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Diabetic Ketoacidosis

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Text of Diabetic Ketoacidosis

  • Diabetic KetoacidosisTopical Formal PresentationRobert R. ZaidGenesys Regional Medical CenterMichigan State University IV8 June 2004

  • Diabetic KetoacidosisBackgroundOne of the most serious acute metabolic complications of diabetesOccurs more commonly in patients with insulin-dependent diabetes mellitus (IDDM)Mortality rate was 100% in 1922 but has since come down to 5% with improvements in health care

    Kitabchi, A. E., Wall, B. M., Diabetic Ketoacidosis, 1995, Medical Clinics of North America, Vol. 79, 1, pg 9

  • Diabetic KetoacidosisBackgroundDefinitionBlood glucose level > 250 mg/dlBlood pH < 7.3Ketones in serum > 5 meq/L

    Hamdy, O., Diabetic Ketoacidosis, http://www.emedicine.com, 2004, Schade, D. E.

  • Diabetic KetoacidosisBackground Initiating factorsInfection Pneumonia and UTI most commonlyInadequate use of insulinNot taking insulinPump blockageMechanical failure of pumpNew onset diabetesMedical, surgical or emotional stressDrugs: Corticosterioids, thiazide diureticsPancreatitisHamdy, O., Diabetic Ketoacidosis, http://www.emedicine.com, 2004, Schade, D. E.

  • Diabetic KetoacidosisPathogenesisEffects of insulin deficiencyAlterations in metabolismCarbohydrates, protein and lipids affectedFluid and electrolytes

    Kitabchi, A. E., Wall, B. M., Diabetic Ketoacidosis, 1995, Medical Clinics of North America, Vol. 79, 1, pg 9

  • Diabetic KetoacidosisPathogenesis: Alterations in metabolismCaused byIneffectiveness of insulinElevations in glucagon, catecholamines & cortisol

    Hepatic gluconeogenesis, glycogenolysis, and lipolysis are affected by this hormone imbalanceFat, liver and muscle can survive without glucoseBrain must maintain use of glucose for starvation

    Kitabchi, A. E., Wall, B. M., Diabetic Ketoacidosis, 1995, Medical Clinics of North America, Vol. 79, 1, pg 9

  • Diabetic KetoacidosisPathogenesis: Alterations in metabolismCatecholamines (unopposed) Promote triglyceride breakdown to FFA and glycerolStimulates gluconeogenesis

    InsulinInhibits gluconeogenesis

  • Diabetic KetoacidosisPathogenesis: Alterations in metabolismHyperglycemia results fromIncreased gluconeogenesisConversion of glycogen to glucoseInadequate use of glucose by peripheral tissues

    Ketone bodies result fromBeta oxidation of FFADecreased concentrations of malonyl coA (an inhibitor of ketogenesis)

  • Key: G- Glucose AA- Amino Acid FA- Fatty acid KET- Ketones TG- Triglycerides

    FedINFedOUTFastINFastOUTDKAINDKAOUTBrain CellGCO2GCO2GCO2Liver CellGAACO2AAFAGKETAAFAGKETMuscle CellGAACO2FAKETCO2AAFAKETCO2AAFat CellGTGFATGFA

  • Diabetic KetoacidosisPathogenesis: Alterations in metabolismHyperglycemia leads toGlycosuria Polyuria (osmotic diuresis)PolydipsiaPolyphagiaWeight lossDehyrdation

    Ketone bodies lead toMetabolic acidosis

    Kitabchi, A. E., Wall, B. M., Diabetic Ketoacidosis, 1995, Medical Clinics of North America, Vol. 79, 1, pg 16

  • Diabetic KetoacidosisPathogenesis: Fluid and ElectrolytesMajor cause of electrolyte loss is due to osmotic diuresisBrought on by excess excretion of glucoseGlucose is restricted to extracellular space pulling water from intracellular spaceNaCl, K are excreted in the urine followed by massive amounts of waterKitabchi, A. E., Wall, B. M., Diabetic Ketoacidosis, 1995, Medical Clinics of North America, Vol. 79, 1, pg 17

  • Diabetic KetoacidosisPathogenesis: Fluid and ElectrolytesInitially plasma sodium concentrations are low or normal despite water losses due to osmotic shift of water Correction of sodiumAdd 1.6 mEq to plasma sodium for every 100 mg of glucose over 100 mg/dl(i.e. Corrected Na+ = (Plasma glucose-100) / 100 * 1.6)

  • Diabetic KetoacidosisPathogenesis: Fluid and ElectrolytesTotal body potassium depletionLoss equals 5-10 mEq / kg body weightPlasma concentrations may be normal or elevated at time of presentation of DKAWater and K are shifted from intracellular to extracellular spaceAcidosis also causes potassium shiftLack of insulin (a promoter of K uptake)Secondary hyperaldosteronism can increase potassium loss

  • Diabetic KetoacidosisPathogenesis: Fluid and ElectrolytesMetabolic acidosisCaused by buffer deficitInduced by ketoacid dissociation at physiologic pHH+ ions are buffered by HCO3Bicarbonate concentration decreases75% - 85% of ketoanions are reabsorbedKetouriaReabsorbtion is directly related to GFRPatients who take in fluids and NaCl at onset of DKA will have better renal function and more ketoanion excretionMetabolism of ketoacids produces HCO3Therefore, excretion of ketoacids results in loss of potential HCO3

  • Diabetic KetoacidosisDiagnosis of DKAStrong assesment of DKAHistory and physical Hyperglycemia (finger stick)Urine Keto-Diastick (positive for ketones)

