Pediatrics Diabetic Ketoacidosis (DKA) from Primary to Intensive Care Wendy Nasser MSN, CPNP-AC/PC Mark Riccioni MSN, CPNP-AC/PC

Pediatrics We have no conflicts of interest to disclose

Page 2 xxx00.#####.ppt 9/21/2015 5:28:21 AM Pediatrics Objectives 1. Describe classic signs and symptoms of DKA in the new onset diabetic. 2. Summarize pertinent lab studies and acute management of DKA. 3. Identify the diabetic child in crisis 4. Describe various fluid management options 4.Explain the role of parental involvement in the care of puberty-aged diabetic children and the effect of decreased readmissions.

Page 3 xxx00.#####.ppt 9/21/2015 5:28:21 AM Pediatrics Case Study

Page 4 xxx00.#####.ppt 9/21/2015 5:28:21 AM Pediatrics Let’s talk about pathophysiology Diabetes Mellitus (DM) is a syndrome that occurs secondary to the body’s inability to maintain energy homeostasis. DM type 1 results from insulin deficiency caused by autoimmune destruction of islet cells in the pancreas and is then manifested by decreased uptake of glucose resulting in high serum glucose.

Page 5 xxx00.#####.ppt 9/21/2015 5:28:21 AM Pediatrics A closer look at Pathophysiology of DM type 1 Due to lack of insulin hormone, Glucose draws water into the serum and into the kidneys. As the osmotic force of glucose builds in the kidneys (above 180), urine output increases (polyuria) and thirst is sensed (polydypsia) along with hunger (polyphagia) and weight loss occurs. As the body becomes more and more dehydrated, increased release of Growth Hormone, Glucagon and epinephrine ensues. Breakdown of fat stores and creation of ketones then results from the imbalance between catabolic (glucagon and epinephrine) and anabolic (insulin) hormones. The buildup of ketones results in ketoacidosis The body senses stress (i.e. acidosis, hyperglycemia, lactic acidosis and poor tissues perfusion) and responds by releasing cortisol, catecholamines and more growth hormone. The worsening imbalance restarts the cycle and the patient becomes more and more intravascularly depleted and symptomatic.

Page 6 xxx00.#####.ppt 9/21/2015 5:28:21 AM Pediatrics Pathophysiology: DM type 2 typically results from insulin resistance and relative insulin deficiency leading to abnormal metabolism of carbohydrates, protein and fat. Type 2 is becoming more prevalent in children with obesity on the rise.

Page 7 xxx00.#####.ppt 9/21/2015 5:28:21 AM Pediatrics Diabetic Ketoacidosis is the most common endocrine metabolic disorder in childhood and adolescence(add bar graph)

Page 8 xxx00.#####.ppt 9/21/2015 5:28:21 AM Pediatrics When all the of the symptoms coalesce Severity on presentation dictates treatment of DKA and degree of treatment required… pH 7.15 HCO3 > or < then 10 Glasco Coma Score (GCS<13) Respiratory status Level of dehydration Electrolyte derangements Age less than 5

Page 9 xxx00.#####.ppt 9/21/2015 5:28:21 AM Pediatrics We can’t forget to correct for lab values! Corrected Na+= Na x (Glucose-100) Osmolarity = 2x (Na+) + (Glu/18) + (BUN/2.8) K+ elevated in 1/3 of cases, do not add to IV fluids if no UOP or serum K+>5.5

Page 10 xxx00.#####.ppt 9/21/2015 5:28:21 AM Pediatrics Fluid Protocol Controversies The common concern during DKA treatment is the potential risk of brain injury to the patient as he/she undergoes correction of acidosis resulting in fluid shifts in the brain In the US, treatment of DKA across institutions varies widely with different fluid protocols in place and no consensus on which protocol is best at protecting patients from harm.

Page 11 xxx00.#####.ppt 9/21/2015 5:28:21 AM Pediatrics But is it all about lab correction? Lab values can be corrected…over time The true question is: can we protect the affected children from the effects of DKA and improve their brain’s recovery and development?

Page 12 xxx00.#####.ppt 9/21/2015 5:28:21 AM Pediatrics Scan and Insert cover of DKA study paper here

Page 13 xxx00.#####.ppt 9/21/2015 5:28:21 AM Pediatrics Concerning data 1% of patients in DKA have clinically overt signs of cerebral edema 50% of affected children die or sustain permanent neurological injury. (Ref 5, 6 from k&G)

Page 14 xxx00.#####.ppt 9/21/2015 5:28:21 AM Pediatrics DKA Fluid Protocol (Kuppermann and Glaser) 2011 Reported that Cerebral edema (CE) resulting from diabetic ketoacidosis (DKA) is the most frequent diabetes-related cause of death in children. Ref (2,4 from k &g)

Page 15 xxx00.#####.ppt 9/21/2015 5:28:21 AM Pediatrics Kuppermann and Glaser’s Preliminary Animal Studies Data from rat studies suggested that decreased cerebral blood flow during DKA may be part of the cause behind DKA-related brain injury The rat models also indicated that the brain metabolic state actually worsens initially during DKA treatment, theorized to be a result of reperfusion injury

Page 16 xxx00.#####.ppt 9/21/2015 5:28:21 AM Pediatrics CT evidence of cerebral edema (Krane, 1985)

Page 17 xxx00.#####.ppt 9/21/2015 5:28:21 AM Pediatrics What is the cause of Cerebral Edema? The study aims to look at the two varying treatment strategies 1. Conservative fluid therapy protocols: CE may result from osmotic shifts caused by rapid rehydration with intravenous fluids drives 2. More liberal and rapid correction of DKA: Cerebral hypo- perfusion may play a prominent role in the development of cerebral injury and CE Best practice has not yet been determined

