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

In adults with cirrhosis, acetaminophen 500 mg every 6 h, up to a maximum of 2 g/day, is the preferred first-line analgesic (Statement 30), and systemic NSAIDs should be avoided (Statement 31). Opioids should be avoided when possible for chronic pain; when necessary, opioid use should be approached with caution and with careful discussion with patients and caregivers, and low-dose oxycodone or hydromorphone can be started in select cases on an as-needed basis and titrated to effect, often in consultation with pain-management experts (Statement 32). First-line opioids are low-dose, short-acting agents with extended dosing intervals: oxycodone 2.5 mg PO q6-8h PRN or hydromorphone 1 mg PO q6h PRN (hydromorphone 0.4 mg IV); the initial prescription should be a 7-day supply of a low-dose short-acting opioid with close follow-up, and extended-release formulations should be avoided. Codeine, morphine, and tramadol should generally be avoided; because morphine is relatively contraindicated in advanced cirrhosis, clinicians should first consider hydromorphone or oxycodone. Methadone should only be used in consultation with a specialist. IV fentanyl is a preferred opioid because of its favorable metabolism, but the transdermal fentanyl patch is problematic for outpatient use because its lowest available dose (12 µg/h) may be too high for patients with cirrhosis, and cachexia is a relative contraindication to the patch. When an opioid is started, prophylactic medications should be considered proactively to prevent constipation and hepatic encephalopathy (e.g., lactulose).

Perform a diagnostic paracentesis in all patients with new-onset ascites that is accessible for sampling, and in any patient with cirrhosis and ascites who is emergently admitted to the hospital for any reason, to rule out SBP even in the absence of signs or symptoms of infection (up to one-third of SBP is asymptomatic). Also perform it whenever a patient with ascites develops signs, symptoms, or laboratory abnormalities suggestive of infection, and in patients with tense ascites and AKI to exclude SBP as the cause. LVP/paracentesis is safe even with coagulopathy: elevated prothrombin time (INR >1.5) or thrombocytopenia (platelets <50×10^9/L) is not a contraindication, and routine transfusion of clotting factors or platelets is NOT recommended, with possible exceptions in disseminated intravascular coagulation, or uremia with thrombocytopenia (where desmopressin may be considered, especially with prior bleeding). The initial laboratory investigation of ascitic fluid should include ascitic fluid neutrophil (PMN) count, ascitic fluid total protein, and ascitic fluid albumin plus a simultaneous serum albumin to calculate the serum-ascites albumin gradient (SAAG). Ascitic fluid culture is not part of that routine initial panel but should be obtained whenever SBP is being evaluated (routinely for inpatients and when secondary bacterial peritonitis is suspected); when cultured, inoculate ≥10 mL of fluid into aerobic and anaerobic blood culture bottles at the bedside, before the first dose of antibiotics. Amylase, cytology, glucose, LDH, and mycobacterial (AFB/ADA) or triglyceride testing are not routinely indicated and should be guided by clinical context (e.g., suspected pancreatic, malignant, secondary-bacterial, tuberculous, or chylous ascites). Interpret SAAG to classify the cause: SAAG ≥1.1 g/dL indicates portal hypertension (~97% accuracy), while SAAG <1.1 g/dL points to non-portal-hypertensive (peritoneal) causes such as peritoneal carcinomatosis, tuberculous peritonitis, nephrotic syndrome, or pancreatic/chylous ascites. Within high-SAAG ascites, use ascitic total protein to distinguish the source: total protein <2.5 g/dL suggests cirrhosis (also massive liver metastasis, late Budd-Chiari), whereas total protein ≥2.5 g/dL suggests a postsinusoidal/cardiac source (heart failure, portal vein thrombosis, sinusoidal obstruction syndrome, early Budd-Chiari), directing workup toward right-heart catheterization, hepatic-vein Doppler, and echocardiography. The diagnosis of SBP is established with an ascitic fluid absolute neutrophil (PMN) count >250/mm^3 (with or without a positive culture, and in the absence of a surgically treatable intra-abdominal source of infection). Spontaneous bacterial empyema (SBE) is the analogous spontaneous infection of a pre-existing hepatic hydrothorax, not a parapneumonic effusion, and is established by the same pleural fluid PMN count >250/mm^3, but only after pneumonia and other secondary causes of the effusion have been excluded; despite the term "empyema" it is managed as an infection with antibiotics, and a chest tube should NOT be placed.

