Esophagus

Introduction

Most foreign material ingested by dogs and cats will either pass uneventfully through the gastrointestinal tract, cause mild vomiting and/or diarrhea, or be dissolved by gastric acid.¹ However, foreign bodies that lodge in the esophagus should be considered an emergency. The longer entrapped foreign bodies are present, the greater the chance of severe esophageal wall damage and possible perforation.² Sharp pointed objects can penetrate the esophageal wall leading to mediastinitis or occasionally broncho-esophageal fistula.³ The most commonly encountered esophageal foreign bodies are bones, rawhide chew toys, dental chews such as Greenies^®, fish hooks, and hairballs.⁴

Because of indiscriminate eating habits, swallowing of incompletely masticated food, and exposure to dental cleaners, foreign bodies occur more commonly in dogs than cats.^3,5,6,7 Hairballs vomited from the stomach can obstruct the esophagus in cats. Foreign bodies can occur in any age animal, but are most common in young dogs, or those frequently given bones or rawhide chew toys.⁸ Foreign body entrapment may be more common in small dogs and terrier breeds.^3,4

Pathophysiology

The esophagus is very distensible and most ingested foreign objects are passed into the stomach. Foreign bodies commonly lodge where the esophagus is restricted from distending: the thoracic inlet, base of the heart, or diaphragmatic hiatus. The entrapped foreign body stimulates secondary peristalsis, which can augment pressure necrosis of the esophageal wall.^9,10 Even though the esophagus is lined by tough stratified squamous epithelium, erosion, ulceration, and perforation can develop if the foreign body is not promptly removed. Fish hooks can lodge anywhere within the esophagus but the pharyngeal portion of the esophagus and heart base are most common.⁶

Clinical Signs

The most common clinical signs associated with esophageal foreign bodies are regurgitation, excess salivation, anorexia, odynophagia, and respiratory signs due to aspiration pneumonia. Foreign body ingestion may be observed or suspected by the owner. Clinical signs develop acutely. With obstructive lesions regurgitation of water occurs and dehydration can quickly develop. Perforation of the esophageal wall may result in pyrexia and depression. Mediastinitis with extension into the pleural cavity will lead to pleural effusion and progressive respiratory distress.
 

Diagnosis

Most esophageal foreign bodies are radiodense and clearly visible on survey radiographs (Figures 17-1A and B). Other common radiographic findings include a soft tissue density surrounding the foreign body (fluid in the esophagus, thickened wall, or localized mediastinitis) and air-filled dilated esophagus cranial to the foreign body.¹¹ Thin poultry bones can be difficult to visualize as they silhouette with ribs and vertebrae.

Although difficult to diagnose in cases with large entrapped bones, the presence of mediastinitis radiographically suggests esophageal perforation. Radiographic findings associated with mediastinitis include: increased mediastinal opacity and widening, extensive fluid density surrounding the foreign body, loss of detail around the mass, or obliteration of the shadow of the caudal vena cava.³

If perforation has occurred, thoracic radiographs taken after esophagoscopy may demonstrate pneumomediastinum. If perforation is suspected on survey radiographs, but cannot be confirmed, an iodine contrast study should be performed. Aqueous organic iodide contrast at 0.5-1.0 ml/kg can be administered.¹² Contrast studies should be performed after foreign body removal, because when the foreign body is still in place it may obstruct the perforation site, blocking leakage of contrast.³
 

