Hiatal Hernia in the Dog: A Clinical Report of Four Chinese Shar Peis
Four Chinese shar pei littermate puppies were presented for vomiting, regurgitation, hypersalivation, and poor growth. Diagnosis of hiatal hernia was made for each of the four dogs based on survey radiographs and barium esophagram studies. All dogs initially underwent medical therapy, to which only one dog responded. All dogs underwent surgical treatment, which included manual hernia reduction followed by phrenoplasty, esophagopexy, and left incisional gastropexy, 5 to 40 days following initiation of medical therapy. The three surgical techniques described eliminated the need to enter the pleural cavity and offered excellent long-term results with no recurrence of clinical signs following surgery.
Introduction
Hiatal hernia is defined as the protrusion of abdominal contents through the esophageal hiatus of the diaphragm into the thorax. Four types of hiatal hernia are described in the human literature, with type I or sliding hiatal hernia being the most common.1 Other, less frequent types include type II or paraesophageal hiatal hernia, where the gastroesophageal junction remains in place, but the fundus slides through the hiatus into the thorax; type III, which is a combination of types I and II; and type IV, which is the most severe form, involving herniation of abdominal contents (including spleen, colon, and jejunum) into the thorax.2,3
Type I hiatal hernia is also the most common form diagnosed in dogs and cats.1,4–6 This condition is mainly observed in young dogs (congenital form) and occasionally in adults (acquired form), with Chinese shar peis and English bulldogs being the most commonly affected breeds.4,7–9 Cats can also be affected; the domestic shorthair breed is overrepresented.7 The acquired form of hiatal hernia is described as a consequence of a traumatic event or in association with severe upper respiratory disease, including brachycephalic syndrome and laryngeal paralysis.10,11
The most common clinical signs associated with hiatal hernia include regurgitation, hypersalivation, vomiting, and slow growth. These signs are also often encountered in other conditions such as reflux esophagitis and megaesophagus.1,9,12,13 These latter two conditions may be associated with or be consequences of hiatal hernia, and their presence is associated with a worse prognosis.2,4,5,9 Type I hiatal hernias can be intermittent; this can hinder diagnostic efforts. Diagnosis is based on a plain radiograph and barium esophagram, with fluoroscopy facilitating detection of intermittent herniation.13–15 Definitive diagnosis of reflux esophagitis requires esophageal endoscopy and biopsy.12
The two main treatment options are medical therapy and surgery. Medical therapy is recommended initially by some authors and includes prokinetics, antacids, and cytoprotective agents.5,7 The goals of medical management are to resolve reflux esophagitis and associated megaesophagus.9 Antacid drugs such as H2 receptor inhibitors and proton pump inhibitors are used to decrease acidity of reflux material, thus alleviating damage to the esophageal mucosa. Aluminum phosphate, through its antacid activity, can also be used as a cytoprotective agent.15,16 Prokinetic agents such as metoclopramide and cisapride increase the rate of gastric emptying and may provide some augmentation to the tone of the lower esophageal sphincter, thus decreasing the rate and the amount of gastroesophageal reflux.7,12 Additionally, cytoprotective agents, such as sucralfate, are used to increase resistance of gastric and esophageal mucosa to injury.7,17,18 Their efficiency depends on environmental conditions such as the pH and appropriate administration.12 Aspiration pneumonia is a complication of regurgitation and must be treated with appropriate therapy.4,9
Surgical management is generally a combination of gastropexy, esophagopexy, and plication of dorsal and/or ventral aspects of the esophageal hiatus to modify the topographic anatomy of the lower esophagus after hiatal hernia reduction (hiatal plication).1–6,8,10 Nissen fundoplication was described for treatment of reflux esophagitis in humans, and it has been used historically in dogs;19 but poor outcomes in this species, despite modification of the original surgery, resulted in discontinuation of this technique.1,4,5
This report describes four cases of hiatal hernia that occurred in all the puppies of a Chinese shar pei litter and outlines a successfully modified surgical treatment used after failure of medical therapy.
