Introduction

There are several reports of hiatal hernias in both dogs and cats, but type of herniation is not always described.^1–18 In small animals, the congenital sliding hiatal hernia (type I) is the most common form, whereas the other congenital hernias (types II and III) have been rarely described.^6,10,15,18 Less than 30 feline cases of hiatal hernias were found in the English literature.^1–12,18 Of those feline cases, type I hiatal hernias appear to be the most common, while types II and III are extremely rare and have been described in only two cats.^6,12

The case described in this article is most representative of a complex congenital type II hiatal hernia that was comprised of a normally positioned esophagogastric junction but paraesophageal herniation of the entire stomach, spleen, greater and lesser omenta, left limb of the pancreas, and the proximal portion of the descending duodenum into the thorax. The purpose of this report was to describe the findings and successful treatment of this complex congenital paraesophageal hernia, which, to the authors' knowledge, has not been documented in either the cat or the dog.

Case Report

A 3 mo old male domestic shorthair weighing 2 kg was evaluated by the emergency service at the Veterinary Medical Center at Michigan State University for acute onset of anorexia, lethargy, abnormal breathing pattern, and a palpable mass within the cranial abdomen. The cat was normal the evening prior to presentation and had no history of previous illnesses. On presentation, the cat was quiet but alert and responsive. The mucous membranes were slightly pale with a normal capillary refill time of <2 sec. On thoracic auscultation, cardiac sounds were decreased on the right side of the thorax but normal on the left. Respiratory sounds could not be auscultated on the caudal aspect of the right hemithorax. The cat was tachypneic and dyspneic with a paradoxical breathing pattern. A large mass effect was palpated in the cranial abdomen. The cranial aspect of this mass effect was difficult to delineate but the caudal aspect was easily palpable. The mass effect was suspicious of either a cranial abdominal mass or cranial displacement of abdominal contents. The remainder of the physical examination was within normal limits.

Routine emergency blood work (consisting of packed cell volume, total solids, venous blood gases, and electrolytes) was unremarkable. Thoracic and abdominal radiographs revealed a severely gas- and fluid-distended stomach that was displaced cranial to the diaphragm and confined mainly to the right hemithorax (Figure 1). There was displacement of the cranial mediastinum and cardiac silhouette towards the left hemithorax. The liver appeared to be in its normal location. There was no evidence of megaesophagus. A mild pulmonary interstitial pattern was also noted and was attributed to hypoinflation. Incidentally, a transitional seventh lumbar vertebra was noted as well. Radiographic findings were consistent with either a diaphragmatic hernia or complex hiatal hernia.

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Based on the radiographic findings, an exploratory celiotomy was performed. The cat was premedicated with buprenorphine^a (0.02 mg IV), induced with a combination of ketamine^b and diazepam^c (IV to effect), and anesthetized routinely with no complications. Cefazolin^d (22 mg/kg IV) was prophylactically administered at the time of induction. After intubation, an orogastric tube was passed to decompress the stomach, and the cat was routinely prepared for abdominal surgery and possible median sternotomy. Anesthesia was maintained with isoflurane^e in O₂ (range, 0.5–2%). During the anesthetic period, hydrocolloids^f, dopamine^g, and IV fluids^h were administered as indicated for cardiovascular support.

A ventral midline celiotomy was performed. The entire stomach, spleen, omentum, and left limb of the pancreas were displaced within the pleural cavity. The descending duodenum and adjacent right limb of the pancreas were found in a left paramedian and cranial location. The proximal aspect of the duodenum, along with the distal common bile duct, were at the level of the defect in the phrenicoesophageal ligament between the ventromedial aspect of the abdominal esophagus and the surrounding pars lumbalis of the diaphragm. The biliary tree appeared severely dilated (Figure 2A). The rest of the diaphragm and remainder of the abdominal organs appeared within normal limits. Most of the greater omentum was successfully reduced with gentle traction, but the defect had to be extended by approximately 5 mm through the left crus of the diaphragm to allow safe reduction of the stomach and spleen. The hernia ring was inspected. The gastroesophageal junction was in its normal location and strongly attached on its dorsal and left lateral aspects to the left crus of the diaphragm. The ventral and right lateral aspect of the phrenicoesophageal ligament was absent, which allowed communication between the peritoneal cavity and the caudal mediastinum (Figure 2B).

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While gentle caudal traction was applied to the stomach, a phrenicoplasty was performed with multiple simple interrupted suturesⁱ between the ventral-most aspect of left and right diaphragmatic crura. The defect was reduced so that only one finger could be passed through the esophageal hiatus. Esophagopexy was then performed by suturing the ventral and right lateral aspects of the esophagus to the surrounding left and right crura of the diaphragm in a simple interrupted suture pattern (Figure 3A). A thoracic tube was then placed through a stab incision in the left pars costalis of the diaphragm and tunneled through to a paramedian stab incision in the left abdominal wall. An incisional gastropexy was then performed between the left gastric fundus and the left transversus abdominis muscle (Figure 3B). The chest tube was aspirated immediately after closure of the abdominal wall until negative pressure was obtained then secured to the skin with a finger trap pattern^j. The abdomen was closed in a routine fashion with a standard three-layer closure. There were neither surgical nor intraoperative complications.

