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366 SECTION VI Gastrointestinal Disease
A
Fig. 35.3 Endoscopic retrograde cholangiopancreatography (ERCP). (A) Normal cholangiogram. Contrast
injected into the biliary tree during ERCP demonstrates the intraductal anatomy of the common bile duct
(CBD), right hepatic duct (RHD), left hepatic duct (LHD), and smaller intrahepatic biliary radicals. (B) Normal pancreatogram. Contrast injected into the pancreatic duct during ERCP defines the intraductal anatomy
throughout the length of the pancreas. (Courtesy of Brian C. Jacobson.)
Fig. 35.4 Endoscopic ultrasound of the gastrointestinal wall. A 12-MHz
ultrasound probe, passed through the accessory channel of an endoscope, demonstrates the normal layers of the rectal wall. The mucosa
(m) appears as a superficial, hyperechoic (white) band and a deeper
hypoechoic (black) band. The submucosa (sm) appears as the next
hyperechoic layer. The muscularis propria (mp) appears hypoechoic, and
the serosa (s) appears as the outermost, hyperechoic layer. (Courtesy
of Brian C. Jacobson.)
B
addition, EUS can image beyond the gastrointestinal tract wall, providing sonographic images of adjacent structures within the mediastinum and upper abdomen, including the pancreas, liver, gallbladder,
mesenteric vessels, lymph nodes, and adrenal glands. High-frequency
EUS catheter probes can be passed through the accessory channel of
a duodenoscope and into the biliary and pancreatic ducts to provide
sonographic images of small tumors and stones. They can likewise be
used through a standard endoscope to evaluate diminutive subepithelial lesions and stage obstructing esophageal cancers. Fine-needle
aspiration (FNA) as well as core biopsy can be performed under EUS
guidance and is the preferred approach to obtaining a tissue diagnosis in many circumstances (e.g., pancreatic masses or cysts, subepithelial lesions of the GI tract, and intra-abdominal or paraesophageal
lymphadenopathy). Technologic advancements such as elastography
and contrast-enhanced harmonic EUS have further enhanced the
diagnostic capability of EUS, particularly in terms of distinguishing
malignancy from benign processes. Furthermore, EUS-guided vascular access provides a unique modality for portal vein sampling and
portal pressure measurements. However, EUS is more than just a diagnostic modality, and the spectrum of EUS-guided therapies is rapidly
expanding. Therapeutic maneuvers that can be performed via EUS
guidance include transluminal drainage of pseudocysts and walledoff pancreatic necrosis, pancreatic cyst ablation, celiac axis neurolysis,
fiducial (technical) placement into solid tumors to guide stereotactic
radiotherapy, and achieving bile duct access or biliary drainage (when
initial attempts at ERCP have failed or surgically altered anatomy precludes standard ERCP.)
this transducer can be placed within the GI lumen, high-resolution
images of the bowel wall can be obtained, revealing distinct layers that
correspond to the mucosa, submucosa, muscularis propria, and serosa
(Fig. 35.4). This technique allows the endoscopist to stage tumor
depths and determine the layer of origin of subepithelial masses. In
“Second Space” and “Third Space” Endoscopy
Recent advancements in endoscopic techniques and equipment have
led to the development of so-called “second-space” and “third-space”
endoscopy procedures within the peritoneal cavity and intramural/
submucosal tissue planes, respectively.
CHAPTER 35 Endoscopic and Imaging Procedures
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Fig. 35.6 Small bowel follow-through. Ingested barium defines the con-
tours of the small and large bowel lumen. A long stricture (S) of the terminal ileum can be seen in this patient with Crohn’s disease. (Courtesy
of Brian C. Jacobson.)
367
Fig. 35.5 Upright plain radiograph of the abdomen. Air in dilated loops
of colon and air-fluid levels can be seen in this patient with a sigmoid
volvulus. (Courtesy of Brian C. Jacobson.)
Natural orifice transluminal endoscopic surgery (NOTES) is an
evolving, minimally invasive field that combines endoscopic and surgical approaches to access the peritoneal cavity. Through the use of
an endoscope, a clinician can access a desired target or organ through
a transgastric, transcolonic, transvaginal or transurethral approach.
Examples of NOTES procedures include cholecystectomy, appendectomy, sleeve gastrectomy, hysterectomy, and hernia repair.
The success and promise of NOTES procedures has led to the
development of “third space” endoscopic interventions within the
intramural tissue planes of the gastrointestinal tract. Such procedures
include full-thickness resection of subepithelial tumors of the GI tract,
as well as peroral endoscopic myotomy (POEM) to treat achalasia and
esophageal motility disorders. By utilizing submucosal endoscopy, the
POEM procedure consists of four steps involving a mucosal incision,
submucosal tunneling, subsequent myotomy, and finally mucosal closure through the placement of clips or sutures. POEM has become a
very popular modality in treating achalasia, due to its long-term efficacy, lack of abdominal incisions, and rapid recovery.
The same principles and techniques of POEM have been used in
the treatment of pyloric dysfunction in patients with gastroparesis in
what is known as gastric POEM (G-POEM). Lately, there has been
a growing body of evidence proposing that pyloric dysfunction may
indeed be a significant contributor to the pathogenesis and symptomatic effects related to gastroparesis. In this context, the need for an
alternative, more effective, and minimally invasive therapeutic modality that can target a subset of patients who exhibit pyloric dysfunction
has emerged. G-POEM has shown promise, but further long-term and
head-to-head studies are needed to see if this modality can emerge as
first-line therapy.
