Crohn Disease

See Inflammatory Bowel Disease for shared epidemiology, classification, clinical features, diagnosis, and medical treatment as originally framed by the colon-focused chapter chunk. This page now also incorporates a full small-bowel-focused treatment of Crohn disease. Content below is from two textbook reference chapters (Sabiston Ch52 - Inflammatory Bowel Disease and Sabiston Ch50 - Small Bowel Anatomy, Physiology, Obstruction & Crohn Disease), not primary literature.

Unlike UC (where surgery is curative), Crohn’s surgery is generally reserved for complications — it does not cure the disease, and recurrence after resection is expected to some degree.

History

First documented case described by Morgagni in 1761. Dalziel (Scottish surgeon) described nine cases of intestinal inflammatory disease in 1913. The landmark 1932 paper by Crohn and colleagues provided the detailed pathologic and clinical description that crystallized this entity and gave it its name.

Incidence and epidemiology

Crohn disease is the most common primary surgical disease of the small bowel. Annual incidence in the US is 3–20 per 100,000 and rising. Estimated direct/indirect US costs exceed $800 million/year. Typically attacks young adults in their 2nd–3rd decades, with a smaller second incidence peak in the 6th decade (bimodal distribution). More common in urban dwellers; earlier reports suggested a higher female predominance but more recent data show roughly equal sex distribution. Risk is about twice as high in smokers as nonsmokers. Some studies show increased incidence in women using oral contraceptives, though more recent studies show no difference. Relatively uncommon worldwide in African Americans, but rates in African Americans in the US are similar to those in Caucasians. Ashkenazi Jews have a 2- to 4-fold higher incidence than age/gender-matched controls. Individuals born in spring months (April–June) are more likely to develop Crohn’s; migrants from low-risk to high-risk regions develop Crohn’s at rates similar to the high-risk region within one generation.

Etiology

Cause remains unknown; most likely contributing factors are infectious, immunologic, and genetic, with environmental/dietary/smoking/psychosocial factors of lesser but non-negligible importance.

• Infectious agents: mycobacterial infections (particularly Mycobacterium paratuberculosis) and enteroadherent E. coli have received the most attention, but neither has been proven causative; antimycobacterial therapy has not reliably ameliorated disease.
• Immunologic factors: humoral and cell-mediated immune responses against intestinal cells suggest an autoimmune phenomenon; cytokines (IL-1, IL-2, IL-8, TNF-α) contribute to the inflammatory response, though it remains controversial whether immune dysregulation is causative or an effect of the disease process.
• Genetic factors: the single strongest risk factor for developing Crohn’s is having a first-degree relative with it. Risk increases 30-fold for siblings, 14- to 15-fold for all first-degree relatives. Dizygotic twin concordance is ~4% vs. 20–50% in monozygotic twins. Genes most strongly/frequently associated: NOD2, MHC, MST1 (3p21); other implicated loci on chromosomes 16q, 5q, 19p, 7q, 3p. NOD2 is associated with decreased Paneth cell antimicrobial peptide expression; heterozygosity confers 2- to 4-fold increased risk, homozygosity 17- to 40-fold. NOD2 also predicts ileal stenosis, fistula, and Crohn-related surgery. CARD15 impairs NF-κB activation and is also useful in distinguishing Crohn’s from UC (more strongly associated with Crohn’s, especially in patients of northern European descent). See Table 50.5 in the source for the full gene-by-phenotype breakdown (diagnosis, prognosis, behavior [stricturing/penetrating/ inflammatory/granulomatous], location, activity, surgery risk, dysplasia/cancer risk, extraintestinal manifestations, pharmacogenetics). More recent genome-wide studies in monozygotic twins have found no reproducible intra-pair differences in whole genome sequence or tissue-specific variants directly in inflamed mucosa, suggesting somatic mutation is not a major driver and simple Mendelian inheritance cannot explain the pattern — multifactorial causation (including environmental factors) is likely.
• Environmental factors: low-risk Asian countries adopting a Western lifestyle have seen rising incidence. Smoking is the single largest environmental risk factor (2-fold increased risk), with smoking-associated single nucleotide polymorphisms identifying a genetic disposition to this environmental risk. Other risk-increasing factors: oral contraceptives, aspirin, NSAIDs, decreased dietary fiber, increased fat intake. Dysbiosis (decreased Bacteroides/Firmicutes, increased Gammaproteobacteria/Actinobacteria) is associated with higher risk; invasive mucosal-adherent E. coli survive within macrophages and induce higher TNF-α production.

Pathology

Most common sites: small intestine and colon. A large multi-institutional study proposed a three-category model (ileal Crohn’s, colonic Crohn’s, ulcerative colitis) for risk stratification of surgical complications and genetic risk scoring by location. Ileal involvement is associated with IL10, CRP, NOD2, ZNF365, STAT3 mutations; ileocolonic with ATG16L1, TCF4, TCF7L2; colonic with HLA, TLR4, TLR1, TLR2, TLR6. Small and large bowel are both involved in ~55% of patients; small bowel disease alone in ~30%; colon alone in ~15%. Disease is characteristically discontinuous and segmental (“skip areas” of normal bowel between diseased segments). Perirectal/perianal involvement occurs in about a third of patients, particularly with colonic involvement. Can involve mouth, esophagus, stomach, duodenum, and appendix, though these are rarely the sole site of disease.

