Esophageal dysfunction in four alpaca crias and a llama cria with vascular ring anomalies

Erica C. McKenzie Department of Clinical Sciences, College of Veterinary Medicine, Oregon State University, Corvallis, OR 97331.

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Bernard Seguin Department of Clinical Sciences, College of Veterinary Medicine, Oregon State University, Corvallis, OR 97331.

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Christopher K. Cebra Department of Clinical Sciences, College of Veterinary Medicine, Oregon State University, Corvallis, OR 97331.

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Marco L. Margiocco Department of Clinical Sciences, College of Veterinary Medicine, Kansas State University, Manhattan, KS 66505.

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David E. Anderson Department of Clinical Sciences, College of Veterinary Medicine, Kansas State University, Manhattan, KS 66505.

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Christiane V. Löhr Department of Biomedical Sciences, College of Veterinary Medicine, Oregon State University, Corvallis, OR 97331.

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Abstract

Case Description—3 alpaca crias and cadavers of an alpaca cria and a llama cria were evaluated for evidence of esophageal dysfunction.

Clinical Findings—All 5 crias were between 3 and 5 months of age when clinical signs developed, and all had a thin body condition when examined. Clinical signs included coughing, regurgitation, and grossly visible esophageal peristaltic waves. A barium esophagram was used to diagnose esophageal obstruction, megaesophagus, and a vascular ring anomaly (VRA). Fluoroscopy was used to evaluate deglutition, esophageal peristalsis, and the extent of esophageal dilation in 1 alpaca cria. A persistent right aortic arch was identified in 1 alpaca cria, and a left aortic arch with right ductus arteriosus or ligamentum arteriosum and an aberrant right subclavian artery were identified in the 4 remaining crias.

Treatment and Outcome—Surgical correction of the VRA was attempted in the 3 live alpaca crias. It was complicated by the conformation and location of each VRA and inaccurate anatomic diagnosis of the VRAs before surgery. Treatment was universally unsuccessful because of intraoperative complications and the persistence of clinical signs after surgery.

Clinical Relevance—Megaesophagus is typically an idiopathic condition in camelids. However, these findings suggested that camelids with esophageal dysfunction during the neonatal period may have a VRA. The prognosis is grave for camelids with VRA, and accurate anatomic diagnosis of the VRA via the use of advanced imaging techniques (eg, angiography, computed tomography, or magnetic resonance imaging) may improve the success of surgical intervention.

Abstract

Case Description—3 alpaca crias and cadavers of an alpaca cria and a llama cria were evaluated for evidence of esophageal dysfunction.

Clinical Findings—All 5 crias were between 3 and 5 months of age when clinical signs developed, and all had a thin body condition when examined. Clinical signs included coughing, regurgitation, and grossly visible esophageal peristaltic waves. A barium esophagram was used to diagnose esophageal obstruction, megaesophagus, and a vascular ring anomaly (VRA). Fluoroscopy was used to evaluate deglutition, esophageal peristalsis, and the extent of esophageal dilation in 1 alpaca cria. A persistent right aortic arch was identified in 1 alpaca cria, and a left aortic arch with right ductus arteriosus or ligamentum arteriosum and an aberrant right subclavian artery were identified in the 4 remaining crias.

Treatment and Outcome—Surgical correction of the VRA was attempted in the 3 live alpaca crias. It was complicated by the conformation and location of each VRA and inaccurate anatomic diagnosis of the VRAs before surgery. Treatment was universally unsuccessful because of intraoperative complications and the persistence of clinical signs after surgery.

Clinical Relevance—Megaesophagus is typically an idiopathic condition in camelids. However, these findings suggested that camelids with esophageal dysfunction during the neonatal period may have a VRA. The prognosis is grave for camelids with VRA, and accurate anatomic diagnosis of the VRA via the use of advanced imaging techniques (eg, angiography, computed tomography, or magnetic resonance imaging) may improve the success of surgical intervention.

A 5-month-old sexually intact female Huacaya alpaca (cria 1) was referred to the Oregon State University Veterinary Teaching Hospital for evaluation of esophageal dysfunction. The cria had a history of intermittent respiratory noise since birth, lethargy, failure to thrive, ptyalism, and coughing since 3 months of age. Physical examination findings included thin body condition (body weight, 20.5 kg [45.1 lb]) and grossly visible peristaltic waves in the esophagus in the distal cervical region (between C3 and C6). Esophagoscopy revealed a narrowing of the intrathoracic portion of the esophagus. Examination of a lateral thoracic radiograph revealed gas distention in the cervical portion of the esophagus with fluid pooling in the caudal portion of the cervical esophagus cranial to the thoracic inlet and ventral displacement of the thoracic portion of the trachea. Examination of a barium esophagram revealed an abrupt truncation of the barium column 1.5 cm cranial to the carina that appeared to be caused by a focal extrinsic esophageal compression (eg, VRA). The esophagus was dilated with ingesta cranial to the truncation and appeared to surround the trachea hemicircumferentially within the thoracic inlet. Examination of a dorsoventral radiographic view revealed that the esophagus was displaced to the right, and the left descending aorta was visible. Thus, these findings reduced the likelihood that the truncation was caused by a PRAA.

