Sheila Razdan

All Publications

• Increasing in-person medical interpreter utilization in the NICU through a bundle of interventions. Journal of perinatology : official journal of the California Perinatal Association Feister, J., Razdan, S., Sharp, D., Punjabi, S., Blecharczyk, E., Escobar, V., Gay, P. M., Scala, M., Bonifacio, S. 2024

  Abstract

  In-person medical interpretation improves communication with patients who have preferred language other than English (PLOE). Multi-dimensional barriers to use of medical interpreters limit their use in the NICU.Medical teams in our NICU were not consistently using in-person medical interpreters, leading to ineffective communication with families with PLOE.Interventions included staff educational sessions and grand rounds regarding equitable language access, distribution of interpreter request cards to families, and allocation of dedicated in-person interpreters for NICU rounds. Interpreter utilization was calculated by total requests per Spanish-speaking person day in the NICU.Interpreter utilization increased five-fold during the intervention period (from 0.2 to 1.0 requests per Spanish-speaking person day).We substantially increased our unit in-person interpreter utilization through a bundle of multifaceted interventions, many of which were low-cost. NICUs should regard dedicated medical interpreters as a critical part of the care team.

  View details for DOI 10.1038/s41372-024-01915-5

  View details for PubMedID 38424233

  View details for PubMedCentralID 1955368

• Disparity drivers, potential solutions, and the role of a health equity dashboard in the neonatal intensive care unit: a qualitative study. Journal of perinatology : official journal of the California Perinatal Association Razdan, S., Hedli, L. C., Sigurdson, K., Profit, J., Morton, C. H. 2023

  Abstract

  Racial/ethnic disparities are well-described in the neonatal intensive care unit (NICU). We explored expert opinion on their etiology, potential solutions, and the ability of health equity dashboards to meaningfully capture NICU disparities.We conducted 12 qualitative semi-structured interviews, purposively selecting a diverse group of neonatal experts. We used grounded theory to develop codes, shape interviews, and conduct analysis.We identified three sources of disparity: interpersonal bias, care process and institutional barriers, and social determinants of health, particularly as they affect parental engagement in the NICU. Proposed solutions included racial/cultural concordance, bolstering hospital-based resources, and policy interventions. Health equity dashboards were viewed as useful but limited, because clinical metrics do not account for many of the aforementioned sources of disparities.Equity dashboards serve as a motivational starting point for quality improvement; future iterations may require novel, qualitative data sources to identify underlying etiologies of NICU disparities.

  View details for DOI 10.1038/s41372-023-01856-5

  View details for PubMedID 38155228

  View details for PubMedCentralID 6503514

• Angiotensin-II Use for Refractory Hypotension in an Infant With Bilateral Renal Agenesis. Pediatrics Razdan, S., Davis, A. S., Tidmarsh, G., Hintz, S. R., Grimm, P. C., Chock, V. Y. 2023

  Abstract

  Infants with congenital bilateral renal agenesis are at significant risk for morbidity and mortality, despite substantial and continuing advances in fetal and neonatal therapeutics. Infants with bilateral renal agenesis may episodically develop severe hypotension that can be refractory to traditional vasopressors. Synthetic angiotensin-II has been successfully used in adult and a few pediatric patients with refractory hypotension but has not been extensively studied in infants. We describe the use of angiotensin-II in treating refractory hypotension in a premature infant with congenital bilateral renal agenesis admitted to the NICU. Within 48 hours, he no longer required other vasopressors. Subsequently, angiotensin-II was gradually weaned and discontinued over 10 days and the patient was ultimately discharged from the hospital. This case demonstrates that angiotensin-II may be a helpful agent to treat refractory hypotension in infants with bilateral renal agenesis.

  View details for DOI 10.1542/peds.2023-062128

  View details for PubMedID 38098437

• Patent foramen ovale in adults with sickle cell disease and stroke. American journal of hematology Razdan, S., Strouse, J. J., Reddy, A., Resar, D. F., Hasan, R. K., Resar, J. R., Naik, R. P., Urrutia, V. C., Lanzkron, S., Resar, L. M. 2016; 91 (9): E358-60

  View details for DOI 10.1002/ajh.24440

  View details for PubMedID 27253454

• Sexual dimorphism in BDNF signaling after neonatal hypoxia-ischemia and treatment with necrostatin-1. Neuroscience Chavez-Valdez, R., Martin, L. J., Razdan, S., Gauda, E. B., Northington, F. J. 2014; 260: 106-19