• Gross pathologic features: thickened, gray-pink or dull purple-red bowel loops, with areas of thick gray-white exudate/fibrosis on the serosa. A striking finding is creeping fat — circumferential mesenteric fat wrapping around the bowel wall (Fig. 50.16). As disease progresses, the bowel wall becomes increasingly thickened, firm, rubbery, and almost incompressible (Fig. 50.17). Uninvolved proximal bowel may dilate secondary to obstruction of the diseased segment. Involved segments are often adherent to adjacent loops/viscera, with internal fistulas common in these areas; mesentery is thickened with enlarged lymph nodes. The earliest gross lesion on opening the bowel is a superficial aphthous ulcer; with progression, ulceration becomes more pronounced and complete transmural inflammation results — ulcers are characteristically linear and may coalesce into transverse sinuses with islands of normal mucosa between, giving the characteristic cobblestone appearance.
• Microscopic features: mucosal/submucosal edema may precede gross changes. Chronic inflammatory infiltrate with extensive edema, hyperemia, lymphangiectasia, intense mononuclear cell infiltration, and lymphoid hyperplasia. Characteristic lesions are noncaseating granulomas with Langerhans giant cells, appearing later in the disease course, found in the bowel wall or regional lymph nodes in 60–70% of patients (Fig. 50.18).

Montreal classification (Table 50.6)

Categorizes patients by:

• Age at diagnosis: A1 ≤16, A2 17–40, A3 >40
• Behavior: B1 nonstricturing/nonpenetrating, B2 stricturing, B3 penetrating (+P modifier for perianal disease, addable to B1–B3)
• Location: L1 ileal, L2 colonic, L3 ileocolonic, L4 isolated upper GI tract (addable to L1–L3)

Developed to provide reproducible staging, predict remission/relapse, and direct therapy.

Clinical manifestations

Can occur at any age; typical patient is a young adult in the 2nd–3rd decade with an insidious onset and slow, protracted course. Characteristic symptomatic periods of abdominal pain and diarrhea interspersed with asymptomatic periods of varying length; over time symptomatic periods become more frequent, severe, and longer-lasting. Most common symptom is chronic diarrhea, followed by intermittent colicky abdominal pain most often in the lower abdomen; pain may be severe and right-lower-quadrant, mimicking acute appendicitis. Unlike UC, bowel movements are typically fewer and stools rarely contain mucus/pus/blood. Systemic symptoms (low-grade fever, weight loss, loss of strength, malaise) present in about a third of patients.

Main intestinal complications are obstruction (from acute exacerbation of active disease or chronic fibrosing lesions narrowing the lumen) and perforation. Free perforation with generalized peritonitis is rare; more commonly, fistulas form between sites of perforation and adjacent structures (small/large bowel, urinary bladder, vagina, stomach, skin — usually at a prior laparotomy site). Localized abscesses can occur near perforation sites. Colitis patients may develop toxic megacolon. Bleeding is typically indolent/chronic, but massive GI bleeding can occasionally occur, particularly in duodenal Crohn’s with chronic ulcer formation.

Cancer risk: long-standing Crohn’s predisposes to small intestine and colon carcinoma, typically arising at sites of chronic inflammation, more commonly in the ileum. Most are not detected until advanced stages with a poor prognosis. Relative risk of small bowel cancer is ~100-fold increased though absolute risk remains small. Colorectal cancer risk with colonic involvement and long disease duration is a greater concern; dysplasia is the putative precursor lesion (as with UC), and patients with long-standing colonic Crohn’s should have an equally aggressive colonoscopic surveillance regimen as extensive UC. Small bowel adenocarcinoma associated with Crohn’s has an aggressive behavior with a strong probability of extracellular mucin; mucinous-appearing/fistulous/adhesion- retraction areas in surgical specimens should always be examined by a pathologist for dysplasia/ malignancy. Extraintestinal cancers (squamous cell carcinoma of vulva/anal canal, Hodgkin and non-Hodgkin lymphoma) may also be more frequent, especially in patients treated with immunomodulators.

Perianal disease (fissure, fistula, stricture, abscess) is common — occurs in 25% of patients with small-bowel-limited disease, 41% with ileocolitis, 48% with colonic involvement alone; may be the sole presenting feature in 5% and may precede intestinal disease onset by months to years.

Extraintestinal manifestations present in ~30% of patients: skin lesions (erythema nodosum, pyoderma gangrenosum — Fig. 50.19), arthritis/arthralgias, uveitis/iritis, aphthous stomatitis, and (less commonly) amyloidosis, pancreatitis, and nephrotic syndrome. These may precede, accompany, or follow the underlying bowel disease.

Diagnosis

No single diagnostic test exists; a multimodal approach (labs, endoscopy, radiology, pathology) is required.

