The week in GI, filtered to what is worth knowing.

Two current US guidelines govern Crohn's disease and should be read together. ACG 2025 (Lichtenstein et al.) remains the reference for diagnosis, mild-to-moderate disease, perianal, postoperative and abscess management. DIAGNOSIS: fecal calprotectin (>50-100 μg/g) separates inflammatory from noninflammatory disease of the colon. Workup is ileocolonoscopy with biopsies, including uninvolved mucosa, plus small-bowel imaging. CTE and MRE are comparable; prefer MRE in patients <35 y and when serial exams are likely. Intestinal ultrasound is an ungraded adjunct. Do routine CRC surveillance in Crohn's colitis. MILD-TO-MODERATE: recommend against oral mesalamine; sulfasalazine only for symptomatic mild colonic CD; ileal-release budesonide 9 mg for induction in ileocecal disease but not for maintenance. MODERATE-TO-SEVERE (AGA Living Guideline, Scott et al., Gastroenterology 2025;169(7):1397-1448, 16 recommendations: 1 strong, 9 conditional, 6 knowledge gaps; updated quarterly, adult outpatients only): RECOMMEND infliximab, adalimumab, ustekinumab, risankizumab, mirikizumab, guselkumab or upadacitinib over no treatment; SUGGEST certolizumab pegol or vedolizumab over no treatment. Advanced-therapy-naive: suggest higher-efficacy agents (infliximab, adalimumab, vedolizumab, ustekinumab, risankizumab, mirikizumab, guselkumab) over lower-efficacy ones (certolizumab pegol, upadacitinib). Prior advanced-therapy (especially anti-TNF) exposure: suggest higher- or intermediate-efficacy agents (adalimumab, risankizumab, guselkumab, upadacitinib; ustekinumab, mirikizumab) over lower-efficacy ones (vedolizumab, certolizumab pegol). Suggest against thiopurine monotherapy for induction; suggest it for maintenance of remission. Suggest SC/IM methotrexate monotherapy; suggest against oral methotrexate. In thiopurine-naive patients starting infliximab, suggest infliximab + thiopurine over infliximab alone. No recommendation on IFX + MTX, adalimumab + immunomodulator, or non-TNF biologic + immunomodulator. After ≥6 months of steroid-free remission on anti-TNF + immunomodulator, suggest withdrawing the immunomodulator and suggest against withdrawing the anti-TNF. SUGGEST upfront advanced therapy over step-up therapy (corticosteroids and/or immunomodulator first). No recommendation on treating to endoscopic vs symptomatic remission. The ACG 2025 moderate-to-severe recommendations (anti-TNF, IFX + thiopurine combination and IL-12/23/IL-23 agents, each strong/moderate; upadacitinib after anti-TNF exposure; steroids for short-term induction only; TPMT/NUDT15 testing before thiopurines) still stand alongside AGA. ACG perianal (infliximab first; drain abscesses and place setons before escalating), postoperative (endoscopy at 6-12 months; anti-TNF strong, vedolizumab conditional in high-risk patients) and intra-abdominal abscess (>2 cm: antibiotics plus drainage, hold immunosuppression) positions are unchanged. THERAPEUTIC ENDOSCOPY (AGA Clinical Practice Update, CGH 2026; details below come from AGA news coverage, not the full text, and are ungraded advice): get cross-sectional imaging before the procedure. Endoscopic balloon dilation is first-line for short strictures (about ≤4-5 cm) with few risk factors (fistula, prestenotic dilation >5 cm, high CRP, prior anti-TNF). Longer or multiple strictures, or ≥3 risk factors, favor surgery.

