Esophagogastric junction opening during relaxation distinguishes nonhernia reflux patients, hernia patients, and normal subjects

BACKGROUND AND AIMS: Flow across the esophagogastric junction (EGJ) is strongly related to opening dimensions. This study aimed to determine whether opening of the relaxed EGJ was altered in patients with gastroesophageal reflux disease (GERD). METHODS: Seven normal subjects (NL), 9 GERD patients without hiatus hernia (NHH), and 7 with hiatus hernia (HH) were studied. Cross-sectional area (CSA) of the relaxed EGJ was measured during low-pressure distention using a modified barostat technique that resulted in filling a compliant bag straddling the EGJ with renograffin to the set pressure. Swallows were imaged fluoroscopically at distensive pressures of 2-12 mm Hg. The diameter of the narrowest point of the EGJ in PA and lateral projections was measured from digitized images. CSA was determined as a function of intrabag pressure. RESULTS: The minimal EGJ opening aperture occurred at the diaphragmatic hiatus in all subjects. At pressures 0 mm Hg, there were significant increases in EGJ CSA both for HH and NHH compared with NL (P < 0.001) and for HH compared with NHH (P < 0.005). This difference may explain the diminished air/water discrimination seen during transient lower esophageal sphincter (LES) relaxation-associated reflux in GERD patients. CONCLUSIONS: Anatomic degradation of the EGJ distinguishes GERD patients from normal subjects, and these changes may impact on both the observed mechanisms of reflux and the constituents of reflux during transient LES relaxation. Therapy focused on EGJ compliance may benefit GERD patients.     

Neuro-regulation of lower esophageal sphincter function as treatment for gastroesophageal reflux disease

The junction between the esophagus and the stomach is a specialized region, composed of lower esophageal sphincter （LES） and its adjacent anatomical structures, the gastric sling and crural diaphragm. Together these structures work in a coordinated manner to allow ingested food into the stomach while preventing reflux of gastric contents across the esophago-gastric junction （EGJ） into the esophagus. The same zone also permits retrograde passage of air and gastric contents into esophagus during belching and vomiting. The precise coordination required to execute such a complicated task is achieved by a finely-regulated high-pressure zone. This zone keeps the junction between esophagus and stomach continuously closed, but is still able to relax briefly via input from inhibitory neurons that are responsible for its innervation. Alterations of the structure and function of the EGJ and the LES may predispose to gastroesophageal reflux disease （GERD）.     

Transient lower esophageal sphincter relaxations do not result from passive opening of the cardia by gastric distention

BACKGROUND & AIMS: Transient lower esophageal sphincter relaxation is the main mechanism for gastroesophageal reflux. Although there is evidence that transient lower esophageal sphincter relaxations are neurally mediated, another school of thought is that transient lower esophageal sphincter relaxations result from gastric distention, which shortens the sphincter to the point where it opens and the pressure decreases. We assessed the relationship of transient lower esophageal sphincter relaxation to gastroesophageal junction opening in an unsedated human model. METHODS: Seven healthy volunteers (6 men and 1 woman, aged 18-53 years) were studied while they were sitting. Manometry was performed by using a sleeve catheter passed through 1 nostril. A 5.3-mm endoscope was placed through the other nostril to obtain a retroflexed view of the cardia. The biopsy channel was connected to a barostat to distend the stomach with air at 15 mm Hg for 30 minutes. Manometric and endoscopic video-recording times were synchronized but scored independently. RESULTS: The transient lower esophageal sphincter relaxation onset invariably preceded gastroesophageal junction opening (median, 5.0 seconds; range, 0.5-20.7 seconds; P < .001). The transient lower esophageal sphincter relaxation nadir also typically occurred before gastroesophageal junction opening (median, 2.1 seconds; range, -4.2 to +19.5 seconds; P < .001). Once open, the gastroesophageal junction moved proximally for the duration of the transient lower esophageal sphincter relaxation. Termination of transient lower esophageal sphincter relaxations occurred about the time the time of gastroesophageal junction closure. CONCLUSIONS: These data refute the hypothesis that transient lower esophageal sphincter relaxations result from passive mechanical distraction of the gastroesophageal junction. Rather, transient lower esophageal sphincter relaxations must occur before the gastroesophageal junction can open.     

