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Inflammatory Bowel Disease & Colon

Crohn vs UC, and the colon emergencies that bleed, obstruct, or infarct

Gastrointestinal·Intestinal & Colorectal Pathology·5 min read·9 high-yield points·Reviewed by Veli Bakalov, MD @HemeOncBuddy
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Crohn disease vs ulcerative colitis

The core contrast. Both are chronic, relapsing inflammatory bowel diseases (IBD) of young patients, but they differ in depth, distribution, and histology. Crohn disease is transmural, with skip lesions anywhere from mouth to anus (favoring the terminal ileum) and noncaseating granulomas. Ulcerative colitis (UC) is mucosal, continuous, confined to the colon, and always involves the rectum. Nearly every other difference follows from depth: transmural inflammation explains why Crohn, not UC, causes fistulae and strictures.

Crohn disease vs ulcerative colitis
FeatureCrohn diseaseUlcerative colitis
LocationMouth to anus; terminal ileum favored; rectum usually sparedColon only; always the rectum, spreading proximally
DistributionSkip lesionsContinuous
DepthTransmuralMucosa and submucosa
Gross / imagingCobblestone mucosa, creeping fat, string signFriable mucosa, pseudopolyps, lead-pipe colon
HistologyNoncaseating granulomasCrypt abscesses (neutrophils in crypts)
ComplicationsStrictures, obstruction, fistulae, abscesses, perianal disease, malabsorptionToxic megacolon, perforation
Signature associationCalcium oxalate kidney stones, gallstonesPrimary sclerosing cholangitis (p-ANCA)
SmokingWorsensProtects
SurgeryNot curative; disease recursColectomy is curative

Treatment overview. Flares are treated with corticosteroids; maintenance uses 5-aminosalicylates (mesalamine, sulfasalazine), especially in UC, immunomodulators such as azathioprine, and biologics such as anti-TNF antibodies (infliximab).

Crohn disease

Distribution and gross findings. Crohn favors the terminal ileum and spares the rectum. Skip lesions alternate with normal bowel, and linear ulcers between swollen mucosa create a cobblestone appearance. Transmural inflammation and fibrosis narrow the terminal ileum, seen as a string sign on barium study, and produce strictures, obstruction, fistulae, abscesses, and perianal disease. Mesenteric fat wraps around the serosa ("creeping fat").

Histology and immunology. Noncaseating granulomas are the histologic hallmark, and the inflammation is Th1/Th17-driven. Bloody diarrhea is less prominent than in UC, while obstruction and malabsorption are common; terminal ileal disease causes B12 deficiency.

Stones from the ileum. Loss of terminal ileal bile acid reabsorption causes fat malabsorption. Unabsorbed fatty acids bind calcium in the gut, leaving oxalate free to be absorbed (enteric hyperoxaluria), which forms calcium oxalate kidney stones. The shrunken bile acid pool also favors cholesterol gallstones.

Extraintestinal disease. Migratory polyarthritis, erythema nodosum, pyoderma gangrenosum, uveitis, oral aphthous ulcers, and ankylosing spondylitis. Most of these also occur in UC.

Ulcerative colitis

Distribution. UC always involves the rectum and spreads continuously and proximally, never beyond the colon and without skip lesions. Because inflammation is limited to the mucosa and submucosa, it causes bloody diarrhea with tenesmus rather than fistulae.

Pathology. Crypt abscesses (neutrophils within crypts) and friable, ulcerated mucosa with pseudopolyps (regenerating islands between ulcers). Long-standing disease flattens the colon and removes haustra, giving a lead-pipe colon on imaging.

Toxic megacolon (massive dilation of an inflamed colon) and perforation are the feared acute complications of UC.

PSC and cancer. UC is strongly associated with primary sclerosing cholangitis: p-ANCA positivity, onion-skin fibrosis of bile ducts, and beading on MRCP, with an added risk of cholangiocarcinoma. UC carries a higher colorectal cancer risk than Crohn, rising with extent and duration of colitis. Smoking paradoxically protects against UC.

Diverticular disease

Diverticulosis. False diverticula (mucosa and submucosa only) herniate through weak points in the muscularis where the vasa recta penetrate, most often in the sigmoid colon. A low-fiber diet raises intraluminal pressure. Usually asymptomatic, diverticulosis is the most common cause of acute, painless lower-GI bleeding (hematochezia) in older adults, because a stretched vas rectum at the diverticulum neck ruptures.

Diverticulitis. Inflammation or microperforation of a diverticulum produces LLQ pain, fever, and leukocytosis ("left-sided appendicitis"). Diagnose with CT; treat with antibiotics covering gram-negatives and anaerobes, and avoid colonoscopy or barium enema acutely because of perforation risk. Complications are abscess, perforation with peritonitis, obstruction from stricture, and fistula.

A colovesical fistula presents with pneumaturia (air in the urine) and recurrent polymicrobial UTIs.

Ischemic colitis and angiodysplasia

Ischemic colitis. Reduced perfusion injures the watershed zones, the splenic flexure and rectosigmoid junction, classically in older patients after hypotension or AAA repair. It causes crampy abdominal pain (postprandial when hypoperfusion is chronic) with bloody diarrhea. Imaging shows thumbprinting from submucosal edema and hemorrhage.

Angiodysplasia. Tortuous, dilated submucosal vessels in the cecum and ascending colon of older adults cause painless hematochezia or occult bleeding with iron deficiency. It is associated with aortic stenosis (Heyde syndrome, in which shear stress across the valve produces acquired von Willebrand deficiency) and with end-stage renal disease.

Colon lesions that bleed, hurt, or infarct
LesionUsual sitePresentationKey clue
DiverticulosisSigmoidPainless hematocheziaLow-fiber diet; most common major LGI bleed
DiverticulitisSigmoidLLQ pain, fever, leukocytosisCT; antibiotics, no acute scope
Ischemic colitisSplenic flexure, rectosigmoidCrampy pain, bloody diarrheaHypotension or AAA repair; thumbprinting
AngiodysplasiaCecum, ascending colonPainless or occult bleedingAortic stenosis (Heyde), ESRD

Appendicitis

Pathogenesis. Appendicitis begins with luminal obstruction, by a fecalith in adults or lymphoid hyperplasia in children. It is the most common indication for emergency abdominal surgery.

  1. Luminal obstructionFecalith (adults) or lymphoid hyperplasia (children)
  2. Distension and ischemiaBacterial overgrowth and invasion of the wall
  3. Periumbilical painVisceral afferents entering at T10
  4. RLQ pain at McBurney pointInflammation reaches the parietal peritoneum
  5. RupturePeritonitis if untreated
Appendicitis progression

Exam signs. McBurney point tenderness (one-third of the way from the anterior superior iliac spine to the umbilicus); psoas sign (pain on hip extension, retrocecal appendix); obturator sign (pain on internal rotation of the flexed hip, pelvic appendix); and Rovsing sign (RLQ pain on LLQ palpation). Treatment is appendectomy.