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Author: Isaac Hassan, MB, ChB, FRCR, DMRD, Former Senior Consultant Radiologist, Department of Radiology, St Bernard's Hospital, Gibraltar

Isaac Hassan is a member of the following medical societies: American Roentgen Ray Society and Royal College of Radiologists

Editors: Bernard D Coombs, MB, ChB, PhD, Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand; David Andrew Nicholson, BM, BS, FRCR, Honorary Lecturer, Department of Radiology, University of Manchester; Consultant Gastrointestinal Radiologist, Department of Radiology, Hope Hospital, Salford Royal Hospital NHS Trust; Robert M Krasny, MD, Consulting Staff, Department of Radiology, The Angeles Clinic and Research Institute; Eugene C Lin, MD, Consulting Staff, Department of Radiology, Virginia Mason Medical Center

Author and Editor Disclosure

Synonyms and related keywords: DU, peptic ulcer, gastric ulcer, Helicobacter pylori, H pylori, Zollinger-Ellison syndrome

Background

Duodenal ulcers (DUs) affect nearly 10% of the adult population at some time (Levine, 2000). DUs account for two thirds of all peptic ulcers, which are defined as mucosal breaks >3 mm, and gastric ulcers account for the rest. Unlike gastric ulcers, which may be malignant in about 5% of cases (Levine, 2000), DUs are almost invariably benign; therefore, treatment with antisecretory drugs can be commenced after radiologic diagnosis, without endoscopy being performed beforehand.

Pathophysiology

The most common cause of DUs is infection with Helicobacter pylori (Pattison et al, 1997; Peek and Blaser, 1997; Suerbaum and Michetti, 2002). About 90% of DUs and 70-75% of gastric ulcers are associated with H pylori infection. The second most common cause of DUs is the use of nonsteroidal anti-inflammatory drugs (NSAIDs), which account for most H pylori–negative ulcers (Lanas et al, 1997).

Severe physiologic stress (eg, burns, surgery, head injury) may induce peptic ulceration. Other causes are relatively rare and include gastrinoma (ie, Zollinger-Ellison syndrome) and radiation- or chemotherapy-induced ulcers. Several diseases are associated with an increased risk of peptic ulceration; these include cirrhosis, chronic pulmonary disease, renal failure, and renal transplantation.

Frequency

United States

About 4.5 million people are affected annually, and approximately 10% of the population has evidence of a DU at some time (Levine, 2000). The prevalence of DU is estimated to be 6-15% in the general population; this is linked to the presence of H pylori. In those infected with H pylori, the lifetime prevalence is approximately 20% (Levine, 2000). Overall, the incidence of DU has been decreasing over the past 3-4 decades.

International

The frequency rates of DUs in other countries are variable and are determined primarily by association with their major causes: H pylori infection and NSAID use.

Mortality/Morbidity

DU causes significant morbidity related to pain. Hospitalization is required mainly for complications such as ulcer hemorrhage, perforation, penetration, and obstruction. The annual rate of any complication in patients of all age groups is approximately 1-2% per ulcer (Levine, 2000).

The mortality rate associated with ulcer hemorrhage has remained about 5% over the past 20 years, despite advances in medical therapy. However, in patients who require surgical intervention for complications, such as perforation and obstruction, the mortality rate is significantly higher in the elderly than in other age groups.

Sex

The prevalence has shifted from a male predominance to similar occurrences in males and females. The lifetime prevalence is approximately 11-14% for men and approximately 8-11% for women (Levine, 2000).

Age

DU rates in younger men are decreasing, but they are increasing in older women. These trends reflect the prevalence of H pylori infection and the use of NSAIDs in older populations.

Anatomy

The duodenum consists of 4 parts. The duodenal bulb, or cap, and the pars superior make up the first part. The second part consists of the descending duodenum, where the duodenal papilla and ampulla of Vater are located. The ampulla of Vater contains the outlet of the conjoined or separate pancreatic and bile ducts. The third part consists of the horizontal duodenum and extends from the second part to the arteriomesenteric bundle, where the superior mesenteric artery crosses anterior to the duodenum. The fourth, or ascending, part extends from this point to the duodenojejunal flexure.

Clinical Details

The patient's history may include the following features:

  • Typically, pain occurs more than 2 hours after meals or at night, and it may be relieved by eating. It is localized in the epigastrium, and it is gnawing, burning, or aching in nature. However, the pain may also be in the right upper abdominal quadrant, chest, or back.
  • Anorexia, weight loss, belching, bloating, nausea, and/or heartburn may occur.
  • Vomiting may be related to partial or complete gastric outlet obstruction.
  • Hematemesis or melena may result from gastrointestinal (GI) bleeding.