The role of transsphincteric pressure and proximal gastric volume in acid reflux before and after fundoplication

BACKGROUND & AIMS: This study was conducted to explore the role of proximal gastric volume and transsphincteric pressure on acid reflux during transient lower esophageal sphincter relaxation (TLESR) in patients with gastroesophageal reflux disease (GERD) both before and after laparoscopic fundoplication. METHODS: Twenty GERD patients were studied before and after fundoplication along with 20 healthy controls. High-resolution manometry and pH recording was performed for 1 hour before and 2 hours following meal ingestion (500 mL/300 kcal). Three-dimensional ultrasonographic images of the stomach were acquired before and every 15 minutes after meal ingestion. RESULTS: Postprandial proximal to total gastric volume distribution ratios were significantly larger in GERD patients before fundoplication (0.57 +/- 0.01; P < .05) and smaller following fundoplication (0.37 +/- 0.01; P < .001) compared with controls (0.46 +/- 0.01). The percentage of TLESRs associated with acid reflux did not relate to proximal gastric volume in any subject group. The transsphincteric pressure profile was different for TLESRs with and without reflux in GERD patients as well as in healthy controls. The pressure gradient across the esophagogastric junction (EGJ) (DeltaEGJp) was greater for TLESRs with acid reflux compared with TLESRs without acid reflux in both GERD patients (11.4 +/- 0.8 vs 8.0 +/- 0.5 mm Hg, respectively; P < .01) and controls (10.6 +/- 0.7 vs 7.1 +/- 0.8 mm Hg, respectively; P < .05). After fundoplication, DeltaEGJp during TLESRs was 7.9 +/- 0.9 mm Hg, and the transsphincteric pressure profile markedly changed. CONCLUSIONS: Although proximal gastric volume plays a key role in eliciting TLESRs, it is not related to the incidence of acid reflux during TLESRs. The transsphincteric pressure gradient is greater in TLESRs associated with acid gastroesophageal reflux.     

High-resolution manometry and impedance-pH/manometry: valuable tools in clinical and investigational esophagology

Both high-resolution manometry (HRM) and impedance-pH/manometry monitoring have established themselves as research tools and both are now emerging in the clinical arena. Solid-state HRM capable of simultaneously monitoring the entire pressure profile from the pharynx to the stomach along with pressure topography plotting represents an evolution in esophageal manometry. Two strengths of HRM with pressure topography plots compared with conventional manometric recordings are (1) accurately delineating and tracking the movement of functionally defined contractile elements of the esophagus and its sphincters, and (2) easily distinguishing between luminal pressurization attributable to spastic contractions and that resultant from a trapped bolus in a dysfunctional esophagus. Making these distinctions objectifies the identification of achalasia, distal esophageal spasm, functional obstruction, and subtypes thereof. Ambulatory intraluminal impedance pH monitoring has opened our eyes to the trafficking of much more than acid reflux through the esophageal lumen. It is clear that acid reflux as identified by a conventional pH electrode represents only a subset of reflux events with many more reflux episodes being composed of less acidic and gaseous mixtures. This has prompted many investigations into the genesis of refractory reflux symptoms. However, with both technologies, the challenge has been to make sense of the vastly expanded datasets. At the very least, HRM is a major technological tweak on conventional manometry, and impedance pH monitoring yields information above and beyond that gained from conventional pH monitoring studies. Ultimately, however, both technologies will be strengthened as outcome studies evaluating their utilization become available.     

Current concepts of the antireflux barrier

The lower esophageal sphincter, crural diaphragm, and phrenoesophageal ligament are the anatomic structures that constitute the antireflux barrier. The intraluminal pressure at the esophagogastric junction (EGJ) reflects the strength of the antireflux barrier. The end-expiratory pressure is a result of the tonic activity of the smooth muscles of the lower esophageal sphincter. The EGJ pressure increases during inspiration owing to the effect of the crural diaphragm. There is a reflex increase in the EGJ pressure during periods of increased intra-abdominal pressure, and the crural diaphragm contributes to this reflex contraction of the EGJ. Based on the contribution of the lower esophageal sphincter and crural diaphragm to the EGJ pressure, a two sphincter hypothesis of the antireflux barrier competence is suggested.     

