Hepatology & Gastroenterology & Internal Medicine & Digestive Surgery
Portal hypertension
Portal hypertension (PH) is defined as a pathological increase in pressure within the portal venous system above 5 mmHg (normal range: 1–5 mmHg), measured indirectly by the hepatic venous pressure gradient (HVPG = blocked suprahepatic pressure − free suprahepatic pressure). A HVPG ≥ 10 mmHg defines clinically significant PHT (CS-PHT), the threshold at which complications—gastroesophageal varices, ascites, hepatic encephalopathy—and at which prophylaxis for variceal bleeding is indicated. A HVPG ≥ 12 mmHg corresponds to the threshold at which the risk of hemorrhage is highest. Liver cirrhosis is by far the most common cause of PHT in developed countries (90% of cases), regardless of etiology (alcohol + HCV + HBV + MASLD/NASH + HAI + CBP + CSP). Other causes—portal vein thrombosis, Budd-Chiari syndrome, schistosomiasis, congenital hepatic fibrosis—are less common but warrant identification because their specific management differs. The pathophysiology involves two interdependent components: increased intrahepatic resistance (fixed component: fibrosis + regenerative nodules; reversible dynamic component: intrahepatic vasoconstriction due to NO deficiency + excess endothelin-1) and splanchnic vasodilation with portal hyperflow (excessive splanchnic NO production → arteriolar vasodilation → increased portal flow). Major complications—variceal bleeding, ascites, hepatic encephalopathy, and bacterial infection (spontaneous bacterial peritonitis)—are the leading causes of mortality in cirrhosis and require structured, sequential management.
Pathophysiology, etiology, and hemodynamic evaluation
- Pathophysiology of portal hypertension — vascular and hemodynamic components: Portal venous system — anatomical overview: portal vein = confluence of the superior mesenteric vein + inferior mesenteric vein + splenic vein → drains the gastrointestinal tract + spleen + pancreas → divides in the liver into right and left branches → hepatic sinusoids → supra→ inferior vena cava + normal portal pressure: 1–5 mmHg + normal portal flow: 1,000–1,500 mL/min; mechanisms of portal hypertension in cirrhosis: increased intrahepatic resistance: structural (fixed) component: fibrosis + regenerative nodules → architectural distortion → reduction in sinusoidal lumen + compression of suprahepatic venules → mechanical increase in resistance + vascular component (dynamic — partially reversible): deficit in endothelial NO production by sinusoidal endothelial cells (decreased eNOS) → intrahepatic vasoconstriction + activation of perisinusoidal stellate cells (HSC) → contraction of the sinusoids → angiotensin II + endothelin-1 → worsening of resistance → the dynamic component accounts for approximately 30–40% of total resistance → therapeutic target for hepatic vasodilators (statins — Zafra 2004 — Hepatology: simvastatin → reduction in HPV) + splanchnic vasodilation and portal hyperflow: excessive NO production in the splanchnic circulation (vasodilation) + prostacyclin + substance P + VIP → splanchnic arteriolar vasodilation → reduction in splanchnic resistance → increased splanchnic blood flow → increased portal flow → worsening of PHT + cirrhogenic cardiac dysfunction: high cardiac output + high heart rate + low systemic vascular resistance → «hyperdynamic syndrome» of cirrhosis → relative central hypovolemia despite plasma volume expansion + activated renin-angiotensin-aldosterone system (RAAS) → sodium and water retention → ascites; definition and measurement of HPP: HPP = blocked suprahepatic pressure (BHP—an indirect reflection of sinusoidal portal pressure)—free suprahepatic pressure (FHP) → technique: superhepatico-venous catheterization → balloon inflated → SHBP measured → balloon deflated → FHP measured → normal SHBP: 1–5 mmHg → PHT: >5 mmHg → subclinical PHT: 5–10 mmHg → PHT-CSP: ≥10 mmHg → threshold for complications + varices: ≥12 mmHg → maximum hemorrhagic threshold → therapeutic target: reduction in SHPV of 20–30 mmHg from baseline OR SHPV <12 mmHg → near elimination of hemorrhagic risk (Bosch 2003 — Journal of Hepatology) → HVPG is the gold standard but is not routinely performed + several non-invasive markers are used in practice (elastography + CBC + transaminases + APRI score + FIB-4)
- Etiology of portal hypertension — classification by level of obstruction: Pre-sinusoidal portal hypertension — blockage upstream of sinusoids: pre-hepatic: portal vein thrombosis (PVT): most common non-cirrhotic cause → thrombophilia workup (JAK2 + FV Leiden + prothrombin G20210A + antithrombin + proteins C and S) + myeloproliferative neoplasms (main cause of non-cirrhotic pre-hepatic portal hypertension) + intra-abdominal infections (pylephlebitis) + chronic pancreatitis → normal HVPG (resistance is upstream of the liver) → frequent esophageal varices but normal liver → better prognosis than in cirrhosis + splenic vein thrombosis → isolated gastric varices + extrinsic compression (pancreatic tumor) + intra-hepatic pre-sinusoidal: schistosomiasis mansoni (portal fibrosis without cirrhosis — major cause in tropical countries) + congenital hepatic fibrosis + diffuse hepatic metastases + sarcoidosis + lymphoma + mastocytosis; sinusoidal portal hypertension — most frequent (cirrhosis): hepatic cirrhosis of any etiology: alcoholic + HCV + HBV + MASLD/NASH + AIH + PBC + PSC + hemochromatosis + Wilson's