Paediatric Diabetic Emergencies

Hypoglycaemia

• Causes
  • Insulin excess
  • Overdose of oral hypogclyaemic in T2DM
  • Intercurrent illness
  • Vigorous exercise
  • Other metabolic/endocrine issues (e.g. Addison’s disease)
• Definition
  • <2.5mmol/L
  • Symptoms may appear <4mmol/L and this should be the aim in all diabetic children

• Treatment
  • ABCDE
  • 2-5mL/kg of glucose 10% IV bolus
  • IM glucagon 0.5U (0.5mg) up to 8yo and 1U (1mg) for older children
  • Followed by glucose infusion and/or oral simple and complex carbohydrate

DKA

• Definition: BSL >11mmol/L, pH <7.3 and bicarbonate <15mmol/L
• Always consider in abdominal pain, tachypnoea, drowsiness, intercurrent infection and secondary enuresis
• May present as first diagnosis of T1DM or secondary to a febrile illness or poor adherence to management
• As obesity becomes more prevalent, T2DM is becoming more common
• T1DM still constitutes 90% of childhood diabetes

Risk factors for DKA in new T1DM

• Younger age (<5)
• Children with first-degree relative with T1DM
• Lower SES
• Glucocorticoids/antipsychotics/diazoxide/immunosuppressant agents all reported to precipitate DKA

Euglycaemic DKA

• Young or partially treated children and pregnant adolescents may present with this
• Relative normoglycaemia is seen in those who were given or took insulin prior to arrival, are starving or had reduced oral intake or those with impaired gluconeogenesis due to liver failure

Resuscitation

• ABCDE
• IV access x 2
• IV fluid bolus if in shock 10-20mL/kg N/saline
• Strict fluid balance
• Hourly obs including neurological
• Hourly blood glucose/ketones
• VBG q2h for first 6 hours then 2-4 hourly 
• Serum urea and electrolytes q2-4hrly for first 12-24 hours
• Nurse head-up

Investigations

• FBC
• Chem20
• Blood ketones
• VBG
• Septic work-up if indicated
• If new diagnosis diabetes: Insulin antibodies, GAD antibodies, coeliac screen (total IgA, angi-gliadin Ab, anti-TTG Ab) and TFT
• Urine ketones and culture

Fluids

• Keep NBM
• Deficit replacement over the next 48 hours + Maintenance/ongoing losses
• N/saline until BSL 12-15mmol/L then add 5% dextrose
• Degree of dehydration
  • None/mild = <4% = no clinical signs
  • Moderate = 4-7% = reduced skin turgor, poor capillary return
  • Severe = >7% = Poor perfusion, rapid pulse, reduced blood pressure i.e. shock

Insulin

• Only initiate after resuscitation complete
• 0.1U/kg/hr at constant rate – Dextrose infusion titrated or increased concentration to 10% to maintain BSL fall of 4-5mmol/L/hr
• Continue until BSL 5-10mmol/L, pH >7.30, bicarb >15 and ketonaemia resolved
• Change to subcutaneous insulin once eating and then cease infusion 30 min after meal
• Only drop insulin rate to 0.05U/kg/hr if BSL remains <5 despite 10% dextrose running at maintenance rate provided the acidosis continues to improve

Potassium

• Initiate once K <5.5, no ECG changes of hyperkalaemia, anuria or severe renal impairment
• Measured serum K goes up by 0.6mmol/L for every 0.1 drop in pH and will therefore drop precipitously as acidosis is corrected
• Initially 40mmol/L of saline and titrate to serum K measured q2-4h for first 12-24 hours of management

Sodium

• Corrected Na = Measured Na + ((Glucose -5.5)/3)
• If hypernatraemia exists (>150mmol/L, slow rehydration to replace deficit over 72 hours

Bicarbonate

• Not indicated unless cardiorespiratory compromise thought to be due to acidosis or marked hyperkalaemia not responsive to usual therapy
• May worsen intracellular acidosis, hypokalaemia and hypernatraemia

