食管功能检查的临床应用

目的 探讨食管腔内压力测定和２４小时食管ｐＨ监测在临床的应用价值。方法 用上述食管功能检查方法对：（１）胃食管反流性疾病采用内、外科不同治疗方法的比较：（２）鉴别食管源性胸痛;（３）评价抗酸药物的作用;以及（４）胆囊切除术后胃食管功能监测等。结果 通过食管功能检查完成了对上述四项内容的验证和评价,取得了良好的效果。结论 食管腔内压力测定和２４小时食管ｐＨ监测是诊断食管功能性疾病是最敏感和特异的检查     

Duodenogastric and gastroesophageal bile reflux

This study reviews current data regarding duodenogastric and gastroesophageal bile reflux-pathophysiology, clinical presentation, methods of diagnosis (namely, 24-hour intraluminal bile monitoring) and therapeutic management. Duodenogastric reflux (DGR) consists of retrograde passage of alkaline duodenal contents into the stomach; it may occur due to antroduodenal motility disorder (primary DGR) or may arise following surgical alteration of gastoduodenal anatomy or because of biliary pathology (secondary DGR). Pathologic DGR may generate symptoms of epigastric pain, nausea, and bilious vomiting. In patients with concomitant gastroesophageal reflux, the backwash of duodenal content into the lower esophagus can cause mixed (alkaline and acid) reflux esophagitis, and lead, in turn, to esophageal mucosal damage such as Barrett's metaplasia and adenocarcinoma. The treatment of DGR is difficult, non-specific, and relatively ineffective in controlling symptoms. Proton pump inhibitors decrease the upstream effects of DGR on the esophagus by decreasing the volume of secretions; promotility agents diminish gastric exposure to duodenal secretions by improving gastric emptying. In patients with severe reflux resistant to medical therapy, a duodenal diversion operation such as the duodenal switch procedure may be indicated.     

Gastric banding interferes with esophageal motility and gastroesophageal reflux

BACKGROUND: Gastroesophageal reflux and progressive esophageal dilatation can develop after gastric banding (GB). HYPOTHESIS: Gastric banding may interfere with esophageal motility, enhance reflux, or promote esophageal dilatation. DESIGN: Before-after trial in patients undergoing GB. SETTING: University teaching hospital. PATIENTS AND METHODS: Between January 1999 and August 2002, 43 patients undergoing laparoscopic GB for morbid obesity underwent upper gastrointestinal endoscopy, 24-hour pH monitoring, and stationary esophageal manometry before GB and between 6 and 18 months postoperatively. MAIN OUTCOME MEASURES: Reflux symptoms, endoscopic esophagitis, pressures measured at manometry, esophageal acid exposure. RESULTS: There was no difference in the prevalence of reflux symptoms or esophagitis before and after GB. The lower esophageal sphincter was unaffected by surgery, but contractions in the lower esophagus weakened after GB, in correlation with preoperative values. There was a trend toward more postoperative nonspecific motility disorders. Esophageal acid exposure tended to decrease after GB, with fewer reflux episodes. A few patients developed massive postoperative reflux. There was no clear correlation between preoperative testing and postoperative esophageal acid exposure, although patients with abnormal preoperative acid exposure tended to maintain high values after GB. CONCLUSIONS: Postoperative esophageal dysmotility and gastroesophageal reflux are not uncommon after GB. Preoperative testing should be done routinely. Low amplitude of contraction in the lower esophagus and increased esophageal acid exposure should be regarded as contraindications to GB. Patients with such findings should be offered an alternative procedure, such as Roux-en-Y gastric bypass.     

Spontaneous rupture and functional state of the esophagus.

