| Popis: |
Diabetic ketoacidosis (DKA) in pregnancy is a rare but serious medical emergency. Its incidence ranges between 0.2%-9% and carries a fetal mortality rate up to 90%. DKA remains to be an extremely rare complication of gestational diabetes (GDM). Early diagnosis and management may be delayed due to its atypical presentation. We present a case of DKA in GDM with no pre-existing diagnosis of type 1 diabetes (T1DM) or type 2 diabetes (T2DM). A 33-year-old African American woman G2P0010 with GDM on insulin diagnosed in current pregnancy, presented at 30-weeks of gestation with a 3-day history of general malaise, altered mentation, and emesis. Severe DKA (blood glucose 920 mg/dL, pH 7.02, anion gap 38, bicarbonate 5.0 mEq/L, and positive serum ketones), systemic inflammatory response syndrome (tachycardia, WBC of 24,000/mcL), and intrauterine fetal demise via ultrasound were determined upon presentation. MICU admission for prompt and vigorous medical management with intravenous fluid resuscitation, insulin and bicarbonate infusions, and broad-spectrum antibiotic therapy was required. Clinical course was complicated by worsening hypokalemia. Spontaneous vaginal delivery of a non-viable fetus occurred at the MICU. After delivery, resolution of DKA was achieved. Once the patient's mentation was back to her baseline, she admitted complete cessation of insulin 1-week prior to admission. Workup revealed negative glutamic acid decarboxylase, islet cell, and zinc transporter-8 autoantibodies in addition to normal C-peptide levels. A new HbA1C of 9% compared to HbA1C of 5.5% at 6 weeks of gestation, made pre-existing T2DM unlikely. Eventually, the patient was downgraded to the medicine wards for continuity of care. DKA in pregnancy is a rare complication typically associated with T1DM. It may occur at near-normal blood glucose levels, known as euglycemic DKA, causing a delay in diagnosis. Physiologic changes during the last trimester of gestation explain the higher incidence of DKA at this stage. These include the relative state of insulin resistance, which in addition to insulin-antagonistic hormones such as human placental lactogen, prolactin, cortisol, and progesterone contribute to this state. Furthermore, a relative accelerated state of starvation with an increase in maternal ketone body formation, and a reduction in the buffering capacity when exposed to ketonemia places gravida women with impaired glucose tolerance at higher risk to develop DKA. Fetal loss may result from reduced uteroplacental perfusion and fetal hypokalemia leading to fatal arrhythmia. The most common precipitating factors of DKA in pregnancy are infection, including COVID-19, insulin therapy non-adherence, steroid use, dehydration, and unrecognized new-onset diabetes which accounts for up to 30% of cases. It has been described that a genetic polymorphism in SLC26A6 gene may increase the susceptibility to develop DKA in GDM. Prevention, early diagnosis, and vigorous medical management of DKA in pregnancy may possibly reduce maternal and fetal mortality. Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m. |
