Poor Gastric Emptying in Patients with Paraesophageal Hernias: Pyloroplasty,Per-Oral Pyloromyotomy,BoTox,or Wait and See?

Abstract

Gastric emptying delay may be caused with both functional and anatomic derangements. Gastroparesis is suspected in patients presenting with certain foregut symptoms without anatomic obstruction. Data are still emerging regarding the best treatment of this condition. In cases where large paraesophageal hernias alter the upper gastrointestinal anatomy, it is difficult to know if gastroparesis also exists. Management of hiatal hernias is also still evolving, with various strategies to reduce recurrence being actively investigated. In this article, we present a systematic review of the existing literature around the management of gastroparesis and the management of paraesophageal hernias when they occur separately. In addition, since there are limited data to guide diagnosis and management of these conditions when they are suspected to coexist, we provide a rational strategy based on our own experience in patients with paraesophageal hernias who have symptoms or studies that raise suspicion for a coexisting functional disorder.

Epidemiology and Symptoms of Gastroparesis

Gastroparesis is a chronic medical condition that is characterized by delayed gastric emptying in the absence of mechanical obstruction.^1–3 The pathophysiology of the disorder remains poorly understood.⁴ Cases of gastroparesis are usually idiopathic; however, the condition may be associated with medical conditions such as diabetes mellitus, Parkinson's disease, or collagen vascular disorders, or as a sequela of viral infections or certain upper gastrointestinal (GI) surgical procedures done in proximity to the vagus nerves.^5,6

Gastroparesis most commonly presents with nonspecific symptoms such as nausea, vomiting, early satiety, bloating, and abdominal pain.^2,7 Although vomiting is a common symptom and patients may present with malnutrition, the condition is not uniformly associated with food restriction, and can even be seen in the overweight population.¹ However, the presence of restrictive or avoidant food intake behaviors is associated with greater symptom intensity.⁸ Cases of gastroparesis may be complicated by the presence of phytobezoars, which may present as a palpable epigastric mass or may worsen the common presenting symptoms.⁶ Phytobezoars may also lead to the formation of gastric ulcers, cause intestinal obstruction, or even lead to gastric perforation.⁶

Gastroparesis can significantly lower the quality of life (QoL) of affected patients.^9,10 Parkman et al⁹ assessed 715 gastroparesis patients using 2 QoL assessment tools. The 36-Item Short Form Health Survey version-2 (SF-36v2)¹¹ was used to assess general mental and physical health, and the Patient Assessment of Upper Gastrointestinal Disorders Quality of Life (PAGI-QoL)¹² was used to assess disease-specific QoL. Gastroparesis patients had lower mental and physical health by the SF-36v2, and lower upper GI QoL by the PAGI-QoL. The investigators demonstrated how QoL is impacted by nausea, vomiting, abdominal pain, psychological factors, anxiety, and other patient-related factors such as smoking.⁹ Yu et al,¹⁰ in another study using the same assessment tools delivered to 1423 adults with gastroparesis, found 64% were not satisfied with the treatments they were receiving and that approximately half expected their symptoms to worsen over time (47%).

The nonspecific nature of the symptoms of gastroparesis makes epidemiological studies difficult.¹³ Jung et al¹³ utilized a medical record linkage system in Olmsted County, Minnesota, and found an age-adjusted incidence of 9.4 per 100,000 for men and 37.8 per 100,000 for women, demonstrating that the condition may be more common in female patients.¹³ Ye et al¹⁴ used a large United States National Claims Database to demonstrate an incidence of “definite gastroparesis” of 21.5 per 100,000, with definite gastroparesis defined as persistence of symptoms more than 3 months after diagnostic gastric scintigraphy. Syed et al,¹⁵ in a population-based study using an aggregated database called the “Explorys,” demonstrated a disease prevalence of 0.16%. These investigators additionally delineated an incidence of 4.59% among patients with type 2 diabetes mellitus and an incidence of 1.31% among patients with type 1 diabetes mellitus.

