Editorial Type: Case Reports
 | 
Online Publication Date: 01 Jul 2009

Nonsurgical Treatment of Gastroesophageal Intussusception in a Puppy

BVSc (Hons), MACVS,
BVSc (Hons), Fellow ACVSc,
BVSc, MACVSc, and
BVetMed, PhD, Fellow ACVSc, MRCVS
Article Category: Other
Page Range: 185 – 190
DOI: 10.5326/0450185
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A 7-week-old, female Siberian husky was presented to Murdoch University Veterinary Hospital with an acute onset of respiratory distress and regurgitation. Thoracic imaging identified an intraluminal esophageal mass with concurrent aspiration pneumonia. Esophagoscopy identified the mass as stomach, and a diagnosis of gastroesophageal intussusception was made. The intussusception was reduced endoscopically, and fixation of the stomach to the abdominal wall was performed using a tube gastropexy. Gastroesophageal intussusception is an uncommon disease in small animals and traditionally has been managed surgically. This case report describes an alternative method of treatment associated with a good outcome in this puppy.

Introduction

Gastroesophageal intussusception (GEI) is a rare disorder15 in which part or all of the stomach invaginates into the thoracic esophagus. In severe cases, additional organs such as the spleen, pancreas, duodenum, and omentum may also involute.2,6,7 Some authors have categorized GEI as a type of hiatal hernia;4 however, GEI can be differentiated from a sliding hiatal hernia by the position of the gastroesophageal junction and a paraesophageal hiatal hernia by the position of the stomach within, rather than adjacent to, the esophagus.2,5,8 Two types of GEI are reported in the literature: a chronic, recurrent form that causes intermittent gastrointestinal signs and an acute, persistent type that results in signs of acute esophageal obstruction and respiratory distress.8,9

The pathogenesis of GEI is not well understood and is likely multifactorial.1 Anatomical abnormalities such as esophageal hiatal enlargement,5 lower esophageal sphincter incompetency, and esophageal motility disorders (such as megaesophagus)1,2 are likely to be involved. In humans, risk factors for the development of GEI include conditions that cause an increase in abdominal pressure, such as pregnancy, obesity, overeating followed by rigorous exercise, and chronic dyspepsia.10 In dogs, increased intraabdominal pressure from disorders such as chronic vomiting or blunt trauma, and negative intrathoracic pressure from inspiratory dyspnea due to chronic upper airway obstruction or severe respiratory disease1 may also be factors. The latter hypothesis is supported by a study of six of 11 Dalmatian puppies that died from acute respiratory distress syndrome (ARDS) and had developed GEI in the terminal stages of disease.11 The development of GEI in a dog with laryngeal paralysis1 and the development of a sliding hiatal hernia in a cat with a laryngeal mass12 also support this association.

The clinical signs of GEI are usually related to esophageal and gastric outflow obstruction and include vomiting, regurgitation, hypersalivation, dysphagia, abdominal discomfort, and occasionally hematemesis.2,4 Concurrent respiratory distress due to the resultant space-occupying intrathoracic mass is often present and may be complicated by secondary aspiration pneumonia. In acute cases, cardiovascular compromise can result from compression of the great thoracic vessels causing reduced venous return, or from endotoxic shock due to gastric ischemia, necrosis, and release of inflammatory mediators.3 Such cases deteriorate rapidly and can be considered gastrointestinal emergencies.6

Diagnosis of GEI is based on a combination of survey and contrast radiography, fluoroscopy, and esophagoscopy. Survey radiographs may suggest GEI if a large soft-tissue mass is visible in the caudodorsal mediastinum, with displacement of the trachea and cardiac silhouette and loss of the gastric shadow. Contrast radiography often will show an intraluminal filling defect and may outline gastric rugal folds. Fluoroscopy identifies esophageal dysmotility, while esophagoscopy may confirm the diagnosis by showing a mass in the distal esophagus—the appearance of which is consistent with gastric mucosa.

Historically, the treatment of choice for a GEI has involved surgical replacement and fixation of the stomach to the abdominal wall via laparotomy.1 In acute cases that are presented as emergencies, immediate stabilization of the animal is required, including oxygen support for dyspnea, correction of electrolyte abnormalities, and appropriate management of dehydration and/or shock. Management of secondary complications, such as aspiration pneumonia and esophageal disease, is also required in the perioperative period. Prognosis in early reports was poor, with a mortality rate of 95% in one study.4 Survival rates have improved in recent years; however, the long-term prognosis often remains guarded because of concomitant esophageal disease.

