Digestive Diseases and Sciences

, Volume 57, Issue 10, pp 2516–2518

Recurrent Duodenal Stricture Secondary to Untreated Crohn’s Disease

Authors

    • Department of SurgeryStanford University School of Medicine
  • Jeffrey A. Norton
    • Department of SurgeryStanford University School of Medicine
Stanford Multidisciplinary Seminars

DOI: 10.1007/s10620-012-2080-0

Cite this article as:
Plerhoples, T.A. & Norton, J.A. Dig Dis Sci (2012) 57: 2516. doi:10.1007/s10620-012-2080-0

Case Presentation and Evolution

A 62-year-old woman presented with a 25-year history of intermittent nausea, vomiting, bloating, and a precipitous 50 pound weight loss over the preceding 7 months.

Her digestive symptoms had begun after she had added wheat germ to her diet during her first child in 1976. At that time, she underwent an esophagogastroscopy (EGD); a gastroenterologist diagnosed her with celiac sprue based on a “flat” biopsy in the absence of supporting antibody studies. Over the next two decades, her symptoms were reasonably controlled without any specific treatment. Five years ago, she developed protracted nausea and vomiting attributed to have a duodenal stricture. A strictureplasty was performed for a circumferential stricture with no associated mass between the second and third portions of the duodenum. The diagnosis of reactive follicular hyperplasia was made based on normal flow cytometry and hyperplastic lymphoid follicies with otherwise normal histology. She did well for several years thereafter, however, her symptoms slowly recurred. Of note, two of the patient’s children had been diagnosed with Crohn’s disease; three had been diagnosed with celiac sprue and one child carried both diagnoses. Her father had died of colon cancer.

Five years post-surgery, she complained of bloating, early satiety, postprandial fullness, heartburn, decreased energy, nausea, and vomiting. Normal celiac antibodies (anti tissue transglutaminase [IgA tTG], endomysial antibody [IgA EMA], IgA antigliadin antibody [IgA AGA], and IgG antigliadin antibody [IgG AGA]), normal total immunoglobulins, and normal liver function tests were present. Duodenal pathology revealed a villus: crypt = 0.5 (normal 3 or greater), an intra-epithelial lymphocyte count increase of 0.41 (normal 0.3 or less), with the enterocyte layer described as having rounded rather than the usual elongated elliptical nuclei. The villi were “squared off” with complete loss of the normal saw-tooth appearance. Moreover, a significant number of neutrophils was present. An EGD showed esophageal and pyloric luminal dilation, with retained food in the antrum and a proximal megaduodenum. Ulcerating inflammatory process was reported in the distal duodenum associated with a tight (7-mm diameter) stricture (Fig. 1). Biopsies of the stricture showed active acute inflammation, with biopsies just beyond the stricture (in the distal duodenum) reported as normal. Colonoscopy was normal although random colonic mucosal biopsies revealed mild inflammation. Upper GI fluoroscopy with small bowel follow-through confirmed these findings with additional report of markedly delayed gastric and proximal duodenal emptying (4 h) (Fig. 2).
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Fig. 1

Endoscopic photograph of the distal duodenum showing an ulcerating inflammatory process associated with a 7-mm diameter stricture

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Fig. 2

Barium upper GI fluoroscopy showing luminal narrowing of the descending duodenum and dilation of the proximal duodenum and stomach

Due to these findings, accompanied by poor oral intake with consequent malnutrition, she underwent exploratory laparotomy, with a dilated stomach and proximal duodenum, proximal to a duodenal stricture but no mass; the duodenum was decompressed distally. Multiple duodenal adhesions to the retroperitoneum and hepatic flexure were lysed; the duodenum was mobilized and bypassed with an antecolic roux-en-Y duodeno-jejunostomy bypass. She did well postoperatively and was discharged on postoperative day 4 able to tolerate a post-surgical diet. She continues to do well having gained 4 pounds in 2 weeks.