Esophageal function was investigated after 1 to 8 years in five consecutive patients surviving spontaneous esophageal rupture (Boerhaave's syndrome) and treated by suturation. Only one patient was symptom free and had almost normal esophageal function as judged by manometry, 24-hour pH monitoring, endoscopy, and barium swallow. In the other four patients reflux symptoms and a severe functional disturbance of the esophagus were observed. In four patients the manometry revealed a lack of propulsive peristaltic movements and esophageal muscular incoordination (particularly in the upper part of the esophagus) closely mimicking those seen in the nonspecific esophageal motility disorder. In 24-hour intraesophageal pH monitoring a pathologic gastroesophageal reflux with long-lasting single reflux periods was observed, suggesting poor esophageal clearance. Also endoscopic and histologic signs of reflux esophagitis were seen in the same four patients. In contrast, lower esophageal sphincter pressure was normal in all five survivors. It is concluded that patients with spontaneous esophageal rupture have a severe disturbance of esophageal motility. The concomitant reflux esophagitis may be caused primarily by the esophageal motility disturbance, which may also contribute to the origin of the rupture.     

食管动力学及24小时食管pH监测在胸痛诊断中的意义

目的探讨食管动力学、24小时食管pH及24小时动态心电图监测对反复发作性胸痛的诊断价值. 方法对46例反复发作胸痛的患者进行食管动力学检测、24小时食管pH及24小时动态心电图监测,根据检查结果,给予相应治疗,并观察近期效果.结果 46例患者中发现非特异性食管功能障碍24例,其中伴有胃食管反流14例、心肌缺血4例;贲门失弛缓症5例,其中伴有胃食管反流1例;弥漫性食管痉挛4例,其中伴有胃食管反流4例、心肌缺血2例;胡桃夹食管(nutcracker esophagus)1例.结论对反复发作性胸痛患者联合食管测压、24小时食管pH和24小时动态心电图监测有助于食管源性及心源性胸痛的诊断,而且对其鉴别诊断亦有帮助.     

Metaplastic columnar mucosa in the cervical esophagus after esophagectomy

OBJECTIVE: To evaluate the pathogenesis of metaplastic processes within the esophagus using a human model in which the exact duration of reflux was known. SUMMARY BACKGROUND DATA: The pathogenesis of Barrett's esophagus (BE) is incompletely understood. Patients undergoing esophagectomy and gastric tube reconstruction represent a good model for studying the pathophysiology of columnar cell metaplasia of the human esophagus because the cervical esophagus is rarely or never exposed to gastric contents before the surgical procedure. METHODS: Thirty-two patients underwent manometry, simultaneous 24-hour pH and bilirubin monitoring, and endoscopy with biopsy 3 to 10.4 years after esophagectomy. The presence of columnar mucosa in the cervical esophagus was confirmed on histologic examination. The findings on endoscopy and histology were related to clinical data and the results of pH and bilirubin monitoring 1 cm proximal to the esophagogastrostomy. RESULTS: Fifteen (46.9%) of the 32 patients had metaplastic columnar mucosa within their cervical esophagus. Metaplasia was significantly more common in patients with a preoperative diagnosis of BE. The length of metaplastic mucosa correlated significantly with the degree of esophageal acid exposure, but the presence of abnormal bilirubin exposure was unrelated to the presence of metaplasia. The prevalence of metaplasia did not change with increasing time. Intestinal metaplasia was found within the columnar-lined segment in three patients 8.5, 9.5, and 10.4 years after esophagectomy. All patients with intestinal metaplasia had abnormal exposure of both acid and bilirubin, but the presence of combined reflux was not significantly higher in these patients compared with patients with nonintestinalized segments of columnar mucosa. CONCLUSIONS: Esophageal columnar metaplasia is a common complication after gastric pull-up esophagectomy. Metaplasia is more likely to develop in patients with previous BE than other patients. Metaplasia develops in response to squamous epithelial injury in predisposed individuals.     

Mixed reflux of gastric and duodenal juices is more harmful to the esophagus than gastric juice alone. The need for surgical therapy re-emphasized.