Case Reports
Three Chinese shar pei littermates were presented successively between January and February 2006 by three different owners. The dogs had histories of varying degrees of vomiting, hypersalivation, and regurgitation. The fourth littermate puppy was presented with a similar history to another practice. The mean age at presentation was 14 weeks, with a range of 10 to 18 weeks. One dog (case no. 1) had concurrent, severe, bilateral carpal valgus. Complete blood count and serum biochemical analysis results were within normal limits in all but one dog, although mild dehydration was suspected based on dried mucous membranes in three dogs. Case no. 1 was presented with the most acute onset of clinical signs, and this was the only dog with a leukocytosis (white blood cell count 37.0 × 103/μL [reference range 5.1 to 13.0 × 103/μL], with 70% neutrophils). Diagnoses of sliding hiatal hernia (in all dogs), concurrent mild pneumonia (in case no. 1 and suspected in case no. 3), and megaesophagus (in case nos. 1, 2, and 3) were made on the basis of survey thoracic radiographs and on the results of contrast esophagrams using barium sulfatea (5 mL/kg body weight) [Figure 1].
All four puppies initially were treated medically with metoclopramideb (0.5 mg/kg body weight per os [PO] q 8 hours), aluminum phosphatec (1.5 mL/kg body weight PO q 8 hours), and ranitidined (5 mg/kg body weight PO q 12 hours). Additionally, amoxicilline (30 mg/kg body weight PO q 12 hours) and enrofloxacinf (5 mg/kg body weight PO q 24 hours) were given to case nos. 1 and 3 for treatment of aspiration pneumonia. Attempts were made also to change feeding habits, including feeding smaller amounts four times a day from an elevated position and using a puppy diet.g Case nos. 1, 2, and 3 did not respond to medical treatment. The condition of case no. 1 deteriorated rapidly, with increased vomiting, dehydration, and progressive weakness; surgical intervention was required 5 days after initiation of medical treatment. Case nos. 2 and 3 underwent medical therapy for 20 and 17 days, respectively, but did not improve clinically. The decision to pursue surgery was based on lack of clinical improvement. Case no. 4 responded to medical therapy in the early period, but it became refractory after 30 days as clinical signs recurred and increased progressively despite medications. Surgery was performed 40 days after initiation of the medical treatment.
Anesthesia was induced in all dogs with propofolh (2 mg/kg body weight intravenously [IV]) after sedation with acepromazinei (0.05 mg/kg body weight IV) and morphinej (0.02 mg/kg body weight IV). Prophylactic amoxicillink (7.5 mg/kg body weight intramuscularly [IM]) was administered at the time of sedation. All dogs were intubated, and anesthesia was maintained with isoflurane in oxygen. Fluidsl (10 mL/kg body weight per hour IV) were administered during the entire procedure until complete recovery from anesthesia.
Surgical treatment of all dogs included a combination of phrenoplasty, esophagopexy, and left fundic gastropexy [Figure 2]. A standard midline celiotomy was performed, followed by complete abdominal exploration. The left hepatic lobes were gently retracted medially after dissection of the left hepatic triangular ligament to expose the esophageal hiatus. Direct observation of the stomach passing through the esophageal hiatus allowed a definitive diagnosis of sliding hiatal hernia in all dogs [Figure 3].
The herniated stomach was reduced by applying gentle manual traction caudally to the gastric fundus [Figure 4]. On palpation, the phrenoesophageal ligament appeared lax, allowing passage of two fingers inside the hiatus. Traction was applied progressively and was maintained with a stay suture placed on the fundic portion of the stomach. The attachment from the medial portion of the left lumbar crus of the diaphragm to the esophagus (commonly termed the phrenoesophageal ligament) was left intact in order to prevent penetration of the pleural cavity.5,20
The phrenoplasty consisted of placing two to three horizontal mattress sutures of 2-0 monofilament nylonm dorsally and ventrally through the esophageal hiatus while avoiding the vagus nerve [Figure 2]. Initially, one or two dorsal sutures were placed with the cardia retracted laterally and ventrally. Then, one or two ventral sutures were placed. This pattern allowed sufficient reduction of the hiatus size without requiring complete dissection of the phrenoesophageal ligament. Efficacy of the plication was assessed by digital palpation, and additional sutures were placed until not more than the tip of a pair of Metzenbaum scissors could be passed into the hiatus.
