Background: There is still limited data on the safety of propofol sedation during ERCP, where deep sedation is mandatory.Objective: We asked if non-anesthetist sedation with propofol is safe for ERCP. Setting: A hospital-based gastroenterology center in Switzerland. Patients and Design: Between November 1997 and October 2007, all ERCP procedures were prospectively assessed regarding patient characteristics, American Society of Anesthesiologists (ASA) status, dosage of propofol, fall of oxygen saturation, need to increase nasal oxygen administration above 2 L/min, need for assisted ventilation, need for endotracheal intubation, feasibility of the ERCP procedure, sedation-related adverse events or death. Intervention: ERCP procedures were performed under deep sedation with propofol, administered by the endoscopy team consisting of 1 physician endoscopist, 1 endoscopy assistant and 1 radiology assistant. Patient monitoring consisted of pulse oxymetry, breathing frequency, electrocardiogram and clinical assessment. Results: During the 10 years period, 1305 ERCP procedures (9 % diagnostic, 91 % therapeutic) were performed (mean patient age 64 years, range 16-98 years). In 36 ERCP procedures (2.7 %, all patients ASA III and IV), sedation was administered by an anesthesiology team. In the remaining 1269 ERCP procedures (97.3 %), propofol sedation was administered by the endoscopy team. During ERCP, patients received a mean propofol dose of 459 mg (range 50 -1990 mg) in addition to 50 mg of meperidine. Oxygen saturation fell below 90% (lowest 70%) in 92 patients (7%), normalizing within 30 seconds by stimulating the patient and increasing the nasal oxygen flow to 4 to 10 L/min. 4 patients (0.3%) required mask ventilation for less than 30 seconds. No endotracheal intubation was necessary, no death occurred. 12 ERCP procedures (0.9%) had to be discontinued due to increasing hypoxemia, danger of aspiration or insufficient sedation level. 6 of these patients underwent successful ERCP when sedation was applied by an anesthesiology team, the other 6 patients underwent surgery. Conclusions: The vast majority of ERCP procedures can safely be performed with propofol sedation administered by an endoscopy team consisting of 1 physician endoscopist, 1 endoscopy assistant and 1 radiology assistant. Only a small minority of patients (usually ASA III and IV patients) need anesthetist sedation for ERCP.

Background: Propofol has been shown to be safe for nonanesthetist use during GI endoscopy. However, published studies involved propofol administration by an additional nurse or used specialized patient monitoring or were carried out in tertiary hospitals.Objective: Considering the downward pressure on reimbursement for endoscopic procedures, we asked how much staff and monitoring is necessary for safe use of propofol.Setting: Two private gastroenterology practices.Patients and Design: A total of 27,061 endoscopic procedures (14,856 EGDs and 12,205 colonoscopies) were prospectively assessed regarding patient characteristics, American Society of Anesthesiologists (ASA) status, dosage of propofol, fall of oxygen saturation below 90%, need to increase nasal oxygen administration above 2 L/min, and need for assisted ventilation.Intervention: Propofol was administered by the endoscopy nurse supervised by the endoscopist. Patient monitoring consisted of only pulse oximetry and clinical assessment.Results: The mean propofol dose for EGD was 161 mg (range 50-650 mg). During colonoscopy patients received a mean propofol dose of 116 mg (30-500 mg) in addition to 25 mg of meperidine. Oxygen saturation fell below 90% (lowest 74%) in 623 procedures (2.3%), normalizing within less than 30 seconds by stimulating the patient and increasing the nasal oxygen flow to 4 to 10 L/min. Six patients (ASA 111) required mask ventilation for less than 30 seconds. No endotracheal intubation was necessary.Limitations: There was no further follow-up regarding adverse events after patient discharge from the endoscopy unit.Conclusions: An endoscopy team, consisting of I physician endoscopist and I endoscopy nurse, can safely administer propofol sedation for GI endoscopy in a practice setting without additional staff or specialized monitoring.

The main duodenal papilla is found inside a diverticulum in 5% to 23% of patients in ERCP series. 1 Osnes M. Myren J. Lotveit T. et al. Juxtapapillary duodenal diverticula and abnormalities by endoscopic retrograde cholangio-pancreatography (ERCP). Scand J Gastroenterol. 1977; 12: 347-351 Crossref PubMed Scopus (32) Google Scholar , 2 Kirk A.P. Summerfield J.A. Incidence and significance of juxtapapillary diverticula at endoscopic retrograde cholangio-pancreatography. Digestion. 1980; 20: 31-35 Crossref PubMed Scopus (58) Google Scholar Identification of the orifice and selective cannulation of each duct can be a complex problem, particularly when the papilla is on the edge of the diverticulum and facing inside it. Technical modifications of the ERCP procedure are required to increase its success. The present report describes the simultaneous use of two endoscopes to gain access to the bile duct.

Patient-controlled analgesia and sedation (PCAS) has the potential advantage over standard sedation of tailoring the level of sedation to individual patients and procedures. Ultra-short acting agents such as propofol and the newer opioids, with their fast onset and short duration of action, are ideal agents for use in PCAS for endoscopy. The majority of trials using PCAS have been performed in colonoscopy and demonstrated PCAS is effective, safe, and yields high patient satisfaction. Target controlled infusion of propofol has shown encouraging results for prolonged upper endoscopy procedures like endoscopic retrograde cholangiopancreatography.

