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Biomedical subjects

R A Hinder

Publications and source records attributed to R A Hinder.

At least 73 records · Page 4Linked to original sources
PubMed1997

Laparoscopic Nissen fundoplication: where do we stand?

Laparoscopic Nissen fundoplication was first performed in 1991. With the increasing number of these procedures being performed it is appropriate to review the published short-term results. A retrospective review of reports on this subject was performed. There were a total of 2453 patients available for review. Twenty-five of 2453 (1.0%) patients had an esophageal or gastric perforation and 28 of 2453 (1.1%) patients required transfusion for bleeding. Forty-nine of 2453 (2%) patients developed a pneumothorax. Two of 2453 (0.1%) patients required a splenectomy. Conversion to the open procedure was necessary in 5.8% (143 of 2453) of patients. The laparoscopic approach is associated with minimal postoperative morbidity. Four of 2453 (0.2%) needed further early surgery for persistent bleeding, 11 of 2453 (0.4%) for a missed perforation, 22 of 2453 (0.9%) for crural disruption, paraesophageal herniation, or gastric volvulus. Four of 2453 (0.2%) patients died of either a missed duodenal perforation, a missed esophageal perforation, ischemic bowel with mesenteric thrombosis, or myocardial infarction. Early postoperative dysphagia occurred in 500 of 2453 (20.3%) patients. Late postoperative dysphagia occurred in 114 of 2068 (5.5%), with the need for dilatation in 72 of 2068 (3.5%). Endoscopy was required for food impaction in 11 of 2068 (0.5%) and re-operation for dysphagia occurred in 18 of 2068 (0.9%). Fifty-seven of 1658 (3.4%) patients developed reflux symptoms and 11 of 1658 (0.7%) required revisional surgery. Satisfaction rates ranged from 87 to 100%. In the short term, laparoscopic fundoplication can be performed with less morbidity and mortality than the open procedure. It is superior to medical therapy. Long-term follow-up is awaited.

Esophagitis, Peptic↗
PubMed1997

Management of ingested foreign bodies within the appendix: a case report with review of the literature.

A case is reported of an elective appendectomy in a patient with known ingestion of a sharp foreign body. The metal drill bit was ingested unintentionally 3 months before presentation at our institution. Plain abdominal films demonstrated the foreign body in the right lower abdominal quadrant. Because the gold dental drill bit was sharp and thought to be lodged in the terminal ileum or cecum, an attempt was made to remove the object during colonoscopy. This attempt was unsuccessful because no drill bit could be detected in the colon or terminal ileum. A laparoscopic exploration was performed, and the foreign body was found to lie in the appendix, after bowel manipulation under fluoroscopic guidance and with direct laparoscopic visualization. A laparoscopic assisted appendectomy was performed. On pathologic examination the drill bit was embedded in the tip of the appendix with signs of intramucosal acute inflammation. Management and indication for surgery of foreign bodies in the appendix are discussed, and we review the related literature. This is the second reported case of a dental drill bit in the appendix causing appendicitis.

Aged↗
PubMed1996

Heller myotomy via minimal-access surgery. An evaluation of antireflux procedures.

BACKGROUND: Myotomy offers the best known cure for achalasia and can now be performed via minimal-access surgery. OBJECTIVE: To examine the questions of surgical approach for Heller myotomy and choice of fundoplication in the setting of minimal-access surgery. DESIGN: Thirty-nine patients with achalasia underwent Heller myotomy via either thoracoscopy or laparoscopy, with either a Dor or a Toupet fundoplication (Heller-Dor and Heller-Toupet procedures, respectively). Manometry, pH analysis, and clinical course were evaluated 3 to 9 months after surgery. Clinical course was reviewed at 11 to 46 months after surgery. SETTING: University hospitals. PATIENTS: Diagnosis of achalasia was based on history and physical examination, contrast radiography, stationary manometry, and 24-hour pH analysis. All patients participated in the clinical evaluations. Twenty-two patients consented to postoperative manometry and 18 to postoperative pH analysis. INTERVENTIONS: Thoracoscopic Heller-Dor procedures (n = 4), laparoscopic Heller-Dor procedures (n = 6), and laparoscopic Heller-Toupet procedures (n = 29). MAIN OUTCOME MEASURES: Hospital stay and recovery time were compared between thoracoscopic and laparoscopic groups. Decrease in the lower esophageal sphincter pressure, 24-hour esophageal pH, postoperative symptoms, and overall satisfaction were compared between the Dor and Toupet groups. RESULTS: Only 1 patient was dissatisfied with the experience. Patients undergoing thoracoscopy had a longer convalescence. No postoperative reflux was identified, although some patients complained of heartburnlike symptoms. Dysphagia and heartburn were more prevalent among patients with Dor fundoplication than among patients with Toupet fundoplication. CONCLUSIONS: Minimal-access myotomy is an excellent intervention for achalasia. The preferred approach is via laparoscopy. Our experience has led us to favor the Toupet over the Dor fundoplication after myotomy.

