1. HARRISON’SGastroenterology and Hepatology
2. Derived from Harrison’s Principles of Internal Medicine, 17th Edition EditorsANTHONY S. FAUCI, MD EUGENE BRAUNWALD, MDChief, Laboratory of Immunoregulation; Distinguished Hersey Professor of Medicine,Director, National Institute of Allergy and Infectious Diseases, Harvard Medical School; Chairman,TIMI Study Group,National Institutes of Health, Bethesda Brigham and Women’s Hospital, BostonDENNIS L. KASPER, MD STEPHEN L. HAUSER, MDWilliam Ellery Channing Professor of Medicine, Robert A. Fishman Distinguished Professor and Chairman,Professor of Microbiology and Molecular Genetics, Department of Neurology,Harvard Medical School; Director, Channing Laboratory, University of California, San FranciscoDepartment of Medicine,Brigham and Women’s Hospital, Boston J. LARRY JAMESON, MD, PhD Professor of Medicine; Vice President for MedicalDAN L. LONGO, MD Affairs and Lewis Landsberg Dean,Scientiﬁc Director, National Institute on Aging, Northwestern University FeinbergNational Institutes of Health, Bethesda and Baltimore School of Medicine, Chicago JOSEPH LOSCALZO, MD, PhD Hersey Professor of Theory and Practice of Medicine, Harvard Medical School; Chairman, Department of Medicine; Physician-in-Chief, Brigham and Women’s Hospital, Boston
3. HARRISON’SGastroenterology and Hepatology Editors Dan L. Longo, MD Scientiﬁc Director, National Institute on Aging, National Institutes of Health, Bethesda and Baltimore Anthony S. Fauci, MD Chief, Laboratory of Immunoregulation; Director, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda Associate Editor Carol A. Langford, MD, MHS Associate Professor of Medicine Cleveland Clinic, Cleveland New York Chicago San Francisco Lisbon London Madrid Mexico City Milan New Delhi San Juan Seoul Singapore Sydney Toronto
5. CONTENTSContributors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ix SECTION III DISORDERS OF THE ALIMENTARY TRACTPreface . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . xiii 13 Diseases of the Esophagus . . . . . . . . . . . . . . . . 112 SECTION I Raj K. Goyal CARDINAL MANIFESTATIONS OF 14 Peptic Ulcer Disease and Related Disorders . . . 125 GASTROINTESTINAL DISEASE John Del Valle 1 Abdominal Pain . . . . . . . . . . . . . . . . . . . . . . . . . 2 15 Disorders of Absorption. . . . . . . . . . . . . . . . . . 152 William Silen Henry J. Binder 2 Oral Manifestations of Disease . . . . . . . . . . . . . . . 8 16 Inﬂammatory Bowel Disease . . . . . . . . . . . . . . 174 Samuel C. Durso Sonia Friedman, Richard S. Blumberg 3 Atlas of Oral Manifestations of Disease . . . . . . . . 21 17 Irritable Bowel Syndrome . . . . . . . . . . . . . . . . 196 Samuel C. Durso, Janet A.Yellowitz, Jane C.Atkinson Chung Owyang 4 Dysphagia. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 27 18 Diverticular Disease and Common Raj K. Goyal Anorectal Disorders . . . . . . . . . . . . . . . . . . . . . 203 Susan L. Gearhart 5 Nausea,Vomiting, and Indigestion . . . . . . . . . . . 33 William L. Hasler 19 Mesenteric Vascular Insufﬁciency . . . . . . . . . . . 213 Susan L. Gearhart 6 Diarrhea and Constipation. . . . . . . . . . . . . . . . . 42 Michael Camilleri, Joseph A. Murray 20 Acute Intestinal Obstruction . . . . . . . . . . . . . . 218 Susan L. Gearhart,William Silen 7 Weight Loss . . . . . . . . . . . . . . . . . . . . . . . . . . . 58 Carol M. Reife 21 Acute Appendicitis and Peritonitis . . . . . . . . . . 222 Susan L. Gearhart,William Silen 8 Gastrointestinal Bleeding . . . . . . . . . . . . . . . . . . 62 Loren Laine SECTION IV 9 Jaundice . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 68 INFECTIONS OF THE ALIMENTARY TRACT Daniel S. Pratt, Marshall M. Kaplan 22 Acute Infectious Diarrheal Diseases10 Abdominal Swelling and Ascites . . . . . . . . . . . . . 77 and Bacterial Food Poisoning. . . . . . . . . . . . . . 228 Robert M. Glickman, Roshini Rajapaksa Joan R. Butterton, Stephen B. Calderwood 23 Clostridium Difﬁcile–Associated Disease, SECTION II Including Pseudomembranous Colitis. . . . . . . . 238 Dale N. Gerding, Stuart Johnson EVALUATION OF THE PATIENT WITH ALIMENTARY TRACT SYMPTOMS 24 Intraabdominal Infections and Abscesses . . . . . . 244 Miriam J. Baron, Dennis L. Kasper11 Approach to the Patient with Gastrointestinal Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 84 25 Helicobacter Pylori Infections . . . . . . . . . . . . . . . 253 William L. Hasler, Chung Owyang John C.Atherton, Martin J. Blaser12 Gastrointestinal Endoscopy . . . . . . . . . . . . . . . . 94 26 Salmonellosis. . . . . . . . . . . . . . . . . . . . . . . . . . 260 Louis Michel Wong-Kee-Song, Mark Topazian David A. Pegues, Samuel I. Miller v
6. vi Contents27 Shigellosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . 270 42 Genetic, Metabolic, and Inﬁltrative Philippe Sansonetti, Jean Bergounioux Diseases Affecting the Liver . . . . . . . . . . . . . . . 434 Bruce R. Bacon28 Infections Due to Campylobacter and Related Species. . . . . . . . . . . . . . . . . . . . . 276 43 Diseases of the Gallbladder and Bile Ducts . . . . 439 Martin J. Blaser Norton J. Greenberger, Gustav Paumgartner29 Cholera and Other Vibrioses . . . . . . . . . . . . . . 281 Matthew K.Waldor, Gerald T. Keusch SECTION VII LIVER TRANSPLANTATION30 Viral Gastroenteritis. . . . . . . . . . . . . . . . . . . . . 289 Umesh D. Parashar, Roger I. Glass 44 Liver Transplantation . . . . . . . . . . . . . . . . . . . . 458 Jules L. Dienstag, Raymond T. Chung31 Amebiasis and Infection with Free-Living Amebas. . . . . . . . . . . . . . . . . . . . . 296 SECTION VIII Sharon L. Reed DISORDERS OF THE PANCREAS32 Protozoal Intestinal Infections 45 Approach to the Patient with and Trichomoniasis . . . . . . . . . . . . . . . . . . . . . 304 Pancreatic Disease . . . . . . . . . . . . . . . . . . . . . . 472 Peter F. Weller Phillip P Toskes, Norton J. Greenberger .33 Intestinal Nematodes . . . . . . . . . . . . . . . . . . . . 312 46 Acute and Chronic Pancreatitis . . . . . . . . . . . . 479 Peter F. Weller,Thomas B. Nutman Norton J. Greenberger, Phillip P. Toskes SECTION V SECTION IX EVALUATION OF THE PATIENT NEOPLASTIC DISEASES OF THE WITH LIVER DISEASE GASTROINTESTINAL SYSTEM34 Approach to the Patient with 47 Gastrointestinal Tract Cancer . . . . . . . . . . . . . . 500 Liver Disease . . . . . . . . . . . . . . . . . . . . . . . . . . 322 Robert J. Mayer Marc Ghany, Jay H. Hoofnagle 48 Tumors of the Liver and Biliary Tree . . . . . . . . 51735 Evaluation of Liver Function . . . . . . . . . . . . . . 332 Brian I. Carr Daniel S. Pratt, Marshall M. Kaplan 49 Pancreatic Cancer . . . . . . . . . . . . . . . . . . . . . . 528 Yu Jo Chua, David Cunningham SECTION VI 50 Endocrine Tumors of the Gastrointestinal DISORDERS OF THE LIVER Tract and Pancreas . . . . . . . . . . . . . . . . . . . . . . 533 AND BILIARY TREE Robert T. Jensen36 The Hyperbilirubinemias. . . . . . . . . . . . . . . . . 340 SECTION X Allan W Wolkoff . NUTRITION37 Acute Viral Hepatitis . . . . . . . . . . . . . . . . . . . . 349 Jules L. Dienstag 51 Nutritional Requirements and Dietary Assessment . . . . . . . . . . . . . . . . . . . . . . . . . . . 55438 Toxic and Drug-Induced Hepatitis . . . . . . . . . . 378 Johanna Dwyer Jules L. Dienstag 52 Vitamin and Trace Mineral Deﬁciency39 Chronic Hepatitis . . . . . . . . . . . . . . . . . . . . . . 390 and Excess . . . . . . . . . . . . . . . . . . . . . . . . . . . 562 Jules L. Dienstag Robert M. Russell, Paolo M. Suter40 Alcoholic Liver Disease . . . . . . . . . . . . . . . . . . 415 53 Malnutrition and Nutritional Assessment . . . . . 577 Mark E. Mailliard, Michael F Sorrell . Douglas C. Heimburger41 Cirrhosis and Its Complications . . . . . . . . . . . . 419 54 Enteral and Parenteral Nutrition Therapy . . . . . 586 Bruce R. Bacon Bruce R. Bistrian, David F. Driscoll
7. Contents vii SECTION XI Appendix OBESITY AND EATING DISORDERS Laboratory Values of Clinical Importance . . . . . 635 Alexander Kratz, Michael A. Pesce, Daniel J. Fink55 Biology of Obesity . . . . . . . . . . . . . . . . . . . . . 600 Jeffrey S. Flier, Eleftheria Maratos-Flier Review and Self-Assessment . . . . . . . . . . . . . . . 65556 Evaluation and Management of Obesity . . . . . . 610 Charles Wiener, Gerald Bloomﬁeld, Cynthia D. Brown, Robert F. Kushner Joshua Schiffer,Adam Spivak57 Eating Disorders . . . . . . . . . . . . . . . . . . . . . . . 619 Index. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 703 B.Timothy Walsh58 The Metabolic Syndrome . . . . . . . . . . . . . . . . 626 Robert H. Eckel
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9. CONTRIBUTORSNumbers in brackets refer to the chapter(s) written or co-written by the contributor.JOHN C. ATHERTON, MD BRIAN I. CARR, MD, PhDProfessor of Gastroenterology; Director,Wolfson Digestive Professor of Medicine,Thomas Jefferson University; Director of theDiseases Centre, University of Nottingham, United Kingdom  Liver Tumor Program, Kimmel Cancer Center, Philadelphia JANE C. ATKINSON, DDS YU JO CHUA, MBBSProgram Director, Clinical Trials Program, Center for Clinical Research Fellow (Medical Oncology), Royal Marsden Hospital,Research, National Institute of Dental and Craniofacial Research, London National Institutes of Health, Bethesda  RAYMOND T. CHUNG, MDBRUCE R. BACON, MD Associate Professor of Medicine, Harvard Medical School; DirectorJames F. King Endowed Chair in Gastroenterology; Professor of of Hepatology, Massachusetts General Hospital; Medical Director,Internal Medicine, Division of Gastroenterology & Hepatology, Liver Transplant Program, Massachusetts General Hospital,St. Louis [41, 42] Boston MIRIAM J. BARON, MD DAVID CUNNINGHAM, MDInstructor in Medicine, Harvard Medical School, Boston  Professor of Cancer Medicine, Institute of Cancer Research; Consultant Medical Oncologist, Head of Gastrointestinal Unit,JEAN BERGOUNIOUX, MD Royal Marsden Hospital, London Medical Doctor of Pediatrics, Unité de Pathogénie MicrobienneMoléculaire, Paris  JOHN DEL VALLE, MD Professor and Senior Associate Chair of Graduate Medical Education,HENRY J. BINDER, MD Department of Internal Medicine, Division of Gastroenterology,Professor of Medicine; Professor of Cellular & Molecular Physiology, University of Michigan Health System,Ann Arbor Yale University, New Haven  JULES L. DIENSTAG, MDBRUCE R. BISTRIAN, MD, PhD Carl W.Walter Professor of Medicine and Dean for MedicalChief, Clinical Nutrition, Beth Israel Deaconess Medical Center; Education, Harvard Medical School; Physician, Gastrointestinal Unit,Professor of Medicine, Harvard Medical School, Boston  Massachusetts General Hospital, Boston [37–39, 44]MARTIN J. BLASER, MD DAVID F. DRISCOLL, PhDFrederick H. King Professor of Internal Medicine; Chair, Assistant Professor of Medicine, Harvard Medical School, Boston Department of Medicine; Professor of Microbiology, New YorkUniversity School of Medicine, New York [25, 28] SAMUEL C. DURSO, MD, MBA Associate Professor of Medicine, Clinical Director, Division ofGERALD BLOOMFIELD, MD, MPH Geriatric Medicine and Gerontology,The Johns Hopkins UniversityDepartment of Internal Medicine,The Johns Hopkins University School of Medicine, Baltimore [2, 3]School of Medicine, Baltimore [Review and Self-Assessment] JOHANNA DWYER, DSc, RDRICHARD S. BLUMBERG, MD Professor of Medicine and Community Health,Tufts UniversityProfessor of Medicine, Harvard Medical School; Chief, Division School of Medicine and Friedman School of Nutrition Science andof Gastroenterology, Hepatology and Endoscopy, Brigham and Policy; Senior Scientist Jean Mayer Human Nutrition ResearchWomen’s Hospital, Boston  Center on Aging at Tufts; Director of the Frances Stern Nutrition Center,Tufts-New England Medical Center Hospital, Boston CYNTHIA D. BROWN, MDDepartment of Internal Medicine,The Johns Hopkins University ROBERT H. ECKEL, MDSchool of Medicine, Baltimore [Review and Self-Assessment] Professor of Medicine, Division of Endocrinology, Metabolism and Diabetes, Division of Cardiology; Professor of Physiology andJOAN R. BUTTERTON, MD Biophysics; Charles A. Boettcher II Chair in Atherosclerosis; ProgramAssistant Clinical Professor of Medicine, Harvard Medical School; Director,Adult General Clinical Research Center, University ofClinical Associate in Medicine, Massachusetts General Hospital, Colorado at Denver and Health Sciences Center; Director LipidBoston  Clinic, University Hospital,Aurora STEPHEN B. CALDERWOOD, MD DANIEL J. FINK,† MD, MPHMorton N. Swartz, MD Academy Professor of Medicine Associate Professor of Clinical Pathology, College of Physicians(Microbiology and Molecular Genetics), Harvard Medical School; and Surgeons, Columbia University, New York [Appendix]Chief, Division of Infectious Diseases, Massachusetts GeneralHospital, Boston  JEFFREY S. FLIER, MDMICHAEL CAMILLERI, MD Caroline Shields Walker Professor of Medicine, Harvard MedicalAtherton and Winifred W. Bean Professor; Professor of Medicine School; Dean of the Faculty of Medicine, Harvard School ofand Physiology, Mayo Clinic College of Medicine, Rochester  Medicine, Boston  † Deceased. ix
10. x ContributorsSONIA FRIEDMAN, MD GERALD T. KEUSCH, MDAssistant Professor of Medicine, Harvard Medical School;Associate Associate Provost and Associate Dean for Global Health, BostonPhysician, Brigham and Women’s Hospital, Boston  University School of Medicine, Boston SUSAN L. GEARHART, MD ALEXANDER KRATZ, MD, PhD, MPHAssistant Professor of Colorectal Surgery and Oncology,The Johns Assistant Professor of Clinical Pathology, Columbia University CollegeHopkins University School of Medicine, Baltimore [18–21] of Physicians and Surgeons;Associate Director, Core Laboratory, Columbia University Medical Center, New York-PresbyterianDALE N. GERDING, MD Hospital; Director,Allen Pavilion Laboratory, New York [Appendix]Assistant Chief of Staff for Research, Hines VA Hospital,Hines; Professor, Stritch School of Medicine, ROBERT F. KUSHNER, MDLoyola University, Maywood  Professor of Medicine, Northwestern University Feinberg School of Medicine, Chicago MARC GHANY, MDStaff Physician, Liver Diseases Branch, National Institute of Diabetes LOREN LAINE, MDand Digestive and Kidney Diseases, National Institutes of Health, Professor of Medicine, Keck School of Medicine, UniversityBethesda  of Southern California, Los Angeles ROGER I. GLASS, MD, PhD MARK E. MALLIARD, MDDirector, Fogarty International Center;Associate Director for Associate Professor and Chief, Division of GastroenterologyInternational Research, National Institutes of Health, Bethesda  and Hepatology, Omaha ROBERT M. GLICKMAN, MD ELEFTHERIA MARATOS-FLIER, MDProfessor of Medicine, New York University School of Medicine, Associate Professor of Medicine, Harvard Medical School; Chief,New York  Obesity Section, Joslin Diabetes Center, Boston RAJ K. GOYAL, MD ROBERT J. MAYER, MDMallinckrodt Professor of Medicine, Harvard Medical School, Stephen B. Kay Family Professor of Medicine, Harvard MedicalBoston; Physician,VA Boston Healthcare and Beth Israel Deaconess School, Dana- Farber Cancer Institute, Boston Medical Center,West Roxbury [4, 13] SAMUEL I. MILLER, MDNORTON J. GREENBERGER, MD Professor of Genome Sciences, Medicine, and Microbiology,Clinical Professor of Medicine, Harvard Medical School; Senior University of Washington, Seattle Physician, Brigham and Women’s Hospital, Boston [43, 45, 46] JOSEPH A. MURRAY, MDWILLIAM L. HASLER, MD Professor of Medicine, Division of Gastroenterology and Hepatology,Professor of Medicine, Division of Gastroenterology, University The Mayo Clinic, Rochester of Michigan Health System,Ann Arbor [5, 11] THOMAS B. NUTMAN, MDDOUGLAS C. HEIMBURGER, MD, MS Head, Helminth Immunology Section; Head, Clinical ParasitologyProfessor of Nutrition Sciences; Professor of Medicine; Director, Unit; Laboratory of Parasitic Diseases, National Institute ofClinical Nutrition Fellowship Program, University of Alabama at Allergy and Infectious Diseases, National Insitutes of Health,Birmingham, Birmingham  Bethesda JAY H. HOOFNAGLE, MDDirector, Liver Diseases Research Branch, CHUNG OWYANG, MDDivision of Digestive Diseases and Nutrition, Professor of Internal Medicine, H. Marvin Pollard CollegiateNational Institute of Diabetes and Digestive and Kidney Diseases, Professor; Chief, Division of Gastroenterology, University ofNational Institutes of Health, Bethesda  Michigan Health System,Ann Arbor [11, 17]ROBERT T. JENSEN, MD UMESH D. PARASHAR, MBBS, MPHChief, Digestive Diseases Branch, National Institute of Diabetes, Lead, Enteric and Respiratory Viruses Team, Epidemiology Branch,Digestive and Kidney Diseases, National Institutes of Health, Division of Viral Diseases, National Center for Immunization andBethesda  Respiratory Diseases, Centers for Disease Control and Prevention, Atlanta STUART JOHNSON, MDAssociate Professor, Stritch School of Medicine, Loyola University, GUSTAV PAUMGARTNER, MDMaywood; Staff Physician, Hines VA Hospital, Hines  Professor of Medicine, University of Munich, Munich, Germany MARSHALL M. KAPLAN, MDProfessor of Medicine,Tufts University School of Medicine; Chief DAVID A. PEGUES, MDEmeritus, Division of Gastroenterology,Tufts-New England Medical Professor of Medicine, Division of Infectious Diseases, David GeffenCenter, Boston [9, 35] School of Medicine at UCLA, Los Angeles DENNIS L. KASPER, MD, MA (Hon) MICHAEL A. PESCE, PhDWilliam Ellery Channing Professor of Medicine, Professor of Clinical Professor of Pathology, Columbia University College ofMicrobiology and Molecular Genetics, Harvard Medical School; Physicians and Surgeons; Director of Specialty Laboratory, New YorkDirector, Channing Laboratory, Department of Medicine, Brigham Presbyterian Hospital, Columbia University Medical Center,and Women’s Hospital, Boston  New York [Appendix]