The increasing number of patients being hospitalized due to gastroparesis in recent years suggests that the incidence of the disorder may be rising.^16,17 These reports, along with likelihood of underdiagnosis due to the nonspecific nature of symptoms,⁵ make gastroparesis a health care problem that requires consideration when addressing foregut symptoms.

Diagnosis of Gastroparesis

To diagnose gastroparesis, exclusion of a mechanical obstruction is necessary. Thus, the initial evaluation of a patient with suspected gastroparesis should include an anatomic assessment by upper GI contrast study and/or esophagogastroduodenoscopy (EGD). Normal appearing anatomy, along with possible retention of gastric contents after a period of fasting, may suggest gastroparesis.¹⁸

The gold standard test for the diagnosis of gastroparesis is gastric scintigraphy.^19–21 Patients consume a radiolabeled meal and are imaged at specific time points, most commonly over 4 hours. Use of radionucleotides for the assessment of gastric emptying dates back to 1966, when Griffith et al²² used Chromium-51. Scintigraphic images were found to directly correlate with the volume of the remaining meal without any need for geometric adjustment.²³

More recently, a Technitium-99 sulfur colloid meal consisting of two large eggs, two slices of bread with jam, and water²³ has been used as a test meal. Another option considered more representative of the typical American meal consists of two scrambled eggs, a slice of whole wheat toast with jam, and milk.²⁴ In the former, gastroparesis is diagnosed if greater than 60% of the meal is present after 2 hours, or if more than 10% is present after 4 hours.²¹ In the latter, retention of more than 75% at 2 hours or 25% at 4 hours is diagnostic of gastroparesis. It is important to note that before a nuclear medicine gastric emptying study, certain factors should be controlled.

Prokinetic agents should be held for 48–72 hours before the study depending on the half-life of the drug.²⁵ Patients should not use tobacco products on the morning of the study.^26,27 Finally, blood glucose should be well controlled,²³ as studies have shown that serum glucose levels of >288 mg/dL can delay gastric emptying compared to patients with normal baseline glucose levels.²⁸ Recently, the United European Gastroenterology (UEG) and the European Society for Neurogastroenterology and Motility (ESNM) groups published a consensus statement on appropriate use of gastric scintigraphy for the diagnosis of gastroparesis substantiated by high levels of evidence.¹⁹

Another diagnostic option with good supporting evidence, according to ESNM, is the stable isotope Gastric Emptying Breathing Test.¹⁹ In this study, patients consume a meal that contains radiolabeled carbon. Through the implementation of mathematical models, the measured end-tidal carbon dioxide at 4 and 6 hours after the meal is used to estimate gastric emptying.^29–32

A Wireless Motility Capsule may also be used for the diagnosis of gastroparesis. According to ESNM, this method has moderate quality supportive evidence, and further research on its use is needed.¹⁹ This capsule can measure and transmit pH, pressure, and temperature data to an external receiver for interpretation.^20,33 Patients consume a low-fat test meal and then the capsule, and then fast for 6 hours. If the capsule passes through the stomach by 5 hours, gastric emptying is considered normal; otherwise, patients are considered to have emptying delay. This test is based on the physiologic alteration of pH as the capsule moves from the acidic environment of the stomach to the alkaline environment of the duodenum.²¹

Management of Gastroparesis

Nutritional strategies

Patients suffering from gastroparesis can present with recurrent vomiting, which may lead to hypokalemic metabolic alkalosis, as well as vitamin and mineral deficiencies, including iron, folate, vitamin B12, vitamin D, vitamin E, and thiamine. These essential nutrients must be replaced as needed.^20,34,35 In addition, patients should be advised to mechanically reduce the size of their meals.²¹ According to a randomized controlled study performed by Olausson et al,³⁶ patients who received a small-particle diet demonstrated improvement of nausea, vomiting, postprandial fullness and bloating.