Treatment

Most esophageal foreign bodies can be successfully removed endoscopically (Figure 17-2).¹¹ If foreign bodies cannot be endoscopically grasped and extracted from the esophagus, they can often be carefully pushed into the stomach with an orogastric tube under endoscopic visualization. In the stomach, gastric acid will dissolve most bones, or foreign bodies can be removed via celiotomy and gastrotomy, or endoscopically, as more room is available for endoscopic manipulation.^5,9,11 Pushing an impacted foreign body into the stomach with an orogastric tube without endoscopic visualization should be performed carefully or not at all, because of the risks of severe mucosal damage or esophageal perforation. Surgery of the esophagus should be avoided if possible because of difficult exposure within the thorax, post-operative morbidity, and frequent complications. Surgical removal is indicated if a foreign body cannot be removed or pushed into the stomach, if the entire tip of a fishhook has penetrated the esophageal wall, or if esophageal perforation is present. A highly successful method of foreign body retrieval using forceps under fluoroscopic guidance has been reported, but is not practical for most practitioners.⁴
 

Large foreign bodies may be so tightly lodged within the esophagus, that flexible endoscopic forceps cannot grasp the object tightly enough for removal. These foreign bodies can often be retrieved using a rigid uterine or rectal biopsy forceps passed along the side of a flexible endoscope.² During removal, large foreign bodies may lodge at the pharynx, but can be delivered by grasping with curved carmalt forceps. Foreign bodies can also be removed using a rigid endoscope and rigid forceps.^5,6,8,11

Esophagoscopy

To perform esophagoscopy, the animal should be positioned in left lateral recumbency.¹³ A mouth speculum must be placed on the left upper and lower canine teeth to protect the endoscope. The tongue should be grasped and the head and neck extended by an assistant. A flexible endoscope is passed over the base of the tongue, through the pharynx dorsal to the endotracheal tube, and into the proximal esophagus. Lubrication is generally not necessary.

The esophageal mucosa is usually collapsed and appears in longitudinal folds.^14-16 It should be distended by insufflating air. The endoscope tip should be centralized within the lumen by adjusting the control knobs. Only minor tip adjustments are necessary, as the esophagus is a relatively straight tube. By advancing the endoscope only when the lumen is clearly visible, the endoscopist can dramatically reduce the risk of esophageal perforation. The endoscope should be advanced until the foreign body is visible. The mucosa surrounding the foreign body should be carefully inspected for erosion, ulceration, or perforation. If perforation is present or suspected, air insufflation should be limited, to avoid producing pneumomediastinum and possibly pneumothorax. Attempts should be made to gently slide the endoscope past the foreign body. This will allow assessment of mucosa not initially visible and help to plan foreign body extraction. The shape, contour, and composition of the foreign body will dictate the type of forceps necessary for extraction. The most helpful forceps are the rat-tooth, wire snare, 4-wire basket, and Roth net.

The foreign body forceps should be passed through the endoscope’s biopsy channel into the lumen of the esophagus and opened by an assistant. An edge of the foreign body should be grasped and the forceps closed. The forceps should be withdrawn to pull the foreign body close to the endoscope’s tip. Air should be insufflated during withdrawal of the endoscope to help dilate the esophagus and prevent damage to the esophageal mucosa as the foreign body is withdrawn.

Fishhooks can be difficult to remove, especially if embedded or if they are treble-barb hooks.⁶ If the tip of the hook is protruding into the lumen, it can be grasped and the entire hook pulled through the mucosa and removed. If the tip of the hook is not visible but appears to be embedded only in the mucosa or submucosa, the hook can be gently torn through the mucosa, creating a superficial laceration that usually heals without complication.⁶ If the hook appears to have passed through the esophageal wall, it should be surgically removed.

Hairballs, or trichobezoars, which occur most often in cats, often tear apart when grasped with foreign-body-retrieval forceps. Because of their tendency to fragment, hairballs may require multiple passes with extraction forceps to completely remove them. In addition, because of space limitations, it is usually not possible to place a wire snare or basket around the center of an esophageal hairball. In some cases, it is easier to push the hairball into the stomach for easier endoscopic manipulation, and where the hairball can be firmly grasped and removed. Esophageal perforation and resulting mediastinitis is a severe complication of esophageal foreign bodies. Small perforations can be managed medically by treating esophagitis, while large perforations require surgical repair and drainage.⁸