Variations in pain threshold, drug tolerance, and visceral sensitivity among patients make it difficult to anticipate the appropriate dose of sedation for gastrointestinal endoscopy. Propofol was recently introduced for sedation in endoscopy and has a rapid onset and offset of action, making it an ideal substance for patient-controlled administration. Several controlled trials have demonstrated that during colonoscopy, patient-controlled application of propofol alone or in combination with various opioids is effective,safe, and yields high patient satisfaction. Target-controlled infusion of propofol has shown encouraging results for prolonged upper endoscopy procedures like endoscopic retrograde cholangio pancreatography.

The clinical spectrum of Sjögren's syndrome is broad, ranging from isolated sicca syndrome to systemic disease including the GI tract.1Sheikh SH Shaw-Stiffel TA The gastrointestinal manifestations of Sjögren's syndrome.Am J Gastroenterol. 1995; 90: 9-14PubMed Google Scholar The case of a patient with Sjögren's syndrome, chronic pancreatitis, and sclerosing cholangitis is described and compared with the 7 previously published cases of this rare triad.2Waldram R Kopelman H Tsantoulas D Williams R. Chronic pancreatitis, sclerosing cholangitis, and sicca complex in two siblings.Lancet. 1975; 1: 550-552Abstract PubMed Scopus (115) Google Scholar, 3Sjögren I Wengle B Korsgren M Primary sclerosing cholangitis associated with fibrosis of the submandibular glands and the pancreas.Acta Med Scand. 1979; 205: 139-141Crossref PubMed Scopus (63) Google Scholar, 4Montefusco PP Geiss AC Bronzo RL Randall S Kahn E McKinley MJ Sclerosing cholangitis, chronic pancreatitis, and Sjögren's syndrome: a syndrome complex.Am J Surg. 1984; 147: 822-826Abstract Full Text PDF PubMed Scopus (162) Google Scholar, 5Versapuech JM LaBayle D Grange D Fischer D Kemeny F D'Hubert E Primary sclerosing cholangitis, chronic pancreatitis and Sjögren's syndrome [in French with English abstract].Ann Med Interne. 1986; 137: 147-154PubMed Google Scholar, 6Barreda F Contardo C Leon A Navarrete J Figueroa R Attanasio F Primary sclerosing cholangitis associated with Sjögren's syndrome, retroperitoneal fibrosis and chronic pancreatitis. Report of a case [in Spanish with English abstract].Rev Gastroenterol Peru. 1989; 9: 106-114PubMed Google Scholar, 7Nieminen U Koivisto T Kahri A Färkkilä M Sjögren's syndrome with chronic pancreatitis, sclerosing cholangitis, and pulmonary infiltrations.Am J Gastroenterol. 1997; 92: 139-142PubMed Google Scholar A Peruvian man developed vitiligo at the age of 34 years. Shortly thereafter, thyroid hormone replacement was initiated because of hypothyroidism. A biopsy of the thyroid gland demonstrated a thyroiditis; the antithyroglobulin antibodies were positive. At age 35 years, the patient was evaluated for chronic pancreatitis and found to have a mass in the tail of the pancreas. FNA disclosed inflammatory changes. Eventually, the tail of the pancreas was resected and a Roux-en-Y pancreaticojejunostomy was performed. At operation, the diagnosis of advanced chronic pancreatitis with atrophy and fibrosis was confirmed. One year later, the patient presented with dry eyes, dry mouth, and salivary gland enlargement. A diagnosis of Sjögren's syndrome was made based on biopsies from a submandibular lymph node and salivary glands. The patient presented 2 years later at our hospital with intermittent right upper quadrant abdominal pain and nausea of 9 months' duration. During episodes of pain, transient elevations of serum transaminases to 10 times the upper normal limit together with mild elevations of bilirubin and of alkaline phosphatase were documented. Furthermore, rheumatoid factor was present and the IgG level was elevated. Additional immunologic tests, including antinuclear antibodies, Anti-SS-A and Anti-SS-B, antimitochondrial antibodies, antineutrophil cytoplasm antibody, tumor markers (AFP, CA 19-9), as well as serologic tests for hepatitis A, B, and C, and HIV, revealed no abnormalities. Transabdominal US demonstrated normal liver parenchyma with findings suggestive of bile duct dilatation. Endoscopic retrograde cholangiography revealed strictures at the hepatic bifurcation and distal common bile duct (Fig. 1). Selective endoscopic cannulation of the bile duct was not possible. The patient underwent percutaneous transhepatic cholangiography (PTC) with balloon dilatation and insertion of bilateral 10F plastic stents. Cytopathologic evaluation of specimens obtained by brushing the bile duct strictures and CT revealed no evidence of malignancy. The bile duct abnormalities were judged to be consistent with a diagnosis of sclerosing cholangitis and treatment with ursodeoxycholic acid (UDCA) was initiated (15 mg per kg body weight). The upper abdominal discomfort resolved and the liver enzyme levels returned to normal levels within a few weeks. PTC with balloon dilatation and stent exchange was repeated after 1 month and the stents were finally removed after 3 months (Fig. 2). Eighteen months later, the patient was still doing well with liver enzyme levels within normal ranges; US revealed normal-appearing liver and bile ducts. Sjögren's syndrome is a chronic autoimmune disorder with a predilection for exocrine glands and is characterized by the classic sicca syndrome (dry eyes, dry mouth, salivary gland enlargement).8Sjögren H Zur Kenntnis der Keratoconjunctivitis sicca (Keratitis filiformis bei Hypofunktion der Tränendrüsen) [German].Acta Ophthalmol. 