Esophageal motility: effects of injection sclerotherapy

The purpose of this project was to evaluate the acute and chronic effects of sclerotherapy on esophageal motility and function. We studied motility in eight patients before and after injection sclerotherapy of esophageal varices. We injected the varices with 5% sodium morrhuate twice during the first week and then at 1, 2, 3, and 6 months. Lower esophageal sphincter pressure, contraction wave amplitude, and duration were not altered by sclerotherapy. However, the length of the high-pressure zone increased significantly from 3.6 +/- 0.3 cm to 4.2 +/- 0.2 cm during the first 3 days after initial treatment, and sclerotherapy caused considerable distortion of peristaltic wave form. Also, esophageal peristaltic velocity decreased in three patients who complained of dysphagia and subsequently developed esophageal stricture. The strictures have responded well to dilatation, and in two patients velocity has even returned toward the baseline value. Reflux esophagitis has not been a problem. Esophageal motility is altered by sclerotherapy of esophageal varices. Stricture formation seems to be reversible after sclerotherapy is stopped or discontinued.     

Manometric evaluation of esophageal motility in patients submitted to prophylactic variceal sclerosis

Summary Sclerotherapy of esophageal varices is an effective hemostatic treatment and may also prevent bleeding. In our study, we examined the effects of prophylactic sclerotherapy on esophageal motility in 15 patients with Child's A cirrhosis of the liver. All the patients underwent three manometric measurements, performed respectively before the sclerotherapy, I week after the eradication of varices, and 3 months later. The results of our study show that prophylactic sclerotherapy of esophageal varices does not significantly change the resting pressure and length of the lower esophageal sphincter. Neither the amplitude nor the duration of the postswallowing esophageal peristaltic waves is significantly influenced by sclerotherapy. However, sclerotherapy produces a significant increase in tertiary contractions in the distal esophagus, which could explain the onset of dysphagia among patients in whom postsclerotherapy stricture is not evident.     

Long-term effects of repeated injection sclerotherapy on esophageal motility and mucosa

Background: Endoscopic sclerotherapy (ST), widely used as treatment of bleeding esophageal varices, might cause motility disturbances of the esophagus as well as mucosal damage. We performed this study to evaluate the long-term effects of repeated sclerotherapy on esophageal motility and mucosa. Methods: Ten patients with liver cirrhosis and bleeding esophageal varices treated with repeated ST were evaluated after the last ST, median 52 months, by esophageal manometry and gastroscopy where forceps biopsies were taken. Results: We found a significant difference in the distal esophageal sphincter intraabdominal length. The distal esophageal sphincter pressure was somewhat lower in the ST group although the difference did not reach statistical significance. There was infiltration of neutrophil leukocytes in biopsies from four patients and normal findings in the rest. Conclusions: Long-term follow-up evaluation showed statistically longer distal esophageal intraabdominal length in the ST group. No mucosal alterations were found at the histopathological investigation. Received: 22 April 1996/Accepted: 20 August 1996     

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.     

The role of esophageal sphincter tonus and of gastric motility in the extent of reflux esophagitis]

Thirty-two patients with symptomatic gastroesophageal reflux disease were investigated by esophagogastroduodenoscopy, 24 h pH monitoring, esophageal manometry and measurement of gastric emptying of solids, in order to elucidate the relative importance of lower esophageal sphincter tone, amount of acid reflux and gastric emptying on the degree of esophagitis. The mechanical competency of lower esophageal sphincter was significantly deranged in patients with moderate/severe esophagitis than in patients with mild esophagitis. The gastric emptying time was significantly delayed in patients with moderate/severe esophagitis than in patients with mild esophagitis. No relationship was observed between amount of acid reflux, lower esophageal sphincter function and gastric emptying time. Our results suggest that resting pressure of lower esophageal sphincter and the gastric motor function play a major role in severity of reflux esophagitis.     

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.     

