Congenital Esophageal Hiatal Hernia in the Chinese Shar-Pei Dog

Transcription

1 Congenital Esophageal Hiatal Hernia in the Chinese Shar-Pei Dog Mary Beth Callan, VMD, Robert J. Washabau, VMD, PhD, H. Mark Saunders, VMD, Larry Kerr, DVM, Caroline Prymak, BVSc, and David Holt, BVSc Esophageal hiatal hernia was diagnosed in 11 young Chinese Shar-Pei dogs between October 1985 and July 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), (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. (Journal of Veterinary Internal Medicine 1993; 7: Copyright by the American College of Veterinary Internal Medicine.) AN ESOPHAGEAL hiatal hernia is a protrusion of abdominal contents through the esophageal hiatus of the diaphragm into the thoracic cavity. It is a relatively uncommon condition affecting both dogs and cats. Two types of esophageal hiatal hernia have been recognized in the dog and cat: 1) sliding hiatal hernia, in which the abdominal segment of the esophagus and parts of the stomach are displaced cranially through the esophageal hiatus,'-'* and 2) paraesophageal hiatal hernia, in which From the Department of Clinical Studies, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA (Callan, Washabau, Saunders, Prymak, and Holt) and the Department of Radiological Sciences, School of Veterinary Medicine, University of California, Davis, CA (Kern). Dr. Kern's present address is the Santa Cruz Veterinary Hospital, 2585 Soquel Drive, Santa Cruz, CA Dr. Prymak's present address is 65 Ordsall Park Road, East Retford, Nottinghamshire, DN22 7PQ England. Accepted February 10, Reprint requests: Robert J. Washabau, VMD, PhD, Department of Clinical Studies, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA Copyright by the American College of Veterinary Internal Medicine /93/ $3.00/0 the abdominal segment of the esophagus and lower esophageal sphincter remain in a fixed position but a portion of the stomach herniates into the mediastinum alongside the thoracic es~phagus.'~ In dogs and cats, sliding hiatal hernia is the most common form. The clinical signs associated with hiatal hernia are vanable and range in severity from infrequent episodes of mild anorexia, hypersalivation, and regurgitation to vomiting, hematemesis, and dyspnea. '-I2 Cardiac arrest can occur when large hernias interfere with cardiopulmonary function. Medical therapies have traditionally been directed toward treatment of presumed reflux esophagitis but usually fail to resolve the clinical signs. Surgical stabilization of the normal anatomy by reduction in the size of the esophageal hiatus, fixation of the esophagus to the diaphragmatic crus (esophagopexy), and left fundic gastropexy has yielded good to excellent results. I Most sliding esophageal hiatal herniae have been reported in animals less than 1 year of age. There are isolated reports of their occurrence in older anirnal~.~~" No breed predilection has been described, although the Chinese Shar-Pei and Chow Chow account for 5 of the 12 previously reported cases in the 210

2 Vd. 7. No. 4, 1993 HIATAL HERNIA IN THE SHAR-PEI 21 1 This article describes a congenital form of sliding esophageal hiatal hernia in 1 I young Chinese Shar-Pei dogs. Materials and Methods Sliding esophageal hiatal hernia was diagnosed in eight young Shar-Pei dogs at the Veterinary Hospital of the University of Pennsylvania between October 1985 and July 199 I. Three cases of sliding esophageal hiatal hernia in young Shar-Pei dogs were diagnosed at the Veterinary Medical Teaching Hospital of the University of California between October 1985 and September The medical records of all patients were reviewed to determine histories, physical examination findings, complete blood counts, serum chemistries, urinalyses, radiographic findings, surgical procedures, and postoperative course. A diagnosis of hiatal hernia was made in all dogs by survey radiographic and/or barium esophagram evidence of displacement of the esophagogastric junction and stomach into the thoracic cavity. Barium esophagrams were also used to assess esophageal motility and, to a lesser extent, caudal esophageal sphincter function in eight