Inflammatory Bowel Disease: Inflammatory Bowel Disease: Crohn Disease Therapy

0:00Welcome to Board Pearls. This is episode two of three of the Inflammatory Bowel Disease chapter, in the Colorectal and Pelvic Floor Disorders module. This episode is Crohn disease and the advanced therapies. A newly diagnosed young woman shows how Crohn disease is classified, which features predict an aggressive course, and how thiopurines are started safely, and an older man with mild ileal disease shows when gentler therapy is enough. A man with ulcerative colitis who needs an advanced therapy but has heart failure and a prior clot shows what each drug class blocks and which comorbidities rule a class out. A woman with colitis, swollen knees, and uveitis shows why extraintestinal disease changes the choice, and a man who wants a fast oral drug shows the Janus kinase inhibitors. A man with a perianal abscess and fistula shows why the abscess is drained before any biologic. A woman with a long stricture shows when to dilate or operate and how to prevent recurrence after surgery, and an older man shows why everyone has a colonoscopy after resection.

1:04Here's the first patient. A nineteen-year-old woman has had right lower abdominal pain, diarrhea, and eighteen pounds of weight loss over four months. She smokes half a pack a day. Ileocolonoscopy shows deep ulcers in the terminal ileum, with a normal colon and rectum. Magnetic resonance, MR, enterography shows thirty centimeters of inflamed ileum, without a stricture, fistula, or abscess. She has no perianal disease. Her C-reactive protein, CRP, and calprotectin are high. Last week she needed prednisone in the emergency department for pain and vomiting.

1:40She has Crohn disease of the terminal ileum. It's transmural, segmental inflammation, and her normal colon and rectum separate it from ulcerative colitis. In Crohn disease, where the disease sits and how it behaves decide how hard to treat, because the same immune response can cause an ileal stricture in one patient, diffuse colitis in another, and complex perianal fistulas in a third. So she's classified first, with the Montreal system.

2:06The Montreal system has three parts. Montreal A is age at diagnosis: A1 under seventeen, A2 seventeen to forty, and A3 over forty. Onset under seventeen is itself a risk marker, because younger patients accumulate more years of disease and tend toward extensive disease and complications. Montreal L is location: L1 the terminal ileum, L2 colon only, L3 ileocolonic, and L4 upper gastrointestinal, GI, involvement from the esophagus to the jejunum, added as a modifier alongside another location.

2:45Location also explains how she was diagnosed. About seventy percent of patients have terminal ileal disease, L1 or L3, which is why ileocolonoscopy with ileal intubation is the key diagnostic test. Montreal B is behavior: B1 inflammatory, B2 stricturing, and B3 penetrating, with fistulas or abscess, and a lower-case p is added for perianal disease. She's A2, L1, B1.

3:15Her behavior today won't stay fixed without treatment. Seventy to eighty percent of patients begin with inflammatory disease, but within ten to twenty years about half of them have moved to stricturing or penetrating disease. Transmural inflammation scars into strictures or burrows into fistulas and abscesses. So the goal of her treatment is to prevent that progression by reaching and holding mucosal healing.

3:39How hard to push depends on how aggressive her disease is likely to be. That decides between step-up therapy, starting mild and escalating, and top-down therapy, starting a biologic early. The features predicting an aggressive course are young age at diagnosis, under thirty and especially under seventeen; deep ulcers; perianal disease; smoking; needing steroids at presentation; extensive small bowel involvement; stricturing or penetrating behavior at diagnosis; a prior bowel resection; and high titers of anti-Saccharomyces cerevisiae antibody, ASCA. She's nineteen, with deep ulcers, smoking, steroids at presentation, and thirty centimeters of small bowel disease.

4:18With several high-risk features, step-up approaches lead to more progression to surgery and complications, so a biologic starts early. In biologic-naive patients with moderate to severe Crohn disease, infliximab with azathioprine works better than either alone. So she's offered that combination, after tuberculosis and hepatitis B screening. Smoking cessation is part of her treatment, because smoking accelerates Crohn disease, raises the rate of strictures and fistulas, and worsens recurrence after surgery.

