Endoscopy, in full.

Diagnose acute pancreatitis (AP) by the Atlanta criteria (2 of 3: characteristic epigastric/LUQ pain, lipase or amylase >3x ULN [lipase preferred for specificity/duration], or characteristic imaging). ACG 2024 stratifies severity risk using SIRS on admission plus bedside risk factors, rising/elevated BUN, rising/elevated hematocrit (>44), obesity (BMI>30), extrapancreatic fluid collections/pleural effusion/infiltrates, altered mental status, and older age/comorbidities, rather than mandating a formal BISAP or APACHE II composite score. Give moderately aggressive lactated Ringer's, most important in the first 6-12 hours, reassessing volume status/BUN/HCT at 6 hours (further aggressive hydration has little added benefit after 24-48h). Start oral low-fat solid food within 24-48h as tolerated in mild disease; if enteral feeding is needed for moderately severe/severe disease, prefer nasogastric over nasojejunal with small-peptide/medium-chain-triglyceride formula and continuous (not bolus/cyclic) feeding; avoid parenteral nutrition if possible. Do not give prophylactic antibiotics, even in severe disease or sterile necrosis; reserve antibiotics for suspected infected necrosis (typically arising 10-14 days in), and choose agents that penetrate pancreatic necrosis while together covering both gut-derived gram-negative enterics and anaerobes, a carbapenem supplies this as monotherapy, whereas a fluoroquinolone or a third-or-higher-generation cephalosporin must be combined with metronidazole; metronidazole alone (anaerobic cover only), or a cephalosporin or a quinolone alone, does not adequately treat infected necrosis. Perform cholecystectomy preferably before discharge for mild acute biliary pancreatitis, and after a second unexplained AP episode even without identified gallstones; reserve ERCP within 24h for AP complicated by cholangitis, with rectal indomethacin +/- pancreatic duct stent and periprocedural hydration to reduce post-ERCP pancreatitis risk. Check triglycerides when gallstones/alcohol are absent (>1000 mg/dL supports a hypertriglyceridemia etiology). For stable pancreatic necrosis, defer surgical, radiological, or endoscopic intervention 4-6 weeks to allow walling-off (step-up approach).

Perform individual gastric risk assessment and staging of precancerous conditions at first-time gastroscopy, irrespective of the patient's country of origin. Use high quality endoscopy with virtual chromoendoscopy (VCE), after proper training, for screening, diagnosis and staging of atrophy and intestinal metaplasia and after endoscopic therapy; VCE guides the biopsy site, with random biopsies taken only when there are no endoscopically suspected changes. Take biopsies from at least two topographic sites, 2 from the antrum/incisura and 2 from the corpus, VCE-guided, in two separate, clearly labeled vials; an additional incisura biopsy is optional, not required. Stage with validated endoscopic classifications of atrophy (e.g. Kimura-Takemoto) or intestinal metaplasia (e.g. EGGIM) to stratify gastric cancer risk (suggestion, weaker than the biopsy recommendation). Follow up patients with extensive endoscopic changes (Kimura C3+ or EGGIM 5+) OR an advanced histological stage that reaches OLGA/OLGIM III/IV, severe atrophy or intestinal metaplasia and/or significant changes in both antrum and corpus rising to stage III/IV, not any intestinal metaplasia or any antrum-plus-corpus involvement on its own, with high quality endoscopy every 3 years, irrespective of country of origin (strong recommendation, moderate quality). Propose NO surveillance for patients with mild to moderate atrophy or intestinal metaplasia restricted to the antrum, in the absence of endoscopic signs of extensive lesions or other risk factors (family history of gastric cancer, incomplete intestinal metaplasia, persistent H. pylori infection), the guideline states this group constitutes most individuals found in clinical practice. Eradicate H. pylori in all patients with precancerous conditions and after endoscopic or surgical therapy. Discontinue or do not start gastric cancer screening or surveillance in asymptomatic individuals over 80, and weigh comorbidities when planning treatment of superficial lesions. Advise smoking cessation; low-dose daily aspirin may be considered for gastric cancer prevention only in selected individuals already at high cardiovascular risk. For visible neoplasia, use ESD for differentiated lesions clinically staged as dysplastic (low or high grade) or intramucosal carcinoma (any size if not ulcerated, or ≤30 mm if ulcerated), with EMR an alternative for Paris 0-IIa lesions ≤10 mm with low likelihood of malignancy. At the population level, endoscopic screening is suggested every 2-3 years in high-risk regions (age-standardized rate >20 per 100,000 person-years), every 5 years in intermediate-risk regions (ASR 10-20) only if cost-effectiveness has been proven, and not at all in low-risk regions (ASR <10).