This case report describes the successful management of an acute onset of esophageal obstruction and respiratory distress secondary to GEI in a puppy, using endoscopic reduction and fixation of the stomach to the abdominal wall with a tube gastropexy.

Case Report

A 7-week-old, 2.5-kg, female Siberian husky was presented to Murdoch University Veterinary Hospital with a 12-hour history of vomiting, regurgitation, and respiratory distress. The owner reported that the puppy had intermittent regurgitation from birth that had lessened in frequency after she began eating solid food the week prior to presentation. Physical examination revealed a body condition score of 3/9, heart rate of 220 beats per minute, and a respiratory rate of 60 breaths per minute with increased inspiratory effort. Increased bronchovesicular lung sounds were auscultated bilaterally, while pyrexia (body temperature 39.3°C), reduced oxygen saturation (SpO2 79%), and a mean arterial blood pressure of 74 mm Hga were also identified.

Survey radiography performed by the referring veterinarian showed a homogeneous soft-tissue mass in the dorsal thorax extending between the diaphragm and the third rib pair. The cranial margin of the mass was smoothly rounded [Figure 1A]. The mass caused marked ventral displacement of the trachea. Contrast radiography demonstrated distension of the cervical and cranial thoracic esophagus and confirmed obstruction of the caudal esophagus by the mass [Figure 1B]. Based on these findings, a diagnosis of esophageal obstruction was made. Possible causes of the obstruction included GEI and esophageal foreign body.

The puppy was initially treated with oxygen support and intravenous fluid resuscitation (5 mL/kg Dextran 70b and 20 mL/kg lactated Ringer’s solutionc) for signs of compensated cardiovascular shock. Once the animal was hemodynamically stable, crystalloid solution was continued intravenously (IV) at a maintenance rate (3.6 mL/kg per hour of lactated Ringer’s solution, supplemented with 2.5% glucose and 20 mmol/L potassium chloride).

The puppy was maintained in an oxygen-rich environment (fraction of inspired oxygen between 40% and 60%). Additional medications included metoclopramided (0.4 mg/kg IV q 8 hours), ranitidinee (2 mg/kg IV q 12 hours), terbutalinef (12 μg/kg subcutaneously q 8 hours), and amoxicilling (24 mg/kg IV q 8 hours).

Thoracic radiography was repeated while the puppy was under sedation with butorphanolh (0.03 mg/kg) and acetylpromazinei (0.004 mg/kg). Ventral displacement of the trachea persisted; however, the entire thoracic esophagus was now filled with a heterogeneous soft-tissue opacity. In the ventral lung fields, patchy consolidation and interstitial infiltrates suggested aspiration pneumonia [Figures 2A, 2B]. Fluoroscopy and contrast radiography were performed after the effects of sedation had resolved and confirmed esophageal dilatation, a caudal esophageal mass, and failure of the contrast medium to enter the gastric lumen.

The following day, the puppy underwent general anesthesia (butorphanol 0.01 mg/kg IV, propofolj 5 mg/kg IV, inhalational isofluranek). Esophagoscopy revealed a dilated, fluid-filled proximal esophagus. A large, intraluminal mass consistent with the mucosal surface of the stomach was observed in the midthoracic esophagus [Figure 3]. Gentle advancement of the endoscope resulted in replacement of this structure into the abdominal cavity. The region of the esophagus where the invaginated stomach had been located was dilated and inflamed, but no evidence of ulceration or adhesions was seen. A percutaneous endoscopic gastrostomy (PEG) tube was placed through the left abdominal wall to attach the stomach to the abdominal wall and to enable enteral nutritional management. After recovery, the puppy’s respiratory rate had improved (44 breaths per minute with reduced inspiratory effort and an SpO2 of 84%), and it continued to improve over the following 24-hour period. Sucralfatel (0.1 g/kg per os [PO]) was administered 12 hours after PEG tube placement, while food and water were withheld for an additional 12 hours. At 24 hours following the procedure, PEG tube feeding was not required, as the puppy ate willingly. Oral feeding from an elevated position was continued during hospitalization, and no further regurgitation occurred. Thoracic radiography was repeated the following day with butorphanol (0.4 mg/kg IV) sedation; radiographs showed a small amount of gas in the cranial thoracic esophagus, resolution of the GEI, and resolving aspiration pneumonia [Figures 4A, 4B].

