handbook of digestive diseases

8/15/2019 Handbook of Digestive Diseases

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Anil Minocha, MD, FACP, FACG

Professor of Medicine

Director of Digestive Diseases University

of Mississippi Medical Center Jackson, Mississippi

An innovative information, education, and management company

6900 Grove Road•

Thorofare, NJ 08086


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Includes bibliographical references.ISBN 1-55642-665-8 (pbk.)1. Digestive organs--Diseases--Handbooks, manuals, etc.[DNLM: 1. Digestive System Diseases--Handbooks. WI 39 M666h 2004] I. Title.RC802.M5673 2004616.3--dc22

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DD!"AT!#N

With pride and love, I dedicate this book to my daughter Geeta,

the light of my life; to my loving parents, Kamla and Ram S. Minocha,for their constant encouragement and dedication that shaped my life;and to my entire Minocha family for their patience, love, andunderstand- ing without which the book could not have beenwritten.


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"#NTNT$

Dedication

....................................................................................................iii Acknowledgments ........................................................................................ix About the Author .........................................................................................xiPreface........................................................................................................xiii

Section One: Common Gastrointestinal ComplaintsChapter 1: Dysphagia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1Chapter 2: Noncardiac Chest Pain . . . . . . . . . . . . . . . . . . . . . . . 8Chapter 3: Nausea and Vomiting . . . . . . . . . . . . . . . . . . . . . . 11Chapter 4: Belching . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16Chapter 5: Hiccups . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17Chapter 6: Dyspepsia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 19Chapter 7: Acute Abdominal Pain . . . . . . . . . . . . . . . . . . . . . . 22Chapter 8: Upper Gastrointestinal Bleeding . . . . . . . . . . . . . . 29Chapter 9: Lower Gastrointestinal Bleeding . . . . . . . . . . . . . . 35Chapter 10: Occult and Obscure Gastrointestinal Bleeding. . . 38Chapter 11: Acute Diarrhea . . . . . . . . . . . . . . . . . . . . . . . . . . . . 42Chapter 12: Traveler’s Diarrhea . . . . . . . . . . . . . . . . . . . . . . . . . 47Chapter 13: Chronic Diarrhea. . . . . . . . . . . . . . . . . . . . . . . . . . . 49Chapter 14: Constipation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 56Chapter 15: Pruritus Ani . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 60Chapter 16: Chronic Rectal Pain Syndromes. . . . . . . . . . . . . . . 62Chapter 17: Fecal Incontinence . . . . . . . . . . . . . . . . . . . . . . . . . . 63

Section Two: NutritionChapter 18: Malnutrition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 69Chapter 19: Enteral Nutrition . . . . . . . . . . . . . . . . . . . . . . . . . . . 73Chapter 20: Parenteral Nutrition . . . . . . . . . . . . . . . . . . . . . . . . 77

Section Three: EsophagusChapter 21: Gastroesophageal Reflux Disease . . . . . . . . . . . . . 85Chapter 22: Barrett’s Esophagus . . . . . . . . . . . . . . . . . . . . . . . . 94

Chapter 23: Esophageal Cancer . . . . . . . . . . . . . . . . . . . . . . . . . 97Chapter 24: Gas-Bloat Syndrome . . . . . . . . . . . . . . . . . . . . . . . 101Chapter 25: Schatzki’s Ring . . . . . . . . . . . . . . . . . . . . . . . . . . . 102Chapter 26: Infectious Esophagitis . . . . . . . . . . . . . . . . . . . . . . 103Chapter 27: Pill Esophagitis . . . . . . . . . . . . . . . . . . . . . . . . . . . 106Chapter 28: Caustic Ingestion . . . . . . . . . . . . . . . . . . . . . . . . . . 108

Section Four: Stomach and Duodenum

Chapter 29: Gastritis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 113Chapter 30: Peptic Ulcer Disease . . . . . . . . . . . . . . . . . . . . . . . 116Chapter 31: Functional Dyspepsia . . . . . . . . . . . . . . . . . . . . . . 121


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Chapter 32: Helicobacter Pylori . . . . . . . . . . . . . . . . . . . . . . . . 123


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vi Contents

Chapter 33: Gastroparesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 127Chapter 34: Gastric Polyps . . . . . . . . . . . . . . . . . . . . . . . . . . . . 130Chapter 35: Gastric Cancer . . . . . . . . . . . . . . . . . . . . . . . . . . . . 133

Section Five: LiverChapter 36: Hepatitis A. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 139Chapter 37: Hepatitis B . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 141Chapter 38: Hepatitis C . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 147Chapter 39: Hepatitis D and E . . . . . . . . . . . . . . . . . . . . . . . . . 155Chapter 40: Primary Biliary Cirrhosis . . . . . . . . . . . . . . . . . . . 156Chapter 41: Primary Sclerosing Cholangitis . . . . . . . . . . . . . . 159

Chapter 42: Alcoholic Liver Disease . . . . . . . . . . . . . . . . . . . . 163Chapter 43: Nonalcoholic Fatty Liver Disease . . . . . . . . . . . . 167Chapter 44: Drug-Induced Liver Disease . . . . . . . . . . . . . . . . 170Chapter 45: Autoimmune Hepatitis . . . . . . . . . . . . . . . . . . . . . 177Chapter 46: Hemochromatosis . . . . . . . . . . . . . . . . . . . . . . . . . 184Chapter 47: Wilson’s Disease . . . . . . . . . . . . . . . . . . . . . . . . . . 188Chapter 48: Alpha1Antitrypsin Deficiency. . . . . . . . . . . . . . . 191Chapter 49: Liver Cirrhosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . 193

Chapter 50: Medical Care of the Cirrhotic Patient . . . . . . . . . 197Chapter 51: Ascites . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 202Chapter 52: Spontaneous Bacterial Peritonitis . . . . . . . . . . . . 206Chapter 53: Hepatic Encephalopathy . . . . . . . . . . . . . . . . . . . 210Chapter 54: Hepatorenal Syndrome. . . . . . . . . . . . . . . . . . . . . 214Chapter 55: Hepatocellular Carcinoma . . . . . . . . . . . . . . . . . . 216Chapter 56: Hepatobiliary Disease During Pregnancy. . . . . . 218Chapter 57: Fulminant Hepatic Failure . . . . . . . . . . . . . . . . . . 224

Chapter 58: Liver Transplantation . . . . . . . . . . . . . . . . . . . . . . 227

Section Six: Gallbladder and PancreasChapter 59: Gallstones. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 231Chapter 60: Acute Pancreatitis . . . . . . . . . . . . . . . . . . . . . . . . . 236Chapter 61: Chronic Pancreatitis . . . . . . . . . . . . . . . . . . . . . . . 241Chapter 62: Pancreatic Cancer . . . . . . . . . . . . . . . . . . . . . . . . . 246Chapter 63: Zollinger-Ellison Syndrome . . . . . . . . . . . . . . . . . 250

Section Seven: Small IntestineChapter 64: Chronic Intestinal Pseudo-Obstruction . . . . . . . . 255Chapter 65: Small Bowel Obstruction . . . . . . . . . . . . . . . . . . . 259Chapter 66: Small Bowel Bacterial Overgrowth . . . . . . . . . . . 263Chapter 67: Lactose Intolerance . . . . . . . . . . . . . . . . . . . . . . . . 267Chapter 68: Celiac Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . 268Chapter 69: Tropical Sprue . . . . . . . . . . . . . . . . . . . . . . . . . . . . 274Chapter 70: Intestinal Lymphangiectasia . . . . . . . . . . . . . . . . 275

Chapter 71: Whipple’s Disease . . . . . . . . . . . . . . . . . . . . . . . . 276


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Contents vii

Section Eight: Large IntestineChapter 72: Acute Appendicitis . . . . . . . . . . . . . . . . . . . . . . . 279Chapter 73: Clostridium Difficile Diarrhea . . . . . . . . . . . . . . . 281

Chapter 74: Irritable Bowel Syndrome. . . . . . . . . . . . . . . . . . . 286Chapter 75: Inflammatory Bowel Disease . . . . . . . . . . . . . . . . 293Chapter 76: Microscopic Colitis . . . . . . . . . . . . . . . . . . . . . . . . 306Chapter 77: Acute Colonic Pseudo-Obstruction . . . . . . . . . . . 309

(Ogilvie’s Syndrome)Chapter 78: Diverticular Disease of the Colon . . . . . . . . . . . . 312Chapter 79: Colorectal Polyps . . . . . . . . . . . . . . . . . . . . . . . . . 318Chapter 80: Colorectal Cancer . . . . . . . . . . . . . . . . . . . . . . . . . 320

Chapter 81: Familial Polyposis/Cancer Syndromes . . . . . . . . 326Chapter 82: Colorectal Cancer Screening. . . . . . . . . . . . . . . . . 333Chapter 83: Anorectal Disorders . . . . . . . . . . . . . . . . . . . . . . . 337Chapter 84: Miscellaneous Colorectal Disorders . . . . . . . . . . 343

Section Nine: Diagnostic and Therapeutic ModalitiesChapter 85: Antibiotic Prophylaxis . . . . . . . . . . . . . . . . . . . . . 347Chapter 86: Esophagogastroduodenoscopy . . . . . . . . . . . . . . 349

Chapter 87: Colonoscopy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 351Chapter 88: Complications of Colonoscopy . . . . . . . . . . . . . . 354Chapter 89: Endoscopic Retrograde . . . . . . . . . . . . . . . . . . . . 355

