There are two major forces acting on the repair of the hiatal hernia that lead to disruption of the repair and ultimate failure: radial tension and axial tension (Fig. 16.1). Radial tension at the hiatus acts upon the diaphragm in a plane perpendicular to the esophagus. This tension results in the movement of crural fibers away from the midline and a widening of the diaphragmatic hiatus. It is opposed by the phrenoesophageal ligament which helps keep the hiatus in place around the esophagus. The dynamic nature of the diaphragm and its constant motion over time causes stretching and even break down of a sutured crural repair with resultant failure and recurrence of the hernia. When the radial forces overcome the forces keeping the hiatus together, the hiatus loosens and allows herniation to occur. When repairing hiatal hernias, increased radial tension is manifested as difficulty re-approximating the left and right crural pillars.

Axial tension is related to the cephalad forces acting on the esophagus both intrinsically and extrinsically and is manifest as the tendency for the gastroesophageal junction (GEJ) to migrate upward into the mediastinum. There is a natural physiologic movement of the GEJ of up to 2.5 cm in non-hernia patients, with the phrenoesophageal membrane acting as an elastic recoil mechanism to return the GEJ to its proper anatomic configuration [8]. When the phrenoesophageal ligament becomes attenuated, the amount of recoil decreases and results in herniation [9]. Additional forces include negative intra-thoracic pressure, positive intra-abdominal pressure, contractile forces of the longitudinal esophageal musculature, and increased intra-gastric pressure. In addition, chronic displacement of the GE junction into the chest combined with fibrosis from recurrent esophagitis can make re-establishment of adequate intra-abdominal esophagus difficult (short esophagus), with resultant axial tension on the repair. After primary repair of a paraesophageal hernia, this axial tension acting on the esophagus continues unopposed and can result in disruption of the hiatal closure or any fixation sutures resulting in intra-thoracic migration of the GEJ and fundoplication.

There are several technical factors at the time of the index operation over which the surgeon has control and which can result in reduced likelihood of recurrence. A full mobilization of the distal esophagus up to or above the inferior pulmonary veins will improve intra-abdominal length and decrease axial tension on the short esophagus. Intra-operative endoscopy with endoscopic confirmation of the squamo-columnar junction will aid in correctly placing the wrap at and above the GE junction rather than too low.

The actual shaping of the fundoplication by utilizing the correct portion of the fundus and bringing it around the esophagus with the proper configuration is critical. If the gastric body rather than the fundus is used to construct the wrap, a type III failure may occur (Fig. 16.2). In order to avoid an overly tight wrap, the fundoplication is most often constructed over a bougie. Data suggests a decrease in post-operative dysphagia with the use of a bougie. There is however a real possibility of dilator perforation during insertion, which is estimated at 1% [10, 11]. In addition, standardization of crural closure has been elusive, and an overly tight cruroplasty may lead to postoperative dysphagia and need for dilation or revision, whereas overly loose closure can be a factor in recurrent herniation.

There are several factors relating to the patients that can affect the rate of recurrence. Paraesophageal hernias occur mainly in the aging population, which is likely related to attenuation of the phrenoesophageal membrane (and perhaps other connective tissue involving the repair) and subsequent recurrence [9]. Factors that put patients at a higher risk of failure are pre-operative (body mass index) BMI >35, unresponsiveness to acid-reducing medications, atypical symptoms, and psychiatric illness [12]. While there is no absolute BMI cutoff beyond which a repair should not be performed, dietary counseling and referral to a bariatric surgeon should be considered for any patients with BMI >35. Post-operatively, tight nausea control should be implemented in order to avoid retching, which can increase intra-abdominal pressure and is a primary factor associated with recurrence. In addition, patients should be counseled to avoid any inordinate heavy lifting, straining or strenuous exercise which could lead to increased intra-abdominal pressure and resultant recurrence.

Anatomic failure can be classified based on the type of failure and it is helpful to identify the type of failure as an indicator of the underlying cause (Fig. 16.2). Increased radial and axial tension can lead to a Type IA failure and is seen when the entire wrap along with the gastroesophageal junction migrates cephalad resulting in an intra-thoracic fundoplication. This is the most common type of failure. A variation on this problem is the so-called slipped Nissen , or Type IB failure in which the wrap remains below the diaphragm but the stomach and the gastroesophageal junction slip upward through the wrap resulting in the GEJ residing within the mediastinum. This failure may occur due to misjudging the location of the true GEJ with the wrap placed low around the cardia instead of the fundus, from increased axial tension due to unrecognized short esophagus, or as a result of chronic stress on the GEJ from intra-gastric pressure. When in doubt, poor placement can be avoided by intraoperative endoscopy and identification of the true junction. Type II failure is analogous to the true paraesophageal hernia. Breakdown of the crural repair sutures with an intact wrap and normally located GEJ can result in intra-thoracic stomach with dysphagia, pain, or potential gastric volvulus despite an appropriately placed wrap. Finally, a defective initial construction of the wrap results in a Type III failure as described above, caused by utilizing the mid-body of the stomach to fashion the wrap rather than the fundus.