A 3-cm incisional esophagopexy was then performed to secure the left side of the esophagus onto the medial portion of the left lumbar crus. An incision was made down to the muscularis of the esophagus and was sutured to a corresponding superficial seromuscular incision performed onto the diaphragm with two simple continuous sutures of 2-0 nonabsorbable, monofilament nylon.m A 4-cm, left incisional fundic gastropexy, securing the stomach to the body wall behind the last rib, was performed using 2-0 nonabsorbable, monofilament nylonm suture [Figures 2, 5].14 Copious lavage with warm, sterile isotonic saline and routine closure completed the surgery. Postoperative care included intravenous fluid therapy and maintenance of the preoperative medications, with the addition of morphinej (0.5 mg/kg body weight subcutaneously [SC]) as needed for pain.
One dog (case no. 3) presented with abdominal distention the day after surgery. Abdominal films taken at this time showed severe, diffuse, intestinal gas accumulation compatible with a functional paralytic ileus. However, the dog ate small amounts of moistened food, and the ileus resolved the following day. All dogs were discharged 1 to 3 days after surgery. Postoperative medical therapy included a combination of the preoperative medication plus oral tramadoln (5 mg/kg body weight) for 4 days. Metoclopramide and ranitidine were discontinued after 1 week, and aluminum phosphate was maintained until suture removal at 15 days postoperatively. All dogs were fed liquid foodo for 2 days postoperatively, followed by 2 weeks of moistened food.p After a 15-day convalescence period, the dogs were given either soft or dry food at the discretion of the owner, and no problems were noted.
The clinical outcomes for the dogs were evaluated at the time of suture removal by the referral veterinarians. The authors obtained follow-up information by telephone conversations with the owners or the referral veterinarians at 2, 4, and 10 months after surgery. All dogs regained weight quickly, and no recurrence of signs was noted in any of them. Radiographs made of case nos. 1 and 3 at 15 and 10 weeks postoperatively, respectively, failed to reveal megaesophagus or residual hiatal hernia and showed resolution of aspiration pneumonia. None of the dogs required further medical management. Long-term outcomes were considered excellent (mean follow-up 10.5 months; range 9 to 11 months).
Discussion
The most common type of hiatal hernia encountered in dogs and cats, including the four dogs reported in this case series, is type I or sliding hiatal hernia, in which the distal portion of the esophagus and parts of the stomach are displaced cranially through the esophageal hiatus into the caudal mediastinum. This displacement is responsible for axial separation between the lower esophageal sphincter and the diaphragmatic esophageal hiatus. Most reports describe hiatal hernia as a congenital condition with symptoms occurring between 2 and 4 months of age, which is the range observed in this report.1,4,5,8,9 Time of onset of clinical signs may relate to transition from liquid to solid diet at weaning; however, it has been reported both earlier and later.2–5 This study supports the higher prevalence of hiatal hernia reported as a congenital condition in Chinese shar peis in comparison with other breeds.4,5,9
Hypersalivation and vomiting were the most dominant clinical signs in this series. Case no. 1 also was presented with mild gastric distension associated with an acute increase of signs, which expedited the decision to perform surgery. No attempt was made to assess esophagitis in this study. A degree of reflux esophagitis was assumed to exist secondary to the hiatal herniation, and medical management was appropriate for this condition.