Cardia↗
PubMed1996

Duodenogastric reflux causes growth stimulation of foregut mucosa potentiated by gastric acid blockade.

We investigated whether duodenogastric reflux (DGR) together with gastroesophageal reflux causes growth stimulation of the foregut mucosa and if additional gastric acid suppression enhances the effect of DGR. DGR was induced in rats using a split gastroenterostomy. A cardiomyotomy was performed across the gastroeophageal junction in order to enhance reflux into the esophagus. DGR rats were divided into six subgroups: DGR, DGR + truncal vagotomy, DGR + omeprazole, DGR + gastrin receptor blockade, DGR + omeprazole + gastrin receptor blockade, and DGR + gastrin. Two sham groups, one with and one without omeprazole treatment, served as controls. DGR significantly increased the weight and DNA content of the esophageal and gastric mucosa, which was further enhanced by vagotomy or omeprazole. Histology revealed foveolar hyperplasia in the stomach and esophageal mucosal hyperplasia in these groups. In addition, severe esophagitis was found in the DGR group receiving omeprazole. Omeprazole without DGR had no growth-stimulating effect on the foregut mucosa. DGR-induced growth stimulation was accompanied by hypergastrinemia. Increased growth in the stomach but not the esophagus was inhibited by gastrin receptor blockade. Gastrin administration did not result in enhancement of DGR-induced growth stimulation of the foregut mucosa. It is concluded that DGR, often present in severe reflux esophagitis, causes mucosal growth of the foregut of rats. This trophic response may explain why severe reflux esophagitis is associated with an increased risk of esophageal adenocarcinoma. DGR-induced growth stimulation of the foregut is potentiated by gastric acid suppression, suggesting that chronic antisecretory medication in gastroesophageal reflux may not always be advisable. Omeprazole + DGR caused severe esophageal damage, which may explain why antisecretory medication may fail to heal severe reflux esophagitis.

Animals↗
PubMed1996

Three-dimensional imaging of the lower esophageal sphincter in healthy subjects and gastroesophageal reflux.

The resting pressure and intraabdominal length are the most important factors which determine competence of the lower esophageal sphincter (LES). The intraabdominal sphincter vector volume (ISVV) is a single value which takes into account both of these measurements. Normal values of ISVV and of the total sphincter vector volume (TSVV) were established in 20 normal subjects. The sensitivity and the specificity of ISVV and TSVV were then evaluated in 81 patients with gastroesophageal reflux disease (GERD) and in 19 normal subjects and were compared with the usual stepwise pullback manometry (SPM) measuring the resting pressure of the LES at the respiratory inversion point. The motorized pullthrough technique was used to perform the vector volume procedure. Normal values of ISVV were 1870-10740 mm Hg2 x mm, and of TSVV 2200-13110 mm Hg2 x mm. The sensitivity of ISVV was 93.8% (p < 0.05), of TSVV 80.2%, and of SPM 81.5%. The specificity of ISVV and TSVV was 89.5% and of SPM 78.9% (not significant). Analysis of the intraabdominal sphincter vector volume is more sensitive than the total sphincter vector volume or standard stationary manometry in establishing a defective LES in patients with GERD. Intraabdominal sphincter vector volume analysis will allow surgeons better to identify patients with a defective LES who may be suitable for antireflux surgery.

Diagnosis, Computer-Assisted↗
PubMed1996

Mechanisms and avoidance of esophageal perforation by anesthesia personnel during laparoscopic foregut surgery.

BACKGROUND: This study retrospectively assesses the mechanisms of 13 esophageal or gastric injuries resulting from dilator or nasogastric tube placement during laparoscopic foregut surgery and is intended to assist in determining methods of prevention. METHODS: Information regarding esophageal or gastric injury during laparoscopic foregut surgery was obtained from six experienced laparoscopic surgeons. The specific mechanisms of injury were determined by discussion with the operating surgeon and review of the operative reports. RESULTS: Eleven cases of esophageal or gastric perforation occurred during bougie insertion and two perforations occurred secondary to nasogastric tube placement during Nissen fundoplication or Heller myotomy. Five perforations required conversion to open operation for repair including two delayed thoracotomies. The 13 injuries occurred during the performance of 1,620 laparoscopic foregut operations for an overall incidence of 0.8%. CONCLUSION: Foregut injury resulting from esophagogastric intubation during laparoscopic surgery is more common than expected. Risk factors include esophageal anatomy, intrinsic pathologic changes of the esophagus, and inexperience. Prevention must focus on close communication between the surgeon and anesthesiologist and safe techniques of dilator insertion.

