Bilateral Basal Ganglia Infarctions in a Neonate Born During Maternal Diabetic Ketoacidosis
| العنوان: | Bilateral Basal Ganglia Infarctions in a Neonate Born During Maternal Diabetic Ketoacidosis |
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| المؤلفون: | Christopher A. Collura, Matthew Stenerson, Aida N. Lteif, Carl H. Rose, William A. Carey |
| المصدر: | Pediatrics. 128:e707-e710 |
| بيانات النشر: | American Academy of Pediatrics (AAP), 2011. |
| سنة النشر: | 2011 |
| مصطلحات موضوعية: | Adult, Brain Infarction, Diabetic ketoacidosis, Pregnancy in Diabetics, Physiology, Placental insufficiency, Diabetic Ketoacidosis, Pregnancy, Diabetes mellitus, medicine, Fetal distress, Humans, Fetus, 3-Hydroxybutyric Acid, Dehydration, business.industry, Basal Ganglia Cerebrovascular Disease, Uterus, Infant, Newborn, Pregnancy Outcome, Placental Insufficiency, medicine.disease, Ketoacidosis, Fetal circulation, Regional Blood Flow, Anesthesia, Pediatrics, Perinatology and Child Health, Female, business |
| الوصف: | Diabetic ketoacidosis (DKA) during pregnancy carries significant risk of intrauterine fetal demise, but little is known about its postnatal sequelae in surviving neonates. We report here the case of an infant who was born to a mother with White's class C diabetes mellitus during an episode of DKA. Throughout pregnancy her glucose control was suboptimal, as evidenced by a predelivery glycosylated hemoglobin level of 8.1%. At 33 weeks' gestation, the mother presented with nausea and vomiting, a serum glucose concentration of 575 mg/dL, and other metabolic derangements consistent with DKA. Despite rehydration and insulin therapy, fetal distress necessitated cesarean delivery. At birth the infant required intubation, but her clinical status quickly improved and she was extubated within the first day of life. However, on day-of-life 4 she exhibited seizure-like activity, and subsequent brain MRI revealed bilateral basal ganglia infarctions. Previous research has revealed that the keto acid β-hydroxybutyrate (β-OHB) can cross the placenta into the fetal circulation and thereafter accumulate in the fetal brain, which leads to severe metabolic derangements. Furthermore, β-OHB accumulates rapidly in the basal ganglia of older children during episodes of DKA, wherein its presence is associated with neuronal injury. We suspect that transplacental transfer of maternal β-OHB led to an acquired ketoacidosis in the fetus and that accumulation of β-OHB contributed to neuronal injury and subsequent infarction of the basal ganglia. Further research is necessary to better characterize neonatal complications of maternal DKA, as well as the possible inclusion of β-OHB levels in the goal-directed treatment of this disease. |
| تدمد: | 1098-4275 0031-4005 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::7e98944a1d9b455a0758ac9ec93f078cTest https://doi.org/10.1542/peds.2010-3597Test |
| رقم الانضمام: | edsair.doi.dedup.....7e98944a1d9b455a0758ac9ec93f078c |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 10984275 00314005 |
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