Complications

• 0.5% of children develop cerebral oedema due to DKA
• Risk factors – Younger age, T1DM, raised serum urea, severe dehydration at presntation, severe acidosis and greater hypocapnoea at presentation
• Warning signs
  • Altered LOC, headache, cranial nerve palsies and seizures
• Treatment
  • Slow rehydration rate to 1/3, IV mannitol 0.5g/kg, intubation and assisted ventilation

DKA Disposition

• ICU admission for:
  • <2yo
  • Coma
  • Cardiovascular compromise
  • Seizures
  • Severe acidosis (pH <7.0, bicarb <5)
  • Signs of cerebral oedema
• Discuss all cases with Endocrine team

New presentation, mildly ill diabetic

• <3% dehydration, no acidosis and no vomiting but BSL >11.1
• May have ketones
• Initial Ix: FBC, Chem20, VBG, GAD antibodies, insulin antibodies, coeliac screen, TFT
• Consider in obese children/acanthosis nigricans: C-peptide, insulin, lipid profile and LFT

• Management
  • 0.25U/kg quick-acting insulin SC stat
    • If within 2 hours of meal, defer and give mealtime dose
    • Halve dose if <4yo
  • Admit all children for diabetic workup and management

Hyperglycaemic, ketotic mildly ill with known diabetes

• If not acidotic, simply need extra subcut insulin to clear ketones
• If on intermittent daily injections (BD or MDI)
  • 10% of total insulin daily dose as SC of rapid-acting insulin in addition to normal insulin regime
  • Monitor BSL and ketones q1-2hrly
  • Can repeat after 2-4 hours if ketones not <1.0
• If on insulin pump therapy
  • Need to assume pump failure
  • Give 20% of total insulin daily dose as SC of rapid-acting insulin (as if pump has failed, has no long-acting insulin onboard) and resite pump with endocrine involvement

Kupperman study

• Clinical trial of fluid infusion rates for paediatric DKA NEJM 2018
• Cerebral oedema <1%
• Clinical question:
  • Does composition or rate of IV fluid resus in paediatric DKA impact neurocognitive function after recovery from ketoacidosis?
• Study design
  • 2×2 0.9% vs. 0.45% vs. rapid vs. slow

• Fast 0.45% or 0.9%
  • Half fluid deficit replaced with 0.45% or 0.9% NaCl in initial 12 hours + Maintenance
  • Remainder of deficit replaced during subsequent 24 hours
  • Assumed 10% fluid deficit and both received initial 10mL/kg 0.9% N/S bolus x 2
• Slow 0.45% or 0.9%
  • Deficit + Maintenance evenly over 48 hours
  • Both groups assumed 5% deficit and both received 10mL/kg 0.9% N/S bolus x 1

• Exclusion: GCS < 11 at time of randomization
• Primary outcome = Number of episodes of GCS <14
• Secondary outcomes
  • Incidence of clinically apparent brain injury
  • Short-term memory loss

• Results
  • 1361 episodes of DKA
  • 48 episodes of GCS <14 (3.5%)
  • 22 episodes requiring hyperosmolar therapy (1.6%)
  • 12 episodes of apparent brain injury (0.9%)
  • No difference in incidence across groups
  • Hyperchloraemic acidosis more common in 0.9% NaCl groups and more common in rapid vs. slow groups
• Only 10% of study population was <6yo which is main group at risk

Risk factors for cerebral oedema in DKA

• Treatment with bicarbonate
• High serum BUN at presentation (severe dehydration)
• Lower PaCO2 levels at presentation (severe metabolic acidosis)
• Failure to serum sodium to rise with therapy
• Large drops in serum osmolality with therapy
• Lower serum bicarbonate (severe metabolic acidosis)
• Younger age at presentation
• Newly diagnosed diabetes (may present late)
• Rate of fluid administration ?? Simply sicker patients get faster fluids ??

Last Updated on November 22, 2021 by Andrew Crofton