Inflammatory Bowel Disease: Inflammatory Bowel Disease: The Pouch and Beyond

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 covers the pouch, cancer surveillance, and the whole patient. A man with an inflamed ileal pouch has pouchitis, and his case shows why pouches get inflamed, what must be excluded first, and what to do when antibiotics stop working. A woman with bleeding from her pouch shows cuffitis, and a man with a fistula and granulomas shows Crohn-like disease of the pouch. A woman with long-standing colitis who feels well shows when dysplasia surveillance starts, how often, which technique, and what happens to a visible lesion, and a man with dysplasia on a random biopsy shows what to do when nothing is visible. A man with back pain and a red eye while his bowel is quiet shows which problems outside the gut follow bowel activity and which run on their own. A woman with a leg ulcer that worsened after debridement shows pyoderma gangrenosum, and a man with a kidney stone shows enteric hyperoxaluria. And a woman about to start a biologic who wants to conceive shows nutrition, vaccines before immunosuppression, and pregnancy, for her and for her partner.

1:12Here's the first patient. A forty-one-year-old man had a total proctocolectomy with an ileal pouch-anal anastomosis two years ago, for extensive ulcerative colitis that failed medical therapy. He also has primary sclerosing cholangitis. For ten days he's had eleven stools a day, up from his usual five, with urgency, cramps, a little blood, and a low-grade fever. He takes no nonsteroidal anti-inflammatory drugs, NSAIDs.

1:38His story suggests acute pouchitis, inflammation of the pouch body, and his operation explains why it happens. About twenty percent of patients with ulcerative colitis need a colectomy over fifteen years. In patients without contraindications, the restorative operation of choice is a total proctocolectomy with an ileal pouch-anal anastomosis, in which the end of the ileum is folded into a J-shaped reservoir and joined to the anal canal. That exposes small bowel lining to the stasis and bacterial load of a colon, and inflammation follows.

2:09Pouchitis is common, and it tends to come back. It affects roughly half of pouch patients within ten years, recurrence is the rule, and five to ten percent develop chronic pouchitis. The mechanism involves an altered pouch microbiome, residual mucosal inflammation, and possibly disease genetics. Pouchitis is markedly more common in pouches made for ulcerative colitis than in those made for familial adenomatous polyposis, where it's rare.

2:34His history also holds the risk factors. They're extensive pancolitis at colectomy, backwash ileitis, primary sclerosing cholangitis, a positive perinuclear antineutrophil cytoplasmic antibody, pANCA, being an ex-smoker, regular NSAID use, and prior extraintestinal manifestations. He had extensive colitis and has primary sclerosing cholangitis, a major amplifier of the risk.

3:01The diagnosis still needs endoscopy with biopsies, because other problems look the same and are treated differently. Acute pouchitis presents with increased frequency, urgency, cramps, bleeding, low-grade fever, and dehydration if severe. But infectious pouchitis, from Clostridioides difficile or cytomegalovirus, CMV, looks the same, and so do cuffitis and Crohn-like disease of the pouch.

3:28Inflammation after a pouch is classified by where it is, and that's what endoscopy shows. Inflammation of the pouch body is pouchitis. Inflammation of the retained rectal cuff is cuffitis. Inflammation of the pouch inlet, the ileum above the pouch, or the perianal tissues suggests Crohn-like disease. It's also classified by course, acute or chronic, and the Pouchitis Disease Activity Index combines clinical, endoscopic, and histologic findings. His pouchoscopy shows an inflamed, ulcerated pouch body with a normal pre-pouch ileum and cuff. His C. difficile test is negative, and his biopsies show no CMV. He has acute pouchitis.

4:10With infection excluded, he gets an antibiotic. The choices are ciprofloxacin one thousand milligrams a day, or metronidazole seven hundred fifty to fifteen hundred milligrams a day, for seven to fourteen days, with combination antibiotics for patients who don't respond to one. He takes ciprofloxacin, and within four days his stools are back to five a day.

4:32Over the next year he relapses within weeks every time ciprofloxacin stops. That's chronic pouchitis, defined as symptoms beyond four weeks despite therapy, or frequent relapse. It comes in two kinds, and the kind decides the treatment. Antibiotic-dependent pouchitis responds but needs antibiotics continuously. It's managed with chronic low-dose ciprofloxacin, tapered to the lowest effective dose, or with rotating ciprofloxacin, metronidazole, rifaximin, tetracycline, amoxicillin-clavulanate, and tinidazole, plus an eight-strain probiotic mixture, the preferred probiotic for maintenance. Antibiotic-refractory pouchitis doesn't respond and needs escalation.