The puppy was discharged 6 days after admission, with medications including ranitidine (2 mg/kg PO q 12 hours), sucralfate (0.1 g/kg PO q 8 hours), and amoxicillin-clavulanic acidm (10 mg/kg PO q 12 hours). The owners were instructed to feed the puppy from an elevated position, and care for the PEG tube site was outlined. Follow-up examination was performed 4 days after discharge, at which time necrosis of the area surrounding the PEG tube was noted. The owner reported intermittent regurgitation of fluid. An esophagram was repeated the following day. Gas and fluid were present within the esophagus, consistent with reduced esophageal motility, but the stomach was located in a normal position in the cranial abdomen. Reassessment 9 days after discharge showed the PEG site to be healing well, but regurgitation remained intermittent, and weight gain was minimal despite a good appetite. The puppy’s daily caloric requirement was recalculated, and a feeding regimen using a highly digestible dietn was introduced over a 3-day period. The puppy was returned for PEG tube removal 24 days after discharge, at which time the owner reported that the regurgitation had resolved completely. Abdominal ultrasound confirmed that the fundus of the stomach was positioned adjacent to the left abdominal wall. The PEG tube was removed without complication while the puppy was under brief inhalation anesthesia with sevoflurane.o

Follow-up evaluation was performed 48 days after discharge. The animal’s body weight had appropriately increased to 5 kg. The gastrostomy site had healed well, and the owner reported no further vomiting or regurgitation. Follow-up via telephone 4 months after initial presentation revealed that the dog continued to remain asymptomatic.

Discussion

Canine GEI is a rare condition with only 30 cases reported in the veterinary literature. These reports predominantly involve large-breed dogs <3 months of age, with a higher incidence in males and German shepherd dogs.4 The case reported here has a similar signalment but differs in that it is a female. Interestingly, a previous case has been reported involving the husky breed, also of the female gender.13

The key to successful treatment of GEI involves the initial identification and treatment of concurrent diseases such as pneumonia, followed by reduction of the intussusception itself. Historically, surgical exploration has been advocated as the method of choice to achieve this. To date, all reported canine cases of GEI in which treatment has been attempted have been managed in this way.3,8,1316 Following surgical reduction, attachment of the stomach to the abdominal wall with either unilateral or bilateral, incisional, circumcostal, or belt loop gastropexies has been performed. Correction of concurrent anatomical abnormalities, such as an enlarged esophageal hiatus, has also been performed during the surgical procedure. Endoscopic reduction of GEI has been previously reported once in a dog.2 In that case, reduction was achieved by insufflating the esophagus while closing off the proximal esophagus. No report was provided as to whether this dog went on to have either surgical or tube gastropexy performed. Endoscopic reduction of GEI was also achieved in a cat17 that subsequently had a surgical gastropexy.

To the authors’knowledge, this is the first case of GEI that has been corrected solely by endoscopic maneuvers. Benefits of this method include avoidance of prolonged general anesthesia in an already compromised animal and providing a method of administering enteral nutrition. A possible disadvantage of this technique is the limitation of having to do a left-sided, unilateral gastropexy; bilateral gastropexies have been advocated by some authors.3,13 Others, however, have had success with left unilateral gastropexies.8 One report16 suggests they may have an anatomical advantage over right-sided gastropexies because of the position of the esophageal hiatus to the left of midline. Contraindications to performing endoscopic reduction would include situations where the gastric wall is compromised or adhesions are present, creating a risk of gastric perforation. Assessment and correction of esophageal hiatal abnormalities are also not possible with this method of correction.

Although the pathogenesis of GEI in small animals is unclear, the veterinary literature has shown a strong association with preexisting esophageal disease. In one report,4 >50% of the 23 dogs with GEI had concurrent megaesophagus or other esophageal abnormalities, and this has been a finding in all feline cases reported.1719 This has been suggested as the reason German shepherd dogs are over-represented,3 as they also have a predisposition for the congenital form of this disease.20,21 In the case presented here, regurgitation had been documented since birth, suggesting the presence of congenital esophageal disease that may have contributed to the development of GEI.