CholangiopancreatographyChapter 90: Endoscopic Ultrasound . . . . . . . . . . . . . . . . . . . . 358Chapter 91: Percutaneous Endoscopic Gastrostomy . . . . . . . 360

and JejunostomyChapter 92: Gastrointestinal Radiology . . . . . . . . . . . . . . . . . . 364

Section Ten: Miscellaneous TopicsChapter 93: AIDS Patients . . . . . . . . . . . . . . . . . . . . . . . . . . . . 373Chapter 94: Food Allergies . . . . . . . . . . . . . . . . . . . . . . . . . . . . 378Chapter 95: Gastrointestinal Cancer Screening . . . . . . . . . . . . 382

and SurveillanceChapter 96: Gastrointestinal Problems. . . . . . . . . . . . . . . . . . . 384

in Systemic DisordersChapter 97: Systemic Manifestations of Gastrointestinal . . . . 391

DiseasesChapter 98: Gastrointestinal Infections . . . . . . . . . . . . . . . . . . 394Chapter 99: Acute Intestinal Ischemia . . . . . . . . . . . . . . . . . . . 403Chapter 100: Chronic Mesenteric Ischemia . . . . . . . . . . . . . . . . 410Chapter 101: Ischemic Colitis . . . . . . . . . . . . . . . . . . . . . . . . . . . 412Chapter 102: Obesity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 416

Index. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .421


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A"%N#&'DG(NT$

This book has been an enormous "solo" project that would not

have been possible without the teachings, assistance, andcooperation of many friends, senior colleagues, teachers, andthought-leaders with whom I have interacted throughout my careerand who have selfless- ly shared their knowledge and wisdom thatcarries me through this day.I am deeply indebted to the numerous expert friends and

colleagues who have reviewed the contents of the book andprovided me with important feedback and helpful suggestions. In

particular, I would like to express my deep sense of gratitude toThomas Abell, MD; Bhupinder Anand, MD; FarshidAraghizadeh, MD; Maher Azzouz, MD; Adil Bharucha, MD; RogerBlake, MD; Alan Buchman, MD; Randall Burt, MD; LawrenceBrandt, MD; Michael Camilleri, MD; Jennifer Christie, MD;Poonputt Chotiprasidhi, MD; Ray Clouse, MD; Sheila Crowe, MD;Richard deShazo, MD; Douglas Drossman, MD; Chris Friedrich,MD, PhD; Susan Galandiuk, MD; Robert Halpert, MD; Harold

Henderson, MD; Jorge Herrera, MD; Peter Kahrilas, MD; BretLashner, MD; Kalyana Lavu, MD; Scott Malinowski, PharmD;Stephen McClave, MD; Roy Orlando, MD; C. S. Pitchumoni, MD;Satish Rao, MD; Douglas Rex, MD; Arvey Rogers, MD; Sitesh Roy,MD; Lawrence Schiller, MD; Reza Shaker, MD; Gagan Sood, MD;and last but not the least, Christina Surawicz, MD. The high qualityof the text is primarily due to their help and guid- ance; the errors areall mine.

I am greatly indebted to my publisher, John Bond, and the acquisi-tions editor, Carrie Kotlar, for providing me with this unique oppor-tunity to contribute to my passion of medical education andhigh quality patient care. Finally, it was the project editor, RobertSmentek, and his team who successfully converted a blandmanuscript into a book that readers can easily read and assimilate. Iam grateful to him for doing his best to make me—and my book—look good.


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A)#*T T+ A*T+#R

Anil Minocha, MD currently serves as Professor of Medicine and

Director, Division of Digestive Diseases at the University ofMississippi Medical Center in Jackson, Mississippi. In addition to anactive involvement in patient care and research, he also serves as theProgram Director for the Gastroenterology Fellowship Program.Dr. Minocha is board-certified in gastroenterology, internal medi-

cine, and geriatrics. In addition to gastroenterology, he is fellowship-trained in clinical pharmacology and medical toxicology. He is also aFellow of the American College of Physicians and American College

of Gastroenterology.Dr. Minocha is the former gastroenterology editor forVeterans Health Systems Journal and a medical editor of theGastroenterology Textbook of eMedicine. He also serves as a manuscriptreviewer for a variety of peer-reviewed medical journals. In additionto writing several books for physicians and the lay public, he hasauthored or coau- thored over 70 publications in peer-reviewedscientific literature.

The author invites any comments or criticisms of the book thatyou might have.


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R-A"

The education of the doctor which goes on after he has his degree is, after

all, the most important part of his education. John Shaw Billings

Medicine is an art, not a science, and our vast fund of knowledgeis increasing exponentially. Time is of the essence when a patient issit- ting in an office waiting for decisions about the plan ofmanagement of his or her digestive complaints, and there may not beenough time to shuffle through the pages of a voluminous text book.

This book ful- fills the need for a quick, concise, complete, and up-to-date source of practical and unclouded clinical information, allowinga physician to develop a plan of action in an expeditious manner inany setting.A unique and distinctive characteristic of this book is that while

many other books may list management options, this bookactually includes decision-making processes, as well as the genericand brand names of the commonly used products for a particular

disorder along with the recommended doses. This feature eliminatesthe need for the physician to read several different books or thePDR for different pieces of information. The bottom line is that this book is a quick, one- stop shop for quickly needed information.

At the end of each chapter, I have also provided pearls that high-light important teaching points and/or common errors to avoidwith respect to that disorder. In addition, each chapter is followed by bibli- ographies for those interested in a more exhaustive reading of

the sub- ject.To achieve the goal of providing a condensed version of the state

of knowledge for a broad audience, I have presented what I think isthe mainstream consensus, while touching on the controversies sur-rounding various issues. While this book is an abbreviated version ofa standard text book, it is by no means a substitute for a referencetext- book or the wisdom of the thought-leaders. Robert Hutchinsononce said, “It is unnecessary—perhaps dangerous—in medicine to

be too clever.” This advice still holds true.As for myself, this book has been a lot of hard work, but it has

been a lot more fun!


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S

E C

!

" #

" #

E

"#((#N GA$TR#!NT$T!NA' "#(,'A!NT$

"hapter

. DysphagiaApproximately 30 to 40 pairs of muscles, and at least six pairs of

nerves, are involved in facilitating the movement of food fromthe mouth to the stomach. Adding to the complexity is the fact that

swallowing has to be coordinated with respiration in order toprevent aspiration. A functional or an anatomic defect at any levelcan lead to dysphagia.

!D(!#'#G/

The overall prevalence of dysphagia in the general population isabout 7%. The prevalence of dysphagia among subjects greater than

50 years of age varies from 16 to 30% and may be as high as 60% inacute hospital wards and nursing homes.

T/$ #- D/$+AG!A

Swallowing function is comprised of three phases:1. Oral

2. Pharyngeal

3. EsophagealDysphagia may be classified into two types:Oropharyngeal dyspha-

gia,in which the problem lies in the oropharynx; andEsophageal dysphagia,in which the problem lies in the esophagus.

"ropharyngeal Dysphagia

AT+#GN$!$

Oropharyngeal dysfunction may be classified into four categories:


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2 Chapter 1

1. Inability or excessive delay in initiating swallowing.

2. Aspiration of food.

3. Nasopharyngeal regurgitation.

4. Presence of food residue after swallowing.

Dysphagia can be caused by numerous factors including:1. Iatrogenic (chemotherapy and neuroleptics, head and neck sur-gery).

2. Infections (diphtheria, botulism, Lyme disease, syphilis, andviral or fungal mucositis).

3. Metabolic causes (amyloidosis, Cushing's syndrome, thyrotox-icosis, Wilson's disease).

4. Myopathic problems (connective tissue disorders, myastheniagravis, myotonic dystrophy, sarcoidosis).

5. Paraneoplastic syndromes.

6. Neurological disorders (brain stem tumors, headtrauma, stroke, cerebral palsy, Huntington's disease, multiplesclerosis, polio and postpolio syndrome, tardive dyskinesia,

Parkinson's disease and dementia).7. Structural causes (cricopharyngeal achalasia, Zenker's divertic-ulum, cervical webs, head and neck tumors).

8. Hyper- and hypothyroidism.

9. Oral ulcerations due to Crohn's and Behcet's disease.

10. Poor dentition and ill-fitting dentures.

Amongst the elderly subjects, the causes are typically neuromus-

cular in origin in approximately 80% of the cases.

"'!N!"A' (AN!-$TAT!#N$

Patients can usually point out the site of the problem (eg, orophar-ynx). They may complain of food accumulating in the mouth, inabili-ty to initiate swallowing, or describe aspiration. Patients mayalso have difficulty with chewing. They may drool and suffer fromaspira- tion, cough, and have choking spells during meals.

Patients complaining of dysphagia for both solids and liquids andtheir ability to expectorate rather than vomit out the foodsuggests oropharyngeal rather than esophageal dysphagia.Oropharyngeal dysphagia should be distinguished from not only

esophageal dysphagia, but also from globus sensation and hyposali-vation or xerostomia. These distinctions can usually be made on the basis of history.

Globus sensation or globus hystericus is a sensation of a lump or

fullness in the throat which does not affect or impede the swallowingprocesses. Swallowing, in fact, may improve the symptoms.


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Dysphagia 3

Oropharyngeal dysphagia due to hyposalivation occurs due toloss of lubrication from saliva.Physical examination involves performing a general physical

examination in addition to an attempt to identify any neuromuscularor systemic disorders that may be causing the dysphagia as well as itscomplications. Assistance by a speech language pathologist isvalu- able.