At 5.5 months of age, cria 1 was anesthetized and positioned in right lateral recumbency. Thoracotomy was performed via the left third intercostal space. A left aortic arch with a persistent right ligamentum arteriosum and retroesophageal RSA were identified. Transection of the ligamentum arteriosum appeared to resolve the compression of the esophagus. However, access to the left aortic arch and RSA was limited and extensively impeded the ability of the surgeon to perform the procedure.

After surgery, a finely chopped and moistened diet was provided to the cria. Cria 1 developed persistent pleural effusion and continued to have intermittent episodes of regurgitation, gurgling respiration, and increased abdominal effort despite changes to the diet. Radiography of the thorax 10 days after surgery revealed pleural effusion, pulmonary atelectasis, and distention of the cranial portion of the esophagus with feed material. Examination of a barium esophagram revealed an esophageal dilation located cranial to the carina and attenuation of the barium column near the base of the heart. Thoracocentesis was used to remove approximately 1,100 μL of white fluid (total protein, 3.1 mg/dL; WBC count, 390 nucleated cells/μL [47% large mononuclear cells, 41% small lymphocytes, and 12% nondegenerate neutrophils]) that was consistent with a chylous effusion. Esophagoscopy was repeated and revealed a pronounced dilation of the lumen of the esophagus cranial to the narrowing of the intrathoracic portion of the esophagus.

Cria 1 was euthanatized 15 days after surgery. Necropsy revealed chylothorax and a focal intrinsic constriction (lumen diameter, < 1 cm) of the intrathoracic portion of the esophagus near the base of the heart that included dilation of the esophagus orad to the stricture and dilation aborad to the stricture. The left cranial lung lobes were adhered to the thoracic wall. Histologic examination of the esophagus revealed fibrosis and small-diameter myofibers (presumably caused by atrophy) of the smooth muscle at the site of constriction and less pronounced atrophy of the smooth muscle in the proximal and distal portions of the esophagus. Wallerian degeneration was observed in nerves located within the periesophageal connective tissue, the dorsal and ventral tracts of the lumbar portion of the spinal cord and spinal nerves, and the cauda equina.

A 7-month-old sexually intact male Huacaya alpaca cria (cria 2) was referred to the Oregon State University Veterinary Teaching Hospital for evaluation of weight loss, coughing, and regurgitation. The cria was reported to have increased respiratory effort after nursing during the neonatal period and was treated for weight loss and pneumonia at 2 months of age. A barium esophagram was performed at 6 months of age to determine the cause of intermittent episodes of regurgitation, coughing, and retching. Examination of the esophagram revealed an esophageal obstruction and megaesophagus. Thereafter, a pelleted ration was provided from an elevated feed bin, but clinical signs did not improve.

Physical examination findings included tachypnea (respiratory rate, 40 breaths/min), pyrexia (rectal temperature, 39.1°C [102.3°F]), and thin body condition (20.5 kg). Waves in the esophagus were visible along the distal cervical region (between C3 and C6). Radiography of the thorax revealed substantial distention of the esophagus and residual feed material within the esophagus extending from the upper to lower esophageal sphincter. Dorsal and right lateral extrinsic compression of the esophagus was observed at the level of the third intercostal space. Pulmonary infiltrates were observed in the caudal and ventral lung fields. Reevaluation of the previously obtained barium esophagram revealed focal compression of the dorsal wall of the esophagus with ablation of the barium column at the level of the third intercostal space (Figure 1). Saccular dilation of the esophagus with accumulation of barium cranial and caudal to the extrinsic compression of the esophagus was observed. Esophagoscopy revealed pooling of fluid and food material within the thoracic portion of the esophagus. Furthermore, a narrowing of the intrathoracic portion of the esophagus made it impossible to pass the endoscope beyond this point. Cria 2 was placed in right lateral recumbency, and fluoroscopy was performed, which revealed normal deglutition, nonprogressive esophageal peristalsis, and esophageal dilation and pooling of barium orad and aborad to the esophageal constriction at the third intercostal space.