Patients presenting with symptoms of gastroparesis should also be advised to reduce the volume and increase the frequency of meals they consume.³⁷ According to the American College of Gastroenterology, gastroparesis patients should consume four to five small meals per day.^18,38 It is important to stress to patients they should restrict fat and fiber in their diet, as these components can delay gastric emptying.³⁹ In addition, patient-related factors known to contribute to gastroparesis, including smoking and alcohol consumption, should be eliminated.³⁴ In cases of diabetic gastroparesis, patients should be advised to limit carbohydrate intake, as acute hyperglycemia can also cause a delay in gastric emptying.³⁹

Gastroparesis may lead to intolerance of oral intake. Additional measures to ensure adequate caloric intake may be needed,³⁹ including dependence on a liquid diet, and in some cases, addition of oral nutritional supplements, enteral nutrition, or even parenteral nutrition.^21,39

Medical strategies

When symptoms of gastroparesis persist, despite the implementation of behavioral and dietary interventions, medications may be utilized. The primary medications used for treatment of gastroparesis are prokinetic agents. The most prescribed prokinetic is metoclopramide.^20,21 Metoclopramide is a dopamine D₂ receptor antagonist and a serotonin 5-HT₄ receptor agonist that has been shown to improve symptoms significantly.^40–42 Treatment of gastroparesis with metoclopramide is presently the only FDA-approved treatment^18,21; however, use of the drug should not exceed 12 weeks as it can induce tardive dyskinesia.⁴³ Another commonly used medication for gastroparesis is domperidone, which is a peripherally acting D₂ receptor antagonist that has equal effectiveness to metoclopramide.^44,45

Unfortunately, the use of this drug is limited due to cardiotoxic side effects, as it tends to prolong the QTc interval.⁴⁶ Other options for the treatment of gastroparesis include macrolide antibiotics like azithromycin, which act on motilin receptors in the GI tract, but their use is limited due to rapid tachyphylaxis and cardiotoxicity.⁴⁷

The GI hormone ghrelin improves gastric emptying.⁴⁸ Therefore, the development of effective ghrelin agonists is a field of great interest for investigators.⁴⁹ Ulimorelin in oral and intravenous formulations was initially produced and tested; however, the lack of symptom response led to the cessation of clinical trials.^50–54 Another ghrelin agonist, Relamorelin,⁵⁰ has demonstrated improved gastric emptying time, nausea, postprandial, and bloating, and seems to have a favorable side-effect profile; however, data for this agent stem from phase-II clinical trials and therefore more data will be required.^55–57 A recent meta-analysis by Hong et al,⁵⁸ which incorporated six randomized controlled trials using ghrelin agonists, demonstrated a statistically significant improvement of overall gastroparesis-related symptoms.

In cases of gastroparesis where a specific symptom predominates, certain drugs targeting that symptom may be used. For example, ondansetron may have a role for severe nausea and emesis,^20,21 or tricyclic antidepressants amitriptyline and nortriptyline may be used for severe abdominal pain.^20,21

Endoscopic strategies

Abnormal pyloric tone has been implicated in the pathogenesis of gastroparesis.⁵⁹ In 1986, Mearin et al⁵⁹ demonstrated that patients with symptoms of gastroparesis have altered pyloric contraction compared to healthy controls. This observation led to the development of various invasive procedures that specifically target the pylorus. Surgical and endoscopic options exist. Today, the most implemented endoscopic procedures include per-oral pyloromyotomy (POP), injection of botulinum toxin (Botox), and endoscopic self-expandable stent placement.

