Network


Latest external collaboration on country level. Dive into details by clicking on the dots.

Hotspot


Dive into the research topics where Ronald Bridges is active.

Publication


Featured researches published by Ronald Bridges.


Canadian Journal of Gastroenterology & Hepatology | 2010

Survey of Access to GastroEnterology in Canada: The SAGE Wait Times Program

Desmond Leddin Mb; Ronald Bridges; David Morgan; Carlo A Fallone; Craig Render; Victor Plourde; James Gray; Connie Switzer; Jim McHattie; Harminder Singh; Eric Walli; Iain Murray; Anthony Nestel; Paul Sinclair; Ying Chen; E. Jan Irvine

BACKGROUND Assessment of current wait times for specialist health services in Canada is a key method that can assist government and health care providers to plan wisely for future health needs. These data are not readily available. A method to capture wait time data at the time of consultation or procedure has been developed, which should be applicable to other specialist groups and also allows for assessment of wait time trends over intervals of years. METHODS In November 2008, gastroenterologists across Canada were asked to complete a questionnaire (online or by fax) that included personal demographics and data from one week on at least five consecutive new consultations and five consecutive procedure patients who had not previously undergone a procedure for the same indication. Wait times were collected for 18 primary indications and results were then compared with similar survey data collected in 2005. RESULTS The longest wait times observed were for screening colonoscopy (201 days) and surveillance of previous colon cancer or polyps (272 days). The shortest wait times were for cancer-likely based on imaging or physical examination (82 days), severe or rapidly progressing dysphagia or odynophagia (83 days), documented iron deficiency anemia (90 days) and dyspepsia with alarm symptoms (99 days). Compared with 2005 data, total wait times in 2008 were lengthened overall (127 days versus 155 days; P<0.05) and for most of the seven individual indications that permitted data comparison. CONCLUSION Median wait times for gastroenterology services continue to exceed consensus conference recommended targets and have significantly worsened since 2005.


Journal of Hepatology | 2000

Familial idiopathic adulthood ductopenia: a report of five cases in three generations

Kelly W. Burak; David C. Pearson; Mark G. Swain; James K. Kelly; Stefan J. Urbanski; Ronald Bridges

BACKGROUND/AIMS Idiopathic adulthood ductopenia is a cholestatic liver disease of unknown etiology. Although most cases are sporadic, familial cases do occur. METHODS We describe a series of adult-onset bile duct depletion involving five members of an extended family spanning three generations. The proband, a 49-year-old man, presented in 1989 with asymptomatic elevation of liver enzyme tests. Investigations for chronic liver disease, including endoscopic retrograde cholangiopancreatography, were negative. Findings on liver biopsy progressed from normal in 1989 to striking loss of interlobular bile ducts in 1992. Ursodeoxycholic acid has resulted in improvement of liver enzyme tests. The probands brother required a liver transplant at age 35 for cryptogenic cirrhosis. The probands sister, age 42, has had intermittent jaundice and elevation of liver enzyme tests since 1971. Her liver biopsy findings progressed from normal in 1975, to striking bile duct damage by 1997. The probands 21-year-old son has elevated liver enzyme tests and a liver biopsy consistent with idiopathic adulthood ductopenia. The probands father had a liver biopsy at age 70 for investigation of a liver mass. It revealed extensive fibrosis and striking bile duct destruction. RESULTS/CONCLUSIONS This is the largest series of familial idiopathic adulthood ductopenia reported, and the first with multiple generations described. Genetics appears to play a role in some cases of adulthood ductopenia. Ursodeoxycholic acid may be beneficial in the treatment of this condition.


Annals of Internal Medicine | 1993

Chronic Active Hepatitis Associated with Trazodone Therapy

Paul L. Beck; Ronald Bridges; Douglas J. Demetrick; James K. Kelly; Samuel S. Lee