DIAGNOSIS: Diagnosis of BE requires intestinal metaplasia in the tubular esophagus (conditional, very-low certainty) AND columnar mucosa of at least 1 cm (conditional, low). Patients with a normal-appearing Z line, or a Z line with <1 cm proximal displacement from the top of the gastric folds and no visible lesion, should NOT undergo routine biopsy. At screening endoscopy with findings consistent with possible BE, obtain at least 8 biopsies, following the Seattle protocol (4-quadrant biopsies every 1-2 cm plus targeted sampling of any visible lesion) for segments longer than 4 cm (conditional, low). The at-least-8-biopsy minimum applies to all screening exams regardless of segment length and is NOT waived for shorter (<=4 cm) segments; when a short segment - typically 1-2 cm, e.g. a single tongue - will not physically support 8 biopsies, obtain at least 4 biopsies per cm of circumferential BE and 1 biopsy per cm of tongues of BE, so that short segments are still adequately sampled and dysplasia or cancer is not missed. Dysplasia of any grade must be confirmed by a SECOND pathologist with expertise in GI pathology (STRONG, low). SURVEILLANCE: Use both high-definition white-light endoscopy AND chromoendoscopy (STRONG, moderate) with a structured biopsy protocol (STRONG, low). Intervals are dictated by degree of dysplasia (conditional, very-low) and by segment length (STRONG, moderate): nondysplastic BE <3 cm - EGD every 5 years; nondysplastic BE >=3 cm - EGD every 3 years. Indefinite for dysplasia (confirmed by a second pathologist), any length - escalate to twice-daily PPI and repeat EGD within 6 months; if still indefinite, EGD annually; if downgraded/upgraded, follow the NDBE or LGD algorithm. Confirmed LGD opting for surveillance - EGD at 6 months, at 12 months from diagnosis, then annually, sampling with 4-quadrant biopsies every 1 cm. MEDICAL: At least once-daily PPI in patients with BE without allergy or other contraindication to PPI use (conditional, VERY-LOW certainty); higher/twice-daily dosing is reserved for those who need it for symptom control, as the incremental antineoplastic benefit of dose escalation is unclear. Suggest AGAINST antireflux surgery as an antineoplastic measure (conditional, low). No recommendation could be made on aspirin plus PPI chemoprevention, on WATS-3D, or on p53 IHC/TissueCypher. ENDOSCOPIC THERAPY: For BE with HGD or intramucosal carcinoma (T1a), EET is recommended over ESOPHAGECTOMY (STRONG, moderate). For confirmed LGD, endoscopic therapy is SUGGESTED to reduce progression to HGD/EAC, with endoscopic surveillance of confirmed LGD explicitly retained as an ACCEPTABLE ALTERNATIVE (conditional, moderate) - this is a shared-decision-making choice, not a mandate. Resect all visible lesions endoscopically BEFORE ablation of the residual segment (conditional, very-low); RFA is the preferred ablative modality; goal is complete eradication of intestinal metaplasia. EET should be performed at high-volume centers (conditional, very-low). T1b (submucosal) cancer: the default is surgical referral for esophagectomy, BUT EET may be considered for sm1 disease (invasion into the upper third of the submucosa, depth <500 micrometers) with low-risk features - well differentiated, <2 cm, no lymphovascular invasion, negative deep margin. Patients with high-risk histology are best treated with esophagectomy unless they are poor surgical candidates, for whom multidisciplinary discussion of alternatives such as ADJUVANT chemoradiation may be appropriate. POST-EET: An endoscopic surveillance program is recommended after successful EET (STRONG, moderate), with intervals set by the BASELINE degree of dysplasia: baseline LGD - 1 year, 3 years, then every 2 years; baseline HGD or T1a - 3, 6, and 12 months, then annually.