NONENDOSCOPIC IMAGING PROCEDURES
Plain Abdominal Radiographs
Plain abdominal radiographs include upright, supine, and lateral decubitus films obtained with standard radiograph equipment and without
the use of contrast agents. Plain films are most useful in the initial evaluation of abdominal pain or nausea and vomiting, particularly when
perforation or obstruction is suspected, and they may reveal evidence
of a pneumoperitoneum, dilated bowel loops and air-fluid levels,
excessive amounts of stool, or displacement of bowel loops. These findings are indicative of a perforation, obstruction or ileus, constipation
or fecal impaction, and volvulus or organ enlargement, respectively
(Fig. 35.5). Calcifications, such as those seen in chronic pancreatitis
and gallstone disease, may also be visible on these radiographs.
Contrast Studies
Contrast agents such as barium or the water-soluble diatrizoate (e.g.,
Gastrografin) can be administered by mouth or rectum to detect
mucosal abnormalities (ulcerations and masses), strictures, herniations, diverticula, and abnormal peristalsis. Contrast agents can be
used alone (single contrast) or with the instillation of air or ingestion of
gas-forming agents (double contrast). The former method is more useful for detecting obstructing lesions and motility disturbances, whereas
the latter method aids in detecting more subtle findings such as small
ulcerations or polyps.
A video esophagogram (also known as modified barium swallow)
entails the filming of a patient’s oral cavity and pharynx during the
ingestion of contrast materials of various thicknesses and textures.
This imaging modality permits careful assessment of a patient’s ability to manipulate a food bolus, swallow effectively, and avoid aspiration events. A video esophagogram is indicated for evaluating patients
with oropharyngeal dysphagia and recurrent aspiration pneumonia. A
standard barium esophagogram (barium swallow) focuses attention on
the esophagus during the ingestion of a bolus of contrast. This study
can detect esophageal rings, webs, strictures, and motility problems
that endoscopy might miss. A barium esophagogram may be useful
for evaluating esophageal dysphagia, either as a complementary test to
endoscopy, or when endoscopy is contraindicated.
An upper GI series includes serial radiographic images as an ingested
contrast agent travels through the esophagus, stomach, and duodenum.
This study can define gastric abnormalities, such as masses, ulcerations,
and mucosal thickening. It is indicated in evaluating abdominal pain and
suspected gastric outlet obstruction. If radiographic imaging continues
as the contrast agent traverses the jejunum and ileum, the study is called
a small bowel follow-through (Fig. 35.6). Indications for a small bowel
follow-through include suspected small bowel obstruction or partial
obstruction from any cause, suspected small bowel mucosal diseases such
as Crohn’s disease, and obscure GI blood loss (although this has been
368 SECTION VI Gastrointestinal Disease
Fig. 35.7 Computed tomography enterography. A long segment of
inflamed terminal ileum is demonstrated in this patient with Crohn’s
disease. (Courtesy of Christopher S. Huang.)
largely replaced by video capsule endoscopy). During this more involved
procedure, a radiologist will obtain multiple films, including spot films, or
close-up views of regions that appear abnormal. Fluoroscopy can be used
to follow a contrast agent during the journey through the small bowel.
Attention is paid not only to structural findings but also to the length of
time required for contrast to reach and enter the colon. For more detailed
small bowel images, enteroclysis can be performed. This method requires
the infusion of concentrated contrast directly into the small bowel
through a nasojejunal tube placed under fluoroscopic guidance. Because
of its invasive nature, as well as the availability of better small bowel imaging techniques, enteroclysis is now rarely performed.
Single- and double-contrast barium enemas can detect colonic strictures, diverticula, polyps, and colonic ulcerations, and they can be therapeutic in reducing a sigmoid volvulus. Double-contrast barium enema
may be used for colorectal cancer screening as a stand-alone test or in
conjunction with flexible sigmoidoscopy, or it may be used to visualize
the proximal colon when colonoscopy cannot be completed for various
reasons. However, it is now infrequently used for these purposes given its
relatively poor sensitivity, as well as availability of computed tomography
colography (“virtual colonoscopy,” discussed later). In general, the upper
GI series and barium enema have been superseded by upper endoscopy
and colonoscopy because the endoscopic procedures offer increased sensitivity for detecting mucosal abnormalities, the ability to obtain mucosal
biopsies, and the potential for resection of identified lesions.
Transabdominal Ultrasound
Ultrasonography is often the first imaging study obtained in the evaluation of suspected biliary colic, jaundice, and abnormal liver tests. Its
use of sound waves to create an image obviates the need for radiation
exposure, and the addition of Doppler techniques permits the assessment of vascular flow. Ultrasound can detect parenchymal abnormalities, such as fatty liver or cirrhosis, focal masses or cysts, ascites, biliary
ductal dilation, gallstones, and large vessel thromboses. It may detect
thickening of the gut wall and areas of intussusception. Ultrasound is
also used to guide needle placement for biopsies or fluid aspiration.
Ultrasound cannot penetrate bone or air, preventing its use as a more
general diagnostic tool for the GI tract.
Computed Tomography, Computed Tomography
Enterography, and Computed Tomography Colography
Computed tomography (CT) uses computer-aided reconstruction of
multiple radiographic images obtained in a circular or helical course
around a patient’s vertical axis. Internal organs are visualized based
on their inherent tissue densities compared with their surroundings.