Perform HCC surveillance in adults with cirrhosis of any etiology who are able to benefit from HCC treatment, accordingly, do not enroll patients with Child-Turcotte-Pugh class C cirrhosis unless they are candidates for (or listed for) liver transplantation, and do not surveil those with life-limiting comorbidity (life expectancy <1-2 years) that transplantation cannot remedy, and in select non-cirrhotic chronic HBV carriers at elevated risk (e.g., active hepatitis/high viral load, family history of HCC, African/African-American ancestry, Asian men >40 and Asian women >50; AASLD references risk scores such as PAGE-B but stops short of mandating a specific numeric cutoff). Surveillance is abdominal ultrasound PLUS serum AFP at ~6-month (semiannual) intervals, a change from prior AASLD guidance, which had left AFP optional (Strong recommendation). Pursue diagnostic evaluation for an AFP ≥20 ng/mL or for a rising AFP, defined as a doubling of AFP or an increase on two consecutive tests even if the absolute value is <20 ng/mL. Any suspicious ultrasound observation ≥1 cm, or an inadequate/limited ultrasound, should be evaluated with multiphasic contrast-enhanced CT or MRI interpreted with CT/MRI LI-RADS. AASLD 2023 stages confirmed HCC using the BCLC framework and links stage to therapy (curative resection, ablation, or transplantation within Milan criteria for very-early/early disease; TACE and other locoregional therapy for intermediate disease; systemic therapy for advanced disease). Its first-line systemic options for advanced HCC with preserved liver function (Child-Pugh A) are atezolizumab+bevacizumab OR durvalumab+tremelimumab (STRIDE) as preferred, with sorafenib, lenvatinib, or durvalumab monotherapy as alternatives when the preferred combinations are contraindicated. After potentially curative therapy, continue surveillance for recurrence given high recurrence risk (AASLD monitors with cross-sectional contrast-enhanced imaging, not ultrasound, in the early post-treatment period).

