The Angelchik prosthesis appears to be effective in preventing gastroesophageal reflux, although its precise mechanism of action remains controversial. In a unique in vitro model, 10 freshly harvested canine esophagogastric specimens were tested for their ability to remain competent against challenges of intragastric pressure under controlled conditions of intra-abdominal pressure, longitudinal esophageal tension, lower esophageal sphincter pressure and overall length and circumference of the cardia (measure of gastric dilatation). Competency of the specimen was assessed by stepwise variation in the overall length of the sphincter, while keeping constant intraabdominal pressure (20 cm H2O), intragastric pressure (20 cm H2O), esophageal tension (physiologic), lower esophageal sphincter pressure (15 cm H2O) and degree of gastric dilatation (3 cm). With each specimen serving as its own control, the effect produced by the application of an Angelchik prosthesis was evaluated. Results consistently demonstrated that at any lower esophageal sphincter length the percent of competency was increased when the prosthesis was applied (P < 0.01). The findings indicate that the Angelchik prosthesis controls reflux by preventing unfolding of the lower esophageal sphincter when challenged by intragastric pressure.
Clinicopathological features of cystic neoplasms of the pancreas were studied in 38 patients of whom 22 had serous cystadenoma, 7 benign mucinous cystadenoma, 7 cystadenocarcinoma, and 2 solid and cystic tumour. Of the latter tumours, one was malignant. Sixteen patients (12 with serous cystadenoma) had previously or simultaneously non-pancreatic malignant disease, mostly of the urogenital tract. There was a female predominance of 29/9 in the series and median age differed between tumour types. Mean tumour sizes were similar in the different tumour types. Compared with the other tumours, serous cystadenomas were more frequently situated in the body or tail of the pancreas. Macroscopically, serous cystadenoma were often indistinguishable from pseudocysts, although the absence of previous pancreatitis, alcohol abuse, and gallstone disease favour the diagnosis of neoplasia. The malignant tumours rarely metastasized and showed a far better prognosis than ductal adenocarcinoma of the pancreas. Since serous cystadenoma occurs in old age (median 76 years), is often without symptoms, and is easily diagnosed histologically, a conservative surgical approach might be considered when symptoms are absent. All other tumours should be excised.
Between 1968 and 1984 liver resection with curative attempt was performed in 22 patients with hilar cholangiocarcinoma. Right lobectomy was performed in 4 patients, extended right lobectomy in 7, left lobectomy in 8, and excision of the median segment segment of the left lobe (segment IV) in 3. Bilio-enteric continuity was restored by hepatocholedochostomy in 17 patients and hepatojejunostomy in 4. (One patient had external transhepatic catheter drainage and no internal bile drainage.) Operative mortality rate was 27% and caused by excessive intraoperative bleeding, sepsis, or liver insufficiency. Postoperative complications occurred in 57% of patients surviving the operation and were due mainly to leakage from the hepatocholedochostomy. Median survival was 6 months, and one third of the patients survived 1 year. Three patients survived 10 years and were among the four patients in whom a tumor-free resection margin was obtained (one of them died in the postoperative phase). It is concluded that resection of hilar cholangiocarcinoma may give long-term survival if a free resection margin is obtained. The importance of a free resection margin indicates that surgery should be aggressive and include liver resection.
Plasmapheresis was used as a complement to conventional therapy in a patient with multiorgan failure and disseminated intravascular coagulation (DIC) following biliary obstruction and septic cholangitis. The patient's remarkable improvement after plasmapheresis suggests a beneficial influence on the pathophysiologic mechanisms. Plasmapheresis is concluded to inhibit DIC and eliminate endotoxins.
Determining whether recurrent chest pain emanates from an esophageal or cardiac disorder presents a formidable challenge even for the most astute clinician. The overlapping response to provocative as well as therapeutic drugs and the often atypical nature and distribution of the pain adds to these difficulties. Evaluation of these patients is difficult, not only because of the overlapping clinical picture, but also because of the danger in using provocative drugs in those with demonstrated coronary artery disease to evoke chest pain [5, 6]. Because of our experience in encountering this situation clinically, we reviewed the records of 24 patients with proven coronary artery disease in whom it was also found necessary to perform complete esophageal diagnostic testing, including 24-h esophageal pH and esophageal manometry. The results of treatment, including simultaneous surgical repair of two disorders, were also analyzed.