OBJECTIVE: The author's goal was to determine the role of duodenal components in the development of complications of gastroesophageal reflux disease. SUMMARY AND BACKGROUND DATA: There is a disturbing increase in the prevalence of complications, specifically the development of Barrett's esophagus among patients with gastroesophageal reflux disease. Earlier studies using pH monitoring and aspiration techniques have shown that increased esophageal exposure to fluid with a pH above 7, that is, of potential duodenal origin, may be an important factor in this phenomenon. METHODS: The presence of duodenal content in the esophagus was studied in 53 patients with gastroesophageal reflux disease confirmed by 24-hour pH monitoring. A portable spectrophotometer (Bilitec 2000, Synectics, Inc.) with a fiberoptic probe was used to measure intraluminal bilirubin as a marker for duodenal juice in the esophagus. Normal values for bilirubin monitoring were established for 25 healthy subjects. In a subgroup of 22 patients, a custom-made program was used to correlate simultaneous pH and bilirubin absorbance readings. RESULTS: Fifty-eight percent of patients were found to have increased esophageal exposure to gastric and duodenal juices. The degree of mucosal damage increased when duodenal juice was refluxed into the esophagus, in that patients with Barrett's metaplasia (n = 27) had a significantly higher prevalence of abnormal esophageal bilirubin exposure than did those with erosive esophagitis (n = 10) or with no injury (n = 16). They also had a greater esophageal bilirubin exposure compared with patients without Barrett's changes, with or without esophagitis. The correlation of pH and bilirubin monitoring showed that the majority (87%) of esophageal bilirubin exposure occurred when the pH of the esophagus was between 4 and 7. CONCLUSIONS: Reflux of duodenal juice in gastroesophageal reflux disease is more common than pH studies alone would suggest. The combined reflux of gastric and duodenal juices causes severe esophageal mucosal damage. The vast majority of duodenal reflux occurs at a pH range of 4 to 7, at which bile acids, the major component of duodenal juice, are capable of damaging the esophageal mucosa.     

Inflammation and specialized intestinal metaplasia of cardiac mucosa is a manifestation of gastroesophageal reflux disease.

OBJECTIVE: The purpose of the study was to test the hypothesis that cardiac mucosa, carditis, and specialized intestinal metaplasia at an endoscopically normal-appearing cardia are manifestations of gastroesophageal reflux disease. SUMMARY BACKGROUND DATA: In the absence of esophageal mucosal injury, the diagnosis of gastroesophageal reflux disease currently rests on 24-hour pH monitoring. Histologic examination of the esophagus is not useful. The recent identification of specialized intestinal metaplasia at the cardia, along with the observation that it occurs in inflamed cardiac mucosa, led the authors to focus on the type and condition of the mucosa at the gastroesophageal junction and its relation to gastroesophageal reflux disease. METHODS: Three hundred thirty-four consecutive patients with symptoms of foregut disease, no evidence of columnar-lined esophagus, and no history of gastric or esophageal surgery were evaluated by 1) endoscopic biopsies above, at, and below the gastroesophageal junction; 2) esophageal motility; and 3) 24-hour esophageal pH monitoring. The patients were divided into groups depending on the histologic presence of cardiac epithelium with and without inflammation or associated intestinal metaplasia. Markers of gastroesophageal reflux disease were compared between groups (i.e., lower esophageal sphincter characteristics, esophageal acid exposure, the presence of endoscopic erosive esophagitis, and hiatal hernia). RESULTS: When cardiac epithelium was found, it was inflamed in 96% of the patients. The presence of cardiac epithelium and carditis was associated with deterioration of lower esophageal sphincter characteristics and increased esophageal acid exposure. Esophagitis occurred more commonly in patients with carditis whose sphincter, on manometry, was structurally defective. Specialized intestinal metaplasia at the cardia was only seen in inflamed cardiac mucosa, and its prevalence increased both with increasing acid exposure and with the presence of esophagitis. CONCLUSION: The findings of cardiac mucosa, carditis, and intestinal metaplasia in an endoscopically normal-appearing gastroesophageal junction are histologic indicators of gastroesophageal reflux disease. These findings may be among the earliest signs of gastroesophageal reflux and contribute to the authors understanding of the pathophysiology of the disease process.     

