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consistent with fibromuscular oesophageal stenosis. The dilated oesophagus showed normal architecture and neural deficits were not seen. The final diagnosis was established as congenital triple fibromuscular oesophageal stenosis, cervical megaoesophagus and aspiration pneumonia.
Discussion
Fig 1: Standing double contrast cervical oesophagography: there is a triple ring-like oesophageal stenosis at the thoracic inlet (arrows). The contrast medium fills the dilated caudal cervical part of the oesophagus and the focally dilated segments between the triple strictures. The intrathoracic oesophagus is not dilated and shows peristaltic activity.
In horses, the incidence of congenital oesophageal stenosis is not known, but it is rarely reported. Extramural oesophageal stenosis caused by vascular ring anomaly entrapment has been documented; persistent right aortic arch seems to be the most common (Petrick et al. 1978; Mackey et al. 1986; Butt et al. 1998; Bauer et al. 2006). Congenital mural oesophageal stenosis in a foal was also described in a single case report and was similar to that in children; a single site is typical (Clabough et al. 1991; Amae et al. 2003; Tillotson et al. 2003). It is obvious that the diagnosis of equine oesophageal stenosis in the early stages of a foal’s life is indicative of a congenital disorder. However, the clear exclusion of acquired stricture is usually not possible. The circular mucosal ulceration of different depths after
long-term oesophageal obstruction, external trauma of the neck, healing of oesophageal rupture or previous oesophageal surgery are possible causes of acquired oesophageal luminal stricture (Stick 2006). The short history of our case and clinical signs present from birth are highly suggestive of a congenital disorder and acquired oesophageal narrowing is less likely. Human congenital oesophageal stenosis is typically
Fig 2: Gross necropsy image of the oesophagus. The larynx is on the right and the thoracic part of the oesophagus is on the left. The cervical oesophagus is dilated (megaoesophagus) and the triple oesophageal stricture is marked by arrows.
cervical part of the oesophagus and 3 regions of concentric oesophageal narrowing of the oesophagus at the cranial thoracic inlet (Fig 1). The thoracic part of the oesophagus was normal. Ultrasonographic examination of the dilated oesophagus showed a distended lumen and the oesophageal wall thickness was 1–2 mm. A presumptive diagnosis of mural or extramural oesophageal stricture and cervical megaoesophagus complicated by aspiration pneumonia was made. The owner refused other diagnostic imaging methods and the foal was discharged. He was treated with antibiotics Doxyhexal1 (doxycycline 10 mg/kg bwt b.i.d. per os) but was not weaned from the dam. After 3 weeks the foal’s clinical status deteriorated and he was subjected to euthanasia. The post mortem examination revealed poor physical
condition. The lungs were dark red and milk was present on cut section. The oesophagus was significantly dilated in the whole cervical region (megaoesophagus). There were no vascular rings identified causing oesophageal entrapment. The oesophagus had 3 sharply demarcated mural strictures (1.5 cm diameter) located at the cranial thoracic aperture (Fig 2). Strictures persisted after the oesophageal lumen was cut open. Histopathological examination of the oesophagus at the sites of multiple lumen narrowing showed mild fibrosis with disarrangement of proliferating smooth muscle fibres,
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associated with other developmental anomalies such as oesophageal atresia with distal tracheoesophageal fistula or tetralogy of Fallot or Down’s syndrome (Amae et al. 2003). No other developmental anomaly was identified in our equine patient. In people, 3 types of congenital oesophageal stenosis
have been described – membranous stenosis, fibromuscular stenosis and tracheobronchial remnants (Nihoul-Fekete et al. 1987). Tillotson et al. (2003) suspected membranous web stenosis in a foal successfully treated by balloon dilation. In our case, histopathological examination of the oesophageal wall at the sites of multiple lumen narrowing showed the presence of mild fibrosis with disarrangement of proliferating smooth muscle fibres. This finding, together with the absence of tracheobronchial cartilaginous tissue, respiratory glands and membranous proliferation in the affected parts of the oesophageal wall, corresponds to the congenital oesophageal stenosis known as fibromuscular stenosis (Nihoul-Fekete et al. 1987). The lower third of the oesophagus is most commonly
affected by fibromuscular stenosis in people (Elhalaby et al. 2006). There is insufficient evidence of congenital oesophageal stenosis location in horses with the cervical as well as the thoracic oesophagus having been described (Clabough et al. 1991; Tillotson et al. 2003). In our case, the triple stricture of the oesophagus was located at the thoracic inlet. This location was described in a case of right subclavian artery anomaly creating an oesophageal entrapment in a mature horse (Viljoen et al. 2012). Vascular anomalies were excluded during post mortem examination in our case. Megaoesophagus within the cranial oesophageal part
remains unexplained in our patient. Two types of megaoesophagus are described in the horse – obstruction induced megaoesophagus caused by retention of food
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