Diagnosis Of Upper Gastrointestinal Bleeding Research Articles

Is variceal bleeding increasing within the UK population?

Introduction The incidence of cirrhosis and mortality from chronic liver disease is increasing, but it is not known whether hospitalisations for variceal bleeding are also increasing. In contrast, hospitalisations for peptic ulcer bleeding are believed to be decreasing due to falling H. pylori and peptic ulcer prevalence. Yet in the UK during the 1990s non variceal hospitalisation rates remained unchanged, and even increased in the elderly, possibly as a consequence of aspirin and NSAID use.1 We therefore aimed to accurately determine trends in hospitalisation rates of variceal haemorrhage and compare these to the current trends of non-variceal haemorrhage. Methods We used hospital episodes statistics which contain all admissions within England, and identified the number of upper gastrointestinal bleeds according to ICD 10 codes between 1999 and 2007. We used the Office of National Statistics mid-year population estimates to derive the population denominators by age and sex. Changes in hospitalisation rates were adjusted for age and sex using Poisson regression. Results 313,111 admissions were identified with a primary diagnosis of upper gastrointestinal haemorrhage. Of these 302,492 (97%) were non-variceal bleeds, and 10,619 (3%) were variceal bleeds (see table 1). Even after adjusting for age and sex there was no increase in the hospitalisation rate of variceal haemorrhage test for trend (p = 0.5). In contrast, there was a slight 0.6% annual increase in the hospitalisation rate of non variceal haemorrhage that persisted despite adjusting for age and gender (annual increase in hospitalisation rate of 0.2%, 95% confidence interval 0.1–0.4%, p = 0.001). Conclusion Hospitalisation rates of variceal haemorrhage are not increasing despite the observed increase in cirrhosis. This could be because of better primary and secondary prevention of bleeding or from the diagnosis of cirrhosis at an earlier stage of the disease process. Patients presenting with upper gastrointestinal haemorrhage are admitted acutely to hospital as standard practice within England so these hospitalisation rates are a useful proxy for population based incidence rates.

The characteristics of adults with upper gastrointestinal bleeding admitted to Tripoli Medical Center: a retrospective case-series analysis

Background: Acute upper gastrointestinal bleeding (UGIB) is a common reason for hospital admissions worldwide. Aetiological causes of UGIB vary according to geographic region and socioeconomic status. However, despite the implementation of early endoscopy as the standard method for the diagnosis and treatment of UGIB, data on the characteristics of patients with UGIB in Libya are still minimal. In this study, we describe patient demographics, aetiological causes for UGIB, and possible risk factors for upper gastrointestinal bleeding in patients admitted to the Gastroenterology Department at Tripoli Medical Center from January 2001 through June 2006.Method: This is a retrospective case-series analysis of all adult patients with upper gastrointestinal bleeding admitted to the Gastroenterology Department at TMC. Patients’ medical records were individually reviewed and relevant data abstracted.Results: A total of 928 cases with diagnoses of UGIB were admitted to Tripoli Medical Center during the study period. Of these cases, 60.3% were males and 39.7% females (3:2) and males were significantly younger than females (49.6 years vs. 53.9 years, p=0.001). The most common cause of UGIB was peptic ulcer (37.1%) of which duodenal ulcer was the most common (30.7% of all UGIB), especially amongst male patients (36.4%). The second most common cause was bleeding due to varices (29.8%), especially amongst females (35.1%). Additionally, smoking and NSAIDs use were reported by 18.6% and 9.7% of cases and both were significantly associated with bleeding due to peptic ulcers.Conclusion: This study has investigated the characteristics of adults with UGIB at a tertiary referral center in Libya. The high frequency of bleeding due to varices amongst females mandates further investigations into the possible underlying hepatic causes and their management, and the potential impact on patient outcome and prognosis.

