Inflammatory Bowel Disease: Pouch Dysplasia EIM Pregnancy

0:00Welcome to Board Pearls. This is episode three of three of the Inflammatory Bowel Disease chapter, in the Colorectal and Pelvic Floor Disorders module. This episode is the long-term complications: the pouch and its inflammations, dysplasia surveillance in long-standing colitis, the extraintestinal manifestations, and pregnancy, where continuing biologics through delivery is usually the right call.

0:23The patient who's weathered induction, settled into maintenance, and lost the colon to a restorative pouch is not done with the disease. The cancer risk is still there, the joints and eyes and skin and liver still carry the same immune dysregulation on their own clocks, and the pregnancy the medication list is suddenly built around is more often answered by continuing biologics than stopping them. This is the longer arc of IBD, and it's mostly what the gastroenterologist owns in clinic between flares.

0:51Start with the pouch. Roughly one in five UC patients comes to colectomy over the years, and the restorative procedure is a total proctocolectomy with an ileal pouch-anal anastomosis, folding the terminal ileum into a J-shaped reservoir joined to the anal canal, sometimes through a short cuff of retained rectal mucosa. The new anatomy is the source of new inflammation, because small-bowel lining is now exposed to colonic-type stasis and bacterial loads it wasn't designed for. About half of pouch patients develop pouchitis within the first decade, recurrence is the rule, and a small fraction settle into chronic pouchitis, and it's far more common when the pouch is done for UC than for familial polyposis, which tells you it isn't just stasis, it's the same immune predisposition meeting a new microbial environment.

1:37The pouch problems sort by location and chronicity, and that sorting is the test of reasoning: inflammation in the pouch body is pouchitis, inflammation in the residual rectal cuff is cuffitis, and inflammation involving the pre-pouch ileum, perianal tissues, or pouch inlet that looks structurally different is the Crohn's-like pouch. Localize before you pick the drug. Acute pouchitis presents within months of pouch use with increased frequency, urgency, cramping, and sometimes bleeding, but the diagnosis isn't by symptom, because infectious pouchitis from C. diff or CMV, cuffitis, and a Crohn's-like pattern all overlap, so pouchoscopy with biopsies is mandatory before escalating. First-line for the typical acute case is a short course of ciprofloxacin or metronidazole, with combination antibiotics reserved for non-responders, and the risk-factor profile is tested directly: extensive pancolitis at colectomy, backwash ileitis, primary sclerosing cholangitis, positive pANCA, ex-smoker status, regular NSAID use, and prior extraintestinal manifestations all raise the risk, with sclerosing cholangitis the most powerful amplifier.

2:44Chronic pouchitis is symptoms persisting beyond four weeks despite therapy or frequent relapse, and it splits into antibiotic-dependent, which responds to a chronic low-dose antibiotic managed with rotating agents to limit resistance, and antibiotic-refractory, which doesn't respond to antibiotics at all and escalates through mesalamine, budesonide, immunomodulators, and biologics, with vedolizumab carrying the strongest randomized evidence and being the favored biologic answer for refractory pouchitis, and anti-TNF and ustekinumab also used. Before escalating immunosuppression, clear the secondary causes, C. diff, CMV, pouch ischemia, NSAIDs, and unrecognized celiac, because CMV pouchitis in particular is treated with ganciclovir and missing it costs the patient a biologic they didn't need. Cuffitis is the same UC inflammation restricted to the retained rectal cuff, where bleeding is the dominant feature and the pouch body looks normal, so the endoscopic localization is the key and the treatment is topical mesalamine, which is the answer for the pouch patient with new bleeding and a normal-appearing pouch body. The Crohn's-like pouch is the harder pattern that changes the long-term plan, with pre-pouch ileitis beyond backwash, perianal fistulas, deep ulcers, granulomas, or inlet strictures, treated like luminal Crohn's with anti-TNF first-line, and pouch failure needing excision or permanent diversion occurs in a minority of these, which is why the diagnosis is consequential. Two more: irritable pouch syndrome is the functional analog with normal endoscopy and histology, treated with antimotility agents and behavioral therapy, and pouch outlet obstruction is the structural analog managed with dilation or revision. And the pouch itself is surveilled for dysplasia, annually in high-risk patients with prior dysplasia or cancer, sclerosing cholangitis, or chronic pouchitis, and every few years otherwise, biopsying the cuff and body separately because cuff dysplasia is more common.