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Immediate postoperative care consisted of IV fluids (3 mL/kg/hr), fentanyl^k (2–5 μg/kg/hr), metoclopramide^l (1 mg/kg/day), and IV injections of famotidine^m (0.5 mg/kg q 12 hr). The chest tube was removed 2 hr after surgery because no significant quantity of air or fluid was obtained from successive aspirations. The following morning the cat was in excellent condition and had a good appetite with no dysphagia, regurgitation, or vomiting observed. The cat was discharged from the hospital 24 hr after surgery. The owner was instructed to administer buprenorphine^a (0.01 mg/kg transbuccally q 6 hr pro re nata) for 5 days. The cat continued to make a full recovery without complications.

The cat was re-examined 3 mo after surgery. The cat was normal postoperatively with no regurgitation, vomiting, or respiratory issues. A three-phase esophagogram revealed normal esophageal motility, no gastroesophageal reflux, and no evidence of a persistent hiatal (paraesophageal) hernia. For complete evaluation of the esophagus and stomach, the cat was premedicated and anesthetized routinely for esophagoscopy. The esophageal mucosa was normal and no signs of gastroesophageal reflux could be identified. The gastric mucosa was similarly within normal limits, and no evidence of residual hiatal hernia could be appreciated at the level of the cardia upon insufflation of the stomach.

The cat was examined again 7 mo postoperatively for an unrelated foreign body obstruction. On exploratory celiotomy for foreign body removal, the phrenicoplasty, esophagopexy, and gastropexy were all unremarkable in appearance. Thirty months after surgery, the cat was reported to be completely normal according to the owner.

Discussion

Three types of hiatal hernias are classically described. In the type I (or sliding) hiatal hernia, the esophagogastric junction can displace cranially into the thorax. The phrenicoesophageal ligament is circumferentially weakened and stretched without focal defect. In the type II (rolling or paraesophageal) hernia, part of the stomach is herniated into the thorax through a focal defect of the phrenicoesophageal membrane. The esophagogastric junction remains attached in its normal position at the level of the hiatus. The type III hiatal hernia combines features of both type I and type II hernias. Less commonly, a type IV (or complex type III) hiatal hernia has been described in which a combination of the sliding and paraesophageal components are present as well as herniation of abdominal organs into the chest cavity.^15,18

While regurgitation is the primary clinical sign reported with sliding hiatal hernia, clinical signs of paraesophageal hernia can be more variable and may depend on the nature of herniated abdominal organs. In this case, the acute onset of anorexia, paradoxical breathing pattern, and lethargy are thought to have mainly resulted from the herniation of gastrointestinal contents and ensuing dilation of the stomach. It is also possible that a secondary biliary obstruction (common bile duct appeared dilated in surgery) may have also contributed to the overall cat's malaise.

Both medical and surgical treatments have been advocated for the management of type I hiatal hernias; however, early surgery is warranted with paraesophageal hernias because of the risk of gastrointestinal obstruction, respiratory compromise, and organ strangulation. The surgical techniques used in this case (i.e., phrenicoplasty, esophagopexy, gastropexy) were similar to those described for sliding hiatal hernia in dogs.^4,13,15,18 Because the esophagogastric junction was still attached to the dorsal and left lateral aspects of the diaphragm (i.e., no sliding), it was unnecessary to caudally translate the esophagus before the phrenicoplasty and esophagopexy. Decompression of the stomach with an orogastric tube was beneficial for reduction of the stomach and other viscera. The phrenicoplasty was performed to reduce the defect in the hiatus, and the esophagopexy was to prevent potential sliding of the abdominal esophagus. To the authors' knowledge, the optimal hiatus size has not been described. In the authors' opinion, the phrenicoplasty should be of sufficient size to prevent recurrence of herniation but should not be excessive in that it impedes migration of a normal food bolus. In the present case, the hiatus size was subjectively reduced until one finger could be inserted through the hiatus. The left incisional gastropexy was performed while exerting gentle caudal traction on the stomach to protect the repair and prevent recurrence. Surgical intervention with those three techniques proved to be very effective as the cat was no longer clinical soon after surgery and had not had any signs of disease for at least 30 mo postoperatively.

Conclusion

This report documents a rare complex congenital type II paraesophageal hiatal hernia in a cat. Surgical intervention with a combination of phrenicoplasty, esophagopexy, and left fundic gastropexy was effective in this case and should be considered as a treatment option if presented with this or similar hiatal hernias.