Surgical treatment of stricture of the esophagus associated with hiatal hernia.
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OBJECTIVE: To analyze and determine the clinical characteristics and diagnostic methods of chronic intestinal pseudo-obstruction(CIP). METHODS: We reviewed the medical records of all 23 patients who diagnosed with CIP in Peking Union Medical College Hospital from 1978 to 2000. RESULTS: Twenty three patients fulfilled the diagnostic criteria (9 male, 14 female, median age 50 years, range 4-75 years). The main symptoms at the presentation were abdominal distension(87%), pain(57%), diarrhea(65%), constipation(48%), vomiting(39%) and weight loss(83%). In this group of CIP patients, the abdominal distension was more common and serious than pain, presenting with diarrhea, weight loss and dismotility in esophagus and stomach. Bowel loops and visible peristaltic waves were seldom observed in the CIP patients. The plain film showed the multiple air-fluid levels (17/20, 85%) and generalized intestinal distention and air in colon. The abnormal findings on the barium contrast examination included intestinal dilation (19/23, 83%), weaken peristalses or/and prolongation of transit time (74%) without mechanical lesions. The pseudo-obstruction involved the small intestine (83%) and colon (39%) that determined according to the radiographic features, abnormal gastrointestinal motor functions, findings of endoscopic examination and laparotomy. Eighteen cases were chronic idiopathic intestinal pseudo-obstruction (1 familial myopathy), 5 were secondary to CTD. CONCLUSIONS: Comparison with the typical mechanical obstruction, the presentations of CIP have some relatively characteristics. The clinical diagnosis of CIP can be confirmed on the basis of typical clinical symptoms and radiographic features, abnormal gastrointestinal motility.
Therapy of inoperable carcinoma of the esophagus and cardia must be based on correction of the dysphagia. On that purpose, a new endoprosthesis (type ESKA-Buess) was used. 57 patients were treated by endoscopic placement of an endoprosthesis. The mortality was 3.5%, patients survived appr. 3 months. All patients experienced a marked improvement in swallowing ability, 61% of our patients could swallow normally. The new endoprosthesis showed no relevant alteration in regard to form and material.
Thirty-three patients with free perforation in Crohn's disease are described. There are 14 males and 19 females in this series with ages ranging from 14 to 79 years. The sites of perforation were 22 of the ileum, nine colonic, one jejunal, and one gastroduodenal. Toxic megacolon coexisted in two. Reperforation occurred in three. Free perforation was the presenting sign of the disease in three. Steroid therapy coexisted in 16 patients but in five was administered for less than 10 days before perforation. Obstruction coexisted in only three patients. There were two deaths. Twenty-two patients were treated with resection and diversion, nine patients with resection and drainage, and two with plication only. No relationship between steroid therapy, duration of disease, toxic dilatation, or obstruction with perforation could be established. Resection of the perforated disease segment is necessary when possible. In contradistinction to previous literature, free perforation in Crohn's disease is not as unusual as heretofore believed.
A wide range of therapeutic methods for treatment of malignant and benign stenoses of the upper gastrointestinal tract is at one's disposal with esophageal mechanical dilatation, laser therapy, insertion of plastic tubes and stent implantation. It has become routine to insert flexible metal stents in the treatment of esophageal carcinoma and tracheoesophageal fistula. Case reports exist describing the use of flexible metal stents in complicated benign esophageal stenoses of stomach and duodenum. Until January 1997 we implanted 18 stents (7 Z-stents[Wilson and Cook], 4 covered and 4 uncovered Ultraflex stents [Boston Scientific], 3 Endocoil stents [Instent]) in 15 patients. We treated patients with esophageal carcinoma, recurrent stenoses after gastrectomy and tracheoesophageal fistula. They were followed by questionnaires. Four days after stent implantation 50% of the patients were able to consume normal solid food, the other half semisolids. The main problem was the stent migration (28%). The decisive factors for stent migration were the quality of surface of the stent and its position in the gastroesophageal junction. The stents which were dislocated in the stomach could easily be extracted endoscopically. The endoscopic extraction of a dislocated Z-stent in the small bowel was impossible. The high rate of stent dislocation (20-30%) in distal stent position (gastroesophageal junction) is not to be tolerated with respect to the purchase price.
Exposure of the mucosal surface of exteriorized chambered fundic segments of dog stomach to p-chloromercuribenzene sulfonate (PCMBS) resulted in predictable gross and microscopic structural changes. The first visible response after PCMBS (10 mM) in isosmotic HCl was an intense release of periodic acid-Schiff-stainable mucus. Within 2 min, radioactive PCMBS was found within cells along the entire depth of the gastric glands. Surface cells at 15 min revealed vacuolization of the cell cytoplasm, dilation of the perinuclear and intercellular spaces, mitochondrial swelling, loss of microvilli, and plasmalemma irregularities. Tight junctions, Golgi, and mucous granules appeared unaltered. However, in advanced injury, mucous granules became less dense and their membranes, which were usually smooth, became fragmented and convoluted at this point. Necrotic parietal cells were extruded into the lumen. Damage, however, only rarely extended into the deeper glandular and connective tissue areas.
