01Approach to the Critical Patient/attcp52

Immediate priorities

›Hemodynamic instability recognition

›Hypotension (SBP <90 mmHg or MAP <65 mmHg)

›Septic shock from pylephlebitis

›Hemorrhagic shock from variceal bleed

›Two large-bore IVs and fluid resuscitation

›Tachycardia with abdominal pain

›Pain out of proportion to exam — hallmark of mesenteric ischemia

›Serum lactate immediately

›Peritoneal signs

›Guarding or rebound tenderness — suggests bowel infarction

›Emergent surgical consultation

›Ischemia identification

›Elevated serum lactate (>2 mmol/l)

›Intestinal ischemia from thrombus extension into mesenteric veins

›10–20% mortality if bowel infarction occurs

›Fever with rigors

›Pylephlebitis (septic PVT) — bacteremia from portal gas

›Blood cultures before antibiotics

›Bloody diarrhea or hematochezia

›Intestinal ischemia or variceal hemorrhage

›Emergent GI consultation

›Airway and GI bleeding

›Hematemesis

›Variceal hemorrhage from portal hypertension

›Airway protection assessment

›Octreotide and banding or sclerotherapy pathway

›Active variceal bleed with altered mental status

02History/hx67

Presenting symptoms

›Abdominal pain

›Most common symptom, present in ~80% of acute cases

›Upper abdominal location typical

›Colicky or constant character

›Pain out of proportion to exam findings

›Classic feature indicating mesenteric ischemia

›Demands urgent lactate and CT angiography

›Associated symptoms

›Nausea, vomiting, anorexia, postprandial fullness

›Mesenteric congestion mechanism

›May precede diagnosis by days to weeks in chronic PVT

›Fever

›Pylephlebitis or bowel ischemia

›Temperature >38.5°C with rigors suggests bacteremia

›GI bleeding

›Hematemesis or melena — variceal hemorrhage

›Hematochezia — intestinal ischemia or ischemic colitis

›Abdominal distension

›Ascites from portal hypertension

›Ileus from mesenteric ischemia

Risk factors

›Local and inflammatory causes

›Recent abdominal surgery

›Splenectomy (highest risk), bariatric surgery, colectomy

›Pancreatitis, appendicitis, diverticulitis, IBD flare

›Intra-abdominal infection

›Cholecystitis, hepatic abscess

03Physical Exam/exam45

Vital signs

›Hemodynamic profile

›Fever (>38.5°C)

›Pylephlebitis, bowel ischemia, or superimposed infection

›Tachycardia

›Sepsis, pain, or hemorrhage

›Hypotension

›Septic shock or hypovolemic shock from variceal bleed

Abdominal examination

›Inspection and palpation

›Distension

›Ascites — portal hypertension or acute hepatic decompensation

›Ileus — mesenteric ischemia

›Tenderness

›Mild relative to reported pain severity — PVT pattern

›Guarding and rebound — bowel infarction, peritonitis

›Organomegaly

›Hepatomegaly in 67% at diagnosis

›Splenomegaly — portal hypertension

›Signs of portal hypertension

›Caput medusae

›Dilated periumbilical veins — flow reversal in portal system

›Ascites

›Fluid wave and shifting dullness

›Spontaneous bacterial peritonitis risk in cirrhosis

›Hemorrhoids

›Inferior and middle rectal venous dilation

04Differential Diagnosis/ddx40

Life-threatening mimics

›Mesenteric arterial ischemia

›ICD-10: K55.0

›More acute onset; arterial source

›CT angiography differentiates from portal venous thrombosis

›Typically older patients with atrial fibrillation or atherosclerosis

›Embolism vs. thrombosis vs. non-occlusive ischemia subtypes

›Budd-Chiari syndrome

›ICD-10: I82.0

›Hepatic vein or IVC thrombosis

›Hepatomegaly, ascites, right upper quadrant pain triad

›Caudate lobe hypertrophy on imaging — distinguishing feature

›Variceal hemorrhage

›ICD-10: I85.01

›Complication of chronic PVT-induced portal hypertension

›Upper GI endoscopy is diagnostic and therapeutic

Abdominal emergencies

›Acute pancreatitis

›ICD-10: K85.9

›Can both mimic and precipitate PVT

›Lipase and amylase elevation; CT Balthazar grading

›Pylephlebitis (septic PVT)

