ESOPHAGEAL HIATAL HERNIA—Some Aspects of Surgical Treatment

Patients with esophageal hiatal hernia often have an array of distressing complaints and physical signs that are difficult to interpret. Physiologic and anatomic studies of the gastroesophageal area in the region of the esophageal hiatus of the diaphragm indicate the existence of a three-in-line sphincter group, consisting of the inferior esophageal constrictor, diaphragmatic pinchcock and cardioesophageal junction. These mechanisms, acting in unison, prevent regurgitation in normal persons.It also can be deduced from clinical, radiologic and experimental data that anatomic disturbances at the esophageal hiatus account for physiologic alterations. A reasonable explanation for the symptoms and signs of esophageal hiatal hernia can be made on the basis of the functional competence of the three-in-line sphincter mechanisms.     

The role of hiatus hernia in GERD

Increased esophageal acid exposure in gastroesophageal reflux disease has several potential causes, some related primarily to physiological dysfunction of the LES and others related to anatomic distortion of the gastroesophageal junction as occurs with hiatus hernia. One attractive feature of implicating hiatal hernias in the pathogenesis of reflux disease is that, like reflux disease, axial hernias become more common with age and obesity. However, the importance of hiatus hernia is obscured by imprecise definition and an all-or-none conceptualization that has led to wide variation in estimates of prevalence among normal or diseased populations. There are at least three potentially significant radiographic features of a hiatus hernia: axial length during distention, axial length at rest, and competence of the diaphragmatic hiatus. Although any or all of these features may be abnormal in a particular instance of hiatus hernia, each is of different functional significance. Grouping all abnormalities of the gastroesophageal junction as "hiatus hernia" without detailing the specifics of each case defies logic. Mechanistically, the gastroesophageal junction must protect against reflux both in static and dynamic conditions. During abrupt increases in intra-abdominal pressure, the crural diaphragm normally serves as a "second sphincter," and this mechanism is substantially impaired in individuals with a gaping hiatus. Large, non-reducing hernias also impair the process of esophageal emptying, thereby prolonging acid clearance time following a reflux event (especially while in the supine posture). These anatomically-determined functional impairments of the gastroesophageal junction lead to increased esophageal acid exposure. Thus, although hiatus hernia may or may not be an initiating factor at the inception of reflux disease, it clearly can act as a sustaining factor accounting for the frequently observed chronicity of the disease.     

Potentialities of computed tomography in the diagnosis of hiatal hernia

An analysis of the results of 98 studies has demonstrated the potentialities of X-ray computed tomography in the diagnosis of hiatal hernia (HH), provided the X-ray computed tomography (XCT) semiotics of HH. It has found that XCT may directly visualize and objectively evaluate anatomic structures, such as diagraphmatic crus and esophageal foremen. It has emphasized that when XCT of abdominal and thoracic organs is performed, it is necessary to include the areas of diagragmatic curs and esophageal foramen into the list of anatomic structures binding for visual assessment and characterization, which in combination with other studies will assist in the early diagnosis of hiatal hernia and eventually expand the potentialities of XCT to a greater extent.     

Full incorporation of Strattice(TM) Reconstructive Tissue Matrix in a reinforced hiatal hernia repair: a case report

ABSTRACT: INTRODUCTION: A non-cross-linked porcine acellular dermal matrix was used to reinforce an esophageal hiatal hernia repair. A second surgery was required 11 months later to repair a slipped Nissen; this allowed for examination of the hiatal hernia repair and showed the graft to be well vascularized and fully incorporated. CASE PRESENTATION: A 71-year-old Caucasian woman presented with substernal burning and significant dysphagia. An upper GI series revealed a type III complex paraesophageal hiatal hernia. She underwent laparoscopic surgery to repair a hiatal hernia that was reinforced with a xenograft (StratticeTM Reconstructive Tissue Matrix, LifeCell, Branchburg, NJ, USA) along with a Nissen fundoplication. A second surgery was required to repair a slipped Nissen; this allowed for examination of the hiatal repair and graft incorporation 11 months after the initial surgery. CONCLUSION: In this case, a porcine acellular dermal matrix was an effective tool to reinforce the crural hiatal hernia repair. The placement of the mesh and method of fixation are believed to be crucial to the success of the graft. It was found to be well vascularized 11 months after the original placement with no signs of erosion, stricture, or infection. Further studies and longterm follow-up are required to support the findings of this case report.     