The 2026 AASLD/IDSA guideline addresses six PICO questions only; it states explicitly that all other 2018 AASLD recommendations for CHB management remain applicable, and that screening/diagnosis were out of scope. Baseline evaluation and the standard treatment indications (cirrhosis with detectable HBV DNA; HBeAg-positive immune-active with ALT >2x ULN and HBV DNA >20,000 IU/mL; HBeAg-negative immune-active with ALT >2x ULN and HBV DNA >2,000 IU/mL; prophylaxis for reactivation risk during immunosuppression) derive from the 2018 document, not this update, which lists 'treatment of HBeAg-positive and -negative immune active CHB with ALT >2x ULN', treatment of children, treatment of cirrhosis, low-level viremia, virologic breakthrough, and special populations (transplant, acute HBV, HCV/HDV/HIV coinfection) as topics 'well covered in previous AASLD 2018 Guidance and for which recommendations have not changed'. Preferred agents remain entecavir, TDF, or TAF. THE SIX 2026 RECOMMENDATIONS: (1) PMTCT, for pregnant persons with HBV DNA >200,000 IU/mL at any time point during pregnancy, regardless of HBeAg status, AASLD RECOMMENDS initiating TDF or TAF at gestational week 28 (STRONG recommendation, MODERATE certainty, the only strong recommendation in the guideline); TDF has a more extensive safety record in pregnancy than TAF. Implementation qualifiers: initiate immediately if care is first sought after week 28; initiate at week 16 if infant HBIG will be unavailable (with subsequent infant vaccination); consider earlier initiation when amniocentesis is anticipated (transmission risk is increased with HBV DNA >2,000,000 IU/mL) or when preterm labor risk is high; continue TDF/TAF if already on it, switch entecavir or other agents to TDF/TAF; if treatment was solely for perinatal prophylaxis it may be discontinued at delivery, with HBV DNA and ALT monitored every 1-3 months for up to 6 months for withdrawal flare and treatment reinitiated if ALT >=5x ULN; use TDF or TAF in breastfeeding persons requiring treatment. (2) HORIZONTAL TRANSMISSION, for HBsAg-positive viremic persons not meeting disease-specific treatment indications who are in high-risk scenarios for transmission to others, AASLD SUGGESTS a shared decision-making approach regarding antiviral treatment (CONDITIONAL, VERY LOW certainty). Qualifiers the guideline stresses: the decision weighs exposure risk and the vaccine/immunity status of contacts, favoring treatment if contacts are unvaccinated, vaccine-nonresponsive, immunocompromised, or of unknown vaccine status; persons requesting treatment for prevention may be prescribed it since risks may not be disclosed; explicitly, people with CHB must NOT be restricted in daily activities, contact sports, school, or professional training and must NOT be required to take antivirals because of transmission risk in those settings; routine contact, shared meals, and hugging are not transmission routes (avoid sharing toothbrushes/razors); most healthcare workers with CHB are NOT high-risk, but those performing SHEA Category III exposure-prone procedures may require antivirals (SHEA target HBV DNA <1000 IU/mL); neither CDC nor SHEA requires disclosure to patients or staff; anti-stigma framing is part of the recommendation. (3) IMMUNE-TOLERANT PHASE, defined as HBeAg-positive, HBV DNA >10^7 IU/mL, and normal ALT; AASLD SUGGESTS antiviral therapy for those over age 40 years, OR with significant liver inflammation (grade >=2) or fibrosis (>=F2) on biopsy or noninvasive tests (CONDITIONAL, VERY LOW certainty). For persons under age 40 who are interested in starting treatment earlier, AASLD suggests shared decision-making weighing risk factors and the benefits and risks of treatment. Accurate phase identification requires persistently normal ALT on >=2 measurements >=6 months apart, using ULN 35 U/L (males) and 25 U/L (females). (4) INDETERMINATE ('grey zone') PHASE, the HBeAg-negative indeterminate phase is defined as HBsAg-positive, HBeAg-negative persons whose ALT and/or HBV DNA fall outside the thresholds for HBeAg-negative immune-active CHB (ALT >2x ULN and HBV DNA >2,000 IU/mL) and outside those for inactive CHB (HBV DNA <2,000 IU/mL with normal ALT), comprising predominantly two subgroups, (I) normal (<ULN) or mildly elevated (<2x ULN) ALT with HBV DNA >=2,000 IU/mL, or (II) elevated ALT (>ULN) with HBV DNA <2,000 IU/mL, with ALT interpreted against ULN 35 U/L (males) and 25 U/L (females) and phase assigned on >=2 ALT and HBV DNA measurements over a 6-12 month period; in adults who are HBsAg-positive, HBeAg-negative, without cirrhosis and in the indeterminate phase so defined, AASLD SUGGESTS antiviral therapy using a shared decision-making approach assessing risks and benefits, and re-evaluating that decision at each follow-up visit if treatment has not been initiated (CONDITIONAL, VERY LOW certainty). Decision-relevant factors include fibrosis stage, age, and sex, e.g. age >40, male sex, and low-normal platelets (<180 k/mm3) favor treatment. (5) DISCONTINUATION, in adults with CHB who are HBeAg-negative, without cirrhosis, with sustained undetectable HBV DNA on nucleos(t)ide analogue therapy, AASLD SUGGESTS NOT withdrawing NA therapy until HBsAg loss (CONDITIONAL, VERY LOW certainty). If a patient nonetheless has a strong desire to stop, shared decision-making applies and ALL of the following must be met: no history of advanced fibrosis/cirrhosis, hepatic decompensation (variceal bleed, ascites, encephalopathy, hepatorenal syndrome), HCC, or extrahepatic HBV complications; if HBeAg-positive at treatment start, HBeAg seroconversion to anti-HBe-positive for >=1 year with undetectable HBV DNA >=2 years; if HBeAg-negative at start, undetectable HBV DNA >=2 years; no HIV or HDV coinfection; quantitative HBsAg <100 IU/mL; and willingness to adhere to frequent monitoring. After stopping, monitor ALT and HBV DNA every 1-3 months for 6 months, then every 3 months for 6-12 months, then every 3-6 months. Restart antivirals IMMEDIATELY if HBV DNA >=10,000 IU/mL (4 log IU/mL) at any time regardless of ALT, OR ALT >=5x ULN regardless of HBV DNA, OR total bilirubin >2.5 mg/dL. (6) HCC SURVEILLANCE (all CONDITIONAL, VERY LOW certainty; modality/interval per AASLD 2023 HCC Practice Guidance), Rec 6: after HBsAg loss, continue surveillance in those with cirrhosis, family history of HCC, men who lost HBsAg after age 40, and women who lost HBsAg after age 50. Rec 7: in HBV-HDV coinfection, surveil adults independent of cirrhosis status; in children, individualize because HCC risk in that population is unknown. Rec 8: in HBV-HIV coinfection, surveil men >=18 years and women >=40 years. Rec 9: in HBV-HCV coinfection, AASLD recommends treating HCV and suggests HCC surveillance per HBV mono-infection criteria. Where a person has more than one coinfection, the surveillance recommendation should follow the coinfection carrying the highest associated risk. The guideline notes that most of its recommendations rest on low or very low certainty evidence and that shared decision-making, not uniform policy, is the intended mode of application.

