Ebook Gastrointestinal imaging: Part 1

(BQ) Part 1 book Gastrointestinal imaging presents the following contents: Pharynx and esophagus, stomach, small bowel, appendix, colon, anorectum, diffuse and vascular liver disease. Invite you to consult.

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Koenraad J. Mortele, MD

Associate Professor of RadiologyHarvard Medical SchoolDepartment of RadiologyBeth Israel Deaconess Medical Center

Boston, Massachusetts

Benjamin M. Yeh, MD

Professor of RadiologyUCSF Department of Radiology and

Biomedical ImagingUniversity of California, San Francisco

San Francisco, California

With Medical Illustrations by

Heike Blum

Medical IllustratorMüenster, Germany

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Library of Congress Cataloging-in-Publication Data

Gastrointestinal imaging (Levy)

Gastrointestinal imaging / edited by Angela D Levy, Koenraad J Mortele, Benjamin M Yeh.

p ; cm.—(Rotations in radiology)

Includes bibliographical references and index.

ISBN 978–0–19–975942–2 (alk paper)

I Levy, Angela D., editor II Mortele, Koenraad J., editor III Yeh, Benjamin, editor IV Title V Series: Rotations in radiology.

[DNLM: 1 Digestive System Diseases—diagnosis 2 Diagnosis, Differential

3 Diagnostic Imaging—methods 4 Diagnostic Techniques, Digestive System WI 141] RC804.D52

616.3′0754—dc23

2014028627

This material is not intended to be, and should not be considered, a substitute for medical or other professional advice Treatment for the conditions described in this material is highly dependent on the individual circumstances And, while this material is designed to offer accurate information with respect to the subject matter covered and to be current as of the time it was written, research and knowledge about medical and health issues is constantly evolving and dose schedules for medications are being revised continually, with new side effects recognized and accounted for regularly Readers must therefore always check the product information and clinical procedures with the most up-to-date published product information and data sheets provided by the manufacturers and the most recent codes of conduct and safety regulation The publisher and the authors make no representations or warranties to readers, express or implied, as to the accuracy or completeness of this material Without limiting the foregoing, the publisher and the authors make no representations or warranties as to the accuracy or efficacy of the drug dosages mentioned in the material The authors and the publisher do not accept, and expressly disclaim, any responsibility for any liability, loss or risk that may be claimed or incurred as a consequence of the use and/or application of any of the contents of this material.

9 8 7 6 5 4 3 2 1

Printed in the United States of America

on acid-free paper

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To my husband Asa, for his love and infinite support.

—ADL

To Dejana, for her infinite love and support, and my four beautiful children, Charlotte, Christophe, Mabel and Mila,

who make me proud every day and remind me of what is truly important in life

—KJM

To my wife, Dr. Z. Jane Wang, and our kids, who inspire us daily

—BMY

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The views expressed in Section 14, Multisystem Disorders

and Syndromes, are those of the authors and do not

neces-sarily reflect the official policy or position of the Uniformed

Services University of the Health Sciences, Department of the Air Force, Navy or Army; Department of Defense or the US Government

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Preface xv

Contributors xvii

Section I: Pharynx and Esophagus

1 Normal Anatomy and Imaging Techniques

of the Pharynx and Esophagus 3

4 Pharyngeal and Esophageal Diverticula 16

Marc S. Levine

A Zenkers and Killian-Jamieson Diverticula 16

B Thoracic Esophageal Diverticula 18

Section II: Stomach

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Section III: Small Bowel

of the Small Bowel 119

Francis J. Scholz and Peter E. Humphrey

21 Congenital and Developmental Abnormalities 124

A Malrotation 124

B Paraduodenal Hernia 126

22 Diverticula of the Small Bowel 130

A Diverticulosis of the Small Bowel 130

B Meckel’s Diverticulum 132

23 Crohn’s Disease 136

24 Other Inflammatory Disorders 142

A Tuberculosis 142

B Small Bowel Parasites 144

C Opportunistic Small Bowel Infections 146

D Nonsteroidal Anti-inflammatory Drug Enteropathy 149

25 Celiac Disease 151

26 Small Bowel Obstruction 156

A Mechanical Small Bowel Obstruction 156

B Closed-Loop Obstruction and Strangulation 159

27 Small Bowel Intussusception 163

31 Benign Tumors of the Small Bowel 180

A Ectopic Pancreas 180

B Brunner Gland Lesions 181

C Adenoma 183

D Lipoma and Hemangioma 184

32 Malignant Tumors of the Small Bowel 187

A Adenocarcinoma of the Small Bowel 187

B Lymphoma of the Small Bowel 189

C Carcinoid Tumor of the Small Bowel 191

D Gastrointestinal Stromal Tumor 193

E Metastases 195

Section IV: Appendix

Mark Knox and Koenraad J. Mortele

A Appendiceal Carcinoid Tumors 209

B Appendiceal Mucinous Cystadenoma 211

37 Inflammatory Bowel Disease 223

Richard M. Gore, Kiran H. Thakrar, Geraldine M. Newmark, Uday K. Mehta, and Jonathan W. Berlin

39 Infectious Colitis 236

41 Benign Colonic Polyps 247

42 Colonic Adenocarcinoma 252

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43 Colonic Obstruction 257

44 Colonic Volvulus 260

Section VI: Anorectum

of the Anorectum 265

Koenraad J. Mortele

46 Retrorectal Developmental Cysts 271

Max J. Lahaye, Geerard L. Beets, Regina G. H Beets-Tan, and Angela D. Levy

47 Perianal Fistula 274

Jaap Stoker

48 Rectal Adenocarcinoma 280

Benjamin M. Yeh and Koenraad J. Mortele

49 Other Anorectal Neoplasms 285

Angela D. Levy and Koenraad J. Mortele

50 Posterior Compartment of the Pelvic Floor 290

Beatriz C Baranski Kaniak, Guilherme Moura

da Cunha, Jin-Young Choi, and Claude

B. Sirlin

53 Disorders of Iron Overload 316

B. Sirlin

54 Cirrhosis 323

B. Sirlin

55 Other Metabolic Disorders 330

da Cunha, Jin-Young Choi, and Claude B. Sirlin

C Liver Infarct 342

57 Portal Vein Disorders 345

da Cunha, Jin-Young Choi, and Claude B. Sirlin

A Bland Thrombosis 345

B Tumoral Thrombosis 348

58 Veno-Occlusive Disorders 354

B. Sirlin

59 Liver Transplantation 361

B. Sirlin

A Pre–liver Transplantation Evaluation 361

B Post–liver Transplantation Complications 363

Section VIII: Focal Liver Disease

60 Cystic Hepatic Tumors 371

Jin-Young Choi, Guilherme Moura da Cunha, Beatriz C Baranski Kaniak, and Claude B. Sirlin

A Simple Hepatic Cysts and Polycystic Liver Disease 371

B Biliary Cystadenoma and Cystadenocarcinoma 374

C Von Meyenberg Complexes 376

61 Benign Liver Tumors 379

A Benign and Premalignant Liver Nodules in the Cirrhotic Liver 397

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63 Uncommon Solid Liver Tumors 413

64 Secondary Liver Tumors 419

66 THEDs: THADs and THIDs 436

67 Trauma 443

Section IX: Gallbladder

A Acute Calculous Cholecystitis 453

B Acute Acalculous Cholecystitis 456

G Gallbladder Perforation and Gallstone Ileus 467

of the Bile Ducts 481

So Yeon Kim, En-Haw Wu, and Benjamin M. Yeh

73 Developmental and Congenital Disorders of the Bile Duct 484

So Yeon Kim, En-Haw Wu, and Benjamin M. Yeh

A Bile Duct Anatomic Variants 484

B Obstructed or Excluded Bile Ducts 515

C Bile Duct Leak 516

Section XI: Pancreas

B Congenital and Genetic Diseases 530

C Other Pancreatic Variants and Pitfalls 532

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C Serous Microcystic Adenoma 556

D Solid Pseudopapillary Tumor 558

83 Pancreatic Ductal Adenocarcinoma 560

Koenraad J. Mortele

84 Other Solid Pancreatic Tumors 565

Koenraad J. Mortele and Angela D. Levy

A Pancreatic Endocrine Tumors 565

B Rare Solid Pancreatic Tumors 569

C Secondary Pancreatic Tumors 571

85 Pancreatic Surgery/Transplant 575

Koenraad J. Mortele and Angela D. Levy

A The Postoperative Pancreas 575

103 Familial Adenomatous Polyposis 679

David Reynolds, Grant Lattin, and Darcy J. Wolfman

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108 Von Hippel-Lindau Syndrome 697

