{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,12]],"date-time":"2026-10-12T14:04:12Z","timestamp":1791813852822,"version":"4.3.4"},"reference-count":27,"publisher":"American Academy of Pediatrics (AAP)","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2004,8,1]]},"abstract":"<jats:p>Objective. To determine the potential contribution of initial hypoglycemia to the development of neonatal brain injury in term infants with severe fetal acidemia.<\/jats:p><jats:p>Methods. A retrospective chart review was conducted of 185 term infants who were admitted to the neonatal intensive care unit between January 1993 and December 2002 with an umbilical arterial pH &amp;lt;7.00. Short-term neurologic outcome measures include death as a consequence of severe encephalopathy and evidence of moderate to severe encephalopathy with or without seizures. Hypoglycemia was defined as an initial blood glucose \u226440 mg\/dL.<\/jats:p><jats:p>Results. Forty-one (22%) infants developed an abnormal neurologic outcome, including 14 (34%) with severe hypoxic ischemic encephalopathy who died, 24 (59%) with moderate to severe hypoxic ischemic encephalopathy, and 3 (7%) with seizures. Twenty-seven (14.5%) of the 185 infants had an initial blood sugar \u226440 mg\/dL. Fifteen (56%) of 27 infants with a blood sugar \u226440 mg\/dL versus 26 (16%) of 158 infants with a blood sugar &amp;gt;40 mg\/dL had an abnormal neurologic outcome (odds ratio [OR]: 6.3; 95% confidence interval [CI]: 2.6\u201315.3). Infants with abnormal outcomes and a blood sugar \u226440 mg\/dL versus &amp;gt;40 mg\/dL had a higher pH (6.86 \u00b1 0.07 vs 6.75 \u00b1 0.09), a lesser base deficit (\u221219 \u00b1 4 vs \u221223.8 \u00b1 4 mEq\/L), and lower mean arterial blood pressure (34 \u00b1 10 vs 45 \u00b1 14 mm Hg), respectively. There was no difference between groups in the proportion of infants who required cardiopulmonary resuscitation (7 [46%] vs 15 [57%]) and those with a 5-minute Apgar score &amp;lt;5 (11 [73%] vs 22 [85%]). By multivariate logistic analysis, 4 variables were significantly associated with abnormal outcome: initial blood glucose \u226440 mg\/dL versus &amp;gt;40 mg\/dL (OR: 18.5; 95% CI: 3.1\u2013111.9), cord arterial pH \u22646.90 versus &amp;gt;6.90 (OR: 9.8; 95% CI: 2.1\u201344.7), a 5-minute Apgar score \u22645 versus &amp;gt;5 (OR: 6.4; 95% CI: 1.7\u201324.5), and the requirement for intubation with or without cardiopulmonary resuscitation versus neither (OR: 4.7; 95% CI: 1.2\u201317.9).<\/jats:p><jats:p>Conclusion. Initial hypoglycemia is an important risk factor for perinatal brain injury, particularly in depressed term infants who require resuscitation and have severe fetal acidemia. It remains unclear, however, whether earlier detection of hypoglycemia, such as in the delivery room, in this population could modify subsequent neurologic outcome.<\/jats:p>","DOI":"10.1542\/peds.114.2.361","type":"journal-article","created":{"date-parts":[[2004,8,14]],"date-time":"2004-08-14T00:53:04Z","timestamp":1092444784000},"page":"361-366","source":"Crossref","is-referenced-by-count":180,"title":["Initial Hypoglycemia and Neonatal Brain Injury in Term Infants With Severe Fetal Acidemia"],"prefix":"10.1542","volume":"114","author":[{"given":"Walid A.","family":"Salhab","sequence":"first","affiliation":[{"name":"From the University of Texas Southwestern Medical Center at Dallas, Department of Pediatrics, Neonatal-Perinatal Medicine, Dallas, Texas"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Myra H.","family":"Wyckoff","sequence":"additional","affiliation":[{"name":"From the University of Texas Southwestern Medical Center at Dallas, Department of Pediatrics, Neonatal-Perinatal Medicine, Dallas, Texas"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Abbot R.","family":"Laptook","sequence":"additional","affiliation":[{"name":"From the University of Texas Southwestern Medical Center at Dallas, Department of Pediatrics, Neonatal-Perinatal Medicine, Dallas, Texas"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jeffrey M.","family":"Perlman","sequence":"additional","affiliation":[{"name":"From the University of Texas Southwestern Medical Center at Dallas, Department of Pediatrics, Neonatal-Perinatal Medicine, Dallas, Texas"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"417","published-online":{"date-parts":[[2004,8,1]]},"reference":[{"key":"2021121006433249900_R1","doi-asserted-by":"crossref","unstructured":"Jones MD, Burd LI, Makowski EI, et al. 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