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1.
J Pediatr ; 276: 114286, 2024 Sep 02.
Artigo em Inglês | MEDLINE | ID: mdl-39233115

RESUMO

OBJECTIVE: To describe our experience utilizing epoprostenol for pulmonary hypertension (PH) in infants with congenital diaphragmatic hernia (CDH) requiring extracorporeal life support (ECLS). STUDY DESIGN: We retrospectively reviewed infants diagnosed with CDH who required ECLS at our institution from 2013 to 2023. Data collected included demographics, disease characteristics, medication administration patterns, and hospital outcomes. We first compared infants who received intravenous epoprostenol and those who did not. Among infants who received epoprostenol, we compared survivors and nonsurvivors. χ² test/Fisher's exact and Mann-Whitney tests were used, with significance defined at P < .05. RESULTS: Fifty-seven infants were included; 40 (70.2%) received epoprostenol. Infants receiving epoprostenol had lower observed/expected total fetal lung volume (O/E TFLV) on magnetic resonance imaging (20 vs 26.2%, P = .042) as well as higher prenatal frequency of liver-up (90 vs 64.7%, P = .023) and "severe" classification (67.5 vs 35.3%, P = .007). Survival with and without epoprostenol was comparable (60% vs 64%, P = .23). Of those receiving epoprostenol, both survivors and nonsurvivors had similar prenatal indicators of disease severity. Most (80%) of hernia defects were classified as type C/D and 68% were repaired <72 hours after ECLS cannulation. The median age at initiation of epoprostenol was day of life 6 (IQR: 4, 7) in survivors and 8 (IQR: 7, 16) in nonsurvivors (P = .012). Survivors had shorter ECLS duration (11 vs 20 days, P = .049). Of nonsurvivors, refractory PH was the cause of death for 13 infants (81%). CONCLUSIONS: In infants with CDH requiring ECLS, addition of epoprostenol appears promising and earlier initiation may affect survival.

2.
J Surg Res ; 302: 568-577, 2024 Aug 22.
Artigo em Inglês | MEDLINE | ID: mdl-39178573

RESUMO

INTRODUCTION: There is a growing body of literature that shows geographic social vulnerability, which seeks to measure the resiliency of a community to withstand unforeseen disasters, may be associated with negative outcomes after traumatic injury. For motor vehicle collisions (MVCs) specifically, it is unknown how the resources of a patient's home environment may interact with resources of the environment where the crash occurred. METHODS: We merged publicly available crash data from the state of Michigan with the Michigan Trauma Quality Improvement dataset. A social vulnerability index (SVI) score was calculated for each ZIP code and was then cross-referenced between the location of the MVC (Crash-SVI) and the patient's home address (Home-SVI). SVI was divided into quintiles, with higher numbers indicating greater vulnerability. Adjusted logistic regression models using least absolute shrinkage and selection operator for feature selection and regularization were performed sequentially using patient, vehicular, and environmental variables to identify associations between Home-SVI and Crash-SVI, with mortality and injury severity score (ISS) greater than 15 (ISS15). RESULTS: Between January 2020 and December 2022, a total of 14,706 patients were identified. Most MVCs (75.3% of all patients) occurred in the second through fourth quintiles of SVI. In all cases, Crash-SVI occurred most frequently within the same quintile as the patient's Home-SVI. Average crash speed limits showed a significant negative association with increasing SVI. On adjusted logistic regression, there were significantly increased odds of mortality for the fifth quintile of Home-SVI in comparison to the first quintile when adjusted for patient factors; but this lost significance after the addition of vehicular or environmental variables. In contrast, there were decreased odds of ISS15 for the highest quintiles of Crash-SVI in all logistic regression models. CONCLUSIONS: Geographic social vulnerability markers were associated with lower MVC-associated injury severity, perhaps in part because of the association with lower speed limit in these areas.

