Laparoscopic Paraesophageal Hernia Repair: Technique, Outcomes, and Management of Complications

Pathophysiology, Incidence, and Clinical Presentation

In normal esophageal anatomy the gastroesophageal junction (GEJ) is located below the hiatal orifice. It is held in place by both the phrenoesophageal ligaments and an aggregate of posterior attachments between the GEJ and cardia of the stomach. The phrenoesophageal ligament is formed from the fascia transversalis on the abdominal aspect of the diaphragm and the endothoracic fascia on the thoracic aspect of the diaphragm. Both leaves then insert on the muscular wall of the esophagus. During normal swallowing-initiated peristalsis, the elastic properties of the phrenoesophageal ligament allow the esophagus to shorten, resulting in slight movement of the GEJ cephalad. Physiologic stressors, such as gastroesophageal reflux, obesity, chronic cough, and normal changes in tissue architecture associated with aging may result in the attenuation and weakening of the ligament, with widening of the hiatal aperture and herniation of the stomach into the chest and the paraesophageal space.

Hiatal hernias are generally classified into four types ( Fig. 26.1 ). Type I is often referred to as a sliding hiatal hernia, with the GEJ frequently moving in and out of the chest. Paraesophageal hernia (PEH) occurs when part or all of the stomach translocates from the abdomen through the esophageal hiatus and into the posterior mediastinum. When the GEJ remains in the normal intraabdominal position, the PEH is a “true” PEH because the fundus of the stomach herniates through an anterolateral weakening of the phrenoesophageal ligament and lies next to the esophagus in the mediastinum. This type of PEH is known as a type II PEH, which is quite uncommon. In the more common type III PEH, the GEJ has also migrated cephalad, likely as a result of some genetic predisposition to this type of hernia and often preceded by long-standing gastroesophageal reflux. It is hypothesized that ongoing reflux leads to fibrotic changes to the esophagus wall, leading to a foreshortening of the esophageal longitudinal muscles and, subsequently, the esophagus itself.

One of the world's most renowned experts on this topic, Dr. Griffith Pearson, measured the length of the esophagus, from the upper esophageal sphincter to the lower esophageal sphincter, in a group of patients with type III PEH and found this to be on average approximately 5 cm shorter than the same measurement in patients without a PEH. Over time, this scarring pulls the GEJ into the posterior mediastinum, along with the proximal stomach, stretching and lengthening the phrenoesophageal ligament and widening the crural aperture. Eventually, the GEJ becomes fixed within the posterior mediastinum with varying degrees of gastric herniation and is known as a type III PEH. Patients with large type III PEH are usually symptomatic and may present with symptoms suggestive of obstruction, including chest pain, early satiety, postprandial bloating, or dysphagia. Anemia, cough, aspiration, and shortness of breath are also common symptoms of the PEH that are often attributed to other causes. When other abdominal organs follow the stomach into the chest, such as omentum, colon, spleen, and/or portions of the pancreas, the hernia is referred to as type IV PEH.

PEHs comprise approximately 5% to 10% of all hiatal hernias, and in addition to their common symptomatology listed previously, they can in extreme situations lead to gastric volvulus with resultant gastric and/or esophageal necrosis, sepsis, and death. Despite frequent symptoms and the potential for significant morbidity associated with acute presentation, there is significant debate regarding the need for and timing of operative intervention, as well as the approach to operation. Part of the reluctance to send patients for elective surgery is the significant morbidity that was associated with historical open operations, which frequently included a thoracotomy and/or thoracoabdominal incisions. Currently, many experienced centers can perform repair of PEH minimally invasively but are still criticized by significant recurrence rates and side effects that may occur. However, a combination of significant minimally invasive esophageal surgery experience and a thorough understanding of the anatomy, pathophysiology, and historical management of PEH may help to provide surgeons with the necessary tools to manage this difficult disease process and provide patients with durable outcomes.

Indications/Contraindications

Over the past decade, the laparoscopic approach for PEH repair has become a standard approach in many centers, enabling PEH to be repaired with less pain, faster recovery, and reduced morbidity. However, it has become clear that only a few centers have published successful outcomes with minimally invasive approaches that have recurrence rates that are reasonably comparable to the best open series. Optimal outcomes with durable results are much more likely to occur when performed by experienced surgeons with significant open and minimally invasive esophageal surgery experience.