5:16He does well for a while on low-dose ciprofloxacin and the probiotic, then stops responding even after a change of antibiotic, so he now has antibiotic-refractory pouchitis. Before escalating, secondary causes are excluded, because more immune suppression won't help a pouch whose problem is something else. Those causes are C. difficile or CMV infection, pouch ischemia, NSAID use, and coexisting celiac disease. CMV pouchitis is treated with ganciclovir or valganciclovir. His tests and medication review are clear.

5:49His escalation options run from topical to systemic. They're oral or topical mesalamine, oral budesonide, a thiopurine, and biologics. Vedolizumab has the strongest randomized evidence for chronic refractory pouchitis and is the preferred biologic. It was approved for chronic pouchitis in Europe in twenty twenty-two, but it isn't approved for pouchitis in the United States. Anti-tumor necrosis factor, anti-TNF, drugs and ustekinumab are also used. He starts vedolizumab and responds over three months.

6:25His pouch also needs cancer surveillance, and his risk sets the interval. High-risk patients are those with prior dysplasia or cancer in the colectomy specimen, primary sclerosing cholangitis, or chronic pouchitis, and they're surveyed every year. Low-risk patients are surveyed every three to five years. He has two high-risk features, so he needs annual pouchoscopy. The cuff and pouch body are biopsied separately, because dysplasia is more common in the cuff and management may differ.

6:52The second patient shows that not every pouch problem is pouchitis. A thirty-seven-year-old woman with a pouch has rectal bleeding and urgency. Her pouchoscopy shows a normal pouch body with inflammation confined to the cuff, the strip of rectal mucosa between the pouch join and the dentate line. She has cuffitis, ulcerative colitis restricted to that remnant. Its symptoms overlap with pouchitis, but bleeding dominates, and biopsies show chronic colitis-type changes. It's the usual cause of bleeding after a pouch when the pouch body looks normal. Because it's colitis, not dysbiosis, it's treated topically, with mesalamine suppositories or enemas, or topical hydrocortisone or budesonide, not antibiotics.

7:37The third patient's pouch shows that the original diagnosis can change. A forty-five-year-old man had a pouch made for presumed ulcerative colitis. He now has inflammation in the ileum above the pouch inlet, more than backwash would explain, a perianal fistula, deep ulcers, and granulomas on biopsy. That's Crohn-like disease of the pouch. Its features are pre-pouch ileitis, perianal fistulas or abscesses, deep ulcers, granulomas, and strictures at the inlet or outlet.

8:07Its causes vary, but its treatment follows Crohn disease. Some cases are an unclassified colitis that has now declared itself as Crohn disease, which is the risk of making a pouch when the type of colitis isn't certain. Others are a surgical complication or true new disease. He's treated like luminal Crohn disease with biologic therapy, an anti-TNF drug first, with infliximab having the most evidence, and ustekinumab or vedolizumab as alternatives. Pouch failure, meaning removal or permanent diversion, occurs in roughly ten to fifteen percent of Crohn-like pouches.

8:41When the pouch looks normal, the cause of symptoms is functional or mechanical. A normal pouchoscopy and normal biopsies in a patient with frequency and urgency is irritable pouch syndrome. It's a functional disorder treated with antimotility drugs and behavioral interventions, not antibiotics. Pelvic floor dyssynergia can involve the pouch-anal segment. Pouch outlet obstruction can be functional or anatomic, from a stricture at the join, a twisted pouch, or retained rectum, and it needs endoscopic evaluation with balloon dilation or surgical revision.

9:13The fourth patient still has her colon, and her question is about cancer. A fifty-year-old woman has extensive ulcerative colitis, Montreal E3. Her bloody diarrhea began nine years ago, but she wasn't diagnosed until seven years ago, after two years of being told it was hemorrhoids. She's in remission on mesalamine. She has no family history of colorectal cancer, no primary sclerosing cholangitis, and no colonoscopy since diagnosis. Her calprotectin is normal. She asks whether she needs another scope when she feels so well.

