1. History
- Key HPI questions: Characterize stool frequency, consistency, presence of blood or mucus; abdominal pain location, severity, and relationship to meals; fever, night sweats, unintentional weight loss; nausea, vomiting, or obstructive symptoms (bloating, inability to pass flatus) [1]
- Symptom characterization: Chronic diarrhea, crampy abdominal pain (often RLQ), fatigue, and anorexia are cardinal features. Rectal bleeding is less common than in UC but occurs with colonic involvement [2]
- Timing and triggers: Ask about recent NSAID use (17–28% relapse rate within 9 days of nonselective NSAIDs in quiescent IBD), antibiotic use, recent infections, dietary changes, psychological stress, and medication nonadherence [1][3-4]
- Medication adherence: Determine current maintenance therapy, last dose of biologic, missed doses, and prior steroid courses (>2/year suggests need for therapy adjustment) [2]
- Important negatives: Travel history, sick contacts, recent C. difficile exposure, recent surgery, symptoms of obstruction (vomiting, obstipation), perianal symptoms (drainage, pain), and urinary symptoms (fistula to bladder) [1][5]
2. Alarm Features
- High fever, persistent vomiting, involuntary guarding, or rebound tenderness → concern for perforation, abscess, or fulminant disease [1][3]
- Signs of intestinal obstruction: Distension, inability to pass flatus, bilious vomiting [6]
- Hemodynamic instability: Tachycardia, hypotension → hemorrhage, sepsis, or severe dehydration [7]
- Cachexia, significant weight loss, failure to thrive → nutritional emergency [6]
- Perianal abscess with systemic signs of infection [6]
- Symptoms refractory to outpatient corticosteroids or biologics → fulminant disease requiring hospitalization [1]
3. Medications
- Acute flare treatment:
- Mild-moderate: Budesonide 9 mg/day (gut-selective, fewer systemic effects) [2]
- Moderate-severe: Prednisone 40 mg/day, taper over ≤3 months (5 mg/week to 20 mg, then 2.5–5 mg/week) [1][8]
- Severe/fulminant (inpatient): IV methylprednisolone 40–60 mg/day [1][3]
- Fulminant/steroid-refractory: Infliximab 5 mg/kg IV (weight-based dosing preferred in high inflammatory burden) [1][3]
- Medications to avoid:
- NSAIDs — may exacerbate disease activity (ACG: strong recommendation to avoid) [1][3]
- Mesalamine — ineffective in Crohn's disease [2][9]
- Corticosteroids should not be used for maintenance [2][9]
- Opioids — use cautiously; risk of ileus and narcotic bowel syndrome
- Medication interactions/cautions:
- Thiopurines (azathioprine/6-MP): check TPMT/NUDT15 before initiation; monitor CBC and LFTs
- Biologics: screen for latent TB and hepatitis B before initiation [2]
- Corticosteroids: increased risk of infections, VTE (5-fold), osteoporosis, hyperglycemia [1][10]
4. Diet
- During acute flare: A low-residue, low-FODMAP approach may reduce symptoms short-term; avoid high-fiber, raw fruits/vegetables if stricturing disease is present [11]
- Hydration: Aggressive oral or IV rehydration; monitor electrolytes, especially with high-output diarrhea
- Exclusive enteral nutrition (EEN): Strongest evidence in pediatric CD for induction; can be used as adjunct in adults, particularly with stricturing complications or preoperatively [11-12]
- Long-term: Transition to a Mediterranean diet (rich in fruits, vegetables, monounsaturated fats, lean protein; low in ultraprocessed foods and added sugar) once symptoms improve — associated with improved biomarkers and quality of life [1][11]
- Avoid: Sugar-sweetened beverages, ultraprocessed foods, excess saturated/trans fats, emulsifiers [11][13]
5. Review of Systems
- GI: Stool frequency/consistency, blood, mucus, tenesmus, urgency, nocturnal diarrhea, nausea/vomiting, dysphagia
- MSK: Joint pain/stiffness (peripheral arthritis in 10–20%; sacroiliitis in 13–50%) [2]
- Dermatologic: Skin nodules (erythema nodosum), non-healing ulcers (pyoderma gangrenosum) [1-2]
- Ophthalmologic: Eye redness, pain, photophobia (uveitis, episcleritis) [2]