Surgical management of esophageal motility disturbances

During the past few decades, knowledge regarding normal and abnormal esophageal behavior has greatly increased because of the introduction of sophisticated techniques of studying esophageal function. As a result, the normal motility patterns of the esophagus are now well known, and conditions characterized by disturbances of esophageal motility can be readily recognized and therapy can be designed along more physiologic lines than heretofore.Motility disturbances of the esophagus can be classified as those involved with the upper esophageal sphincter and those involving the body of the esophagus and lower esophageal sphincter. Cricopharyngeal myotomy has played an increasing role in the management of abnormalities of function of the upper esophageal sphincter, particularly in patients with hypertension of the upper esophageal sphincter or incoordination of the upper esophageal sphincter as seen in pharyngoesophageal diverticulum. Esophagomyotomy has also found a useful place in the management of symptomatic patients with esophageal achalasia, in whom I believe it is the primary treatment of choice. Results of a properly performed myotomy suggest that an ancillary antireflux maneuver is not necessary. Although diffuse spasm of the esophagus and hypertensive sphincter represent different forms of esophageal motility disorders characterized by hypermotility rather than hypomotility, in properly selected patients a long esophagomyotomy has been useful in relieving the disabling symptoms of pain and dysphagia exhibited by most of these persons.Hypotension of the lower esophageal sphincter is now recognized as an underlying mechanism responsible for gastroesophageal reflux in a variety of disease states. Thus reflux and its debilitating sequence of ulcerative esophagitis and stricture formation should now be viewed as a physiologic abnormality rather than a strictly anatomic abnormality such as may occur in the presence of diaphragmatic hernia. Treatment is primarily medical and is designed to minimize the occasions of reflux and its effects by reducing gastric acids. Only in a small percentage of patients is surgical treatment in the form of an antireflux procedure required.     

Motility and mucosal hemodynamics of the lower esophagus after transabdominal esophageal transection for esophageal varices]

Lower esophageal motility and mucosal hemodynamics were investigated in 20 patients who underwent transabdominal esophageal transection for esophageal varices (ET), to evaluate their association with reflux esophagitis and variceal recurrence. In the manometric study with microtransducer catheter, maximum swallowing pressure in the lower esophagus of the patients was significantly lower than that of the healthy controls (20 cases) (26.1 +/- 20.5mmHg vs. 80.0 +/- 10.0mmHg: p < 0.01), while high pressure zone pressure did not differ between the two groups. In comparison between patients with and without esophagitis (E(+) and E(-)), maximum swallowing pressure of E(+) was statistically lower than that of E(-) (12.4 +/- 18.7mmHg vs. 31.0 +/- 19.1mmHg: p < 0.05). In the hemodynamic study by reflectance spectrophotometry, the index of esophageal mucosal blood volume (IHb) and the index of oxygen saturation of hemoglobin (ISo2) of E(+) and E(-) were no different from those in the patients with non-operated esophageal varices (10 cases). Although there was no correlation between the recurrence of RC-sign and mucosal microcirculation, the patients with larger varices tended to have a higher IHb and a patients with F1-varices had significantly lower ISo2 than the patients without varices. This study indicated that the poor clearance ability after ET may lead to reflux esophagitis and the patients with variceal recurrence had the congested mucosal microcirculation, compared to those without variceal recurrence.     

Efficacy of Medical Therapy and Antireflux Surgery to Prevent Barrett’s Metaplasia in Patients With Gastroesophageal Reflux Disease

OBJECTIVE: To investigate whether Barrett's metaplasia may develop despite effective medical therapy. SUMMARY BACKGROUND DATA: Gastroesophageal reflux disease has a multifactorial etiology. Therefore, medical treatment may not prevent complications of reflux disease. METHODS: Eighty-three patients with reflux disease and mild esophagitis were prospectively studied for the development of Barrett's metaplasia while receiving long-term therapy with proton pump inhibitors and cisapride. Only patients who had effective control of reflux symptoms and esophagitis were included. The surveillance time was 2 years. The outcome of these 83 patients was compared with that of 42 patients in whom antireflux surgery was performed with a median follow-up of 3.5 years. RESULTS: Twelve (14.5%) patients developed Barrett's while receiving medical therapy; this was not seen after surgery. Patients developing Barrett's had a weaker lower esophageal sphincter and peristalsis before treatment than patients with uncomplicated disease. CONCLUSIONS: Antireflux surgery is superior to medical therapy in the prevention of Barrett's metaplasia. Therefore, patients with reflux disease who have a weak lower esophageal sphincter and poor esophageal peristalsis should undergo antireflux surgery, even if they have only mild esophagitis.     

Evaluation of lower esophageal sphincter function in infants and children following esophageal surgery

Esophageal manometry was performed before and after the operations for esophageal disorders in children to evaluate lower esophageal sphincter (LES) function and motility of the esophagocardiac region in each disease. Patients who underwent radical operations for gross C-type esophageal atresia (EA) and those with hiatal hernias considered to have gastroesophageal reflux (GER) showed reduction in LESP and LESL and eosphagocardiac motor abnormalities. Lower esophageal sphincter pressure and length, and motility of the esophagocardiac region improved in six patients who underwent an antireflux operation. Abnormal esophageal waves in EA patients persisted even after improvements in LES function by the antireflux operation and were considered to be a congenital problem, as the literature suggests. Effects of surgical intervention on the esophagus on the LES function were studied. Lower esophageal sphincter and esophagocardiac function were preserved, and GER did not develop after Livaditis' procedure for EA or esophageal transection and sectioning the esophageal branch of the vagus nerve for esophageal varices. Anatomic abnormalities that lead to LES dysfunction are considered to cause GER.     

