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Author’s Accepted Manuscript image

Imaging Manifestations of Peptic Ulcer Disease on


Computed Tomography

Arthur H. Baghdanian, Armonde A. Baghdanian,


Shilpa Puppala, Michele Tana, Michael A. Ohliger

www.elsevier.com/locate/bios

PII: S0887-2171(17)30128-2
DOI: https://doi.org/10.1053/j.sult.2017.12.00210.4103/0971-3026.20295710.1016/S0140-6736(15)0027
710.1148/radiology.178.3.199441210.1055/s-2007-100543310.1016/S0140-6736(09)60938-
710.1001/archsurg.140.2.20110.1016/S0140-6736(16)32404-710.1007/s13244-017-0562-
510.1148/radiographics.21.suppl_1.g01oc01s14710.2214/ajr.182.4.182092710.1148/radiol.246106
014-0207-910.1111/1754-
9485.1240810.1097/SLA.0b013e3181b975b810.1148/radiology.153.3.649447110.1007/s00261-00
x10.1111/j.1440-1673.2004.01364.x10.4021/gr2009.10.132110.3348/kjr.2009.10.1.6310.1007/s00
Reference: YSULT795
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Cite this article as: Arthur H. Baghdanian, Armonde A. Baghdanian, Shilpa
Puppala, Michele Tana and Michael A. Ohliger, Imaging Manifestations of
Peptic Ulcer Disease on Computed Tomography, Seminars in Ultrasound, CT,
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Imaging Manifestations of Peptic Ulcer Disease on Computed Tomography

Baghdanian, AH; Baghdanian, AA; Puppala, S; Tana, M; Ohliger, MA

Arthur H. Baghdanian, MD

UCSF Department of Radiology and Biomedical Imaging

San Francisco, California

Armonde A. Baghdanian, MD

UCSF Department of Radiology and Biomedical Imaging

San Francisco, California

Shilpa Puppala, MD

UCSF Department of Radiology and Biomedical Imaging

San Francisco, California

Michele Tana, MD

UCSF Department of Gastroenterology

San Francisco, California

Michael A. Ohliger, MD PHD

UCSF Department of Radiology and Biomedical Imaging

San Francisco, California


Corresponding author:

Arthur Baghdanian, MD

University of California, San Francisco

Department of Radiology & Biomedical Imaging

505 Parnassus Avenue

Room L374, Box 0628

San Francisco, CA 94143

Office: 415-353-1628 Fax: 415-353-8589

Email: arthur.baghdanian@ucsf.edu

www.radiology.ucsf.edu

Peptic ulcer disease

ABSTRACT:

Although the overall prevalence of peptic ulcer disease (PUD) has decreased in modern times, its

actual incidence may be underestimated due to the non-specific clinical presentations patients’

manifest. The potential lethal complications that can result from PUD include life threatening

abdominal hemorrhage and bowel perforation that result in significant morbidity and mortality.

CT imaging historically lacks specificity in detecting PUD related pathology in the stomach and

proximal small bowel segments. Therefore, these are potential pitfalls in the radiologist’s search
pattern on abdominopelvic CT imaging. This article highlights imaging features of

uncomplicated PUD on CT imaging in order to allow for early detection of this disease process

on imaging and the prevention of potential high-grade complications by recommending

esophagogastroduodenoscopy.

INTRODUCTION:

Early detection of peptic ulcer disease (PUD) can prevent serious potential complications such as

life-threatening hemorrhage and bowel perforation (1). Peptic ulcer-related perforation is

considered a surgical emergency with a mortality of up to 30% (2). The gold standard for

diagnosing peptic ulcer disease is esophagogastroduodenoscopy. However, it is not commonly

used to evaluate patients in the emergency setting given the non-specific clinical presentation of

peptic ulcer disease and the more invasive nature of endoscopic examinations. By contrast, CT

of the abdomen and pelvis is frequently ordered in the emergency department to help exclude

acute abdominal processes. Given the historic lack of specificity of CT imaging in diagnosing

PUD, the stomach and duodenum may be overlooked segments in the a radiologists’ search

pattern (3). With advances in CT technology, radiologists who are familiar with subtle findings

of acute uncomplicated PUD may prevent complications such as hemorrhage or bowel

perforation by recommending urgent upper endoscopy.

