A case of nasopharyngeal stenosis with secondary hiatal hernia is described. An 8-year-old castrated male domestic shorthair cat was referred for a chronic upper respiratory problem and presumptive vomiting. Despite conservative management by the primary care veterinarian, the cat's condition progressed. The cat was presented to an emergency facility prior to referral to a specialty hospital. On presentation, inspiratory stridor was evident. Thoracic radiography revealed a hiatal hernia. Computed tomography indicated pharyngeal edema and probable nasopharyngeal stenosis. Endoscopy confirmed the presence of nasopharyngeal stenosis consistent with either stricture or choanal atresia. Balloon dilation of the choana was performed. The hiatal hernia regressed spontaneously post-resolution of the nasopharyngeal stenosis. The cat remained asymptomatic at recheck 3 months later.

Esophageal hiatal hernia was diagnosed in 11 young Chinese Shar-Pei dogs between October 1985 and July 1991. The dogs ranged in age from 2 to 11 months and included 3 females and 8 males. The most common clinical signs were regurgitation, vomiting, and hypersalivation. Physical examination was normal in 6 dogs; abnormal physical examination findings in the other 5 dogs included fever, dehydration, hypersalivation, and pulmonary wheezes and crackles. Laboratory evaluation was significant only for neutrophilia in 5 dogs. A diagnosis of hiatal hernia was made on the basis of survey thoracic radiographic and/or barium esophagram findings of displacement of the esophagogastric junction and stomach into the thoracic cavity; the diagnosis was confirmed by surgery in 9 dogs and at necropsy in 2 dogs. Megaesophagus (n = 7), gastroesophageal reflux (n = 4), and esophageal hypomotility (n = 1) were additional findings in some dogs. Aspiration pneumonia was diagnosed in 7 of the dogs. Medical therapies formulated for the therapy of presumed reflux esophagitis generally failed to resolve the clinical signs associated with the hiatal hernia. Hiatal herniae were surgically repaired in 9 of the Shar-Peis by various combinations of diaphragmatic crural apposition, fixation of the esophagus to the diaphragmatic crus (esophagopexy), and left fundic tube gastropexy. Eight of the animals survived surgery, six of which have been asymptomatic since surgery (19 to 36 months). The megaesophagus, esophageal hypomotility, and bronchopneumonia resolved in all of these dogs.

The thoracic bellows mechanism consists of the rib cage and the diaphragm. The purpose of this study was to determine if nontraumatically acquired lesions of the bellows were secondary to underlying disease. Abnormalities of the bellows, specifically stress fractures of the ribs and hiatal hernia, were found in 21 dogs and cats with underlying cardiopulmonary disease, neuromuscular disease, or metabolic disease. A case-control study of Bulldogs demonstrated that hiatal hernia was associated with the more severe manifestations of brachycephalic syndrome. Stress fractures occurred mostly in females and in cats, and involved multiple ribs. Fractures were usually related to severe respiratory effort, but also occurred in association with metabolic disease. Hiatal hernia was also associated with severe respiratory effort, but may be exacerbated if a neuromuscular disorder affecting the diaphragm is present. Abnormalities of the thoracic bellows, such as rib stress fractures and hiatal hernia, may be signs of underlying disease, rather than being primary causes of disease.

Clinical signs of esophageal hiatal hernia in four dogs and one cat included regurgitation, vomiting, hematemesis, hypersalivation, dysphagia, and dyspnea. Thoracic radiographs, esophagram, and fluoroscopy were used to demonstrate cranial displacement of the esophagogastric junction and part of the stomach through the esophageal hiatus. Other findings included megaesophagus, esophageal hypomotility, gastroesophageal reflux, and pneumonia. Medical therapy failed to resolve the clinical signs. Reduction in size of the esophageal hiatus, fixation of the esophagus to the diaphragmatic crus (esophagopexy), and a left fundic gastropexy were performed. Surgical results were considered good to excellent.

Paraesophageal hiatal herniation and pyloric obstruction were diagnosed in a pup with a history of vomiting. Findings of contrast radiography included esophageal reflux, delayed gastric emptying time, and paraesophageal herniation. Exploratory celiotomy revealed increased firmness of the pylorus and a primary defect in the esophageal hiatus, which allowed gastric herniation. Nissen fundoplication was performed following reconstruction of the esophageal hiatus, and pyloroplasty was performed to relieve the gastric outlet obstruction. Pyloric biopsy findings were consistent with a diagnosis of chronic gastritis. Recovery from surgery was initially unremarkable; however, the dog died suddenly 3 weeks after surgery. Necropsy revealed a large diaphragmatic hernia adjacent to the esophageal hiatus; the hernia had resulted in incarceration of the abdominal organs. The hiatal hernia reconstruction remained intact and was not the cause of the diaphragmatic disruption.