Obesity: a challenge to esophagogastric junction integrity

BACKGROUND & AIMS: The aim of the current study was to analyze the relationship between obesity and the morphology of the esophagogastric junction (EGJ) pressure segment using high-resolution manometry. METHODS: Two hundred eighty-five patients (108 men, aged 18-87) were studied. A solid-state manometric assembly with 36 circumferential sensors spaced 1 cm apart was placed transnasally, and simultaneous intra-esophageal and intragastric pressures were measured over 6-8 respiratory cycles. Separation of the lower esophageal sphincter (LES) and crural diaphragm was quantified by measuring the distance between the two EGJ elements during inspiration. The association between anthropometric variables and pressure values were examined using univariate and multivariate analysis. RESULTS: There was a significant correlation of body mass index (BMI) and waist circumference (WC) with intragastric pressure (inspiration, BMI [r = 0.57], WC [r = 0.62] P < .0001; expiration, BMI [r = 0.58], WC [r = 0.64], P < .0001) and gastroesophageal pressure gradient (GEPG) (inspiration, BMI [r = 0.37], WC [r = 0.43], P < .0001; expiration, BMI [r = 0.24], WC [r = 0.26], P < .0001). Multivariate analysis adjusting for age, gender, and patient type did not alter the direction or magnitude of this relationship. In addition, obesity was associated with separation of the EGJ pressure components (BMI, r = 0.17, P < .005; WC, r = 0.21, P < .001). CONCLUSIONS: Obese subjects are more likely to have EGJ disruption (leading to hiatal hernia) and an augmented GEPG providing a perfect scenario for reflux to occur. Whether or not weight loss can reverse these abnormalities is unknown.     

Electrical and mechanical inhibition of the crural diaphragm during transient relaxation of the lower esophageal sphincter

Electrical and mechanical correlates of crural diaphragm activity during swallow-induced and transient lower esophageal sphincter relaxation were monitored in 12 healthy subjects. Simultaneous esophageal manometric, pH, and crural diaphragm electromyogram recordings were performed for 1 hour in the postprandial period. Swallow-induced lower esophageal sphincter relaxation was associated with minimal inhibition of the crural diaphragm, but transient lower esophageal sphincter relaxation was accompanied by marked inhibition of the crural diaphragm. The degree of lower esophageal sphincter relaxation appeared to correlate with the degree of crural diaphragm inhibition during transient lower esophageal sphincter relaxation. Inhibition of crural diaphragm during transient lower esophageal sphincter relaxation may play an important role in facilitating flow across the gastroesophageal junction.     

Mean pressure obtained by modified rapid pull-through technique used to assess lower esophageal sphincter function

Lower esophageal sphincter pressure, length of sphincter, and contraction of the crural diaphragm are determinants of esophageal function. Mean pressure manometrics in modified rapid pull-through reflects these three factors. Reproducibility and interobserver variability were studied to assess this method's efficacy and were compared with the maximum expiratory pressure in station pull-through in 44 individuals divided into three groups: achalasia, gastroesophageal reflux, and healthy volunteers. Mean pressure in rapid pull-through showed high reproducibility, no significant differences (14.4 ± 8.4 vs 12.6 ± 8.2 mm Hg) between two measurements, and a high correlation coefficient (r = 0.9). Interobserver variability was lower than that seen for maximum expiratory pressure (P < 0.001). Mean pressure was lower than maximum expiratory pressure in patients with achalasia (21.1 ± 7 vs 30.7 ± 8.6 mm Hg). Both methods showed identical sensitivity to establish a hypotensive sphincter in patients with reflux (73%). We think that mean pressure obtained by rapid pull-through is a good methodology to assess lower esophageal sphincter competence. It is rapid, simple, shows good reproducibility and low interobserver variability, and is clinically valid.     