D!AGN#$!$

The underlying cause is usually apparent in most cases on the basis of clinical assessment. A videofluoroscopic evaluation of

oropharyngeal function is of paramount importance. A nasalendoscopy is performed in some centers which helps identify notonly the structural lesions of the oropharynx, but also assesses theswallowing function and the oropharyngeal reflexes. Presence orabsence of aspiration can also be determined by this technique. Adirect or indirect laryngoscopy should be performed in patientssuspected of having structural oropharyngeal lesions. Manometryand mano-fluorography is used in select centers, but their clinical

contribution is limited.TRAT(NT

Treatment depends upon the cause and the goal of feeding if thecause can not be effectively treated. Three types of dysfunction can becategorized:1. Severe dysfunction with the risk for severe aspirationrequiring nonoral feeding and even tracheotomy.

2. Structural dysfunction amenable to cricopharyngeal myotomy.3. Dysfunction amenable to dietary modification and swallowingtherapy.

reat$ent of Str%ct%ral Pro&le$s

Endoscopic dilatation is carried out for cricopharyngeal strictures.Surgery or chemoradiation therapy may be useful in oropharyngealtumors.The significance of cricopharyngeal bar identified on radiography

is controversial, although cricopharyngeal myotomy may relieve dys-phagia in select cases. Cervical osteophytes are common inelderly subjects; surgery should only be undertaken in patients withsevere dysphagia in whom all other causes have been excluded andconser- vative management has failed.Small lateral pharyngeal diverticula can be seen in patients with or

without dysphagia; improvement in dysphagia may occur after surgi-

cal ligation or removal of these diverticula. Diverticulectomy is under-taken for Zenker's diverticulum along with cricopharyngeal myotomyto prevent recurrence. Endoscopic myotomy has also been used.


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4 Chapter 1

Dilatation or myotomy for cervical esophageal webs yields mixedresults.

reat$ent of Patients at 'isk for Aspiration

In patients with high risk of aspiration pneumonia, gastrostomyfeedings may be required; however, its benefit remains to beestab- lished since the risk of aspiration of oropharyngeal secretionsis not reduced by gastrostomy. In severe cases, surgicalprocedures to reduce or eliminate aspiration may be needed. Jejunalfeeding may or may not improve airway safety.

Manage$ent of Patients (ith Cardiovasc%lar Accident

Most stroke-related dysphagia improves in 10 to 15 days.Although it may be better to avoid gastrostomy during this period,considerations of risks, costs, and benefits of transfer of thepatient from the hospital to a nursing home may overshadow theclinical considerations and lead to early gastrostomy placement inselect cases.

S(allo(ing herapy

This includes dietary modification and adjustments in theswallowing posture or swallowing technique. The goal is tostrengthen the weak oropharyngeal muscles in order to improve thespeed and coor- dination of the swallowing processes with minimalaspiration. While dietary modifications have the strongest scientific basis for its effec- tiveness, swallowing therapy is frequently used because of biological plausibility, low cost, and no risk.

Esophageal Dysphagia

AT+#GN$!$

Esophageal dysphagia may be caused by a variety of disorders, forexample, strictures or narrowing due to gastroesophageal reflux dis-ease (GERD), esophageal rings, tumors, lye ingestion, pill esophagitis,radiation and infectious esophagitis; mediastinal diseases(enlarged heart, aortic aneurysm, lung tumors, mediastinal masses,lymphoma); infections (tuberculosis and histoplasmosis); and

motility disorders (achalasia, scleroderma, etc).

"'!N!"A' -AT*R$

Patients usually complain of dysphagia primarily to solidfoods, whereas those with neuromuscular disorders have dysphagiato both solids and liquids. Patients are only 70% accurate in localizingthe site of the problem. In the remainder, they point to the neck. The

location pointed out by the patient suggests that the lesion is either ator above that site and it is only rarely below that site.


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Dysphagia 5

Schat)ki*s 'ing

Patients usually have intermittent and nonprogressive dysphagia.This often occurs during a meal in a restaurant, and as such, the term

Steak-house syndrome has been used. Patients may go without symp-toms for months or even years between the episodes.

Esophageal Strict%re

Benign strictures cause gradually progressive dysphagia with ahistory of heartburn obtained in 75% of the cases. In contrast,malignant strictures may cause rapidly progressive dysphagia, and isassociated with weight loss. Ingestion of medications like doxycycline,

potassium, nonsteroidal anti-inflammatory drugs (NSAIDs),quinidine, or alen- dronate suggest the possibility of stricture due topill-esophagitis.Patients who are immune-compromised are more likely to get

infectious esophagitis due toCandida, Cytomegalovirus (CMV), or Herpes simplexvirus, although odynophagia is more likely underthese circumstances than dysphagia alone. Infectious esophagitisdoes not typically cause a severe stricture.

#e%ro$%sc%lar Dysf%nction

Collagen vascular disorders like scleroderma and systemic lupuserythematosus (SLE) cause neuromuscular dysfunction resultingin dysphagia to both solids and liquids. Achalasia presents withlong- standing dysphagia; weight loss may be present in some cases.

Physical Findings

Physical examination is unremarkable in many cases. It is impor-tant to assess the nutritional status as well as to look for any systemicdisorder or signs of malignancy.

! N$T!GAT!#N$

+ari%$ S(allo( vs Endoscopy

Barium swallow with a barium pill is more sensitivethan endoscopy for detection of esophageal narrowing, especiallyif the lumen is greater than the diameter of the endoscope. It alsoprovides information on causes of extrinsic compression.Some experts consider endoscopy to be a more cost effective first

step and proceed directly to esophagogastroduodenoscopy (EGD)rather than performing a barium study. Endoscopic evaluation is rec-ommended for patients with esophageal dysphagia not only to estab-

lish and confirm the diagnosis of an obstruction, inflammation, infec-tion, or malignancy, but also for therapeutic purposes (ie, biopsiesand esophageal dilatation can be undertaken if necessary).


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6 Chapter 1

'ole of Esophageal Mano$etry

Esophageal manometry is useful in cases of suspected esophagealmotility disorders like achalasia, diffuse esophageal spasm (DES) and

collagen vascular diseases. Manometry should be used selectivelysince its effect upon altering the outcome in neuromuscular disordersexcept achalasia is controversial.Findings in achalasia include esophageal aperistalsis and failure of

the lower esophageal sphincter to relax in response to swallow.Secondary achalasia as a manifestation of cancer of the lung or gastriccardia needs to be ruled out before treating achalasia as idiopathic.

'adion%clide St%diesEsophageal transit scintigraphy is primarily used for research pur-

poses.

TRAT(NT

Treatment depends upon the cause.

+enign Strict%reStrictures are treated with aggressive acid suppression as well as

esophageal dilation. Simple strictures greater than 12.0 mm in sizecan be dilated using mercury bougies, polyvinyl bougies, or balloons. Complex strictures which are narrow or tortuous should be dilated using dilators over the guide wire or through-the-scope(TTS) balloon dilators. Aggressive acid suppression should continuefor patients in whom dysphagia resolves and no further dilation is

needed.If dysphagia persist or returns, repeat endoscopy should be under-

taken to confirm the presence of any mucosal lesions as well as for arepeat dilatation. Patients may continue to require dilatation intermit-tently on as needed basis.In patients in whom dysphagia persists despite repeated dilation

or returns quickly, consider a local injection ofcorticosteriods. Intralesional injection of corticosteroid involves

injection of triamci- nolone (Kenalog 40.0 mg/mL) 0.25 mL ineach of four quadrants. Other experts dilute the drug and give 0.5mL (1:1 dilution with ster- ile saline) or 1 mL (1:3 dilution) into eachquadrant at the narrowest region of the stricture.Self-bougienage and surgery are undertaken as a last resort.

Schat)ki*s 'ing

Patients should be treated by using a single large dilator for dis-

ruption of the ring along with aggressive acid suppression. Althoughthere is no good scientific data, I do not recommend a graded dilation


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Dysphagia 7

starting with smaller diameter and advancing to larger diameter.Repeated dilatation on an as needed basis may be required.If dysphagia persists or returns quickly, manometry should be

considered to look for a treatable motility disorder. Repeat endoscopyshould be undertaken to confirm healing of esophagitis and to lookfor persistence of the ring. If the ring is persistent, furtherabrupt dilatation, pneumatic dilation, endoscopic therapy, or surgeryshould be considered.

Achalasia

Treatment depends upon patient preference, skill of the endo-

scopist and the surgeon, as well as the patient's condition (ie, whetherthe patient is good or poor operative risk). Both pneumatic dilatationand surgical myotomy are effective and can be undertaken in patientswho are good operative risks. Patients who fail pneumaticdilation once are candidates for repeat dilation using a largerdiameter balloon for a total of up to three pneumatic dilatations.Persistent failure of pneumatic dilation should prompt surgicalmyotomy.

Patients who are poor operative risks may be considered for med-ical therapy using nitrates or calcium channel blockers and periodicdilation with a large diameter dilator.If dysphagia persists or is quick to return, injection of botulinum

toxin into the lower esophageal sphincter should be undertaken. Theeffect of botulinum toxin usually lasts for about 6 months andthen treatment can be repeated. If dysphagia persists despite botulinum toxin, consider gastrostomy, pneumatic dilation, or

surgical myotomy.Patients with a severely dilated esophagus due to longstanding

achalasia may not benefit from above measures andfrequently require esophagectomy.

