Clinical Gastroenterology 3e by Nicholas J Talley


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The third edition of Clinical Gastroenterology focuses on both common and uncommon problems as they present in clinical practice. Australian and international contributors have provided specialist content with a practical and problem-based approach to the subject. There is good use of decision trees to assist in patient assessment and treatment, clear illustrations suitable for patient education, and extensive use of summary tables to highlight key points to guide general practitioners, specialist trainees and medical students.

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Clinical Gastroenterology 3e by Nicholas J Talley

  1. 1. 3eClinicalGastroenterologyA practical problem based approachNicholas Talley
  2. 2. Clinical gastroenterologyA practical problem-based approach
  3. 3. Clinical gastroenterology A practical problem-based approach Editor Nicholas J Talley Pro Vice-Chanceller and Professor, Faculty of Health, University of Newcastle, NSW, Australia Adjunct Professor of Medicine, Mayo Clinic, USA Adjunct Professor, University of North Carolina, USA Adjunct Professor of Gastroenterology, Karolinska Institute, Stockholm, SwedenSydney Edinburgh London New York Philadelphia St Louis Toronto
  4. 4. Churchill Livingstone is an imprint of Elsevier Elsevier Australia. ACN 001 002 357 (a division of Reed International Books Australia Pty Ltd) Tower 1, 475 Victoria Avenue, Chatswood, NSW 2067This edition © 2011 Elsevier AustraliaThis publication is copyright. Except as expressly provided in the Copyright Act 1968and the Copyright Amendment (Digital Agenda) Act 2000, no part of this publicationmay be reproduced, stored in any retrieval system or transmitted by any means (includingelectronic, mechanical, microcopying, photocopying, recording or otherwise) without priorwritten permission from the publisher.Every attempt has been made to trace and acknowledge copyright, but in some cases thismay not have been possible. The publisher apologises for any accidental infringementand would welcome any information to redress the situation.This publication has been carefully reviewed and checked to ensure that the content is asaccurate and current as possible at time of publication. We would recommend, however, thatthe reader verify any procedures, treatments, drug dosages or legal content described in thisbook. Neither the author, the contributors, nor the publisher assume any liability for injuryand/or damage to persons or property arising from any error in or omission from this publication.National Library of Australia Cataloguing-in-Publication Data_________________________________________________________________________________________Author: Talley, Nicholas Joseph.Title: Clinical gastroenterology : a practical problem-based approach / Nicholas Talley.Edition: 3rd ed.ISBN: 9780729539487 (pbk.)Notes: Includes bibliographies and index.Subjects: Gastrointestinal system--Diseases. Gastroenterology. Digestive organs--Diseases. Gastrointestinal system--Diseases--Diagnosis.Dewey Number: 616.33_________________________________________________________________________________________Publisher: Sophie KalinieckiDevelopmental Editor: Neli BryantPublishing Services Manager: Helena KlijnProject Coordinator: Geraldine MintoEdited by Joy WindowProofread by Sarah Newton-JohnCover and internal design by Trina McDonaldIndex by Annette MuskerIllustrations for 3rd edition by TNQ Books and Journals Pvt. Ltd.; other illustrations by Alan LaverTypeset by TNQ Books and Journals Pvt. Ltd.Printed by China Translation & Printing Services Ltd.
  5. 5. DedicationThis edition of Clinical Gastroenterology is dedi-cated to the late Christopher J Martin, Founda-tion Professor of Surgery, University of Sydneyat Nepean Hospital, 1993–2006. Chris was aworld-class oesophagologist and gastrointestinalsurgeon; the Whiteley–Martin Research Unit atNepean Hospital, which studies upper gastroin-testinal cancer, was named after him. v
  6. 6. ForewordIt is a great honour and privilege to write the great deal of care and foresight to develop anForeword for the third edition of Clinical gastro- educational forum using this approach. Again,enterology: a practical problem-based approach, Professor Talley and his colleagues have doneedited by Professor Nicholas J Talley. This book a remarkable job of incorporating the problem-has proven to be a wonderful addition to our based learning approach into all of theireducational repertoire in gastroenterology. A chapters. His team of largely Australian doctorsmyriad of books and educational electronic tools and colleagues with whom he has interacted in(e.g. Up-to-Date) exist to help the practitioner with the Mayo Clinic system in the United States ofdisease-oriented questions. However, very few America have done a really stellar job in adheringeducational media bring us back to the patient. to the goals and objectives of this learningIn this wonderful book, Professor Talley and approach. Obviously the success of this book iscolleagues focus on symptom-based medicine. highlighted by the need for a third edition. FromAfter all, it is symptoms and the sense of feeling my perspective this book will ultimately be usedunwell which brings patients to the practitioner worldwide by medical students and practitionersfor relief and improvement in their health. In our trying to understand the relationship betweencurrent era of applying a barrage of imaging and symptoms and pathophysiological processes inendoscopic technologies to patient’s problems, we gastrointestinal diseases. Professor Talley andoften lose track of a rational and symptom-based his colleagues simply need to be congratulatedapproach in evaluating a patient’s symptoms. on helping to promote outstanding education inIndeed this is one of the few books to address these gastroenterology!issues from a presenting complaint perspective. In addition to its erudite approach to the Gregory Gores MD, FACPpatient, this book also employs problem-based Reuben R Eisenberg Professor of Medicinelearning methodology. This is a highly successful Chair, Division of Gastroenterology andeducational tool to improve recognition and Hepatologyretention of medical information. It takes a 18 November 2010 vii
  7. 7. ContentsForeword viiPreface xiContributors xiii 1 Heartburn, regurgitation and 11 Constipation 130 non-cardiac chest pain 1 N Talley K DeVault 12 Perianal pain 141 2 Difficulty swallowing and pain on D Lubowski and D Kozman swallowing 15 13 Acute diarrhoea 158 I Cook V Duncombe and J Almeida 3 Hiccups, sore mouth and 14 Chronic diarrhoea and fatty stools 174 bad breath 27 V Duncombe and J Almeida N Talley 15 Inflammatory bowel disease 190 4 Acute abdominal pain 37 M Picco M Cox 16 Faecal incontinence (leakage 5 When to test for Helicobacter of stool) 206 pylori and what to do with a D Lubowski and D Kozman positive test 66 N Talley 17 Loss of appetite and loss of weight 220 6 Indigestion (chronic epigastric N Talley pain or meal-related discomfort) 73 J Tack 18 Food allergies and intolerance 238 G Whelan and P Allen 7 Chronic lower abdominal pain or discomfort 88 19 Palpable asymptomatic J Kellow abdominal masses 246 N Tait 8 Wind and gas 100 P Kerlin 20 Abdominal distension 263 M Cox 9 Nausea and vomiting 106 N Talley 21 Lumps in the groin and hernia 271 N Talley10 Vomiting blood, black stools, blood per rectum, occult 22 Rectal/perianal mass and bleeding 115 colorectal cancer 279 M Weltman and N Phung M Weltman and N Phung ix
  8. 8. Contents23 Jaundice and pruritus 293 27 Obesity and anti-obesity medical A Keegan and surgical management 375 CD Smith24 Abnormal liver function test results 307 A Keegan and N Talley 28 Patient preparation and principles of sedation in gastrointestinal25 Management of end-stage liver endoscopy 381 disease and liver transplantation 346 I Norton and A Gupta M Leise and K Watt Index 39126 Abdominal incidentalomas 356 N Tait and S Lynchx