The very first POP procedure was described by Khashab et al⁶⁰ in 2013. Using an endoscope and following the principles of submucosal endoscopy and the techniques used during esophageal per-oral endoscopic myotomy (POEM) for the treatment of achalasia, the team was able to divide the inner circular and oblique muscle fibers of the pylorus.⁶⁰ The patient had a normalized postoperative gastric emptying study and great improvement in symptoms. Spadaccini et al,⁶¹ in a recent meta-analysis, demonstrated POP is feasible and associated with improvement of symptoms in 83.9%. Similarly, Yan et al,⁶² in their meta-analysis, reported POP was 100% technically successful and associated with significant improvements in gastric cardinal symptom index and gastric emptying time.

The endoscopic injection of Botox has been studied as a potential alternative for the treatment of refractory gastroparesis.^63–69 Botox is a toxin that prevents the release of acetylcholine in the neuromuscular junction and causes inhibition of muscle activity.⁷⁰ The toxin has been used in the treatment of other GI conditions marked by muscular hypertonicity, such as esophageal achalasia⁷¹ and anal fissures.⁷² In an initial assessment of the efficacy of Botox for the treatment of gastroparesis, Bromer et al⁶⁴ found 43% of patients responded for an average of 5 months. Similar results were reported by Miller et al,⁶⁶ who found patients demonstrated improved gastric emptying and symptoms.

However, the two studies failed to demonstrate superiority of the Botox compared to injection of normal saline, raising concerns for the true effectiveness.^65,67 In addition, there is high concern that repeated Botox injections may lead to fibrosis of the pylorus and that could limit the safety of future endoscopic or surgical procedures.²¹

In 2013, Clarke et al⁷³ suggested endoscopic transpyloric stenting. They used this technique in 3 patients and demonstrated all had improvement of symptoms. Khashab et al,⁷⁴ in a subsequent study of 30 patients with severe refractory gastroparesis, verified stenting was technically feasible, with 75% of patients having symptom improvement and 69% gastric emptying improvement. However, the use of self-expanding stents can cause major complications like bleeding, perforation, and stent migration.⁷⁵

Surgical strategies

The most used surgical technique for the treatment of refractory gastroparesis is the Heineke-Mikulicz pyloroplasty, a procedure during which a longitudinal full-thickness gastroduodenotomy is performed to divide the pylorus and then the opening is transversely sutured.⁷⁶ Toro et al⁷⁶ demonstrated 82% of patients having laparoscopic pyloroplasty reported postoperative symptom improvement. Similarly, Hibbard et al. demonstrated a series of minimally invasive pyloroplasties with symptom response that was durable for more than 3 months.⁷⁷ Shada et al⁷⁸ demonstrated 90% of gastroparesis patients treated with laparoscopic pyloroplasty had postoperative improvement or normalization of gastric emptying time.

Pyloroplasty can also be performed robotically. Bajpai et al⁷⁹ showed that laparoscopic and robotic pyloroplasty had similar 90-day outcomes and that robotic cases had shorter mean operative time and hospital length of stay. Pyloroplasty can sometimes cause obstruction of the gastric outlet.⁸⁰ This obstruction could be acute, because of the inclusion of the pyloric back wall in the suture line, or chronic, due to fibrosis.⁸⁰ In addition, pyloroplasty may result in GI leak with associated abscess and/or sepsis.⁸⁰

Strategies under investigation

Dysfunction of the interstitial cells of Cajal and cellular changes in the enteric neurons have been implicated in the pathophysiology of gastroparesis.⁸¹ Therefore, investigators have developed an implantable gastric electrical stimulator, a device that resembles a pacemaker, to deliver high-frequency, low-energy impulses to the gastric wall.^20,21 This device may provide a sustained antiemetic effect through prokinetic and antiarrhythmic mechanisms⁸²; over time, patients may demonstrate improvement in QoL and GI hormonal levels.⁸¹ Laine et al⁸³ demonstrated that the use of a high-frequency stimulator led to the improvement of symptoms in 79% of patients, with subsequent regain of weight.