Grant Lattin and Darcy J. Wolfman

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We are privileged to practice radiology and abdominal

imag-ing in an era that includes classic radiologic techniques—such

as radiography, fluoroscopy, and nuclear medicine—as well

as modern state-of the-art high-resolution ultrasound,

multidetector computed tomography, magnetic resonance

imaging, positron emission tomography computed

tomog-raphy, and the advanced postprocessing techniques that

can be applied to these imaging data The combination of

these diagnostic radiologic and imaging modalities makes

it possible to provide the most accurate and comprehensive

diagnostic information to patients and their physicians in

a manner that allows for the optimal treatment and

man-agement of gastrointestinal diseases However, for those

learning and practicing radiology and abdominal imaging,

the amount of information they must acquire about these

diseases can be overwhelming Furthermore, it has been

difficult to find a relatively short single-volume reference

that concisely encapsulates the most important clinical

and pathologic information on gastrointestinal diseases as

well as all of the radiologic and imaging modalities used to

study them

Therefore the goal of our textbook is to provide a prehensive but easy-to-read resource that highlights the

com-most important clinical, pathologic, radiologic, and

imag-ing manifestations of gastrointestinal diseases It is

pri-marily designed to be used during training on radiology

rotations where gastrointestinal diseases are imaged and

to place diagnostic considerations into clinical context

Because all radiologic and imaging modalities are

dis-cussed with each disease, this textbook can be used during

fluoroscopy, computed tomography, magnetic resonance

imaging, and ultrasound rotations; for exam preparation; and as a reference by practicing radiologists

As part of the Rotations in Radiology series,

Gastrointestinal Imaging provides a comprehensive review

of gastrointestinal diseases through its organization by organ and disease The book is organized into sections that cover all of the hollow and solid gastrointestinal organs, the peritoneal cavity and abdominal wall; finally, there is

a multisystem section that covers diseases affecting tiple organs and organ systems Each major section con-tains a chapter on normal anatomy, imaging techniques, and principles of interpretation for each specified organ For each disease, a concise definition and summary of the clinical, pathologic, and imaging manifestations is pro-vided, followed by a bulleted differential diagnosis that highlights the differences between diseases, a summary

mul-of key points, and a brief review mul-of current management The chapters are heavily illustrated with images that show the most important radiologic and imaging features Anatomic illustrations highlight the key anatomical fea-tures that are important for understanding imaging con-cepts and disease classification

All chapters are authored by internationally known radiologists who have published authoritative works in their fields of expertise We greatly thank them for taking the time

to contribute to this book It is essential that they pass their knowledge and expertise on to those using this textbook who are in residency training, studying for exams, or simply referencing material for clinical practice In short, this text provides the most current imaging concepts and theory for the wide range of diseases of the gastrointestinal tract

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Geerard L. Beets, MD, PhD

Professor of Surgery

Department of Surgery

Maastricht University Medical Centre

Maastricht, The Netherlands

Regina G. H Beets-Tan, MD, PhD

Professor of Radiology

Department of Radiology

Maastricht University Medical Centre

Maastricht, The Netherlands

Guilherme Moura da Cunha, MD

Liver Imaging Group

Dept of Radiology

University of California

San Diego, California

Clinica de Diagnostico por Imagem - CDPI

Evanston HospitalEvanston, Illinois

Peter E. Humphrey, MD

Northwest ImagingKalispell Regional Medical CenterKalispell, Montana

Beatriz C Baranski Kaniak, MD

Liver Imaging GroupDepartment of RadiologyUniversity of California, San Diego

VA Healthcare SystemSan Diego, California

Jonathan Keung, MD

Department of RadiologyWalter Reed National Military Medical CenterBethesday, Maryland

So Yeon Kim, MD

Department of Radiology and Research Institute

of RadiologyUniversity of Ulsan College of MedicineAsan Medical Center

Seoul, Korea

Mark Knox, MBBCh, BAO

Department of Radiology

St James’s HospitalDublin, Ireland

Max J. Lahaye, MD, PhD

Department of RadiologyMaastricht University Medical CentreMaastricht, The Netherlands

Grant Lattin, MD

Assistant Professor of RadiologyDepartment of RadiologyUniformed Services UniversityBethesda, Maryland

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Université Libre de Bruxelles

Erasme University Hospital

Lahey Hospital and Medical CenterBurlington, Massachusetts

Claude B. Sirlin, MD

Liver Imaging GroupDepartment of RadiologyUniversity of California, San DiegoSan Diego, California

Jaap Stoker, MD

Professor of RadiologyDepartment of RadiologyAcademisch Medisch CentrumUniversiteit van AmsterdamAmsterdam, The Netherlands

Eric Sturgill, MD

Department of RadiologyNaval Medical Center PortsmouthPortsmouth, Virginia

Kiran H. Thakrar, MD

Professor of RadiologyChief GI RadiologyDepartment of RadiologyNorth Shore University Health SystemUniversity of Chicago

Evanston HospitalEvanston, Illinois

Darcy J. Wolfman, MD

Assistant Professor of RadiologyUniformed Services University of the Health SciencesDepartment of Radiology

Walter Reed National Military Medical CenterBethesda, Maryland

En-Haw Wu, MD

UCSF Department of Radiology and Biomedical ImagingChang Gung Memorial Hospital

Linkou, Taiwan

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Pharynx and Esophagus

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Normal Anatomy and Imaging

Techniques of the Pharynx and

Esophagus

Marc S. Levine

Introduction

Pharyngoesophagography is a valuable technique for

dem-onstrating a wide range of functional and structural lesions

of the pharynx and esophagus The pharyngeal portion of

the study enables evaluation of swallowing dysfunction

as well as a variety of morphologic abnormalities in the

pharynx The esophageal portion is equally valuable for

detecting esophageal dysmotility, gastroesophageal reflux

disease, infectious esophagitis, esophageal carcinoma, and

other morphologic abnormalities of the esophagus

Pharynx

Pharyngeal Examination

The oral and pharyngeal phases of swallowing function are

evaluated by having the patient initially swallow a bolus of

high-density barium; the patient is then viewed in the

fron-tal and lateral positions If the patient is unable to stand,

he or she may be placed in a speech therapy chair for this

examination Video or DVD recordings of swallowing are

obtained and later reviewed in slow motion to carefully

assess all phases of swallowing Spot images of the

phar-ynx are also obtained, again with the patient in frontal and

lateral positions, during suspended respiration and

phona-tion to assess for structural abnormalities of the pharynx

(Figure 1-1) Phonation expands the pharyngeal lumen,

sometimes permitting the detection of findings that are not

visible when the pharynx is collapsed (see Figure 1-1A and

B) If a Zenker’s diverticulum, cervical esophageal

stric-ture, or tumor is suspected, rapid-sequence imaging may

be performed to better assess the cervical esophagus and

pharyngoesophageal junction Modified barium swallows

use various consistencies of barium to assess the presence

and degree of laryngeal penetration or aspiration in patients

who are at risk for aspiration or have known swallowing

dif-ficulties These modified swallows are usually performed in

conjunction with speech pathologists who can employ a

variety of compensatory strategies (e.g., placing the head in

a chin-tuck position) to improve swallowing function

Normal Pharyngeal Anatomy

The pharynx, a tube composed of skeletal muscle, has a squamous epithelial lining The oropharynx extends in a craniocaudad direction from the soft palate to the pharyngo-epiglottic folds The anterior wall of the oropharynx extends

to the base of the tongue, and the posterior wall abuts the upper cervical spine The hypopharynx is the portion of the pharynx that is associated with the larynx The hypophar-ynx extends craniocaudally from the pharyngoepiglottic folds to the pharyngoesophageal segment (Figure 1-2)

The anterior wall of the hypopharynx is formed by the epiglottic and arytenoid cartilages, piriform sinuses, and surrounding thyroid cartilage The posterior wall of the hypopharynx is bordered by the cervical spine The crico-pharyngeus muscle forms the junction of the pharynx and esophagus, also termed the pharyngoesophageal segment

The palatine fossae are bounded by the anterior and posterior tonsillar pillars, also known as the paired palato-glossal and palatopharyngeal folds The vertical surface of the tongue is nodular because of the underlying circumval-late papillae and lingual tonsil The valleculae are potential spaces created by a fold of tissue that extends posteriorly to the epiglottis (the median glossoepiglottic fold) The vallecu-lae disappear when the epiglottis inverts during swallowing

The piriform sinuses form the anterior portion of the lower hypopharynx They are pear-shaped spaces created

by protrusion of the larynx into the pharynx These spaces are open posteriorly to the remainder of the hypopharynx The aryepiglottic folds and mucosa overlying the muscu-lar process of the arytenoid cartilages form the medial boundaries of the piriform sinuses

Normal Pharyngeal Function

Swallowing is arbitrarily divided into four tion and bolus preparation, (2) the oral phase, (3) the pha-ryngeal phase, and (4) the esophageal phase During the oral phase, a bolus is selected and brought to the lips by volitional activity A liquid is sucked or poured into the mouth A solid

phases: (1) inges-is placed on top of the tongue Liquids do not require much oral manipulation and therefore are easily transferred to the