An alternative explanation for the persistent regurgitation is that this puppy initially had the chronic intermittent form of GEI, which then developed into the acute, persistent form. In contrast to feline cases of GEI, which are more often the chronic intermittent type,1719 the acute form is much more common in the dog.3,68,14,16 However, two canine cases of the chronic intermittent form have been described. One case affected a 2-year-old pug that had previously been diagnosed and treated for a sliding hiatal hernia.15 The second case involved an 8-week-old female Siberian husky,13 similar to the case reported here.

Unfortunately, it is impossible to confirm which theory might be correct in the case of this report, because no imaging of the puppy had been performed prior to the presentation with acute disease. Clinically, the animal had complete resolution of the regurgitation, suggesting either spontaneous resolution of congenital esophageal disease or chronic intermittent GEI.

Conclusion

Gastroesophageal intussusception is an unusual condition predominantly affecting young, large-breed dogs. It should be considered as a differential diagnosis when an animal exhibits signs of acute or chronic esophageal obstruction, especially with concurrent respiratory distress. Endoscopic intervention may provide an alternative to surgical correction of GEI.

Surgivet 9200 series; Smiths Medical PM, Inc., Waukesha, WI 53186

Dextran 70; Baxter Healthcare, Old Toongabbie, New South Wales 2146 Australia

Compound sodium lactate Hartmann’s solution; Baxter Healthcare, Old Toongabbie, New South Wales 2146 Australia

Metomide; Delvet, Seven Hills, New South Wales 2147 Australia

Zantac; Glaxo Smith Kline, Boronia, Victoria 3113 Australia

Bricanyl; Astra Zeneca, North Ryde, New South Wales 2113 Australia

Amoxicillin; CSL Ltd., Parkeville, Victoria 3052 Australia

Torbugesic; Fort Dodge, Baulkham Hills, New South Wales 2153 Australia

A.C.P. 2; Delvet, Seven Hills, New South Wales 2147 Australia

Fresofol; Pharmatel Fresenius Kabi Hornsby, New South Wales 2077 Australia

I.S.O.; VCA, Kings Park, New South Wales 2148 Australia

Carafate; Aspen Pharmacare, St. Leonards, New South Wales 2065 Australia

Clavulox; Pfizer, West Ryde, New South Wales 2114 Australia

Science Diet puppy; Hills, North Ryde, New South Wales 2113 Australia

SevoFlo; Advanced Aneasthesia Specialists, Gladesville, New South Wales 2111 Australia

Acknowledgments

The authors acknowledge the emergency and critical care staff that cared for this animal during its time in the intensive care unit. The authors also acknowledge colleagues in the medicine, diagnostic imaging, anesthesia, and surgical departments for their advice and input, as well as Balcatta Veterinary Hospital for the referral and imaging of this case. The authors thank Professor John Bolton for his help with preparing the digital images for this article.

Figure 1A—. Survey left lateral radiograph of the thorax. Note a large soft-tissue opacity (M) with a rounded, smooth cranial margin occupying most of the thoracic esophagus. Gas distends the esophagus at the cranial aspect of the mass. The trachea (arrow) is markedly ventrally displaced.Figure 1A—. Survey left lateral radiograph of the thorax. Note a large soft-tissue opacity (M) with a rounded, smooth cranial margin occupying most of the thoracic esophagus. Gas distends the esophagus at the cranial aspect of the mass. The trachea (arrow) is markedly ventrally displaced.Figure 1A—. Survey left lateral radiograph of the thorax. Note a large soft-tissue opacity (M) with a rounded, smooth cranial margin occupying most of the thoracic esophagus. Gas distends the esophagus at the cranial aspect of the mass. The trachea (arrow) is markedly ventrally displaced.
Figure 1A Survey left lateral radiograph of the thorax. Note a large soft-tissue opacity (M) with a rounded, smooth cranial margin occupying most of the thoracic esophagus. Gas distends the esophagus at the cranial aspect of the mass. The trachea (arrow) is markedly ventrally displaced.

Citation: Journal of the American Animal Hospital Association 45, 4; 10.5326/0450185

Figure 1B—. Left lateral projection of the thorax. Liquid barium has been administered per os; it distends the cranial esophagus and confirms obstruction of the caudal esophagus by the soft-tissue mass (M).Figure 1B—. Left lateral projection of the thorax. Liquid barium has been administered per os; it distends the cranial esophagus and confirms obstruction of the caudal esophagus by the soft-tissue mass (M).Figure 1B—. Left lateral projection of the thorax. Liquid barium has been administered per os; it distends the cranial esophagus and confirms obstruction of the caudal esophagus by the soft-tissue mass (M).
Figure 1B Left lateral projection of the thorax. Liquid barium has been administered per os; it distends the cranial esophagus and confirms obstruction of the caudal esophagus by the soft-tissue mass (M).