Current Advancement on the Dynamic Mechanism of Gastroesophageal Reflux Disease

Gastroesophageal reflux disease (GERD) is a common clinical disease associated with upper gastrointestinal motility disorders. Recently, with improvements in living standards and changes in lifestyle and dietary habits, the incidence of GERD has been increasing yearly. However, the mechanism of GERD has not been fully elucidated due to its complex pathogenesis, and this had led to unsatisfactory therapeutic outcomes. Currently, the occurrence and development of GERD involve multiple factors. Its pathogenesis is mainly thought to be related to factors, such as lower esophageal sphincter pressure, transient lower esophageal sphincter relaxation, crural diaphragmatic dysfunction, hiatus hernia, and impaired esophageal clearance. Therefore, explaining the pathogenesis of GERD more clearly and systematically, exploring potential and effective therapeutic targets, and choosing the best treatment methods have gradually become the focus of scholars'' attention. Herein, we reviewed current advancements in the dynamic mechanism of GERD to better counsel patients on possible treatment options.     

The problem of the acquired short esophagus; report of 18 patients

A shortened esophagus is probably acquired, rather than congenital, in the great majority of cases. The process by which the shortening develops, as described by Allison and his coworkers, begins with esophageal hiatal hernia, followed by esophagitis caused by the irritation of acids from the stomach, then recurrent ulceration and healing which forms scar tissue which little by little shortens the esophagus. Obesity and relaxation of the supporting musculotendinous structures which accompany advancing years probably are contributory factors in production of esophageal hiatal hernia. Fifteen of a series of 18 patients noted the onset of symptoms on or after the age of 45. Roentgen examination of the esophagus and stomach is indispensable in establishing a diagnosis of acquired short esophagus. Esophagoscopic examination is even more important. In some cases endoscopic differentiation between acute inflammation and carcinoma is difficult. In such circumstances examination of a biopsy specimen taken from the gastric mucosa immediately distal to the area of inflammation or stricture may be helpful. Results in eight patients with advanced esophageal shortening and stricture who were treated conservatively indicate that this should be tried before surgical treatment is considered. For patients with esophageal hiatal hernia accompanied by shortening of the esophagus that is just beginning to produce symptoms, early repair is indicated, since the condition is progressive and the surgical problem is much simpler in the early stages.     

THE PROBLEM OF THE ACQUIRED SHORT ESOPHAGUS—Report of 18 Patients

A shortened esophagus is probably acquired, rather than congenital, in the great majority of cases. The process by which the shortening develops, as described by Allison and his coworkers, begins with esophageal hiatal hernia, followed by esophagitis caused by the irritation of acids from the stomach, then recurrent ulceration and healing which forms scar tissue which little by little shortens the esophagus.Obesity and relaxation of the supporting musculotendinous structures which accompany advancing years probably are contributory factors in production of esophageal hiatal hernia. Fifteen of a series of 18 patients noted the onset of symptoms on or after the age of 45.Roentgen examination of the esophagus and stomach is indispensable in establishing a diagnosis of acquired short esophagus. Esophagoscopic examination is even more important. In some cases endoscopic differentiation between acute inflammation and carcinoma is difficult. In such circumstances examination of a biopsy specimen taken from the gastric mucosa immediately distal to the area of inflammation or stricture may be helpful.Results in eight patients with advanced esophageal shortening and stricture who were treated conservatively indicate that this should be tried before surgical treatment is considered. For patients with esophageal hiatal hernia accompanied by shortening of the esophagus that is just beginning to produce symptoms, early repair is indicated, since the condition is progressive and the surgical problem is much simpler in the early stages.     