Report of a Case: Pseudoaneurysm of the Cystic Artery With Hemobilia Treated by Arterial Embolization

We report a case of hemobilia caused by pseudoaneurysm of the cystic artery in a 71-year-old woman who presented with fever and epigastric colicky pain with jaundice. Liver function tests showed signs of obstructive jaundice. On the second day, patient had a massive hematemesis and melena with hypovolemic shock. Hemobilia was diagnosed by endoscopically visualizing bleeding from the papilla of Vater. An emergent angiography demonstrated the presence of a pseudoaneurysm in the cystic artery. Selective embolization of the cystic artery was then performed to interrupt the blood flow into the pseudoaneurysm. Immediately after embolization, patient was hemodynamically stabilized. Although the patient did not undergo cholecystectomy after embolization due to severe co-morbidities, no signs of ischemic gallbladder have been observed. Hemobilia should be included in the differential diagnosis of upper gastrointestinal bleeding with unknown etiology. Embolization could be an option for pseudoaneurysms of the cystic artery especially in high-risk patients. J Med Cases. 2011;2(4):178-183 doi: https://doi.org/10.4021/jmc249w

The aetiology, management and clinical outcome of upper gastrointestinal bleeding among patients admitted at the Kilimanjaro Christian Medical Centre in Moshi, Tanzania

Upper gastro-intestinal (GI) bleeding is a life-threatening emergency that results in high morbidity and mortality and therefore requires admission to hospital for urgent diagnosis and management. The aim of this study was to determine the causes of upper GI bleeding and clinical outcome of patients admitted to medical department with the diagnosis of upper GI bleeding. A retrospective study of records of all upper GI bleeding patients who were admitted to medical department, Kilimanjaro Christian Medical Centre (KCMC) from January 2007 to December 2008 was conducted. A total of 130 patients (13-96 years old) were enrolled in the study, whereby 73 (56.2%) were males. The causes of bleeding, all endoscopically diagnosed included oesophageal varices in 55 (42.3%) cases, followed by duodenal ulcers 20 (15.4%), hemorrhagic/erosive gastritis 10 (7.7%), gastric ulcer 6 (4.6%) and Mallory Weiss tear 2 (1.5%). No cause was identified in the remaining 27 % of cases. Conservative medical therapy alone was carried out in 52.3% of the patients. Endoscopic therapy was used in 61 (46.9%) of patients. Only 2 (1.5%) patients underwent surgical intervention. The overall mortality at discharge was 17%, while 107 (82%) patients were discharged improved. In conclusion, the commonest causes of upper GI bleeding are oesophageal varices and duodenal ulcer. Most cases of upper GI bleeding were successfully treated with pharmacologic and endoscopic treatment. The high mortality may be influenced by delayed presentation to health facilities, and comorbidities. There is a need for strengthening preventive programmes and conducting studies to identify predictors of outcome of upper GI bleeding to develop evidence based management protocols.

Prevalencia de nueva hemorragia por úlcera péptica en pacientes tratados con inhibidores de la bomba de protones por vía intravenosa

Background and objective The aim of this study is to assess the prevalence of peptic ulcer rebleeding by comparing patients who received omeprazole versus pantoprazole i.v. as well as to study the costs of each treatment. Patients and methods Retrospective and observational study. Information was gathered on sex and age of the patients, the diagnosis of upper gastrointestinal bleeding (UGB) according to the classification of Forrest, the type of proton pump inhibitor (PPI) i.v. used and the treatment regimen, presence or absence of rebleeding, mortality and data on health costs through a pharmacoeconomic cost-effectiveness analysis. Results We included 807 patients, 490 of whom (60.7%) received pantoprazole and 317 (39.3%) omeprazole. There was no difference between the average age of both groups, 61.2 years vs 62.3, p = 0.544; sex, 71% men vs 68.6%, P = .78; the percentage of patients within Forrest I was 35.1% vs 42%, P = .05, in grade II was 50.2% vs 40.4%, P = .006 and in grade III was 14.7% vs 17.7%, P = .259. The number of vials per day of treatment was significantly lower in the pantoprazole group from the third to fifth day, with no differences in the first two days and the sixth. There was rebleeding in 8.2% of patients treated with pantoprazole and 11.7% with omeprazole, P = .098. 2.2% of patients treated with pantoprazole died vs 2.6% treated with omeprazole, P = .086. The expected cost of a patient treated with pantoprazole was 2188.25 € vs 3279.02 € with omeprazole, P < .001. Conclusions While the results of the administration of omeprazole vs pantoprazole i.v. in patients with UGB are similar, the latter turns out to have a better cost-effectiveness profile.

