Clinical Focus

  • Neonatal-Perinatal Medicine

Professional Education

  • Board Certification: American Board of Pediatrics, Neonatal-Perinatal Medicine (2014)
  • Fellowship: Loma Linda University Neonatal-Perinatal Medicine Fellowship (2011) CA
  • Board Certification: American Board of Pediatrics, Pediatrics (2008)
  • Residency: Driscoll Childrens Hospital at Texas AandM Pediatric Residency (2008) TX
  • Medical Education: PSG Institute of Medical Sciences and Research (2001) India

All Publications

  • Catecholamine-resistant hypotension and myocardial performance following patent ductus arteriosus ligation JOURNAL OF PERINATOLOGY Noori, S., McNamara, P., Jain, A., Lavoie, P. M., Wickremasinghe, A., Merritt, T. A., Solomon, T., Sekar, K., Attridge, J. T., Swanson, J. R., Gillam-Krakauer, M., Reese, J., Poindexter, B. B., Brook, M., Auchus, R. J., Clyman, R. I., PDA Ligation Hypotension Trial Inv 2015; 35 (2): 123–27


    We performed a multicenter study of preterm infants, who were about to undergo patent ductus arteriosus ligation, to determine whether echocardiographic indices of impaired myocardial performance were associated with subsequent development of catecholamine-resistant hypotension following ligation.A standardized treatment approach for hypotension was followed at each center. Infants were considered to have catecholamine-resistant hypotension if their dopamine infusion was > 15 μg kg(-1)min(-1). Echocardiograms and cortisol measurements were obtained between 6 and 14 h after the ligation (prior to the presence of catecholamine-resistant hypotension).Forty-five infants were enrolled, 10 received catecholamines (6 were catecholamine-responsive and 4 developed catecholamine-resistant hypotension). Catecholamine-resistant hypotension was not associated with decreased preload, shortening fraction or ventricular output. Infants with catecholamine-resistant hypotension had significantly lower levels of systemic vascular resistance and postoperative cortisol concentration.We speculate that low cortisol levels and impaired vascular tone may have a more important role than impaired cardiac performance in post-ligation catecholamine-resistant hypotension.

    View details for DOI 10.1038/jp.2014.151

    View details for Web of Science ID 000348751900009

    View details for PubMedID 25118721

    View details for PubMedCentralID PMC4310792

  • Hypotension following Patent Ductus Arteriosus Ligation: The Role of Adrenal Hormones JOURNAL OF PEDIATRICS Clyman, R. I., Wickremasinghe, A., Merritt, A., Solomon, T., McNamara, P., Jain, A., Singh, J., Chu, A., Noori, S., Sekar, K., Lavoie, P. M., Attridge, J. T., Swanson, J. R., Gillam-Krakauer, M., Reese, J., DeMauro, S., Poindexter, B., Aucott, S., Satpute, M., Fernandez, E., Auchus, R. J., Patent Ductus Arteriosus Ligation 2014; 164 (6): 1449-+


    To test the hypothesis that an impaired adrenal response to stress might play a role in the hypotension that follows patent ductus arteriosus (PDA) ligation.We performed a multicenter study of infants born at <32 weeks' gestation who were about to undergo PDA ligation. Serum adrenal steroids were measured 3 times: before and after a cosyntropin (1.0 μg/kg) stimulation test (performed before the ligation), and at 10-12 hours after the ligation. A standardized approach for diagnosis and treatment of postoperative hypotension was followed at each site. A modified inotrope score (1 × dopamine [μg/kg/min] + 1 × dobutamine) was used to monitor the catecholamine support an infant received. Infants were considered to have catecholamine-resistant hypotension if their greatest inotrope score was >15.Of 95 infants enrolled, 43 (45%) developed hypotension and 14 (15%) developed catecholamine-resistant hypotension. Low postoperative cortisol levels were not associated with the overall incidence of hypotension after ligation. However, low cortisol levels were associated with the refractoriness of the hypotension to catecholamine treatment. In a multivariate analysis: the OR for developing catecholamine-resistant hypotension was OR 36.6, 95% CI 2.8-476, P = .006. Low cortisol levels (in infants with catecholamine-resistant hypotension) were not attributable to adrenal immaturity or impairment; their cortisol precursor concentrations were either low or unchanged, and their response to cosyntropin was similar to infants without catecholamine-resistant hypotension.Infants with low cortisol concentrations after PDA ligation are likely to develop postoperative catecholamine-resistant hypotension. We speculate that decreased adrenal stimulation, rather than an impaired adrenal response to stimulation, may account for the decreased production.

    View details for DOI 10.1016/j.jpeds.2014.01.058

    View details for Web of Science ID 000336503200042

    View details for PubMedID 24636853

    View details for PubMedCentralID PMC4035426

  • Use of propranolol for treatment of hemangiomas in PHACE syndrome JOURNAL OF PERINATOLOGY Solomon, T., Ninnis, J., Deming, D., Merritt, T. A., Hopper, A. 2011; 31 (11): 739–41


    We report the case of a 29-week preterm infant with PHACE (posterior fossa malformations, hemangionas, arterial anomalies, cardiac anomalies, eye anomalies) syndrome. PHACE syndrome is a neurocutaneous disorder with large facial segmental hemangionas associated with anomalies of the brain, eye, heart and aorta. The hemangiomas in our patient were problematic, distorting the airway and interfering with respirations to the point of requiring mechanical ventilation. Consultation with several different centers with medical expertize in treatment of congenital hemangiomas revealed different views on the best management strategy. In this infant, the hemangiomas progressed with failure to involute despite currently recommended therapy including corticosteroids and vincristine. Therefore, the infant was treated with propranolol and had significant regression of the hemangiomas. The use of propranolol for the treatment of infantile hemangiomas is reviewed.

    View details for DOI 10.1038/jp.2011.28

    View details for Web of Science ID 000296590600008

    View details for PubMedID 22037156