AR'$

❍

Although not applicable to all cases, patients with oropharyn-

geal dysphagia usually have more difficulty swallowing liq-uids than solids. Patients with esophageal dysphagia presentwith the same degree of difficulty for solids and liquids orwith solid foods more than liquids.

❍

Feeding through gastrostomy does not reduce the incidence ofaspiration pneumonia in patients with oropharyngeal dyspha-gia.

❍

Barium swallow with a barium pill is superior to endoscopyfor detecting esophageal stricture; however, endoscopywithout performing a barium study may be more cost-


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8 Chapter 1effective.


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8 Chapter 2

)!)'!#GRA+/

Lind CD. Dysphagia: evaluation and treatment.Gastroenterol Clin North Am. 2003;32(2):553-75.

"hapter

1 #oncardiac Chest PainNoncardiac chest pain (NCCP) is defined as an angina-like

substernal chest pain unrelated to the heart. Since microvascularangina is one of the etiologies contributing to NCCP, angina-likechest pain may be a more appropriate term.

!D(!#'#G/

As many as 35% of coronary angiograms performed in the UnitedStates are entirely normal. Based on the magnitude of coronaryangiograms performed annually, the incidence of new cases of NCCPis about 500,000 per year. However, this may be an underestimation because it includes only the cases where cardiac catheterization has been performed, whereas many patients undergo less invasive work-up. This disorder accounts for as much as $2 billion cost annually tothe health care system.

AT+#+/$!#'#G/

The esophagus is believed to be involved in as many as 60% of thecases. The mechanisms involved are not well understood andmay include the presence of noxious stimulus in the esophagus, alowering of sensory pain threshold, or an abnormality of thenervous system. GERD plays a predominant role. Esophageal motilitydisorders are found only in a minority of cases and there is apoor relationship between symptoms and the occurrence of anepisode of esophageal dysmotility. Visceral hypersensitivity may beinvolved. These patients have lower pain threshold to balloondistention compared to controls.Although termed NCCP, cardiac causes may still cause “noncar-

diac” chest pain. There is a high prevalence of microvascular anginaor syndrome X. Other potential cardiac etiologies include pericarditis

and mitral valve prolapse.


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Psychiatric disorders include panic disorder, anxiety, and somati-zation. Musculoskeletal disorders like fibromyalgia and costochondri-tis occur in about 10% of cases.

No single etiology may be able to explain the chest pain for mostpeople since there is a high frequency of psychiatric, esophageal, andcardiac abnormalities overlapping in many of the same patients.

"'!N!"A' -AT*R$

Patients complain of a substernal, squeezing chest pain, whichmay be associated with nausea and vomiting. This pain may possibly

radiate to the jaw, neck, back, or arms. It is frequently difficult todistinguish a cardiac from a noncardiac source. An esophagealetiology is suggested by pain without radiation, lasting for severalhours and days, and has a positive response to antacids and acid-suppressive therapy. Association with dysphagia, regurgitation,and heartburn also points to GERD.

D!AGN#$!$

History and physical examination cannot reliably distinguish between cardiac and noncardiac source of pain. Cardiac etiology mustalways be excluded first since both cardiac and esophageal etiologymay coexist in the same patient, and a cardiac cause can befatal. Cardiac evaluation appropriate for age and risk factorsshould be undertaken including a noninvasive or invasive test,although coronary angiography is standard.

Once a cardiac etiology has been excluded, attention should focuson the esophagus with the predominant target beingGERD. Esophageal tests available include 24-hour pH monitoring,upper endoscopy, esophageal manometry, and provocative testing.A 24- hour pH monitoring combined with symptom analysisprovides the best diagnostic yield. The role of impedanceplethysmography is evolving.The usefulness of esophageal manometry is controversial because

of the lack of temporal relationship between episodes of dysmotilityand the pain. Provocative tests like Bernstein’s test and edrophoniumtest are usually not done these days. These provocative tests have lowsensitivity but high specificity of 70 to 90%. Balloon distention testattempts to identify patients with visceral hyperalgesia.A proton pump inhibitor (PPI) test using a twice a day dose of a

PPI has a highly positive predictive value if the patient’s symptomsabate in 14 days. In the absence of an esophageal diagnosis, a psychi-

atric evaluation may be required.


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D!--RNT!A' D!AGN#$!$

In addition to the common potential causes of NCCP, one should

not forget other conditions like biliary colic and peptic ulcer disease.Chest pain may also occur as the result of chronic obstructivepul- monary disease (COPD) and asthma.

(ANAG(NT

Management includes identification of the cause, exclusion ofa cardiac etiology, and reassurance about an excellent prognosis.

GERD responds well to treatment with acid suppressive therapy.Beta-blockers, nitrates, and calcium channel blockers have been triedfor esophageal motility disorders, as well as for microvascular anginawith limited success. Studies using smooth muscle relaxantshave shown conflicting results.Musculoskeletal conditions respond to the use of appropriate

anal- gesics and NSAIDs. Tricyclic antidepressants, as well as selectivesero- tonin reuptake inhibitors (SSRIs), are effective for panic

disorder.Low doses of tricyclic antidepressants like imipramine (Tofranil20.0 to 50.0 mg/day) or amitriptyline (Elavil 25.0 to 50.0 mg/day) areeffective in reducing the severity and frequency of chest pain episodesirrespective of the underlying cause of pain.Cognitive behavioral therapy has been shown to be of benefit.

Thoracic longitudinal myotomy has been used in rare cases of severerefractory chest pain due to nutcracker esophagus.

$*GG$TD $TRATG/

A rational approach to management includes exclusion of cardiacetiology as the first step. Once a cardiac etiology has been excluded,attempts should be made to classify the pain into esophageal, muscu-loskeletal,and/orpsychological causes. If an esophageal etiology issuspected, an empiric trial of a twice-a-day PPI should be undertaken.

In responders, the treatment may be continued as maintenance.In nonresponders, an EGD and/or 24-hour pH monitoring withsymptom analysis should be done. If the 24-hour pH monitoring andEGD are normal, an empiric trial with tricyclic antidepressantsis appropriate. Esophageal manometry and provocative testingshould be undertaken in selected cases if tricyclicantidepressants fail. Calcium channel blockers may be tried if asevere motility disorder other than achalasia is identified.

In patients whose clinical features suggest musculoskeletal etiolo-gy, look for trigger points and the reproducibility of the chest pain.


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Anti-inflammatory and local therapies are helpful in such cases. If apsychological dysfunction is suspected, panic disorder anddepres- sion should be ruled out. A short course of benzodiazepines

may be appropriate but long-term management may requireassistance from a mental health professional.

R#GN#$!$

Long-term mortality of patients in whom coronary angiogram has been normal is less than 1% at 10 years. However, the morbidityis high because of frequent visits to the physicians, as well as the

emergency rooms; frequent coronary angiograms; limitation ofactivity and inability to work; and continued use of health careresources despite negative cardiac evaluation.

AR'$

❍

Cardiac etiology must always be excluded to a reasonabledegree of certainty since both gastroesophageal reflux disease

and coronary artery disease may coexist in the same patient.

❍

Gastroesophageal reflux disease, and not esophageal spasm, isthe predominant esophageal cause of noncardiac chest pain.

❍ Gastroesophageal reflux disease is the most common treatablecause of noncardiac chest pain.

)!)'!#GRA+/

Minocha A. Non-cardiac chest pain: where does it start?PostGraduate Medicine. 1996;100:107-114.

"hapter

2 #a%sea and o$iting

Nausea is a sensation of impending vomiting whereas vomitingitself is a well-coordinated motor act that results in expulsion ofupper gastrointestinal (GI) contents in retrograde fashion. Vomitingis usually, but not always, preceded by nausea.


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12 Chapter 3

Rumination occurs when the gastric contents come up to theoropharynx followed by chewing again and are then reswallowed. Itis effortless and occurs in the absence of the coordinated neuromus-

cular activity seen in vomiting; in humans, it is often labeled aspseudorumination.Cyclic vomiting syndrome is characterized by repeated and per-

sistent episodes of nausea and vomiting lasting for hours ordays. Patients are symptom-free between the episodes. There is oftena personal or family history of migraine.

AT+#GN$!$

Nausea is usually associated with the disruptions of normalelectromechanical function along with an increase of endogenous epi-nephrine and norepinephrine as well as other changes of theauto- nomic nervous system (ANS).Vomiting is a protective reflex that is normally regulated by a

combination of neural, hormonal, and GI factors. Multiple well-coordinated events occur during the act of vomiting, including

relaxation of the stomach and the lower esophageal sphincter,retrograde contraction in the distal stomach and proximal small bowel, contraction of abdominal muscles, along with contraction ofcricopharyngeus followed by its relaxation just before vomiting.

T!#'#G/

Nausea and vomiting can be conceptualized as due to

central, extrinsic (to the gut) or intrinsic/enteric causes. Thedifferential diagnosis is complex and diverse and includesinfectious or eosinophilic gastroenteritis, postoperative vomiting,alcoholism, congestive heart failure, cyclic vomiting syndrome,pregnancy, mechanical obstruction (gastric outlet obstruction,intestinal obstruction), infections, dysmotility (GERD,gastroparesis, intestinal pseudo-obstruction), endocrine andmetabolic disorders (diabetes mellitus, hypo- and

hyperthyroidism, hypo- and hyperparathyroidism, Addison’s dis-ease, and renal failure), medications (chemotherapy, NSAIDs, digox-in, antidepressants and psychotropic agents), radiation therapy, intra-abdominal inflammatory conditions (peptic ulcer, cholecystitis, pan-creatitis, hepatitis, Crohn’s disease), central nervous system(CNS) disorders (brain tumor, abscess, meningitis or infarction,motion sickness, labyrinthitis, Meniere’s disease), andpsychogenic disorders (anxiety neurosis, depression, anorexia-

bulimia syndrome).


