Paraesophageal hernias comprise approximately 5% to 15% of all hiatal hernias and are challenging hernias to repair. Most commonly, these occur in patients age >50 to 60 years. The natural history of paraesophageal hernia repair has not been systematically studied, but, in general, many patients present with a longstanding history of hiatal hernia. Therefore, it’s likely that these progressively enlarge over time. While they can be asymptomatic, some patients present with acute gastric outlet obstruction and/or gastric ischemia that requires emergency surgical intervention. In this chapter, the clinical presentation, diagnostic evaluation, and surgical technical aspects and resultant outcomes of paraesophageal hernia repair will be presented.

The classification of hiatal hernia is illustrated by the radiographic studies shown in Figure 24-1. Type I hernias are sliding hiatal hernias defined by the location of the gastroesophageal (GE) junction above the diaphragm. Types II, III, and IV are different types of paraesophageal hernias. In type II paraesophageal hernias (PEHs), the GE junction is in a normal position and a portion of the upper stomach, usually the fundus, is herniated alongside the esophagus through the hiatus. Type II PEHs account for a relatively small percentage of cases. The most common type of PEH is type III, in which there is a combined sliding and paraesophageal component. These hernias can be quite large, with most of the stomach, if not the entire stomach, in the chest and associated volvulus. Type IV PEHs are those in which some other organ besides the stomach is herniated into the chest, most commonly the colon, but also possibly the small bowel, pancreas, and duodenum.

Because of the large size of the defect and extent of herniation, the stomach may undergo rotation within the hernia sac. Most commonly, this consists of organoaxial volvulus in which the stomach rotates along the axis of the organ. This type of volvulus results in the greater curvature being flipped upward and at a higher position in the mediastinum than the lesser curvature (Fig. 24-2A). The stomach can also rotate along the axis of its mesentery (mesoaxial volvulus). Mesoaxial volvulus is associated with a higher risk of gastric ischemia because of the twisting of the mesentery, which can compromise venous return and gastric blood flow (Fig. 24-2B).

Patients with PEH may be completely asymptomatic, but more often, they have a variety of symptoms depending on the extent of the herniation. There may be a longstanding history of hiatal hernia that has been managed medically. Postprandial fullness, discomfort, and pain, especially after eating a larger meal, are some of the most common symptoms associated with PEH. These symptoms occur because the herniated segment does not empty properly, and therefore, with a larger meal, the stomach becomes distended, which leads to discomfort. Typical heartburn and regurgitation symptoms of gastroesophageal reflux disease (GERD) may be present but are less common, likely because these patients may still have a competent lower esophageal sphincter. Patients may also have dysphagia either because of associated esophageal dysmotility or because the large hernia compresses the distal esophagus. Approximately 25% of patients present with anemia from gastrointestinal bleeding. The bleeding is usually occult and discovered incidentally on a routine blood count. Anemia in this setting is typically due to Cameron lesions, which are superficial erosions or ulcerations in the proximal stomach that can be secondary to constriction of the stomach at the hiatal defect and friction from movement across the hiatus, which can lead to occult blood loss. PEH may also be detected incidentally on plain chest radiographs as shown in Figure 24-3 or on computed tomography (CT) scan done for chest pain or other reasons (Fig. 24-4).

Up to 20% of patients with PEH present with gastric volvulus. While gastric volvulus can be asymptomatic, it can also develop acutely and lead to gastric outlet obstruction with acute onset of chest or epigastric pain, nausea, and emesis. In some cases, the volvulus may lead to gastric ischemia and strangulation. Most patients who present with acute gastric outlet obstruction can be temporized with nasogastric decompression. However, some patients require emergency surgery to reduce the stomach and avoid progression to gastric strangulation. Inability to pass a nasogastric tube should raise concern for gastric volvulus with possible gastric ischemia.

The diagnosis and evaluation of a patient with a PEH typically involve a multistep process and numerous tests once the diagnosis is suspected.¹ When the diagnosis is suspected, the initial evaluation should consist of a barium esophagram and esophagogastroduodenoscopy (EGD). The barium swallow may be useful in defining the anatomy, the type of hiatal hernia, and in particular, the relationship of the GE junction to the diaphragm. If the GE junction is located more than 5 cm above the hiatus, then the patient may have a shortened esophagus (Fig. 24-5). This is a very useful initial test as it typically yields a significant amount of information about the anatomy and function of the esophagus and stomach.

Further diagnostic evaluation should be carried out that consists of an upper gastrointestinal endoscopy to assess for mucosal lesions and other upper gastrointestinal pathology including the presence of Cameron ulcers and to evaluate the stomach. Factors evaluated at the time of EGD include the size of the hernia, which is often appreciated with retroflexed view. In acute presentations, an EGD can be used to assess the viability of stomach if there is concern for ischemia.

Because patients with PEH may have associated esophageal dysmotility or hypomotility from longstanding reflux and the large hernia, high-resolution esophageal manometry is advisable for most patients to identify this condition and for selection of the proper type of fundoplication to be done at the time of repair. In some cases, it may be difficult for the manometry catheter to pass through the GE junction and assess the lower esophageal sphincter, which can be compressed by the herniated contents. In general, a 24-hour pH test is not indicated for PEH because the presence of the hernia is sufficient objective evidence of the underlying pathology and the results do not typically alter the surgical approach.

