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EQUINE VETERINARY EDUCATION / AE / MAY 2015


The endoscopic appearance of the oesophagus was


abnormal in several ways in the first 3 examinations. The dilation proximal to the stricture did not seem to be related only to the distal obstruction but seemed to be at least partially related to dysfunction of the musculature in the oesophageal wall. There was no visible peristalsis and the inner lining did not have the longitudinal striations typical of the longitudinal muscles of the normal oesophagus. The appearance of the oesophagus in the last endoscopy strengthens this assumption since, although the stricture was still present, the proximal oesophagus was much less dilated, peristalsis was observed and the longitudinal striations were evident. This indicated that the function of the proximal oesophagus has improved. There may have been 2 dysfunctional problems, the stricture itself (perhaps muscular spasm) and the dilation of the proximal oesophagus that may have not been caused only by the stricture, as mentioned before. A suggested sequence of events that may explain the clinical improvement is as follows: the balloon dilation resulted in improvement in the stricture site, which resulted in the immediate clinical improvement, then the proximal dilation cause by the stricture improved and finally the normal function returned to the proximal oesophagus and allowed for the further clinical improvement. In the early stages of the described case, the stricture completely obstructed the passage of fluids. The appearance resembled a muscular circular contraction. After resolution of the clinical signs of milk regurgitation, the final endoscopy revealed improvement in the ability of the stenotic site to expand and fluids were able to pass freely through it. This also suggested the presence of a functional problem that was improving and not necessarily an anatomical obstruction. Dysfunction of the oesophagus causing megaoesophagus, without an accompanying stenosis or stricture, has been previously reported in weanling foals, although the dysfunction was probably congenital in these cases (Rohrbach and Rooney 1980; Clark et al. 1987; Broekman and Kuiper 2002). Since manometric examination of the oesophagus was not performed in the described filly, the muscular and neurological function could not be truly assessed. Idiopathic muscular hypertrophy of the oesophagus has been described in horses as an uncommon cause of oesophageal obstruction or rupture (Benders et al. 2004; Cathcart et al. 2013). This oesophageal abnormality is characterised by hypertrophy of the smooth muscle and is usually an incidental finding on post mortem examination. The aetiology of the abnormality is not clear, but it has never been described in neonatal foals. Since the filly in this report survived and did not require surgery, this abnormality could not be ruled in or out although thickening of the oesophageal wall was not observed on the CT scan. Oesophageal ectasia, a congenital dilatation of the oesophagus which is not accompanied by stenosis or stricture, has previously been described in a foal (Rohrbach and Rooney 1980). Oesophageal achalasia, a neuromuscular dysfunction causing flaccid dilatation of the oesophagus accompanied by narrowing of the distal portion was suspected but not proven in a weanling colt (Bowman et al. 1978). Both abnormalities may be clinically similar to the presented case, however, the presence of the stricture and its location precludes these abnormalities. A diverticulum of the oesophagus (Craig et al. 1989; Feige et al. 2000) and an intramural inclusion cyst (Sams et al. 1993) were other possible differential diagnoses but were ruled out by the CT scan and the improvement observed in the last endoscopy. A spasmotic


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dysfunction of the oesophagus causing chest pain and dysphagia is described in human patients (Tutuian and Castell 2006). This condition is not congenital and its aetiology is unclear although abnormalities in endogenous nitric oxide function are suspected. Treatment options include: proton pump inhibitors, calcium channel inhibitors, peppermint oil, visceral analgesia, botulism toxin injection, balloon dilation and myotomy. This condition and most of these treatments have not been described in horses. It is possible that a similar focal dysfunction was the cause for the constriction in the oesophagus in the described filly. The improvement seen in the filly with the use of the balloon dilation might be similar to that seen in some human patients treated for spasmodic obstruction in same manner. Since there was no clear evidence of an anatomical


cause for the stricture, conservative rather than surgical treatment was chosen. Initially, an attempt to medically induce dilatation of the muscle at the site of the stricture was chosen. In the first 2 days of hospitalisation the filly was treated with oxytocin and N-butylscopolammonium (NBB). The use of oxytocin to relax the striated muscle of the oesophagus for the possible treatment of acute oesophageal obstructions (‘choke’) has been previously examined with conflicting results. In the study by Meyer et al. (2000) several doses of i.v. oxytocin were shown to cause intramural pressure reduction due to relaxation of the striated muscle located in the proximal two-thirds of the oesophagus. Contrary to these results, the study by Wooldridge et al. (2002) demonstrated no effect of oxytocin on the equine oesophageal musculature. Oxytocin was used in this case at the dose of 0.11 u/kg bwt as described by Meyer et al. (2000), who found that the peak relaxation effect of this dose of oxytocin occurred within 15 min of administration. The oxytocin treatment did not seem to have any lasting effect on the oesophageal obstruction in the described case. N-butylscopolammonium is an anticholinergic smooth muscle relaxant that has been shown to cause relaxation of the muscles of the rectum in normal horses (Luo et al. 2006) and bronchodilation in horses suffering from recurrent airway obstruction (Couetil et al. 2012). Its effect on the equine oesophagus musculature has not been studied. N-butylscopolammonium was used empirically in this case in the hope it would cause relaxation of the smooth muscle fibres located in the muscularis mucosa of the oesophagus and help facilitate dilatation of the stricture site. No effect of the NBB administration was observed in the described filly. Since an endoscopic examination was not performed within the time period of maximal effect of both oxytocin and NBB (the second endoscopy was performed >24 h after the last treatments) a transient effect on the stricture could not be ruled out; however, a long lasting effect was not observed. In hindsight, the use of these medications during the bougienage sessions might have been beneficial, but this was not considered at the time. Since the pharmacological treatments were unsuccessful


and no obvious anatomical abnormality was diagnosed as the cause for the stricture, balloon bougienage was used in an attempt to facilitate oesophageal dilatation. The described case is the first report of some success in the use of balloon bougienage for the treatment of congenital oesophageal stenosis or stricture in a neonatal foal. Attempts to dilate oesophageal strictures with the same method have been anecdotally described in horses with variable results. Knottenbelt et al. (1992) described one unsuccessful attempt


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