A histopathological study of esophageal atresia and tracheoesophageal fistula

Dutta, Hemonta Kumar; Mathur, Manu; Bhatnagar, Veereshwar

doi:10.1016/s0022-3468(00)90209-4

Cited by 38 publications

(23 citation statements)

References 7 publications

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“…Immunohistochemical studies with Actin showed agenesia of muscularis mucosae and an evident disarrangement of muscle bundles in the UEP [11] and, histologically, complete disorganization of muscularis mucosae and muscularis propria in the DES [12]. From the above findings, it can be inferred that EA/TEF is accompanied by a development failure of some mesodermal-derived buds in connection with a diagonal deviation of the esophago-tracheal septum.…”

Section: Discussionmentioning

confidence: 99%

Intramural Ganglion Structures in Esophageal Atresia: A Morphologic and Immunohistochemical Study

Zuccarello

Spada

Turiaco

et al. 2009

International Journal of Pediatrics

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Introduction and Aim. Disorders of esophageal motility causing dysphagia and gastroesophageal reflux are frequent in survivors to esophageal atresia (EA) and distal tracheoesophageal fistula (TEF). The aim of the present study was to investigate the histologic and immunohistochemical features in both esophageal atretic segments to further understand the nature of the motor disorders observed in these patients. Material and Methods. Esophageal specimens from 12 newborns with EA/TEF and 5 newborns dead of unrelated causes were examined. The specimens were fixed in 5% buffered formalin, included in paraffin and cut in 5 micron sections that were stained with hematoxilin and eosin (H and E), and immunohistochemical stainings for Actin, S-100 protein, Neurofilament, Neuron-Specific-Enolase, Chromogranin A and Peripherin were evaluated under the microscope. Results. In controls, the distribution of the neural elements was rather homogenous at both levels of the esophagus. In contrast, the atretic segments showed quantitative and qualitative differences between them with sparser nervous tissue in the distal one in comparison with the proximal one and with controls. Conclusions. These results further support the assumption that histomorphological alterations of the muscular and nervous elements within the esophageal wall might contribute to esophageal dysmotility in patients surviving neonatal operations for EA/TEF.

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Section: Discussionmentioning

confidence: 99%

Intramural Ganglion Structures in Esophageal Atresia: A Morphologic and Immunohistochemical Study

Zuccarello

Spada

Turiaco

et al. 2009

International Journal of Pediatrics

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“…15 Other researchers have reported cases in which the fistula tract contains tissue of respiratory origin, such as tracheobronchial remnants or even pulmonary sequestrations. [16][17][18][19] The respiratory lineage of the fistula tract could account for the consistently poor motility seen after standard repair of EA/TEF. As we work to define the molecular signaling anomalies of both the rodent and human models of EA/TEF, perhaps we can gain some understanding of how to better treat or even prevent this anomaly.…”

Section: Discussionmentioning

confidence: 99%

Aberrant fibroblast growth factor receptor 2 signalling in esophageal atresia with tracheoesophageal fistula

Spilde

Bhatia

Mehta

et al. 2004

Journal of Pediatric Surgery

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“…Analysis of esophageal innervation in dead EA newborn has reported abnormalities in the Auerbach plexus (plexus hypoplasia and abnormal interganglionic network) (34). Other studies have also reported hypoplasia of esophageal innervation or smooth muscle (35, 36) or interstitial cells of Cajal (37) in the proximal pouch (36, 38, 39), distal esophagus (36, 37, 39, 40), or in the fistula (35, 41). Animal studies in a rat adriamycin model of EA have similarly shown abnormal vagal and intrinsic innervation of the esophagus (36, 42).…”

Section: Etiology Of the Esophageal Dysmotilitymentioning

confidence: 98%

Dysmotility in Esophageal Atresia: Pathophysiology, Characterization, and Treatment

Fauré

Grunder

2017

Front. Pediatr.

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Esophageal dysmotility is almost universal after esophageal atresia (EA) repair and is mainly related to the developmental anomaly of the esophagus. Esophageal dysmotility is involved in the pathophysiology of numerous symptoms and comorbidities associated with EA such as gastroesophageal reflux disease, aspiration and respiratory complications, and symptoms of dysphagia and feeding disorders. High-resolution esophageal manometry (HREM) has facilitated the characterization of the dysmotility, but there is an incomplete correlation between symptoms and manometrical patterns. Impedance coupled to HREM should help to predict the clinical outcome and therefore personalize patient management. Nowadays, the management of esophageal dysmotility in patients with EA is essentially based on treatment of associated inflammation related to peptic or eosinophilic esophagitis.

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A histopathological study of esophageal atresia and tracheoesophageal fistula

Cited by 38 publications

References 7 publications

Intramural Ganglion Structures in Esophageal Atresia: A Morphologic and Immunohistochemical Study

Intramural Ganglion Structures in Esophageal Atresia: A Morphologic and Immunohistochemical Study

Aberrant fibroblast growth factor receptor 2 signalling in esophageal atresia with tracheoesophageal fistula

Dysmotility in Esophageal Atresia: Pathophysiology, Characterization, and Treatment

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