11. Contributors xiDANIEL S. PRATT, MD MARK TOPAZIAN, MDAssistant Professor of Medicine, Harvard Medical School; Director, Associate Professor of Medicine, Mayo College of Medicine,Liver- Billary-Pancreas Center, Massachusetts General Hospital, Rochester Boston [9, 35] PHILLIP P. TOSKES, MDROSHINI RAJAPAKSA, MD, BA Professor of Medicine, Division of Gastroenterology, HepatologyAssistant Professor, Department of Medicine, Gastroenterology, New and Nutrition, University of Florida College of Medicine,York University Medical Center School of Medicine and Hospitals Gainesville [45, 46]Center, New York  MATTHEW K. WALDOR, MD, PhDSHARON L. REED, MD Professor of Medicine (Microbiology and Molecular Genetics),Professor of Pathology and Medicine; Director, Microbiology and Channing Laboratory, Brigham and Women’s Hospital, HarvardVirology Laboratories, University of California, San Diego Medical Medical School, Boston Center, San Diego  B. TIMOTHY WALSH, MDCAROL M. REIFE, MD Professor of Psychiatry, College of Physicians & Surgeons, ColumbiaClinical Associate Professor of Medicine, Jefferson Medical College, University; Director, Eating Disorders Research Unit, New YorkPhiladelphia  Psychiatric Institute, New York  PETER F. WELLER, MDROBERT M. RUSSELL, MD Professor of Medicine, Harvard Medical School; Co-Chief,Director, Jean Mayer USDA Human Nutrition Research Center on Infectious Diseases Division; Chief,Allergy and InﬂammationAging at Tufts University; Professor of Medicine and Nutrition,Tufts Division;Vice-Chair for Research, Department of Medicine, BethUniversity, Boston  Israel Deaconess Medical Center, Boston [32, 33]PHILIPPE SANSONETTI CHARLES WIENER, MDProfesseur á l’Institut Pasteur, Paris, France  Professor of Medicine and Physiology;Vice Chair, Department of Medicine; Director,JOSHUA SCHIFFER, MD Osler Medical Training Program,Department of Internal Medicine,The Johns Hopkins University The Johns Hopkins University School of Medicine, BaltimoreSchool of Medicine, Baltimore [Review and Self-Assessment] [Review and Self-Assessment]WILLIAM SILEN, MD ALLAN W. WOLKOFF, MDJohnson and Johnson Distinguished Professor of Surgery, Emeritus, Professor of Medicine and Anatomy and Structural Biology;Harvard Medical School, Boston [1, 20, 21] Director, Belfer Institute for Advanced Biomedical Studies; Associate Chair of Medicine for Research; Chief, Division of Hepatology,MICHAEL F. SORRELL, MD Albert Einstein College of Medicine, Bronx Robert L. Grissom Professor of Medicine, University of NebraskaMedical Center, Omaha  LOUIS MICHEL WONG-KEE-SONG, MD Assistant Professor of Medicine, Division of GastroenterologyADAM SPIVAK, MD and Hepatology, Mayo College of Medicine, Rochester Department of Internal Medicine,The Johns Hopkins UniversitySchool of Medicine, Baltimore [Review and Self-Assessment] JANET A.YELLOWITZ, DMD, MPH Associate Professor; Director, Geriatric Dentistry,The Johns HopkinsPAOLO M. SUTER, MD, MS University School of Medicine, Baltimore Professor of Medicine, Medical Policlinic, Zurich, Switzerland 
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13. PREFACEHarrison’s Principles of Internal Medicine (HPIM) has long This book is aimed at bringing together the chap-been a major source of information related to the prac- ters of HPIM related to gastroenterology and hepatol-tice of medicine for many practitioners and trainees.Yet ogy in a conveniently sized book for a focused studyin its aim to cover the broad spectrum of medicine, the of this medical subspecialty. The book is organizedbook has become nearly 3000 pages in length and is into 58 chapters and 11 sections: (I) Cardinal Manifes-pushing the envelope of “portability.” HPIM has tations of Gastrointestinal Disease; (II) Evaluation ofspawned several offspring tailored to diverse uses for the Patient with Alimentary Tract Symptoms; (III)sources of medical information. The entire book plus a Disorders of the Alimentary Tract; (IV) Infections oflarge cache of supplemental visual and textual informa- the Alimentary Tract; (V) Evaluation of the Patienttion is available as Harrison’s Online, a component of with Liver Disease; (VI) Disorders of the Liver andMcGraw-Hill’s Access Medicine offering. A condensed Biliary Tree; (VII) Liver Transplantation; (VIII) Disor-version of HPIM, called Harrison’s Manual of Medicine, ders of the Pancreas; (IX) Neoplastic Diseases of thehas been published in print format suitable for carrying Gastrointestinal System; (X) Nutrition; and (XI) Obe-in a white coat pocket and in several electronic formats sity and Eating Disorders.(PDA, Blackberry, iPhone). A companion to HPIM that The information presented here is contributed byserves as a study guide for standardized tests in medicine, physician/authors who have personally made notableHPIM Self-Assessment and Board Review, is an effective advances in the ﬁelds of their expertise. The chaptersteaching tool that highlights important areas of medi- reﬂect authoritative analyses by individuals who havecine discussed in HPIM. Harrison’s Practice is another been active participants in the amazing surge of newelectronic information source, organized by medical information on genetics, cell biology, pathophysiology,topic or diagnosis with information presented in a con- and treatment that has characterized all of medicine insistent structured format for ease of ﬁnding speciﬁc the last 20 years. In addition to the didactic value of theinformation to facilitate clinical care and decision-making chapters, a section of test questions, answers, and anat the bedside. All of these products retain the broad explanation of the correct answers is provided to facilitatespectrum of topics presented in the HPIM “mother learning and assist the reader in preparing for standard-book” in variable degrees of depth. ized examinations. In 2006, for the first time, the Editors of HPIM Gastroenterology and hepatology, like many otherexperimented with extracting portions of HPIM that were areas of medicine, are changing rapidly. Novel technolo-focused on a speciﬁc subspecialty of internal medicine. gies of imaging, development of new drugs, and theThe products of that effort, Harrison’s Endocrinology, Har- application of molecular pathogenesis information torison’s Rheumatology, and Harrison’s Neurology in Clinical detect disease early and prevent disease in people at riskMedicine, were very well-received by audiences keenly in- are just a few of the advances that have made an impactterested in the respective subspecialities of internal medi- on the practice of gastroenterology. Physicians are nowcine. Accordingly, we are expanding the effort to include applying endoscopic techniques in ways that were oncebooks focused on other specialties. unimaginable including performing operations success- According to a report from the National Institute of fully without an incision; operations that once requiredDiabetes and Digestive and Kidney Diseases, for every major surgery with attendant morbidity and expense.100 residents of the United States, there were 35 ambu- The pace of discovery demands that physicians under-latory care contacts and 5 overnight hospital stays at take nearly continuous self-education. It is our hope thatwhich a digestive disease diagnosis was noted. In 2004, this book will help physicians in this process.digestive diseases accounted for more than 236,000 We are grateful to Kim Davis and James Shanahan atdeaths. Thus, training in the disciplines of gastroenterol- McGraw-Hill for their help in producing this book.ogy and hepatology is essential to any primary carephysician or general internist and even to practitioners Dan L. Longo, MDof other internal medicine subspecialties. Anthony S. Fauci, MD xiii
14. NOTICE Medicine is an ever-changing science. As new research and clinical experi- ence broaden our knowledge, changes in treatment and drug therapy are required.The authors and the publisher of this work have checked with sources believed to be reliable in their efforts to provide information that is complete and generally in accord with the standards accepted at the time of publica- tion. However, in view of the possibility of human error or changes in med- ical sciences, neither the authors nor the publisher nor any other party who has been involved in the preparation or publication of this work warrants that the information contained herein is in every respect accurate or complete, and they disclaim all responsibility for any errors or omissions or for the results obtained from use of the information contained in this work. Readers are encouraged to conﬁrm the information contained herein with other sources. For example and in particular, readers are advised to check the prod- uct information sheet included in the package of each drug they plan to administer to be certain that the information contained in this work is accu- rate and that changes have not been made in the recommended dose or in the contraindications for administration. This recommendation is of particular importance in connection with new or infrequently used drugs. Review and self-assessment questions and answers were taken from Wiener C, Fauci AS, Braunwald E, Kasper DL, Hauser SL, Longo DL, Jameson JL, Loscalzo J (editors) Bloomﬁeld G, Brown CD, Schiffer J, Spivak A (contributing editors). Har- rison’s Principles of Internal Medicine Self-Assessment and Board Review, 17th ed. New York, McGraw-Hill, 2008, ISBN 978-0-07-149619-3.The global icons call greater attention to key epidemiologic and clinical differences in the practice of medicinethroughout the world.The genetic icons identify a clinical issue with an explicit genetic relationship. xiv
15. SECTION I CARDINALMANIFESTATIONS OFGASTROINTESTINAL DISEASE
16. CHAPTER 1 ABDOMINAL PAIN William Silen ■ Some Mechanisms of Pain Originating in the Abdomen . . . . . . 2 ■ Referred Pain in Abdominal Diseases . . . . . . . . . . . . . . . . . . . . 4 ■ Metabolic Abdominal Crises . . . . . . . . . . . . . . . . . . . . . . . . . . . 5 ■ Neurogenic Causes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5 ■ Further Readings . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7The correct interpretation of acute abdominal pain is the type and amount of material to which the peritonealchallenging. Since proper therapy may require urgent surfaces are exposed in a given time period. For example,action, the unhurried approach suitable for the study of the sudden release into the peritoneal cavity of a smallother conditions is sometimes denied. Few other clinical quantity of sterile acid gastric juice causes much moresituations demand greater judgment, because the most pain than the same amount of grossly contaminated neu-catastrophic of events may be forecast by the subtlest of tral feces. Enzymatically active pancreatic juice incitessymptoms and signs. A meticulously executed, detailed more pain and inﬂammation than does the same amounthistory and physical examination are of great impor- of sterile bile containing no potent enzymes. Blood andtance.The etiologic classiﬁcation in Table 1-1, although urine are often so bland as to go undetected if their con-not complete, forms a useful basis for the evaluation of tact with the peritoneum has not been sudden and mas-patients with abdominal pain. sive. In the case of bacterial contamination, such as in The diagnosis of “acute or surgical abdomen” is not pelvic inﬂammatory disease, the pain is frequently of lowan acceptable one because of its often misleading and intensity early in the illness until bacterial multiplicationerroneous connotation. The most obvious of “acute has caused the elaboration of irritating substances.abdomens” may not require operative intervention, and The rate at which the irritating material is applied tothe mildest of abdominal pains may herald an urgently the peritoneum is important. Perforated peptic ulcercorrectable lesion. Any patient with abdominal pain of may be associated with entirely different clinical picturesrecent onset requires early and thorough evaluation and dependent only on the rapidity with which the gastricaccurate diagnosis. juice enters the peritoneal cavity. The pain of peritoneal inﬂammation is invariably accentuated by pressure or changes in tension of the peritoneum, whetherSOME MECHANISMS OF PAIN produced by palpation or by movement, as in coughingORIGINATING IN THE ABDOMEN or sneezing. The patient with peritonitis lies quietly in bed, preferring to avoid motion, in contrast to the patientInﬂammation of the Parietal Peritoneum with colic, who may writhe incessantly.The pain of parietal peritoneal inﬂammation is steady Another characteristic feature of peritoneal irritationand aching in character and is located directly over the is tonic reﬂex spasm of the abdominal musculature, local-inﬂamed area, its exact reference being possible because ized to the involved body segment. The intensity of theit is transmitted by somatic nerves supplying the parietal tonic muscle spasm accompanying peritoneal inﬂamma-peritoneum. The intensity of the pain is dependent on tion is dependent on the location of the inﬂammatory 2