1933; 11: 1-151Google Scholar Focal lymphocytic infiltration of the exocrine glands leads to irreversible destruction and atrophy and to diminished or absent glandular secretions. As many exocrine glands are related to the GI tract, Sjögren's syndrome can involve any part of the gut. Pancreatic involvement is common in Sjögren's syndrome and accounts for some cases of autoimmune chronic pancreatitis.9Nishimori I Yamamoto Y Okazaki K Morita M Onodera M Kino J et al.Identification of autoantibodies to a pancreatic antigen in patients with idiopathic chronic pancreatitis and Sjögren's syndrome.Pancreas. 1994; 9: 374-381Crossref PubMed Scopus (62) Google Scholar Abnormal exocrine pancreatic function has been documented in up to one third of patients with Sjögren's syndrome.1Sheikh SH Shaw-Stiffel TA The gastrointestinal manifestations of Sjögren's syndrome.Am J Gastroenterol. 1995; 90: 9-14PubMed Google Scholar Liver involvement is present in about 10% of patients, with primary biliary cirrhosis being the most frequently associated hepatic disorder.10Skopouli FN Barbatis C Moutsoupoulos HM Liver involvement in primary Sjögren's syndrome.Br J Rheumatol. 1994; 33: 745-748Crossref PubMed Scopus (120) Google Scholar The association of sclerosing cholangitis, however, with Sjögren's syndrome and with chronic pancreatitis is rare. Since 1975, 7 patients have been described in published reports.2Waldram R Kopelman H Tsantoulas D Williams R. Chronic pancreatitis, sclerosing cholangitis, and sicca complex in two siblings.Lancet. 1975; 1: 550-552Abstract PubMed Scopus (115) Google Scholar, 3Sjögren I Wengle B Korsgren M Primary sclerosing cholangitis associated with fibrosis of the submandibular glands and the pancreas.Acta Med Scand. 1979; 205: 139-141Crossref PubMed Scopus (63) Google Scholar, 4Montefusco PP Geiss AC Bronzo RL Randall S Kahn E McKinley MJ Sclerosing cholangitis, chronic pancreatitis, and Sjögren's syndrome: a syndrome complex.Am J Surg. 1984; 147: 822-826Abstract Full Text PDF PubMed Scopus (162) Google Scholar, 5Versapuech JM LaBayle D Grange D Fischer D Kemeny F D'Hubert E Primary sclerosing cholangitis, chronic pancreatitis and Sjögren's syndrome [in French with English abstract].Ann Med Interne. 1986; 137: 147-154PubMed Google Scholar, 6Barreda F Contardo C Leon A Navarrete J Figueroa R Attanasio F Primary sclerosing cholangitis associated with Sjögren's syndrome, retroperitoneal fibrosis and chronic pancreatitis. Report of a case [in Spanish with English abstract].Rev Gastroenterol Peru. 1989; 9: 106-114PubMed Google Scholar, 7Nieminen U Koivisto T Kahri A Färkkilä M Sjögren's syndrome with chronic pancreatitis, sclerosing cholangitis, and pulmonary infiltrations.Am J Gastroenterol. 1997; 92: 139-142PubMed Google Scholar In all of these cases, the same triad was present as in the present case (Table 1). Table 1Comparison of current patient with published cases of Sjögren's syndrome, chronic pancreatitis, and sclerosing cholangitisYear of publicationPresent case19752Waldram R Kopelman H Tsantoulas D Williams R. Chronic pancreatitis, sclerosing cholangitis, and sicca complex in two siblings.Lancet. 1975; 1: 550-552Abstract PubMed Scopus (115) Google Scholar19752Waldram R Kopelman H Tsantoulas D Williams R. Chronic pancreatitis, sclerosing cholangitis, and sicca complex in two siblings.Lancet. 1975; 1: 550-552Abstract PubMed Scopus (115) Google Scholar19793Sjögren I Wengle B Korsgren M Primary sclerosing cholangitis associated with fibrosis of the submandibular glands and the pancreas.Acta Med Scand. 1979; 205: 139-141Crossref PubMed Scopus (63) Google Scholar19844Montefusco PP Geiss AC Bronzo RL Randall S Kahn E McKinley MJ Sclerosing cholangitis, chronic pancreatitis, and Sjögren's syndrome: a syndrome complex.Am J Surg. 1984; 147: 822-826Abstract Full Text PDF PubMed Scopus (162) Google Scholar19865Versapuech JM LaBayle D Grange D Fischer D Kemeny F D'Hubert E Primary sclerosing cholangitis, chronic pancreatitis and Sjögren's syndrome [in French with English abstract].Ann Med Interne. 1986; 137: 147-154PubMed Google Scholar19896Barreda F Contardo C Leon A Navarrete J Figueroa R Attanasio F Primary sclerosing cholangitis associated with Sjögren's syndrome, retroperitoneal fibrosis and chronic pancreatitis. Report of a case [in Spanish with English abstract].Rev Gastroenterol Peru. 1989; 9: 106-114PubMed Google Scholar19977Nieminen U Koivisto T Kahri A Färkkilä M Sjögren's syndrome with chronic pancreatitis, sclerosing cholangitis, and pulmonary infiltrations.Am J Gastroenterol. 1997; 92: 139-142PubMed Google ScholarAge, gender37, male31, female36, male43, male48, female63, male30, female32, maleManifestationP→S→CS→P→CP→C→SS→P→CS→P→CP→C→SS→P→CP→S→CAdditional organsThyroid, skinLungsAutoimmune featuresRf, IgGEos, LMILMIRf, EosRf, HLA B8Rf, LCCOriginPeruvianSiblingSiblingPeruvianTherapyStent, UDCAMCTMCTPrednisoloneSurgerySurgerySurgeryUDCAP, Pancreatitis; C, cholangitis; S, Sjögren's syndrome; Rf, rheumatoid factor; Eos, eosinophilia; LCC, low complement components; LMI, leukocyte migration inhibition in the presence of bile antigen; UDCA, ursodeoxycholic acid; MCT, medium chain triglycerides. Open table in a new tab Except for one, all were in the fourth or fifth decade of life when the syndrome complex became fully developed. In most cases, sclerosing cholangitis was the last clinical manifestation recognized. In addition to the triad of Sjögren's syndrome, pancreatitis, and cholangitis, our patient also had vitiligo and autoimmune thyroiditis. The patient of Nieminen et al.7Nieminen U Koivisto T Kahri A Färkkilä M Sjögren's syndrome with chronic pancreatitis, sclerosing cholangitis, and pulmonary infiltrations.Am J Gastroenterol. 