  9. 9. Preface ‘We expect too much of the student and we of current, important references. Every chapter try to teach him too much. Give him good has been carefully revised and edited to ensure methods and a proper point of view, and all the material is current, reflects best practice and other things will be added, as his experience is easy to understand. A new two-colour layout grows.’ Sir William Osler enhances the readability of the text and tables. Five new chapters have been added covering whenWelcome to the 3rd edition of Clinical gastroenter- to test and treat Helicobacter pylori, inflammatoryology: a practical problem-based approach! The bowel disease, obesity, preparing for endoscopylast edition was published in 2006, and it is very and sedation, and management of end-stage livergratifying to see its success translate into another disease and liver transplant.edition so soon. The production of a 3rd edition This is an international textbook withof a textbook normally indicates it has survived contributors from Australia, Europe and the USA,childhood and adolescence and has reached all of whom are experts in the field; I remainadulthood, reflecting its acceptance as a valuable very grateful for their efforts. We have relied oneducation tool. The editor and authors have feedback from peer reviewers and readers as westrived to ensure that this new edition remains a have prepared this new edition; please do notlearning gem. hesitate to contact us with your suggestions and The aim of the book is unchanged: to provide an recommendations.up-to-date, systematic, highly integrated yet very We have missed the input of the late Professorpractical account of gastroenterology, hepatology, Christopher Martin into this edition, but believeendoscopy and gastrointestinal surgery. With the book will live up to his high standards.this in mind, the book retains its clinical focus, Gastroenterology is an exciting hands-onstarting with a common (or uncommon but specialty that has seen very considerable advancesimportant) problem, and working through the over the past few decades. Whether you are aassessment, differential diagnosis, pathophysiology medical student, resident, registrar or generaland management, complementing a problem- practitioner, this volume will provide valuablebased learning approach now so popular around management guidance when you next encounter athe world. particular gastrointestinal symptom, sign, laboratory A number of new features have been added in test or x-ray.this edition. Each chapter now starts off with acase to set the scene and illustrate some essential Nicholas J Talleyprinciples. At the end of each chapter is a list of Newcastle, December 2010key points to promote learning, followed by a list xi
  10. 10. ContributorsPatrick Allen MBBChBAO, MRCP, BSc Paul Kerlin BA, MBBS (Hons), MD, FRACP,Consultant Gastroenterologist, Causeway FACG, FAICD, AGAFHospital, Northern Trust, NI, UK Clinical Professor of Medicine Gastroenterologist and Hepatologist, the WesleyJohn Almeida MD, DNB, FRACP Hospital, Auchenflower, Qld, AustraliaConsultant Gastroenterologist, Prince of WalesHospital, Randwick, Sydney, NSW, Australia Daniel R Kozman MBBS, FRACS Colorectal Surgeon, St George Hospital andIan Cook MBBS, MD (Syd), FRACP Bankstown Hospital, NSW, AustraliaProfessor of Medicine, University of New SouthWales Michael D Leise MDDirector, Gastrointestinal Motility Service and Instructor in Medicine, Division ofSwallow Centre Gastroenterology and Hepatology, Mayo Clinic,Department of Gastroenterology and Hepatology Rochester, MN, USASt George Hospital, Sydney, NSW, Australia David Z Lubowski MBBCh, FRACSMichael Cox MBBS, MS, FRACS Associate Professor of Surgery, University ofProfessor and Head of Surgery New South WalesHead of Upper Gastro-Intestinal Surgical Unit Head, Department of Colorectal Surgery,Head of Whitely-Martin Research Centre, St George Hospital, Sydney, NSW, AustraliaNepean Hospital, Sydney, NSW, Australia Scott A Lynch MD, MPH, FAAFPKenneth R DeVault MD Director, Bariatric Center, Bariatric Medicine,Professor and Chair, Department of Medicine, Mayo Clinic, Jacksonville, Florida, USAMayo Clinic, Jacksonville, Florida, USA Ian Norton MBBS, PhD, FRACPV Duncombe MD, MSc, FRACP Senior Staff Specialist, Royal North ShoreConsultant Gastroenterologist, Prince of Wales Hospital, NSW, AustraliaHospital, Randwick, Sydney, NSW, Australia Clinical Associate Professor, University of Sydney, NSW, AustraliaArun Gupta MBBSGastroenterology Advanced Trainee, Royal North Nghi Phung MBBS, PhD, FRACP, FAChAMShore Hospital, NSW, Australia Senior Staff Specialist, Westmead Hospital, NSW, AustraliaAndrew Keegan MBBS, BSc (Med), PhD, FRACPAdjunct Associate Professor, Sydney Medical Michael F Picco MD, PhDSchool Nepean, University of Sydney Assistant Professor of MedicineConsultant Gastroenterologist, Nepean Hospital, Consultant, Department of Medicine,NSW, Australia Mayo Clinic, Jacksonville, Florida, USAJohn Kellow MD, FRACP C Daniel Smith MD, FACSAssociate Professor and Head, Professor and Chair, Department of SurgeryDiscipline of Medicine, Sydney Medical School Surgeon-in-Chief, Mayo Clinic, Jacksonville,Northern Director, Gastrointestinal Investigation Florida, USAUnit, Royal North Shore Hospital, Sydney, NSW xiii
  11. 11. ContributorsJan Tack MD, PhD Greg Whelan AM, MD, MBBS, MSc, FRACP,Professor of Medicine, Translational Research FAFPHM, FAChAMCenter for Gastrointestinal Disorders Professor of Addiction Medicine, Monash(TARGID), University of Leuven, Leuven, University, Melbourne, Vic, AustraliaBelgium Medical Director, Addiction Rehabilitation Service, The Melbourne Clinic, Vic, AustraliaNoel Tait MBBS, FRACSProfessor of Surgery, University of Wollongong, Kymberly DS Watt MD, FRCPCNSW, Australia Associate Professor of MedicineConsultant General Surgeon, Wollongong Division of Gastroenterology and Hepatology,Hospital, NSW, Australia Mayo Clinic and Foundation, Rochester, MN, USANicholas J Talley MD, PhD, FRACP, FAFPHM,FRCP, FACP, FACG, AGAFPro Vice-Chancellor, Faculty of Health,University of Newcastle, NSW, AustraliaMartin Weltman MBBCh, PhD, FRACP, FAChAMDirector of Endoscopy, Nepean Hospital, NSW,AustraliaHead of Department Gastroenterology andHepatology Services, Nepean Hospital, NSW,Australiaxiv
  12. 12. 1 Heartburn, regurgitation and non-cardiac chest painCase allow the examiner to determine if the patient isA 52-year-old male presents with intermittent, describing heartburn, acid regurgitation, belching,retrosternal burning. This tends to occur after bloating, abdominal pain, halitosis or even flatus.meals, but occasionally is worsened by exercise. He Some patients even use the work ‘gas’ to describegets relief with drinking water and with antacids. indigestion.The symptom has been present for years, but has Heartburn, regurgitation and, to a lesser extent,become progressively more severe over the past 6 chest pain are symptoms that imply oesophagealmonths. He has also developed what he describes disease. The type of oesophageal diseaseas ‘slow swallowing’, which on further questioning responsible for these symptoms can often besounds like mild dysphagia to solids that happens anticipated on the basis of history alone. Physicalabout once a week. He has gained 10 kg in the examination rarely contributes to the diagnosis.past year and has no evidence of gastrointestinal Heartburn and regurgitation will be discussedbleeding. His examination is unremarkable except together as they often co-exist in patients withfor mild obesity (BMI = 31) and his stool has no gastro-oesophageal reflux disease (GORD). Chestoccult blood. He had a normal exercise stress test pain does not imply a particular disease process,as part of a recent executive physical. but rather