The GI lumen is usually opacified by having the patient drink an oral
contrast agent. In addition, intravenous contrast agents can be administered to highlight regions with increased blood flow, thereby improving detection of pathologic lesions, such as tumors and areas of active
inflammation. CT can detect parenchymal lesions, such as tumors,
cysts, and abscesses, as well as define the size, shape, and characteristics
of parenchymal organs, such as the liver and spleen. Vascular abnormalities, such as perigastric varices or large vessel thromboses, and
intra-abdominal fluid, such as ascites, can also be seen with CT. The caliber and contour of the GI tract wall are demonstrated by CT, aiding in
the diagnosis of inflammatory lesions, such as colitis, diverticulitis, and
appendicitis. CT can also be used to guide needle biopsies of abdominal
masses and to place electrodes into tumors for ablative therapies such as
radiofrequency ablation. The use of CT to guide placement of drainage
catheters has made possible the percutaneous treatment of intra-abdominal abscesses, pseudocysts, and pancreatic necrosis.
CT enteroclysis and CT enterography are two emerging techniques
developed to provide better images of the small intestine. CT enteroclysis uses a nasojejunal tube to deliver contrast into the small intestine, whereas CT enterography uses an orally ingested low-density
intraluminal contrast to distend the lumen and highlight the small
intestinal mucosa (Fig. 35.7). With the advancement of this technology
and its ability to reconstruct images in multiple planes, both luminal
and extraluminal information can be obtained.
CT can also be used to obtain high-resolution images of the colon.
CT colonography, or virtual colonoscopy, makes use of special image
reconstruction software to create accurate visualization of the colonic
lumen, provided that the patient has completed a bowel-cleansing
regimen identical to that used for colonoscopy (although techniques
that do not require such preparation are being developed). These CT
images are 70% to 90% sensitive for detecting polyps or masses within
the colon, helping to determine which patients need therapeutic colonoscopy. CT colonography is considered an acceptable option for
colorectal cancer screening in average risk individuals but is primarily
used to complete colonic visualization in the setting of an incomplete
colonoscopy (due to technical reasons or obstructing pathology).
Magnetic Resonance Imaging and Magnetic
Resonance Cholangiopancreatography
Similar to CT, magnetic resonance imaging (MRI) provides multiple cross-sectional images of the abdomen and pelvis. These images
are created using powerful field magnets to orient small numbers of
nuclei within the body in such a way as to produce a measurable magnetic moment. MRI therefore avoids radiation exposure but requires
the patient to lie nearly motionless, and often within a small enclosed
tube, for prolonged periods. MRI can visualize parenchymal lesions
such as masses and cysts and may better characterize abnormalities
seen on CT, such as hemangiomas, hepatic focal nodular hyperplasia,
and fatty liver. MRI is also helpful in better characterizing perirectal
abscesses and fistulas in Crohn’s disease. Special rectal MRI probes
or coils can provide detailed images of rectal cancer used for tumor
staging, as well as evaluate the anal sphincters in patients with fecal
incontinence.
MRI of the biliary and pancreatic ducts (magnetic resonance chol-
angiopancreatography, MRCP) is a noninvasive method that can detect
ductal dilation, strictures, stones (Fig. 35.8), pancreatic parenchymal
changes in chronic pancreatitis, and congenital ductal abnormalities,
such as pancreas divisum. Magnetic resonance angiography is a magnetic resonance method for visualizing blood vessels and serves as an
important noninvasive tool for evaluating patients with suspected
mesenteric ischemia, vasculitis, and other vascular anomalies.
CHAPTER 35 Endoscopic and Imaging Procedures
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Fig. 35.8 Magnetic resonance cholangiopancreatography. Several
stones are visualized within the common bile duct, appearing as
hypointense filling defects on T2-weighted images. (Courtesy of Christopher S. Huang.)
Visceral Angiography
Angiography is an invasive technique whereby a catheter is introduced
into a blood vessel, and intravascular contrast is injected during fluoroscopic imaging to visualize the vessel’s lumen. Visceral angiography
is used for evaluating mesenteric vessels in the setting of GI bleeding
and suspected mesenteric ischemia. For GI bleeding, angiography is
sensitive enough to detect 1 to 1.5 mL per minute of blood loss. Once
the site of bleeding has been localized, the radiologist can infuse vasopressin (a vasoconstrictor) or embolize the vessel using tiny coils or
gelatin sponges to ensure hemostasis. In the setting of mesenteric
ischemia, angiography permits localization of a vascular stenosis or
obstruction, followed by possible therapeutic interventions (e.g., balloon angioplasty, stent placement, infusion of vasodilators and thrombolytics). Other indications for angiography include the placement
of transjugular intrahepatic portosystemic shunts (TIPS) in cirrhotic
patients with intractable variceal bleeding or refractory ascites and for
chemoembolization of liver tumors.
Radionuclide Imaging
Technetium-99m (
in GI imaging. Its 6-hour half-life and ready availability make it
ideal for clinical use.
use in several imaging techniques.
99m
and
Tc-labeled red blood cell scanning are two distinct methods that can be used to detect active GI bleeding. The latter uses
the patient’s own blood cells to carry the radionuclide throughout
the body. These methods can detect as little as 0.05 to 0.4 mL per
minute of blood loss. However, localization of the site of bleeding is
less accurate with these methods compared with angiography.
scans are often performed before angiography to document ongoing bleeding before subjecting a patient to the more invasive, less
sensitive study. A
to diagnose a hepatic hemangioma with an almost 100% positive
predictive value.
Cholescintigraphy using
the most commonly performed liver study in nuclear medicine. The
radionuclide is taken up by the liver, is excreted into bile, and passes
through the biliary tree into the gallbladder and duodenum. Failure
to visualize the gallbladder during a hepatobiliary IDA scan may
99m
Tc) is currently the major radionuclide used
99m
Tc is used to label various substances for
99m
Tc-labeled red blood cell scan can also be used
99m
99m
Tc-sulfur colloid scanning
Tc-iminodiacetic acid (IDA) analogs is
99m
Tc
369
indicate cholecystitis secondary to cystic duct obstruction by a gallstone. Meckel’s diverticulum can be a source of abdominal pain and
bleeding, but it can be difficult to visualize with standard endoscopic
and radiographic imaging. The agent
99m
Tc-pertechnetate has a high
affinity for gastric mucosa and is therefore used to demonstrate the
presence of this congenital anomaly.