Esophageal dilatation (ED) in neonates is rare. In the present case, ED was detected in a chest radiograph following repair of congenital diaphragmatic hernia (CDH) in a term neonate. A roentgenographic swallow study on the seventh day of life demonstrated ED and a sub-diaphragmatic stomach. The infant thrived adequately on enteral feeding. A swallow study on the twentieth day of life showed a normal-width esophagus with gastroesophageal reflux and small hiatus hernia. The longstanding herniated stomach in the fetus apparently caused kinking, edema, and obstruction of the gastroesophageal junction. This led to a significant ED and concealment of gastroesophageal reflux. We aim to arouse awareness about the occurrence of ED with CDH, and about its benign course under conservative management.
BACKGROUND: The aim of our study is to observe the outcome of pharyngocolonic anastomosis in esophageal reconstruction for diffuse corrosive esophageal stricture involving hypopharynx. METHODS: This is a retrospective report of the experience and results of 14 patients undergoing esophageal reconstruction with pharyngocolonic anastomosis without resection of the strictured intrathoracic esophagus. The left colonic segment was pulled up to the neck through the substernal space in all patients. RESULTS: There was no operative or hospital death. Postoperative complications included cervical anastomotic leakage in 4 patients, rupture of abdominal incision in 1 patient, and aspiration pneumonia in 2 patients. The length of follow-up ranged from half a year to 10 years, with an average of 4 years. Anastomotic stenosis occurred in 2 patients. One patient was improved after dilatation and the other was relieved by plastic operation. One patient began to have vomiting after meals 7 months after surgery and was found to have redundant abdominal colon graft, which was corrected with a side-to-side anastomosis between the colon and the stomach. CONCLUSIONS: A successful reconstruction for hypopharyngoesophageal stricture requires a sufficiently large hypopharyngocolonic anastomosis and a technique of good anastomosis. From our experience, this procedure is shown to be safe and effective.
The histopathology of the portal vein in human extrahepatic portal vein obstruction (EHPVO) in the form of cavernomatous transformation of the portal vein is well documented. However, a similar detailed histopathology has not been documented in experimental EHPVO, even though the model has been in existence for many years. An experimental model of EHPVO was created by partial ligation of the portal vein in 20 rats. A control group of 11 sham operated (SO) rats was also studied. Development of portal hypertension was confirmed by measurement of intrasplenic pulp pressure (19.7 + 7.1 cm normal saline vs 12.9 + 1.1 cm of normal saline in SO rats). Histopathological evidence included varices in the oesophagus and congestion in the submucosa and mucosa of the stomach and capillarization of sinusoids in the spleen. Animals were killed at 22-265 days post-ligation. While SO animals showed mild focal sinusoidal congestion and a normal portal vein, the experimental group of animals with EHPVO showed oedema around the portal vein, multiple dilated vascular channels near the hilum resembling cavernomatous transformation and severe sinusoidal congestion. Jejunum and kidneys showed congested veins in the experimental group. None of the SO animals showed this change. Thus experimental EHPVO does reproduce some histological changes observed in human EHPVO.
OBJECTIVE: Stricture formation resulting in impedance of gastric emptying is a relatively common complication after gastric surgery that involves anastomosis creation or pyloroplasty. Treatment of the stenosis with fluoroscopically guided balloon dilatation avoids further surgery. Accordingly, we report our experience with 32 dilating procedures in 24 consecutive patients who had the postoperative complication of obstruction at a surgically created gastric outlet. MATERIALS AND METHODS: Out of our series of approximately 650 fluoroscopically guided balloon dilatations, 32 procedures were performed on 24 patients with anastomotic strictures or pyloric narrowing after gastric surgery (vertical banded gastroplasty or gastric bypass surgery [n = 15], partial esophagectomy with esophagogastrostomy and pyloroplasty [n = 6], and partial gastrectomy with gastrojejunostomy [n = 3]). The group included 13 men and 11 women ranging from 32 to 79 years old (mean, 51 years). Diameters of the balloons chosen ranged from 10 to 20 mm, depending on the size of the surgically created anastomosis or pyloroplasty. Indications for balloon dilatation were clinical and radiographic evidence of gastric outlet obstruction. The procedures were done between 13 days and 10 years (mean, 14 months) after gastric surgery. The result of each procedure was assessed by evaluating clinical outcome (relief or recurrence of symptoms) during the follow-up period of 2 days to 36 months (mean, 8 months) after the procedure. RESULTS: In 17 of the 24 patients, the obstructive symptoms were treated successfully with a single dilatation procedure, and symptoms did not recur during follow-up ranging from 1 to 36 months (mean, 11 months). In the other seven patients, the procedure was considered unsuccessful because the patients experienced recurrent obstruction within 2 days to 13 weeks (mean, 3 weeks) after the initial procedure. In one of these, symptoms were relieved by a second procedure. Repeat dilatations in the other six patients were unsuccessful, and all six eventually required surgical revision for definitive treatment. No complicating perforations were noted as a result of dilatation. CONCLUSION: Our experience shows that fluoroscopically guided balloon dilatation is a simple and safe technique for treating obstructive symptoms caused by strictures occurring after gastric surgery. In the majority of patients, symptoms are relieved with a single balloon dilatation, eliminating the need for further surgery. However, patients whose obstructive symptoms recur after the initial balloon dilatation procedure are less likely to benefit from further dilatations and usually require surgery.