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Nausea andVomiting 13

"'!N!"A' -AT*R$

History often provides clues to the underlying cause. Acute onset

of symptoms occurs due to infections, medications, or acute exacerba-tion of a chronic medical condition like diabetes mellitus. A numberof patients with diabetic gastropathy (which can include bothdelayed and rapid emptying) present with cyclical symptoms, muchlike the migraine-related cyclic vomiting syndrome.Chronic nausea and vomiting is seen in patients with gastropare-

sis, intestinal pseudo-obstruction and related GI neuromuscular dis-orders; most have dyspeptic symptoms regularly.

Abdominal pain is seen in infectious and inflammatory conditionslike peptic ulcer disease, cholecystitis, or pancreatitis.Vomiting soon after eating points to gastroparesis, gastric

outlet obstruction, or pseudorumination. Vomitus containingundigested food from several hours or days before suggests outletobstruction or a primary esophageal disorder such as achalasia.Feculent vomitus suggests intestinal obstruction or gastrocolic fistula.Complaint of abdominal distention suggests intestinal obstruction.

Upper GI bleed may occur because of the underlying cause of vomit-ing (eg, peptic ulcer, pancreatitis) or a result of forceful vomiting caus-ing a Mallory-Weiss tear.

! N$T!GAT!#N$

These are tailored according to the clinical presentation andthe pathology suspected. Anatomic disorders such as peptic

ulceration or partial small bowel obstruction (SBO) must always be considered, realizing that the presentation of SBO orintusseception may not be straightforward.Studies include CBC, comprehensive metabolic profile, serum

amylase, and lipase, as well as abdominal x-ray series. Rightupper quadrant ultrasound and HIDA scan are helpful inhepatobiliary and pancreatic disorders. Miscellaneous tests done inselect cases include pregnancy test, thyroid function tests, serologic

markers for collagen vascular disorders, dedicated small bowel barium study, and an abdominal CT scan. GI motor functionand physiology can be assessed by gastric emptying time andelectrogastrography, along with small intestinal manometry.


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14 Chapter 3

TRAT(NT

General Manage$ent Management includes nutritional and symptomatic therapy in

addition to the treatment of underlying cause. A low-residue, low-fat,and predominantly liquid diet is helpful. The underlyingdisorder should be aggressively corrected (eg, correction ofhyperglycemia in diabetes mellitus). In addition to other possibleindications of underlying disorders, patients with evidence ofdehydration should be hos- pitalized.

Prokinetics

Prokinetic agents (metoclopramide 10.0 to 20.0 mg qid, domperi-done 10.0 to 30.0 mg qid, and cisapride 10.0 to 20.0 mg qid) are usefulas antiemetics especially in cases of gastroparesis. Erythromycinis effective as a prokinetic, but suffers from tachyphylaxis;other macrolide analogues are being investigated. Tegaserod alsohas sig- nificant effects on the upper GI tract, although it is currently

approved in the United States for constipation-predominant irritable bowel syndrome (IBS) in females. See Chapter 33 for details ontreatment of gastroparesis.

Sy$pto$atic Control

Nonspecific control of symptoms is achieved by using antiemetics.Combination of drugs with different mechanisms of action is benefi-cial in severe cases. Serotonin antagonists like ondansetron (Zofran) 4

to 10.0 mg IV or 8.0 mg PO tid, dolasetron 12.5 mg IV, or granisetron(Kytril) 10.0 mcg/kg IV qd or 1.0 mg PO bid are effective; the latterare primarily used for chemo-/radiation-induced or postoperativevomit- ing.Phenothiazines (promethazine 25.0 mg PO/IV q 4 to 6 hours or

8.0 to 15.0 mg/h IV infusion; prochlorperazine 5.0 to 10.0 mg POqid or5.0-10.0 mg IV q 6 hours) alone or in combination with other agents

are useful in a variety of disorders. The dose should be titrated to theside effect of sedation.Muscrinic agents are used primarily in motion sickness. Options

include scopolamine (Transderm Scop) 1 patch 4 hours prior to eventand meclizine (Antivert 25.0 to 50.0 mg starting before trip) andrepeated every day as needed.Other options of antiemetics include trimethobenzamide (Tigan

300.0 mg PO tid or 200.0 mg IM tid), dronabinol (Marinol), and

droperidol (Inapsine); the use of the latter is limited by its side effects.


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Nausea andVomiting 15

Acid-S%ppression

This is frequently undertaken especially in severe cases. H2RAs or

PPIs may be used depending upon the severity of symptoms.

Miscellaneo%s reat$ents

Tricyclic antidepressants and sumatriptan are reported to be help-ful in cyclic vomiting syndrome, as they can be in migraine. Clonidinemay be helpful in some patients with gastroparesis.Powdered ginger-root (250.0 mg qid), pyridoxine (10.0 to 50.0 mg

PO q 6 hours), doxylamine (Unisom 25.0 mg PO bid), acupuncture,and acupressure are beneficial in nausea and vomitingassociated with pregnancy. Refractory cases of hyperemesisgravidarum may benefit from a short-course of corticosteroids andparenteral nutrition.Patients with chronic symptoms who are unable to tolerate oral

feeds may need enteral feedings via a jejunostomy tube with or with-out a venting gastrostomy. Some patients may be candidates forimplantable gastric electrical stimulation (GES) device. Surgical resec-

tions and drainage procedures are not helpful. Psychiatric evaluationmay be needed in select patients.

"#('!"AT!#N$

Fluid and electrolyte disturbances, malnutrition, purpura, loss ofdental enamel, dental caries, esophagitis, Mallory-Weiss tear, andeven Boerhaave’s syndrome may be seen. Many patients with chronicnausea and vomiting may suffer from complications of long-termintravenous access including thrombosis and infection.

AR'$

❍ Nausea and vomiting are symptoms and aggressive effortsshould be made to define and treat the underlying disorder.

❍

Many patients have an underlying GI neuromuscular disease.

❍ Gastric electrical stimulation device is useful in severe gastro-paresis.

)!)'!#GRA+/

Quigley EM, Hasler WL, Parkman HP. AGA technical review on nauseaand vomiting.Gastroenterology. 2001;120(1):263-86.

Rashed H, Abell TL, Familoni BO, Cardoso S. Autonomic function incyclic vomiting syndrome and classic migraine.Dig Dis Sci.

1999;44:74s-78s.


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16 Chapter 4

Koch KL, Frissora CL. Nausea and vomiting during pregnancy.Gastroenterol Clin North Am. 2003;32(1):201-34.

"hapter

3 +elching Dictionaries describe belching or eructation as “the voiding of gas

or a small quantity of acidic fluid from the stomach throughthe mouth.” Aerophagia means swallowing of air. It primarilyoccurs while eating, drinking, chewing gum, and smoking, andincreases exponentially during anxiety. Belching in anxious persons isan extension of “normal” aerophagia and belching. While breathing in, the patients suck air into the esophagus in addition tothe trachea.

AT+#GN$!$

Normally the air in stomach is passed downstream into the intes-tines. Belching occurs when the stomach air, instead of going down,goes up into the esophagus and is expelled through the mouth. As inGERD, this process requires that the lower esophageal sphincter(LES) relax to allow the regurgitation of air upward into the esopha-gus and then out through the mouth making a sound.

Belching after a meal, especially a big meal, may be normal.It occurs as a result of air being swallowed while eating. In addition,a lot of swallowed air accumulates in the stomach in betweenmeals. The food once it reaches the stomach, displaces the air alreadypresent there. Postparandial belching is facilitated by LESrelaxation from foods like onions, mint, tomatoes, and alcohol.Cultural acceptance of belching varies. While considered to

be uncouth in the western society, a belch after a hearty meal is

considered to be a compliment for the chef in some Easterncultures.Chronic belching is generally not due any organic disorder. Rather,

it is a learned process, albeit subconsciously. In most cases, air is swal-lowed into the esophagus as described above, but ispromptly expelled out as a belch even before it has had a chance toreach the stomach. This develops into a habit in anxious persons. Magenblase syndromeis a poorly defined disorder that involves

increased fullness and bloating due to a collection of gas in the stom-ach after a meal as described above. The symptoms resolve after the


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17 Chapter 4patient belches.


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Hiccups 17

"'!N!"A' -AT*R$

Many patients believe that the belching is an indicator of disease

of the digestive system. Frequently, they ascribe relief of theirdigestive symptoms actually caused by other disorders to belching.Measures to decrease aerophagia frequently prescribed in chronic

belching (but which may be of limited benefit) include eating slowly;not chewing gum; and avoiding carbonated beverages, mint, onions,chocolates, and alcohol. Stress reduction and relaxation is the key.

AR'$

❍

Belching is a normal phenomenon and is an extension of “nor-mal” aerophagia and belching.

)!)'!#GRA+/

Rao SS. Belching, bloating, and flatulence. How to help patients who havetroublesome abdominal gas.Postgrad Med. 1997;101(4):263-9, 275-8.

"hapter

4 .icc%psThese commonly occur after a large meal or alcohol ingestion, and

are frequently subjected to numerous home-remedies.

AT+#GN$!$

Hiccups occur as a result of intermittent and involuntaryspas- modic contraction of inspiratory muscles associated withabrupt airway closure at the glottis, which produces the audiblesound.