Gastric emptying studies are useful for the evaluation of patients
with suspected gastroparesis. Patients are given a
99m
Tc-sulfur colloid-labeled standardized meal (consisting of liquid egg whites, toast,
jam/jelly, and water) and are imaged at 0, 1, 2, and 4 hours after meal
ingestion. Gastric retention of greater than 10% at 4 hours is highly
sensitive and specific for delayed gastric emptying.
Radionuclide imaging studies are also useful for the detection,
staging, and monitoring of certain neoplasms such as neuroendocrine
tumors (NETs). Most well-differentiated NETs express somatostatin
receptors and can therefore be detected with radiolabeled somatostatin
analogues such as 111-In pentetreotide and 68-Ga DOTATATE.
PROSPECTUS FOR THE FUTURE
Through continued technologic advances, improvements in both
endoscopic and radiologic image quality and resolution will also continue. In addition, the gastrointestinal lumen will no longer be regarded
as a boundary to therapeutic endoscopy. Examples of expected innovations include the following:
• The continued expansion of endoscopic procedures beyond the walls
of the GI tract, providing a less invasive approach to treatment of
diseases traditionally managed surgically.
• “Second-space”and“third-space”endoscopytechniquesarelikely
to be refined further, and bariatric endoscopy techniques are likely
to become more widely performed.
• Further development of computer-aided diagnosis (or “articial
intelligence”) for colonoscopy with automated polyp detection and
characterization.
SUGGESTED READINGS
ASGE Technology Committee, Aslanian HR, Sethi A, et al.: ASGE guideline
for endoscopic full-thickness resection and submucosal tunnel endoscopic
resection, VideoGIE 4(8):343–350, 2019.
Byrne MF, Jowell PS: Gastrointestinal imaging: Endoscopic ultrasound,
Gastroenterology 122:1631–1648, 2002.
DiSario JA, Petersen BT, Tierney WM, et al.: Enteroscopes, Gastrointest Endosc
66:872–880, 2007.
Fletcher JG, Huprich J, Loftus EV, et al.: Computerized tomography
enterography and its role in small-bowel imaging, Clin Gastroenterol
Hepatol 6:283–289, 2008.
Gore RM, Levine MS: Textbook of gastrointestinal radiology, ed 2, Philadelphia,
2000, Saunders.
Mishkin DS, Chuttani R, Croffie J, et al.: ASGE Technology Status Evaluation
Report: Wireless capsule endoscopy, Gastrointest Endosc 63:539–545, 2006.
Muguruma N, Tanaka K, Teramae S, Takayama T: Colon capsule endoscopy:
toward the future, Clin J Gastroenterol 10(1):1–6, 2017.
Riff BP, DiMaio CJ: Exploring the small bowel: update on deep enteroscopy,
Curr Gastroenterol Rep 18(6):28, 2016.
Schneider M, Höllerich J, Beyna T: Device-assisted enteroscopy: A review
of available techniques and upcoming new technologies, World J
Gastroenterol 25(27):3538–3545, 2019.
Shah SL, Perez-Miranda M, Kahaleh M, Tyberg A: Updates in Therapeutic
Endoscopic Ultrasonography, J Clin Gastroenterol 52(9):765–772, 2018.
Thrall JH, Ziessman HA: Nuclear Medicine: The Requisites, ed 2, St. Louis,
2000, Mosby.
36
Esophageal Disorders
Harlan Rich, Zilla Hussain, Neal D. Dharmadhikari
INTRODUCTION
The esophagus is a muscular tube that serves as conduit for the passage of solids and liquids into the stomach. It averages 23 to 25 cm
in length and descends from the pharynx, at the lower border of the
cricoid cartilage, to the stomach, at the cardiac orifice. Its descent is
generally vertical and follows anterior to the vertebral column through
the diaphragm and into the abdomen.
The esophagus is made up of four strata: mucosa, submucosa,
muscularis externa, and adventitia. The stratified squamous nonkeratinized mucosa also contains the lamina propria and smooth muscle
muscularis mucosae. Esophageal cardiac glands, in the lamina propria, produce mucous secretions that coat the lining of the esophagus. The submucosal layer contains esophageal glands, mucous and
serous cells, and the Meissner, or submucosal, plexus. The muscularis
externa is composed of an inner circular and outer longitudinal muscle layer. The upper third is mostly skeletal muscle innervated by the
vagus nerve, while the lowest third is predominantly smooth muscle
innervated by the enteric nervous system. The middle third is a mix of
both skeletal and smooth muscle. The Auerbach, or myenteric, plexus
is located between the inner circular and outer longitudinal layers.
The outermost layer of the esophagus is the adventitia. A serosal layer
covers the short segment of the abdominal esophagus across the diaphragm to the gastric cardia.
Sphincters are found at each end of the esophagus: the upper esophageal sphincter (UES) and the lower esophageal sphincter (LES). The
UES is composed of three striated skeletal muscles: cricopharyngeus,
thyropharyngeus, and cranial cervical esophagus. It maintains a degree
of muscular activity at rest and relaxes during swallowing, vomiting, or
belching. Opening of the UES occurs both via relaxation of these muscles and the pulling open of the sphincter via the superior and inferior
hyoid and posterior pharyngeal muscles. The LES is a zone of circular,
smooth muscle that maintains tonic contraction at rest and relaxes
during swallowing, vomiting, and belching. The LES is supported by
a functional external sphincter composed of the right crus of the diaphragm, which surrounds the esophagus as it enters the abdomen.