a group of disorders and will be He is started on omeprazole 20 mg daily and discussed separately.scheduled for an upper endoscopy due to his In this chapter, the features of and approachdysphagia and duration of disease. The endoscopy to symptoms best described as heartburn andis performed after he was on the omeprazole for regurgitation will be outlined and associated4 weeks and demonstrates a 3 cm hiatal hernia symptoms supporting the diagnosis of GORD andwith a lower oesophageal ring of about 15 mm its complications will be discussed. Thereafter,diameter. There is no evidence of Barretts a practical guide to the use of investigations tooesophagus. Dilation is performed to 20 mm. On confirm the clinical diagnosis will be presentedfollow-up questioning, he states that his reflux as well as an outline of the principles of clinicalsymptoms are 90% improved on the omeprazole management. Similarly, a practical approach toand his dysphagia has resolved. He is counselled the diagnosis and management of chest pain willon dietary changes including, most importantly, be discussed.smaller meals with lower fat content with a goalto improve both his weight and reflux symptoms. HeartburnIn 4 months, he returned with recurrent Heartburn is a pain or discomfort typicallysymptoms after stopping his omeprazole. He was described as burning in nature. Its primarycounselled that he probably would need long- position is usually lower retrosternal, deep toterm maintenance, and the surgical and medical the xiphisternum. Heartburn commonly radiatesoptions were reviewed. He elected to remain on upwards, retrosternally, occasionally as far as theomeprazole and quickly became asymptomatic. neck. There may be associated epigastric pain. The timing of heartburn is characteristic. ItHistory occurs intermittently, either postprandially or‘Indigestion’ is a commonly used but poorly when the patient bends forward or lies flat in bed,understood term that means different things when the gastric contents are level with, or above,to different patients. Careful questioning may the lower end of the oesophagus. When it occurs 1
  13. 13. 2 Clinical gastroenterology: a practical problem-based approachpostprandially, it is most commonly in the early one-third of the population at least once a month;postprandial period, 5 to 30 minutes after a meal. 10% have daily heartburn. Only a minority of thoseThe postural changes that initiate heartburn do so with reflux symptoms present for medical raising the level of the gastric contents abovethe level of the gastro-oesophageal junction. The Regurgitationduration of an individual attack, when untreated, Regurgitation is the second ‘typical’ symptomrarely exceeds an hour. of GORD. Patients with regurgitation often, but Factors that precipitate an attack vary not always, also have heartburn. Although theconsiderably from patient to patient. For some, two symptoms can be closely linked temporally,the size of the meal is important, such that it will heartburn tends to be more frequent.occur with large meals but not small meals. For Regurgitation describes the intermittent, suddenothers, particular foodstuffs will precipitate an and often spontaneous sensation of materialattack. Foodstuffs more commonly incriminated moving from the stomach proximally towards theinclude curries, garlic, red wine, fatty foods, oesophagus and throat. Individual patients tendchocolate and citrus juice. The combination of to regurgitate about the same volume of bolusa meal and lying down can be additive in effect. each time. The usual precipitants of heartburnSome patients will describe waking from sleep for a particular patient are also the precipitants ofwith severe heartburn a few hours after retiring to acid regurgitation. They include meals (especiallybed, particularly following dietary indiscretions. larger meals), assumption of a horizontal posture,Attacks may occur when the patient lies on rises in intraabdominal pressure, and belching.the right side but not on the left side or supine. Food regurgitation is described as the predominantExercise, either isometric, including straining, form of regurgitation by some patients. This willor isotonic, such as brisk walking or running, obviously occur mostly after eating. Regurgitationcan trigger heartburn. Retrosternal burning pain occurring within the first 30–60 minutes after athat is triggered by exercise needs to be closely meal usually will not be acidic in character, whilescrutinised to ensure that symptoms of coronary regurgitation occurring more distant in time fromischaemia are not being overlooked. a meal will usually be acidic. Regurgitation may Response to medication is often predictive of persist in a treated patient even if the heartburnwhether the patients complaints are secondary has resolved with acid GORD and, therefore, qualify as heartburn. ‘Waterbrash’ is a term used to describe theRetrosternal burning pain that is not at least partially sudden appearance of a volume of salty or tastelessrelieved by appropriate medication is unlikely to be fluid in the mouth. It is the result of salivary glandcaused by the reflux of acid into the oesophagus, stimulation in response to gastro-oesophagealunless there is some other strong evidence reflux or peptic ulcer disease. At times, it issupporting reflux as the cause of the symptom. difficult to distinguish from regurgitation, butHeartburn is usually relieved within several since both are reflux symptoms, that distinctionminutes by antacids. Discomfort relieved within is not always critical. There are several othermuch shorter periods or after much longer periods symptoms that can be confused with less likely to be secondary to gastro-oesophageal Rumination is the effortless return of food into thereflux. Similarly, heartburn usually improves oesophagus or mouth. This usually occurs duringwith agents that diminish gastric secretion of acid meals and the food is often reswallowed. Patientssuch as H2-receptor antagonists and proton pump with bulimia are also occasionally misdiagnosedinhibitors, although relief with these agents is not as having GORD. Finally, burping and belchingas immediate as the relief produced by antacids. involve the ‘reflux’ of air, not liquids, and can The time course, severity and frequency of also be confused with regurgitation. Patients withheartburn will vary considerably from patient to rumination, bulimia and aerophagia (excessivepatient. Some patients have the recent onset of belching and burping) can usually be diagnosedsymptoms, while others will have symptoms dating with a carefully taken history and will, at times,back over many years; some describe symptoms as have false positive ambulatory reflux testing.occasional only, while others are inconveniencedmany times a day. It is important to ask about Complications of acid regurgitationnocturnal symptoms since those patients may Severe acid regurgitation can be associated withhave more severe mucosal disease, a poorer health- other problematic symptoms including chokingrelated quality of life and more difficult to treat attacks, cough, asthma, hoarseness of voice, a fouldisease. Heartburn is very common, reported by taste in the mouth in the morning, bad breath, a
