INTRODUCTION

Colorectal diseases encompassing congenital, traumatic, inflammatory, or neoplastic pathologies are common. In most cases, a multidisciplinary approach is used to diagnose colorectal diseases, and these modalities include clinical history, physical examination, laboratory tests, imaging studies, endoscopic examination, and pathology. Corrective endoscopy and surgery play an essential role in treating these diseases in patients with indications and without contraindications. Macroscopic and microscopic examination of the samples, either biopsies or resection specimens, provides valuable information on the diseases. First, it may help diagnose the disease in the biopsy to guide subsequent management and treatment. Second, it may help confirm a diagnosis in endoscopically or surgically resected specimens. Third, a more thorough histological examination of the resected specimen may help validate the performance of other noninvasive diagnostic modalities. Last but not least, it is an integral component of clinical trials in patients with colorectal diseases. Due to the scope of this book, this chapter will focus on the histopathological features of perforation, anastomotic leaks, abscesses, and strictures features most commonly seen in inflammatory bowel disease (IBD). IBD is an umbrella term used to describe two distinct forms of intestinal inflammation, ulcerative colitis (UC) and Crohn’s disease (CD). In contrast to other inflammatory conditions affecting the gastrointestinal tract, where specific etiological factors can be identified, the precise causative factors for most cases of IBD remain largely unknown. Although traditionally considered distinct, UC and CD share important common pathophysiological processes, manifested by chronic, immune-mediated inflammation and associated with abdominal pain, diarrhea, gastrointestinal tract bleeding, fever, etc. The natural history of IBD is characterized by remissions and exacerbations of intestinal and extraintestinal disease variably with the development of complications like perforations, abscesses, strictures, fistulas, and anastomotic leaks. ^, Awareness of the flares and complications of IBD clinically and pathologically helps narrow the differentials and guide patient management. Similar complications can also occur in other colorectal diseases, and sometimes the histomorphology might be similar too; however, a strong multidisciplinary approach and review of additional pathology material would help in arriving at the diagnoses in most cases. In this section, we review the clinical features, macroscopic and microscopic features of perforations, anastomotic leaks, abscesses, fistula, and strictures complicating IBD.

PERFORATIONS

Macroscopic Findings in Perforation

Macroscopic findings in perforation depend on the interval between the injury and the surgery. In an acutely perforated bowel (such as a car accident or gunshot wound) resected by surgery, there may be only a transmural defect with fresh hemorrhage. If there is a lapse of time between the perforation and the surgery, macroscopically, the areas of perforation can be seen as transmural defects in the wall with fibrinous or fibrinopurulent exudates over the serosal surface. Sometimes, due to adhesions, the sites of perforation may not be visible grossly ( Fig. 10.1 ). In CD, other features like strictures, cobblestone appearance of the mucosa, inflammatory pseudopolyps, and concomitant fissures and fistulas may be seen. UC classically involves the rectum with more variable, continuous involvement of the rest of the colon. Perforations complicating UC occur commonly in the setting of toxic megacolon where the bowel wall is dilated and thinned out. The serosal surface at the sites of perforation demonstrates fibrinopurulent exudate.

Macroscopic picture of a resected small bowel with walled-off perforation. The perforation site is indicated by the forceps and the short black stitch. Fat wrapping is present. The mucosa reveals evidence of enteritis.

(Photo courtesy Dr. Yan Huang, the Sixth Affiliated Hospital of Sun Yat-Sen University of Medical Sciences, Guangzhou, China). (Courtesy of Dr. Yan Huang, the First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China).

Microscopic Findings in Perforation

Microscopically, the perforation involving CD can occur anywhere in the gastrointestinal tract, but most commonly in the small bowel. Normal small bowel has well-defined mucosa, muscularis mucosae , submucosa, muscularis propria, and serosa ( Fig. 10.2A ). Perforation in CD usually occurs in the background of chronic active enteritis ( Fig. 10.2B ), ulcerations, fissures ( Fig. 10.2B ), and sinus tracts ( Fig. 10.2C ). Dense transmural lymphoid aggregates ( Fig. 10.2D ), neural hypertrophy ( Fig. 10.2E ), muscular hypertrophy, mural fibrosis ( Fig. 10.2C ), and mesenteritis ( Fig. 10.2D ) that characterize CD classically may be seen in the adjoining areas. In some cases of perforation, the mucosa may have quiescent enteritis ( Fig. 10.2F ). In UC, the inflammation away from the perforated site tends to be more mucosal and submucosally restricted ( Fig. 10.3 ). Perforation secondary to infectious enterocolitis is characterized by transmural necrosis and exuberant inflammation ( Fig. 10.4 ). The site of perforation irrespective of the etiology usually demonstrates intense acute inflammation and granulation tissue on the mesentery and serosal aspect ( Fig. 10.5A and B ); multinucleated giant cells may be present, as also the “pulse granulomas/hyaline ring granulomas” ( Fig. 10.5C ).

Histology of normal small bowel and diseased small bowel in Crohn’s disease. (A) Normal histology of the small bowel includes well-formed villi, mucosa, muscularis mucosae , submucosa, muscularis propria , and serosa. (B) Crohn’s disease with chronic active enteritis, ulceration, fissuring ulcer, and lymphoid inflammation. (C) Crohn’s disease is characterized by mural fibrosis and serosal fibrosis.(D) Mesenteric fat atrophy and fibrosis, corresponding to fat wrapping on macroscopic examination. (E) Neural hypertrophy in the submucosa and muscularis propria . (F) In some cases, the overlying mucosa may only show quiescent enteritis and submucosal fibrosis.

Histopathology in ulcerative colitis. (A) Ulcerative colitis is characterized by diffuse and superficial inflammation confined to the mucosa and in some cases, superficially portion of the submucosa. (B) Chronic active colitis (i.e., chronic inflammation, architectural distortion, and active inflammation) in ulcerative colitis.

Bowel perforation due to infection enteritis. (A) The perforation site shows a defect lined by necrosis and inflammation. (B) The intermediate power view reveals necrosis and inflammation at the perforation site.

Histopathological examination of a perforated bowel. (A) Regardless of the etiology of perforation, the mesentery at or near the perforation may show fibrin, necrosis, and fibrosis. (B) Similarly, the serosa may show similar changes including fibrin deposition, necrosis, mesothelial hyperplasia, and fibroblastic proliferation. (C) Sometimes, pulse/hyaline ring granulomas may be indicative of a current or even remote history of perforation.

Differential Diagnosis of Perforation

The differential diagnosis of perforation includes infections, medications/chemicals, malignancy, ischemia, and obstruction, among others. However, a strong clinical correlation and examination of the areas not involved by perforation help in narrowing the differential diagnosis significantly. For example, perforations caused by ischemia will show ischemic-like changes in the adjacent mucosa, such as mucosal necrosis/ulceration ( Fig. 10.6A ), crypt atrophy ( Fig. 10.6B ), submucosal edema, submucosal fibrosis, and muscular atrophy, pseudomembranous exudate ( Fig. 10.6C ) as well as pseudo-signet ring cells ( Fig. 10.6D ). In general, the inflammation in chronic ischemia is less prominent than in CD.

Chronic ischemic injury may perforate the bowel. (A) The adjacent mucosa may show ulceration and submucosal fibrosis, but the muscularis propria is usually atrophic. (B) The mucosa may be atrophic and the surface epithelium shows regenerative changes. (C) Sometimes, pseudomembranes with volcanic eruptions resembling Clostridium difficile -associated colitis may be seen. (D) Degenerated goblet cells resembling signet ring cells (pseudosignet ring cells) can be seen.

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