Alterations confined to the gastro-oesophageal junction: the relationship between low LOSP, TLOSRs, hiatus hernia and acid pocket

The gastro-oesophageal junction is a specialised segment of the gut designed to prevent reflux of gastric contents into the oesophagus. This task is fulfilled by two structures, i.e. the lower oesophageal sphincter and the crural diaphragm, which generate a high pressure zone. Especially during low pressure at the junction, as in case of long-lasting transient lower oesophageal sphincter relaxations, reflux can occur but mainly if a positive pressure gradient exists between stomach and the oesphagogastric junction. Although patients with gastro-oesophageal reflux disease have increased oesophageal acid exposure compared to controls, the number of transient relaxations is not increased compared to healthy controls. Instead, the risk to have acid reflux is at least doubled in patients, especially in those with a hiatal hernia, most likely as a result of the supradiaphragmatic position of the acid pocket. In hiatal hernia patients, the acid pocket is indeed often trapped in the hernia above the diaphragm. Which factors exactly determine the physical composition (liquid or gas) and the proximal extent of the refluxate however requires further research.     

Transient Lower Esophageal Sphincter Relaxations and Gastroesophageal Reflux Episodes in Healthy Subjects and GERD Patients During 24 Hours

Still little is known about the 24-hr pattern of transient lower esophageal sphincter relaxations (TLESRs), particularly in patients with GERD. The aim of our study was to evaluate the 24-hr esophageal and LES motor pattern and esophageal pH and to identify the relationship between TLESRs and gastroesophageal reflux in healthy subjects and in GERD patients. Ten healthy subjects and nine patients with esophagitis (grade I–II) underwent a 24-hr pH manometric recording by means of a portable electronic device. The recording aimed at identifying the temporal relationships between reflux episodes and LES motor events. The GERD patients showed a greater number of either reflux episodes or TLESRs during the 24 hr as compared to controls. While most refluxes occurred during TLESRs in both groups, a small percentage of TLESRs was followed by reflux episodes in healthy people, with only a slight increase in GERD patients. In conclusion, although representing an important motor pattern during gastroesophageal reflux both in healthy subjects and in patients with GERD, TLESR could probably be considered one of the pathophysiologic mechanisms of gastroesophageal reflux more than the primary cause of reflux episodes.     

下食管括约肌运动和功能与胃食管反流病

目的　观察胃食管反流病 (GERD)患者与对照组餐前、餐后食管pH情况 ,下食管括约肌(LES )运动模式的变化以及酸反流事件与一过性下食管括约肌松弛 (TLESR )、低LES压力 (LESP)的关系。方法　两组受试者均接受连续性 4h食管压力测定 (分别为空腹和餐后 1、2、3h)和食管pH监测 (GERD组检测 4h ,对照组检测 2 4h)。结果　GERD组酸反流事件明显高于对照组 (P <0 0 5 )。两组间TLESR发生率差异无显著性 (P >0 0 5 ) ,但与空腹比较 ,两组餐后 1h和 2hTLESR发生率明显增多 ;GERD组伴有酸反流的TLESR明显高于对照组 (P <0 0 0 1)。 4 3% (2 9/ 6 8)的酸反流事件发生在TLESR期间。 31% (2 1/ 6 8)的酸反流事件出现于低LESP状态中。结论　GERD是多因素参与的病理过程。LES运动形式变化和功能不全是GERD的重要背景因素。     

High-resolution manometry of the EGJ: an analysis of crural diaphragm function in GERD

AIM: High-resolution manometry (HRM) provides a spatially enhanced, dynamic representation of the esophagogastric junction (EGJ) high-pressure zone making it possible to isolate the crural diaphragm (CD) contraction from expiratory lower esophageal sphincter (LES) pressure. This study compared CD function of subjects with and without gastroesophageal reflux disease (GERD). METHODS: A total of 75 asymptomatic controls and 156 GERD patients (EGD or pH monitoring positive) underwent HRM. The EGJ axial pressure profile was analyzed over five respiratory cycles to quantify the position and contractile vigor of the CD relative to the LES. Correlations between EGJ HRM attributes and GERD status were examined. RESULTS: GERD patients had significantly greater CD-LES separation compared with either controls or EGD-/pH- patients. GERD patients also had significantly less inspiratory augmentation of EGJ pressure (EGD-/pH+, 11.5 +/- 1.9 mmHg; EGD+, 10.0 +/- 1.2 mmHg) compared with controls (16.9 +/- 1 mmHg) or EGD-/pH- patients (16.7 +/- 0.2 mmHg). Using a logistic regression model that simultaneously examined expiratory LES pressure, LES-CD separation, and inspiratory EGJ augmentation while controlling for age and BMI, only inspiratory augmentation had a significant independent association with GERD. CONCLUSIONS: HRM characterization of EGJ morphology correlates with the objective demonstration of GERD. Although both LES pressure and LES-CD separation are associated with GERD, the strongest association and the only independent predictor of GERD as a categorical outcome in a logistic regression analysis was impaired CD function as indicated by reduced inspiratory augmentation of EGJ pressure.     