Figure 1—
Figure 1—

Barium esophagram obtained from a 7-month-old sexually intact male Huacaya alpaca cria (cria 2) with weight loss, coughing, and regurgitation. Notice the focal ablation of the barium column near the third intercostal space and the saccular dilations (arrows) of the esophagus orad and aborad to the extrinsic compression of the esophagus caused by a PRAA.

Citation: Journal of the American Veterinary Medical Association 237, 3; 10.2460/javma.237.3.311

Cria 2 was anesthetized and positioned in left lateral recumbency. Thoracotomy was performed via the right fourth intercostal space. A PRAA with a left ligamentum arteriosum was observed in the thoracic cavity. The cria was repositioned in right lateral recumbency, and thoracotomy was then performed via the left fourth intercostal space. The ligamentum arteriosum was ligated and transected. A catheter with an inflatable cuff was passed through the oral cavity into the esophagus and advanced to the level of the constriction. The cuff of the catheter was inflated (bougienage) in an attempt to increase the diameter of the lumen of the esophagus at the site of the constriction. Endoscopy performed during the surgery revealed a subjective increase in luminal diameter subsequent to bougienage at the stricture site.

Cria 2 recovered from anesthesia. It was provided small quantities of finely chopped feed. After consumption of the feed, the cria had grossly visible peristaltic waves in the esophagus and respiratory distress followed by regurgitation of the feed. Radiography performed 48 and 96 hours after surgery revealed consolidation of the ventral lung field, substantial dilation of the esophagus, and feed material within the esophagus extending from the thoracic inlet to the lower esophageal sphincter. Additionally, deviation of the dorsal esophageal wall with a banding effect was observed at the level of the third and fourth intercostal spaces, and there was narrowing of the trachea at the level of the third intercostal space. Cria 2 was euthanatized 4 days after surgery. Necropsy findings were consistent with PRAA, megaesophagus secondary to constriction caused by the PRAA, and aspiration pneumonia. The circumference of the distal portion of the esophagus was 18 cm, and the lumen of the esophagus was filled with feed. The circumference of the esophagus at the site of constriction where bougienage was performed during surgery was 7.5 cm. Histologic examination of tissues was not performed.

A 4-month-old sexually intact female Huacaya alpaca cria (cria 3) with a 3-week history of choking, which was first noticed at the time of weaning, and weight loss was evaluated at the Kansas State University Veterinary Medical Teaching Hospital. Physical examination findings included a thick white discharge from the oral and nasal passages and increased intensity of lung sounds during auscultation of the thorax. Cardiac murmur was not detected. Esophageal peristaltic waves along the neck were grossly visible, and regurgitated fluid and feed material were observed in the cria's pen.

Radiography of the neck and thorax revealed an ingesta-filled focal dilation of the esophagus cranial to the base of the heart and ventral deviation of the trachea caused by distention of the esophagus. Examination of a dorsoventral radiographic view of the thorax revealed a prominent left aortic arch that extended cranially to the middle of the second intercostal space as well as a second elliptical soft tissue structure located to the right of the trachea at the level of the fourth rib. Examination of a barium esophagram revealed distention of the cervical and cranial thoracic portions of the esophagus and a conical narrowing of a focal segment of the intrathoracic portion of the esophagus cranial to the base of the heart (Figure 2). Examination of a dorsoventral radiographic view of the thorax revealed a sigmoid deviation of the lumen of the esophagus with a right lateral deviation observed at the cranial aspect of the left aortic arch and a left lateral deviation 1 rib space caudal, which was at the location of an ellipseshaped soft tissue structure that was suspected to be a PRAA. The lumen of the esophagus tapered cranial to this second deviation (ie, left lateral deviation) at the level of the fifth intercostal space. These radiographic findings were considered evidence of the presence of a double aortic arch. Esophagoscopy revealed a stricture of the intrathoracic portion of the esophagus and pulsation of the surrounding vasculature along the esophagus. Echocardiographic examination findings were unremarkable, and arterial blood gas analysis results were within the reference ranges.

Figure 2—
Figure 2—

Barium esophagram obtained from a 4-month-old sexually intact female Huacaya alpaca cria (cria 3) with a 3-week history of choking. Notice the distention of the cervical and cranial thoracic portions of the esophagus and conical narrowing (arrow) of a focal segment of the intrathoracic portion of the esophagus orad to the base of the heart caused by compression from an aberrant RSA.