The impact of reflux composition on mucosal injury and esophageal function

The components of refluxed gastric juice are known to cause mucosal injury, but their effect on esophageal function is less appreciated. Our aim was to determine the effect of acid and/or bile on mucosal injury and esophageal function. From 1993–2004, 402 patients with reflux symptoms had 24-hour pH and Bilitec monitoring, manometry, and endoscopy with biopsies. Mucosal injury (esophagitis or Barrett’s esophagus) and esophageal function (lower esophageal sphincter [LES] characteristics and body contractility) in patients with acid reflux, bile reflux, or both were compared with patients without reflux. Reflux was present in 273/402 patients; of these, 37 (13.5%) had increased exposure to bile, 82 (30.0%) had increased exposure to acid, and 154 (56.4%) had increased exposure to both. Mucosal injury was most common with increased mixed acid and bile exposure, followed by acid alone, and was uncommon with bile alone (P<0.0001). Functional deterioration paralleled mucosal injury (P<0.0001). Mixed acid and bile exposure was present in more than half of patients with reflux and was associated with the most severe mucosal injury and the greatest deterioration of esophageal function. This suggests that composition of gastric juice is the primary determinant of inflammatory mucosal injury and subsequent loss of esophageal function. Presented at the Forty-Sixth Annual Meeting of The Society for Surgery of the Alimentary Tract, Chicago, Illinois, May 14–19, 2005 (oral presentation).     

Carcinogenesis in reflux disease--in search for bile-specific effects

Bile reflux may play a key role for esophageal carcinogenesis in reflux disease. In search for bile-specific effects, the animal model of esophageal cancer was applied in a mutagenesis assay. Big Blue transgenic mice were operated with microsurgical techniques. Seven had total gastrectomy with esophagojejunostomy creating esophageal reflux of bile and five had a sham operation. After 24 weeks, the mutation frequency (MF) was measured through standard Big Blue mutagenesis assay in the esophageal mucosa and the duodenum as control. Esophageal reflux resulted in esophagitis in the distal esophagus. The MF in esophageal mucosa was 1.6 times higher in animals with reflux than in sham-operated animals; it was identical in the duodenum. In conclusion, the mutagenic potential of bile reflux has been confirmed. However, mechanisms of carcinogenesis in the esophageal cancer model other than chronic inflammation could not be identified because of the only moderately increased MF.     

Effect of different fractions of alkaline reflux on the gastric stump and the esophagus: an experimental research on pigs

An experimental study was conducted to evaluate the effect of different fractions (bile and pancreaticoduodenal secretions) on the gastric stump and esophageal mucosa. Twenty pigs underwent partial gastrectomy (two-third distal) and cardiomyotomy in order to induce free gastroesophageal reflux. Then, reconstruction of the alimentary tract was performed to assess the effects of different types of alkaline reflux. A combined (biliary and pancreaticoduodenal) reflux, an isolated biliary reflux, and an isolated pancreaticoduodenal reflux were induced, respectively, in three different groups of five pigs each. In a control group a Roux-en-Y gastrojejunostomy was performed. Nine months later, the animals were sacrificed, the esophagus and the gastric stump were removed for histologic examination. The results show that the most severe histopathological lesions are determined by combined alkaline reflux; on the other hand, separated fractions can induce only mild changes on the gastric stump and esophageal mucosa.     