Probable Interaction Between Warfarin and Marijuana Smoking

To report a probable interaction between warfarin and marijuana smoking, resulting in increased international normalized ratio (INR) values and bleeding complications. A 56-year-old white male had been receiving chronic warfarin therapy for 11 years after mechanical heart valve replacement. He was admitted to the hospital with a diagnosis of upper gastrointestinal bleeding. Upon admission, his INR value was supratherapeutic at 10.41, and his hemoglobin level was 6.6 g/dL. He received 4 units of fresh frozen plasma and one 10-mg dose of oral vitamin K; his INR was 1.8 the next day. He was discharged 7 days after admission. Fifteen days after hospital discharge, he was readmitted with a constant nosebleed and increased bruising. His INR value was 11.55. After treatment, he was discharged with an INR value of 1.14. The patient smoked marijuana more frequently throughout the period of these 2 hospitalizations due to his depression. He was counseled by the pharmacist on the potential interaction of warfarin and marijuana. The patient decided to stop smoking marijuana after the third counseling session. During the 9 months that he did not smoke marijuana, his INR values ranged from 1.08 to 4.40 with no significant bleeding complications. Marijuana may increase warfarin anticoagulant effect by inhibiting its metabolism, and to a lesser extent, displacing warfarin from protein-binding sites. Other causes (eg, nonadherence) of the patient's increased INR were ruled out. Using the Horn Drug Interaction Probability Scale, our patient's warfarinmarijuana interaction appeared to be probable. To our knowledge, there have been no other reported cases of warfarin-marijuana interaction. While more clinical reports would be useful to confirm this interaction, clinicians should be aware of its probability so as to manage patients appropriately.

Hemobilia as a Late Complication After Blunt Abdominal Trauma: A Case Report and Review of the Literature

Bleeding within the biliary tree, called hemobilia, is a rare complication after blunt hepatic trauma. To report on a patient who developed hemobilia 1 month after a blunt abdominal injury and to discuss the diagnosis and treatment of hemobilia. A 17-year-old boy presented with upper gastrointestinal bleeding caused by hemobilia 1 month after a blunt liver injury. Angiography revealed a pseudoaneurysm of the right hepatic artery, which was successfully treated with embolization. The diagnosis of hemobilia first requires consideration of the diagnosis, particularly in patients with previous abdominal trauma. Hemobilia should be included in the differential diagnosis of upper gastrointestinal bleeding. Investigations of choice include computed tomography scan followed by angiography. During angiography, treatment can be done by endovascular embolization.

Endoscopic Hemoclipping Therapy for Gastric Angiodysplasia in a Child

Gastric angiodysplasia is a very rare cause of upper gastrointestinal bleeding in children and adolescents and is considered to be a vascular abnormality with a developmental cause. Gastric angiodysplasia can be managed with various endoscopic methods, including argon plasma coagulation, electrocoagulation, heater probe, sclerotherapy, band ligation, and hemoclipping therapy. We describe a case of gastric angiodysplasia in a 12-year-old boy with hematemesis and melena. Gastroduodenoscopy showed a typical lesion of angiodysplasia with oozing on the posterior wall of the gastric body. We successfully performed endoscopic hemoclipping therapy to heal the bleeding lesion, and no recurrence of bleeding was observed on follow-up. Gastric angiodysplasia should be included in the differential diagnosis of upper gastrointestinal bleeding in children.