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oropharynx In contrast, solids must be chewed and mixed

with saliva to achieve a satisfactory consistency for

swallow-ing Once the bolus is prepared, the tongue collects and sizes

the bolus and transfers it into the oropharynx The tongue

tip rises to appose the hard palate, and the midtongue forms

an inclined plane that directs the bolus into the oropharynx The velopharyngeal portal is closed as the soft palate rises to appose the posterior pharyngeal wall, and the superior con-strictor muscle contracts to appose the soft palate

Epiglottic tilt is accomplished by contraction of the suprahyoid muscles, thyrohyoid muscle, and intrinsic epiglottic muscles Elevation of the hyoid bone by the suprahyoid muscle group pulls on the hyoepiglottic liga-ment attached to the lower portion of the epiglottic carti-lage Hyoid elevation tilts the upper epiglottis toward the horizontal in a fulcrum-like motion Contraction of the aryepiglottic and oblique arytenoid muscles and thyroepi-glottic muscles then inverts the epiglottis

The epiglottis acts as a stream diverter, directing the bolus into the lateral swallowing channels The tilting epi-glottis also helps cover the laryngeal vestibule The larynx closes in a retrograde fashion; the true vocal cords close at the beginning of the swallow, followed by the false vocal cords and remainder of the laryngeal vestibule A portion of the bolus that has entered the laryngeal vestibule therefore is pushed back into the hypopharynx by retrograde laryngeal closure The bolus flows through the pharynx by a combi-nation of gravity, elevation of the pharynx over the bolus, tongue push, and sequential contraction of the constrictor muscles Although the upper esophageal sphincter relaxes at the beginning of a swallow, the pharyngoesophageal segment does not open until the bolus reaches the lower hypopharynx Elevation of the larynx and pharynx pulls the anterior wall

of the pharyngoesophageal segment anteriorly Tongue base retraction, constrictor contraction, and gravity then increase bolus pressure to open the pharyngoesophageal segment

Figure 1-1 Double-contrast images of the pharynx (A) Lateral spot image of the pharynx during suspended respiration shows the normal anatomy of the pharynx (B) Repeat lateral spot image of the pharynx during phonation better distends the pharynx, showing enlarged palatine tonsils (small black arrows) (C) Frontal spot image of the pharynx during suspended respiration also shows the palatine tonsils (small black arrows) indenting the lateral walls of the pharynx (Large black arrows denote epiglottis, large white arrows denote valleculae, and small white arrows denote piriform sinuses.)

Figure 1-2 Normal pharyngeal anatomy The pharynx

is composed of the nasopharynx, oropharynx, and

hypopharynx The hypopharynx extends craniocaudally from

the pharyngoepiglottic folds to the pharyngoesophageal

segment The pharyngoesopheal segment forms the junction

between the hypopharynx and the esophagus

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Esophageal Examination

Barium esophagograms are generally performed as

bipha-sic examinations that include both upright double-contrast

views with a high-density barium suspension and prone

single-contrast views with a low-density barium

suspen-sion The patient first ingests an effervescent agent and

then rapidly gulps high-density barium in the upright left

posterior oblique (LPO) position, in which double-contrast

views of the esophagus are obtained (Figure 1-3) The

patient is then placed in a recumbent right-side-down position for double-contrast views of the gastric cardia and fundus (Figure 1-4)

After the double-contrast phase of the examination is completed, the patient is placed in the prone right ante-rior oblique position and asked to take discrete swallows

of a low-density barium suspension to evaluate esophageal motility Esophageal dysmotility is thought to be present when abnormal peristalsis is detected on two or more of five separate swallows The patient then rapidly gulps the low-density barium suspension to optimally distend the esophagus (particularly the distal esophagus) in order to rule out rings or strictures that could be missed on the double-contrast portion of the examination (Figure 1-5) Finally, the patient is turned from a supine to a right lateral position to assess for spontaneous gastroesophageal reflux

or reflux induced by a Valsalva maneuver or water-siphon test The water-siphon test is performed with the patient

in a supine right posterior oblique position The distal esophagus is observed fluoroscopically while the patient takes several swallows of water If reflux is identified, the height of the refluxed barium column and clearance time should be noted

Barium tablets with a standard diameter of 12.5 mm are useful for the detection of subtle esophageal stric-tures in patients with dysphagia While in an upright or near upright position, the patient should swallow the tab-let with water Normally the tablet will pass through the esophagus in less than 20 seconds

Figure 1-3 Normal double-contrast view of the esophagus

with the patient in an upright left-posterior-oblique position

Note the smooth, featureless appearance of the esophageal

mucosa en face

Figure 1-4 Normal gastric cardia A lateral right-side-down

view of the gastric fundus shows the cardiac rosette as

multiple stellate folds radiating to a central point (arrow) at

the gastroesophageal junction

Figure 1-5 Normal single-contrast view of the esophagus with the patient in a prone right-anterior-oblique position Prone views are best for optimally distending the esophagus

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Normal Esophageal Anatomy

On double-contrast views, the esophagus normally

has a smooth, featureless appearance en face and a thin

white etching where it is seen in profile (see Figure 1-3)

Occasionally collapsed or partially collapsed views (also

known as mucosal relief views) may show the normal

longitudinal folds as thin, straight, delicate structures no

more than 1 to 2 mm in width

The gastric cardia can often be recognized by the ence of three or four stellate folds that radiate to a cen-

pres-tral point at the gastroesophageal junction, also known as

the cardiac rosette (see Figure 1-4) In some patients with

tumor involving the cardia, these lesions may be manifest

by distortion, effacement, or obliteration of this normal

anatomic landmark

Normal Esophageal Motility

Esophageal motility is best evaluated with the patient in

the prone or right anterior oblique recumbent position,

so as to negate the effect of gravity After the pharyngeal

phase of swallowing, barium enters the esophagus through

a relaxed upper esophageal sphincter The normal primary

peristaltic wave propagates toward the stomach, effacing

the esophageal lumen as it progressively strips the barium

bolus from the esophagus through a relaxed lower

esopha-geal sphincter into the gastric fundus At fluoroscopy, the

peristaltic wave has an inverted-V shape at the top of the

barium column The primary wave is sometimes disrupted

at or near the level of the aortic arch, with retrograde

pas-sage of a small amount of barium proximally as a normal

finding in older patients This phenomenon is also known

as proximal escape Esophageal dysmotility disorders may

be characterized by weakened or absent primary

peristal-sis, prolonged transit time greater than 30 seconds, large

amounts of proximal escape, or to-and-fro motion of the

barium column; it is sometimes associated with a variable

number of nonperistaltic contractions or lower esophageal

sphincterdysfunction

Suspected Aspiration or Perforation

If there is concern that a patient may aspirate

dur-ing a fluoroscopic examination, barium or a nonionic

water-soluble contrast agent should be used because ionic

water-soluble contrast agents have high osmolality and

therefore draw fluid into the lungs when aspirated,

plac-ing the patient at risk for severe, even life-threatenplac-ing

is identified, the examination should immediately be repeated with barium because barium is denser and more radiopaque and is better at defining small, subtle perfora-tions that are likely to be missed with water-soluble con-trast agents

Key Points

■ Fluoroscopic examination of the pharynx enables evaluation of the oral and pharyngeal phases of swallowing as well as the anatomic structures of the pharynx

■ Barium esophagograms are performed as biphasic studies to evaluate the esophageal mucosa, anatomy, and motility

■ Barium or a nonionic water-soluble contrast material

is the preferred contrast agent in patients who are at risk for aspiration

■ A water-soluble contrast agent should be employed

as the initial contrast medium in patients with pected perforation If no leak is detected with a water-soluble contrast agent, the examination should immediately be repeated with barium to rule out subtle leaks that might otherwise be missed

sus-Further Reading

Dodds WJ, Stewart ET, Logemann JA Physiology and ogy of the normal oral and pharyngeal phases of swallowing

radiol-AJR 1990;154:953–963.

Donner MW, Bosma JF, Robertson DL Anatomy and physiology

of the pharynx Gastrointest Radiol 1985;10:196–212.

Herlinger H, Grossman R, Laufer I, et al The gastric

car-dia in double-contrast study: its dynamic image AJR

Rubesin SE Pharynx: normal anatomy and examination

techniques In: Gore RM, Levine MS, eds Textbook of Gastrointestinal Radiology 3rd ed Philadelphia, Pa: WB

Saunders, 2008:235–252.