Trazodone (Desyrel, Bristol-Myers Squibb Canada, Montreal, Quebec) is a nontricyclic antidepressant that has been available in North America since the early 1980s. Three previous cases of hepatic injury associated with this drug have been reported [1-3]. In two cases, the patients had been taking trazodone only briefly, and the biopsy specimens confirmed acute injury. In the third case, a patient had taken trazodone for 7 months and showed liver chemistry abnormalities for 6 months after drug cessation. However, no liver biopsy was done in that case. We describe a patient who developed chronic active hepatitis in association with trazodone therapy. Case Report A 75-year-old Asian woman came to the emergency department with jaundice. She had noted the onset of dark urine and pale stools 3 weeks previously, and her family noticed that she was jaundiced 1 week before. She reported nausea and anorexia that had started approximately 8 months before the onset of jaundice, concomitant with the initiation of a course of trazodone therapy, 150 mg daily, prescribed for depression. She had no previous history of jaundice, blood transfusion, intravenous drug abuse, parenteral drug therapy, acupuncture treatment, or alcohol use. She had no significant past medical problem other than a cholecystectomy 15 years previously. The only medication she was taking was trazodone. She reported no history of herbal medicine ingestion. The physical examination at admission was unremarkable except for jaundice. No hepatosplenomegaly, abdominal tenderness, or ascites were present. Stigmata of chronic liver disease were absent. A rectal examination showed guaiac-negative pale stool. The hemoglobin concentration was 136 g/L. The prothrombin time and partial thromboplastin times were elevated at 13.9 s and 40.8 s, respectively (normal, < 11.7 s and < 36 s, respectively). The bilirubin level was 306 mol/L (normal, < 20 mol/L), with a conjugated bilirubin level of 175 mol/L (normal, < 5 mol/L). Initial liver enzyme levels were as follows: alanine aminotransferase, 15.55 kat/L (normal, < 0.58 kat/L); aspartate aminotransferase, 14.05 kat/L (normal, < 0.53 kat/L); -glutamyltransferase, 6.33 kat/L (normal, < 0.58 kat/L); and alkaline phosphatase, 2.4 kat/L (normal, < 2.4 kat/L). Results of chest and abdominal radiographs and an abdominal ultrasound scan were normal. Serologic tests for hepatitis A virus (IgM anti-HAV) and hepatitis B surface and e antigens were negative. An assay for IgM antibody against hepatitis B core antigen was also negative, but IgG antibodies against hepatitis B surface and core antigens were detected. Serologic test results for hepatitis C virus were negative using a first-generation enzyme-linked immunosorbent assay (Ortho Diagnostics, Raritan, New Jersey) and, subsequently, a second-generation recombinant immunoblot assay (Ortho). Serologic tests for Q fever, cytomegalovirus, and herpes simplex, Epstein-Barr, and varicella zoster viruses were all negative. Serologic tests for antimitochondrial, antismooth muscle, and antinuclear antibodies were also negative. The prothrombin time and partial thromboplastin times remained elevated despite a 3-day course of therapy with subcutaneous vitamin K. Because of the abnormal coagulation factors, a transjugular approach was used for liver biopsy. Measurements of hepatic venous pressures done in conjunction with biopsy showed a modestly elevated hepatic venous pressure gradient (corresponding to portal pressure) of 9 mm Hg (normal, 1 to 4 mm Hg). The liver tissue was fragmented and nodular and showed a pattern consistent with chronic active hepatitis (Figure 1). Between the nodules there was reticulin condensation but no deposition of elastica, indicating that the lesion was relatively recent. The portal tracts were expanded by an infiltrate of lymphocytes and plasma cells, with erosion of limiting plates and portoportal and portocentral bridging necrosis. Eosinophils were rare. The parenchyma showed thickening of liver cell plates, occasional acidophil bodies, mild focal inflammation, low-grade parenchymal and reticuloendothelial hemosiderosis, and no -1-antitrypsin bodies or metallothionein. Centrilobular areas showed liver cell dropout and lipofuscin-laden macrophages that stained strongly positive with diastase-periodic acid-Schiff. Immunostains for hepatitis B surface and core antigens were negative. Figure 1. Liver specimen showing the pattern of chronic active hepatitis. Trazodone therapy was discontinued and within 1 week the patients nausea and anorexia had resolved. Ten days after stopping the drug, the aminotransferase enzyme levels had markedly decreased and by 4 weeks had returned to normal. The prothrombin and partial thromboplastin times returned to normal within 2 weeks. The bilirubin and -glutamyltransferase levels were slow to decrease but gradually declined, returning to normal approximately 6 months after the last dose of trazodone. The patient has been followed for 2 years since resolution and has showed no further clinical or laboratory evidence of hepatic dysfunction. Discussion To our knowledge, this is the first reported case of trazodone-induced chronic active hepatitis. Chu and colleagues [1] described a case of acute trazodone-induced hepatotoxicity. Their patient developed an exfoliative, macular, pruritic rash and elevated liver enzyme levels 3 weeks after starting a course of trazodone therapy (500 mg daily). The liver biopsy specimen showed a mixed hepatocellular-cholestatic pattern [1]. Sheikh and Nies [2] described a patient who developed intrahepatic cholestasis 2 weeks after starting trazodone therapy (50 mg daily). In these two patients, symptoms resolved rapidly after discontinuation of therapy, and liver enzyme levels returned to normal within 8 weeks of stopping trazodone. Longstreth and Hershman [3] described a patient who developed jaundice, pruritus, nausea, leukonychia, and elevated liver enzyme levels after a 7-month course of trazodone therapy (200 mg daily). The patients symptoms and jaundice rapidly resolved after cessation of trazodone. The liver enzyme levels were nearly normal 5 weeks after stopping the drug, but there were an intermittent slight elevations of the aspartate aminotransferase and alkaline phosphatase levels for as long as 6 months after the discontinuation of trazodone therapy [3]. It is possible that the patient had drug-induced chronic hepatitis, especially given the prolonged abnormalities in liver enzyme levels; however, because a liver biopsy was not done, this remains speculative. In our case, both bilirubin and -glutamyltransferase levels remained elevated until 6 months after cessation of the drug, probably reflecting the chronicity of the hepatotoxic process. Given the extensive damage that the biopsy specimen showed, this slow resolution of all liver chemistry abnormalities was not surprising. Chronic active hepatitis has many causes. However, we are confident that the chronic hepatitis in our patient was caused by trazodone. Hepatitis B serologic test results were consistent with remote past exposure to hepatitis B but not with ongoing viral infection, which was confirmed by the negative immunostains on the biopsy specimen. The serologic and biopsy findings effectively ruled out other causes of chronic hepatitis. Finally, the temporal relation of the symptoms and liver enzyme abnormalities to the starting and stopping of the drug strongly implicates trazodone as the cause of the chronic hepatitis. We suggest that clinicians be alert to the possibility of hepatic injury in patients taking this medication.