  14. 14. 1 Heartburn, regurgitation and non-cardiac chest pain 3sore tongue, dental caries and nasal aspiration. ● slow progression in severity over months toSome patients complain of waking up episodically years; andwith a sensation of choking such that they will ● minimal to no weight loss.cough vigorously, but rarely produce sputum, get There are patients with symptoms of dysphagiaup out of bed and even go to an open window to and reflux for whom an organic cause will not becatch their breath. These symptoms subside fairly found by endoscopy or barium swallow; dysphagiarapidly. For some, the history suggesting episodic in these cases may be caused by a motor disorder oftracheal aspiration will be less dramatic. They may the oesophageal body. It is usually not clear whetherdescribe a chronic cough, perhaps worse in the this dysmotility is due to chronic reflux or if motilitymorning, but without sudden exacerbations. When is the primary problem. If confirmation is requiredthat is the case, other causes of cough will need to (after more serious disease has been excluded bybe considered and excluded as part of a respiratory barium testing or endoscopy), an oesophagealwork-up. Asthma usually has an allergic basis manometry and ambulatory reflux test may bebut, occasionally, can be precipitated by gastro- required. Alternatively, resolution of dysphagia afteroesophageal reflux. Such patients may present later a trial of proton pump inhibitor therapy is nearlyin life without any obvious cause for obstructive diagnostic of a reflux association.airways disease. In these patients, the symptomsof gastro-oesophageal reflux are commonly not Examinationsevere. Acid regurgitation can result in a chemicallaryngitis and cause hoarseness of voice. Usually A typical history of heartburn or acid regurgitationthe regurgitation occurs at night so hoarseness is is usually sufficient to diagnose GORD. There aremost evident in the morning, and gradually settles no specific signs on physical examination thatas the day passes. Similarly, waking up with a foul support the clinical diagnosis. Deep epigastrictaste in the mouth or bad breath can be attributed tenderness may be present, but is not specificto nocturnal gastro-oesophageal reflux. Nasal and is not of any particular clinical significance.aspiration is a particularly unpleasant consequence The role of the examination in GORD is mainly toof regurgitation, again usually occurring at night. exclude other issues such as pulmonary disease, cardiac auscultation abnormalities and severeProblems with swallowing tenderness (unlikely to be present with GORD).Odynophagia Pathophysiology of GORDGORD is one of the causes of odynophagia (pain The oesophagus and the stomach are separatedon swallowing). It is usually reported in response by a high-pressure zone produced by tonicto hot or cold foodstuffs (see Ch 2). contraction of specialised smooth muscle of the lower oesophageal sphincter (LOS) and the phasicDysphagia contraction of the cural diaphragm. In normalThe sensation of obstructed swallowing is unusual individuals, this functional barrier is maintainedin patients with heartburn and regurgitation except to allow antegrade flow with swallowingand, when present, is worthy of special clinical and retrograde flow with belching and vomiting.attention. Oesophageal stenosis secondary to Reflux is likely when the LOS has a very lowsevere, long-standing erosive peptic oesophagitis basal pressure. In patients with a weak sphincter,is the most common cause of reflux-induced increases in intraabdominal pressure can easilydysphagia. An undiagnosed oesophageal overcome that pressure and produce pathologicalcarcinoma should be considered in appropriate amounts of reflux. On the other hand, most patientsclinical settings. It is the implied severity of the with reflux have relatively normal pressure and itreflux disease and the possibility of malignancy is felt that the LOS tends to relax at inappropriatethat makes investigation by barium swallow and times, leading to reflux (transient LOS relaxations).upper gastrointestinal endoscopy mandatory in Hiatus herniation predisposes to reflux as a resultthese patients. The features of dysphagia usually of a dissociation of a weak LOS with the addedassociated with a benign stenosis secondary to pressure provide by the diaphragm. In addition,peptic oesophagitis are: a hernia predisposes to inadequate clearance of● exclusively for solids (not liquids); gastric contents away from the lower oesophagus.● experienced at the lower end of the sternum; Most of the fluid volume of refluxate is promptly● little variation in severity from day to day given cleared from the oesophagus by one or more swallows. the same-sized bolus; Small amounts of residual acid are neutralised by
  15. 15. 4 Clinical gastroenterology: a practical problem-based approachweakly alkaline saliva with subsequent swallows. certain patients (particularly older patients withClearance is delayed during sleep when swallowing is chronic symptoms) should undergo endoscopy toless reliably triggered by reflux. Smoking exacerbates screen for Barretts oesophagus.the effects of reflux by inhibiting salivation, thereby The characteristic endoscopic signs of refluxdelaying acid clearance. oesophagitis are shown in Table 1.1 and Figure Repeated and prolonged exposure to gastric 1.1. As mentioned above, there is only a weaksecretions can result in erosion and ulceration of correlation between the severity of oesophagealthe oesophageal mucosa. The occurrence of injury, acidification and the degree of peptic oesophagitis.expressed as erosive oesophagitis, is dependent On the other hand, it is clear that more severeon three factors: (1) duration of exposure; (2) the grades of esophagitis are more difficult to heal.chemical composition of the refluxate; and (3) Oesophagitis should never be diagnosed based onthe natural resistance of the individual. Thereby, anything short of mucosal erosion and never shouldwe can explain several well-known clinical be based on erythema of the distal oesophagus.observations. First, the severity of oesophagitis The diagnostic endoscopic examination is alwaystends to be worse when oesophageal acidification carried as far as the first part of the duodenumis prolonged, and reducing gastric acid secretion looking for incidental pathology. The finding of apromotes healing of peptic oesophagitis.Secondly, two patients with similar levels of Table 1.1 Classification of reflux at endoscopyreflux, as measured by pH monitoring, may (Los Angeles—LA—System)have marked differences in mucosal appearanceat endoscopy. One may have severe erosive Grade Featureoesophagitis while the other, a normal-looking Grade A At least one mucosal break (erosion)mucosa. The role of bile and pancreatic juice in each ≤ 5 mmproducing oesophagitis in patients with an intact Grade B At least one mucosal break > 5 mm butLOS and pylorus is limited. This mechanism is of not continuous between the tops of twoconsiderable importance in patients without an mucosal foldsintact pylorus. Heartburn, on the other hand, is dependent Grade C At least one mucosal break that is continuous between the tops ofprimarily on mucosal sensitivity, not 2 mucosal folds, but which is notmucosal ulceration. Thus, some patients with circumferential (< 75%)symptomatically severe heartburn may have no Grade D Circumferential mucosal break (≥ 75%)peptic oesophagitis, while others with no heartburncan present with a peptic stricture secondary to long-standing peptic oesophagitis. Therefore, the severityof heartburn is a poor predictor of oesophagitis.This is a particular problem in older patients whooften present with advanced oesophageal damagedespite relatively modest symptoms.Investigation of Heartburn and AcidRegurgitationUpper gastrointestinal endoscopyThe finding of peptic oesophagitis at endoscopyconfirms that symptoms of heartburn andregurgitation are due to GORD. On the otherhand the absence of oesophagitis in no wayexcludes GORD. Patients with typical symptomsthat occur occasionally and that are completelycontrolled by simple measures, such as attentionto lifestyle (see below) or antacids, do not needupper endoscopy. On the other hand, patients Figure 1.1 Endoscopic view of linear erosive pepticwith reflux symptoms and alarm features (such oesophagitis (Grade D) of the distal vomiting, bleeding, weight loss or dysphagia) From plate 20-4 of the online edition of the Merckshould always be investigated. In addition, Manual, with permission from Dr D Martin.