4:49She's already on prednisone, and the steroid plan depends on where the disease is. For mild to moderate disease of the ileum or right colon, budesonide nine milligrams a day is the preferred induction steroid. Eighty to ninety percent of it is cleared on first pass through the liver, so the terminal ileum and right colon see a high dose while the body sees little. It beats mesalamine four grams a day and is about as good as prednisolone for mild to moderate ileocecal disease.

5:18Budesonide has two limits that follow from its design. It doesn't work for left-sided colonic Crohn disease, because its controlled-release formulation doesn't reach the distal colon. And six milligrams a day doesn't maintain remission beyond about six months, so it can't stand in for an immunomodulator or biologic.

5:36Her disease is extensive enough that systemic steroids were needed. Extensive or severe disease gets prednisone forty to sixty milligrams a day, tapered over six to eight weeks. Steroid dependence, a flare whenever the dose drops below ten milligrams, and steroid refractoriness both mean escalation, because long-term steroids in Crohn disease are linked to infection, bone disease, and higher mortality.

6:02Five-aminosalicylic acid, five-ASA, plays almost no part in her plan. Sulfasalazine has a small benefit in mild colonic Crohn disease, through its sulfapyridine part acting on the colon, and mesalamine has even less. Neither works for small bowel disease, and neither is used for maintenance.

6:20Before her azathioprine starts, it has to be made safe. Azathioprine, two to two and a half milligrams per kilogram a day, and six-mercaptopurine, one to one and a half, work through six-thioguanine nucleotides, which stop proliferating lymphocytes. Onset takes eight to twelve weeks, so thiopurines maintain remission after another drug has induced it, and they aren't used for induction.

6:45A genetic test comes before the first dose. Thiopurine methyltransferase, TPMT, testing, by genotype or activity, is mandatory, because low activity builds up cytotoxic metabolites and causes severe marrow suppression at standard doses. Absent activity means no drug, and intermediate activity means half the dose. NUDT15 testing is added in patients of Asian, Hispanic, or Native American ancestry, because those variants also predict toxicity and a TPMT test doesn't detect them.

7:20The side effects explain the monitoring. They're marrow suppression and liver injury; early idiosyncratic pancreatitis, which means stopping the drug; nausea and infection; non-melanoma skin cancer, which calls for sun protection; a modest absolute rise in non-Hodgkin lymphoma; and the rare hepatosplenic T-cell lymphoma in young men on a thiopurine with an anti-TNF drug. A blood count and liver tests every three to four months are required.

7:46One interaction can be used on purpose. Allopurinol shifts thiopurine metabolism toward six-thioguanine and away from six-methylmercaptopurine. So a low-dose thiopurine with allopurinol can turn a non-responder into a responder, under expert supervision. Her TPMT activity is normal, and she starts infliximab and azathioprine while her prednisone is tapered.

8:10Her response is judged by her mucosa, not her symptoms. The Crohn Disease Activity Index, CDAI, defines remission under one hundred fifty, mild disease one hundred fifty to two hundred twenty, moderate to severe two hundred twenty to four hundred fifty, and severe over four hundred fifty. The Harvey-Bradshaw Index is a simpler clinical score. But the CDAI correlates poorly with the mucosa, and an ulcerated ileum in a patient who feels well still goes on to stricture.

8:39So treat-to-target uses objective markers. They're endoscopic healing, fecal calprotectin, and MR enterography, with endoscopic scores such as the Simple Endoscopic Score for Crohn Disease, SES-CD, and the Crohn Disease Endoscopic Index of Severity, CDEIS.

8:57The second patient shows that low-risk disease can start gently. A sixty-two-year-old man who doesn't smoke has fifteen centimeters of mildly inflamed terminal ileum with shallow ulcers, a normal CRP, and no perianal disease. Older age, limited ileal inflammatory disease, no smoking, a normal CRP, and mild endoscopic findings put him in the low-risk group. He can start with budesonide induction and add an immunomodulator or biologic only if his disease recurs or progresses. The risk group isn't fixed, and if he ever declares a stricture or a perianal fistula, he moves into the high-risk group.