Scope: this primary document covers portal hypertension and varices in cirrhosis ONLY. Everything else in the current entry (HCC surveillance, transplant referral, nutrition, vaccination, ascites/SBP/HE/HRS/ACLF management) belongs to the separate documents listed as supporting sources and must not be attributed to this guidance. Risk-stratify compensated advanced chronic liver disease (cACLD) with non-invasive tests before defaulting to endoscopy. By vibration-controlled transient elastography, liver stiffness (LSM) under 10 kPa excludes cACLD, 10 to 14.9 kPa is suggestive and warrants further testing, and 15 kPa or above rules cACLD in. Clinically significant portal hypertension (CSPH, i.e. HVPG above 10 mm Hg) is ruled in non-invasively by LSM at or above 25 kPa alone, or LSM 20 to 24.9 kPa with platelets below 150 x 10^9/L, or LSM 15 to 19.9 kPa with platelets below 110 x 10^9/L. Where spleen stiffness measurement is available, values below 21 kPa argue against CSPH and above 50 kPa argue for it. These non-invasive cutoffs are conditional probability thresholds, not universal diagnostic rules, and hold only when their derivation conditions are met. They were established in compensated advanced chronic liver disease of viral (treated or untreated HBV/HCV), alcohol-related, or non-obese (BMI under 30) MASLD etiology, and are not validated for and should not be applied to cholestatic (e.g. PBC, PSC), vascular, or other etiologies, in which different cutoffs apply. They also require a technically reliable liver stiffness measurement by vibration-controlled transient elastography, fasting, at least 10 valid acquisitions, and an IQR/median ratio below 30 percent, and are confounded by factors that raise liver stiffness independently of fibrosis, including ALT flares or acute hepatitis, extrahepatic cholestasis, hepatic congestion (right heart failure), and recent food intake; Baveno VII recommends confirming an LSM-based rule-in on a repeat measurement obtained on a separate day. The spleen stiffness cutoffs apply only to a dedicated 100 Hz spleen module, carry a higher technical failure rate, are machine-dependent, and are not interchangeable with values obtained using the standard 50 Hz liver probe. Where these population or acquisition conditions are not met, the numeric thresholds do not reliably classify CSPH, and HVPG measurement or endoscopy is required rather than a non-invasive determination. Preserve the gray zone: LSM 15 to 25 kPa without a qualifying platelet count is explicitly indeterminate (roughly 40 to 60 percent of cACLD patients) and calls for HVPG and/or endoscopy rather than assumption in either direction. Once CSPH is established, offer a non-selective beta-blocker, carvedilol preferred at 12.5 mg/day, to lower portal pressure and prevent FIRST decompensation, on the strength of PREDESCI. This is a treat-the-pressure strategy rather than a treat-the-varices one: because a patient already on NSBB for CSPH would not have management changed by the finding, screening endoscopy becomes unnecessary for most such patients. Screening EGD is still indicated where elastography is unavailable, technically difficult, or gives discordant results, and for patients who do not meet non-invasive criteria. Standard beta-blocker contraindications (severe asthma, advanced heart block, bradyarrhythmias) continue to apply. For varices needing treatment managed endoscopically, band ligation is repeated every 2 to 4 weeks until obliteration, with surveillance endoscopy at 6 months and annually thereafter. Gastric/cardiofundal varices are treated with cyanoacrylate injection or EUS-guided coil embolization rather than banding, with hepatology involvement. In acute variceal hemorrhage, consider preemptive (early) TIPS within 24 to 72 hours in high-risk patients: Child-Turcotte-Pugh class B with score above 7 and active bleeding at endoscopy despite vasoactive therapy, or CTP class C with score 10 to 13. Keep the document's own qualifier: there is no established universal MELD or CTP cutoff at which TIPS is mandatory, and the decision is case-by-case with hepatology consultation. Statin use in compensated cirrhosis is NOT a recommendation traceable to this document; the current entry's statin sentence needs its own source or removal. Verification note: the Hepatology full text is paywalled (402/403 on direct fetch). Document identity, title, year, volume, pages and authorship were confirmed via Crossref and PubMed metadata; the numeric thresholds above were corroborated from two independent peer-reviewed commentaries on this specific guidance and match the Baveno VII rule-of-five, but were not read verbatim from the primary PDF. A human should confirm the exact guidance-statement wording against the full text before this entry is treated as quotation-grade.