  16. 16. 1 Heartburn, regurgitation and non-cardiac chest pain 5chronic duodenal ulcer is significant as this may Summation of the duration of episodes over anbe the underlying cause of gastro-oesophageal extended period, usually 24–48 hours, gives areflux symptoms (see Ch 5). measure of the underlying pathophysiological process, which can be used to score the severity ofOesophageal biopsy at upper the disease. Further, a correlation between symptomsgastrointestinal endoscopy and episodes of oesophageal acidification can beBiopsy of a normal-appearing oesophagus was once established (see Fig 1.2). The test is not required forsuggested to aid in the diagnosis of GORD, but is diagnosis in the majority of patients with typicalnot advocated by most experts in adult GORD. symptoms of reflux in whom the diagnosis canMicroscopic changes suggestive of GORD include: be made either endoscopically or, if there is no● relative increase in papillary height; oesophagitis, on the basis of a successful therapeutic● relative increase in thickness of the basal layer trial with a course of antisecretory treatment. of the epithelium; Recently, another technology has been● the presence of intraepithelial neutrophils and developed that has the potential to measure eosinophils. not only acid reflux, but also the reflux of other These microscopic findings can be relatively substances with a more neutral pH. This technologydifficult to quantify on routine biopsy specimens takes advantage of the conductivity of refluxedand the diagnostic value of these findings continues liquid and is measured with a specially designedto be disputed, so biopsy is not recommended catheter that not only measures the movement ofroutinely. Recently, some experts have suggested that fluid using impedance, but also measures pHobtaining midoesophageal biopsies in patients (acid reflux). The exact role of this testing remainswith any unexplained oesophageal symptom to be completely defined, but has been suggested(especially dysphagia) to search for histological to be of particular benefit in patients requiringevidence of eosinophilic oesophagitis (Ch 2). testing while on acid suppression. When contemplating performing an ambulatoryUpper gastrointestinal radiology reflux test, two questions must be answered: shouldBefore the establishment of flexible upper the test be done on or off acid-supression therapygastrointestinal endoscopy, upper gastrointestinal and should impedance monitoring be included?contrast radiology with barium was the initial Off-therapy testing is the best way to determineinvestigation for dyspepsia and reflux symptoms. if the patient has pathological gastro-oesophagealIt has been downgraded to a second-line reflux. This testing can be performed with eitherinvestigation, mainly because it is not a sensitive a tube-based or tubeless system. If, on the otherdetector of oesophageal mucosal damage. It does, hand, the question is of ongoing reflux on therapy,however, offer complementary information, some experts advocate a combined impedance pHwhich is sometimes useful. Some advocate test. An alternative, especially in the patient withroutine radiological testing in any patient with either no or a modest response to therapy, is todysphagia. It also allows better definition of the stop medications and do a pH test off therapy. Thepresence and size of a hiatus hernia, which may application of the concept of pretest probabilitybe important if surgery for reflux is contemplated. is important in that decision-making process. IfThe demonstration of barium refluxing into the the patient is believed to have reflux and a non-oesophagus is neither specific nor sensitive for the acid contribution to symptoms is to be excluded,presence of pathological acid reflux. on-therapy, impedance pH testing makes sense. If on the other hand, the patient is not believed toAmbulatory reflux monitoring have reflux (often the case when there is a minimalEpisodes of gastro-oesophageal reflux result in response to therapy), stopping therapy and doingacidification of the distal oesophagus. Neutral pH is an off-therapy test is most reasonable. A negativerestored by oesophageal peristalsis. These episodes off-therapy pH test and a failed therapeutic trialcan be monitored and recorded by placement of a provide the best evidence that reflux is not thepH microelectrode in the distal oesophagus. In the cause of an individual patients symptoms.past this test required prolonged nasal intubation,which is unpleasant. That discomfort can now Bernstein testingbe avoided by attaching the pH electrode to the Bernstein testing is a test of mucosal sensitivitylower oesophageal mucosa endoscopically. The pH that is of mostly historical interest, although it mayrecording then occurs by telemetry. The electrode be available in a few referral centres. It involvessubsequently detaches and passes spontaneously. transnasal oesophageal intubation and perfusion
  17. 17. 6 Clinical gastroenterology: a practical problem-based approach A BFigure 1.2
  18. 18. 1 Heartburn, regurgitation and non-cardiac chest pain 7Figure 1.2 24-hour oesophageal pH testing (pH probe 5 cm above lower oesophageal sphincter) A:Pathological upright reflux. The lines indicate the times at which the patient had reflux symptoms. These eventsall coincide with a decrease in pH to below pH 4. The symptoms of this patient are clearly caused by reflux.B: Pathological reflux during sleep. During sleep, in particular, the oesophageal pH persists longer at a low valuedue to disordered oesophageal clearance. A symptom index over 50% ([no. of symptoms with pH under 4 ÷ totalno. symptoms] × 100%) is considered significant. The symptom-associated probability (SAP) is a more optimalmethod to estimate if acid reflux episodes are linked to symptoms. The 24-hour recording is divided into 2-minperiods, and the 2-min periods before onset of symptoms identified for evidence of reflux (pH under 4.0). Theprobability (P) that events are unrelated is calculated (using Fishers exact test). SAP = (1.0 – P) × 100%From Smout AJPM, Akkermans LMA. Normal and disturbed motility of the gastrointestinal tract. Petersfield:Wrightson Biomedical Publishing; 1972, with permission.of the distal oesophageal mucosa with dilute (0.1 Patient-directed therapyM) hydrochloric acid alternating with placebo For most of the population who have occasional,(normal saline). The test is considered positive if mild symptoms of reflux, intermittent, patient-the acid produces the patients symptoms and the directed treatment is all that is required. Suchsaline does not. It can be complementary to pH treatment involves lifestyle changes including:monitoring in patients whose atypical symptoms, ● weight loss, if overweight or in the face ofparticularly chest pain, are infrequent and do not recent weight gain;occur during a pH-monitoring study. ● avoidance of large meals, particularly beforeOesophageal manometry retiring to bed at night;This test has no routine diagnostic role in the ● postural advice including elevation of the headevaluation of symptoms of GORD unless antireflux of the bed by insertion of 20 cm blocks undersurgery is being considered, where manometry the bed head and avoidance of bending;is used to exclude achalasia and to tailor the ● avoiding drugs, cigarettes, alcohol andtightness of the repair. It may sometimes be useful foodstuffs that might precipitate the evaluation of patients with symptomsof dysphagia in addition to those of heartburn Box 1.1 Effectiveness of drugs forand regurgitation, where a barium swallow and gastro-oesophageal refluxendoscopy have been normal and the dysphagiaremains unexplained (see Ch 2). Twice-daily proton pump Most effective inhibitorsTreatment Once-daily proton pump inhibitor combined withClinical management of heartburn and H2-receptor antagonistregurgitation Once-daily proton pump inhibitorsThe intensity of reflux symptoms varies from Standard-dose H2-receptora mild, occasional discomfort, for which the antagonistspatient may want little more than antacid and Antacids Least effectivereassurance, to a daily, incapacitating pain thatprevents normal activity. Management needsto be commensurate with the magnitude of the Table 1.2 Features of clinical managementclinical problem. Unlike duodenal ulceration, of gastro-oesophageal refluxGORD is usually a persistent condition withoutexacerbations and remissions. Drug therapy Patient-directed Doctor-directedhas a hierarchy (see Box 1.1). Oesophagitis treatment treatmentindicates a need for therapy to heal the mucosa Weight loss, if overweight Continue lifestyle measuresand maintain healing; virtually all patients Avoidance of large meals of low-levelwith severe oesophagitis (LA grade C and D Postural advice such as eleva- Regular or on-demand full- tion of bed head at night dose H2-receptor antagonistoesophagitis; see Table 1.1) will relapse if Avoidance of foodstuffs that or proton pump inhibitormedical therapy is stopped, as will most (80%) precipitate reflux High-dose proton pumpwith milder oesophagitis. A review of the clinical On-demand antacids or inhibitormanagement principles for patients with gastro- H2-receptor antagonists for Endoscopic or laparoscopic breakthrough symptoms antireflux therapyoesophageal reflux is presented in Table 1.2.