9:46She does, because years of extensive colitis raise her colorectal cancer risk whatever her symptoms. Long-standing colonic inflammatory bowel disease, IBD, raises the risk through chronic inflammation. It produces oxidative damage to deoxyribonucleic acid, DNA, epigenetic changes, and microsatellite or chromosomal instability. That creates a field of dysplasia across the inflamed colon rather than a single polyp.

10:16The biology also explains why the lesions are hard to see. In colitis-associated cancer, TP53 mutates early and APC later, the reverse of the sporadic sequence. That's one reason these cancers often don't arise from a classic adenoma, and why flat lesions must be sought. In extensive ulcerative colitis, the cumulative cancer risk rises with time, to roughly eighteen percent at thirty years, and primary sclerosing cholangitis compounds it substantially. Feeling well doesn't protect her, because the risk comes from years of disease.

10:51Her timing is counted from her first symptoms. In extensive ulcerative colitis, and in Crohn colitis involving more than a third of the colon, surveillance colonoscopy begins eight to ten years after the onset of symptoms, not diagnosis, because her colon was inflamed during the undiagnosed years. Counting from diagnosis she's at seven years, but from symptoms she's at nine and due now. In primary sclerosing cholangitis with IBD, surveillance begins immediately at the diagnosis of the liver disease and is yearly from the start, because the cancer risk is higher and comes earlier.

11:25Her interval after that depends on her risk. High-risk patients are surveyed every year. They have primary sclerosing cholangitis, prior dysplasia, a family history of colorectal cancer, dense pseudopolyposis, active inflammation, or a stricture. Intermediate-risk patients, with extensive disease and no other risk factors, are surveyed every two to three years. For low-risk patients, with limited disease, sustained remission, and no family history, every five years can be considered.

11:55The exam has to be timed to remission, because active inflammation hides dysplasia. An exam that finds active colitis doesn't count, and it's repeated once the disease is controlled. She's in remission, so her exam can go ahead now.

12:09The technique has to find flat dysplasia, which random sampling misses. The older approach took thirty-two random biopsies, four quadrants every ten centimeters, sampling blindly. An international consensus on surveillance for colorectal endoscopic neoplasia in IBD replaced it with high-definition white light colonoscopy plus chromoendoscopy. A dye, methylene blue at zero point one to zero point four percent or indigo carmine at zero point one three to zero point four percent, is sprayed onto the lining. It pools in surface contours and reveals subtle flat lesions that white light misses, and each gets a targeted biopsy.

12:50Chromoendoscopy changes what else is needed. Random biopsies can be omitted with chromoendoscopy, though some centers keep a few in high-risk patients, such as those with primary sclerosing cholangitis or prior dysplasia. Virtual chromoendoscopy with narrow-band imaging is an acceptable alternative with high-definition equipment and an experienced endoscopist, with comparable sensitivity in expert hands.

13:16Anything found is described in the same consensus terms, because the description decides the management. The old term DALM, dysplasia-associated lesion or mass, is retired. A visible lesion is described by shape, either polypoid, meaning pedunculated or sessile, or non-polypoid, meaning flat, depressed, or ulcerated. It's also described by whether it's endoscopically resectable. Her chromoendoscopy finds a fifteen-millimeter flat, non-polypoid lesion in the sigmoid with clear borders and no signs of submucosal invasion.

13:51What happens to a lesion is decided by grade, visibility, and resectability. Visible resectable dysplasia, with clear margins and no submucosal invasion, is removed completely by an experienced operator, using endoscopic mucosal resection or submucosal dissection. It's then surveyed at three to six months and yearly after that. Visible dysplasia that isn't resectable, with poor margins, submucosal invasion, ulceration, or multifocality, goes to proctocolectomy.

14:23Her lesion is removed by mucosal resection and shows low-grade dysplasia with clear margins. Every dysplasia diagnosis is confirmed by a second gastrointestinal pathologist, because interobserver variability is significant, and hers is confirmed. She's now high risk, with colonoscopy at three to six months, then yearly.

14:43The fifth patient shows that invisible dysplasia is harder. A fifty-five-year-old man with long-standing pancolitis had high-grade dysplasia on a random biopsy. An experienced endoscopist using high-definition chromoendoscopy finds no visible lesion. Invisible high-grade dysplasia carries a synchronous cancer risk of about forty percent, so he's referred for proctocolectomy.