Diagnose acute pancreatitis (AP) by the Atlanta criteria (2 of 3: characteristic epigastric/LUQ pain, lipase or amylase >3x ULN [lipase preferred for specificity/duration], or characteristic imaging). ACG 2024 stratifies severity risk using SIRS on admission plus bedside risk factors, rising/elevated BUN, rising/elevated hematocrit (>44), obesity (BMI>30), extrapancreatic fluid collections/pleural effusion/infiltrates, altered mental status, and older age/comorbidities, rather than mandating a formal BISAP or APACHE II composite score. Give moderately aggressive lactated Ringer's, most important in the first 6-12 hours, reassessing volume status/BUN/HCT at 6 hours (further aggressive hydration has little added benefit after 24-48h). Start oral low-fat solid food within 24-48h as tolerated in mild disease; if enteral feeding is needed for moderately severe/severe disease, prefer nasogastric over nasojejunal with small-peptide/medium-chain-triglyceride formula and continuous (not bolus/cyclic) feeding; avoid parenteral nutrition if possible. Do not give prophylactic antibiotics, even in severe disease or sterile necrosis; reserve antibiotics for suspected infected necrosis (typically arising 10-14 days in), and choose agents that penetrate pancreatic necrosis while together covering both gut-derived gram-negative enterics and anaerobes, a carbapenem supplies this as monotherapy, whereas a fluoroquinolone or a third-or-higher-generation cephalosporin must be combined with metronidazole; metronidazole alone (anaerobic cover only), or a cephalosporin or a quinolone alone, does not adequately treat infected necrosis. Perform cholecystectomy preferably before discharge for mild acute biliary pancreatitis, and after a second unexplained AP episode even without identified gallstones; reserve ERCP within 24h for AP complicated by cholangitis, with rectal indomethacin +/- pancreatic duct stent and periprocedural hydration to reduce post-ERCP pancreatitis risk. Check triglycerides when gallstones/alcohol are absent (>1000 mg/dL supports a hypertriglyceridemia etiology). For stable pancreatic necrosis, defer surgical, radiological, or endoscopic intervention 4-6 weeks to allow walling-off (step-up approach).

Distinguish benign from malignant biliary strictures using cross-sectional imaging (MRI/MRCP preferred over contrast-enhanced CT) plus laboratory tests, interpreting CA19-9 after biliary decompression and never relying on tumor markers alone; check serum IgG4 when IgG4-related sclerosing cholangitis is suspected (HISORt criteria). Per the ESGE 2024 diagnostic work-up guideline, tissue-acquisition strategy now branches by stricture location rather than following one linear sequence: for DISTAL extrahepatic strictures with jaundice and no pancreatic mass, combined same-session EUS-guided tissue acquisition (EUS-TA, end-cutting FNB needle) plus ERCP-based tissue acquisition (standard brush cytology plus fluoroscopy-guided biopsy) is the strongly preferred first-line approach; for PERIHILAR strictures, obtain brush cytology plus fluoroscopy-guided biopsy at index ERCP, escalate indeterminate strictures to cholangioscopy-guided biopsy (with intraductal ultrasound/confocal laser endomicroscopy selectively), and reserve EUS-TA for cases where ERCP-based sampling is insufficient and curative resection is not feasible and/or extraluminal disease is accessible; escalate any positive or indeterminate feature to multidisciplinary tumor board. Manage benign anastomotic and chronic-pancreatitis strictures with a fully-covered self-expanding metal stent for 6-12 months (multiple plastic stents when FCSEMS is contraindicated, hepaticojejunostomy if refractory). Treat cholangitis with biliary obstruction as an indication for urgent biliary drainage, but do not instrument every obstructed sector: for hilar or multisegmental strictures (Bismuth II-IV), ESGE suggests draining ≥50% of the liver volume and avoiding opacification of biliary ducts that will not be drained (weak recommendation, low-quality evidence), because post-ERCP cholangitis frequently complicates injection of obstructed ducts that are not subsequently drained, whereas drainage of >50% of liver volume is associated with less cholangitis and longer survival; ESGE suggests antibiotic prophylaxis before biliary stenting in selected patients (e.g., immunocompromised patients, expected incomplete biliary drainage; weak recommendation, moderate-quality evidence), with a full antibiotic course if adequate drainage is not achieved during the procedure. Direct etiology-specific care for Strasberg bile-duct injuries, post-transplant strictures (ASGE 2023: ERCP preferred over PTBD, covered SEMS preferred over multiple plastic stents), IgG4-sclerosing cholangitis, Mirizzi syndrome, and choledochal cysts.