Canadian Journal of Gastroenterology & Hepatology | 2013

The 2012 Sage Wait Times Program: Survey of Access to Gastroenterology in Canada

Desmond Leddin; David Armstrong; Mark Borgaonkar; Ronald Bridges; Carlo A Fallone; Jennifer J. Telford; Ying Chen; Palma Colacino; Paul Sinclair

BACKGROUND Periodically surveying wait times for specialist health services in Canada captures current data and enables comparisons with previous surveys to identify changes over time. METHODS During one week in April 2012, Canadian gastroenterologists were asked to complete a questionnaire (online or by fax) recording demographics, reason for referral, and dates of referral and specialist visits for at least 10 consecutive new patients (five consultations and five procedures) who had not been seen previously for the same indication. Wait times were determined for 18 indications and compared with those from similar surveys conducted in 2008 and 2005. RESULTS Data regarding adult patients were provided by 173 gastroenterologists for 1374 consultations, 540 procedures and 293 same-day consultations and procedures. Nationally, the median wait times were 92 days (95% CI 85 days to 100 days) from referral to consultation, 55 days (95% CI 50 days to 61 days) from consultation to procedure and 155 days (95% CI 142 days to 175 days) (total) from referral to procedure. Overall, wait times were longer in 2012 than in 2005 (P<0.05); the wait time to same-day consultation and procedure was shorter in 2012 than in 2008 (78 days versus 101 days; P<0.05), but continued to be longer than in 2005 (P<0.05). The total wait time remained longest for screening colonoscopy, increasing from 201 days in 2008 to 279 days in 2012 (P<0.05). DISCUSSION Wait times for gastroenterology services continue to exceed recommended targets, remain unchanged since 2008 and exceed wait times reported in 2005.


Canadian Journal of Gastroenterology & Hepatology | 2012

Canadian Digestive Health Foundation Public Impact Series 5: Pancreatitis in Canada. Incidence, prevalence, and direct and indirect economic impact

Christopher W. Teshima; Ronald Bridges; Richard N. Fedorak

The Canadian Digestive Health Foundation initiated a scientific program to assess the incidence, prevalence, mortality and economic impact of digestive disorders across Canada in 2009. The current article presents the updated findings from the study concerning pancreatitis.