T!#'#G!" -A"T#R$

Prolonged hiccups may be caused by foreign bodies in theear canal, cervical tumors, neurologic disorders, diabetes, uremia,alcoholism, and inflammatory or neoplastic lesions in the chest liketuber- culosis, pleurisy, and cancer. Medications like corticosteroidsand benzodiazepines have been implicated, but convincing evidenceis lacking.GI causes include GERD, and gastric outlet obstruction. GERD is

frequently the result—and not the cause—of hiccups.


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18 Chapter 5

"'!N!"A' -AT*R$

Most hiccups are short-lived and resolve spontaneously. Chronic

hiccups are defined as those persisting for greater than 48hours. Prolonged and persistent hiccups can persist for days,and even months to years, creating problems of chronic fatigue,sleep disturbances, depression, weight loss, and even suicide.

! N$T!GAT!#N$

These should be tailored to the overall presentation. Thesemay include CBC, comprehensive metabolic profile, upper-endoscopy, laryngoscopy, x-rays,and/or CT of the chest andabdomen. An MRI of the brain may be undertaken as last resort.No cause is found in majority of the cases. Fluoroscopy should beperformed to evaluate diaphragmatic movements.

TRAT(NT

Treatment should be directed at the cause. However, no cause can

be identified in many cases.

.o$e 'e$edies

These include breath holding, drinking water, rebreathing into a bag, and Valsalva maneuver.

Medical reat$ent

Pharyngeal stimulation with a nasogastric tube may be of benefit.

Firm pharyngeal stimulation in a fasting state has beenadvocated. Medications used include baclofen (5.0 to 20.0 mgtid), metoclopramide, chlorpromazine, haloperidol, amitriptyline,carbamazepine, dilantin, and nifedipine.

S%rgery

Phrenic nerve ablation may be needed in select cases. Phrenicnerve stimulation by surgically placed electrodes is in its infancy.

AR'$

❍

Most hiccups are short-lived and resolve spontaneously or inresponse to simple home remedies.

❍

Majority of chronic hiccups are idiopathic in origin.


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Dyspepsia 19

)!)'!#GRA+/

Friedman NL. Hiccups: a treatment review. Pharmacotherapy.1996;16(6):986-95.

Thompson DF, Landry JP. Drug-induced hiccups. Ann Pharmacother.1997;31(3):367-9.

"hapter

6 Dyspepsia

Dyspepsia is defined as an upper abdominal discomfort that may be associated with nausea, vomiting, fullness, bloating, or early sati-ety. Although some experts include heartburn as one of the associa-tions, the presence of heartburn alone is not considered to be dyspep-sia.

!D(!#'#G/

Prevalence estimates vary depending upon the population studiedand the definition used. Annual prevalence is estimated to be 25%.The number increases to 40% if patients with frequent heartburn arealso included.

T!#'#G/

As many as 15% to 25% of the patients with dyspepsia have pep-tic ulcer disease, while GERD is the cause in 5% to 15%. Biliary tractdisease, pancreatitis, medications, gastroparesis, infections,and malignancies are rare causes. As many as 50% to 80% of thepatients are characterized as functional dyspepsia (see Chapter 31).

"'!N!"A' -AT*R$

Three patterns of symptoms are described:1. Ulcer-like dyspepsia characterized by burning or epigastricpain relieved with antacids or acid blockers.

2. Dysmotility like dyspepsia has predominance of nausea, vom-iting, bloating, and early satiety.

2. Unspecified or mixed.

There is a marked overlap between the three groups, and abouthalf of the patients can be classified into more than onesubgroup.


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20 Chapter 6

Symptoms alone have poor predictive value for the diagnosis foundduring endoscopy.Physical examination is usually unremarkable. Epigastric tender-

ness may be seen in some cases. Presence of occult blood in stool rais-es concerns for a slowly bleeding peptic ulcer disease or malignancy.

D!AGN#$!$

CBC, comprehensive metabolic profile (including liver functiontests), and thyroid function tests are usually normal. Inyoung patients, multiple strategies for investigating dyspepsia in the

absence of alarm symptoms (ie, weight loss and bleeding) have beensuggest- ed and remain embroiled in controversy. Various optionsinclude:1. Empiric trial of antisecretory drug therapy.

2. Initial endoscopy.

3. Noninvasive serological testing for H. pylori(Hp) followed bytreatment if positive.

4. Empiric eradication of Hp.

5. Testing for Hp in patients undergoing endoscopy, ultimatelyeradicating it if infection is present.

Endoscopy is the standard for the diagnosis of mucosaldisease including ulcers, reflux esophagitis, and cancer, but it isexpensive, invasive, and not cost-effective in young patientswithout alarm symptoms. Empiric treatment with acid suppressionprovides rapid symptomatic relief in large number of patients;

however, a high rate of symptom recurrence and the possibility ofinappropriate long-term medication use make this option lessdesirable.Empiric eradication of Hp results in financial savings, but is

not favored by most experts. Testing for Hp and performingendoscopy in patients with a positive test is not cost-effective.Testing for Hp and eradicating it, if positive, is the initial step rec-

ommended by many professional societies for patients younger than

45 years of age without any alarm symptoms. This strategy increasesthe chances of antibiotic resistance.Barium studies are cheaper than endoscopy, but less accurate for

the diagnosis of peptic ulcer disease, and are not routinelyrecom- mended. Gallbladder ultrasound in patients withdyspeptic symptoms but without typical biliary pain should beavoided, since the presence of gallstones in such patients can leadto unnecessary surgery. Although gastroparesis is found in 30 to

80% of the patients, prokinetic drugs provide inconsistent relief ofsymptoms.


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Dyspepsia 21

D!--RNT!A' D!AGN#$!$

Patients with a duodenal ulcer typically have pain 2 to 5

hours after meals or on an empty stomach. They also tend towake up around midnight with pain. However, the classicsymptoms tend to occur in less than 50% of the patients. About 20%of the patients report weight gain.GERD manifests with heartburn and regurgitation; symptoms are

often relieved with antacids.Patients with gastric malignancy usually have alarm features like

weight loss, bleeding, anemia,and/or dysphagia, in addition

to abdominal pain. Gastroparesis may be seen in patients with ahistory of diabetes mellitus, hypo- or hyperthyroidism, andhyperparathy- roidism. Medications associated with dyspepsiainclude iron, NSAIDs, bisphosphonates, and antibiotics. Althoughscientific data is lacking, food intolerances are frequently implicated by the patients.

Biliary pain is acute, severe, epigastric, and/or right upperquadrant pain lasting for at least 1 hour and may radiate to back or

scapula; it is associated with nausea, vomiting, sweating, andrestlessness. The patient is typically pain-free between the episodes.Cholelithiasis by itself does not cause dyspeptic symptoms in the

absence of biliary colic or other complications. Although there isa huge overlap of functional dyspepsia and IBS, patients with IBShave disturbed bowel habit in addition to the abdominal pain.

R "#((NDD AR#A"+

If history suggests GERD, biliary pain, IBS, aerophagia, or medica-tion-induced symptoms, then the patient should be managed appro-priately by targeting the diagnosis.The various strategies for management of uninvestigated dyspep-

sia continue to be mired in controversy and should be tailored to theindividual patient and the likelihood of Hp infection. Patientsless than 45 years of age presenting with dyspeptic symptoms, but

without predominant GERD symptoms, ingestion of NSAIDs, or anyother alarm symptoms (weight loss, bleeding, recurrent vomiting,anemia, or dysphagia) should be tested for Hp using a noninvasivetest. Hp eradication should be carried out in patients who testpositive for it. Patients who do not respond to Hp eradication therapyshould undergo endoscopy.Patients who initially test negative for Hp should undergo an

empiric trial of acid suppression, preferably a proton pump inhibitor.

If symptoms persist despite acid suppressive therapy or if symptomsoccur rapidly after cessation of treatment, endoscopy should be per-


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41/560

22 Chapter 7

Because the incidence of peptic ulcer disease due to Hp is declin-ing, some experts recommend acid suppression as the initial step, fol-lowed by testing for Hp in patients who fail to resolve with acid sup-

pressive therapy.

AR'$

❍ Majority of patients with typical symptoms of peptic ulcer dis-ease are found to have functional dyspepsia.

❍

Investigation of dyspepsia should be based upon the patient’sage and clinical features including presence or absence of

alarm symptoms.

)!)'!#GRA+/

Delaney BC, Moayyedi P, Forman D. Initial management strategiesfor dyspepsia. Cochrane Database Syst Rev. 2003;(2):CD001961.

"hapter

5 Ac%te A&do$inal PainThe abdomen is a Pandora’s box. Abdominal pain may be visceral,

somatoparietal, or referred. History and physical examination

lack sensitivity and specificity in localizing the source of thepain. A rational approach to management requires anunderstanding of the mechanisms, as well as the causes andassociations of the pain, typical patterns, and typical clinicalpresentations. The majority of patients do not present with a typicalpicture, especially elderly subjects and the immune-comprised host.

"A*$$ #- A!N )/ '#"AT!#N

• Right upper quadrant pain: hepatitis, cholecystitis, biliary colic,cholangitis, pancreatitis, pneumonia, subdiaphragmaticabscesses.

• Right lower quadrant pain: appendicitis, pelvic inflammatorydisease, ectopic pregnancy, inguinal hernia.

• Epigastric pain: peptic ulcer disease, GERD, gastritis, pancreati-tis, myocardial infarction, pericarditis, ruptured aorticaneurysm.