17. TABLE 1-1 3 SOME IMPORTANT CAUSES OF ABDOMINAL PAIN PAIN ORIGINATING IN THE ABDOMEN CHAPTER 1 Parietal peritoneal inﬂammation Vascular disturbances Bacterial contamination Embolism or thrombosis Perforated appendix or other perforated Vascular rupture viscus Pressure or torsional occlusion Pelvic inﬂammatory disease Sickle cell anemia Chemical irritation Abdominal wall Abdominal Pain Perforated ulcer Distortion or traction of mesentery Pancreatitis Trauma or infection of muscles Mittelschmerz Distension of visceral surfaces, e.g., by hemorrhage Mechanical obstruction of hollow viscera Hepatic or renal capsules Obstruction of the small or large Inﬂammation of a viscus intestine Appendicitis Obstruction of the biliary tree Typhoid fever Obstruction of the ureter Typhlitis PAIN REFERRED FROM EXTRAABDOMINAL SOURCE Cardiothoracic Pneumothorax Acute myocardial infarction Empyema Myocarditis, endocarditis, pericarditis Esophageal disease, spasm, rupture, inﬂammation Congestive heart failure Genitalia Pneumonia Torsion of the testis Pulmonary embolus Pleurodynia METABOLIC CAUSES Diabetes Familial Mediterranean fever Uremia Porphyria Hyperlipidemia C1-esterase inhibitor deﬁciency (angioneurotic edema) Hyperparathyroidism Acute adrenal insufﬁciency NEUROLOGIC/PSYCHIATRIC CAUSES Herpes zoster Spinal cord or nerve root compression Tabes dorsalis Functional disorders Causalgia Psychiatric disorders Radiculitis from infection or arthritis TOXIC CAUSES Lead poisoning Black widow spiders Insect or animal envenomations Snake bites UNCERTAIN MECHANISMS Narcotic withdrawal Heat strokeprocess, the rate at which it develops, and the integrity of Obstruction of Hollow Viscerathe nervous system. Spasm over a perforated retrocecal The pain of obstruction of hollow abdominal viscera isappendix or perforated ulcer into the lesser peritoneal classically described as intermittent, or colicky. Yet thesac may be minimal or absent because of the protective lack of a truly cramping character should not be mislead-effect of overlying viscera. A slowly developing process ing, because distention of a hollow viscus may produceoften greatly attenuates the degree of muscle spasm. Cat- steady pain with only very occasional exacerbations. It isastrophic abdominal emergencies such as a perforated not nearly as well localized as the pain of parietal peri-ulcer may be associated with minimal or no detectable toneal inﬂammation.pain or muscle spasm in obtunded, seriously ill, debili- The colicky pain of obstruction of the small intestinetated elderly patients or in psychotic patients. is usually periumbilical or supraumbilical and is poorly
18. 4 localized. As the intestine becomes progressively dilated of continuous, diffuse pain in a patient likely to have with loss of muscular tone, the colicky nature of the vascular disease is quite characteristic of occlusion of the pain may diminish. With superimposed strangulating superior mesenteric artery. Abdominal pain with radia-SECTION I obstruction, pain may spread to the lower lumbar region tion to the sacral region, ﬂank, or genitalia should always if there is traction on the root of the mesentery.The col- signal the possible presence of a rupturing abdominal icky pain of colonic obstruction is of lesser intensity aortic aneurysm. This pain may persist over a period of than that of the small intestine and is often located in several days before rupture and collapse occur. the infraumbilical area. Lumbar radiation of pain is com- mon in colonic obstruction. Abdominal Wall Cardinal Manifestations of Gastrointestinal Disease Sudden distention of the biliary tree produces a steady rather than colicky type of pain; hence the term biliary Pain arising from the abdominal wall is usually constant colic is misleading. Acute distention of the gallbladder and aching. Movement, prolonged standing, and pressure usually causes pain in the right upper quadrant with accentuate the discomfort and muscle spasm. In the case radiation to the right posterior region of the thorax or of hematoma of the rectus sheath, now most frequently to the tip of the right scapula, and distention of the encountered in association with anticoagulant therapy, a common bile duct is often associated with pain in the mass may be present in the lower quadrants of the epigastrium radiating to the upper part of the lumbar abdomen. Simultaneous involvement of muscles in other region. Considerable variation is common, however, so parts of the body usually serves to differentiate myositis that differentiation between these may be impossible. of the abdominal wall from an intraabdominal process The typical subscapular pain or lumbar radiation is fre- that might cause pain in the same region. quently absent. Gradual dilatation of the biliary tree, as in carcinoma of the head of the pancreas, may cause no pain or only a mild aching sensation in the epigastrium REFERRED PAIN IN ABDOMINAL or right upper quadrant. The pain of distention of the DISEASES pancreatic ducts is similar to that described for disten- tion of the common bile duct but, in addition, is very Pain referred to the abdomen from the thorax, spine, or frequently accentuated by recumbency and relieved by genitalia may prove a vexing diagnostic problem, the upright position. because diseases of the upper part of the abdominal cav- Obstruction of the urinary bladder results in dull ity such as acute cholecystitis or perforated ulcer are fre- suprapubic pain, usually low in intensity. Restlessness quently associated with intrathoracic complications. A without speciﬁc complaint of pain may be the only sign most important, yet often forgotten, dictum is that the of a distended bladder in an obtunded patient. In con- possibility of intrathoracic disease must be considered in trast, acute obstruction of the intravesicular portion of every patient with abdominal pain, especially if the pain the ureter is characterized by severe suprapubic and is in the upper part of the abdomen. Systematic ques- ﬂank pain that radiates to the penis, scrotum, or inner tioning and examination directed toward detecting aspect of the upper thigh. Obstruction of the uretero- myocardial or pulmonary infarction, pneumonia, peri- pelvic junction is felt as pain in the costovertebral angle, carditis, or esophageal disease (the intrathoracic diseases whereas obstruction of the remainder of the ureter is that most often masquerade as abdominal emergencies) associated with ﬂank pain that often extends into the will often provide sufﬁcient clues to establish the proper same side of the abdomen. diagnosis. Diaphragmatic pleuritis resulting from pneu- monia or pulmonary infarction may cause pain in the right upper quadrant and pain in the supraclavicular Vascular Disturbances area, the latter radiation to be distinguished from the A frequent misconception, despite abundant experience referred subscapular pain caused by acute distention of to the contrary, is that pain associated with intraabdomi- the extrahepatic biliary tree. The ultimate decision as to nal vascular disturbances is sudden and catastrophic in the origin of abdominal pain may require deliberate and nature.The pain of embolism or thrombosis of the supe- planned observation over a period of several hours, dur- rior mesenteric artery, or that of impending rupture of ing which repeated questioning and examination will an abdominal aortic aneurysm, certainly may be severe provide the diagnosis or suggest the appropriate studies. and diffuse.Yet just as frequently, the patient with occlu- Referred pain of thoracic origin is often accompa- sion of the superior mesenteric artery has only mild nied by splinting of the involved hemithorax with respi- continuous diffuse pain for 2 or 3 days before vascular ratory lag and decrease in excursion more marked than collapse or ﬁndings of peritoneal inﬂammation appear. that seen in the presence of intraabdominal disease. In The early, seemingly insigniﬁcant discomfort is caused addition, apparent abdominal muscle spasm caused by by hyperperistalsis rather than peritoneal inﬂammation. referred pain will diminish during the inspiratory phase Indeed, absence of tenderness and rigidity in the presence of respiration, whereas it is persistent throughout both
19. respiratory phases if it is of abdominal origin. Palpation present in a patient at rest.The demonstration of irregu- 5over the area of referred pain in the abdomen also does larly spaced cutaneous pain spots may be the only indi-not usually accentuate the pain and in many instances cation of an old nerve lesion underlying causalgic pain. CHAPTER 1actually seems to relieve it.Thoracic disease and abdom- Even though the pain may be precipitated by gentle pal-inal disease frequently coexist and may be difﬁcult or pation, rigidity of the abdominal muscles is absent, andimpossible to differentiate. For example, the patient with the respirations are not disturbed. Distention of theknown biliary tract disease often has epigastric pain dur- abdomen is uncommon, and the pain has no relation-ing myocardial infarction, or biliary colic may be ship to the intake of food.referred to the precordium or left shoulder in a patient Pain arising from spinal nerves or roots comes and Abdominal Painwho has suffered previously from angina pectoris. goes suddenly and is of a lancinating type. It may be Referred pain from the spine, which usually involves caused by herpes zoster, impingement by arthritis,compression or irritation of nerve roots, is characteristi- tumors, herniated nucleus pulposus, diabetes, or syphilis.cally intensiﬁed by certain motions such as cough, It is not associated with food intake, abdominal disten-sneeze, or strain, and is associated with hyperesthesia tion, or changes in respiration. Severe muscle spasm, asover the involved dermatomes. Pain referred to the in the gastric crises of tabes dorsalis, is common but isabdomen from the testes or seminal vesicles is generally either relieved or is not accentuated by abdominal pal-accentuated by the slightest pressure on either of these pation. The pain is made worse by movement of theorgans.The abdominal discomfort is of dull aching char- spine and is usually conﬁned to a few dermatomes.acter and is poorly localized. Hyperesthesia is very common. Pain due to functional causes conforms to none of the aforementioned patterns. The mechanism is hard toMETABOLIC ABDOMINAL CRISES deﬁne. Irritable bowel syndrome (IBS) is a functional gastrointestinal disorder characterized by abdominal painPain of metabolic origin may simulate almost any other and altered bowel habits. The diagnosis is made on thetype of intraabdominal disease. Several mechanisms may basis of clinical criteria (Chap. 17) and after exclusion ofbe at work. In certain instances, such as hyperlipidemia, demonstrable structural abnormalities. The episodes ofthe metabolic disease itself may be accompanied by an abdominal pain are often brought on by stress, and theintraabdominal process such as pancreatitis, which canlead to unnecessary laparotomy unless recognized. C1- pain varies considerably in type and location. Nauseaesterase deﬁciency associated with angioneurotic edema and vomiting are rare. Localized tenderness and muscleis often associated with episodes of severe abdominal spasm are inconsistent or absent. The causes of IBS orpain.Whenever the cause of abdominal pain is obscure, a related functional disorders are not known.metabolic origin always must be considered. Abdominalpain is also the hallmark of familial Mediterranean fever. The problem of differential diagnosis is often notreadily resolved.The pain of porphyria and of lead colic Approach to the Patient: ABDOMINAL PAINis usually difﬁcult to distinguish from that of intestinalobstruction, because severe hyperperistalsis is a promi- Few abdominal conditions require such urgent oper-nent feature of both. The pain of uremia or diabetes is ative intervention that an orderly approach need benonspeciﬁc, and the pain and tenderness frequently shift abandoned, no matter how ill the patient. Only thosein location and intensity. Diabetic acidosis may be pre- patients with exsanguinating intraabdominal hemor-cipitated by acute appendicitis or intestinal obstruction, rhage (e.g., ruptured aneurysm) must be rushed toso if prompt resolution of the abdominal pain does not the operating room immediately, but in suchresult from correction of the metabolic abnormalities, an instances only a few minutes are required to assess theunderlying organic problem should be suspected. Black critical nature of the problem. Under these circum-widow spider bites produce intense pain and rigidity of stances, all obstacles must be swept aside, adequatethe abdominal muscles and back, an area infrequently venous access for ﬂuid replacement obtained, and theinvolved in intraabdominal disease. operation begun. Many patients of this type have died in the radiology department or the emergency room while awaiting such unnecessary examinationsNEUROGENIC CAUSES as electrocardiograms or abdominal ﬁlms. There are no contraindications to operation when massive intraabdominalCausalgic pain may occur in diseases that injure sensory hemorrhage is present. Fortunately, this situation is rela-nerves. It has a burning character and is usually limited tively rare.These comments do not pertain to gastroin-to the distribution of a given peripheral nerve. Normal testinal hemorrhage, which can often be managed bystimuli such as touch or change in temperature may be other means (Chap. 8).transformed into this type of pain, which is frequently
20. 6 Nothing will supplant an orderly, painstakingly deﬁnitive plan has been formulated; obfuscation of the detailed history, which is far more valuable than any lab- diagnosis by adequate analgesia is unlikely. oratory or radiographic examination. This kind of his- In the examination, simple critical inspection of theSECTION I tory is laborious and time-consuming, making it not patient, e.g., of facies, position in bed, and respiratory especially popular, even though a reasonably accurate activity, may provide valuable clues. The amount of diagnosis can be made on the basis of the history information to be gleaned is directly proportional to alone in the majority of cases. Computer-aided diagno- the gentleness and thoroughness of the examiner. Once sis of abdominal pain provides no advantage over a patient with peritoneal inﬂammation has been clinical assessment alone. In cases of acute abdominal examined brusquely, accurate assessment by the next Cardinal Manifestations of Gastrointestinal Disease pain, a diagnosis is readily established in most instances, examiner becomes almost impossible. Eliciting whereas success is not so frequent in patients with rebound tenderness by sudden release of a deeply pal- chronic pain. IBS is one of the most common causes of pating hand in a patient with suspected peritonitis is abdominal pain and must always be kept in mind cruel and unnecessary. The same information can be (Chap. 17). The location of the pain can assist in nar- obtained by gentle percussion of the abdomen rowing the differential diagnosis (see Table 1-2); (rebound tenderness on a miniature scale), a maneuver however, the chronological sequence of events in the that can be far more precise and localizing. Asking the patient’s history is often more important than empha- patient to cough will elicit true rebound tenderness sis on the location of pain. If the examiner is sufﬁ- without the need for placing a hand on the abdomen. ciently open-minded and unhurried, asks the proper Furthermore, the forceful demonstration of rebound questions, and listens, the patient will usually provide tenderness will startle and induce protective spasm in a the diagnosis. Careful attention should be paid to the nervous or worried patient in whom true rebound extraabdominal regions that may be responsible for tenderness is not present.A palpable gallbladder will be abdominal pain. An accurate menstrual history in a missed if palpation is so brusque that voluntary muscle female patient is essential. Narcotics or analgesics spasm becomes superimposed on involuntary muscular should not be withheld until a deﬁnitive diagnosis or a rigidity. TABLE 1-2 DIFFERENTIAL DIAGNOSES OF ABDOMINAL PAIN BY LOCATION RIGHT UPPER QUADRANT EPIGASTRIC LEFT UPPER QUADRANT Cholecystitis Peptic ulcer disease Splenic infarct Cholangitis Gastritis Splenic rupture Pancreatitis GERD Splenic abscess Pneumonia/empyema Pancreatitis Gastritis Pleurisy/pleurodynia Myocardial infarction Gastric ulcer Subdiaphragmatic abscess Pericarditis Pancreatitis Hepatitis Ruptured aortic aneurysm Subdiaphragmatic abscess Budd-Chiari syndrome Esophagitis RIGHT LOWER QUADRANT PERIUMBILICAL LEFT LOWER QUADRANT Appendicitis Early appendicitis Diverticulitis Salpingitis Gastroenteritis Salpingitis Inguinal hernia Bowel obstruction Inguinal hernia Ectopic pregnancy Ruptured aortic aneurysm Ectopic pregnancy Nephrolithiasis Nephrolithiasis Inﬂammatory bowel disease Irritable bowel syndrome Mesenteric lymphadenitis Inﬂammatory bowel disease Typhlitis DIFFUSE NONLOCALIZED PAIN Gastroenteritis Diabetes Mesenteric ischemia Malaria Bowel obstruction Familial Mediterranean fever Irritable bowel syndrome Metabolic diseases Peritonitis Psychiatric disease