• Laboratory: serologic markers — perinuclear antineutrophil cytoplasmic antibody (and target proteins BPI, lactoferrin, cathepsin G, elastase), anti-Saccharomyces cerevisiae antibody (ASCA), anti-CBir1 (outer membrane porin of flagellin), OmpC-IgG (outer membrane porin of E. coli) — can predict IBD development even in patients thought low-risk, and ASCA helps differentiate Crohn’s from UC. CRP and ESR are nonspecific and have largely been abandoned as primary markers. Fecal calprotectin (sensitivity 69%, specificity 82% for small bowel inflammation at >140 ng/mL) and fecal lactoferrin (sensitivity 69%, specificity 79% at >6 ng/mL) are useful screening tools for early small bowel Crohn’s; calprotectin correlates with CRP and ESR, while lactoferrin correlates only with CRP.
• Radiology: CT enterography (CTE) or MR enterography (MRE) are often used as initial assessment — both accurate for disease activity/bowel damage; MRE may be superior for detecting strictures and ileal wall enhancement, though CTE is used more for cost/availability. Barium enema historically used to identify features like the Kantor string sign (long narrowed terminal ileum segments, Fig. 50.20) in long-standing disease; segmental/irregular involvement and fistulas also visible. CTE is useful for demonstrating transmural thickening and extramural complications (Fig. 50.22). Ultrasound has limited value, especially for disease proximal to the terminal ileum (misses up to 67% in one study), but may help assess undiagnosed RLQ pain.
• Endoscopy: ileocolonoscopy with terminal ileum biopsy is the gold standard. May show aphthous ulcers with granularity and normal-appearing surrounding mucosa; discrete ulcers/cobblestoning and discontinuous segments favor Crohn’s over UC. Balloon enteroscopy (single-, double-balloon, spiral) allows evaluation of small bowel beyond ileocolonoscopy reach; double-balloon is the most established technique (240–360 cm enteral intubation vs. 90–150 cm for push enteroscopy or 50–80 cm for ileocolonoscopy), with ~1% complication risk (pancreatitis, perforation, bleeding). CDEIS or SES-CD scoring used to define extent/severity once diagnosis is confirmed. Capsule endoscopy (FDA-approved 2001) is useful for superficial mucosal abnormalities (≥3 ulcers without NSAID use is the most common abnormal-finding criterion); limited by capsule retention risk (13% in Crohn’s vs. 1–2.5% general population); severity measured by the CECDAI/Niv score.
• Differential diagnosis: bacterial (Salmonella, Shigella), intestinal TB, and protozoal (amebiasis) infections can mimic Crohn’s as an ileitis; in the immunocompromised host, rare mycobacterial and CMV infections. Acute distal ileitis may mimic early Crohn’s but can also be unrelated, caused by Campylobacter or Yersinia — these usually resolve spontaneously and should not be biopsied/resected if noted incidentally at surgery. Crohn colitis vs. ulcerative colitis distinction can be difficult in 5–10% of patients (see Table 50.7 for a detailed symptom/radiologic/proctoscopic comparison) — UC almost always involves the rectum most severely with continuous proximal extension and does not extend deep into the bowel wall; Crohn’s may be worse on the right side, sometimes spares the rectum, and shows skip lesions, linear/deep/scattered ulceration, and (unlike UC) frequent anal fissure/fistula/abscess.

Management

Medical therapy

No cure exists. Medical therapy aims for steroid-free remission and prevention of exacerbations/ complications; endoscopic healing has emerged as the therapeutic goal given its poor correlation with symptoms alone. Surgery is advocated for neoplastic/preneoplastic lesions, obstructing stenoses, suppurative complications, or medically intractable disease. Narcotic analgesia should be avoided except perioperatively given tolerance/abuse potential in chronic disease. Clinical remission = Crohn Disease Activity Index (CDAI) below 150 (Box 50.4, 8 clinical factors); response = drop of 100 points. CDAI 150–220 = mild-moderate; 220–450 = moderate-severe (after failure of first-line therapy); >450 = severe fulminant disease with failed medical therapy and obstruction/peritonitis/ abscess complications.

• Aminosalicylates (sulfasalazine, mesalamine): sulfasalazine’s benefit is mainly in colonic disease; its use for small bowel Crohn’s maintenance has fallen out of favor. Mesalamine (4 g/day) demonstrated efficacy without increased side effects; rare interstitial nephritis (1%) requires periodic renal monitoring.
• Corticosteroids: fast-acting/effective for inducing remission but not ideal for maintenance. Budesonide (9 mg/day) has high first-pass hepatic metabolism, targeting the ileum/right colon while mitigating systemic steroid effects; more effective than placebo or mesalamine for mild- moderate active ileal disease and is the preferred primary treatment there. Prednisone for moderate-severe disease; >50% of patients (particularly smokers) become “steroid dependent,” with chronic use causing osteoporosis and increased relapse rates. High-dose (40–60 mg/day) until symptom resolution and weight gain resumption; parenteral for severe disease once abscess is excluded. No standard taper; generally 5–10 mg/week to 20 mg, then 2.5–5 mg weekly to cessation. DEXA scan, calcium, and vitamin D supplementation, with consideration of bisphosphonates, are warranted once steroid therapy begins.
• Antibiotics: metformin-era metronidazole initially reported effective but later found no better than placebo for inducing remission; ciprofloxacin, rifaximin, clofazimine, ethambutol, isoniazid, and rifabutin have varying success. Clear role in septic complications and perianal disease; mechanism of action in Crohn’s unclear; long-term use limited by side effects. May help as adjuncts for perianal disease, enterocutaneous fistulas, or active colonic disease, but not recommended for maintenance or remission induction.
• Immunosuppressive agents: azathioprine (AZT), 6-mercaptopurine (6-MP), and methotrexate (MTX) effective for maintenance therapy in moderate-severe disease; AZT/6-MP for maintaining steroid-induced remission, weekly IV MTX for both induction and maintenance. Slow onset requires steroid bridging until transition is complete. Relatively safe; most common side effects are pancreatitis, hepatitis, fever, rash; more concerning are chronic liver disease, bone marrow suppression, and malignant transformation potential. Thiopurine methyltransferase (TPMT) genetic polymorphisms affect AZT/6-MP metabolism — decreased TPMT activity carries significantly increased fatal bone marrow suppression risk; genotype testing may help identify predisposed patients. Other agents: cyclosporine and FK-506 (tacrolimus) — FK-506 effective for fistula improvement (not remission) in severe/steroid-refractory perianal disease; cyclosporine not found efficacious except in uncontrolled studies at low dose.
• Anti-TNF therapy: considered a breakthrough. Infliximab (chimeric monoclonal anti-TNF-α) effective and safe as monotherapy for moderate-severe disease, effective for both induction and maintenance; ~two-thirds of patients achieve perianal fistula closure, though not every fistulizing/ extraintestinal-disease patient responds. Other FDA-approved anti-TNF agents: adalimumab (humanized IgG1, self-administrable), certolizumab (humanized antibody fragment linked to PEG, does not cross the placenta/excrete in breast milk — preferred in pregnancy/nursing). Similar safety profiles across the three: increased risk of TB reactivation, invasive fungal/opportunistic infection, demyelinating CNS lesions, latent MS activation, CHF exacerbation, and possible increased melanoma risk. Flare on anti-TNF therapy prompts measurement of serum drug concentration and antidrug antibodies to guide dose increase, agent switch (same class), or class switch. Smoking cessation is an important adjunct — smoking is an independent predictor of needing maintenance biologic therapy.
• Novel therapies: leukocyte trafficking inhibitors, interleukin inhibitors, antiadhesion molecule antibodies — often used after anti-TNF failure/intolerance. Natalizumab (anti-α4 integrin) effective for induction/maintenance but withdrawn after progressive multifocal leukoencephalopathy cases, later reinstated for refractory disease. Vedolizumab (humanized anti-α4β7 integrin, blocks MadCAM-1 interaction) more gut-specific, avoids the neurologic side effects of less selective α4 inhibitors, but has slow onset of action; approved 2014 for anti-TNF/ immunosuppressant nonresponders. Ustekinumab (humanized IgG1 anti-IL-12/23, targets shared p40 subunit) shown effective in anti-TNF-refractory disease with similar efficacy in two large trials; approved 2016. Other agents in development target NF-κB, MAPK, and PPAR-γ signaling with variable/ still-developing results.
• Nutritional therapy: variable success; chemically defined elemental diets shown in some studies to reduce disease activity (particularly small-bowel-localized disease) and reduce corticosteroid- induced toxicities; liquid polymeric diets similarly effective and more palatable. Standard elemental diets have not reliably prevented relapse, with few exceptions. TPN useful in active disease but complication rates exceed enteral nutrition; primary role is questionable, but there is a secondary role in replenishing nutrient stores, allowing protein synthesis/healing, and preparing patients for surgery.
• Smoking cessation: implication as a causative factor has been hard to prove, but smoking clearly worsens disease course — associated with late bimodal-onset disease, increased relapse/maintenance failure, and severity in a linear dose-response relationship. Tobacco exposure independently predicts need for maintenance biologic therapy.

