Interdisciplinary structural follow-up of surgical newborns: a prospective evaluation

Gischler, Saskia J.; Mazer, Petra; Duivenvoorden, Hugo J.; Dijk, Monique van; Bax, N. M. A.; Hazebroek, F. W. J.; Tibboel, Dick

doi:10.1016/j.jpedsurg.2008.12.034

Cited by 110 publications

(142 citation statements)

References 29 publications

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“…After screening of title/abstract followed by full text, 23 papers 6,7,[25][26][27][28][29][30][31][32][33][34][35][36][37][38][39][40][41][42][43][44] reporting on 895 children met our inclusion and exclusion criteria and were selected for systematic review (Table 1). There was a wide range in follow-up duration and time of assessment from 12 months up to 60 months of age.…”

Section: Resultsmentioning

confidence: 99%

“…However, for noncardiac congenital anomalies (NCCA), there are limited data regarding the impact on neurodevelopmental outcomes, and results from existing studies are contradictory. Laing et al 6 reported a concerning rate of up to 50% mild to significant neurodevelopmental delay in these children; conversely Gischler et al 7 found no delay in cognitive outcome in this group. The latter did find a significant delay in motor development, however.…”

mentioning

confidence: 75%

“…Meta-analysis in 498 infants showed a cognitive development score of 0.5 SD below the population reference mean, expressed as MDI score of 92 ± 13 (mean ± SD) 6,7,25,26,28,29,31,[36][37][38]40,41 (Fig 2A), with data from BSID-II and -III at 12 and 24 months of age. Onesample t tests demonstrated that the mean MDI was significantly lower than the healthy population mean of 100 (P < .001; 95%, confidence interval [CI] 91.7-94.2).…”

Section: Meta-analysismentioning

confidence: 92%

“…6,7,25,26,28,29,31,[36][37][38][39][40][41] This metaanalysis in 511 children resulted in a motor development score of 0.6 SD below the population average, indicated by the PDI score of 91 ± 14 (Fig 3A). One-sample t tests demonstrated that the mean PDI was significantly lower than the healthy population mean of 100 (P < .001; 95% CI 89.8-92.1).…”

Section: Meta-analysismentioning

confidence: 94%

“…A higher number of congenital anomalies also significantly increased the risk of neurodevelopmental delay. 7,30,37 Neuroimaging with either cerebral ultrasonography, CT, or MRI scanning was reported in 11 studies, 7,26,27,31,34,35,[40][41][42]45,47 and 10 of these articles reported solely on CDH. In 7 studies, 7,34,[40][41][42]45,47 the correlation between brain damage and neurodevelopmental outcome was not explored, and in 4 studies, 26,27,31,35 no significant correlation was found.…”

Section: Risk Factorsmentioning

confidence: 99%

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Neurodevelopmental Outcomes After Neonatal Surgery for Major Noncardiac Anomalies

et al. 2016

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Section: Resultsmentioning

confidence: 99%

mentioning

confidence: 75%

Section: Meta-analysismentioning

confidence: 92%

Section: Meta-analysismentioning

confidence: 94%

Section: Risk Factorsmentioning

confidence: 99%

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Neurodevelopmental Outcomes After Neonatal Surgery for Major Noncardiac Anomalies

et al. 2016

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Infantile hypertrophic pyloric stenosis in patients with esophageal atresia

Kate

Brouwer

Bever

et al. 2020

Birth Defects Research

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Background: Patients born with esophageal atresia (EA) have a higher incidence of infantile hypertrophic pyloric stenosis (IHPS), suggestive of a relationship. A shared etiology makes sense from a developmental perspective as both affected structures are foregut derived. A genetic component has been described for both conditions as single entities and EA and IHPS are variable components in several monogenetic syndromes. We hypothesized that defects disturbing foregut morphogenesis are responsible for this combination of malformations. Methods: We investigated the genetic variation of 15 patients with both EA and IHPS with unaffected parents using exome sequencing and SNP arraybased genotyping, and compared the results to mouse transcriptome data of the developing foregut. Results: We did not identify putatively deleterious de novo mutations or recessive variants. However, we detected rare inherited variants in EA or IHPS disease genes or in genes important in foregut morphogenesis, expressed at the proper developmental time-points. Two pathways were significantly enriched (p < 1 × 10 −5): proliferation and differentiation of smooth muscle cells and self-renewal of satellite cells. Conclusions: None of our findings could fully explain the combination of abnormalities on its own, which makes complex inheritance the most plausible genetic explanation, most likely in combination with mechanical and/or environmental factors. As we did not find one defining monogenetic cause for the EA/IHPS phenotype, the impact of the corrective surgery could should be further investigated.

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Lung function, exercise tolerance, and physical growth of children with congenital lung malformations at 8 years of age

Hijkoop

Schoonhoven

Rosmalen

et al. 2019

Pediatric Pulmonology

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Objective To improve counseling on congenital lung malformations (CLM) by describing long‐term outcomes of children either operated on or managed by observation. Study design We analyzed lung function (spirometry), exercise tolerance (Bruce treadmill), and physical growth of 8‐year‐old children with CLM who participated in our longitudinal prospective follow‐up program. The data are shown as median standard deviation scores (SDS) with IQR, or estimated marginal means (95% CI) on the basis of general linear models. Results Twenty‐nine (48%) of the 61 children had required surgery at a median age of 108 (IQR: 8‐828) days, and 32 (52%) were managed by observation. In the surgery group, all lung function measurements (except for forced vital capacity [FVC]) were significantly below 0 SDS, with median FEV1 −1.07 (IQR: −1.70 to −0.56), FEV1/FVC −1.49 (−2.62 to −0.33), and FEF25%‐75% −1.95 (−2.57 to −0.63) (all P < 0.001). Children in the observation group had normal FEV1 and FVC, whereas FEV1/FVC (−0.81 (−1.65 to −0.14)) and FEF25%‐75% (−1.14 (−1.71 to −0.22)) were significantly below 0 SDS (both P < 0.001). Mean exercise tolerance was significantly below 0 SDS in both groups (observation: −0.85 (95% CI: −1.30 to −0.41); surgery: −1.25 (−1.69 to −0.80)); eight (28%) children in the observation group and ten (40%) in the surgery group scored <−1 SDS. Physical growth was normal in both groups. Conclusion Children with CLM may be at risk for reduced lung function and exercise tolerance, especially those who required surgery. As little pulmonary morbidity was found in children with asymptomatic CLM, this study supports a watchful waiting approach in this group.

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Interdisciplinary structural follow-up of surgical newborns: a prospective evaluation

Cited by 110 publications

References 29 publications

Neurodevelopmental Outcomes After Neonatal Surgery for Major Noncardiac Anomalies

Neurodevelopmental Outcomes After Neonatal Surgery for Major Noncardiac Anomalies

Infantile hypertrophic pyloric stenosis in patients with esophageal atresia

Lung function, exercise tolerance, and physical growth of children with congenital lung malformations at 8 years of age

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