1997; 92: 139-142PubMed Google Scholar had additional pulmonary infiltrates that disappeared during treatment of the sclerosing cholangitis. None of the patients had inflammatory bowel disease, which is frequently associated with primary sclerosing cholangitis.11Angulo P Lindor KD. Primary sclerosing cholangitis.Hepatology. 1999; 30: 325-332Crossref PubMed Scopus (231) Google Scholar It is tempting to speculate that the sclerosing cholangitis associated with pancreatitis and Sjögren's syndrome might result from pathogenic mechanisms that differ from those related to inflammatory bowel disease. P, Pancreatitis; C, cholangitis; S, Sjögren's syndrome; Rf, rheumatoid factor; Eos, eosinophilia; LCC, low complement components; LMI, leukocyte migration inhibition in the presence of bile antigen; UDCA, ursodeoxycholic acid; MCT, medium chain triglycerides. Elevations of serum autoantibodies, including SS-A and SS-B, are typical in patients with Sjögren's syndrome.1Sheikh SH Shaw-Stiffel TA The gastrointestinal manifestations of Sjögren's syndrome.Am J Gastroenterol. 1995; 90: 9-14PubMed Google Scholar Interestingly, none the 8 patients with Sjögren's, chronic pancreatitis, and sclerosing cholangitis had these abnormalities. However, some markers of disordered immune function were present in almost all patients including a positive test for rheumatoid factor,4Montefusco PP Geiss AC Bronzo RL Randall S Kahn E McKinley MJ Sclerosing cholangitis, chronic pancreatitis, and Sjögren's syndrome: a syndrome complex.Am J Surg. 1984; 147: 822-826Abstract Full Text PDF PubMed Scopus (162) Google Scholar, 5Versapuech JM LaBayle D Grange D Fischer D Kemeny F D'Hubert E Primary sclerosing cholangitis, chronic pancreatitis and Sjögren's syndrome [in French with English abstract].Ann Med Interne. 1986; 137: 147-154PubMed Google Scholar, 7Nieminen U Koivisto T Kahri A Färkkilä M Sjögren's syndrome with chronic pancreatitis, sclerosing cholangitis, and pulmonary infiltrations.Am J Gastroenterol. 1997; 92: 139-142PubMed Google Scholar elevated IgG level, eosinophilia,2Waldram R Kopelman H Tsantoulas D Williams R. Chronic pancreatitis, sclerosing cholangitis, and sicca complex in two siblings.Lancet. 1975; 1: 550-552Abstract PubMed Scopus (115) Google Scholar, 4Montefusco PP Geiss AC Bronzo RL Randall S Kahn E McKinley MJ Sclerosing cholangitis, chronic pancreatitis, and Sjögren's syndrome: a syndrome complex.Am J Surg. 1984; 147: 822-826Abstract Full Text PDF PubMed Scopus (162) Google Scholar a decreased complement components,7Nieminen U Koivisto T Kahri A Färkkilä M Sjögren's syndrome with chronic pancreatitis, sclerosing cholangitis, and pulmonary infiltrations.Am J Gastroenterol. 1997; 92: 139-142PubMed Google Scholar HLA B8,5Versapuech JM LaBayle D Grange D Fischer D Kemeny F D'Hubert E Primary sclerosing cholangitis, chronic pancreatitis and Sjögren's syndrome [in French with English abstract].Ann Med Interne. 1986; 137: 147-154PubMed Google Scholar or leukocyte migration inhibition in the presence of bile antigen.2Waldram R Kopelman H Tsantoulas D Williams R. Chronic pancreatitis, sclerosing cholangitis, and sicca complex in two siblings.Lancet. 1975; 1: 550-552Abstract PubMed Scopus (115) Google Scholar An altered immunologic response to a common antigenic determinant of the duct cells of salivary glands, the pancreas, and the bile ducts may play a role in the pathogenesis of this triad. Circulating immune complexes containing the pancreatic antigen against SP3-1 monoclonal antibody have been found in patients with idiopathic chronic pancreatitis and Sjögren's syndrome.12Onodera M Okazaki K Morita M Nishimori I Yamamoto Y Immune complex specific for the pancreatic duct antigen in patients with idiopathic chronic pancreatitis and Sjögren sydrome.Autoimmunity. 1994; 19: 23-29Crossref PubMed Scopus (7) Google Scholar SP3-1 recognizes an antigen in duct cells of various exocrine organs, including pancreas and salivary glands, as well as bile ducts. Later studies demonstrated that carbonic anhydrase II is one candidate target antigen recognized during the autoimmune pathophysiology of idiopathic chronic pancreatitis and Sjögren's syndrome.13Kino-Ohsaki J Nishimori I Morita M Okazaki K Yamamoto Y Onishi S et al.Serum antibodies to carbonic anhydrase I and II in patients with idiopathic chronic pancreatitis and Sjögren's syndrome.Gastroenterology. 1996; 110: 1579-1586Abstract Full Text Full Text PDF PubMed Scopus (216) Google Scholar Bile duct epithelia also contain an abundance of carbonic anhydrase II, and antibodies to this enzyme have been detected in the sera of patients with autoimmune cholangitis.14Gordon SC Quattrociocchi-Longe TM Khan BA Kodali VP Chen J Silverman AL et al.Antibodies to carbonic anhydrase in patients with immune cholangiopathies.Gastroenterology. 1995; 108: 1802-1809Abstract Full Text PDF PubMed Scopus (100) Google Scholar These data provide evidence that a common immunologic process may lead to the triad of pancreatitis, cholangitis, and Sjögren's syndrome. The fact that two of the affected patients were siblings2Waldram R Kopelman H Tsantoulas D Williams R. Chronic pancreatitis, sclerosing cholangitis, and sicca complex in two siblings.Lancet. 