Advanced therapy, monitoring, and post-surgical management (BSG 2025 guideline)

The medical-therapy subsection above is textbook-level (mechanism/class only, no trial evidence or positioning) — until this ingest, Crohn’s had no primary-guideline backing at all in this wiki, unlike Ulcerative Colitis (which gained full guideline coverage from ACG 2025 - Ulcerative Colitis Guideline and AGA 2024 - Moderate-to-Severe UC Pharmacotherapy Guideline earlier in the same ingest session). This subsection adds GRADE-based recommendations from BSG 2025 - IBD Guidelines (Adults) — see that page for full detail; only headline positioning is repeated here.

Advanced therapy roster (all “conditional” strength recommendations, certainty/magnitude noted):

Agent	Recommendation	Certainty / magnitude	Notes
Adalimumab	Suggested	Moderate / moderate	Combination with a purine analogue recommended — lowers NNT for remission 4→2
Infliximab	Suggested	Moderate / moderate	Combination with a purine analogue recommended — ~20% higher maintenance magnitude than monotherapy
Ustekinumab	Suggested	Moderate / moderate	Usable after purine analogue and/or anti-TNF failure
Risankizumab	Suggested	Low / small	SEQUENCE trial: non-inferior to ustekinumab for remission at wk 24, superior for endoscopic remission at wk 48 (anti-TNF-experienced patients)
Upadacitinib	Suggested	Low / small	First oral agent effective for both induction and maintenance in Crohn’s; reserved for after anti-TNF failure given VTE/MACE boxed warning
Vedolizumab	NOT suggested	Low / trivial	Genuine disease-specific divergence from its favorable UC positioning — trivial effect size across all direct Crohn’s trial evidence regardless of biologic exposure status; not precluded case-by-case, but not a guideline-endorsed default
Antibiotics	NOT suggested	High / trivial	No individual agent/combination robustly studied; small class-wide induction effect only
Probiotics	NOT suggested	Very low	Insufficient evidence

Therapeutic drug monitoring — adds concrete numbers to what the disease page previously only covered qualitatively (TPMT testing above): target purine analogue metabolites 6-TGN 235–450 pmol/8×10⁸ RBCs, MMP <5700 pmol/8×10⁸ RBCs, checked ~4 weeks after starting and 3-monthly alongside FBC/U&E/LFT. PANTS-study-derived anti-TNF trough targets at later time points (week 14+): 6.1–10.0 mg/L for infliximab, 10.1–12.0 mg/L for adalimumab — evidence insufficient to formally recommend routinely targeting these levels, but useful context for dose-escalation decisions on secondary loss of response.

Exclusive enteral nutrition (EEN): well-established in pediatric Crohn’s (~73% remission, intention-to-treat) but not formally graded for adults — Cochrane data show no difference vs. steroids without allowing firm conclusions (very low certainty). Best-supported adult use is preoperatively: ~6 weeks preoperative EEN associated with lower postoperative abscess/leak rates and lower CRP in observational studies. Practical protocol: whole-protein/peptide/elemental formulas equally efficacious: gradual volume increase to a target ~25–30 kcal/kg/day energy, 1 g/kg/day protein; refeeding-syndrome bloods (K, phosphate, Mg) monitored daily while ramping in at-risk patients; continue 6–8 weeks once established to induce mucosal healing.

Withdrawal of therapy: infliximab withdrawal after ≥1 year of stable remission is not suggested — both RCTs examining this (SPARE, STOP-IT) showed materially elevated relapse risk on withdrawal (roughly 1 in 3 patients relapse within 1–2 years, though retreatment on relapse is usually effective). By contrast, withdrawing the immunomodulator while continuing anti-TNF is not associated with a significant relapse-risk increase, if attempted after >2 years of combination therapy and >6 months of corticosteroid-free remission.

Non-surgical stricture management: CREOLE study found adalimumab avoided escalation to steroids/dilation/surgery in 64% of symptomatic ileal strictures at 24 weeks (a prognostic score using clinical + MRE features predicts response) — relevant alongside the strictureplasty/resection decision-making in “Specific problems” below. Endoscopic balloon dilation is appropriate for ileocolonic anastomotic strictures <4cm without sharp angulation, though most patients need repeat dilation.