Citation: Journal of the American Veterinary Medical Association 237, 3; 10.2460/javma.237.3.311

Figure 3—
Figure 3—

Photograph of the right lateral aspect of the esophagus from a cadaver of a 6-month-old sexually intact female Suri alpaca cria (cria 4). Notice the left aortic arch (aorta), aberrant RSA, and the patent RDA (overlying the forceps) that caused entrapment of the esophagus.

Citation: Journal of the American Veterinary Medical Association 237, 3; 10.2460/javma.237.3.311

The cria was anesthetized and positioned in right lateral recumbency. Thoracotomy and resection of the fourth left rib were performed. The vasculature observed during radiography was not apparent via this approach. Therefore, the cria was repositioned in left lateral recumbency, and thoracotomy and resection of the fourth right rib were performed. Large vessels were identified and thought to be consistent with the vasculature observed during radiography. Structures surrounding these vessels were dissected to enable the surgeon to definitively define the vasculature. Unfortunately, the vasculature was inadvertently perforated, and the cria died because of exsanguination via hemorrhage through the perforation.

Necropsy findings included the identification of a left aortic arch and an aberrant RSA. The aberrant RSA originated from the aorta at a point 4 cm distal to the left subclavian artery, continued dorsally over the esophagus to the right, and caused compression of the esophagus, with moderate esophageal dilation cranial to the point of compression. Additionally, a patent RDA extended through a space between the pulmonary artery and the aberrant RSA. A ductus arteriosum originated from the pulmonary artery at a point 3 cm distal to the expected location of a left ductus arteriosum.

Postmortem examination was performed on 2 crias (crias 4 and 5) at the Oregon State University Veterinary Teaching Hospital. Cria 4 was a 6-month-old sexually intact female Suri alpaca with a history of intermittent regurgitation and loss of body condition beginning at 5 months of age. A barium esophagram was obtained by the referring veterinarian; evaluation of the esophagram revealed a focal ventral deviation of the trachea at the level of the third rib, barium accumulation at the level of the thoracic inlet, distention of the esophagus, and a focal region of narrowing of the lumen of the esophagus at the level of the third rib. These findings were consistent with an extrinsic dorsal compression of the esophagus. The caudal thoracic portion of the esophagus appeared normal. A tentative diagnosis of megaesophagus caused by a VRA was made by the referring veterinarian, and the cria was euthanatized. A left aortic arch was detected during necropsy. Additionally, an aberrant RSA was identified originating from the aorta at a point 3 cm distal to the origin of the left subclavian artery. An RDA extended through a space between the descending aorta and the right pulmonary artery at a point 1 cm distal from the origin of the RSA. The esophagus was dilated cranial to the ligamentum arteriosum.

Cria 5 was a 7-month-old sexually intact female llama that had intermittent episodes of choking and gurgling that began at 3 months of age. No abnormality was identified during physical examination by a referring veterinarian, and examination of a radiographic view of the pharynx and proximal portion of the esophagus revealed no abnormalities. The owner attempted to feed the cria a moist small particle feed, but the clinical signs persisted. At 5 months of age, evaluation of a barium esophagram revealed dilation of the cervical and thoracic portions of the esophagus cranial to the base of the heart and focal compression of the esophagus near the base of the heart. A tentative diagnosis of VRA was made. At 7 months of age, the cria had a thin body condition and a green liquid was observed around the mouth and nares, and the cria was euthanatized. Necropsy findings included a normal left aortic arch with an aberrant RSA originating at a point 3.5 cm distal to the left subclavian artery. An RDA originated at a point 1.3 cm distal to the origin of the RSA, extended through a space between the aorta and the right pulmonary artery, and caused compression of the esophagus. The circumference of the esophagus cranial and caudal to the ductus arteriosum was 11 and 5.5 cm, respectively.

To acquire an understanding of the frequency of VRAs and the relationship between VRA and megaesophagus in camelids, records were retrieved and reviewed for all camelids submitted to the Oregon State University Teaching Hospital or Veterinary Diagnostic Laboratory for necropsy from July 2002 to July 2009 (n = 366 camelids). In addition to the 5 crias reported here, 6 llamas and 4 alpacas with megaesophagus were detected during necropsy. Three of those 4 alpacas were ≤ 1 year old. One of these 3 young alpacas was a 2month-old cria with a VRA that consisted of a 1-cm-wide membranous band of tissue that originated from the right dorsal aspect of the aorta to the dorsomedial aspect of the right caudal lung lobe and crossed the esophagus caudal to the base of the heart. Most of the membranous band was formed by a thin-walled blood vessel that bifurcated near the aorta. It could not be definitively determined from the record if this vessel was the cause of the clinical signs of megaesophagus. However, the esophageal lumen was narrow enough that it would not allow the person performing the necropsy to pass a finger through the esophagus at the point where the membranous band crossed the esophagus. All 6 llamas and the 1 remaining alpaca were ≥ 5 years old, and VRA was not detected in any of these adult camelids.