Similar results were reported by Hedjoudje et al⁸⁴ in a retrospective analysis, which found gastric stimulation was associated with improvement in abdominal bloating, early satiety, vomiting, QoL, and body mass index at 10-year follow up. However, guidelines from with UEG and ESNM reported evidence for use of gastric electrical stimulation as Grade B, suggesting more studies are needed.¹⁹

Improvement of gastric emptying with fundoplication

Interestingly, gastric emptying is improved after fundoplication procedures.^85–90 Farrell et al⁹⁰ demonstrated that gastroesophageal reflux patients with concomitant gastroparesis, who underwent fundoplication alone, had 38% improvement in nuclear medicine gastric emptying time, whereas those undergoing fundoplication and pyloroplasty had a 70% improvement. Similar results were demonstrated by Le Page and Martin,⁸⁵ who found 67% of patients who underwent fundoplication, along with partial sleeve gastrectomy, had an improvement in gastric emptying time of solids. The same observation was made in the pediatric population by Estevão-Costa et al,⁸⁹ who found that gastric emptying was significantly faster in the postoperative setting. Fundoplication reduces retrograde movement across the esophagogastric junction and/or food trapping above the diaphragm in hiatal hernias, thereby delivering gastric contents more effectively to the antrum for improved gastric emptying.⁹⁰

Epidemiology and Symptoms of Paraesophageal Hernias

Hiatal herniation refers to the protrusion of abdominal viscera through the esophageal hiatus of the diaphragm.⁹¹ The organ that most commonly herniates into the mediastinum is the stomach; however, other abdominal viscera may also herniate. Kohn et al. defined hiatal herniation as “a protrusion of any abdominal structure other than the esophagus into the thoracic cavity through a widening of the hiatus.”⁹² Hiatal hernias are classified into four types, based primarily on the location of the gastroesophageal junction.⁹³ Type I hiatal hernias, also called “sliding hiatal hernias,” are the most common type and involve the gastroesophageal junction moving axially through the esophageal hiatus.⁹³

Type II hiatal hernias occur when the gastroesophageal junction remains in place and the gastric fundus rolls alongside the esophagus.⁹³ Type III hiatal hernias represent a combination of the two aforementioned types, with both the gastroesophageal junction and the fundus present.⁹³ Type IV hiatal hernias demonstrate the features of type III hernias, with the addition of another abdominal organ protruding into the hiatal hernia sac.⁹³ Type II–IV hiatal hernias are collectively referred to as “paraesophageal hernias,”⁹⁴ and are of clinical importance since such hernias may present with ischemia, volvulus, or obstruction.⁹⁴ About 90% of paraesophageal hernias are type III hiatal hernias, with the least common being type II.⁹²

The true prevalence of paraesophageal hernias is largely unknown due to the vagueness or absence of symptoms in many cases.⁹⁵ Recent reports estimate the incidence between 15% and 20% of the overall population.⁹⁶ Commonly, hiatal hernias are noted as an incidental finding during evaluation for some other condition.⁹⁵ The presence of hiatal hernias has been associated with conditions that increase intra-abdominal pressure, such as obesity, chronic obstructive pulmonary disease, and chronic constipation.⁹⁷

Symptoms of paraesophageal hernias are classified as obstructive and nonobstructive.⁹³ Nonobstructive symptoms may include symptoms associated with gastroesophageal reflux disease, whereas obstructive symptoms may include dysphagia, early satiety, regurgitation, epigastric pain, chest pain, and shortness of breath from mechanical compression or due to pneumonitis as a result of microaspirations.^93,96

Diagnosis

According to the guidelines published by the Society of American Gastrointestinal and Endoscopic Surgeons (SAGES) in April 2013,⁹² many imaging modalities may assist in the diagnosis of paraesophageal hernia. The first test in evaluation of paraesophageal hernia is typically a barium swallow.^91–93,95 Fluoroscopic assessment allows for the delineation of the esophagogastric anatomy and gives information about the motility of the esophagus.^92,93 Alternatively, diagnosis may be made by plain chest radiography, in which air-fluid levels or visceral gas may be noted.⁹² Computerized tomography scan may be preferred in emergent presentations of suspected acute gastric volvulus,⁹² or in chronic presentations when planning an operation for a large hiatal hernia to delineate all contents of the hernia sac.⁹³

