← Issue №10/ week of Sep 6, 2026/Hepatology

Spleen stiffness measurement rules out high-risk varices in patients with chronic portal vein thrombosis without cirrhosis.

From GI Signals issue №10: what this paper found, what it changes, and where it sits against the current standard of care, reviewed by Simon Mathews, MD.

Hepatology retrospective · n=346 · Sep 1, 2026 · J Hepatology · IF 40.1

Spleen stiffness measurement rules out high-risk varices in patients with chronic portal vein thrombosis without cirrhosis.

New evidenceportal hypertensionvariceal bleedingbiomarker
Clinical takeawayConsider using SSM-VCTE ≤40 kPa to avoid screening endoscopy in chronic PVT without cirrhosis, as it reliably excludes HRV in this population.
What it foundSSM-VCTE ≤40 kPa ruled out high-risk varices (HRV) with 97% sensitivity and 96-97% NPV in chronic PVT without cirrhosis, sparing 41-43% of endoscopies with 3-5% HRV missed.
ContextChallenges current practice of mandatory endoscopy in all chronic PVT patients without cirrhosis, offering a non-invasive alternative with high accuracy.
Emergingsuggested applicable standard· American Association for the Study of Liver Diseases (AASLD), "Diagnosis, Evaluation, and Management of Ascites, Spontaneous Bacterial Peritonitis and Hepatorenal Syndrome: 2021 Practice Guidance" (Biggins et al.), Hepatology, 2021

Decision at stakewhether to perform screening endoscopy for high-risk varices in patients with chronic portal vein thrombosis without cirrhosis

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.

From our summary of this standard, unedited — the part the paper bears on. marks omitted text. Our wording, not the guideline's; read the source for its own text.

Our full summary of this standard

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.

American Association for the Study of Liver Diseases (AASLD), "Diagnosis, Evaluation, and Management of Ascites, Spontaneous Bacterial Peritonitis and Hepatorenal Syndrome: 2021 Practice Guidance" (Biggins et al.), Hepatology, 2021 · reviewed 2026-07-23 ↗
Moga L … ERN RARE-LIVER; a study of VALDIG, an EASL consortium · Journal of Hepatology · IF 40.1 · PubMed ↗Permalink
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