21. As in history taking, sufﬁcient time should be spent In rare instances, barium or water-soluble contrast study 7in the examination. Abdominal signs may be minimal of the upper part of the gastrointestinal tract maybut nevertheless, if accompanied by consistent symp- demonstrate partial intestinal obstruction that may CHAPTER 1toms, may be exceptionally meaningful. Abdominal elude diagnosis by other means. If there is any questionsigns may be virtually or totally absent in cases of of obstruction of the colon, oral administration of bar-pelvic peritonitis, so careful pelvic and rectal examina- ium sulfate should be avoided. On the other hand, intions are mandatory in every patient with abdominal pain. cases of suspected colonic obstruction (without perfo-Tenderness on pelvic or rectal examination in the ration), contrast enema may be diagnostic.absence of other abdominal signs can be caused by In the absence of trauma, peritoneal lavage has Abdominal Painoperative indications such as perforated appendicitis, been replaced as a diagnostic tool by ultrasound, CT,diverticulitis, twisted ovarian cyst, and many others. and laparoscopy. Ultrasonography has proved to be Much attention has been paid to the presence or useful in detecting an enlarged gallbladder or pan-absence of peristaltic sounds, their quality, and their creas, the presence of gallstones, an enlarged ovary,frequency. Auscultation of the abdomen is one of the or a tubal pregnancy. Laparoscopy is especially help-least revealing aspects of the physical examination of ful in diagnosing pelvic conditions, such as ovariana patient with abdominal pain. Catastrophes such as cysts, tubal pregnancies, salpingitis, and acute appen-strangulating small intestinal obstruction or perforated dicitis. Radioisotopic scans (HIDA) may help differ-appendicitis may occur in the presence of normal entiate acute cholecystitis from acute pancreatitis. Aperistaltic sounds. Conversely, when the proximal CT scan may demonstrate an enlarged pancreas, rup-part of the intestine above an obstruction becomes tured spleen, or thickened colonic or appendicealmarkedly distended and edematous, peristaltic sounds wall and streaking of the mesocolon or mesoappen-may lose the characteristics of borborygmi and dix characteristic of diverticulitis or appendicitis.become weak or absent, even when peritonitis is not Sometimes, even under the best circumstances withpresent. It is usually the severe chemical peritonitis all available aids and with the greatest of clinical skill, aof sudden onset that is associated with the truly deﬁnitive diagnosis cannot be established at the timesilent abdomen. Assessment of the patient’s state of of the initial examination. Nevertheless, despite lackhydration is important. of a clear anatomic diagnosis, it may be abundantly Laboratory examinations may be of great value in clear to an experienced and thoughtful physician andassessment of the patient with abdominal pain, yet surgeon that on clinical grounds alone operation iswith few exceptions they rarely establish a diagnosis. indicated. Should that decision be questionable, watch-Leukocytosis should never be the single deciding fac- ful waiting with repeated questioning and examinationtor as to whether or not operation is indicated. A will often elucidate the true nature of the illness andwhite blood cell count >20,000/␮L may be observed indicate the proper course of action.with perforation of a viscus, but pancreatitis, acutecholecystitis, pelvic inﬂammatory disease, and intestinalinfarction may be associated with marked leukocytosis. FURTHER READINGSA normal white blood cell count is not rare in cases of ASSAR AN, ZARINS CK: Ruptured abdominal aortic aneurysm: Aperforation of abdominal viscera.The diagnosis of ane- surgical emergency with many clinical presentations. Postgradmia may be more helpful than the white blood cell Med J 85:268, 2009count, especially when combined with the history. CERVERO F, LAIRD JM: Visceral pain. Lancet 353:2145, 1999 FORD AC et al: Yield of diagnostic tests for celiac disease in individuals The urinalysis may reveal the state of hydration or with symptoms suggestive of irritable bowel syndrome: Systematicrule out severe renal disease, diabetes, or urinary review and meta-analysis.Arch Intern Med 169:651, 2009infection. Blood urea nitrogen, glucose, and serum JAMES AW et al: Portomesenteric venous thrombosis after laparoscopicbilirubin levels may be helpful. Serum amylase levels surgery:A systematic literature review.Arch Surg 144:520, 2009may be increased by many diseases other than pan- JONES PF: Suspected acute appendicitis: Trends in management overcreatitis, e.g., perforated ulcer, strangulating intestinal 30 years. Br J Surg 88:1570, 2001obstruction, and acute cholecystitis; thus, elevations of LYON C, CLARK DC: Diagnosis of acute abdominal pain in older patients.Am Fam Physician 74:1537, 2006serum amylase do not rule out the need for an opera- RICHARDSON WS et al: The role of diagnostic laparoscopy fortion.The determination of the serum lipase may have chronic abdominal conditions: An evidence-based review. Surggreater accuracy than that of the serum amylase. Endosc 23:2073, 2009 Plain and upright or lateral decubitus radiographs of SILEN W: Cope’s Early Diagnosis of the Acute Abdomen, 21st ed. Newthe abdomen may be of value in cases of intestinal York and Oxford: Oxford University Press, 2005obstruction, perforated ulcer, and a variety of other SMITH JE, HALL EJ: The use of plain abdominal x-rays in the emer-conditions. They are usually unnecessary in patients gency department. Emerg Med J 26:160, 2009 TAIT IS et al: Do patients with abdominal pain wait unduly long forwith acute appendicitis or strangulated external hernias. analgesia? J R Coll Surg Edinb 44:181, 1999
22. CHAPTER 2 ORAL MANIFESTATIONS OF DISEASE Samuel C. Durso ■ Diseases of the Teeth and Periodontal Structures . . . . . . . . . . . 8 Tooth and Periodontal Structure . . . . . . . . . . . . . . . . . . . . . . . . 8 ■ Diseases of the Oral Mucosa . . . . . . . . . . . . . . . . . . . . . . . . . 10 ■ Nondental Causes of Oral Pain . . . . . . . . . . . . . . . . . . . . . . . . 17 ■ Diseases of the Salivary Glands . . . . . . . . . . . . . . . . . . . . . . . 18 ■ Dental Care of Medically Complex Patients . . . . . . . . . . . . . . . 18 ■ Halitosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 19 ■ Aging and Oral Health . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 19 ■ Further Readings . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20As primary care physicians and consultants, internists are gum line and covered with bonelike cementum. Dentin, aoften asked to evaluate patients with disease of the oral material that is denser than bone and exquisitely sensitivesoft tissues, teeth, and pharynx. Knowledge of the oral to pain, forms the majority of the tooth substance.milieu and its unique structures is necessary to guide Dentin surrounds a core of myxomatous pulp containingpreventive services and recognize oral manifestations of the vascular and nerve supply.The tooth is held ﬁrmly inlocal or systemic disease (Chap. 3). Furthermore, internists the alveolar socket by the periodontium, supporting struc-frequently collaborate with dentists in the care of tures that consist of the gingivae, alveolar bone, cemen-patients who have a variety of medical conditions that tum, and periodontal ligament.The periodontal ligamentaffect oral health or who undergo dental procedures that tenaciously binds the tooth’s cementum to the alveolarincrease their risk of medical complications. bone. Above this ligament is a collar of attached gingiva just below the crown. A few millimeters of unattached or free gingiva (1–3 mm) overlap the base of the crown,DISEASES OF THE TEETH AND forming a shallow sulcus along the gum-tooth margin.PERIODONTAL STRUCTURESTOOTH AND PERIODONTAL STRUCTURE Dental Caries, Pulpal and Periapical Disease, and ComplicationsTooth formation begins during the sixth week ofembryonic life and continues through the ﬁrst 17 years Dental caries begin asymptomatically as a destructiveof age. Tooth development begins in utero and contin- process of the hard surface of the tooth. Streptococcusues until after the tooth erupts. Normally all 20 decidu- mutans, principally, along with other bacteria colonizeous teeth have erupted by age 3 and have been shed by the organic buffering ﬁlm on the tooth surface to pro-age 13. Permanent teeth, eventually totaling 32, begin to duce plaque. If not removed by brushing or the naturalerupt by age 6 and have completely erupted by age 14, cleaning action of saliva and oral soft tissues, bacterialthough third molars (wisdom teeth) may erupt later. acids demineralize the enamel. Fissures and pits on the The erupted tooth consists of the visible crown cov- occlusion surfaces are the most frequent sites of decay.ered with enamel and the root submerged below the Surfaces adjacent to tooth restorations and exposed roots 8
23. are also vulnerable, particularly as teeth are retained in resorption of the alveolar bone. A role for the chronic 9an aging population. Over time, dental caries extend to inﬂammation resulting from chronic periodontal diseasethe underlying dentin, leading to cavitation of the in promoting coronary heart disease and stroke has been CHAPTER 2enamel and ultimately penetration to the tooth pulp, proposed. Epidemiologic studies demonstrate a moder-producing acute pulpitis. At this early stage, when the ate but signiﬁcant association between chronic peri-pulp infection is limited, the tooth becomes sensitive to odontal inﬂammation and atherogenesis, though a causalpercussion and hot or cold, and pain resolves immedi- role remains unproven.ately when the irritating stimulus is removed. Should Acute and aggressive forms of periodontal disease arethe infection spread throughout the pulp, irreversible pul- less common than the chronic forms described above. Oral Manifestations of Diseasepitis occurs, leading to pulp necrosis. At this late stage However, if the host is stressed or exposed to a newpain is severe and has a sharp or throbbing visceral qual- pathogen, rapidly progressive and destructive disease ofity that may be worse when the patient lies down. Once the periodontal tissue can occur. A virulent example ispulp necrosis is complete, pain may be constant or inter- acute necrotizing ulcerative gingivitis (ANUG), or Vincent’smittent, but cold sensitivity is lost. infection, characterized as “trench mouth” during World Treatment of caries involves removal of the softened War I. Stress, poor oral hygiene, and tobacco and alcoholand infected hard tissue; sealing the exposed dentin; and use are risk factors. The presentation includes suddenrestoration of the tooth structure with silver amalgam, gingival inﬂammation, ulceration, bleeding, interdentalcomposite plastic, gold, or porcelain. Once irreversible gingival necrosis, and fetid halitosis. Localized juvenilepulpitis occurs, root canal therapy is necessary, and the periodontitis, seen in adolescents, is particularly destruc-contents of the pulp chamber and root canals are tive and appears to be associated with impaired neu-removed, followed by thorough cleaning, antisepsis, and trophil chemotaxis. AIDS-related periodontitis resemblesﬁlling with an inert material. Alternatively, the tooth ANUG in some patients or a more destructive form ofmay be extracted. adult chronic periodontitis in others. It may also pro- Pulpal infection, if it does not egress through the duce a gangrene-like destructive process of the oral softdecayed enamel, leads to periapical abscess formation, tissues and bone that resembles noma, seen in severelywhich produces pain on chewing. If the infection is malnourished children in developing nations.mild and chronic, a periapical granuloma or eventually aperiapical cyst forms, either of which produces radiolu- Prevention of Tooth Decay and Periodontalcency at the root apex. When unchecked, a periapical Infectionabscess can erode into the alveolar bone, producing Despite the reduced prevalence of dental caries andosteomyelitis; penetrate and drain through the gingivae periodontal disease in the United States, due in large(parulis or gumboil); or track along deep fascial planes, part to water ﬂuoridation and improved dental care,producing a virulent cellulitis (Ludwig’s angina) involv- respectively, both diseases constitute a major publicing the submandibular space and ﬂoor of the mouth. health problem worldwide and for certain groups. TheElderly patients, those with diabetes mellitus, and internist should promote preventive dental care andpatients taking glucocorticoids may experience little or hygiene as part of health maintenance. Special popula-no pain and fever as these complications develop. tions at high risk for dental caries and periodontal dis- ease include those with xerostomia, diabetics, alcoholics,Periodontal Disease tobacco users, those with Down’s syndrome, and thosePeriodontal disease accounts for more tooth loss than with gingival hyperplasia. Furthermore, patients lackingcaries, particularly in the elderly. Like dental caries, dental care access (low socioeconomic status) and thosechronic infection of the gingiva and anchoring struc- with reduced ability to provide self-care (e.g., nursingtures of the tooth begins with formation of bacterial home residents, those with dementia or upper extremityplaque. The process begins invisibly above the gum line disability) suffer at a disproportionate rate. It is importantand in the gingival sulcus. Plaque, including mineralized to provide counseling regarding regular dental hygieneplaque (calculus), is preventable by appropriate dental and professional cleaning, use of fluoride-containinghygiene, including periodic professional cleaning. Left toothpaste, professional ﬂuoride treatments, and use ofundisturbed, chronic inﬂammation ensues and produces electric toothbrushes for patients with limited dexterity,a painless hyperemia of the free and attached gingivae and to give instruction to caregivers for those unable to(gingivitis) that typically bleeds with brushing. If ignored, perform self-care. Internists caring for international stu-severe periodontitis occurs, leading to deepening of the dents studying in the United States should be aware ofphysiologic sulcus and destruction of the periodontal the high prevalence of dental decay in this population.ligament. Pockets develop around the teeth and become Cost, fear of dental care, and language and cultural dif-ﬁlled with pus and debris. As the periodontium is ferences may create barriers that prevent some fromdestroyed, teeth loosen and exfoliate. Eventually there is seeking preventive dental services.