dogs. The diagnosis of hiatal hernia was confirmed by surgery in nine dogs and at necropsy in two dogs. All surviving animals were reexamined and radiographically evaluated 4 to 6 weeks postoperatively. Except for one dog (no. 11) who was seen periodically for recurrent gastrointestinal problems, all surviving dogs had long-term follow-up evaluation by telephone contact with pet owners. None of the eight dogs diagnosed at the University of Pennsylvania were directly related. The three dogs diagnosed at the University of California came from one breeder, but a pedigree analysis could not be obtained. TABLE 1. Findings in 1 1 Shar-Pei Dogs With Hiatal Hernia Dog Sex Age (mo) Clinical Signs Radiographic Findings Outcome I M 4 regurgitation hiatal hernia Asymptomatic 2 I mo after surgery megaesophagus 2 M 4 vomiting hiatal hernia Euthanatized (no surgery) dysphagia megaesophagus dyspnea 3 4 F F M 4 regurgitation hiatal hernia Died before surgery anorexia megaesophagus 4 regurgitation hiatal hernia Died 24 h after surgery anorexia coughing 3 vomiting hiatal hernia Euthanatized 24 d after surgery hypersalivation M I M 8 M 9 F 3 regurgitation hiatal hernia Asymptomatic 36 mo after surgery, then lost to follow-up coughing 4 vomiting hiatal hernia Asymptomatic 22 mo after surgery hypersalivation megaesophagus 3 regurgitation hiatal hernia Asymptomatic 18 mo after surgery, then lost to follow-up nasal discharge megaesophagus 2 vomiting hiatal hernia Asymptomatic 18 mo after surgery, then lost to follow-up regurgitation megaesophagus hypersalivation nasal discharge 10 M 2 vomiting hiatal hernia Asymptomatic 19 mo after surgery megaesop hagus I1 M II vomiting hiatal hernia Recurrent gastrointestinal problems 24 mo after surgery

3 212 CALLAN ET AL. Journal of Veterinary Internal Medicine Historical Findings Results Eleven Shar-Pei dogs, eight males and three females less than 1 year of age, were investigated for evidence of hiatal hernia. The historical findings included regurgitation (n = 6), vomiting (n = 6), hypersalivation (n = 3), anorexia (n = 2), nasal discharge (n = 2), coughing (n = 2), dysphagia (n = l), hematemesis (n = l), and dyspnea (n = 1). Clinical signs of vomiting and regurgitation were present for 2 to 3 weeks in most dogs, and their frequency ranged from intermittent (once every few days) to constant (after each meal). The dog diagnosed at 11 months of age had mild episodes of vomiting beginning at 3 months of age, but was not investigated until the signs became more severe, at 1 1 months of age (Table 1). Physical Examination The physical examination was normal in 6 of the 11 dogs. Abnormal physical examination findings in the remaining 5 dogs included hypersalivation (n = 3), dehydration (n = 3), pulmonary crackles or wheezes (n = 3), fever (n = 2), and decreased body weight (n = 2). Hematology, Serum Chemistry, Urinalysis The hematologic abnormalities were limited to a mature neutrophilia ( 15,624 to 25,972 polymorphonuclear leukocytes/pl) in five of the eleven dogs. No abnormalities were demonstrated in the serum chemistries or urinalyses in any dogs. Sz irvej, R adiographv A hiatal hernia was tentatively diagnosed by survey radiographs in all 1 1 dogs (Fig 1). The survey radiographic finding consistent with this diagnosis was the presence of FIG. 1. Right lateral survey thoracic radiograph of dog no. 7 showing caudodorsal gas-filled intrathoracic soft-tissue opacity. The appearance is most compatible with the diagnosis of hiatal hernia. FIG. 2. Right lateral barium esophagram of dog no. 2 showing hiatal hernia and generalized megaesophagus. a caudodorsal gas-filled intrathoracic soft-tissue opacity (n = 11). Additional survey radiographic findings were suspected megaesophagus (n = 7) and dependent alveolar consolidation consistent with (n = 7). Barium Esophagram A partially herniated stomach was identified fluoroscopically in eight animals (Fig 2). Generalized megaesophagus was confirmed in seven animals, and esophageal hypomotility was observed in one animal. Gastroesophageal reflux of barium paste occurred in four animals. Medical Management Medical therapies formulated