Gastroesophageal scintigraphy to assess the severity of gastroesophageal reflux disease.

Thirty-six (36) patients with symptomatic gastroesophageal reflux were studied. Symptoms of heartburn, regurgitation and dysphagia were scored as to their severity and compared to quantitative tests of gastroesophageal reflux. Patients were studied with the acid reflux test, fiberoptic endoscopy, esophageal mucosal biopsy with a pinch forceps, esophageal manometry and radioisotopic gastroesophageal scintigraphy. Symptoms were scored according to an arbitrary grading system as mild, moderate, or severe. There were significant correlations between symptoms scores and both the degree of endoscopic esophagitis and the gastroesophageal reflux indices as measured by the radioisotopic scintiscan, but not with the degree of histologic esophagitis or lower esophageal sphincter pressure. Review of the findings suggests the following profile for patients who might require antireflux surgery: severe symptoms, presence of endoscopic esophagitis; resting lower esophageal sphincter pressure below 10 mmHg; and gastroesophageal reflux index above 10%.     

Specificity and sensitivity of objective diagnosis of gastroesophageal reflux disease

To evaluate the diagnostic value of different tests for gastroesophageal reflux disease, a test population was constructed from 45 patients with symptoms of heartburn and regurgitation with or without esophagitis and 45 healthy subjects, who never experienced heartburn, regurgitation, or swallowing discomfort. The test population underwent esophagoscopy, standard acid reflux test, 24-hour pH monitoring, and manometry of the lower esophageal sphincter. Sensitivity, specificity, positive predictive value, negative predictive value, and the accuracy of the tests and test combinations were calculated. Esophagoscopy had a sensitivity of 62%, that is, only 62% of patients with the disease have evidence of mucosal damage on endoscopy. Manometric measurements of the lower esophageal sphincter had a sensitivity of 84%, a specificity of 89%, and an accuracy of 87%. Twenty-four hour esophageal pH monitoring had a sensitivity, specificity, and accuracy of 96%. The results show that 24-hour pH monitoring can detect gastroesophageal reflux disease with an accuracy of 96% by measuring an increase in esophageal acid exposure. Manometry of the lower esophageal sphincter can detect a mechanically deficient sphincter as a cause of the disease with an accuracy of 87%. The test combination of 24-hour monitoring and motility studies can select patients with an accuracy of 91% who have an increase in esophageal exposure to gastric juice because of a deficient cardia. Antireflux surgery is designed to reduce esophageal exposure to gastric juice in patients with a deficient sphincter by creating a mechanical antireflux mechanism at the cardia. Therefore it is necessary to determine the mechanical status of the sphincter with manometry before surgery in such patients. Thus the indications for antireflux surgery are (1) uncontrolled symptoms of increased esophageal exposure to gastric juice; (2) a documented increase in esophageal exposure to gastric juice by 24-hour pH monitoring; and (3) a mechanically defective sphincter on motility with a pressure of 6 mm Hg or less, an overall length of 2 cm or less, and an abdominal length of 1 cm or less.     

The treatment of gastroesophageal reflux disease with laparoscopic Nissen fundoplication: prospective evaluation of 100 patients with "typical" symptoms.