Canadian Journal of Gastroenterology & Hepatology | 2005

Well differentiated intrahepatic cholangiocarcinoma in the setting of biliary papillomatosis: A case report and review of the literature

Heather Cox; Michael Ma; Ronald Bridges; Estifanos Debru; Oliver F. Bathe; Francis Sutherland; Elijah Dixon

A 64-year-old man presented with long-standing, vague, epigastric abdominal pain. History, physical examination and laboratory studies were noncontributory. However, serial computed tomography scans revealed a rapidly progressive mass in segment 2 of the liver. Surprisingly, surgical pathology revealed a well-differentiated intrahepatic cholangiocarcinoma associated with biliary papillomatosis (BP). BP is a rare, benign and potentially fatal disease of the intra- and extrahepatic bile ducts. It is typified by numerous multicentric papillary fronds arising from biliary columnar epithelium. Most patients present with symptoms of jaundice and cholangitis. Although a benign disease, a review of the literature demonstrated that BP often recurs after surgical resection, carries a poor prognosis and has a moderately high malignant transformation rate. Treatment options for BP include surgical resection, transplant, ablation, stenting and/or bypass.


Canadian Journal of Gastroenterology & Hepatology | 2002

Leptomeningeal carcinomatosis secondary to gastroesophageal adenocarcinoma: A case report and review of the literature

Ayman A. Abdo; Sylvain Coderre; Ronald Bridges

BACKGROUND Leptomeningeal carcinomatosis (LC) is a rare metastatic complication of solid tumours. It has been mainly described in association with breast cancer, lung cancer and melanoma. CASE PRESENTATION A patient presenting with progressive solid food dysphagia with documented adenocarcinoma of the lower esophagus and gastroesophageal junction is reported. One month after the initial diagnosis, the patient developed gradual onset of increasing headache and progressive decrease in the level of consciousness. Computed tomography of the head showed evidence of meningeal enhancement, and cerebrospinal fluid examination showed the presence of adenocarcinoma cells, making the diagnosis of LC. The patient died one month after LC was diagnosed. DISCUSSION LC is a poor prognostic sign in solid organ malignancies. It usually presents with headache, altered level of consciousness and focal neurological deficits. Diagnosis is established by finding malignant cells in the cerebrospinal fluid and supported by marked meningeal enhancement on computed tomography of the brain. A review of the English literature found only three reported cases of LC secondary to esophageal malignancy. CONCLUSION A case of LC complicating esophageal and gastroesophageal junction malignancy is described. A high index of suspicion and early diagnosis may influence the poor outcome of these patients.


Canadian Journal of Gastroenterology & Hepatology | 2012

Indicators of safety compromise in gastrointestinal endoscopy

Mark Borgaonkar; Lawrence Hookey; Roger Hollingworth; Ernst J. Kuipers; Alan Forster; David Armstrong; Alan N. Barkun; Ronald Bridges; Rose M Carter; Chris de Gara; Caroline Dubé; Robert Enns; Donald G. MacIntosh; Sylvaine Forget; Grigorios I. Leontiadis; Jonathan Meddings; Peter B. Cotton; Roland Valori

INTRODUCTION The importance of quality indicators has become increasingly recognized in gastrointestinal endoscopy. Patient safety requires the identification and monitoring of occurrences associated with harm or the potential for harm. The identification of relevant indicators of safety compromise is, therefore, a critical element that is key to the effective implementation of endoscopy quality improvement programs. OBJECTIVE To identify key indicators of safety compromise in gastrointestinal endoscopy. METHODS The Canadian Association of Gastroenterology Safety and Quality Indicators in Endoscopy Consensus Group was formed to address issues of quality in endoscopy. A subcommittee was formed to identify key safety indicators. A systematic literature review was undertaken, and articles pertinent to safety in endoscopy were identified and reviewed. All complications and measures used to document safety were recorded. From this, a preliminary list of 16 indicators was compiled and presented to the 35-person consensus group during a three-day meeting. A revised list of 20 items was subsequently put to the consensus group for vote for inclusion on the final list of safety indicators. Items were retained only if the consensus group highly agreed on their importance. RESULTS A total of 19 indicators of safety compromise were retained and grouped into the three following categories: medication-related - the need for CPR, use of reversal agents, hypoxia, hypotension, hypertension, sedation doses in patients older than 70 years of age, allergic reactions and laryngospasm⁄bronchospasm; procedure-related early - perforation, immediate postpolypectomy bleeding, need for hospital admission or transfer to emergency department from the gastroenterology unit, instrument impaction, severe persistent abdominal pain requiring evaluation proven to not be perforation; and procedure-related delayed - death within 30 days of procedure, 14-day unplanned hospitalization, 14-day unplanned contact with a health provider, gastrointestinal bleeding within 14 days of procedure, infection or symptomatic metabolic complications. CONCLUSIONS The 19 indicators of safety compromise in endoscopy, identified by a rigorous, evidence-based consensus process, provide clear outcomes to be recorded by all facilities as part of their continuing quality improvement programs.


