Contemporary postoperative imaging practices among pediatric surgeons for image-guided central venous line placement: A survey of the American Pediatric Surgical Association.
- 作者列表："Cunningham AJ","Krishnaswami S","Radu S","Hamilton NA
BACKGROUND/PURPOSE:Rare life-threatening complications after central venous line (CVL) placement in children may encourage the routine use of postoperative imaging, despite multiple studies demonstrating the limited utility of this practice. The aim of this study was to investigate the nature of this discordance. METHODS:A 10-question survey was sent to 1,239 members of the American Pediatric Surgical Association (APSA) addressing contemporary practices regarding CVL placement and postoperative imaging. RESULTS:Five hundred eighteen (42%) surveys were completed. The majority of respondents routinely obtain a chest radiograph (CXR) after image-guided CVL placement (52%). Years in practice, operative volume, and practice type were not statistically associated with postoperative CXR usage (all p > 0.05). 'Routine' users were more likely to cite "standard of care" (p < 0.001), position verification (p < 0.001), and complication identification (p < 0.001) as indications for use than those who use CXR selectively. CONCLUSION:Routine use of postoperative CXR after image-guided CVL placement remains common among pediatric surgeons. Significant variation exists in the indication for this study, with considerable disagreement between 'selective' and 'routine' users. Consideration should be given for an APSA standardized guideline utilizing a clinically-driven approach to CVL placement and postoperative imaging to align with evidence-based practice. LEVEL OF EVIDENCE:N/A - descriptive analysis of survey results.
背景/目的: 儿童中心静脉线 (CVL) 置入后罕见的危及生命的并发症可能鼓励术后影像学的常规使用，尽管多项研究证明这种做法的效用有限。本研究的目的是调查这种不一致的性质。 方法: 向美国小儿外科协会 (APSA) 的 1,239 名成员发送了一项 10 个问题的调查，讨论了关于 CVL 放置和术后成像的当代实践。 结果: 完成了 42% 项调查。大多数受访者在图像引导 CVL 放置后常规获得胸片 (CXR) (52%)。实践年限、手术量和实践类型与术后 CXR 使用无统计学关联 (均 p> 0.05)。“常规” 用户更可能引用 “护理标准” (p <0.001) 、位置验证 (p <0.001) 和并发症识别 (p <0.001) 作为适应症的使用比那些选择性使用 CXR 的人。 结论: 小儿外科医生在影像引导下放置 CVL 后常规使用术后 CXR 仍然很常见。本研究的适应症存在显著差异，“选择性” 和 “常规” 用户之间存在相当大的分歧。应考虑使用临床驱动的 CVL 放置和术后成像方法的 APSA 标准化指南，以与循证实践保持一致。 证据水平: N/A-调查结果的描述性分析。
METHODS:BACKGROUND:Preterm birth is a risk factor for elevated blood pressure in childhood and the development of hypertension and cardiometabolic disease in adulthood; however, mechanisms for the development of both are poorly understood. Rapid weight gain early in childhood may serve as a driver directly and indirectly through cortisol levels found to be elevated in early childhood in individuals born preterm. OBJECTIVES:The objective of this pilot study was to examine the effect sizes of the relationships between weight gain and blood pressure in toddlers born very preterm. A secondary aim was to note any mediating effect of cortisol on the relationships between weight gain and blood pressure. METHODS:A cross-sectional design with a convenience sample of 36 toddlers who were born very preterm was used to examine the relationships between postnatal weight gain, cortisol, and blood pressure at follow-up. RESULTS:Many of the participants experienced rapid weight gain in the first 12 months of life. Mean systolic and diastolic readings were 94 and 56.6, respectively. Diastolic blood pressure readings were obtained from 23 participants and the majority were elevated. Weight gain was associated with diastolic blood pressure with a medium effect size. A mediating role with cortisol was not supported.Although findings need to be validated in a larger sample, the blood pressure elevations in this sample were alarming. If readings continue to amplify as these children age, the fact that elevations are already present during the toddler period could indicate more significant cardiovascular disease in adulthood for this population. Rapid weight gain in early life may be a driver for elevated blood pressure even during early childhood in individuals born preterm.
METHODS:This article presents a case series of n = 21 models of fetal cardiovascular anatomies obtained from post mortem microfocus computed tomography (micro-CT) data. The case series includes a broad range of diagnoses (e.g., tetralogy of Fallot, hypoplastic left heart syndrome, dextrocardia, double outlet right ventricle, atrio-ventricular septal defect) and cases also had a range of associated extra-cardiac malformations (e.g., VACTERL syndrome, central nervous system anomalies, renal anomalies). All cases were successfully reconstructed from the microfocus computed tomography data, demonstrating the feasibility of the technique and of the protocols, including in-house printing with a desktop 3D printer (Form2, Formlabs). All models were printed in 1:1 scale as well as with the 5-fold magnification, to provide insight into the intra-cardiac structures. Possible uses of the models include education and training.
METHODS:Abstract Background Congenital heart disease (CHD) affects ~ 1% of live births and is the most common birth defect. Although the genetic contribution to the CHD has been long suspected, it has only been well established recently. De novo variants are estimated to contribute to approximately 8% of sporadic CHD. Methods CHD is genetically heterogeneous, making pathway enrichment analysis an effective approach to explore and statistically validate CHD-associated genes. In this study, we performed novel gene and pathway enrichment analyses of high-impact de novo variants in the recently published whole-exome sequencing (WES) data generated from a cohort of CHD 2645 parent-offspring trios to identify new CHD-causing candidate genes and mutations. We performed rigorous variant- and gene-level filtrations to identify potentially damaging variants, followed by enrichment analyses and gene prioritization. Results Our analyses revealed 23 novel genes that are likely to cause CHD, including HSP90AA1, ROCK2, IQGAP1, and CHD4, and sharing biological functions, pathways, molecular interactions, and properties with known CHD-causing genes. Conclusions Ultimately, these findings suggest novel genes that are likely to be contributing to CHD pathogenesis.