Gastrointestinal Bleeding E-Book

• Herausgeber: John Wiley & Sons
• Kategorie: Fachliteratur
• Sprache: Englisch

Seitenzahl: 572

Veröffentlichungsjahr: 2012

Beschreibung

There have been many advances in the management of this condition since the first edition of Gastrointestinal Bleeding. This new edition, thoroughly revised and restructured, includes the latest updates on all areas of the field of GI Bleeding, systematically covering all the areas of the GI tract, from upper GI to lower GI, through to small bowel bleeding. It fully covers the different types of bleeding that can occur, from peptic ulcer through to variceal bleeding and looks at new developments and pioneering techniques in the field, including endoscopy and balloon-enteroscopy. A methodology section describes the latest design of clinical trials in GI bleeding and this edition now highlights the new guidelines on UGIB (Upper gastrointestinal bleeding). This new edition of Gastrointestinal Bleeding is an invaluable purchase for all gastroenterologists, both in training and fully qualified.

Leseprobe

Contents

Cover

Title Page

Copyright

List of Contributors

Part I: General Approach to Upper and Lower GI Bleeding

Chapter 1: Gastrointestinal Bleeding: Presentation, Differential Diagnosis and Epidemiology

Causes of Upper Gastrointestinal Bleeding

Peptic Ulcer and Gastro-Duodenal Erosions

Gastroesophageal Varices

Mallory-Weiss Syndrome

Angiodysplasia

Gastric Antral Vascular Ectasia

Dieulafoy's Lesion

Lower Gastrointestinal Bleeding

References

Chapter 2: Gastrointestinal Bleeding: Resuscitation, ICU Care and Risk Stratification

Initial Management

Fluid or Blood Replacement

Emptying Gastric Content

Correct Bleeding Diathesis

Pharmacological Treatment Before Endoscopy

Risk Stratification

Lower Gastrointestinal Bleeding

References

Chapter 3: Gastrointestinal Bleeding: Antiplatelets and Anticoagulants

Antiplatelet Agents

Aspirin

Risk factors for upper GI bleeding in aspirin users

Clopidogrel

Double Antiplatelet Agent Therapy

Discontinuation of Aspirin During Acute Peptic Ulcer Bleeding

Interaction Between Antiplatelet Agent and Proton Pump Inhibitors

Anticoagulants

References

Part II: Peptic Ulcer Bleeding

Chapter 4: Peptic Ulcer Bleeding: Endoscopic Diagnosis, Endoscopic Therapy and Pharmacotherapy

Introduction

Endoscopy Timing and Preparation

Endoscopy

Pharmacotherapy

Conclusions

References

Chapter 5: Peptic Ulcer Bleeding: Surgery and Radiology

Introduction

Indications for Transcatheter Arterial Embolization and Surgical Treatment

Transcatheter Arterial Embolization

Surgery

TAE Versus Surgery

Conclusions

References

Part III: Variceal Bleeding

Chapter 6: Variceal Bleeding: Endoscopic Diagnosis, Endoscopic Therapy and Pharmacotherapy

Introduction

Prediction of Cirrhotic Patients at Risk of Variceal Bleeding

Primary Prophylaxis of Esophageal Variceal Bleeding (Primary Prevention)

Treatment of an Active Bleed

Prevention of Recurrent Variceal Bleeding (Secondary Prevention)

Summary

Conclusions

References

Chapter 7: Variceal Bleeding: Surgery and Radiology

Introduction

TIPS

Surgical Shunt

Primary Prophylaxis of First Esophageal Variceal Bleed

Rescue Therapies for Acute Variceal Bleeding

Prevention of Recurrent Variceal Bleeding (Secondary Prophylaxis)

Complications of TIPS

Complications Related to Portasystemic Shunting

Orthotopic Liver Transplantation

Summary

Conclusion

References

Part IV: Other Causes of Upper GI Bleeding

Chapter 8: Other Causes of Upper Gastrointestinal Bleeding

Erosive Causes of Upper Gastrointestinal Bleeding

Drug Induced Erosion

Mechanical Erosions

Inflammatory Erosions

Angiodysplasia

Dieulafoy Lesion

Vasoenteric Fistula

Portal Hypertensive Gastropathy

Gastric Antral Vascular Ectasia

Hereditary Vascular Anomalies

Vasculitides and Systemic Disorders

Ischemia of the Digestive Tract

Neoplastic Lesions

Polyps

Adeno- and Squamous Cell Carcinoma

Lymphoma

Mesenchymal Tumors

Kaposi's Sarcoma

Primary Malignant Melanoma

Neuroendocrine Tumor

Metastatic Tumor

Traumatic or Iatrogenic Bleeding

Miscellaneous Causes of Bleeding

Conclusion

References

Part V: Lower GI Bleeding

Chapter 9: Lower GI Bleeding: Endoscopic, Radiological and Surgical Diagnosis and Management