9:36The third patient needs an advanced therapy, and his other illnesses narrow the options. A fifty-eight-year-old man has moderate to severe ulcerative colitis. He's failed mesalamine and can't get below fifteen milligrams of prednisone without bleeding again. He has heart failure, New York Heart Association class three, and he had a deep vein thrombosis two years ago. He has no joint, skin, or eye symptoms and has never had a biologic.

10:04He has steroid-dependent ulcerative colitis, so he needs an advanced therapy, and his heart and his clot decide which. Choosing starts with what each class blocks, because the target predicts both strengths and risks. Anti-tumor necrosis factor, anti-TNF, drugs block TNF-alpha. Vedolizumab blocks alpha-four beta-seven integrin, which steers lymphocytes into the gut. Ustekinumab blocks interleukins twelve and twenty-three, IL-12 and IL-23, together, while risankizumab and mirikizumab block IL-23 alone.

10:38The two oral classes act differently. Janus kinase, JAK, inhibitors block signaling inside the cell, downstream of many cytokine receptors. Sphingosine-1-phosphate, S1P, receptor modulators trap lymphocytes in lymph nodes. Anti-TNF drugs remain the broadly effective foundation, the newer agents match or beat them in particular settings, and the classes are told apart mostly by safety.

11:05The anti-TNF drugs differ mainly in form and approval. Infliximab is a chimeric antibody given intravenously at five milligrams per kilogram at weeks zero, two, and six, then every eight weeks. It's increased to ten milligrams per kilogram or given every four to six weeks for an inadequate response. Adalimumab is fully human and subcutaneous: one hundred sixty milligrams at week zero, eighty at week two, then forty every two weeks. Biosimilars of both are clinically equivalent.

11:42Two anti-TNF drugs are each approved for only one disease, because their trials in the other failed. Certolizumab pegol, a pegylated antibody fragment, is given subcutaneously at four hundred milligrams at weeks zero, two, and four, then every four weeks, and it's approved for Crohn disease only. Golimumab is given subcutaneously at two hundred milligrams at week zero, one hundred at week two, then every four weeks, and it's approved for ulcerative colitis only.

12:10Any anti-TNF drug needs screening first, because reactivation of latent infection can be fatal. Tuberculosis screening uses an interferon-gamma release assay, or a purified protein derivative, PPD, skin test with a chest film. Hepatitis B screening uses surface antigen, core antibody, and surface antibody. Latent tuberculosis gets isoniazid for at least a month before starting, and hepatitis B gets entecavir or tenofovir alongside. Hepatitis C is screened but doesn't rule the drugs out.

12:44His comorbidities now rule classes out. Anti-TNF drugs carry serious bacterial infection, including Listeria and Legionella, and invasive fungal infection, such as histoplasmosis, coccidioidomycosis, and blastomycosis in endemic areas. They also carry drug-induced lupus, demyelinating disease, worsening heart failure, and lymphoma. They're avoided in multiple sclerosis and in class three or four heart failure, which rules them out for him.

13:12The JAK inhibitors are ruled out for him too. They carry a boxed warning for serious infection, especially shingles, major adverse cardiovascular events, malignancy, thrombosis, and mortality, from post-marketing data on tofacitinib in rheumatoid arthritis. So they're avoided with clot risk and in older patients with heart disease, and he has both. S1P modulators exclude severe heart failure, so they're out as well.

13:38That leaves a gut-selective drug or an IL-23 drug. Vedolizumab blocks alpha-four beta-seven, which carries lymphocytes into the gut mucosa by binding mucosal addressin cell adhesion molecule one, MAdCAM-1. So systemic immunosuppression is minimal, and trial safety was close to placebo. Natalizumab blocks alpha-four broadly, in the gut and central nervous system, and causes progressive multifocal leukoencephalopathy. No such cases have been reported in otherwise healthy inflammatory bowel disease, IBD, patients on vedolizumab.