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Pharyngeal Disorders

Marc S. Levine

Neuromuscular Disorders

Most patients with swallowing dysfunction have neural or

muscular disorders that alter the timing of events or

mus-cular contraction in the oropharynx rather than causing

structural damage Cerebrovascular accidents are among

the most common causes of neuromuscular dysfunction

About one fourth of patients with strokes have dysphagia

In general, left-sided strokes alter the oral phase of

swal-lowing, whereas right-sided strokes alter the pharyngeal

phase The corticobulbar pathways in the internal

cap-sule may be damaged by large hemispheric strokes or

small-vessel disease Acute strokes or small-vessel

dis-ease—resulting from hypertension, diabetes, or other

causes—can also affect the swallowing center in the pons

and medulla

Diseases that directly damage motor neurons in the swallowing center or cranial nerves in the skull base may

cause bulbar palsy, with oral and pharyngeal swallowing

difficulties Destruction of lower motor neurons occurs in

amyotrophic lateral sclerosis and in 10% of patients with

acute poliomyelitis The latter patients may have

progres-sive disintegration of axon terminals in surviving but

overworked residual motor neurons, with pharyngeal

weakness due to postpolio muscular atrophy Unilateral

pharyngeal paresis is often caused by destruction of motor

nerves at the skull base or in the neck from tumor, trauma,

or surgery Abnormal transmission at the myoneural

junc-tion in myasthenia gravis may cause dysphagia, which is

exacerbated by prolonged swallowing

Dysphagia from inflammatory or endocrine-related myopathies is potentially treatable Dermatomyositis and

polymyositis directly damage intrinsic or extrinsic

mus-cles of the pharynx Pharyngeal muscle myopathy may

be caused by a variety of endocrine disorders, including

hyper- or hypothyroidism and Cushing’s syndrome

The end result of these various neuromuscular ders is poor timing of oral and pharyngeal events or abnor-

disor-mal oropharyngeal movement A bolus may be directed

normally but still enter the larynx or vestibule because

of poor timing Laryngeal penetration is defined as

pas-sage of the bolus into the laryngeal vestibule just before or

during swallowing Abnormal tongue motion, pharyngeal

contraction, or epiglottic tilt may also lead to laryngeal

penetration Abnormal oral or pharyngeal movement may

result from a structural abnormality or neuromuscular disorder Abnormal epiglottic tilt or pharyngeal muscular contraction may also lead to stasis in the valleculae or pir-iform sinuses respectively Marked stasis in the piriform sinuses may cause the retained bolus to overflow into the larynx through the interarytenoid notch after swallowing Thus overflow aspiration is defined as retained barium in the valleculae or piriform sinuses overflowing into the laryngeal vestibule while the patient is breathing nor-mally Aspiration may also result from the regurgitation

of esophageal contents into the pharynx

Structural Disorders

Lymphoid Hyperplasia

Lymphoid hyperplasia of the lingual or palatine tonsils

is a nonspecific response to aging, allergies, and repeated infections Lymphoid hyperplasia of the lingual tonsil at the posteroinferior tongue base may appear on barium studies as multiple small, smooth-surfaced, ovoid nod-ules symmetrically distributed over the vertical surface

of the tongue base, often extending into the valleculae and vallecular surface of the epiglottis When this lym-phoid hyperplasia is focal or mass-like, it can mimic the appearance of tumor at the base of the tongue (Figure 2-1) Therefore patients with asymmetric nodularity or mass lesions at the tongue base should undergo further investi-gation to differentiate lymphoid hyperplasia of the lingual tonsil from malignant tumor

Pharyngeal and Cervical Esophageal Webs

Webs are thin folds that usually arise from the anterior wall

of the proximal cervical esophagus or geal segment Cervical esophageal webs are common findings of uncertain etiology An association with gastro-esophageal reflux disease has been reported Asymmetric scarring of the cervical esophagus from radiation or other causes can also lead to the development of webs

pharyngoesopha-Webs are thin (1 to 2 mm in thickness) folds arising from the anterior wall of the pharyngoesophageal seg-ment or proximal cervical esophagus A web may appear

on barium studies as a radiolucent bar in the barium pool

or as a thin structure etched in white by barium Some

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webs extend circumferentially, with a deeper shelf on

their anterior surface (Figure 2-2A) Patients with

dys-phagia usually have webs that compromise the lumen of

the cervical esophagus by more than 50% Obstruction is

manifest by dilatation of the cervical esophagus above the

web or a so-called jet phenomenon in which a thin column

of barium is seen spurting through the web (Figure 2-2B)

Benign Cysts and Tumors

Retention cysts are common benign lesions found at the tongue base or in the valleculae, piriform sinuses, and aryepiglottic folds These cysts are lined by squamous epithelium and filled with desquamated debris They typ-ically appear on barium studies as smooth-surfaced hemi-spheric masses that protrude into the pharyngeal lumen (Figure 2-3) Granular cell tumors, ectopic thyroid tissue, and thyroglossal duct cysts may occasionally be manifest

by similar findings at the base of the tongue

Benign pharyngeal tumors such as lipomas, bromas, hamartomas, and oncocytomas are uncommon Like retention cysts, these tumors may appear on barium studies as smooth submucosal masses protruding into the pharyngeal lumen

neurofi-Squamous Cell Carcinoma

In the United States, squamous cell carcinoma of the tongue, pharynx, and larynx is five times more common than squamous cell carcinoma of the esophagus Ninety percent of these tumors are nonkeratinizing squamous cell carcinomas Almost all of these lesions develop in moderate or heavy abusers of alcohol, tobacco, or both The signs, symptoms, treatment, and prognosis depend on the location of the tumor in the pharynx Most patients have a recent onset of symptoms, including hoarseness and dysphagia The overall 5-year survival rate for these patients is 20% to 40%

The radiographic findings of squamous cell carcinoma

of the pharynx are similar to those of malignant tumors elsewhere in the gastrointestinal tract The normal contour

of the involved structure is disrupted by a protrusion into the lumen or by an area of ulceration extending outside the expected luminal contour (Figure 2-4) Intraluminal

Figure 2-1 Lymphoid hyperplasia of lingual tonsil Lateral

spot image of the pharynx shows focal lobulation of the

posteroinferior tongue base and adjacent valleculae

(arrows) due to lymphoid hyperplasia of the lingual tonsil This

appearance could be mistaken for a polypoid carcinoma of

the tongue base

Figure 2-2 Cervical esophageal web (A) Lateral spot image of the cervical esophagus during swallowing shows a thin, smooth, circumferential area of narrowing (arrow) due to a cervical esophageal web (B) Frontal spot image during swallowing shows a jet phenomenon (arrow) due to barium spurting through the narrowed segment of the web

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tumor can appear on a scout view as an area of increased

soft tissue radiopacity replacing the normally air-filled

lumen or, after oral barium, as a radiolucent filling defect

in the barium pool The irregular mucosal surface of the tumor may show a granular, nodular, ulcerated, or lobu-lated contour or by barium-etched lines in an unexpected configuration or location The distensibility and mobility

of the involved structure may also be compromised

The palatine tonsil is the most common site of involvement by squamous cell carcinoma of the pharynx Tonsillar tumors can spread to the posterior pharyngeal wall, soft palate, and base of the tongue Lymph node metastases are found in about 50% of patients Squamous cell carcinomas of the tongue base are usually advanced tumors that have already spread deep into the intrinsic

or extrinsic muscles of the tongue These tumors can also invade the palatine tonsils, valleculae, or pharyngoepi-glottic folds Lymph node metastases are present in about 70% of patients

The supraglottic laryngeal structures tis, aryepiglottic folds, mucosa overlying the muscular process of the arytenoid cartilages, false vocal cords, and laryngeal ventricle) arise from the pharyngobuc-cal anlage, forming a portion of the anterior wall of the hypopharynx Supraglottic cancers are often clas-sified as a subtype of laryngeal rather than pharyngeal tumors These lesions frequently cause coughing and choking The supraglottic region has an extensive lym-phatic bed; supraglottic cancers therefore tend to spread throughout the supraglottic region into the preepiglot-tic space Cervical lymphadenopathy is detected in one third to one half of patients

(epiglot-Squamous cell carcinomas of the piriform sinuses are usually bulky masses that, in 70% to 80% of patients, have already spread to lymph nodes at the time of presenta-tion Tumors of the medial piriform sinus may invade the ipsilateral aryepiglottic fold, arytenoid and cricoid carti-lage, and paraglottic space, often resulting in hoarseness Tumors of the lateral piriform sinus may invade the thy-roid cartilage, thyrohyoid membrane, and neck, including the carotid sheath

Squamous cell carcinomas of the posterior pharyngeal wall are large, bulky tumors that cause few symptoms, often presenting as painless neck masses resulting from metasta-ses to cervical lymph nodes More than half of these patients have lymph node metastases at the time of diagnosis These exophytic tumors may spread superiorly or inferiorly into the nasopharynx or cervical esophagus, respectively, and posteriorly into the retropharyngeal space

Lymphoma

About 10% of pharyngeal malignancies are non-Hodgkin’s lymphomas arising in the lymphoid tissue of Waldeyer’s ring, including the adenoids, palatine tonsils, and lingual tonsil Hodgkin’s disease involving the pharynx is uncom-mon, even though Hodgkin’s disease is often first detected

in cervical lymph nodes Patients with pharyngeal phoma frequently present with a neck mass, and cervical lymph nodes are initially involved in 60% of cases

lym-Figure 2-3 Benign retention cyst Frontal spot image of

the pharynx shows a small (5 mm in diameter), smooth

submucosal lesion (arrow) arising from the superior aspect

of the right piriform sinus due to a benign retention cyst

Figure 2-4 Carcinoma of the pharynx Frontal spot image of

the pharynx shows an advanced ulcerated carcinoma (black

arrows) obliterating the left piriform sinus Note that the tumor

mass extends into the right piriform sinus (white arrows)

