Dka in pregnancy

z4th triage visit with complaint of nausea & zAnti-emetics not workingzRecently treated for UTI, but delayed in zType I DM diagnosed age 21zInitial diagnosis of DKA in pregnancyzMultiple admissions with DKAzPoor compliance 1. 1997 SVD 2. 1999 primary LTCS secondary to failure zFamily Hx: NonezSocial Hx: No toxic habits zMedications: {Lantus 27 units qhs {NovoLog 13 units qac {Macrobid 100 mg daily (day 2 of her course) { MSAFP within normal limits{ 24-hour urine protein 154 mg{ Hemoglobin A1C of 5.2 zPatient was comfortable and in no distresszVS: T 37.1 P 96 BP 124/68 R 22 zPositive fetal heart tones zWeight 75 kgzSerum glucose 163 mg/dL zUrine dip +glucose zHyperemesiszOndansetron and IV normal salinezBlood sample unable to be drawn after hours of hydration and was discharged home zReturns to triage same dayzComplaints of nausea and vomiting, zOn further questioning, reports increase in urinary frequency and general malaise over the past few days zBecause of her nausea and vomiting this zDyspnic, alert and oriented x 3zVS: T 37.4 P 118 BP 102/55 R 41 zOxygen saturation 99% zPositive fetal heart toneszHEENT: Oral mucous membranes zLungs: clear to auscultation bilaterally zBack: no CVA tenderness zAbdomen: soft, nontender, nondistended, zExtremities: no edemazSerum glucose 413 mg/dL z CBC: Wbc 23 Hct 32 Plt 358 bands 13 (↑)z Electrolytes: Na 135 K 3.9 Cl 109 HCO3 10 z Anion gap 19
z ABG: pH 7.18 PaCO2 18 HCO3= 7; PaO2=
z Base excess -20
z Urinalysis: +Leuk, +glucose, +ketones, -nitrite
z EKG: sinus tachycardia with a few nonspecific
z Describe the major metabolic changes of DKAz Describe the major causative factors for DKAz List clinical signs and symptoms of DKAz Choose laboratory and diagnostic studies z Discuss medical management of DKAz Discuss potential complications and prognosis to zIV fluid 1000mL NS for one hour zContinuous IVF half NS at 250ccz10 unit bolus of insulin continued at 5 units zIntravenous antibioticzSerum glucose checked hourly zDextrose added to IVF when serum z Hydration was continued until acidosis resolvedz Serum phosphate and potassium were replacedz Started on a diabetic diet and resumed z Ultrasound performed showing a live fetus z Presumed cause of DKA from an untreated UTI z Discharged home hospital day #4 in stable {Case reports on gestational DM and type II DM zLack of insulin or insulin utilization at zDerangement of carbohydrate, protein and (glucagon, catecholamines, cortisol, growth hormone) zHyperglycemiazMetabolic acidosis zElevated plasma ketones zDehydration INSULIN DEFICIENCY
z Hyperventilation (increase in minute ventilation z Mild respiratory alkalosis z Increase in urinary excretion of bicarbonate z Emesis (common in first trimester) induces z Decrease insulin sensitivity (56% at 36 weeks placental lactogen, progesterone, and cortisol) z State of accelerated starvation (metabolism is modified to breakdown fats over carbohydrates) zInfectionzStresszEmesiszPoor compliancezUndiagnosed diabetes zHyperglycemia (>250 mg/dL)zAcidosis (arterial pH <7.3)zAnion gap (>12 mEq/L)zIncreased base deficit (>4 mEq/L)zKetonemia (≥1:2 dilution)zSome patients (36 percent in one series) may zPerinatal mortality has dropped from about zHypoxemia (volume depletion and acidosis may lead to decreased uterine blood flow) zMetabolic acidosis (glucose and ketones {Absence of baseline heart rate variability{Persistent late decelerations {Non-reassuring biophysical profile maternal condition has been shown to improve the fetal status z Emergency cesarean delivery could worsen the maternal condition and should be avoided z After having corrected the maternal metabolic condition, a non-reassuring fetal heart rate may require intervention.
zVolume replacement (saline) zStop ketogenesis (insulin)zElectrolyte replacement zManagement of acid-base disturbancezIdentify and treat underlying cause { 1000mL 0.9% NaCl over one hour { 500mL 0.45% NaCl next four to six hours { 250mL 0.45% NaCl { Add 5% dextrose when serum glucose reaches 250- { Correct 75% of estimated fluid deficit over first 24 { Continue IV fluid until acidosis is corrected (base { 0.1-0.2 units/kg regular insulin IV bolus followed continuous infusion at a rate of 5-10 units/hour { Goal of therapy is a reduction of glucose by about 75 { If glucose does not decrease by 20% within first 2 { May decrease to 2 units/hour when serum glucose { Maintain between 4 and 5 mEq/L{ If normal value, may add 20 mEq/L to fluid to maintain { Serum potassium initially may be normal or high because of a shift from the intracellular to extracellular space due to hyperosmolality and acidosis { Potassium should not routinely be given in initial fluids because in a volume contracted state with no insulin present it can rise quickly and cause arrhythmias z Search for precipitating causez Check serum glucose hourlyz Check arterial blood gas, electrolytes, and z Careful monitoring of vital signs, urine z Fetal monitoring if over 24 weeks’ gestation z Carroll MA, Yeomans, ER. Diabetic ketoacidosis in pregnancy. Crit Care z Maislos M, Harman-Bohem I, Weitzman S. Diabetic ketoacidosis. A rare complication of gestational diabetes. Diabetes Care 1992;16:661–2 z Bernstein IM, Catalano PM. Ketoacidosis in pregnancy associated with the parenteral administration of terbutaline and betamethasone: a case report. J z Catalano PM, Tyzbir ED, Roman NM, et al. Longitudinal changes in insulin release and insulin resistance in nonobese pregnant women. Am J Obstet z Laffel L: Ketone bodies: A review of physiology, pathophysiology, and application of monitoring to diabetes. Diab Metab Res Rev 1999; 15:412– z Cullen, MT, Reece, EA, Homko, CJ. The changing presentations of diabetic ketoacidosis during pregnancy. Am J Perinatol 1996; 13:449 z Chaunhan SP, Perry KG JR et al. Diabetic ketoacidosis complicating pregnancy. J Perinatol. 1996 May-Jun;16(3 Pt 1):173-5
z Chauhan SP, Perry KG Jr. Management of diabetic ketoacidosis in the obstetric patient. Obstet Gynecol Clin North Am 1995;22:143–55 z Hughes AB: Fetal heart rate changes during diabetic ketosis. Acta Obstet z Hagay AJ, Weissman A, et al. Reversal of fetal distress following intensive treatment of maternal diabetic ketoacidosis. Am J Perinatol 1994; 11:430- z Moore TR: Diabetes in pregnancy. In: Maternal Fetal Medicine Principles and Practice. Fifth Edition. Creasy RK, Resnid R, Iams JD. Philadelphia, z Enis ED, Kreisberg, RA: Ketoacidosis and Hyperosmolarity. In: Diabetes Mellitus: A Fundamental and Clinical Text, 2nd Edition D. LeRoith, SI, Taylor & HM Olefsky (Eds.) Philedelphia, Lippincott, Williams & Wilkins, z Kamalakannan D, Baskar V et al. Diabetic ketoacidosis in pregnancy.
Postgrad Med J. 2003 Aug;79(934):454-7


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