for the therapy of presumed reflux esophagitis included metoclopramide 0.5 to 1.0 mg/kg/d intravenously for 3 to 7 days (n = 4), cimetidine 5 to 10 mg/kg intravenously, two to three times per day for 3 to 9 days (n = 4), and sucralfate suspension 20 mg/kg orally four times daily for 5 days (n = 1). None of these therapies were believed to significantly diminish the frequency or seventy of clinical signs. Antibiotic therapy for based on bacterial culture and sensitivity testing of isolates derived from transtracheal washings was instituted in eight dogs preoperatively. Surgical Technique Using a technique described by us previously,' the hiatal hernia was surgically repaired in 9 of the 11 dogs. The most common surgical repair was transabdominal diaphragmatic crural apposition, esophagopexy, and left fundic tube gastropexy (n = 6). A slightly different surgical technique was used in 3 dogs: serosal gastropexy rather than tube gastropexy (n = l), diaphragmatic crural apposition and esophagopexy without gastropexy

4 VOl. 7. NO. 4, 1993 HIATAL HERNIA IN THE SHAR-PEI 213 (n = I), and transthoracic diaphragmatic crural apposition and esophagopexy (n = 1). Postoperative Course Of the nine Shar-Pei dogs treated surgically, six have been asymptomatic since surgery ( 19 to 36 months). The megaesophagus, esophageal hypomotility, and aspiration pneumonia resolved in all of these dogs (as determined by survey radiography and barium esophagram) 4 to 6 weeks postoperatively. Of the three remaining dogs, one died 24 hours after surgery of pneumonia and septicemia, one was euthanatized 24 days after surgery because of gastric dilation and persistent vomiting, and one developed chronic gastric dilation and paraesophageal hiatal hernia. Of the two dogs not treated surgically, one was euthanatized at the request of the owner, and the other died of and shock while being prepared for surgery. Necropsy Findings Two of the eleven Shar-Pei dogs did not have surgical correction of the hiatal hernia. One dog was euthanatized at the request of the owner. Necropsy of this dog showed herniation of the cardia and fundus through the hiatus of the diaphragm into the thoracic cavity. There was no gross anatomic or histological evidence of esophagitis in this dog. Another dog died of cardiopulmonary arrest while being prepared for emergency surgery (for an acute large gastric herniation). Herniation of the cardia, fundus, and corpus into the thoracic cavity was found at necropsy. Severe bronchopneumonia was also present. There was no gross anatomic or histological evidence of esophagitis in this dog. Of the nine Shar-Pei dogs treated surgically, one dog died of cardiopulmonary arrest 24 hours after surgery. This animal was being medically treated for severe pneumonia when it acutely developed a large herniation of the gastric fundus and corpus requiring emergency surgery. Necropsy in this patient showed an intact herniorrhaphy but also revealed a severe, necrotizing bronchopneumonia in all lung lobes. The esophagus was normal on both gross anatomic and histological examination. Another dog was euthanatized 24 days after surgery at the request of the owner because of persistent vomiting. The herniorrhaphy in this patient was intact at necropsy. No other lesions were found. The esophagus was normal on both gross anatomic and histological examination. Discussion Sliding esophageal hiatal hernia was diagnosed in 11 young Shar-Pei dogs at two veterinary teaching hospitals during a 6-year period. Ten of these dogs were diagnosed between 2 and 4 months of age; one dog was not diagnosed until 11 months of age. The occurrence of hiatal hernia in young dogs of this breed suggests that the condition is a congenital anomaly. The diaphragm develops as a complete structure in the early dog embryo by fusion of mesodermal and endodermal element^.'