The trachea in children with tracheo‐oesophageal fistula

Wailoo, M P; Emery, John L.

doi:10.1111/j.1365-2559.1979.tb03014.x

Cited by 161 publications

(66 citation statements)

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“…In the adriamycin-induced rat model, the trachea develops directly from the upper foregut rather than as a separate bud or anterior extension of the foregut. The high incidence of tracheomalacia found in this model (unpublished results) and in humans (Wailoo and Emery, 1979) may be secondary to the fact that the tracheal primordium is abnormal. Certainly, we observed that at day 12 the upper foregut appeared histologically more like primitive esophagus than normal trachea in that it had simple columnar epithelium.…”

Section: Discussionmentioning

confidence: 58%

Timing and embryology of esophageal atresia and tracheo-esophageal fistula

et al. 1997

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Background: The embryology of tracheo-esophageal anomalies is controversial. The development of an adriamycin-treated animal model has enabled improved understanding of the embryogenesis of these anomalies. Using this model, we aimed to describe the events leading to esophageal atresia and tracheo-esophageal fistula.Methods: Timed-pregnant Sprague-Dawley rats were injected daily with adriamycin intraperitoneally at a dose of 2 mg/Kg on days 6-9 of gestation. Histological sections were prepared from 96 experimental and 34 control rat embryos at 11-14 days gestation (plug day ‫؍‬ day 0).Results: The tracheal bud failed to develop normally from the foregut, leaving the foregut to give origin to both bronchi and differentiate into the respiratory system, and then continue as a fistula to the lower esophageal segment. Dorsal pouching of the proximal foregut, which is seen clearly on day 13, is responsible for the development of the upper esophageal segment.Conclusions: We conclude that failure of the tracheal bud to develop normally from the primitive foregut is the main event which leads to the tracheo-esophageal anomalies. As the proximal part of the primitive foregut develops primarily into a trachea rather than an esophagus, the anomaly of the esophagus could be described as agenesis instead of atresia. Anat. Rec. 249:240-248, 1997. Key words: embryology; esophageal atresia; tracheo-esophageal fistula; notochordThe first clinical description of esophageal atresia was by Durston in 1670, while tracheo-esophageal fistula was reported by Gibson in 1697 (Myers, 1991).Despite awareness of these conditions, only recently has it been investigated in embryos. There are many theories regarding the embryogenesis of esophageal atresia but most fail to explain the combination of atresia and fistula. Part of the difficulty has been the lack of a reproducible animal model of esophageal atresia and other tracheo-esophageal anomalies, but now the adriamycin-induced fetal rat model (Thompson et al., 1978;Diez-Pardo et al., 1996;Qi et al., 1996) provides us with a model of esophageal atresia and tracheo-esophageal fistula.By comparing the morphological changes which occur in the treated rats and normal controls, we aimed to determine the embryological deviations that produce esophageal atresia and tracheo-esophageal fistula. MATERIALS AND METHODSTimed-pregnant Sprague-Dawley rats from a colony maintained at the Royal Children's Hospital were used. The day a vaginal plug was found was considered day 0 of gestation. The rats were housed individually in solid-bottom plastic cages on sawdust bedding at a controlled temperature of 21°C and humidity of 55%, with a 12L:12D photoperiod. Standard laboratory chow and water were allowed ad libitum. Treated animals were injected daily with adriamycin (David Bull Laboratories, Melbourne) at a dose of 2 mg/Kg intraperitoneally (i.p.) on days 6-9 of gestation (four injections). Animals were euthanized using carbon dioxide inhalation overdose. Ninety-six experimental and 34 control embryo...

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Section: Discussionmentioning

confidence: 58%

Timing and embryology of esophageal atresia and tracheo-esophageal fistula

et al. 1997

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“…Its pathogenesis is also conjectural, despite careful histopathological 13,14 and endoscopic 11 studies. TM is easily categorized as primary when no other lesions exist outside the trachea.…”

Section: Discussionmentioning

confidence: 99%

“…3 Subsequent studies on this subject also support the concept of TM in esophageal atresia being a primary abnormality. 13,2,14 Its significance on the management of EA is obvious, as 16%-20% of children suffer from symptomatic tracheomalacia, which together with gastroesophageal reflux is an important cause of late morbidity. 16 Our own finding of two patients with esophageal atresia and TM, out of a total of approximately 40 EA treated in the period, is probably an underrepresentation.…”

Section: Discussionmentioning

confidence: 99%

Etiology and Management of Tracheomalacia: Experience with 37 Children

et al. 1997

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Tracheomalacia (TM) is a recognized cause of stridor in infancy and childhood. Its link to chronic respiratory failure in children is also known.1 Although laryngomalacia is considered the most common cause of upper airway obstruction in children, TM is increasingly being diagnosed either as an intrinsic deficiency of tracheal structure 2,3 or secondary to a spectrum of surgical lesions of the mediastinum, chest wall and the esophagus. 4 One study considers bronchopulmonary dysplasia (BPD), following prolonged ventilation for hyaline membrane disease, to be the most frequent reason for "primary" tracheomalacia. 5Of increasing interest is TM's association with esophageal atresia (EA). A number of reviews have emphasized its significance in children who suffer recurrent pulmonary problems after the repair of tracheoesophageal fistula. 6,7 There have also been advances in the field of diagnostics, i.e., fiberoptic endoscopy, and cine CT scan, 8,9 and surgical treatment by aortopexy has improved the survival and prognosis of many critically ill children with TM. 10Our interest in the subject was triggered by two surgical children. One of them had EA repaired as a newborn, but continued to suffer from recurrent attacks of pneumonia and apneic spells. Following the diagnosis of TM and aortopexy at the age of 18 months, he improved partially. The other child had aberrant innominate artery, apparently compressing the trachea; exploration did not establish this as the cause, but subsequent bronchoscopy showed TM.In this paper we describe our experience with tracheomalacia from 1986 to 1994 at King Fahd Hospital of the University, Al-Khobar, Saudi Arabia, with a brief review of its etiology and management. Patients and MethodsWe reviewed the records of 45 infants and children in whom one of the discharge diagnosis (ICD-9 World Health Organization) was tracheomalacia. Eight were excluded: in seven the diagnosis of TM was suspected but not proven on bronchoscopy, and in one, the child became asymptomatic after the excision of bronchogenic cyst even though bronchoscopic findings suggested TM.The information recorded included the diagnosis on admission; the age at diagnosis of TM; indication for assisted ventilation and the period of ventilation; associated anomalies; the results of imaging, including esophagogram, CT scan and angiography when performed; timings and findings on bronchoscopy, and the outcome. The patients were classified as primary or secondary tracheomalacia according to groups proposed by Benjamin in 1984 11 and modified by Greenholz et al. in 1986. 12 Only descriptive statistics were used for calculating average, range and standard deviation. ResultsThe ages of children, at the time TM was diagnosed, ranged from 21 days to 38 months, with an average age of 8.5 (SD 9.8) months (median=5; range=0-38). Male to female ratio was equal.Thirty out of 37 children were primary with abnormality confined to the trachea alone: the admission diagnoses were prematurity and hyaline membrane disease (HMD) in 15, meconium...

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“…Wailoo and Emery [5] noted a spectrum of tracheomalacia in an autopsy study of 40 children, involving the whole length in 10%, half of the trachea in 47%, and the short segment of the fistula in 22%. A lengthening of the membranous muscle went along with a shortening of cartilage length.…”

Section: Commentmentioning

confidence: 99%