Clinical Focus


  • Neonatal-Perinatal Medicine

Academic Appointments


Professional Education


  • Board Certification: American Board of Pediatrics, Neonatal-Perinatal Medicine (2005)
  • Fellowship, Boston Children's Hospital, Neonatal-Perinatal Medicine (2002)
  • MPH, Harvard TH Chan School of Public health, Clinical Effectiveness (2001)
  • Board Certificaton, American Board of Pediatrics, Pediatrics (1999)
  • Residency, Columbia Presbyterian Medical Center, Pediatrics (1999)
  • Internship, Columbia Presbyterian Medical Center, Pediatrics (1997)
  • Medical Education: Albert Einstein College of Medicine (1996) NY

All Publications


  • Effect of bilirubin on visuocortical development in preterm infants. Journal of perinatology : official journal of the California Perinatal Association Good, W. V., Wong, R. J., Norcia, A. M., Hou, C., Cellucci, J., McGovern, M. Q., Wong-Kee-You, A., Acevedo Munares, G., Richburg, D., Loveridge-Easther, C., Lee, J. S., DeJesus, L., Slagle, T., Stevenson, D. K., Bhutani, V. K. 2025

    Abstract

    To determine if visuocortical development in premature infants with high bilirubin levels is more adversely affected than that in full-term infants.57 preterm infants were managed using institutional guidelines for hyperbilirubinemia. At 12-months corrected age, Vernier acuity, contrast sensitivity, and grating acuity measured using the sweep visual evoked potential (sVEP) were correlated to total serum/plasma bilirubin (TSB) levels in the first week of life.As TSB levels increased, Vernier acuity worsened in infants <34 weeks' gestation compared with those >34 to <37 weeks' gestation (p < 0.001). Contrast sensitivity varied as a function of TSB levels (Spearman correlation 0.63, p < 0.001). Grating acuity was unaffected.Vernier acuity in preterm infants <34 weeks' gestation is more vulnerable to the effects of bilirubin, suggesting that the extrastriate visual cortex is primarily affected by bilirubin. Therefore, guidelines for management of hyperbilirubinemia in preterm infants (<34 weeks' gestation) should be revised.

    View details for DOI 10.1038/s41372-025-02213-4

    View details for PubMedID 39910190

    View details for PubMedCentralID 4197714

  • Treatment and prevention of necrotizing enterocolitis. Seminars in neonatology : SN Lee, J. S., Polin, R. A. 2003; 8 (6): 449-59

    Abstract

    Necrotizing enterocolitis (NEC) is the most common serious, acquired gastrointestinal disorder in the newborn infant. Although many variables are associated with development of NEC, only prematurity has been consistently identified in case-controlled studies. Traditionally, the diving seal reflex has been invoked as the mechanism responsible for ischaemic injury and necrosis. Intestinal ischaemia is likely to be the final common pathway in NEC; however, it is due to the release of vasoconstricting substances, such as platelet activating factor, rather than perinatal asphyxia. Bacteria and/or bacterial toxins are likely to have a key role in the pathogenesis of NEC by fostering production of inflammatory mediators. The role of feeding practices in the pathogenesis of NEC remains controversial. Treatment of infants with NEC generally includes a regimen of bowel rest, gastric decompression, systemic antibiotics and parenteral nutrition. Infants with perforation are generally operated upon; however, there has been recent interest in primary peritoneal drainage as an alternative. Prevention of NEC still remains elusive. Avoidance of preterm birth, use of antenatal steroids and breast-milk feeding are practices that offer the greatest potential benefits. Use of any other strategy should await further trials.

    View details for DOI 10.1016/S1084-2756(03)00123-4

    View details for PubMedID 15001117

    View details for PubMedCentralID PMC7128229