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The palatine tonsil is the primary site of involvement

by pharyngeal lymphoma in 40% to 60% of patients, the

nasopharynx in 18% to 28%, and the lingual tonsil in 10%

Multiple sites are involved in about 25% of patients, but the

hypopharynx is rarely involved by this tumor Pharyngeal

lymphomas typically appear on barium studies as large,

bulky, lobulated masses Nevertheless the mucosal surface

may be relatively smooth because of the submucosal

loca-tion of these tumors

Radiation Change

Patients with carcinoma of the larynx or pharynx are

com-monly treated with radiation therapy Chronic radiation

injury to the pharynx is characterized by vascular

dam-age with mucosal atrophy and fibrosis of muscle and

sub-mucosal tissue Radiation edema and fibrosis appears on

barium studies as a smooth, bulbous enlargement of the

epiglottis, smooth thickening of the aryepiglottic folds,

flattening and truncation of the valleculae, and atrophy

of the soft palate (Figure 2-5) Radiation fibrosis leads to

decreased or absent epiglottic tilt and poor closure of the

laryngeal vestibule with laryngeal penetration (see Figure 2-5) Paresis of the constrictor muscles may result in poor clearance from the hypopharynx with overflow aspiration

Further Reading

Apter AJ, Levine MS, Glick SN Carcinomas of the base of the tongue: diagnosis using double-contrast radiography of the

pharynx Radiology 1984;151:123–126.

Ekberg O, Nylander G Double contrast examination of the

pharynx Gastrointest Radiol 1985;10:263–271.

Gordon AR, Levine MS, Redfern RO, et al Cervical

esopha-geal webs: association with gastroesophaesopha-geal reflux Abdom Imaging 2001;26:574–577.

Gromet M, Homer MJ, Carter BL Lymphoid hyperplasia at the

base of the tongue Radiology 1982;144:825–828.

Quillen SP, Balfe DM, Glick SN Pharyngography after head and neck irradiation: differentiation of postirradiation edema

from recurrent tumor AJR 1993;161:1205–1208.

Rubesin SE, Glick SN The tailored double-contrast

pharyngo-gram Crit Rev Diagn Imaging 1988;28:133–179.

Rubesin SE, Laufer I Pictorial review: principles of double

con-trast pharyngography Dysphagia 1991;6:170–178.

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Achalasia is a motility disorder characterized by absent

pri-mary peristalsis in the body of the esophagus and decreased

relaxation of the lower esophageal sphincter (LES) There

are two types: primary and secondary Primary achalasia

is an idiopathic form of achalasia caused by degeneration

of esophageal ganglion cells in Auerbach’s plexus, whereas

secondary achalasia is an acquired condition caused by

neoplastic or infectious infiltration of the ganglion cells

Demographic and Clinical Features

Primary achalasia typically occurs in young or

middle-aged adults who present with long-standing

dysphagia that slowly progresses over a period of years

Affected individual are usually able to maintain their

weight by modifying their diets, even in advanced disease

In contrast, secondary achalasia is most frequently caused

by malignant tumors involving the gastroesophageal

junc-tion; therefore affected patients tend to be elderly

individ-uals (over 60 years of age) who present with a recent onset

of dysphagia (less than 6 months) and weight loss Thus it

is usually possible to differentiate these conditions on the

basis of the clinical history and presentation

Pathology

Primary achalasia is an idiopathic condition resulting from

the degeneration of ganglion cells in the distal esophagus

and at the gastroesophageal junction In contrast,

second-ary achalasia is an acquired condition caused by malignant

tumor in North America and by Chagas disease in South

America Many patients with secondary achalasia have

tumor that directly infiltrates the gastroesophageal

junc-tion, destroying the ganglion cells in this region In North

America, as many as 75% of patients with secondary

acha-lasia are found to have a carcinoma of the cardia or fundus

as the cause of this condition Carcinoma of the lung, breast,

and pancreas and other malignant tumors can also

metas-tasize to the gastroesophageal junction, causing secondary

achalasia Other patients may develop secondary achalasia

because of tumor involving the vagus nerve, dorsal motor nucleus of the vagus nerve, or brain stem Still other patients have tumors that secrete a vasoactive substance, producing

a paraneoplastic syndrome that mimics achalasia

Imaging Features

Primary achalasia is characterized on barium studies by a dilated, flaccid esophagus with absent primary peristalsis and tapered, beaklike narrowing of the distal esophagus at

or directly adjacent to the gastroesophageal junction due

to incomplete opening of the LES (Figure 3-1) In advanced disease, the esophagus can become massively dilated and

have a tortuous distal configuration (also known as a

sig-moid esophagus) (Figure 3-2) Barium studies typically

reveal a standing column of barium in the thoracic agus with markedly delayed emptying into the stomach Some patients with achalasia have associated nonperistal-tic contractions of varying severity in the esophagus, a

esoph-condition known as vigorous achalasia.

Secondary achalasia is also characterized on barium studies by absent peristalsis and beak-like narrowing of the distal esophagus (Figure 3-3) In secondary achalasia, how-ever, the esophagus is much less dilated because of rapid progression of disease Moreover, in secondary achalasia, the length of the narrowed segment is often considerably greater than that in primary achalasia because of spread of tumor into the distal esophagus (see Figure 3-3) The nar-rowed distal esophagus may also be asymmetric, nodular,

or ulcerated because of underlying tumor in this region

In patients with secondary achalasia caused by mary carcinoma of the cardia, barium studies may reveal other signs of malignant tumor, with an ulcerated, pol-ypoid, or infiltrating lesion in the cardia and fundus In patients with markedly delayed emptying of barium from the esophagus, the stomach paradoxically may empty more rapidly than it fills, limiting evaluation of the cardia and fundus In such cases, the patient can be asked to sip additional barium in a recumbent, left-side-down position

pri-to facilitate radiologic evaluation of the proximal spri-tomach

Computed tomography (CT) of the chest can also be

a useful imaging test for differentiating primary from ondary achalasia In primary achalasia, CT typically reveals

sec-a dilsec-ated esophsec-agus with distsec-al nsec-arrowing sec-and no evidence

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of esophageal wall thickening or mediastinal adenopathy

In secondary achalasia, however, CT may reveal marked thickening of the distal esophagus, an eccentric soft tissue mass at the gastric cardia, and mediastinal adenopathy

Differential Diagnosis

■ Peptic stricture: A tapered peptic stricture in the tal esophagus may resemble achalasia but primary peristalsis is preserved, and peptic strictures are almost always associated with hiatal hernias

dis-■ Extrinsic compression by an ectatic or aneurysmal descending thoracic aorta: This indentation may also cause tapered narrowing of the distal esophagus, but the dilated aorta will displace the distal esophagus and is often calcified and esophageal peristalsis is preserved

Common Variants

When left-posterior-oblique double-contrast radiographs are obtained in the upright position, some patients may experience transient spasm of the LES, seen as a tapered narrowing of the distal esophagus that is indistinguish-able from the narrowing in achalasia In such cases, how-ever, the distal esophagus opens normally and primary peristalsis is normal on prone right-anterior oblique

Figure 3-1 Primary achalasia Upright double-contrast view

of the esophagus shows tapered, beak-like narrowing of the

distal esophagus (arrow) due to incomplete opening of the

LES, with a standing column of barium proximally and slow

emptying of barium into the stomach There was no primary

peristalsis in the body of the esophagus at fluoroscopy This

constellation of findings is characteristic of achalasia

Figure 3-2 Advanced primary achalasia with sigmoid

esophagus This patient has a massively dilated esophagus

with a tortuous distal configuration (also known as a sigmoid

esophagus) and considerable retained debris Also note

tapered narrowing of the distal esophagus just above the

gastroesophageal junction (arrow) These findings are

characteristic of long-standing achalasia

Figure 3-3 Advanced gastric carcinoma at the gastric cardia causing secondary achalasia This patient has a longer segment of narrowing and greater angulation than

is typically seen in primary achalasia There is also marked narrowing and irregularity of the proximal stomach due to encasement by an advanced scirrhous carcinoma invading the distal esophagus (arrow), producing an achalasia-like appearance

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radiographs Affected individuals also have no esophageal

symptoms Transient spasm of the LES in the upright

posi-tion is therefore believed to be a common variant of little

or no clinical importance

Management/Clinical Issues

Patients with primary achalasia may be treated by

botu-linum toxin injection, pneumatic dilatation of the LES,

or laparoscopic surgical myotomy for relief of dysphagia

Rarely, patients with end-stage achalasia may require an

esophagogastrectomy and gastric pull-through for

amelio-ration of symptoms In contrast, patients with secondary

achalasia require a tumor workup for diagnosis and staging

of the underlying malignant tumor responsible for their

■ Sigmoid esophagus with end-stage disease

■ No esophageal wall thickening, mass at cardia, or mediastinal adenopathy on CT

■ Treatment with botulinum toxin injection, matic dilatation, or laparoscopic myotomy

pneu-Secondary Achalasia

■ Malignant tumor

■ Elderly patients (over 60 years of age)

■ Recent onset of dysphagia (less than 6 months)

■ Substantial weight loss

■ Less esophageal dilatation

■ Longer segment of distal esophageal narrowing

■ Asymmetry, nodularity, or ulceration of narrowed segment

■ Tumor involving gastric cardia/fundus

■ Esophageal wall thickening, mass at cardia, or astinal adenopathy on CT

medi-■ Need for tumor workup for diagnosis and staging of underlying malignancy

Further Reading

1 Ott DJ Motility disorders of the esophagus In: Gore RM,

Levine MS, eds Textbook of Gastrointestinal Radiology 3rd

ed Philadelphia, Pa: WB Saunders, 2008:323–335.

