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EQUINE VETERINARY EDUCATION / AE / MAY 2015
Case Report
Congenital oesophageal stricture in an Arabian filly treated by balloon dilation
D. Berlin*, K. Shaabon and D. Peery The Koret School of Veterinary Medicine – Veterinary Teaching Hospital, The Hebrew University of Jerusalem, Rehovot, Israel. *Corresponding author email:
dalia.berlin@
mail.huji.ac.il
Keywords: horse; congenital; foal; oesophagus; stenosis; stricture; balloon dilation
Summary Congenital oesophageal stricture was diagnosed via endoscopy in a 3-day-old Arabian filly suffering from nasal milk regurgitation. Vascular ring anomaly or other extramural, intramural or intraluminal causes were not identified on radiographs or on a computed tomography scan; thus a functional abnormality was suspected. The filly was treated with antibiotics for aspiration pneumonia and was fed milk through an indwelling nasoesophageal tube. Two sessions of balloon bougienage at the stenotic site, under sedation, resulted in marked clinical improvement and thereafter the filly was gradually reintroduced to suckling from the mare. The filly was discharged from the hospital after 17 days and on follow-up there were no reports of food regurgitation even after the introduction of solid food. The filly was still doing well in the latest follow-up at age 11 months.
Introduction
Congenital laryngeal and pharyngeal abnormalities resulting in milk regurgitation are routinely observed in neonatal foals (Altmaier and Morris 1993; Holcombe et al. 2012). Oesophageal anomalies are far less common in neonatal foals and are encountered more frequently in older foals as a result of gastroesophageal reflux and ulceration (Murray et al. 1988). The most common congenital oesophageal anomalies in foals are related to vascular ring anomalies mainly, but not exclusively, persistent aortic arches (Bartels and Vaughan 1969; van der Linde-Sipman et al. 1979; Mackey et al. 1986; Butt et al. 1998; Smith 2004; Bauer et al. 2006). Functional and stenotic anomalies are rarely reported or suspected (Craig et al. 1989; Clabough et al. 1991). This case report describes the clinical presentation, diagnostic methods, treatment, progression and final outcome of a neonatal Arabian filly affected by an unusual congenital oesophageal stenosis/stricture.
Case report
A 3-day-old, 45 kg bodyweight, Arabian filly was referred to the Koret School of Veterinary Medicine – Veterinary Teaching Hospital (KSVM-VTH) with a complaint of milk regurgitation since birth. Gestation length was 333 days and the pregnancy and parturition were uneventful. The mare had had 2 previous normal pregnancies and foals. After parturition the filly was strong and began suckling within 2 h. The owners noticed intermittent milk dripping from the mouth and nostrils. On the second day, the filly seemed weaker and was treated with i.v. fluids, plasma and cefquinome (2 mg/kg bwt, i.m., Cobactan 2.5%1), by the attending veterinarian. When her condition did
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not improve by the following day, she was referred to the hospital for further diagnosis and treatment.
Initial examination and treatment
On presentation, the filly was able to stand but was weak and dehydrated. She was tachypnoeic (40 breaths/min) with normal heart rate (80 beats/min) and normal body temperature (38.5°C). White foam was seen dripping from her mouth and nostrils and crackling sounds were heard on auscultation of the lungs and trachea. After suckling from the mare, a large amount of milk flowed from her mouth and nostrils. Complete blood count showed leucopenia (2.91 × 109/l, reference range [rr] 5.1–10.1 × 109/l) with a normal red blood cells count (9.37 × 1012/l, rr 7.2–12.0 × 1012/l), packed cell volume (38%, rr 32–50%) and total solids (6.2 g/l, rr 5.5–7.5 g/l). The only abnormality on a biochemistry panel was elevated total bilirubin (43 mg/l, rr 5.0–12 mg/l). Endoscopy of the pharynx and larynx was performed without sedation (endoscope diameter 9 mm). Mild collapse of the pharynx with oedematous arytenoid cartilages were observed and milk was present in the trachea. The epiglottis had a normal appearance and normal laryngeal function was demonstrated upon swallowing. Dorsal displacement of the soft palate was not observed during the examination and there were no anatomical abnormalities such as a cleft palate. Initial diagnosis was of mild pharyngeal weakness and dysfunction. A feeding tube2 (12 French, 108 cm) was inserted through
one of the nostrils into the oesophagus under endoscopic guidance at the pharynx and when a syringe was attached to the tube in order to confirm the presence of vacuum, a large amount of milk was aspirated from the oesophagus. An immediate second endoscopy was performed and this time the scope was inserted into the oesophagus. At a distance of approximately 70 cm from the nostril opening, a marked dilatation of the oesophageal lumen was observed, no peristalsis was observed in this region and the normal oesophageal longitudinal mucosal folds were absent. At the distal end of the dilatation, at a depth of 75 cm, a concentric, complete mucosal obstruction resembling a closed cervix was observed that did not allow the passage of the endoscope (Fig 1). The stricture area was not dynamic and no peristalsis seemed to pass through it. On a left lateral chest radiograph the oesophageal dilation was clearly demonstrated while the stricture, marked by the tip of the feeding tube, was located over the caudal aspect of the base of the heart at the level of the eighth intercostal space (Fig 2). There was mixed alveolar and interstitial pattern in the lung field, mainly in the cranioventral and caudal aspects, suggestive of pneumonia.
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