PREVALENCE:

The prevalence of PUD has decreased in modern times in part because of widespread proton

pump inhibitor (PPI) use and in part because of the early diagnosis and treatment of H. pylori

infections. H. pylori is a gram-negative spiral bacillus that infects gastric epithelium and is a
major cause of peptic ulcer formation. H. pylori infection still remains the most common cause

of PUD, responsible for 70% of gastric ulcers and 95% of duodenal ulcers (4). More frequent use

of non-steroidal anti-inflammatory drugs (NSAIDs) has led to a further increase in the

prevalence PUD, responsible for the most of the remaining 30% of gastric ulcers (4). NSAID use

has also been associated with an increased rate of bleeding complications of PUD (5, 6).

Predisposing factors for peptic ulcer disease include corticosteroid use, physiological stress,

inflammatory bowel disease, and Zollinger-Ellison syndrome (7). In addition, smoking and

alcohol consumption lead to the development of more severe PUD and delayed healing of treated

disease (2).

PATHOPHYSIOLOGY:

Formation of peptic ulcers is related to destruction of the mucosal barrier that protects the gastric

or duodenal mucosa as well as excessive acid production (2, 8). H. pylori only infects gastric

epithelium and is commonly localized to the stomach antrum below the mucosal coat of the

stomach (4). H. pylori inhibits the negative feedback response to increases in gastrin production

and acid secretion (7). This can lead to excessive acid entering the duodenal bulb resulting in

duodenal metaplasia and potential H. pylori colonization (7). NSAID-related ulcer formation is

induced from production of free radicals as well as inhibition of prostaglandin production

resulting in damage to the bowel mucosa and loss of the protective effect of prostaglandins on

the mucosal barrier of the stomach leading to eventual mucosal irritation and ulcer formation (9).
CLINICAL PRESENTATION:

Patients with peptic ulcer disease may present with abdominal pain, GI bleeding, early satiety,

bloating, and nausea (7, 10). Patients may initially present with pain during fasting that improves

with food consumption. Chronic ulcers (as well as acute ulcer disease in diabetics) may not have

any associated abdominal pain and present only after serious complications have occurred (7).

Patients with complications of PUD disease such as bleeding may present with hematemesis,

hematochezia, and/or hypotension (2). Perforated peptic ulcer disease patients usually present

with severe abdominal pain and physical exam signs of peritonitis (2).

ANATOMY AND LOCATION of PUD:

Peptic ulcers occur in both the stomach and duodenum. The stomach is divided into the gastric

cardia, fundus, body, antrum, and pylorus. All aspects of the stomach are covered by visceral

peritoneum. The incisura angularis is an acute angle indentation along the lesser curvature of the

stomach wall and marks the division of the stomach body and the antrum (Fig. 1). Gastric ulcers

typically occur at the gastric antrum, with the lesser curvature being the most common location

(7). Peptic ulcers can also occur along the greater curvature of the stomach with the use of

NSAIDs (5).

The duodenum has no mesentery and is only partially covered by peritoneum (11). The

duodenum is divided into four parts: the first portion of the duodenum is the duodenal bulb,

extending superiorly from the pyrloris. The bulb is the only portion of the duodenum that is

covered on all surfaces by visceral peritoneum; the remaining portions of the duodenum are

retroperitoneal. The second portion of the duodenum descends inferiorly, and contains the
pancreatic duct and common bile duct. The third (horizontal) portion, crosses midline in the

retroperitoneum at the level of the second lumbar vertebral body. The fourth portion of the

duodenum extends from the aorta to the Ligament of Treitz (11).

The most common location of duodenal ulcers is in the duodenal bulb, representing 95% of

duodenal ulcers (7, 12, 13). Post-bulbar ulcers (ulcers distal to the duodenal bulb) are rare and

occur in only 3-5% of patients. When post-bulbar ulcers are seen, rare etiologies such as

Zollinger-Ellison Syndrome or Crohn’s disease should be considered (7, 12, 13). In addition,

post-bulbar ulcers are in closer proximity to the gastroduodenal artery and therefore have an

increased risk of hemorrhage when compared to bulbar ulcers (13).