Together, the LES and the functional external sphincter contribute to
a high-pressure zone, preventing the regurgitation of gastric contents.
Relaxation of the LES occurs when vagal efferent impulses activate
myenteric neurons that release nonadrenergic, noncholinergic neurotransmitters, predominantly nitric oxide, and vasoactive intestinal
polypeptide.
Swallowing requires the synchronization of voluntary and involuntary processes. Food mixes with saliva in the mouth and then is
pushed back into the oral pharynx by the tongue. Once food enters
the oral pharynx the glottis closes, protecting the airway. The bolus
is then pushed to the esophagus where the UES is located. The UES
relaxes, allowing food to enter the esophagus and then immediately
closes, preventing the regurgitation of food. The bolus spends 8 to
13 seconds in the esophagus. Primary peristaltic waves, activated by
central sequential firing mechanisms in the striated esophagus, and a
latency gradient through the smooth muscle esophagus activated by
vagal impulses, allow the bolus to travel through the esophagus. The
pressure created by these waves ranges from 40 to 180 mm Hg. The
pressure varies by the bolus’s location in the esophagus, consistency,
volume, and temperature. The LES relaxes and peristaltic waves push
the bolus into the stomach.
SYMPTOMS OF ESOPHAGEAL DISEASE
Heartburn and regurgitation are two of the most common symptoms
of esophageal disease and are defining features of gastroesophageal
reflux disease (GERD). Heartburn is described as a burning sensation
in the chest but can also be described as chest pain. Regurgitation is
the sensation of food or liquid moving up and down the esophagus or
as a sour taste in the mouth.
Dysphagia describes difficulty swallowing and can be characterized
by trouble initiating a swallow or a bolus of material feeling stuck in
the neck or chest while swallowing. The etiology of dysphagia can be
mechanical or functional in nature. Odynophagia is pain with swallowing. Globus sensation is the feeling of something “stuck” or “tightness” in the esophagus. This symptom may be unrelated to swallowing,
separating it from dysphagia.
Chest pain can be a manifestation of esophageal disease, but cardiac
disease should always be considered. Chest pain related to cardiac disease, or angina, can have characteristics similar to those associated with
esophageal-related chest pain. A careful history and physical examination with appropriate diagnostic studies can help distinguish the etiology of chest pain.
DIAGNOSTIC STUDIES OF THE ESOPHAGUS
Radiology
Barium esophagography, a video fluoroscopic procedure, can be used
to assess dysphagia and can diagnose structural abnormalities in the
esophagus or altered motility. When performed with a speech therapist
(a modified barium swallow), it can be used to study the swallowing
mechanism in more detail. A timed barium esophagogram can be used
to assess esophageal emptying.
Computed tomography (CT) and magnetic resonance imaging
(MRI) can often be used to define anatomy further and assess disease
outside the lumen and beyond the mucosa. Positron emission tomography (PET) can be used to evaluate the esophagus but is typically used
to evaluate malignant pathology when there is concern for metastasis.
370
CHAPTER 36 Esophageal Disorders
mmHg
Time (s)
Length along the esophagus (cm)
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371
200.0
UES
-180
-160
-140
-120
-100
- 80
- 60
- 50
- 40
- 30
- 20
- 10
- 0
-14.0
Fig. 36.1 High-resolution manometry (HRM) of normal esophageal peristalsis. HRM catheter consisting of 36
pressure sensors is inserted via the nares into the stomach to provide a complete physiologic pressure map
of the hypopharynx, upper esophageal sphincter (UES), esophagus, lower esophageal sphincter (LES) and
stomach. The Y-axis represents with sensor location; whereas the X-axis represents time. The color variation
represents the different pressures along the length of the catheter at a given time and location. The resting
UES and LES are shown as horizontal color bands. The relaxations of the UES (*) and LES (**) are shown as
decreases in pressures (corresponding to approximately 20 mm Hg on color-pressure bar). The LES opens
shortly after the UES relaxes with the onset of a wet swallow. Esophageal primary peristalsis is shown as a
diagonal color band running from the UES to the LES. The onset of the swallow is seen on HRM as the high
pressure contraction in the proximal, striated esophagus, followed by a lower pressure segment corresponding to the transition zone and a subsequent increase in pressure in the smooth muscle esophagus.
Onset of swallow
***
Striated esophagus
Transition zone
Smooth
muscle
esophagus
LES
10 sec
1
5
10
15
20
25
30
35
Endoscopy and Endoscopic Imaging
Esophagogastroduodenoscopy (EGD, upper endoscopy) allows for
a direct visualization of the mucosal surface of the esophagus, stomach, and duodenum. An endoscope is a flexible fiberoptic tube with a
camera that can be used for the diagnosis, screening, monitoring, and
treatment of various pathologies. Endoscopes have additional channels through which a variety of endoscopic tools (i.e., forceps, dilators,
injection needles, hemostatic tools) can be used to sample or treat the
visualized area.
Endoscopic ultrasound (EUS) incorporates an ultrasound probe
on the end of an endoscope. This ultrasound allows for imaging and
biopsy across the wall of the esophagus and other nearby anatomical
structures.
Manometry
Esophageal manometry is a physiologic evaluation of esophageal contractile function. High-resolution manometry is the diagnostic gold standard
for the diagnosis of motility disorders. It utilizes a catheter lined with 20
to 36 pressure sensors at 1-cm intervals that is inserted via the nasal passage to the gastric body. The sensors record and compute the frequency
and pressures of esophageal peristaltic waves and LES and UES function.
