The effect of hiatus hernia on gastro-oesophageal junction pressure.
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BACKGROUND: Hiatus hernia and lower oesophageal sphincter hypotension are often viewed as opposing hypotheses for gastro-oesophageal junction incompetence. AIMS: To examine the interaction between hiatus hernia and lower oesophageal sphincter hypotension. METHODS: In seven normal subjects and seven patients with hiatus hernia, the squamocolumnar junction and intragastric margin of the gastro-oesophageal junction were marked with endoscopically placed clips. Axial and radial characteristics of the gastro-oesophageal junction high pressure zone were mapped relative to the hiatus and clips during concurrent fluoroscopy and manometry. Responses to inspiration and abdominal compression were also analysed. RESULTS: In normal individuals the squamocolumnar junction was 0.5 cm below the hiatus and the gastro-oesophageal junction high pressure zone extended 1.1 cm distal to that. In those with hiatus hernia, the gastro-oesophageal junction high pressure zone had two discrete segments, one proximal to the squamocolumnar junction and one distal, attributable to the extrinsic compression within the hiatal canal. Inspiration and abdominal compression mainly augmented the distal one. Simulation of hernia reduction by algebraically summing the proximal segment pressures with the hiatal canal pressures restored normal maximal pressure, radial asymmetry, and dynamic responses of the gastro-oesophageal junction. CONCLUSIONS: Hiatus hernia reduces lower oesophageal sphincter pressure and alters its dynamic responsiveness by spatially separating pressure components derived from the intrinsic lower oesophageal sphincter and the extrinsic compression of the oesophagus within the hiatal canal. (+info)
Simultaneous pyloric and colonic obstruction associated with hiatus hernia in a weightlifter: a case report.
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Hiatus hernia is usually attributed to conditions that cause a chronic increase in intra-abdominal pressure such as multiple pregnancies and obesity. A 30-year-old man, a weightlifter, had a massive hiatus hernia causing both high and low gastrointestinal obstruction but no involvement of the gastroesophageal junction or fundus. The onset of the obstruction is attributed to an extreme increase in intra-abdominal pressure caused by the action of lifting weights. (+info)
Reflux esophagitis and its relationship to hiatal hernia.
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We performed this study to evaluate the prevalence of reflux esophagitis and/or hiatal hernia in patients referred to a medical center and to examine the relationship between endoscopic reflux esophagitis and hiatal hernia. The study was carried out in 1,010 patients referred to Yong Dong Severance Hospital for upper gastrointestinal endoscopy because of symptoms related to the gastrointestinal tract from September 1994 to March 1996. The presence of hiatal hernia was defined as a circular extension of the gastric mucosa of 2 cm or more above the diaphragmatic hiatus. Reflux esophagitis was found in 5.3% of patients, hiatal hernia in 4.1%, duodenal ulcer in 7.2% and gastric ulcer in 8.2%. The prevalence rates of reflux esophagitis and hiatal hernia in males were significantly higher than those in females. Thirty-two percent of patients with reflux esophagitis had hiatal hernia. In patients without reflux esophagitis, hiatal hernia was found in only 2.5% (p<0.01). There was no significant association between the presence of hiatal hernia and the degree of esophagitis on endoscopy. Duodenal ulcer was the second most common endoscopic abnormality found in patients with reflux esophagitis. The prevalence rate of reflux esophagitis and/or hiatal hernia at a medical center is relatively low compared to peptic ulcer disease and other reports from the Western countries. Our study confirms the close association between reflux esophagitis and hiatal hernia. (+info)
Pulmonary embolism following laparoscopic antireflux surgery: a case report and review of the literature.
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Deep venous thrombosis and pulmonary embolism are concerning causes of morbidity and mortality in patients undergoing general surgical procedures. Laparoscopic surgery has gained rapid acceptance in the past several years and is now a commonly performed procedure by most general surgeons. Multiple anecdotal reports of pulmonary embolism following laparoscopic cholecystectomy have been reported, but the true incidence of deep venous thrombosis and pulmonary embolism in patients undergoing laparoscopic surgery is not known. We present a case of pulmonary embolism following laparoscopic repair of paraesophageal hernia. The literature is then reviewed regarding the incidence of pulmonary embolism following laparoscopic surgery, the mechanism of deep venous thrombosis formation, and the recommendations for deep venous thrombosis prophylaxis in patients undergoing laparoscopic procedures. (+info)
Familial hiatal hernia in a large five generation family confirming true autosomal dominant inheritance.