Circadian esophageal motor function in patients with gastroesophageal reflux disease

Effective esophageal peristalsis is a major determinant of esophageal clearance function and may contribute to the development of complications in gastroesophageal reflux disease. Using 24-hour ambulatory esophageal manometry, we compared the circadian esophageal motor activity of normal volunteers to that of patients with increased esophageal exposure to gastric juice and various grades of mucosal injury (no mucosal injury, esophagitis, stricture, or Barrett's esophagus). The prevalence of a mechanically defective lower esophageal sphincter, esophageal acid exposure time, and the frequency of nonperistaltic esophageal contractions during the supine, upright, and meal periods increased with increasing severity of mucosal injury. The median amplitude of esophageal contractions was compromised only in patients with a mechanically defective sphincter. This was particularly so in patients with stricture or Barrett's esophagus and was associated with an increased frequency of ineffective contractions (less than 30 mm Hg). These data show that esophageal motor function deteriorates with increasing severity of mucosal injury. This appears to be caused by persistent reflux of gastric juice across a mechanically defective lower esophageal sphincter. The need for surgical correction of a mechanically defective sphincter before the loss of esophageal body function is implicated.     

Complications of gastroesophageal reflux disease. Role of the lower esophageal sphincter, esophageal acid and acid/alkaline exposure, and duodenogastric reflux.

The factors contributing to the development of esophageal mucosal injury in gastroesophageal reflux disease (GERD) are unclear. The lower esophageal sphincter, esophageal acid and acid/alkaline exposure, and the presence of excessive duodenogastric reflux (DGR) was evaluated in 205 consecutive patients with GERD and various degrees of mucosal injury (no mucosal injury, n = 92; esophagitis, n = 66; stricture, n = 19; Barrett's esophagus, n = 28). Manometry and 24-hour esophageal pH monitoring showed that the prevalence and severity of esophageal mucosal injury was higher in patients with a mechanically defective lower esophageal sphincter (p less than 0.01) or increased esophageal acid/alkaline exposure (p less than 0.01) as compared with those with a normal sphincter or only increased esophageal acid exposure. Complications of GERD were particularly frequent and severe in patients who had a combination of a defective sphincter and increased esophageal acid/alkaline exposure (p less than 0.01). Combined esophageal and gastric pH monitoring showed that esophageal alkaline exposure was increased only in GERD patients with DGR (p less than 0.05) and that DGR was more frequent in GERD patients with a stricture or Barrett's esophagus. A mechanically defective lower esophageal sphincter and reflux of acid gastric juice contaminated with duodenal contents therefore appear to be the most important determinants for the development of mucosal injury in GERD. This explains why some patients fail medical therapy and supports the surgical reconstruction of the defective sphincter as the most effective therapy.     

Does delayed gastric emptying contribute to gastroesophageal reflux disease?

We studied 76 patients with symptoms of heartburn, regurgitation, or both and 38 asymptomatic control subjects by measuring the gastric emptying of technetium-99m-labeled oatmeal. In addition, we performed 24-hour esophageal pH monitoring and manometric studies of the esophagus on all study participants. Endoscopy was performed on all patients. Patients with proved reflux on 24-hour pH monitoring, in comparison to those without reflux and the control subjects, had a shorter lower esophageal segment with a lower pressure and more esophagitis. Delayed gastric emptying occurred with equal frequency in patients with and without reflux. Esophageal reflux was not associated with delayed gastric emptying. Delayed emptying was associated with less esophagitis than found in those with normal gastric emptying, suggesting that the prolonged presence of food in the stomach may have a buffering effect on gastric acidity. We concluded that delayed emptying is not a major factor in the pathophysiology of gastro-esophageal reflux disease and that therapy aimed at speeding gastric emptying cannot be supported by our results.     

Barrett's esophagus in children. Diagnosis and management.