3.
Am J Surg ; 236: 115757, 2024 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-38719679

RESUMO

INTRODUCTION: National Institute of Health (NIH) funding is a "gold-standard" of achievement; we examined trends in NIH-funded pediatric surgeons. METHODS: NIH Research Portfolio Online Reporting Tools (RePORT) was queried for American Pediatric Surgical Association (APSA) members (2012 vs 2022). Demographics and time-to-award (TTA) from fellowship were compared. Number of grants, funding allotment, award classification, administering institutes/centers, research type were studied. RESULTS: Thirty-eight (4.6%) APSA members were NIH-funded in 2012 compared to 37 (2.9%) in 2022. Of funded surgeons in 2022, 27% were repeat awardees from 2012. TTA was similar (12 vs 14years, p=0.109). At each point, awards were commonly R01 grants (40 vs 52%, p â€‹= â€‹0.087) and basic science-related (76 vs 63%, p = â€‹0.179). Awardees were predominantly men (82% in 2012 vs 78% in 2022, p=0.779) and White (82% in 2012 vs 76% in 2022, p=0.586). Median amount per grant increased: $254,980 (2012) to $364,025 (2022); by $96,711 for men and $390,911 for women. Median awards for White surgeons increased by $215,699 (p=0.035), and decreased by $30,074 for non-White surgeons, though not significantly (p=0.368). CONCLUSION: The landscape of NIH-funded pediatric surgeons has remained unchanged between time points. With a substantial number of repeat awardees, predominance of R01 grants, and a median TTA over a decade after fellowship graduation, the phenotypes of early career pediatric surgeon-scientists are facing academic endangerment.


Assuntos
Pesquisa Biomédica , National Institutes of Health (U.S.) , Humanos , Estados Unidos , National Institutes of Health (U.S.)/economia , Masculino , Feminino , Pesquisa Biomédica/estatística & dados numéricos , Pesquisa Biomédica/economia , Cirurgiões/estatística & dados numéricos , Pediatria , Apoio à Pesquisa como Assunto/estatística & dados numéricos , Bolsas de Estudo/estatística & dados numéricos , Distinções e Prêmios , Especialidades Cirúrgicas/estatística & dados numéricos , Fenótipo
4.
J Pediatr Surg ; 2023 Sep 29.
Artigo em Inglês | MEDLINE | ID: mdl-37867043

RESUMO

INTRODUCTION: Thoracoscopic CDH repair is increasingly performed for Type A and small Type B defects that are amenable to primary repair. However, the thoracoscopic approach is controversial for larger defects necessitating a patch due to technical complexity, intraoperative acidosis, and recurrence risk. We aim to compare clinical outcomes between thoracoscopic and open patch repair of Type B/C defects, using a standardized technique. METHODS: This is a single-center retrospective review of thoracoscopic and open CDH patch repairs January 2017-December 2021. We excluded primary repairs, Type D hernias, repairs on ECMO, recurrent repairs. Various preoperative, intraoperative, and postoperative variables were compared. Primary outcome was recurrence rate. Secondary outcomes included intraoperative pH and pCO2, operative time, and complication rates. RESULTS: Twenty-nine patients met inclusion criteria (open = 13, thoracoscopic = 16). The open cohort had lower o/e total fetal lung volume (29 vs 41.2%, p = 0.042), higher preoperative peak inspiratory pressures (24 vs 20 cm H2O, p = 0.007), were more frequently Type C defects (92.3 vs 31%, p = 0.002) and had liver "up" in left-sided hernias (46 vs 0%, p < 0.0001). Intraoperatively, median lowest pH and highest pCO2 did not differ; neither did overall median pH or pCO2. Operative times were similar (153 vs 194 min, p = 0.113). No difference in recurrence rates was identified, however postoperative complications were higher in the open group. There were no mortalities. CONCLUSIONS: Although we demonstrate higher disease severity of patients undergoing open repair, thoracoscopic patch repair for Type B/C defects is safe and effective in patients with favorable physiologic status, alleviating concerns for intraoperative acidosis, operative length, and risk of recurrence. LEVEL OF EVIDENCE: II.

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