INTRODUCTION — Diverticula are sac-like protrusions of the bowel wall and occur throughout the small and large bowel. Small bowel diverticula are usually asymptomatic and are discovered incidentally. While rare, the symptomatic complications may be severe and life threatening. This topic will review the clinical manifestations, diagnosis, and management of small bowel diverticula with the exception of Meckel's diverticulum. The clinical manifestations, diagnosis, and management of Meckel's diverticulum, the epidemiology and pathophysiology of colonic diverticular disease, the treatment of diverticulitis, and diverticular bleeding are discussed separately. (See "Lower gastrointestinal bleeding in children: Causes and diagnostic approach", section on 'Meckel's diverticulum' and "Colonic diverticulosis and diverticular disease: Epidemiology, risk factors, and pathogenesis" and "Clinical manifestations and diagnosis of acute colonic diverticulitis in adults" and "Colonic diverticular bleeding".)
EPIDEMIOLOGY AND CLASSIFICATION — Small bowel diverticula can occur anywhere in the small bowel but are most often found in the duodenum. In one retrospective review of 208 patients with symptomatic small bowel diverticulosis, diverticula were located in the duodenum in 79 percent, in the jejunum or ileum in 18 percent, and in all three segments in 3 percent [1]. Sixty percent of patients with small bowel diverticula have concurrent colonic diverticula [2].
Duodenal diverticula have been reported in 2 to 5 percent of patients undergoing barium studies of the upper gastrointestinal tract, 7 percent of patients undergoing endoscopic retrograde cholangiopancreatography, and up to 20 percent in autopsy series [3]. The incidence increases with age but has no sex predilection [4]. The most common duodenal location is near the papilla of Vater, while less than 10 percent of duodenal diverticula are located in the first and fourth part of the duodenum [1,3].
Jejunoileal diverticula are rare and reported to affect 0.5 to 2.3 percent of individuals in radiographic series and up to 7 percent in autopsy studies [5]. They are more commonly reported in men with the highest incidence in the sixth and seventh decades of life.
Small bowel diverticula are classified as congenital or acquired based on the etiology. Diverticula can be also classified as intra- and extraluminal and based on their anatomic location as duodenal, jejunal, ileal, or jejunoileal. The vast majority of diverticula are extraluminal and acquired. Intraluminal and Meckel diverticula are congenital.
ETIOPATHOGENESIS
Duodenal diverticula — Duodenal diverticula are thought to be acquired as a result of herniation through a defect caused by the entrance of large vessels supplying the bowel wall [3,6,7]. A combination of increased intraluminal pressures and intrinsic weakness of the muscular layer is thought to play a role.
Extraluminal duodenal diverticula, located 2 to 3 cm adjacent to the ampulla, are also known as juxtapapillary or periampullary diverticula. These are associated with an increased risk of choledocholithiasis with bilirubin-containing pigment stones [8]. Explanatory mechanisms include primary intraductal stone formation from biliary stasis due to extrinsic diverticular common bile duct (CBD) compression, duodenal content biliary reflux through an incompetent sphincter of Oddi, and stasis-associated bacterial contamination of CBD allowing deconjugation of bilirubin glucuronide and precipitation of bile salts [3,7]. (See 'Obstructive jaundice/recurrent pancreatitis' below.)
Intraluminal duodenal diverticula are rare congenital anomalies, known as "windsock diverticula," resulting from an incomplete canalization of the foregut, producing a duodenal diaphragm or web during embryonic development [9]. Intraluminal diverticula are lined on both sides with duodenal mucosa, and an eccentric opening is usually proximal in the sac.
Jejunoileal diverticula — Jejunoileal diverticula are usually multiple and localized to the proximal jejunum. Distal jejunum and ileum are less frequently affected [10]. Jejunoileal diverticula may be composed of mucosa and submucosa only, or of all layers of the jejunal wall. The etiology is unclear, but intestinal dysmotility and high intraluminal pressures are thought to play a role. They are frequently associated with intestinal dysmotility conditions, such as progressive systemic sclerosis, visceral neuropathies, and myopathies. Familial aggregation has been described in case series, suggesting that some cases may be heritable [11,12]. In patients with visceral myopathy, atrophy of the jejunal wall and increased luminal pressure may lead to the protrusion of the mucosa through defects in the lamina muscularis mucosae, where the supplying blood vessels, vasa recta, penetrates the bowel wall, resulting in the formation of diverticula on the mesenteric side of the bowel [13].