Liquid barium esophagography was done in 29 clinically normal Chinese Shar Pei pups and observed fluoroscopically, beginning when they were approximately 3 months old and repeated periodically until they were at least 18 months old, if possible. Of these dogs, 69% had relatively slow stimulation of secondary waves, 48% had generalized poor esophageal tone or motility, and 38% had esophageal redundancy. Sequential studies revealed apparent improvement with age for those dogs initially showing slow motility, provided that redundancy was not also present. Another group of 9 Chinese Shar Pei pups had histories of either regurgitation or vomiting. Five of these had hiatal hernia and 2 had megaesophagus.

OBJECTIVE To provide a detailed discussion of the aetiology and pathophysiology of hiatal hernia in both humans and small animals, and review current medical and surgical treatments. DESIGN Review article. SUMMARY Hiatal hernia is not completely understood in humans or animals. It has a complex multifactorial aetiology and pathophysiology. A primary disturbance of the lower oesophageal sphincter has not been shown in humans or animals. Knowledge of pathophysiology is necessary to institute appropriate treatment. Medical and/or surgical therapy is not indicated in asymptomatic cases. Medical treatment should be used for up to 1 month in stable cases of sliding hiatal hernia. Paraoesophageal hiatal hernias and any large sliding hiatal hernia should be considered for prompt surgical treatment. Surgical techniques used depend on the type of hiatal hernia present. Surgical treatment of hiatal hernia cases should be performed by experienced surgeons, and must include hiatal closure and gastropexy. The Nissen fundoplication procedure has been discontinued in the veterinary field due to poor success rates, coupled with the published view that there is a marked difference in pathophysiology between humans and dogs. Reported complications associated with the original Nissen fundoplication technique are identical in the human and veterinary literature. There have been no complications reported with use of the modified or 'floppy' Nissen fundoplication in dogs. Both oesophagopexy and Nissen fundoplication require further evaluation in small animals.

OBJECTIVE To determine long-term outcome of medical and surgical treatment of hiatal hernia (HH) in dogs and cats. DESIGN Retrospective case series. ANIMALS 22 dogs and 5 cats. PROCEDURE Medical records of dogs and cats with HH were reviewed. Outcomes of treatment were obtained from reexamination or owner questionnaires. RESULTS The most common breeds affected were English Bulldog and domestic shorthair cat. Mean age of all dogs and cats was 4 years. Hiatal hernia was diagnosed by use of contrast radiography of the esophagus (n = 19), fluoroscopy (7), or esophagoscopy (1). Eight of 15 dogs and cats treated medically for 30 days had complete resolution of signs. Of the 7 in this group that did not respond, 1 died on the 10th day of medical treatment and the remaining 6 were treated surgically. Eight of 10 dogs that underwent hiatal plication, esophagopexy, and gastropexy responded favorably. Four of 7 dogs that underwent fundoplication did well. However, 3 of these dogs did not have clinical signs. Fundoplication was successful in only 1 of 4 dogs with clinical signs. CLINICAL IMPLICATIONS Dogs and cats with clinical signs of reflux esophagitis associated with HH should undergo conservative treatment for 30 days. Most will be managed successfully by use of drugs, dietary alterations, or both. Those that do not respond to conservative treatment will likely require surgery. The best prognosis after, surgery appears to be associated with the esopagopexy technique.

The diagnosis and management of surgical diseases of the esophagus are discussed. Esophageal foreign bodies, strictures, esophagobronchial fistulas, diverticula, gastroesophageal intussusception, hiatal hernias, and megaesophagus are included in the discussion.

A one-year-old, male, smooth-haired standard dachshund was presented with a history of chronic hypersalivation, dysphagia, puffing of the cheeks on expiration, and inspiratory stridor. Oral examination revealed a moderately thickened tongue radix and that the normal intrapharyngeal opening was obliterated. A 7 mm long, midline palatal slit was the only communication between the naso- and oropharynx. The soft palate was fused to the caudal pharyngeal wall. A concurrent hiatal hernia was diagnosed on thoracic radiographs. The soft palate abnormality was surgically corrected and the hiatal hernia was managed medically. On follow-up evaluations, the clinical signs had markedly improved, and the hiatal hernia was no longer visible on survey thoracic radiographs.