24. 10 Developmental and Systemic Disease DISEASES OF THE ORAL MUCOSA Affecting the Teeth and Periodontium Malocclusion is the most common developmental prob- InfectionSECTION I lem, which, in addition to a problem with cosmesis, can Most oral mucosal diseases involve microorganisms interfere with mastication unless corrected through (Table 2-1). orthodontic techniques. Impacted third molars are com- mon and occasionally become infected. Acquired prog- Pigmented Lesions nathism due to acromegaly may also lead to malocclusion, as may deformity of the maxilla and mandible due to See Table 2-2. Cardinal Manifestations of Gastrointestinal Disease Paget’s disease of the bone. Delayed tooth eruption, receding chin, and a protruding tongue are occasional Dermatologic Diseases features of cretinism and hypopituitarism. Congenital syphilis produces tapering, notched (Hutchinson’s) See Tables 2-1, 2-2, and 2-3. incisors and ﬁnely nodular (mulberry) molar crowns. Enamel hypoplasia results in crown defects ranging from Diseases of the Tongue pits to deep ﬁssures of primary or permanent teeth. See Table 2-4. Intrauterine infection (syphilis, rubella), vitamin deﬁciency (A, C, or D), disorders of calcium metabolism (malabsorp- tion, vitamin D–resistant rickets, hypoparathyroidism), pre- HIV Disease and AIDS maturity, high fever, or rare inherited defects (amelogenesis See Tables 2-1, 2-2, 2-3, and 2-5. imperfecta) are all causes. Tetracycline, given in sufﬁciently high doses during the ﬁrst 8 years, may produce enamel Ulcers hypoplasia and discoloration. Exposure to endogenous pigments can discolor developing teeth: erythroblastosis Ulceration is the most common oral mucosal lesion. fetalis (green or bluish-black), congenital liver disease Although there are many causes, the host and pattern of (green or yellow-brown), and porphyria (red or brown lesions, including the presence of systemic features, nar- that ﬂuoresces with ultraviolet light). Mottled enamel occurs row the differential diagnosis (Table 2-1). Most acute if excessive ﬂuoride is ingested during development.Worn ulcers are painful and self-limited. Recurrent aphthous enamel is seen with age, bruxism, or excessive acid expo- ulcers and herpes simplex infection constitute the sure (e.g., chronic gastric reﬂux or bulimia). majority. Persistent and deep aphthous ulcers can be Premature tooth loss resulting from periodontitis is idiopathic or seen with HIV/AIDS. Aphthous lesions seen with cyclic neutropenia, Papillon-Lefèvre syn- are often the presenting symptom in Behçet’s syndrome. drome, Chédiak-Higashi syndrome, and leukemia. Similar-appearing, though less painful, lesions may occur Rapid focal tooth loosening is most often due to infec- with Reiter’s syndrome, and aphthous ulcers are occa- tion, but rarer causes include histiocytosis X, Ewing’s sionally present during phases of discoid or systemic lupus sarcoma, osteosarcoma, or Burkitt’s lymphoma. Early loss erythematosus. Aphthous-like ulcers are seen in Crohn’s of primary teeth is a feature of hypophosphatasia, a rare disease (Chap. 16), but unlike the common aphthous inborn error of metabolism. variety, they may exhibit granulomatous inﬂammation Pregnancy may produce severe gingivitis and local- histologically. Recurrent aphthae in some patients with ized pyogenic granulomas. Severe periodontal disease celiac disease have been reported to remit with elimina- occurs with Down’s syndrome and diabetes mellitus. tion of gluten. Gingival hyperplasia may be caused by phenytoin, calcium Of major concern are chronic, relatively painless channel blockers (e.g., nifedipine), and cyclosporine. ulcers and mixed red/white patches (erythroplakia and Idiopathic familial gingival ﬁbromatosis and several syndrome- leukoplakia) of more than 2 weeks’ duration. Squamous related disorders appear similar. Removal of the medica- cell carcinoma and premalignant dysplasia should be tion often reverses the drug-induced form, though considered early and a diagnostic biopsy obtained. The surgery may be needed to control both. Linear gingival importance is underscored because early-stage malig- erythema is variably seen in patients with advanced HIV nancy is vastly more treatable than late-stage disease. infection and probably represents immune deﬁciency High-risk sites include the lower lip, ﬂoor of the mouth, and decreased neutrophil activity. Diffuse or focal gingi- ventral and lateral tongue, and soft palate–tonsillar pillar val swelling may be a feature of early or late acute complex. Signiﬁcant risk factors for oral cancer in West- myelomonocytic leukemia (AML) as well as of other ern countries include sun exposure (lower lip) and lymphoproliferative disorders. A rare, but pathognomonic, tobacco and alcohol use. In India and some other Asian sign of Wegener’s granulomatosis is a red-purplish, gran- countries, smokeless tobacco mixed with betel nut, ular gingivitis (strawberry gums). slaked lime, and spices is a common cause of oral cancer.
25. TABLE 2-1 11 VESICULAR, BULLOUS, OR ULCERATIVE LESIONS OF THE ORAL MUCOSA CHAPTER 2 CONDITION USUAL LOCATION CLINICAL FEATURES COURSE Viral Diseases Primary acute herpetic Lip and oral mucosa Labial vesicles that rupture and crust, Heals spontaneously in gingivostomatitis (buccal, gingival, and intraoral vesicles that quickly 10–14 days. Unless [herpes simplex virus lingual mucosa) ulcerate; extremely painful; acute secondarily infected, (HSV) type 1, rarely gingivitis, fever, malaise, foul odor, lesions lasting >3 weeks Oral Manifestations of Disease type 2] and cervical lymphadenopathy; are not due to primary occurs primarily in infants, children, HSV infection and young adults Recurrent herpes Mucocutaneous Eruption of groups of vesicles that may Lasts about 1 week, but labialis junction of lip, coalesce, then rupture and crust; condition may be pro- perioral skin painful to pressure or spicy foods longed if secondarily infected. If severe, topical or oral antiviral may reduce healing time Recurrent intraoral Palate and gingiva Small vesicles on keratinized Heals spontaneously in herpes simplex epithelium that rupture and about 1 week. If severe, coalesce; painful topical or oral antiviral may reduce healing time Chickenpox Gingiva and oral Skin lesions may be accompanied by Lesions heal spontaneously (varicella-zoster mucosa small vesicles on oral mucosa that within 2 weeks virus) rupture to form shallow ulcers; may coalesce to form large bullous lesions that ulcerate; mucosa may have generalized erythema Herpes zoster Cheek, tongue, Unilateral vesicular eruptions and Gradual healing without (reactivation of gingiva, or palate ulceration in linear pattern following scarring unless secondarily varicella-zoster virus) sensory distribution of trigeminal infected; postherpetic nerve or one of its branches neuralgia is common. Oral acyclovir, famciclovir, or valacyclovir reduce healing time and postherpetic neuralgia Infectious Oral mucosa Fatigue, sore throat, malaise, fever, Oral lesions disappear mononucleosis and cervical lymphadenopathy; during convalescence; no (Epstein-Barr virus) numerous small ulcers usually appear treatment though gluco- several days before lymphadenopathy; corticoids indicated if gingival bleeding and multiple tonsillar swelling petechiae at junction of hard and compromises airway soft palates Herpangina (coxsack- Oral mucosa, Sudden onset of fever, sore throat, and Incubation period 2–9 days; ievirus A; also possi- pharynx, tongue oropharyngeal vesicles, usually in fever for 1–4 days; bly coxsackie B and children under 4 years, during recovery uneventful echovirus) summer months; diffuse pharyngeal congestion and vesicles (1–2 mm), grayish-white surrounded by red areola; vesicles enlarge and ulcerate Hand, foot, and mouth Oral mucosa, Fever, malaise, headache with Incubation period 2–18 disease (coxsack- pharynx, palms, oropharyngeal vesicles that become days; lesions heal sponta- ievirus A16 most and soles painful, shallow ulcers; highly neously in 2–4 weeks common) infectious; usually affects children under age 10 Primary HIV infection Gingiva, palate, and Acute gingivitis and oropharyngeal Followed by HIV serocon- pharynx ulceration, associated with febrile version, asymptomatic HIV illness resembling mononucleosis infection, and usually and including lymphadenopathy ultimately by HIV disease (Continued)
26. 12 TABLE 2-1 (CONTINUED ) VESICULAR, BULLOUS, OR ULCERATIVE LESIONS OF THE ORAL MUCOSA CONDITION USUAL LOCATION CLINICAL FEATURES COURSESECTION I Bacterial or Fungal Diseases Acute necrotizing Gingiva Painful, bleeding gingiva characterized Debridement and diluted ulcerative gingivitis by necrosis and ulceration of gingival (1:3) peroxide lavage (“trench mouth,” papillae and margins plus provide relief within 24 h; Vincent’s infection) lymphadenopathy and foul odor antibiotics in acutely ill Cardinal Manifestations of Gastrointestinal Disease patients; relapse may occur Prenatal (congenital) Palate, jaws, tongue, Gummatous involvement of palate, Tooth deformities in syphilis and teeth jaws, and facial bones; Hutchinson’s permanent dentition incisors, mulberry molars, glossitis, irreversible mucous patches, and ﬁssures on corner of mouth Primary syphilis Lesion appears Small papule developing rapidly into a Healing of chancre in 1–2 (chancre) where organism large, painless ulcer with indurated months, followed by enters body; may border; unilateral lymphadenopathy; secondary syphilis in occur on lips, chancre and lymph nodes containing 6–8 weeks tongue, or tonsillar spirochetes; serologic tests positive area by third to fourth weeks Secondary syphilis Oral mucosa fre- Maculopapular lesions of oral mucosa, Lesions may persist from quently involved 5–10 mm in diameter with central several weeks to a year with mucous ulceration covered by grayish patches, primarily membrane; eruptions occurring on on palate, also at various mucosal surfaces and skin commissures of accompanied by fever, malaise, and mouth sore throat Tertiary syphilis Palate and tongue Gummatous inﬁltration of palate or Gumma may destroy tongue followed by ulceration and palate, causing complete ﬁbrosis; atrophy of tongue papillae perforation produces characteristic bald tongue and glossitis Gonorrhea Lesions may occur Most pharyngeal infection is More difﬁcult to eradicate in mouth at site asymptomatic; may produce than urogenital infection, of inoculation or burning or itching sensation; though pharyngitis usually secondarily by oropharynx and tonsils may be resolves with appropriate hematogenous ulcerated and erythematous; saliva antimicrobial treatment spread from a viscous and fetid primary focus elsewhere Tuberculosis Tongue, tonsillar A painless, solitary, 1–5 cm, irregular Autoinoculation from area, soft palate ulcer covered with a persistent pulmonary infection usual; exudate; ulcer has a ﬁrm undermined lesions resolve with border appropriate antimicrobial therapy Cervicofacial Swellings in region Infection may be associated with an Typically swelling is hard actinomycosis of face, neck, and extraction, jaw fracture, or eruption of and grows painlessly; ﬂoor of mouth molar tooth; in acute form resembles multiple abscesses with an acute pyogenic abscess, but draining tracks develop; contains yellow “sulfur granules” penicillin ﬁrst choice; (gram-positive mycelia and their surgery usually necessary hyphae) Histoplasmosis Any area of the Nodular, verrucous, or granulomatous Systemic antifungal therapy mouth, particularly lesions; ulcers are indurated and necessary to treat tongue, gingiva, or painful; usual source hematogenous palate or pulmonary, but may be primary Candidiasis (Table 2-3) (Continued)
27. TABLE 2-1 (CONTINUED ) 13 VESICULAR, BULLOUS, OR ULCERATIVE LESIONS OF THE ORAL MUCOSA CHAPTER 2 CONDITION USUAL LOCATION CLINICAL FEATURES COURSE Dermatologic Diseases Mucous membrane Typically produces Painful, grayish-white collapsed vesicles or Protracted course with remis- pemphigoid marked gingival ery- bullae of full-thickness epithelium with sions and exacerbations; thema and ulceration; peripheral erythematous zone; gingival involvement of different sites other areas of oral lesions desquamate, leaving ulcerated area occurs slowly; glucocorticoids Oral Manifestations of Disease cavity, esophagus, may temporarily reduce and vagina may be symptoms but do not control affected the disease Erythema Primarily the oral Intraoral ruptured bullae surrounded by an Onset very rapid; usually idio- multiforme minor mucosa and the skin inﬂammatory area; lips may show hemor- pathic, but may be associated and major of hands and feet rhagic crusts; the “iris,” or “target,” lesion with trigger such as drug (Stevens-Johnson on the skin is pathognomonic; patient may reaction; condition may last syndrome) have severe signs of toxicity 3–6 weeks; mortality with EM major 5–15% if untreated Pemphigus vulgaris Oral mucosa and skin; Usually (>70%) presents with oral lesions; With repeated occurrence of sites of mechanical fragile, ruptured bullae and ulcerated oral bullae, toxicity may lead to trauma (soft/hard areas; mostly in older adults cachexia, infection, and death palate, frenulum, lips, within 2 years; often control- buccal mucosa) lable with oral glucocorticoids Lichen planus Oral mucosa and skin White striae in mouth; purplish nodules on White striae alone usually skin at sites of friction; occasionally causes asymptomatic; erosive lesions oral mucosal ulcers and erosive gingivitis often difﬁcult to treat, but may respond to glucocorticoids Other Conditions Recurrent aphthous Usually on nonkera- Single or clusters of painful ulcers with Lesions heal in 1–2 weeks but ulcers tinized oral mucosa surrounding erythematous border; lesions may recur monthly or several (buccal and labial may be 1–2 mm in diameter in crops times a year; protective barrier mucosa, ﬂoor of (herpetiform), 1–5 mm (minor), or with orabase and topical mouth, soft palate, 5–15 mm (major) steroids give symptomatic lateral and ventral relief; systemic glucocorticoids tongue) may be needed in severe cases Behçet’s syndrome Oral mucosa, eyes, Multiple aphthous ulcers in mouth; inﬂammatory Oral lesions often ﬁrst manifes- genitalia, gut, and ocular changes, ulcerative lesions on genitalia; tation; persist several weeks CNS inﬂammatory bowel disease and CNS disease and heal without scarring Traumatic ulcers Anywhere on oral Localized, discrete ulcerated lesions with red Lesions usually heal in 7–10 mucosa; dentures fre- border; produced by accidental biting of days when irritant is removed, quently responsible mucosa, penetration by a foreign object, or unless secondarily infected for ulcers in vestibule chronic irritation by a denture Squamous cell Any area in the mouth, Ulcer with elevated, indurated border; failure Invades and destroys underlying carcinoma most commonly on to heal, pain not prominent; lesions tend to tissues; frequently metasta- lower lip, tongue, and arise in areas of erythro/leukoplakia or in sizes to regional lymph nodes ﬂoor of mouth smooth atrophic tongue Acute myeloid Gingiva Gingival swelling and superﬁcial ulceration Usually responds to systemic leukemia (usually followed by hyperplasia of gingiva with treatment of leukemia; occa- monocytic) extensive necrosis and hemorrhage; deep sionally requires local radiation ulcers may occur elsewhere on the mucosa therapy complicated by secondary infection Lymphoma Gingiva, tongue, Elevated, ulcerated area that may proliferate Fatal if untreated; may indicate palate and tonsillar rapidly, giving the appearance of traumatic underlying HIV infection area inﬂammation Chemical or thermal Any area in mouth White slough due to contact with corrosive Lesion heals in several weeks burns agents (e.g., aspirin, hot cheese) applied if not secondarily infected locally; removal of slough leaves raw, painful surfaceNote: CNS, central nervous system.