- Oral: Aphthous ulcers [2]
- Urologic: Pneumaturia, fecaluria (enterovesical fistula), recurrent UTIs [5]
- Gynecologic: Vaginal stool discharge (rectovaginal fistula) [5]
- Constitutional: Fatigue, fever, weight loss, night sweats
6. Collateral History and Family History
- Family history of IBD: First-degree relatives have a significantly increased risk; ask about family history of Crohn's, UC, colorectal cancer, and other autoimmune conditions (celiac disease, psoriasis, rheumatoid arthritis, ankylosing spondylitis) [1]
- Collateral: Confirm medication adherence, functional status, nutritional intake, and psychosocial stressors from family/caregivers
- Social context: Smoking status (critical — smoking increases flare risk with OR 1.56), substance use, occupational impact, mental health screening [1-2]
7. Risk Factors
- Smoking — strongest modifiable risk factor: increased flares (OR 1.56), surgery (OR 1.68), steroid dependence, and penetrating phenotype [1-3]
- NSAID use — associated with exacerbations in meta-analyses restricted to low-bias studies (RR ~1.53) [1][13]
- Medication nonadherence — common precipitant of flare
- Prior steroid dependence or biologic failure [14]
- Extensive disease (>40 cm ileal involvement, pancolitis), deep ulcers, prior resections, perianal disease, young age at diagnosis — all markers of aggressive phenotype [9]
- Psychological stress — associated with relapse in observational studies [4]
- Western diet high in ultraprocessed foods, saturated fats, and emulsifiers [11][13]
8. Differential Diagnosis
The critical first step in any Crohn's flare presentation is to rule out infection mimicking a flare: [2]
- Clostridioides difficile infection — most important mimic; test all patients with flare symptoms [2][15]
- CMV colitis — especially in immunosuppressed patients [15]
- Bacterial enteritis (E. coli, Salmonella, Campylobacter, Norovirus) [2]
- Small intestinal bacterial overgrowth (SIBO) — especially post-resection or with strictures [1]
- Bile acid diarrhea — post-ileal resection [1-2]
- Intestinal obstruction from fibrotic stricture (not active inflammation) [2]
- Intra-abdominal abscess [6]
- Intestinal tuberculosis — caseating granulomas, endemic exposure [5]
- Medication-related adverse effects (e.g., from immunomodulators) [1]
- Disorders of gut-brain interaction (IBS overlap) — symptoms without objective inflammation [1]
- Celiac disease, endometriosis — can mimic CD symptoms [1][5]
9. Past Medical History
- Prior Crohn's phenotype: Montreal classification — location (L1-L4), behavior (B1 stricturing, B2 penetrating, B3 inflammatory), perianal modifier [9]
- Surgical history: Prior resections (length, location), anastomotic complications, short bowel syndrome risk
- Previous flare frequency and steroid courses — >2 courses/year indicates need for therapy escalation [2]
- Biologic history: Prior agents, reasons for discontinuation, drug levels/antibodies, immune-mediated vs. mechanistic failure [2]
- Comorbidities: VTE history, osteoporosis, hepatobiliary disease (PSC), nephrolithiasis, cholelithiasis [1][3]
- Vaccination status: Especially relevant before initiating or escalating immunosuppression [2]
10. Physical Exam
- Vitals: Fever, tachycardia, orthostatic hypotension (dehydration/hemorrhage) [1][7]
- General: Cachexia, pallor, dry mucous membranes, nutritional status [2]
- Abdominal exam:
- RLQ tenderness (terminal ileum involvement)
- Palpable mass (phlegmon or abscess) [5]
- Distension, high-pitched bowel sounds (obstruction)
- Peritoneal signs (guarding, rebound) → surgical emergency [1][3]
- Perianal exam: Fistula openings, abscess, skin tags, fissures, drainage — do not omit [5-6]
- Skin: Erythema nodosum (tender, raised nodules on shins), pyoderma gangrenosum (painful ulcers with violaceous borders — do not debride) [2]
- Eyes: Conjunctival injection, scleral injection (episcleritis/uveitis) [2]
- Joints: Swelling, tenderness of large joints (knees, hips, shoulders); sacroiliac tenderness [2]