OBJECTIVE: To determine the local prevalence and optimal therapy for children with Barrett's esophagus (BE), the authors studied children with esophageal strictures or gastroesophageal reflux (GER), or both, to diagnose BE and to follow after therapy. SUMMARY BACKGROUND DATA: Barrett's esophagus is seldom reported in children and therapeutic recommendations are unclear. Barrett's esophagus usually develops during the mucosal reparative process after acid-reflux injury to the esophageal mucosa. Risk factors for BE include conditions that are associated with GER such as mental retardation, esophageal stricture, esophageal atresia, and reversed gastric tube esophagoplasty. Barrett's syndrome increases the risk of esophageal adenocarcinoma by 30 to 40 times. METHODS: All children with the risk factors had repeated esophagoscopy and multiple mucosal biopsies before and after therapy. RESULTS: Eleven children have been documented with BE. The initial diagnoses were: GER, 5; esophageal atresia, 4; nasogastric intubation, 1; lye ingestion, 1. A gastric tube esophagoplasty had been performed in three patients with BE in the esophagus proximal to the anastomosis. Three children with mid-esophageal strictures and long segments of BE had total resection with colic interposition. An additional two patients with tight stricture were treated with colic-patch esophagoplasty without resection. The final three patients were treated with fundoplication alone. CONCLUSIONS: Barrett's esophagus can be caused by acid from gastric tubes but responds to H2 blockers and diet. Resection eliminates BE; esophagoplasty only controls the stricture and must be accompanied by fundoplication. Barrett's esophagus persists in patients with fundoplication alone if reflux control is incomplete. The authors conclude that acid reflux must be controlled to treat BE successfully or the involved segment must be resected. Esophagogastrostomy apparently predisposes to BE.     

Laparoscopic partial posterior fundoplication provides excellent intermediate results in GERD patients with impaired esophageal peristalsis.

BACKGROUND: Gastroesophageal reflux disease (GERD) is frequently associated with impaired esophageal peristalsis, and many authorities consider this condition not suitable for Nissen fundoplication. METHODS: To investigate the outcome of antireflux surgery in the presence of impaired esophageal peristalsis, 78 consecutive GERD patients with poor esophageal contractility who underwent laparoscopic partial posterior fundoplication were studied. A standardized questionnaire, upper gastrointestinal endoscopy, esophageal manometry, and 24-hour pH monitoring were performed preoperatively and at a median of 31 months (range 6-57 months) postoperatively. Esophageal motility was analyzed for contraction amplitudes in the distal two thirds of the esophagus, frequency of peristaltic, simultaneous, and interrupted waves, and the total number of defective propagations. In addition, parameters defining the function of the lower esophageal sphincter were evaluated. RESULTS: After antireflux surgery, 76 patients (97%) were free of heartburn and regurgitation and had no esophagitis on endoscopy. The rate of dysphagia decreased from 49% preoperatively to 10% postoperatively (P < .001). Features defining impaired esophageal body motility improved significantly after antireflux surgery. The median DeMeester score on 24-hour esophageal pH monitoring decreased from 33.3 to 1.1 (P < .001). CONCLUSIONS: Partial posterior fundoplication provides an effective antireflux barrier in patients with impaired esophageal body motility. Postoperative dysphagia is diminished, probably because of improved esophageal body function.     

Duodenogastric reflux potentiates the injurious effects of gastroesophageal reflux

Experimental studies have shown that the severity of esophageal mucosal injury in gastroesophageal reflux disease is related to the reflux of both gastric and duodenal juice. The purpose of this study was to determine whether duodenal juice potentiates esophageal injury in patients with reflux disease or, inf act, causes no harm allowing acid and pepsin to do the damage. A total of 148 consecutive patients who had no previous gastric or esophageal surgery underwent endoscopy and biopsy, manometry, and 24-hour esophageal pH and bilirubin monitoring. Esophageal injury was defined by the presence of erosive esophagitis, stricture, or biopsy-proved Barrett's esophagus. Exposure to duodenal juice, identified by the absorbance of bilirubin, was defined as an exposure time exceeding the ninety-fifth percentile measured in 35 volunteers. To separate the effects of gastric and duodenal juice, patients were stratified according to their acid exposure time. One hundred patients had documented acid reflux on pH monitoring, and in 63 of them it was combined with reflux of duodenal juice. Patients with combined reflux (50 of 63) were more likely to have injury than patients without combined reflux (22 of 37; P < 0.05). When the acid exposure time was greater than 10%, patients with injury (n = 40) had a greater exposure to duodenal juice (median exposure time 17.2% vs. 1.1%, P = 0.006) than patients without injury (n = 5), but there was no difference in their acid exposure (16.9% vs. 13.4%). Patients with dysplasia of Barrett's epithelium (n = 9) had a greater exposure to duodenal juice (median exposure time 30.2% vs. 7.2%, P = 0.04) compared to patients without complications (n = 25), whereas acid exposure was the same (16.4% vs. 15%). Duodenal juice adds a noxious component to the refluxed gastric juice and potentiates the injurious effects of gastric juice on the esophageal mucosa.     