28. 14 TABLE 2-2 PIGMENTED LESIONS OF THE ORAL MUCOSA CONDITION USUAL LOCATION CLINICAL FEATURES COURSESECTION I Oral melanotic Any area of the mouth Discrete or diffuse localized, Remains indeﬁnitely; no growth macule brown to black macule Diffuse melanin Any area of the mouth Diffuse pale to dark-brown Remains indeﬁnitely pigmentation pigmentation; may be physiologic (“racial”) or due to smoking Cardinal Manifestations of Gastrointestinal Disease Nevi Any area of the mouth Discrete, localized, brown to black Remains indeﬁnitely pigmentation Malignant Any area of the mouth Can be ﬂat and diffuse, painless, Expands and invades early; melanoma brown to black, or can be raised metastasis leads to death and nodular Addison’s disease Any area of the mouth, Blotches or spots of bluish-black Condition controlled by adrenal but mostly buccal to dark-brown pigmentation steroid replacement mucosa occurring early in the disease, accompanied by diffuse pigmentation of skin; other symptoms of adrenal insufﬁciency Peutz-Jeghers Any area of the mouth Dark-brown spots on lips, buccal Oral pigmented lesions remain syndrome mucosa, with characteristic indeﬁnitely; gastrointestinal distribution of pigment around polyps may become malignant lips, nose, eyes, and on hands; concomitant intestinal polyposis Drug ingestion Any area of the mouth Brown, black, or gray areas of Gradually disappears following (neuroleptics, oral pigmentation cessation of drug contraceptives, minocycline, zidovudine, quinine derivatives) Amalgam tattoo Gingiva and alveolar Small blue-black pigmented areas Remains indeﬁnitely mucosa associated with embedded amalgam particles in soft tissues; these may show up on radiographs as radiopaque particles in some cases Heavy metal Gingival margin Thin blue-black pigmented line Indicative of systemic pigmentation along gingival margin; rarely seen absorption; no signiﬁcance (bismuth, mercury, except for children exposed to for oral health lead) lead-based paint Black hairy tongue Dorsum of tongue Elongation of ﬁliform papillae of Improves within 1–2 weeks with tongue, which become stained gentle brushing of tongue or by coffee, tea, tobacco, or discontinuation of antibiotic if pigmented bacteria due to bacterial overgrowth Fordyce “spots” Buccal and labial Numerous small yellowish spots Benign; remains without mucosa just beneath mucosal surface; no apparent change symptoms; due to hyperplasia of sebaceous glands Kaposi’s sarcoma Palate most common, Red or blue plaques of variable Usually indicative of HIV but may occur in any size and shape; often enlarge, infection or non-Hodgkin’s other site become nodular and may lymphoma; rarely fatal, but ulcerate may require treatment for comfort or cosmesis Mucous retention Buccal and labial Bluish-clear ﬂuid-ﬁlled cyst due to Benign; painless unless cysts mucosa extravasated mucous from traumatized; may be removed injured minor salivary gland surgically
29. TABLE 2-3 15 WHITE LESIONS OF ORAL MUCOSA CHAPTER 2 CONDITION USUAL LOCATION CLINICAL FEATURES COURSE Lichen planus Buccal mucosa, Striae, white plaques, red Protracted; responds to tongue, gingiva, and areas, ulcers in mouth; topical glucocorticoids lips; skin purplish papules on skin; may be asymptomatic, sore, or painful; lichenoid drug reactions may look Oral Manifestations of Disease similar White sponge Oral mucosa, vagina, Painless white thickening of Benign and permanent nevus anal mucosa epithelium; adolescent/early adult onset; familial Smoker’s leuko- Any area of oral White patch that may May or may not resolve with plakia and smoke- mucosa, sometimes become ﬁrm, rough, or cessation of habit; 2% less tobacco related to location of red-ﬁssured and ulcerated; develop squamous cell lesions habit may become sore and carcinoma; early biopsy painful but usually painless essential Erythroplakia with Floor of mouth com- Velvety, reddish plaque; High risk of squamous cell or without white mon in men; tongue occasionally mixed with cancer; early biopsy patches and buccal mucosa white patches or smooth essential in women red areas Candidiasis Any area in mouth Pseudomembranous type Responds favorably to (“thrush”): creamy white antifungal therapy and curdlike patches that reveal correction of predisposing a raw, bleeding surface causes where possible when scraped; found in sick infants, debilitated elderly patients receiving high doses of glucocorticoids or broad-spectrum antibiotics, or in patients with AIDS Erythematous type: ﬂat, red, Course same as for sometimes sore areas in pseudomembranous type same groups of patients Candidal leukoplakia: Responds to prolonged nonremovable white antifungal therapy thickening of epithelium due to Candida Angular cheilitis: sore Responds to topical ﬁssures at corner of mouth antifungal therapy Hairy leukoplakia Usually lateral tongue, White areas ranging from Due to EBV; responds to rarely elsewhere on small and ﬂat to extensive high dose acyclovir but oral mucosa accentuation of vertical recurs; rarely causes folds; found in HIV carriers discomfort unless in all risk groups for AIDS secondarily infected with Candida Warts Anywhere on skin and Single or multiple papillary Lesions grow rapidly and (papillomavirus) oral mucosa lesions, with thick, white spread; consider keratinized surfaces squamous cell carcinoma containing many pointed and rule out with biopsy; projections; cauliﬂower excision or laser therapy; lesions covered with may regress in HIV normal-colored mucosa or infected patients on multiple pink or pale bumps antiretroviral therapy (focal epithelial hyperplasia)Note: EBV, Epstein-Barr virus.
30. 16 TABLE 2-4 ALTERATIONS OF THE TONGUE TYPE OF CHANGE CLINICAL FEATURESSECTION I Size or Morphology Changes Macroglossia Enlarged tongue that may be part of a syndrome found in developmental conditions such as Down syndrome, Simpson-Golabi-Behmel syndrome, or Beckwith-Wiedemann syndrome may be due to tumor (hemangioma or lymphangioma), metabolic disease (such as primary amyloidosis), or endocrine disturbance (such as acromegaly or cretinism) Cardinal Manifestations of Gastrointestinal Disease Fissured (“scrotal”) Dorsal surface and sides of tongue covered by painless shallow or deep ﬁssures that tongue may collect debris and become irritated Median rhomboid Congenital abnormality of tongue with ovoid, denuded area in median posterior portion of the glossitis tongue; may be associated with candidiasis and may respond to antifungals Color Changes “Geographic” tongue Asymptomatic inﬂammatory condition of the tongue, with rapid loss and regrowth of ﬁliform (benign migratory papillae, leading to appearance of denuded red patches “wandering” across the surface of the glossitis) tongue Hairy tongue Elongation of ﬁliform papillae of the medial dorsal surface area due to failure of keratin layer of the papillae to desquamate normally; brownish-black coloration may be due to staining by tobacco, food, or chromogenic organisms “Strawberry” and Appearance of tongue during scarlet fever due to the hypertrophy of fungiform papillae plus “raspberry” tongue changes in the ﬁliform papillae “Bald” tongue Atrophy may be associated with xerostomia, pernicious anemia, iron-deﬁciency anemia, pellagra, or syphilis; may be accompanied by painful burning sensation; may be an expression of erythematous candidiasis and respond to antifungals TABLE 2-5 ORAL LESIONS ASSOCIATED WITH HIV INFECTION LESION MORPHOLOGY ETIOLOGIES Papules, nodules, plaques Candidiasis (hyperplastic and pseudomembranous)a Condyloma acuminatum (human papillomavirus infection) Squamous cell carcinoma (preinvasive and invasive) Non-Hodgkin’s lymphomaa Hairy leukoplakiaa Ulcers Recurrent aphthous ulcersa Angular cheilitis Squamous cell carcinoma Acute necrotizing ulcerative gingivitisa Necrotizing ulcerative periodontitisa Necrotizing ulcerative stomatitis Non-Hodgkin’s lymphomaa Viral infection (herpes simplex, herpes zoster, cytomegalovirus) Mycobacterium tuberculosis, Mycobacterium avium-intracellulare Fungal infection (histoplasmosis, cryptococcosis, candidiasis, geotrichosis, aspergillosis) Bacterial infection (Escherichia coli, Enterobacter cloacae, Klebsiella pneumoniae, Pseudomonas aeruginosa) Drug reactions (single or multiple ulcers) Pigmented lesions Kaposi’s sarcomaa Bacillary angiomatosis (skin and visceral lesions more common than oral) Zidovudine pigmentation (skin, nails, and occasionally oral mucosa) Addison’s disease Miscellaneous Linear gingival erythemaa a Strongly associated with HIV infection.
31. Less common etiologies include syphilis and Plummer- from dental or periodontal structures, but not referred 17Vinson syndrome (iron deﬁciency). pain. The most common nondental origin is myofascial Rarer causes of chronic oral ulcer such as tuberculosis, pain referred from muscles of mastication, which CHAPTER 2fungal infection, Wegener’s granulomatosis, and midline become tender and ache with increased use. Many suf-granuloma may look identical to carcinoma. Making the ferers exhibit bruxism (the grinding of teeth, often dur-correct diagnosis depends on recognizing other clinical ing sleep) that is secondary to stress and anxiety. Temporo-features and biopsy of the lesion. The syphilitic chancre mandibular disorder is closely related. It predominantlyis typically painless and therefore easily missed. affects females ages 15–45. Features include pain, limitedRegional lymphadenopathy is invariably present. Con- mandibular movement, and temporomandibular joint Oral Manifestations of Diseaseﬁrmation is achieved using appropriate bacterial and sounds. The etiologies are complex, and malocclusionserologic tests. does not play the primary role once attributed to it. Disorders of mucosal fragility often produce painful Osteoarthritis is a common cause of masticatory pain.oral ulcers that fail to heal within 2 weeks. Mucous mem- Anti-inﬂammatory medication, jaw rest, soft foods, andbrane pemphigoid and pemphigus vulgaris are the major heat provide relief. The temporomandibular joint isacquired disorders. While clinical features are often dis- involved in 50% of patients with rheumatoid arthritis andtinctive, immunohistochemical examination should be is usually a late feature of severe disease. Bilateral preau-performed for diagnosis and to distinguish these entities ricular pain, particularly in the morning, limits range offrom lichen planus and drug reactions. motion. Migrainous neuralgia may be localized to the mouth.Hematologic and Nutritional Disease Episodes of pain and remission without identiﬁable cause and absence of relief with local anesthesia areInternists are more likely to encounter patients with important clues. Trigeminal neuralgia (tic douloureux) mayacquired, rather than congenital, bleeding disorders. involve the entire branch or part of the mandibularBleeding after minor trauma should stop after 15 min or maxillary branches of the ﬁfth cranial nerve andand within an hour of tooth extraction if local pressure is produce pain in one or a few teeth. Pain may occurapplied. More prolonged bleeding, if not due to contin- spontaneously or may be triggered by touching the lipued injury or rupture of a large vessel, should lead to or gingiva, brushing the teeth, or chewing. Glossopharyngealinvestigation for a clotting abnormality. In addition to neuralgia produces similar acute neuropathic symptomsbleeding, petechiae and ecchymoses are prone to occur at in the distribution of the ninth cranial nerve. Swallow-the line of vibration between the soft and hard palates in ing, sneezing, coughing, or pressure on the tragus of thepatients with platelet dysfunction or thrombocytopenia. ear triggers pain that is felt in the base of the tongue, All forms of leukemia, but particularly acute pharynx, and soft palate and may be referred to the tem-myelomonocytic leukemia, can produce gingival bleed- poromandibular joint. Neuritis involving the maxillarying, ulcers, and gingival enlargement. Oral ulcers are a and mandibular divisions of the trigeminal nerve (e.g.,feature of agranulocytosis, and ulcers and mucositis are maxillary sinusitis, neuroma, and leukemic inﬁltrate) isoften severe complications of chemotherapy and radia- distinguished from ordinary toothache by the neuro-tion therapy for hematologic and other malignancies. pathic quality of the pain. Occasionally phantom pain fol-Plummer-Vinson syndrome (iron deﬁciency, angular lows tooth extraction. Often the earliest symptom ofstomatitis, glossitis, and dysphagia) raises the risk of oral Bell’s palsy in the day or so before facial weakness devel-squamous cell cancer and esophageal cancer at the post- ops is pain and hyperalgesia behind the ear and side ofcricoidal tissue web. Atrophic papillae and a red, burning the face. Likewise, similar symptoms may precede visibletongue may occur with pernicious anemia. B-group vit- lesions of herpes zoster infecting the seventh nerveamin deﬁciencies produce many of these same symp- (Ramsey-Hunt syndrome) or trigeminal nerve. Posther-toms as well as oral ulceration and cheilosis. Cheilosis petic neuralgia may follow either condition. Coronarymay also be seen in iron deﬁciency. Swollen, bleeding ischemia may produce pain exclusively in the face andgums, ulcers, and loosening of the teeth are a conse- jaw and, like typical angina pectoris, is usually repro-quence of scurvy. ducible with increased myocardial demand. Aching in several upper molar or premolar teeth that is unrelievedNONDENTAL CAUSES OF ORAL PAIN by anesthetizing the teeth may point to maxillary sinusitis.Most but not all oral pain emanates from inﬂamed or Giant cell arteritis is notorious for producinginjured tooth pulp or periodontal tissues. Nonodonto- headache, but it may also produce facial pain or soregenic causes may be overlooked. In most instances throat without headache. Jaw and tongue claudicationtoothache is predictable and proportional to the stimulus with chewing or talking is relatively common. Tongueapplied, and an identiﬁable condition (e.g., caries, abscess) infarction is rare. Patients with subacute thyroiditis oftenis found. Local anesthesia eliminates pain originating experience pain referred to the face or jaw before the
32. 18 tender thyroid gland and transient hyperthyroidism are disorders, Sjögren’s syndrome, sarcoidosis, tuberculosis, appreciated. lymphadenitis, actinomycosis, and Wegener’s granulo- Burning mouth syndrome (glossodynia) is present in matosis. Bilateral nontender parotid enlargement occursSECTION I the absence of an identiﬁable cause (e.g., vitamin B12 with diabetes mellitus, cirrhosis, bulimia, HIV/AIDS, deﬁciency, iron deﬁciency, Plummer-Vinson syndrome, and drugs (e.g., iodide, propylthiouracil). diabetes mellitus, low-grade Candida infection, food sen- Pleomorphic adenoma comprises two-thirds of all sali- sitivity, or subtle xerostomia) and predominantly affects vary neoplasms.The parotid is the principal salivary gland postmenopausal women. The etiology may be neuro- affected, and the tumor presents as a ﬁrm, slow-growing pathic. Clonazepam, alpha-lipoic acid, and cognitive mass.Though benign, recurrence is common if resection Cardinal Manifestations of Gastrointestinal Disease behavioral therapy have beneﬁted some. is incomplete. Malignant tumors such as mucoepider- moid carcinoma, adenoid cystic carcinoma, and adeno- DISEASES OF THE SALIVARY GLANDS carcinoma tend to grow relatively fast, depending upon grade. They may ulcerate and invade nerves, producing Saliva is essential to oral health. Its major components, numbness and facial paralysis. Neutron-beam radiation water and mucin, serve as a cleansing solvent and lubri- therapy is an effective treatment; 5-year survival is about cating ﬂuid. In addition, it contains antimicrobial factors 68% for malignant salivary gland tumors. (e.g., lysozyme, lactoperoxidase, secretory IgA), epider- mal growth factor, minerals, and buffering systems. The DENTAL CARE OF MEDICALLY major salivary glands secrete intermittently in response COMPLEX PATIENTS to autonomic stimulation, which is high during a meal but low otherwise. Hundreds of minor glands in the lips Routine dental care (e.g., extraction, scaling and clean- and cheeks secrete mucus continuously. Consequently, ing, tooth restoration, and root canal) is remarkably safe. oral function becomes impaired when salivary function The most common concerns regarding care of dental is reduced. Dry mouth (xerostomia) is perceived when patients with medical disease are fear of excessive bleed- salivary ﬂow is reduced by 50%.The most common eti- ing for patients on anticoagulants, infection of the heart ology is medication, especially drugs with anticholiner- valves and prosthetic devices from hematogenous seed- gic properties, but also alpha and beta blockers, calcium ing of oral ﬂora, and cardiovascular complications result- channel blockers, and diuretics. Other causes include ing from vasopressors used with local anesthetics during Sjögren’s