Formation of downhill esophageal varices as a rare but serious complication of hemodialysis access: a case report and comprehensive literature review

Proximal or "downhill" esophageal varices are a rare complication of superior vena caval (SVC) obstruction. Few reports describe downhill varices in dialysis patients with catheter-related SVC occlusion. We studied a case of downhill esophageal varices in a dialysis patient from our center and reviewed the published literature on presentation, evaluation and treatment in other dialysis patients (MEDLINE database search). Including our current case, we identified eight reports of dialysis patients with downhill varices. All cases were recognized after presentation with gastrointestinal bleeding, in contrast to low reported bleeding rates of downhill varices in non-dialysis patients. Localized edema and superficial venous engorgement (signs of SVC occlusion) were each observed in four of eight patients. The duration of hemodialysis dependence ranged from 2.5 to 23 years, and dialysis access history included multiple central venous catheters when described (seven cases). Central venous imaging by direct, magnetic resonance or computerized tomographic venography documented SVC stenosis in all cases. Management included percutaneous transluminal angioplasty of the SVC with or without stenting in five of eight patients, three of whom developed restenosis during observation. Successful surgical venous bypass was performed in one patient after failed percutaneous venoplasty. Varices were treated with band ligation in four of eight cases without reported complications. Although rare, downhill esophageal varices should be considered in the differential diagnosis of upper gastrointestinal hemorrhage in dialysis patients exposed to central venous catheters. Diagnosis should prompt radiographic evaluation of SVC patency. Treatment requires timely and coordinated care by specialists in endovascular interventions and gastrointestinal endoscopy.

Successful management of Mallory‐Weiss syndrome in a haemophilia A patient with inhibitor by recombinant activated factor VII

The development of factor VIII (FVIII) inhibitors is the most serious clinical complication in the replacement therapy with FVIII concentrates for haemophilia A patients. Except for the case with low responding inhibitor, the main haemostatic treatment for acute bleeding is a bypassing therapy with either activated prothrombin complex concentrates (APCCs) or recombinant activated factor VII (rFVIIa). Upper gastrointestinal (GI) tract haemorrhage is not rare and is life-threatening in some cases because of massive bleeding. In such cases, effective bypassing therapy should be initiated immediately. However, there are few practical guidelines and recommendations for the bypassing therapy in such a severe bleeding from upper GI tract. Mallory-Weiss syndrome is a relatively rare bleeding condition in patients with haemophilia, characterized by bleeding from tears in the mucosa at the junction of the stomach and oesophagus, resulting from abrupt increase of intraperitoneal pressure usually caused by severe coughing or vomiting. The syndrome is often associated with a history of heavy alcohol use [1]. Hiatal hernia and ageing have been reported as predisposing factors [2]. In this report, we present a young haemophilia A patient with inhibitor in whom Mallory-Weiss syndrome occurred without any trigger, history of alcohol consumption or cirrhosis. A 21-year-old haemophilia A patient with hightitre inhibitor presented nausea and vomiting without blood in the evening of September 5, 2007. As the patient had developed inhibitor at 7 years of age, he had been treated with APCC. Afterwards, immune tolerance induction therapy was provided but without success. The patient had received regular infusion of rFVIIa (94 lg kg thrice weekly) because of frequent episodes of joint bleeding. The following morning, a tarry stool developed. As hematemesis developed in the evening, the patient was admitted to Akashi Municipal Hospital with the clinical diagnosis of upper GI haemorrhage. His body weight was 51.0 kg. Physical findings at admission were not remarkable and digestive symptoms such as vomiting and haematochezia were not significant. Haemoglobin level was 12.0 g dL on admission, suggesting blood loss from GI tract was mild. The patient had no history of alcohol consumption, liver cirrhosis, or viral hepatitis. Bolus infusion of rFVIIa was administered at the dose of 6.0 mg (118 lg kg). Famotidine, a histamine H2-receptor antagonist, was also given intravenously. Furthermore, to be on a safer side, FEIBA (3000 U) was administered twice, at midnight and on the next morning as it was still possible that rFVIIa had not been enough to restrain upper GI haemorrhage. The patient complained of no nausea or abdominal pain during this time, which indicated that the haemostatic therapy was effective. Oral ingestion was started from the noon meal on the following day. However, bloody vomit developed again in the late afternoon and a blood test revealed progressive anaemia (Hb 8.2 g dL). The history of initial vomiting of non-bloody emesis followed by recurrent episodes of hematemesis was suggestive of Mallory-Weiss syndrome. Emergency endoscopy of the upper GI tract revealed haemorrhage at gastro-oesophageal junction, which led to the diagnosis of Mallory-Weiss syndrome (Fig. 1 left). Two Correspondence: Yoshihiko Sakurai, MD, PhD, Department of Pediatrics, Nara Medical University School of Medicine, 840 Shijo-cho, Kashihara, Nara 634-8522, Japan. Tel.: +81 744 29 8881; fax: +81 744 24 9222; e-mail: ysakurai@naramed-u.ac.jp