Post-surgical recurrence prevention (see also “Prognosis” below for the older Fig. 50.25 textbook algorithm this refines): anti-TNF (infliximab or adalimumab) or vedolizumab is suggested after ileocolonic resection for patients with significant recurrence risk factors (young age at diagnosis, active smoking, penetrating disease, perianal disease, multiple prior surgeries), by patient preference, or with endoscopic evidence of recurrence at 6 months — recommended to start within 90 days post-surgery where indicated (NMA data: adalimumab HR 0.1, infliximab HR 0.36, for preventing clinical relapse vs. placebo — a notably more proactive stance than “wait for 6-month scope, then decide” alone). 5-ASA and purine analogue monotherapy are not suggested for this purpose — trivial effect size (NNT 13–14) despite reaching statistical significance in some trials. Endoscopic recurrence is still best assessed by ileocolonoscopy at 6 months post-resection using the Rutgeerts score, as the textbook algorithm below describes.

Perioperative optimization: laparoscopic resection should be considered for localised ileocaecal disease when not responding to or relapsing after medical therapy, or by patient preference; malnutrition screening/correction (immune-enhancing nutritional supplements reduce postoperative complications, OR 0.26 in a meta-analysis) as part of preoperative optimisation; corticosteroids stopped/minimised preoperatively where possible (≥20mg prednisolone associated with increased complications; equivalent IV hydrocortisone given if steroid-dependent and NPO). Immunosuppressive agents (purine analogues, methotrexate) and biologics can be continued perioperatively — reassuring large observational data (PUCCINI, French REMIND studies) found no significant postoperative infection increase with anti-TNF exposure regardless of drug concentration or timing; similarly reassuring (smaller) data for vedolizumab and ustekinumab. JAK inhibitor perioperative safety data are limited (one retrospective series: 13.2% VTE rate after tofacitinib exposure before colectomy in ulcerative colitis — prolonged VTE prophylaxis suggested; no Crohn’s-specific data yet). Pharmacological VTE prophylaxis recommended for essentially all IBD patients admitted for acute illness or surgery, extended post-discharge after major abdominal surgery per UK practice.

Surgical treatment (colonic-focused, from the Inflammatory Bowel Disease chapter chunk)

Approximately 70% of patients will require surgical resection within 15 years after diagnosis. Indications for surgery include failure of medical treatment, bowel obstruction, fistula or abscess formation, steroid dependence, and dysplasia or malignancy.

Indications for surgery:

• Failure to grow in children (as with UC).
• Obstruction secondary to fibrostenotic disease.
• Perforating disease with associated abscess or phlegmon.
• Symptomatic fistulas — a relative indication covering many fistula types. A symptomatic ileosigmoid fistula causing diarrhea from bypassed bowel is a clear example. Enterocutaneous fistulas are not automatically an indication unless associated with obstruction/significant discomfort; the same is true of enteroenteric fistulas.
• Significant abdominal pain associated with obstruction.
• Cancer or dysplasia — as with UC, an indication for resection; because Crohn’s disease (like UC) can be multifocal in the colon, total proctocolectomy is preferred over segmental resection when dysplasia/cancer is the indication.

Surgical options (colonic):

• Ileocolic resection — the single most common operation for Crohn’s (the ileocecal area is involved in nearly half of patients — Fig. 50.23). Because the terminal ileum sits near several pelvic structures, a proximal perforation can track into the sigmoid colon (far more common) or bladder, producing an ileosigmoid or ileovesical fistula. Lends itself well to a laparoscopic approach, except with extensive fistulizing disease or a significant phlegmon making dissection of the right colon mesentery/terminal ileum off retroperitoneal structures difficult. Margin selection: choose bowel that feels grossly normal and has a normal-thickness bowel-mesenteric junction — a palpable, discrete mesenteric junction is a good indicator the lumen there is free of significant Crohn’s inflammation. Anastomotic technique: hand-sewn end-to-end is preferred by the Colon and Rectum chapter’s authors over side-to-side stapled, since it’s easier to evaluate/dilate endoscopically if disease recurs; the anastomosis should be made very wide. (See “Anastomotic technique” below for the Small Bowel chapter’s more detailed, somewhat contrasting discussion.)
• Segmental colon resection — increasingly used over the last two decades, for two reasons: (1) recognition of the colon’s role in water absorption plus the likelihood of repeat operations over a Crohn’s patient’s lifetime, and (2) newer, more potent medications allowing better postoperative suppression of recurrence. Best suited to isolated colonic strictures with relatively normal, distensible “skipped” segments in between. Carries a meaningfully higher recurrence risk than more extensive resection, so should always be paired with postoperative chemoprophylaxis.
• Subtotal colectomy with ileorectal anastomosis — suited to patients with relative rectal sparing and an otherwise diseased colon; segmental resection is preferable when there are areas of normal intervening colon. Also carries a higher recurrence rate. Depending on the amount of retained rectum, an ileal pouch–rectal anastomosis can reduce postoperative bowel-movement frequency; may require temporary diversion (loop ileostomy) to support healing depending on anastomotic height.
• Proctocolectomy with IPAA — historically only a passing mention for Crohn’s, now considered more often given newer immunosuppressive options, in educated patients without obvious perianal disease who understand the higher morbidity risk and less favorable functional results (more bowel movements) compared with IPAA for UC, and the higher risk of needing conversion to an end ileostomy if fistulizing disease develops. Technique is the same as for UC — see the dedicated procedure page.

Cancer risk (surgical implication): if a cancer is identified, total colectomy (not segmental resection) should be performed — colonic procarcinogenic mutations can track along the colon, and the risk of a subsequent cancer elsewhere in the colon is high.