Physical examination findings may include the following:

  • In uncomplicated DU, clinical findings are few and nonspecific.
  • Epigastric tenderness may be present.
  • Guaiac-positive stool may result from occult blood loss.
  • Melena results from acute or subacute GI bleeding.
  • A succussion splash results from partial or complete gastric outlet obstruction. This classic physical sign is elicited by placing a hand over the patient's stomach and making short, sudden, dipping movements to detect the movement of fluid or splash.

Preferred Examination

  • Begin the evaluation with history taking and physical examination.
  • Perform blood tests, including a full blood count and liver function tests.
  • Inspect the stool, and test it for occult blood.
  • Perform either fiberoptic endoscopy or a double-contrast barium study of the upper GI tract.
    • Endoscopy has become the diagnostic procedure of choice for patients with suspected DU. However, endoscopy is more invasive and costly than double-contrast barium study.
    • Double-contrast examinations of the upper GI tract remain a useful alternative to endoscopy but have a lower sensitivity, especially in the detection of small DUs.
  • Test for the presence of H pylori infection. This is essential in all patients with peptic ulcers.
    • Endoscopic or invasive tests include rapid urease, histopathologic, and culture tests.
      • Rapid urease tests are considered the endoscopic diagnostic tests of choice. In gastric mucosal biopsy specimens, H pylori is detected by testing for the bacterial product urease. If H pylori is present, bacterial urease converts urea to ammonia, which changes the pH and produces a color change.
      • Histopathologic evaluation, often considered the criterion standard in the diagnosis of H pylori, requires a trained pathologist.
      • Cultures are used mainly in research studies.
    • Nonendoscopic or noninvasive tests include H pylori antibody detection and urea breath tests.
      • Levels of antibodies, such as immunoglobulin G (IgG), to H pylori can be measured in serum, plasma, or whole-blood samples. Whole-blood test samples are obtained with finger sticks, but the results are less reliable than those of other methods.
      • Urea breath tests are used to detect H pylori infection by testing for the enzymatic activity of bacterial urease. The patient ingests a test meal of urea, labeled with the heavy isotope carbon-13 (13C) or the radioactive isotope 14C. In the presence of urease produced by H pylori, carbon dioxide (labeled with 13C or 14C) is produced in the stomach and absorbed into the bloodstream. It then diffuses into the lungs and is exhaled.
      • Testing of exhaled air detects labeled carbon and proves urease activity and the presence of H pylori infection. The test is extremely specific and has a higher sensitivity than the serologic assay.

Limitations of Techniques

Endoscopy with biopsy has a sensitivity of as high as 95%, but small ulcers in the base of the duodenal bulb may be missed. In the presence of gastric outlet or proximal duodenal obstruction, the endoscope may be unable to pass through the stenosis, and the full extent and cause of the obstruction may not be defined.

Single-contrast barium studies may cause as many as 40% of small ulcers to be missed, but double-contrast barium images depict as many as 95% of ulcers larger than 10 mm (Levine, 2000); these results are comparable to those of endoscopy . However, the sensitivity of double-contrast barium examination decreases with smaller ulcers and recurrent ulcers in a deformed duodenal bulb; therefore, it is not reliable in the detection of duodenitis or duodenal erosions. Barium studies have a disadvantage because biopsy specimens cannot be obtained to test for H pylori infection or to evaluate a suspicious lesion.



Cholecystitis, Acalculous
Cholecystitis, Acute
Cholelithiasis
Crohn Disease
Gastric Ulcer
Gastroesophageal Reflux
Gastrointestinal Bleeding, Upper
Pancreatitis, Acute
Pancreatitis, Chronic
Tuberculosis, Gastrointestinal
Zollinger-Ellison Syndrome


Findings

Most DUs are depicted as round or ovoid pools of barium. About 5% may be linear. Most are smaller than 1 cm in diameter. Giant DUs, defined as those > 2 cm in diameter, have an increased risk of perforation, obstruction, and bleeding. Multiple ulcers occur in about 15% of patients (Levine, 2000); Zollinger-Ellison syndrome should be considered in these patients.

About 95% of DUs occur in the duodenal bulb (Levine, 2000), and the rest occur in the postbulbar duodenum, which consists of the proximal 2 cm of the descending duodenum above the ampulla of Vater. As many as half of all DUs occur in the anterior wall of the bulb.

Technique of double-contrast barium study

Biphasic examination combines the advantages of the double-contrast views of the duodenum using high-density barium with the advantages of the prone or erect compression views using low-density barium to show ulcers in the anterior wall of the bulb. Intravenous (IV) glucagon 0.1 mg and effervescent granules are administered as part of the double-contrast examination, which is followed by the acquisition of single-contrast compression views with low-density barium.