The high-resolution manometry pressures are used to generate esophageal
pressure topographies represented by color-coded, pressure-space-time
plots. These objective metrics are applied to the Chicago Classification to
diagnose esophageal motility disorders (Fig. 36.1).
Esophageal pH Monitoring
Esophageal wireless pH monitoring and catheter-based reflux testing
are diagnostic tools used to study reflux disease. The wireless pH capsule is typically positioned 5 cm above the LES. The capsule measures
the pH at the site for 24 to 48 hours in the ambulatory setting. The data
are then reported as a percentage of the day the pH remains below 4. A
combined impedance-pH probe measures acid and non-acid reflux as
well as the direction of transit of a food or fluid bolus.
STRUCTURAL DISORDERS
Cricopharyngeal Bars
A cricopharyngeal bar is a radiographic finding consisting of a prominent posterior indentation of the esophagus at the level of the cricopharyngeus that is often asymptomatic but can contribute to dysphagia.
The prominence is thought to be due to muscle spasm or impairment of
muscle compliance at the UES. Cricopharyngeal bars can be managed
via surgical and nonsurgical interventions. Nonsurgical options include
dilation at the site or injection of botulinum toxin. Surgical management
technique occurs via cricopharyngeal myotomy.
Diverticula
Diverticula of the esophagus are outpouchings contained within layers of
the esophageal wall. True diverticula involve all layers to the esophageal
wall, whereas false diverticula are limited to the submucosa and mucosa.
372 SECTION VI Gastrointestinal Disease
Pharyngoesophageal
diverticulum (midthoracic)
Pharyngoesophageal
diverticulum (Zenker)
diverticulum
(esophagoscopic view)
Traction
diverticulum
(esophagoscopic
view)
Azygos vein
Traction
Stomach
Fig. 36.2 Esophageal diverticula.
All diverticula are further categorized by their location. They are classified as proximal or pharyngoesophageal (Zenker’s and Killian-Jamieson)
diverticula, mid-esophageal or traction or parabronchial diverticula,
Epiphrenic
diverticulum
(viewed from
right side)
and epiphrenic diverticula. The prevalence of Zenker’s diverticula (ZD)
ranges from 0.01% to 0.11%, and the majority of patients are diagnosed
in their sixth to eighth decades of life. The prevalence of the other types of
CHAPTER 36 Esophageal Disorders
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373
diverticula are unknown but are far less common than Zenker’s diverticula (Fig. 36.2).
ZD forms in the Killian triangle, an area of sparse musculature
bordered by the cricopharyngeus and thyropharyngeus muscles in the
posterior pharyngeal wall. As a result of diminished compliance of the
cricopharyngeus muscle and the UES, the hypopharynx is exposed to
increased intra-bolus pressures while swallowing, causing the ZD to
form. ZD are false diverticula. Parabronchial diverticula are likely associated with mediastinal fibrosis, which is often due to inflammation
of the mediastinum caused by other pathology (i.e., fungal infections,
tuberculosis). Traction on the esophageal wall causes these diverticula
to form. Long-standing distal esophageal obstruction can lead to the
formation of pulsion diverticula either through anatomic abnormalities or motility disorders. Diffuse esophageal spasm has been associated
with parabronchial diverticula, whereas achalasia has been associated
with epiphrenic diverticula. The latter two are true diverticula.
Patients with ZD often present with oropharyngeal dysphagia but can
also suffer from complete esophageal obstruction. Classically, these patients
will complain of dysphagia with regurgitation and halitosis. Parabronchial
and epiphrenic diverticula are most often asymptomatic and diagnosed as
incidental findings on imaging. The complications of these diverticula are
typically related to their underlying disorders (i.e., motility disorders).
Diverticula are diagnosed using barium swallow, endoscopy, and
computed tomography. Manometry can also be used to diagnose
underlying motility issues that contribute to diverticula formation.
Symptomatic ZD should be treated. Smaller ZD can be treated with
cricopharyngeal myotomy alone. Larger ZD may need additional interventions, including diverticulum suspension or diverticulectomy. Endoscopic
cricopharyngeal myotomy is an alternative to surgical approaches.
Parabronchial and epiphrenic diverticula are most successfully addressed
by treating the underlying disorder (i.e., motility disorders or strictures).
They can also involve extended myotomy and diverticulectomy.
Rings and Webs
Esophageal rings are areas of narrowing in the esophageal lumen. An
“A” ring is a muscular ring found in the upper part of the phrenic
ampulla at the area of highest pressure in the LES and is defined by
smooth muscle hypertrophy with normal surface epithelium. A “B”
(or Schatzki) ring is a mucosal ring at the squamocolumnar junction
with squamous epithelium above the ring and columnar epithelium
below. This ring can lead to luminal narrowing and dysphagia. Their
etiology and pathophysiology are poorly understood.
Patients with Schatzki ring often complain of dysphagia to solid
food that is chronic and intermittent. The diameter of the ring is
inversely associated with the incidence and symptoms. A barium
swallow with a full column technique is the best modality to diagnose
Schatzki rings. An endoscope can visualize Schatzki rings but can miss
rings with larger diameters.
The treatment of all esophageal rings is mechanical dilation. This
can be performed with Savary dilators or radial expanding balloon
dilators. There is a high rate of reoccurrence after treatment and a scant
11% of patients are symptom free after 3 years. However, repeated
dilations can be performed without increasing the complication rate.
An esophageal web is a thin, membranous tissue covered with
squamous epithelium that reduces the size of the esophageal lumen.