^ Incomplete formation of the diaphragmatic esophageal hiatus would be expected to lead to the development of clinical signs early in life. The delayed onset of clinical signs at 2 to 4 months of age in Shar-Pei dogs may relate to the transition at weaning from a liquid diet to a diet comprising digestible and indigestible solids and/or to the development of esophageal dilation. Survey radiography was diagnostic of hiatal hernia in all 11 dogs. The survey radiographic finding consistent with this diagnosis was the presence of a caudodorsal gas-filled intrathoracic soft-tissue opacity. Barium esophagram, performed to assess esophageal motility and caudal esophageal sphincter function, delineated the hiatal hernia, and thus confirmed the diagnosis in 8 dogs. Although these findings would suggest that the disorder can be diagnosed by survey thoracic radiographs alone, other investigators have emphasized the importance of performing a barium esophagram in documenting the disorder,i5 particularly in patients with sliding hiatal hernia in which the esophagus and stomach may only intermittently be displaced. Barium esophagram should certainly be performed in a young Shar-Pei dog with survey radiographic findings of megaesophagus to rule out idiopathic megaesophagus (see below). Many of the animals affected by hiatal hernia also had varying degrees of megaesophagus. One animal also had esophageal hypomotility. The pathogeneses of the megaesophagus and esophageal hypomotility were presumed to be and esophagitis, although a primary esophageal motility disorder could not be excluded. The latter possibility seemed less likely because the megaesophagus and esophageal hypomotility resolved in all dogs after surgical restoration and stabilization of normal anatomy. It is important to note, however, that a congenital form of idiopathic megaesophagus has been previously described in a litter of Shar-Pei dogs.16 The animals described in that report had histories identical to the patients described in our report, i.e., regurgitation, vomiting, and hypersalivation in 3- to 4- month-old puppies. Thus, the clinical signs of regurgitation, vomiting, and hypersalivation in a young Shar-Pei dog could easily be attributed to a primary esophageal motility disorder. Our experience with hiatal hernia in the young Shar-Pei dog, however, suggests that megaesophagus is a common complication of hiatal hernia. The finding of megaesophagus in a young Shar-Pei dog should therefore raise a high index of suspicion of an underlying hiatal hernia. As suggested above, barium contrast examination of the caudal esophageal sphincter, esophageal hiatus, and cardia should always be performed in any young Shar-Pei dog with evidence of megaesophagus or esophageal hypomotility.

5 214 CALLAN ET AL. Journal of Veterinary Internal Medicine Pneumonia was a relatively common complication (64% of the cases) of esophageal hiatal hernia in the Shar- Pei dog. The pneumonia was attributed to vomiting and aspiration of food contents into the lung in all dogs. Eight of the nine dogs who underwent surgery were treated with antibiotics for several days before corrective surgery. Surgery was well tolerated, and the aspiration pneumonia eventually resolved in all of these dogs. One dog, in which surgery had been delayed while treating severe pneumonia, required emergency surgery because of herniation of the gastric fundus and corpus into the thoracic cavity. The animal died 24 hours after surgery because of, pulmonary failure, and septicemia. These findings suggest that delaying surgery to treat is not detrimental to patient outcome. Indeed, patient outcome may be improved by delaying surgery in such instances. Emergency surgery should probably be considered only in those patients in which a large hernia impairs cardiopulmonary function. Many of the animals in this study were initially managed medically. The various medical therapies were formulated to provide a diffusion bamer to peptic mucosal digestion (e.g., sucralfate), improve the tone of the caudal esophageal sphincter (e.g., metoclopramide), neutralize or suppress gastric acid secretion (e.g., antacids or H, receptor antagonists), and decrease the gastric emptying time (e.g., liquid meals and metoclopramide). These medical therapies were formulated in the belief that reflux esophagitis contributed to the symptomatology. Indeed, esophagitis has been previously reported as a complication of hiatal hernia.,.' It should be emphasized, however, that although of barium was observed in several patients, esophagitis was not documented in any of the dogs. Further, gastroesophageal reflux has been documented as a normal physiological occurrence in the dog."