Postoperative complications and recurrence: many Crohn’s patients are on immunosuppressive medications at the time of surgery and are hypoalbuminemic from protein-losing enteropathy — both raise infectious-complication risk. Steroids and biologics administered within several months preoperatively both increase infectious complication risk (opinions differ on the relative risk by drug class); this should prompt an explicit discussion with the patient about the possibility of a temporary diverting stoma if an anastomosis is being considered. Recurrence risk factors: smoking, age <30 at Crohn’s onset, and having already had 2 or more operations for fistulizing disease. Early, intensive medical therapy started soon after surgery may reduce recurrence risk. Regular endoscopic surveillance of the lower GI tract is important to catch recurrent disease before it becomes therapy-resistant fibrosis.

Surgical treatment (small-bowel-focused, from this chapter chunk)

Surgery does not cure Crohn’s; the goal has shifted from radical resection to an operation achieving inflammation-free margins with minimal surgery — removing just grossly inflamed tissue (i.e., dilation or strictureplasty to increase luminal diameter), ignoring adjacent areas of bowel that are clearly diseased if not causing a complication. Fistulizing disease rarely requires operative intervention unless the fistula involves the bladder, vagina, or skin, in which case a bowel resection with fistulotomy may be needed. Early in the history of surgical therapy, wider resections were performed hoping for cure or significant remission; this instead led to a greater incidence of recurrence and short bowel syndrome (a devastating surgical complication). Operative treatment of a complication should be limited to the segment of bowel involved with the complication — no attempt should be made to resect more bowel, even when grossly evident disease is apparent elsewhere. Frozen section is unreliable and should be performed only when malignant disease is suspected. Even after resection of a diseased segment, endoscopic recurrence occurs in up to 70–90% within 1 year.

Primary anastomosis vs. initial ostomy with delayed reconstruction: an important decision given that Crohn’s patients are often malnourished, on intensive immunosuppressive therapy, or presenting with intraabdominal sepsis. Standard surgical principles direct the decision: patients with adequate nutrition and minimal intraabdominal sepsis can safely undergo primary anastomosis at the initial operation, whereas malnourished/septic patients are best served by diversion if possible. Surgery is safe for patients on perioperative infliximab or immunosuppression, per large case series, though caution is still warranted in the setting of high-dose immunosuppression.

Anastomotic technique: creating a wider anastomosis with a stapled functional end-to-end technique may decrease fecal stasis and subsequent bacterial overgrowth implicated in anastomotic recurrence. A randomized controlled trial comparing side-to-side stapled vs. end-to-end anastomosis found no difference in overall complication rates, anastomotic leak rates, or symptomatic recurrence rates, with only a slight increase in endoscopic recurrence with end-to-end (43% vs. 38%). A newer antimesenteric functional end-to-end hand-sewn technique (Kono-S anastomosis) was created to minimize anastomotic restenosis and demonstrated a significantly lower rate of stenosis and recurrence in one trial. Although further RCTs are needed, this is a promising novel surgical approach that may decrease the need for additional biologic therapy.

Laparoscopic surgery is safe and feasible in appropriately selected patients (e.g., localized abscesses, simple intraabdominal fistulas, perianastomotic recurrent disease, disease limited to the distal ileum). A large comparative study evaluating laparoscopic colectomy for Crohn colitis found significantly shorter median operative time, earlier return of bowel function, and shorter hospital stay vs. open. Multiple RCTs confirm more rapid recovery of bowel function and shorter hospital stay with similar disease recurrence rates vs. open procedures; long-term follow-up shows improved body image/cosmesis satisfaction and less incisional hernia incidence with laparoscopic ileocolonic resection. The LIR!C trial (randomized multicenter) found laparoscopic resection of uncomplicated ileocecal disease (terminal ileum <40 cm) that had failed steroid treatment could be an alternative to anti-TNF therapy.

Specific problems (small bowel)