  19. 19. 8 Clinical gastroenterology: a practical problem-based approach A foodstuff checklist includes spicy foods, agents in this category, leaving acid suppression asalcohol, fatty foods, chocolates, nuts, tomatoes, essentially the only medical therapy for well as many others. Rather than prohibit Some patients will have symptoms and/or‘everything’ and risk losing patient compliance, oesophagitis that do not respond to standard dosesit is wiser to establish with the patient which of proton pump inhibitors. A common approach isfoodstuffs they recognise as triggers, ask them to increase the dose to twice daily (before meals)to avoid these, go through the checklist to for an additional 4–8 weeks to see if the disease isidentify triggers that the patient might not have brought under control. This approach has not beenpreviously considered and recognised, and then tested in well-designed trials and it is not clear whatask the patient to establish relationships between proportion of patients will respond. An additionalsymptoms and triggers so that they might be nocturnal dose of H2-receptor antagonists may beavoided in the future. In addition, some aspects of assistance, but benefits often wear off if givenof the ‘reflux diet’ such as lower volume, lower fat continuously. An alternative is to study the patientand weight loss will provide added health benefits using ambulatory reflux testing to either confirmbeyond the improvement in reflux symptoms. control of acid (on therapy testing) or to determine Of these various lifestyle changes, only weight if they actually have the disease (off-therapy testingreduction has the potential to change the natural or perhaps combined impedance/pH testing). Thehistory of the disease. Thus, some patients can addition of a prokinetic agent is an attractiveclearly identify a critical weight above which they concept, but none of the currently available agentsexperience symptoms and below which they are have been proven to be effective as either monofree of symptoms. It makes good sense to encourage or ‘add-on’ therapy in this situation. There arethese patients to stay below their critical weight. several agents in development that may inhibitInterestingly, even patients of normal weight transient LES relaxation. Some of the possibilitiesmay develop reflux symptoms when they gain to be considered when a patient is ‘failing’ protonweight but do not become overweight or obese. pump inhibitor therapy are outlined in Table 1.3.Additionally, patients on low-level treatment Patients for whom medical therapy results inmay benefit from intermittent medication for incomplete resolution of symptoms (especiallysymptoms. The medication could be antacids if regurgitation) can achieve that end point withshort-term (about 30 minutes) relief is required, antireflux surgery. Nevertheless, the majority ofor an H2-receptor antagonist or proton pump patients presenting for surgery present becauseinhibitor if relief for several hours is required. they are keen to achieve long-term cure, withoutDoctor-directed treatmentWhen patients present to a physician, they often Table 1.3 Failure of proton pump inhibitor therapyhave tried the above manoeuvres. In some, it may to control gastro-oesophageal reflux symptoms:be reasonable to simply emphasise the above and management approachsee if they can manage their symptoms on their Mechanismown. On the other hand, most patients will be to consider Managementtreated with a prescription medication. Misdiagnosis Review history and The end point of therapy should be complete investigations.or near-complete resolution of symptoms. H2-receptor antagonists have an onset of action that Not taken before Advise taking 30 minutes prior meals to a rapid, but rate of symptom relief is about 50%when standard doses are taken twice daily. There Inadequate dosing Trial twice-daily no evidence that greater than standard doses Nocturnal acid Twice-daily proton pumpprovide additional benefit. Proton pump inhibitors breakthrough inhibitor; if that fails, H2-receptortaken once daily provide a higher rate of symptom antagonist before bed asrelief (60–80%) and endoscopic healing (80–90%), needed; consider surgery.but have a somewhat slower onset of action. Once Acid hypersecretion Exclude Zollinger-Ellisonsymptom relief is achieved an attempt to step down syndrome.the dose or change to an ‘as needed’ approach is Drug resistance Very rare; switch to H2-receptorreasonable. If the patients relapse at that point, antagonist or consider surgery.they are likely to need long-term treatment. Whilea prokinetic would seem to be a rational approach Oesophageal Add a low-dose tricyclic hypersensitivity GORD, there are no available, safe and effective
  20. 20. 1 Heartburn, regurgitation and non-cardiac chest pain 9need for continuing medical therapy and (see Fig 1.3A) and then wrapping of the lowerfollow-up. Most report the loss of reflux symptoms oesophageal sphincter region with the gastricwithout the need to take medication from the day fundus (see Fig 1.3B). There is still debate as toof surgery. There is complete control in up to 90% whether the fundoplication should be completeof patients with typical symptoms that responded as shown in Figure 1.3B, or whether the wrapto acid suppression in the hands of an experienced should be incomplete—surrounding less thansurgeon. However, in some studies up to 50% of the 360° circumference of the lower oesophagealcases eventually will have reintroduction of acid sphincter. Current data suggest that patientssuppression therapy over the long term. The risk having the so-called incomplete fundoplicationof postoperative sequelae has limited the more are more satisfied with the outcome because ofwidespread utilisation of antireflux surgery. The an apparent reduction in sequelae, even thoughmore troublesome of these are painful abdominal the long-term control of reflux might not bedistension (gas bloat), persistent dysphagia and, quite as good as with complete fundoplication.less commonly, persistent diarrhoea. Endoscopic therapies to treat gastro-oesophageal The surgical approach for most will be reflux, including radiofrequency therapy, injectionlaparoscopic. This conveys the advantages of less of biopolymer and endoscopic sewing around thepostoperative pain and early return to full activity. lower oesophageal sphincter, have been studied.The procedure involves an initial restoration of Of these, the systems that place sutures to formnormal anatomical relationships by reduction of a ‘plication’ at the LOS are the only currentlythe commonly associated sliding hiatus hernia available options, while most of the others Sliding RollingFigure 1.3A Schematic representation of a sliding hiatus hernia (left) and a paraoesophageal hernia (right). (a) (b) (c)Figure 1.3B Schematic representation of the Nissen fundoplication operation. From Smout AJPM, AkkermansLMA. Normal and disturbed motility of the gastrointestinal tract. Petersfield: Wrightson Biomedical Publishing; 1972,with permission.
  21. 21. 10 Clinical gastroenterology: a practical problem-based approachhave been removed because of lack of efficacy, ● a malignant stenosis in a patient with GORD;unacceptable side effects or both. ● dysphagia due to another problem not related to reflux (misdiagnosed achalasia or eosinophilicMaintenance therapy oesophagitis, for example).Once a patients symptoms are controlled, they It is often helpful to define the presence andcan be entered into a program of ‘maintenance’ in site of stenosis radiologically. Subsequently,order to keep those symptoms under control. Some the presence or absence of an oesophagealpatients can be ‘stepped down’ to less complete malignancy must be established or disproved byacid suppression (from high dose proton pump upper gastrointestinal endoscopy and biopsy ofinhibitor to standard dose or from standard dose the stenosis and any mucosal irregularity. Onceproton pump inhibitor to H2-receptor antagonist malignancy is excluded, oesophageal dilatationor antacid therapy) and a few can discontinue may be performed to relieve dysphagia. Thetreatment altogether, especially if they adhere dilatation may need to be staged if the stenosis isto lifestyle changes. On the other hand, many very narrow and additional care must be taken ifpatients require the same therapy that they needed the oesophagus has the typical ringed appearanceto achieve remission in order to maintain that associated with eosinophilic esophagitis.remission. Assuming the patient has symptoms or endoscopy suggestive of GORD, they should start a protonRisks of long-term acid suppression pump inhibitor to achieve symptom controlWhen they were first introduced, the use of proton and healing. With this therapy, restenosis is lesspump inhibitors was limited to a short period of common. Antireflux surgery should be consideredtime. Subsequently, concerns over the potential for those who require repeated dilatations oradverse effects of proton pump inhibitor-induced have poor control of heartburn and regurgitation.hypergastrinaemia were discounted and long- These patients are sometimes unsuitable for aterm therapy was approved. Acid suppressants laparoscopic operation, as oesophageal fibrosishave been very safe, but recently a few concerns may render the oesophagus short as well as narrow.have arisen. In addition to aiding digestion, Some surgeons will perform a Collis gastroplastygastric acid helps to eliminate ingested bacteria. (oesophageal lengthening procedure) combinedInfections that