Abbreviations
ACG
American College of Gastroenterology
AGA
American Gastroenterological Association
ASA
American Society of Anesthesiologists
ASGE
American Society for Gastrointestinal Endoscopy
CAN
colitis-associated neoplasia
CD
Crohn’s disease
EGD
esophagogastroduodenoscopy
EUS
endoscopic ultrasound
IBD
inflammatory bowel disease
IUS
intestinal ultrasound
GI
gastrointestinal
GLP-1
glucagon-like peptide
ICV
ileocecal valve
NASPGHA
North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition
NSAID
nonsteroidal antiinflammatory drug
PSC
primary sclerosing cholangitis
UC
ulcerative colitis
VCE
video capsule endoscopy
Introduction
Endoscopy with histology plays a major role in the diagnosis, disease monitoring, assessment of treatment response, neoplasia surveillance, and therapy in inflammatory bowel disease (IBD) . Any part of the diseased gastrointestinal (GI) tract is accessible to various modalities of endoscopy. Colonoscopy with ileoscopy (or ileocolonoscopy) and esophagogastroduodenoscopy (EGD) are the two most commonly used diagnostic tools in IBD, along with capsule endoscopy, deep enteroscopy, ileoscopy, and pouchoscopy. Endoscopy is accurate in grading the degree of mucosal inflammation, which has been considered the gold standard for quantifying the severity of mucosal inflammation and assessment of mucosal healing to medical therapy in IBD. Endoscopic features, such as the distribution of inflammation and characteristics of ulcers, help differentiate phenotypes of IBD and between IBD and IBD-like conditions. White-light, magnified, and chromoendoscopy are routinely used for the surveillance of dysplasia in patients with IBD at risk. Interventional IBD or endoscopic therapy plays a growing role in the management of IBD- or IBD surgery-associated complications, such as strictures and anastomotic leaks .
Setup for inflammatory bowel disease endoscopy
Patients with IBD often have active disease, concurrent use of corticosteroids and other immunosuppressive medications, partial bowel obstruction, or altered bowel anatomy due to surgery. In patients with severe Crohn’s disease (CD) or ulcerative colitis (UC) or these undergoing therapeutic endoscopy, preprocedure abdominal imaging is recommended to delineate intramural, and intra- and extraluminal anatomy. Before endoscopy, we should avoid medicines that may cause bowel inflammation, including sodium phosphate-based bowel preparations and nonsteroidal antiinflammatory drugs .
Asymptomatic patients with IBD undergoing routine diagnostic or surveillance lower GI endoscopy typically require an 8-hour solid-food fast and a 2-hour liquid fast. Special attention should be paid to these with the use of glucagon-like peptide-1 (GLP-1) receptor agonists (such as semaglutide, exenatide, tirzepatide, liraglutide, albiglutide, dulaglutide, and lixisenatide) for the treatment of type 2 diabetes mellitus and weight loss. GLP-1 agonists, particularly with long-term use, are often associated with GI adverse effects, such as nausea, vomiting, bloating, and delayed gastric emptying, raising the concern about the risk of regurgitation and aspiration during and postendoscopy. In elective endoscopy a Consensus-Based Guidance document from the American Society of Anesthesiologists (ASA) lets the treatment team to consider holding off GLP-1 agonists on the day for patients on daily dosing of the GI procedure/surgery and holding off GLP-1 agonists a week prior to the procedure/surgery for patients on weekly dosing. For patients requiring urgent or emergent GI procedures, standard practice is to proceed and treat the patient as “full stomach” and manage accordingly . Due to the lack of data to support stopping GLP-1 agonists prior to elective endoscopy a multisociety statement from the American Gastroenterological Association, American Association for the Study of Liver Diseases, American College of Gastroenterology, American Society for Gastrointestinal Endoscopy, and North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition called for more data on the impact associated with stopping these therapies prior to undergoing upper GI endoscopy or other moderate to deep sedated procedures is unknown at this time . At this point, this author recommends that patients with IBD undergoing endoscopy (especially postoperative endoscopy and therapeutic endoscopy) with conscious sedation or monitored anesthesiology care may follow ASA’s consensus guideline, that is, holding off GLP-1 agonists on the day in patients on daily dosing; and holding off the agents a week before the procedure/surgery in those patients on weekly dosing.
If patients are undergoing endoscopy and simultaneously taking those medications, the information should be documented in the endoscopy report and the submitted script to histopathological evaluation. Insufflation of carbon dioxide (due to its great absorption feature), rather than room air, is also strongly recommended in endoscopy for patients with IBD . There is no published consensus on antibiotic prophylaxis in IBD endoscopy. This has experienced gas leakage or transient bacteremia can occur in diagnostic and therapeutic endoscopy of the diverted bowel ( Fig. 2.1 ). One of the mechanisms for the adverse sequelae is the presence of friable, compromised mucosa from diversion-associated deficiency in nutrients (particularly short-chain fatty acids). Therefore prophylactic antibiotic use is recommended in therapeutic endoscopies in the diverted bowel .
Diversion-associated bowel inflammation. (A) Diffuse friable mucosa in the diverted rectum (i.e., Hartmann pouch) in a patient with Crohn’s disease and a diverting long-term ileostomy. Tissue biopsy resulted in excessive bleeding controlled by the spray of hemostatic gel. (B) Mucosal breakdown even after gentle carbon dioxide insufflation during endoscopy in a separate patient with a diverted rectum.
