A challenging case: Acute-on-chronic vomiting in a German shepherd


A 2-year-old intact male German shepherd was referred to the Kansas State University Veterinary Medical Teaching Hospital for evaluation of a three-day history of lethargy, diarrhea, anorexia, and vomiting.

Vital Stats


  • 2-year-old intact male German shepherd

History and presenting complaints

  • Lethargy, diarrhea, anorexia, and vomiting of three days' duration

  • 22-month history of intermittent vomiting

Physical examination findings

  • Underweight

  • Prolonged capillary refill time

  • Slight abdominal pain on palpation

  • Wavelike movement in the ventral neck as the dog inhaled and exhaled

Initial suspicions

  • Toxin ingestion

  • Gastrointestinal torsion

  • Foreign body

  • Gastrointestinal ulceration

  • Esophageal disease

A 2-year-old intact male German shepherd was referred to the Kansas State University Veterinary Medical Teaching Hospital for evaluation of a three-day history of lethargy, diarrhea, anorexia, and vomiting. The owner also reported that the dog had vomited bile-colored liquid every two to three weeks and had had a difficult time gaining weight beginning at 2 months of age. Several months before this evaluation, a veterinarian had examined the dog because of the vomiting and had prescribed cimetidine (5 mg/kg orally b.i.d.).

Three days before referral, the dog had begun vomiting several times a day. The day before referral, the vomitus had become bloody and had increased in volume, and the owner had taken the dog to an emergency clinic. The results of a complete blood count, serum chemistry profile, and coagulation panel had been within reference ranges. Abdominal radiographs had revealed no abnormalities. The emergency veterinarian suspected gastrointestinal ulceration and had instituted treatment with famotidine (2 mg/kg subcutaneously b.i.d.), sucralfate (1 g orally t.i.d.), and metoclopramide (0.4 mg/kg subcutaneously t.i.d.). The next day, the dog had been depressed and continued vomiting large amounts of bloody fluid, so it was referred to the Kansas State University Veterinary Medical Teaching Hospital.


On presentation, the dog was depressed and underweight (90.6 lb [41.2 kg]) and had a body condition score of 3 on a scale of 9, a temperature of 101.5 F (38.6 C), a heart rate of 120 beats/min, and a respiratory rate of 48 breaths/min. The dog had tacky mucous membranes with a capillary refill time of greater than two seconds and was estimated to be 7% dehydrated. The dog's pulse quality was normal.

Abdominal palpation caused mild discomfort, but no abnormalities were palpated. The dog was not experiencing dyspnea, but we saw an abnormal inward and outward wavelike motion in the ventral cervical area as the dog inhaled and exhaled. We also heard the sound of moving fluid originating from the cervical area from as far as several feet away.

Our differential diagnoses for the hematemesis included toxin ingestion, gastrointestinal torsion, a foreign body, and ulceration. We thought a coagulation disorder was unlikely because no abnormalities were identified on the previous day's coagulation profile. Because of the fluid sound and abnormal motion in the cervical area, we suspected esophageal disease, and our differential diagnoses were megaesophagus (congenital or acquired), an esophageal foreign body, esophagitis, or an esophageal stricture. The recent abdominal radiographs were noted to be unremarkable, but they were not available for us to view at the time of referral. The differential diagnosis list was narrowed to toxin ingestion, gastrointestinal torsion, a foreign body, gastrointestinal ulceration, and esophageal disease.


We performed a complete blood count, a serum chemistry profile, a urinalysis, and an abdominal and thoracic radiographic examination. The complete blood count (Table 1) revealed an elevated hematocrit, an elevated hemoglobin, an elevated red blood cell count, and a leukocytosis with a segmented neutrophilia, lymphopenia, and monocytosis. Abnormal results of the serum chemistry profile (Table 1) included an elevated blood urea nitrogen concentration, hypokalemia, and hypochloremia. These findings were attributed to and consistent with vomiting, anorexia, and dehydration. The elevated blood glucose concentration was most likely a physiologic response (glucocorticoid-associated) to stress.

Table 1 : Laboratory Test Results

The results of a urinalysis on a sample collected by cystocentesis revealed a specific gravity of 1.052 (reference range = 1.015 to 1.045), mild hematuria (3+ blood), and mild proteinuria (4+ protein). The urine specific gravity indicated that the dog was concentrating urine appropriately in the face of dehydration. We attributed the hematuria to the collection method, and we did not consider the proteinuria to be clinically relevant because the urine was concentrated and hematuria was present. We submitted a urine sample for bacterial culture, which resulted in no growth.

