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Diabetic Ketoacidosis Management

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Diabetic Ketoacidosis Management. Heidi Chamberlain Shea, MD Endocrine Associates of Dallas. Goals of Discussion. Pathophysiology of DKA Biochemical criteria for DKA Treatment of DKA Prevention of DKA Hyperosmolar Nonketoic Syndrome. Epidemiology. Annual incidence in U.S. - PowerPoint PPT Presentation

Text of Diabetic Ketoacidosis Management

  • Diabetic Ketoacidosis ManagementHeidi Chamberlain Shea, MDEndocrine Associates of Dallas

  • Goals of DiscussionPathophysiology of DKABiochemical criteria for DKATreatment of DKA Prevention of DKAHyperosmolar Nonketoic Syndrome

  • EpidemiologyAnnual incidence in U.S. 5-8 per 1000 diabetic subjects2.8% of all diabetic admissions are due to DKAOverall mortality rate ranges from 2-10%Higher is older patients

  • DKAPrecipitating FactorsFailure to take insulinFailure to increase insulinIllness/InfectionPneumoniaMIStrokeAcute stressTraumaEmotional

    Medical StressCounterregulatory hormonesOppose insulinStimulate glucagon releaseHypovolmemiaIncreases glucagon and catecholaminesDecreased renal blood flowDecreases glucagon degradation by the kidney

  • Diabetic KetoacidosisDue to:Severe insulin deficiencyExcess counterregulatory hormonesGlucagonEpinephrineCortisolGrowth hormone

  • Role of InsulinRequired for transport of glucose intoMuscleAdiposeLiverInhibits lipolysisAbsence of insulinGlucose accumulates in the bloodLiver Uses amino acids for gluconeogenesisConverts fatty acids into ketone bodiesAcetone, Acetoacetate, -hydroxybutyrateIncreased counterregulatory hormones

  • Counterregulatory Hormones - DKA

  • Insulin DeficiencyGlucose uptakeProteolysisLipolysisAmino AcidsGlycerolFree Fatty AcidsGluconeogenesisGlycogenolysisHyperglycemiaKetogenesisAcidosisOsmotic diuresisDehydration

  • Signs and Symptoms of DKAPolyuria, polydipsiaEnuresisDehydrationTachycardiaOrthostasisAbdominal painNauseaVomiting

    Fruity breathAcetoneKussmaul breathingMental status changesCombativeDrunkComa

  • Lab FindingsHyperglycemiaAnion gap acidosis(Na + K) (Cl + Bicarb) >12Bicarbonate
  • Differential Diagnosis Anion Gap AcidosisAlcoholic ketoacidosisLactic acidosisRenal failureEthylene glycol or methyl alcohol poisoningStarvation in late pregnancy or lactation (rare)

  • Atypical PresentationsDKA can be present with BS
  • Treatment of DKAInitial hospital managementReplace fluid and electrolytesIV Insulin therapyGlucose administrationWatch for complicationsDisconnect insulin pumpOnce resolvedConvert to home insulin regimenPrevent recurrence

  • Treatment of DKAFluids and ElectrolytesFluid replacementRestores perfusion of the tissuesLowers counterregulatory hormonesAverage fluid deficit 3-5 litersInitial resuscitation1-2 liters of normal saline over the first 2 hoursSlower rates of 500cc/hr x 4 hrs or 250 cc/hr x 4 hours When fluid overload is a concernIf hypernatremia develops NS can be used

  • Treatment of DKAFluids and ElectrolytesHyperkalemia initially presentResolves quickly with insulin dripOnce urine output is present and K
  • Treatment of DKAInsulin TherapyIV bolus of 0.1-0.2 units/kg (~ 10 units) regular insulinFollow with hourly regular insulin infusionGlucose levels Decrease 75-100 mg/dl hourMinimize rapid fluid shiftsContinue IV insulin until urine is free of ketones

  • Treatment of DKAGlucose AdministrationSupplemental glucoseHypoglycemia occursInsulin has restored glucose uptake Suppressed glucagonPrevents rapid decline in plasma osmolalityRapid decrease in insulin could lead to cerebral edemaGlucose decreases before ketone levels decreaseStart glucose when plasma glucose
  • Insulin-Glucose Infusion for DKA

  • Complications of DKAInfectionPrecipitates DKAFeverLeukocytosis can be secondary to acidosisShockIf not improving with fluids r/o MIVascular thrombosisSevere dehydrationCerebral vesselsOccurs hours to days after DKAPulmonary EdemaResult of aggressive fluid resuscitation

    Cerebral EdemaFirst 24 hoursMental status changesTx: MannitolMay require intubation with hyperventilation

  • Once DKA ResolvedTreatmentMost patients require 0.5-0.6 units/kg/dayPubertal or highly insulin resistant patients0.8-1.0 units/kg/dayLong acting insulin1/2-2/3 daily requirementNPH, Levemir or LantusShort acting insulin1/3-1/2 given at mealsRegular, Humalog, Novolog or ApidraGive insulin at least 2 hours prior to weaning insulin infusion.

  • Prevention of DKASick Day RulesNever omit insulinCut long acting in halfPrevent dehydration and hypoglycemiaMonitor blood sugars frequentlyMonitor for ketosisProvide supplemental fast acting insulinTreat underlying triggersMaintain contact with medical team

  • Goals of DiscussionPathophysiology of DKABiochemical criteria for DKATreatment of DKA Prevention of DKAHyperosmolar Nonketoic Syndrome

  • Hyperosmolar Nonketotic SyndromeExtreme hyperglycemia and dehydrationUnable to excrete glucose as quickly as it enters the extracellular spaceMaximum hepatic glucose output results in a plateau of plasma glucose no higher than 300-500 mg/dlWhen sum of glucose excretion plus metabolism is less than the rate which glucose enters extracellular space.

  • Hyperosmolar Nonketotic SyndromeExtreme hyperglycemia and hyperosmolarityHigh mortality (12-46%)At riskOlder patients with intercurrent illnessImpaired ability to ingest fluidsUrine volume fallsDecreased glucose excretionElevated glucose causes CNS dysfunction and fluid intake impairedNo ketonesSome insulin may be presentExtreme hyperglycemia inhibits lipolysis

  • Hyperosmolar Nonketotic Syndrome PresentationExtreme dehydrationSupine or orthostatic hypotensionConfusion comaNeurological findingsSeizuresTransient hemiparesisHyperreflexiaGeneralized areflexia

  • Hyperosmolar Nonketotic Syndrome PresentationGlucose >600 mg/dlSodiumNormal, elevated or lowPotassiumNormal or elevatedBicarbonate >15 mEq/LOsmolality >320 mOsm/L

  • Hyperosmolar Nonketotic Syndrome TreatmentFluid repletionNS 2-3 liters rapidlyTotal deficit = 10 litersReplete in first 6 hoursInsulinMake sure perfusion is adequate Insulin drip 0.1U/kg/hrTreat underlying precipitating illness

  • Clinical ErrorsFluid shift and shock Giving insulin without sufficient fluidsUsing hypertonic glucose solutionsHyperkalemiaPremature potassium administration before insulin has begun to act HypokalemiaFailure to administer potassium once levels fallingRecurrent ketoacidosis Premature discontinuation of insulin and fluids when ketones still presentHypoglycemiaInsufficient glucose administration

  • ConclusionSuccessful management requiresJudicious use of fluidsEstablish good perfusionInsulin dripSteady declineComplete resolution of ketosisElectrolyte replacementFrequent neurological evaluations High suspicion for complicationsDetermine etiology to avoid recurrent episodes

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