II. Epidemiology

  1. Incidence: 0.5 to 3% of diabetes in pregnancy
    1. Type 1 Diabetes represents 85% of cases
    2. Type 2 Diabetes represents 15% of cases!

III. Pathophysiology

  1. Normal Pregnancy: Glucose is made available to the fetus
    1. Placenta releases hormonal signals
      1. Human placental lactogen (hPL)
      2. Human Placental Growth Hormone (hPGH)
    2. Glucose level increase is stimulated by hPL and hPGH via several mechanisms
      1. Increased Insulin release from Pancreas
      2. Increased hepatic lipolysis
      3. Increased hepatic Gluconeogenesis
      4. Decreased muscle Glucose utilization
  2. DKA in Pregnancy: Glucose continues to be made available to the fetus
    1. Fetal utilization of Glucose does not rely on maternal Insulin
      1. Results in a relatively normal maternal Glucose despite DKA
    2. Multiple factors lead to DKA in Pregnancy
      1. Factors are similar to non-pregnant DKA (Insulin Deficiency, Stress Response)
      2. Pregnancy has the added factor of Insulin Resistance
    3. Stress Triggers in pregnancy
      1. Infection (25% of cases)
      2. Vomiting (25% of cases)
      3. Corticosteroids (21%)
      4. Medication erros
      5. Trauma

IV. Precautions

  1. DKA in Pregnancy is a high risk condition for mother and fetus
  2. DKA in Pregnancy is easily missed
    1. Serum Glucose is rarely >200 mg/dl (Euglycemic DKA is typical)
    2. Minute Ventilation in pregnancy is 40% higher resulting in baseline pH 7.44, PaCO2 30, Bicarb 18-22

VI. Labs

VII. Diagnosis

  1. Keep a high index of suspicion!
    1. Laboratory findings are often underwhelming despite significant DKA
  2. Diabetic Ketoacidosis
    1. Serum Anion Gap >12
    2. ABG pH <7.3
    3. Serum bicarbonate <15 to 20 mEq/L
    4. Serum Glucose may be elevated
      1. Serum Glucose is only elevated in 50% of cases,
      2. Serum Glucose is rarely >200 mg/dl in DKA in Pregnancy
    5. Serum Ketones (Beta-Hydroxybutyrate) elevated
    6. Positive Urine Ketones
      1. Urine Ketones are not a normal finding in pregnancy
  3. Normal pregnancy (for comparison)
    1. pH 7.44
    2. PaCO2 30 mmHg
    3. Serum Bicarbonate 18-22
    4. Anion Gap <12

VIII. Management

  1. Consult maternal-fetal medicine
  2. See Diabetic Ketoacidosis
  3. Intravenous Fluid Resuscitation (initial 1-2 L IV)
  4. Replace Serum Potassium in Hypokalemia
  5. Initiate Insulin bolus and Insulin Drip
    1. Unlike non-pregnant DKA, Insulin bolus is preferred in DKA of pregnancy
  6. Add dextrose to replacement fluids (e.g. D5LR) if Serum Glucose <250 mg/dl
    1. Most cases of DKA in Pregnancy are euglycemic
  7. Initiate continuous Fetal Monitoring if Gestational age >24 weeks
  8. As with non-pregnant DKA evaluate for underlying triggers (e.g. infection)
  9. Intensive Monitoring in first 4 hours
    1. Hourly Urine Output
    2. Vital Signs every 15 minutes
  10. Repeat labs every 2 hours until Ketones are cleared
    1. Basic metabolic panel (chem8)
    2. Beta-Hydroxybutyrate
    3. Venous Blood Gas periodically as needed
  11. Transition to SQ Bolus Insulin when Anion Gap is closed, Serum Ketones cleared and oral fluids tolerated
    1. Give long-acting subcutaneous Insulin (e.g. Insulin Glargine)
    2. Discontinue Insulin Drip at 2 hours after long-acting Insulin started

IX. Complications

  1. Critical Maternal Illness (as with DKA in general population)
  2. Fetal Mortality (up to 16%)
  3. Preterm Birth (46%)
  4. Neurodevelopmental complications

X. References

  1. Wernimont (2023) Diabetic Ketoacidosis in Pregnancy: Pearls for Non-Obstetricians, M-Health Fairview Emergency Department Lecture, attended 7/13/2023
  2. Má (2016) Saudi J Anaesth 10(2):238-9 +PMID: 27051381 [PubMed]
  3. de Alencar (2019) Clin Pract Cases Emerg Med 4(1):26-28 +PMID: 32064418 [PubMed]

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