- Oral: Aphthous ulcers [2]
- Psoas sign: Pain with hip extension → consider psoas abscess adjacent to terminal ileum [2]
11. Lab Studies
Per WSES and ACG guidelines, the following labs are recommended in the emergency/acute setting: [1][15]
- CBC with differential: Anemia (iron deficiency or chronic disease), leukocytosis, thrombocytosis [1][5]
- CMP: Electrolytes (hypokalemia, hyponatremia from diarrhea), renal function (dehydration, AKI), albumin (nutritional status/inflammation severity) [15]
- CRP: Most useful acute inflammatory marker in CD; correlates with endoscopic activity better than ESR. Note: up to 40% of patients with mild inflammation may have normal CRP [1][15]
- ESR: Complementary but less specific [1]
- Fecal calprotectin: Sensitive marker of intestinal inflammation; >250 μg/g correlates with active disease; <250 μg/g correlates with endoscopic remission [1][5]
- Stool studies: Cultures, ova and parasites, C. difficile toxin assay (mandatory) [2][15]
- LFTs/lipase: Rule out hepatobiliary complications, pancreatitis [15]
- Lactate: If concern for sepsis or bowel ischemia
- Blood cultures: If febrile
- Biologic drug trough and anti-drug antibody levels: If on biologic therapy — guides decision between dose optimization vs. switching [2]
- Micronutrients (outpatient): Iron, ferritin, vitamin D, B12, folate, zinc [5]
12. Imaging
- First-line (ED setting): Contrast-enhanced CT abdomen/pelvis — key study for detecting abscesses, fistulae, obstruction, perforation, and bleeding source [15]
- Preferred for younger patients (<35 years) and serial monitoring: MR enterography (MRE) — equivalent sensitivity to CT without radiation; preferred for assessing disease extent and complications [2][5][15]
- Point-of-care ultrasound (POCUS): Can identify free fluid, abscess, bowel wall thickening, and distension in the ED when CT is not immediately available [15]
- Intestinal ultrasound: Emerging modality with high sensitivity (83–95%) for terminal ileal inflammation; correlates with SES-CD [5]
- When imaging is unnecessary: Mild flare with known disease distribution, no alarm features, and biomarker-confirmed inflammation may not require acute imaging
13. Special Tests
- CDAI (Crohn's Disease Activity Index): Mild-moderate 220–450; severe/fulminant >450 — used in clinical trials and severity stratification [1][3][9]
- SES-CD (Simple Endoscopic Score for Crohn's Disease): Remission 0–2, mild 3–6, moderate 7–15, severe ≥16 [3]
- Flexible sigmoidoscopy: Can be performed in the acute setting to assess distal disease activity, obtain biopsies, and rule out CMV [15]
- Therapeutic drug monitoring (TDM): Drug trough levels and anti-drug antibodies for biologics — distinguishes immune-mediated failure (high antibodies, undetectable drug) from mechanistic failure (therapeutic levels, no antibodies) [2]
- TPMT/NUDT15 genotyping: Before initiating thiopurines
14. ECG
- Indications: Tachycardia, electrolyte abnormalities (hypokalemia, hypomagnesemia from chronic diarrhea), chest pain, or hemodynamic instability
- Findings to watch for: Prolonged QTc (electrolyte derangements), sinus tachycardia (dehydration, sepsis, anemia), ST changes (rare pericarditis as EIM) [1]
- Not routinely required in uncomplicated flares
15. Assessment
Severity stratification per ACG 2025 guidelines: [1]
- Mild-moderate: Ambulatory, tolerating oral intake, no systemic toxicity, no obstruction/abscess/fistula
- Moderate-severe: Failed mild-moderate treatment, or presents with fever, significant weight loss, abdominal tenderness, nausea/vomiting, anemia, elevated CRP/calprotectin, deeper ulcers on endoscopy
- Severe/fulminant: Persistent symptoms despite outpatient steroids/biologics, high fevers, peritoneal signs, cachexia, obstruction, or abscess — usually requires hospitalization
Key clinical pearl: In chronic, long-standing CD, symptoms may not represent active inflammation but rather structural damage (dysmotility, bile acid diarrhea, SIBO, visceral hypersensitivity). Objective confirmation of inflammation with biomarkers or imaging is essential before escalating therapy. [1-2]