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• Periumbilical pain: ruptured aortic aneurysm, early appendici-tis, gastroenteritis, SBO.

• Left upper quadrant pain: pancreatitis, gastric ulcer, acute gastri-tis, splenic infarction, abscess.

• Left lower quadrant: diverticulitis, pelvic inflammatory disease,ectopic pregnancy, inguinal hernia, inflammatory bowel dis-ease (IBD), IBS.

• Diffuse abdominal pain: gastroenteritis, mesenteric ischemia,metabolic causes (diabetic ketoacidosis and porphyria), malar-ia, bowel obstruction, peritonitis, IBS.

R!N"!'$ #- '#"A'!AT!#N #- A!N

1. Most digestive pain is focused in the midline, except in thegall- bladder and ascending and descending colon.

2. Pain is perceived in the spinal segment consistent with thelocation at which the nerves enter the spinal cord. Since nervesfrom the small intestine enter the spinal cord between T8 and

L1, its pain is felt in the periumbilical region.3. Pain may be perceived in the cutaneous dermatomesharing the same spinal cord level as the visceral input. Thuspain of cholecystitis may be felt in the scapular region. Onceperitoneal inflammation occurs, the pain then localizes to theright upper quadrant.

4. Abdominal pain may arise from extra-abdominal sites (eg,

Herpes zoster, myocardial infarction, pneumonia, esophagitis,uremia, porphyria, acute adrenal insufficiency, sickle cell ane-mia, hypersensitivity reaction to insect bites, lead poisoning,muscular contusion, or heat stroke).

5. The specificity for associations of pain with its location is thehighest for epigastric pain seen with gastroduodenal diseases,right subcostal and right upper quadrant pain seen in hepatobiliary diseases, and mid-lower abdominal pain due to gyne-

cological causes.

+!$T#R/

History is of paramount importance and provides important clues.

Pain Characteristics

Dull, aching, and poorly localized visceral pain usually arises from

distention or spasm of a hollow organ (eg, early intestinal obstruction


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or choledocholithiasis). Pain that is sharp and localized occurs due toperitoneal irritation, as seen in acute appendicitis.Pain of pancreatitis is steady with a gradual worsening, whereas a

rupture of viscous with acute peritonitis is sudden in onset and quick-ly reaches its maximal intensity.Burning or gnawing pain occurs in GERD or peptic ulcer disease,

whereas colicky pain is seen in gastroenteritis and intestinal obstruc-tion.

Pain Severity

The severity of the pain provides few clues since it depends upon

subjective report from the patient, as well as host factors like age andimmune-status. In general, pain of mesenteric ischemia, biliary colic,and renal colic is severe, whereas patients with gastroenteritis tend topresent with a less severe pain.

Pain 'adiation

Pain due to pancreatitis radiates to the back, while renal colic painradiates to the groin.

Associated Factors

Patients with chronic mesenteric ischemia tend to developpain within 1 hour of eating. In contrast, patients with duodenalulcer get relief upon eating and the pain recurs within a fewhours once the stomach is empty. Diffuse cramps associated withdiarrhea may point to gastroenteritis. Pain associated withabdominal distension may suggest intestinal obstruction.

+/$!"A' 7A(!NAT!#N

General E/a$ination

Vital signs provide vital information. This includes measurementof orthostatic changes if possible. Hypotension and shock may beseen in patients with intestinal obstruction, peritonitis, and bowel

infarction because of third-spacing and intravascular volumedepletion. Presence of jaundice points to hepatobiliary disease.

!nspection

Inspection includes observing the patient’s position, as well as hisor her general level of comfort. Patients with pancreatitis are usuallyseen sitting up and leaning forward to relieve their pain. Patients withperitonitis lie still on their back since motion causes pain.

Patients with renal colic are restless and in agony.


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Abdominal distention and audible bowel sounds may be appreci-ated. High pitch bowel sounds may be heard in early intestinalobstruction.

A%sc%ltation

Bowel sounds are absent in advanced peritonitis and intestinalpseudo-obstruction. Early bowel obstruction may manifest withthe high pitched bowel sounds. Presence of bowel sounds doesnot exclude intestinal pseudo-obstruction.

Perc%ssion

Gentle percussion is less painful and is the preferred method fortesting rebound tenderness, rather than deep palpation andwith- drawal. Percussion also helps to identify ascites, liverspan, and abdominal mass.

Palpation

Distract the patient while performing palpation, especially if apsy- chogenic component is suspected. Guarding and rigidity are

seen in patients with peritoneal inflammation, but it may be localizedin case of localized peritonitis due to diverticular abscess orappendicitis.A rectal and pelvic examination is part of complete physical exam-

ination of patients with acute abdominal pain. A rectal exam identify-ing fecal impaction may provide the diagnosis of obstruction in elder-ly subjects. Tenderness on rectal exam may be elicited in retrocecalappendicitis as well as pelvic inflammatory disease. Stools should be

check for occult blood.

! N$T!GAT!#N$

The depth and breadth of work-up depends upon the clues fromthe history and physical examination, and whether patient is stable.Lack of findings on history and physical examination in elderly andimmune-compromised subjects should be interpreted with caution.

A CBC and differential may point towards an infectious or inflam-matory process. A comprehensive metabolic profile can help excludemetabolic causes. Liver function tests, serum amylase, lipase, abdom-inal x-rays, chest x-ray, EKG, and urinalysis are usually obtained ini-tially. A urine pregnancy test should be done in women of child-bear-ing age.Abdominal x-ray series including chest x-ray, supine, and upright

abdominal x-ray may provide clues to evidence of obstruction or per-

foration. A CT scan is helpful when the differential diagnosis includesa variety of infectious, inflammatory, and ischemic


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Ultrasound is helpful when a gallbladder disease or a gynecologicaldisease is suspected. Ultrasound also aids in the evaluation ofsus- pected appendicitis, although a CT scan is the test of choice. An

MRI does not play any role in the investigation of acute abdominalpain with the exception of MRCP, which helps evaluate the bile ductsand pancreatic ducts.

"#((#N A"*T A)D#(!NA' A!N

$/NDR#($

1. Biliary colic: Uncomplicated cholelithiasis is usually asympto-

matic. Biliary colic usually occurs due to impaction of stone inthe cystic duct frequently preceded by a fatty meal. The pain isnot colicky but steady. It is usually deep and aching, but can besharp and severe. There is transient elevation of liver enzymes.AST/ALT may go as high as 1800IU/L. Pancreaticenzymes may be elevated. The pain lasts for a few hoursand then resolves completely. Persistence of pain beyond 6hours should raise a suspicion for cholecystitis. Persistence ofthe abnormal liver tests raises the possibility of a persistentstone in the common bile duct or alternate etiologies.

2. Acute cholecystitis: Pain is localized in the right upper quadrantor epigastrium and may be referred to the scapula. Thereis associated nausea, vomiting, and fever. Physical examshows tenderness in right upper quadrant. Murphy’s signmay be positive. HIDA scan shows a lack of filling of

gallbladder.3. Acute cholangitis: It results from impaction and obstruction ofthe bile duct and is characterized by fever, jaundice, andabdominal pain. Labs show elevated serum bilirubin and alka-line phosphatase. Ultrasound may show a dilated common bileduct.

4. Acute pancreatitis: The most common causes are alcoholism andgallstones. A bout of acute pancreatitis usually arises 1 to

3 days after drinking. Patients complain of pain in the upperabdomen, which may be in the right upper quadrant, epigas-trium, or left abdomen with radiation to the back. Pain is rapidin onset and reaches maximum intensity within an hour. Acutepancreatitis may be painless in about 5% of thecases. Pancreatic enzymes are elevated. Serum amylase rises2 to 12 hours after onset of symptoms and declines over thenext 3 to5 days. In contrast, serum lipase persists much longer. Greaterthan 3-fold increase in serum ALT suggest a biliary etiology.


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CT scan is superior to ultrasound for evaluation ofpancreas (see Chapter 60).


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5. Splenic abscess and infarct: Pain occurs in the left upperquadrant and is associated with fever and tenderness. Itshould be considered in patients with risk for embolism

(eg, atrial fibrilla- tion).

6. Acute appendicitis: Initially the pain is periumbilical, whicheventually localizes to the right lower-quadrant with evidenceof localized peritoneal signs. Occasionally patients may com-plain of generalized abdominal pain. Patients with a retrocecalappendix may only complain of dull achy pain withoutany localized tenderness. A good history and physical

examination is usually sufficient for diagnosis in most cases.A urinalysis should be obtained to exclude urinary tractinfection. Pelvic cultures may be helpful in sexually-active menstruating women. A pregnancy test should bedone in women of child- bearing age to exclude ectopicpregnancy. Of note, 30% of patients with acute appendicitisdo not show any leukocytosis; however, most of them do showleft shift. Imaging studies are only required if the diagnosis is

in doubt. A CT scan is the test of choice (see Chapter 72).7.Diverticular disease: Uncomplicated diverticulosis is asympto-matic. Painful diverticular disease may present with abdomi-nal cramps, bloating, and a feeling of incomplete ordifficult evacuation and irregular defecation. Physical examis unremarkable. Diverticulitis on the other hand occurs as aresult of microscopic or macroscopic perforation of thediverticulum, which quickly seals off. Most patients present

with a left lower- quadrant pain. In Asian countries, right-sided diverticulitis is more common. Patients may present tothe physician several days after the onset which helps todistinguish it from any other abdominal complaints.Localized tenderness is seen. CBC shows leukocytosis.Endoscopic evaluation and barium enema are relativelycontraindicated especially in acute severe diverticulitis andthe treatment is usually based on clinical grounds. The studies

are only undertaken if the diagnosis is in doubt. However,once an episode of acute diverticulitis is resolved, patientshould undergo a colonoscopic evaluation in about 4 to8 weeks to exclude any other disorder mimicking diverticulitisincluding a malignancy (see Chapter 78).