The majority of post-bulbar duodenal ulcers occur on the anterior duodenal wall, just proximal

to ampulla. Duodenal ulcers can demonstrate inward bowing of the opposing wall due to edema,

reactive tissue, and spasm at the site of ulcer disease which can obscure an outpouching

indicative of an ulcer crater. Therefore, this inflammatory process can lead to difficulty in the

detection of ulcer craters that are a specific feature demonstrated on fluoroscopic imaging (13).

IMAGING FEATURES of PUD

Fluoroscopy:

Radiologists should be aware of the features of peptic ulcers on upper GI fluoroscopy, as it

continues to be a valued modality in the radiology armamentarium (14). Peptic ulcers in the

stomach and duodenum have similar features on double contrast barium upper GI series. Benign

ulcers appear as radiopaque outpouchings of the bowel wall when barium fills the ulcer crater

(Figs. 1,2). Benign ulcers also have a smooth ulcer mound, symmetric radiating mucosal folds
extending to the central ulcer and an ulcer depth greater than its width. The Hampton line is a

radiolucent line that traverses the ulcer neck resulting from overhanging edematous mucosa (4).

A secondary feature of PUD in the stomach or duodenum is luminal narrowing on upper GI

series resulting from bowel wall edema in the setting of gastritis or duodenitis. Complications of

peptic ulcer disease such as perforation can be diagnosed when administered oral contrast is seen

outside the bowel lumen (Fig. 3).

CT Imaging:

In an early study, Jacobs et al. concluded that CT is not diagnostically useful in the detection of

uncomplicated PUD (3). However, advances in CT imaging have allowed for increased

sensitivity in early ulcer detection to prevent development of more complicated disease (15). As

described by Kitchen et al. there are both indirect and direct CT imaging features of peptic ulcer

disease (15). Furthermore, there is increased accuracy in duodenal ulcer detection by correlation

of axial images with coronal reformations that allows a clearer depiction of ulcers as they can

appear more obvious in profile and may be missed if only using the axial plane (16).

CT imaging features of uncomplicated PUD:

Indirect signs:

The following indirect CT imaging signs may raise the suspicion for underlying peptic ulcers,

permitting early diagnosis and intervention. Gastritis and duodenitis are seen on CT imaging as

submucosal edema leading to bowel wall thickening, reflecting the inflammatory effects of H.

pylori infection or NSAIDs (3, 15, 17). There are a variety of alternative causes of gastric or

duodenal wall thickening that the radiologist should be aware of including trauma, under-

distention, inflammatory bowel disease, or lymphoma. An additional clue to the presence of


PUD is asymmetric thickening of the bowel wall (Fig. 4) (15). Furthermore, thickening in the

common locations of PUD such as the gastric antrum or the anterior wall of the duodenal bulb

should also raise suspicion for peptic ulcers.

CT imaging is limited in its evaluation for the gastric or duodenal fold thickening that has been

classically seen on upper gastrointestinal series (UGI) studies (15). An added benefit of CT is

evaluation for mucosal hyperenhancement resulting from bowel wall hyperemia (Figs. 4, 5).

Since other etiologies of bowel inflammation can also have similar imaging features, this is a

non-specific finding and should be correlated with the patient’s clinical presentation (15, 17). In

addition, inflammatory stranding in the adjacent fat or free fluid adjacent to the stomach or

duodenum should also raise concern for the possibility of PUD (Figs. 6, 7) (11, 15-18).

