MANAGEMENT OF DIABETIC KETOACIDOSIS IN CHILDREN S.V. DELPORT Paediatric Endocrine and Diabetes Unit

DIABETIC KETOACIDOSIS Type 1 DM – epidemic Current trends in RSA All population groups Peaks 4-6 years and 10-14 years 80 new cases/year (RCCH or GSH) 85% in DKA

DIABETIC KETOACIDOSIS Deficiency of circulating insulin Increased counter-regulating hormones Catecholamines Glucogon Cortisol Growth hormone Increased catabolic state Increased glucose production Impaired glucose utlilization

CONSEQUENCES Hyperglycaemia Osmotic diuresis Stress hormone production Dehydration Electolyte imbalance Stress hormone production Inducing further insulin resistance Ketosis Acidosis

CLINICAL MANIFESTATION OF DKA Dehydration Rapid, sighing (Kussmaul) breathing Nausea, vomiting, abdominal pain Progressive obtundation Fever (presence of infection)

CLINICAL MANIFESTATION OF DKA (Biochemical) Hyperglycaemia > 11mmol/L Venous blood gas PH < 7.3 Bicarbonate < 15 mmol/L Ketonaemia/ketonuria

ASSESSMENT OF SEVERITY   Mild Moderate Severe haemodynamic status normal perfusion normal BP BP (poor peripheral pulses) perfusion hydration dehydration 5% dehydration > 10% dehydration > 10% Level of consciousness fully conscious, alert drowsy depressed level of consciousness acidosis pH > 7.3 pH < 7.3 pH <7.1

GOALS OF THERAPY Correct dehydration Correct acidosis & reverse ketosis Restore blood glucose to near normal Avoid complications of therapy Identify and treat precipitating event

MANAGEMENT OF DKA Fluid Therapy Resuscitation Oxygen 100% by face mask Treat shock first Normal saline 0.9% 10 ml / kg over 10 – 30 minutes Reassess. Repeat if peripheral pulses remain poor   Insert nasogastric tube if there is vomiting ± impaired consciousness If the referral centre is more than 1 hour away, 0.9% saline should continue at 10 ml/ kg/ hr for 1– 2 hours, then at a rate of 5 ml/ kg/ hr Proceed to step 2 when hypovolaemia corrected.

Fluid Therapy continued 2. Rehydration requirements = Maintenance + Deficit + excess urine losses (if known)   Maintenance 0 - 2 yrs 80 ml/kg/24 hrs 3 - 5 70 ml/kg/24 hrs 6 - 9 60 ml/kg/24 hrs 10 - 14 50 ml/kg/24 hrs adult (>15) 30 ml/kg/24 hrs + Deficit 5 % dehydrated 50 ml/kg over 48 hrs 10 % dehydrated 100 ml/kg over 48 hrs + Excess urine losses replace urine losses in excess of 2 ml/kg/hour = urine output (ml/kg/hr) – 2 ml/kg/hour ______________________________________________________________________ 3. Reassess patient and review fluid therapy calculations frequently Note: Children < 5% dehydrated, with a pH ³ 7.3, who are clinically well, may tolerate oral rehydration and subcut insuli

MANAGEMENT (cont) Insulin therapy Insulin infusion 1-2 hours after fluids once shock corrected Actrapid HM or Humulin R Bolus NOT recommended When infusion not possible hourly or 2 hourly short or rapid acting analog

INSULIN INFUSION Optimal method: Continuous low-dose IV insulin infusion by syringe pump, not by gravity controller 0.1 units/kg/hour Consider 0.05 units/kg/hour if < 5 years of age Calculation: For 0.1units/kg/hr patient weight <25kg : mix 25units insulin solution in 100ml voluven/saline run insulin solution at (0.4 x patient's mass in kg) ml/hr patient weight >25kg : mix 50units insulin solution in 100 ml voluven/saline run insulin solution at (0.2 x patient's mass in kg) ml/hr

MANAGEMENT (cont) Potassium Phosphate Acidosis start after resuscitation Serum K < 4.5 No elevated Ts on ECG Phosphate falls once treatment started Depleted by diuresis Insulin promotes entry to cells Acidosis fluid no bicarbonate

MONITORING BG – hourly ward glucometer 2-4 hour VBG, glucose, U & E, ketones, Pi Urine volume LOC (GCS – children’s) BP, RR, HR, hydration ECG Treatment (IVF, K, Pi, Insulin)

MORTALITY and MORBIDITY DKA mortality 0.15% to 0.3% Cerebral oedema 60% to 80% DKA deaths Local experience 0.07 (12 years: 2/2880) 100% cerebral oedema 10% - 25% residual morbidity

CEREBRAL OEDEMA Incidence 0.5 – 0.9% Mortality 21-24% Pathogenesis Increased risk – demographics Younger age Hyponatraemia at onset Longer duration of symptoms

CEREBRAL OEDEMA Risk factors at diagnosis / during treatment Greater hypocapnia Elevated urea More sever acidosis at presentation Bicarbonate Attenuated rise in Na Greater volume of fluid in first 4 hours Insulin bolus or in 1st hour

CEREBRAL OEDEMA Warning signs and symptoms Headache and reduced HR Change in neurological status Specific neurological signs Rising BP Decreased O2 saturation

TREATMENT of CEREBRAL OEDEMA Reduce rate of fluid administration Give mannitol 0.5- 1g/kg over 20 minutes (repeat 30 minutes to 2hrs) Hypertonic saline (3%) 5-10ml/kg Elevate head of bed IPPV with hyperventilaton

DKA – KEY POINTS Caused by insulin deficiency Managed in centre with expertise Begin fluid replacement before starting insulin therapy Volume expansion only to restore peripheral circulation Subsequent fluid should rehydrate evenly over 48 hours Begin insulin 1-2 hours after starting fluid replacement therapy

DIABETIC KETOACIDOSIS