For right upper quadrant pain, characterize the pattern (acute vs chronic, post-meal vs unrelated, with vs without fever/jaundice) and triage acute red-flag presentations (Murphy sign, Charcot's triad, painless jaundice with weight loss, pregnancy with LFT/coagulation derangement) to the ED. Obtain labs (CBC, CMP with LFTs, lipase, urinalysis, pregnancy test in reproductive-age women) and RUQ ultrasound as first imaging, then direct further workup by ultrasound findings, cholecystectomy for acute cholecystitis, MRCP for suspected choledocholithiasis based on risk stratification (e.g., high-risk criteria including CBD dilation >6 mm, bilirubin >4 mg/dL, or gallstone pancreatitis), CCK-HIDA/GBEF for acalculous functional gallbladder disorder, and cross-sectional imaging for liver masses or other pathology.

DIAGNOSIS (patient must be on a gluten-containing diet). Serologic testing consists of TTG-IgA plus, if IgA deficiency has not previously been excluded, concurrent total IgA; if IgA deficiency is present, measure an IgG-based serology (DGP-IgG and/or TTG-IgG). This algorithm, previously restricted to those >=2 years, now applies to adults and children at ANY age. An elevated TTG-IgA should proceed to EGD with duodenal biopsy. A negative TTG-IgA in a non-IgA-deficient patient adequately rules out CD only when pretest probability is low or moderate; in symptomatic patients whose pretest suspicion is high (>5%), EGD with duodenal biopsy should be performed irrespective of serologic result. ACG recommends EGD with multiple duodenal biopsies to confirm the diagnosis in both children and adults with suspicion of CD (STRONG recommendation, moderate quality; 1 dissent); sampling should be 1 or 2 biopsies from the bulb (9-o'clock or 12-o'clock position) and at least 4 from the distal duodenum. Lymphocytic duodenosis (>=25 IELs/100 epithelial cells) without villous atrophy is NOT specific for CD. NONBIOPSY PATHWAY (CONDITIONAL recommendation, moderate quality): a combination of high-level TTG-IgA (>10x ULN) with a positive EMA in a SECOND blood sample is suggested as reliable for diagnosis in CHILDREN, and only if the family agrees with the no-biopsy strategy; in SYMPTOMATIC ADULTS unwilling or unable to undergo upper GI endoscopy the same criteria may be considered AFTER THE FACT, as a diagnosis of 'likely CD', ACG does not endorse a prospective no-biopsy pathway in adults, noting a >=10-fold TTG-IgA elevation carries a PPV of only ~95% in adults, which may be unacceptably low given lifelong treatment implications. HLA-DQ2/DQ8 is not required for diagnosis but is useful for serology-histology discrepancy or in patients already on a GFD; if negative, CD is ruled out. TREATMENT AND MONITORING. Strict lifelong GFD. A visit with a dietitian after diagnosis is MANDATORY, with subsequent visits as needed to reinforce education and adherence encouraged; interview with a dietitian experienced in the GFD is the standard of care for assessing adherence. ACG RECOMMENDS consumption of gluten-free oats (STRONG recommendation, moderate quality), with the qualifier that gluten contamination of oats, variable toxicity across oat varieties, and a small risk of immune reaction to avenin require monitoring for oat tolerance (monitoring intervals are not known). ACG