Calculation of esophagogastric junction vector volume using three‐dimensional high‐resolution manometry

Lower esophageal sphincter vector volume (V‐V) was developed in the late 1980s by Bombeck, as a quantification of sphincter integrity used to select reflux patients with a defective valve who may benefit from surgery. Its calculation required motorized pull‐through of an 8‐lumen water perfused manometry catheter with subsequent computerized reconstruction of sphincter morphology. Recently, a three‐dimensional high‐resolution manometry (3D‐HRM) assembly (Given Imaging, Duluth, GA, USA) has been developed with the potential to assess real‐time V‐V. The aim of this study was to assess the feasibility of the calculation of V‐V using the 3D‐HRM assembly and to compare measures of its value using real‐time 3D‐HRM to simulated analogous measures. Eight asymptomatic controls (4F, ages 26–49) were studied in a supine position with a solid‐state 3D‐HRM assembly positioned across the esophagogastric junction (EGJ). The 9‐cm 3D segment comprised 12 rings of 8 radially dispersed pressure sensors, each 2.5 mm long and spaced 7.5 mm apart on center. Recordings were done during normal respiration: (i) with the 3D‐HRM segment in a stationary position across the EGJ; and (ii) during a station pull‐through of the 3D‐HRM segment withdrawing it across the EGJ at 5‐mm increments with each position held for 30 seconds. EGJ cross‐sectional vector areas (CSVAs) were computed using the irregular polygon area formula: , and n = 8 radial sensors. V‐V was computed as the sum of CSVAs at inspiration and end‐expiration by three methods: real‐time 3D‐HRM, three‐station composite, and single‐sensor ring measurements. There were no statistic differences among the methods, and all methods showed significant differences between inspiration and expiration. Calculation of real‐time V‐V is feasible using the 3D‐HRM. Moreover, the results of this study highlighted the potential primary role of the diaphragmatic hiatus in the pathophysiology of gastroesophageal reflux disease and the underrecognized but crucial role of the crural repair during the antireflux surgery.     

Increased inspiratory esophagogastric junction pressure in systemic sclerosis:An add-on to antireflux barrier

AIM:To investigate crural diaphragm(CD)function in systemic sclerosis(SSc)using high-resolution manometryand standardized inspiratory maneuvers.METHODS:Eight SSc volunteers(average age,40.1years;one male)and 13 controls(average age,32.2years;six males)participated in the study.A highresolution manometry/impedance system measured the esophagus and esophagogastric junction(EGJ)pressure profile during swallows and two respiratory maneuvers:sinus arrhythmia maneuver(SAM;the average of six EGJ peak pressures during 5-s deep inhalations)and threshold maneuver(TM;the EGJ peak pressures during forced inhalation under 12 and 24 cm H2O loads).Inspiratory diaphragm lowering(IDL)was taken as the displacement of the EGJ high-pressure zone during the SAM.RESULTS:SSc patients had lower mean lower esophageal sphincter pressure than controls during normal breathing(19.7±2.8 mm Hg vs 32.2±2.7 mm Hg,P=0.007).Sinus arrhythmia maneuver pressure was higher in SSc patients than in controls(142.6±9.4 mm Hg vs 104.6±13.8 mm Hg,P=0.019).Sinus arrhythmia maneuver pressure normalized to IDL was also higher in SSc patients than in controls(83.8±13.4 mm Hg vs37.5±6.9 mm Hg,P=0.005).Threshold maneuver pressures normalized to IDL were also greater in SSc patients than in controls(TM 12 cm H2O:85.1±16.4mm Hg vs 43.9±6.3 mm Hg,P=0.039;TM 24 cm H2O:85.2±16.4 mm Hg vs 46.2±6.6 mm Hg,P=0.065).Inspiratory diaphragm lowering in SSc patients was less than in controls(2.1±0.3 cm vs 3±0.2 cm,P=0.011).CONCLUSION:SSc patients had increased inspiratory EGJ pressure.This is an add-on to EGJ pressure and indicates that the antireflux barrier can be trained.     