1975; 1: 550-552Abstract PubMed Scopus (115) Google Scholar and that our patient as well that of Barreda et al.6Barreda F Contardo C Leon A Navarrete J Figueroa R Attanasio F Primary sclerosing cholangitis associated with Sjögren's syndrome, retroperitoneal fibrosis and chronic pancreatitis. Report of a case [in Spanish with English abstract].Rev Gastroenterol Peru. 1989; 9: 106-114PubMed Google Scholar were Peruvians may indicate a genetic or endemic infectious factor that may enhance susceptibility to this immune-mediated disease. The factor(s) that might trigger the immune reactions in Sjögren's syndrome remain unknown, but viral infections have repeatedly been suggested as possibilities.15Flescher E Talal N Do viruses contribute to the development of Sjögren's syndrome.Am J Med. 1991; 90: 283-285Abstract Full Text PDF PubMed Scopus (55) Google Scholar Therapy was initiated for bile duct obstruction in all patients when cholestasis became evident. The two siblings in the 1975 report of Waldram et al.2Waldram R Kopelman H Tsantoulas D Williams R. Chronic pancreatitis, sclerosing cholangitis, and sicca complex in two siblings.Lancet. 1975; 1: 550-552Abstract PubMed Scopus (115) Google Scholar were treated with medium-chain triglycerides, which improved symptoms, although tests of liver function remained abnormal. In 1 patient, the sclerosing cholangitis responded well to treatment with prednisolone.3Sjögren I Wengle B Korsgren M Primary sclerosing cholangitis associated with fibrosis of the submandibular glands and the pancreas.Acta Med Scand. 1979; 205: 139-141Crossref PubMed Scopus (63) Google Scholar The patients of Montefusco et al.,4Montefusco PP Geiss AC Bronzo RL Randall S Kahn E McKinley MJ Sclerosing cholangitis, chronic pancreatitis, and Sjögren's syndrome: a syndrome complex.Am J Surg. 1984; 147: 822-826Abstract Full Text PDF PubMed Scopus (162) Google Scholar Versapuech et al.5Versapuech JM LaBayle D Grange D Fischer D Kemeny F D'Hubert E Primary sclerosing cholangitis, chronic pancreatitis and Sjögren's syndrome [in French with English abstract].Ann Med Interne. 1986; 137: 147-154PubMed Google Scholar and Barreda et al.6Barreda F Contardo C Leon A Navarrete J Figueroa R Attanasio F Primary sclerosing cholangitis associated with Sjögren's syndrome, retroperitoneal fibrosis and chronic pancreatitis. Report of a case [in Spanish with English abstract].Rev Gastroenterol Peru. 1989; 9: 106-114PubMed Google Scholar underwent biliary surgery with temporary external biliary drainage, which resulted in improvement in cholestasis and symptoms. Nieminen et al.7Nieminen U Koivisto T Kahri A Färkkilä M Sjögren's syndrome with chronic pancreatitis, sclerosing cholangitis, and pulmonary infiltrations.Am J Gastroenterol. 1997; 92: 139-142PubMed Google Scholar reported that their patient with obstructive jaundice responded well to treatment with UDCA. This dihydroxy bile acid is increasingly used for the treatment of chronic cholestatic liver disease. In primary biliary cirrhosis, UDCA has been shown to slow long-term progression and to reduce the need for liver transplantation.16Poupon RE Poupon R Balkau B. Ursodiol for the long-term treatment of primary biliary cirrhosis.N Engl J Med. 1994; 330: 1342-1347Crossref PubMed Scopus (444) Google Scholar In primary sclerosing cholangitis, treatment with UDCA may result in improvement in biochemical tests of liver function, at least in the short term. However, this treatment was not accompanied by beneficial changes in clinical outcomes in a large controlled trial.17Lindor KD. Ursodiol for primary sclerosing cholangitis.N Engl J Med. 1997; 336: 691-695Crossref PubMed Scopus (533) Google Scholar Favorable results have been reported with nonoperative radiologic or endoscopic dilatation and temporary stent insertion for management of symptoms attributed to the presence of dominant stricture(s) in patients with primary sclerosing cholangitis.18May GR Bender CE LaRusso NF Wiesner RH. Nonoperative dilatation of dominant strictures in primary sclerosing cholangitis.AJR Am J Roentgenol. 1985; 145: 1061-1064Crossref PubMed Scopus (90) Google Scholar, 19Lee JG Schutz SM England RE Leung JW Cotton PB. Endoscopic therapy of sclerosing cholangitis.Hepatology. 1995; 21: 661-667PubMed Google Scholar In our patient, stricture dilatation and temporary insertion of biliary stents together with treatment with UDCA was based on encouraging results of similar treatment in an uncontrolled trial in patients with primary sclerosing cholangitis.20Stiehl A Rudolph G Sauer P Benz C Stremmel W Walker S et al.Efficacy of ursodeoxycholic acid treatment and endoscopic dilatation of major duct stenoses in primary sclerosing cholangitis. An 8-year prospective study.J Hepatol. 1997; 26: 560-566Abstract Full Text PDF PubMed Scopus (170) Google Scholar The triad of chronic pancreatitis, sclerosing cholangitis, and Sjögren's syndrome is a rare but well-defined entity that is probably caused by autoimmune mechanisms. Outcome is dominated by the progression of sclerosing cholangitis. Extrahepatic involvement with the latter, as in the present case, is often readily amenable to endoscopic or interventional radiologic therapy. Considering the assumed autoimmune pathogenesis of this syndrome, immunosuppressive treatment may also be beneficial. We thank Rudolf W. Ammann, MD, for his assistance in the search for published cases.