OBJECTIVE: To evaluate prospectively the outcome of laparoscopic fundoplication in a large cohort of patients with typical symptoms of gastroesophageal reflux. SUMMARY BACKGROUND DATA: The development of laparoscopic fundoplication over the past several years has resulted in renewed interest in the surgical treatment of gastroesophageal reflux disease (GERD). METHODS: One hundred patients with typical symptoms of GERD were studied. The study was limited to patients with positive 24-hour pH studies and "typical" symptoms of GERD. Laparoscopic fundoplication was performed when clinical assessment suggested adequate esophageal motility and length. Outcome measures included assessment of the relief of the primary symptom responsible for surgery; the patient's and the physician's evaluation of outcome; quality of life evaluation; repeated upper endoscopy in 30 patients with presurgical esophagitis; and postsurgical physiologic studies in 28 unselected patients, consisting of 24-hour esophageal pH and lower esophageal sphincter manometry. RESULTS: Relief of the primary symptom responsible for surgery was achieved in 96% of patients at a mean follow-up of 21 months. Seventy-one patients were asymptomatic, 24 had minor gastrointestinal symptoms not requiring medical therapy, 3 had gastrointestinal symptoms requiring medical therapy, and 2 were worsened by the procedure. Eighty-three patients considered themselves cured, 11 were improved, and 1 was worse. Occasional difficulty swallowing not present before surgery occurred in 7 patients at 3 months, and decreased to 2 patients by 12 months after surgery. There were no deaths. Clinically significant complications occurred in four patients. Median hospital stay was 3 days, decreasing from 6.3 in the first 10 patients to 2.3 in the last 10 patients. Endoscopic esophagitis healed in 28 of 30 patients who had presurgical esophagitis and returned for follow-up endoscopy. Twenty-four-hour esophageal acid exposure had returned to normal in 26 of 28 patients studied after surgery. Lower esophageal sphincter pressures had also returned to normal in all patients, increasing from a median of 5.1 mmHg to 14.9 mmHg. CONCLUSIONS: Laparoscopic Nissen fundoplication provides an excellent symptomatic and physiologic outcome in patients with proven gastroesophageal reflux and "typical" symptoms. This can be achieved with a hospital stay of 48 hours and a low incidence of postsurgical complications.     

Obesity and Gastro-esophageal Acid Reflux: Physiopathological Mechanisms and Role of Gastric Bariatric Surgery

Background: Controversial findings about the relationships between obesity and gastro-esophageal reflux have been reported, as well as about the effects of weight loss and bariatric surgery on reflux. The aims of this study were to evaluate esophageal motility and gastro-esophageal acid circadian patterns in obese patients and to test the effects of vertical banded gastroplasty (VBG) on these parameters. Methods: 14 obese subjects (BMI 36-53 kg/m²), 4 men, 10 women, 27-61 years old, admitted for elective bariatric surgery, underwent clinical evaluation, upper endoscopy, esophageal manometry and gastroesophageal pH monitoring. Evaluations were repeated 6 to 12 months after gastric surgery that consisted of a VBG (7 patients), accompanied in the other 7 patients with an anti-reflux procedure (fundoplication). Manometric and pH-metric findings in the obese patients were compared with a normal-weight control group before and after the two different surgical treatments. Results: Gastro-esophageal reflux was significantly more frequent in obese (57.1%) than in control group (7.1%). Esophageal motility in obese subjects was not different from controls. After VBG alone, we found a reduction in basal lower esophageal sphincter (LES) pressure and an increase of acid reflux. When VBG was accompanied by fundoplication, basal LES pressure increased and acid reflux frequency decreased. Conclusions: Obesity is associated with gastroesophageal reflux. VBG reduced weight, but not gastro-esophageal acid reflux. Therefore, in our population, this operation cannot be considered as an antireflux procedure.     

A 15-year experience of injection sclerotherapy in adult patients with extrahepatic portal venous obstruction.

OBJECTIVE: The authors report a 15-year experience with injection sclerotherapy in the management of adult and teenage patients with esophageal varices due to extrahepatic portal venous obstruction (EHPVO). SUMMARY BACKGROUND DATA: Extrahepatic portal venous obstruction is an uncommon cause of esophageal varices and is associated with normal liver function. Effective control of variceal bleeding is the major factor influencing survival. The results of surgery have been unsatisfactory, and therefore, more conservative management policies have been adopted. METHODS: Fifty-five patients with proven EHPVO underwent repeated injection sclerotherapy via either a modified rigid esophagoscope under general anaesthesia or a fiber-optic endoscope under light sedation, using ethanolamine oleate as the sclerosant. RESULTS: Esophageal varices were eradicated in 44 patients after a median number 6 injections (range 1-17) over a mean of 12.5 months (range 1-48). The mean follow-up was 6.8 years (range 1.1-14.6 years). Eleven patients were admitted on eighteen occasions with bleeding from esophageal varices before eradication and there were seven bleeding episodes in six patients from recurrent varices after initial eradication. Complications related to sclerotherapy included injection site leak (6), stenosis (11) and mucosal ulceration (32) during 362 injection sclerotherapy episodes. Four patients died during the study period. CONCLUSIONS: Injection scelotherapy is the treatment of choice in most patients with EHPVO.     

Endoscopic noninvasive manometry of esophageal varices: Prognostic significance

Our study attempts to establish a relation between the pressure in the esophageal varices and the clinical outcome in 18 patients in whom sclerotherapy for bleeding esophageal varices was performed. The measured pressure was compared to the endoscopic findings. Before sclerotherapy, a noninvasive manometric measurement was performed on the varices using a spheric membrane manometer fixed at the tip of an endoscope. Twelve of our 18 patients suffered repeated hemorrhage which led to death in five. We discovered a relation between the measured pressure and the outcome. Beside this, we measured the highest pressures in the largest varices. The relation that seems to exist between the pressure in the esophageal varices, the endoscopic findings, and the severity of the portal hypertension may provide new opportunities for research in this field.     