have a small increased incidence with a Nissen fundoplication in that proton pump inhibitor-treated patients include Patients with oesophageal involvement fromClostridium difficile , community-acquired scleroderma are usually readily identifiable bypneumonia and perhaps travellers diarrhoea. the characteristic appearance of their handsAcid aids in the absorption of several nutrients and face. These patients have a hypomotile(iron, calcium and vitamin B12), although oesophageal body in addition to a failure of theclinically significant insufficiencies are very rare. lower oesophageal sphincter. Aggressive high-Recent studies have found a very small increase level medical therapy is to be preferred overin hip fractures in proton pump inhibitor-treated surgical therapy. Oesophageal dysmotility is notpatients. Finally, there is no direct cardiovascular isolated to scleroderma and may occur with manyrisk with acid suppression, although a negative other rheumatologic and non-rheumatologicalinteraction between proton pump inhibitors conditions (long-standing diabetes, for example).and the antiplatelet drug clopidogrel has beensuggested. Hiatus hernia A hiatus hernia is a protrusion of intraabdominalClinical management of dysphagia contents through the oesophageal hiatus in theassociated with reflux symptoms diaphragm. Two main types of hiatus hernia are recognised radiologically (see Fig 1.3A).Dysphagia is a ‘warning’ symptom (red flag) inthe patient with reflux and must be respected as Routine (sliding or fixed) hiatus herniasuch. The possibilities include: This type of hernia is extremely common (in 10–● a benign distal oesophageal stricture secondary 15% of the population) and often asymptomatic. to GORD; Its prevalence increases with age. It occurs● a benign distal oesophageal stricture secondary as a result of circumferential telescoping of to GORD associated with a motility disorder the segment of stomach that lies just distal to (either primary or perhaps associated with a the lower oesophageal sphincter through the rheumatological condition such as scleroderma) oesophageal hiatus. This type of hernia is not
  22. 22. 1 Heartburn, regurgitation and non-cardiac chest pain 11prone to obstruction or strangulation, so specific is not likely to be performed on clinical grounds.surgical treatment of the hernia is not required; As a consequence, many patients remain unawarewhen it is found incidentally in association with that they carry this malignant predispositionGORD, attention should be directed at treatment and present at a more advanced stage.of the reflux disease. Herniae are more common in The columnar lining of Barretts oesophagusmore severe grades of esophagitis and are almost is salmon pink in colour and has a matt surfaceuniversally present in patients with Barretts texture, distinguishing it from stratified squamousoesophagus. epithelium, which is pearly pink in colour and shiny in texture. Histological confirmation isParaesophageal (rolling) hernia necessary and specialised intestinal metaplasia inThis type of hernia is less common. It can range in the oesophagus is the hallmark finding.size from just a small knuckle of fundus protruding Development of adenocarcinoma in Barrettsalongside the non-displaced lower oesophageal oesophagus is a staged process that occurs oversphincter to the whole stomach twisted and several years. The precursors of invasive carcinomarotated within the posterior mediastinum. With (low-grade and high-grade dysplasia) can belarger herniae, there is a tendency for the lower detected reliably only by histological examinationoesophageal sphincter to be displaced proximally of multiple samples of the columnar epithelium.with the stomach. Such herniae should not be There are no reliable serological markers or eventhought of as mixed herniae as the main component endoscopic appearances, although advances inis usually the paraesophageal component. These endoscopic imaging may change that in the nextherniae can cause dysphagia and uncommonly few years. There is no evidence that control ofretrosternal pain due to ischaemia of the entrapped continuing reflux, after the metaplastic epithelialportion of stomach. There may be associated change has occurred, stops progression down thevomiting due to obstruction at either the lower dysplastic pathway, even though this is appropriateoesophagus or at the gastric outlet. Early satietyand weight loss form part of a milder obstructivesyndrome. Large herniae can cause dyspnoea byoccupying part of the thoracic cavity, which wouldotherwise be available for expansion of the lungs.The only effective treatment is surgical repair ofthe hernia, but this is currently recommendedonly for patients with symptoms or complicationsfrom the hernia. There seems to be a higher thanexpected recurrence of herniae after repair of theparaesophageal type.Barretts oesophagusOne of the consequences of long-term gastro-oesophageal reflux is a metaplastic transformationof the stratified squamous epithelium of the distaloesophagus to a columnar type epithelium. Theaffected oesophagus is termed Barretts or columnar-lined oesophagus. The significance of Barrettsoesophagus is its predisposition to malignantchange. Clinically, much effort is expended toidentify and treat such patients before they presentclinically with an adenocarcinoma of the distaloesophagus (Fig 1.4), when the outlook is likely to bepoor (Ch 17). It has been suggested that patients withthe following characteristics are at greatest risk ofdeveloping Barretts oesophagus and subsequentlyoesophageal adenocarcinoma: long-term refluxsymptoms, male sex, Caucasian race and positive Figure 1.4 Adenocarcinoma of the distalfamily history. Despite that, some patients will have oesophagus (arising in Barretts mucosa) on bariumreflux symptoms that are so minor that an endoscopy swallow.
  23. 23. 12 Clinical gastroenterology: a practical problem-based approachfor control of reflux symptoms. Preliminary data any significant help in separating the two. Signs ofsuggest that aspirin may slow the progression of heart disease such as cardiac murmurs and cardiacBarretts oesophagus to dysplasia and is safe when failure, or manifestations of peripheral vascularcombined with a proton pump inhibitor. disease such as bruits and absent pulses, increase The aim of the management strategy of patients the likelihood that the pain is cardiac in origin.with Barretts oesophagus is to identify patients When there is any doubt investigation iswith high-grade dysplasia. These patients are very initially focused on the heart. All patientslikely to proceed in the near future to invasive should have an electrocardiogram (ECG) andadenocarcinoma. In patients with non-dysplastic cardiac enzymes measured if they are examinedBarretts, it is recommended that endoscopic while they are having pain. Those without painsurveillance be conducted every 2–3 years, with at the time of interview and normal resting ECGbiopsies (in each quadrant at 2-cm intervals) along should have an exercise stress ECG performed.the length of the Barretts mucosa. If low-grade The extent of further cardiac investigationdysplasia is identified, the interval should be will depend on clinical judgment. This mightshortened to at least yearly with a more intensive include echocardiography, radionuclide studiesbiopsy pattern (each quadrant every 1 cm). If high- and coronary angiography. Although coronarygrade dysphagia is found and confirmed, there angiography remains the gold standard, itsis a high risk of underlying adenocarcinoma and performance is sometimes delayed because of itsremoval of the Barretts epithelium is generally invasive nature and slight risk of complications.recommended. The traditional approach has been The inconvenience and risk obviously need tosurgical resection of the oesophagus. If performed, be weighed against the likelihood that coronaryas much of the oesophagus as possible should be disease will be uncovered and the likelihood thatremoved to prevent recurrence of Barretts in the the findings will change the clinical management.residual segment. Recently, endoscopic ablative One of the advantages of performing coronarytechniques have been developed and are becoming angiography that reveals normal coronary arteriesa recognised alternative in patients with dysplastic is that both patient and doctor can be reassuredBarretts epithelium. that sudden death becomes very much less likely. Once the patient is determined to not haveNon-cardiac Chest Pain occlusive disease of the coronary arteries, severalNon-cardiac chest pain is a diagnosis reached by other conditions (below) need to be considered.excluding myocardial ischaemia as the cause ofpain by a combination of history taking, physical Microvascular anginaexamination and one or more investigations. Microvascular angina is a cause of ischaemicHistorically, cardiac pain due to ischaemia is chest pain in the presence of normal coronaryprimarily retrosternal in position. It may radiate to arteries; abnormalities may be found onthe neck and jaw, and/or down one or both arms. non-invasive cardiac function testing (e.g.It is pain that is severe in intensity, crushing in radionuclide ventriculography or thalliumnature and usually not prolonged in duration. It is exercise scintigraphy). It appears these patientscommonly precipitated by exercise and causes the have survival rates similar to controls and the painpatient to stop exercising. Patients with cardiac pain will, at times, respond to nitrates and/or calciumare more likely to have evidence of arterial disease channel the lower limbs and cerebral arteries, and cardiacrisk factors such as hypertension, diabetes mellitus, Musculoskeletal conditionsobesity, hypercholesterolaemia and tobacco Early in the clinical evaluation, before invasiveuse. Severe retrosternal chest pain that radiates cardiac investigations are performed, thethrough to the back should lead to consideration of possibility that the chest pain is musculoskeletaldissection of a thoracic aortic aneurysm. in origin should be considered. A history of chest Chest pain of oesophageal origin is more likely wall injury might indicate a sternal be prolonged, to radiate through to the back, to Palpation of the anterior chest wall may revealbe precipitated by eating, and to be associated with focal tenderness suggestive of costochondritis.dysphagia, heartburn and regurgitation. In spite ofthese differences, chest pain of oesophageal origin Panic attackscannot be distinguished from cardiac chest pain Panic attacks can cause chest pain. They resultwith any degree of certainty on the basis of history in discrete periods of intense fear that occuralone. Further, physical examination is rarely of abruptly with at least four of the following
