Abbreviations
ATZ
anal transition zone
CD
Crohn’s disease
GI
gastrointestinal
IBD
inflammatory bowel disease
ICV
ileocecal valve
NSAID
non-steroidal anti-inflammatory drugs
PSC
primary sclerosing cholangitis
SCAD
segmental colitis-associated diverticulosis
UC
ulcerative colitis
Introduction
Crohn’s disease (CD) can affect any part of the gastrointestinal (GI) tract, while classic ulcerative colitis (UC) only involves the colon and rectum. Distinction between inflammatory bowel disease (IBD) and other inflammatory, medication-related, neoplastic, and organ transplantation–related disease conditions is discussed in separate chapters. The identification of normal endoscopic features of the esophagus, stomach, small and large intestines, and anorectum is critical for the diagnosis and differential diagnosis of IBD. In addition, there are “normal variations” in endoscopy of the GI tract. Some of these variations can mimic IBD, IBD-associated complications, and other inflammatory or neoplastic conditions.
Esophagus
The inner layer of the esophagus is covered with whitish squamous cells, in contrast to the salmon-color columnar epithelia in the stomach. The longitudinal vascular pattern is visible, especially in the distal esophagus, close to the esophagogastric junction ( Fig. 3.1 A). A congenital cervical inlet patch is occasionally found in the proximal esophagus ( Fig. 3.1 B). The cervical inlet patch consists of the ectopic gastric mucosa. Acid secretion from ectopic gastric mucosa may lead to esophagitis, ulcer, web, or stricture, mimicking CD of the esophagus.
Normal and abnormal esophagus. (A) Normal distal esophagus and esophagogastric junction. Small linear vasculature is seen; (B) cervical inlet patch in the proximal esophagus, which is covered with pinkish gastric columnar mucosa ( green arrow ); (C) Glycogenic acanthosis with small white epithelial nodules throughout the esophagus ( blue arrow ); (D) Candida esophagitis with white plaques in a patient with Crohn’s disease and renal transplantation and use of systemic corticosteroids.
Glycogenic acanthosis in the esophagus is characterized by multifocal plaques of hyperplastic squamous epithelium with intracellular glycogen deposits. Glycogenic acanthosis should be differentiated from Candida esophagitis ( Fig. 3.1C and D ).
Linear white specks are occasionally seen in the normal esophagus ( Fig. 3.2 A), which should be differentiated from white plaques in those with Candida esophagitis. Patients with esophageal spasms, a functional disorder of the esophagus, may present with linear furrows and esophageal rings ( Fig. 3.2 B), resembling that seen in eosinophilic esophagitis ( Fig. 3.2C and D ). The distinction can be made by histologic evaluation.
Normal esophagus and eosinophilic esophagitis. (A) Linear white specks ( green arrow ) with no clinical significance; (B) Pseudolinear furrows ( yellow arrow ) in a patient with Crohn’s disease, resembling eosinophilic esophagitis. (C) Eosinophilic esophagitis with linear furrows, erosions, and Schatzki ring; (D) Eosinophilic infiltration in eosinophilic esophagitis.
Stomach
IBD rarely involves the stomach. One of the endoscopic features of CD of the stomach is the presence of “bamboo joints” thatwas initially described by Japanese investigators, as shown in Fig. 4.4 in Chapter 4, Crohn’s disease: inflammatory type . Patients with normal stomachs may have a similar endoscopic appearance ( Fig. 3.3 A). Therefore histologic evaluation is critical.
Stomach in Crohn’s disease. (A) “Bamboo-joint” appearance in the normal stomach, resembling that seen in gastric Crohn’s disease ( green arrow ); (B) Fundic gland polyps in the body of the stomach; resulting from long-term use of proton pump inhibitors in a non-inflammatory bowel disease patient; (C) Extensive fundic gland polyps in a Crohn’s disease patient with short-gut syndrome; (D) Antral gastritis in ulcerative colitis patient with H. pylori infection.
With the extensive use of proton pump inhibitors in the general population, fundic gland polyps are commonly seen in the stomach ( Fig. 3.3 B). However, the presence of fundic gland polyps may reflect the body’s compensatory reaction to various stimuli, such as short-gut syndrome in CD ( Fig. 3.3 C). Antral gastritis in IBD is also common, which is not necessarily a part of the disease ( Fig. 3.3 D), with etiologies such as Helicobacter pylori infection and the use of nonsteroidal anti-inflammatory drugs .
Duodenum
The duodenum is a common location of CD of the upper GI tract. CD of the duodenum may present with nonulcerative inflammation, ulcers, or strictures. The distinction between the inflammatory phenotype of CD and “normal” variations of the duodenum sometimes is difficult on endoscopy.
The duNodenum bulb in healthy individuals can have various appearances. The bulbar mucosa can be granular or nodular in a non-disease setting. Granularity and nodularity of the bulbar mucosa mainly consist of Bruner’s glands or Brunner’s gland hyperplasia ( Figs. 3.4 A and B and 3.5 ). Subtle erosions can hide between nodular bulb mucosa ( Fig. 3.4 C and D)
Normal and abnormal duodenum bulb on white light ( left panel ) and narrow-band imaging ( right panel ). (A and B) Granular and nodular mucosa with short villi; (C and D) Subtle erosions in a patient with Crohn’s disease.