2 Woodfield CA, Levine MS, Rubesin SE, et al Diagnosis of

primary versus secondary achalasia: reassessment of clinical

and radiographic criteria AJR 2000;175:727–731.

B Diffuse Esophageal Spasm

Definition

Diffuse esophageal spasm is an uncommon esophageal motility disorder characterized by intermittent weaken-ing or absence of primary peristalsis with simultaneous, repetitive nonperistaltic contractions in the esophagus More than 50% of patients with diffuse esophageal spasm have associated dysfunction of the LES; therefore diffuse esophageal spasm and achalasia are thought to represent opposite ends of a spectrum of related motility disorders

Diffuse esophageal spasm is a disease of the elderly; most patients with this condition are over 60 years of age Affected individuals typically present with substernal chest pain, dysphagia, or both The chest pain is thought to be caused by multiple repetitive nonperistaltic contractions

of moderate to marked intensity (i.e., esophageal spasm)

In contrast, the dysphagia is most likely caused by LES dysfunction with incomplete opening of the sphincter—a frequent finding in patients with diffuse esophageal spasm

Pathology

The cause of diffuse esophageal spasm is unknown This condition typically involves the smooth muscle portion of the esophagus at or below the level of the aortic arch In some patients, the esophageal wall may become markedly thick-ened owing to hypertrophy and thickening of the muscula-ris propria As indicated earlier, there is often associated LES dysfunction with incomplete opening of the sphincter, as in patients with achalasia It has therefore been postulated that the latter patients have a transitional form of diffuse esopha-geal spasm that may progress over time to classic achalasia

Imaging Features

Diffuse esophageal spasm appears on esophagography by intermittently weakened or absent primary esophageal peristalsis associated with multiple repetitive nonperistal-tic contractions of varying intensity With severe disease, there may be lumen-obliterating or near lumen-obliterating

nonperistaltic contractions, producing a classic corkscrew

esophagus (Figure 3-4) However, most patients have

non-peristaltic contractions of mild to moderate severity that

do no obliterate the lumen (Figure 3-5) Therefore the absence of a corkscrew esophagus on barium studies in no way excludes this diagnosis The majority of patients with diffuse esophageal spasm also have impaired opening of the LES with the tapered, beak-like narrowing of the distal esophagus typically associated with achalasia (see Figure 3-5) In patients with achalasia, however, primary peri-stalsis is absent on all swallows, whereas in patients with diffuse esophaeal spasm, primary peristalsis is present on

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some swallows Thus it is possible to differentiate these ditions on the basis of the radiographic findings.

con-Differential Diagnosis

■ Presbyesophagus: A form of esophageal dysmotility associated with aging Barium studies may reveal intermittent weakening or absence of primary peri-stalsis with mild to moderate nonperistaltic con-tractions in the mid- and distal thoracic esophagus but no LES dysfunction These patients are usually asymptomatic, whereas patients with diffuse esoph-ageal spasm present with chest pain, dysphagia, or both

■ Vigorous achalasia: May closely resemble diffuse esophageal spasm with LES dysfunction, but peri-stalsis is absent on all swallows in these patients

Common Variants

More than 50% of patients with diffuse esophageal spasm have a variant of this condition associated with LES dys-function Incomplete opening of the sphincter is seen as a tapered, beak-like narrowing identical to that in patients with achalasia However, other typical radiologic and manometric features of diffuse esophageal spasm enable differentiation from true achalasia

When patients with diffuse esophageal spasm present with chest pain because of multiple severe nonperistal-tic contractions in the esophagus, treatment with cal-cium channel blockers or other agents has sometimes been recommended to decrease esophageal spasm, although such treatment has had limited success When these patients present with dysphagia because of incom-plete opening of the LES, however, they usually have a marked clinical response to botulinum toxin injection, endoscopic balloon dilatation, or laparoscopic surgical myotomy

■ Incomplete opening of the LES in most patients

■ Chest pain, dysphagia, or both

■ Chest pain caused by severe nonperistaltic contractions

■ Dysphagia caused by LES dysfunction

■ Calcium channel blockers for treatment of chest pain

■ Botulinum toxin injection or endoscopic dilatation for LES dysfunction

Figure 3-5 Diffuse esophageal spasm with LES dysfunction

Mild-to-moderate nonperistaltic contractions in the lower

third of the thoracic esophagus indicate diffuse esophageal

spasm Beak-like narrowing of the distal esophagus due

to incomplete opening of the LES is also seen (arrow)

Dysfunction of the LES is found on barium students in more

than 50% of patients with diffuse esophageal spasm

Figure 3-4 Diffuse esophageal spasm Severe, near

lumen-obliterating nonperistaltic contractions in the lower

third of the thoracic esophagus produce a corkscrew

appearance Real-time intermittent absence of primary

peristalsis in the thoracic esophagus was also observed

in this patient with typical radiographic findings of diffuse

esophageal spasm

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Further Reading

1 Ott DJ Motility disorders of the esophagus In: Gore RM,

Levine MS, eds Textbook of Gastrointestinal Radiology 3rd

ed Philadelphia, Pa: WB Saunders, 2008:323–335.

2 Prabhakar A, Levine MS, Rubesin SE, et al Relationship

between diffuse esophageal spasm and lower esophageal sphincter dysfunction on barium studies and manometry in

14 patients AJR 2004;183:409–413.

C Gastroesophageal Reflux Disease

Definition

Patients with gastroesophageal reflux disease (GERD)

often have a distinct form of esophageal dysmotility

char-acterized by intermittently weakened or absent primary

peristalsis in the thoracic esophagus—a finding on barium

studies that should suggest the possibility of underlying

GERD in patients with reflux symptoms

Because this form of esophageal dysmotility occurs in

patients with underlying GERD, affected individuals

typi-cally present with signs and symptoms of reflux, including

heartburn, indigestion, regurgitation, and dysphagia The

presence of this dysmotility may exacerbate the patient’s

reflux symptoms by delaying clearance of refluxed acid from

the esophagus and increasing the degree of esophagitis

Pathology

Some patients with esophageal dysmotility associated

with GERD have underlying reflux esophagitis, whereas

others have gastroesophageal reflux without morphologic

evidence of esophagitis It is therefore uncertain whether

the dysmotility results from weakening of esophageal

peristalsis by refluxed acid in the esophagus or from actual

inflammation of the distal esophagus due to reflux

esoph-agitis Whatever the explanation, abnormal peristalsis in

patients with GERD impairs clearance of refluxed acid

from the esophagus, leading to a vicious cycle with

pro-gressively more severe reflux esophagitis

Imaging Features

The esophageal dysmotility of GERD is characterized on

barium studies by variable weakening and/or intermittent

absence of primary peristalsis in the distal or mid- and

dis-tal thoracic esophagus without associated nonperisdis-taltic

contractions The latter observation is particularly helpful

for differentiating this form of dysmotility from that

asso-ciated with aging (i.e., presbyesophagus), in which multiple

nonperistaltic contractions of varying severity are also

detected in the mid- and distal esophagus The presence of abnormal motility without nonperistaltic contractions on barium studies therefore should elicit a careful search for underlying GERD and its sequelae Cricopharyngeal hyper-trophy may also be seen in GERD and appears as a posterior impression at the posterior pharyngoesophageal junction

■ Scleroderma: Appears on barium studies as absent primary peristalsis in the portion of the thoracic esophagus lined by smooth muscle (below the aortic arch); it is due to smooth muscle atrophy and fibrosis

In these patients, however, peristalsis will be absent

When the typical dysmotility of GERD is observed on barium studies, patients should probably be treated with proton pump inhibitors for relief of reflux symptoms If a patient’s symptoms fail to improve, 24-hour ambulatory esophageal pH monitoring may be performed to deter-mine whether the dysmotility is secondary to underlying reflux disease

■ A common radiographic sign of GERD

■ May exacerbate effects of refluxed acid in the esophagus

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Zenkers diverticulum is a focal mucosal outpouching from

the posterior wall of the lower hypopharynx just above the

cricopharyngeus (i.e., the pharyngoesophageal junction)

