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Salt Lake City, UT, United States

Christensen R.D.,Women and Newborns Clinical Program | Baer V.L.,Women and Newborns Clinical Program | Yaish H.M.,University of Utah

Background A recent NHLBI conference concluded that platelet (PLT) transfusions of neonates must become more evidence based. One neonatal disorder for which transfusions are given is a poorly defined entity, the "thrombocytopenia of perinatal asphyxia." To expand the evidence base for this entity, we performed a multicentered, retrospective analysis of neonates with perinatal asphyxia. Study Design and Methods We analyzed records of term and late preterm neonates with perinatal asphyxia defined by a cord blood pH of not more than 6.99 and/or base deficit of at least 16 mmol/L. From these we identified neonates with at least two PLT counts of fewer than 150 × 109/L in the first week of life and described the severity, nadir, and duration of the thrombocytopenia. Results Thrombocytopenia occurred in 31% (117/375) of neonates with asphyxia versus 5% of matched nonasphyxiated controls admitted to a neonatal intensive care unit (p < 0.0001). Twenty-one of the 117 asphyxiated neonates were excluded from the remaining analysis due to disseminated intravascular coagulation or extracorporeal membrane oxygenation. Nadir PLT counts of the remaining 96 were on Day 3 (75 × 109/L; 90% confidence interval, 35.7 × 109-128.6 × 109/L) and normalized by Days 19 to 21. PLT counts after asphyxia roughly correlated inversely with elevated nucleated red blood cell count (NRBC) counts at birth. Thirty of the 96 received at least one PLT transfusion, all given prophylactically, none for bleeding. Conclusions We maintain that the thrombocytopenia of perinatal asphyxia is an authentic entity. Its association with elevated NRBC counts suggests that hypoxia is involved in the pathogenesis. Because PLT counts are only moderately low, the condition is transient, and bleeding problems seem rare, we speculate that PLT transfusions should not be needed for most neonates with this condition. © 2014 AABB. Source

Marin S.J.,Arup | Christensen R.D.,Women and Newborns Clinical Program | Baer V.L.,Women and Newborns Clinical Program | Clark C.J.,Arup | And 2 more authors.
Therapeutic Drug Monitoring

Umbilical cord tissue was studied as a means of detecting prenatal exposure to nicotine. This was accomplished by comparing the presence and concentration of nicotine as well as nicotine metabolites in both umbilical cord tissue and paired meconium samples with maternal smoking histories obtained by self-report. Nicotine and metabolites (cotinine, 3-hydroxycotinine, nornicotine, and anabasine) were detected and quantitated using liquid chromatography-tandem mass spectroscopy. Between June and September 2009, 19 women with a tobacco exposure history (either first- or second-hand tobacco smoke exposure during pregnancy) were consented for the study. A questionnaire was completed to document nicotine exposure during each trimester of pregnancy. All infants were delivered at term (38 weeks or greater) and paired umbilical cord tissue (10-cm segment or greater) and meconium were obtained. Nicotine and 3-hydroxycotinine were most prominent in meconium, whereas cotinine and 3-hydroxycotinine were most prominent in the umbilical cord. Concentrations of all three analytes were generally higher in meconium. Nornicotine was detected only in meconium, at very low concentrations, and anabasine was not detected in either specimen. All analyte concentrations were lowest when the mother stated she quit smoking early in pregnancy or had only second-hand exposure, and detection was poor if exposure was limited to the first or second trimesters. Although different nicotine and metabolite patterns exist in meconium versus umbilical cord tissue, this work indicates that either specimen can be used to detect third-trimester fetal nicotine exposure. Copyright © 2011 by Lippincott Williams & Wilkins. Source

Jensen J.D.,Institute for Healthcare Delivery Research | Henry E.,Institute for Healthcare Delivery Research | Silver R.M.,University of Utah | Christensen R.D.,Women and Newborns Clinical Program
American Journal of Perinatology

