • Failure of corrected Na to rise (or a falling corrected Na) suggests excessive free water administration and is a risk factor for cerebral edema8 9

6. Hypoglycemia in Children

6.1 Definition and Thresholds

AgeHypoglycemia ThresholdCritical Sample Threshold
Neonate (0-48 hours)<40 mg/dL (guideline varies; some use <45)Obtain critical sample before correction if glucose <50
Neonate (>48 hours)<50 mg/dLSame
Infant/child<60 mg/dL (symptomatic) or <50 mg/dL (any)Obtain critical sample before correction when etiology unknown

6.2 Treatment

ScenarioTreatmentNotes
NeonateD10W 2-4 mL/kg IV push, followed by D10W maintenance at 5-8 mg/kg/min glucose infusion rateNEVER use D25W or D50W in neonates (hyperosmolar, risk of cerebral injury and phlebitis)
Infant/toddlerD25W 2-4 mL/kg IV pushD25W = 250 mg/mL dextrose
Older child/adolescentD50W 1-2 mL/kg IV push (max 25 g)D50W = 500 mg/mL dextrose
No IV accessGlucagon 0.03 mg/kg IM/SC (min 0.1 mg, max 1 mg) or 0.5 mg IM (<25 kg) / 1 mg IM (≥25 kg)Onset 10-20 minutes; may cause nausea; less effective in glycogen-depleted states (malnutrition, hepatic disease)
Mild, alert, tolerating POOral glucose: juice, glucose tablets, or glucose gel (15-30 g of rapid-acting carbohydrate)Recheck glucose in 15 minutes


  1. Subcommittee on Febrile Seizures. “Febrile Seizures: Guideline for the Neurodiagnostic Evaluation of the Child with a Simple Febrile Seizure.” Pediatrics. 2011;127(2):389-394. DOI: 10.1542/peds.2010-3318 ↩︎ ↩︎

  2. Steering Committee on Quality Improvement and Management, Subcommittee on Febrile Seizures. “Febrile Seizures: Clinical Practice Guideline for the Long-term Management of the Child with Simple Febrile Seizures.” Pediatrics. 2008;121(6):1281-1286. DOI: 10.1542/peds.2008-0939 ↩︎

  3. Glauser T, Shinnar S, Gloss D, et al. “Evidence-Based Guideline: Treatment of Convulsive Status Epilepticus in Children and Adults: Report of the Guideline Committee of the American Epilepsy Society.” Epilepsy Curr. 2016;16(1):48-61. DOI: 10.5698/1535-7597-16.1.48 ↩︎ ↩︎

  4. Kapur J, Elm J, Chamberlain JM, et al. “Randomized Trial of Three Anticonvulsant Medications for Status Epilepticus (ESETT).” N Engl J Med. 2019;381(22):2103-2113. DOI: 10.1056/NEJMoa1905795 ↩︎ ↩︎ ↩︎

  5. Freedman SB, Vandermeer B, Milne A, et al. “Diagnosing Clinically Significant Dehydration in Children with Acute Gastroenteritis Using Noninvasive Methods: A Meta-Analysis.” J Pediatr. 2015;166(4):908-916.e6. DOI: 10.1016/j.jpeds.2014.12.029 ↩︎ ↩︎ ↩︎ ↩︎

  6. World Health Organization. The Treatment of Diarrhoea: A Manual for Physicians and Other Senior Health Workers, 4th rev. Geneva: WHO; 2005. URL: https://www.who.int/publications/i/item/9241593180 ↩︎ ↩︎ ↩︎

  7. Moritz ML, Ayus JC. “Prevention of Hospital-Acquired Hyponatremia: Do We Have the Answers?” Pediatrics. 2011;128(5):980-983. DOI: 10.1542/peds.2011-2015 ↩︎ ↩︎

  8. Wolfsdorf JI, Glaser N, Agus M, et al. “ISPAD Clinical Practice Consensus Guidelines 2018: Diabetic Ketoacidosis and the Hyperglycemic Hyperosmolar State.” Pediatr Diabetes. 2018;19(Suppl 27):155-177. DOI: 10.1111/pedi.12701 ↩︎ ↩︎ ↩︎ ↩︎

  9. 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 ↩︎ ↩︎ ↩︎ ↩︎