15:07Invisible low-grade dysplasia is more controversial, and the decision is shared. Its historical synchronous cancer risk was about twenty percent, with progression to high-grade dysplasia or cancer at roughly zero point eight percent a year. It's managed either by close chromoendoscopic surveillance every three to six months by an experienced endoscopist, or by proctocolectomy. The choice depends on the patient, multifocality, and other risk factors such as primary sclerosing cholangitis or prior strictures.

15:37A few other findings during surveillance have their own rules. Inflammatory pseudopolyps aren't dysplasia and need only a representative biopsy, but dense pseudopolyposis hides dysplasia and warrants closer follow-up. Strictures in long-standing colitis carry a risk of malignancy and need thorough biopsy, and a stricture the colonoscope can't pass prompts cross-sectional imaging and consideration of surgery. Dysplasia in Crohn colitis follows the same principles. A sporadic adenoma in colitic mucosa can be managed by polypectomy with surveillance if the surrounding mucosa is free of dysplasia.

16:14The sixth patient's bowel is quiet, but his problems are outside it. A thirty-year-old man has Crohn colitis in endoscopic remission on vedolizumab. For eight months he's had low back pain that's worst in the morning, with an hour of stiffness, eases with exercise, and alternates between his buttocks. Last week his right eye became painful and red around the iris, with light sensitivity and blurred vision. His stools are normal, and his calprotectin is low.

16:43He has two extraintestinal manifestations of IBD, axial spondyloarthritis and anterior uveitis, while his bowel is in remission. About half of IBD patients develop at least one extraintestinal manifestation, from immune dysregulation that targets tissues outside the gut, and having one makes a second more likely. What decides treatment is whether each one follows bowel activity or runs on its own.

17:09The two groups are fixed. Type one peripheral arthritis, erythema nodosum, and episcleritis track the bowel and settle when it's treated. Axial spondyloarthritis, type two peripheral arthritis, anterior uveitis, and primary sclerosing cholangitis run independently. Pyoderma gangrenosum may or may not parallel the bowel. Both of his problems are the independent kind, so controlling his gut won't fix them.

17:36His back pain is inflammatory: worse at rest, better with activity, with morning stiffness and alternating buttock pain. Musculoskeletal problems are the most common extraintestinal manifestation, affecting up to half of patients. Axial spondyloarthritis occurs in one to twenty-six percent of IBD patients depending on definition, more often in men, independent of bowel activity. It can progress to ankylosing spondylitis with sacroiliitis and, in advanced cases, a fused, bamboo-like vertebral column.

18:08A genetic marker raises his risk but doesn't make the diagnosis. Human leukocyte antigen B27, HLA-B27, raises the risk of ankylosing spondylitis in IBD about twentyfold. But most carriers never develop it, and fewer than half of IBD patients carry it, so it's a risk marker, not a diagnosis.

18:29His eye is the urgent part. Anterior uveitis, or iritis, causes eye pain, light sensitivity, blurred vision, and redness around the iris called ciliary flush. It's independent of the bowel, needs immediate ophthalmology referral, and is treated with topical and systemic steroids, with biologics when refractory. Pain, light sensitivity, and any loss of vision mean same-day ophthalmology, and he goes today.

18:58The other eye problems differ in urgency, and the symptoms tell them apart. Episcleritis, the most common IBD eye problem, causes redness without visual change, tracks bowel activity, and is treated with topical steroids plus bowel control. Scleritis causes deep eye pain and threatens vision, needs immediate referral, and is treated systemically.

19:20His axial disease is treated with physical therapy, NSAIDs used cautiously because they can trigger IBD flares, and biologics. Infliximab, adalimumab, golimumab, and certolizumab are effective for ankylosing spondylitis. Two drugs used for ankylosing spondylitis are avoided in IBD: etanercept, which doesn't work in IBD, and interleukin seventeen, IL-17, inhibitors, which may worsen it. Colectomy doesn't improve axial arthritis, though it improves the type one peripheral arthritis of ulcerative colitis.

19:55His current drug explains why his gut is quiet while the rest flares. Vedolizumab blocks lymphocyte traffic into the gut only, which makes it safe but gives it minimal effect outside the gut. When extraintestinal disease is prominent, an anti-TNF drug is preferred, and anti-TNF drugs also treat refractory uveitis. He switches to adalimumab after negative tuberculosis and hepatitis B screening and starts physical therapy. His eye improves with steroid drops, and over three months his morning stiffness eases.