In contrast, Killian-Jamieson diverticulum is a focal

muco-sal outpouching from the anterolateral wall of the cervical

esophagus just below the cricopharyngeus

Zenkers diverticulum is most commonly found in elderly

patients who present with dysphagia, halitosis,

regurgita-tion of undigested food, choking, hoarseness, a neck mass,

or recurrent aspiration pneumonias Other patients with

Zenkers diverticulum are asymptomatic Although most

patients with Killian-Jamieson diverticulum are

asymp-tomatic, some may complain of dysphagia Regurgitation

of undigested food and aspiration pneumonia is less

com-mon in these patients because the diverticulum is located

below the cricopharyngeus

Pathology

Zenkers diverticulum is an acquired mucosal herniation

through an area of congenital muscle weakness in the

crico-pharyngeal muscle (also known as Killians dehiscence) just

above the cricopharyngeus This opening is found in about

one-third of people at autopsy and is thought to develop

between the thyropharyngeus and cricopharyngeus

mus-cles or between the oblique and horizontal fibers of the

cricopharyngeus itself The pathogenesis of Zenkers

diver-ticulum is uncertain, but many patients have

cricopharyn-geal dysfunction with elevated upper esophacricopharyn-geal sphincter

pressures and decreased relaxation of the sphincter during

swallowing It has therefore been postulated that

cricopha-ryngeal dysfunction predisposes to the development of a

Zenkers diverticulum In turn, chronic gastroesophageal

reflux disease (GERD) may predispose to the development

of cricopharyngeal dysfunction in these patients

In contrast, a Killian-Jamieson diverticulum is an acquired mucosal herniation through a triangular area

of weakness (also known as the Killian-Jamieson space)

in the anterolateral cervical esophagus just below the copharyngeus The Killian-Jamieson space is bounded superiorly by the inferior border of the cricopharyngeus, anteriorly by the cricoid cartilage, and inferomedially by the suspensory ligament of the esophagus Transient pro-trusions through the Killian-Jamieson space are called

cri-lateral proximal cervical esophageal pouches, whereas

persistent protrusions are called lateral proximal cervical

esophageal diverticula, also known as Killian-Jamieson

pouches and diverticula, respectively

Imaging Features

When detected on barium studies, a Zenkers lum appears on frontal views as a persistent barium-filled sac in the midline below the tips of the piriform sinuses (Figure 4-1A) On lateral views during swallowing, the opening of the Zenkers diverticulum above the incom-pletely opened pharyngoesophageal segment is often surprisingly broad The sac then courses behind the pha-ryngoesophageal segment and proximal cervical esopha-gus (Figure 4-1B) Barium within the diverticulum can be regurgitated into the lower hypopharynx during breath-ing or additional swallowing, but overflow aspiration is relatively uncommon

diverticu-The Killian-Jamieson diverticulum, which is about one third as common as Zenkers diverticulum, has a characteristic radiographic appearance It tends to be uni-lateral (usually on the left) or occasionally bilateral The diverticulum appears on barium studies as a persistent 3–

to 20-mm outpouching with a distinct neck (Figure 4-2) The diverticulum extends lateral to the cervical esophagus

on frontal views (see Figure 4-2) and overlaps the cervical esophagus on lateral views In contrast, Zenkers diver-ticulum is in the midline on frontal views and posterior

to the cervical esophagus on lateral views (see Figure 4-1) When barium is regurgitated from a Killian-Jamieson diverticulum, it enters the cervical esophagus below the cricopharyngeus), so there is less risk of aspiration than

in patients with a Zenkers diverticulum

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■ Sealed-off perforation from pharyngoesophageal junction or cervical esophagus

Pitfalls and Mimics

Barium trapped above a prematurely closed or pletely opened cricopharyngeus may resemble a small

incom-Zenkers diverticulum and has been termed a pseudo ‒ Zenkers diverticulum In such patients, however, no diver-

ticulum is seen during swallowing The sac-like structure appears only when the barium is trapped above the cri-copharyngeus after swallowing Within a few moments, this barium usually enters the cervical esophagus and the apparent diverticulum disappears It is not known whether a pseudo‒Zenkers diverticulum can progress to

a true Zenkers diverticulum Early closure and plete opening of the cricopharyngeus has also been asso-ciated with gastroesophageal reflux disease (GERD)

incom-Management/Clinical Issues

In symptomatic patients, Zenkers diverticulum can be treated by endoscopic diverticulotomy, in which the par-tition between the diverticulum and cervical esophagus

is opened at endoscopy to facilitate emptying from the

Figure 4-1 Zenkers diverticulum (A) Frontal spot image of the pharynx shows a large round diverticulum filled with barium (arrows)

in the midline just below the piriform sinuses (B) Lateral spot image of the pharynx shows the Zenkers diverticulum (white arrows)

arising from a wide neck just above a prominent cricopharyngeus (black arrow) that fails to open normally during swallowing

Note that the diverticulum extends inferiorly, compressing the posterior wall of the adjacent cervical esophagus These findings

are characteristic of a Zenkers diverticulum

Figure 4-2 Lateral cervical diverticulum (Killian-Jamieson

diverticulum) Frontal spot image of the pharynx and

cervical esophagus during swallowing shows filling of a

tiny diverticulum (arrow) that arises from a discrete neck

on the left lateral wall of the cervical esophagus below the

cricopharyngeus These findings are characteristic of a lateral

cervical esophageal diverticulum

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diverticulum Alternatively, surgical diverticulopexy may

be performed by inverting the diverticulum to improve

emptying Finally, surgical diverticulectomy may be

per-formed as a definitive treatment option Killian-Jamieson

diverticulum is usually discovered as an incidental finding

in asymptomatic patients, but patients with dysphagia may

occasionally require surgical resection of the diverticulum

■ Dysphagia, halitosis, or recurrent aspiration

■ Findings on barium study pathognomonic

■ Treatment options: endoscopic diverticulotomy, gical diverticulopexy and surgical diverticulectomy with cricopharyngeal myotomy

sur-Killian-Jamieson Diverticulum

■ Anterolateral outpouching from cervical esophagus just below the cricopharyngeus

■ Usually no symptoms

■ Findings on barium study pathognomonic

■ Diverticulectomy only for large diverticulum ing dysphagia

caus-Further Reading

Brady AP, Stevenson GW, Somers S, et al Premature contraction

of the cricopharyngeus: new sign of gastroesophageal reflux

disease Abdom Imaging 1995;20:225–228.

Delahunty JE, Margulies SE, Alonso UA, et al The relationship

of reflux esophagitis to pharyngeal pouch (Zenker’s

diver-ticulum) Laryngoscope 1971;81:570–577.

Ekberg O, Nylander G Lateral diverticula from the

pharyngo-esophageal junction area Radiology 1983;146:117–122.

Frieling T, Berges W, Lubke HJ, et al Upper esophageal sphincter

function in patients with Zenker’s diverticulum Dysphagia

1988;3:90–92.

Knuff TE, Benjamin SB, Castell DO Pharyngoesophageal (Zenker’s)

diverticulum: a reappraisal Gastroenterology 1982;82:734–736.

Rubesin SE, Levine MS Killian-Jamieson diverticula:

radio-graphic findings in 16 patients AJR 2001;177:85–89.

Rubesin SE Structural abnormalities of the pharynx In: Gore

RM, Levine MS, eds Textbook of Gastrointestinal Radiology

3rd ed Philadelphia, Pa: WB Saunders, 2008:271–308.

B Thoracic Esophageal Diverticula

Definition

Thoracic esophageal diverticula may be classified as pulsion

or traction diverticula The more common pulsion diverticula

result from esophageal dysmotility with increased minal pressures in the esophagus, whereas traction diver-ticula are caused by scarring in the soft tissues surrounding the esophagus The latter diverticula usually develop in the midesophagus or distal esophagus above the gastroesopha-

intralu-geal junction (i.e., epiphrenic diverticulum) Other patients

may develop tiny outpouchings from the esophagus known

as esophageal intramural pseudodiverticula.