  Abstract

  Brain injury due to neonatal hypoxia-ischemia (HI) is more homogenously severe in male than in female mice. Because, necrostatin-1 (nec-1) prevents injury progression only in male mice, we hypothesized that changes in brain-derived neurotrophic factor (BDNF) signaling after HI and nec-1 are also sex-specific providing differential conditions to promote recovery of those more severely injured. The increased aromatization of testosterone in male mice during early development and the link between 17-β-estradiol (E2) levels and BDNF transcription substantiate this hypothesis. Hence, we aimed to investigate if sexual differences in BDNF signaling existed in forebrain and diencephalon after HI and HI/nec-1 and their correlation with estrogen receptors (ER). C57B6 mice (p7) received nec-1 (0.1μl [8μM]) or vehicle (veh) intracerebroventricularly after HI. At 24h after HI, BDNF levels increased in both sexes in forebrain without evidence of tropomyosin-receptor-kinase B (TrkB) activation. At 96h after HI, BDNF levels in forebrain decreased below those seen in control mice of both sexes. Additionally, only in female mice, truncated TrkB (Tc.TrkB) and p75 neurotrophic receptor (p75ntr) levels increased in forebrain and diencephalon. In both, forebrain and diencephalon, nec-1 treatment increased BDNF levels and TrkB activation in male mice while, nec-1 prevented Tc.TrkB and p75ntr increases in female mice. While E2 levels were unchanged by HI or HI/nec-1 in either sex or treatment, ERα:ERβ ratios were increased in diencephalon of nec-1-treated male mice and directly correlated with BDNF levels. Neonatal HI produces sex-specific signaling changes in the BDNF system, that are differentially modulated by nec-1. The regional differences in BDNF levels may be a consequence of injury severity after HI, but sexual differences in response to nec-1 after HI may represent a differential thalamo-cortical preservation or alternatively off-target regional effect of nec-1. The biological significance of ERα predominance and its correlation with BDNF levels is still unclear.

  View details for DOI 10.1016/j.neuroscience.2013.12.023

  View details for PubMedID 24361177

  View details for PubMedCentralID PMC3950408

• Patent foramen ovale in patients with sickle cell disease and stroke: case presentations and review of the literature. Case reports in hematology Razdan, S., Strouse, J. J., Naik, R., Lanzkron, S., Urrutia, V., Resar, J. R., Resar, L. M. 2013; 2013: 516705

  Abstract

  Although individuals with sickle cell disease (SCD) are at increased risk for stroke, the underlying pathophysiology is incompletely understood. Intracardiac shunting via a patent foramen ovale (PFO) is associated with cryptogenic stroke in individuals without SCD. Recent evidence suggests that PFOs are associated with stroke in children with SCD, although the role of PFOs in adults with stroke and SCD is unknown. Here, we report 2 young adults with SCD, stroke, and PFOs. The first patient had hemoglobin SC and presented with a transient ischemic attack and a subsequent ischemic stroke. There was no evidence of cerebral vascular disease on imaging studies and the PFO was closed. The second patient had hemoglobin SS and two acute ischemic strokes. She had cerebral vascular disease with moyamoya in addition to a peripheral deep venous thrombosis (DVT). Chronic transfusion therapy was recommended, and the DVT was managed with warfarin. The PFO was not closed, and the patients' neurologic symptoms were stabilized. We review the literature on PFOs and stroke in SCD. Our cases and the literature review illustrate the dire need for further research to evaluate PFO as a potential risk factor for stroke in adults with SCD.

  View details for DOI 10.1155/2013/516705

  View details for PubMedID 23956892

  View details for PubMedCentralID PMC3730376

• Necrostatin decreases oxidative damage, inflammation, and injury after neonatal HI. Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism Northington, F. J., Chavez-Valdez, R., Graham, E. M., Razdan, S., Gauda, E. B., Martin, L. J. 2011; 31 (1): 178-89

  Abstract

  Necrostatin-1 inhibits receptor-interacting protein (RIP)-1 kinase and programmed necrosis and is neuroprotective in adult rodent models. Owing to the prominence of necrosis and continuum cell death in neonatal hypoxia-ischemia (HI), we tested whether necrostatin was neuroprotective in the developing brain. Postnatal day (P)7 mice were exposed to HI and injected intracerebroventricularly with 0.1 μL of 80 μmol necrostatin, Nec-1, 5-(1H-Indol-3-ylmethyl)-(2-thio-3-methyl) hydantoin, or vehicle. Necrostatin significantly decreased injury in the forebrain and thalamus at P11 and P28. There was specific neuroprotection in necrostatin-treated males. Necrostatin treatment decreased necrotic cell death and increased apoptotic cell death. Hypoxia-ischemia enforced RIP1-RIP3 complex formation and inhibited RIP3-FADD (Fas-associated protein with death domain) interaction, and these effects were blocked by necrostatin. Necrostatin also decreased HI-induced oxidative damage to proteins and attenuated markers of inflammation coincidental with decreased nuclear factor-κB and caspase 1 activation, and FLIP ((Fas-associated death-domain-like IL-1β-converting enzyme)-inhibitory protein) gene and protein expression. In this model of severe neonatal brain injury, we find that cellular necrosis can be managed therapeutically by a single dose of necrostatin, administered after HI, possibly by interrupting RIP1-RIP3-driven oxidative injury and inflammation. The effects of necrostatin treatment after HI reflect the importance of necrosis in the delayed phases of neonatal brain injury and represent a new direction for therapy of neonatal HI.

  View details for DOI 10.1038/jcbfm.2010.72

  View details for PubMedID 20571523

  View details for PubMedCentralID PMC3049482