›ICD-10: K75.1

›Septic thrombophlebitis of portal or mesenteric veins

›Gas in portal venous system on CT — pathognomonic finding

›Bacteremia — Bacteroides, E. coli, Klebsiella most common

›Acute appendicitis, diverticulitis

›ICD-10: K37, K57.32

05Laboratory Tests/lt61

Essential initial labs

›Complete blood count with differential

›Leukocytosis

›Ischemia, infection, or pylephlebitis

›Left shift suggests bacteremia

›Thrombocytosis

›MPN screen — essential thrombocythemia, polycythemia vera

›Thrombocytopenia

›Cirrhosis with hypersplenism

›Threshold for anticoagulation: platelets <50 x10^9/L requires individualized risk assessment

›Coagulation studies

›PT/INR and aPTT

›Baseline before anticoagulation

›INR unreliable in cirrhosis (does not reflect hemostatic balance)

›Anti-Xa level

›LMWH monitoring in renal impairment or obesity

›Comprehensive metabolic panel

›Renal function (creatinine, BUN)

›Guides DOAC dosing and safety

›AKI common in sepsis and hepatorenal syndrome

›Hepatic panel (AST, ALT, bilirubin, albumin, ALP)

›Usually preserved in acute PVT without cirrhosis

›Severely deranged in acute liver failure from extensive thrombosis

Ischemia and infection markers

›Serum lactate

›Intestinal ischemia marker

›Elevated lactate (>2 mmol/l) — critical red flag for bowel ischemia

›10–20% mortality from bowel infarction

06Diagnostic Tests/dt87

Scoring Systems

›Yerdel classification of PVT in cirrhosis

›Grade I: partial thrombosis of main portal vein (<50%)

›High spontaneous recanalization rate, may observe

›Grade II: thrombosis >50% of main portal vein including complete occlusion

›Significant hemodynamic impact; anticoagulation recommended

›Grade III: complete thrombosis with proximal mesenteric vein occlusion

›High risk of intestinal ischemia; urgent anticoagulation and surgical evaluation

›Grade IV: complete thrombosis of main PV and entire mesenteric vein

›Cavernous transformation in chronic disease; usually not anticoagulated

›AGA/AASLD severity framework

›Recent (<6 months), minimally occlusive (<50%)

›~40% spontaneous recanalization; may observe

›Recent (<6 months), >50% occlusive or extensive

›94% flow reduction at 50% occlusion (Poiseuille's law); anticoagulate

›Chronic (>6 months) with cavernous transformation

›Low recanalization potential; manage portal hypertension complications

›Baveno VII consensus criteria

›Anticoagulation recommended for acute non-cirrhotic PVT immediately

›Continue for 6 months minimum

›Indefinite if permanent prothrombotic state

MRI

›MRI abdomen with and without contrast

›Indications

›CT contrast contraindicated (renal impairment, allergy)

›Characterization of uncertain thrombus on CT

›Monitoring recanalization on anticoagulation

›Performance characteristics

›Specificity 98% for portal vein thrombosis

›Comparable accuracy to CT for thrombus extent and bowel viability

›Protocol specifics

›Gadolinium-enhanced sequences for vascular filling defects

›T2-weighted sequences for bowel wall edema and ischemia

›Diffusion-weighted imaging for bowel infarction

›Findings in acute PVT

›Intraluminal hypointense signal on T1 (thrombus)

›Portal vein expansion without enhancement

›Findings in chronic PVT

›Portal cavernoma — serpiginous collaterals replacing main portal vein

›Splenomegaly and gastroesophageal varices

›Tumor thrombus differentiation

›Arterial enhancement within thrombus — HCC tumor thrombus

›No enhancement — bland thrombus

CT

›CT abdomen and pelvis with IV contrast

›Gold standard for comprehensive PVT evaluation

›~90% accuracy for diagnosis

›Assesses thrombus extent into mesenteric veins

›Evaluates bowel viability and identifies infarction

›Protocol

›Triphasic or portal venous phase imaging

›Arterial phase for tumor thrombus differentiation (arterial enhancement = HCC)