14:15Vedolizumab's strengths and weaknesses both follow from its target. It works in both diseases, and in a head-to-head trial in moderate to severe ulcerative colitis it beat adalimumab at one year. It's three hundred milligrams intravenously at weeks zero, two, and six, then every eight weeks, with a subcutaneous maintenance form. Response often takes six to ten weeks, so it isn't the first choice in acute severe disease. In Crohn disease it may work less well in the small bowel, so it isn't the first choice for severe small bowel disease either. And it has little effect on joint, skin, or eye disease.

14:51None of those weaknesses applies to him. He starts vedolizumab after negative screening, and his prednisone is tapered over three months.

15:00Ustekinumab would also have been reasonable. It blocks the p40 subunit shared by IL-12 and IL-23 and is approved for both diseases. It's given as a weight-based intravenous induction, two hundred sixty milligrams under fifty-five kilograms, three hundred ninety for fifty-five to eighty-five, and five hundred twenty above eighty-five, then ninety milligrams subcutaneously every eight weeks. It works after anti-TNF failure, has low immunogenicity, and has no boxed warning.

15:28The newer IL-23 drugs are more selective. Risankizumab and mirikizumab block only the p19 subunit of IL-23, preserving IL-12 signaling, which may improve the infection profile. Both are approved for both diseases, with intravenous induction and subcutaneous maintenance, and mirikizumab gained its Crohn approval in January twenty twenty-five. IL-23 signaling is why these drugs work across both diseases.

15:57The fourth patient shows how extraintestinal disease changes the choice. A thirty-year-old woman with moderate to severe ulcerative colitis has swollen knees and recurrent anterior uveitis. She needs an anti-TNF drug, because vedolizumab won't touch her joints or eyes. Her interferon-gamma release assay is positive with a clear chest film, so she has latent tuberculosis and takes isoniazid for a month before infliximab.

16:23The fifth patient fits the class the third patient couldn't take. A thirty-four-year-old man with ulcerative colitis has no cardiac or clotting history, has failed infliximab, and wants a fast oral drug. He fits a JAK inhibitor, which works within days to weeks, orally, and after anti-TNF failure. Tofacitinib blocks JAK one, two, and three and is approved for ulcerative colitis. It's ten milligrams twice daily for eight to sixteen weeks, then five milligrams twice daily, with escalation back to ten for sustained response in patients without clot risk.

16:59The other JAK inhibitors are more selective. Upadacitinib is JAK one-selective and approved for both diseases: forty-five milligrams daily for eight weeks, then fifteen or thirty. Filgotinib is another JAK one inhibitor, with ulcerative colitis approval outside the United States. The recombinant zoster vaccine comes first, because shingles reactivates in one and a half to five percent of patients on this class. JAK inhibitors raise lipids, cause anemia and lymphopenia, and can raise creatine phosphokinase, CPK, so lipids, blood counts, and CPK are monitored.

17:39The S1P modulators are oral drugs for ulcerative colitis, and their effect on the heart shapes how they're started. Ozanimod internalizes the S1P one receptor, trapping lymphocytes in nodes and lowering blood lymphocyte counts by design. It's titrated over seven days, from zero point two three milligrams to zero point four six, then zero point nine two from day eight. It needs a baseline electrocardiogram, ECG, and is avoided with second- or third-degree heart block, symptomatic bradycardia, a recent heart attack, or severe heart failure.

18:12Its other screening follows its other risks. It needs a baseline eye exam for macular edema, liver tests, varicella antibody status with vaccination if seronegative, and screening for active infection, because it raises infection risk, including shingles. Etrasimod is a related drug with ulcerative colitis approval.

18:32Pulling the choice together, safety decides first, then efficacy among what's left. Network meta-analyses suggest infliximab and upadacitinib lead for ulcerative colitis induction, and ustekinumab and adalimumab have similar results in Crohn disease. Prior failures, whether the drug is oral, injected, or infused, insurance, and extraintestinal disease matter too. For a patient hoping to conceive, anti-TNF drugs, vedolizumab, and ustekinumab have the most reassuring pregnancy data, and JAK inhibitors are avoided.