Discussion

Crohn’s disease (CD) can cause transmural inflammation in any portion of the gastrointestinal tract, from mouth to anus. Initial complaints can include fatigue, diarrhea, abdominal pain, weight loss, and fever ranging to fistula and stricture-associated symptoms extraintestinal manifestations, such as arthritis or rashes. Endoscopic (EGD, colonoscopy, or videocapsule) or other imaging studies (barium studies, CT, or MRI) are useful for making a diagnosis. Focal ulcerations with both acute and chronic inflammation are usually present in the mucosa. Granulomas are present in only about 30 % of patients, a finding that is considered diagnostic if other causes of granulomatous disease are excluded such as yersinia, Behçet’s disease, tuberculosis, and lymphoma. The diagnosis is supported with serologic markers, most notably perinuclear anti-neutrophil cytoplasmic antibody (pANCA) and anti-saccharomyces cerevisiae antibody (ASCA) [1]. Other markers, such as the antibody to Escherichia coli outer membrane porin (anti-OmpC) and C-reactive protein (CRP) may also be elevated in patients with CD [2, 3]. CD patients may have a lower risk of celiac disease than in the general population [4].

Mechanical obstruction of the stomach or duodenum is accompanied by intractable post-prandial nausea and vomiting, heartburn, and malnutrition. Foregut obstructions of this type were classically associated with peptic ulcer disease, in particular pyloric channel and duodenal ulcers complicating pyloro-duodenal scarring. Due to improved medical treatment and prevention of ulcers, other etiologies including malignancy, post-surgical changes, pancreatitis, gastric volvulus, and CD have assumed more etiological importance. Gastroduodenal manifestations occur in 4% of patients with CD, although histological confirmation is present in less than 40%, usually as focal gastritis. Involvement of the proximal duodenum is more likely [5]. Granulomatous inflammation is present in less than half of patients [6]. Symptoms of duodenal CD are typically controlled medically with compounding controlled release. Formulations of sulfasalazine and mesalazine with pH-dependent release, with steroids and immunomodulatory drugs reserved for severe disease. Gastric outlet obstruction due to CD often requires non medical intervention such as endoscopic dilation or surgical management.

Endoscopic balloon dilation is primarily suited for short, focal and endoscopically-accessible lesions; it may abrogate the need for surgical management in over half of these patients, although many patients may require repeated dilations [7]. Patients with multiple, longer or endoscopically-inaccessible strictures require consideration of several surgical options, including strictureplasty (Heineke-Mikulicz or Finney) or bypass. Strictureplasty has the benefit of preserving bowel functioning, although its benefits may be temporary, often requiring re-operation. Bypass options (including gastro-jejunostomy, duodeno-jejunostomy, and gastro-duodenostomy) are preferred over resections and require fewer reoperations. Minimally invasive version of these operation techniques are generally safe and are associated with shorter hospital stays and decreased perioperative complications [8].

This patient greatly benefited from surgery twice: first as a strictureplasty and second as a duodeno-jejunostomy. However, the diagnosis of CD as a cause of the stricture has been elusive. If she were treated for CD after her first operation she may have been able to avoid re-stricturing and the need for second surgery. This is common with solitary duodenal Crohn’s, where an absence of disease at other sites makes the diagnosis more challenging. This patient will be treated for Crohn’s, which should allow her to reduce the likelihood of another (recurrent) duodenal stricture and obstruction.

Key Points

  • Flat villi on duodenal endoscopic mucosal biopsies are not always related to gluten sensitive enteropathy.

  • Duodenal Crohn’s disease, albeit rare, should be considered in the differential diagnosis of gastroduodenal outlet obstruction.

  • The treatment of duodenal Crohn’s disease with stricture formation involves endoscopic balloon dilation, strictureplasty, or bypass surgery, followed by aggressive medical therapy in order to prevent recurrences.

Copyright information

© Springer Science+Business Media, LLC 2012