EQUINE VETERINARY EDUCATION / AE / MAY 2015


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were not performed due to financial constraints. Chest radiographs revealed resolution of the pneumonia. The filly was discharged from the hospital on the same day, 17 days after admission. The owner was instructed to observe for food regurgitation when the filly started eating solid food. On repeated phone conversations 2, 4, 7 and 10 months after discharge, the owner reported that the filly was doing well, growing at a normal rate, eating hay and grains and no food was observed in the nostrils at any time. Since the filly was doing so well at home, the owner declined the suggestion for endoscopic follow-up, thus long-term evaluation of the oesophageal stricture was not available.


Discussion


Fig 4: Images from the final endoscopy of the oesophagus, on the day of discharge. a) The stricture is still present; however, the proximal oesophagus has a more normal appearance, with the longitudinal folds apparent. b) Dilation of the lumen in the stricture site during a peristaltic wave.


megaoesophagus and stricture were unchanged. This second attempt in balloon bougienage was performed in the same manner and seemed to be slightly more successful as an occasional small opening in the stricture with a concentric expansion of the lumen would appear and then collapse again. The slightly larger opening in the stricture site allowed for better and easier positioning of the balloon catheter and the balloon was inflated with 20 ml and was kept in place for a maximum of 20 s before it would slip away as before. On the next day (ninth day of hospitalisation), there was less foam coming out of the mouth and nostrils and the filly was allowed to nurse once from the mare after manual milking followed by elevation of her head and neck for several minutes. No milk was seen in the nostrils or the mouth after this suckling. On Day 10, the i.v. catheter was removed and the antibiotic treatment was changed to cefquinome (2 mg/kg bwt, i.m., s.i.d. Cobactan 2.5%1). The filly was allowed to nurse twice after milking with no signs of milk regurgitation. During the following 6 days the filly was gradually allowed to nurse more frequently and for longer periods until Day 16, when she was nursing from the mare with no restrictions and without any difficulty or milk regurgitation. Repeated endoscopy on Day 17, revealed marked improvement in the general appearance of the proximal oesophagus. There was very mild dilation with normal looking longitudinal mucosal folds and normal peristalsis was observed. The stricture was still present; however, during the normal peristalsis waves in the oesophagus, transient dilatations and opening of the lumen at the stricture site were observed (Fig 4). There was no milk accumulation in the oesophagus, pharynx or trachea. Further bougienage sessions


Dysphagia accompanied by milk regurgitation in neonatal foals is not an uncommon phenomenon. Most causes are related to pharyngeal or laryngeal anomalies such as dorsal displacement of the soft palate, cleft palate, pharyngeal dysfunction (weakness or paresis) and anomalies of the epiglottis (Altmaier and Morris 1993; Holcombe et al. 2012). Food regurgitation due to oesophageal congenital anomalies are far less common. There are only a few detailed case reports describing congenital oesophageal abnormalities causing obstruction in neonatal foals. Most of these cases describe vascular ring anomalies, mainly a persistent right aortic arch (Bartels and Vaughan 1969; van der Linde-Sipman et al. 1979; Mackey et al. 1986; Butt et al. 1998; Bauer et al. 2006). One case report described an unusual vascular ring anomaly (VRA) causing oesophageal obstruction, which was not a persistent right aortic arch and could not be fully identified on a post mortem examination (Smith 2004). The case described here presents a congenital oesophageal stricture that could not be explained by a VRA despite the use of advanced diagnostic tools such as the CT scan. There is one detailed previous report of a foal with a suspected congenital oesophageal stenosis where a VRA or other anatomical anomalies were not identified (Clabough et al. 1991). Craig et al. (1989) described 61 equine cases of various oesophageal disorders. Six out of the 18 cases with oesophageal strictures were foals aged 1–9 months. The report states that the clinical signs in all the foals began within 2 weeks of parturition. Although definitive diagnosis was not described for any of the strictures, the authors deduced that the strictures were most probably congenital (3 foals survived in the long term). Knottenbelt et al. (1992) described 5 foals with cervical oesophageal strictures, 3 of which were aged 3–4 weeks and all were apparently normal at birth. Acquired oesophageal strictures in mature horses are


mostly related to chronic ulceration causing secondary fibrosis and stricture (Craig et al. 1989; Feige et al. 2000). The condition could be acquired in neonatal foals as well and may be related to gastric ulceration and reflux oesophagitis (Murray et al. 1988). In the presented case, on endoscopic examination no mucosal abnormalities were observed in the oesophagus or the stomach. There were no signs of ulceration, hypertrophy or scarring, so it was not likely that the lesion was acquired in origin. In agreement with the findings and conclusions described in the case reported by Clabough et al. (1991), the oesophageal obstruction in the described case is most appropriately defined as a stenosis or functional stricture since a clear anatomical abnormality in the wall of the oesophagus was not identified.


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