Hemobilija

The phenomenon now known as haemobilia was first recorded in XVII century by well known anatomist from Cambridge, Francis Glisson and his description was published in Anatomia Hepatis in 1654. Until today etiology, clinical presentation and management are clearly defined. Haemobilia is a rare clinical condition that has to be considered in differential diagnosis of upper gastrointestinal bleeding. In Western countries, the leading cause of haemobilia is hepatic trauma with bleeding from an intrahepatic branch of the hepatic artery into a biliary duct (mostly iatrogenic in origin, e.g. needle biopsy of the liver or percutaneous cholangiography). Less common causes include hepatic neoplasm; rupture of a hepatic artery aneurysm, hepatic abscess, choledocholithiasis and in the Orient, additional causes include ductal parasitism by Ascaris lumbricoides and Oriental cholangiohepatitis. Clinical presentation of heamobilia includes one symptom and two signs (Quinke triad): a. upper abdominal pain, b. upper gastrointestinal bleeding and c. jaundice. The complications of haemobilia are uncommon and include pancreatitis, cholecystitis and cholangitis. Investigation of haemobilia depends on clinical presentation. For patients with upper gastrointestinal bleeding oesophagogastroduodenoscopy is the first investigation choice. The presence of blood clot at the papilla of Vater clearly indicates the bleeding from biliary tree. Other investigations include CT and angiography. The management of haemobilia is directed at stopping bleeding and relieving biliary obstruction. Today, transarterial embolization is the golden standard in the management of heamobilia and if it fails further management is surgical.

Nonvariceal upper gastrointestinal bleeding

Nonvariceal upper gastrointestinal bleeding (NUGB) remains a major medical problem even after advances in medical therapy with gastric acid suppression and cyclooxygenase (COX-2) inhibitors. Although the incidence of upper gastrointestinal bleeding presenting to the emergency room has slightly decreased, similar decreases in overall mortality and rebleeding rate have not been experienced over the last few decades. Many causes of upper gastrointestinal bleeding have been identified and will be reviewed. Endoscopic, radiographic and angiographic modalities continue to form the basis of the diagnosis of upper gastrointestinal bleeding with new research in the field of CT angiography to diagnose gastrointestinal bleeding. Endoscopic and angiographic treatment modalities will be highlighted, emphasizing a multi-modality treatment plan for upper gastrointestinal bleeding.