›Acute PVT findings

›Central lucency within expanded, sharply defined portal vein

›Absent filling of portal vein lumen on venous phase

›Bowel wall thickening, pneumatosis intestinalis, or free air (ischemia/infarction)

›Chronic PVT findings

›Portal cavernoma — serpiginous collaterals at porta hepatis

›Splenomegaly, varices, ascites

›Bile duct compression from cavernoma (portal biliopathy)

›Septic PVT (pylephlebitis)

›Gas within portal venous system

›Hepatic microabscesses

›Limitations

›Contrast nephropathy risk in renal impairment

›Radiation exposure — use MRI for follow-up imaging when possible

Ultrasound

›Doppler ultrasound of portal vasculature

›First-line imaging modality for PVT

›Sensitivity 73–93%, specificity 92–99% (2025 meta-analysis)

›No radiation; bedside capability; low cost

›Diagnostic findings

›Hyperechoic intraluminal material in portal vein

›Absent or diminished flow on color Doppler

›Portal vein dilation (>13 mm)

›Chronic PVT findings

›Portal cavernoma — multiple tortuous collateral vessels at porta hepatis

›Hepatopetal collateral flow (reversed from normal)

›Limitations

›Operator dependent

›Limited by bowel gas and body habitus

›Cannot fully assess mesenteric vein extension

›If Doppler negative but clinical suspicion high, proceed to CT with contrast

›Point-of-care ultrasound role

›Detection of ascites — paracentesis guidance

›Splenomegaly and hepatomegaly assessment

›Inferior vena cava assessment for volume status

›Endoscopic ultrasound (EUS)

›Superior to transabdominal ultrasound for portal vein visualization

›Useful in obese patients or when bowel gas limits transabdominal views

›Can assess portal biliopathy and bile duct compression

07Disposition/dispo30

Admission criteria

›Mandatory admission indications

›Signs of intestinal ischemia

›Pain out of proportion, elevated lactate, peritoneal signs

›ICU-level admission; urgent surgical consultation

›Hemodynamic instability

›Septic shock from pylephlebitis

›Hemorrhagic shock from variceal bleed

›IV anticoagulation initiation requirement

›Acute symptomatic PVT with significant thrombus burden

›LMWH dose monitoring and transition planning

›Pylephlebitis

›IV antibiotics, monitoring for hepatic abscess formation

Discharge criteria

›Safe discharge parameters

›Hemodynamically stable with pain controlled

›Tolerating oral intake; no signs of ischemia

›Lactate normalized

›Anticoagulation established

›DOAC initiated or LMWH self-injection teaching complete

›Patient able to perform self-injection (LMWH) if applicable

›Follow-up arranged

›Gastroenterology or hepatology within 1–2 weeks

›Hematology referral if thrombophilia suspected

›Repeat imaging plan (CT or MRI in 3 months)

Transfer criteria

›Transfer triggers

›Bowel infarction requiring emergency surgery

08Treatment/t101

Anticoagulation — LMWH

›Enoxaparin (LMWH) — first-line for acute PVT

›Dosing

›1 mg/kg subcutaneously every 12 hours (therapeutic)

›Weight-based dosing; adjust for renal impairment (CrCl <30 ml/min: 1 mg/kg once daily)

›Monitoring

›Anti-Xa level 4 hours after third dose if obesity, renal impairment, or pregnancy

›Target anti-Xa 0.6–1.0 IU/ml for twice-daily dosing

›Advantages

›Best evidence base; highest recanalization rates (OR 8.4 vs. control)

›Preferred in transplant candidates (short half-life, procedural flexibility)

›Avoid long-term UFH (higher HIT risk in this population)

›Duration

›Bridge to DOAC or VKA after clinical stabilization (typically 5–10 days)

›Continue as monotherapy in transplant candidates for procedural flexibility

Anticoagulation — DOACs

›Direct oral anticoagulants

›Rivaroxaban

›15 mg orally twice daily with food for 21 days

›Followed by 20 mg once daily with evening meal

›Meta-analysis: 87% recanalization vs. 44% without treatment

›Dabigatran

›150 mg orally twice daily after minimum 5 days of parenteral anticoagulation

›110 mg twice daily if age >80 years or concomitant P-glycoprotein inhibitors

›Safety in cirrhosis

›Reasonable in CTP class A and B

›Limited safety data in CTP class C — avoid or use with caution

›Comparable recanalization to LMWH; lower bleeding than warfarin

›Contraindications

›CrCl <15 ml/min (rivaroxaban) or <30 ml/min (dabigatran)