All dogs were treated medically with a combination of metoclopramide, aluminum phosphate, and ranitidine at the recommended doses. In addition to medications, dietary habits may be modified to reduce the effects of megaesophagus or decreased esophageal motility. Changing dietary habits includes feeding a small amount of a low-fat diet in an elevated position. This feeding regimen enhances esophageal emptying, particularly in cases of megaesophagus.14 Decreasing fat content in the meal potentially increases gastric outflow rate and therefore theoretically reduces the risk of gastroesophageal reflux. The rationale for a conservative trial for 30 days was proposed based on literature reports.7,9,13 Despite the fact that other investigators do not consider medical treatment an option in Chinese shar peis, the authors chose, with owner consent, to try medical therapy first.21 This report provides further confirmation for early surgical intervention in the Chinese shar pei with hiatal hernia, as medical management was unsuccessful in all puppies.
The exact etiology for hiatal hernia is not completely understood, but it is likely multifactorial.9–11 Although heritability of hiatal hernia has not been definitively documented, the hypothesis of a partially heritable trait (as has been shown in humans) is supported by this report as well as others that support a familial condition in Chinese shar peis.2,4,22 According to the breeder, the bitch was in good health and did not have any adverse event during her pregnancy. This was the first litter of both the bitch and stud, and although they did not have any clinical signs of hiatal hernia, they were not evaluated specifically for this by a veterinarian.
Primary lower esophageal sphincter incompetence has not been demonstrated in dogs, nor people, but secondary sphincter disturbance is thought to be responsible for a significant part of the etiopathogenesis.4,5,8,9 By definition, sliding hiatal hernia is an abnormal topographic anatomy of the most distal part of the esophagus, including the lower esophageal sphincter. Therefore, the most commonly proposed mechanism that is responsible for an axial separation between the lower esophageal sphincter and the diaphragm is an anatomical abnormality of the esophageal hiatus of the diaphragm. This axial separation removes several reinforcement mechanisms of the lower esophageal sphincter that are directly related to the distal esophageal topography, including the pinching effect of the right crus of the diaphragm on the distal esophagus during diaphragm contraction, the “flap valve” effect produced by the angle of insertion of the esophagus into the stomach, and the “flutter valve” effect from positive pressure exerted on the short abdominal esophagus.4–7,9,10,22,23
A recent histological study failed to prove the presence of a consistent, histologically distinct, abdominal portion of the esophagus in healthy dogs using the phrenoesophageal ligament as the landmark for determining the separation between thorax and abdomen.20 The validity of a flutter valve effect on the distal esophagus is therefore questionable. This study provides support for a previously formulated hypothesis, which proposes that creating an abdominal esophagus by completely dissecting the phrenoesophageal ligament is not a restoration of the normal anatomy but rather a modification of the anatomy that manipulates gastroesophageal physiology in a beneficial manner.6,23 A comparative histological study of the phrenoesophageal ligament in normal and affected dogs may enhance understanding of this area in animals with hiatal hernia. Microscopic evidence of hypertrophy or hyperlaxity of the phrenoesophageal ligament may be present, which could correlate with the gross aspect of the phrenoesophageal ligament seen in this case series.
