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Paraesophageal Hernia Paraesophageal Hernia a, b Dmitry Oleynikov, MD *, Jennifer M. Jolley, MD KEYWORDS Hiatal Paraesophageal Nissen fundoplication Hernia Laparoscopic KEY POINTS A paraesophageal hernia is a common diagnosis with surgery as the mainstay of treatment. Accurate arrangement of ports for triangulation of the working space is important. The key steps in paraesophageal hernia repair are reduction of the hernia sac, complete dissection of both crura and the gastroesophageal junction, reapproximation of the hiatus, and esophageal lengthening to achieve at least 3 cm of intra-abdominal esophagus. On-lay mesh with tension-free reapproximation of the hiatus. Anti-reflux procedure is appropriate to restore lower esophageal sphincter (LES) competency. INTRODUCTION Hiatal hernias were first described by Henry Ingersoll Bowditch in Boston in 1853 and then further classified into 3 types by the Swedish radiologist, Ake Akerlund, in 1926.1,2 In general, a hiatal hernia is characterized by enlargement of the space be- tween the diaphragmatic crura, allowing the stomach and other abdominal viscera to protrude into the mediastinum. The cause of hiatal defects is related to increased intra-abdominal pressure causing a transdiaphragmatic pressure gradient between the thoracic and abdominal cavities at the gastroesophageal junction (GEJ).3 This pressure gradient results in weakening of the phrenoesophageal membrane and widening of the diaphragmatic hiatus aperture. Conditions that are associated with increased intra-abdominal pressure are those linked with all abdominal wall hernias, including obesity, pregnancy, chronic constipation, and chronic obstructive pulmo- nary disease with chronic cough. There has even been a potential genetic component discovered in the development of hiatal hernias. Specific familial clusters across gen- erations have been identified, indicating a possible autosomal dominant mode of a Center for Advanced Surgical Technology, University of Nebraska Medical Center, 986245 Nebraska Medical Center, Omaha, NE 68198-6245, USA; b Department of Surgery, University of Nebraska Medical Center, 986245 Nebraska Medical Center, Omaha, NE 68198-6245, USA * Corresponding author. E-mail address: [email protected] Surg Clin N Am 95 (2015) 555–565 http://dx.doi.org/10.1016/j.suc.2015.02.008 surgical.theclinics.com 0039-6109/15/$ – see front matter Ó 2015 Elsevier Inc. All rights reserved. 556 Oleynikov & Jolley Abbreviations EGD Esophagogastroduodenoscopy GEJ Gastroesophageal junction GERD Gastroesophageal reflux disease GI Gastrointestinal LES Lower esophageal sphincter LUQ Left upper quadrant PEH Paraesophageal hernia inheritance. Certain evidence has linked a collagen-encoding COL3A1 gene and an altered collagen-remodeling mechanism in the formation of hiatal hernias.4 This link indicates that there may be both genetic and acquired factors that contribute to the development of hiatal hernias. Although hiatal hernias were originally only classified into 3 types, the current clas- sification scheme defines 4 types of hiatal or paraesophageal hernias (PEHs).1 These types are listed next: Type 1: Sliding hernia, the GEJ migrates into the thorax Type 2: True PEH or rolling hernia, the herniation of the gastric fundus through a weakness in the phrenoesophageal membrane, the GEJ remains in the normal anatomic location Type 3: Combination of types 1 and 2, the herniation of the GEJ and stomach into the chest (occasionally they can be larger and are sometimes termed giant PEHs) Type 4: Includes other intra-abdominal viscera, such as colon, small bowel, omen- tum, or spleen along with the stomach migrating into the chest Type 1, or sliding hiatal hernias, are the most common type and account for approx- imately 95% of hiatal hernias. The other 3 types combine to make up the remaining 5% of hiatal hernias.1 All can be approached with similar preoperative and operative stra- tegies when patients are symptomatic. CLINICAL PRESENTATION Although the true prevalence of these hernias is difficult to determine because they are often asymptomatic or poorly defined, more recent epidemiologic studies have shown them to be more common than previously recognized in the Western population.4 Typical patients are female and elderly, more commonly in or beyond their sixth decade of life. They may present with vague symptoms of intermittent epigastric pain and postprandial fullness. Sliding hiatal hernias are most commonly associated with gastroesophageal reflux disease (GERD). Large hiatal defects tend to present with symptoms of progressive intolerance to solids/liquids with regurgitation, nausea, and vomiting. These defects can also present with symptoms related to the space they occupy, such as chest pain and respiratory problems caused by