Direct signs:

The following direct signs of PUD can lead to an accurate diagnosis when evaluating the

stomach and duodenum on CT imaging. CT imaging features of focal outpouching of the

mucosal bowel lining resulting from the crater of the ulcer is a more specific feature for ulcer

disease (Figs. 6, 8-11) (15, 19). An additional feature is focal disruption of mucosal

enhancement resulting from the ulcer crater eroding through the epithelial lining of the mucosal

layer into the submucosal layer or muscularis propria (Figs. 5, 6, 9, 12, 13, 14). Therefore,

although lack of bowel distention on CT imaging may limit visualization of an ulcer crater,

absence of mucosal enhancement is an added clue that there is an underlying peptic ulcer in the

bowel wall. In the setting of peptic ulcers this feature may be more obvious since underlying

gastritis or duodenitis may result in a trilaminar appearance of the bowel wall allowing the

radiologist to better scrutinize the mucosa for interrupted enhancement (15, 19-21).
CT imaging features of complicated PUD:

As Wang et al. describe, the complications of PUD are bleeding, perforation, and less commonly

gastric outlet obstruction and fistulization to adjacent organs (10, 18). One of the more serious

complications of PUD is hemorrhage, which occurs in 15% of patients (10). Clinically, patients

may present with hematemesis, melena, hematochezia, or hemodynamic instability. Active

bleeding can be diagnosed on CT imaging as active vascular contrast extravasation, although

slow or intermittent hemorrhage may not be seen and therefore correlation with patient

symptoms and hemodynamic state is necessary (10). Blood products may accumulate adjacent to

the site of ulceration or seen as hyperdense material within the stomach or duodenal lumen (Figs.

9, 10). Ulcers can erode into the left gastric and gastroduodenal artery and lead to massive

hemorrhage (Fig. 11). Rarely gastric ulcers can also erode into the splenic artery, also leading to

massive hemorrhage (22).

Although peptic ulcer-related bowel perforations are less common than hemorrhage, perforation

is the most common indication for surgery and has increased mortality (2). Perforated peptic

ulcer disease is a surgical emergency with a mortality rate of up to 30% (2). The most common

cause of non-traumatic gastric perforation is PUD, the second being ulcerated gastric

malignancies (1, 20, 23). Clinical signs of perforation involve guarding on abdominal exam,

severe upper abdominal pain, and rebound tenderness (1). On CT imaging, features of free

intraabdominal air with the above described irregularities of the duodenum or stomach such as

focal wall thickening, discontinuity of the mucosa, fat stranding, and free fluid adjacent to the

gastric wall are suggestive of PUD-related perforation (Figs. 6, 7, 12) (11). Additional features
include extraluminal oral contrast when it is administered prior to performing CT scanning. Tiny

foci of air adjacent to the gastric or duodenal wall may be the sole sign of a perforated ulcer (11).

Perforated gastric ulcers along the lesser/greater curvatures and along the anterior wall can

perforate into the peritoneal space. Ulcers along the posterior surface of the stomach can

perforate into the lesser sac, which is located posterior to the stomach and anterior to the

pancreas (1). Duodenal perforation can extend either into the peritoneal or extraperitoneal space

(11, 16, 17). Free intraperitoneal air may also be seen tracking adjacent to the falciform ligament

or ligamentum teres (16). Contained perforations can occur and may initially present without

pneumoperitoneum (Fig. 13) (15).

Perforation related to gastric malignances is rarely seen (1). CT imaging features of perforation

related to gastric malignancy is similar to the findings discussed above in addition to abnormal

gastric wall thickening and enhancement related to tumor invasion into the gastric submucosa

and serosa resulting in loss of the trilaminar enhancement of the bowel loops (Fig. 15) (1).

Secondary clues to gastric malignancy involves adjacent lymphadenopathy or distal metastatic

disease (1).

Stricture and Fistulization:

Gastric outlet obstruction can result from peptic ulcer disease. It occurs in 5-8% of ulcer related

complications (8, 12). Gastric outlet obstruction resulting from peptic ulcer related fibrosis from

chronic inflammatory changes near the antrum and pylorus (7). Gastric adenocarcinoma and

duodenal tumors can involve the gastric pylorus also resulting in gastric outlet obstruction, and

should be considered when an enhancing mass is seen invading into the wall of the stomach (1).
Although rare, ulcers can lead to fistulization to adjacent organs such as the pancreas, biliary

tree, gall bladder or liver (Fig. 14) (10).