The webs can be congenital or acquired. Congenital webs are rare.
Acquired esophageal webs are associated with Plummer-Vinson syndrome (iron deficiency anemia, glossitis, koilonychia, and esophageal/
pharyngeal carcinoma).
Patients with esophageal webs will present with dysphagia. The
webs are diagnosed by barium swallow or endoscopy. Lifestyle
modifications are encouraged to reduced symptoms, but some patients
must be treated with mechanical dilation similar to the treatment for
Schatzki rings.
Malignancy
Esophageal cancer is the seventh most common cancer and the sixth
leading cause of cancer-related mortality worldwide. The five-year survival rate after diagnosis is 15% to 20%. The incidence of esophageal
cancer varies by region. In developed countries, the incidence of squamous cell cancer (SCC) has fallen and adenocarcinoma has become
the leading type. However, SCC remains more prevalent worldwide.
The major risk factors for developing SCC are alcohol and tobacco use.
There are other carcinogens which, similar to alcohol and tobacco, are
thought to lead to inflammation and dysplasia. Tobacco is a moderate risk factor for the adenocarcinoma. Obesity and body mass index
remain the strongest risk factors for the development of esophageal
adenocarcinoma. Obesity can predispose patients to GERD and
Barrett esophagus, which also cause adenocarcinoma. The progression
of gastrointestinal reflux disease to adenocarcinoma is described in a
subsequent section (Fig. 36.3).
With esophageal cancer, patients often complain of progressive
dysphagia and weight loss. Depending on the progression of symptoms, they may also present with anemia or other symptoms. The
treatment of esophageal cancer depends on progression and staging
but can involve chemotherapy, radiation, surgery, and/or palliative
measures.
Hiatal Hernias
A hiatal hernia results in abdominal contents, such as the stomach,
becoming displaced above the diaphragm. Hiatal hernias are subcategorized into four types: type I (sliding hiatal hernia), type II (paraesophageal hernia; the proximal stomach protrudes up through the
diaphragm along the distal esophagus), type III (a combination of type
I and type II), and type IV (herniation of other abdominal organs).
Sliding hiatal hernias are the most common variety. Types II through
IV are considered variations of paraesophageal hernias (Fig. 36.4).
Sliding hernias are a result of laxity in the phrenoesophageal membrane, a membrane that anchors the esophagus to the diaphragm. This
results in a widening of the hiatal tunnel, allowing the gastric cardia
to herniate into the thorax. Increasing age and obesity often contribute to the decreasing elasticity of the phrenoesophageal membrane.
Paraesophageal hernias are caused by defects in this membrane.
Hernias may be diagnosed by plain film, barium swallow studies,
cross-sectional imaging, and endoscopy. Asymptomatic hiatal hernias
rarely need to be treated. If a type I hiatal hernia is associated with
GERD, then medical or surgical treatment should be considered. The
course of treatment would focus on treating the symptoms of GERD.
Paraesophageal hernias (type II-IV) are prone to complications
including volvulus, obstruction, incarceration, and perforation and
should be treated expediently because continued enlargement will lead
to worsening symptoms and complications.
GASTROESOPHAGEAL REFLUX DISEASE AND
SEQUELAE
A consensus (the Montreal consensus, specifically) amongst a panel
of world experts defined GERD as “a condition which develops when
the reflux of stomach contents causes troublesome symptoms and/
or complications.” This definition includes symptomatic syndromes
and syndromes with esophageal injury but does not include functional
heartburn.
374 SECTION VI Gastrointestinal Disease
ABCD
Fig. 36.3 Histologic progression of Barrett esophagus with no dysplasia (A) to low-grade (B) dysplasia, high-
grade dysplasia (C), and esophageal adenocarcinoma (D).
Pathophysiology and Symptoms
The pathophysiology of GERD is determined by numerous factors
including gastric acid–esophageal mucosa interaction, incompetence
of the gastroesophageal junction, decrease in esophageal mucosal
defenses, and altered sensory mechanisms that interpret the symptoms.
Numerous modalities can be used to help diagnose and manage
GERD, but often history is enough to diagnose and begin treatment.
The symptoms that are characteristic of GERD include heartburn and
regurgitation. Chest pain can also be a presenting symptom but should
be distinguished from cardiac chest pain. Patients can also present with
less common, atypical symptoms such as dysphagia, dyspepsia, epigastric pain, bloating, nausea, and belching.
Diagnosis
The diagnosis of GERD is established using history of symptoms,
objective testing (endoscopy and esophageal pH monitoring), and
patient responsiveness to therapy. A proton pump inhibitor (PPI) trial
is a method that may be used to diagnose GERD in patients with typical symptoms without concerning features that may include dysphagia, odynophagia, weight loss, anemia, nausea, or vomiting. A lack of
response to PPIs does not exclude the diagnosis of GERD, and atypical
symptoms are not as reliable at predicting response. Therefore, objective testing with endoscopy or esophageal pH monitoring should be
considered in patients who do not respond to PPIs.
Endoscopy provides direct visualization of the esophageal lumen and
evaluation of the esophageal mucosa in patients with suspected GERD.
It can demonstrate objective findings suggestive of GERD such as erosive
esophagitis, strictures, and Barrett esophagus. Not all symptomatic patients
will have evidence of erosions or mucosal damage, which can limit the
diagnostic specificity of endoscopy. Endoscopy allows for biopsy of the
mucosa, which is helpful in screening for Barrett esophagus, but can also
aid in establishing another diagnosis. Eosinophilic esophagitis may have a
similar presentation and biopsy can be used to differentiate between GERD
without erosions and eosinophilic esophagitis. Biopsy is not recommended
to diagnose GERD in patients with heartburn and normal endoscopy.