syndrome, chronic parotitis, salivary duct dental treatment. Experience conﬁrms that the risks of obstruction, diabetes mellitus, HIV/AIDS, and irradia- any of these complications are very low. tion for head and neck cancer. Management involves Patients undergoing tooth extraction or alveolar and eliminating or limiting drying medications, preventive gingival surgery rarely experience uncontrolled bleed- dental care, and supplementing oral liquid. Sugarless ing when warfarin anticoagulation is maintained within mints or chewing gum may stimulate salivary secretion the therapeutic range currently recommended for pre- if dysfunction is mild. When sufﬁcient exocrine tissue vention of venous thrombosis, atrial ﬁbrillation, or remains, pilocarpine or cevimeline has been shown to mechanical heart valve. Embolic complications and increase secretions. Commercial saliva substitutes or gels death, however, have been reported during subtherapeu- relieve dryness but must be supplemented with ﬂuoride tic anticoagulation. Therapeutic anticoagulation should applications to prevent caries. be conﬁrmed before and continued through the proce- Sialolithiasis presents most often as painful swelling dure. Likewise, low-dose aspirin (e.g., 81–325 mg) can but in some instances as just swelling or pain. The be safely continued. obstructing stone produces spasm upon eating. Conserv- Patients at high or moderate risk for bacterial endo- ative therapy consists of local heat, massage, and hydra- carditis should maintain optimal oral hygiene, including tion. Promotion of salivary secretion with mints or ﬂossing, and have regular professional cleaning. Prophy- lemon drops may ﬂush out small stones. Antibiotic treat- lactic antibiotics are recommended for all at-risk ment is necessary when bacterial infection in suspected. patients who undergo dental and oral procedures likely In adults, acute bacterial parotitis is typically unilateral and to cause signiﬁcant bleeding and bacteremia. Should most commonly affects postoperative patients within the unexpected bleeding occur, antibiotics given within 2 h ﬁrst 2 weeks of surgery. Staphylococcus aureus is the most following the procedure provide effective prophylaxis. common bacterial agent. Dehydration, advanced age, Hematogenous bacterial seeding from oral infection and chronic debilitating disease are major risks. Chronic can undoubtedly produce late prosthetic joint infection bacterial sialadenitis results from lowered salivary secre- and therefore requires removal of the infected tissue (e.g., tion and recurrent bacterial infection. When suspected drainage, extraction, root canal) and appropriate antibi- bacterial infection is not responsive to therapy, the dif- otic therapy. However, evidence that late prosthetic joint ferential diagnosis should be expanded to include infection occurs following routine dental procedures is benign and malignant neoplasms, lymphoproliferative lacking. For this reason, antibiotic prophylaxis is not
33. recommended before dental surgery in patients with Helicobacter pylori gastritis can also produce ammoniac 19orthopedic pins, screws, and plates. It is, however, advised breath. If no odor is detectable, then pseudohalitosis orwithin the ﬁrst 2 years after joint replacement for even halitophobia must be considered. These conditions CHAPTER 2patients who have inﬂammatory arthropathies, immuno- represent varying degrees of psychiatric illness.suppression, type 1 diabetes mellitus, previous prostheticjoint infection, hemophilia, or malnourishment. Concern often arises regarding the use of vasocon- AGING AND ORAL HEALTHstrictors in patients with hypertension and heart disease.Vasoconstrictors enhance the depth and duration of While tooth loss and dental disease are not normal con- sequences of aging, a complex array of structural and Oral Manifestations of Diseaselocal anesthesia, thus reducing the anesthetic dose andpotential toxicity. If intravascular injection is avoided, 2% functional changes occurs with age that can affect orallidocaine with 1:100,000 epinephrine (limited to a total health. Subtle changes in tooth structure (e.g., dimin-of 0.036 mg epinephrine) can be used safely in those ished pulp space and volume, sclerosis of dentinalwith controlled hypertension and stable coronary heart tubules, altered proportions of nerve and vascular pulpdisease, arrhythmia, or congestive heart failure. Precau- content) result in diminished or altered pain sensitivity,tion should be taken with patients taking tricyclic anti- reduced reparative capacity, and increased tooth brittle-depressants and nonselective beta blockers as these drugs ness. In addition, age-associated fatty replacement ofmay potentiate the effect of epinephrine. salivary acini may reduce physiologic reserve, thus Elective dental treatments should be postponed for at increasing the risk of xerostomia.least 1 month after myocardial infarction, after which Poor oral hygiene often results when vision fails orthe risk of reinfarction is low provided the patient is when patients lose manual dexterity and upper extremitymedically stable (e.g., stable rhythm, stable angina, and ﬂexibility.This is particularly common for nursing homefree of heart failure). Patients who have suffered a stroke residents and must be emphasized, since regular oralshould have elective dental care deferred for 6 months. cleaning and dental care have been shown to reduce theIn both situations, effective stress reduction requires incidence of pneumonia. Other risks for dental decaygood pain control, including the use of the minimal include limited lifetime ﬂuoride exposure and preferenceamount of vasoconstrictor necessary to provide good by some older adults for intensely sweet foods when tastehemostasis and local anesthesia. and olfaction wane. These factors occur in an increasing Bisphosphonate therapy can be associated with proportion of persons over age 75 who retain teeth thatosteonecrosis of the jaw. Most patients affected have have extensive restorations and exposed roots. Withoutreceived high-dose aminobisphosphonate therapy for assiduous care, decay can become quite advanced yetmultiple myeloma or metastatic breast cancer and have remain asymptomatic. Consequently, much or all of theundergone tooth extraction or dental surgery. Intra-oral tooth can be destroyed before the process is detected.lesions appear as exposed yellow-white hard bone Periodontal disease, a leading cause of tooth loss, isinvolving the mandible or maxilla.Two-thirds are painful. indicated by loss of alveolar bone height. Over 90% ofPatients about to receive aminobisphosphonate therapy Americans have some degree of periodontal disease byshould receive preventive dental care that reduces the age 50. Healthy adults who have not experienced signif-risk of infection and need for future dentoalveolar icant alveolar bone loss by the sixth decade do not typi-surgery. cally develop signiﬁcant worsening with advancing age. Complete edentulousness with advanced age, though less common than in previous decades, is still present inHALITOSIS approximately 50% of Americans age ≥85. Speech, mas- tication, and facial contours are dramatically affected.Halitosis typically emanates from the oral cavity or nasal Edentulousness may also worsen obstructive sleep apnea,passages.Volatile sulfur compounds resulting from bacte- particularly in those without symptoms while wearingrial decay of food and cellular debris account for the dentures. Dentures can improve speech articulation andmalodor. Periodontal disease, caries, acute forms of gin- restore diminished facial contours. Mastication is restoredgivitis, poorly ﬁtting dentures, oral abscess, and tongue less predictably, and those expecting dentures to improvecoating are usual causes. Treatment includes correcting oral intake are often disappointed. Dentures require peri-poor hygiene, treating infection, and tongue brushing. odic adjustment to accommodate inevitable remodelingXerostomia can produce and exacerbate halitosis. Pock- that leads to a diminished volume of the alveolar ridge.ets of decay in the tonsillar crypts, esophageal diverticu- Pain can result from friction or traumatic lesions producedlum, esophageal stasis (e.g., achalasia, stricture), sinusitis, by loose dentures. Poor ﬁt and poor oral hygiene may per-and lung abscess account for some instances. A few sys- mit candidiasis to develop. This may be asymptomatic ortemic diseases produce distinctive odors: renal failure painful and is indicated by erythematous smooth or gran-(ammoniacal), hepatic (ﬁshy), and ketoacidosis (fruity). ular tissue conforming to an area covered by the appliance.
34. 20 ACKNOWLEDGMENT GUEIROS LA et al: Impact of ageing and drug consumption on oral The author acknowledges the contribution to this chapter by the health. Gerodontology 26:297, 2009 previous author, Dr. John S. Greenspan. LITTLE JW et al (eds): Dental Management of the Medically Compromised Patient, 6th ed. St. Louis, Mosby, 2002SECTION I REGEZI JA, SCIUBBA JJ: Oral Pathology: Clinical Pathologic Correlations, FURTHER READINGS 4th ed. Philadelphia, Saunders, 2002 BAUM BJ et al: Aquaporin-1 gene transfer to correct radiation-induced SPAHR A et al: Periodontal infection and coronary heart disease. Role salivary hypofunction. Handb Exp Pharmacol 190:403, 2009 of periodontal bacteria and importance of total pathogen burden DURSO SC: Interaction with other health team members in caring in the coronary event and periodontal disease (CORODONT) for elderly patients. Dent Clin North Am 49:377, 2005 study.Arch Intern Med 166:554, 2006 GONSALVES WC et al: Common oral conditions in older persons. Am WOO SB et al: Systematic review: Bisphosphonates and osteonecrosis Cardinal Manifestations of Gastrointestinal Disease Fam Physician 78:845, 2008 of the jaws.Ann Intern Med 144:753, 2006
35. CHAPTER 3 ATLAS OF ORAL MANIFESTATIONS OF DISEASE Samuel C. Durso ■ Janet A. Yellowitz ■ Jane C. AtkinsonThe health status of the oral cavity is linked to cardiovas- outstanding clinical photographs illustrating many of thecular disease, diabetes, and other systemic illnesses. Thus, conditions discussed in Chap. 2, Oral Manifestations ofthere is signiﬁcant clinical value in examining the oral Disease. Conditions affecting the teeth, periodontal tis-cavity for signs of disease.This chapter presents numerous sues, and oral mucosa are all represented.FIGURE 3-1 FIGURE 3-2Gingival overgrowth secondary to calcium channel blocker use. Oral lichen planus. 21
36. 22SECTION I Cardinal Manifestations of Gastrointestinal Disease FIGURE 3-3 FIGURE 3-6 Erosive lichen planus. Severe periodontitis. FIGURE 3-4 A Stevens-Johnson syndrome—reaction to nevirapine. B FIGURE 3-5 FIGURE 3-7 Inﬂamed palate. Angular cheilitis.
37. 23 CHAPTER 3 Atlas of Oral Manifestations of DiseaseFIGURE 3-8 FIGURE 3-10Sublingual leukoplakia. Traumatic lesion inside of cheek. FIGURE 3-11 Sublingual keratosis.ABFIGURE 3-9A. Epulis (gingival hypertrophy) under denture. B. Epulis FIGURE 3-12ﬁssuratum. Oral carcinoma.
38. 24SECTION I Cardinal Manifestations of Gastrointestinal Disease FIGURE 3-13 FIGURE 3-16 Healthy mouth. Gingival recession. FIGURE 3-14 FIGURE 3-17 Geographic tongue. Heavy calculus and gingival inﬂammation. FIGURE 3-15 FIGURE 3-18 Moderate gingivitis. Severe gingival inﬂammation and heavy calculus.
39. 25 CHAPTER 3 Atlas of Oral Manifestations of Disease FIGURE 3-19 FIGURE 3-22 Heavy plaque and gingival inﬂammation. Severe periodontal disease, missing tooth, very mobile teeth.FIGURE 3-20 FIGURE 3-23Ulcer on lateral border of tongue—potential carcinoma. Salivary stone.FIGURE 3-21 FIGURE 3-24Osteonecrosis. A. Calculus. B. Teeth cleaned.
40. 26SECTION I Cardinal Manifestations of Gastrointestinal Disease FIGURE 3-25 Traumatic ulcer. FIGURE 3-27 White coated tongue—likely candidiasis. FIGURE 3-26 Fissured tongue.
41. CHAPTER 4 DYSPHAGIA Raj K. Goyal Physiology of Swallowing . . . . . . . . . . . . . . . . . . . . . . . . . . . . 27 Pathophysiology of Dysphagia . . . . . . . . . . . . . . . . . . . . . . . . 28 ■ Further Readings . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 32Dysphagia is deﬁned as a sensation of “sticking” or bolus then activates oropharyngeal sensory receptorsobstruction of the passage of food through the mouth, that initiate the deglutition reﬂex.The deglutition reﬂexpharynx, or esophagus. However, it is often used as an is centrally mediated and involves a complex series ofumbrella term to include other symptoms related to swal- events. It serves both to propel food through the phar-lowing difﬁculty. Aphagia signiﬁes complete esophageal ynx and the esophagus and to prevent its entry into theobstruction, which is usually due to bolus impaction and airway. When the bolus is propelled backward by therepresents a medical emergency. Difﬁculty in initiating a tongue, the larynx moves forward and the upperswallow occurs in disorders of the voluntary phase of swal- esophageal sphincter (UES) opens. As the bolus moveslowing. However, once initiated, swallowing is completed into the pharynx, contraction of the superior pharyngealnormally. Odynophagia means painful swallowing. Fre- constrictor against the contracted soft palate initiates aquently, odynophagia and dysphagia occur together. peristaltic contraction that proceeds rapidly downward toGlobus pharyngeus is the sensation of a lump lodged in the move the bolus through the pharynx and the esophagus.throat. However, no difﬁculty is encountered when swal- The lower esophageal sphincter (LES) opens as the foodlowing is performed. Misdirection of food, resulting in nasal enters the esophagus and remains open until the peri-regurgitation and laryngeal and pulmonary aspiration staltic contraction has swept the bolus into the stomach.during swallowing, is characteristic of oropharyngeal dys- Peristaltic contraction in response to a swallow is calledphagia. Phagophobia, meaning fear of swallowing, and primary peristalsis. It involves inhibition followed byrefusal to swallow may occur in hysteria, rabies, tetanus, and sequential contraction of muscles along the entire swal-pharyngeal paralysis due to fear of aspiration. Painful lowing passage.The inhibition that precedes the peristalticinﬂammatory lesions that cause odynophagia may also contraction is called deglutitive inhibition. Local distentioncause refusal to swallow. Some patients may feel the food of the esophagus from residual food activates secondaryas it goes down the esophagus.This esophageal sensitivity peristalsis.is not associated with either food sticking or obstruction. Muscles of the oral cavity, pharynx, UES, and cervical esophagus are striated and are directly innervated by the lower motor neurons carried in the cranial nerves. OralPHYSIOLOGY OF SWALLOWING cavity muscles are innervated by the Vth and the VIIthThe process of swallowing begins with a voluntary cranial nerves and the tongue muscles by the XIIth cra-(oral) phase that includes a preparatory phase during nial nerve. Pharyngeal muscles are innervated by thewhich a food bolus suitable for swallowing is prepared IXth and the Xth cranial nerves.and a transfer phase during which the bolus is pushed The UES consists of constrictor and dilator muscles.into the pharynx by contraction of the tongue. The The constrictor muscles include the cricopharyngeus 27