Two current US guidelines govern Crohn's disease and should be read together. ACG 2025 (Lichtenstein et al.) remains the reference for diagnosis, mild-to-moderate disease, perianal, postoperative and abscess management. DIAGNOSIS: fecal calprotectin (>50-100 μg/g) separates inflammatory from noninflammatory disease of the colon. Workup is ileocolonoscopy with biopsies, including uninvolved mucosa, plus small-bowel imaging. CTE and MRE are comparable; prefer MRE in patients <35 y and when serial exams are likely. Intestinal ultrasound is an ungraded adjunct. Do routine CRC surveillance in Crohn's colitis. MILD-TO-MODERATE: recommend against oral mesalamine; sulfasalazine only for symptomatic mild colonic CD; ileal-release budesonide 9 mg for induction in ileocecal disease but not for maintenance. MODERATE-TO-SEVERE (AGA Living Guideline, Scott et al., Gastroenterology 2025;169(7):1397-1448, 16 recommendations: 1 strong, 9 conditional, 6 knowledge gaps; updated quarterly, adult outpatients only): RECOMMEND infliximab, adalimumab, ustekinumab, risankizumab, mirikizumab, guselkumab or upadacitinib over no treatment; SUGGEST certolizumab pegol or vedolizumab over no treatment. Advanced-therapy-naive: suggest higher-efficacy agents (infliximab, adalimumab, vedolizumab, ustekinumab, risankizumab, mirikizumab, guselkumab) over lower-efficacy ones (certolizumab pegol, upadacitinib). Prior advanced-therapy (especially anti-TNF) exposure: suggest higher- or intermediate-efficacy agents (adalimumab, risankizumab, guselkumab, upadacitinib; ustekinumab, mirikizumab) over lower-efficacy ones (vedolizumab, certolizumab pegol). Suggest against thiopurine monotherapy for induction; suggest it for maintenance of remission. Suggest SC/IM methotrexate monotherapy; suggest against oral methotrexate. In thiopurine-naive patients starting infliximab, suggest infliximab + thiopurine over infliximab alone. No recommendation on IFX + MTX, adalimumab + immunomodulator, or non-TNF biologic + immunomodulator. After ≥6 months of steroid-free remission on anti-TNF + immunomodulator, suggest withdrawing the immunomodulator and suggest against withdrawing the anti-TNF. SUGGEST upfront advanced therapy over step-up therapy (corticosteroids and/or immunomodulator first). No recommendation on treating to endoscopic vs symptomatic remission. The ACG 2025 moderate-to-severe recommendations (anti-TNF, IFX + thiopurine combination and IL-12/23/IL-23 agents, each strong/moderate; upadacitinib after anti-TNF exposure; steroids for short-term induction only; TPMT/NUDT15 testing before thiopurines) still stand alongside AGA. ACG perianal (infliximab first; drain abscesses and place setons before escalating), postoperative (endoscopy at 6-12 months; anti-TNF strong, vedolizumab conditional in high-risk patients) and intra-abdominal abscess (>2 cm: antibiotics plus drainage, hold immunosuppression) positions are unchanged. THERAPEUTIC ENDOSCOPY (AGA Clinical Practice Update, CGH 2026; details below come from AGA news coverage, not the full text, and are ungraded advice): get cross-sectional imaging before the procedure. Endoscopic balloon dilation is first-line for short strictures (about ≤4-5 cm) with few risk factors (fistula, prestenotic dilation >5 cm, high CRP, prior anti-TNF). Longer or multiple strictures, or ≥3 risk factors, favor surgery.