Mild esophagitis and erosions will heal quickly without complications. Food should be withheld for 24 hours followed by frequent feeding of small quantities of a gruel diet for 2-3 days. The gruel can be gradually thickened, the meal volume increased, and the feeding frequency decreased if regurgitation does not occur. Moderate or severe esophagitis and ulceration require more intensive medical management and a longer period of “resting the esophagus” by withholding oral food intake. In some cases, a percutaneous gastrostomy tube can be placed to provide nutrition while promoting esophageal healing and bypassing the esophagus. Cimetidine (10 mg/kg TID), ranitidine (2 mg/kg BID or TID), or famotidine (0.5 mg/kg BID) or a proton pump antagonist such as omeprazole (1 mg/kg SID) should be given to reduce gastric acid production and prevent further esophageal damage from gastroesophageal reflux. Metoclopramide (0.2-0.4 mg/ kg TID) can help increase gastroesophageal tone and reduce gastric reflux. Sucralfate suspension can bind to and coat eroded or ulcerated esophageal mucosa (1 gm/25 kg TID-QID). If severe mucosal damage is present, broad-spectrum antibiotics should be given for 1-2 weeks. Medical treatments should be continued for 1 week after normal feeding has been resumed. After the esophagus has healed, oral feeding can be started as described above. Until oral feeding begins, medications (except sucralfate) must be given parenterally or via the PEG tube.

Prognosis

The overall prognosis is good, but is dependent on the type of foreign body, the duration of time present, the degree and severity of esophageal damage, and the development of perforation.⁴ The longer a foreign body is impacted within the esophagus, the harder it is to remove and the greater chance for perforation. Large perforations warrant a poor prognosis, despite aggressive surgical care.³ Most cases with esophagitis, that receive appropriate medical care, will heal without complications.^8,10 Stricture formation following foreign body retrieval of bones is uncommon and is more likely following perforation or when severe damage to the esophageal wall has occurred, or after impaction of a dental chew.⁷ Animals with severe esophagitis or ulceration should be endoscopically reevaluated in 7-10 days to assess stricture formation, which if present can be dilated with balloon catheters.

References

1. Leib M. Diseases of the esophagus. In: Leib M, Monroe W, eds. Practical Small Animal Internal Medicine. Philadelphia: W B Saunders; 1997:633-652.
2. Jones BD. Management of Esophageal Foreign Bodies. In: Kirk RW, Bonagura JD, ed. Current Veterinary Therapy XI. Philadelphia: W B Saunders Company; 1992:577-580.
3. Parker NR, Walter PA, Gay J. Diagnosis and Surgical management of esophageal perforation. J Am Anim Hosp Assoc 1989;25:587-594.
4. Moore A. Removal of oesophageal foreign bodies in dogs: use of the fluoroscopic method and outcome. J Sm Anim Pract 2001;42:227-230.
5. Pearson H. Symposium on Conditions of the Canine Oesophagus - I Foreign Bodies in the Oesophagus. J Sm Anim Pract 1966;7:107-116.
6. Michels GM, Jones BD, Huss BT, et al. Endoscopic and surgical retrieval of fishhooks from the stomach and esophagus in dogs and cats: 75 cases (1977-1993). J Am Vet Med Assoc 1995;207:1194-1197.
7. Leib MS, Sartor LL, Esophageal foreign body obstruction caused by a dental chew treat in 31 dogs (2000-2006). J Am Vet Assoc 2008; 232:1021-1025.
8. Ryan WW, Greene RW. The Conservative Management of Esophageal Foreign Bodies and Their Complications: A Review of 66 Cases in Dogs and Cats. J Am Anim Hosp Assoc 1975;11:243-249.
9. Spielman BL, Shaker EH, Garvey MS. Esophageal foreign body in dogs: a retrospective study of 23 cases. J Am Anim Hosp Assoc 1992;28:570-574.
10. Zimmer JF. Canine Esophageal Foreign Bodies: Endoscopic, Surgical, and Medical Management. J Am Anim Hosp Assoc 1984;20:669-677.
11. Houlton EF, Herrtage ME, Taylor PM, et al. Thoracic oesophageal foreign bodies in the dog: a review of ninety cases. J Sm Anim Pract 1985;26:521-536.
12. Moon M, Myer W. Gastrointestinal contrast radiology in small animals. Sem Vet Med Surg 1986;1:121-143.
13. Leib MS. Endoscopic Examination of the Dog and Cat. In: Jensen SL, Gregersen H, Moody FG, Shokouh-Amiri MH, eds. Essentials of Experimental Surgery: Gastroenterology. Amsterdam: Harwood Academic Publishers; 1994.
14. Tams TR. Esophagoscopy. In: Tams TR, ed. Small Animal Endoscopy. St. Louis: C V Mosby; 1990:47-88.
15. Guilford WG. Upper gastrointestinal endoscopy. Vet Clin North Am: Sm Anim Pract 1990;20:1209-1227.
16. Guilford W, Jones BD. Gastrointestinal endoscopy of the dog and cat. Vet Med Rep 1990;2:140-150.
     