The American Journal of Gastroenterology | 2016

Defining Benchmarks for Adenoma Detection Rate and Adenomas Per Colonoscopy in Patients Undergoing Colonoscopy Due to a Positive Fecal Immunochemical Test

Robert J. Hilsden; Ronald Bridges; Catherine Dube; S. Elizabeth McGregor; Christopher Naugler; Sarah M Rose; Alaa Rostom; Steven J. Heitman

Objectives:Although there is an accepted benchmark for adenoma detection rate (ADR) in average risk screening colonoscopy, a benchmark for ADR or the associated quality indicator, adenomas per colonoscopy (APC), for colonoscopies performed for a positive fecal immunochemical test (FIT+) has not been established. The purpose of this study was to propose methods for establishing a benchmark ADR and APC for FIT+ patients.Methods:In this historical cohort study, we included 15,329 patients aged 50–74 years who underwent a colonoscopy at Alberta Health Services’ Colon Cancer Screening Centre, Calgary, Canada, from 1 January 2014 to 30 June 2015 for either investigation of a positive FIT or average risk screening. Using meta-regression, we estimated for FIT+ patients the ADR and APC that corresponded to (Method #1: minimally acceptable) an ADR of 25% in average risk individuals, (Method #2: standard of care) the average ADR or APC in all FIT+ patients, and (Method #3: aspirational) the average FIT+ ADR or APC in colonoscopies performed by endoscopists with an ADR of ≥35% in average risk patients.Results:At least one adenoma was detected in 30% of average risk patients and 58% of FIT+ patients. The calculated benchmark FIT+ ADRs for the three methods were 55, 60, and 65%, respectively. The calculated benchmarks for FIT+ APC were 1.2, 1.4, and 1.7, respectively. To account for expected random variation in individual endoscopists’ ADR or APC, we propose using the upper bound of the 95% confidence interval of an endoscopist’s ADR or APC to determine if they fall below a given benchmark.Conclusions:We have proposed methods of defining benchmarks for ADR and APC in FIT+ patients that go beyond the current “minimally acceptable” threshold currently recommended in average risk patients. These new thresholds represent results obtained by all peers and by a group of expert adenoma detectors defined in an independent patient cohort (average risk). Because the true adenoma burden in FIT+ patients could vary based on factors such as the threshold used to define a positive FIT, screening programs or endoscopy units may need to calculate their own benchmarks using local data.


Canadian Journal of Gastroenterology & Hepatology | 1997

Use of Axathioprine for Nongranulomatous Ulcerative Jejunoileitis

Robert Enns; Thomas Lay; Ronald Bridges

Nongranulomatous ulcerative jejunoileitis (NGUJI) is a rare, often fatal disorder that produces multiple nonmalignant small bowel ulcerations. A 55-year-old woman with presumed celiac disease presented with steroid-refractory diarrhea, weight loss and abdominal pain. A laparotomy was performed to exclude the possibility of a lymphomatous disorder, and multiple nonmalignant small bowel ulcerations were discovered. Despite a combination of treatment with total parenteral nutrition (TPN) and prednisone 30 mg/day she continued to deteriorate. The addition of azathioprine to her treatment regimen resulted in marked clinical and biochemical improvement. Her enteroscopy normalized, and she was able to discontinue TPN and reduce her steroid requirements. Although azathioprine has been used occasionally to treat refractory sprue, there have been no reports of its use in NGUJI. In this case, azathioprine played a key role in the management of NGUJI and should be considered a treatment option for patients with this disorder.

Collaboration


Dive into the Ronald Bridges's collaboration.

Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar

David Armstrong

University of Southern California

View shared research outputs
Top Co-Authors

Avatar
Researchain Logo
Decentralizing Knowledge