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Gastroenterology›Condition·Updated Apr 17, 2026·v1

Inflammatory Bowel Disease

Inflammatory Bowel Disease (IBD) encompasses chronic immune-mediated conditions (Crohn's and Ulcerative Colitis) requiring lifelong management. Treatment has evolved toward achieving transmural healing using biologics and small molecules. Early identification of complications like strictures or ASUC is vital for reducing morbidity.

High Evidence115 references·3,719 words·15 min read·v1
GastroenterologyIBDCrohn's DiseaseUlcerative ColitisBiologics

Quick Reference

RxDrug of choiceInfliximab (UC/CD), EEN (Pediatric CD induction)
AltAlternativesUstekinumab, Vedolizumab, Upadacitinib, Filgotinib
⊘AvoidLive vaccines while on biologics; NSAIDs (may trigger flares)
DxTest of choiceColonoscopy with biopsy (Diagnosis); IUS/MRE (Monitoring)
ScKey scoreMontreal Classification (Adults); PUCAI/wPCDAI (Pediatric)
→When to referAcute severe colitis, suspected stricture/obstruction, perianal fistulas, growth failure, or failure of first-line biologics
IBD is a systemic inflammatory disease requiring a treat-to-target approach focused on transmural healing via biologics, small molecules, or nutritional induction.
Inflammatory Bowel Disease (IBD) is a chronic, relapsing, immune-mediated systemic disorder characterized by persistent gastrointestinal inflammation and cyclical tissue damage. It primarily encompasses two distinct clinical entities: [[Crohn's disease]] (CD), which features transmural inflammation and can involve any segment of the GI tract, and [[ulcerative colitis]] (UC), which is limited to continuous mucosal inflammation of the colon and rectum. The global prevalence is rising, particularly in newly industrialized nations, and the disease now affects a significant number of older adults. Modern management has shifted from symptom-based control to a 'treat-to-target' paradigm, aiming for objective transmural healing to prevent structural bowel damage and reduce surgical requirements. This approach utilizes a tiered strategy of induction and maintenance with biologics, small molecules, and nutritional therapies.

Overview and Recommendations

Background

  • •Recognize IBD as a heterogeneous group of idiopathic inflammatory conditions, primarily and , driven by a complex interplay of genetic susceptibility, environmental triggers, and dysregulated immune responses. While CD is characterized by 'skip lesions' and transmural involvement, UC typically presents with continuous mucosal inflammation starting from the rectum.
  • •Identify the global epidemiological shift where IBD prevalence is increasing worldwide, now affecting over 5 million individuals with UC alone. While traditionally a disease of young adults, the 'elderly-onset' population (≥60 years) is the fastest-growing demographic, presenting unique challenges due to comorbidities and increased frailty.
  • •Understand the systemic nature of IBD, which extends beyond the gut to include extraintestinal manifestations (EIMs) such as , uveitis, and primary sclerosing cholangitis. IBD is also associated with an increased risk of atherosclerotic cardiovascular disease (ASCVD) and venous thromboembolism (VTE), particularly during active flares.
  • •Note the importance of phenotypic variants such as perianal fistulizing Crohn's disease (pfCD) and acute severe ulcerative colitis (ASUC). ASUC is a life-threatening emergency requiring rapid hospitalization and intensive medical rescue to avoid emergency colectomy.
  • •Consider the role of genetic drivers like the NOD2 gene, which is found in approximately 40% of Caucasian CD patients and is linked to related multisystem disorders such as Yao syndrome (YAOS) and Blau syndrome.

Evaluation

  • •Suspect IBD in patients presenting with chronic diarrhea (especially nocturnal), hematochezia, abdominal pain, weight loss, or unexplained growth failure in pediatric populations. Always ask about a family history of IBD and the presence of extraintestinal symptoms like joint pain or skin rashes.
  • •Obtain baseline inflammatory biomarkers, specifically C-reactive protein (CRP) and fecal calprotectin. Fecal calprotectin is highly sensitive for intestinal inflammation and is used to differentiate IBD from functional disorders like (IBS).
  • •Order a complete blood count (CBC) and iron studies to screen for anemia, which is the most common systemic complication. Also, check albumin levels as hypoalbuminemia can indicate severe disease and predict poor response to certain biologics like infliximab.
  • •Perform a thorough physical examination, including a digital rectal exam and inspection of the perianal area for skin tags, fistulas, or abscesses, which are highly suggestive of Crohn's disease.
  • •Utilize (IUS) as a first-line, non-invasive tool to assess bowel wall thickness (BWT). A BWT > 3 mm is a key indicator of active inflammation and can be used for longitudinal monitoring without radiation exposure.
  • •Order Magnetic Resonance Enterography (MRE) or CT Enterography (CTE) to evaluate for small bowel involvement, strictures, or penetrating disease (fistulas/abscesses) that cannot be reached by standard endoscopy.
  • •Perform a with multiple biopsies from both inflamed and non-inflamed segments. Histological features such as crypt abscesses in UC or non-caseating granulomas in CD are diagnostic hallmarks.
  • •Classify the disease using the Montreal Classification for adults or the Paris Classification for pediatric patients to standardize the description of disease location, behavior, and age at onset.
  • •Rule out infectious mimics, particularly Clostridioides difficile, which has a high prevalence (up to 28%) in IBD patients on biologics and can trigger or exacerbate flares.
  • •Screen for baseline sarcopenia and nutritional deficiencies using EWGSOP2 criteria, as muscle loss is a significant predictor of poor outcomes and incident IBD.
  • •Evaluate for perianal disease using pelvic MRI, which is the reference standard for classifying complex branching fistulas, or transperineal ultrasonography (TPUS) as a non-invasive alternative.
  • •Assess for psychological comorbidities, including anxiety and depression, which are highly prevalent and closely correlated with disease activity, especially in adolescents.