Discussion

Vascular ring anomalies arise from the deranged maturation of the aortic arch system in the developing embryo and result in entrapment of the thoracic portion of the trachea, esophagus, or both by a vascular or ligamentous structure.1 The development and conformation of the many variations of VRA have been described in humans1 and other animals.2,3 In most patients, a VRA results from a singular or combined aberration of the aortic arches, the ducti arteriosum, and the subclavian arteries.1,3 Examination of a cria that was euthanatized for reasons attributable to another disease confirmed that the RSA does not typically originate directly from the aorta and that the anatomic construction of the aortic arch of South American camelids is similar to that of dromedaries (Camelus dromedarius).4

Vascular ring anomalies have been reported in a wide variety of animal species, including cats,2 dogs,2 horses,5,6 and cattle,7,8 and dogs are most frequently affected. In 95% of dogs with VRA, the most common inciting cause is the interaction between a PRAA and the left ligamentum arteriosum.9 In approximately onethird of these dogs, there is concurrent retroesophageal positioning of the left subclavian artery, which may contribute to compression of the esophagus.9 Other forms of VRA, which include a double aortic arch, left aortic arch with RDA or ligamentum arteriosum, and anomalies of the subclavian arteries, are rare in animals but have been reported.9–16

Vascular ring anomalies appear to be rare in herbivores, and most clinical reports5–8,17–22 of this condition comprised a PRAA with left ligamentum arteriosum. Concurrent abnormalities of the ductus arteriosus and subclavian arteries rarely have been reported, and anomalies associated with a left aortic arch are atypical in all species in which VRAs are described.9,14,18,19 A VRA was reported in a foal23 with a left aortic arch, in an alpaca cria13 with a left aortic arch and RDA, and in 2 German Shepherd Dog littermates13 with a left aortic arch and RDA. However, in the present clinical report of 5 crias, 4 (crias 1, 3, 4, and 5) had a left aortic arch with persistence of the right ligamentum arteriosum or ductus arteriosus; additionally, all 4 of these crias had an aberrant RSA, which was the major cause of the extrinsic compression of the esophagus in cria 3. The importance of these findings, apart from being a rarely described anomaly, is that a definitive (crias 1 and 3) or suspected (cria 2) left aortic arch in each cria greatly complicated the surgical approach used.

A thorough diagnostic evaluation to determine the conformation of a VRA before an attempted surgical intervention and the involvement of an experienced surgeon is critical for minimizing the length of time for the procedure and trauma induced during surgery and to facilitate relief of extrinsic compression on the esophagus by all anomalous or aberrant anatomic structures.12,13 Although most VRAs are accessible via a left-sided thoracotomy or during thoracoscopy, a double aortic arch with a hypoplastic right aortic arch, a left aortic arch with a persistent right ligamentum arteriosum or RDA, and an aberrant RSA are more readily accessible via a right-sided surgical approach.24–26 Therefore, use of advanced imaging techniques is strongly recommended before an attempted surgical intervention in camelids with VRA. Advanced imaging techniques rarely have been used to investigate VRA in veterinary patients, and this may be attributable to the restricted availability of equipment and the expectation that PRAA is the cause of megaesophagus in most animals. However, angiography during computed tomography has been used to successfully identify PRAA and other more complex VRAs in dogs,27,28 and magnetic resonance imaging is considered a valuable procedure in humans with VRA.1

Clinical signs of esophageal dysfunction began when the crias of the present clinical report were between 3 and 5 months of age and included coughing, weight loss, regurgitation, and grossly evident esophageal abnormalities. Interestingly, cardiac murmurs were not detected in crias with patent anomalous structures in the present report. It is possible that cardiac murmurs were simply not audible at the time of examination. Careful auscultation of the thorax was performed because of the strong suspicion of VRA, and it may have been possible that the small diameter of the lumen of the anomalous structures was a contributing factor to the absence of an audible cardiac murmur.