The lateral and ventrodorsal abdominal radiographs revealed a cranially displaced spleen. At the cranial edge of the lateral radiograph, part of the caudal thorax was visible, revealing a large soft tissue structure (Figure 1). The stomach was not visible within the abdomen. The thoracic radiographs demonstrated severe gas distention of the cranial thoracic esophagus, consistent with megaesophagus; microcardia was also present (Figures 2-4). An ovoid, 14- x 18-cm soft tissue mass was present on the midline in the area of the caudal thoracic esophagus (Figure 3).

Figures 1-4

Based on the radiographic findings, we diagnosed a gastroesophageal intussusception. Our other differential diagnoses were a paraesophageal hernia, a hiatal hernia, an esophageal luminal mass, and a foreign body. Paraesophageal and hiatal hernias were less likely because the mass appeared to be an intraluminal esophageal mass. An esophageal mass such as a granuloma or neoplasia seemed less likely than a gastroesophageal intussusception because the stomach could not be seen in the abdomen. The severe megaesophagus was most likely a congenital or acquired condition, and megaesophagus can be a predisposing factor for a gastroesophageal intussusception. The intussusception could only have been present for a short time. The microcardia was consistent with hypovolemia.


We initiated intravenous fluid therapy (380 ml/hr) with lactated Ringer's solution to stabilize the dog hemodynamically before performing abdominal exploratory surgery, which was scheduled for early the next morning. General anesthesia was induced with propofol (5 mg/kg intravenously) and maintained with isoflurane. Positive pressure ventilation was required. We initiated an intravenous continuous rate infusion of fentanyl (5 µg/kg/hr) and lidocaine (50 µg/kg/hr).

A ventral midline incision was made from the xiphoid to the pubis. On exploration, the stomach was completely invaginated within the esophagus; the duodenum was the first portion of the gastrointestinal tract located on the abdominal side of the diaphragm. No other organs were displaced into the esophagus. The esophageal hiatus had no visible abnormalities. The spleen was displaced cranially. Gentle traction was applied to reduce the stomach into its normal position, but a diaphragmatic incision about 2 cm in length at the level of the esophageal hiatus was required to reduce the stomach into the abdominal cavity. A ventral longitudinal incision in the esophagus about 2 cm wide was also made to free the congested stomach.

Once the stomach was reduced, its viability was assessed. The serosal surfaces of the fundus and cardia were dark-red to purple. The pyloric antrum and pylorus were normal in color. The wall of the stomach felt slightly thickened, and wall motility was normal, so stomach resection was deemed unnecessary. The spleen looked grossly normal and was no longer displaced. The rest of the abdominal exploratory surgery revealed no other abnormalities.

The incision in the esophagus was closed in a two-layer, simple continuous pattern with 3-0 polydioxanone suture. An incisional gastropexy at the level of the pyloric antrum was performed to attach the stomach to the right body wall with 0 polydioxanone suture. The abdominal and thoracic cavities were copiously lavaged with 0.9% sterile saline solution. The diaphragm incision was closed with 0 polydioxanone suture in a simple continuous pattern. An enterostomy tube (8-F infant feeding tube) was placed aborally in the proximal jejunum. A 24-F thoracostomy tube was placed at the right eighth intercostal space. The abdomen was closed in a routine manner.


After surgery, the dog received nasal oxygen insufflation (5 L/min), cefazolin (22 mg/kg intravenously t.i.d.), enrofloxacin (10 mg/kg intravenously once daily), famotidine (0.5 mg/kg intravenously b.i.d.), and sucralfate (1 g orally t.i.d.). The fentanyl infusion was continued for 24 hours. The lidocaine infusion was also continued for 24 hours for its anesthetic and prokinetic effects. Continuous telemetric monitoring was performed, and no arrhythmias were noted. The chest tube was aspirated every four to six hours. The dog recovered well from surgery and was bright, alert, and normothermic the next day. The urinary catheter placed after surgery was removed the next morning.

Twenty-four hours after surgery, one-fourth of the patient's required caloric intake was calculated for CliniCare Canine/Feline Liquid Diet (Abbott Animal Health) and was fed through the jejunostomy tube as a continuous rate infusion. The fentanyl and lidocaine infusions were discontinued. Pain was controlled with morphine (0.5 mg/kg subcutaneously q.i.d.).