Introduction

Clinical Evaluation

Acute Severe Hemorrhage

Acute Self-Limiting/Intermittent Hemorrhage

Chronic/Intermittent Bleeding

Specific Conditions

References

Part VI: Small Bowel Bleeding

Chapter 10: Small Bowel Bleeding

Epidemiology and Terminology

Etiology

Diagnosis

Guidelines, Algorithms and Integrative Approach to Small Bowel Bleeding

References

Part VII: GI Bleeding of Unknown Origin

Chapter 11: Gastrointestinal Bleeding of Unknown Origing

Introduction

Definitions

Etiology

Patient's Evaluation and Assessment

Investigations

Comparative Studies

Diagnostic Approach to Patients with OGIB

Conclusions

References

Part VIII: Methodology and Guidelines

Chapter 12: Design of Clinical Trials in Gastrointestinal Bleeding

Introduction

Example of An Observational Study: The UK Comparative Audit of Upper Gastrointestinal Bleeding and the Use of Blood (9)

Example of a Randomized Controlled Trial (RCT): Intravenous Esomeprazole for Prevention of Recurrent Peptic Ulcer Bleeding (10)

Conclusion

References

Chapter 13: Guidelines and Consensus on Gastrointestinal Bleeding

Introduction

Defining a Need for the Creation or Updating of Guidelines

The Multidimensional Process of Guideline Development

Quantifying the Strength of the Recommendations and Corresponding Evidence

Operational Aspects of the CPG Development Process

Conclusion

References

Index

This edition first published 2012, © 2012 by Blackwell Publishing Ltd

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Library of Congress Cataloging-in-Publication Data

Gastrointestinal bleeding / edited by Joseph J.Y. Sung, Ernst J. Kuipers, Alan N. Barkun. – 2nd ed.

p.; cm.

Includes bibliographical references and index.

ISBN 978-1-4051-9555-3 (hardback)

I. Sung, Joseph J. Y. (Joseph Jao Yiu), 1959- II. Kuipers, Ernst J. III. Barkun, Alan.

[DNLM: 1. Gastrointestinal Hemorrhage–diagnosis. 2. Gastrointestinal Hemorrhage–therapy. WI 143]

LC classification not assigned

616.3′3–dc23

2011031413

List of Contributors

Disaya Chavalitdhamrong CURE Digestive Diseases Research Center David Geffen School of Medicine at UCLA and Divisions of Digestive Diseases UCLA Medical Center and West Los Angeles VA Medical Center Los Angeles, CA, USA

I. Lisanne Holster Department of Gastroenterology and Hepatology Erasmus MC University Medical Center Rotterdam, The Netherlands

Caroline M. den Hoed Department of Gastroenterology and Hepatology Erasmus MC University Medical Center Rotterdam, The Netherlands

Ana Ignjatovic Wolfson Unit for Endoscopy St Mark's Hospital, Imperial College London London, UK

Vipul Jairath NHS Blood and Transplant and Translational Gastroenterology Unit John Radcliffe Hospital Oxford, UK

John T. Jenkins Department of Colorectal Surgery St Mark's Hospital, Imperial College London, London, United Kingdom

Dennis M. Jensen CURE Digestive Diseases Research Center David Geffen School of Medicine at UCLA and Divisions of Digestive Diseases UCLA Medical Center and West Los Angeles VA Medical Center Los Angeles, CA, USA

Thomas O.G. Kovacs CURE Digestive Diseases Research Center David Geffen School of Medicine at UCLA and Divisions of Digestive Diseases UCLA Medical Center and West Los Angeles VA Medical Center Los Angeles, CA, USA

Larry H. Lai Institute of Digestive Disease The Chinese University of Hong Kong Hong Kong, China

Johan F. Lange Department of Surgery Erasmus MC University Medical Centre Rotterdam, the Netherlands