*" The occurrence and severity of reflux esophagitis with hiatal hernia depends on two important factors: I) the occurrence of gastroesophageal reflux is significantly increased in young animals (as in animals in this study) because of developmental immaturity of the caudal esophageal and, 2) the seventy of reflux esophagitis with hiatal hernia in the dog depends to a large extent upon the composition of the refluxed material.2'.22 For example, erosive esophagitis only occurs with maximal gastric stimulation in the absence of duodenogastric reflux.,' Unfortunately, medical therapies formulated for the treatment of reflux esophagitis were not effective in ameliorating the clinical signs in four patients described in this report. These results and the results from a previous study' at our hospital suggest that medical therapies formulated for the treatment of presumed reflux esophagitis may not be effective in treating this disorder. The inadequate response to medical therapy may have been a consequence of the degree of herniation and apparent permanent displace- ment of the herniated stomach in many of these patients. Further investigation will be needed to determine the ultimate utility of medical therapies in the treatment of hiatal hernia. Surgical stabilization of the hiatus was curative in six of the nine dogs who underwent surgery. The most commonly used surgical technique was transabdominal diaphragmatic crural apposition, esophagopexy, and left fundic tube gastropexy. The results of this study and of a previous report' suggest that an antireflux procedure (e.g., fundoplication) is not a necessary component of the surgical repair. Further, antireflux procedures have historically been associated with many postoperative complication^.^,^^' Our experience with hiatal hernia in the Shar-Pei dog suggests that such a procedure should be considered only when there is manometrically proved incompetence of the caudal esophageal sphincter. Three animals experienced postoperative problems. One animal died in the immediate postoperative period of complications of. The other two animals had persistent vomiting and/or regurgitation for varying periods of time after surgical correction. These signs were attributed to chronic gastric dilation and delayed gastric emptying of solids (shown radiographically) in both dogs, and to the subsequent development of a paraesophageal hiatal hernia in one dog. Gastroparesis could have developed in these patients for one of several reasons. First, the surgery (i.e., crural apposition and esophagopexy) could have interfered with gastric vagal innervation. Truncal vagotomy in the dog permanently slows the propagation of the pacesetter potential in the corpus and antrum and, therefore, the gastric emptying of solid^.^^,^^ Alternatively, placement of the gastrostomy tube at the site of the gastric pacemaker in the gastric corpus could have disrupted the normal propagation of the pacesetter potential. Other studies suggest, however, that recovery of the pacesetter potential occurs by 14 days postoperati~ely.~~?~~ Therefore, it seems unlikely that the persistent vomiting/regurgitation in these two dogs can be explained by permanent disruption of the pacesetter potential. Finally, hiatal hernia may merely be one manifestation of a more diffuse gastrointestinal motility disorder in this breed. In that regard, idiopathic megaesophagus'6 as well as an ill-defined enter~pathy,~ have been described previously in the Shar- Pei dog. In summary, sliding esophageal hiatal hernia seems to be a congenital disorder in the Chinese Shar-pei dog. Regurgitation, vomiting, and hypersalivation are common clinical signs associated with this disorder. Survey thoracic radiographs were diagnostic of the disorder in all animals. Barium esophagram further delineated the hiatal hernia and aided in evaluation of esophageal motility in those animals in which the study was performed. Esophageal hypomotility and megaesophagus are potential complications of hiatal hernia that should not be