Adult↗
PubMed1996

The hypertensive lower esophageal sphincter.

BACKGROUND: This study defines the entity of the hypertensive lower esophageal sphincter (HLES) and its treatment, including surgical implications. METHODS: Esophageal manometry was performed on 1,300 patients. Of these, 53 (4%) had HLES with resting pressure > 26.5 mm Hg, defined as the upper limit of normal resting LES pressure. Thirty-two of these patients had 24-hour esophageal pH studies. The response to treatment was assessed. RESULTS: Fourteen patients (26%) with HLES had achalasia. Of the remaining 39 (74%), 25 had an isolated HLES with normal esophageal body motility, 5 had a nonspecific esophageal motility disorders (NEMD), 4 were post-Nissen fundoplication, 3 had a nutcracker esophagus, and 2 had diffuse esophageal spasm (DES). Nineteen percent of HLES patients had gastroesophageal reflux on pH studies. Eighty-two percent of HLES patients responded well to symptom-directed medical therapy. Two patients with esophageal body dysmotility responded well to an esophageal myotomy with a partial fundoplication. CONCLUSIONS: Patients with the HLES form a heterogeneous group. Gastroesophageal reflux in HLES patients is not uncommon. Patients with HLES respond well to medical therapy. Carefully selected patients require surgery.

Adolescent↗
PubMed1996

Laparoscopic technique of proximal selective vagotomy.

Proximal selective vagotomy (PSV) is an effective, definitive therapy for peptic ulcer disease of the duodenum. Long-term studies have shown that ulcer recurrence occurs in less than 10% of patients if the operation is performed by an experienced surgeon. Since PSV does not influence gastric emptying, side effects such as diarrhea, gastric stasis or the dumping syndrome are rare. Due to this favorable experience, PSV is our preferred technique for the laparoscopic approach to peptic ulcer disease. We have performed this operation in 13 patients. Indications were chronic duodenal ulceration unresponsive to medical therapy, chronic duodenal ulceration combined with reflux esophagitis, and reflux esophagitis due to gastric acid hypersecretion. In patients with reflux esophagitis PSV was performed in addition to an antireflux procedure. Laparoscopic PSV can be performed more accurately than the open procedure since it allows for better visualization with less possibility of missing small vagal connections to the parietal cells such as the 'criminal nerve'. The median duration of operation was 3 hours. There were no serious peri- or postoperative complications. The median time of postoperative hospital stay was 3 days. During the median follow-up of 27 months no recurrence of duodenal or esophageal ulceration was encountered and none of the patients complained of epigastric pain, diarrhea or dumping symptoms.

Adult↗
PubMed1995

An intraluminal surgical approach to the management of gastric bezoars.

Trichobezoars are difficult to remove endoscopically, often cause nausea and vomiting, and can result in small-bowel obstruction. A patient with a trichobezoar presented to our clinic with symptoms of partial small-bowel obstruction. Multiple attempts at flexible endoscopic removal were unsuccessful. Two large-diameter percutaneous gastrostomies with an inflatable balloon and distal foam-rubber stent to assure intragastric positioning were introduced under general anesthesia. Visualization was provided by a 0 degree panavision laparoscope placed through one of the gastrostomies. The bezoar was removed through the second gastrostomy using standard laparoscopic instruments. The patient made an uneventful recovery. This is the first reported case of percutaneous removal of a trichobezoar. We conclude large-diameter gastrostomies may serve as a port of access for numerous other intraluminal procedures.

Bezoars↗
PubMed1995

In vitro free radical production in rat esophageal mucosa induced by nicotine.

Oxidative stress induced by nicotine was investigated in the esophageal mucosa of rats. The homogenized mucosa was incubated for 30 min with 50, 100, 200, 400, and 800 ng/mg protein/ml nicotine or with 200 ng/mg protein/ml nicotine for 15, 30, 45, and 60 min. Esophageal mucosa was also incubated for 30 min with 200 ng/mg protein/ml nicotine with or without the scavengers superoxide dismutase (SOD), catalase, SOD+catalase, inactivated SOD, inactivated catalase, or albumin. Incubation with 0.9% NaCl served as control. There was a strong correlation between chemiluminescence and the nicotine dose (r = 0.75) or the nicotine incubation time (r = 0.77). Thirty-minute incubation of the esophageal mucosa with 200 ng/mg protein/ml nicotine increased chemiluminescence 5.5-fold and lipid peroxidation 3.3-fold. This response was dampened by SOD or catalase and abolished by SOD+catalase. Inactivated enzymes or albumin had no scavenging effect. These results demonstrate that nicotine causes oxidative stress to the esophageal mucosa.

