Introduction
Background
Duodenal ulcers (DUs) affect nearly 10% of the adult population at some time.1 DUs account for two thirds of all peptic ulcers, which are defined as mucosal breaks of 3 mm or greater, and gastric ulcers account for the rest.
Double-contrast upper gastrointestinal series. Posterior wall duodenal ulcer.
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.
Unlike gastric ulcers, which may be malignant in about 5% of cases,1 DUs are almost invariably benign; therefore, treatment with antisecretory drugs can be commenced after radiologic diagnosis, without endoscopy being performed beforehand.2,3
Pathophysiology
The most common cause of duodenal ulcers (DUs) is infection with Helicobacter pylori.4,5,6 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.7
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.8
Frequency
United States
About 4.5 million people are affected annually, and approximately 10% of the population has evidence of a duodenal ulcer (DU) at some time.1 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%.1 Overall, the incidence of DU has been decreasing over the past 3-4 decades.
International
The frequency rates of duodenal ulcers (DUs) in other countries are variable and are determined primarily by association with their major causes: H pylori infection and NSAID use.
Mortality/Morbidity
Duodenal ulcer (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.1
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.1
Age
Duodenal ulcer (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.
Presentation
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 duodenal ulcer (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 duodenal ulcer (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 (13 C) or the radioactive isotope14 C. In the presence of urease produced by H pylori, carbon dioxide (labeled with13 C or14 C) 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.
- Endoscopic or invasive tests include rapid urease, histopathologic, and culture tests.
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 mm1 ; 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.
Differential Diagnoses
More on Duodenum, Ulcers |
 Overview: Duodenum, Ulcers |
| Imaging: Duodenum, Ulcers |
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References
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Newton EB, Versland MR, Sepe TE. Giant duodenal ulcers. World J Gastroenterol. Aug 28 2008;14(32):4995-9. [Medline].
Ramakrishnan K, Salinas RC. Peptic ulcer disease. Am Fam Physician. Oct 1 2007;76(7):1005-12. [Medline].
Pattison CP, Combs MJ, Marshall BJ, et al. Helicobacter pylori and peptic ulcer disease: evolution to revolution to resolution. AJR Am J Roentgenol. Jun 1997;168(6):1415-20. [Medline]. [Full Text].
Peek RM Jr, Blaser MJ. Pathophysiology of Helicobacter pylori-induced gastritis and peptic ulcer disease. Am J Med. Feb 1997;102(2):200-7. [Medline].
Suerbaum S, Michetti P. Helicobacter pylori infection. N Engl J Med. Oct 10 2002;347(15):1175-86. [Medline].
Lanas A, Serrano P, Bajador E, et al. Evidence of aspirin use in both upper and lower gastrointestinal perforation. Gastroenterology. Mar 1997;112(3):683-9. [Medline].
Love JW. Peptic ulceration may be a hormonal deficiency disease. Med Hypotheses. 2008;70(6):1103-7. [Medline].
Levine MS, Kelly MR, Laufer I, et al. Gastrocolic fistulas: the increasing role of aspirin. Radiology. May 1993;187(2):359-61. [Medline].
Horton KM, Fishman EK. MDCT and 3-dimensional computed tomography imaging of small bowel neoplasms: current concept in diagnosis. J Comput Assist Tomogr. Jan-Feb 2004;28(1):106-16.
Husain S, Ahmed AR, Johnson J, Boss T, O'Malley W. CT scan diagnosis of bleeding peptic ulcer after gastric bypass. Obes Surg. Nov 2007;17(11):1520-2. [Medline].
Ghekiere O, Lesnik A, Hoa D, Laffargue G, Uriot C, Taourel P. Value of computed tomography in the diagnosis of the cause of nontraumatic gastrointestinal tract perforation. J Comput Assist Tomogr. Mar-Apr 2007;31(2):169-76. [Medline].
Kim JH, Shin JH, Di ZH, Ko GY, Yoon HK, Sung KB. Benign duodenal strictures: treatment by means of fluoroscopically guided balloon dilation. J Vasc Interv Radiol. Apr 2005;16(4):543-8. [Medline].
El-Nakeeb A, Fikry A, Abd El-Hamed TM, Fouda EY, El Awady S, Youssef T, et al. Effect of Helicobacter pylori eradication on ulcer recurrence after simple closure of perforated duodenal ulcer. Int J Surg. Dec 6 2008;[Medline].
Carucci LR, Levine MS, Rubesin SE, et al. Upper gastrointestinal tract barium examination of postbulbar duodenal ulcers. AJR Am J Roentgenol. Apr 2004;182(4):927-30. [Full Text].
Ford AC, Delaney BC, Forman D, et al. Eradication therapy in Helicobacter pylori positive peptic ulcer disease: systematic review and economic analysis. Am J Gastroenterol. Sep 2004;99(9):1833-55. [Medline].
Horton KM, Fishman EK. Multidetector-row computed tomography of the duodenum: technique and clinical applications. Crit Rev Comput Tomogr. 2004;45(5-6):309-34.
Jayaraman MV, Mayo-Smith WW, Movson JS, et al. CT of the duodenum: an overlooked segment gets its due. Radiographics. Oct 2001;21 Spec No:S147-60. [Medline]. [Full Text].
Lang EK. Transcatheter embolization in management of hemorrhage from duodenal ulcer: long-term results and complications. Radiology. Mar 1992;182(3):703-7. [Medline].
Lanza FL. NSAIDs and the gastrointestinal tract. Abdom Imaging. Jan-Feb 1997;22(1):1-4. [Medline].
Levine MS, Creteur V, Kressel HY, et al. Benign gastric ulcers: diagnosis and follow-up with double-contrast radiography. Radiology. Jul 1987;164(1):9-13. [Medline].
Levine MS, Rubesin SE, Herlinger H, et al. Double-contrast upper gastrointestinal examination: technique and interpretation. Radiology. Sep 1988;168(3):593-602. [Medline].
Rodriguez HP, Aston JK, Richardson CT. Ulcers in the descending duodenum. Postbulbar ulcers. Am J Roentgenol Radium Ther Nucl Med. Oct 1973;119(2):316-22. [Medline].
Further Reading
Related eMedicine topics
Duodenal Ulcers (from Gastroenterology)
Peptic Ulcer Disease
Gastritis and Peptic Ulcer Disease
Peptic Ulcer: Surgical Perspective
Gastric Ulcers
Clinical guidelines
Dyspepsia: A National Clinical Guideline
American Gastroenterological Association Medical Position Statement: Evaluation of Dyspepsia
Clinical trials
Study of Esomeprazole 20 mg or 40 mg vs Placebo Effectiveness on the Occurrence of Peptic Ulcers in Subjects on LDA (Oberon)
Keywords
duodenal ulcer, duodenum ulcer, DU, peptic ulcer, gastric ulcer, Helicobacter pylori, H pylori, Zollinger-Ellison syndrome