Mechanisms of gastroesophageal reflux in critically ill mechanically ventilated patients

BACKGROUND & AIMS: Gastroesophageal reflux is a major problem in mechanically ventilated patients and may lead to pulmonary aspiration and erosive esophagitis. Transient lower esophageal sphincter relaxations are the most common mechanism underlying reflux in nonventilated patients. The mechanisms that underlie reflux in critically ill ventilated patients have not been studied. The aim of this study was to determine the mechanisms underlying gastroesophageal reflux in mechanically ventilated patients in the intensive care unit. METHODS: In 15 mechanically ventilated intensive care unit patients, esophageal motility, pH, and intraluminal impedance (11/15 patients) were recorded for 1 hour before and 5 hours during continuous nasogastric feeding. RESULTS: Basal lower esophageal sphincter pressure was uniformly low (2.2 +/- 0.4 mmHg). The median (interquartile range) acid exposure (pH <4) was 39.4% (0%-100%) fasting and 32% (7.5%-94.2%) fed. Acid reflux occurred in 10 patients, but slow drifts in esophageal pH were also an important contributor to acid exposure. If esophageal pH decreased to pH <4, it tended to remain so for prolonged periods. A total of 46 acid reflux events were identified. Most (55%) occurred because of absent lower esophageal sphincter pressure alone; 45% occurred during straining or coughing. CONCLUSIONS: Gastroesophageal reflux in mechanically ventilated patients is predominantly due to very low or absent lower esophageal sphincter pressure, often with a superimposed cough or strain. These data suggest that measures that increase basal LES pressure may be useful to prevent reflux in ventilated patients.     

The effect of intravenous diazepam on esophageal motility in normal subjects

Controversy exists over whether diazepam can be used for sedation during esophageal manometry studies without affecting the results. To evaluate the effect of diazepam, 20 healthy asymptomatic volunteers were studied using a standard manometry protocol employing an Arndorfer capillary infusion system. Following a baseline manometry, each subject received 0.1 mg/kg diazepam intravenously over 1 min and underwent repeat manometry 5 min after completion of the injection. All manometry recordings were coded and read blindly. The amplitude of the lower esophageal sphincter was significantly reduced by diazepam from 26.2±10.9 and 30.0±10.9 mm Hg to 18.8±7.6 and 24.5±9.7 mm Hg by rapid and station pull-through methods, respectively (P<0.01 all both methods). Esophageal contraction wave duration was significantly increased following diazepam at 3, 8, and 13 cm above the lower esophageal sphincter (P<0.01 all levels). There was a trend toward increased contraction wave amplitude following diazepam administration in the lower three fourths of the esophagus. On the basis of these results, we conclude that diazepam sedation may produce misleading results when used during esophageal manometric testing. It is recommended that diazepam not be used in manometric studies of normal subjects or patients with reflux esophagitis and that manometric findings in patients with hypertensive or spastic disorders be interpreted with caution if diazepam is given as a premedication.     