Identifying and defining symptoms is one of the most important steps in treating recurrent hernias. Many patients experience new symptoms after an otherwise satisfactory primary hernia repair, such as gas-bloat, hyper-flatulence, or mild dysphagia even in the absence of documented anatomical defects or technical errors. Without investigations it may be difficult to determine which symptoms are due to the physiologic effects of the wrap versus the effects of a recurrence. It is imperative then to obtain a good symptomatic history detailing exactly when the symptoms started, progression, and temporal relation to oral intake. Symptomatic management is the first step in the early postoperative period unless there is strong reason to suspect disorder of the repair. For persistent, progressive, or atypical symptoms, objective studies will be needed to determine the presence and correlation of anatomic defects with symptoms.

The most common post-operative symptoms related to recurrence are heartburn, regurgitation, dysphagia, and pain [13]. Any of these may be the result of the repair itself. For example, the sensation of heartburn may be caused by esophageal distension or spasm secondary to the effect of the wrap rather than failure of the repair. However, if any of these symptoms persist beyond the first 3 months, a focused workup should be implemented in order to identify any possible recurrence and assist therapeutic decision-making.

It is reasonable to start with two-phase esophagography. This test will help elucidate esophageal and gastric anatomy including an obstructing repair, anatomic recurrence and its classification, intra-thoracic wrap migration, and strictures or other anatomic abnormalities and is the most sensitive test for recurrent herniation (Fig. 16.3) [14]. It can also provide useful information on the basic function of the gastroesophageal junction and valve, visualizing both transit and reflux, though it is less reliable with regard to recurrent reflux. The pylorus can be examined as well in order better identify vagal injury and resultant hypertonicity of the sphincter mechanism. Anatomic recurrence is commonly defined as 2 or more cm of stomach and/or GEJ above the diaphragmatic crura although several variations of the diagnostic criteria exist [15].

Endoscopy is important in the workup in order to visualize any intra-luminal abnormalities. Erosions, esophagitis, or gastritis can be identified and help reinforce the diagnoses of reflux and recurrence. A recurrent hiatal hernia can be seen and the configuration of the gastroesophageal flap valve based on the Hill system can be graded (Fig. 16.4). The presence of a stricture or narrowing may prompt additional manometric evaluation. Rarely, erosion of suture or mesh into the lumen will be detected.

Manometry is not an essential part of the evaluation of recurrent PEH, but may prove useful in certain circumstances. If pre-operative manometry is available and the patient denies any new dysphagia, then repeat manometric evaluation is unlikely to add any additional usefulness. However, if the patient has new-onset dysphagia or there is uncertainty surrounding the patient’s esophageal motility, then manometry should be performed to rule out any esophageal motility disorders of the esophageal body or the reconstructed GEJ, to help determine optimal reconstruction.

Objective evaluation of reflux in the form of 24-h pH monitoring is vital to identify the presence of acid reflux, especially if anatomic recurrence is subtle or absent and the etiology of symptoms is unclear. In the case of large recurrent anatomic defects clearly attributable to the patient’s symptoms, pH monitoring is less helpful as re-operation is likely regardless of the pH study outcome. Any patients with symptoms of reflux and a positive DeMeester score in the setting of anatomic recurrence should be considered for revisional surgery.

If there is concern for vagus nerve injury or impaired gastric motility, a gastric emptying study is helpful in determining gastric function. The incidence of gastroparesis requiring a gastric emptying procedure can be as high as 12% after re-operation and increases with each subsequent recurrence [16]. A patient who gives a history of nausea or extended bloating after meals should make the surgeon suspicious for gastric emptying issues. If a gastric emptying test shows delayed gastric emptying, careful consideration must be given to the management of abnormal gastric emptying in the setting of previous hernia repair. If on endoscopy the pylorus is dysfunctional, a trial of endoscopic botulinum toxin may improve emptying and signal a good chance of success for pylorplasty or pyloromyotomy at the time of reoperation [17]. If the sphincter mechanism is functional without increased tone or obstruction, however, then pro-motility agents may be attempted.

Although once the mainstay of re-operative hiatal hernia repair, the open approach has been largely supplanted by laparoscopic paraesophageal hernia repair over the last 20 years. Compared to the open trans-abdominal and trans-thoracic approaches, laparoscopy has been shown to decrease hospital length of stay, postoperative pain, and respiratory complications while offering similar outcomes [18, 19]. In experienced hands, the laparoscopic approach is safe even in the setting of previous laparoscopy or even laparotomy with low conversion rates of around 7% [20, 21]. It has been shown that results with reoperation are superior in experienced centers, however, and typically these operations should be performed only by surgeons experienced in re-operative repair [22]. If there is concern for ischemia, perforation or gross spillage, however, an open approach may be warranted [23]. Important key steps relating to re-operative paraesophageal hernia repair will be discussed in this section (Table 16.2).