When evaluating a patient with a PEH for possible surgery, the physician should be familiar with the full spectrum of associated symptoms because less than 5% of patients are truly asymptomatic when questioned thoroughly. Repair is generally recommended for all symptomatic patients. The management of a truly asymptomatic hernia remains a topic of debate. The incidence of a truly asymptomatic PEH is uncommon, and often patients billed as asymptomatic frequently do suffer from significant symptoms such as shortness of breath that may not be attributed to the hernia. Often these symptoms have occurred insidiously and patients have learned to live with these troublesome limitations and symptoms. In the previous era of primarily open repair, some studies estimated that the risk of life-threatening complications from a PEH was greater than 25% within a relatively short-term follow-up. More recently, it has been recognized that life-threatening events are much less common and some authors have created risk-benefit algorithms to support the notion that life-threatening events are lower than the risk of undergoing repair. However, when analyzing the findings of these studies, it is important to make note of the definition of minimally symptomatic or asymptomatic used; in the paper by Stylopoulos, minimal symptoms were defined as “heartburn that did not affect patient quality of life.” In our experience, the vast majority of patients with radiographic findings of large PEH will have obstructive symptoms, including dysphagia, postprandial bloating, and chest pain and may not suffer from actual heartburn. On occasion, elderly patients in our clinics may deny difficulty swallowing but, when questioned further, will report significant and unintentional weight loss over the previous 5 to 10 years and substantial changes to their diet to avoid hard and sometimes even soft solids.

When these hernias progress to requiring semiurgent, nonelective repair in our series, as well as by other surgeons, they are associated with a significantly increased risk of perioperative morbidity and mortality. In our series of 662 patients who underwent laparoscopic repair of a giant PEH, patients admitted electively for laparoscopic repair had a postoperative mortality rate of 0.5% compared with 7.5% for patients who underwent urgent repair. This can be markedly higher when patients present with gastric necrosis, massive hemorrhage, or severe aspiration pneumonia, albeit the incidence of these more life-threatening situations is less common. Thus, when evaluating patients who may be minimally symptomatic, it is important to keep these data in mind. The risk of perioperative mortality and/or morbidity with elective and nonelective operation can be estimated to some degree by the size of the PEH, the patient's functional status, the presence of comorbid conditions, and the patient's symptom complex. In patients with age-adjusted Charleston Comorbidity Index scores of 5 or less, perioperative morbidity and mortality with elective laparoscopic repair is low and increases dramatically when performed urgently. Furthermore, patients with very large PEH were much more likely to have obstructive symptoms and to present urgently when compared with patients with smaller (<75% gastric herniation) PEH. Urgent presentations often occur in patients in whom the presence of the PEH was known much earlier. As such, we recommend elective surgical repair for most patients who have minimal symptoms and very large PEH because of the higher risk of mortality or complications after emergency surgery.

Relative contraindications to laparoscopic PEH repair include conditions that might preclude or increase the risk of all laparoscopic surgery, such as portal hypertension, significant hematologic clotting disorders, and contraindications to surgery in general, such as inadequate cardiovascular function or the inability to tolerate general anesthesia. All of these relative contraindications must be weighed against the complications of an incarcerated, necrotic stomach or the morbidity of an urgent repair for acute problems. Age itself should not be considered a complication because most of these patients are elderly and will be even less likely to tolerate urgent or emergent surgery but typically do very well with elective laparoscopic repair.

Preoperative Assessment

PEH can be visualized with a variety of radiographic studies. We consider the barium esophagram as the gold standard for evaluating PEH because it is inexpensive, low risk, and provides an accurate assessment of the degree of gastric herniation and the anatomic relationship between the stomach, GEJ, and diaphragmatic hiatus. When combined with video imaging, the barium esophagram provides useful information on reflux and esophageal motility. In less experienced hands, endoscopic evaluation can be difficult due to changes in the anatomic orientation of the esophagus, stomach, and diaphragm. In cases of a large volvulized PEH navigating the endoscope through the GEJ, stomach, and pylorus can be challenging. Computed tomography (CT) scans can provide complementary data and are often useful in identifying type IV hernias and evaluating coexisting pathology. However, we do not routinely require a CT scan prior to surgery. Additional studies, such as 24-hour pH monitoring and manometry, are used selectively in patients with smaller PEH (~30% to 50%). Although these functional tests are important when evaluating patients with smaller hernias, they provide less reliable information in patients with larger PEH. Furthermore, in contrast to sliding hiatal hernias, objective evidence of reflux disease is not necessary prior to repair of a symptomatic PEH.

Manometric assessment of the lower esophageal sphincter in large PEH is frequently difficult and at times inaccurate due to proximal displacement of the GEJ, tortuosity, and inability to position the catheter into the distal stomach. However, obtaining a simple manometric analysis of the body of the esophagus can be quite helpful in assessing the esophageal peristaltic wave and contractions to help determine the type of fundoplication as part of PEH repair. Preoperative or intraoperative endoscopy is always performed by the operating surgeon to evaluate gastric and esophageal viability and to identify associated abnormalities, such as Barrett esophagus, strictures, diverticula, esophageal malignancy, and the location of the GEJ. It is critical for the surgeons to perform their own endoscopy, if not prior to surgery, then at a minimum, the day of surgery, and not rely on the findings on endoscopy reported by others, because important features can be missed or underestimated when unaccustomed to endoscopic evaluation of a PEH.