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.     

Total duodenal diversion for treatment of reflux esophagitis uncontrolled by repeated antireflux procedures.

The operations of Nissen, Hill, and Belsey are adequate in controlling esophaegeal reflux in the majority of patients. In a small percentage however, objective and subjective evidence of esophagitis persists in spite of repeated operations to restore lower esophageal sphincter competency. These failures are then usually treated by operative procedures of great magnitude involving organ interposition. Repeated antireflux operations directed to the gastroesophageal area may in some instances result in impairment of blood supply with an increased risk of both esophageal and gastric fistulae. In the past many observers have felt that reflux esophagitis resulted solely from the effects of acid-pepsin secretions bathing the distal esophagus. Recently experimental and clinical data have indicated the importance of duodenal contents in the etiology and perpetuation of reflux esophagitis. During a recent two year period, 6 patients with persistent reflux esophagitis uncontrolled by repeated antireflux procedures have been seen on our service. These 6 patients, underwent 12 unsuccessful antireflux operations elsewhere. Three of the 6 patients had also been subjected to vagotomy-antrectomy for a coexisting duodenal ulcer. A marked lowering of gastric acidity took place but esophageal reflux and esophagitis persisted. These three patients were treated on our service by takedown of the Billroth I anastomosis, closure of the duodenal stump and diversion of the duodenal contents into a Roux-en-Y limb. Three other patients who had undergone unsuccessful antireflux procedures alone were subjected to antral resection, Roux-en-Y diversion and transthoracid vagotomy. This simplified appraoch to the treatment of persistent esophageal reflux uncontrolled by repeated antireflux procedures has given satisfactory results. The operation should be considered when technical considerations preclude further surgical attempts to perform another effective antireflux operation. Total duodenal diversion should, however, not be considered as the primary operation for the patient suffering from reflux esophagitis. However, in circumstances discussed above this direct approach appears preferable to major resectional procedures.     

Effects of total fundoplication on function of the esophagus after myotomy for achalasia

Twelve patients underwent distal esophageal myotomy for achalasia. After denuding the esophageal mucosa over 50 percent of its circumference, a short (2 cm) total fundoplication was performed over a size 56 mercury bougie. Clinical evaluation showed marked symptomatic improvement. Obstructive symptoms are minimal, and no reflux symptoms were noted. Manometric documentation showed a significant decrease in resting esophageal and lower esophageal sphincter pressure. Contraction pressure was also lowered, and peristalsis returned in 36 percent of the waves in the proximal esophagus. Radiologic and scanning documentation revealed slow emptying without evidence of significant reflux. Endoscopic evaluation revealed no esophagitis after 19 months' follow-up.     

Vertical banded gastroplasty as an antireflux procedure

Vertical banded gastroplasty creates a channel by two applications of the TA-90 stapler from an end-to-end anastomosis window above the crow's foot to the angle of His, against a 32 F. tube along the lesser curvature. The caudad end of the channel is restricted by a 5 cm collar. Thirty-one obese patients more than 45 kg overweight were studied by interview, barium swallow, endoscopy, and manometry. These procedures were repeated 13 +/- 5.5 weeks postoperatively, after resolution of operative edema and before extensive weight loss. Preoperative symptoms included heartburn in 24 patients, regurgitation in 17 patients, and aspiration in 2 patients, and barium swallow demonstrated hiatal hernia in 7 patients and reflux in 7 patients (5 with hiatal hernia). In addition, endoscopy detected mild esophagitis in 3 patients, and hiatal hernia in 11 patients. Postoperatively, the incidence of heartburn decreased in all patients, barium swallow showed slow channel emptying but no hiatal hernia or reflux, and endoscopy did not identify any esophagitis. Preoperative lower esophageal sphincter pressure was 14.5 +/- 7.2 mm Hg. Postoperatively, the vertical banded gastroplasty channel had an initial peak (collar) pressure of 19.2 +/- 7.8 mm Hg (p less than 0.01 compared with preoperative lower esophageal sphincter pressure), a channel pressure of 9.5 +/- 6 mm Hg, a lower esophageal sphincter pressure of 20.1 +/- 7.7 mm Hg (p less than 0.005), and a channel length of 6.8 +/- 1.4 cm. Vertical banded gastroplasty creates a high pressure channel, inhibiting reflux of gastric juice without the need for any additional procedure.