16. Treatment Plan
Initial stabilization (ED/inpatient)
- IV fluid resuscitation, electrolyte correction
- NPO if obstruction suspected; otherwise, diet as tolerated
- VTE prophylaxis with subcutaneous heparin — IBD patients have a ~3-fold increased VTE risk; prophylactic anticoagulation reduces VTE (HR 0.62) without increasing bleeding [6][16-17]
- Pain management: acetaminophen preferred; avoid NSAIDs; use opioids sparingly
Medical therapy by severity
Post-induction
- Assess maintenance therapy adherence and efficacy; check biologic drug levels and antibodies [2]
- If immune-mediated failure → switch drug class; if mechanistic failure → switch mechanism of action [2]
- Early biologic initiation (infliximab + immunomodulator) in moderate-severe CD is associated with superior steroid-free remission at 1 year (79% vs 15% with step-up) [8]
- For biologic-experienced patients with inadequate response, moderate-certainty evidence supports adalimumab, risankizumab, or guselkumab over vedolizumab or ustekinumab [8]
Complications requiring specific management
- Abscess: Percutaneous drainage (if ≥3 cm) + IV antibiotics, then reassess for surgery vs. medical therapy [6]
- Obstruction with active inflammation: IV corticosteroids + bowel rest; surgical consultation [1][6]
- Perianal disease: Multidisciplinary approach — surgical drainage of abscess, seton placement, combined with medical therapy [6]
17. Disposition
Admission criteria (per AGA 2026 Best Practice Advice): [6]
- Severe disease refractory to outpatient treatment
- Suspected complications: obstruction, abscess, perforation, hemorrhage
- Significant nutritional risk or failure to thrive
- Hemodynamic instability, sepsis
- Inability to tolerate oral intake or medications
- Need for IV corticosteroids or inpatient biologic infusion
Observation indications
- Partial bowel obstruction responding to conservative management
- Moderate dehydration requiring IV fluids with expected improvement
Discharge criteria: [6]
- Stability of treatment response achieved before discharge
- Tolerating oral intake and medications
- Pain controlled with oral analgesics
- Clear discharge transition plan with outpatient GI follow-up established
- VTE prophylaxis plan addressed (consider extended prophylaxis in high-risk patients) [10][18]
Specialist consultation triggers
- GI: All admitted patients; outpatient urgent referral for moderate-severe flares
- Surgery: Obstruction not resolving with medical therapy, abscess requiring drainage, perforation, hemorrhage, fulminant disease not responding to medical rescue therapy
- Ophthalmology: New eye symptoms (uveitis, scleritis)
- Dermatology: Pyoderma gangrenosum (avoid debridement)
18. Follow Up / Return Precautions
- Follow-up timing: GI follow-up within 1–2 weeks of ED visit or discharge; sooner if on new steroid taper or biologic initiation
- Symptoms requiring immediate return:
- Worsening abdominal pain, distension, or inability to pass gas/stool
- High fever (>38.5°C / 101.3°F)
- Bloody stools with hemodynamic symptoms (lightheadedness, syncope)
- Signs of perianal abscess (increasing pain, swelling, drainage)
- Inability to tolerate oral fluids or medications
- Patient counseling:
- Smoking cessation — quitting reduces flare risk to that of nonsmokers and decreases need for steroids and surgery [1][19]
- Do not stop maintenance medications without discussing with GI
- Avoid NSAIDs; use acetaminophen for pain [3]
- Steroid tapers should not be self-adjusted
- Expected recovery: Mild-moderate flares typically improve within 1–2 weeks of steroid initiation; severe flares may require weeks of inpatient management and therapy optimization [1][8]
Images
References
1. ACG Clinical Guideline: Management of Crohn's Disease in Adults. — Lichtenstein GR, Loftus EV, Afzali A, et al. The American Journal of Gastroenterology. 2025.