To evaluate the influence of the composition of refluxed material in the pathogenesis of esophagitis, a dog model was used to allow esophageal reflux of gastric secretions, duodenal pancreaticobiliary secretions, and a combination of both. Control dogs had only an esophageal incision. Incompetence of the cardia was established in five other groups by transecting the distal sphincter and creating a hiatal hernia. Two groups received moderate or maximal histamine stimulation of gastric secretion. A gastroje-junostomy, pyloromyotomy, and duodenal closure distal to the papilla were added in the other three groups, creating duodenogastric reflux; two were stimulated with histamine and one had a truncal vagotomy and no histamine. Radiologic, manometric, and pH studies showed that incompetence of the cardia was obtained. The dogs were killed 4 wk postoperatively and evaluated for gross and microscopic evidence of esophagitis. Erosive esophagitis was found only in dogs with reflux of gastric juice following maximal acid stimulation. Microscopic reflux changes in esophageal mucosa were seen in all groups; again, changes were most pronounced in dogs with maximal gastric stimulation. The combination of duodenogastric reflux and moderate gastric stimulation produced more significant alterations in microscopic reflux criteria than did moderate gastric stimulation alone. Our conclusions are as follows: In a dog model of gastroesophageal reflux of various combinations of gastric and duodenal secretory components, erosive esophagitis occurred only with maximal gastric stimulation in the absence of duodenogastric reflux. All reflux combinations, however, produced some degree of microscopic changes, suggesting they could eventually cause gross changes with a lengthened experimental time span.
Pressure and abdominal length of the distal esophageal sphincter are important factors in maintaining competency of the cardia against challenges of intraabdominal pressure. Some patients with normal distal esophageal sphincter pressure and position may have reflux which could be due to the inability of the cardia to overcome challenges of intragastric pressure. Three experimental studies and one clinical study were designed to evaluate this problem. The results showed that the resistance to flow through the cardia is related to the integrated effect of distal esophageal sphincter pressure and length; the ratio of distal esophageal sphincter to intragastric pressure necessary to maintain competency is inversely related to the length of sphincter present; gastric dilatation has an adverse effect on the degree of competency achieved by a given distal esophageal sphincter length; and patients with an overall distal esophageal sphincter length of 2 cm or less measured at rest in the fasting state are subject to reflux caused by gastric dilatation, increased intragastric pressure independent of intraabdominal pressure, or both.
In construction of the eosphagojejunostomy after total gastrectomy, the EEA stapled (US Surgical Corporation, Norwalk, CT) and the two-layer interrupted 3-0 Dexon anastomoses are compared concerning the radiological appearance, breaking strength, circulation, and collagen concentration. Thirty female pigs were used. After total gastrectomy and Roux-en-Y preparation, the pigs were randomized to achieve sutured or stapled anastomoses. 141Ce-labeled microspheres were used for measurements of anastomotic blood flow. After the pigs were killed, the breaking strength of the anastomosis was recorded, the collagen content determined, and an anastomotic index calculated comparing two perpendicular diameters in the anastomosis and 5 cm above. Breaking strength, leakage frequency, and anastomotic index were the same in the two groups. One week after surgery, there was a significant increase in anastomotic circulation (p less than 0.05) in both the sutured and the stapled anastomoses compared to controls. Collagen increased equally with time in the two groups (p less than 0.01). The stapled esophagojejunostomy was faster to perform (20 min) than the sutured (28 min) (p less than 0.05).
To evaluate function of the normal and pathologic esophageal body under more physiologic conditions than those utilized for traditional laboratory testing, manometry was performed before and during eating using a catheter assembly containing three peripheral transducers. Studies were evaluated from seven normal volunteers, 18 typical achalasia patients (eight before and 10 after esophagomyotomy), and eight patients with diffuse esophagcal spasm (DES) as characterized by frequent simultaneous and repetitive contractions. In the preprandial period, all had similar frequencies of esophagcal contractions, although there was a wide range. During eating, the frequency of contractions increased in all groups; however, the contraction frequency in unoperated achalasia patients, 12.7 ± 5.0 contractions/min, significantly exceeded the frequency in normal volunteers of 4.9 ± 1.3 contractions/min, p < 0.01. The frequency was lower in operated achalasia patients, 9.4 ± 6.5 contractions/min, but still exceeded that of normal volunteers, p < 0.01. Patients with DES also had more frequent contractions, 10.5 ± 9.7 contractions/ min, than did the normal volunteers, p < 0.01. The mean pressure of esophagcal contractions for both achalasia groups was similar and was significantly lower than for the normal volunteers. Pressure in the DES patients was intermediate. It is concluded that patients with achalasia have lower pressure but more frequent contractions than normal volunteers during eating, and this spasm-like activity may be a more important pathophysiologic factor in their dysphagia than previously recognized. Esophagomyotomy does decrease the frequency of these contractions. Frequency, but not pressure, of contractions differs from normal in patients with DES.
