1017 e1 eT A B LE 85 1 La b o ra to ry M o n it o ri n g S ch ed u le R ec o m m en d at io n La bo ra to ry A na ly si s DK A Co nfi rm ed Ho ur 1 Ho ur 2 Ho ur 3 Ho ur 4 Ho ur 5 Ho ur 6 Ho ur 7 Ho u[.]
X X X X X BUN Creatinine Magnesiumc X Hour X X X Hour X Hour X X X X X X X X X Hour X Hour If the patient has fever or other symptoms suggesting infection, blood cultures, chest radiograph, and urinalysis should be considered Bacterial infections, however, are infrequent causes of DKA in children bOHB, b-Hydroxybutyrate; BUN, blood urea nitrogen; DKA, diabetic ketoacidosis a Repeat glucose every hour while on insulin drip; send first glucose to the lab as well for serum glucose b Repeat sodium and bOHB every hours while on insulin drip When bOHB measurement is not available or is impractical, calculation of the anion gap can also be used to track resolution of DKA c May repeat these labs every hours until normalized, especially while on insulin drip X X X X X X X X X X Hour bOHBb X Hour X X X X X X X Hour X X X X Hour Blood gas (capillary, venous, or arterial) Phosphorus Calcium X X Bicarbonate c X Chloride c X Potassium Sodium Glucose b DKA Confirmed a Laboratory Analysis eTABLE Laboratory Monitoring Schedule Recommendation 85.1 X X X Hour 10 X Hour 11 X X X Hour 12 1017.e1 1018 S E C T I O N V I I I Pediatric Critical Care: Metabolic and Endocrine DKA in adolescents treated with intensive management regimens was 2.8 per 100 patient-years, significantly lower than the incidence in those treated conventionally (4.7 per 100 patient-years) Although this is an older study, it was a time- and resource-intensive study representing a more idealized situation than often encountered in the overall pediatric diabetes population.46 In a more recent study from the Barbara Davis Center for Childhood Diabetes in Denver, the overall incidence of DKA was per 100 person-years In that study, factors associated with higher incidence included older age, higher HbA1C (relative risk [RR] of 1.68 per 1% increase in HbA1C in younger children and 1.43 in older children), higher reported insulin dose, Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM-4) psychiatric diagnoses, and “underinsurance” reflecting lower socioeconomic status.47 A multinational study based on registries and audits showed DKA frequency at 5% in Austria and Germany, 6.4% in England and Wales, and 7.1% in the United States 48 In some studies, DKA is documented to occur with a two- to fivefold increased risk in children and adolescents on continuous subcutaneous insulin infusion therapy (CSII) compared with subcutaneous injections, particularly in the first year of initiation of CSII.48,49 However, lower rates of DKA are achievable for those on CSII with adequate training and resources T2DM has been occurring with increasing frequency in older children and adolescents Certain racial/ethnic groups in the United States are disproportionately affected, including Native Americans, Hispanics, and African Americans DKA can be the clinical presentation of T2DM in youth, estimated at 5% to 10%.34 Youth with T2DM may also present with hyperglycemic hyperosmolar syndrome (HHS), also referred to as hyperosmotic hyperglycemic nonketotic coma (described more fully later) Morbidity and Mortality Associated With Diabetic Ketoacidosis Mortality in children presenting with DKA is approximately 0.25% to 0.30%.45 Most of the mortality in DKA occurs in children with cerebral edema, accounting for 57% to 87% of deaths Neurologic sequelae of DKA are described later Other causes of morbidity and mortality include sepsis and secondary infection, electrolyte abnormalities (e.g., hypokalemia), arrhythmias, rhabdomyolysis, cerebral infarction, thrombosis, pneumomediastinum, subcutaneous emphysema, and pulmonary edema Management Guidelines (Fig 85.1) Fluids Restoration of adequate peripheral perfusion and hemodynamic stability with bolus administration of IV fluids (0.9% saline or other isotonic fluids) should begin as soon as possible Typical patients require an initial fluid bolus of 10 to 20 mL/kg Repeated boluses may be necessary if ongoing hemodynamic instability is present Studies have shown that clinical assessments of dehydration severity in children with DKA tend to be inaccurate.50–52 The average degree of dehydration for most patients is approximately 7% to 9% of body weight This figure should be used as a basis for determining the total volume of fluids to be replaced The estimated fluid deficit, along with maintenance fluid requirements, should be replaced over 24 to 48 hours using 0.45% to 0.90% saline, generally initially with 0.90% saline, then transitioning to 0.45% saline after several hours Replacement of ongoing urinary fluid losses is usually unnecessary because osmotic diuresis typically resolves rapidly after beginning DKA treatment However, in circumstances of persistently high urine output, or profuse vomiting or diarrhea, replacement of ongoing losses may be considered Whether variations in IV fluid administration protocols might contribute to risk of cerebral injuries resulting from DKA has been a topic of debate A recent large prospective multicenter study, the Pediatric Emergency Care Applied Research Network (PECARN) Fluid Therapies Under Investigation in DKA (FLUID) Trial, assessed neurologic and neurocognitive outcomes of children with DKA treated with fluid regimens that varied in rate of administration and sodium content.53,54 This study found no differences in acute or postrecovery outcomes of children treated with 0.45% versus 0.90% NaCl content fluids nor in children treated with more rapid versus slower fluid infusions The study findings suggest that a range of fluid protocols can be safely used to treat children with DKA and that fluid infusions should not be restricted because of concerns about causing cerebral injury (CI) IV fluid administration should be adjusted according to each patient’s hemodynamic state and fluid balance Insulin Insulin should be administered intravenously via continuous infusion An infusion rate of 0.1 U/kg per hour is typically used Lower insulin dosages (0.025–0.05 U/kg per hour) are used in some centers To date, there have been few studies comparing standard insulin dosages with lower dosages These studies generally have not found substantive differences in outcomes but have involved small sample sizes or have been retrospective and nonrandomized.55,56 A larger prospective study is necessary Insulin administration results in resolution of acidosis and hyperglycemia via suppression of ketogenesis and hepatic glucose output (gluconeogenesis) and promotion of peripheral glucose uptake An initial bolus or loading dose of insulin is not recommended Maximal suppression of ketogenesis is achieved rapidly with an insulin infusion (0.05–0.10 U/kg per hour).56–58 Even in the absence of insulin administration, the serum glucose concentration often decreases substantially with initial rehydration, reflecting improvements in renal perfusion and decreased counterregulatory hormone concentrations.15 This decline in glucose concentration during the initial period of rehydration should not be interpreted as indicating excessive insulin administration Serum glucose concentrations typically normalize before ketosis and acidosis resolve To continue insulin administration at dosages sufficient to allow resolution of ketosis, dextrose should be added to the IV fluids Transition to dextrose-containing fluids should occur when the serum glucose concentrations decline below approximately 250 mg/dL The “two-bag system” for dextrose administration allows a rapid response to changes in serum glucose concentration and is cost-effective.59 Two bags of IV fluids with identical electrolyte content but different dextrose content (0% and 10%) are administered simultaneously with the relative rates of administration frequently adjusted to increase or decrease the dextrose concentration while maintaining a constant overall rate of administration of fluid and electrolytes Electrolytes Serum potassium concentrations often decline rapidly during treatment and potassium replacement is mandatory Typical 1019 CHAPTER 85 Diabetic Ketoacidosis DIABETIC KETOACIDOSIS (DKA) PATHWAY OVERVIEW PHASE 1: Early electrolyte adjustment/rehydration Assessment DKA suspected -Monitor GCS and neurological status every hour up to 24 hours if presenting pH