Pediatic Diabetic KetoAcidosis DR TARIQ AL THOBITI

Pediatric Diabetic Ketoacidosis Children with Diabetes specially type I ,remain at risk for developing diabetic ketoacidosis (DKA). Children who are type I diabetics have incidence of DKA of 8/100 patients. In children younger than 19 years old , DKA is the admitting diagnosis in 65% of all hospital admissions of patients with diabetes mellitus.

Pediatric Diabetic Ketoacidosis The overall mortality rate for children in DKA is not unimpressive. Range of mortality is between 0.15 – 0.31 % The mortality associated with cerebral edema may approach 20-50 % The incidence of neurologic morbidity is significant and reported in 35-40% of survivors. Cerebral edema has largely been a complication of treatment in the pediatric population.

Pathophysiology of Diabetes Type I

Pediatric Diabetic Ketoacidosis DEFINITION: Hyperglycemia >200mg/dl = 11 mmol/l Acidosis ph<7.3 Bicarbonate < 15 meq/l Ketonemia (Beta hydroxy butyrate and acetoacetate) >3 mmol/l Ketonuria

Pediatric Diabetic Ketoacidosis ETIOLOGY: Error in insulin management at home or inadequate insulin administration. Secondary to child or parental non-compliance because of emotional and psychological stress Insulin pump malfunction Infections Pre-pubertal and pubertal phase

Pediatric Diabetic Ketoacidosis

Pediatric Diabetic Ketoacidosis Clinical Presentation: Sometimes can be challenging and subtle requiring high degree of suspicion. Classically: Polyuria, Polydipsia, weight loss also abdominal pain,nausea,vomiting. Physical examination: Dry mucous membranes, tachycardia, delayed capillary refill, hypo-perfusion,hypothermia,kussmaul’s breathing, diffuse abdominal pain.

Pediatric Diabetic Ketoacidosis Management: 1- Fluids:Carefully regulated treatment plan to prevent the most lethal complication of DKA  cerebral edema 2- Electrolytes: A- serum sodium: As serum glucose fall with therapy , serum sodium should rise to normal or above normal level. Clinicians should consider the possibility of pseudohyponatremia that may result from elevated glucose. Corrected Na level: Na decreased 1.6mEq/l for each 100mg/dl rise in glucose

Pediatric Diabetic Ketoacidosis Management: 2- Electrolytes: B- serum potassium: At initial presentation in DKA, normally they have high or normal potassium level even though total body potassium stores are depleted (extra-cellular shift of potassium) CAUSES: High plasma osmolalityosmotic shift of water to ECFpotassium follows this gradient hyperkalemia Acidosis Insulin deficiencyglycogenolysis and proteolysisworsen osmotic gradient.

Pediatric Diabetic Ketoacidosis Management: 2- Electrolytes: B- serum potassium: Potassium is lost from the body via 3 routes: vomiting, urinary loss. Massive volume depletion2ryhyperaldosteronismincreased excretion of potassium through kidney. C- Serum phosphate: Renal excretion of phosphate + rapid entry of phosphate intracellularly hypophosphatemia Phosphous replacement if level below 1 mg/dl as it may cause muscle weakness and insult diaphragmatic tissues. Always keep in mind that phosphorus administration may cause hypocalcemia.

Pediatric Diabetic Ketoacidosis Management: 3- Insulin and glucose: Although there is consensus that blood sugar level must be greater than 200 mg/dl for patient to be in DKA , there are some infrequent reports of euglycemic DKA. Reasons: 1- Fasting child. 2- Poor nutrient intake Insulin is crucial in the treatment of pediatric DKA as it suppresses lipolysis and ketogenesis. Care should be taken to avoid precipitous drop in glucose level, should not drop at a rate faster than 100mg/dl/hr to decrease the risk of cerebral oedema.

Pediatric Diabetic Ketoacidosis Management: 4- Acidosis and bicarbonate: There is absolutely no role for bicarbonate administration in DKA patientsleads to cerebral oedema (paradoxical CNS acidosis). Indications for bicarbonate administration: 1- Severe academia with pH <<6.9 2- Life threatening hyperkalemia with ECG changes.

Pediatric Diabetic Ketoacidosis Complications of DKA: 1- Hypoglycemia: 2ry to insulin infusion Do hourly blood glucose check. Treatment: various types of IV dextrose 2- Hypokalemia: 2ry to insulin therapy which shifts potassium intracellularly. Potassium losses from the body via: vomiting, urinary loss. Massive volume depletion2ry hyperaldosteronismincreased excretion of potassium through kidney. It is prudent to add some potassium chloride to IVF according to protocol.

Pediatric Diabetic Ketoacidosis Complications of DKA: 3- Cerebral edema: It is a multifactorial process (cerebral oligemia,hyperemia.inflammation, cyto-toxic insult) Overhydration leads to cerebral edema. bicarbonate administration in DKA patientsleads to cerebral oedema (paradoxical CNS acidosis). Rapid drop in glucose level leads to osmotic shiftcerebral edema Failure of correction of Na with treatment Epidemiologically patients with high blood urea concentrations are at risk. Epidemiologically patients with severe hypocapnia are at risk for cerebral edema.

Pediatric Diabetic Ketoacidosis Complications of DKA: 3- Cerebral edema: Clinically: Altered mental status Headache Vomiting Bradycardia Hypertension Irregular breathing Seizures Anisocoria

The story of Hamad

The story of Hamad Hamad is a 12 years old boy who was fit and well , presented to the A/E with severe vomiting , abdominal pain , drowsiness and shortness of breath, low grade fever. He had polyuria and Polydipsia . He had no past medical history of note and he takes no medications . His elder sister had celiac disease and his mother had hypothyroidism .