›Pregnancy (Category X — use LMWH instead)

›Active significant bleeding or platelets <50 x10^9/L (relative)

Anticoagulation — Warfarin (VKA)

›Vitamin K antagonist

›INR target 2.0–3.0

›Effective for PVT recanalization

›INR monitoring unreliable in cirrhosis (synthetic dysfunction)

›Initiation

›Overlap with LMWH for minimum 5 days until INR >2.0 on two consecutive days

›Loading dose 5–10 mg orally on day 1

›Monitoring

›Weekly INR during initiation, monthly when stable

›Increased drug and dietary interactions in liver disease

›Role

›Second-line when DOACs unavailable or contraindicated

›Less convenient; cumbersome monitoring burden

Anticoagulation duration

›Duration framework

›Reversible etiology (surgery, pancreatitis)

›3–6 months minimum

›Permanent prothrombotic state (MPN, antiphospholipid syndrome)

›Indefinite anticoagulation

›Cirrhosis with PVT

›6 months minimum; continue until transplant if listed

›Reimage every 3 months to assess recanalization

›Chronic PVT with cavernoma

›Anticoagulation generally not beneficial

›Focus on portal hypertension complications management

›Recurrence risk

›Up to 38% rethrombosis after anticoagulation withdrawal

›Continue in transplant candidates even after recanalization

Management of pylephlebitis

›Septic portal vein thrombosis

›Empiric IV antibiotics

›Piperacillin-tazobactam 3.375 g IV every 6 hours

›Alternative: ceftriaxone 2 g IV once daily plus metronidazole 500 mg IV every 8 hours

›Duration: 4–6 weeks total (IV until clinical improvement, then oral transition)

›Anticoagulation concurrent with antibiotics

›LMWH therapeutic dosing — reduces thrombus propagation

›Evidence supports anticoagulation plus antibiotics over antibiotics alone

›Source control

›Treat underlying source (appendicitis, diverticulitis, cholecystitis)

›Hepatic abscess drainage if present

Portal hypertension and variceal bleeding

›Variceal hemorrhage management

›Octreotide

›50 mcg IV bolus followed by 50 mcg/hour continuous infusion

›Continue for 3–5 days after initial control

›Antibiotics prophylaxis

›Ceftriaxone 1 g IV daily for 7 days (Class I recommendation)

›Reduces bacterial infection, rebleeding, and mortality

›Endoscopic variceal ligation (EVL)

›First-line endoscopic therapy for acute variceal hemorrhage

›Band ligation preferred over sclerotherapy (lower complication rate)

›Non-selective beta-blockers for prophylaxis

›Propranolol 20 mg orally twice daily; titrate to reduce resting HR by 25%

›Or carvedilol 6.25 mg orally twice daily

›Note: meta-analysis showed increased PVT incidence in cirrhosis (OR 4.62) with beta-blockers — ensure PVT ruled out before starting

Interventional procedures

›Transjugular intrahepatic portosystemic shunt (TIPS)

›Indications

›Cirrhotic patients with symptomatic portal hypertension and PVT

›Failed anticoagulation after 3–6 months

›Recurrent variceal hemorrhage with PVT

›Outcomes

›Recanalization in 81% in prospective data

›Reduces portal pressure and allows anticoagulation with lower bleeding risk

›Contraindications

›Severe hepatic encephalopathy, CTP class C without transplant plan

›Complete cavernous transformation of portal vein (technical limitation)

›Catheter-directed thrombolysis/thrombectomy

›Salvage therapy indications

›Failed systemic anticoagulation after 2–4 weeks

›Severe acute PVT with mesenteric ischemia and no surgical indication

›Catheter-directed tPA infusion via superior mesenteric artery approach

›Surgical thrombectomy

›Rare; reserved for bowel resection concurrent with thrombectomy

›High morbidity; hepatology and surgical co-management required

09Special Populations/sp57

Pregnancy

›PVT in pregnancy

›Incidence and risk

›Pregnancy is an independent risk factor (hypercoagulable state)