6 Vol. 7. NO. 4, 1993 HIATAL HERNIA IN THE SHAR-PEI 215 confused with a primary esophageal motility disorder. Aspiration pneumonia is another important complication of hiatal hernia that is best mananged before corrective surgery. Medical therapies formulated for the treatment of presumed reflux esophagitis are minimally effective. The condition is best treated surgically by diaphragmatic crural apposition, esophagopexy, and left fundic tube gastropexy. An antireflux procedure (e.g., fundoplication) is not a necessary component of the surgery. References 1. 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 1989; 18: Ellison GW, Lewis DD, Phillips L, et al. Esophageal hiatal hernia in small animals: literature review and a modified surgical technique. J Am Anim Hosp Assoc 1987; 23: Peterson SL. Esophageal hiatal hernia in a cat. J Am Vet Med Assoc 1983; 183: Ackerman NA. Esophageal hiatal hernia in a dog. J Am Vet Radio1 SOC 1982; 23: Dhein CRM, Rawlings CA, Rosin E, et al. Esophageal hiatal hernia and eventration of the diaphragm with resultant gastroesophageal reflux. J Am Anim Hosp Assoc 1980; l6: Robotham GR. Congenital hiatal hernia in a cat. Feline Pract 1979; 9: Iwasaki M, De Martin BW, Alvarage J, et al. Congenital hiatal hernia in adog. Mod Vet Pract 1977; 58: Alexander JW, Hoffer RE, MacDonald JM, et al. Hiatal hernia in the dog: a case report and review of the literature. J Am Anim HOSP ASSOC 1975; Gaskell CJ, Gibbs C, Pearson H. Sliding hiatal hernia with reflux esophagitis in two dogs. J Small Anim Pract 1974; 15: Frye FL. Hiatal diaphragmatic hernia and tricholithiasis in a golden cat. Vet Med/Small Anim Clinician 1972; 67: Kluth GA, Kennea TL. A case of hiatus hernia in a boxer dog. Vet Rec 1964; Waldron DR, Moon M, Leib MS, et al. Oesophageal hiatal hernia in two cats. J Small Anim Pract 1990; 31: Miles KG, Pope ER, Jergens AE. Paraesophageal hiatal hernia and pyloric obstruction in a dog. J Am Vet Med Assoc 1988; 193: Noden DM, de Lahunta A. The Embryology of Domestic Animals. Developmental Mechanisms and Malformations. Baltimore: Williams & Wilkins, 1985; Suter PF. Thoracic Radiography: A Text Atlas of Thoracic Diseases of the Dog and Cat. Wettswil (Switzerland): PF Suter, 1984; Knowles KE, O Brien DP, Amann JF. Congenital idiopathic megaesophagus in a litter of Chinese Shar-peis: Clinical, electrodiagnostic, and pathological findings. J Am Anim Hosp Assoc 1990; 26~ Patrikios J, Martin CJ. Dent J. Relationship of transient lower esophageal sphincter relaxation to postprandial gastroesophageal reflux and belching in dogs. Gastroenterology 1986; 90~ Martin CJ, Patrikios J, Dent J. Abolition of gas reflux and transient lower esophageal sphincter relaxation by vagal blockade in the dog. Gastroenterology 1986; 9 1 : Hillemeier C, Gryboski J, McCallum R, et al. Developmental characteristics of the lower esophageal sphincter in the kitten. Gastroenterology 1985; 89: Cohen S. Developmental characteristics of lower esophageal sphincter function. Gastroenterology 1974; 67: Evander A, Little AG, Riddell RH, et al. Composition of the refluxed material determines the degree of reflux esophagitis in the dog. Gastroenterology 1987; 93: Baue AE, Hoffer RE. The effects of experimental hiatal hernia and histamine stimulation on the intrinsic esophageal sphincter. Surg Gynecol Obstet 1967; 125: Kelly KA, Code CF. Effect of transthoracic vagotomy on canine gastric electrical activity. Gastroenterology 1969; 57: Holle GE, Reiser SB, Frey KW. Effect of selective proximal vagotomy without and with pyloroplasty on gastroduodenal motility. Am J Physiol 251 (Gastrointest Liver Physiol 14) 1986; G752-G Bedi BS, Kelly KA, Holley KE. Pathways of propagation of the canine gastric pacesetter potential. Gastroenterology 1972; Kelly KA, Code CF. Canine gastric pacemaker. Am J Physiol 1971; 220: Williams DA. Markedly subnormal serum cobalamin in Shar-pei dogs with signs of gastrointestinal disease. Proc 9th ACVIM Forum 1991; 888.