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Dka diabetic ketoacidosis managment

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Text of Dka diabetic ketoacidosis managment

  • DIABETIC KETOACIDOSIS

    PRESENTED BY:

    DR. Eyad Hamad Miskawisupervised by : Dr. Eyas Saleh

  • Definition of Diabetic Ketoacidosis**

  • Pathogenesis of DKAInsulinDeficiencyBeta-cellfailureD/CInsulin Glucotoxicity

  • Carbohydrate Metabolism in DKA Relative or absolute insulin deficiencyglucose output

    glycogenolysisliverglucose uptakemuscle

  • Increased Glucose Production in DKA

  • Increased Production of Ketones in DKALipolysisFFAGlycerolKetogenesisB-OH-BAcetoacetate

    TG

  • Diagnostic Criteria for DKA DKA Mild Moderate SeverePlasma glucose (mg/dl)pHAnion gap Bicarbonate (mEq/l)Urine ketones*Serum ketones*Effective serum Osmol (mOsm/kg)Alteration in sensoriaor mental obtundation

    >2507.25-7.3 >10 15-18positivepositivevariable

    alert>2507.0-1210- 25012

  • Clinical Presentation of DKASignHypothermiaTachycardiaTachypneaKussmaul breathingIleusAcetone breathAltered sensoriumSymptomsPolydipsiaPolyuriaWeaknessWeight lossNausea Vomiting Abdominal painThe onset of DKA is usually relative short, ranging from hours to a day or two.

  • Causes of DKA

    Stressful precipitating event that results in increased catecholamines, cortisol, glucagon.Infection (pneumonia, UTI)AlcoholStrokeMyocardial InfarctionPancreatitisTraumaMedications (steroids)Non-compliance with insulin

  • Immediate determination of blood glucose by finger stick, and serum ketones (3-BH) by finger stick or urinary ketones.

    Laboratory studies:ABGsCBC with differentialCMP (glucose, electrolytes, bicarbonate, BUN, creatinine)Serum ketonesUrinalysis Bacterial cultures*Cardiac enzymes*

    Initial Laboratory Studies* If clinically indicated

  • Replacement of fluids lossesCorrection of hyperglycemia/metabolic acidosisReplacement of electrolytes lossesDetection and treatment of precipitating causesConversion to a maintenance diabetes regimen (prevention of recurrence)Management of DKA

  • Fluid TherapyAssume 10-15% dehydrationBegin with a 10-20 ml/kg bolus of NSReplace calculated deficit evenly over 36 hours - generally 1.5 x maintenance for the next several hours is appropriateDo not exceed 40ml /kg in the initial 4 hoursDouble bag systemNS at 1.5 x M until glucose below 300 mg/dlD10 NS to be mixed with NS to achieve desired glucose concentration

  • Insulin bolus ??Insulin bolus or not ?Insulin should be started about an hour after IV fluid replacement is started to allow for checking potassium levels and because insulin may be more dangerous and less effective before some fluid replacement has been obtained.Although the incidence of life-threatening hypokalemia due to aggressive insulin administration is very low, there is little to no advantage in starting insulin prior to rehydration and evaluation of serum potassium levels. Initial bolus of insulin does not change overall management of DKA

  • Insulin TherapyIV infusion with basal rate 0.1 U/kg/hrIdeal glucose decline is about 50-100 mg/hrContinue insulin until urinary (blood) ketones are cleared and anion gap is closed

  • Blood Glucose monitoring in DKACheck initial blood glucose q1h.Goal decrease in blood glucose is 50-75mg/dl/hrOnce stable(3consecutie values decrease in target range)change blood glucose monitoringq2h.Resume q1h blood glucose monitoring for each change in the insulin infusion rate.Add dextrose5% to IV fluid when blood glucose
  • CHANGING THE INSULIN INFUSION RATEDecrease IV insulin by 50%if blood glucose decrease by >100mg/dl/hr in any 1hr periodIncrease insulin drip by 50%/hr if change in blood glucose is
  • Transition to Subcutaneous InsulinPatients with DKA should be treated with IV insulin until ketoacidosis is resolved.

    Criteria for resolution of DKA:BG 200 mg/dLSerum bicarbonate level 18 mEq/LVenous pH 7.3 and anion gap closed

  • WHEN TO STOP IV INSULINWhen the condition is stable, pH exceeds 7.3, and bicarbonate is greater than 18 mEq/L, the patient is allowed to eat a meal preceded by the usual subcutaneous (SC) dose of regular insulin.

  • Potassium replacement

  • SodiumPseudohyponatremia, add 1.6 mEq of Na to every 100mg/dL of glucose above normal Expect that the Na+ level will rise during treatmentIf Na+ does not rise, true hyponatremia may be present (risk of cerebral edema) and should be treated

  • Bicarbonate Bicarbonate should be used only when there is severe depression of the circulatory system or cellular metabolism Not recommended unless pH 7.0 Bicarbonate administration leads to increased cerebral acidosisHCO3- + H+ = CO2 + H2O. Bicarbonate passes the BBB slowly CO2 diffuses freelyexacerbating cerebral acidosis and cerebral depression

  • Bicarbonate Bicarbonate should be used only when there is severe depression of the circulatory system or cellular metabolism Not recommended unless pH
  • A 10 y/o male (~30 kg) presents to the ED with a one-day history of emesis and lethargy.Vitals show T 37C, HR 110, RR 25, BP 99/65. Patient is lethargic, but oriented. Exam reveals the odor of acetone on the breath, dry lips, but otherwise unremarkableLabs: pH 7.05, PaCO2 20, HCO3 9 , PaO2 100, BE -20, Na+ 133, K + 5.2, Cl 96, CO2 8, BS 600. Urine shows 4+ glucose and large ketonesCase Scenario #1

  • How much fluid would you administer as a bolus?What is the value of anion gap ? Would you administer bicarbonate?What is the true serum sodium?How much insulin would you administer?What IVF would you start? At what rate?Case Scenario #1

  • Answers 600 cc over 20 min28 highNo cardiovascular collapse and therefore there is no justification for the administration of bicarbonate.

    133 +(600-100)= 1420.1*30= 3u/hr1.5*(10*100+10*50+10*20)= 2550cc q 24 hrs

  • Pearls on DKADiagnosis : pH < 7.3 , RBS > 300, Hco3 < 15Correct dehydration over 48 hours Bolus fluid only with hemodynamic compromise Sodium bicarbonate when pH
  • THANK YOU

    ********10 - 20 cc/kg bolus of NS would be adequate. Though the patient is dehydrated (dry lips), his hemodynamics are good, with acceptable vitals and good perfusion. There would be no reason to administer more than 20 cc/kg fluids.

    While this patient is clearly acidemic, he is NOT in impending cardiovascular collapse and therefore there is no justification for the administration of bicarbonate. In fact, administration of bicarbonate has been associated with the development of cerebral edema.

    The true serum sodium is 143 133 + 0.016[700-100]

    Insulin is generally started at 0.1 u/kg/hr. Therefore, in this 30 kg patient, an insulin infusion of 3 u/hr of regular insulin should be initiated.

    IVF of 2/3 NS or NS should be started at ~ 2400 cc/m2/day, which is approximately 1.5 x maintenance

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