A 20 year old female with past medical history of poorly controlled type 1 diabetes, anorexia, and depression presents to the Emergency Department due to abdominal pain, nausea, and shortness of breath. She is noted
to have an elevated blood glucose of 512 and chemistry reveals bicarb <6, beta hydroxybuterate 9.90, and pH 6.88. You have diagnosed diabetic ketoacidosis (DKA) and plan to start treatment for it when you note a beta hCG of 1380.
DKA in pregnancy is considered an obstetrical emergency and is one of the leading causes of fetal loss. 0.5-10% of diabetic women will experience DKA during their pregnancy1,2. While the maternal mortality is low at <1% (though higher than in non-pregnant patients2), there are significant effects on the fetus including increased risk of preterm delivery and a perinatal mortality with reports ranging from 9-35%1,2,3. The hyperglycemia and acidosis of DKA both contribute to these poor outcomes. Maternal hyperglycemia leads to fetal hyperglycemia and due to osmotic forces this leads to a fetal diuresis and therefore fetal volume depletion3. Maternal acidemia combined with maternal diuresis results in decreased uterine blood flow and placental perfusion which therefore decreases oxygen delivery to the fetus1.
The pregnant state predisposes diabetics to worsening glycemic control and therefore DKA1. Pregnancy is a state of relative insulin deficiency due to lower maternal fasting glucose levels. The pregnant woman is in a lipolytic state with an increased baseline of free fatty acids in the blood. Common symptoms such as vomiting during pregnancy can contribute to the development of DKA4. Additionally, the physiologic tachypnea of pregnancy decreases the ability to buffer ketoacids via respiratory compensation and therefore makes the acidosis state less tolerable2,4.
The presentation of DKA is the same in this population as the general population, though euglycemic DKA is more frequent5. It has been reported that up to 36% of pregnant DKA patients have a blood glucose <200 mg/dL3. The treatment is also the same as in the general population with the addition of considering fetal heart rate monitoring and early consultation with a high risk obstetric team and an endocrinologist. Patients often require ICU level of care. Abnormalities in fetal heart rate tracing including repetitive decelerations and absence of variability will often occur but resolve as maternal acidosis improves1. DKA alone is not an indication for delivery as morbidity and mortality can be decreased via in utero resuscitation of the fetus by aggressive treatment of the mother’s DKA. The condition of the mother and fetus as well as the fetal gestational age must all be taken into account when considering early delivery1.
Ashley Mogul is a third year resident and the Academic Chief at Stony Brook.
@JustAMogul
References:
Ecker, JL. Pregestational diabetes mellitus: Obstetrical issues and management. In: UpToDate, Barss V (Ed), UpToDate, Waltham, MA, 2018.
Morton-Eggleston, EB & Seely, EW. Pregestational diabetes: Preconception counseling, evaluation, and management. In: UpToDate, Barss V (Ed), UpToDate, Waltham, MA, 2018.
Clardy, PF & Reardon, CC. Critical illness during pregnancy and the postpartum period. In: UpToDate, Finlay G (Ed), UpToDate, Waltham, MA, 2018.
Nyce, AL, Lubkin, CL, & Chansky, ME. “Diabetic ketoacidosis”. Tintinalli’s Emergency Medicine: A comprehensive study guide. Ed. Tintinalli, JE. McGraw-Hill Education. 2016.
Hirsch, IB & Emmett M. Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Clinical features, evaluation, and diagnosis. In: UpToDate, Mulder JE (Ed), UpToDate, Waltham, MA, 2018.