4:45That brings up the larger surveillance question long-standing IBD raises. Decades of colonic inflammation drive a dysplasia-to-cancer sequence different from the sporadic one, with the tumor-suppressor mutation occurring early rather than late, and the cancer risk rising with disease duration, with sclerosing cholangitis compounding it substantially and changing when surveillance begins. In extensive UC and in Crohn's colitis involving more than a third of the colon, surveillance colonoscopy begins eight to ten years after the onset of symptoms, not the date of diagnosis, and that distinction is tested because it changes the start by years in a patient diagnosed late, whereas in sclerosing cholangitis with IBD, surveillance begins immediately at the diagnosis of the cholangitis, because the cancer risk there is markedly higher and earlier and waiting eight years would miss the cancers. After the first exam, the interval is risk-stratified: annually for high-risk patients, meaning sclerosing cholangitis, prior dysplasia, a family history of colorectal cancer, dense pseudopolyposis, active inflammation, or a stricture; every couple of years for intermediate-risk extensive disease; and up to five years for low-risk limited disease in sustained remission. The exam is performed in remission whenever possible, because active inflammation obscures the dysplasia signal, so if active inflammation is found, you control the disease and repeat.

6:10How to look has changed: instead of many random biopsies, the current approach is high-definition white light plus chromoendoscopy, spraying dye onto the mucosa to highlight contour and reveal subtle flat lesions white light misses, with targeted biopsies of any visible lesion, and random biopsies can be omitted when chromoendoscopy is done, though many centers keep some in the highest-risk patients. Visible lesions are described simply as polypoid or non-polypoid and as endoscopically resectable or not. What to do with each finding falls along grade, visibility, and resectability. Visible dysplasia that's endoscopically resectable with clear margins is removed completely by endoscopic resection, with follow-up surveillance in a few months then annually. Visible dysplasia that isn't resectable, because of poor margins, submucosal invasion, or multifocality, is referred for proctocolectomy. Invisible high-grade dysplasia, meaning a positive random biopsy with no visible lesion on a good chromoendoscopy exam, carries a high synchronous cancer risk, so the answer is proctocolectomy. Invisible low-grade dysplasia is the more controversial category, managed either with close surveillance by an experienced endoscopist using chromoendoscopy or with proctocolectomy, the choice driven by multifocality and concurrent risk factors, and all dysplasia should be confirmed by a second pathologist because interobserver variability is real. A few sub-points: inflammatory pseudopolyps aren't dysplasia and don't need resection beyond a representative biopsy, though dense pseudopolyposis raises the risk of missed dysplasia; strictures in long-standing colitis carry malignancy risk and need thorough biopsy, and one that can't be passed prompts imaging and consideration of surgery; and a sporadic adenoma in colitic mucosa can be managed by polypectomy with surveillance if the surrounding mucosa is clean.

8:07The third part is the multisystem face of IBD. About half of patients develop at least one extraintestinal manifestation, and having one makes a second more likely, and the boards split them on one question: some parallel luminal disease activity and resolve when the bowel is treated, and others run independent of bowel activity and need their own management, which decides whether the gastroenterologist owns the problem or a referral is part of the answer. Musculoskeletal disease is the most common. Peripheral arthritis splits into two types: the first is pauciarticular, affecting a few large joints, parallels bowel activity, and is self-limited, treated with the underlying IBD plus cautious NSAIDs or sulfasalazine; the second is polyarticular, affects small joints, runs independent of bowel activity, is associated with uveitis, and is chronic, treated with sulfasalazine, methotrexate, or a biologic. Axial spondyloarthropathy is more common in men and runs independent of bowel activity, presenting with inflammatory back pain that's worse at rest and better with activity, progressing toward ankylosing spondylitis, and HLA-B27 raises that risk markedly though most carriers never develop it, so it's a risk marker, not a near-certain predictor. Treatment is physical therapy, cautious NSAIDs, and biologics, and here two drug facts matter: etanercept works for the spondylitis but not for IBD, so it's not the answer when both coexist, and IL-17 inhibitors used in spondylitis can worsen IBD and are avoided. The teaching trap is clean: colectomy improves the bowel-tracking peripheral arthritis but does not improve axial arthritis, which runs on its own clock.

9:52Dermatologic manifestations sort into reactive and disease-specific lesions. Erythema nodosum is the most common, tender nodules on the shins that parallel disease activity and resolve with bowel-directed therapy. Pyoderma gangrenosum is harder, a pustule that breaks down into an ulcer with violaceous undermined borders, demonstrating pathergy where lesions worsen at sites of trauma, commonly on the legs or around a stoma, with variable activity tracking, treated from potent topical steroids or tacrolimus through systemic agents and biologics for refractory disease. Sweet syndrome is the rare neutrophilic eruption with fever, and metastatic Crohn's is cutaneous granulomas distant from the gut. Ocular manifestations are where misclassification has real consequences: episcleritis is the most common, parallels disease activity, doesn't threaten vision, and responds to topical therapy, while scleritis is deeper, threatens vision, and earns immediate ophthalmology referral, and anterior uveitis runs independent of bowel activity with eye pain, photophobia, and blurring, earning immediate referral and systemic steroids with anti-TNF for refractory disease, so the board move on an eye complaint is to ask about photophobia and vision change before deciding whether topical management is enough. Hepatobiliary disease is dominated by primary sclerosing cholangitis, which complicates a small percentage of UC and fewer Crohn's patients but is present in most sclerosing cholangitis patients, preferentially affects extensive UC, runs independent of bowel activity, and links directly back to surveillance because it mandates annual colonoscopy from its diagnosis, with the fuller framework in chapter twenty. Other hepatobiliary points: gallstones are more common in ileal Crohn's from impaired bile-salt absorption, and drug-induced hepatitis and pancreatitis follow the thiopurines, methotrexate, and mesalamine. Renal manifestations include calcium oxalate stones, the renal phenotype of ileal Crohn's with an intact colon and fat malabsorption, through enteric hyperoxaluria, where malabsorbed fat binds luminal calcium so oxalate is left free for colonic absorption and the kidney concentrates it.