The mechanical basis of impaired esophageal emptying postfundoplication

Fundoplication (FP) efficacy is a trade-off between protection against reflux and postoperative dysphagia from the surgically altered mechanical balance within the esophagogastric segment. The purpose of the study was to contrast quantitatively the mechanical balance between normal and post-FP esophageal emptying. Physiological data were combined with mathematical models based on the laws of mechanics. Seven normal controls (NC) and seven post-FP patients underwent concurrent manometry and fluoroscopy. Temporal changes in geometry of the distal bolus cavity and hiatal canal, and cavity-driving pressure were quantified during emptying. Mathematical models were developed to couple cavity pressure to hiatal geometry and esophageal emptying and to determine cavity muscle tone. We found that the average length of the hiatal canal post-FP was twice that of NC; reduction of hiatal radius was not significant. All esophageal emptying events post-FP were incomplete (51% retention); there was no significant difference in the period of emptying between NC and post-FP, and average emptying rates were 40% lower post-FP. The model predicted three distinct phases during esophageal emptying: hiatal opening (phase I), a quasi-steady period (phase II), and final emptying (phase III). A rapid increase in muscle tone and driving pressure forced normal hiatal opening. Post-FP there was a severe impairment of cavity muscle tone causing deficient hiatal opening and flow and bolus retention. We conclude that impaired esophageal emptying post-FP follows from the inability of distal esophageal muscle to generate necessary tone rapidly. Immobilization of the intrinsic sphincter by the surgical procedure may contribute to this deficiency, impaired emptying, and possibly, dysphagia.     

Esophagogastric junction distensibility: a factor contributing to sphincter incompetence

To quantify the effect of hiatus hernia (HH) on esophagogastric junction (EGJ) distensibility, eight normal subjects and nine gastroesophageal reflux disease (GERD) patients with HH were studied with concurrent manometry, fluoroscopy, and stepwise controlled barostatic distention of the EGJ. The minimal barostatic pressure required to open the EGJ during the interswallow period was determined. Thereafter, barium swallows were imaged in 5-mmHg increments of intrabag pressure. EGJ diameter and length were measured at each pressure during deglutitive relaxation. The EGJ opening diameter was greater in hernia patients compared with normal subjects during deglutitive relaxation at all pressures, and EGJ length was 23% shorter. EGJ opening pressure among hernia patients was lower than normal subjects during the interswallow period. In conclusion, the EGJ of GERD patients with HH was more distensible and shorter than normal subjects. These findings partially explain why HH patients are predisposed to reflux by mechanisms other than transient lower esophageal sphincter relaxations, sustain greater volumes of refluxate, and have a reduced ability to discriminate gas from liquid reflux.     

Evaluation of 100 Esophageal Motility Studies at a University Medical Center

100 esophageal motility studies on 88 consecutive patients referred to the University of California Medical Center were analyzed. Diagnoses of achalasia, diffuse spasm of the esophagus, scleroderma, hiatal hernia and other conditions were made from the motility tracings. The motility tests have been found to be most helpful in differentiating various disorders of swallowing and thoracic pain of unknown cause.     

SURGICAL TREATMENT OF ESOPHAGEAL HIATUS HERNIA BY TRANSTHORACIC HERNIOTOMY: A PRELIMINARY REPORT

In view of the extensive operation required for repair of hiatus hernia by transthoracic or abdominal approach, herniotomy was done in three cases. Objectives were to (a) widen the esophageal hiatus, (b) remove the hernial sac, (c) cut the structures of the omentum and lesser curvature so that the stomach would lie flat in the chest, and (d) fix the stomach at the new level.After the operation, all three patients were free of the symptoms of indigestion of which they had previously complained.     

Surgical treatment of esophageal hiatus hernia by transthoracic herniotomy; a preliminary report

In view of the extensive operation required for repair of hiatus hernia by transthoracic or abdominal approach, herniotomy was done in three cases. Objectives were to (a) widen the esophageal hiatus, (b) remove the hernial sac, (c) cut the structures of the omentum and lesser curvature so that the stomach would lie flat in the chest, and (d) fix the stomach at the new level. After the operation, all three patients were free of the symptoms of indigestion of which they had previously complained.     