Background and Study Aims: Patients and Methods: Results: Conclusions:

QUESTION UNDER STUDY To assess whether patient or adenoma characteristics at index colonoscopy could be predictors of metachronous adenomas and of advanced metachronous adenomas at first surveillance colonoscopy. METHODS This retrospective study evaluated polypectomies of 372 adenomas in 214 patients who underwent a first follow-up colonoscopy after a median of 17 months. Logistic regression analysis was used to assess the association of baseline patient and adenoma characteristics with the development of any metachronous adenomas and of advanced adenomas (>1.0 cm, or villous component, or severe dysplasia, or early cancer). RESULTS Eighty-one patients (38%) demonstrated 130 metachronous adenomas including 21 cases (10%) with advanced adenomas. The presence of more than 2 baseline adenomas was significantly associated with the finding of adenomas at follow-up (odds ratio 2.44, 95% confidence interval 1.27-4.68, p = 0.010). Patient age (>or= 60 versus <60) and size of largest adenoma (>1.0 cm versus

BACKGROUND AND STUDY AIMS To assess whether polyp histological type can be predicted by patient characteristics and endoscopic polyp findings. PATIENTS AND METHODS 1681 polyps in 494 patients were categorized as advanced adenomas (villous component or severe dysplasia or early cancer) or insignificant polyps. Chi-squared tests were used to analyze whether polyp histological type could be predicted based on patient age (< 60 vs. > or = 60 years), gender, family history of colon polyps or cancer, presence of anemia, polyp size (< or = 5 mm vs. > 10 mm), and location (left- vs. right-sided). RESULTS Insignificant polyp histology (n = 1337) correlated with patient age < 60 years (P = 0.0026), lack of anemia (P< 0.0001), polyp size < or = 5 mm (P < 0.0001), and right-sided location (P= 0.0058). Stepwise inclusion of these parameters demonstrated that the association of a < or = 5 mm right-sided polyp in a patient < 60 years yielded the highest combined predictive value (96.2%) for an insignificant polyp. Conversely, age > or = 60 years, presence of anemia, polyp size > 10 mm, or left-sided location, as single or combined parameters, demonstrated a maximum predictive value of only 75.4% for an advanced adenoma. CONCLUSIONS A small right-sided polyp in a young patient is associated with a small risk (3.8 %) for advanced adenomatous tissue, indicating that histological investigation of such a polyp might not always be necessary. However, the recent recognition of flat adenomas and "mini" de novo colon carcinomas in the European population also may limit the usefulness of small polyp diameters in the exclusion of severe polyp histology.