Forty-eight hours after surgery, the dog remained bright, alert, and normothermic, and we removed the chest tube because only a small amount of fluid had been removed. The liquid diet continuous rate infusion was increased to half the required daily caloric intake.

Three days after surgery, the dog was still bright and alert but had vomited blood (not regurgitated) several times and had a temperature of 103 F (39.4 C). Our differential diagnoses for the recurrence of vomiting and the pyrexia were gastrointestinal necrosis, infection, sepsis, and pneumonia. We instituted an intravenous continuous rate infusion of metoclopramide (0.05 mg/kg/hr).

Four days after surgery, the dog's vomiting frequency increased despite the metoclopramide, and the dog's temperature increased to 104.2 F (40.1 C). Our differential diagnoses were pneumonia, sepsis, gastrointestinal necrosis, and leakage. Thoracic radiography (Figure 5) revealed an alveolar pattern most consistent with bronchopneumonia in the left cranial, right middle, and right cranial lung lobes. The severe megaesophagus was still evident in the cranial thoracic esophagus. Results of a complete blood count (Table 1) showed a leukocytosis, neutrophilia with a regenerative left shift, mild lymphopenia, and a monocytosis. Abnormal results of a serum chemistry profile (Table 1) included hypoproteinemia, hypoalbuminemia, hypocholesterolemia, and decreased alanine transaminase and elevated alkaline phosphatase activities. We considered measuring serum acetylcholine receptor antibody concentrations because myasthenia gravis can cause megaesophagus, but we elected not to because of the dog's declining condition and the time needed to receive the results.

Figure 5

At this time, we thought the dog had aspiration pneumonia associated with megaesophagus. We recommended performing a transtracheal wash and bacterial culture, but the owner declined. Our treatment for the patient's aspiration pneumonia included nasal oxygen (5 L/min), nebulization of saline solution, coupage every four to six hours, and antibiotic therapy. We increased the frequency of enrofloxacin administration (10 mg/kg intravenously b.i.d.). Since the dog was not improving with the cefazolin therapy, we discontinued it and began ampicillin therapy (24 mg/kg intravenously t.i.d.).

Five days after surgery, the dog became very depressed, tachypneic (120 breaths/min), remained febrile (104.5 F [40.3 C]), and began vomiting large amounts of bloody fluid. Thoracic radiography revealed no changes in appearance from the previous day. Results of an arterial blood gas analysis (sample obtained while the dog was receiving supplemental oxygen) indicated hypoxemia (PO2 = 60 mm Hg [normal = 90 to 100 mm Hg]; PCO2 = 25 mm Hg [normal = 36 to 40 mm Hg]; SPO2 = 91% [normal = 95% to 100%]). The owners elected euthanasia because of the poor prognosis associated with aspiration pneumonia and megaesophagus.

A gross necropsy was performed. The jejunostomy and gastropexy sites were intact. The stomach serosa was dark-red to black, but the mucosa appeared normal. The esophageal serosa and mucosa were dark-red to black, but the mucosa was intact. The sutures were intact in the esophagus; however, when tested, fluid leaked through a small portion of the suture line. The diaphragm incision was also intact. The mediastinum contained about 1 L of serosanguineous fluid. The esophagus was markedly dilated, measuring more than 16 cm in circumference (Figure 6). The cranial lung lobes were atelectatic. There was no gross evidence of aspiration pneumonia, but a histologic examination was not performed.

Figure 6


Gastroesophageal intussusception is a rare gastrointestinal emergency, and the cause is not completely understood. It seems to be more common in young dogs, usually less than 3 months of age. Males seem to be more commonly affected, as do large-breed dogs, especially German shepherds, possibly because of the higher incidence of hereditary megaesophagus.1-4 Esophageal disease is frequently associated with gastroesophageal intussusception, suggesting that abnormalities such as megaesophagus, abnormal esophageal motility, and esophageal hiatus laxity may be important contributing factors to gastroesophageal intussusception.2-6