20:29Had his joint pain been peripheral, its pattern would have decided whether bowel control was enough. Type one is pauciarticular, fewer than five large joints such as knees and ankles. It parallels bowel activity, comes with other extraintestinal problems, and is self-limited, so it's treated by treating the bowel, plus short courses of cautious NSAIDs or sulfasalazine. Type two is polyarticular, in the small joints such as the knuckles. It's independent of the bowel, associated with uveitis but not other extraintestinal problems, and chronic, so it's treated with sulfasalazine, methotrexate, or an anti-TNF drug or a Janus kinase, JAK, inhibitor.

21:11Of the independent manifestations, primary sclerosing cholangitis matters most to the gastroenterologist, because it changes surveillance. It complicates about five percent of patients with ulcerative colitis, and less often Crohn disease, and about three-quarters of patients with it have ulcerative colitis. It favors extensive colitis, is independent of bowel activity, can precede or follow bowel symptoms by years, and mandates yearly surveillance colonoscopy from its diagnosis.

21:40The liver and pancreas have other IBD links, mostly from drugs and bile salts. Gallstones are more common in ileal Crohn disease because of bile salt loss. Thiopurines and methotrexate can cause drug-induced hepatitis, and autoimmune hepatitis can overlap. Pancreatitis can come from azathioprine, six-mercaptopurine, or five-aminosalicylic acid, five-ASA, from gallstones, from autoimmune disease, or rarely from granulomatous Crohn involvement of the pancreas.

22:12The seventh patient shows that the skin has its own patterns, and that one of them is made worse by care. A forty-four-year-old woman with ulcerative colitis had a shin pustule that broke down into a painful ulcer with violaceous, undermined edges, and it worsened after a nurse debrided it. That's pyoderma gangrenosum. The worsening after trauma is pathergy, also seen in Behcet disease. It favors the legs and the skin around a stoma, and because trauma worsens it, it isn't debrided.

22:43Her treatment depends on how extensive it is. Limited lesions get high-potency topical steroids or topical tacrolimus. More extensive disease gets oral prednisone, dapsone, cyclosporine or tacrolimus, or azathioprine. Refractory disease gets an anti-TNF drug or an inhibitor of interleukins twelve and twenty-three.

23:04The other skin problems differ in how they relate to the bowel. Erythema nodosum is the most common IBD skin problem, in ten to twenty percent. It's deep, tender, red nodules on the front of the lower legs, parallels bowel activity, and clears when the bowel is treated. Sweet syndrome is rare, with fever and tender red plaques from neutrophil infiltrates, and it's treated with steroids. Metastatic Crohn disease is skin nodules with non-caseating granulomas far from the gut, often on the abdominal wall, limbs, or vulva, and it's treated with systemic therapy and metronidazole.

23:38The eighth patient shows how the kidney is affected through the gut. A thirty-eight-year-old man with ileal Crohn disease and an intact colon has a calcium oxalate stone. His diseased ileum malabsorbs fat. The unabsorbed fatty acids bind calcium in the gut, oxalate is left free, and the colon absorbs it, so urinary oxalate rises. That's enteric hyperoxaluria, and it needs both steatorrhea and an intact colon. The other kidney problems in IBD are secondary amyloid A, AA, amyloidosis, from deposits of serum amyloid A protein, presenting with proteinuria, and interstitial nephritis from five-ASA.

24:21The last patient brings the whole picture together before a new drug. A twenty-nine-year-old woman has ileal Crohn disease and had forty centimeters of terminal ileum resected three years ago. She's on methotrexate and about to start an anti-TNF drug for a flare. She and her partner want to conceive within the year. She's tired. Her hemoglobin is nine point six with a low ferritin, her B12 is low, and her vitamin D is low. She's never had chickenpox or the varicella vaccine.

24:49Her fatigue has a cause in her blood counts. She has iron deficiency anemia and B12 and vitamin D deficiency, and each follows where her disease is. Iron deficiency anemia is common in both diseases, from chronic blood loss in ulcerative colitis and from impaired absorption plus inflammation in Crohn disease. Oral iron is poorly tolerated during active inflammation, so intravenous iron, as iron sucrose, ferric carboxymaltose, or ferric derisomaltose, is often needed, as it is in her flare.