Onset of the clinical signs of esophageal dysfunction likely coincided with an increased intake of solid food by weaned crias. However, onset of the clinical signs of esophageal dysfunction caused by VRAs has been reported in a mature llama17 and in mature animals of other species.6,29 A list of differential diagnoses for camelids with esophageal dysfunction include primary megaesophagus, esophageal obstruction, and congenital or acquired esophageal stricture.30,31 An initial diagnostic evaluation for camelids with esophageal dysfunction should include radiography, which may be used to identify aspiration pneumonia, dilation or impaction of the esophagus, and ventral deviation or compression of the trachea. Although dorsoventral or ventrodorsal radiographic views are not consistently obtained in large animals, these can provide critical information regarding VRAs and should be obtained in all appropriately sized animals.9 Evaluation of a dorsoventral radiographic view allowed identification of the aortic structures in the left side of the thorax and reduced the probability of a PRAA in crias 1 and 3. Additionally, evaluation of a dorsoventral radiographic view revealed a left lateral deviation consistent with a PRAA that was subsequently diagnosed in cria 2 during thoracotomy.

The use of a contrast agent during radiographic imaging of the esophagus is a critical component for determining the cause of esophageal dysfunction in veterinary patients. In the present clinical report, a barium esophagram was an appropriate diagnostic tool for use in determining the cause of an extrinsic esophageal compression and identifying a VRA in all 5 crias. The characteristic findings of esophageal dysfunction during evaluation of a barium esophagram included a tapering of the barium column near the base of the heart, ventral deviation of the dorsal wall of the esophagus, and mild to severe esophageal dilation cranial to the location of the esophageal stricture. Esophageal dilation was also observed caudal to the location of the esophageal stricture during examination of a barium esophagram; furthermore, this phenomenon has been reported in a llama17 with a VRA and in animals of other species2,32 and may represent damage to surrounding nervous structures or obstruction to physiologic regurgitation in camelids. Persistent esophageal dilation after surgical correction of a VRA is common in dogs despite an improvement in clinical signs.33 In the present clinical report, esophageal dilation and dysfunction continued in 2 crias after surgery and was associated with continued stricture of the esophagus in the region of the VRA (cria 1) and impaired esophageal motility (cria 2). The logistic restrictions associated with providing a liquid or slurry diet to camelids also complicated the recovery of these crias after surgery.

Additional diagnostic procedures that may be used in camelids thought to have a VRA include esophagoscopy and fluoroscopy for the assessment of deglutition, esophageal diameter, and esophageal peristalsis.1 Transthoracic echocardiography should be used to rule out concurrent cardiac defects and to identify a patent RDA. A patent RDA was not detected during echocardiography in cria 3, which may have been because of the small size of the RDA.20,34 Thus, echocardiography may have limitations for identifying and characterizing the anatomy of the aortic arch and its branches. Although these diagnostic techniques have not been used extensively in camelids, angiography and transesophageal echocardiography may be better for use in identifying and characterizing the anatomy of the aortic arch and its branches. Successful thoracoscopic correction of PRAA has been reported in dogs35,36; therefore, thoracoscopy might be a useful procedure for confirming the appropriate surgical approach before thoracotomy when advanced imaging techniques are not available.

Respiratory noise or distress associated with direct tracheal constriction is a common clinical sign in humans with VRAs and may occasionally be detected in domestic animals with VRAs.6,14,34,37 Although it was not possible to determine whether these signs resulted from tracheal constriction, respiratory abnormalities were detected in crias 1 and 2 during the neonatal period. Aspiration pneumonia, compression of the trachea by a dilated esophagus, and obstruction of the nasal cavities with regurgitated feed material may also cause respiratory dysfunction in camelids with a VRA.13,17 Respiratory distress may develop or the animal may suddenly die if the esophagus becomes dilated and impacted with feed or bedding material, and this has been reported in a cria with a VRA.13 Thus, a VRA should be considered as a cause for respiratory noise or difficulty breathing in crias in the neonatal and juvenile period.

Complications associated with VRAs in camelids include aspiration pneumonia, esophageal obstruction, negative energy balance, anemia, and dyspnea. Additionally, surgical correction of a VRA may be associated with hemorrhage, chylothorax, pleural adhesions, exacerbation of pneumonia, and persistent esophageal dysfunction. The prognosis is grave for survival and improvement of esophageal function after surgical correction of a VRA in camelids; death has been reported for every camelid with a VRA. Early recognition and correction of a VRA in camelids may improve the prognosis for recovery, as has been reported34,37 for other species. However, clinical signs typically appear during the juvenile period, particularly after weaning, and substantial esophageal dysfunction is likely to be already present. Additionally, the fibrous nature of the typical camelid diet complicates dietary management in patients with a VRA. Nutrition provided partially or completely by parenteral methods, administration of broad-spectrum antimicrobials, anti-inflammatory treatments, and esophageal prokinetic drugs (eg, metoclopramide) should be considered in crias undergoing surgery to correct a VRA. Intraoperative esophagoscopy would be an important tool for evaluation of the success of surgical transection of the VRA and attempts to relieve fibrous esophageal constrictions through dissection and bougienage.2,25