8.Nephrolithiasis: There is a wide spectrum of pain which may beminimal to severe, eventually requiring hospitalization and

parenteral pain control. Pain waxes and wanes in paroxysmslasting from 10 to 60 minutes. Pain may be in the flank or mayradiate to the testicle or tip of the penis or labia. The location of


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the pain can change as the stone migrates. A CT scan is the testof choice. Ultrasound may be undertaken in patients who wishto avoid radiation especially pregnant women or women of

child bearing age.

9.Pelvic inflammatory disease: It is characterized by lower abdomi-nal pain especially during menstruation or sexual intercourse.It occurs more commonly between the ages of 15 and 25 years.Those at risk include African Americans, those with multiplesex partners, and those with a male sex partner who has a sex-ually transmitted disease. Pain is usually bilateral. Additional

features may include uterine bleeding, new onset of vaginaldischarge, proctitis, fever, and chills. Ectopic pregnancy, rup-tured ovarian cyst, torsion of the fallopian tubes,and endometriosis should be excluded.

10. Chronic mesenteric ischemia: There is postparandial pain associ-ated with weight loss and sometimes nausea, vomiting,and diarrhea. It may be seen in patients with atherosclerosis ormay be a manifestation of systemic vasculitis. Angiography

is the test of choice (see Chapter 100).11. Acute mesenteric ischemia: Abdominal pain is acute, severe, dif-

fuse, and out of proportion to the physical findings. There may be frank hematochezia or only heme-positive stools.Angiography provides diagnosis as well as therapeutic options(see Chapter 99).

12. Acute intestinal obstruction: It causes acute, severe, and diffuseabdominal pain. Etiologies include adhesions, incarceratedhernia, intussusception, or volvulus. Adhesions account for 80to 95% of the cases. Fecal impaction may sometimes present asobstruction especially in case of elderly or those withneuro- logical or developmental disorders. Patientscomplain of abdominal pain, nausea, vomiting, abdominaldistention, and lack of passage of flatus. Abdominal x-rayseries shows dilated bowel with multiple air-fluid levels (see

Chapter 77).

(ANAG(NT

General Meas%res

Stable patients seen in ambulatory settings usually do not requireany aggressive investigations. Patients with acute abdomen, onthe other hand, should go to the emergency room and be admitted.They should take nothing by mouth. Intravenous fluids andelectrolytes are


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Upper Gastrointestinal Bleeding 29

8

administered while the investigations are pending. A surgical consultshould be obtained.

Pain Control Narcotics for pain control should be avoided early in thecase because they cloud the assessment and decision-makingprocess. Patients with biliary colic or acute cholecystitis get benefitfrom parenteral NSAIDs like ketorolac (15.0 to 30.0 mg IV or IM q 6hours).

Specific Manage$ent

Treatment beyond intravenous fluids and pain control dependsupon the etiology of the pain. Patients with evidence of diffuse peri-tonitis required emergent surgical consultation.

AR'$

❍

Typical clinical and laboratory features of acute abdominalpain may be absent in about 30% of the cases, especially in eld-

erly and immune-compromised subjects.

❍

Rectal and pelvic exam should be performed in all casesof acute abdomen.

❍ A pregnancy test should be performed in all women of child- bearing age.

)!)'!#GRA+/

Sharp HT. The acute abdomen during pregnancy.Clin Obstet Gynecol.2002;45(2):405-13.

Gore RM, Miller FH, Pereles FS, Yaghmai V, Berlin JW. Helical CT in theevaluation of the acute abdomen. Am J Roentgenol.2000;174(4):901-13.

"hapter

Upper Gastrointestinal +leeding

Upper GI bleeding is a major cause of morbidity and mortality, aswell as utilization of health care resources. It accounts for over100 hospitalizations per 100 000 population and is more common in

males. The elderly are especially at high-risk.


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30 Chapter 8

T!#'#G/

Peptic ulcer disease accounts for 55% of the cases. Risk factors for

bleeding in peptic ulcer disease include Hp infection, NSAIDs, severestress of sickness in ICU patients (stress gastropathy), andgastric hyperacidity.Varices are the cause in 14% of upper GI hemorrhage and variceal

bleeding carries a mortality rate of 30% for each episode.Arteriovenous malformations are the diagnosis in 6%,whereas Mallory-Weiss tears, erosions, and tumors each are the causein about

5% cases.Uncommon causes of upper GI bleed include Dieulafoy’s lesion,gastric antral vascular ectasia (GAVE), portal hypertensive gastropa-thy, hemobilia, hemosuccus pancreaticus, and upper GI tumors.

"'!N!"A' -AT*R$

Patients usually present with hematemesis or coffee ground-likeemesis and/or melena. Instillation of 50 to 100 mL of blood intothe stomach results in melena; on the other hand, patients losing 100mL of blood per day may have normal appearing stools.

D!AGN#$!$

Gastric lavage of frank blood or coffee ground-like material isdiagnostic. However, lavage may be negative if the bleeding hasstopped or the source of bleeding is beyond the pylorus and

the pylorus is closed.The presence of bilious material on gastric lavage suggests

that there is no active upper GI bleeding. Hematochezia may be seenin 5 to 10% of the patients with severe upper GI hemorrhage. Suchcases are usually accompanied by hemodynamic compromise.Endoscopy is undertaken for diagnostic as well as therapeuticpurposes.

! N!T!A' (ANAG(NT

Rapid assessment of hemodynamic status and resuscitation aremore important than the precise diagnosis of the cause of bleed.Large bore intravenous access should be accomplished quickly.Stat labs should be drawn for at least a CBC, basic metabolic panel,and coagulation profile. Patients with shock, orthostatichypotension, drop of hematocrit greater than 6%, transfusion

requirement of greater than two units, or continued active bleedingshould be admitted to the ICU for close monitoring. Aggressive


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Upper Gastrointestinal Bleeding 31resuscitation with stabilization as much as possible is essential tominimize complications.


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32 Chapter 8

ransf%sions

Elderly patients or those with severe comorbidity likecoronary artery disease should have blood transfusions to

maintain a hematocrit above 30%. Young and otherwise healthysubjects may be trans- fused to the extent of 20% or above.

Patients with continued bleeding in the presence of coagulopathy(INR greater than 1.5) or low platelet count less than 50000/mm2 should be given fresh frozen plasma and plateletsrespectively.

'ole of Gastric 0avage

The impact of nasogastric lavage on the outcome remains to be established. Gastric lavage using a large-bore orogastric tuberemoves blood and blood clots and facilitates endoscopy as well asreduces the risk for aspiration. Use of prokinetic prior to endoscopymay accom- plish the same objective.

Air(ay Protection

Endotracheal intubation should be considered in patients with

continuing active bleed and altered mental status.

!nitial Medical Manage$ent Octreotide is effective in controlling active variceal bleeding due to

varices and reducing risk for rebleeding after endoscopic controlof the hemorrhage. Its role in nonvariceal upper GI hemorrhage iscon- troversial and I recommend its use as an adjunctive treatment before endoscopy or if endoscopy is unsuccessful or unavailable. I

also recommend intravenous PPI infusion to be started as soonas possible prior to endoscopy.

$"!-!" D!AGN#$!$

EGD allows a precise diagnosis as well as opportunity for thera-peutics. A single dose of metoclopramide 20.0 mg IV or erythromycin250.0 mg IV may be given 20 to 120 minutes prior to endoscopy to

has- ten gastric emptying of the blood and clots, thereby improvingvisi- bility and the quality of endoscopic visualization.Angiography or RBC bleeding scan may occasionally be helpful.

Endoscopic ultrasound may help distinguish between gastric varicesand large gastric folds. Upper GI barium studies are contraindicatedin the presence of acute GI bleed.


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Upper Gastrointestinal Bleeding 33

TRAT(NT #- )'D!NG *'"R$

'isk Stratification

Endoscopy allows for risk stratification of the patients. For exam-ple, patients with active arterial bleeding are likely to rebleed in 90%of the cases on medical management alone, nonbleeding visible vesselin 50%, and adherent clot in about 25% of cases. On the other hand,an ulcer with a clean base rebleeds in less than 5% of the cases.Persistent oozing from an ulcer without a visible vessel has arebleeding rate of

10 to 20%.

Endoscopic Strategy +ased on 'isk Stratification

Endoscopic therapy improves outcome in patients with active bleeding as well as nonbleeding visible vessels. Ulcers with aclean base or flat pigmented spot should not be treatedendoscopically. The management of adherent clot is controversial.Clots that can not be removed by aggressive irrigation carry a 25%

risk for rebleeding. While some experts manage these patientsmedically, others attempt to remove the clot by ensnaring andthen treating it based on the underlying ulcer pathology.

Endoscopic reat$ents

Endoscopic treatments for bleeding peptic ulcers include electro-coagulation, injection therapy, hemostatic clips, a fibrin sealant orglue, or cauterization. Usually a combination of injection therapy with

epinephrine1/10 000 locally followed by thermal coagulation is per-formed. Endoscopic clips control bleeding in the manner similar tosurgical ligation. The role for fibrin sealant needs to be defined.

!atrogenic Co$plications

Treatment related complications include aspiration, hypoventila-tion, hypo

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