Two current US guidelines govern Crohn's disease and should be read together. ACG 2025 (Lichtenstein et al.) remains the reference for diagnosis, mild-to-moderate disease, perianal, postoperative and abscess management. DIAGNOSIS: fecal calprotectin (>50-100 μg/g) separates inflammatory from noninflammatory disease of the colon. Workup is ileocolonoscopy with biopsies, including uninvolved mucosa, plus small-bowel imaging. CTE and MRE are comparable; prefer MRE in patients <35 y and when serial exams are likely. Intestinal ultrasound is an ungraded adjunct. Do routine CRC surveillance in Crohn's colitis. MILD-TO-MODERATE: recommend against oral mesalamine; sulfasalazine only for symptomatic mild colonic CD; ileal-release budesonide 9 mg for induction in ileocecal disease but not for maintenance. MODERATE-TO-SEVERE (AGA Living Guideline, Scott et al., Gastroenterology 2025;169(7):1397-1448, 16 recommendations: 1 strong, 9 conditional, 6 knowledge gaps; updated quarterly, adult outpatients only): RECOMMEND infliximab, adalimumab, ustekinumab, risankizumab, mirikizumab, guselkumab or upadacitinib over no treatment; SUGGEST certolizumab pegol or vedolizumab over no treatment. Advanced-therapy-naive: suggest higher-efficacy agents (infliximab, adalimumab, vedolizumab, ustekinumab, risankizumab, mirikizumab, guselkumab) over lower-efficacy ones (certolizumab pegol, upadacitinib). Prior advanced-therapy (especially anti-TNF) exposure: suggest higher- or intermediate-efficacy agents (adalimumab, risankizumab, guselkumab, upadacitinib; ustekinumab, mirikizumab) over lower-efficacy ones (vedolizumab, certolizumab pegol). Suggest against thiopurine monotherapy for induction; suggest it for maintenance of remission. Suggest SC/IM methotrexate monotherapy; suggest against oral methotrexate. In thiopurine-naive patients starting infliximab, suggest infliximab + thiopurine over infliximab alone. No recommendation on IFX + MTX, adalimumab + immunomodulator, or non-TNF biologic + immunomodulator. After ≥6 months of steroid-free remission on anti-TNF + immunomodulator, suggest withdrawing the immunomodulator and suggest against withdrawing the anti-TNF. SUGGEST upfront advanced therapy over step-up therapy (corticosteroids and/or immunomodulator first). No recommendation on treating to endoscopic vs symptomatic remission. The ACG 2025 moderate-to-severe recommendations (anti-TNF, IFX + thiopurine combination and IL-12/23/IL-23 agents, each strong/moderate; upadacitinib after anti-TNF exposure; steroids for short-term induction only; TPMT/NUDT15 testing before thiopurines) still stand alongside AGA. ACG perianal (infliximab first; drain abscesses and place setons before escalating), postoperative (endoscopy at 6-12 months; anti-TNF strong, vedolizumab conditional in high-risk patients) and intra-abdominal abscess (>2 cm: antibiotics plus drainage, hold immunosuppression) positions are unchanged. THERAPEUTIC ENDOSCOPY (AGA Clinical Practice Update, CGH 2026; details below come from AGA news coverage, not the full text, and are ungraded advice): get cross-sectional imaging before the procedure. Endoscopic balloon dilation is first-line for short strictures (about ≤4-5 cm) with few risk factors (fistula, prestenotic dilation >5 cm, high CRP, prior anti-TNF). Longer or multiple strictures, or ≥3 risk factors, favor surgery.

This standard applies to MASLD: hepatic steatosis on imaging or biopsy, at least one cardiometabolic criterion, no other liver disease, and alcohol below the MetALD range. The AGA 2026 MetALD update sets MetALD at about 140-350 g/week of alcohol in women and 210-420 g/week in men, averaged over at least 3 months. MASLD therefore means under about 140 g/week (women) or 210 g/week (men), and drinking above the MetALD range is ALD. Assess alcohol use in every patient with steatotic liver disease at diagnosis and at least once a year, by interview, a validated questionnaire (e.g., AUDIT-C) and/or biomarkers such as phosphatidylethanol (PEth). Advise every patient with steatotic liver disease to stop drinking. Screen people with type 2 diabetes, people with overweight or obesity plus at least one more metabolic risk factor, and anyone with incidental steatosis or raised aminotransferases. Use FIB-4 first. A score below 1.3 (below 2.0 at age 65 or older) is low risk: the patient stays in primary care and repeats FIB-4 every 1-2 years. A score at or above the cutoff goes to a second-line test: VCTE, or ELF if elastography is not available. VCTE below 8 kPa is low risk. VCTE of 8 kPa or more, or ELF of 9.2 or more, means clinically significant fibrosis is likely and the patient should be referred to hepatology. Read liver stiffness with caution if the patient is actively drinking. Reserve biopsy for discordant or unclear results. Lifestyle change is the base of treatment for everyone: at least 5% weight