›Postpartum period has the highest risk (especially first 6 weeks)

›OCP use in reproductive-age women — leading acquired risk factor

›Anticoagulation in pregnancy

›LMWH is the agent of choice throughout pregnancy

›Enoxaparin 1 mg/kg subcutaneously twice daily

›Does not cross the placenta

›DOACs — absolutely contraindicated in pregnancy (teratogenic, Category X)

›Warfarin — first trimester contraindicated (fetal warfarin embryopathy)

›May be used in 2nd and 3rd trimester with risks and benefits discussed

›Delivery planning

›Switch from LMWH to UFH 36–37 weeks gestation for deliverability

›Neuraxial anesthesia timing relative to last dose of anticoagulation

›Hematology and maternal-fetal medicine co-management

›Postpartum

›Continue anticoagulation for minimum 6 weeks postpartum

›Thrombophilia testing after delivery and anticoagulation discontinuation

Geriatric

›PVT in older adults (age >65 years)

›Epidemiology

›Higher prevalence of malignancy-associated PVT (HCC, pancreatic cancer)

›More frequent comorbidities limiting anticoagulation (bleeding history, falls)

›Higher prevalence of CKD — impacts DOAC selection and dosing

›Anticoagulation considerations

›Renal function decline affects DOAC clearance

10Background/b67

Epidemiology

›Prevalence and incidence

›General population incidence

›2.7 per 100,000 person-years overall

›Among most common splanchnic vein thromboses

›Cirrhosis-related PVT

›Prevalence 1% in compensated cirrhosis; up to 20% in transplant candidates

›Incidence increases with severity of portal hypertension

›NASH-associated cirrhosis increasingly common etiology

›Non-cirrhotic PVT

›~30% have concurrent systemic thrombophilic disorder

›Risk factors absent in up to 35% of cases (idiopathic)

›MPNs account for ~25% (JAK2 V617F mutation)

›Demographics

›Bimodal distribution

›Neonates (umbilical vein catheterization)

›Adults peak in 5th–6th decade (cirrhosis, MPN)

›Mortality

›Intestinal infarction carries 10–20% mortality

›Uncomplicated acute PVT with anticoagulation: excellent prognosis

Pathophysiology

›Virchow's triad applied to PVT

›Stasis

›Slow portal flow (<10–15 cm/s) in cirrhosis

›Portal hypertension reduces mesenteric venous return

›Endothelial injury

›Post-surgical — splenectomy disrupts splenic vein flow

›Inflammatory — pancreatitis, appendicitis, IBD cause adjacent vessel wall injury

›Hypercoagulability

›Inherited — Factor V Leiden, prothrombin mutation, protein C/S deficiency

›Acquired — MPN (clonal thrombocytosis, erythrocytosis), antiphospholipid syndrome, PNH

›Consequences of PVT

›Portal hypertension development

›Obstruction increases pre-sinusoidal pressure

›Cavernous transformation — collateral portal channels form over weeks to months

›Varices, ascites, splenomegaly, hypersplenism

›Mesenteric ischemia

›Extension into superior mesenteric vein reduces intestinal perfusion

›Bowel wall edema progresses to transmural infarction

›94% flow reduction at 50% portal occlusion per Poiseuille's law

›Portal biliopathy

›Cavernoma compresses common bile duct

›Causes obstructive cholestasis in chronic PVT

Therapeutic Considerations

›Anticoagulation decision framework

›Non-cirrhotic acute PVT

›Anticoagulation recommended immediately per Baveno VII

›Goal: prevent mesenteric extension and achieve recanalization

›Recanalization rate: LMWH 44–87%, DOACs 87%, warfarin ~30–40%

›Cirrhotic PVT

›Individualized based on thrombus burden, transplant candidacy, bleeding risk

›Anticoagulate if >50% occlusive, extends to mesenteric veins, or transplant candidate

›AGA 2025 Clinical Practice Update supports anticoagulation in most cirrhotic PVT