A case of gastric duplication communicating with the pancreatic duct system is reported. The clinical presentation consisted of abdominal pain with recurrent acute pancreatitis. The histopathological examination showed that the duplication was lined with normal pyloric mucosa. In the tubular structure, connecting the duplication to the pancreatic ducts, an increase in the number of serotonin-positive cells was found. The pancreas showed dilatation of the duct system and chronic pancreatitis.
Dieulafoy disease is an unusual cause of gastrointestinal (GI) hemorrhage that can be fatal. It arises from an abnormally large eroded submucosal artery commonly located in the proximal stomach. Since this disease first described in 1884, it has been rarely discussed in radiology literature. We describe a case of an elderly patient with multiple medical problems presented with upper and lower GI hemorrhage. Repeated upper GI endoscopies revealed a large fundal clot but otherwise were unremarkable. Angiography showed anomalous short gastric artery originating normally from the splenic artery. The latter was embolized with microcoils and Gelfoam. Following embolization, the frequency and amount of bleeding decreased although did not totally stop and the patient underwent elective partial gastrectomy. The diagnosis was made histologically. Therefore, Dieulafoy disease can represent a diagnostic and therapeutic challenge. It should be suspected if a patient with GI hemorrhage is found to have extravasation from a dilated tortuous artery that appears normal otherwise with no associated large draining veins. Transcatheter selective arterial embolization has a reported role in the literature as a less invasive therapeutic option compared to surgery.
BACKGROUND: In 1989, we predicted an increasing number of esophagectomies for megaesophagus and for recurrent symptoms after prior esophagomyotomy or balloon dilatation for achalasia. Patient selection in this group is challenging, as the potential operative morbidity of an esophagectomy must be weighed against the expected clinical outcome after a redo esophagomyotomy or alternative procedures designed to salvage the native esophagus. METHODS: The hospital records of 93 patients undergoing esophagectomy for achalasia during the past 20 years were reviewed retrospectively and the results of operation assessed using our prospectively established Esophageal Resection Database and follow-up information obtained through personal contact with the patients. RESULTS: Patient age averaged 51 years. Indications for esophagectomy included tortuous megaesophagus (64%), failure of prior myotomy (63%), and associated reflux stricture (7%). Ninety-four percent of the patients underwent a transhiatal esophagectomy. Stomach was used as the esophageal substitute in 91% cases. Intraoperative blood loss averaged 672 mL. Postoperative length of stay averaged 12.5 days. Major complications included anastomotic leak (10%), recurrent laryngeal nerve injury (5%), delayed mediastinal bleeding requiring thoracotomy (2%), and chylothorax (2%). There were 2 hospital deaths (2%) from respiratory insufficiency and sepsis. Follow-up has averaged 38 months. In all, 95% of patients eat well; nearly 50% have required an anastomotic dilatation; troublesome regurgitation has been rare; and 4% have refractory postvagotomy dumping. CONCLUSIONS: Esophagectomy, preferably through a transhiatal approach, is generally safe and effective therapy in selected patients with achalasia. Unique technical considerations include difficulty encircling the dilated cervical esophagus, deviation of the esophagus into the right chest, large aortic esophageal arteries, and adherence of the exposed esophageal submucosa to the adjacent aorta after prior myotomy.