Laparoscopic antireflux surgery in the treatment of gastroesophageal reflux in patients with Barrett esophagus

BACKGROUND: Patients with gastroesophageal reflux and Barrett esophagus may represent a group of patients with poorer postoperative outcomes. It has been suggested that such patients should undergo open rather than laparoscopic antireflux surgery. HYPOTHESIS: The laparoscopic approach to antireflux surgery is appropriate treatment for patients with Barrett esophagus who have symptomatic gastroesophageal reflux disease. METHODS: The outcome of 757 patients undergoing laparoscopic surgery for gastroesophageal reflux disease from January 1, 1992, through December 31, 1998, was prospectively examined. Barrett esophagus was present in 81 (10.7%) of these patients (58 men and 23 women). The outcome for this group of patients was compared with that of patients undergoing surgery who did not have Barrett esophagus. RESULTS: The types of operation performed were similar for the 2 patient groups. The mean +/- SD length of columnar mucosa was 47.4 +/- 43.6 mm. The average +/- SD operation time was 79.0 +/- 33.4 minutes. Conversion to open surgery occurred in 6 patients. Postoperative outcomes were as follows. Esophageal manometry and 24-hour pH studies before and after laparoscopic fundoplication demonstrated a significant increase in lower esophageal sphincter resting and residual relaxation pressures and a significant decrease in distal esophageal acid exposure. Four patients have developed high-grade dysplasia or invasive cancer within 4 years of their antireflux surgery, and all of these have subsequently undergone esophageal resection. CONCLUSIONS: The outcome of laparoscopic antireflux surgery is similar for patients with Barrett esophagus compared with other patients with gastroesophageal reflux disease. This suggests that laparoscopic surgery is appropriate treatment for this patient group.     

Surgical management of the gastroesophageal reflux syndrome in childhood

Gastroesophageal reflux (GER) is a common cause of repeated emesis, failure to thrive, repeated pulmonary infection, and asthma in infants and children. During a 14-year period 270 children underwent gastroesophageal fundoplication for symptomatic reflux. The 24-hour esophageal pH monitoring is the most accurate test available to verify the presence of GER and is also helpful in evaluating the results of fundoplication. Transabdominal fundoplication may be performed with a low risk of complications. The most frequent complication requiring reoperation is paraesophageal hiatus hernia (6/270 patients), which should be repaired in almost all instances when symptoms develop. Closure of the crura posterior to the esophagus greatly reduces the incidence of this problem. Esophageal motility disorders occur in more than 35% of patients with symptomatic reflux and militate against performing a tight antireflux operation. Approximately 50% of patients with symptomatic reflux have associated gastric motility disorders. Radionuclide studies with 99mTC sulfur colloid in semisolid feedings have determined the magnitude of gastric retention after a feeding and have been helpful in identifying children who require a pyloroplasty with or without fundoplication. Pyloroplasty is performed simultaneously with fundoplication in approximately 10% of patients with symptomatic reflux when the lower esophageal sphincter pressure is low and the esophageal pH monitor shows reflux. The excellent clinical results achieved by fundoplication with or without pyloroplasty and the low morbidity and mortality rates indicate that these procedures should be used early in the management of infants and children who suffer symptomatic GER.