Pulsion diverticula are much more common than traction diverticula In most cases the diverticula are detected as inci-dental findings in patients who have no esophageal symp-toms However, a large epiphrenic diverticulum near the gastroesophageal junction may fill with debris, causing dys-phagia, regurgitation, or aspiration Because pulsion diver-ticula are usually associated with esophageal dysmotility, especially diffuse esophageal spasm, affected individuals may present with dysphagia or chest pain because of their under-lying motility disorder Traction diverticula and esophageal intramural pseudodiverticula are usually detected as inciden-tal findings, although patients with pseudodiverticula may have dysphagia because of associated esophageal strictures

Pathology

A pulsion diverticulum results from mucosal herniation through the wall of the esophagus; therefore pulsion diver-ticula do not contain a muscular lining In contrast, a traction diverticulum is a true diverticulum containing all layers of the esophageal wall, including a muscularis propria Pulsion diverticula are often associated with fluoroscopic or mano-metric findings of esophageal dysmotility, especially diffuse esophageal spasm It has therefore been postulated that these diverticula result from increased intraluminal pressures in the esophagus In contrast, traction diverticula are usually caused by scarring and volume loss in the perihilar regions from prior surgery, radiation therapy to the chest, or granu-lomatous diseases such as tuberculosis or histoplasmosis involving perihilar lymph nodes Finally, esophageal intra-mural pseudodiverticula consist pathologically of dilated excretory ducts of deep mucous glands in the esophagus

Imaging Features

Pulsion diverticula appear on barium studies as multiple rounded outpouchings from the distal or midesophagus that have wide necks (Figure 4-3) Because these diver-ticula lack a muscular lining, they often do not empty completely when the esophagus collapses and may be associated with other radiographic findings of esophageal motor dysfunction Although most patients with pulsion diverticula are asymptomatic, a giant epiphrenic diver-ticulum near the gastroesophageal junction may fill with debris, causing dysphagia, regurgitation, or aspiration (Figure 4-4)

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In contrast, traction diverticula typically appear

as solitary outpouchings from the midesophagus that have a triangular or tented appearance or a flat base with angulated margins due to traction on the divertic-ulum by a fibrotic process in the adjacent mediastinum (Figure 4-5) Because they contain a muscular lining, traction diverticula tend to empty their contents when the esophagus collapses at fluoroscopy Thus it is usu-ally possible to distinguish traction diverticula from pulsion diverticula on the basis of the radiographic findings

Esophageal pseudodiverticula typically appear on esophagography as tiny 2- to 5-mm flask-shaped out-pouchings in longitudinal rows parallel to the esophagus

or as tiny collections of barium that may not cate with the lumen (Figure 4-6) The pseudodiverticula classically have a diffuse distribution in the esophagus and are sometimes associated with strictures in the upper or midesophagus However, it is more common

communi-to have an isolated cluster of pseudodiverticula in the distal esophagus in the region of a peptic stricture In such cases, the pseudodiverticula most likely occur as a sequela of scarring from reflux esophagitis Occasionally longitudinal tracking may be seen in the wall of the esophagus between two or more adjacent pseudodiver-ticula (see Figure 4-6)

Figure 4-4 Giant epiphrenic diverticulum A frontal spot image

from a barium swallow shows a large amount of residual

barium filling a giant diverticulum (white arrows) arising from

the right lateral wall of the distal esophagus Also note barium

in a second tiny diverticulum (black arrow) more distally This

patient presented with dysphagia due to retention of food

within the diverticulum

Figure 4-3 Pulsion diverticulum Double-contrast view of the

esophagus shows a smooth round pulsion diverticulum (white

arrow) arising from a wide neck on the left lateral wall of the

distal esophagus Note multiple nonperistaltic contractions

(black arrows) in this patient with diffuse esophageal spasm

associated with the development of a pulsion diverticulum

Figure 4-5 Traction diverticulum Double-contrast view shows

a midesophageal diverticulum that has a flat base and angled margins (arrows) This most likely represents a traction diverticulum due to mediastinal scarring with retraction

of the adjacent esophageal wall This patient had normal esophageal motility

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Pitfalls and Mimics

When viewed en face on double-contrast esophagrams,

esophageal intramural pseudodiverticula can sometimes

be mistaken for tiny ulcers When viewed in profile,

how-ever, they often appear to be floating or levitating outside

the wall of the esophagus without apparent

communica-tion with the lumen (see Figure 4-6), whereas true

esopha-geal ulcers are almost always seen to communicate directly

with the lumen This sign is therefore extremely helpful for

differentiating esophageal intramural pseudodiverticula

from ulcers

Patients with pulsion diverticula in the esophagus are

usually treated for their underlying esophageal motility

disorders (especially diffuse esophageal spasm), which are likely to be responsible for their symptoms Surgical repair may involve an associated longitudinal myotomy

to reduce local intraluminal pressure Traction diverticula and esophageal intramural pseudodiverticula rarely require specific treatment When the pseudodiverticula are associ-ated with strictures, however, these individuals may present with dysphagia, which is relieved by esophageal dilatation procedures

Key Points

Pulsion Diverticulum

■ Usually multiple

■ Mid- or distal esophagus

■ Rounded outpouching with discrete neck

■ Remains filled when esophagus collapses

■ Associated with diffuse esophageal spasm

Traction Diverticulum

■ Usually solitary

■ Midesophagus at level of pulmonary hila

■ Triangular outpouching with wide base

■ Empties when esophagus collapses

■ Associated with surgery, radiation, or tous disease in lungs

granuloma-Esophageal Intramural Pseudodiverticula

■ Dilated excretory ducts of deep mucous glands

■ Tiny flask-shaped outpouchings

■ Longitudinal rows parallel to long axis of esophagus

■ Often floating or levitating outside esophagus out direct communication

with-■ Longitudinal intramural tracking between pseudodiverticula

■ Associated with strictures, especially peptic tures in distal esophagus

stric-Further Reading

1 Levine MS Miscellaneous abnormalities of the esophagus

In: Gore RM, Levine MS, eds Textbook of Gastrointestinal Radiology 3rd ed Philadelphia, Pa: WB Saunders,

2008:465–493.

2 Levine MS, Moolten DN, Herlinger H, et al Esophageal

intramural pseudodiverticulosis: a reevaluation AJR

1986;147:1165–1170.

Figure 4-6 Esophageal intramural pseudodiverticulosis

A prone right-anterior-oblique single-contrast view of the

esophagus shows innumerable tiny pseudodiverticula (white

arrows) arising from the wall of the lower and midthoracic

esophagus Note that many of the pseudodiverticula appear

to be floating or levitating outside the wall without apparent

communication with the lumen—a finding characteristic

of these structures Also note intramural tracking of barium

(black arrows) between some of the diverticula These tracks

can sometimes be mistaken for flat ulcers

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Candida esophagitis is by far the most common cause of

infectious esophagitis, typically occurring in

immunocom-promised patients A fulminant form of candidiasis is

some-times encountered in patients with AIDS Nevertheless, these

patients typically have an excellent response to treatment

with antifungal agents, even in the presence of severe disease

About 75% of patients with Candida esophagitis are

immu-nocompromised secondary to underlying malignancy;

treatment with radiation, chemotherapy, or steroids; or

other causes However, the remaining 25% of patients have

local esophageal stasis due to such conditions as achalasia

and scleroderma, which enable the fungal organisms to

overgrow and colonize the esophagus, leading to subsequent

esophagitis Only about 50% of patients with candidiasis

have oropharyngeal candidiasis (i.e., thrush), so the absence

of oropharyngeal disease in no way excludes this diagnosis

Patients with Candida esophagitis typically present with

odynophagia or dysphagia Even in patients with severe

dis-ease, however, there is usually a marked and rapid response

to treatment with antifungal agents such as fluconazole; thus

Candida esophagitis is a readily treatable disease.

Pathology

Candida esophagitis is characterized

histopathologi-cally by heaped-up areas of necrotic epithelial debris and

colonies of Candida albicans on the mucosa The lesions

are recognized grossly as white exudates and plaques

that have a distinctive endoscopic appearance Although

single-contrast barium studies have little value in patients

with suspected candidiasis, double-contrast barium

stud-ies have sensitivitstud-ies as high as 90% for detecting Candida

esophagitis in relation to endoscopy, primarily because

of the ability of such studies to demonstrate mucosal

plaques Thus only mild cases are likely to be missed on

the double-contrast examination

Imaging Features

Candida esophagitis is usually manifest on

double-contrast studies by discrete plaque-like lesions in the esophagus (Figure 5-1) The plaques may appear as linear or irregular filling defects that tend to be oriented longitudinally in relation to the long axis of the esopha-gus and are separated by segments of normal interven-ing mucosa During the past two decades, a much more fulminant form of candidiasis has been encountered

in patients with AIDS, who may present with a grossly

irregular or shaggy esophagus caused by innumerable

coalescent plaques and pseudomembranes with ping of barium between the lesions (Figure 5-2) Some

trap-of these plaques may eventually slough, producing one

or more deep ulcers superimposed on a background of diffuse plaque formation Occasionally AIDS patients may present with the shaggy esophagus of candidiasis

as the initial manifestation of their disease; therefore the examining radiologist may be the first to suggest that the patient has AIDS

■ Glycogenic acanthosis: A benign, degenerative dition characterized by accumulation of glycogen in the squamous epithelial cells lining the esophagus This condition appears on double-contrast studies in the form of discrete nodules, but they tend to have a more rounded appearance than the plaques of candi-diasis These patients also are elderly individuals who are not immunocompromised and have no esopha-

con-geal symptoms; thus differentiation from Candida

esophagitis is usually possible based on the clinical and radiographic findings

■ Reflux esophagitis: May be manifest by a nodular mucosa, but the nodules have poorly defined bor-ders and the nodularity extends proximally from the gastroesophageal junction as a continuous area of disease

■ Superficial spreading carcinoma: May be manifest by confluent nodules and plaques in a focal distribution, enabling differentiation from the discrete plaques and nodules of candidiasis

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