Additional information about the esophageal and gastric pathology can be derived from EGD, in which the direct visualization of the mucosa can detect the presence of esophagitis, Barrett's esophagus, or of Cameron's ulcers, which are mucosal ulcerations at the level of the diaphragm.^93,94 Twenty-four-hour pH study and esophageal manometry are utilized selectively to assess the presence of pathologic reflux and to determine the function of the esophagus.^92–94 pH-metry can help correlate symptoms with the occurrence of reflux episodes, and esophageal manometry can rule out major motility abnormalities that may alter the surgical approach.^92,93

Management of Paraesophageal Hernias

The treatment of symptomatic paraesophageal hernias usually involves operation.⁹² Open paraesophageal hernia repairs were initially performed through the chest or the abdomen; however, minimally invasive techniques developed in the 1990s and shifted the approach to laparoscopic operations in most centers.⁹⁸ Köckerling et al⁹⁹ queried the “Herniamed Registry” and found 17,328 elective hiatal hernia repairs from 2010 to 2019. Of these, 96.4% were laparoscopic repairs. Similar results were shown when Swiss surgeons were surveyed on their preferred approach to type III hiatal hernias.¹⁰⁰ Gerdes et al¹⁰⁰ reported there is clear consensus among surgeons that hiatal hernia repair is best performed laparoscopically.

Various reports have also highlighted the improved outcomes of laparoscopic repair compared with open approaches. For example, Fullum et al¹⁰¹ analyzed the National Inpatient Sample dataset to demonstrate that laparoscopic repair of paraesophageal hernias is associated with lower mortality rates. Others have analyzed robotic surgery for the treatment of hiatal hernias. Warren et al¹⁰² reported that 114 patients who underwent robotic hiatal hernia repair had significantly shorter length of hospital stay compared with patients repaired laparoscopically, and lower rates of recurrence.¹⁰² More supporting data are expected in the near future.

Despite the clear consensus on the management of symptomatic paraesophageal hernias by surgery, there is no such consensus regarding the treatment of asymptomatic paraesophageal hernias.⁹² Initial reports by Hill¹⁰³ and Skinner and Helsey¹⁰⁴ reported high mortality of procedures performed on an emergent basis, and therefore suggested paraesophageal hernias should be surgically repaired once identified regardless of the presence or absence of symptoms. However, in the early 2000s, Stylopoulos et al¹⁰⁵ used a decision analysis model to demonstrate that elective paraesophageal hernia repairs for minimally symptomatic or asymptomatic patients were more likely than not to lead to worse outcomes compared to a watchful waiting (WW) strategy.

Similar results were demonstrated a decade later by Jung et al,¹⁰⁶ who used a similar statistical model to confirm that patients with asymptomatic paraesophageal hernia are better managed by WW. Oude Nijhuis et al,¹⁰⁷ in a single-center experience of 293 patients who were managed using WW, demonstrated 1.6% overall mortality, hernia-related complications in 8.1%, and only a 1.1% rate of emergency surgery. These investigators provided a case series supporting the use of WW as a safe option for asymptomatic or minimally symptomatic patients.

Implementation of techniques to reduce recurrence and reoperation

Laparoscopic repair of symptomatic paraesophageal hernias may be associated with radiographic hernia recurrence in 12%–42%.^108–110 Several factors have been associated with increased risk of recurrence, including obesity, chronicity of the hernia, and type of hernia.¹¹¹ Thus, surgeons have utilized adjunctive measures to reduce the recurrence rate; however, there is no clear consensus regarding best practice. According to the SAGES guidelines for the management of paraesophageal hernias, evidence supporting routine use of a fundoplication at the time of paraesophageal hernia repair is weak.⁹² Fundoplication can prevent postoperative reflux, but may contribute to postoperative dysphagia.¹¹² Likewise, existing data do not support a particular type of fundoplication. Andolfi et al,¹¹³ in a recent review of literature, found most surgeons prefer 360° fundoplication and reserve partial fundoplication for patients with esophageal dysmotility; however, the authors were unable to demonstrate a specific manometric profile guiding use of a partial fundoplication.