It is unclear whether neonates born to women with thrombocytopenia during pregnancy are themselves at increased risk for thrombocytopenia at birth. In the current retrospective study, platelet count reference ranges were developed for pregnant women according to trimester, and correlations were sought between the platelet counts of mothers at delivery and their neonates. During the study period, 92,518 platelet counts were recorded on 41,887 pregnant women. A progressive shift toward lower platelet counts in a similarly shaped histogram occurred during pregnancy, with the lower reference range (2.5 percentile) for platelets during the third trimester being 113×10 9/L. Among 11,797 maternalneonatal pairs following delivery, no correlation was observed between maternal and neonatal counts. However, if the mother's lowest count was <50×10 9/L, the relative risk of any degree of thrombocytopenia in their neonate was 4.6 (95% confidence interval [CI], 1.8 to 33.3) and the relative risk of severe neonatal thrombocytopenia was 7.8 (95% CI, 1.8 to 33.3). The results of the current study demonstrate that platelet counts >75×10 9/L in pregnant women were not associated with an increased risk of neonatal thrombocytopenia, and maternal platelet counts of <50×10 9/L were accompanied by an almost fivefold risk increase of neonatal thrombocytopenia. Copyright © 2011 by Thieme Medical Publishers, Inc. Source

Christensen R.D.,University of Utah | Baer V.L.,Women and Newborns Clinical Program | Henry E.,Primary Childrens Hospital | Snow G.L.,Statistical Data Center | And 2 more authors.

BACKGROUND: Thrombocytopenia is common among small-for-gestational-age (SGA) neonates abstract (birth weight ,10th percentile reference range), but several aspects of this thrombocytopenia are unclear, including the incidence, typical nadir, duration, association with preeclampsia, mechanism, and risk of death. METHODS: Using 9 years of multihospital records, we studied SGA neonates with 2 platelet counts ,150 000/mL in their first week. RESULTS: We found first-week thrombocytopenia in 31% (905 of 2891) of SGA neonates versus 10% of non-SGA matched controls (P , .0001). Of the 905, 102 had a recognized cause of thrombocytopenia (disseminated intravascular coagulation, early-onset sepsis, or extracorporeal membrane oxygenation). This group had a 65% mortality rate. The remaining 803 did not have an obvious cause for their thrombocytopenia, and we called this thrombocytopenia of SGA. They had a mortality rate of 2% (P , .0001) and a mean nadir count on day 4 of 93 000/mL (SD 51 580/mL, 10th percentile 50 000/mL, 90th percentile 175 000/mL). By day 14, platelet counts were 150 000/mL in more than half of the patients. Severely SGA neonates (,1st percentile) had lower counts and longer thrombocytopenia duration (P , .001). High nucleated red cell counts at birth correlated with low platelets (P , .0001). Platelet transfusions were given to 23%, and counts typically more than tripled. Thrombocytopenia was more associated with SGA status than with the diagnosis of maternal preeclampsia. CONCLUSIONS: SGA neonates with clearly recognized varieties of thrombocytopenia have a high mortality rate. In contrast, thrombocytopenia of SGA is a hyporegenerative condition of moderate severity and 2 weeks' duration and is associated with evidence of intrauterine hypoxia and a low mortality rate. Copyright © 2015 by the American Academy of Pediatrics. Source

Nussenzveig R.H.,University of Utah | Christensen R.D.,Women and Newborns Clinical Program | Prchal J.T.,University of Utah | Yaish H.M.,University of Utah | Agarwal A.M.,University of Utah

We evaluated a neonate with severe jaundice but a negative family history. Spherocytes were present and suspected hereditary spherocytosis was confirmed by osmotic fragility and eosin-5-maleimide erythrocyte staining. We found he was a compound heterozygote for two pathogenic mutations in the gene encoding α-spectrin: a previously reported αLEPRA inherited from his asymptomatic mother, and a novel α-spectrin mutation in intron 45 +1 disrupting the consensus splice site, from his asymptomatic father. © 2014 S. Karger AG, Basel. Source

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