Management

  • •Adopt a 'treat-to-target' strategy aiming for transmural healing (TMH), defined by the normalization of bowel wall thickness on ultrasound, rather than just symptomatic relief. TMH is associated with superior long-term outcomes and lower surgery rates.
  • •Induce remission in moderate-to-severe UC using Guselkumab 200 mg or 400 mg IV at weeks 0, 4, and 8, or initiate anti-TNF therapy such as Infliximab 5 mg/kg IV.
  • •Manage Acute Severe Ulcerative Colitis (ASUC) with inpatient IV Methylprednisolone 60 mg/day. If no response is seen by day 3 (e.g., PUCAI score > 45 in children), initiate rescue therapy with Infliximab 5 mg/kg or Cyclosporine.
  • •Utilize personalized dosing models (e.g., iDose) for Infliximab in ASUC to account for high drug clearance in patients with high inflammatory burdens, aiming to maximize colectomy-free survival.
  • •Administer Exclusive Enteral Nutrition (EEN) as first-line induction therapy for pediatric Crohn's disease. Provide 100% of daily caloric requirements via liquid formula for 6 to 8 weeks to induce mucosal healing and avoid steroid toxicity.
  • •Transition to maintenance therapy with Subcutaneous (SC) Infliximab 120 mg every 2 weeks, which often achieves higher colonic tissue concentrations than IV administration.
  • •Consider Ustekinumab for Crohn's disease, induced with a weight-tiered IV dose (e.g., 6 mg/kg for patients ≥40 kg) and maintained with 90 mg SC every 8 weeks, especially in patients with symptomatic ileal strictures.
  • •Employ small molecule JAK inhibitors like Upadacitinib 15-30 mg daily or Filgotinib 200 mg daily for refractory UC cases that have failed biologic therapy.
  • •Monitor therapy using Therapeutic Drug Monitoring (TDM) to assess drug trough levels and the development of anti-drug antibodies (ADAs), particularly when clinical response is lost.
  • •Address iron deficiency anemia with IV Iron (e.g., Ferric Carboxymaltose 1000 mg) rather than oral iron during active flares to ensure better absorption and avoid GI irritation.
  • •Implement bone protection for patients on prolonged corticosteroids, including Calcium 1000–1200 mg/day and Vitamin D 800–1000 IU/day, to mitigate the risk of osteoporosis and fractures.
  • •Refer for surgical consultation early in cases of uncomplicated ileocaecal CD; laparoscopic ileocaecal resection is a valid alternative to Infliximab with high rates of long-term therapy-free remission.
  • •Manage fibrostenotic strictures with Endoscopic Balloon Dilation (EBD) or Endoscopic Stricturotomy (ESt) for short (< 5 cm) accessible lesions before considering surgical resection.
  • •Maintain maintenance therapy throughout pregnancy to prevent flares, as active disease is the greatest risk to the fetus. Anti-TNFs, Vedolizumab, and Ustekinumab are generally considered safe during gestation.
  • •Avoid live vaccines in patients on biologics or immunosuppressants. Ensure all age-appropriate vaccinations and screenings (e.g., TB, Hepatitis B/C) are completed prior to starting advanced therapies.

Board Review — High Yield

  • •ASCA vs pANCA — Anti-Saccharomyces cerevisiae antibodies (ASCA) are associated with Crohn's; pANCA is more common in Ulcerative Colitis.
  • •Transmural vs Mucosal — Crohn's involves the full thickness of the bowel wall (transmural); UC is limited to the mucosa and submucosa.
  • •Skip Lesions — Characteristic of Crohn's disease, where areas of inflammation are separated by normal-appearing mucosa.
  • •Crypt Abscesses — A classic histological finding in Ulcerative Colitis representing neutrophils within the colonic crypts.
  • •Toxic Megacolon — A surgical emergency defined by colonic dilation > 6 cm associated with systemic toxicity.
  • •Exclusive Enteral Nutrition (EEN) — The preferred first-line induction therapy for pediatric Crohn's disease, superior to steroids for mucosal healing.
  • •Rutgeerts Score — Used to assess the risk of endoscopic recurrence in Crohn's disease after ileocaecal resection.
  • •NOD2/CARD15 — The first gene associated with Crohn's disease susceptibility, particularly ileal involvement.

Deep Dive — Evidence Details

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