Studies of abnormalities of the lower esophageal sphincter during esophageal emptying based on a fully coupled bolus–esophageal–gastric model

The aim of this work was to develop a fully coupled bolus–esophageal–gastric model based on the immersed boundary–finite element method to study the process of esophageal emptying across the esophagogastric junction (EGJ). The model included an esophageal segment, an ellipsoid-shaped stomach, a bolus, and a simple model of the passive and active sphincteric functions of the lower esophageal sphincter (LES). We conducted three sets of case studies: (1) the effect of a non-relaxing LES; (2) the influence of the tissue anisotropy in the form of asymmetrical right- and left-sided compliance of the LES segment; and (3) the influence of LES and gastric wall stiffness on bulge formation of the distal esophageal wall. We found that a non-relaxing LES caused sustained high wall stress along the LES segment and obstruction of bolus emptying. From the simulations of tissue anisotropy, we found that the weaker side (i.e., more compliant) of the LES segment sustained greater deformation, greater wall shear stress, and a greater high-pressure load during bolus transit. In the third set of studies, we found that a right-sided bulge in the esophageal wall tends to develop during esophageal emptying when LES stiffness was decreased or gastric wall stiffness was increased. Hence, the bulge may be partly due to the asymmetric configuration of the gastric wall with respect to the esophageal tube. Together, the observations from these simulations provide insight into the genesis of epiphrenic diverticula, a complication observed with esophageal motility disorders. Future work, with additional layers of complexity to the model, will delve into the mechanics of gastroesophageal reflux and the effects of hiatus hernia on EGJ function.     

Gastritis of the Herniated Stomach in Patients with Esophageal Hiatus Hernia

Seven illustrative cases of gastritis of the herniated stomach in patients with sliding esophageal hiatus hernia are reported. Five had superficial gastritis (three mild, one moderate and one severe); two had atrophic gastritis. Gastritis was present in two patients whose mucosa appeared normal at esophagoscopy. Interstitial hemorrhage into the lamina propria was present in four of the seven biopsy specimens. The possibility that interstitial hemorrhage may be related to the development of gastric erosions is considered. The pathogenesis of this form of gastritis is discussed.     

FAMILIAL DIAPHRAGMATIC HERNIA

Familial occurrence of diaphragmatic hiatal hernia has been reported often. Herein reported is a family in which eight of eleven children had hiatal hernia.Hiatal hernia must be considered as a possible etiological factor in all upper abdominal, cardiac or respiratory disturbances from infancy to senility. The lesion may be present in a patient who has none of the symptoms usually associated with such defects.Conservative treatment is indicated unless serious symptoms definitely referred to the hernia are present and not adequately controlled by conservative means.     

Familial diaphragmatic hernia

Familial occurrence of diaphragmatic hiatal hernia has been reported often. Herein reported is a family in which eight of eleven children had hiatal hernia. Hiatal hernia must be considered as a possible etiological factor in all upper abdominal, cardiac or respiratory disturbances from infancy to senility. The lesion may be present in a patient who has none of the symptoms usually associated with such defects.Conservative treatment is indicated unless serious symptoms definitely referred to the hernia are present and not adequately controlled by conservative means.     

Recurrent achalasia in a child with Williams-Beuren syndrome

Williams-Beuren syndrome is a multysistem genetic disorder caused by the 1.6Mb hemizygous deletion involving the elastin gene in the region q11.23 of chromosome 7. The phenotype of Williams-Beuren syndrome is extremelly variable but the most common findings include cardiovascular disease, distinctive facies, mental retardation, a specific congitive profile, endocrine abnormalities, growth retardation and connective tissue abnormalities. Although gastrointestinal difficulties are one of the most constant and prominent finding of the syndrome, including gastro-esophageal reflux (GER), poor suckling, vomiting, constipation, prolonged colic, rectal prolapse, inguinal, umbilical and hiatal hernia, there have been no reports of achalasia in association with Williams-Beuren syndrome in the literature. We present the case of a boy with Williams-Beuren syndrome, achalasia and recurrent postoperative stenosis of the cardia. After Heller myotomy, the boy developed severe restenosis of the cardia with abundant adhesions which repeated after every treatment, five times in periods shorter than one month. Eventually, he developed GER, errosive gastritis and hiatal hernia which led to severe malnutrition and failure to thrive. Although the genetic defect causing Williams-Beuren syndrome might not be the direct cause of achalasia we suggest that the frequent development of severe restenosis of cardia due to tight adhesions could be the consequence of elastin gene haploinsufficiency and altered structure and function of elastic fibers in esophageal connective tissue. This case highlights the importance of early diagnosis of esophageal motor disorders in childhood which should be included in the differential diagnosis when a child with Williams-Beuren syndrome presents with dysphagia and/or regurgitation.     