CLINICAL MANIFESTATIONS
Typical presentation — Most patients with small bowel diverticula are asymptomatic. Patients with small bowel diverticula, particularly jejunoileal diverticula, may present with early satiety, bloating, and chronic upper abdominal discomfort and diarrhea/steatorrhea due to bacterial overgrowth [14]. (See "Approach to the adult patient with suspected malabsorption", section on 'Clinical presentation' and "Small intestinal bacterial overgrowth: Etiology and pathogenesis", section on 'Anatomic disorders'.)
Duodenal diverticulosis most commonly presents with postprandial epigastric abdominal cramping pain and vomiting due to partial or intermittent duodenal obstruction.
Complications — Patients with small bowel diverticulosis may also present with symptoms due to a complication [6]. Approximately 5 percent of patients with duodenal diverticula and up to 10 percent of patients with jejunoileal diverticula develop complications [15].
Small bowel obstruction — Small intestinal obstruction may occur due to a volvulus or enterolith impaction, resulting in nausea, vomiting, cramping abdominal pain, obstipation (ie, inability to pass flatus or stool), and abdominal distention [16-18]. (See 'Complications' above.)
Although intestinal pseudoobstruction has been reported in patients with jejunoileal diverticula, this is likely due to an associated jejunoileal dyskinesia rather than the diverticulum itself [16,19-22]. (See "Etiologies, clinical manifestations, and diagnosis of mechanical small bowel obstruction in adults", section on 'Clinical presentations'.)
Acute diverticulitis — Patients with acute small bowel diverticulitis may present with midepigastric or periumbilical pain and fever or with signs of complications such as abscess, fistula, or perforation. A diverticular abscess may be noted on abdominal CT scan at initial presentation or may develop subsequently. Patients with diverticular perforation usually present with acute surgical abdomen. In rare cases, enterocutaneous fistula may form as a complication to diverticulitis [23-25]. (See "Clinical manifestations and diagnosis of acute colonic diverticulitis in adults", section on 'Acute complications'.)
Gastrointestinal bleeding — Bleeding may occur secondary to diverticulitis with ulceration, rupture of a jejunal diverticulum into the lumen, diverticulosis with associated trauma, or arteriovenous malformations [26-30]. Hemorrhage from duodenal diverticula usually presents with hematemesis and melena, whereas jejunoileal diverticula usually present with hematochezia [31]. A small bowel diverticular bleed should be considered in patients with overt upper gastrointestinal tract bleeding but no clear source on forward-viewing upper endoscopy. In such cases, a duodenoscopy may visualize an extraluminal duodenal diverticula. (See "Evaluation of suspected small bowel bleeding (formerly obscure gastrointestinal bleeding)".)
Obstructive jaundice/recurrent pancreatitis — Periampullary duodenal diverticula can cause bile duct obstruction leading to obstructive jaundice with or without stones, recurrent acute pancreatitis episodes, or cholestasis secondary to intradiverticular bezoar [32-34].
DIAGNOSIS — Small bowel diverticulosis is often diagnosed incidentally in patients undergoing upper endoscopy or abdominal imaging for evaluation of upper gastrointestinal symptoms [35,36]. (See 'Clinical manifestations' above and "Small intestinal bacterial overgrowth: Clinical manifestations and diagnosis", section on 'Evaluation to determine the etiology'.)
Imaging — On contrast imaging of the gastrointestinal tract (eg, upper gastrointestinal series with small bowel follow-through or computed tomography [CT]/magnetic resonance [MR] enterography), small bowel diverticula appear as globular outpouchings [37,38]. Complications of diverticulitis can also be visualized on abdominal CT scan/MR imaging. (See "Clinical manifestations and diagnosis of acute colonic diverticulitis in adults", section on 'Imaging'.)
Endoscopy — Extraluminal small bowel diverticula appear as a blind saccular outpouching of the bowel wall. Duodenal diverticula are best identified on duodenoscopy as they can be missed with a forward-viewing endoscope. Intraluminal duodenal diverticula have a polypoid appearance. The diverticular orifice is usually visualized proximally, and the diverticular fundus protrudes distally into the duodenal lumen [9].
Differential diagnosis — The differential diagnosis varies based on the clinical presentation.
●The differential diagnosis of diarrhea and malabsorption due to small intestinal bacterial overgrowth includes other causes of chronic diarrhea (eg, celiac disease, irritable bowel syndrome) and is discussed in detail separately. (See "Approach to the adult with chronic diarrhea in resource-abundant settings", section on 'Etiology' and "Small intestinal bacterial overgrowth: Clinical manifestations and diagnosis", section on 'Differential diagnosis'.)