Common clinical signs of gastroesophageal intussusception include regurgitation, vomiting, hematemesis, hypersalivation, abdominal discomfort, and dyspnea.3 Along with the stomach, other abdominal organs can invaginate into the esophagus, including the spleen, duodenum, pancreas, and omentum.3,5 In addition to obstructing the esophagus, gastroesophageal intussusception can cause respiratory and cardiovascular dysfunction by acting as a space-occupying mass in the thorax.2-4 The intussusception can impair caudal lung lobe expansion and compress the great vessels in the thorax, compromising perfusion to various organs and venous return to the heart, leading to a state of obstructive shock and death.3

Gastroesophageal intussusception can be diagnosed by obtaining plain or contrast radiographs. A soft tissue opacity mass may be located in the caudal thoracic mediastinal area. The gas bubble in the stomach's normal anatomical location will be absent. If contrast medium is used, it may show a filling defect in the caudal esophagus, with no contrast present in the normal anatomical location of the stomach.3-5 If the diagnosis is still questionable, esophagoscopy can be performed, although it may not be possible to pass the endoscope into the stomach or rugal folds may be viewed within the esophagus.2-5,7

Initial therapy includes correcting fluid and electrolyte abnormalities. If indicated, initial therapy may also include antibiotics and analgesics. Once gastroesophageal intussusception is diagnosed, immediate surgical correction is required. Reduce the stomach invagination, and assess affected organs for viability (i.e. observe serosal color, wall texture, vascular patency, and presence of motility). Necrotic tissue can range in color from green to black, will often feel thin, may lack peristaltic activity, and, if incised, may not display normal bleeding. If you are unsure about the viability of a portion of the stomach, remove or invaginate it.8 Also secure the stomach with a gastropexy so that it will stay within the abdominal cavity. Incisional, belt-loop, and circumcostal gastropexies can prevent recurrence of invagination.2-5 In some cases, it may be beneficial to perform more than one gastropexy—more specifically, one on the left body wall with the idea that the esophageal hiatus is to the left of midline, so securing the stomach in this manner will have an advantage over right-sided gastropexies.2,4 Fundoplication or alteration of the esophageal hiatus are other methods that may prevent recurrence.2,5,7 Fundoplication involves apposing the fundus of the stomach to the esophagus, and alteration of the hiatus involves narrowing the hiatus. These procedures are not routinely performed and may have negative effects in patients with megaesophagus by creating more resistance for food to pass easily into the stomach.

After surgical correction, most patients require management of their megaesophagus-related sequelae and esophageal and gastric mucosal damage. If aspiration pneumonia is present, administer appropriate antibiotics based on bacterial culture and antimicrobial sensitivity testing results or a good empirical selection until the patient is stable enough to obtain a sample by transtracheal wash. Nasal oxygen and nebulization may also be indicated.2 In patients with evidence of severe esophagitis and gastritis, placing a feeding tube such as a jejunostomy tube will allow the esophageal and gastric mucosa time to rest and provide a method of supplying nutrients to the patient. Administering H2 receptor blockers and other mucosal protectants will also aid in mucosal healing.3 Dogs with megaesophagus should be fed small frequent meals while being held in an upright position to facilitate passage of ingesta into the stomach.

The prognosis in dogs with gastroesophageal intussusception is typically guarded to poor. A review of literature published in 1984 revealed a mortality rate of 95%.3 An unfavorable prognosis is most likely attributable to the fact that this is a relatively rare condition with limited awareness, resulting in delayed or incorrect diagnosis; that death can occur rapidly after clinical signs appear; and that secondary complications such as aspiration pneumonia can mask a correct diagnosis and worsen the prognosis.3

This case was challenging because an early diagnosis of esophageal disease was hindered by the dog's history of chronic vomiting, allowing the eventual development of a severe condition with an unfavorable outcome. The cause of the vomiting, or the vomiting itself, could have been a predisposing factor for the development of gastroesophageal intussusception in this dog, as people with a history of physical exertion and peptic disease are predisposed to gastroesophageal intussusception.9 It is reasonable to speculate that this dog's history of chronic vomiting may have also involved chronic regurgitation.

It is important to differentiate between vomiting and regurgitation because they can result from vastly different disease processes. This differentiation can be accomplished by taking a detailed history and performing a complete physical examination. Regurgitation is not preceded by signs of nausea or retching (forceful contraction of abdominal muscles), the regurgitated material should not contain bile, and, if the material is pH-tested, it should have a value of 7 or higher. Further diagnostic tests to rule out regurgitation may include radiography (plain and contrast) and endoscopy.

