EQUINE VETERINARY EDUCATION / AE / MAY 2015


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Case Report


Congenital triple oesophageal stricture and megaoesophagus in a neonatal colt


B. Bezdekova*†, M. Skoric‡ and M. Pekarkova§ †Equine Clinic, Faculty of Veterinary Medicine, University of Veterinary and Pharmaceutical Sciences Brno, Brno, Czech Republic; ‡Department of Pathology and Parasitology, Faculty of Veterinary Medicine, University of Veterinary and Pharmaceutical Sciences Brno, Brno, Czech Republic; and §UK-VET sro, Praha, Czech Republic. *Corresponding author email: bbezdekova@vfu.cz


Keywords: foal; dysphagia; aspiration pneumonia; contrast radiographs


Summary Congenital oesophageal stenosis is rarely described in horses. This case report describes a neonatal colt with signs of a milky nasal discharge and cervical swelling present from birth. The diagnostic evaluation revealed a triple oesophageal stricture, identified as congenital fibromuscular oesophageal stenosis. A megaoesophagus was seen cranial to the strictures, but its aetiology remains unexplained. To the authors’ knowledge, multiple oesophageal stenosis together with megaoesophagus has not previously been described in the horse.


Introduction


The incidence of human congenital oesophageal stenosis is estimated at 1 in 23,000–50,000 live births (Rowe et al. 1995). In horses, the incidence of congenital oesophageal stenosis is not known, but it is rarely reported. Acquired forms of oesophageal strictures are more common in the horse and can be caused by external or internal trauma such as long-term oesophageal obstruction, which can produce circumferential ulceration, or a kick from another horse, nasogastric tube trauma, oesophageal surgery or oesophageal healing following rupture (Fubini et al. 1999). Clinical signs of congenital stenosis appear shortly after birth. In addition to vascular entrapments of the oesophagus (vascular ring abnormalities), simple congenital stenosis has also been described (Steward and Reinertson 1983; Clabough et al. 1991; Tillotson et al. 2003). These cases were not accompanied by a megaoesophagus. Membranous stenosis, fibromuscular stenosis and tracheobronchial remnants are described histologically in human congenital oesophageal stenosis (Nihoul-Fekete et al. 1987). In equine simple congenital stenosis the mucosal and submucosal layers of the oesophagus appear to be involved, which could be similar to membranous webs in man (Stick 1987; Clabough et al. 1991; Tillotson et al. 2003). Therefore those lesions could be suitable candidates for balloon dilation (Tillotson et al. 2003). Idiopathic congenital megaoesophagus has been described as a functional oesophageal disorder in the horse and the Friesian breed is predisposed to its occurrence (Broekman and Kuiper 2002). The other possible functional disorders described as congenital are oesophageal agangliosis and achalasia (Klein et al. 1989). This report documents a case of congenital triple oesophageal stricture with cranial megaoesophagus. To the authors’ knowledge, a similar case has not previously been reported in the scientific literature.


Case description


An 11-day-old, 41 kg Akhal Teke colt was referred to the Equine Clinic, Faculty of Veterinary Medicine, University of Veterinary and Pharmaceutical Sciences Brno because of bilateral milky nasal discharge, which was first seen on the second day after his birth. Intermittent swelling on the left part of his neck was observed during suckling, suspected of being an enlarged oesophagus. On admission, the colt was bright, alert and in good


condition physically. Temperature was slightly elevated (38.6°C), the respiratory rate and the heart rate were normal (26 breaths/min; 62 beats/min). Mucous membranes were pink, and capillary refill time was 1.5 s. Lung auscultation revealed harsh sounds bilaterally during inspiration and expiration. On tracheal auscultation, intraluminal fluid sound could be heard, suggesting milk aspiration into the lower airways. Normal intestinal borborygmi were heard bilaterally in the abdomen. When the colt suckled from the mare’s udder, dilation of the cervical oesophagus was noted. Immediately after suckling, bilateral milky discharge was seen and hand palpation of the dilated oesophagus caused its increase. Clinical pathology showed a normal level of IgG (>8.0 g/l),


hyperfibrinogenaemia (4.74 g/l; reference range [rr] 1.5– 3.0 g/l), hyperbilirubinaemia (80.0 μmol/l; rr 1.7–39.0 μmol/l), increased bile acids (37.2 μmol/l; rr for age 2 weeks 11.3– 30.6 μmol/l [Barton and LeRoy 2007]), mature neutrophilia (9.76 × 109/l [88%]; rr 5.1–8.7 × 109/l [50–75%]) and lymphopenia (0.927 × 109/l [9%]; rr 1.6–5.1 × 109/l [25–50%]). Endoscopic examination was performed without medical


restraint using a 140 cm, 9mm diameter fibrescope. This ruled out upper airway developmental pathology. Milk was present within the upper and lower airways. The larynx was normal but the cervical part of the oesophagus contained a large amount of milk and its peristaltis was poor. The thoracic oesophagus showed normal peristaltic waves. Oesophageal mucosal appearance was normal and no obvious narrowing of the oesophageal lumen could be identified. The stomach was partially filled with milk and the nonglandular mucosa surface was normal. The pyloric antrum and pylorus were not examined. Standing chest radiographs showed a patchy alveolar lung pattern caudoventrally consistent with aspiration pneumonia. A nasogastric tube (diameter 12 mm) was inserted into the


foal’s oesophagus and it reached the stomach normally. Plain and double contrast radiographic examination of the oesophagus using barium contrast and air insufflation was done, and showed a moderate to severely gas-dilated


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