PEH repair can be challenging for a number of reasons, including the large amount of herniated contents, the presence of a large hiatal defect that must be closed, need to excise a large hernia sac, the possibility of a shortened esophagus, and often distorted anatomy. In addition, these patients are frequently older with more comorbidities and accompanying obesity, which can increase the difficulty and risks of surgical repair.

PEHs may be repaired either via an open abdominal, open thoracic, or laparoscopic transabdominal approach. Over the past 20 years, laparoscopic PEH repair has largely replaced these other approaches except in the rare, unstable patient who does not tolerate a pneumoperitoneum or the septic patient with gastric necrosis. The operation may be segmented into 3 primary steps, the details of which are provided in Table 24-1: (1) dissection and reduction of the hernia sac and stomach into the abdomen; (2) closure of the crural/hiatal defect; and (3) creation of the fundoplication. Patient preparation should consist of a single dose of intravenous antibiotic (first-generation cephalosporin unless allergic), lower leg compression devices and subcutaneous heparin for thromboembolic prophylaxis, and placement of a urinary catheter. The patient is typically positioned on a bean bag mattress that is well padded and with the legs on spreader bars so the surgeon can stand between the legs.

Step 1. Dissection of the Hernia Sac and Reduction of the Herniated Contents

At initial laparoscopic exploration, one may attempt to reduce the herniated contents, but this is often difficult to achieve without first dissecting the hernia sac (Fig. 24-6). One should use gentle traction and avoid forcible reduction because of the risk of tearing or perforating the stomach. An advanced energy device (most commonly an ultrasonic coagulator) facilitates dissection of the hernia sac and mobilization of the upper stomach and esophagus. The dissection can begin either on the anatomic right or left side of the stomach. The authors prefer to begin by dividing the gastrohepatic ligament up to the right crus of the diaphragm. The hepatic branch of the vagus nerve can be divided, but one should take care to identify (and preserve) a replaced left hepatic artery, which can be present in up to 30% of cases. The phrenoesophageal membrane and edge of the hernia sac are then incised anteriorly, and the plane between the sac and the mediastinum should be developed and then extended toward the right and left crura (Fig. 24-7). This maneuver is critical for beginning to reduce contents out of the mediastinum and can largely be done by blunt dissection. The dissection of the sac continues along the right side down to the base of the crura and into the retroesophageal space until the left crus has been identified. It is important to preserve the thin fascial layer over the crura, which provides strength for the subsequent crural closure. Once the right side has been freed up and the retroesophageal window started, the left anterior phrenoesophageal and gastrophrenic attachments can be divided, which allows one to begin to reduce the sac out of the left side of the mediastinum. At this point, it is often preferable to open the gastrosplenic omentum beginning at the level of the upper body of the stomach and dividing it up to the left crus, taking the short gastric vessels with an ultrasonic coagulator (Fig. 24-8). With large PEHs, the short gastric pedicle is often elongated, which can make this step in the operation easier than with conventional hiatal hernia repair. The short gastrics should be taken close to the stomach to avoid injury near their entry into the spleen, which can be difficult to control, and also to avoid leaving redundant tissue on the fundus for the subsequent fundoplication. The attachments at the base of the left crus are then divided, and at this point, one should visualize a completed retroesophageal window (Fig. 24-9).

Next, the dissection is carried back into the mediastinum where the esophagus is mobilized circumferentially, taking care to identify and preserve both anterior and vagal nerve trunks, which can be distorted in their location by the large hernia (Fig. 24-10). Retraction on the esophagus and upper stomach during mediastinal mobilization can be accomplished either by placing a grasper in the retroesophageal window or by a Penrose drain placed around the esophagus at the hiatus.

It is often helpful at this point to excise the hernia sac, which is usually larger on the left anterior side (Fig. 24-11). The hernia sac may serve as a lead point for possible hernia recurrence, and in some small studies, excision of the hernia sac has been associated with a reduced hernia recurrence rate.²

When excising the sac, one must be careful to avoid injuring the anterior vagus nerve, which can be closely applied to the base of the sac. In some cases, there is also redundant sac to excise on the anatomic right side, and care should be taken there to identify and preserve the posterior vagus nerve during that step.

Once the contents are completely reduced and the esophagus has been extensively mobilized, a determination should be made as to whether or not there is adequate intra-abdominal length of 2.5 to 3 cm or more. If not, then an esophagogastric lengthening procedure may need to be performed, as described below. Other precautions include the importance of proper traction and countertraction to expose the relevant anatomy at each stage in the operation. One should also be careful with the use of energy near the esophagus, stomach, and vagus nerves because of the risk of direct thermal spread to those structures.

Step 2: Closure of the Hiatal Defect

Once the hernia has been reduced and the esophagus has been fully mobilized, the hiatal defect should be repaired. The crura should be closed with interrupted nonabsorbable sutures, preferably 0 polyester-type sutures (Fig. 24-12). The closure should begin posteriorly with either simple interrupted or figure of 8 sutures or a combination thereof. Some surgeons prefer to use pledgeted sutures to buttress the closure. If mesh is to be used, it should be placed at this step in the operation. It may be necessary with larger defects to also place a crural closure stitch anterior to the esophagus because of increasing tension posteriorly. In cases in which there is a wide defect that cannot be closed primarily, a relaxing incision can be made in the right crus to bring the crura together at the midline. This defect from the relaxing incision would then need to be covered with some type of mesh, as will be discussed below.