Helicobacter pylori (H. pylori) besiedelt den menschlichen Magen bei 15–30% der westlichen Bevölkerung, und die Infektionsrate in den Entwicklungsländern ist noch deutlich höher [1]. Ob es sich dabei um ein Pathogen handelt oder nicht, war noch vor 15 Jahren umstritten. Die Antwort auf die Frage, wann eine Helicobacter-pylori-Infektion behandelt werden soll, ist bis heute ein Beispiel für die Schwierigkeit, aus noch ungenügenden Daten Konsequenzen für die praktische Tätigkeit abzuleiten. In unserer Praxis stellen wir fest, dass die frühere Zurückhaltung betreffend Behandlung von H. pylori heute eher ins Gegenteil auszuschlagen droht. Als Beispiel seien Patienten mit erhöhtem Titer auf H. pylori erwähnt, welche bei fehlendem Absinken des Titers oft mehrfach antibiotisch behandelt werden. In der vorliegenden Übersicht sollen deshalb die wichtigsten Situationen der Praxis beleuchtet werden, in welchen sich die Frage betreffend Behandlung der H.-pylori-Infektion stellt. Die grosse Flut an teils widersprüchlichen Daten und Interpretationen zwingt zu einer subjektiven Wertung und einer Beschränkung der besprochenen Themen. Die abgegebenen Empfehlungen basieren grösstenteils auf internationalen Konsensus-Richtlinien [2–6].

Background: Nasoenteral feeding tube placement with the Seldinger technique using transoral endoscopy is a tedious procedure. This study compared the transoral approach with a new technique that uses a transnasal endoscope without the need for a mouth-to-nose wire transfer. Methods: Critically ill patients requiring nasoenteral feeding tube placement were randomly assigned to the transoral technique using a standard upper endoscope (n = 80) or the transnasal method using a 5.3 mm fiberscope (n = 80). Procedure time, medication requirement, technical difficulty, patient tolerance, and radiologic tube position were assessed. Results: The two groups were similar with regard to baseline medication, endoscopic findings, as well as overall technical difficulty and patient tolerance. The transnasal technique required less procedure time (median 8.0 versus 12.0 minutes, p < 0.001) and less relaxant medication (p = 0.029). Furthermore, it caused fewer circulatory (p = 0.040) and respiratory (p = 0.016) alterations regardless of the application of sedative or relaxant medication. The transnasal endoscope was inferior with respect to passage through the pylorus (p = 0.003) and duodenum (p = 0.020). These differences were significant in univariate hypothesis testing. Bonferroni correction for multiple testing of data removed the significance at p > 0.0031. Both techniques achieved similar rates of successful tube placement in the small bowel (86% versus 84%, p = 0.82). Conclusion: Transnasal endoscopy allows accurate placement of nasoenteral feeding tubes in critically ill patients and is superior to transoral endoscopy in terms of procedure time, medication requirement, and safety. (Gastrointest Endosc 2000;52:506-10.)

Background and Study Aims: A new technique has been described which combines abdominal helical computed tomography (CT) scanning and virtual reality computer technology, known as virtual colonoscopy (VC); the reconstructed images provide a simulation of the interior of the colon as viewed by endoscopy, We compared VC with conventional colonoscopy in patients with suspected or known colonic neoplasia.Patients and Methods: A total of 38 patients, in whom there was a high likelihood of colonic polyps or cancer, underwent a noncontrast helical CT scan of the abdomen and pelvis after regular colonoscopy bowel preparation,The images were reconstructed into a VC presentation and compared with the subsequent conventional colonoscopy in a blinded manner.Results: Conventional colonoscopy identified a total of 24 polyps 5 mm or greater. VC correctly identified five of 13 polyps 5-9 mm in size, and ten of II lesions greater than or equal to 10 mm in diameter. The reasons for four missed lesions were identified as being secondary to a collapsed rectum in two patients and stool in the right colon in two patients, The sensitivity and specificity per patient of VC for lesions greater than or equal to 5 mm were 66.7% and 75.0% respectively, and for lesions greater than 1 cm were 90.0% and 82.1%, respectively.Conclusions: Virtual colonoscopy is feasible, well tolerated, and capable of detecting most lesions seater than 10 mm in diameter, This technique is continuing to be developed and warrants further evaluation as a diagnostic and screening tool in colorectal neoplasia.