19:06The sixth patient has Crohn disease that has reached the perianal tissues. A twenty-six-year-old man with Crohn disease of the colon and rectum, diagnosed two years ago, has had throbbing perianal pain for five days and a fever of thirty-eight point four. An opening beside the anus drains pus, with a tender, warm swelling next to it. He smokes. He's been on mesalamine only, because his bowel symptoms were mild. His gastroenterologist wants to start infliximab today.

19:32He has perianal Crohn disease with a fistula and, from the fever and the warm swelling, an abscess. Transmural inflammation near the anus tunnels into the surrounding tissue. It produces fistulas, usually trans-sphincteric or complex with several branches, plus abscesses, fissures, and skin tags, and untreated, scarring of the sphincters ends in incontinence.

19:55His colonic disease made this more likely. Perianal disease develops in about twenty-five to thirty-five percent of Crohn patients, more often with colonic and rectal disease, as he has. It adds a p to his Montreal behavior and, with smoking, puts him in the high-risk group, so mesalamine was never going to be enough. His treatment has a surgical part for the sepsis and the tracts and a medical part for the inflammation.

20:19The anatomy is defined first, with pelvic magnetic resonance imaging, MRI. It shows whether each tract is simple, a single tract, or complex, with branches; where any abscess sits; and how the tracts relate to the sphincters. It's preferred over endoanal ultrasound because it separates branching tracts, and a tract that isn't found isn't drained. His MRI shows a trans-sphincteric fistula with a second branch, a complex fistula, and a three-centimeter abscess beside it.

20:49So the infliximab waits. A biologic is never started before an abscess is drained, because suppressing the immune system around a closed collection of pus can turn a local infection into sepsis. The sequence is fixed: pelvic MRI or endoscopic ultrasound to define the anatomy; examination under anesthesia by a colorectal surgeon, with drainage and placement of setons; then dose-optimized anti-TNF therapy.

21:17A seton is what makes the immunosuppression safe. It's a non-absorbable suture threaded through the fistula tract and left there, keeping it open and draining so pus can't build up again. He needs two, one through each branch.

21:33Once he's drained, the medical part heals the fistula. It pairs antibiotics, metronidazole two hundred fifty to five hundred milligrams three times daily, with or without ciprofloxacin five hundred milligrams twice daily, for four to twelve weeks, with an anti-TNF drug. Antibiotics alone aren't the treatment. Infliximab has the strongest evidence for fistula healing. In perianal disease it's dose-optimized, often starting at ten milligrams per kilogram, with the interval shortened if needed, rather than escalating only after the standard dose fails. Adalimumab and certolizumab are alternatives, and vedolizumab and ustekinumab have less robust perianal data.

22:13Adding an immunomodulator improves outcomes, and his age and sex decide which. In a young man, a thiopurine with an anti-TNF drug compounds lymphoma risk, including hepatosplenic T-cell lymphoma, so methotrexate is preferred. It's twenty-five milligrams weekly by injection for induction and fifteen weekly for maintenance, with folic acid one milligram daily to reduce mouth sores and low blood counts. It's injected because oral absorption from inflamed bowel is variable.

22:42Methotrexate has its own cautions and one extra benefit. It's teratogenic and contraindicated in men or women planning conception within three to six months. Cumulative liver injury is a concern with obesity or diabetes, and pneumonitis is rare but serious. It also treats the peripheral arthritis of IBD, which makes it attractive when that's present.

23:04The surgeon drains his abscess and places two setons. He starts metronidazole and ciprofloxacin, his screening is negative, and he starts infliximab ten milligrams per kilogram with weekly methotrexate, plus smoking cessation support. Setons are removed once medical therapy has reduced the inflammation, usually at three to six months, with the biologic continued, because pulling them too early lets an inflamed tract close over and form a new abscess. Three months later his drainage has stopped, a repeat MRI shows less inflammation, and the setons come out.

23:36If his disease had failed all of that, further options exist. Mesenchymal stem cells, darvadstrocel, are injected into complex fistulas, approved in Europe and increasingly used in the United States. Severe disease that fails everything may need diversion, a loop ileostomy or end colostomy, and finally proctectomy.