  24. 24. 1 Heartburn, regurgitation and non-cardiac chest pain 13symptoms: chest pain, palpitations, sweating, aetiology is more likely. The diagnostic optiontrembling, shortness of breath, choking, nausea, is to either perform an ambulatory reflux test ordizziness, feelings of unreality or detachment, offer a trial of proton pump inhibitor (PPI). The sofear of losing control, fear of dying, paraesthesia called ‘PPI-test’ is a short-term (7–14 day) trial ofand flushes or chills. a twice daily proton pump inhibitor that seems to have a reasonable sensitivity and specificity whenOesophageal conditions compared to ambulatory pH testing. An ambulatoryOesophageal conditions that can cause non-cardiac reflux test should be considered ‘positive’ if therechest pain, in order of importance, include: is excess reflux or if symptoms occur in correlation● GORD (most common); with episodes of reflux. If proton pump inhibitor treatment is effective, it should obviously continue.● non-specific motility disorder or hypertensive The role of endoscopy in patients without typical lower oesophageal sphincter (uncertain symptoms in unclear, but the finding of erosive significance); oesophagitis may clinch the diagnosis.● high pressure ‘nutcracker’ oesophagus If the patient fails a treatment trial or if the (uncertain significance); symptoms are clearly related to swallowing,● diffuse oesophageal spasm (rare); and an oesophageal motility test may be of benefit● achalasia (rare). although the minority of patients will have These conditions can be diagnosed either by a clearly definable motility disturbance. Theendoscopy and pH monitoring in the case of GORD, manometric characteristics of motor disordersand by oesophageal manometry in the remainder. that may cause non-cardiac chest pain are shownUnfortunately it is often difficult to be sure that in Table 1.4. Unfortunately, manometry hasthe oesophageal condition diagnosed is indeed the significant limitations in this clinical settingcause of the pain, as will be discussed below. as it is performed in a laboratory over a short The program of investigation for patients time frame (which is standard) and the chancedeemed to have non-cardiac chest pain that might that the abnormal manometric findings willbe oesophageal in origin will depend on how be observed, except in the case of achalasia, issignificant the symptoms are in terms of both their low. This likelihood can be increased by usingseverity and frequency. Some patients will do well provocative agents, such as edrophonium, orif reassured that their heart is not the cause of their extending the period of observation utilisingsymptoms. GORD should be the first consideration a portable ambulatory manometry system.for the aetiology of oesophageal pain. If the patient Effective therapy for diffuse oesophageal spasm,has co-existing heartburn or regurgitation, a reflux nutcracker oesophagus, non-specific motility Table 1.4 Manometric features of oesophageal motility disorders that may be associated with non-cardiac chest pain Disorder Features Achalasia (see Ch 2) ● Incomplete relaxation of the lower oesophageal sphincter ● Aperistalsis of the oesophageal body Diffuse oesophageal spasm ● Simultaneous contractions (> 10%) ● High-amplitude contractions (> 180 mmHg) ● Repetitive synchronous oesophageal body contractions (> 2 peaks) ● Prolonged oesophageal body contractions (> 6 s) Nutcracker oesophagus ● High-amplitude peristaltic contractions (> 180 mmHg) ● Prolonged oesophageal body contractions (> 6 s) Hypertensive lower oesophageal sphincter Elevated lower oesophageal sphincter pressure (> 45 mmHg) Non-specific motility disorder One or more of the following: ● non-transmitted contractions (> 20%); ● repetitive oesophageal body contractions (> 2 peaks); ● prolonged oesophageal body contractions (> 6 s); ● low-amplitude peristalsis (< 30 mmHg); ● frequent spontaneous contractions.
  25. 25. 14 Clinical gastroenterology: a practical problem-based approachdisorder and hypertensive lower oesophageal Fortunately, most patients with Barrettssphincter is currently not available. Therapeutic oesophagus do not progress and patients intrials of nitrates or a calcium channel blocker are surveillance programs for Barretts oesophagusworthwhile, but should be discontinued if there is usually progress slowly allowing for effectiveno apparent response. intervention using endoscopic or surgical A group of patients will remain for whom no approaches.diagnosis will be achieved after all investigations ● The oesophagus may be the cause of chest painhave been completed and therapeutic trials similar to angina.undertaken. These patients probably have ● Cardiac causes should be carefully excluded invisceral hypersensitivity, a variant of irritable any patient with chest pain prior to consideringbowel syndrome. For the sufferer of chest an oesophageal origin.pain, there is likely to be a significant degree ● Reflux is the most common cause of non-of anxiety because of the fear of possible cardiac chest pain, with some other patientssudden death. Clearly, these patients need to be suffering from spastic oesophageal motilityreassured sympathetically that it is very unlikely disorders such as nutcracker oesophagus orthat their condition, although distressing, diffuse oesophageal spasm.will be progressive or fatal and that continuedobservation is quite appropriate. Some of these Further readingpatients will benefit from antidepressant therapy Cremonini F, Wise J, Moayyedi P, et al. Diagnostic(e.g. low-dose tricyclic antidepressant). and therapeutic use of proton pump inhibitors in non-cardiac chest pain: a metaanalysis. Am JKey Points Gastroenterol 2005; 100:1226–1232.● Heartburn, regurgitation or both are the cardinal Dent J, El-Serag HB, Wallander MA, et al. Epidemiology symptoms of gastro-oesophageal reflux disease of gastro-oesophageal reflux disease: a systematic review. Gut 2005; 54:710–717. (GORD). DeVault KR, Castell DO; American College of● Other GORD-related symptoms may include Gastroenterology. Updated guidelines for the choking attacks, cough, asthma, hoarseness of diagnosis and treatment of gastroesophageal reflux voice, a foul taste in the mouth in the morning, disease. Am J Gastroenterol 2005; 100:190–200. bad breath, a sore tongue, dental caries and DeVault KR, Talley NJ. Insights into the future of gastric acid suppression. Nature Rev Gastroenterol Hepatol nasal aspiration. 2009; 6:524–532.● Dysphagia related to reflux is usually caused by El-Serag H, Becher A, Jones R. Systematic review: a benign stricture, but endoscopy is required persistent reflux symptoms on proton pump to rule out malignant causes and also allows inhibitor therapy in primary care and community dilation of any stricture. studies. Aliment Pharmacol Ther 2010; 32:720–737. Johnson DA, Fennerty MB. Heartburn severity● Endoscopy is required in GORD patients underestimates erosive esophagitis severity in with alarm features such as vomiting, elderly patients with gastroesophageal reflux disease. bleeding, weight loss or dysphagia. Patients Gastroenterology 2004; 126:660–664. with long-standing symptoms are at risk for Kahrilas PJ, Shaheen NY, Vaezi MF, et al. American Barretts oesophagus and should also undergo Gastroenterological Association Institute technical endoscopy. review on the management of gastroesophageal reflux disease. Gastroenterology 2008; 135:1392–413.● Ambulatory reflux testing is used to confirm Sharma P, McQuaid K, Dent J et al. A critical review of the or refute reflux in difficult cases, particularly diagnosis and management of Barretts esophagus: when surgery is being considered. the AGA Chicago Workshop. Gastroenterology 2004;● The combination of lifestyle changes and 127:310–330. medical therapy (usually with a once-daily Shaheen NJ, Sharma P, Overholt BF, et al. Radiofrequency ablation in Barretts esophagus with dysplasia. New proton pump inhibitor) will control GORD in Engl J Med 2009; 360:2277–2288. the vast majority of patients. Wang KK, Sampliner RE. Updated guidelines 2008 for● Barretts oesophagus is a consequence of GORD the diagnosis, surveillance and therapy of Barretts and places patients at an increased risk of esophagus. Am J Gastroenterol 2008; 103:788–797. developing adenocarcinoma of the oesophagus.