James Y.W. Lau Institute of Digestive Disease The Chinese University of Hong Kong Hong Kong, China

Irene M. Mulder Department of Surgery Erasmus MC University Medical Centre Rotterdam, the Netherlands

Brian P. Saunders Department of Colorectal Surgery St Mark's Hospital, Imperial College London, London, United Kingdom

Ernest G. Seidman McGill Center for IBD Research Montreal General Hospital Montreal, Canada

Daniela E. Serban Pediatric Clinic II Emergency Hospital for Children University of Medicine and Pharmacy “Iuliu Haieganu” Cluj-Napoca, Romania

Part I

General Approach to Upper and Lower GI Bleeding

Chapter 1

Gastrointestinal Bleeding: Presentation, Differential Diagnosis and Epidemiology

Joseph Sung

Institute of Digestive Disease, The Chinese University of Hong Kong, Hong Kong, China

Upper gastrointestinal bleeding (UGIB) represents a substantial clinical and economic burden, with reported incidence ranging from 48–160 cases per 100,000 adults per year (1–3). UGIB commonly presents with hematemesis and/or melena. In cases of severe UGIB, hematochezia (bright red or maroon colored blood per rectum) can be found. Depending on the speed of blood loss, hemodynamic status may be affected in different ways. In patients with severe blood loss in a short period of time, resting tachycardia (pulse > 100 beats per minute), hypotension (systolic blood pressure <100 mmHg) and postural drop in blood pressure (drop in systolic blood pressure of >20mmHg on standing) are evident, leading to dizziness and loss of consciousness in some cases. In patients with mild to modest blood loss over a longer duration of presentation, anemia, malaise and postural changes in pulse and blood pressure are common.

The incidence and prevalence of uncomplicated peptic ulcer have declined in recent years, largely due to the availability of treatments to eradicate Helicobacter pylori (H. pylori), and to the decreasing prevalence of H. pylori infection (4, 5). However, the use of acetylsalicylic acid (ASA) and other non-steroidal anti-inflammatory drugs (NSAIDs) that are associated with adverse gastrointestinal events is becoming more widespread. The mass vaccination against viral hepatitis B in newborns has also led to a decrease in cirrhosis and portal hypertension in high prevalence countries in Asia. As a result, the incidence of variceal hemorrhage due to viral hepatitis has declined, although alcoholic cirrhosis remains an important medical emergency.

Causes of Upper Gastrointestinal Bleeding

The most common causes of upper GI bleeding are depicted in large scale surveys (Table 1.1) (6, 7). Peptic ulcer disease usually constitutes slightly over 50% and esophagogastric varices 15–20% (Fig. 1.1). The other important conditions leading to UGIB include Mallory-Weiss tear, angiodysplasias and vascular ectasias, Dieulafoy's lesion, tumors of the upper gastrointestinal tract. In as many as 20% of patients, the diagnosis cannot be ascertained. On the other hand, in around 10% of patients, more than one source of bleeding may be identified.

Table 1.1 Incidence of upper gastrointestinal hemorrhage associated with peptic ulcer disease.

Fig. 1.1 Common causes of upper gastrointestinal bleeding (Modified from Silverstein et al. (3) with permission from Elsevier.)

Peptic Ulcer and Gastro-Duodenal Erosions

Both peptic ulcers and erosions are defined as a breach of the gastroduodenal mucosa as a result of peptic injuries. Differentiation of ulcers from erosions on endoscopic appearance is often based on the size (at least 5mm) and the presence of appreciable depth in ulcers. Both lesions are mainly caused by Helicobacter pylori infection and the use of non-steroidal anti-inflammatory drugs. With the wide use of aspirin and other anti-platelet agents as prophylaxis against coronary heart disease, cerebrovascular accident and prevention of cancer, the incidence of peptic ulcers related to these drugs are expected to rise. Stress related ulcers develop in patients who are hospitalized for major illness and life-threatening non-bleeding medical conditions. The risk of stress ulcer bleeding is probably higher in those who have respiratory failure and those with a bleeding diathesis. It has also been known that these patients have a higher mortality than those admitted to hospital with primary UGIB. The incidence varies widely in different countries and cohort studies. In recent years, however, evidence suggests that there is an increasing trend of peptic ulcer not related to H. pylori infection or NSAID, so-called non-HP non-NSAID ulcers (8). These patients are older and their risk of recurrent bleeding is higher and associated with higher mortality. The etiology behind this non-HP non-NASID ulcers remains unclear.