To assess the histopathologic features of fundic gland polyps (FGP) of the stomach, 83 specimens from 25 patients were examined. In nine patients, FGP were associated with an inherited adenomatous polyposis syndrome; the other 16 patients had nonsyndromic FGP. FGP were microscopically characterized by the presence of fundic glands with variably disordered architecture, a feature not previously emphasized. Disordered architecture, found in 80 of 83 specimens (96%), comprised a spectrum of abnormalities, ranging from prominent glandular and cellular budding, found in 51 biopsies (61%), to irregular tortuous glands, noted in 61 biopsies (75%), to microcysts lined by fundic epithelium, seen in 72 biopsies (87%). The continuous range of these changes suggested that FGP arise through progressive formation and unfolding of secondary glandular buds, to result in cystic dilatation. No differences were found between syndromic and nonsyndromic FGP with respect to histologic features or mucin histochemistry, including presence of O-acylated sialomucins.
OBJECTIVE: To report a rare case of carcinoma erysipelatoides on the laryngeal skin caused by stomach adenocarcinoma. CLINICAL PRESENTATION AND INTERVENTION: A 48-year-old male, who had undergone a gastrectomy 18 months prior to admission for stage IIIA gastric adenocarcinoma, presented with a reddish induration of the cervical skin, lymphadenopathy in both supraclavicular areas and widespread subcutaneous nodules. Abdominal computerized tomography and chest radiography did not reveal any organ metastasis or peritoneal carcinomatosis. A biopsy of the induration revealed atypical epithelial cells with edema and dilatation of lymphatics. The patient was given combination chemotherapy of etoposide, adriamycin, and cisplatin, and significant improvement was observed over the cervical area after three courses. The patient tolerated the systemic chemotherapy well and has been followed for two months. CONCLUSION: We recommend combination chemotherapy in patients with cutaneous metastasis of gastric adenocarcinoma as a safe and effective treatment.
Rarely can a clinical diagnosis of cancer of the esophagus and stomach be made while the lesion is still early. By the time the patient has symptoms and reports them to the physician, these tumors are usually invasive. In high-risk populations, screening if feasible and patients with vague symptoms can be aggressively studied. Technical advances have aided in screening high risk individuals. Double contrast radiography and direct exfoliative cytology with brush smears have increased the diagnostic accuracy. In patients with esophageal strictures dilatation followed by biopsy has proven useful and safe. Gastric secretory studies of acidicity, pepsin, enzymes and tumor markers are not sensitive enough to be helpful. Serial studies of serum pepsinogen I in a high-risk individual may be of value, but this still needs confirmation. Most surgeons agree that preoperative staging can be helpful in predicting patients in whom a palliative procedure should be planned rather than a curative approach.
Tapeworm cysts were identified in liver of Wistar rats and it induced fibrosarcoma in liver and gastroenteropathy in stomach and intestine. The tapeworm larva was confirmed as Strobilocercus fasciolaris by PCR linked mitochondrial DNA sequencing. Light microscopy, special staining (masson trichrome) and immunoflouresence supported the diagnosis of fibrosarcoma. Infiltration of plasma cells, macrophages and eosinophils were observed in the liver section. Gastric mucosal hyperplasia, dilation of gastric glands with secretion, intestinal mucosal cell hyperplasia, proliferation of duodenal submucosal glands were confirmed by light microscopy and supported by PAS, AB staining. The concomitant development of hepatic sarcoma and gastroenteropathy by larvae of Taenia taeniaeformis (S. fasciolaris) infection is very rare and is the first reported case in Wistar rats to our knowledge.
Dietary factors can modulate visceral sensitivity and are suggested to interact with neuroimmune pathways. To determine whether daily low-level exposure to a food contaminant (diquat) alters sensitivity to gastric distension (GD) and the role of mast cells and tachykinin receptors activation, two series of experiments were conducted in eight groups of eight male Wistar rats (200-250 g) receiving daily doses of either diquat (0.1 mg/kg per day orally) or water for 21 days. In the first series, rats were sacrificed at the end of treatments and the gastric mucosal mast cell (MMC) number was histologically quantified. In the second series, after 21 days of treatment the cardiovascular depressor (CVD) response and corresponding gastric volumes were recorded under GD (from 10 to 40 mmHg). Doxantrazole (5 mg/kg intraperitoneally (i.p.)), a mast cell stabilizer, and SR 140333 (1 mg/kg i.p.) and MEN 11420 (0.1 mg/kg intravenously), respectively NK1 and NK2 receptor antagonists, were administered before GD. Before and after GD, blood samples were taken to measure blood histamine and the gastric MMC number was determined after sacrifice. Diquat treatment increased the MMC number. In diquat-treated rats, GD increased the CVD response and blood histamine level and induced MMC degranulation. Doxantrazole did not modify the hypersensitivity to GD but prevented mast cell degranulation. Both NK1 and NK2 receptor antagonists blocked the enhanced CVD response induced by diquat and prevented mast cell degranulation. None of the drugs had any effect in control animals. Prolonged exposure to a food contaminant at doses possibly found in food increases gastric sensitivity to distension, activates tachykinin receptors and results in MMC degranulation after GD.