Chronic cough and gastroesophageal reflux.

We reviewed the charts of 20 patients with chronic cough of unknown cause who had been referred to a tertiary care respiratory centre from 1980 to 1984 to determine whether gastroesophageal reflux (GER) was a contributing factor. Fifteen of the patients complained of symptoms suggestive of GER: radiologic investigation of the upper gastrointestinal tract revealed hiatus hernia and GER in four, hiatus hernia alone in three, GER alone in two, decreased esophageal peristalsis in one and normal findings in four. Fibreoptic bronchoscopy in the four former smokers and one nonsmoker showed diffuse mucosal erythema. A chest x-ray film in one patient showed an infiltrate at the base of the right lung; transbronchial biopsy revealed vegetable material, which confirmed pulmonary aspiration. A 3-month course of medical antireflux treatment (dietary and lifestyle changes, elevation of the head of the bed and administration of cimetidine, antacid and metoclopramide) relieved the chronic cough in 14 of the 20 patients. Of the remaining patients one was lost to follow-up and five had GER confirmed by means of esophagoscopy, esophageal motility testing and long-term intraesophageal pH monitoring; four of the five patients underwent fundoplication and were asymptomatic 3 months after surgery. Antireflux therapy should be considered in patients with chronic cough when other causes have been ruled out, even if there are no GER symptoms. If the treatment fails, full investigation for GER is recommended; if GER is confirmed, surgery should be considered.     

Defining GERD

"It is not the death of GERD that I seek, but that it turns from its evil ways and follows the path of righteousness." The reflux world is fully aware of what GERD is and what GERD does. What the world does not know, however, is the answer to the most important yet least asked question surrounding GERD's raison-d'etre: Why is GERD here and why do we have it? What GERD is: abnormal gastric reflux into the esophagus that causes any type of mischief. What GERD does: causes discomfort and/or pain with or without destroying the mucosa; causes stricture or stenosis, preventing food from being swallowed; sets the stage for the development of esophageal adenocarcinoma; invades the surrounding lands to harass the peaceful oropharyngeal, laryngeal and broncho-pulmonary territories; reminds us that we are not only human, but that we are dust and ashes. Why GERD is here: We propose three separate and distinct etiologies of GERD, and we offer the following three hypotheses to explain why, after 1.5 million years of standing erect, we have evolved into a species (specifically Homosapiens sapiens) that is destined to live with the scourge of GERD. Hypothesis 1: congenital. The antireflux barrier, comprising the smooth-muscled lower esophageal sphincter, the skeletal-muscled right crural diaphragm and the phreno-esophageal ligament does not completely develop due to a developmental anomaly or incomplete gestation. Hypothesis 2: acute trauma: The antireflux barrier in adults suffering acute traumatic injury to the abdomen or chest is permanently disrupted by unexpected forces, such as motor vehicle accidents (with steering wheel crush impact), blows to the abdomen (from activities such as boxing, etc.), heavy lifting or moving (e.g., pianos, refrigerators) or stress positions (e.g., hand stands on parallel gym bars). The trauma creates a hiatal hernia that renders the antireflux mechanism useless and incapable of preventing GERD. Hypothesis 3: chronic trauma: The antireflux barrier in children and adults is gradually weakened over time as a result of chronic straining to defecate and straining in an unphysiologic position, both of which stem from our modern day habits of eating a low-fiber diet and living on the high-seated toilet. We suggest that the chronic traumatic hiatal hernia is (a) the cause of more than 90 percent of the GERD that stalks the Western world; (b) is a direct result of abandoning the popular and worldwide practice of squatting to socialize, eat and defecate; and (c) is our just reward for adopting the "civilized" high sitting position on chairs and modern toilets.     

ENDOSCOPY IN HERNIA AT THE ESOPHAGEAL HIATUS

Endoscopy is useful for confirming diagnosis of hiatal hernia as made by x-ray examination, for establishing the diagnosis when x-ray examinations do not disclose the herniation, and for observation of resultant abnormalities in the affected area. The authors'' experience with gastroscopy and esophagoscopy in hiatal hernia is reported and the techniques and usual findings in these procedures are summarized.