Duodenum bulb with nodular mucosa from Brunner’s gland hyperplasia. (A and B) Localized Brunner’s gland hyperplasia in the anterior wall of the duodenum bulb; (C) Brunner’s gland hyperplasia was highlighted with lysozyme ( green ) on immunofluorescence. Paneth cells in the intestinal epithelia are highlighted with human-defensing-5 ( red ).
The duodenum cap is located in the junction between the bulb and the second portion of the duodenum, which is a common place for strictures in CD of the upper GI tract ( Fig. 3.6 ). Positioning the endoscope’s tip at the cap or duodenum sweep can be challenging.
Normal and abnormal duodenum cap. (A and B) Duodenum cap is presented between the bulb and 2nd portion ( green arrows ) (C) Strictured duodenum cap resulting from Crohn’s disease ( yellow arrow ); (D) Subtle Crohn’s stricture at the cap that was missed by previous upper endoscopies.
The second to fourth portions of the normal duodenum are characterized by the folds, villi, and occasionally lacteals, which are different from the bulbar mucosa. The villi can be highlighted with image-enhanced endoscopy ( Fig. 3.7 ) Lacteals may present with punctate white spots which mostly represent some degree of intestinal lymphangiectasia ( Fig. 3.8 A and B,) . Diffuse white duodenum mucosa, however, may be associated with nonspecific inflammation, infections (such as Whipple’s disease), or lymphoma . In between the white mucosa, there may be erythematous mucosa with short villi resulting from mucin depletion from IBD, the use of non-steroidal anti-inflammatory drugs ( Fig. 3.8 C and D). Nodules or polypoid lesions can be seen in the duodenum in the healthy or diseased ( Fig. 3.9 )
New. Normal 2nd portion of the duodenum. (A) Duodenum mucosa with visible villi; (B) The mucosal villi were highlighted with narrow-band and magnified imaging; (C) Histologic demonstration of the duodenum villi.
Normal and abnormal mucosa in the 2nd portion of the duodenum. (A and B) Diffuse or spotted white duodenum from lacteals. Lymphangiectasia with a white nodule is highlighted ( green arrow ); (C) Patchy erythema from mucin depletion of epithelia; (D) Chronic inflammation, loss of duodenal villi, and attenuation of the duodenal epithelium with surface erosion ( blue arrows ), (H&E stain, 100x; Courtesy of H. Mabel Ko, MD, of Columbia University).
Nodular lesions at the duodenum in the healthy and diseased. (A). Gastric (fundic) hereteropia with nodules in the 2nd part of the duodenum in a healthy individual; (B) Duodenitis with erythema and nodules in a patient with Crohn’s disease; (C) Diffuse flat polyps in the duodenum in a patient with familial adenomatous polyposis; (D) Diffuse duodenitis with mucosal nodularity in a patient with ulcerative colitis and ileal pouch-anal anastomosis.
A proper evaluation of the size of the lumen and luminal contents of the duodenum may yield some diagnostic clues. Dilated lumen of the duodenum may result from distal obstruction, small bowel bacterial overgrowth, and gastroenteritis. A pool of luminal secretion with dilated duodenum or other parts of the small intestine can be a sign of small bowel bacterial overgrowth ( Fig. 3.10 ).
The lumen and luminal contents of the duodenum in the healthy and diseased. (A) Normal-sized lumen of the 2nd portion of the duodenum in a healthy individual; (B) Minimum amount of bile or other secretions on the surface of the duodenal mucosa in a healthy individual; (C) Dilated lumen of the duodenum with excessive luminal secretions from a patient with small bowel bacterial overgrowth; (D) Slightly dilated lumen of the duodenum with mucosal erythema in a patient with acute gastroenteritis.
Duodenum papilla may present in different shapes and sizes ( Fig. 3.11 A and B). The papilla and surrounding areas are common locations for familial adenomatous polyposis ( Fig. 3.6 B). Patients with ulcerative colitis, or primary sclerosing cholangitis (PSC) or IgG4-associated systemic disorders may present with diffuse duodenitis or mucinous discharge from intraductal papillary mucinous neoplasm ( Fig. 3.11 C-new). Ampullary adenomas can occur in patients with long-standing small bowel CD ( Fig. 3.11 D-new) Ampullary lesions may explain some “idiopathic pancreatitis” in CD .
Duodenum papilla in the healthy and inflammatory bowel disease. (A) Normal duodenum papilla ( green arrow ); (B) Normal-appearing papilla on narrow-band imaging ( blue arrow ) with histology showing low-grade dysplasia in a patient with familial adenomatous polyposis; (C) Mucin discharge from intraductal papillary mucinous neoplasm in a patient with ulcerative colitis; (D) Ampullary tubulovillous adenoma in a patient with long-standing small bowel Crohn’s disease.
Jejunum
Normal jejunum contains plicae circulares (muscular flaps or valves of Kerckring) and villi ( Fig. 3.11 A). Diseases limited to jejunum only are rare. CD and its postoperative changes are examples ( Figs. 3.11 B, C, and D). ( Fig. 3.12 ).