suggests AGAINST routine use of gluten detection devices in food or biospecimens (conditional, low quality; 1 dissent), and finds INSUFFICIENT EVIDENCE to recommend for or against probiotics (evidence gap). ACG suggests setting a goal of intestinal healing as an end point of GFD therapy, advocating individualized discussion of goals beyond clinical and serological remission (CONDITIONAL recommendation, low quality). Follow-up may require multiple visits in the first year (e.g. 3, 6, and 12 months) and regular visits (e.g. twice a year or yearly) thereafter, tracking symptoms and TTG or DGP serology; other tests may include CBC, ALT, AST, vitamins A/D/E/B12, copper, zinc, folic acid, ferritin, and iron, with follow-up bloodwork individualized to verify correction of values abnormal at baseline. Preventive care includes vaccines and DXA. Symptoms improve within days of strict adherence (diarrhea improved in 80% within 60 days), but mucosal healing lags: median time from GFD onset to mucosal healing in adults is 3 years, so it is reasonable to consider a follow-up biopsy in adults after 2 years of starting a GFD, in the ABSENCE of symptoms, after shared decision-making; children heal faster (95% within 2 years), altering the risk-benefit calculus. Repeat biopsy is the only reliable method to document mucosal healing, seroconversion correlates poorly. Upper endoscopy with biopsies is also indicated for lack of clinical response or relapse of symptoms despite a GFD. VACCINATION: ACG suggests vaccination to prevent pneumococcal disease in patients with CD (CONDITIONAL recommendation, low quality), because increased pneumococcal risk is attributed to hyposplenism (frequently subclinical) present in roughly one-third of patients. The regimen follows CDC recommendations by age, immunization record, and comorbidity: for an adult with CD and functional asplenia not previously vaccinated or with unknown history, 1 dose of PCV15 (followed by PPSV23 at least 1 year later) or 1 dose of PCV20 (no PPSV23 indicated); for an adult with CD and no other condition carrying a specific CDC recommendation, ACG suggests 1 dose of PCV20 alone, or 1 dose of PCV15 first and then consider PPSV23 at least 1 year later. NONRESPONSIVE CD (NRCD): defined as persistent symptoms, signs, or laboratory abnormalities typical of CD despite 6-12 MONTHS of dietary gluten avoidance. Evaluation should review and confirm the initial diagnosis of CD, assess for inadvertent gluten exposure (via expert dietitian assessment and serology, positive serologies despite 12 months of GFD suggest ongoing gluten ingestion), assess for a coexisting functional disorder, and selectively test based on clinical suspicion for food intolerances (e.g. lactose, fructose), pancreatic insufficiency, microscopic colitis, and small intestinal bacterial overgrowth, among others. REFRACTORY CD (RCD) is a separate, rarer entity (<1% of patients outside referral centers): ongoing malabsorptive symptoms and signs with villous atrophy despite strict adherence to a GFD for MORE THAN 12 months and absence of other disorders including overt lymphoma; initial assessment centers on distinguishing RCD type 1 from type 2 by CD3/CD8 immunostains, T-cell receptor clonality by PCR, and/or flow cytometry of duodenal biopsies.