loss improves steatosis, and 10% or more is usually needed for fibrosis to improve. Pharmacotherapy is recommended for adults with non-cirrhotic MASH and F2-F3 fibrosis (by non-invasive tests or biopsy), alongside structured lifestyle intervention and optimised management of comorbidities. The NIT ranges that stand in for F2-F3 differ by society. AASLD uses VCTE 8-15 kPa, MRE 3.1-4.4 kPa or ELF 9.2-10.5. EASL-EASD-EASO 2026 frames the treatable high-risk group as, for example, VCTE 10-20 kPa, MRE 3.1-5.0 kPa or ELF 9.8-11.3. Two drugs are approved: resmetirom (80 mg oral daily, or 100 mg at body weight of 100 kg or more; AASLD Oct 2024 guidance) and semaglutide 2.4 mg subcutaneously once weekly (FDA accelerated approval Aug 2025, AASLD Nov 2025 guidance; in ESSENCE, MASH resolved without fibrosis worsening in 62.9% vs 34.3% on placebo). EASL-EASD-EASO 2026 says to choose between them by patient preference, risks and cardio-renal-metabolic profile. Semaglutide may be preferred with obesity, type 2 diabetes, established cardiovascular disease or high cardiovascular risk. Resmetirom may be prioritised without obesity, or when the patient is already on or cannot tolerate a GLP-1 receptor agonist. On semaglutide, monitoring includes nutrition and sarcopenia assessment, and fibrosis NITs are used over time to judge response. In MASH cirrhosis, resmetirom and semaglutide appear safe but should not be used as MASH-targeted treatment until liver-related benefit is shown. Pioglitazone or vitamin E remain options under the AASLD 2023 guidance. Neither resmetirom nor semaglutide has been formally studied in MetALD. Manage cardiometabolic risk in every patient whatever the fibrosis stage, including statins for ASCVD and control of glucose and blood pressure. On semaglutide, watch for GI side effects and rare risks (AKI, gallbladder disease, pancreatitis, retinopathy, loss of lean mass). For MetALD, treat moderate or severe alcohol use disorder with medication plus behavioural therapy, correct micronutrient deficiencies (folate, thiamine, vitamin D), and do not offer bariatric or endobariatric procedures. HCC surveillance with ultrasound, with or without AFP, every 6 months is indicated only when cirrhosis is present.

This standard applies to MASLD: hepatic steatosis on imaging or biopsy, at least one cardiometabolic criterion, no other liver disease, and alcohol below the MetALD range. The AGA 2026 MetALD update sets MetALD at about 140-350 g/week of alcohol in women and 210-420 g/week in men, averaged over at least 3 months. MASLD therefore means under about 140 g/week (women) or 210 g/week (men), and drinking above the MetALD range is ALD. Assess alcohol use in every patient with steatotic liver disease at diagnosis and at least once a year, by interview, a validated questionnaire (e.g., AUDIT-C) and/or biomarkers such as phosphatidylethanol (PEth). Advise every patient with steatotic liver disease to stop drinking. Screen people with type 2 diabetes, people with overweight or obesity plus at least one more metabolic risk factor, and anyone with incidental steatosis or raised aminotransferases. Use FIB-4 first. A score below 1.3 (below 2.0 at age 65 or older) is low risk: the patient stays in primary care and repeats FIB-4 every 1-2 years. A score at or above the cutoff goes to a second-line test: VCTE, or ELF if elastography is not available. VCTE below 8 kPa is low risk. VCTE of 8 kPa or more, or ELF of 9.2 or more, means clinically significant fibrosis is likely and the patient should be referred to hepatology. Read liver stiffness with caution if the patient is actively drinking. Reserve biopsy for discordant or unclear results. Lifestyle change is the base of treatment for everyone: at least 5% weight loss improves steatosis, and 10% or more is usually needed for fibrosis to improve. Pharmacotherapy is recommended for adults with non-cirrhotic MASH and F2-F3 fibrosis (by non-invasive tests or biopsy), alongside structured lifestyle intervention and optimised management of comorbidities. The NIT ranges that stand in for F2-F3 differ by society. AASLD uses VCTE 8-15 kPa, MRE 3.1-4.4 kPa or ELF 9.2-10.5. EASL-EASD-EASO 2026 frames the treatable high-risk group as, for example, VCTE 10-20 kPa, MRE 3.1-5.0 kPa or ELF 9.8-11.3. Two drugs are approved: resmetirom (80 mg oral daily, or 100 mg at body weight of 100 kg or more; AASLD Oct 2024 guidance) and semaglutide 2.4 mg subcutaneously once weekly (FDA accelerated approval Aug 2025, AASLD Nov 2025 guidance; in ESSENCE, MASH resolved without fibrosis worsening in 62.9% vs 34.3% on placebo). EASL-EASD-EASO 2026 says to choose between them by patient preference, risks and cardio-renal-metabolic profile. Semaglutide may be preferred with obesity, type 2 diabetes, established cardiovascular disease or high cardiovascular risk. Resmetirom may be prioritised without