Bleeding from gastroduodenal ulcers stop in 90% of cases by the time patients arrive to hospital. However, recurrent bleeding occurs in 30–50% of cases if appropriate treatment is not given.

Incidence of Peptic Ulcer Bleeding

A systematic review of upper gastrointestinal bleeding in 11 studies in Europe, reported on the incidence of complications associated with peptic ulcer extrapolated to the general population (Table 1.1) (9). Reported annual incidences of hemorrhage in the general population ranged from 0.019% (10) to 0.057% (11). A UK database study reported an annual incidence of 0.079% (12). However, this study was confined to individuals older than 60 years, and could therefore not be extrapolated to the population as a whole. Two national audits from the UK extended the analysis to include all causes of upper gastrointestinal hemorrhage and found a higher incidence. Blatchford and colleagues reported an annual incidence of 0.172% (95% CI: 0.165–0.180) in Scotland in 1992/1993 (13). Similarly, an audit performed during a four-month period in hospitals in the UK found an annual incidence of 0.103% (14). In this study, the annual incidence increased from 0.023% in individuals aged under 23 years to 0.485% in individuals aged over 75 years.

The few studies that have examined time trends in peptic ulcer hemorrhage reported no significant change in incidence over time. Bardhan and colleagues observed only a slight decrease in the annual incidence of hemorrhage in the UK, from 0.021% during 1990–1994 to 0.019% during 1995–2000 (10). Van Leerdam and colleagues similarly reported a statistically non-significant decrease in the incidence of both gastric and duodenal ulcer hemorrhage from 1993/4 to 2000 (2). However, Lassen and colleagues reported a slight increase in the annual incidence of hemorrhage in Denmark, from 0.055% in 1993 (95% CI: 0.049–0.062) to 0.057% in 2002 (5). Taha and colleagues studied the incidence of all upper gastrointestinal hemorrhage in individuals taking ASA 75 mg/day in Scotland (15). The annual incidence increased from 0.015% in 1996 to 0.018% in 1999 and 0.027% in 2002.

Mortality of Peptic Ulcer Disease

Mortality after peptic ulcer hemorrhage ranges from 1.7% to 10.8%, depending on the reported series and the average mortality is 8.8%. Increasing age, comorbid illness, hemodynamic shock on presentation, recurrent bleeding and need for surgery are important predictors of mortality in peptic ulcers bleeding after therapeutic endoscopy (16). Furthermore, delay in treatment for over 24 hours may be an important management issue. Recently, two studies from the US indicated that patients admitted after hours exhibited a higher mortality; although observational studies, the authors suggested this association may be related to lower rates of early intervention (17, 18).

However, not all cases of mortality are related to uncontrolled hemorrhage. In a single-center audit from Hong Kong which included 10,428 cases of confirmed peptic ulcer bleeding, only 25% of patients died from bleeding-related cause (e.g. uncontrolled bleeding, died on surgery, post-surgical complication endoscopy related complications, and death within 48 hours after endoscopy) (19). Comorbid illnesses such as cardiac, pulmonary, or cerebrovascular diseases, multi-organ failure or sepsis, and terminal malignancy constituted the majority of causes of death in this series. Therefore, the management of patients with peptic ulcer bleeding should not be focusing only on the control of hemorrhage. It is important to provide supportive care and management of patients' cardiopulmonary conditions. Drugs such as antiplatelet agents and anticoagulants which might be related to the development of peptic ulcer bleeding are often discontinued during UGIB. The early resumption of these drugs should be considered, balancing the risks and benefits of these treatments (20).