●The differential diagnosis of abdominal pain and the evaluation of abdominal pain are discussed in detail, separately. (See "Causes of abdominal pain in adults" and "Evaluation of the adult with abdominal pain".)
MANAGEMENT
Asymptomatic patients — Patients with asymptomatic small intestinal diverticulosis do not require any treatment.
Symptomatic patients — The management in symptomatic patients is based on the clinical presentation:
●Small intestinal bacterial overgrowth – Diarrhea and malabsorption due to small intestinal bacterial overgrowth is treated with antibiotic therapy. The management of small intestinal bacterial overgrowth is discussed in detail separately. (See "Small intestinal bacterial overgrowth: Management".)
●Acute diverticulitis – Management of patients with acute uncomplicated diverticulitis typically includes a restricted diet and antibiotics. Surgical management is reserved for small bowel diverticulitis complicated by bowel perforation. This may require open or laparoscopic-assisted resection of the involved segment. For symptomatic intraluminal duodenal diverticula, duodenotomy and excision are usually necessary for removal, although endoscopic resection has also been successful [9]. Complication rates are usually low with these procedures [14,35]. However, in one series, postoperative complications were higher in symptomatic patients as compared with patients in which diverticula were found incidentally during surgery (26 versus 8 percent) [39]. The management of acute diverticulitis and its complications is similar to patients with acute colonic diverticulitis and is discussed in detail, separately. (See "Acute colonic diverticulitis: Medical management".)
●Small bowel diverticular bleeding – The management of small bowel diverticular bleeding includes resuscitation and, if the bleeding does not stop spontaneously, identification and treatment of the bleeding site. The management of upper gastrointestinal bleeding is discussed in detail, separately. (See "Approach to acute upper gastrointestinal bleeding in adults" and "Approach to acute lower gastrointestinal bleeding in adults".)
●Obstruction – Small bowel obstruction from enterolith impaction of diverticula may be treated with enterotomy and stone extraction or manual crushing and milking the stone distally into the colon, which has been reported to be successful [20]. The management of small bowel obstruction is discussed in detail, separately. (See "Management of small bowel obstruction in adults", section on 'Surgical causes of small bowel obstruction'.)
●Choledocholithiasis – Choledocholithiasis due to juxtapapillary diverticula can be successfully treated by endoscopic retrograde cholangiopancreatography with sphincterotomy and stone removal followed by laparoscopic cholecystectomy [33,40].
SUMMARY AND RECOMMENDATIONS
●Epidemiology – Small bowel diverticula are usually asymptomatic and often discovered incidentally. Small bowel diverticula can occur anywhere in the small bowel but are most often found in the duodenum. (See 'Epidemiology and classification' above.)
●Pathogenesis – Duodenal diverticula usually occur near the papilla of Vater. The vast majority of duodenal diverticula are extraluminal and are thought to be acquired as a result of herniation, where the supplying blood vessels penetrates the mucosa. Intraluminal diverticula are rare and congenital. Jejunal diverticula are usually multiple and localized to the proximal jejunum. They are frequently associated with disorders of intestinal motility, such as progressive systemic sclerosis, visceral neuropathies, and myopathies. (See 'ETIOPATHOGENESIS' above.)
●Clinical features
•Most patients with small bowel diverticula are asymptomatic. Patients with small bowel diverticula, particularly jejunoileal diverticula, may present with early satiety, bloating, chronic upper abdominal discomfort and diarrhea/steatorrhea due to bacterial overgrowth. (See 'Clinical manifestations' above.)
•Patients with small bowel diverticulosis can also present with complications including small bowel obstruction, diverticular bleeding, and diverticulitis. Acute small bowel diverticulitis may be complicated by abscess, perforation, or enterocutaneous fistula. (See 'Complications' above and 'Acute diverticulitis' above.)
●Diagnosis – Small bowel diverticular disease is usually not suspected clinically, and often diagnosed incidentally on imaging or endoscopy. Intraluminal duodenal diverticula may have a polypoid appearance, while extraluminal small bowel diverticula appear as a blind saccular outpouching of the bowel wall. Duodenal diverticula are best identified on duodenoscopy as they can be missed with a forward-viewing endoscope. (See 'Diagnosis' above.)
●Management – Patients with asymptomatic small intestinal diverticulosis does not require treatment. The management in symptomatic patients is based on the clinical presentation. Surgical management is reserved for bowel perforation, fistula, or abscess and in patients with refractory gastrointestinal bleeding. (See 'Management' above.)
ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Vladan Milovic, MD, PhD, and Ellionore Järbrink-Sehgal, MD, PhD, who contributed to earlier versions of this topic review.
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