Page 18 xxx00.#####.ppt 9/21/2015 5:28:21 AM Pediatrics Aspiring for Safe Change Several institutions across the country are currently collaborating in Kuppermann and Glaser’s study with the overall goal to optimize DKA treatment and prevent neurological injury. The hope is that collaboration of data acquisition will improve therapy and enhance long-term neurocognitive outcomes for children with diabetes

Page 19 xxx00.#####.ppt 9/21/2015 5:28:21 AM Pediatrics Determining “best practice” is complicated at best Children in the study are assigned to one of several fluid protocols all of which are used at some hospitals in the US The aim is to determine which protocol has the best outcomes while nothing new or “experimental” is utilized

Page 20 xxx00.#####.ppt 9/21/2015 5:28:21 AM Pediatrics DKA Fluid Study Protocol Kuppermann and Glaser A1A2B1B2 Standard bolus10cc/kg NS Additional bolus 10cc/kg NS Assumed fluid deficit 10% of body weight 5% of body weight Deficit replacement ½ over 12 hrs, ½ over next 24 hrs (plus maintenance) evenly over 48 hrs (plus maintenance) Fluid for deficit replacement ½ NSNS½ NSNS

Page 21 xxx00.#####.ppt 9/21/2015 5:28:21 AM Pediatrics DKA Fluid Study Overview: Child is diagnosed with DKA and consented to participate in study Child is randomized to 1 of 4 fluid treatment protocols Child’s mental status is closely monitored for overt signs of cerebral edema or DKA complications DKA is converted and treatment terminated 3-month follow up for neurocognitive testing is obtained

Page 22 xxx00.#####.ppt 9/21/2015 5:28:21 AM Pediatrics Traditional Texas Children’s Hospital DKA Protocol The Two-Bag System

Page 23 xxx00.#####.ppt 9/21/2015 5:28:21 AM Pediatrics Calculating IVF rate in DKA Determine the number of IV boluses the patient received prior to start of correction Subtract the total amount of fluid given from the total 24h volume to be given for correction (2500/m2/d – total IV boluses)=correction volume to be given in 24h. Divide the result by 24 to reveal the hourly rate in ml/h

Page 24 xxx00.#####.ppt 9/21/2015 5:28:21 AM Pediatrics TCH 2-bag system protocol Bag A: LR + KPO4 2mmol/100ml + KCL 1.5mEq/100ml Bag B: D10LR + KPO4 2mmol/100ml + KCL 1.5mEq/100ml Total IVF ml/h= Bag A ml/h + Bag B ml/h dependent on blood glucose Blood Glucose >300__ml/h (100% bag A) __ml/h (75% bag A) __ml/h (25% bag B) __ml/h (50% bag A) __ml/h (50% bag B) __ml/h (25% bag A) __ml/h (75% bag B) Blood Glucose <150__ml/h (100% bag B)

Page 25 xxx00.#####.ppt 9/21/2015 5:28:21 AM Pediatrics Insulin Administration Insulin drips are recommended for patients less than or equal to 5yo if HCO3 </=15mEq/L or if </= 12mEq/L and older than 5 years of age Recommended dose is 0.1units/kg/hr If patient is less than 5 years of age or “Hyper osmolar” the recommended dose is 0.05units/kg/hr

Page 26 xxx00.#####.ppt 9/21/2015 5:28:21 AM Pediatrics Extenuating Circumstances that Affect the Titration of Correction When pH is not improving, the insulin gtt may have to be titrated up If glucose is decreasing too quickly (more than 100mg/dL per hour), the correction must be slowed down and the patient must be monitored closely

Page 27 xxx00.#####.ppt 9/21/2015 5:28:21 AM Pediatrics Intensive Monitoring Labs required for IVF titration and correction: Gucose q1h Lytes q2h x2 then q4h Initial blood gas Q1h vitals and neuro vitals Strict I&Os

Page 28 xxx00.#####.ppt 9/21/2015 5:28:21 AM Pediatrics Insulin Administration Without mental status changes on initial presentation, subcutaneous insulin can be given if HCO3 is greater than 15mEq/L in patients 5yo or younger, or greater than 12mEq/L in patients older than 5yo If 2-bag system is required, once HCO3 is greater than or equal to 15, the patient can be converted to subcutaneous therapy

Page 29 xxx00.#####.ppt 9/21/2015 5:28:21 AM Pediatrics The role of parental involvement in the care of puberty-aged diabetic children and the effect of decreased readmissions

Page 30 xxx00.#####.ppt 9/21/2015 5:28:21 AM Pediatrics Criteria for Discharge Corrected acidosis and return to “neurological baseline” Completion of Diabetes education and agreement of responsible adult who assumes responsibility of minor’s welfare Completed Endocrine Social Work consult to determine barrier to resources and medications Follow up appointment is scheduled with Endocrinologist

Page 31 xxx00.#####.ppt 9/21/2015 5:28:21 AM Pediatrics Case Study

Page 32 xxx00.#####.ppt 9/21/2015 5:28:21 AM Pediatrics Questions??

Page 33 xxx00.#####.ppt 9/21/2015 5:28:21 AM Pediatrics Bkgd 255 Text/Lines Shadows 128 Title Text 255 Fill Fill Accent Accent Primary Palette Starter Page 1 [36pt bold] palette/guides Text [Arial 28pt] ‐ Text [Arial 22pt] Text [Arial 22pt] Work area (Guide set 2.87)   Work area (Guide set 2.27) Work area  (Guide set 4.51) Work area (Guide set 4.51)  Guide for Title and Appendix page  (Guide set 1.38) Doc ID, Time stamp and page number only shows up in grayscale printing, location is here, to edit go into slide master, this info will appear on every page, except Cover and Appendix pages 

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