obesity, or when the patient is already on or cannot tolerate a GLP-1 receptor agonist. On semaglutide, monitoring includes nutrition and sarcopenia assessment, and fibrosis NITs are used over time to judge response. In MASH cirrhosis, resmetirom and semaglutide appear safe but should not be used as MASH-targeted treatment until liver-related benefit is shown. Pioglitazone or vitamin E remain options under the AASLD 2023 guidance. Neither resmetirom nor semaglutide has been formally studied in MetALD. Manage cardiometabolic risk in every patient whatever the fibrosis stage, including statins for ASCVD and control of glucose and blood pressure. On semaglutide, watch for GI side effects and rare risks (AKI, gallbladder disease, pancreatitis, retinopathy, loss of lean mass). For MetALD, treat moderate or severe alcohol use disorder with medication plus behavioural therapy, correct micronutrient deficiencies (folate, thiamine, vitamin D), and do not offer bariatric or endobariatric procedures. HCC surveillance with ultrasound, with or without AFP, every 6 months is indicated only when cirrhosis is present.

This standard applies to MASLD: hepatic steatosis on imaging or biopsy, at least one cardiometabolic criterion, no other liver disease, and alcohol below the MetALD range. The AGA 2026 MetALD update sets MetALD at about 140-350 g/week of alcohol in women and 210-420 g/week in men, averaged over at least 3 months. MASLD therefore means under about 140 g/week (women) or 210 g/week (men), and drinking above the MetALD range is ALD. Assess alcohol use in every patient with steatotic liver disease at diagnosis and at least once a year, by interview, a validated questionnaire (e.g., AUDIT-C) and/or biomarkers such as phosphatidylethanol (PEth). Advise every patient with steatotic liver disease to stop drinking. Screen people with type 2 diabetes, people with overweight or obesity plus at least one more metabolic risk factor, and anyone with incidental steatosis or raised aminotransferases. Use FIB-4 first. A score below 1.3 (below 2.0 at age 65 or older) is low risk: the patient stays in primary care and repeats FIB-4 every 1-2 years. A score at or above the cutoff goes to a second-line test: VCTE, or ELF if elastography is not available. VCTE below 8 kPa is low risk. VCTE of 8 kPa or more, or ELF of 9.2 or more, means clinically significant fibrosis is likely and the patient should be referred to hepatology. Read liver stiffness with caution if the patient is actively drinking. Reserve biopsy for discordant or unclear results. Lifestyle change is the base of treatment for everyone: at least 5% weight loss improves steatosis, and 10% or more is usually needed for fibrosis to improve. Pharmacotherapy is recommended for adults with non-cirrhotic MASH and F2-F3 fibrosis (by non-invasive tests or biopsy), alongside structured lifestyle intervention and optimised management of comorbidities. The NIT ranges that stand in for F2-F3 differ by society. AASLD uses VCTE 8-15 kPa, MRE 3.1-4.4 kPa or ELF 9.2-10.5. EASL-EASD-EASO 2026 frames the treatable high-risk group as, for example, VCTE 10-20 kPa, MRE 3.1-5.0 kPa or ELF 9.8-11.3. Two drugs are approved: resmetirom (80 mg oral daily, or 100 mg at body weight of 100 kg or more; AASLD Oct 2024 guidance) and semaglutide 2.4 mg subcutaneously once weekly (FDA accelerated approval Aug 2025, AASLD Nov 2025 guidance; in ESSENCE, MASH resolved without fibrosis worsening in 62.9% vs 34.3% on placebo). EASL-EASD-EASO 2026 says to choose between them by patient preference, risks and cardio-renal-metabolic profile. Semaglutide may be preferred with obesity, type 2 diabetes, established cardiovascular disease or high cardiovascular risk. Resmetirom may be prioritised without obesity, or when the patient is already on or cannot tolerate a GLP-1 receptor agonist. On semaglutide, monitoring includes nutrition and sarcopenia assessment, and fibrosis NITs are used over time to judge response. In MASH cirrhosis, resmetirom and semaglutide appear safe but should not be used as MASH-targeted treatment until liver-related benefit is shown. Pioglitazone or vitamin E remain options under the AASLD 2023 guidance. Neither resmetirom nor semaglutide has been formally studied in MetALD. Manage cardiometabolic risk in every patient whatever the fibrosis stage, including statins for ASCVD and control of glucose and blood pressure. On semaglutide, watch for GI side effects and rare risks (AKI, gallbladder disease, pancreatitis, retinopathy, loss of lean mass). For MetALD, treat moderate or severe alcohol use disorder with medication plus behavioural therapy, correct micronutrient deficiencies (folate, thiamine, vitamin D), and do not offer bariatric or endobariatric procedures. HCC surveillance with ultrasound, with or without AFP, every 6 months is indicated only when cirrhosis is present.