Principles
Ileocolonoscopy is considered a standard practice in the evaluation of IBD, as a majority of patients with CD have disease in the distal or terminal ileum, representing L1 or L3 phenotypes in the Montreal classification , and all patients with UC have diseased bowel, including backwash ileitis, within the reach of ileocolonoscopy. For the diagnosis and differential diagnosis of IBD the value of ileocolonoscopy is beyond the quantification of severity and distribution of the bowel inflammation. Description of active endoscopic mucosal inflammation should include features of edema, erythema, exudates, friability, erosions, ulcers, and spontaneous bleeding. In addition, the location and length of the bowel involved and the number, size, shape, and depth of ulcers should also be documented. Furthermore, abnormalities resulting from chronic inflammatory injury should be evaluated and documented, including stricture, fistula, postinflammatory polyps, mucosal scars or bridges, and stiffness or distensibility of the bowel wall ( Fig. 2.2 ). Finally, disease status in surgically altered bowel in IBD, such as ileostomy, ileal pouch, stricturoplasty, and ileocolonic anastomosis, should be reported in endoscopy.
The description of inflammatory bowel disease (IBD) endoscopy is beyond the quantification of mucosal inflammation. It should also include other features. (A) Extensive mucosal scar with “lead piping” (or loss of the haustra) of the lumen of the left colon, resulting from long-term ulcerative colitis (UC) treated with biological agents. (B) A separate patient with UC has a stiff rectum with reduced distensibility.
UC is characterized by the presence of diffuse inflammation of the rectum with proximal extension. At the same time, CD is featured with a segmental disease with often sparing of the rectum ( Fig. 2.3 ). Mucosal patterns of the terminal ileum and proximal colon, along with features of the ileocecal valve (ICV) and histology, may help distinguish CD from UC with backwash ileitis. Endoscopic characteristics favoring the diagnosis of CD ileitis include discrete ulcers and strictures of the terminal ileum or ICV. In contrast, diffuse colitis and ileitis with the continuous pattern across a widely patent ICV are the features of UC with backwash ileitis, which is common in patients with concurrent primary sclerosing cholangitis (PSC) ( Fig. 2.4 ).
Distribution of mucosal inflammation in ulcerative colitis (UC) and Crohn’s disease. Diffuse colitis with erythema, exudates, and friability in the colon (A) and rectum (B) in a patient with UC. Diffuse colitis with erythema, erosions, and exudates in the colon (C) with sparing of the rectum (D) in a separate patient with Crohn’s colitis.
Distribution of ileitis in ulcerative colitis (UC) and Crohn’s disease (CD). Diffuse colitis with granular, flat mucosa and loss of vascularity in the terminal ileum (i.e., backwash ileitis) (A) and widely patent or a “Fish Mouth” configuration of the ileocecal valve (B) in a patient with UC. Linear ulcers and mucosal edema of the terminal ileum (C) and ulcerated, strictured, and deformed ileocecal valve (D) in a separate patient with CD.
Conventional white-light colonoscopy and image-enhanced endoscopy, such as virtual or dye-based chromoendoscopy , are the standard care for surveillance of colitis-associated neoplasia (CAN). Adequate control of inflammation and bowel preparation are prerequisites for accurate detection of CAN.
Techniques of tissue biopsy
Endoscopic features of IBD and non-IBD enterocolitides, such as infectious enterocolitis, drug-induced enterocolitis, ischemic colitis, and radiation colitis, overlap. Endoscopy alone provides only a limited value in distinguish among those enterocolitides. In contrast, endoscopic tissue biopsy with histopathological evaluation is critical for the diagnosis and differential diagnosis of CD and UC, and other enterocolitides. In addition, the importance of the index colonoscopy with intubation of the terminal ileum, photodocumentation, and segmental biopsies is never overemphasized in the evaluation of IBD and its mimics. For example, one distinctive feature of the differential diagnosis between UC and Crohn’s colitis is the distribution of disease (continuous pattern in UC vs segmental disease with rectal sparing in CD) ( Fig. 2.3 ) before the initiation of medical therapy. At ileocolonoscopy for the evaluation of IBD or IBD-like conditions, at least four topographic locations should be biopsied, including the terminal ileum, right colon, left colon, and rectum, and separately labeled ( Fig. 2.5 ) .
Topographic location of tissue biopsy in colonoscopy. For the diagnosis and differential diagnosis and differential diagnosis of inflammatory bowel disease, at least four segments of lower gastrointestinal tract during colonoscopy, particularly index colonoscopy, that is, terminal ileum, right colon, left colon, and rectum (blue arrows) .
The endoscopist should exert extreme caution when patients have deep ulcers in the bowel or severe bowel inflammation resulting from IBD or IBD-like conditions, as the risk of bleeding or perforation is high. The endoscopist should avoid the biopsy of the ulcer base and perform balloon dilation or stricturotomy of deeply ulcerated strictures ( Fig. 2.6 ). The endoscopist should use carbon dioxide for insufflation, minimize air administration.
Crohn’s disease-associated strictures. (A) Nonulcerated stricture at the terminal ileum. (B) Colonic stricture with deep ulceration.
The endoscopist should be familiar with the orientation of the bowel anatomy, which is particularly important for tissue biopsy and endoscopic therapy during lower GI endoscopy ( Fig. 2.7 ). Location of biopsy at endoscopy is determined by various factors, including the purpose and pretest probabilities of diagnosis. For example, biopsy of distal anterior rectum is taken for the evaluation rectal prolapse, rectal prolapse, rectocele, or radiation injury from brachytherapy (e.g., for prostate cancer), while biopsy of the posterior wall of the rectum is for the diagnosis of IBD proctitis ( Fig. 2.8 A), and biopsy for the evaluation of IBD should be in the lateral or posterior wall of the rectum ( Fig. 2.8B ). The location of linear, longitudinal ulcers indicates site of the mesenteric edge ( Fig. 2.9 ).