Loss of the secondary sphincter mechanisms may increase reflux of gastric contents into the esophagus. The effect of gastroesophageal reflux depends on individual susceptibility, as signs can range from absent to severe in affected dogs.12 A reasonable assumption is that reflux esophagitis, when present, plays a role in the clinical signs, but its role as a primary cause for hiatal hernia is questionable. First, medical therapy addressing reflux esophagitis fails to resolve signs in numerous dogs, including the ones in this report; secondly, dogs that are presented with hiatal hernia without reflux esophagitis have been reported.7,9
The presence of megaesophagus is not clearly described as a consequence of hiatal hernia.5,10 Development of megaesophagus can be related to reflux esophagitis, but congenital forms of megaesophagus—hypomotile and redundant esophagus—have been reported in Chinese shar peis.4,6,10,24 Therefore, these conditions may be associated rather than simply concurrent with hiatal hernia. Megaesophagus may increase the effect of gastroesophageal reflux and the occurrence of regurgitation by reducing esophageal clearance.5 The spontaneous resolution of megaesophagus after corrective surgeries, as observed in case nos. 1 and 3, tends to support the fact that megaesophagus can be a secondary lesion rather than a primary or concurrent disease.4,5,10
Nissen fundoplication was an early technique adapted from the human literature for treatment of lower esophageal dysfunction with hiatal hernia.19,25 It has been associated with a high rate of complications in dogs and is currently not recommended.4,5,7,10 The modified or “floppy” Nissen fundoplication was subsequently developed, and good outcomes have been reported.9 The rationale for using sphincter enhancement techniques is to decrease the rate and the amount of gastroesophageal reflux responsible for the most severe symptoms.9 The mechanism of reduction of gastroesophageal reflux by Nissen and floppy Nissen fundoplication is partially related to the anatomical suppression of the vagus nerve plexus present around the lower esophageal sphincter. Vagal input is responsible for relaxation of the latter. Surgical separation between the esophagus and the diaphragm is performed during fundoplication procedures (gastroesophageal mobilization), and this is responsible for vagal input suppression at that level.26 Fundoplication techniques are more demanding, and complication rates are higher than those with repositioning techniques.4,5,7,9,10 Therefore, a rationale for application of sphincter enhancement techniques would be failure to respond to previous phrenoplasty, esophagopexy, or gastropexy surgery.9 None of the dogs in this study required additional surgery.
A recent study on barrier pressure (i.e., the pressure exerted by the lower esophageal sphincter and the associated secondary sphincters to prevent gastroesophageal reflux) at the gastroesophageal junction on anesthetized dogs showed that left tube gastropexy performed on healthy dogs increased barrier pressure significantly in the immediate postoperative period.27 This finding could partially explain the success rate observed with this procedure in association with hiatus attenuation. If the barrier pressure of the lower esophageal sphincter is increased, the risk of gastroesophageal reflux decreases, as does the associated reflux esophagitis. The initial technique used a Foley catheter to perform a tube gastropexy of the fundus to the left body wall.4–6 The advantage of using a tube gastropexy is the ability to tube-feed anorexic dogs; however, a tube gastropexy is more time consuming and has more associated complications than an incisional gastropexy.14 The authors used an incisional gastropexy, and all dogs were eating well the day after surgery.
Hiatal attenuation, with or without a complete dissection of the phrenoesophageal ligament, seems important in restoring a more physiological topography of the lower esophagus. Techniques proposed for treatment of hiatal hernia traditionally imply entering the pleural cavity during the hiatus dissection, thus necessitating assisted ventilation.4–6 A previously described technique for hiatal attenuation involves a complete dissection of the phrenoesophageal ligament followed by a reconstruction of the dorsal and ventral aspects of the hiatus, reducing the diaphragmatic defect.1,4–6
The surgical technique used to treat these dogs involves minimal dissection of the phrenoesophageal ligament, allowing hiatal reduction and avoiding pleural cavity penetration. This technique was used to reduce surgical time and anesthetic risk. Hernia reduction and herniorrhaphy are still recommended to avoid the risk of reherniation. To the authors’ knowledge, no study has evaluated the relative contribution of hiatal plication, esophagopexy, and left fundic gastropexy. It could be argued that the left fundic gastropexy is solely responsible for the good outcome associated with this procedure used to treat congenital hiatal hernia. Although the long-term effect of the gastropexy on a growing puppy has not been evaluated, and the duration of its effect is unknown, the esophagopexy is also recommended to prevent later recurrence of herniation in case the gastropexy effect decreases with time or fails in the short term.
The relatively simple surgical technique described here permits utilization in most current private practices, as it does not require assisted ventilation and could thus decrease the perioperative complications, such as those associated with a thoracic drainage tube and pneumothorax. Despite this consideration, assisted ventilation may be necessary and should be available in cases of thoracic intrusion during hernia reduction.