Esophagojejunostomy after total gastrectomy was attempted in 27 operations with the EEA stapling device (U.S. Surgical Corp., Norwalk, Conn.). After removal of the specimen the anastomosis is performed with an end-to-side technique with insertion of the cartridge and its central rod through the open jejunal end. The 28 mm wide cartridge was used in 24 anastomoses and the 25 mm wide cartridge was used in two. In one case the 25 mm cartridge tore the distal esophagus, and the anastomosis had to be sutured manually. The median operation time was 305 minutes (range, 205 to 560 minutes), and the time to perform the anastomosis was 20 minutes (range, 15 to 60 minutes). Anastomotic leakage occurred in three patients, two of whom were stapled with the 25 mm cartridge. All healed with conservative treatment. One patient developed a stricture at the anastomotic site due to recurrence of the tumor. There was one hospital death. Median hospital stay was 16 days (range, 8 to 71 days) and median survival time was 11 months. It is concluded that the EEA stapler allows the construction of a fast and reliable esophagojejunostomy with good functional results after total gastrectomy for gastric cancer.
In 39 patients with severe attacks of acute pancreatitis, a longitudinal study was done with respect to the influence of peritoneal lavage on objective prognostic signs (WBC, blood-glucose, serum-calcium, hematocrit, serum-creatinine, arterial pO2, base deficit); amylase activities in peritoneal fluid, serum, and urine; serum-hemoglobin, serum-Na, serum-K, and plasma-insulin. In addition to standard care in the ICU, half of the patients (N = 19) were randomly treated with peritoneal lavage. Peritoneal lavage did not influence overall mortality (13%), incidence of major complications (36%), or hospital stay (23 +/- 7 days). None of the prognostic signs was significantly influenced by lavage. Amylase concentration in peritoneal fluid was significantly reduced in the lavaged group after 6 hours compared to 24 hours in controls. Serum and urinary amylase decreased 12 hours earlier in the lavaged group, indicating an efficiency of the lavage procedure per se. Still, this study did not reveal any beneficial clinical effects of peritoneal lavage in acute pancreatitis.
Basal pressure and relaxation of the lower oesophageal sphincter (LOS) as well as amplitude, duration and propagation velocity of peristaltic waves in the distal third of oesophagus were measured in 15 healthy adults (nine men and six women). A highly standardised technique was used employing manometric equipment including a low-compliance pneumohydraulic infusion system and a triple lumen recording catheter. After establishment of baseline manometry values the catheter was positioned with its distal orifice in the lower oesophageal sphincter. In 10 subjects 0.2 mg/kg body weight of morphine sulphate was then injected subcutaneously. In five others equal volume of saline was given. The manometric data were analysed blindly. Repeated manometric evaluations were carried out 15, 30, 45, 60, and 75 minutes after the injection. Morphine increased slightly LOS-pressure and significantly (p less than 0.001) decreased LOS-relaxation, the maximal effect occurring 30 minutes after the injection. Amplitude of peristaltic waves increased slightly but insignificantly, whereas propagation velocity and duration were uninfluenced. The results of this study suggest that pharmacologic doses of morphine influence normal function of the LOS and possibly the distal oesophagus. The role of endogenous opiates in this respect, however, awaits further studies. It is suggested that abnormalities in opioid neurotransmission may explain some of the non-specific oesophageal motility disorders.
In short-term experiments (25 or 72 h) oral trypsin inhibitor administration to pancreatitic rats significantly decreased survival rate, whereas oral trypsin administration had no effect in this respect. Neither treatment influenced the activities of amylase in serum, pancreatic tissue or ascites. Trypsin given in excess together with the trypsin inhibitor abolished the deleterious effects on survival caused by the trypsin inhibitor. In a long-term experiment in healthy rats oral trypsin inhibitor ingestion caused a significant increase in pancreatic wet weight, protein concentration and activities of amylase, lipase and trypsinogen in pancreatic tissue; again, trypsin administration had no effect. The data support the idea that oral trypsin inhibitor administration causes release of cholecystokinin (CCK) or CCK-like factors from the intestine by interfering with the negative feedback regulation exerted by intraluminal trypsin. The results of the short-term experiments further indirectly suggest that even small amounts of trypsin within the intestine - as in acute pancreatitis - can exert the feedback regulation. Finally, the results of the long-term experiment suggest that oral administration of trypsin does not exert any suppressive effects on pancreatic wet weight and pancreatic enzyme content.