Per the 2024 ADQI-ICA joint consensus (which updates the 2015 ICA-AKI criteria referenced in AASLD 2021), in a patient with cirrhosis and ascites: DIAGNOSE HRS-AKI when all of (a) cirrhosis with ascites; (b) AKI by KDIGO/ICA criteria, serum creatinine rise ≥0.3 mg/dL (26.5 µmol/L) within 48h or ≥50% from a baseline known or presumed within the prior 7 days, and/or urine output ≤0.5 mL/kg/h for ≥6h (strong recommendation, grade A); (c) absence of improvement in serum creatinine and/or urine output within 24h following adequate volume resuscitation WHEN CLINICALLY INDICATED, the consensus recommends AGAINST systematic 48h albumin administration as a diagnostic requisite (strong recommendation, grade D), and only where volume status is equivocal is a single fluid challenge (250-500 mL crystalloid, or 1-1.5 g/kg of 20-25% albumin) assessed within 24h; and (d) absence of strong evidence for an alternative primary cause of AKI (e.g., septic shock requiring vasopressors, acute glomerular injury, obstruction, or nephrotoxin-induced AKI) (not graded). HRS-AKI is a phenotype specific to advanced cirrhosis and ascites: coexisting CKD, tubular injury or proteinuria do NOT exclude it, and it may coexist with, or be superimposed on, other AKI etiologies rather than requiring pure exclusion. TREAT: immediately on diagnosis start a vasoconstrictor plus 20-25% albumin (strong recommendation, grade A). Terlipressin is first-line, continuous IV infusion 2-12 mg/day, titrated up by ≥2 mg/day every 24h to a maximum 12 mg/day if serum creatinine has not fallen ≥25%; or IV bolus 1-2 mg every 6h, escalated from 1 mg to 2 mg every 6h on that same ≥25% serum-creatinine response threshold, with the 12 mg/day maximum applying only to continuous infusion and not to bolus dosing. If terlipressin is unavailable or contraindicated, norepinephrine (continuous infusion 0.5-3 mg/h, up-titrated 0.5 mg/h every 4h to raise MAP ≥10 mmHg; requires ICU care and a central line) may be more appropriate. Midodrine 7.5-15 mg PO every 8h plus octreotide 100-200 µg SC every 8h with albumin is third-line, considered only if terlipressin is contraindicated AND transfer to ICU for norepinephrine is not possible. Give 20-25% albumin 20-40 g/day with any vasoconstrictor, adjusted daily to volume status and withheld for fluid overload/pulmonary edema. Discontinue vasoconstrictors when serum creatinine returns to within 0.3 mg/dL of baseline, for a severe adverse reaction, if kidney function does not improve after 48h at maximum tolerated dose, if RRT is indicated, or at a maximum of 14 days of therapy (strong recommendation, grade B). Initiation of RRT should be individualized to clinical context and anticipated or observed life-threatening AKI-related complications (best-practice statement) rather than framed strictly as a transplant-bridge measure. Recommend expedited evaluation for liver transplantation following an episode of AKI (best-practice statement); LT in selected patients is the definitive treatment for HRS-AKI regardless of vasoconstrictor response (strong recommendation, grade A), with vasoconstrictors serving as a bridge to transplantation or renal recovery rather than a cure.