The SAGES guideline stressed the importance of surgeons ensuring an intra-abdominal esophageal length of 2–3 cm, given strong evidence doing so decreases hiatal hernia recurrence.⁹² If sufficient esophageal length cannot be achieved, an esophageal lengthening procedure may be used, most commonly a Collis gastroplasty.¹¹⁴ Recent reports demonstrate the safety of the Collis gastroplasty.^115,116 Weltz et al¹¹⁵ performed a retrospective analysis of 480 fundoplication patients and found addition of the lengthening procedure does not add to morbidity and mortality. Lu et al¹¹⁶ reported that patients who undergo Collis gastroplasty during fundoplication do not have an increased risk of postoperative dysphagia.

The SAGES guideline found there is strong evidence that use of mesh reinforcement over diaphragmatic crural repair is associated with lower hiatal hernia recurrence rates.⁹² The acceptance of this by practicing surgeons is demonstrated in reports by Gerdes et al,¹⁰⁰ who analyzed surgical trends in the treatment of type III hiatal hernias in Switzerland, and by Frantzides et al,¹¹⁷ who surveyed SAGES members. However, the type of mesh utilized was not uniform in these studies.^100,117 Superiority of mesh compared to traditional suture cruroplasty was additionally demonstrated in a meta-analysis performed by Memon et al,¹¹⁸ who found reoperation rate was significantly higher in nonmesh patients. Asti et al¹¹⁹ also found a significantly higher chance of operation failure at 12 months.

In addition, in a meta-analysis performed by Tam et al,¹²⁰ higher rates of recurrence were noted in the suture cruroplasty arm than the mesh-augmented arm. Mesh can be either absorbable or nonabsorbable. Nonabsorbable mesh has been associated with severe complications like esophageal erosion and dysphagia.¹²¹ Absorbable mesh, despite having reduced adhesion formation and facilitating revascularization with decreased inflammatory response, has been associated with increased rates of gas-bloat syndrome.¹²²

Use of pledgets for suture reinforcement is another area of investigation. Weitzendorfer et al,¹²³ in a recently published retrospective review, concluded that the use of pledgets is justified and safe. Kang et al¹²⁴ reported that despite their nonutilization of mesh, pledgets on cruroplasty sutures led to high satisfaction at long-term follow-up with a low recurrence rate of 6.7%.

Another adjunctive technique that may help improve durability of paraesophageal hernia repairs is the utilization of a gastrostomy tube for gastropexy. The latest guidelines published by SAGES support the use of gastrostomy with a strong level of evidence.⁹² A recent report, however, by Yheulon et al¹²⁵ using data from the American College of Surgeons National Surgical Quality Improvement Program (ACS-NSQIP), found that patients receiving a gastrostomy at the time of paraesophageal hernia repair had not only longer hospitalization but also more chance of preoperative factors such as malnutrition and respiratory disease. Clearly, a randomized controlled trial of use of gastrostomy at the time of paraesophageal hernia repair will be needed for firm conclusions to be drawn.

Paraesophageal Hernias with Suspected Functional Diagnoses

We have reviewed gastroparesis and paraesophageal hernias in isolation, but the purpose of this article is to discuss the possibility of both these conditions occurring concomitantly. In this section, we will elaborate on our historical and contemporary approach to this particular subgroup of patients with anatomic evidence of a paraesophageal hernia and symptoms and/or radiographic evidence of possible gastroparesis.