Introduction

The hiatus of the esophagus is that portion of the diaphragm that allows the esophagus and vagus nerves to pass between the thoracic and abdominal cavities. A hiatal hernia (HH) can allow the protrusion of an abdominal structure(s) through an enlarged hiatus and into the thoracic cavity. The most common HH in the dog and cat is the axial hiatal hernia, which implies a cranial displacement of the gastroesophageal junction through the hiatus into the caudal mediastinum¹ (Figure 17-3A). Various amounts of stomach may reside within the thorax as well as other viscera that may move cranially. Most of the time this is a “sliding” hiatal hernia whereby the viscera is not fixed and moves back and forth between the thorax and abdomen.

Paraesophageal hernias occur when the esophagaogastric junction remains in its normal position below the diaphragm. (Figure 17-3B). However, the fundus and other parts of the stomach as well as other abdominal viscera can move through the hiatus into the mediastinum alongside the esophagus.

Hiatal hernias can be congenital or acquired, although the congenital type may not become symptomatic until adulthood.^2,3 There appears to be a congenital predisposition in the Chinese Shar Pei breed. This breed has also been shown to have an increased incidence of esophageal motility disorders and esophageal redundancy, although these can be incidental radiographic findings not associated with any clinical signs.^4,5 Acquired hiatal hernias are often associated with some form of trauma although there is some evidence to suggest that they can occur in dogs and cats with no history of trauma but in association with cardio- pulmonary, neuromuscular, or metabolic disease.⁶

Pathophysiology

The terminal esophagus (abdominal portion) incorporates the lower esophageal sphincter (LES) and extends approximately 2 cm below the diaphragm. Normally, the LES relaxes to allow a bolus of food or liquid to pass into the stomach and quickly closes to prevent excessive gastroesophageal reflux (GER). Any change to the normal anatomic relationship between the LES, the hiatus, and the phrenicoesophageal ligament can disrupt the high pressure zone (unrelated to the cranial displacement of the LES) and contribute to excessive GER by impairing the competency of the sphincter.^7,8 Other anatomic factors that may contribute to excessive GER include the loss of the oblique angle at which the stomach and esophagus join and the distortion of the muscular sling produced by the lesser curvature of the stomach.⁸ In most cases of hiatal hernia in the dog and cat, a primary disorder of the LES is unlikely.⁷

Trauma, a well-recognized cause of acquired HH, may result in weakening of the attachments at the hiatus. Hiatal hernias have been seen associated with chronic diaphragmatic herniation.^2,9 However, non-traumatic causes may be related to the “bellows” effect of the thorax.⁶ Brachycephalic breeds such as the Bulldog have been shown to have a relationship between more severe forms of the brachycephalic syndrome and hiatal hernias.⁶ It is speculated that severe inspiratory disorders can result in negative intraesophageal and intrapleural pressure, leading to the esophagus and stomach being drawn into the thorax, worsening a mild preexisting hiatal hernia and associated signs.^6,10