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 is unchanged and still follows the separate ESGE diagnostic guideline (Endoscopy 2025;57:166-185). Start with MRI/MRCP plus laboratory tests, read CA19-9 only after decompression, and check IgG4 when IgG4-related sclerosing cholangitis is suspected. For distal extrahepatic strictures with no pancreatic mass, do combined same-session EUS-guided tissue acquisition plus ERCP brushing and biopsy. For perihilar strictures, sample by ERCP first and move to cholangioscopy-guided biopsy if the result is indeterminate. Do not place an uncovered SEMS (USEMS) until malignancy is confirmed. Management now follows the 2026 ESGE biliary stricture management guideline, which replaces the 2018 stenting guideline and brings it into line with the 2022 therapeutic EUS guideline. Benign: post-cholecystectomy strictures get temporary multiple plastic stents (MPSs), exchanged every 3-4 months with as many stents as possible, for about 12 months. A fully covered SEMS (FCSEMS) is an option only if the stricture is more than 2 cm below the hepatic confluence or the patient will not comply with repeated ERCPs. Anastomotic strictures after liver transplant get MPSs, or a temporary FCSEMS if more than 2 cm below the confluence. Nonanastomotic post-transplant strictures that can be treated endoscopically get MPSs plus balloon dilation if needed. Chronic pancreatitis strictures get a temporary 8-10 mm FCSEMS for 6-12 months. High-grade PSC strictures get balloon dilation alone, with no stent, because stenting adds no benefit and may add adverse events. Endotherapy is indicated for a benign stricture with liver tests raised for more than 1 month and/or cholangitis. Malignant distal: drain before surgery only selectively (cholangitis, severe jaundice or pruritus, delayed surgery). When drainage is needed before surgery or neoadjuvant therapy, or for palliation, place a 10-mm SEMS endoscopically. Endoscopic drainage is preferred over surgery or PTBD for inoperable obstruction. Malignant hilar: manage in high-volume centres with a hepatobiliary multidisciplinary team (MDT). ERCP is preferred over PTBD for preoperative drainage. Palliate Bismuth I-II with ERCP. For Bismuth III-IV, ERCP or ERCP combined with EUS-guided drainage (EUS-BD) is preferred over primary PTBD, with PTBD as a complement if needed. For proven Bismuth II-IV, aim to drain more than 50%, ideally 70% or more, of the viable nonatrophic liver volume using several routes as needed. Use plastic stents when the drainage strategy is undefined or the centre is not expert. USEMS are for expert centres when the diagnosis is proven, the tumour is unresectable, and complete drainage is predicted. After failed or unfeasible ERCP, EUS-BD is recommended over PTBD. Use hepaticogastrostomy (EUS-HGS) if there is a duodenal stricture, and EUS-HGS or choledochoduodenostomy (EUS-CDS) if there is not. PTBD is used if EUS-BD fails. In surgically altered anatomy, benign disease gets enteroscopy-assisted ERCP first; malignant disease gets enteroscopy-assisted ERCP or EUS-BD. Give antibiotics before ERCP in selected cases: predicted incomplete drainage, hilar strictures, immunocompromised patients, PSC, cholangioscopy. This follows the ESGE ERCP-adverse-events guideline. Etiology-specific care (Strasberg injuries, IgG4-SC, Mirizzi, choledochal cysts) is unchanged.

Address the specific underlying cause of persistent or new post-cholecystectomy symptoms after narrowing the heterogeneous differential (retained/CBD stone, sphincter of Oddi dysfunction, bile leak/duct injury, bile acid diarrhea, functional dyspepsia/IBS, GERD). First exclude time-sensitive early postoperative complications, bile leak/duct injury, obstructing retained/CBD stone, biliary obstruction or cholangitis, and treat red-flag features (jaundice, fever, sepsis, or early-onset/worsening pain) as warranting prompt evaluation rather than reassurance; only then reassure that most symptoms settle within 6-12 months, avoid empiric reoperation, and obtain multidisciplinary GI + HPB surgery input for refractory or atypical cases.