Conclusion
To the authors’ knowledge, this is the first report of an entire litter of Chinese shar peis affected with hiatal hernia. This supports the suspicion of an inherited condition in this breed; congenital hiatal hernia is also supported in the human literature.22 However, genetic evaluation would be necessary to prove this hypothesis. The poor success rate associated with medical management of these Chinese shar peis, plus reports by other authors, suggest that surgery should be initiated as soon as the animal is stable without significant investment in medical therapy.21 Surgical management involves several stabilization procedures including left fundic gastropexy, esophagopexy, and esophagal hiatus plication. Penetration into the pleural cavity is not necessary, as the authors obtained excellent long-term results after surgical treatment in these four dogs; the outcomes were also consistent with those reported in previous studies.
Micropaque; Guebert Co., Villepinte, 93420, France
Primperid; CEVA Santé animale, Libourne, 33500, France
Phosphaluvet; Boerhinger Ingelheim France S.A.S., Reims, 51100, France
Zantac; GlaxoSmithKline, Marly le Roi, 78160, France
Suramox; Virbac, Carros, 06510, France
Baytril; Bayer Animal Health AG, Leverkusen, 51373, Germany
Vet complex premier age; Virbac, Carros, 06510, France
Rapinovet; Schering-Plough Animal Health, Welwyn Garden City, Hertfordshire, AL7, United Kingdom
Vetranquil; CEVA Santé animale, Libourne, 33500, France
Morphine Lavoisier; Laboratoire Chaix et Du Marais, Paris, 75017, France
Duphamox LA; Fort Dodge Animal Health, Southampton, SO14, United Kingdom
Ringer’s lactate; Bayer, Lcverkuscn, 51373, Germany
Ethilon; Ethicon, Inc., Johnson & Johnson Co., Somerville, NJ 08876
Contramal; Grünenthal, Stolberg, 06547, Germany
Fortol; Intervet, Beaucouze, 49070, France
a/d; Hill’s Pet Nutrition S.N.C., Sophia-Antipolis, 06560, France
Citation: Journal of the American Animal Hospital Association 44, 6; 10.5326/0440335
Citation: Journal of the American Animal Hospital Association 44, 6; 10.5326/0440335
Citation: Journal of the American Animal Hospital Association 44, 6; 10.5326/0440335
Citation: Journal of the American Animal Hospital Association 44, 6; 10.5326/0440335
Citation: Journal of the American Animal Hospital Association 44, 6; 10.5326/0440335
Preoperative, right lateral thorax radiograph of the esophagram from case no. 1. Note the megaesophagus (E), gas-filled stomach (S), and the herniated cardia and proximal part of the stomach (H). Note also the presence of a small amount of barium in the pyloric antrum (B).
Schematic representation of the stabilization procedures. After transection of the left triangular ligament, the liver (L) is retracted to the right side of the abdomen to facilitate exposure of the esophageal hiatus. The herniated stomach (S) is reduced. The dorsal sutures of the phrenoplasty (not shown) are then placed, followed by placement of the ventral sutures (double arrow). The vagus nerve (V) must be identified and avoided. The esophagopexy (arrowhead) is performed on the medial aspect of the left lumbar crus of the diaphragm (D). Finally, the gastropexy (arrow) is performed on the left side, maintaining caudal traction on the stomach.
Intraoperative view of the right abdomen from the right side before hiatal hernia reduction. The fundus (F) can be clearly seen, but the cardia and proximal stomach are passing through the esophageal hiatus (arrow) of the diaphragm (D).
Intraoperative view following manual reduction of the hernia. Gentle caudal traction applied on the gastric fundus (arrow) achieved progressive reduction of the hernia. The stomach is pulled until the gastroesophageal ligament (PEL) is completely exposed.
Intraoperative view after stabilization procedures. The left fundic gastropexy (arrow) pulls the stomach (S) slightly caudally. The esophagopexy (arrowhead) is visible adjacent to the left hepatic lobe (L). The phrenoplasty is not visible. Note the absence of dissection of the phrenoesophageal ligament, which is left intact (PEL).