lung compression or aspiration. These respiratory issues may include shortness of breath, asthma, and bronchitis. Other unpredictable symptoms that may be revealed with a thorough his- tory include hoarseness, cough, laryngitis, and pharyngitis.4 An unusual cause of gastrointestinal (GI) bleeding and iron deficiency anemia is Cameron lesions related to hiatal hernias. These lesions are linear gastric ulcers or erosions located on the gastric mucosal folds at the diaphragmatic impression of large hiatal hernias.5 Cameron lesions are prevalent in 5% of patients with a hiatal hernia discovered on up- per endoscopy, and the risk of one existing increases with hernia size.5 More acute complications of PEHs are mechanical problems, such as gastric obstruction, Paraesophageal Hernia 557 volvulus, incarceration, and strangulation, which require urgent surgical intervention. These problems may be seen in patients who present with obstructive symptoms of new-onset dysphagia, chest pain, and early satiety. There is a well-known triad, Borchardt triad, associated with gastric volvulus that one should look for in patients: epigastric pain, inability to vomit, and failure to pass a nasogastric tube into the stom- ach.2 Some long-term effects of hiatal hernias are the development of severe reflux with associated erosive esophagitis, Barrett esophagus, and an increased risk of sub- sequent esophageal cancer.4 All symptomatic patients are recommended to undergo PEH repair if deemed to be a good surgical candidate. PREOPERATIVE EVALUATION Hiatal hernias may be discovered incidentally on lateral chest radiographs as a retro- cardiac bubble or during the work-up of unexplained upper GI symptoms, cardiac, or respiratory symptoms. The evaluation of these patients should follow a standard pro- tocol in all instances including a complete history and physical. The history may reveal symptoms that were not previously apparent. The physical examination of these patients is usually unremarkable unless they are having acute complications related to the hiatal hernia. The best diagnostic study to determine the presence and size of the hernia is an upper GI barium study. It can also demonstrate associ- ated esophageal motility dysfunction or stricture/stenosis related to long-standing GERD.4 Esophagogastroduodenoscopy (EGD) is essential to evaluating esophageal length and the mucosa of the herniated stomach for any other abnormal pathology, such as ulcers, esophagitis, gastritis, Barrett esophagus, or neoplasms. EGDs should be performed on all patients who are being evaluated for PEH repair in order to better understand the important anatomic landmarks specific to each patient. Esophageal manometry is also essential to assess esophageal motility and lower esophageal sphincter (LES) characteristics (pressure, relaxation, and location), which may alter the operative approach with regard to the choice of fundoplication performed. Although not essential in the preoperative evaluation, an esophageal pH study can help to provide a quantitative analysis of reflux episodes by correlating pH with a pa- tient’s subjective complaints of reflux.3 Often, because these patients are elderly, they have significant comorbidities that require further evaluation, specifically with re- gard to the assessment of cardiac and respiratory status. With the help of anes- thesia, cardiology, and pulmonology preoperative consultations, the necessary additional studies (such as cardiac stress tests or pulmonary function tests) are ob- tained. All of these examinations help to determine whether or not patients are suit- able surgical candidates. TREATMENT Most patients who are found to be symptomatic from a hiatal hernia will have experi- enced little relief for their upper GI symptoms with over-the-counter antacids, hista- mine receptor antagonists, or proton pump inhibitors. Although it is good to continue these medications to help control symptoms, the definitive management of PEHs is surgery. Historically PEHs were treated with a thoracotomy or laparotomy; but the laparoscopic transabdominal approach has become the gold standard for repair of all hiatal hernias. The first laparoscopic PEH repair was reported in 1991 and continues to evolve with respect to variations in technique, including removal or reduction of the hernia sac, the use of mesh to reinforce the cruroplasty, and whether or not to incorporate an antireflux procedure. Despite these controversies in practice, certain basic tenants exist in laparoscopic hiatal hernia repair: reduction of the hernia 558 Oleynikov & Jolley sac and its contents, complete dissection of both crura and the GEJ, tension-free reapproximation of the hiatus, and adequate mobilization of the esophagus to achieve at least 3 cm of intra-abdominal
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