›Recanalization rates

›LMWH: OR 8.4 vs. control in meta-analysis

›DOACs: 87% vs. 44% without treatment in meta-analysis

›Spontaneous recanalization without treatment: ~40% in cirrhotic patients

›Bleeding risk in cirrhosis

›Cirrhosis is not inherently a bleeding disorder — rebalanced hemostasis

›Reduced procoagulant factors balanced by reduced anticoagulant proteins

›Thromboelastography (TEG) better reflects true hemostatic balance than INR

›Platelet threshold

›Anticoagulation with platelets <50 x10^9/L requires individualized assessment

›Variceal hemorrhage risk

›Screen with EGD before initiating anticoagulation in cirrhotic patients

›Treat varices with EVL or beta-blocker prophylaxis first

›TIPS role

›TIPS achieves 81% PVT recanalization in prospective cohort data

›Reduces portal pressure enabling safer anticoagulation

›Preferred in cirrhotic patients with both PVT and portal hypertension complications

11Patient Discharge Instructions/pdi29

copy discharge instructions

›Portal Vein Thrombosis — Discharge Instructions

›What you were treated for

›A blood clot in the portal vein, the large vein that carries blood to your liver

›This can affect blood flow to your intestines and liver

›Your medications

›Take your blood thinner exactly as prescribed — do not skip doses

›If taking injectable medication (enoxaparin), inject as instructed

›If taking a pill blood thinner (rivaroxaban or dabigatran), take with food as directed

›Do not stop your blood thinner without talking to your doctor

›Activity restrictions

›Avoid contact sports or activities with high fall or injury risk while on blood thinners

›You may resume normal daily activities as tolerated

›Diet and lifestyle

›If prescribed warfarin, maintain consistent vitamin K intake (do not dramatically change green vegetable intake)

›If you have liver disease and ascites, limit sodium to less than 2 grams per day

›Stay well hydrated; avoid excessive alcohol

›Follow-up appointments

›Gastroenterology or hepatology within 1–2 weeks

›Repeat imaging (CT or MRI) in 3 months to assess clot response

›Blood work as directed to monitor kidney function and blood thinner levels

›Return to Emergency Department immediately for

›Worsening or new severe abdominal pain

›Vomiting blood or black tarry stools

›Bright red blood in stool

›Fever above 38.5°C or chills

›Lightheadedness, fainting, or feeling that you may pass out

›New confusion or difficulty thinking clearly

12References/r48

Guidelines and key sources

›ACG Clinical Guideline: Disorders of the Hepatic and Mesenteric Circulation

›Simonetto DA, Singal AK, Garcia-Tsao G, et al.

›American Journal of Gastroenterology. 2020

›DOI: 10.14309/ajg.0000000000000486

›Comprehensive management framework for PVT including anticoagulation and variceal management

›AASLD Practice Guidance: Vascular Liver Disorders, Portal Vein Thrombosis, and Procedural Bleeding

›Northup PG, Garcia-Pagan JC, Garcia-Tsao G, et al.

›Hepatology. 2021

›DOI: 10.1002/hep.31646

›Anticoagulation safety in cirrhosis, bleeding risk stratification

›AGA Clinical Practice Update on Management of Portal Vein Thrombosis in Patients With Cirrhosis

›Davis JPE, Lim JK, Francis FF, Ahn J.

›Gastroenterology. 2025

›Linkinghub.elsevier.com/retrieve/pii/S0016-5085(24)05664-6

›Expert review on DOAC use and updated anticoagulation thresholds in cirrhosis

›Portal Vein Thrombosis: Diagnosis, Management, and Endpoints for Future Clinical Studies

›Elkrief L, Hernandez-Gea V, Senzolo M, et al.

›Lancet Gastroenterology and Hepatology. 2024

›PMID: 38996577

›Comprehensive landmark review including classification and treatment evidence synthesis

›Portal Vein Obstruction: Epidemiology, Pathogenesis, Natural History, Prognosis and Treatment

›Kumar A, Sharma P, Arora A.

›Alimentary Pharmacology and Therapeutics. 2015

›DOI: 10.1111/apt.13019

›Epidemiology and pathophysiology reference

›Diagnostic Performance of Ultrasound, CT and MRI in Portal Vein Thrombosis

›Girardi L, Zarka F, Pradier M, et al.

Evidence & Review

Evidence & Review