Evaluate for achalasia any patient with dysphagia to solids and liquids, regurgitation, or chest pain, and specifically consider it in patients presumed to have GERD who do not respond to acid suppression (strong recommendation, very low quality). Diagnose with high-resolution manometry using esophageal pressure topography rather than conventional line tracings (strong, high). Subtype by Chicago Classification (I, II, III), this is a conditional recommendation (low quality): subtyping may inform prognosis and treatment choice, with type II having the most favorable outcomes and type III requiring a longer/tailored myotomy; ACG does not make subtyping mandatory for diagnosis. Always perform upper endoscopy in suspected achalasia to exclude pseudoachalasia from an obstructing mass; use cross-sectional imaging and/or endoscopic ultrasound in difficult cases (ACG states this as narrative guidance, not a numbered recommendation, and specifies no biopsy protocol). FLIP is described as complementary, useful in patients who cannot tolerate manometry and as an arbiter in difficult cases where manometry fails to diagnose achalasia despite high clinical suspicion, not as a required confirmatory test. TREATMENT: pneumatic dilation is superior to medical therapy for symptom relief and esophageal emptying (strong, very low). PD and laparoscopic Heller myotomy are both effective and equivalent short- and long-term for patients who are candidates for definitive therapy (strong, high). POEM and LHM give comparable symptomatic improvement (strong, moderate). POEM and PD give comparable symptomatic improvement in type I or II (conditional, low). For type III, tailored POEM or LHM is recommended as a more efficacious disruptive LES therapy than PD (strong, moderate), ACG does NOT single out POEM over LHM for type III. When surgical myotomy is performed, add fundoplication: myotomy with fundoplication is superior to myotomy alone for controlling distal esophageal acid exposure (strong, moderate), using either Dor or Toupet (conditional, moderate). Botulinum toxin injection is first-line therapy for patients unfit for definitive therapy (strong, moderate), and prior botulinum toxin does not significantly compromise subsequent myotomy performance or outcomes (strong, low). POEM carries a higher incidence of GERD than LHM with fundoplication or PD (strong, moderate). Do not place stents for long-term dysphagia (strong, low). Reserve esophagectomy for surgically fit patients with megaesophagus who have failed other interventions (strong, low), and consider Heller myotomy before esophagectomy in patients who failed PD and POEM when the anatomy is conducive and there is evidence of incomplete myotomy (strong, very low). FOLLOW-UP: use timed barium esophagram as the first-line test to evaluate continued or recurrent symptoms after definitive therapy (strong, very low); the Eckardt score alone or HRM alone should not be used to define treatment failure. Do not obtain routine gastrografin esophagram after dilation, reserve it for clinical suspicion of perforation (strong, low). RETREATMENT: PD is appropriate and safe after failed surgical myotomy or POEM (strong, moderate), and POEM is safe in patients who previously underwent PD or LHM (strong, low). SURVEILLANCE: ACG recommends AGAINST routine endoscopic surveillance for esophageal carcinoma in patients with achalasia (strong, low), although risk is elevated (~1 cancer per 300 patient-years), absolute numbers are low, an estimated >400 endoscopies would be needed to detect one cancer, and surveillance has not demonstrated improved survival.

Suspected small-bowel bleeding (SSBB), bleeding between the ampulla of Vater and the ileocecal valve, suspected when GI bleeding persists after negative upper and lower endoscopy. Small-bowel capsule endoscopy (SBCE) is recommended as the FIRST-LINE examination, before other endoscopic and radiological tests (strong, moderate). ESGE does NOT recommend routine second-look endoscopy prior to SBCE in suspected small-bowel bleeding or iron-deficiency anemia (strong, low). In OVERT suspected small-bowel bleeding, perform SBCE as soon as possible after the bleeding episode, ideally within 48 hours, to maximize diagnostic and therapeutic yield (strong, high). Device-assisted enteroscopy (DAE) is recommended to confirm and possibly treat lesions identified by SBCE (strong, high); in overt suspected small-bowel bleeding, DAE should optimally be performed within 48-72 hours of the bleeding episode (strong, high). Where SBCE is unavailable or contraindicated, DAE and/or dedicated small-bowel cross-sectional imaging may be considered first, depending on availability, expertise and clinical suspicion (weak, low). After a HIGH-QUALITY NEGATIVE SBCE, ESGE recommends conservative management (strong, moderate), the 2015 wording qualified this as patients without ongoing bleeding evidenced by overt bleeding or