Sonnenberg studied mortality data from non-European countries including Argentina, Australia, Chile, Hong Kong, Japan, Mexico, Singapore and Taiwan (21) (Fig. 1.2). The age-standardized death rates in individual countries were tracked from 1971 to 2004. In all countries, there was a decline in gastric and duodenal ulcer mortality. The risk of dying from gastric and duodenal ulcer increased in consecutive generations born between the mid- and end of the nineteenth century and decreased in all subsequent generations. The peak mortality of gastric and duodenal ulcers occurred at the turn of the last century (Fig. 1.1). This decline in mortality which preceded the advent of endoscopic and pharmacological treatment is attributed to the decline in H. pylori infection. The bell shaped peak of ulcer occurrence among consecutive generations born between 1850 and 1950 is related to the interaction between a declining H. pylori infection and an advancing age of patients from these countries. In Europe, The data from the past 50–80 years show striking similarity (22) (Fig. 1.3). The risk of dying from gastric and duodenal ulcers increased among consecutive generations born during the second half of the nineteenth century until shortly before the turn of the twentieth century and then decreased in all subsequent generations. The time trends of gastric ulcer incidence preceded those of duodenal ulcer by 10–30 years. The increase in consumption of NSAID and introduction of potent anti-secretory medications have not affected the long-term downward trends of ulcer mortality. The birth-cohort pattern is the most predominant factor influencing the temporal change of peptic ulcer mortality, probably related to H. pylori carriage rate.

Fig. 1.2 Time trends of standardized cohort mortality ratio (SCMR) of gastric ulcer (GU) and duodenal ulcer (DU) from Japan, Australia, US and UK (Reproduced from Sonnenberg (21) with permission from Wiley-Blackwell.)

Fig. 1.3 Time trends of standardized cohort mortality ratio (SCMR) of gastric ulcer (GU) and duodenal ulcer (DU) from European countries (Reproduced from Sonnenberg (21) with permission from Wiley-Blackwell.)

Gastroesophageal Varices

Gastroesophageal varices are often, but not always, the result of portal hypertension. Bleeding from gastroesophageal varices is now widely accepted as a phenomenon of “explosion” instead of “erosion.” Varices develop usually when portal pressure builds up to above 20 mmHg and with a hepatic venous pressure gradient exceeding 12 mmHg, it is associated with a greater risk of continued or recurrent bleeding (23). Thus the risk of hemorrhage is related to the size of the varices, wall thickness and intra-variceal pressure. Several groups have confirmed that variceal size is the most important prognostic factor for variceal bleeding (24, 25). Red color signs, which include cherry-red spots and red wale markings, are also associated with more advanced grades of varices and a higher risk of hemorrhage. These signs are thought to represent focal weakness or “blowouts” in the variceal wall. Fibrin clots or “white nipple signs” are occasionally seen over the variceal columns which have recently bled. Beside the gross appearance of varices, patients with decompensated cirrhosis definitely fare worse than those with compensated liver function. Portal vein thrombosis is another poor prognostic indicator. The risk of bleeding from varices is related to the Child-Pugh score, not just because of more severe portal hypertension, but also because of other factors such as nutritional deficiency, coagulopathy and increased fibrinolysis in advanced liver disease. Recently, an association between bacterial infection and failure to control bleeding has been observed and a causal relationship implicated (26). Prophylactic antibiotic administration to cirrhotics with variceal bleeding results in reduced morbidity and mortality when infection is brought under control (27). A diurnal periodicity of variceal bleeding has also been observed. Bleeding episodes occur more frequently in the early morning and late evening, probably as a result of hyperdynamic blood flow in the portal system after meals.

Varices in direct continuity with the esophagus along the lesser and greater curves of the stomach are called gastroesophageal varices (GOV) types 1 and 2 respectively. Isolated gastric varices in the fundus (IGV1) occur less frequently than GOVs (10% vs 90%) but cause bleeding more often than either GOVs or isolated gastric varices at other loci in the stomach (IGV2).

Several prognostic indices have been developed to predict which patients with esophageal varices are likely to bleeding (28). Some of these are based on clinical parameters, others combined with endoscopic features, and the rest use a combination of endoscopic features, biochemical parameters and echo-Doppler ultrasound findings. The most widely used index is still the North Italian Endoscopic Club Index (NIEC Index) (24). This index is based on (1) severity of liver disease (Child-Pugh class), (2) size of varices and (3) presence of red markings on the varices. Based on this scoring system, cirrhotic patients are classified into one of six possible risk classes, each with a prediction rate of bleeding. The NIEC index has been prospectively validated in independent series. Yet, with the best prognostic index, one only predicts less than 40% of subsequent variceal bleeding. Obviously, many factors predisposing to variceal bleeding remain unknown.

