Long-term evaluation of esophageal function in patients treated at birth for esophageal atresia

Tomaselli, V.; Volpi, M.; Dell'Agnola, C. A.; Bini, Marta; Rossi, Alfredo; Indriolo, A.

doi:10.1007/s00383-002-0887-z

Cited by 79 publications

(47 citation statements)

References 11 publications

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“…However, the prevalence of dysphagia in the age groups 5–11 and 12–18 years was lower than other literature reports, although our population was similar to those in previously published studies [12, 13, 18, 23]. In general, dysphagia in children is underreported as stated in literature [19].…”

Section: Discussionsupporting

confidence: 83%

“…So far, this subdivision has not been applied before in dysphagia prevalence studies in children with OA [12, 13, 18, 23]. In our results, oropharyngeal dysphagia was present in children with repaired OA based on review of medical records.…”

Section: Discussionmentioning

confidence: 55%

“…Despite this improved survival, significant numbers of children with repaired OA still have to deal with short- and long-term morbidity. This has led to increased interest in the identification of morbidity in these patients [10–12, 21, 23]. …”

Section: Introductionmentioning

confidence: 99%

“…Dysphagia is a common problem [12, 20, 23]. Due to the dysphagia, many children develop adaptive feeding behaviours [11, 20].…”

Section: Introductionmentioning

confidence: 99%

“…Two issues limit the up-to-date knowledge of dysphagia in this population. First, different definitions are used to describe dysphagia [10, 14, 20], which probably explains the wide variability in prevalence of 45 to 70 % [12, 13, 18, 23]. Second, dysphagia can occur in one or more phases of the swallowing process, respectively, the oral, pharyngeal and oesophageal phase.…”

Section: Introductionmentioning

confidence: 99%

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Dysphagia in children with repaired oesophageal atresia

et al. 2016

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Dysphagia is a common problem in children with repaired oesophageal atresia (OA). Abnormalities in the oropharyngeal and oesophageal phase have hardly been studied. The aims of this study were to assess the prevalence of dysphagia in children with repaired OA and to identify and differentiate oral and pharyngeal dysphagia based on videofluoroscopic swallow study (VFSS) findings in a limited number of children in this cohort. Medical records of 111 patients, born between January 1996 and July 2013 and treated at the Radboudumc Amalia Children’s Hospital, were retrospectively reviewed. The prevalence of dysphagia was determined by the objective and modified Functional Oral Intake Scale (FOIS) in four age groups. The first performed VFSS of 12 children was structurally assessed. The prevalence of dysphagia was 61 of 111 patients (55 %) in age group <1 year. In age group 1–4, 5–11 and 12–18 years, the prevalence of dysphagia decreased from 54 of 106 (51 %) patients to 11 of 64 (17 %) and 5 of 24 (21 %) patients. The 12 VFSS’s reviews revealed oral dysphagia in 36 % and pharyngeal dysphagia in 75 %.Conclusions: This study highlights dysphagia as an important problem in different age groups of children with repaired OA. Furthermore, our study shows the presence of oropharyngeal dysphagia in this population. This study emphasizes the need to standardize the use of objective dysphagia scales, like the modified FOIS, to provide a careful follow-up of children with repaired OA. What is Known: • Prevalence of dysphagia in children with repaired oesophageal atresia varies widely (ranges from 45 to 70 %) in literature. • Oral, pharyngeal and oesophageal dysphagia require different treatment approaches. What is New: • We determined dysphagia based on functional oral intake and provide an overview of change in dysphagia prevalence and severity over time in children with repaired OA. • Our study shows that dysphagia, including oropharyngeal dysphagia, is highly prevalent in young children with repaired OA and improves with time.

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Section: Discussionsupporting

confidence: 83%

Section: Discussionmentioning

confidence: 55%

Section: Introductionmentioning

confidence: 99%

“…Dysphagia is a common problem [12, 20, 23]. Due to the dysphagia, many children develop adaptive feeding behaviours [11, 20].…”

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Dysphagia in children with repaired oesophageal atresia

et al. 2016

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The Effect of Adriamycin Exposure on the Notochord of Mouse Embryos

Hajduk

May

Puri

et al. 2012

Birth Defects Research Pt B

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The notochord has important structural and signaling properties during vertebrate development with key roles in patterning surrounding tissues, including the foregut. The adriamycin mouse model is an established model of foregut anomalies where exposure of embryos in utero to the drug adriamycin leads to malformations including oesophageal atresia and tracheoesophageal fistula. In addition to foregut abnormalities, treatment also causes branching, displacement, and hypertrophy of the notochord. Here, we explore the hypothesis that the notochord may be a primary target of disruption leading to abnormal patterning of the foregut by examining notochord position and structure in early embryos following adriamycin exposure. Treated (n = 46) and control (n = 30) embryos were examined during the crucial period when the notochord normally delaminates away from the foregut endoderm (6-28 somite pairs). Transverse sections were derived from the anterior foregut and analyzed by confocal microscopy following immunodetection of extracellular matrix markers E-cadherin and Laminin. In adriamycin-treated embryos across all stages, the notochord was abnormally displaced ventrally with prolonged attachment to the foregut endoderm. While E-cadherin was normally detected in the foregut endoderm with no expression in the notochord of control embryos, treated embryos up to 24 somites showed ectopic notochordal expression indicating a change in characteristics of the tissue; specifically an increase in intracellular adhesiveness, which may be instrumental in structural changes, affecting mechanical and signaling properties. This is consistent with disruption of the notochord leading to altered signaling to the foregut causing abnormal patterning and congenital foregut malformations.

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