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1 Athina Sikavitsas DO Children's Emergency Services University of Michigan Discuss DKA Presentation Assessment Treatment I have no financial disclosures 1

2 6 Y/O male presents with vomiting and abdominal pain for past couple of days Felt warm Had been feeling tired prior to vomiting Clothes look looser on him Appears distressed Alert and somewhat anxious Noted tachypnea RR: 30 HR: 170, BP: 85/45 Cool extremities Diffuse abdominal pain Dry mucous membranes 2

3 Vomiting: Viral illness Appendicitis Other GI illness Sepsis Dehydrated IV obtained : 20 cc/kg bolus Labs: glucose: 497 Bicarb:5 Lactate: 5, ph:7.01 WBC:25K,HB:15 3

4 DKA New onset? Per 2014 International Society for Pediatric and Adolescent Diabetes guidelines, pediatric DKA will be defined as patients < 18 YO(cared for by pediatric services) with presenting serum glucose of > 200, venous ph < 7.30 or serum bicarbonate of < 15 with presence of ketones in either the blood and urine. 4

5 Polyuria, polydipsia, polyphagia Weight loss Fatigue Nausea/ vomiting Abdominal pain (paralytic ileus) Fruity odor to breath Hyperventilation (Kussmaul resp.) Evidence dehydration-hr, cap refill, turgor Mental status- altered, coma The clinical disturbances seen in kids in DKA are manifestations of loss of normal hormonal control of: 1. carbohydrate metabolism 2. protein metabolism 3. Fat metabolism 5

6 Hyperglycemia Acidosis Increased K (however low actual stores) Lactic acidosis Pseudohyponatremia 6

7 Dehydration: most DKA are about 10% dehydrated Kussmaul breathing Electrolyte abnormalities Mental status changes: Cerebral edema Cerebral edema is the most devastating and overt form of cerebral injury in DKA (CIDKA), accounting for up to 90% of pediatric DKA deaths. 3,4 Thoughts that there potential contributing mechanisms for CIDKA.inflammation and vasogenic factors 7

8 The figure is excerpted from Dr. Elliot Krane s publication and indicates that the peak onset of cerebral edema is oft 6-18 hours after initiation of treatment. These data were confirmed by Glaser et al in Case control studies indicate that pediatric patients receiving sodium bicarbonate in the early phases of DKA, those presenting with severe acidosis and dehydration and those whose corrected serum sodium decrease during treatment (Glaser et al 2001, Durward et al 2011) are at highest risk of developing overt cerebral edema. Hyperglycemia raises osmolality of ECF Lowers serum sodium by dilution As insulin corrects hyperglycemia, serum sodium should rise Failure of serum sodium to rise appropriately may be sign of increased risk for cerebral edema 8

9 For each 100 mg /dl increase in blood glucose, serum Na+ will measure 1.6 meq/dl lower If glucose is 497,serum sodium may be 132 for our patient on lab results All pts in DKA are potassium depleted Insulin and correction of acidosis will drive K+ back into cells Serum K+ levels will drop Almost all pts will require K+ replacement Close monitoring is needed 9

10 Prevent depletion of RBC 2,3 DPG which will improve tissue oxygenation as acidosis is resolving May be useful in patients with anemia, CHF, pneumonia, hypoxia Phosphate therapy increased 2,3 DPG in treated group at 48 hrs. (N/S) Glucose and acidosis rates of correction were not improved Treated group had significantly lower plasma ionized calcium Tetany has been reported in pediatric patients given all replacement as KPO4 Fisher and Kitabihi

11 Correct dehydration IV Fluids Stop catabolism/ restore normoglycemia Insulin Correct electrolytes replacement (Na, Cl, K, phos) Correct acidosis/ reverse ketosis Insulin and IVF, Avoid complications of treatment Establish IV (2 if possible). Labs venous blood gas with electrolytes, CBC, Comp, Magnesium, Phosphorus, HgbA1C. Fluid bolus with isotonic fluids NS - 20ml/kg. Consider repeat 20 ml/kg ONLY if hemodynamics (especially blood pressures) are unstable. Goal of fluid resuscitation is to assure perfusion and restore blood pressure NOT to normalize HR and mentation. NO insulin bolus. NO sodium bicarbonate UNLESS patient hypotensive or in cardiopulmonary arrest. 11

12 Very important to monitor Q1 hour neuro checks in initial resuscitation Cerebral edema is a most worrisome outcome/presentation If concern for neuro status: consider 3%saline bolus (5cc/kg) Recheck blood glucose (hourly) Goal glucose mg/dl. Start/continue insulin infusion DO NOT bolus insulin Regular Humulin Insulin at 0.1 units/kg/hour. Consider start at 0.05 units/kg/hr in infants or toddlers < 3yo with new onset DKA or in patients demonstrating extreme insulin sensitivity. IV fluids with electrolytes at 1.5 x Maintenance 12

13 Infusion rates: If Glucose > 250 run Bag #1 at 100% of ordered fluid rate (1.5 x Maintenance) If Glucose between , run Bag #1 at 50% of ordered fluid rate (0.75 x Maintenance) and Bag #2 at 50% of ordered fluid rate (0.75 x Maintenance) If Glucose between , run Bag #2 at 100% or ordered fluid rate (1.5 x Maintenance) 13

14 Insulin infusion is NOT to be discontinued while the patient is in DKA. For patients with rapidly dropping glucose, dextrose content should be increased so that infusion can be maintained. If, after dextrose concentration is increased, glucose remains low, consider dropping infusion to 0.05 U/kg/hr but all attempts should be made NOT to stop the infusion until DKA is resolved. 14

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16 Treated with above protocol guidelines Time for correction? Up to 24 hours 16

17 In children with diabetes Risk 1-10/100 person years Poor metabolic control/history of DKA Psychiatric disorders Peripubertal and adolescent girls Unstable family situation Pump therapy failure Patients are told to check all three sites Do nut disconnect pump unless sure they are in DKA TROUBLESHOOTING: 1. TUBING 2. INFUSION SET 3.NEEDLE 4.PUMP 17

18 Recognition of DKA Rehydration is important Insulin helps to restore catabolic state and not stopped until DKA resolved Careful monitoring of electrolytes and replacement Risk of Cerebral edema is most concerning 18

19 Koves,IH,Leu,MG et al; Improving Care for Pediatric Diabetic Ketoacidosis. Pediatrics 2014;134;e848 Glaser N,Barnett,P et al; Pediatric Emergency Medicine Collaborative Research Committee of the American Academy of Pediatrics. Risk factors for cerebral edema in children with diabetic acidosis. N Engl J Med 2001;344(4): Wolfsdorf JI,Allgrove J,Craig ME,etal; ISPAD Clinical practice Consensus Guideline 2014 Compendium: Diabetic ketoacidosis and hyperglycemic hyperosmolar state. Pediatr Diabetes 2014(suppl20): Dunger DB,Sperling MA et al; Predicting Cerebral edema during diabetic ketoacidosis. N Engl J Med. 2001;344 (4) Decourcey DD, Steil GM,etal; Increasing use of hypertonic saline over mannitol in the treatment of symptomatic cerebral edema in pediatric diabetic ketoacidosis: an 11-year Retrospective Analysis of Mortality. Pediatric Critical Care Medicine 2013:14(7)