The vital threat of an upper gastrointestinal bleeding: Risk factor analysis of 121 consecutive patients

To analyze the importance in predicting patients risk of mortality due to upper gastrointestinal (UGI) bleeding under today's therapeutic regimen. From 1998 to 2001, 121 patients with the diagnosis of UGI bleeding were treated in our hospital. Based on the patients' data, a retrospective multivariate data analysis with initially more than 270 single factors was performed. Subsequently, the following potential risk factors underwent a logistic regression analysis: age, gender, initial hemoglobin, coumarines, liver cirrhosis, prothrombin time (PT), gastric ulcer (small curvature), duodenal ulcer (bulbus back wall), Forrest classification, vascular stump, variceal bleeding, Mallory-Weiss syndrome, RBC substitution, recurrent bleeding, conservative and surgical therapy. Seventy male (58%) and 51 female (42%) patients with a median age of 70 (range: 21-96) years were treated. Their in-hospital mortality was 14%. While 12% (11/91) of the patients died after conservative therapy, 20% (6/30) died after undergoing surgical therapy. UGI bleeding occurred due to duodenal ulcer (n = 36; 30%), gastric ulcer (n = 35; 29%), esophageal varicosis (n = 12; 10%), Mallory-Weiss syndrome (n = 8; 7%), erosive lesions of the mucosa (n = 20; 17%), cancer (n = 5; 4%), coagulopathy (n = 4; 3%), lymphoma (n = 2; 2%), benign tumor (n = 2; 2%) and unknown reason (n = 1; 1%). A logistic regression analysis of all aforementioned factors revealed that liver cirrhosis and duodenal ulcer (bulbus back wall) were associated risk factors for a fatal course after UGI bleeding. Prior to endoscopy, only liver cirrhosis was an assessable risk factor. Thereafter, liver cirrhosis, the location of a bleeding ulcer (bulbus back wall) and patients' gender (male) were of prognostic importance for the clinical outcome (mortality) of patients with a bleeding ulcer. Most prognostic parameters used in clinical routine today are not reliable enough in predicting a patient's vital threat posed by an UGI bleeding. Liver cirrhosis, on the other hand, is significantly more frequently associated with an increased risk to die after bleeding of an ulcer located at the posterior duodenal wall.

Live liver donor mortality

The review article by Middleton et al.1 published in the January 2006 issue of Liver Transplantation has an inaccuracy in the last row of Table 1. The reference quoting Beavers et al.2 included 2 donor deaths (1 from Hamburg3 and the other North Carolina4). The review by Beavers et al.2 did report our live donor liver transplantation experience of the late 1990s,5, 6 but we did not have any donor mortality in that period. Only in the year 2004, was a 50-yr-old female right liver donor was readmitted 10 weeks after surgery for fever, chills, and hematemesis. She did not have a history of peptic ulcer and was asymptomatic after the donor operation. Tachycardia, hypotension, and anemia all pointed to the diagnosis of upper gastrointestinal bleeding. She developed convulsion and cardiac arrest upon upper endoscopy. Attempts of resuscitation were futile. Postmortem revealed a duodenocaval fistula that was conducive to an air embolism during upper endoscopy, resulting in the rapid demise of the donor. She had received 2 weeks of H2 antagonist after the donor operation. This was a late donor mortality.7 All of the other live liver donors in our series are well. It is also worth noting that the review by Beavers et al.2 did not mention any donor mortality from Argentina or Korea. See Ching Chan MS*, Sheung Tat Fan MS, MD, PhD, DSc*, * Department of Surgery, University of Hong Kong, Hong Kong, China

Reappraisal of Upper Gastrointestinal Bleeding Prevalence in Acute Myocardial Infarct Patients Undergoing Urgent Coronary Angiography