Most variceal bleeding temporarily stops by the time patient arrives hospital. Without proper treatment, however, recurrent bleeding occurs in 30–40% within the next two to three days and up to 60% within one week (29). The risk of recurrent bleeding is presumably related to changes in hemodynamics of the portal system including an increase in portocollateral resistance after hypotension, increased splanchnic blood flow stimulated by blood in the gut, and an increase in portal venous pressure as a result of overzealous volume expansion during resuscitation. After the index bleeding, mortality is highest in the first five days and returns to baseline levels by three to four months (29). This is the critical time window for optimal treatment to improve survival of variceal bleeders. Complications related to bleeding and the treatment of bleeding substantially contribute to the mortality such as sepsis, hepatic encephalopathy, renal failure, and aspiration.

Mallory-Weiss Syndrome

Mallory-Weiss Syndrome is a longitudinal mucosal laceration in the distal esophagus and proximal stomach. Although initially considered a rare cause of upper GI bleeding, the condition is being diagnosed more frequently and now accounts for 3–14% of patients presenting with UGIB (30). The prognosis of the condition is generally good, with only 5% of patients presenting with hemodynamic instability, and a small proportion with hematochezia. Mallory-Weiss syndrome can co-exist with other bleeding lesions, such as ulcers or varices, which could have caused the bleeding when esophageal mucosa is further damaged in vomiting. A transient increase in the pressure gradient between the intrathoracic and intragastric portion of the gastroesophageal junction, often caused by retching, is thought to create the tear. In up to 50% of patients with Mallory-Weiss syndrome, a hiatal hernia is present. However whether the presence of a hiatal hernia is etiologic to the tear or not is not clear. Retrograde intussusception of the stomach into the esophagus has been suggested as a mechanism for the pathogenesis of a Mallory-Weiss tear. The classic history of a Mallory-Weiss Syndrome is antecedent retching or emesis, initially presenting with clear vomitus, followed subsequently by hematemesis. Although antecedent retching was previously thought to be a prerequisite for the syndrome, it is actually reported in only 30–50% of patients. A significant proportion of these patients report alcohol binging. The Mallory-Weiss Syndrome may also associated with a variety of other antecedent events that give rise to an increase in intra-abdominal pressure, such as blunt abdominal trauma, hiccupping, retching during endoscopy, coughing, parturition, epileptic convulsions, straining, and even bowel preparation for colonoscopy. Predisposing conditions to the development of a Mallory-Weiss Syndrome include a hiatal hernia and, perhaps, advanced age (30).

Angiodysplasia

Angiodysplasiae are etctatic, dilated, thin-walled vessels in the gastrointestinal tract. They occur mostly in the stomach and less frequently in the small bowel and colon. They account for 5–7% of patients presenting with gastrointestinal bleeding. Often found in patients with advanced age, angiodysplasias are associated with chronic renal failure, hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu Syndrome), chronic mucosal ischemia, and prior radiation therapy. The previous belief that angiodysplasia was related to aortic valve disease has been a subject of hot debate (31, 32). The diagnosis can be made by visualizing small, punctate, bright red, vascular mucosal lesions during endoscopy.

Platelet dysfunction associated with chronic renal failure has been postulated as a cause for recurrent bleeding. Endoscopic treatment using thermal coagulation can be successful but the multiplicity and involvement of sites not easily accessible, often in the small bowel, make its management difficult. Estrogen-progesterone treatment has been used to prevent recurrent bleeding from angiodysplasia but efficacy not proven by clinical studies.

Gastric Antral Vascular Ectasia

Gastric antral vascular ectasia (GAVE), also known as “watermelon stomach,” is an uncommon acquired vascular malformation distinct from portal hypertensive gastropathy (33). The diagnosis is made by a distinctive endoscopic appearance, characterized by longitudinal, vascular antral gastric folds converging like stripes of a watermelon onto the pylorus. Most patients present with chronic occult blood loss and transfusion-dependent anemia. Approximately 30% of patients with GAVE syndrome have cirrhosis but portal hypertension is not an absolute necessity for the development of this condition. Antral predilection for GAVE and the diffuse nature of portal hypertensive gastropathy distinguish the two entities. There is some evidence to suggest that GAVE may actually be associated with autoimmune diseases. As the lesion is superficial, often involving a large surface in the stomach, cautery with argon plasma coagulation often represents a particularly well adapted therapeutic option. The treatment might need to be repeated for several sessions before eradication can be achieved.