• Acute ileitis (nonstricturing, nonpenetrating): presents with acute RLQ pain mimicking acute appendicitis; at exploration the appendix is normal but the terminal ileum is edematous, beefy red, with a thickened mesentery and enlarged lymph nodes. This is a self-limited manifestation of early Crohn’s, but is often unrelated — bacteriologic agents such as Campylobacter and Yersinia can cause acute ileitis. Intestinal resection should not be performed. In the absence of appendix or cecal inflammation, appendectomy should still be performed (in the absence of clear disease at the appendix/cecum) to eliminate the appendix as a future source of RLQ pain confusion.
• Stricturing disease: intestinal obstruction is the most common indication for surgical therapy in Crohn’s, often partial, with nonoperative management indicated initially. Success of nonoperative management can often be predicted by symptom chronicity at the affected site; distinguishing acute exacerbation from chronic stricture can use stool lactoferrin/calprotectin (favor acute inflammation) or genetic markers (e.g., NOD2, TLR4, CX3CR1, which may predict success of medical therapy). For a chronic strictured segment, medical therapy is rarely effective; operative intervention is required for complete obstruction and for partial obstruction not resolving with nonoperative management. The treatment of choice for intestinal obstruction in Crohn’s is segmental resection of the involved segment with primary reanastomosis — may involve segmental resection and primary anastomosis of a short ileal segment, or an ileocecectomy if both ileum and cecum are involved (Fig. 50.23).
• Strictureplasty: in selected patients with obstruction from single or multiple strictures, an option that widens the lumen while avoiding intestinal resection. Performed via a longitudinal incision through the narrowed area followed by transverse closure — Heineke-Mikulicz style for shorter segments (Fig. 50.24A), or a Finney-pyloroplasty-style/side-to-side isoperistaltic technique for longer diseased segments (>10 cm, Fig. 50.24B). Best used in patients with multiple short areas of narrowing over long segments, those who have had several prior resections, and those with chronic fibrous obstruction. Preserves intestinal length with complication and recurrence rates comparable to resection/reanastomosis. Given concerns about carcinoma at chronically strictured segments, full-thickness biopsy with frozen section at the stricture site has been advocated at the time of strictureplasty to rule out malignant disease before performing it. Contraindications (Box 50.5): excessive tension due to rigid/thickened bowel segments, perforation, fistula/abscess formation at the intended strictureplasty site, hemorrhagic strictures, multiple strictures within a short segment, malnutrition/hypoalbuminemia (<2.0 g/dL), and suspicion of cancer at the intended site.
• Bypass procedures: historically common, now largely reserved for specific circumstances — two types exist, exclusion bypass (proximal transected ileum anastomosed to transverse colon end-to-side, with or without a distal mucous fistula from the retained ileal segment) and continuity (simple) bypass (side-to-side ileotransverse colonic anastomosis without transection). Currently, bypass with exclusion is used only for severe gastroduodenal Crohn’s not amenable to strictureplasty, older poor-risk patients, patients who’ve had several prior resections and cannot afford to lose more bowel, and select ileocecal-disease patients with an abscess/phlegmon densely adherent to the retroperitoneum where resection would risk entering an abscess or endangering a normal structure.
• Penetrating disease: fistula and abscess formation in Crohn’s are relatively common, usually involving adjacent small bowel, colon, or other surrounding viscera (e.g., bladder). A radiographically demonstrable enteroenteral fistula with no sepsis/complications is not itself an indication for surgery. Penetrating disease is particularly sensitive to anticytokine therapy, and a conservative surgical approach to fistula is most appropriate. Enterocutaneous fistulas may develop but are rarely spontaneous, more often following resection or drainage of intraabdominal abscesses; treatment entails fistula outflow reduction, infection prevention, and nutrition/skin care optimization; if conservative management fails, excision of the fistula tract and primary anastomosis is preferred, with preoperative optimization important given that penetrating disease patients tend to have longer operative times, higher reoperation rates, increased length of stay, and more postoperative complications. If fistula forms between two or more adjacent loops of diseased bowel, the involved segments should be excised; if fistula involves an adjacent normal organ (bladder, colon), only the diseased small bowel segment and fistulous tract need be resected, with the defect in the normal organ simply closed. Most patients with ileosigmoid fistulas do not necessarily require resection of the sigmoid unless it is also found to have Crohn’s disease, in which case it should be resected along with the diseased small bowel segment.
• Perforation: free perforation into the peritoneal cavity is uncommon in Crohn’s. Typically, penetration presents as a localized abscess densely adherent to the diseased segment of bowel rather than free perforation. In cases of free perforation, the segment of involved bowel should be resected, and in the presence of minimal contamination a primary anastomosis can be performed; if generalized peritonitis is present, a safer option may be to create an ostomy until intraabdominal sepsis is controlled, restoring continuity after 4–6 weeks. Abscesses without free perforation can be treated with percutaneous drainage and antibiotics; however, fistula or uncontrolled sepsis may develop, requiring resection with or without primary anastomosis. An abscess smaller than 3 cm, in a patient not on biologics and without an associated fistula, can be treated with antibiotics alone; abscesses not meeting these criteria should undergo percutaneous drainage — early treatment of an abscess is key to resolution regardless of drainage route.
• Gastrointestinal bleeding: anemia from chronic blood loss is common; life-threatening hemorrhage is rare. Hemorrhage is more common with colonic than small bowel Crohn’s. As with other complications, the involved segment should be resected and intestinal continuity restored. Arteriography may help localize bleeding before surgery. For bleeding associated with duodenal Crohn’s, endoscopic intervention is usually successful; duodenotomy with oversewing of the bleeding ulcerative area is indicated if endoscopy fails.
• Urologic complications: occur in up to a third of patients, most commonly ureteral obstruction secondary to ileocolic disease with retroperitoneal inflammatory compression. Surgical treatment of the primary intestinal disease is adequate in most patients; in a few cases of long-standing inflammatory disease, periureteric fibrosis may be present and require ureterolysis with or without ureteral stenting.
• Colorectal disease: the same principle applies to patients with disease limited to the colon as to those with disease limited to the small bowel — surgical resection should be limited to the main segment involved. Indications for surgery include lack of response to medical management and complications of Crohn colitis (obstruction, hemorrhage, perforation, toxic megacolon). Depending on the diseased segments, procedures commonly include segmental colectomy with colocolonic anastomosis, total abdominal colectomy with ileorectal anastomosis, total proctocolectomy with ileoanal anastomosis, and (in patients with extensive perianal and rectal disease) abdominoperineal resection with end ileostomy. Strictureplasty has limited usefulness in colonic Crohn disease, and concerns of malignant transformation at an area of colonic obstruction should limit its application. A particularly troubling problem after abdominoperineal resection in Crohn patients is delayed healing of the perineal wound — more than half of perineal wounds remain open at 6 months. Persistent nonhealing wounds require excision with secondary closure; large cavities/sinuses may need well-vascularized muscle pedicles (gracilis, semimembranosus, rectus abdominis) or omentum, or an inferior gluteal myocutaneous flap. Continence-preserving operations such as IPAA or continent ileostomy (Kock pouch) may be considered in very carefully selected patients with Crohn’s isolated to the colon after thorough counseling about increased anastomotic failure/wound complication risk — these procedures should never be considered in patients with evidence of terminal ileal or perianal disease, which carry a significantly increased recurrence rate in the pouch, fistulas to the anastomosis, and peripouch abscesses.
• Perianal disease: fissures and fistulas are common, particularly with colonic involvement. Treatment should be nonoperative unless an abscess or complex fistula develops, and even then surgery should be cautious and limited to the specific problem with minimal tissue loss. Nonsuppurative, chronic fistulization or fissuring is treated with antibiotics, immunosuppressive agents (AZT or 6-MP), and infliximab, which has shown the best results in fistula closure as it is most widely supported by evidence; cyclosporine or FK-506 have shown some benefit in several uncontrolled studies. Wide excision of abscesses or fistulas is not indicated; more conservative interventions, including liberal placement of drainage catheters and noncutting setons, are preferable. Definitive fistulotomy is indicated for most patients with superficial, low transsphincteric, and low intersphincteric fistulas, recognizing that some degree of anal stenosis may occur as a result of chronic inflammation. High transsphincteric, suprasphincteric, and extrasphincteric fistulas are usually treated with noncutting setons. Fissures are usually lateral, relatively painless, large, and indolent, and often respond to conservative management. Abscesses should be drained, but large excisions of tissue should not be performed. Advancement flap closure of perineal fistulas may be required in certain cases. Selective construction of diverting stomas has good results combined with optimal medical therapy to induce remission of inflammation. Proctectomy is infrequent but required in a subset of patients with persistent, unremitting disease despite conservative medical and surgical therapy. Primary-guideline update (BSG 2025 - IBD Guidelines (Adults)): workup should combine pelvic MRI with exam under anaesthesia (± endoanal ultrasound) by an experienced colorectal surgeon — proctitis at assessment predicts worse fistula-healing outcomes (OR 2.85). Infliximab is suggested as first-line biologic for perianal Crohn’s, started as soon as adequate sepsis drainage is achieved (pooled anti-TNF data: RR 1.94 for fistula induction of remission, RR 1.79 for maintenance, vs. placebo) — consistent with, and now evidence-graded, what the textbook content above already taught. The PISA-II trial (the only perianal Crohn’s surgical RCT since the prior BSG guideline) found MRI-assessed fistula closure higher with combined surgery (advancement flap/LIFT) plus anti-TNF than anti-TNF alone (12% vs 9%). Refractory disease significantly affecting quality of life should be offered faecal stream diversion — reversal rates are low and proctectomy may ultimately still be required. A phase III mesenchymal stem cell therapy trial (Cx601/darvadstrocel + fibrin glue) failed its primary combined-remission endpoint at 24 weeks despite promising phase II data — not yet a viable option outside trials.
• Duodenal disease: occurs in fewer than 5% of Crohn patients, most commonly in the duodenal bulb. Operative intervention is uncommon; the primary indication for surgery is duodenal obstruction not responding to medical therapy, with endoscopic balloon dilation and surgery being the mainstays of treatment. Gastrojejunostomy to bypass the disease, rather than duodenal resection, is the procedure of choice. Strictureplasty has been performed successfully in selected patients and may avoid the marginal ulceration and diarrhea associated with gastrojejunostomy.