Infusion manometry and detection of sphincteric function of crural diaphragm

The principles of infusion manometry in the measurement of lower esophageal sphincter (LES) pressure were laid down in the mid-1960s by L.D. Harris and his coworkers. Dodds and his colleagues were largely responsible for the improvements and advent of the low-compliance manometry. Using side-hole manometry, it is possible to detect accurate LES pressure that correlates with the strength of the antireflux barrier. The LES pressure as measured by the side-hole manometry, shows respiration-induced pressure oscillations. These pressure oscillations were initially thought to be due to the influence of abdominal and thoracic pressures on the LES. However, it was later pointed out that these pressure oscillations were due to the relative motion of the point pressure sensor (side hole of the manometric catheter) and the LES during respiration. Recent studies suggest that active contraction of the crural diaphragm during inspiration is responsible for the pressure oscillations observed in the cat LES pressure tracings. The use of the sleeve device in the measurement of LES pressure during contraction of the diaphragm has been described recently. Using the principles of manometry and sleeve device, it is now possible to identify two lower esophageal sphincters: the smooth muscle LES, traditionally known as the LES, and crural diaphragm, which we have referred to as the external lower esophageal sphincter. The purpose of the following paper is to summarize the general principles of the infusion manometry in the measurement of intraluminal pressure, specifically the LES pressure. The recently developed technique of detection of the sphincteric function of the crural diaphragm by the sleeve device will be discussed. In the last paragraph the limitations of manometry in detection of the muscular contractile activity are described.     

Acidity surrounding the squamocolumnar junction in GERD patients: "acid pocket" versus "acid film"

AIM: This study aimed to localize the gastric-to-esophageal pH transition point relative to the squamocolumnar junction (SCJ) and esophagogastric junction (EGJ) high-pressure zone in controls and GERD patients. METHODS: Ten controls and 10 GERD patients were studied. Subjects had an endoclip placed at the SCJ prior to a pH catheter pull-through (upright and supine) during concurrent fluoroscopy before and after consuming a standardized meal. Six controls and 6 GERD patients also underwent concurrent manometry. The relative positions of the SCJ, EGJ high-pressure zone, and pH transition points were analyzed. RESULTS: Most controls and GERD patients exhibited an unbuffered acidified segment in the proximal stomach postprandially. The proximal pH transition point was confined distal to the SCJ in control subjects, regardless of posture or meal state. GERD patients exhibited a more proximal pH transition point, extending above the SCJ and EGJ high-pressure zone in the supine position, especially postprandially. However, the high-pressure zone was intact. CONCLUSION: A short segment of unbuffered acidity of unknown volume exists after meals in the proximal stomach. In controls, the unbuffered acidic segment is contained distal to the SCJ while in the GERD patients it extended into and even across the EGJ high-pressure zone. However, this extension through the EGJ in GERD patients occurred in the context of an intact sphincter suggesting that this is best conceptualized as an acid "film" rather than a "pocket." This observation may help explain the propensity of the distal esophageal mucosa to lesions of reflux disease.     

Impaired bolus transit across the esophagogastric junction in postfundoplication dysphagia

OBJECTIVES: This study assessed the effect of fundoplication on liquid and solid bolus transit across the esophagogastric junction (EGJ) in relation to EGJ dynamics and dysphagia. METHODS: Twelve patients with gastro-esophageal reflux disease (GERD) were studied before and after fundoplication. Concurrent high-resolution EGJ manometry and fluoroscopy were performed whilst swallowing liquid barium and a solid bolus. The EGJ transit time, EGJ opening duration, transit efficacy, and EGJ relaxation were measured. During the test symptoms of dysphagia were scored using a visual analog scale. RESULTS: The minimal opening aperture at fluoroscopy was located at the manometric EGJ in all subjects. Fundoplication markedly reduced the EGJ opening diameter from 1.0 +/- 0.1 to 0.6 +/- 0.1 cm (p < 0.01) and rendered deglutative EGJ relaxation incomplete. After fundoplication, a higher intrabolus pressure was found (p < 0.05) associated with a reduced axial bolus length (p < 0.001). EGJ transit time increased from 6.9 +/- 0.9 to 9.8 +/- 1.0 s for liquids (p < 0.01) and from 2.8 +/- 0.5 to 5.8 +/- 0.8 s (p < 0.01) for solids after fundoplication. No relation between EGJ transit and dysphagia scores was observed before fundoplication. In contrast, EGJ transit time significantly correlated with dysphagia scores both during liquid (r = 0.84; p < 0.01) and solid (r = 0.69; p < 0.05) bolus transit following fundoplication. CONCLUSIONS: Fundoplication patients exhibit a restricted hiatal opening and an incomplete deglutative EGJ relaxation. To facilitate EGJ transit despite these altered EGJ dynamics a higher intrabolus pressure is created by augmented bolus compression. Fundoplication increases EGJ transit time, the degree of which is associated with postoperative dysphagia.