The exact cause of this dog's megaesophagus was unknown, but it is likely that the megaesophagus was present before the gastroesophageal intussusception. Initial abdominal radiographs of this dog were not available for viewing. They may have been considered to be normal because the caudal thorax may not have been included in the study, the lack of the gastric gas bubble in the cranial abdomen may have been overlooked, or the gastroesophageal intussusception was possibly not present at that time. The rarity of this condition and a generalized low level of awareness may have allowed this condition to persist for up to 24 hours before the proper diagnosis was made and appropriate treatment was initiated. The focus on the history of vomiting and not considering esophageal disease undoubtedly had a negative effect on the eventual outcome.

Another challenging aspect of this case was the postoperative management. We think that the dog's recovery from an already severe condition was hindered by its respiratory disease (aspiration pneumonia), leading to a state of hypoxemia. Thoracic radiographs taken five days after surgery showed patterns consistent with bronchopneumonia. There was no obvious gross evidence of pneumonia on necropsy, but it was not ruled out by a histologic examination. We think that aspiration pneumonia was present based on clinical and radiographic signs. If a transtracheal wash or bronchoalveolar lavage had been performed, the results of the cytology and culture would have helped rule pneumonia in or out. A pulmonary thromboembolism could have caused the radiographic changes as well.10

Another differential diagnosis for the dog's postoperative clinical signs could have been esophageal leakage. If leakage through the esophageal incision had been suspected, another surgery could have been performed to repair the esophagus. Although leakage of the thoracic esophagus was considered, the expected pleural effusion was not seen radiographically. The fluid may have been difficult to see if it was contained in the caudal mediastinal space, as noted at necropsy. If negative culture results had been attained after a transtracheal wash or bronchoalveolar lavage, esophageal leakage would have been more strongly considered.


Gastroesophageal intussusception is a relatively rare condition, but this case demonstrates the importance of considering esophageal disease when confronted with a history of chronic vomiting. The outcome depends on being able to recognize possible esophageal disease promptly so that appropriate diagnostic steps are taken to arrive at an early and correct diagnosis. ?

Ralph P. Millard, DVM*

Brenda Jo Salinardi, DVM, MS, DACVS**

Department of Clinical Sciences

College of Veterinary Medicine

Kansas State University

Manhattan, KS 66506

Current addresses:

*Department of Veterinary Clinical Sciences

College of Veterinary Medicine

University of Minnesota

St. Paul, MN 55108

**Department of Clinical Sciences

College of Veterinary Medicine

Oregon State University

Corvallis, OR 97331


1. Washabau RJ, Holt DE. Esophageal pathophysiology. In: Slatter D, ed. Textbook of small animal surgery. 3rd ed. Philadelphia, Pa: WB Saunders Co, 2003;530-533.

2. Graham KL, Buss MS, Dhein CR, et al. Gastroesophageal intussusception in a Labrador retriever. Can Vet J 1998;39:709-711.

3. Leib MS, Blass CE. Gastroesophageal intussusception in the dog: a review of literature and a case report. J Am Anim Hosp Assoc 1984;20:783-790.

4. Clark GN, Spodnick GJ, Rush JE, et al. Belt loop gastropexy in the management of gastroesophageal intussusception in a pup. J Am Vet Med Assoc 1992;201:739-742.

5. von Werthern CJ, Montavon PM, Fluckiger MA. Gastro-oesophageal intussusception in a young German shepherd dog. J Small Anim Pract 1996;37:491-494.

6. Greenfield CL, Quinn MK, Coolman BR. Bilateral incisional gastropexies for treatment of intermittent gastroesophageal intussusception in a puppy. J Am Vet Med Assoc 1997;211:728-730.

7. Applewhite AA, Cornell KK, Selcer BA. Diagnosis and treatment of intussusceptions in dogs. Compend Contin Educ Pract Vet 2002;24:110-125.

8. Fossum TW. Surgery of the stomach. In: Small animal surgery. 2nd ed. St. Louis, Mo: Mosby, 2002;337-368.

9. Gowen GF, Stoldt HS, Rosato FE. Five risk factors identify patients with gastroesophageal intussusception. Arch Surg 1999;134:1394-1397.

10. Johnson LR, Lappin MR, Baker DC. Pulmonary thromboembolism in 29 dogs: 1985-1995. J Vet Intern Med 1999;13:338-345.

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