Citation: Journal of the American Animal Hospital Association 45, 4; 10.5326/0450185

Figures 2A, 2B—. Left lateral (A) and ventrodorsal (B) projections of the thorax. The thoracic esophagus is markedly distended by a heterogeneous, soft-tissue opacity (M) causing ventral displacement of the trachea (arrow). The well-defined margin of the mass seen in the previous study is no longer visible, perhaps due to the accumulation of fluid in the cranial esophagus. In the periphery of the right cranial and caudal lung lobes, an alveolar lung pattern is present. In the left lung, a dense interstitial pattern is present. These changes are consistent with aspiration pneumonia.Figures 2A, 2B—. Left lateral (A) and ventrodorsal (B) projections of the thorax. The thoracic esophagus is markedly distended by a heterogeneous, soft-tissue opacity (M) causing ventral displacement of the trachea (arrow). The well-defined margin of the mass seen in the previous study is no longer visible, perhaps due to the accumulation of fluid in the cranial esophagus. In the periphery of the right cranial and caudal lung lobes, an alveolar lung pattern is present. In the left lung, a dense interstitial pattern is present. These changes are consistent with aspiration pneumonia.Figures 2A, 2B—. Left lateral (A) and ventrodorsal (B) projections of the thorax. The thoracic esophagus is markedly distended by a heterogeneous, soft-tissue opacity (M) causing ventral displacement of the trachea (arrow). The well-defined margin of the mass seen in the previous study is no longer visible, perhaps due to the accumulation of fluid in the cranial esophagus. In the periphery of the right cranial and caudal lung lobes, an alveolar lung pattern is present. In the left lung, a dense interstitial pattern is present. These changes are consistent with aspiration pneumonia.Figures 2A, 2B—. Left lateral (A) and ventrodorsal (B) projections of the thorax. The thoracic esophagus is markedly distended by a heterogeneous, soft-tissue opacity (M) causing ventral displacement of the trachea (arrow). The well-defined margin of the mass seen in the previous study is no longer visible, perhaps due to the accumulation of fluid in the cranial esophagus. In the periphery of the right cranial and caudal lung lobes, an alveolar lung pattern is present. In the left lung, a dense interstitial pattern is present. These changes are consistent with aspiration pneumonia.Figures 2A, 2B—. Left lateral (A) and ventrodorsal (B) projections of the thorax. The thoracic esophagus is markedly distended by a heterogeneous, soft-tissue opacity (M) causing ventral displacement of the trachea (arrow). The well-defined margin of the mass seen in the previous study is no longer visible, perhaps due to the accumulation of fluid in the cranial esophagus. In the periphery of the right cranial and caudal lung lobes, an alveolar lung pattern is present. In the left lung, a dense interstitial pattern is present. These changes are consistent with aspiration pneumonia.Figures 2A, 2B—. Left lateral (A) and ventrodorsal (B) projections of the thorax. The thoracic esophagus is markedly distended by a heterogeneous, soft-tissue opacity (M) causing ventral displacement of the trachea (arrow). The well-defined margin of the mass seen in the previous study is no longer visible, perhaps due to the accumulation of fluid in the cranial esophagus. In the periphery of the right cranial and caudal lung lobes, an alveolar lung pattern is present. In the left lung, a dense interstitial pattern is present. These changes are consistent with aspiration pneumonia.