Bulbar ulcers

Bulbar ulcer craters are depicted as well-defined round or ovoid pools of barium that can be seen en face or in profile (see Images 1-5); they are often surrounded by a smooth mound of edematous mucosa. Radiating folds converge to the edge of the crater (see Image 3). Ulcers in the anterior wall may be detected as a ring shadow (see Image 4), with barium coating the edge of the unfilled ulcer crater. These craters are filled on prone or erect compression views. The duodenal bulb is often deformed by edema and spasm associated with the ulcer or by scarring from a previous ulcer (see Images 6-7). Small ulcers may not be detected in a deformed bulb.

Postbulbar ulcers

Postbulbar ulcers are usually located in the medial wall of the proximal descending duodenum above the ampulla of Vater (see Images 8-9) and are prone to bleeding. Detection of the ulcer niche or crater is often difficult because of the associated edema and spasm, which may also cause indentation of the lateral wall of the descending duodenum opposite the ulcer. This indentation may lead to stricture formation as a result of fibrosis and may mimic a carcinoma of the duodenum.

Ulcer healing

Healing is often rapid, with a decrease in the size of the ulcer and a change from a round to a linear configuration. Healing may lead to scarring, with radiating mucosal folds converging to the site of the previous ulcer. Bulbar deformity results from asymmetrical scarring and retraction during healing (see Images 6-7). Pseudodiverticula result from the expansion of normal segments of the cap between areas of fibrosis. If present, the typical cloverleaf appearance of the scarred bulb is caused by multiple pseudodiverticula formation.

Complications of duodenal ulceration

  • Hemorrhage occurs in 20-30% of ulcers (Levine, 2000).
    • Endoscopy is the investigation of choice, with a sensitivity of more than 90% in the detection of the bleeding site (Levine, 2000).
    • Double-contrast barium studies are limited by poor mucosal coating in the presence of bleeding. Nevertheless, the bleeding site may be detected in as many as 75% of cases (Levine, 2000). A filling defect resulting from a blood clot, food debris, or granulation tissue may be seen at the base of the barium-filled ulcer.
  • Gastric outlet obstruction occurs in 5% of patients with peptic ulcers (Levine, 2000).
    • It is most common in DUs but also occurs in antral or pyloric channel ulcers. Peptic ulcers account for two thirds of cases of gastric outlet obstruction in adults (Levine, 2000).
    • The images typically show narrowing and deformity of the pylorus or duodenal cap (see Image 10).
    • Nasogastric suction of the large gastric residue (see Image 11) may be required before performing the upper GI series.
    • The descending duodenum may be obstructed by fibrosis caused by a postbulbar ulcer (see Image 9).
    • Less common causes of gastric outlet (or proximal duodenal) obstruction include malignancy (see Image 12), such as carcinoma of the duodenum (see Image 13); large duodenal adenomas (see Image 14); Crohn disease; tuberculosis; mural hematoma; and extrinsic compression caused by pancreatic lesions.
  • Perforation occurs in as many as 10% of patients with peptic ulcer disease (Levine, 2000).
    • Most perforations arise from ulcers in the anterior aspect of the duodenal cap.
    • In 75% of cases, free gas is present in the peritoneum (Levine, 2000); this is best shown on an erect chest radiograph (see Image 15).
    • A water-soluble contrast upper GI series may demonstrate the presence and site of the perforation or whether it has sealed.
    • Subphrenic collections are common sequelae of a perforated DU. Occasionally, they may be shown on an erect chest radiograph (see Image 16), but they are best assessed with ultrasonography or computed tomography (CT) scanning (see Image 17).
  • Penetrating posterior wall DUs result in a walled-off perforation.
    • An abscess may form in the lesser sac.
    • The pancreas is involved in two thirds of cases (Levine, 2000).
  • Fistulas may be present (Levine et al, 1993).
    • Duodenocolic fistulas are usually caused by invasion of the second part of the duodenum by a carcinoma of the hepatic flexure or ascending colon. Rarely, they may be a result of a penetrating ulcer of the duodenal bulb or postbulbar region that has caused erosion into the adjacent colon.
    • Choledochoduodenal fistulas (Levine et al, 1993) may occur. About 95% of these are associated with complications of biliary tract calculi. Only 5% of these fistulas are a result of DUs that cause erosion into the common bile duct. Abdominal radiographs may show gas in the biliary tree.