Animals↗
PubMed1995

Free radical scavengers prevent reflux esophagitis in rats.

Free radical damage in reflux esophagitis of rats induced by 24-hr duodenojejunal ligation was studied. Oxygen free radicals were selectively blocked. Groups were: sham operation, reflux, reflux + superoxide dismutase (SOD), catalase, dimethylthiourea, allopurinol, and inactivated SOD or inactivated catalase alone or in the combination SOD + catalase or SOD + catalase + dimethylthiourea + allopurinol. Macroscopic esophagitis was inhibited only by SOD, alone or in combination with other agents. Esophageal mucosal lipid peroxidation was 10-fold increased in the reflux group compared to the sham group (P < 0.05). This response was damped by SOD > catalase (P < 0.05) but not by the inactivated enzymes, dimethylthiourea or allopurinol. SOD + catalase showed no significant improvement on SOD alone. Total inhibition of lipid peroxidation was achieved by combining all scavengers. Total glutathione (GSH) in the esophageal mucosa was stimulated by reflux. This response was inhibited by scavengers equivalent to their efficacy in preventing lipid peroxidation. It is concluded that reflux esophagitis is associated with free radical release with O2- being the main source. Free radicals appear to stimulate GSH production in this prolonged oxidative stress.

Animals↗
PubMed1995

Esophagitis in Sprague-Dawley rats is mediated by free radicals.

Free radical-mediated esophagitis was studied during duodenogastroesophageal reflux (mixed reflux) or acid reflux in rats. The influence of reflux on esophageal glutathione levels was also examined. Mixed reflux caused more gross mucosal injury than acid reflux. Gross mucosal injury occurred in the mid-esophagus. Total glutathione (GSH) in the esophageal mucosa of control rats was highest in the distal esophagus. The time course of esophageal GSH in rats treated by mixed reflux showed a significant decrease 4 hr after initiation of reflux, followed by a significant increase from the 12th hour on. Mucosal GSH was increased in both reflux groups after 24 hr but significantly more so in the mixed than in the acid reflux group. The free radical scavenger superoxide dismutase (SOD) prevented esophagitis and was associated with decreased GSH levels. GSH depletion by buthionine sulfoximine (BSO) prevented esophagitis and stimulated SOD production in the esophageal mucosa. It is concluded that gastroesophageal reflux is associated with oxidative stress in the esophageal mucosa. The lower GSH levels in the mid-esophagus may predispose to damage in this area. Duodenogastroesophageal reflux causes more damage than pure acid reflux. Oxidative stress leads to GSH depletion of the esophageal mucosa in the first few hours following damage but then stimulates GSH production. GSH depletion by BSO does not worsen esophagitis since it increases the esophageal SOD concentration.

Animals↗
PubMed1995

Free radical production in nicotine treated pancreatic tissue.

The ability of nicotine to induce oxidative stress in the pancreatic tissue of rats was investigated. Homogenized pancreatic tissue of Sprague-Dawley rats was incubated with nicotine in a dose of 200 ng/mg protein/ml for 15, 30, 45, and 60 min or was incubated for 30 min with nicotine in a dose of 50, 100, 200, 400, and 800 ng/mg protein/ml. Pancreatic tissue was also incubated with 200 ng/mg protein/ml nicotine with or without the scavengers superoxide dismutase (SOD), catalase, SOD+catalase, inactivated SOD, inactivated catalase, or albumin. Incubation with 0.9% NaCl served as control. There was a positive correlation between the duration of nicotine incubation and chemiluminescence (r = 0.6) or lipid peroxidation (r = 0.71) and also between the nicotine dose and chemiluminescence (r = 0.54) or lipid peroxidation (r = 0.66). Thirty minutes incubation of pancreatic tissue with nicotine in a dose of 200 ng/mg protein/ml increased chemiluminescence 5 fold and lipid peroxidation 2.5 fold. This response was dampened by SOD or catalase and abolished by SOD+catalase. Inactivated enzymes or albumin had no scavenging effect. These results demonstrate that nicotine causes oxidative stress to the pancreatic tissue of rats.

Animals↗
PubMed1995

Reflux esophagitis in humans is mediated by oxygen-derived free radicals.