Figures 2A, 2B—. Left lateral (A) and ventrodorsal (B) projections of the thorax. The thoracic esophagus is markedly distended by a heterogeneous, soft-tissue opacity (M) causing ventral displacement of the trachea (arrow). The well-defined margin of the mass seen in the previous study is no longer visible, perhaps due to the accumulation of fluid in the cranial esophagus. In the periphery of the right cranial and caudal lung lobes, an alveolar lung pattern is present. In the left lung, a dense interstitial pattern is present. These changes are consistent with aspiration pneumonia.Figures 2A, 2B—. Left lateral (A) and ventrodorsal (B) projections of the thorax. The thoracic esophagus is markedly distended by a heterogeneous, soft-tissue opacity (M) causing ventral displacement of the trachea (arrow). The well-defined margin of the mass seen in the previous study is no longer visible, perhaps due to the accumulation of fluid in the cranial esophagus. In the periphery of the right cranial and caudal lung lobes, an alveolar lung pattern is present. In the left lung, a dense interstitial pattern is present. These changes are consistent with aspiration pneumonia.Figures 2A, 2B—. Left lateral (A) and ventrodorsal (B) projections of the thorax. The thoracic esophagus is markedly distended by a heterogeneous, soft-tissue opacity (M) causing ventral displacement of the trachea (arrow). The well-defined margin of the mass seen in the previous study is no longer visible, perhaps due to the accumulation of fluid in the cranial esophagus. In the periphery of the right cranial and caudal lung lobes, an alveolar lung pattern is present. In the left lung, a dense interstitial pattern is present. These changes are consistent with aspiration pneumonia.Figures 2A, 2B—. Left lateral (A) and ventrodorsal (B) projections of the thorax. The thoracic esophagus is markedly distended by a heterogeneous, soft-tissue opacity (M) causing ventral displacement of the trachea (arrow). The well-defined margin of the mass seen in the previous study is no longer visible, perhaps due to the accumulation of fluid in the cranial esophagus. In the periphery of the right cranial and caudal lung lobes, an alveolar lung pattern is present. In the left lung, a dense interstitial pattern is present. These changes are consistent with aspiration pneumonia.Figures 2A, 2B—. Left lateral (A) and ventrodorsal (B) projections of the thorax. The thoracic esophagus is markedly distended by a heterogeneous, soft-tissue opacity (M) causing ventral displacement of the trachea (arrow). The well-defined margin of the mass seen in the previous study is no longer visible, perhaps due to the accumulation of fluid in the cranial esophagus. In the periphery of the right cranial and caudal lung lobes, an alveolar lung pattern is present. In the left lung, a dense interstitial pattern is present. These changes are consistent with aspiration pneumonia.Figures 2A, 2B—. Left lateral (A) and ventrodorsal (B) projections of the thorax. The thoracic esophagus is markedly distended by a heterogeneous, soft-tissue opacity (M) causing ventral displacement of the trachea (arrow). The well-defined margin of the mass seen in the previous study is no longer visible, perhaps due to the accumulation of fluid in the cranial esophagus. In the periphery of the right cranial and caudal lung lobes, an alveolar lung pattern is present. In the left lung, a dense interstitial pattern is present. These changes are consistent with aspiration pneumonia.
Figures 2A, 2B Left lateral (A) and ventrodorsal (B) projections of the thorax. The thoracic esophagus is markedly distended by a heterogeneous, soft-tissue opacity (M) causing ventral displacement of the trachea (arrow). The well-defined margin of the mass seen in the previous study is no longer visible, perhaps due to the accumulation of fluid in the cranial esophagus. In the periphery of the right cranial and caudal lung lobes, an alveolar lung pattern is present. In the left lung, a dense interstitial pattern is present. These changes are consistent with aspiration pneumonia.