25:19Her B12 deficiency follows her ileal disease and resection, because B12 is absorbed only in the terminal ileum. So she needs parenteral B12, one thousand micrograms intramuscularly weekly for four weeks, then monthly. Folate deficiency complicates sulfasalazine and methotrexate, which is why folic acid is built into both regimens. Vitamin D deficiency contributes to bone disease and is supplemented.

25:45Other deficiencies depend on how much bowel is affected. Zinc deficiency from severe diarrhea causes dermatitis and altered taste. Extensive small bowel disease or resection causes fat-soluble vitamin loss. Her forty centimeters is under the one hundred centimeter threshold, so any diarrhea from the resection would be bile acid diarrhea. A resection over one hundred centimeters would make it fatty and make her fat-soluble vitamins a priority. She gets intravenous iron, B12 injections, and vitamin D.

26:14Her bones are protected next, because IBD and steroids both thin them. Calcium and vitamin D are given, and a bone density scan by dual-energy x-ray absorptiometry is indicated with prolonged corticosteroids, in postmenopausal women, in men over fifty, and in anyone with a low-trauma fracture. A T-score below minus two point five means a bisphosphonate, which is also considered with prolonged steroid exposure. She has limited steroid exposure and no fracture, so she gets calcium and vitamin D now.

26:45Nutrition support is kept for specific situations. Enteral and parenteral nutrition are reserved for severe undernutrition, except in children with Crohn disease, where exclusive enteral nutrition is a primary therapy. Short bowel syndrome may need specialized nutrition and teduglutide, a glucagon-like peptide two, GLP-2, analog.

27:06Her vaccines have to be settled before the anti-TNF drug starts, and what matters is whether each is live. Live vaccines are contraindicated during biologic therapy and for three months after stopping it, so they're given at least four weeks before a biologic starts. The live vaccines are measles-mumps-rubella, varicella, yellow fever, oral typhoid, intranasal influenza, and the old live shingles vaccine, largely replaced by the recombinant one.

27:32She's not immune to varicella, so she needs the varicella vaccine at least four weeks before her anti-TNF drug. That's a real delay in a flare, which is why vaccine status deserves attention well before a biologic is needed.

27:46Inactivated vaccines are safe during biologic therapy and recommended. They're injected influenza yearly; pneumococcal conjugate vaccine, PCV, fifteen or twenty, followed by pneumococcal polysaccharide vaccine, PPSV, twenty-three per current schedules; recombinant zoster for adults fifty and older, or nineteen and older on immunosuppressants, which includes her; human papillomavirus, HPV, through age forty-five; hepatitis A and B; meningococcal vaccine, especially before complement inhibitor therapy; tetanus, diphtheria, and pertussis, Tdap; and coronavirus disease, COVID-19, vaccination with boosters.

28:23Two of those vaccines matter more with specific drugs. Hepatitis B vaccination is critical because biologics raise the risk of reactivation, so non-immune patients are vaccinated after screening. Before a JAK inhibitor, the recombinant zoster vaccine is given regardless of age, because shingles reactivates in one and a half to five percent of patients on JAK therapy.

28:44Her pregnancy plan starts from one fact. Disease activity at conception is the single best predictor of pregnancy outcome, and active disease threatens a pregnancy more than most medications. A patient who stops her drugs to protect the baby and then flares has put the pregnancy at greater risk. So the order is remission first, then conception, on drugs safe to continue.

29:05Most IBD medications continue through pregnancy, with a few exceptions that affect her. Methotrexate is teratogenic and stops three to six months before conception in either parent. Tofacitinib and upadacitinib are avoided in pregnancy, which also makes an anti-TNF drug a better fit than a JAK inhibitor for her flare. Sulfasalazine continues with mandatory folic acid. Anti-TNF drugs, vedolizumab, and ustekinumab have the most reassuring pregnancy data.

29:34Her drug choice also affects her baby's vaccines. The anti-TNF drugs other than certolizumab, plus vedolizumab and ustekinumab, cross the placenta in the third trimester. So an exposed infant carries the drug for months and shouldn't receive live vaccines until it clears, typically by six months for anti-TNF and interleukin twenty-three drugs. The live vaccine that matters is rotavirus, given in the first months of life. Certolizumab pegol crosses the placenta minimally, so it's sometimes preferred in late pregnancy, and an exposed infant can receive rotavirus on schedule.