Esophageal pH monitoring with or without impedance may objectively demonstrate the presence of abnormal esophageal acid exposure,
non-acid reflux, reflux frequency, and symptoms associated with reflux.
Management
Lifestyle modifications are a part of the initial therapy for GERD.
Patients are counseled on behaviors that may improve symptoms
and recommendation of avoidance of foods that trigger symptoms.
Weight loss is advised for overweight and obese patients. Weight
gain, even in patients with normal BMI, can provoke new GERD
symptoms. Other behavior modifications include tobacco cessation, raising the head of the bed, and avoiding recumbent position
for at least 2 hours after a meal. The common foods that can trigger heartburn and regurgitation include coffee, alcohol, chocolate,
fatty foods, citrus, and spicy foods. It is important that all lifestyle
modifications be tailored to each patient’s symptoms and disease
course.
When lifestyle modifications fail, medical interventions should
be attempted. Medications that can treat GERD include antacids,
histamine-receptor antagonists (H2 blockers), and PPIs. Patients
often utilize over-the-counter antacids to provide symptom relief of
GERD. These antacids work to neutralize gastric hydrochloric acid
and inhibit pepsin. With the advent of H2 blockers and PPIs, antacid
use has declined, but a smaller cohort of patients will continue using
them for heartburn. H2 blockers reversibly bind to histamine H2
receptors, preventing histamine released during a meal from binding to receptors on ECL and parietal cells. PPIs are superior to H2
blockers because they essentially irreversibly block the hydrogen-potassium ATPase that secretes hydrochloric acid from the gastric parietal cells. They have been shown to contribute to esophageal healing
and have decreased relapse rates when compared to H2 blockers. In
addition, PPIs have also been shown to be superior for heartburn
relief.
Surgical options can be considered for GERD or esophagitis refractory to medical therapy, when patients suffer side effects of medical
therapy, exhibit noncompliance, or need correction of a concomitant
large hiatal hernia. The surgical options for treatment include laparoscopic fundoplication or bariatric surgery. Laparoscopic fundoplication involves “wrapping” the fundus of the stomach around the end of
the esophagus to help repair and provide support to the LES. Bariatric
surgery with gastric bypass in obese patients with GERD can also be
used to treat GERD.
CHAPTER 36 Esophageal Disorders
Type I
Type II
Type III
Type IV
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375
Sliding hiatal hernia
Ai
Hatus
Esophagus
Gastroesophageal
junction
GEJ
*
Fundus
Diaphragm
Paraesophageal hernia
Esophagus
Gastroesophageal
Aii
junction
Herniated
Fundus
Gastric fundus
herniated
through hiatus
fundus
Aiii
Herniated
fundus
Gastro-
esophageal
junction
Mixed
Esophagus
Paraesophageal hernia
Esophagus Herniated
Aiv
stomach
Herniated
colon
Bi
Bii
Ci Cii
Fig. 36.4 Anatomic drawings (row A), barium contrast radiography (row B), and endoscopic (i-iii) and com-
puted tomographic (iv) views (row C) of Type I or sliding hiatal hernia (column 1), Type II PEH (column 2),
Type III PEH (column 3), and Type IV PEH (column 4). Pane Bi: *, sliding hiatal hernia. Pane Bii: True paraesophageal hernia adjacent to GEJ. Separation between GEJ and diaphragm noted, consistent with a small
adjacent hiatal hernia. White arrow: Barium tablet present. Black arrows: Widened hiatus. Pane Biii: White
arrow: Gastroesophageal junction. Black arrows: Widened diaphragmatic hiatus. Pane Biv: Herniated, intra-
thoracic stomach with herniation of duodenum. This stomach is flipped in an organoaxial rotation. Pane Ci:
Sliding hiatal hernia. Pane Cii: Separate PEH present, herniated through laxity in phrenoesophageal membrane. Lax diaphragmatic hiatus also present. Pane Ciii: Image taken from the diaphragmatic hiatus (black
arrows). Herniation of GEJ noted with large adjacent fundus/PEH (white asterisk). Pane Civ: Coronal com-
puted tomography (CT) image of an intrathoracic stomach with herniated loops of colon (white arrows). GEJ,
Gastroesophageal junction; PEH, paraesophageal hernia.
Extraesophageal Manifestations of GERD
GERD contributes to several extraesophageal manifestations including respiratory, laryngopharyngeal, and dental symptoms. Respiratory
symptoms include pulmonary disease (asthma, idiopathic pulmonary
fibrosis, bronchitis, etc.), cough, wheezing, and shortness of breath.
Laryngeal symptoms present as hoarseness, throat pain, globus, choking, postnasal drip, laryngeal and tracheal stenosis, and laryngospasm.
Dental erosions can also be a result of GERD.
Non-GERD causes of extraesophageal manifestations should be con-
sidered prior to associating the symptoms with GERD. Diagnostic tools are
Biii Biv
*
Ciii
unable to provide reliable evidence of causality between GERD and extraesophageal symptoms. In addition, PPIs have not shown a clear therapeutic
benefit in the treatment of these symptoms. The diagnosis of GERD, as
described previously, can help with the association, but the presence or
absence of GERD cannot reliably establish it as cause of extraesophageal
symptoms. Clinicians often rely on symptom association analysis to find a
temporal association between reflux symptoms and other symptoms.
Acid suppression with a PPI is still used to treat extraesophageal symptoms when typical GERD symptoms are present. When typical GERD
symptoms are not present, reflux monitoring is considered prior to
Civ
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