Diagnose MASLD by hepatic steatosis on imaging (or biopsy) plus at least one cardiometabolic criterion and exclusion of competing etiologies (significant alcohol use, other liver disease), then risk-stratify fibrosis using a sequential non-invasive approach: FIB-4 first, followed by a second-line imaging-based test (VCTE, MRE, or ELF) for indeterminate/high-risk FIB-4, with liver biopsy reserved for discordant or unclear cases. Lifestyle modification (≥7-10% weight loss, Mediterranean diet, exercise) remains the foundation for all patients. For adults with MASH and F2-F3 fibrosis identified by non-invasive tests (VCTE 8-15 kPa, MRE 3.1-4.4 kPa, or ELF 9.2-10.5) rather than biopsy, AASLD now gives dedicated, updated practice guidance on both FDA-approved pharmacotherapies: resmetirom (Oct 2024 update) and semaglutide 2.4mg/week subcutaneous (Nov 2025 update, following August 2025 accelerated FDA approval based on ESSENCE trial data: 62.9% vs 34.3% MASH resolution without fibrosis worsening; 36.8% vs 22.4% ≥1-stage fibrosis improvement). Pioglitazone or vitamin E remain options per the 2023 base guidance. Manage cardiometabolic risk with statins for ASCVD reduction plus glycemic and blood-pressure control; for semaglutide specifically, routine hepatic panels are recommended only as clinically indicated (no discontinuations for LFT elevation in ESSENCE), with monitoring for GI adverse effects and rare risks (AKI, gallbladder disease, pancreatitis, thyroid C-cell tumors, retinopathy progression, lean mass loss). HCC surveillance with ultrasound and AFP every 6 months remains indicated only if cirrhosis is present.

For heartburn or regurgitation persisting despite PPI therapy, current practice (ACG 2022 GERD guideline, still the operative ACG guideline, plus the AGA 2022 personalized-GERD CPU) is to first optimize the PPI: confirm adherence, dose 30-60 minutes before meals, escalate to twice-daily dosing or switch agents for an 8-week trial. Empiric escalation to vonoprazan/P-CAB is NOT a routine pre-testing step: the AGA 2024 P-CAB clinical practice update advises against P-CABs as first-line therapy and reserves them for PPI failure with confirmatory GERD evidence (LA grade B or worse erosive esophagitis, biopsy-proven Barrett's, peptic stricture, or acid exposure time >6%). If symptoms persist after optimization, perform EGD (ideally 2-4 weeks off PPI when GERD is unproven) with esophageal biopsies to exclude EoE (>=15 eos/hpf; the ACG 2025 EoE guideline has removed the PPI trial from the diagnostic pathway) and then physiologic testing per Lyon Consensus 2.0: in unproven GERD, ambulatory reflux monitoring OFF therapy, applying Lyon 2.0's modality-specific thresholds -- on catheter-based single-day (24-hour) pH or pH-impedance, AET >6% is conclusive for GERD, 4-6% is inconclusive, and <4% argues against GERD; on prolonged wireless (Bravo, up to 96-hour) monitoring, AET >6% on >=2 days is conclusive for GERD while AET <4% on all days excludes it, and a study meeting neither threshold is inconclusive (the number of days with AET <4% carries prognostic weight for PPI discontinuation) -- and, in either modality, a normal-AET (<4%) study with positive symptom association indicates reflux hypersensitivity or, without it, functional heartburn; in previously proven GERD, pH-impedance ON optimized therapy, where AET >4% plus >80 reflux episodes defines actionable refractory GERD (MNBI <1500 ohms supportive, >2300 ohms against). High-resolution manometry per Chicago Classification 4.0 (still current) excludes achalasia and major motility disorders and is required before anti-reflux surgery. Therapy is phenotype-directed: surgical or endoscopic anti-reflux intervention for confirmed refractory pathologic reflux, and neuromodulators with or without brain-gut behavioral therapy for reflux hypersensitivity and functional heartburn.

