Starvation Ketoacidosis in the Third Trimester of Pregnancy

ABSTRACT

Introduction: Starvation ketoacidosis represents one of the three metabolic acidoses caused by the accumulation of ketone bodies within the bloodstream. Outside of late pregnancy, it is a relatively rare condition. In late pregnancy, the placental production of the hormones estrogen, cortisol, and human placental lactogen combined with increased lipolysis causes greater insulin resistance and an overall catabolic state which improves nutrient availability for vital fetal growth. However, this also allows for a magnified response to fasting that results in increased ketone production and in rare cases “accelerated starvation.” In this case, we present a 25-year-old pregnant patient who presented with nausea, vomiting, and poor oral intake, who was found to be in starvation ketoacidosis. Case Description A 25-year-old G2P1001 cis female with a previous medical history of migraines presented at 33 weeks gestation with nausea, vomiting, and poor oral intake for four days prior to admission in the setting of COVID-19 infection. Patient presented hemodynamically stable and in no acute distress. Fetal non stress test on admission was reactive. Initial lab work revealed a glucose of 95, anion gap of 21, and a bicarbonate level of 7. A beta hydroxybutyrate (BHB) level was elevated at 5.26. Arterial blood gas showed a pH of 7.2 and a PCO2 of 23, consistent with an anion gap metabolic acidosis. Urinalysis revealed 3+ ketones. Overall labs were consistent with starvation ketoacidosis and the patient was immediately resuscitated with dextrose containing intravenous fluids and an insulin drip to help shunt away from ketoacidosis. Her BHB rapidly downtrended to 1.28 within 12 hours and within 24 hours it normalized. Her metabolic acidosis continued to improve throughout her hospitalization. She was able to tolerate a regular diet prior to being discharged home. A few weeks later, she had an uncomplicated full term delivery of a healthy baby. Discussion: Starvation ketoacidosis outside of pregnancy is rare and takes at least two weeks to manifest as a mild ketoacidosis. In pregnancy, patients are in an insulin resistant state which increases with gestational age, making them prone to ketoacidosis particularly in the second and third trimesters. Ketoacidosis in pregnancy is not only harmful for the pregnant individual, but for the developing fetus as well. Ketones can cross the placental barrier, leading to neurological impairment and even fetal demise if the acidosis is not addressed quickly. Prompt treatment with IV fluids, dextrose, and insulin is imperative to prevent neurodevelopmental compromise. Patients with appropriate and timely treatment can continue on to have uncomplicated pregnancies and deliveries.