Degree of Confidence

Single-contrast barium studies may cause as many as 40% of small ulcers to be missed, but double-contrast barium images depict as many as 95% of ulcers larger than 10 mm; these results are comparable to those of endoscopy. However, the sensitivity of double-contrast barium examination decreases with smaller ulcers and recurrent ulcers in a deformed duodenal bulb. Double-contrast barium examination is not reliable in the detection of duodenitis or duodenal erosions.

False Positives/Negatives

Ulcers may be obscured by edema, spasm, or scarring. False-positive results are caused by pseudodiverticula and small pools of barium in a deformed bulb resulting from previous peptic ulceration.



Findings

CT scanning has little role in the primary detection of DUs. However, primary inflammatory processes of the duodenum, such as ulcers, duodenitis, and secondary involvement from pancreatitis, can reliably be diagnosed with CT scanning (Horton and Fishman, Crit Rev Comput Tomogr, 2004). Careful CT scanning technique and three-dimensional imaging can help optimize detection of abnormalities and disease, as well as help with surgical planning. They include the use of oral contrast, preferably water, as well as IV contrast.

CT scanning also has a role in the detection of subphrenic and other collections that may occur after perforation of a DU (see Image 15).



Findings

Ultrasonography may indicate the presence of a giant DU. Its main role is in the detection of other causes of upper abdominal pain such as that caused by gallstones and pancreatitis. This modality also depicts subphrenic and other collections resulting from a perforated DU.



Transcatheter embolization may be used to treat bleeding DUs. Terminal muscular-branch vessel embolization is more effective than gastroduodenal artery embolization in the initial and long-term control of bleeding. Terminal vessels may be occluded with 6-cyanoacrylate, but duodenal stenosis is a late complication in one quarter of all patients.

Fluoroscopically guided balloon (15 or 20 mm in diameter) dilatation may be used for benign duodenal strictures caused by peptic ulcers, Crohn disease, or postoperative adhesion (Kim et al, 2005). Duodenal perforation may occur, necessitating emergency surgery.

Medical/Legal Pitfalls

  • Failure to diagnose and effectively treat duodenal ulceration.
  • Failure to diagnose and treat the complications of duodenal ulceration such as hemorrhage, gastric outlet obstruction, and perforation
  • The treatment of elderly patients is a special concern.



Media file 1:  Double-contrast upper gastrointestinal series. Posterior wall duodenal ulcer.
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Media type:  X-RAY

Media file 2:  Same patient as in Image 1. Lateral view of a posterior wall ulcer.
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Media type:  X-RAY

Media file 3:  Double-contrast upper gastrointestinal series. Anterior wall ulcer in a duodenal cap.
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Media type:  X-RAY

Media file 4:  Same patient as in Image 3. Lateral view of an anterior wall duodenal ulcer.
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Media type:  X-RAY

Media file 5:  Duodenal cap ulcer in a patient with a short history of symptoms.
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Media type:  X-RAY

Media file 6:  Deformity of duodenal cap caused by recurrent ulceration. Single-contrast view.
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Media type:  X-RAY

Media file 7:  Same patient as in Image 6. Double-contrast view.
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Media type:  X-RAY

Media file 8:  Postbulbar ulcer.
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Media type:  X-RAY

Media file 9:  Same patient as in Image 8. Single-contrast view.
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Media file 10:  Gastric outlet obstruction caused by deformed duodenal cap from recurrent peptic ulceration.
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Media type:  X-RAY

Media file 11:  Large volume of residual gastric juice in gastric outlet obstruction. Note the fluid level (arrow) between the barium and gastric juice. Nasogastric aspiration before radiographic examination aids assessment of these cases.
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Media type:  X-RAY

Media file 12:  Obstruction as a result of marked narrowing of the first and second parts of the duodenum. Laparotomy demonstrated malignant infiltration of the duodenum caused by adenocarcinoma of the gallbladder.
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Media type:  X-RAY

Media file 13:  Upper gastrointestinal series. Annular shouldered stricture caused by carcinoma in the second part of the duodenum.
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Media type:  X-RAY

Media file 14:  Large 2-cm adenoma in the descending part of the duodenum.
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Media type:  CT

Media file 15:  Chest radiograph. Free gas under the diaphragm caused by a perforated duodenal ulcer.
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Media type:  X-RAY

Media file 16:  A gas-fluid level is seen under the right diaphragm as a result of a subphrenic collection caused by a perforated duodenal ulcer.
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Media type:  X-RAY

Media file 17:  This computed tomography scan shows a large, right subphrenic collection.
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Media type:  CT



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Duodenum, Ulcers excerpt

Article Last Updated: Dec 20, 2006