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BACKGROUND: Familial hiatal hernia has only rarely been documented. AIMS: To describe the pattern of inheritance of familial hiatal hernia within an affected family. SUBJECTS: Thirty eight members of a family pedigree across five generations. METHODS: All family members were interviewed and investigated by barium meal for evidence of a hiatal hernia. RESULTS: Twenty three of 38 family members had radiological evidence of a hiatal hernia. No individual with a hiatal hernia was born to unaffected parents. In one case direct male to male transmission was shown. CONCLUSIONS: Familial inheritance of hiatal hernia does occur. Evidence of direct male to male transmission points to an autosomal dominant mode of inheritance. (+info)
Laparoscopic fundoplication failures: patterns of failure and response to fundoplication revision.
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OBJECTIVE: To determine rates and mechanisms of failure in 857 consecutive patients undergoing laparoscopic fundoplication for gastroesophageal reflux disease or paraesophageal hernia (1991-1998), and compare this population with 100 consecutive patients undergoing fundoplication revision (laparoscopic and open) at the authors' institution during the same period. SUMMARY BACKGROUND DATA: Gastroesophageal fundoplication performed through a laparotomy or thoracotomy has a failure rate of 9% to 30% and requires revision in most of the patients who have recurrent or new foregut symptoms. The frequency and patterns of failure of laparoscopic fundoplication have not been well studied. METHODS: All patients undergoing fundoplication revision were included in this study. Symptom severity was scored before and after surgery by patients on a 4-point scale. Evaluation of patients included esophagogastroscopy, barium swallow, esophageal motility, 24-hour ambulatory pH, and gastric emptying studies. Statistical analysis was performed with multiple chi-square analyses, Fisher exact test, and analysis of variance. RESULTS: Laparoscopic fundoplication was performed in 758 patients for gastroesophageal reflux disease and in 99 for paraesophageal hernia. Median follow-up was 2.5 years. Thirty-one patients (3.5%) have undergone revision for fundoplication failure. The mechanism of failure was transdiaphragmatic herniation of the fundoplication in 26 patients (84%). In 40 patients referred from other institutions, after laparoscopic fundoplication, only 10 (25%) had transdiaphragmatic migration (p < 0.01); a slipped or misplaced fundoplication occurred in 13 patients (32%), and a twisted fundoplication in 12 patients (30%). The failure mechanisms of open fundoplication (29 patients) followed patterns previously described. Fundoplication revision procedures were initiated laparoscopically in 65 patients, with six conversions (8%). The morbidity rate was 4% in laparoscopic procedures and 9% in open ones. There was one death, from aspiration and adult respiratory distress syndrome after open fundoplication. A year or more after revision operation, heartburn, chest pain, and dysphagia were rare or absent in 88%, 78%, and 91%, respectively, after laparoscopic revision, and were rare or absent in 91%, 83%, and 70%, respectively, after open revision, but 11 patients ultimately required additional operations for continued or recurrent symptoms, 3 after open revision (17%), and 8 after laparoscopic fundoplication (11%). CONCLUSIONS: Laparoscopic fundoplication failure is infrequent in experienced hands; the rate may be further reduced by extensive esophageal mobilization, secure diaphragmatic closure, esophageal lengthening (applied selectively), and avoidance of events leading to increased intraabdominal pressure. When revision is required, laparoscopic access may be used successfully by the laparoscopically experienced esophageal surgeon. (+info)
Gastric volvulus in childhood.
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Gastric volvulus is an uncommon condition more so in the paediatric age group. The cause of gastric volvulus may be idiopathic or secondary to various congenital or acquired conditions. In this short series of three patients, one had volvulus which was due to ligamentous laxity and mobile spleen, second had congenital postero-lateral diaphragmatic defect and the third had hiatus hernia. (+info)
Defining GERD.
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"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. (+info)