42. 28 and inferior pharyngeal constrictor muscles. The dilator Oral and Pharyngeal (Oropharyngeal) Dysphagia muscles include a number of suprahyoid muscles includ- Oral-phase dysphagia is associated with poor bolus for- ing the geniohyoid muscle. The constrictor muscles are mation and control, so that food may either drool out ofSECTION I innervated by the Xth cranial nerve and the dilator the mouth or overstay in the mouth or the patient may muscles are innervated by the XIIth and also the Vth experience difﬁculty in initiating the swallowing reﬂex. and the VIIth cranial nerves. The UES remains closed Poor bolus control may also lead to premature spillage owing to the elastic properties of its wall and to neuro- of food into the pharynx and aspiration into the genic tonic contraction of the cricopharyngeus muscle. unguarded larynx and/or nasal cavity. Pharyngeal-phase Inhibition of the vagal excitatory activity in the central dysphagia is associated with stasis of food in the pharynx Cardinal Manifestations of Gastrointestinal Disease nervous system relaxes the cricopharyngeus, and con- due to poor pharyngeal propulsion and obstruction at traction of the dilator muscles opens the UES by caus- the UES. Pharyngeal stasis leads to nasal regurgitation ing upward and forward displacement of the larynx. and laryngeal aspiration during or after a swallow. Nasal The neuromuscular apparatus for peristalsis is differ- regurgitation and laryngeal aspiration during the process ent in cervical and thoracic parts of the esophagus. The of swallowing are hallmarks of oropharyngeal dysphagia. cervical esophagus, like the pharyngeal muscles, is com- Oropharyngeal dysphagia may be due to mechanical posed of striated muscles and is innervated by lower causes, including a variety of developmental abnormali- motor neurons in the vagus (Xth cranial) nerve. Peristal- ties, head and neck tumors, radiation therapy, and sis in the cervical esophagus is due to sequential activa- inﬂammatory processes (Table 4-1). tion of the vagal motor neurons in the nucleus Oropharyngeal motor dysphagia results from impair- ambiguus. ment of the voluntary effort required in bolus preparation In contrast, the thoracic esophagus and LES are com- or neuromuscular disorders affecting bolus preparation, posed of smooth-muscle ﬁbers and are innervated by initiation of the swallowing reﬂex, timely passage of excitatory and inhibitory neurons within the esophageal food through the pharynx, and prevention of entry of myenteric plexus. Neurotransmitters of the excitatory food into the nasal and the laryngeal opening. Paralysis nerves are acetylcholine and substance P, and of the of the suprahyoid muscles leads to loss of opening of the inhibitory nerves are vasoactive intestinal peptide (VIP) UES and severe dysphagia. Because each side of the and nitric oxide. Separate groups of parasympathetic pharynx is innervated by ipsilateral nerves, a unilateral preganglionic nerve ﬁbers in the Xth cranial nerve aris- lesion of motor neurons leads to unilateral pharyngeal ing from its dorsal motor nucleus project onto the paralysis. inhibitory and excitatory postganglionic myenteric neu- Neuromuscular disorders causing dysphagia are listed rons. Patterned activation of inhibitory followed by in Table 4-1. They include a variety of cortical and excitatory vagal pathways is responsible for peristalsis, suprabulbar disorders, lesions of the cranial nerves in which consists of a sequence of inhibition (deglutitive their nuclei in the brainstem or their course to the mus- inhibition) followed by contraction. The LES relaxes, cles, defects of neurotransmission at the motor end with deglutitive inhibition, at the onset of esophageal plates, and muscular diseases. Some of these disorders peristalsis. also involve laryngeal muscles and vocal cords, causing The LES is closed at rest because of its intrinsic myo- hoarseness. genic tone, inﬂuenced by excitatory and inhibitory Since the oropharyngeal phase of swallowing lasts no nerves. The function of the LES is supplemented by the more than a second, rapid-sequence videoﬂuoroscopy is striated muscle of the diaphragmatic crura, which sur- necessary to permit detection and analysis of abnormali- rounds the LES and acts as an external LES. ties of oral and pharyngeal function. However, such studies can only be performed in a fully conscious and PATHOPHYSIOLOGY OF DYSPHAGIA cooperative patient. A videoﬂuoroscopic swallowing Based on anatomic site of involvement, dysphagia may study (VFSS) using barium of different consistencies be divided into oral, pharyngeal, and esophageal dyspha- may reveal difﬁculties in the oral phase of swallowing. gia. Normal transport of an ingested bolus through the The pharynx is examined to detect stasis of barium in swallowing passage depends on the size of the ingested the valleculae and pyriform sinuses and regurgitation of bolus and size of the lumen, the force of peristaltic con- barium into the nose and tracheobronchial tree. Pharyn- traction, and deglutitive inhibition, including normal geal contraction waves and opening of UES with a swal- relaxation of UES and LES during swallowing. Dyspha- low are carefully monitored. Manometric studies may gia caused by a large bolus or a narrow lumen is called demonstrate reduced amplitude of pharyngeal contrac- mechanical dysphagia, whereas dysphagia due to weakness tions and reduced UES pressure without further fall in of peristaltic contractions or to impaired deglutitive pressure on swallowing (see Fig. 13-3). General treat- inhibition causing nonperistaltic contractions and ment consists of maneuvers to reduce pharyngeal stasis impaired sphincter relaxation is called motor dysphagia. and to enhance airway protection under the direction of
43. TABLE 4-1 a trained swallow therapist. Feeding by a nasogastric 29 OROPHARYNGEAL DYSPHAGIA tube or an endoscopically placed gastrostomy tube may be necessary for nutritional support; however, these CHAPTER 4 OROPHARYNGEAL MECHANICAL DYSPHAGIA maneuvers do not provide protection against aspiration I. Wall defects of salivary secretions. Gastrostomy tube feeding may A. Congenital actually increase gastroesophageal reﬂux and lead to 1. Cleft lip, cleft palate more aspiration. Jejunostomy tube feeding may lessen 2. Laryngeal clefts B. Post surgical reﬂux. II. Intrinsic narrowing Dysphagia resulting from a cerebrovascular accident Dysphagia A. Inﬂammatory usually improves with time, although often not com- 1. Viral (herpes simplex, varicella-zoster, pletely. Patients with myasthenia gravis and polymyositis cytomegalovirus) may respond to treatment of the primary disease. 2. Bacterial (peritonsillar abscess) Cricopharyngeal myotomy is usually not helpful. Exten- 3. Fungal (Candida) 4. Mucocutaneous bullous diseases sive operative procedures to prevent aspiration are rarely 5. Caustic, chemical, thermal injury needed. Death is often due to pulmonary complications. B. Web A cricopharyngeal bar results from failure of the 1. Plummer-Vinson syndrome cricopharyngeus to relax but with normal activity of the C. Strictures suprahyoid muscles on swallowing. Barium swallow 1. Congenital micrognathia shows a prominent projection on the posterior wall of 2. Caustic ingestion 3. Post-radiation the pharynx at the level of the lower part of the cricoid D. Tumors cartilage (see Fig. 13-1). A transient cricopharyngeal bar 1. Benign is seen in up to 5% of individuals without dysphagia 2. Malignant undergoing upper gastrointestinal studies; it can be pro- III. Extrinsic compression duced in normal individuals during a Valsalva maneuver. A. Retropharyngeal abscess, mass A persistent cricopharyngeal bar may be caused by B. Zenker’s diverticulum C. Thyroid disorders ﬁbrosis in the cricopharyngeus. Cricopharyngeal myotomy D. Vertebral osteophytes may be helpful in severely symptomatic case with func- OROPHARYNGEAL MOTOR DYSPHAGIA tional evidence of obstruction by the cricopharyngeus muscle, but is contraindicated in the presence of gastroe- I. Diseases of cerebral cortex and brainstem sophageal reﬂux because it may lead to pharyngeal and A. With altered consciousness or dementia pulmonary aspiration. Globus pharyngeus mainly occurs 1. Dementias including Alzheimer’s disease 2. Altered consciousness, metabolic encephalopathy, in individuals with emotional disorders, particularly in encephalitis, meningitis, cerebrovascular accident, women. Results of barium studies and manometry are brain injury normal. Treatment consists primarily of reassurance. B. With normal cognitive functions Some patients with globus pharyngeus have associated 1. Brain injury reﬂux esophagitis, and they may respond to treatment of 2. Cerebral palsy the esophagitis. 3. Rabies, tetanus, neurosyphilis 4. Cerebrovascular disease 5. Parkinson’s disease and other extrapyramidal lesions Esophageal Dysphagia 6. Multiple sclerosis (bulbar and pseudobulbar palsy) 7. Amyotrophic lateral sclerosis (motor neuron disease) In an adult, the esophageal lumen can distend up to 4 cm 8. Poliomyelitis and post-poliomyelitis syndrome in diameter. When the esophagus cannot dilate beyond II. Diseases of cranial nerves (V, VII, IX, X, XII) 2.5 cm in diameter, dysphagia to normal solid food can A. Basilar meningitis (chronic inﬂammatory, neoplastic) occur. Dysphagia is always present when the esophagus B. Nerve injury C. Neuropathy (Guillain-Barré syndrome, familial cannot distend beyond 1.3 cm. Circumferential lesions dysautonomia, sarcoid, diabetic and other causes) produce dysphagia more consistently than do lesions that III. Neuromuscular involve only a portion of circumferences of the esophageal A. Myasthenia gravis wall, as uninvolved segments retain their distensibility.The B. Eaton-Lambert syndrome esophageal causes of mechanical dysphagia are listed in C. Botulinum toxin Table 4-2. Common causes include carcinoma, peptic D. Aminoglycoside and other drugs IV. Muscle disorders and other benign strictures, and lower esophageal ring. A. Myositis (polymyositis, dermatomyositis, sarcoidosis) Esophageal motor dysphagia may result from abnormali- B. Metabolic myopathy (mitochondrial myopathy, thyroid ties in peristalsis and deglutitive inhibition due to diseases myopathy) of the esophageal striated or smooth muscle. C. Primary myopathies (myotonic dystrophy, oculopha- Diseases of the striated muscle often also involve the ryngeal myopathy) cervical part of the esophagus, in addition to affecting
44. 30 TABLE 4-2 ESOPHAGEAL DYSPHAGIA ESOPHAGEAL MECHANICAL DYSPHAGIASECTION I I. Wall defects 3. Pill-induced A. Congenital 4. Inﬂammatory (Crohn’s disease, Candida, B. Tracheoesophageal ﬁstula mucocutaneous lesions) II. Intrinsic narrowing 5. Ischemic A. Inﬂammatory esophagitis 6. Postoperative 1. Viral (herpes simplex, varicella-zoster, 7. Post-radiation Cardinal Manifestations of Gastrointestinal Disease cytomegalovirus) 8. Congenital 2. Bacterial D. Tumors 3. Fungal (Candida) 1. Benign 4. Mucocutaneous bullous diseases 2. Malignant 5. Caustic, chemical, thermal injury III. Extrinsic compression 6. Eosinophilic esophagitis A. Vascular compression (dysphagia lusoria, aberrant B. Webs and rings right subclavian artery, right-sided aorta, left atrial 1. Esophageal (congenital, inﬂammatory) enlargement, aortic aneurysm) 2. Lower esophageal mucosal ring (Schatzki’s ring) B. Posterior mediastinal mass 3. Eosinophilic esophagitis C. Postvagotomy hematoma and ﬁbrosis 4. Host-versus-graft disease, mucocutaneous disorders C. Benign strictures 1. Peptic 2. Caustic ESOPHAGEAL MOTOR DYSPHAGIA I. Disorders of cervical esophagus 2. Enhanced muscle contraction (see oropharyngeal motor dysphagia, Table 4-1) a. Hypertensive peristalsis (nutcracker II. Disorders of thoracic esophagus esophagus) A. Diseases of smooth muscle or excitatory nerves b. Hypertensive LES, hypercontracting LES 1. Weak muscle contraction or LES tone B. Disorders of inhibitory innervation a. Idiopathic 1. Diffuse esophageal spasm b. Scleroderma and related collagen vascular 2. Achalasia diseases a. Primary c. Hollow visceral myopathy b. Secondary (Chagas’ disease, carcinoma, d. Myotonic dystrophy lymphoma, neuropathic intestinal pseudo- e. Metabolic neuromyopathy (amyloid, alcohol?, obstruction syndrome) diabetes?) 3. Contractile (muscular) lower esophageal ring f. Drugs: anticholinergics, smooth muscle relaxants Note: LES, lower esophageal sphincter. the oropharyngeal muscles. Clinical manifestations of weakness is often associated with symptoms of gastroe- the cervical esophageal involvement are usually over- sophageal reﬂux disease (GERD). Dysphagia due to loss shadowed by those of the oropharyngeal dysphagia. of the inhibitory innervation is typically not associated Diseases of the smooth-muscle segment involve the with GERD but may be associated with chest pain. thoracic part of the esophagus and the LES. Dysphagia The causes of esophageal motor dysphagia are also occurs when the peristaltic contractions are weak or listed in Table 4-2; they include scleroderma of the absent or when the contractions are nonperistaltic. Loss of esophagus, achalasia, DES, and other motor disorders. peristalsis may be associated with failure of LES relax- ation. Weakness of contractile power occurs due to mus- cle weakness, as in scleroderma or impaired cholinergic Approach to the Patient: effect. Nonperistaltic contractions and failure of LES DYSPHAGIA relaxation occur due to impaired inhibitory innervation. Figure 4-1 shows an algorithm of approach to a patient In diffuse esophageal spasm (DES), inhibitory innervation with dysphagia. only to the esophageal body is impaired, whereas in acha- HISTORY The history can provide a presumptive lasia inhibitory innervation to both the esophageal body diagnosis in >80% of patients. The site of dysphagia and LES is impaired. Dysphagia due to esophageal muscle
45. DYSPHAGIA 31 Difficulty in initiating a swallow, misdirectional food causing coughing, choking, or nasal regurgitation CHAPTER 4 Yes No (+ Localized to throat) (+ Localized to chest or throat) Oropharyngeal dysphagia Esophageal dysphagia Dysphagia Neuromuscular findings Dysphagia to solids or liquids Yes No SOLIDS AND LIQUIDS SOLIDS ONLY Oropharyngeal Oropharyngeal Esophageal Esophageal Motor dysphagia Mechanical dysphagia Motor dysphagia Mechanical dysphagia Mental status • ENT Evaluation • Barium swallow • Esophagoscopy • Esophageal motility • Barium swallow • Esophagoscopy IMPAIRED NORMAL + Prominent heartburn Episodic or progressive FIGURE 4-1 - VFSS Yes No EPISODIC PROGRESSIVE Approach to the patient with dysphagia. ENT, ear, Lower nose, and throat; VFSS, Oral phase Pharyngeal phase esophageal ring Carcinoma videoﬂuoroscopic swallow- abnormalities abnormalities Scleroderma Achalasia ing study.described by the patient helps to determine the site mechanical dysphagia with a lumen that is notof esophageal obstruction; the lesion is at or below severely narrowed. In advanced obstruction, dyspha-the perceived location of dysphagia. gia occurs with liquids as well as solids. In contrast, Associated symptoms provide important diagnostic motor dysphagia due to achalasia and DES is equallyclues. Nasal regurgitation and tracheobronchial aspi- affected by solids and liquids from the very onset.ration with swallowing are hallmarks of pharyngeal Patients with scleroderma have dysphagia to solidsparalysis or a tracheoesophageal ﬁstula. Tracheo- that is unrelated to posture and to liquids whilebronchial aspiration unrelated to swallowing may be recumbent but not upright. When peptic stricturedue to achalasia, Zenker’s diverticulum, or gastroe- develops in patients with scleroderma, dysphagiasophageal reﬂux. becomes more persistent. Association of laryngeal symptoms and dysphagia The duration and course of dysphagia are helpfuloccurs in various neuromuscular disorders. The pres- in diagnosis. Transient dysphagia may be due to anence of hoarseness may be an important diagnostic inﬂammatory process. Progressive dysphagia lasting aclue. When hoarseness precedes dysphagia, the pri- few weeks to a few months is suggestive of carcinomamary lesion is usually in the larynx; hoarseness fol- of the esophagus. Episodic dysphagia to solids lastinglowing dysphagia may suggest involvement of the several years indicates a benign disease characteristicrecurrent laryngeal nerve by extension of esophageal of a lower esophageal ring.carcinoma. Sometimes hoarseness may be due to Severe weight loss that is out of proportion to thelaryngitis secondary to gastroesophageal reflux. degree of dysphagia is highly suggestive of carcinoma.Hiccups may rarely occur with a lesion in the distal Chest pain with dysphagia occurs in DES andportion of the esophagus. Unilateral wheezing with related motor disorders. Chest pain resembling DESdysphagia may indicate a mediastinal mass involving may occur in esophageal obstruction due to a largethe esophagus and a large bronchus. bolus. A prolonged history of heartburn and reﬂux The type of food causing dysphagia provides useful preceding dysphagia indicates peptic stricture. A his-information. Difﬁculty only with solids implies tory of prolonged nasogastric intubation, ingestion of
46. 32 caustic agents, ingestion of pills without water, previ- procedure of choice. Videoendoscopy is currently per- ous radiation therapy, or associated mucocutaneous formed only in specialized centers. Otolaryngoscopic diseases may provide the cause of esophageal stricture. and neurologic evaluation are also usually required.SECTION I If odynophagia is present, candidal, herpes, or pill- If esophageal mechanical dysphagia is suspected on induced esophagitis should be suspected. clinical history, barium swallow and esophagogas- In patients with AIDS or other immunocompro- troscopy with or without mucosal biopsies are the mised states, esophagitis due to opportunistic infec- diagnostic procedures of choice. In some cases, CT tions such as Candida, herpes simplex virus, or examination and endoscopic ultrasound may be use- cytomegalovirus and to tumors such as Kaposi’s sar- ful. For motor esophageal dysphagia, barium swallow, Cardinal Manifestations of Gastrointestinal Disease coma and lymphoma should be considered. esophageal manometry, esophageal pH, and imped- ance testing are useful diagnostic tests. Esophagogas- PHYSICAL EXAMINATION Physical examination is troscopy is also often performed in patients with important in oral and pharyngeal motor dysphagia. motor dysphagia to exclude an associated structural Signs of bulbar or pseudobulbar palsy, including abnormality (Chap. 13).