Hiatal hernias are caused by weakening of the muscles in the phrenoesophageal membrane and widening or enlargement of the hiatal tunnel. Surgical procedures of the hiatus or congenital malformation can also be to blame. Asymptomatic hiatal hernias are usually an incidental finding diagnosed by gastroenterologists or radiologists.1 There are four types of hiatal hernias: Type I, or sliding hernia, allows a portion of the gastric cardia to herniate upward into the chest1 and accounts for 95% of hiatal hernias. Types II, III, and IV are considered paraesophageal hernias and make up the other 5% of hernia diagnoses.1,2
Paraesophageal hernias are larger than sliding hernias and allow a greater portion of the stomach to herniate into the chest. Type II hernias result from a localized defect in the phrenoesophageal membrane, but the gastroesophageal (GE) junction remains attached to the preaortic fascia and the median arcuate ligament;1 the gastric fundus is the most likely area to herniate into the chest. Type II hernias can become larger over time, eventually allowing the entire stomach to herniate into the chest. Type III hernias are a combination of types I and II. Type IV hernias are associated with a large defect in the phrenoesophageal membrane that allows other organs, ie, the colon, spleen, and small intestine, to enter the hernia sac.1,2
Paraesophageal hernias can cause symptoms like those of gastroesophageal reflux disease (GERD) and create more serious problems if not appropriately treated.3,4 Some of the larger and more insidious hernias can cause the stomach to rotate on its longitudinal axis, causing a volvulus. This may result in acute severe postprandial pain and is a medical emergency requiring immediate surgical intervention.
CASE
A 64-year-old female with a long history of GERD was seen in our office for a newly diagnosed large paraesophageal hernia that was demonstrated on CT (Figure 1). (A bronchogenic cyst that also appears on the CT has been followed. The size of the cyst remains stable, and the patient is asymptomatic.) During her medical interview, the patient complained mainly of early satiety, regurgitation of food, and some epigastric discomfort in the postprandial period. Her medications included esomeprazole (Nexium) 40 mg in conjunction with rabeprazole (Aciphex) 20 mg twice a day, but these provided only minimal to no relief of her symptoms. The medical history included varicose veins and hypercholesterolemia.
On physical examination, the patient appeared healthy and younger than her stated age. Pulmonary, cardiovascular, and abdominal examinations were unremarkable. All other systems were within normal limits. A barium swallow examination revealed a large type III sliding paraesophageal hernia with reflux of contrast from the stomach to the esophagus (Figure 2). Because she was exhibiting signs and symptoms attributable to her hernia, surgical repair was considered reasonable treatment. Possible risks, complications, and likely outcomes of surgical intervention were discussed in detail with her. She freely consented to surgery, and informed consent was obtained.
Surgical procedure The patient was taken to the OR and draped and prepped using sterile technique. A 10-mm laparoscopic port was made using a #15 blade at a point one-third the distance from the xiphoid to the umbilicus. The abdomen was entered using the Hasson technique.5 A 10-mm 30-
degree laparoscope was then used to explore the abdomen. An additional 10-mm port was placed three fingers below the xiphoid, and two 5-mm ports were placed below the costal margin on the left. An atraumatic liver retractor was placed to retract the lateral lobe of the liver for direct visualization. A large paraesophageal hernia was clearly visualized. The hernia sac was then reduced using hand-over-hand technique. The right diaphragmatic crus was defined; dissection was begun with division of the gastrohepatic ligament and extended up to define the right crus. Further dissection was carried up to define the left crus down to the gastrosplenic ligament. The esophagus was mobilized superiorly from the mediastinum, and the short gastric vessels were divided using a harmonic scalpel. The entire hernia sac was taken down along with the gastroesophageal fat pad. Care was taken not to injure either of the vagus nerves. Although the esophagus was optimally mobilized, the surgeon felt that the patient had a short esophagus, with the GE junction being proximal to the diaphragmatic hiatus. In order to minimize the risk of recurrent hernia, the surgeon recommended a Collis-Nissen fundoplication.6
Fundoplication is the process by which part of the stomach is brought around the esophagus to form a partial or complete wrap. The purpose of this is to recreate the mechanics of the GE junction and minimize reflux.
In patients with a short esophagus, an esophageal lengthening procedure may be required to ensure that the wrap remains in the abdomen after fundoplication. An example of an esophageal lengthening procedure is the Collis creation of the neoesophagus from the proximal stomach. A Keith needle with 2-0 silk was used to pass the anvil of the circular EEA 21-mm stapler (Ethicon Endo-Surgery, Inc, Cincinnati, Ohio) from the back of the stomach to the front of the stomach, with a 48-Fr bougie dilator in place along the lesser curve of the stomach. The circular EEA 21-mm stapler was fired, and the EZ 45-mm linear stapler (Ethicon) was then used to complete esophageal lengthening. The circular EEA 21-mm stapler produces a circular defect in the stomach wall, which allows completion of the gastroplasty with the EZ 45-mm linear stapler to create a tension-free intra-abdominal neoesophagus.7 The EZ 45-mm linear stapler produces two rows of three staples on either side of the deploy stapler. With a 48-Fr bougie dilator in place, crural stitches were placed to approximate the diaphragmatic crura.
Fundoplication was then performed, with a flexible retractor bringing the stomach back behind the neoesophagus; two interrupted sutures were used to create a loose fundoplication over the bougie dilator. No tension was noted at the fundoplication site. Mesh or a patch of Gore-Tex can be used to reinforce closure of a large crural defect, but no mesh was used in this patient. The bougie dilator was then removed and a nasogastric tube was introduced into the esophagus and passed down into the stomach without issue. A Blake drain was directed into the mediastinum through the esophageal hiatus and draped over the staple line of the Collis-Nissen. Each of the ports and the liver retractor were removed under direct visualization. The drain was sewn in place, and the port incisions were closed. The incisions were washed and dried, and dressings were placed. No intraoperative complications occurred.