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 as soon as possible in any patient with new-onset ascites that can be sampled. Also perform one in any patient with cirrhosis and ascites who is admitted to hospital. AASLD 2021 says this applies to emergent admission for any reason. AGA 2025 BPA 2 names admission for ascites- or encephalopathy-related symptoms. The tap rules out SBP even without signs of infection, because up to one-third of SBP is asymptomatic. Repeat it whenever signs, symptoms or labs suggest infection, and in tense ascites with AKI. Paracentesis is safe with coagulopathy: INR >1.5 or platelets <50×10^9/L is not a contraindication, and routine FFP or platelet transfusion is not recommended. Possible exceptions are DIC, and uremia with thrombocytopenia, where desmopressin may be considered. Initial fluid testing: neutrophil (PMN) count, total protein, and ascitic albumin with a same-day serum albumin to calculate the SAAG. AGA 2025 adds Gram stain and culture to the initial panel for new-onset ascites and hospitalized patients. AASLD 2021 treats culture as part of the SBP workup rather than the routine panel. Either way, inoculate ≥10 mL into aerobic and anaerobic blood-culture bottles at the bedside before antibiotics. Amylase, cytology, glucose, LDH, AFB/ADA and triglycerides are ordered only for a clinical reason. SAAG ≥1.1 g/dL means portal hypertension (~97% accuracy). SAAG <1.1 g/dL points to a non-portal-hypertensive cause: carcinomatosis, TB peritonitis, nephrotic syndrome, pancreatic or chylous ascites. Within high-SAAG ascites, total protein <2.5 g/dL suggests cirrhosis (also massive liver metastases or late Budd-Chiari). Total protein ≥2.5 g/dL suggests a cardiac or postsinusoidal cause (heart failure, portal vein thrombosis, SOS, early Budd-Chiari), so work up with echocardiography, hepatic-vein Doppler or right-heart catheterization. SBP is diagnosed by ascitic PMN >250/mm^3, with or without a positive culture, once a surgically treatable source has been excluded. SBE is diagnosed by pleural fluid PMN >250/mm^3 in a hepatic hydrothorax after pneumonia and other secondary causes are excluded. It is treated with antibiotics and no chest tube.

Perform HCC surveillance with abdominal ultrasound PLUS serum AFP every ~6 months (semiannual, not annual) in adults with cirrhosis of any etiology who could benefit from HCC treatment: Child-Turcotte-Pugh A or B, and CTP C only if a liver-transplant candidate or listed. Do not surveil patients whose life expectancy is <1-2 years from comorbidity that neither transplantation nor HCC therapy can remedy, and weigh the physical, psychological and financial harms of surveillance case by case. Also surveil selected non-cirrhotic chronic HBV carriers: Asian men >40 and women >50 from endemic regions, people of African origin at younger ages, family history of HCC, or high viral load/active hepatitis. AGA 2026 endorses PAGE-B (intermediate/high risk at ≥10) and REAL-B to stratify these patients. Patients with HCV cirrhosis stay in surveillance after SVR. Patients without cirrhosis from other causes are NOT surveilled because incidence is too low (≤F3 fibrosis, MASLD without cirrhosis, HCV cured before cirrhosis), though fibrosis staging uncertainty warrants individual discussion. CT/MRI are not routine surveillance tools. Abbreviated MRI, GALAD and other blood biomarkers are investigational and should not replace ultrasound+AFP. Multicancer blood detection tests should not be used. Recall per AASLD 2023: AFP ≥20 ng/mL or a rising AFP (doubling, or a rise on two consecutive tests even below 20), any ultrasound observation ≥1 cm, or an inadequate ultrasound triggers multiphasic contrast CT or MRI read with LI-RADS. Treatment per AASLD 2023 is BCLC-linked: resection, ablation or transplant within Milan criteria for very-early/early disease, TACE and other locoregional therapy for intermediate disease, systemic therapy for advanced disease. Preferred first-line systemic therapy in Child-Pugh A is atezolizumab+bevacizumab or durvalumab+tremelimumab (STRIDE); sorafenib, lenvatinib or durvalumab monotherapy are the alternatives. BEACON-HCC (AASLD/HCC-LIVE, Hepatology 2026) is a Delphi consensus framework for treatment allocation that complements BCLC; it does not replace it. Under BEACON-HCC, macrovascular invasion does not automatically mean systemic therapy, and EBRT/SBRT and TARE are primary options. Continue post-treatment surveillance with contrast-enhanced cross-sectional imaging early after curative therapy.

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.

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.

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.