Dieulafoy's Lesion

A Dieulafoy's lesion, also known as cirsoid aneurysm or submucosal arterial malformation, is a rare cause of upper GI bleeding. The lesion was named “exulceratio simplex” by the French surgeon Georges Dieulafoy in 1896. The condition can cause significant bleeding and is often difficult to diagnose. The true incidence is unknown, but in one series, it accounted for 1–5.8% of cases presenting with GI bleeding. A Dieulafoy's lesion consists of an abnormally large submucosal artery, a “caliber-persistent artery,” protruding through a minute 2–5 mm mucosal defect. The diameter of the abnormal and often tortuous artery ranges from 1 to 3 mm, almost 10 times the diameter of normal arteries in the submucosa. Dieulafoy's lesions can be found along the entire GI tract, most commonly in the stomach (74%), duodenum (14%), colon (5%), gastric anastomosis (5%), small bowel (1%), and esophagus (1%). The proximal stomach is by far the most common site, classically described in the proximal lesser curvature within 6 cm of the gastroesophageal junction (34). For reasons which are still unclear, Dieulafoy's lesion is more commonly found in the older individuals.

Lower Gastrointestinal Bleeding

Lower GI bleeding arises from a source distal to the ligament of Treitz. It accounts for 10–20% of acute GI bleeding. It is usually suspected when patients complain of hematochezia or passing blood clot instead of melena. Common causes of colonic bleeding include diverticular hemorrhage, angiodysplasia, radiation colo-proctitis, colonic polyps, carcinoma, and inflammatory bowel diseases (35) (Fig. 4). One emerging cause of lower GI bleeding relates to the increasing use of aspirin and NSAID in the elderly population. It is estimated that one-third of aspirin/non-aspirin NSAID induced ulcers or erosions occur beyond the level of the duodenum (36). The other important cause of lower GI bleeding would be related to bowel ischemia. This is usually found in the elderly patients as a result of heart failure, hypotension and cardiac arrhythmia. In a review of several large studies that include almost 1,600 patients with acute lower GI bleeding, the three most common causes of lower GI bleeding were diverticulosis, bowel ischemia, and anorectal conditions such as hemorrhoid, anal fissures and rectal ulcers (37).

Fig. 1. 4 Common causes of lower gastrointestinal bleeding (Modified from Zuckerman and Prakash (35) with permission from Elsevier.)

Studies on lower gastrointestinal bleeding are much fewer than that of upper gastrointestinal bleeding. The severity of lower GIB is variable but past publications suggested the overall mortality to be low. A large-scale population-based study in Spain indicated that, while the incidence of upper gastrointestinal complication is declining, a rising trend of lower GI complications increased from 20/100,000 to 33/100,000 (38) (Fig. 1.5). This trend is attributed to the advancing age of patients, the higher number of comorbidities of the population and a decreased therapeutic effectiveness beyond the duodenum. With the development of balloon-assisted enteroscopy and wireless capsule endoscopy, there will be more cases of lower gastrointestinal bleeding confirmed with an identifiable cause.

Fig. 1.5 Time trend of upper and lower gastrointestinal bleeding and the associated mortality by year and by age groups (Modified from Lanas et al. (38) with permission from Wiley-Blackwell.)

Hospitalization due to the lower gastrointestinal bleeding was found mostly in patients older than 60 years of age. Mortality is relatively uncommon. Unlike the case of upper gastrointestinal bleeding which is found more commonly in males, in lower gastrointestinal bleeding, there is no gender difference between males and females. It will be a challenge to improve patient care in the future unless we develop new strategies to reduce the number of lower GI bleeding as well as reducing their associated mortality.

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Chapter 2

Gastrointestinal Bleeding: Resuscitation, ICU Care and Risk Stratification

Joseph Sung

Institute of Digestive Disease, The Chinese University of Hong Kong, Hong Kong, China

Initial Management

The goals of managing a patient with acute GI bleeding are first to resuscitate; second, to control active bleeding; and third, to prevent recurrence of hemorrhage. The importance of resuscitation in the initial management of gastrointestinal bleeding cannot be over-emphasized.

Significant GI bleeding is indicated by syncope, continuous hematemesis and tachycardia, significant drop in systolic blood pressure, postural hypotension and requirement of blood or intravenous fluid to maintain blood pressure. Patients over age 60 and with multiple underlying diseases are at higher risk of negative outcomes. Those admitted for other medical problems (e.g. heart or respiratory failure, or cerebrovascular bleed) and who develop gastrointestinal bleeding during hospitalization also exhibit a higher risk of dying from the condition.