23:57The seventh patient's Crohn disease has scarred instead of tunneling. A thirty-five-year-old woman has had ileal Crohn disease for twelve years. For three months she's had cramping pain and bloating after meals, and she's vomited twice. She smokes a pack a day and has never had surgery. MR enterography shows a twelve-centimeter stricture of the terminal ileum that runs across the ileocecal valve into the cecum, with dilated bowel above it, little enhancement to suggest active inflammation, and no abscess or fistula.

24:26She has stricturing Crohn disease with partial small bowel obstruction. She's moved from Montreal B1 to B2, the natural history in action, which puts her in the high-risk group. What to do depends on how much of the stricture is inflammation and how much is scar. Many strictures are mixed, and active inflammation around a stricture is treated medically before any dilation or surgery, because medical therapy alone may open a partly inflammatory stricture.

24:54Her MR enterography answers that question. A thick, brightly enhancing wall points to inflammation and medical therapy first. Hers shows little enhancement, so it's mostly fibrotic, and drugs won't open it. MR enterography also rules out an abscess, fistula, or active inflammation, each of which would close off a mechanical option.

25:14A fibrotic stricture needs a mechanical fix, and dilation is the least invasive. Endoscopic balloon dilation suits short, accessible strictures, typically under four to five centimeters, without active inflammation, fistula, or dysplasia. Its response rate is reasonable, but about half recur within a year. At twelve centimeters, hers is far too long.

25:36That leaves surgery, and the choice is to save the bowel or remove it. Crohn disease recurs, and repeated resections risk short bowel syndrome, so short fibrotic strictures are treated with stricturoplasty, which widens the segment without removing it. Heineke-Mikulicz, a lengthwise incision closed crosswise, suits strictures up to about ten centimeters. Finney, a side-to-side join, suits strictures up to about twenty-five. Michelassi, an isoperistaltic side-to-side stricturoplasty, is for very long strictures.

26:09Stricturoplasty has firm limits. It isn't done with active inflammation at the stricture, an abscess, dysplasia, or cancer, or for a colonic stricture, where resection is preferred. Her ileal length might have suited a Finney, but her stricture crosses the valve into the cecum, so the surgeon performs an ileocolonic resection.

26:26Her surgery isn't the end, because Crohn disease comes back. After ileocolonic resection without preventive therapy, recurrence is nearly universal. Endoscopic recurrence is seen in seventy to ninety percent at one year, at the new terminal ileum at the join, the neoterminal ileum. Symptoms lag well behind, reaching about sixty percent of patients by ten years, and surgical recurrence rises over decades. So waiting for symptoms means treating recurrence that has been building for a long time.

26:56Whether she gets preventive therapy is decided at surgery by risk. High-risk features are smoking, age under thirty, fistulizing or penetrating disease, two or more prior resections, perianal disease, and a short interval since the last surgery, and these patients start preventive therapy within four weeks. Low-risk patients are older, at a first operation for a short fibrotic stricture under ten to twenty centimeters, non-smokers, with disease for more than ten years, and they can be observed.

27:29She's thirty-five, at her first operation, with twelve years of disease and a fibrotic stricture, but she smokes a pack a day, which makes her high risk. Stopping smoking is the single modifiable factor that meaningfully reduces postoperative recurrence. An anti-TNF drug started within four weeks of surgery is the most effective prophylaxis, with thiopurines and metronidazole as alternatives. She joins a cessation program, her screening is negative, and she starts adalimumab three weeks after surgery.

27:59Everyone, whatever the risk group, has ileocolonoscopy six to twelve months after surgery, graded with the Rutgeerts score. I-zero is no lesions. I-one is fewer than five aphthous lesions. I-two is five or more lesions in the neoterminal ileum, or lesions confined to the anastomosis. I-three is diffuse aphthous ileitis with diffusely inflamed mucosa. I-four is diffuse inflammation with larger ulcers, nodules, or stricturing.