Ulcerated Malignancy:

Gastric cancer is the third most common gastrointestinal malignancy and is most commonly

gastric adenocarcinoma (95%). Gastric carcinomas can have various morphological appearances

including: an intraluminal polyploid mass, an infiltrative mass invading the wall of the stomach

into adjacent structures, or an ulcerated mass. On CT imaging, gastric masses can be difficult to

see in a non-distended stomach; however, an irregular contour to the stomach wall or an

abnormal enhancing tissue extending into the stomach wall should raise a radiologist’s suspicion

(Fig. 15). In the duodenum, adenocarcinoma is the most common malignant tumor. Duodenal

malignancy is most common near the ampulla and can also present as a polyploid, ulcerated, or

circumferential mass (4, 24).

Incidence of missed gastroduodenal ulcers

Allen et al. analyzed the incidence of missed gastroduodenal ulcers in cases of endoscopically

proven gastroduodenal ulcer cases. Their study had blinded readers interpret 114 CT

examinations, 50% of which had endoscopic evidence of gastroduodenal ulcer disease. At least

one of two readers detected 42% of endoscopically-proved ulcers on CT. False positive rate was

only 7%, suggesting ulcers can be detected with high specificity if they are actively sought out.

At the same time, the primary radiology interpretation detected an ulcer in only 5% of cases

(25). Therefore, there is a clear need for radiologists to be aware of the various features of the

PUD and scrutinize the stomach and duodenum as part of their search pattern in order to allow

early detection and prevent potential complications.


CONCLUSION:

Although the stomach and duodenum are sometimes overlooked by radiologists, knowledge of

the above described features on CT and other imaging may help radiologists combine both direct

and indirect findings of PUD to prevent dangerous complications such as bleeding and

perforation. Findings of PUD described above include gastric and duodenal wall thickening,

irregular mucosal hyper-enhancement or lack of enhancement as well as bowel wall

outpouchings. Familiarity with the imaging manifestations of PUD on CT can help radiologists

alert referring providers to the presence of uncomplicated PUD.

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a. b.
Figure 1. (a) Single contrast upper GI series demonstrates an outpouching (arrow) of the
duodenal bulb consistent with a peptic ulcer. The incisura angularis along the lesser curvature is
visualized demarcating the separation of the body and antrum of the stomach (arrow head). (b)
On additional view the heaped up edematous mucosa of the ulcer mound (star) is causing a
circumferential radiolucent ring around the outpouching (arrow) of the ulcer crater.
a. b.
Figure 2. Double contrast upper GI series demonstrates a focal outpouching filled with contrast
(a, b; arrow) consistent with a gastric ulcer at the gastric antrum.

a. b.
Figure 3. Single contrast fluoroscopic images demonstrating extra-luminal oral contrast
extending outside the bowel lumen consistent with a bowel perforation at the duodenal bulb
(arrow; a, b).
a. b.
Figure 4. Contrast enhanced abdominopelvic CT demonstrates abnormal stomach wall
thickening adjacent to the pylorus (arrow, a, b). Review of the coronal reformation demonstrates
the profile of the ulcer crater which was not as conspicuous on axial imaging as well as
inflammatory stranding in the adjacent fat (star) (b).

a. b.
c.
Figure 5. 50-year-old male presented with abdominal pain for four days. (a) Contrast enhanced
CT on initial presentation demonstrated duodenal wall thickening with mucosal enhancement
and submucosal edema (star) of the duodenal bulb. In addition, there was focal discontinuity of
mucosal enhancement (arrow). Patient was discharged from the ER with omeprazole. (b, c) Four
days later the patient presented with peritonitis. Contrast enhanced CT demonstrated sequelae of
bowel perforation with free fluid, peritoneal enhancement (arrow) and hypoperfusion complex of
the bowel loops.

a. b.
Figure 6. 44-year-old male presented with severe abdominal pain. (a) Abdominopelvic CT with
IV and oral contrast demonstrated a focal outpouching (black arrow) of the duodenal bulb. There
was inflammatory stranding seen in the fat adjacent to the duodenum (white arrow). (b) 8 hours
later the patient developed worsening abdominal pain and a repeat CT with IV and oral contrast
demonstrated fat stranding and ill-defined free fluid adjacent to the duodenal site of ulcer disease
(star). A focus of gas can be seen adjacent to the liver (arrow) and the patient was diagnosed with
a perforated peptic ulcer.