Background: Magnetic resonance (MR) imaging is uniquely sensitive to temperature changes. This preliminary study assessed the feasibility of real-time MR-monitoring of the endoscopic laser application in an interventional scanner. Methods: The procedures were performed with a MRcompatible endoscope (XGIF-MR30C, Olympus, Tokyo, Japan) in two domestic pigs in an interventional 0.5 Tesla MR-system (Signa SP, General Electric Medical, Schenectady, NY, USA) with a 56 cm gap permitting vertical access to the animal. Both the endoscopic view and the MR-images were simultaneously visible on two liquid crystal monitors within the scanner. An external circular balloon filled with gadolinium rendered the endoscope tip visible for MR-imaging. A 10 meter long 365 μm bare laser fiber connected to a Nd:YAG laser located outside the scanner room was inserted through the accessory channel of the endoscope. Laser applications were performed in the rectum (n=5) and the transverse colon (n=1) with energy outputs ranging between 1200 and 1950 Joules delivered at a power of 5 Watts during 4 to 6.5 minutes. The laser induced temperature changes were visualized using a color-coded subtraction technique based on amplitude alterations of T1-weighted gradient echo sequences enabling an image update every 3 seconds in a single axial, sagittal or coronal plane. The animals were sacrificed and the macroscopic coagulation sizes were compared with the lesion sizes seen at real-time MR.Results: The endoscope did not cause any artifacts at continuous MR-imaging. The sizes of the macroscopic coagulation zones of the laser induced lesions were correctly predicted by the color-coded MR-images in a 5 mm lesion in the transverse colon and two 10 mm and 15 mm lesions in the rectum. One lesion was underestimated (5 mm instead of 15 mm) by MR. The lack of a visible pre-treatment lesion inherent with the healthy animal model complicated the accurate MR-localization of the intended laser application sites. This resulted in the failed MR-delineation of two 10 mm laser lesions. Conclusion: Real-time MR-monitoring of endoscopic laser application in an interventional scanner is feasible. This new technique may allow future safe and predictable destruction of gastrointestinal tumors with fewer treatment sessions.

A 61-year-old man was admitted with complaints of crampy abdominal pain and bloody stools. Eleven years earlier he had an aortobifemoral bypass done for an abdominal aortic aneurysm. CT showed an aneurysm at the proximal margin of the aortic graft extending to the third portion of the duodenum (A , arrow ). The patient was referred to our hospital for surgical repair of a suspected aortoenteric fistula. On arrival, there were no signs of GI bleeding. EGD was normal. Colonoscopy, however, demonstrated a segmental colitis in the sigmoid colon. This lesion, consistent with ischemic colitis, was interpreted as the cause of the rectal bleeding.

Background: There are conflicting recommendations regarding the prophylactic use of antibiotics in patients undergoing placement of percutaneous endoscopic gastrostomy tubes. The purpose of this decision analysis was to assess the cost-effectiveness of antibiotic prophylaxis in percutaneous endoscopic gastrostomy,Methods: A decision tree was modeled using the data of 7 published prospective placebo-controlled trials. Infectious complications were classified as grade I (requiring local care), grade II (requiring intravenous antibiotics), or grade III (requiring surgery), Medication costs were estimated from the United States average wholesale prices of the 1998 Red Book. Physician and facility costs were estimated based on the 1998 Medicare costs, A one-way sensitivity analysis was performed by varying the probability rates of the complications associated with percutaneous endoscopic gastrostomy and the costs of their treatment.Results The average cost of prophylactic antibiotics was $13.10, Antibiotic prophylaxis led to expected cost savings of $76.72 per percutaneous endoscopic gastrostomy, A sensitivity analysis suggested that antibiotic prophylaxis for percutaneous endoscopic gastrostomy was the preferred strategy unless the average probability of grade III complications dropped below an improbably low threshold value of 0.09%,Conclusion: Antibiotic prophylaxis in percutaneous endoscopic gastrostomy is a cost-effective strategy.

BACKGROUND AND STUDY AIMS Endoscopic laser therapy involves a risk of perforation, mainly because the depth of tissue destruction is not visible. Magnetic resonance (MR) imaging is capable of showing temperature changes, and is therefore suitable for monitoring thermal therapies such as laser. This animal study assessed the feasibility of real-time MR monitoring of endoscopic laser applications in the gastrointestinal tract. MATERIALS AND METHODS The procedures were carried out using an MR-compatible endoscope in three live pigs in a 0.5-Tesla interventional MR system. Nd:YAG laser applications were performed in the lower gastrointestinal tract (n = 7) and upper gastrointestinal tract (n = 5), and were monitored using real-time color-coded T1-weighted gradient echo sequences. The postmortem macroscopic tissue coagulation sizes were compared with the lesion diameters seen on real-time MR. RESULTS The endoscope did not cause any artifacts during continuous MR imaging. Ten of the twelve laser lesions were visible with temperature-sensitive MR imaging, and their sizes correlated well with the diameters of the postmortem macroscopic coagulation zones (r = 0.76, P = 0.009). Two laser lesions were not visible on MR due to technical limitations inherent with the healthy animal model. CONCLUSIONS The formation of endoscopic laser lesions in the porcine gastrointestinal tract can be accurately visualized using real-time temperature-sensitive MR imaging. This new technique has the potential to spare healthy tissue while ensuring full treatment coverage of the targeted lesion with fewer therapy sessions.