continued transfusion requirement, and the 2022 update carries this qualifier as a separate companion recommendation: for patients with a high-quality negative SBCE who have ONGOING overt bleeding or a continued need for blood transfusions, ESGE recommends further investigation using repeat SBCE, DAE, or dedicated small-bowel cross-sectional imaging (strong, moderate). SBCE is also recommended first-line in iron-deficiency anemia when small-bowel evaluation is indicated (strong, high), and after unremarkable or nondiagnostic dedicated small-bowel cross-sectional imaging if likely to influence management (strong, low). CROHN'S DISEASE: in SUSPECTED Crohn's with negative ileocolonoscopy, SBCE is the initial small-bowel modality ONLY in the absence of obstructive symptoms or known bowel stenosis (strong, high); in that group ESGE explicitly does NOT recommend routine cross-sectional imaging or a patency capsule before SBCE (strong, HIGH quality). With obstructive symptoms or known stenosis, dedicated cross-sectional imaging (MRE/MR-enteroclysis or CTE/CT-enteroclysis) is used FIRST (strong, moderate), and a patency capsule is recommended before SBCE in suspected Crohn's with obstructive symptoms (strong, low), even when cross-sectional imaging is negative. In ESTABLISHED Crohn's, a patency capsule before SBCE is recommended to decrease the retention rate (strong, moderate). SMALL-BOWEL TUMORS: SBCE is recommended where there is increased risk of a small-bowel tumor (strong, moderate); ESGE does NOT recommend specific investigations before SBCE in suspected small-bowel tumor UNLESS the patient is considered at risk of capsule retention (strong, low). If imaging has ALREADY demonstrated a suspected small-bowel tumor, DAE is preferred over SBCE (strong, low). Cross-sectional imaging is recommended for staging and operability when SBCE shows a tumor with high diagnostic certainty (strong, low); where the capsule diagnosis is uncertain, biopsy sampling AND tattooing of the location by DAE is recommended (strong, low); for a subepithelial mass, confirm by DAE and/or cross-sectional imaging per local availability/expertise (strong, low). SBCE is NOT recommended for follow-up of treated small-bowel tumors, for lack of data (strong, low). PATENCY/RETENTION generally: GI obstruction is an absolute contraindication to SBCE. If the patency capsule is egested intact, retention of a real capsule is unlikely; if not egested within 30 hours, cross-sectional imaging (not plain abdominal radiography) is favored to localize it. In Peutz-Jeghers syndrome, routine patency capsule use is NOT recommended and should be considered case-by-case.

ACG 2025 makes 19 GRADE-rated statements plus non-graded key concepts. DIAGNOSIS: EoE is diagnosed by symptoms of esophageal dysfunction plus at least 15 eos/hpf in at least 1 hpf on esophageal biopsy, after evaluating for non-EoE disorders that cause or potentially contribute to esophageal eosinophilia (strong recommendation, low-quality evidence). A PPI trial is NOT a diagnostic criterion and the term PPI-REE is abandoned; PPIs are positioned purely as a treatment. Obtain at least 6 esophageal biopsies from at least 2 esophageal levels (e.g., proximal/mid and distal), targeting endoscopic findings if possible (strong, low). Use a systematic endoscopic scoring system such as the EoE Endoscopic Reference Score (EREFS) at every endoscopy (strong, low). Quantify eosinophil counts, not merely report them as above threshold, on biopsies from every endoscopy performed for EoE (strong, low), since serial counts gauge anti-inflammatory effect; the guideline notes eosinophil density (~60 eos/mm2) may be preferable for cross-setting comparison but that this has not yet been adopted in practice. Key concept: perform the diagnostic endoscopy off treatment (no dietary restriction and no PPI) to maximize diagnostic sensitivity. TREATMENT, the three anti-inflammatory options do NOT carry equal recommendation strength: swallowed topical steroids are recommended (STRONG, moderate evidence); PPIs are suggested (CONDITIONAL, low); empiric food elimination diet is suggested (CONDITIONAL, low). Because the field lacks comparative efficacy trials, the guideline states the choice among them is individualized to disease characteristics and patient preference within a shared decision-making framework, and advises that a single anti-inflammatory therapy be selected initially. Either fluticasone propionate or budesonide is a reasonable initial topical steroid (conditional, low); options include the FDA-approved budesonide oral suspension, the EMA-approved budesonide orodispersible tablet, and off-label asthma preparations adapted for esophageal delivery. Administer topical steroids after meals or at bedtime with nothing to eat or drink for 30-60 minutes to maximize esophageal dwell time; in young children prefer a slurry/suspension over an inhaler device. Dosing (Table 6): high-dose PPI, adults, double the approved reflux dose per day (e.g., omeprazole 20 mg twice daily or 40 mg daily or PPI equivalent); children, 2 mg/kg/day (or 1 mg/kg twice daily). Budesonide, adults 2-4 mg/day, divisible twice daily (approved budesonide oral suspension dosing is 2 mg twice daily); children 1-2 mg/day by age/height/weight. Fluticasone, adults 1,760 mcg/day in divided doses; children 110-880 mcg/day in divided doses. Currently available allergy testing (skin prick, patch, or serum Ig panels) is NOT suggested to direct elimination diets (conditional, very low). Providers MAY consider starting with a less-restrictive empiric elimination (1FED or 2FED) as the initial diet choice, incorporating patient preference through shared decision-making, and should collaborate with a dietician or nutritionist; after an initial dietary response a structured food reintroduction process is advised, with endoscopy and biopsy after each food reintroduced, because symptoms alone must not be used to determine food triggers. BIOLOGICS: dupilumab is suggested for EoE in individuals 12 years of age or older who are nonresponsive to PPI therapy (conditional, moderate) and, as a separate statement, for pediatric patients aged 1-11 years weighing at least 15 kg who are nonresponsive to PPI therapy (conditional, low). Dosing: 15 to <30 kg, 200 mg subcutaneously every other week; 30 to <40 kg, 300 mg subcutaneously every other week; >=40 kg, 300 mg subcutaneously weekly. Key concept: use dupilumab as step-up therapy in difficult-to-treat patients, and consider it in patients with multiple atopic conditions that would independently meet requirements for its use; the guideline explicitly states its position in the treatment algorithm is still being determined. No recommendation can be made for or against cendakimab, benralizumab, lirentelimab, mepolizumab, or reslizumab. Omalizumab is suggested AGAINST (conditional, low), as are cromolyn and montelukast (conditional, very low). DILATION: endoscopic dilation is suggested as an ADJUNCT to medical therapy for esophageal strictures causing dysphagia (conditional, low). Dilation alone does not affect underlying inflammatory disease activity, so in fibrostenotic EoE it should occur in conjunction with effective medical or dietary anti-inflammatory therapy. Use a start-low-and-go-slow approach: begin with a dilator size that may underestimate esophageal caliber, relook after dilation, and work to larger sizes until a mucosal disruption ('dilation effect') or the target diameter is reached. In adults and adolescents, a goal luminal diameter that relieves dysphagia and food impaction, typically at least 16 mm, should be achieved over one or more sessions, depending on initial luminal caliber and the effect observed during dilation. Dilation technique may be chosen by stricture characteristics and endoscopist preference. MAINTENANCE: continuation of EFFECTIVE dietary or pharmacologic therapy is advised to prevent recurrence of symptoms, histologic inflammation, and endoscopic abnormalities, notably graded STRONG despite low-quality evidence, because disease activity almost universally recurs when treatment is stopped. For patients on pharmacologic treatment, providers should consider identifying the lowest effective dose for long-term use, with any dose-reduction decision individualized. MONITORING AND RESPONSE: evaluate treatment response with symptomatic AND endoscopic AND histologic outcomes (strong, low); providers are advised NOT to monitor symptoms alone, since symptoms do not strongly correlate with endoscopic or histologic disease activity. Perform endoscopy to assess response 8-12 weeks after starting a new therapy such as PPI, topical steroid, or food elimination diet; for dupilumab the assessment interval may range from 12 to 24 weeks based on clinical trial findings. Providers MAY consider using a histologic response threshold of <15 eos/hpf, with the improvement in eosinophil count interpreted in the context of other histologic features, endoscopic findings, and symptoms, the guideline frames this as a 'may consider' key concept rather than a fixed target. Follow-up should be individualized and at shorter intervals for patients with complications (food impaction, perforation, strictures requiring dilation, malnutrition); repeat endoscopy after any treatment change such as dose reduction; care gaps of 2 years or more are associated with progression to fibrostenosis. PEDIATRIC-SPECIFIC: in children with EoE and dysphagia, an esophagram is suggested to evaluate fibrostenotic disease (conditional, very low); evaluation by a feeding therapist and/or dietician is suggested as an adjunctive intervention in children with feeding dysfunction (conditional, very low); growth, development including eating skills, and nutrition are treatment goals in children in addition to symptomatic, endoscopic, and histologic goals.