A nine-week-old, female Australian Shepherd dog weighing five kg was presented to the Emergency Department of the University of Veterinary Medicine Vienna, Austria, with a three-day history of profuse vomiting and regurgitation. No clinical signs had been noticed before the acute onset of disease. The puppy had been purchased from a breeder one week prior to presentation. The primary veterinarian suspected a hiatal hernia based on thoracic and abdominal positive contrast radiographs. The puppy had been fed solid food for a couple of weeks without any difficulty, had been healthy from birth, and was the largest puppy of the litter. Initial physical examination revealed lethargy, a body condition score of four out of nine, reduced skin turgor, increased vesicular lung sounds and abdominal tenderness on palpation. Other parameters were within normal limits. A fecal test for parvoviral antigen (IDEXX SNAP® test) was negative. Clinicopathologic findings on blood examination were metabolic alkalosis (pH 7.51 [reference value 7.351-7.463], HCO3 38.6 mmol/L [reference value 18-24 mmol/L]), hypokalemia (2.9 mmol/L [reference value 3.6-5.6 mmol/L]), both likely attributable to the vomiting, and a mild, stress- induced hyperglycemia (132 mg/dl [reference value 55-100 mg/dl]). Thoracic radiographs in left lateral recumbency showed a contrast-filled esophagus, due to a barium contrast study performed by the referring veterinarian 4 hours previously. A diverticulum of the esophagus in the cranial mediastinum was suspected with severe esophageal distention in the caudal portion of the mediastinum. An intraluminal soft-tissue mass with traces of barium contrast and rugal folds was visible in the caudal thorax. The trachea was displaced ventrally, and the stomach silhouette was not visible in the cranial abdomen. There was no evidence of lung consolidation or infiltration, although esophageal obstruction caused by gastroesophageal intussusception (GEI) was strongly suspected. Initial treatment for dehydration, and electrolyte imbalances from the regurgitation and vomiting consisted of intravenous saline supplemented with potassium chloride (6 ml/kg/h) to balance dehydration and hypokalemia, ranitidine (2 mg/kg IV BID, Ulsal Injectable, Gebro Pharma GmbH, Fieberbrunn, A) as gastric protectant, maropitant (1 mg/kg IV SID, Cerenia Injectable, Pfizer Animal Health Austria GmbH, Vienna, A) as antiemetic, and amoxicillin-clavulanic acid (22 mg/kg IV BID, Clavamox Injectable, 550 mg, Sandoz GmbH, Vienna, A) to prevent possible aspiration pneumonia. Esophageal endoscopy was performed under general anesthesia (butorphanol 0.1 mg/kg IV, Butomidor Injectable, 10 mg/ml, Richter Pharma AG, Wels, A; propofol 5 mg/kg IV, Propofol „Fresenius“ 1% with MCT Injectable, Fresenius Kabi Austria GmbH, Graz, A; and inhalational isoflurane). Inspection of the esophagus with a flexible videoendoscope (Olympus GIF 165) revealed accumulation of intraluminal fluid, food particles and contrast media in the cranial and midsection of the esophagus, while the caudal third of the esophagus appeared distended and obstructed by an intraluminal mass consistent with the stomach. Uncomplicated gastric reposition was achieved by advancement of the endoscope against the gastric mucosa. Closure of the gastric cardia appeared incomplete. The caudal esophagus remained dilated with the mucosa macroscopically intact. To prevent repeated dislocation of the stomach and to allow for nutrition bypassing the esophagus, a percutaneous endoscopic gastrostomy (PEG) tube (mushroom/Pezzar style silicone catheter, Surgivet, Smiths Medical, Dublin, OH, USA) was placed in the left abdominal wall. Inspection of the cranial and middle parts of the esophageal lumen after removal of its contents failed to demonstrate the presence of the radiographically suspected cranial diverticulum. Based on endoscopic findings the final diagnosis was GEI with secondary esophageal dilation. After an uneventful recovery from anesthesia, the patient’s condition improved. Partial parenteral nutrition, a metoclopramide constant rate infusion (CRI, 0.01 mg/kg/h, Paspertin 10 mg Injectable, Abbott Products GmbH, Hannover, D) to prevent vomiting and a lidocaine CRI (0.05 mg/kg/h, Xylanaest purum 1% Injectable, Gebro Pharma GmbH, Fieberbrunn, A) as analgetic and radical scavenger were added to the therapeutic regimen. Twelve hours after endoscopy, lidocaine was progressively reduced and discontinued. A mucosal protectant (sucralfate, 0.1 g/kg PO TID, Ulcogant oral suspension 1 g/5 ml, Merck S.L., Mollet Del Valles, E) was administered, along with small amounts of water. Feeding via the PEG tube was withheld for another 24 hours to prevent possible mucosal irritation caused by gastroesophageal reflux or vomiting. Thoracic radiographs in left lateral recumbency taken 36 hours after gastric repositioning showed resolution of the gastroesophageal intussusception. The esophagus still appeared dilated, and an interstitial and mild alveolar lung pattern was identified and thought to be from aspiration pneumonia. Thirty-six hours after endoscopy, enteral nutrition was initiated via PEG tube using a bland diet. The dog was clinically normal, playful, tolerated oral water and sucralfate well. Over the next days, blood values returned to normal and oral feeding from an elevated position was gradually introduced. Although neither vomiting nor regurgitation were observed, thoracic radiographs in left lateral recumbency nine days after initial presentation showed persisting caudal esophageal dilation. The patient was discharged nine days after admission. The owner was instructed to offer incrementally increasing small portions of food formed to meatballs from an elevated position five times daily and was taught how to use the PEG tube to maintain the dog’s nutrition. Ranitidine, sucralfate and amoxicillin-clavulanic acid were prescribed as oral medications. The dog remained clinically unremarkable, gained weight and size quickly, and the PEG tube was removed two weeks after discharge as oral feedings covered the patient’s nutritional demands. Thoracic radiographs in left lateral recumbency repeated at five weeks, four months and eight months after discharge revealed persistent esophageal dilatation, absence of abnormal lung patterns, and the patient continues to tolerate commercially available dog food and treats without difficulty. Thoracic radiographs in left lateral recumbency eight months after initial presentation show the esophagus is still dilated with a slight distension cranial to the heart. There is a striped luminal pattern in the caudal section consistent with a narrower lumen of the esophagus. The stomach is filled with contrast medium.