    Definitive diagnosisArterial blood gas (pH and bicarbonate) which show a metabolic acidosis

  • Diabetic KetoacidosisDiagnosis of DKA History and physicalClinical presentationPolyuria, polydipsia, weight lossNausea, vomitting, abdominal painPhysical examinationSigns of volume depletionDecreased skin turgorDry axilla and oral mucosaLow jugular venous pressureHypotensionFruity odor (exhaled acetone)Kussmaul respirations

  • Diabetic KetoacidosisDefinitive diagnosis Hyperglycemia>250 mg/dLBicarbonate
  • Diabetic KetoacidosisDefinitive diagnosis - initial workupBlood chemistryGlucose by finger stickBlood and urine ketones (nitroprusside)CBC w/ differentialArterial blood gasUAInfusion of 1 L of 0.9% NaClKitabchi, A. E., Wall, B. M., Diabetic Ketoacidosis, 1995, Medical Clinics of North America, Vol. 79, 1, pg 17

  • Diabetic KetoacidosisTreatment - goalsImprove circulatory volume and perfusionDecrease serum glucoseClear serum of ketoacids at steady rateCorrect electrolyte imbalancesKitabchi, A. E., Wall, B. M., Diabetic Ketoacidosis, 1995, Medical Clinics of North America, Vol. 79, 1, pg 17

  • Diabetic KetoacidosisTreatment - goalsFluid and electrolytesInitial fluid Isotonic saline (restricted to extracellular space)1 L 0.9% saline in first hourPlasma osmolality can be used to estimate severity of dehydration2 (Na+) (mEq/L) + glucose (mg/dL) / 18 + BUN (mg/dL) / 2.8Stupor and coma can occur w/ osmolality > 340 mOsm/kg H20Kitabchi, A. E., Wall, B. M., Diabetic Ketoacidosis, 1995, Medical Clinics of North America, Vol. 79, 1, pg 17

  • Diabetic KetoacidosisTreatment - goalsFluid and electrolytesSubsequent fluid replacementHypotonic saline (0.45% NaCl) at 200 to 1000mL/hIn DKA, H20 loss exceeds NaCl lossHypotonic saline is similar to fluids lost in DKABoth compartments will gradually be replacedDextrose should be added to fluids if glucose < 200 mg/ dLAllow for continued insulin administration until ketonemia is controlledSome studies show that fluid replacement before insulin does not effect the severity of DKAAllows for reductions in blood glucose and potassium concentrations before insulin therapy

    Kitabchi, A. E., Wall, B. M., Diabetic Ketoacidosis, 1995, Medical Clinics of North America, Vol. 79, 1, pg 17

  • Diabetic KetoacidosisTreatment Fluids and electrolytesFluid and electrolytesAdvantages of early rehydrationRestores circulatory volumeDiminish concentration of catecholamines, glucagon

    Complications of fluid therapyExcessive therapy may result in ARDSCerebral edemaHyperchloremic acidosis

    Kitabchi, A. E., Wall, B. M., Diabetic Ketoacidosis, 1995, Medical Clinics of North America, Vol. 79, 1, pg 17

  • Diabetic KetoacidosisTreatment Insulin therapyConscious, non-obtunded patientInitial priming dose0.3 to 0.4 U / kg given IV given SCSubsequent insulinER7 units / hour IVGeneral floorHourly injections of insulin SCEnsures that nurse sees patient on hourly basisICU7 units/ hour IV per hourKitabchi, A. E., Wall, B. M., Diabetic Ketoacidosis, 1995, Medical Clinics of North America, Vol. 79, 1, pg 17

  • Diabetic KetoacidosisTreatment Potassium therapyPotassium decreases after insulin therapyInsulin causes potassium to enter cellsExtracellular fluid volume expansion Resolution of acidemiaNegative potassium balance from DKAHypokalemia is life threateningKitabchi, A. E., Wall, B. M., Diabetic Ketoacidosis, 1995, Medical Clinics of North America, Vol. 79, 1, pg 17

  • Diabetic KetoacidosisTreatment Potassium therapyPotassium should not be added to initial first liter of saline (0.9%)Patients are initially hyperkalemicAddition of K+ without insulin can cause a dangerous increase in extracellular potassiumCardiac arrythmias

    Kitabchi, A. E., Wall, B. M., Diabetic Ketoacidosis, 1995, Medical Clinics of North America, Vol. 79, 1, pg 17

  • Diabetic KetoacidosisTreatment Potassium therapyRequirements for potassium therapyPatient is making urineSerum potassium is less than 5.5Potassium replacement20 to 30 mEq per L of IV fluid2/3 KCL, 1/3 KP04 to replace phosphorusPatients with severe hypokalemia at admission may need more aggressive potassium replacement May need potassium added to first liter of fluidDo not exceed 40 mEq/ hourCheck potassium level every 1 to 2 hours initiallyKitabchi, A. E., Wall, B. M., Diabetic Ketoacidosis, 1995, Medical Clinics of North America, Vol. 79, 1, pg 17

  • Diabetic KetoacidosisTreatment Bicarbonate therapyControversialMost literature shows no benefit to using bicarbonate with patients who have DKANo differences in reduction of glucose or ketoanionMay increase hypokalemiaFor patients with pH < 7.0, they may benefit from bicarbonate therapypH 6.9-7.0 may give 44 mEq of bicarbpH
  • Diabetic KetoacidosisTreatment Phosphate therapyAt presentation serum phosphate may be nor

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