The esophagitis that results from HH and GER is caused by the reflux of acidic gastric contents along with pepsin. Esophagitis can induce vomiting (less likely) or regurgitation. The regurgitation is usually intermittent and the contents of the regurgitated material can be blood-tinged and contain undigested food, clear liquid, and foam.

Differential diagnoses for reflux esophagitis associated with HH would include congenital megaesophagus, and acquired megaesophagus due to dysautomonia, myasthenia gravis, neoplasia, foreign bodies, lead poisoning, hypothyroidism, hypoadrenocorticism, and polymyositis.
 

Diagnosis

To some degree, signalment is important as the Chinese Shar Peis and English bulldogs appear to be predisposed to HH.^4,6 However, most animals with the congenital form of HH will have signs before they are 1 year of age, although diagnosis may be delayed.¹¹ Animals with the acquired form of HH may develop signs at any age.

Not all animals with a HH are symptomatic and hernias may be identified on thoracic radiographs as incidental findings.² Animals with symptomatic HH will consistently have regurgitation and pain from esophagitis, may have hypersalivation, anorexia, and aerophagia. Odonydysphagia, chronic weight loss, and a soft moist cough may be seen. Coughing may indicate aspiration which in severe cases results in aspiration pneumonia.

Physical examination signs may be limited to increased lung sounds (if aspiration is a problem), a thin body condition, and possibly hypersalivation. In addition, the affected animal may be febrile and dehydrated.

The most helpful diagnostic tools are radiography and endoscopy. Survey radiographs of the thorax usually demonstrate a megaesophagus and an abnormal soft tissue density in the caudodorsal thorax. With sliding hernias, however, repeat radiographs may be necessary to finally demonstrate the displaced viscera. The gas within the stomach will help identify any gastric displacement and pneumonia may be seen.

A barium contrast esophagram should be performed as it helps identify the gastroesophageal junction and/or gastric rugal folds. The degree of megaesophagus can be defined better with the aid of contrast material. Fluoroscopy is useful in demonstrating the intermittent (sliding) nature of the hernia. The presence of gastroesophageal reflux and the severity of hypomotility can also be analyzed. If a paraesophageal hernia is present, the gastroesophageal junction remains in its normal position while the stomach and other displaced viscera are displaced cranially into the thorax along with and adjacent to the distal esophagus.

Endoscopy will assist in identifying not only the HH but secondary inflammatory changes of the distal esophagus as well. Endoscopy may demonstrate enlargement of the hiatal opening, cranial displacement and dilatation of the cardia, and rugal folds of the stomach.¹² Visualization of the cardia and gastroesopahgeal junction is often easiest with the scope in the retroflex position.¹²

Medical Therapy

The goal of medical therapy is to alleviate the signs caused by reflux esophagitis and any aspiration pneumonia that may be present. Animals with minimal symptomatology may benefit from dietary modification alone. Modification should include a soft diet low in fat, decreasing the volume of food given at each meal while increasing the frequency of feeding, and feeding from an elevated position. Some obese animals will also benefit by losing weight.

In those cases that fail to respond to dietary changes, raising the gastric pH with an H2-receptor antagonist will help neutralize the effects of gastric secretions on the esophageal mucosa and decrease the esophagitis. The improvement in esophagitis indirectly helps increase the tone of the LES thereby diminishing the amount of GER. A proton-pump inhibitor (omeprazole, Prilosec, Astra Zeneca) can be substituted for the H2-receptor antagonist. A prokinetic drug such as metoclopramide (Reglan, Wyeth Pharmaceuticals) or cisapride can be used to help increase the LES tone and hasten gastric emptying resulting in less GER. Cytoprotective agents such as sucralfate (Carafate, Hoechst Marion Roussel) has been shown to be effective by coating the distal esophagus and providing protection against the effects of gastric acid, pepsin, and bile salts. This is given as a slurry or suspension when used for esophagitis.