BACKGROUND: Oxidative stress in reflux esophagitis was investigated before and after antireflux surgery. PATIENTS AND METHODS: Oxidative stress was studied in the distal and proximal esophagus of control patients (without esophagitis, but with other gastrointestinal disorders), of patients with various grades of esophagitis (including Barrett's esophagus), and in patients who had a Nissen fundoplication. Oxidative stress was assessed by chemiluminescence, lipid peroxidation (LP), and by measuring superoxide dismutase (SOD). RESULTS: Chemiluminescence and LP increased with the degree of esophagitis and was highest in patients with Barrett's esophagus; SOD decreased with damage, except in cases of Barrett's esophagus associated with mild esophagitis. Chemiluminescence and LP in reflux patients were higher in the distal than in the proximal esophagus, and SOD was lower, whereas no such difference was found in controls. Findings after Nissen fundoplication were similar to those of controls. CONCLUSIONS: Reflux esophagitis is mediated by free radicals depleting SOD. Barrett's esophagus is a severe form of oxidative damage; in some patients, high SOD levels may prevent severe esophagitis. Antireflux surgery prevents oxidative damage.

Barrett Esophagus↗
PubMed1995

Pathologic duodenogastric reflux associated with persistence of symptoms after cholecystectomy.

BACKGROUND: The aim of this study was to determine whether increased duodenogastric reflux contributes to postcholecystectomy symptoms. METHODS: Gastric pH monitoring, hepatobiliary scintigraphy, gastric emptying scans, and gastric acid analysis were performed in asymptomatic (n = 10) and in symptomatic (n = 27) patients after cholecystectomy. Normal subjects (n = 20), patients with dyspepsia related to gastric acid hypersecretion (n = 20), patients with reflux gastritis after gastric surgery (n = 10), and patients with confirmed primary pathologic duodenogastric reflux (n = 10) were studied as controls. Symptomatic patients also underwent upper gastrointestinal endoscopy. RESULTS: Symptomatic patients had significantly increased interprandial gastric exposure to pH < 3 compared with asymptomatic subjects, which correlated well with a high incidence of hepatobiliary scans positive for abnormal duodenogastric reflux and chronic gastritis on endoscopy. Gastric alkaline exposure in symptomatic patients was similar to that seen in patients with primary pathologic duodenogastric reflux and patients with duodenogastric reflux related to gastric surgery. Gastric acid secretion and gastric emptying were not altered. Five patients tested before and after laparoscopic cholecystectomy showed that nocturnal gastric alkalization was enhanced after operation. CONCLUSIONS: This study suggests that excessive duodenogastric reflux may be responsible for persistence of symptoms after cholecystectomy.

Adult↗
PubMed1995

Profound duodenogastric reflux causes pancreatic growth in rats.

Although duodenogastric reflux is a physiological event, excessive reflux may be a pathogenetic factor in several diseases of the foregut, including cancer. Long term profound duodenogastric reflux produces pancreatic and gastric tumours in rats. The trophic effect of surgically induced duodenogastric reflux on the pancreas was investigated and the mechanisms involved were examined. Rats with profound reflux from a split gastroenterostomy were compared with sham operated and unoperated controls after two and six weeks. In the six week experiment, one reflux and one sham group were given the cholecystokinin (CCK) receptor antagonist devazepide (25 nmol/kg/h). Duodenogastric reflux caused a significant increase in pancreatic weight, DNA, and plasma CCK and gastrin concentrations at both two and six weeks. Devazepide substantially reduced the pancreatic weight increase after six weeks but did not abolish it completely. CCK and gastrin were not affected by devazepide. These results suggest that CCK is largely responsible for the pancreatic growth induced by reflux but another factor may also be involved. The trophic effect of duodenogastric reflux may contribute to the increased incidence of pancreatic cancer reported after gastric surgery.

Animals↗
PubMed1995

The technique of laparoscopic Nissen fundoplication.

Patients with severe GERD resistant to medical therapy are benefited greatly by laparoscopic fundoplication provided that there is careful preoperative patient selection and evaluation. Preoperative evaluation should include contrast esophagography, EGD with biopsies, stationary manometry, and 24-hour pH analysis. Significant esophageal shortening or severe dysplasia are contraindications to laparoscopic fundoplication. A short, loose Nissen fundoplication should be performed in patients with adequate esophageal body function, whereas patients with esophageal dysmotility should be offered a partial fundoplication such as the Toupet procedure. If these guidelines are followed, long-term good results can be expected, with minimal complications, and all of the advantages of the minimally invasive approach.

Follow-Up Studies↗