2. Management of Crohn Disease: A Review. — Cushing K, Higgins PDR. The Journal of the American Medical Association. 2021.
3. ACG Clinical Guideline: Management of Crohn's Disease in Adults. — Lichtenstein GR, Loftus EV, Isaacs KL, et al. The American Journal of Gastroenterology. 2018.
4. Environmental Factors in the Relapse and Recurrence of Inflammatory Bowel Disease: A Review of the Literature. — Martin TD, Chan SS, Hart AR. Digestive Diseases and Sciences. 2015.
5. Crohn's Disease. — Dolinger M, Torres J, Vermeire S. Lancet. 2024.
6. AGA Clinical Practice Update on Inpatient Management of Adults With Inflammatory Bowel Disease: Expert Review. — Cohen-Mekelburg S, Hashash JG, Loftus EV, Rubin DT. Gastroenterology. 2026.
7. The Management of Emergency Hospital Visits for Inflammatory Bowel Diseases: A French National Expert Consensus Report. — Hébuterne X, Peyrin-Biroulet L, Hausfater P. Digestive and Liver Disease : Official Journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver. 2020.
8. Management of Crohn Disease in Adults. — Choden T, Levine E, Davis AM. The Journal of the American Medical Association. 2026.
9. AGA Clinical Practice Guidelines on the Medical Management Of Moderate to Severe Luminal and Perianal Fistulizing Crohn's Disease. — Feuerstein JD, Ho EY, Shmidt E, et al. Gastroenterology. 2021.
10. Venous Thromboembolism in Inflammatory Bowel Disease. — Cheng K, Faye AS. World Journal of Gastroenterology. 2020.
11. AGA Clinical Practice Update on Diet and Nutritional Therapies in Patients With Inflammatory Bowel Disease: Expert Review. — Hashash JG, Elkins J, Lewis JD, Binion DG. Gastroenterology. 2024.
12. Newer Biologic and Small-Molecule Therapies for Inflammatory Bowel Disease. — Baumgart DC, Le Berre C. The New England Journal of Medicine. 2021.
13. Lifestyle, Behaviour, and Environmental Modification for the Management of Patients With Inflammatory Bowel Diseases: An International Organization for Study of Inflammatory Bowel Diseases Consensus. — Ananthakrishnan AN, Kaplan GG, Bernstein CN, et al. The Lancet. Gastroenterology & Hepatology. 2022.
14. Predictors of relapse in patients with Crohn's disease in remission after 1 year of biological therapy. — Molnár T, Lakatos PL, Farkas K, et al. Alimentary Pharmacology & Therapeutics. 2013.
15. WSES-AAST Guidelines: Management of Inflammatory Bowel Disease in the Emergency Setting. — De Simone B, Davies J, Chouillard E, et al. World Journal of Emergency Surgery : WJES. 2021.
16. Consensus Statements on the Risk, Prevention, and Treatment of Venous Thromboembolism in Inflammatory Bowel Disease: Canadian Association of Gastroenterology. — Nguyen GC, Bernstein CN, Bitton A, et al. Gastroenterology. 2014.
17. Effectiveness and Safety of Prophylactic Anticoagulation Among Hospitalized Patients With Inflammatory Bowel Disease. — Dawwas GK, Cuker A, Schaubel DE, Lewis JD. Blood Advances. 2024.
18. Venous Thromboembolic Events in Inflammatory Bowel Diseases: A Review of Current Evidence and Guidance on Risk in the Post-Hospitalization Setting. — Murthy SK, Robertson McCurdy AB, Carrier M, McCurdy JD. Thrombosis Research. 2020.
19. ACG Clinical Guideline Update: Preventive Care in Inflammatory Bowel Disease. — Farraye FA, Melmed GY, Lichtenstein GR, et al. The American Journal of Gastroenterology. 2025.