The story of Hamad Hamad was severely dehydrated with reduced skin turgor , dry mucous membranes and a GCS of 13 . Generally he was emaciated .throat congested. His abdomen was mildly tender with no guarding or rigidity . No other significant finding on exam His vitals were BP 70/35 HR 140 , RR 35 . Temp 37.9 Orally and Sats 100 % on air . Hamad is 35 kg

What do you think is going on with Hamad ???

What investigations would you like to order to Hamad??

The story of Hamad Blood glucose Urinary/plasma ketones Serum electrolytes BUN/Cr CBC, blood C/S, throat swab and culture Blood gas

What you would expect to find??? Elevated blood glucose (500mg/dl) Low bicarbonate level Anion gap metabolic acidosis Urine dipsticks positive for glucose and ketones

What you would expect to find??? Sodium: low Osmotic flux of water into extracellular space reduces serum sodium concentration (pseudohyponatremia) Actual sodium: 1.6mEq/L per 100mg/dL rise in glucose Potassium: Level varies depending on urinary loss and severity of acidosis. Potassium moves extracellularly in exchange for hydrogen ions Typical hyperkalemia on presentaion Total body stores are depleted due to urinary loss

What you would expect to find??? Phosphate Depleted in the setting of DKA Serum level may not accurately represent total body stores

What you would expect to find??? Hamad Blood gas (VBG) : pH 7.05 Pco2 20 pO2 60 Bicarb 4 BE – 20 Urea 11.0 mmol/l sodium 126 mmol/l K 6.5 mmol/l

What management would you give Hamad Goals of correction: Dehydration Electrolytes deficits Hyperglycemia Acidosis Infection

Fluid Replacement

What type ???

Fluids Normal Saline has the best evidence , consider half saline if hypernatremia .

How much ??? For initial resuscitation 10 ml/kg in first hour , can be repeated for the 2nd hour No K in bolus bags Add KCL when level drop below 5 meq/l

Insulin

Hamad is in the resus. Room--what and when ???? Give Hamad fluid bolus first . Remember he need at least 2 cannulas . While you prepare the insulin for Hamad . One hour may have elapsed . Dilute 50 unit of insulin in 500 ml of N.saline and prepare infusion pump in a rate depends on Hamad weight . ( in hamad it will be 35 ml per hour ) 0.05-0.1 unit/kg/hr

What next?? Electrolytes and venous pH should be initially evaluated hourly for the first three to four hours and then every two hours. When clinically appropriate, the frequency of measurement can be reduced to every four to six hours. Monitor blood glucose hourly during the initial four to six hours of fluid and insulin therapy

What next?? Measure and record fluid input and output accurately. If the patient is neurologically impaired or it is difficult to ascertain urine output, a urine catheter should be placed. Clinical parameters including heart rate, respiratory rate, blood pressure, oxygen saturation, and neurologic status should be monitored continuously. In patients with severe DKA or altered mental status, frequent neurologic examinations are recommended

Hamad initial sodium is low ???? Corrected serum Na = 132

Serum sodium is not going in the right direction for Hamad , It did not rise up .

HYPONATREMIA If the serum sodium fails to rise appropriately, consideration should be given to increasing the sodium concentration in the infused fluids and decreasing their rate of administration according to protocol. The patient should be carefully monitored for early signs of cerebral edema

Hamad Initial Potassium is 6.5 ????

High Potassium Start IVF with normal saline (plain). Check K again after fluid resuscitation and Insulin . Very likely it will come down . If the potassium level is below 5 mEq/L , add 40 mEq/lit of potassium chloride to IVF.

High Potassium If the potassium level is greater than 6 mEq/L, do not administer potassium supplement. Continue monitoring. ECG was abnormal,with signs of hyperkalemia!!!! What are the signs???

It is still 6.1 after fluids ????

Management of hyperkalemia Restrict K in IVF Stabilize myocardium: Calcium chloride 10-20mg/kg IV OR Calcium gluconate 100-200 mg/kg IV Shift potassium intra-cellularly: Na HCO3 1-2 mmol/kg IV Glucose/Insulin infusionRegular insulin 0.1 unit/kg +D25% 2ml/kg over 30 min Enhance Elimination: Kayexalate PO/PR :0.5-1 gm/kg Ventolin nebulizer

What if the initial K is less than 3.5 ( rare ) Patient at risk of hypokalemic arrest (put the patient in continuous ECG Monitoring ). Delay insulin infusion Replace K vigorously and safely The maximum recommended rate of IV potassium replacement is usually 0.5-1 mEq/kg/hour over 2 hours. The serum potassium concentrations should be monitored hourly and the replacement adjusted as needed.

Hamad in 1st 6 hrs Hamad started to have: Intensifying headache Altered consciousness Recurrent vomiting Slow heart rate No ophthalmoplegia No anisocoria No Posturing No seizures

Now What Happened ….???

BRAIN EDEMA

Now How can we help you Hamad ????? Don’t delay treatment for further evaluation or CT of the brain Reduce the rate of fluid adminstration Position head at 30 degrees Mannitol 0.5-1 gm/kg IV first dose and a second one in 15 min 3% N.saline Intubation and Hyperventilation to attain PaCO2 of 30 RSI: Lidocaine + Midazolam + Rocuronium

Course of Hamad Illness The physical examination always include careful search for infection that may have precipitated DKA. Hamad was covered with IV antibiotics

After 24 hrs in PICU: Hamad Bl/Pr now 110/70 More hydrated Blood Glusose 120 He is not acidotic

Follow Up Hamad was extubated and recovered He was told he had diabetes and this is one of its complications He will always remember he had an episode of Diabetic Ketoacidosis

And He will always remember to take his insulin

Any Questions

THANK YOU