28:27The score decides what happens next. Rutgeerts i-two or higher predicts clinical recurrence and is the point to escalate therapy, without waiting for i-three, i-four, or symptoms. Her colonoscopy at nine months shows two small aphthous lesions, i-one. She's stopped smoking, feels well, and stays on adalimumab.

28:47The last patient shows why the colonoscopy is universal. A sixty-four-year-old man who has never smoked, with twenty years of Crohn disease, had his first resection for an eight-centimeter fibrotic ileal stricture, with no perianal or penetrating disease. He's low risk and observed without preventive therapy. He feels well, but his colonoscopy at seven months shows more than five aphthous lesions in the neoterminal ileum, Rutgeerts i-two, so he starts an anti-TNF drug before any symptoms.

29:13Here are the traps the boards set in these patients. Not every new patient is treated the same, and a young patient with deep ulcers and early steroid need isn't stepped up slowly. Budesonide isn't used for left-sided colonic disease or for maintenance. A steroid-dependent patient isn't left on prednisone. Mesalamine isn't used for small bowel Crohn disease. A thiopurine isn't started without TPMT testing, and NUDT15 isn't skipped in higher-risk ancestries. Thiopurines don't induce remission. And response isn't judged by the CDAI alone.

29:46The advanced therapy traps follow. An anti-TNF drug isn't started without tuberculosis and hepatitis B screening. Anti-TNF drugs aren't given in class three or four heart failure or multiple sclerosis. A JAK inhibitor isn't given with heart disease or a clot history, or without the zoster vaccine. Vedolizumab isn't the choice for acute severe disease or prominent extraintestinal disease. Ozanimod isn't started without an ECG and an eye exam. And certolizumab isn't used for ulcerative colitis, or golimumab for Crohn disease.

30:24The perianal traps come next. A biologic isn't started before an abscess is drained. Endoanal ultrasound isn't relied on for branching fistulas. Setons aren't pulled early. And a complex fistula isn't treated with standard infliximab dosing or with antibiotics alone.

30:43The stricture and postoperative traps close the list. An actively inflamed stricture isn't dilated or operated on first, and a stricture longer than about five centimeters isn't dilated. Stricturoplasty isn't done in the colon or with an abscess, dysplasia, or cancer. A high-risk patient doesn't go without preventive therapy, and smoking cessation isn't overlooked. The six-to-twelve-month colonoscopy isn't skipped. And escalation doesn't wait past Rutgeerts i-two.

31:14So, start to finish. Classify Crohn disease by Montreal age, location, and behavior. Half of inflammatory disease progresses to strictures or fistulas within ten to twenty years unless the mucosa heals. High-risk features call for early biologic therapy with an immunomodulator, and low-risk ileal disease can start with budesonide.

31:36Check TPMT and, where relevant, NUDT15 before thiopurines, and use injected methotrexate as the alternative, especially in young men. Treat to objective targets, not symptoms.

31:49Choose an advanced therapy by safety first. Anti-TNF drugs need tuberculosis and hepatitis B screening and are avoided in advanced heart failure and demyelinating disease. Vedolizumab is gut-selective and slow. Ustekinumab and the IL-23 drugs work in both diseases. JAK inhibitors are fast and oral but carry clot, cardiovascular, infection, and cancer warnings. S1P modulators need an ECG and an eye exam.

32:20Define perianal disease with pelvic MRI. Drain the abscess and place setons before any biologic, then give antibiotics with dose-optimized infliximab and an immunomodulator, removing setons at three to six months.

32:35Treat inflammation around a stricture first, dilate only short accessible strictures, and use stricturoplasty rather than repeated resection outside the colon. After ileocolonic resection, start an anti-TNF drug within four weeks in high-risk patients, stop smoking, and scope everyone at six to twelve months, escalating at Rutgeerts i-two.

32:58Episode three is the ileal pouch and its problems, dysplasia surveillance in colitis, the disease outside the gut, and the whole patient: nutrition, vaccines, and pregnancy.

33:09For 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 two of three of chapter fourteen, and I'll see you in the next one.