If the hiatal hernia is small and there is minimal displacement of abdominal contents, the reflux esophagitis is not severe and medical treatment alone is often effective. However, animals that remain symptomatic in spite of aggressive medical therapy will require surgical intervention. Some owners may also choose surgery initially because of their inability to comply with the rigorous requirements of medical therapy.

Surgical Therapy

Veterinary surgeons have historically performed plication of the gastric fundus around the distal esophagus to reverse the effects on GER caused by a hiatal hernia.^3,10 However, Prymak and colleagues advised against this as a component of surgical therapy for hiatal hernia since a LES disorder is not thought to be the primary problem associated with an HH.⁷ Surgical repositioning of the displaced stomach and gastroesophageal junction to its normal abdominal location, reduction in size of the esophageal hiatus by plication of the lumbar crus of the diaphragm, and esophagopexy/gastropexy are the procedures associated with the greatest degree of success and fewest complications.⁷

A cranial midline celiotomy is performed to access the cranial abdomen, diaphragm, and distal esophagus. The stomach and esophagus are gently retracted caudally while standing on the left side of the animal that is placed in dorsal recumbency. An assistant maintains slight caudal traction on the stomach and esophagus that helps reposition the distal esophagus below the diaphragm. The small intestine is packed in warm saline-soaked laparotomy pads outside the abdominal cavity to the right of the midline. The triangular ligament of the liver is incised and the liver lobes retracted laterally toward the right side of the abdomen to aid in visualization of the esophageal hiatus. The ventral portion of the esophagus is carefully dissected away from the phrenicoesophageal ligament to allow the caudal portion of the esophagus and the LES to be withdrawn into the abdomen. During this dissection, the ventral trunk of the vagus nerve and blood vessels should be avoided. The right and left crura of the diaphragm are then approximated (hiatal plication) with polypropylene or monofilament synthetic suture to reduce the hiatus to a diameter of 1-2 cm, or to the size, which would allow the passage of one finger adjacent to the esophagus.⁷ Polypropylene or a monofilament synthetic suture is preferred for the plication (Figure 17-4A).

The esophagus is then “fixed” to the diaphragm to maintain the LES in the abdominal cavity caudal to the esophageal hiatus. This esophagopexy is accomplished by placing 2 sutures on each side of the hiatal opening between the diaphragm and the tunica muscularis along the ventrolateral surface of the esophagus, again taking care to avoid the vagus nerve (Figure 17-4B). Finally, a left-sided incisional gastropexy is performed while the fundus is under a slight amount of caudal traction. The incision on the abdominal wall is made slightly caudal to the incision on the fundus of the stomach so that when traction is applied to the fundus, the two incisions will be in alignment. In cats, the abdominal wall incision for gaqstropexy is placed more caudally to ensure a moderate amount of traction on the fundus when the abdominal wall and gastric incision are aligned.

Postoperative Care

The animal is maintained on medical therapy and special feeding techniques as described under medical therapy for 2-3 weeks postoperatively. If aspiration pneumonia is a concurrent problem, antibiotics, coupage, oxygen therapy, and nebulization may be necessary. Some degree of regurgitation may continue postoperatively but usually resolves in 3-7 days. If reflux esophagitis is severe, a tube gastrostomy can be performed at the time of hiatal hernia repair and the animal fed in this manner until regurgitation is absent and esophagitis has decreased. Resolution of the megaesophagus and improved esophageal motility has been documented as early as 7 days after hiatal hernia correction.⁷

In most cases, the prognosis following hiatal hernia correction is good. Some animals may still require feeding from an elevated position and small frequent feedings especially if there is a generalized gastrointestinal motility disorder.¹³