Vascular ring anomalies are a rarely reported cause of megaesophagus in camelids and are typically associated with weight loss and signs of esophageal dysfunction in crias ≤ 6 months after birth. Furthermore, VRAs may cause a substantial megaesophagus condition in neonatal or juvenile camelids. The majority (4/5) of the crias in the present clinical report had a left aortic arch with an RDA or ligamentum arteriosum accompanied by an aberrant RSA. Minimum assessment of these patients should include a CBC, serum biochemical analysis, radiography of the thorax, and a barium esophagram with lateral and dorsoventral or ventrodorsal radiographic views. Surgical intervention has been unsuccessful in all camelids with a VRA. When surgery is to be attempted for the correction of a VRA, it should be preceded by use of advanced imaging techniques or thoracoscopy to identify the underlying cause or causes. Additionally, pertinent recommendations on breeding management should be provided to owners of affected crias because of evidence that suggests a genetic basis for VRAs in other species.13,38

ABBREVIATIONS

PRAA

Persistent right aortic arch

RDA

Right ductus arteriosus

RSA

Right subclavian artery

VRA

Vascular ring anomaly

References

  • 1.

    Hernanz-Schulman M. Vascular rings: a practical approach to imaging diagnosis. Pediatr Radiol 2005;35:961979.

  • 2.

    Ellison GW. Vascular ring anomalies in the dog and cat. Compend Contin Educ Pract Vet 1980;2:693705.

  • 3.

    VanGundy T. Vascular ring anomalies. Compend Contin Educ Pract Vet 1989;11:3646.

  • 4.

    Smuts MMS, Bezuidenhout AJ. The heart and arteries. In: Anatomy of the dromedary. New York: Oxford University Press, 1987;142167.

  • 5.

    Mackey VS, Large SM, Breznock EM, et al. Surgical correction of a persistent right aortic arch in a foal. Vet Surg 1986;15:325328.

  • 6.

    Butt TD, MacDonald DG, Crawford WH, et al. Persistent right aortic arch in a yearling horse. Can Vet J 1998;39:714715.

  • 7.

    Rooney JR II, Watson DF. Persistent right aortic arch in a calf. J Am Vet Med Assoc 1956;129:57.

  • 8.

    Roberts SJ, Kennedy PC. Delehanty DD. A persistent right aortic arch in a Guernsey bull. Cornell Vet 1953;43:537542.

  • 9.

    Buchanan JW. Tracheal signs and associated vascular anomalies in dogs with persistent right aortic arch. J Vet Intern Med 2004;18:510514.

    • Search Google Scholar
    • Export Citation
  • 10.

    Vianna ML, Krahwinkel DJ Jr. Double aortic arch in a dog. J Am Vet Med Assoc 2004;225:12221224.

  • 11.

    Moonan N, Mootoo NF, Mahler SP. Double aortic arch with a hypoplastic left arch and patent ductus arteriosus in a dog. J Vet Cardiol 2007;9:5961.

    • Search Google Scholar
    • Export Citation
  • 12.

    Hurley K, Miller MW, Willard MD, et al. Left aortic arch and right ligamentum arteriosum causing esophageal obstruction in a dog. J Am Vet Med Assoc 1993;203:410412.

    • Search Google Scholar
    • Export Citation
  • 13.

    Holt D, Heldmann E, Michel K, et al. Esophageal obstruction caused by a left aortic arch and an anomalous right patent ductus arteriosus in two German Shepherd littermates. Vet Surg 2000;29:264270.

    • Search Google Scholar
    • Export Citation
  • 14.

    McCandlish IAP, Nash AS, Peggram A. Unusual vascular ring in a cat: left aortic arch with right ligamentum arteriosum. Vet Rec 1984;114:338340.

    • Search Google Scholar
    • Export Citation
  • 15.

    Griffiths D. Three cases of aberrant right subclavian artery in the dog. Acta Vet Scand 1989;30:355357.

  • 16.

    House AK, Summerfield NJ, German AJ, et al. Unusual vascular ring anomaly associated with a persistent right aortic arch in two dogs. J Small Anim Pract 2005;46:585590.

    • Search Google Scholar
    • Export Citation
  • 17.

    Butt TD, MacDonald DG, Crawford WH. Persistent right aortic arch in a mature llama. Vet Rec 2001;148:118119.

  • 18.