11:57Nutrition follows the disease distribution, which organizes the whole list. Iron deficiency is common, from blood loss in UC and impaired absorption plus inflammation in Crohn's, with oral iron poorly tolerated during active disease so intravenous iron is often necessary. B12 deficiency follows ileal Crohn's or terminal-ileum resection because B12 absorption is restricted to the terminal ileum, replaced parenterally. Folate deficiency complicates sulfasalazine and methotrexate, so supplementation is built into both. Vitamin D deficiency contributes to bone disease, so supplementation is routine, with bone-density screening and bisphosphonates for patients on prolonged steroids or with fractures. Zinc deficiency from severe diarrhea gives dermatitis and altered taste, fat-soluble vitamin deficiency follows extensive small-bowel disease, and enteral or parenteral nutrition is reserved for severe undernutrition or as primary therapy in pediatric Crohn's, with short-bowel patients sometimes needing a GLP-2 analog.

12:58Vaccinations are the move the gastroenterologist has to make before biologics start, because the window narrows once therapy begins, and the organizing rule is that live vaccines are contraindicated during biologic therapy and for three months after stopping, so they're given at least four weeks before initiation, the live list being measles-mumps-rubella, varicella, yellow fever, oral typhoid, and intranasal influenza. Inactivated vaccines are safe during therapy and recommended throughout: inactivated influenza annually, pneumococcal on the current schedule, the recombinant zoster vaccine for older adults and for younger patients on JAK inhibitors, HPV through the mid-forties, hepatitis A and B with hepatitis B especially critical because biologics raise reactivation risk, and meningococcal before complement inhibitor therapy. And infants exposed to a biologic in utero have one added rule: live vaccines including rotavirus are deferred until the transferred drug clears, typically by around six months, except after certolizumab, which crosses minimally so infant rotavirus vaccination can proceed.

14:04Pregnancy in IBD is where the medication instinct often runs the wrong way, and the rule is simple: active disease threatens the pregnancy more than active medication, and disease activity at conception is the single best predictor of outcome, so the conversation about which drugs to continue is the same as the one about achieving remission before conception. Most IBD medications continue throughout pregnancy, the exceptions being methotrexate, which is teratogenic and stopped several months before conception in either parent, and the JAK inhibitors, which are avoided. Sulfasalazine continues with mandatory folic acid, with the counseling point that it causes reversible oligospermia in the male partner. The biologics other than certolizumab cross the placenta in the third trimester, so the infant avoids live vaccines until the drug clears, while certolizumab crosses minimally and is sometimes preferred in late pregnancy, with the fuller framework in chapter thirty-five.

15:00So hold this episode by remembering that IBD isn't finished when the flare resolves. The pouch creates its own disease pattern, located in the body, the cuff, or the inlet and chronic, refractory, or Crohn's-like, and the localization decides the drug. Long-standing colitis carries a real cancer risk, with surveillance starting when symptoms began rather than when the diagnosis was made, except in sclerosing cholangitis where it starts immediately, and the exam looks for visible flat lesions with chromoendoscopy, resecting what can be resected and removing the colon when dysplasia can't be cleared. The extraintestinal manifestations either track the bowel or they don't, and that distinction tells you whether bowel-directed therapy is the answer. Vaccines have to land before biologics start, especially the live ones. And the pregnant patient is almost always better off continuing her biologic than stopping it, because the disease is the threat.

15:52The next chapter moves from inflammatory disease of the colon to neoplastic disease of the colon: the screening start age and the menu of modalities, the molecular subtypes that change treatment, the post-polypectomy surveillance intervals, and the selective role of antibiotics in uncomplicated diverticulitis.

16:09For the full chapter, the practice vignettes, and the topic-tagged question bank, head to board pearls dot com. You'll find the rest of the series on Apple Podcasts, Spotify, or wherever you listen to podcasts. That brings us to the end of episode three of three of chapter fourteen, and I'll see you in the next one.