Purpose: Acute myocardial infarct (MI) patients have never been targeted as patients at high risk for clinically significant gastrointestinal bleeding (CSGB). Because of the stress attributed to this condition and the related therapeutic procedures, the hemodynamic changes and the intensive use of early combined anticoagulant treatments, we believe that this population is at an increased risk for upper gastrointestinal bleeding. The objective of this study is to evaluate the prevalence of CSGB in acute MI patients undergoing urgent coronary angiography using the criteria currently used in the gastroenterological literature. Methods: Using the archives of the Centre Hospitalier Universitaire de Sherbrooke, a historic cohort of all patients diagnosed with a MI who also underwent a coronary angiography between April 1996 and April 2003 was reviewed (1174 patients). Patients with a concurrent diagnosis of upper gastrointestinal bleeding (79 patients) were then selected and screened for CSGB criteria. Patients undergoing non-urgent (>72 hours after diagnosis) and non-therapeutic intended urgent coronary angiography were excluded. All anticoagulant medication and acid-suppressing drugs were listed in the remaining. Results: Clinically significant gastrointestinal bleeding showed an increasing trend through the years with an prevalence of 4.4% in the latest 2 years. A total of 25 cases of clinically significant gastrointestinal bleeding were identified through the six years reviewed with about half the cases (11 cases) in the latest two years. Of these, 92% received a minimum of 3 anticoagulant drugs and nearly half received 4 or more agents. A glycoprotein IIbIIIa inhibitor was administered in 11 of the 25 patients and clopidogrel was used in an increasing trend since 1999. Interestingly, only a quarter of the patients received acid-suppressing agents before their bleeding. Conclusions: Patients undergoing urgent coronary angiography for an acute MI seem to be at high risk for clinically significant gastrointestinal bleeding. The use of early combined multiple anticoagulant drugs could explane the number of bleeding episodes. These results indicate a possible new indication for gastroprotective therapy. A prospective study evaluating the effect of gastroprotective measures in this population is currently undertaken.

Long-term Outcome of Helicobacter pylori–Negative Idiopathic Bleeding Ulcers: A Prospective Cohort Study

Helicobacter pylori-negative idiopathic ulcers are increasingly recognized. The secular trend and long-term outcome of this condition are unknown. We prospectively studied consecutive patients with bleeding gastroduodenal ulcers from January to December 2000. The incidence and etiology of ulcers during this period were compared with that between September 1997 and August 1998. H. pylori-negative idiopathic ulcers were defined as negative tests for H. pylori, no exposure to analgesics within 4 weeks, and absence of other risk factors for ulcers. After the ulcers had healed, patients with H. pylori-negative idiopathic ulcers and patients with H. pylori ulcers who received eradication therapy were followed up for 12 months without anti-ulcer drugs. Six hundred thirty-eight patients had bleeding ulcers: 213 (33.4%) were H. pylori ulcers, and 120 (18.8%) were H. pylori-negative idiopathic ulcers (vs 480 [50.3%] H. pylori ulcers and 40 [4.2%] H. pylori-negative idiopathic ulcers in 1997-1998; P < .001). H. pylori-negative idiopathic ulcers accounted for 16.1% of patients who were admitted for bleeding and 42.4% of patients who bled while in the hospital (P < .0001); 28.3% of patients with H. pylori-negative idiopathic ulcers had histologic evidence of past H. pylori infection. The probability of recurrent ulcer complications in 12 months was 13.4% (95% CI: 7.3%-19.5%) in patients with H. pylori-negative idiopathic ulcers and 2.5% (95% CI: 0.4%-4.6%) in patients with H. pylori ulcers who received eradication therapy (P = .0002). The incidence of H. pylori-negative idiopathic bleeding ulcers is rising. These ulcers are prone to recurrent complications.

Acute necrotizing esophagitis: a large retrospective case series.

Acute necrotizing esophagitis is a rarely described entity. Its incidence has not yet been established, and its multifactorial etiology remains unknown. The aim of the present study was to establish the incidence, clinical presentation, endoscopic course, accompanying factors, and pathogenesis of the condition. A retrospective analysis of clinical, laboratory, endoscopic and histological data and the clinical course in 29 patients with acute necrotizing esophagitis was carried out over a 5-year period. Acute necrotizing esophagitis was observed in 29 of 10 295 upper gastrointestinal endoscopies (0.28 %) carried out during the 5-year period. The average age of the patients was 75.24 years (range 40 - 91), and they were predominantly male. Eighty-three percent of the patients had comorbid conditions. In all cases, acute necrotizing esophagitis became evident with upper gastrointestinal bleeding, without hemodynamic stabilization in the majority of cases (75.9 %). The lesions predominantly affected the lower two-thirds of the esophagus (59 %), and there were coexisting abnormal endoscopic findings in 83 % of cases. Empirical supportive therapy, including oral nutritional rest, omeprazole, sucralfate (15 cases) and broad-spectrum antibiotics (7 cases) was provided. The condition resolved in all patients. Ten patients in the group died of other causes (coexisting illnesses). Acute necrotizing esophagitis was more commonly recognized than has previously been reported. It is a serious clinical entity that should be considered in the differential diagnosis of upper gastrointestinal bleeding, particularly in elderly patients. The prognosis depends more on the patient's advanced age and on comorbid illnesses than on the course of the esophageal lesions, which resolved in all patients in this series.