Citation: Journal of the American Animal Hospital Association 45, 4; 10.5326/0450185

Figure 3—. Endoscopic view of the thoracic esophagus. A soft-tissue mass (M) is seen within the lumen of the esophagus (arrows).Figure 3—. Endoscopic view of the thoracic esophagus. A soft-tissue mass (M) is seen within the lumen of the esophagus (arrows).Figure 3—. Endoscopic view of the thoracic esophagus. A soft-tissue mass (M) is seen within the lumen of the esophagus (arrows).
Figure 3 Endoscopic view of the thoracic esophagus. A soft-tissue mass (M) is seen within the lumen of the esophagus (arrows).

Citation: Journal of the American Animal Hospital Association 45, 4; 10.5326/0450185

Figures 4A, 4B—. Right lateral (A) and ventrodorsal (B) projections of the thorax. A small, focal gas bubble is present in the midthoracic esophagus, dorsal to the heart (arrow). The caudal thorax is unremarkable. Aspiration pneumonia has resolved.Figures 4A, 4B—. Right lateral (A) and ventrodorsal (B) projections of the thorax. A small, focal gas bubble is present in the midthoracic esophagus, dorsal to the heart (arrow). The caudal thorax is unremarkable. Aspiration pneumonia has resolved.Figures 4A, 4B—. Right lateral (A) and ventrodorsal (B) projections of the thorax. A small, focal gas bubble is present in the midthoracic esophagus, dorsal to the heart (arrow). The caudal thorax is unremarkable. Aspiration pneumonia has resolved.Figures 4A, 4B—. Right lateral (A) and ventrodorsal (B) projections of the thorax. A small, focal gas bubble is present in the midthoracic esophagus, dorsal to the heart (arrow). The caudal thorax is unremarkable. Aspiration pneumonia has resolved.Figures 4A, 4B—. Right lateral (A) and ventrodorsal (B) projections of the thorax. A small, focal gas bubble is present in the midthoracic esophagus, dorsal to the heart (arrow). The caudal thorax is unremarkable. Aspiration pneumonia has resolved.Figures 4A, 4B—. Right lateral (A) and ventrodorsal (B) projections of the thorax. A small, focal gas bubble is present in the midthoracic esophagus, dorsal to the heart (arrow). The caudal thorax is unremarkable. Aspiration pneumonia has resolved.
Figures 4A, 4B—. Right lateral (A) and ventrodorsal (B) projections of the thorax. A small, focal gas bubble is present in the midthoracic esophagus, dorsal to the heart (arrow). The caudal thorax is unremarkable. Aspiration pneumonia has resolved.Figures 4A, 4B—. Right lateral (A) and ventrodorsal (B) projections of the thorax. A small, focal gas bubble is present in the midthoracic esophagus, dorsal to the heart (arrow). The caudal thorax is unremarkable. Aspiration pneumonia has resolved.Figures 4A, 4B—. Right lateral (A) and ventrodorsal (B) projections of the thorax. A small, focal gas bubble is present in the midthoracic esophagus, dorsal to the heart (arrow). The caudal thorax is unremarkable. Aspiration pneumonia has resolved.Figures 4A, 4B—. Right lateral (A) and ventrodorsal (B) projections of the thorax. A small, focal gas bubble is present in the midthoracic esophagus, dorsal to the heart (arrow). The caudal thorax is unremarkable. Aspiration pneumonia has resolved.Figures 4A, 4B—. Right lateral (A) and ventrodorsal (B) projections of the thorax. A small, focal gas bubble is present in the midthoracic esophagus, dorsal to the heart (arrow). The caudal thorax is unremarkable. Aspiration pneumonia has resolved.Figures 4A, 4B—. Right lateral (A) and ventrodorsal (B) projections of the thorax. A small, focal gas bubble is present in the midthoracic esophagus, dorsal to the heart (arrow). The caudal thorax is unremarkable. Aspiration pneumonia has resolved.
Figures 4A, 4B Right lateral (A) and ventrodorsal (B) projections of the thorax. A small, focal gas bubble is present in the midthoracic esophagus, dorsal to the heart (arrow). The caudal thorax is unremarkable. Aspiration pneumonia has resolved.

Citation: Journal of the American Animal Hospital Association 45, 4; 10.5326/0450185

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Copyright: Copyright 2009 by The American Animal Hospital Association 2009
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Figure 1A

Survey left lateral radiograph of the thorax. Note a large soft-tissue opacity (M) with a rounded, smooth cranial margin occupying most of the thoracic esophagus. Gas distends the esophagus at the cranial aspect of the mass. The trachea (arrow) is markedly ventrally displaced.


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Figure 1B

Left lateral projection of the thorax. Liquid barium has been administered per os; it distends the cranial esophagus and confirms obstruction of the caudal esophagus by the soft-tissue mass (M).


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Figures 2A, 2B

Left lateral (A) and ventrodorsal (B) projections of the thorax. The thoracic esophagus is markedly distended by a heterogeneous, soft-tissue opacity (M) causing ventral displacement of the trachea (arrow). The well-defined margin of the mass seen in the previous study is no longer visible, perhaps due to the accumulation of fluid in the cranial esophagus. In the periphery of the right cranial and caudal lung lobes, an alveolar lung pattern is present. In the left lung, a dense interstitial pattern is present. These changes are consistent with aspiration pneumonia.


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Figure 3

Endoscopic view of the thoracic esophagus. A soft-tissue mass (M) is seen within the lumen of the esophagus (arrows).


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Figures 4A, 4B

Right lateral (A) and ventrodorsal (B) projections of the thorax. A small, focal gas bubble is present in the midthoracic esophagus, dorsal to the heart (arrow). The caudal thorax is unremarkable. Aspiration pneumonia has resolved.


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