Stage cholangiocarcinoma with multiphasic MRI/MRCP plus CT chest/abdomen/pelvis, obtain tissue via ERCP brush cytology with FISH, cholangioscopy-directed biopsy, or EUS-FNA (avoiding primary perihilar tumor sampling if liver transplant is being considered due to theoretical seeding risk), and manage through a multidisciplinary tumor board with treatment stratified by tumor location: resect (anatomic hepatectomy for intrahepatic, hemihepatectomy with bile duct resection for perihilar, Whipple for distal) with adjuvant capecitabine (category 1, per BILCAP) when resectable. For unresectable or metastatic disease, first-line systemic therapy is gemcitabine plus cisplatin combined with a PD-L1/PD-1 checkpoint inhibitor, either durvalumab (TOPAZ-1) or pembrolizumab (KEYNOTE-966), both listed as category 1 preferred options by NCCN; comprehensive molecular/genomic profiling is recommended for all unresectable/metastatic candidates for systemic therapy to identify actionable targets (e.g., FGFR2 fusions, IDH1 mutations, HER2 amplification) for later-line therapy. Selected unresectable early-stage perihilar tumors may undergo neoadjuvant chemoradiation and liver transplant per the Mayo Clinic protocol at experienced centers, and jaundice or cholangitis is managed with biliary drainage (ERCP preferred over PTC).

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.

Confirm unintentional weight loss (≥5% body weight over 6-12 months, office-weighed) and triage into a three-bucket framework, decreased intake, malabsorption, or hypermetabolic, to direct the evaluation. Obtain first-tier labs (CBC, CMP with LFTs, TSH, glucose/A1c, lipase, CRP/ESR, nutritional and iron studies, HIV, and a universal celiac panel) plus mechanism-directed imaging and endoscopy, prioritizing urgent EGD, colonoscopy, or pancreas-protocol CT when malignancy red flags are present. Assess for malnutrition early and initiate nutritional support concurrently with the diagnostic workup, as clinically indicated. Reserve multidisciplinary/PET-CT review for refractory undiagnosed cases.

In adults with chronic idiopathic constipation, the AGA-ACG panel makes 10 GRADE-based pharmacological recommendations, and the strength tier is part of the recommendation. Unqualified as to prior therapy: STRONG recommendation (moderate certainty) for polyethylene glycol; STRONG recommendation (moderate certainty) for bisacodyl or sodium picosulfate, but explicitly qualified as short-term or rescue therapy; CONDITIONAL suggestion for fiber supplementation (low certainty), magnesium oxide (very low certainty), and senna (low certainty). Reserved for patients who do not respond to, fail, or are intolerant of over-the-counter agents: STRONG recommendation (moderate certainty) for linaclotide, plecanatide, and prucalopride; CONDITIONAL suggestion for lubiprostone (low certainty) and lactulose (very low certainty). The guideline states no specific doses, no mandatory ordering algorithm, and no fixed trial duration; it notes only that nonpharmacological therapies 'often represent the initial steps in management' and directs clinicians to shared decision making incorporating patient preference, cost, and availability. The guideline explicitly does not cover anorectal evacuation disorders, referring those to the ACG 2021 benign anorectal guideline.

PEG remains the standard for durable enteral access in patients unable to swallow safely or meet nutritional needs orally, placed by the pull (Gauderer-Ponsky) technique, and ASGE 2024 now suggests PEG over IR-guided gastrostomy for initial placement in normal foregut anatomy. A single prophylactic IV dose of a beta-lactam antibiotic (e.g., cefazolin) is given before placement. Post-procedure bowel rest is no longer recommended: feeding may start within 3-4 hours of uncomplicated placement (ESGE 2021, strong/high-quality; ASGE 2024, strong/moderate), medications may be given immediately, and routine gastric residual volume checks are not indicated. Buried bumper prophylaxis is daily site care with DAILY inward tube mobilization and a loose external bumper kept 1-2 cm from the abdominal wall (ESGE 2021), not weekly rotation. Antiplatelet agents, including dual antiplatelet therapy, need not be routinely withheld for PEG; anticoagulant management is individualized by multidisciplinary discussion of bleeding versus thrombotic risk. In malignant dysphagia, either transoral pull PEG or direct (introducer) PEG is acceptable with counseling about implantation metastasis and periodic site examination. Device selection among PEG, PEG-J, DPEJ, surgical gastrostomy, and parenteral nutrition remains multidisciplinary, and a goals-of-care discussion before placement, including avoiding routine PEG in advanced dementia in favor of careful hand feeding (AGA 2020 / Choosing Wisely), is unchanged.