30:09Her year follows that plan. She receives the varicella vaccine and her inactivated vaccines, including hepatitis B, and stops methotrexate. Her tuberculosis and hepatitis B screening is negative, and she starts adalimumab five weeks after the varicella vaccine. Six months later she's in remission, with methotrexate well behind her, and she and her partner begin trying to conceive. She stays on adalimumab through pregnancy, and her baby's rotavirus vaccine is deferred.

30:37Her partner's drugs matter too. He's a thirty-one-year-old man with ulcerative colitis who takes sulfasalazine. It continues around pregnancy, but it causes reversible low sperm counts in about sixty percent of men, so it's raised now rather than after a year of trying. If he took methotrexate, he'd stop it three to six months before they try.

30:57Here are the traps the boards set in these patients. Pouchitis isn't treated without endoscopy and biopsies, and C. difficile and CMV aren't overlooked. Bleeding from the cuff isn't pouchitis. Pre-pouch ileitis, fistulas, or granulomas point to Crohn-like disease. Refractory pouchitis isn't escalated before infection, ischemia, NSAIDs, and celiac disease are rechecked. Vedolizumab isn't approved for pouchitis in the United States. And irritable pouch isn't treated with antibiotics.

31:30The surveillance traps follow. The surveillance clock starts at symptom onset, not diagnosis, and primary sclerosing cholangitis doesn't wait eight years. Surveillance isn't done during a flare. Random biopsies aren't a substitute for chromoendoscopy. The term DALM is retired, and a second pathologist confirms every dysplasia read. And invisible high-grade dysplasia goes to surgery, not surveillance.

31:57The extraintestinal traps come next. Axial disease, uveitis, and primary sclerosing cholangitis don't settle with the bowel. Colectomy won't fix back pain. IL-17 inhibitors and etanercept aren't used in IBD. Vedolizumab isn't relied on for prominent extraintestinal disease. Anterior uveitis and scleritis need urgent referral. Pyoderma gangrenosum isn't debrided. And ileal Crohn disease with an intact colon causes oxalate stones.

32:29The whole-patient traps close the list. Oral iron isn't used in active inflammation, and oral B12 isn't used after ileal resection. A live vaccine isn't given on a biologic or less than four weeks before one. Recombinant zoster isn't skipped before a JAK inhibitor. A biologic isn't stopped in pregnancy to let the disease flare. Methotrexate and JAK inhibitors don't continue while trying to conceive, and the father's methotrexate counts too. And an infant exposed to an anti-TNF drug other than certolizumab doesn't get rotavirus on schedule.

33:03So, start to finish. Inflammation after a pouch is classified by location and course. Acute pouchitis gets ciprofloxacin or metronidazole after endoscopy excludes infection, cuffitis, and Crohn-like disease. Chronic pouchitis is antibiotic-dependent or antibiotic-refractory, and refractory disease is escalated to a biologic, with vedolizumab best supported, after secondary causes are excluded.

33:30Cuffitis is treated topically, Crohn-like disease is treated like Crohn disease, and a normal pouch with symptoms is irritable pouch. Survey the cuff and pouch separately, yearly in high-risk patients.

33:43Colitis surveillance starts eight to ten years after symptoms in extensive disease, and at diagnosis in primary sclerosing cholangitis, using high-definition chromoendoscopy in remission. Resect visible resectable dysplasia. Send non-resectable visible dysplasia and invisible high-grade dysplasia to proctocolectomy, and confirm every read with a second pathologist.

34:07Classify extraintestinal problems by whether they track the bowel. Anti-TNF drugs treat axial disease and uveitis, and vedolizumab doesn't reach beyond the gut. Uveitis and scleritis need urgent ophthalmology, pyoderma isn't debrided, and ileal Crohn disease with an intact colon causes oxalate stones.

34:27Replace what the disease takes, by location. Give live vaccines at least four weeks before immunosuppression and inactivated vaccines throughout. In pregnancy, active disease is the main risk. Aim for remission at conception, stop methotrexate in either parent three to six months ahead, avoid JAK inhibitors, continue most others, and delay live vaccines in an infant exposed to a biologic, except certolizumab.

34:55That completes the Inflammatory Bowel Disease chapter. The next chapter is colorectal cancer, polyps, and diverticular disease.

35:04For 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.