Prognosis

Crohn disease is a chronic inflammatory disorder that is not medically or surgically curable; therefore therapeutic approaches aim to induce and maintain symptomatic control, improve quality of life, and minimize long-term complications. Approximately 71% of patients require surgery within 10 years of diagnosis, and 50% require a second procedure within 20 years. Symptomatic recurrence varies from 40% to 80%; endoscopic recurrence is much higher, with up to 90% of patients having visible lesions within 5 years. Smoking cessation is the only clearly modifiable risk factor. Surgery is generally indicated when the patient fails to respond to medical therapy or develops complications; multiple studies show significant quality-of-life improvement after surgical intervention. Although postsurgical recurrence is high, algorithms using careful endoscopic surveillance combined with maintenance immunomodulators, anti-TNF antibodies, anti-integrin therapy, and even investigational traditional Chinese medicine all play a role in preventing postoperative recurrence (Fig. 50.25’s algorithm stratifies patients by predicted risk of clinical recurrence — “high”-risk patients go straight to anti-TNF or AZT/6-MP with surveillance endoscopy, “low”-risk patients start with 3 months of metronidazole before surveillance endoscopy — with therapy escalated or continued based on whether endoscopic recurrence is found). Standardized mortality rates increase in patients whose disease began before age 20 and in those who have had disease for longer than 13 years. Long-term survival studies suggest a death rate approximately two to three times higher than the general population, most commonly related to chronic wound complications and sepsis. Gastrointestinal cancer is the leading cause of disease-related deaths in Crohn patients; other causes include sepsis, thromboembolic complications, and electrolyte disorders.

Open items / gaps

• Medical management now has primary-guideline backing (see “Advanced therapy, monitoring, and post-surgical management” above, from BSG 2025 - IBD Guidelines (Adults)) — this was the wiki’s single biggest IBD gap and is now closed. Not yet cross-checked against any Crohn’s-specific ACG or AGA guideline (only UC-specific versions of those have been ingested). Note vedolizumab’s Crohn’s-specific “not suggested” stance is a genuine efficacy finding, not a guideline-methodology disagreement — see BSG 2025 - IBD Guidelines (Adults)‘s limitations note for why this differs from vedolizumab’s favorable UC positioning.
• No primary trial data yet on segmental vs. more extensive resection recurrence rates specifically (as opposed to the general post-surgical advanced-therapy recommendations now added above), or on specific postoperative chemoprophylaxis regimen head-to-head efficacy beyond what’s summarized above.
• Perianal Crohn’s fistula management now has a dedicated subsection above (setons, fistulotomy, infliximab, diverting stoma, proctectomy), but LIFT and other anal-fistula-specific surgical techniques familiar from cryptoglandular fistula management are not discussed by either source chapter — worth checking primary literature if this becomes clinically relevant.
• The Colon and Rectum chapter chunk’s preference for hand-sewn end-to-end ileocolic anastomosis and this Small Bowel chapter chunk’s more nuanced discussion (stapled functional end-to-end vs. hand-sewn end-to-end vs. Kono-S) are not fully reconciled here — both are presented as the respective source chapters describe them; worth flagging if primary-literature ingest later clarifies current practice consensus.
• Short bowel syndrome, mentioned here only as a historical cautionary consequence of overly wide resection, is not yet developed as its own topic — expected later in this same chapter (Miscellaneous Problems section).