In some cases where resolution of clinical signs is not complete, a primary LES disorder may exist. These cases may benefit from a fundoplication which is a valvuloplasty technique designed to increase the tone of the LES and decrease reflux.^3,14 This procedure is technically demanding and requires an experienced surgeon to achieve good results. This surgery may also be associated with serious complications such as gastric dilation, stricture, and dysphagia.^15-19
 

References

1. Kelly KA. Physiology of the gastrointestinal tract. New York: Raven Press, 1981, 281.
2. Lorinson D, Bright RM. Long-term outcome of medical and surgical treatment of hiatal hernias in dogs and cats: 27 cases (1978-1996). J Am Vet Med Assoc 213: 381, 1998.
3. Ellison GW, Lewis DD, Phillips L et al: Esophageal hiatal hernia in small animals: literature review and a modified surgical technique. J Amer Anim Hosp Assoc 23:391, 1987.
4. Stickle R, Sparschu G, Love N et al. Radiographic evaluation of esophageal function in Chinese Shar Pei pups. J Amer Vet Med Assoc 201:81, 1992.
5. Sivacolundhu RK, Read RA, Marchevsky AM. Hiatal hernia controversies-a review of pathophysiology and treatment options. Aust Vet J 80:48, 2002.
6. Hardie EM, Ramirez III O, Clary EM et al. Abnormalities of the thoracic bellows: Stress fractures of the ribs and hiatal hernia. J Vet Intern Med 12: 279, 1998.
7. Prymak C, Saunders HM, Washabau RJ. Hiatal hernia repair by restoration and stabilization of normal anatomy: an evaluation in four dogs and one cat. Vet Surg 18:386, 1989.
8. Henderson RD. Gastroesophageal function in hiatus hernia. Can J of Surg 15:63, 1972.
9. Pratschke KM, Hughes JML, Skelly C, et al. Hiatal herniation as a complication of chronic diaphragmatic herniation. J Small Anim Pract 39:33, 1998
10. Sontag SJ, O’Connell S, Khandewal S et al. Most asthmatics have gastrointestinal reflux with or without bronchodilator therapy. Gastro-enter 99:613, 1990.
11. Hedlund CS. Hiatal hernia. In Fossum TW, ed.: Small Animal Surgery 2nd ed. Philadelphia. Mosby, Inc, 2002: p 326.
12. Johnson SE, Sherding RG: Diseases of the esophagus and disorders of swallowing. In Birchard SJ & Sherding RG eds. Saunders Manual of Small Animal Practice 2nd ed. Philadelphia. W B Saunders 2000 p 727.
13. Knowles KE, O’Brien DP, Amann FJ. Congenital idiopathic megaesophagus in a litter of Chinese shar peis: clinical, electrodiagnostic, and pathologic findings. J Amer Anim Hosp Assoc 26:313, 1990
14. Prymak C: Esophageal hiatal hernia repair In Bojrab MJ, ed. Current techniques in small animal surgery. 4th ed. Baltimore. Williams and Wilkins, 1998, p 197.
15. Gaskell CJ, Gibbs C, Pearson H: Sliding hiatal hernia with reflux esophagitis in two dogs. J Small Anim Pract 15:503, 1974.
16. Waldron DR, Moon M, Leib MS, et al. Esophageal hiatal hernia in two cats. J Small Anim Pract 31:259, 1990.
17. Earlam RJ, Ellis FH. Repair of experimental hiatal hernia in dogs. Arch Surg 95:585, 1967.
18. Donahue PE, Bombeck CT. The modified Nissen fundoplication reflux presentation without gas bloat. Chir Gasroenterol 11:15, 1977.
19. Stanghellini V, Malagelada JR. Gastric manometric abnormalities in patients with dyspeptic symptoms after fundoplication. Gut 27:790, 1985.