a. b.
Figure 7. 80-year-old male presented with abdominal pain. A non-contrast CT shows
inflammatory fat stranding adjacent (arrow) to the duodenum (a). The next morning the patient
had persistent abdominal pain. A repeat CT study demonstrated free air consistent with a bowel
perforation (b).

a. b.
Figure 8. 55-year-old with a history of NSAID use presented with abdominal pain. Contrast
enhanced axial CT demonstrated a focal outpouching at the lesser curvature of the stomach
(arrow) consistent with a gastric ulcer on axial (a) and coronal images (b).
a. b.

c. d.
Figure 9. 60-year-old male initially presented with non-specific symptoms of abdominal pain.
(a) Contrast enhanced axial CT without oral contrast demonstrated a focal outpouching (arrow)
of the duodenal bulb. One week later the patient presented with hematemesis, syncope and
anemia. (b) Contrast enhanced axial CT without oral contrast demonstrated the same
outpouching (arrow) of the bowel lumen consistent with an ulcer in the duodenal bulb.
Hyperdense material consistent with hemorrhage was seen in the duodenal lumen (star). Patient
was taken to endoscopy and two ulcers spurting blood were seen. Epinephrine was injected and a
ligature was placed and patient was transferred to interventional radiology. (c) Celiac angiogram
demonstrated active bleeding in the duodenal lumen (arrow). (d) Contrast enhanced CT with IV
and oral contrast after embolization demonstrated the coiled gastroduodenal artery.
a. b.
Figure 10. CT angiogram can be helpful in diagnosing active arterial bleeding. Contrast
enhanced abdominopelvic CT in the arterial phase demonstrated active contrast extravasation
(arrow; a) related to the ulcer seen on image b (arrow).

a. b.
Figure 11. (a) Contrast enhanced CT shows the ulcer crater as an outpouching (white arrow)
adjacent to the gastroduodenal artery (black arrow) at which time the patients hemoglobin was
13. Five days later the patient presented with hemodynamic instability related to peptic ulcer
bleeding, hemoglobin on repeat presentation was 8. (b) Repeat conrast enhanced CT again
demonstrates the ulcer crater (white arrow) and adjacent inflamamtory changes extending to the
gastroduodenal artery (black arrow).
Figure 12. Contrast enhanced CT in the coronal plain demonstrates mucosal discontinuity (white
arrow) as well as free air both in the wall of the duodenum and adjacent to the liver (black
arrows).

Figure 13. 57-year-old male presented to ED with hematochezia. (a) Coronal contrast enhanced
axial CT of the abdomen pelvis demonstrated mucosal discontinuity consistent with a focal
contained perforation at the 2nd portion of the duodenum (arrow). (b) Follow up contrast
enhanced coronal CT abdomen pelvis study with intravenous and oral contrast again showed the
focal perforation (arrow) and free air (star) which were seen on initial imaging.
a. b.

c. d.
Figure 14. Patient presented to emergency department with non-specific abdominal pain. (a)
Axial contrast enhanced abdominopelvic CT image demonstrated fat stranding adjacent to the
duodenum (star) and a focal outpouching (arrow) in the duodenum consistent with a duodenal
ulcer. (b) A tract is seen extending from the ulcer to the common bile duct (arrow) as well as
pneumobilia on the coronal reformation (arrow head). (c) Again, shown is a tract extending from
the duodenum to the common bile duct (arrow) concerning for a fistula to the duodenum. (d)
Patient was taken to ERCP and found to have a large duodenal ulcer which had fistulized to the
common bile duct (arrow).
Figure 15. 41-year-old male presented with colicky abdominal pain. Contrast enhanced axial CT
demonstrated an outpouching of the gastric antrum (arrow). The wall of the ulcer demonstrates
enhancement to the serosal level. Patient was found to have poorly differentiated gastric
adenocarcinoma.

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