    Peters M, Koch R, Kämmerling J, et al. Persistent right aortic arch in a yearling captive wood bison (Bison bison athabascae). J Zoo Wildl Med 2002;33:386388.

    • Search Google Scholar
    • Export Citation
  • 19.

    van den Ingh TS, van der Linde-Sipman JS. Right aortic arch in a lamb and two pigs. Vet Q 1986;8:3740.

  • 20.

    van der Linde-Sipman JS, Goedegebuure SA, Kroneman J. Persistent right aortic arch associated with a persistent left ductus arteriosus and an interventricular septal defect in a horse. Tijdschr Diergeneeskd 1979;104:189194.

    • Search Google Scholar
    • Export Citation
  • 21.

    Petrick SW, Roos CJ, van Niekerk J. Persistent right aortic arch in a horse. J S Afr Vet Assoc 1978;49:355358.

  • 22.

    Bartels JE, Vaughan JT. Persistent right aortic arch in the horse. J Am Vet Med Assoc 1969;154:406409.

  • 23.

    Smith TR. Unusual vascular ring anomaly in a foal. Can Vet J 2004;45:10161018.

  • 24.

    McFaul R, Millard P, Nowicki E. Vascular rings necessitating right thoracotomy. J Thorac Cardiovasc Surg 1981;82:306309.

  • 25.

    Kyles AE. Esophagus. In: Slatter D, ed. Textbook of small animal surgery. 3rd ed. Philadelphia: Saunders, 2003;577582.

  • 26.

    Hedlund CS, Fossum TW. Surgery of the digestive system. In: Fossum TW, ed. Small animal surgery. St Louis: Mosby Elsevier, 2007;405409.

    • Search Google Scholar
    • Export Citation
  • 27.

    Joly H, D'Anjou MA, Huneault L. Imaging diagnosis—CT angiography of a rare vascular ring anomaly in a dog. Vet Radiol Ultrasound 2008;49:4246.

    • Search Google Scholar
    • Export Citation
  • 28.

    Pownder S, Scrivani PV. Non-selective computed tomography angiography of a vascular ring anomaly in a dog. J Vet Cardiol 2008;10:125128.

    • Search Google Scholar
    • Export Citation
  • 29.

    Fingeroth JM, Fossum TW. Late-onset regurgitation associated with persistent right aortic arch in two dogs. J Am Vet Med Assoc 1987;191:981983.

    • Search Google Scholar
    • Export Citation
  • 30.

    Watrous BJ, Pearson EG, Smith BB, et al. Megaesophagus in 15 llamas: a retrospective study (1985–1993). J Vet Intern Med 1995;9:9299.

  • 31.

    Clabough DL, Roberts MC, Robertson I. Probable congenital esophageal stenosis in a Thoroughbred foal. J Am Vet Med Assoc 1991;199:483485.

    • Search Google Scholar
    • Export Citation
  • 32.

    Clifford DH, Ross JN Jr, Waddell ED, et al. Effect of persistent aortic arch on the ganglial cells of the canine esophagus. J Am Vet Med Assoc 1971;158:14011410.

    • Search Google Scholar
    • Export Citation
  • 33.

    Muldoon MM, Birchard SJ, Ellison GW. Long-term results of surgical correction of persistent right aortic arch in dogs: 25 cases (1980–1995). J Am Vet Med Assoc 1997;210:17611763.

    • Search Google Scholar
    • Export Citation
  • 34.

    Isakow K, Fowler D, Walsh P. Video-assisted thoracoscopic division of the ligamentum arteriosum in two dogs with persistent right aortic arch. J Am Vet Med Assoc 2000;217:13331336.

    • Search Google Scholar
    • Export Citation
  • 35.

    MacPhail CM, Monnet E, Twedt DC. Thoracoscopic correction of persistent right aortic arch in a dog. J Am Anim Hosp Assoc 2001;37:577581.

  • 36.

    Bonnard A, Auber F, Fourcade L, et al. Vascular ring abnormalities: a retrospective study of 62 cases. J Pediatr Surg 2003;38:539543.

  • 37.

    Longo-Santos LR, Maksoud-Filho JG, Tannuri U, et al. Vascular rings in childhood: diagnosis and treatment [in Portuguese]. J Pediatr (Rio J) 2002;78:244250.

    • Search Google Scholar
    • Export Citation
  • 38.

    Gunby JM, Hardie RJ, Bjorling DE. Investigation of the potential heritability of persistent right aortic arch in Greyhounds. J Am Vet Med Assoc 2004;224:11201122.

    • Search Google Scholar
    • Export Citation
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