Risk factors for upper gastrointestinal bleeding among end-stage renal disease patients

The risk of upper gastrointestinal bleeding (UGIB) is increased among end-stage renal disease (ESRD) patients compared to the general population. However, correlates of UGIB among ESRD patients remain unknown. We conducted a cohort study of dialysis patients to ascertain risk factors for UGIB. Data from the United States Renal Data System Dialysis Morbidity and Mortality Studies, Waves 2-4 were used to identify risk factors for incident UGIB among ESRD patients. First hospitalizations for UGIB were identified using hospital diagnosis codes between 12/31/93 and 12/31/99. Cox regression was used to estimate the association between predictors of interest and first diagnosis of UGIB. Cases of UGIB (698) were observed over 30648 patient years of follow-up. Before adjustment for confounding factors, increasing age, diabetes, former and current smoking, cardiovascular disease (CVD), lower serum albumin, malnutrition, and inability to ambulate independently were associated with an increased risk of UGIB, while African Americans and transplant patients had a lower risk of UGIB. After adjustment, African American race was associated with a lower risk of UGIB (RR = 0.90; 0.82, 0.98), while current smoking (RR = 1.11; confidence interval 1.03, 1.19), history of CVD (RR = 1.32; 1.10, 1.59), and inability to ambulate independently (RR = 1.32; 1.07, 1.63) were associated with a higher risk of UGIB. Age, gender, diabetes, lower serum albumin, nourishment, treatment modality, aspirin use, nonsteroidal anti-inflammatory drug (NSAID) use, and antiplatelet or anticoagulant medication use were not found to be significantly related to the risk of UGIB after adjustment for potential confounding factors. CVD, current smoking, and risk factors suggesting more disability are associated with a greater risk of UGIB among patients with ESRD.

Upper Gastrointestinal Bleeding in the Medical Intensive Care Unit (MICU) Doha, Qatar: A one-year survey

Upper gastrointestinal bleeding is a common problem and is an important cause of morbidity and mortality. Between June 1999 to May 2000 eight hundred and sixty patients were admitted to the Medical Intensive Care Unit, Hamad Medical Corporation, 102 of whom (11.8%) were admitted with a diagnosis of upper gastrointestinal bleeding. The most common nationality was Qatari (42.2%) and the most common age group was between 50-60years old (28.4%). The most frequent cause of bleeding was peptic ulcer disease (50 patients) followed by variceal bleeding. Our results are compatible with other reports.

Hemorragia masiva por hiperplasia nodular de glándulas de Brunner en el síndrome antifosfolipídico

Gastrointestinal hemorrhage is an exceptional complication of antiphospholipid syndrome and most reported cases are secondary to ischemic lesions. Brunner's gland hyperplasia is an infrequent and usually asymptomatic condition that has been associated with chronic renal failure. We report a patient with primary antiphospholipid syndrome who, after mechanic heart valve replacement and while in a state of drug-induced anticoagulation, experienced a life-threatening upper gastrointestinal hemorrhage due to nodular hyperplasia of Brunner's glands. This entity may be considered in the differential diagnosis of upper gastrointestinal bleeding in patients with antiphospholipid syndrome, most of whom are treated with oral anticoagulatory drugs, and particularly in patients with chronic renal failure.