When a patient presents with upper GI symptoms, despite medical therapies, we initiate a complete anatomic and physiologic workup of the esophagus and stomach. As described in the above section on paraesophageal hernias, we typically start with anatomic assessment with an upper GI contrast study and an upper endoscopy. The size and type of any hiatal hernia, as well as mucosal evidence of gastroesophageal reflux or Cameron's ulcerations can be determined. Retained food on EGD may raise the suspicion of gastroparesis. In situations where the hiatal hernia is not significantly obstructive, and there is no severe esophagitis (Los Angeles Grade C or D), we obtain 24-hr pH impedance testing, preferably off PPIs. In most cases, we also obtain esophageal manometry. We also query patients about the presence of symptoms associated with gastroparesis, such as prominent regurgitation or emesis. If these situations, we obtain a solid-phase nuclear medicine gastric emptying study.

When there is a substantial paraesophageal hernia, many of the above studies may be less reliable than usual. A large hiatal hernia may alter esophageal transit, impact measures of relaxation at the lower esophageal sphincter due to external pressure, or delay gastric emptying. The surgeon will always form a surgical plan to address anatomic issues by repairing the paraesophageal hernia, but it is less clear in which cases functional derangements such as esophagogastric junction outflow obstruction (EGJOO) or gastroparesis also require intervention during the same anesthetic.

Regarding cases of paraesophageal hernias with possible EGJOO, we previously utilized preoperative endoscopic Botox injection into the lower esophageal sphincter as a means to predict which patients were likely to benefit from a cardiomyotomy at the time of hiatal hernia repair. We also performed posterior partial fundoplications to allow easier access for a staged myotomy if one was not performed at the primary operation. The development of POEM has opened up the possibility for a staged approach to EGJOO after paraesophageal hernia repair, with postoperative repeat esophageal manometry testing if dysphagia persists, and POEM if indicated. Recently, we have begun to explore use of endoscopic impedance planometry for intraoperative assessment of lower esophageal distensibility after the reduction of paraesophageal hernia, with consideration of concomitant cardiomyotomy in cases highly suspicious for intrinsic EGJOO.

For cases of paraesophageal hernias with possible gastroparesis, historically, we have implemented pyloroplasty for situations where the anatomy is not significantly obstructive and the half-emptying time on solid-phase gastric scintigraphy is >120 minutes. This approach added risk of leak at the pyloroplasty site and potential for dumping syndrome. Here again, advances in endoscopic interventions have changed our strategy.

Today, we address the anatomy first, with a laparoscopic repair of the paraesophageal hernia with the knowledge that staged POP is available if needed for persistent gastroparesis. To protect the paraesophageal hernia repair and fundoplication, we will add a percutaneous endoscopic gastrostomy for the dual benefits of gastropexy and perioperative venting to control nausea and bloating. Patients who have persistent symptoms of poor gastric emptying can have repeat EGD and gastric emptying assessment, and can be treated with POP before removal of the gastrostomy, if indicated. This staged approach allows reassessment after correction of the anatomy and elimination of reflux, and in most cases, the patient is spared pyloroplasty.

Conclusion

Mechanical obstruction caused by paraesophageal hernias makes the diagnosis of gastroparesis difficult or impossible. Therefore, we advocate for a staged approach based on our experience and the advent of endoscopic pyloric interventions. Such a strategy will spare many patients from an unnecessary pyloroplasty. We advise primary management of the paraesophageal hernia to relieve existing obstruction, with consideration of gastrostomy for perioperative control of nausea and bloating. If symptoms of delayed gastric emptying persist, then we employ the standard diagnostic and endoscopic therapies with confidence, with POP being our procedure of choice.

Footnotes

Authors' Contributions

D.N.V.: writing—original draft and writing—review and editing.

T.M.F.: conceptualization, writing—original draft, writing—review and editing, supervision, and project administration.

Disclosure Statement

No competing financial interests exist.

Funding Information

No funding was received for this article.

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