disease + A1AT + Budd-Chiari syndrome: obstruction of hepatic veins → sinusoidal and post-sinusoidal portal hypertension + veno-occlusive disease (VOD) / sinusoidal obstruction syndrome (SOS): complication of bone marrow transplant (intense chemotherapeutic conditioning) → sinusoidal portal hypertension + toxins: irbesartan + chronic vitamin A; post-sinusoidal portal hypertension — blockage downstream of sinusoids: Budd-Chiari syndrome (thrombosed hepatic veins) + constrictive pericarditis + severe right heart failure (chronic congestive heart failure → cardiac portal hypertension → cardiomegaly + jugular vein distension + high SAAG gradient >11 g/L + high brachial pressure) + risk factors for complications: HVPG ≥10 mmHg → risk of developing varices + HVPG ≥12 mmHg → risk of active bleeding + platelets <100 × 10⁹/L + TP bas + hepatic elastography ≥20–25 kPa → correlates with HPCS
Complications and Management
| Complication / area | Data, modalities and protocols | Key studies and recommendations |
|---|---|---|
| Esophageal varices — primary and secondary prophylaxis Endoscopic screening - non-selective beta-blockers - propranolol - carvedilol - elastic band ligation - HVPG - thresholds - NSBBs |
Screening for esophageal varices: upper gastrointestinal endoscopy (EGD): screening recommended upon diagnosis of cirrhosis → Baveno classification (D'Amico 2010 — Journal of Hepatology): small varices (grade 1: <5 mm + grade 2: 5–15 mm) + large varices (grade 3: >15 mm) + risk factors for bleeding: grade 3 + red signs (red spots + linear varices) + Child C cirrhosis → the Baveno VI criteria (de Franchis 2015 — Journal of Hepatology) allow endoscopy to be avoided if: elastometry <20 kPa + platelets >150 × 10⁹/L → no varices to treat with a negative predictive value of 99% → reduction in unnecessary endoscopies; primary prophylaxis of variceal bleeding: small varices without risk factors: no prophylactic treatment → endoscopic follow-up every 1–2 years → small varices with red signs OR Child-Pugh Class C cirrhosis: non-cardioselective beta-blockers (NSBBs) → large varices: NSBBs OR elastic banding (banding) → propranolol 10–20 mg twice daily → titration until HR reduction of 25 bpm or target HR 55 bpm + or carvedilol 6.25 mg twice daily → advantage: additional alpha-blocker → reduction in intrahepatic resistance + reduction in portal flow → Stanley 2015 — Lancet (CARVE RCT): carvedilol vs. elastic banding for primary prevention → carvedilol superior in reducing HCV + survival → carvedilol preferred for primary prevention if no contraindications → nadolol: not available in Canada → mechanism of NSBBs: β1 → reduction in HR + cardiac output → β2 → splanchnic vasoconstriction (blockade of vasodilator β2 receptors) → reduction in portal flow → contraindications of NSBBs: severe asthma + high-grade AV block + severe bradycardia + symptomatic hypotension + severe COPD → caution in refractory ascites (risk of arterial hypotension → hepatorenal syndrome) → Mandorfer 2014 — Hepatology: NSBBs in refractory ascites → increased mortality (ongoing debate) → caution + endoscopic elastic ligation (banding): alternative to NSBBs for large varices → 2–4-week sessions until eradication + quarterly endoscopic follow-up → efficacy similar to NSBBs for primary prophylaxis (Gluud 2012 — Cochrane); secondary prophylaxis (after a first bleeding episode): combination of NSBBs + elastic banding: Villanueva 2006 — Hepatology + D'Amico 2009 — Alimentary Pharmacology and Therapeutics: meta-analysis → combination superior to either alone → 40–50% reduction in bleeding recurrence → reduced mortality → standard of care post-variceal bleeding + hemodynamic goal: reduction in VOPH of 20 mmHg compared to baseline OR VOPH <12 mmHg → near-elimination of recurrence risk + TIPS (Transjugular Intrahepatic Portosystemic Shunt) for secondary prophylaxis: if BBs fail + ligation or persistent PVP ≥20 mmHg → mechanical reduction of portal pressure + early TIPS (≤72 hours after a hemorrhagic episode in Child B patients with active bleeding or Child C patients <14 points) → Garcia-Pagan 2010 — NEJM: Early TIPS → 61% reduction in 1-year mortality in patients at high risk of recurrence → therapeutic breakthrough + covered TIPS (polytetrafluoroethylene — PTFE): Tripodi 2010 + Bureau 2004 — Hepatology: PTFE TIPS vs. bare TIPS (Dacron) → better patency + less encephalopathy → PTFE is the current standard | Garcia-Pagan 2010 — NEJM (RCT on early TIPS): TIPS within 72 hours + high risk (Child B + active bleeding + Child C <14) → 1-year mortality: 14 % vs. 39 % → 61% reduction in % → therapeutic breakthrough + Stanley 2015 — Lancet (CARVE RCT): carvedilol vs. elastic ligation for primary prophylaxis → carvedilol superior + de Franchis 2015 — Journal of Hepatology (Baveno VI): criteria for avoiding endoscopy: LSM <20 kPa + platelets >150 × 10⁹/L → NPV 99% % + Villanueva 2006 — Hepatology: NSBBs + ligation → superior to either alone in secondary prophylaxis → D'Amico 2009 — APT: meta-analysis confirmation + Gluud 2012 — Cochrane: ligation vs. NSBBs in primary prophylaxis → similar efficacy + Bosch 2003 — Journal of Hepatology: target IAP <12 mmHg or 20% reduction → near elimination of bleeding risk + Bureau 2004 — Hepatology: PTFE TIPS vs. bare → PTFE superior in patency + Mandorfer 2014 — Hepatology: NSBBs in refractory ascites → increased mortality → caution |
| Acute variceal hemorrhage — emergency management Terlipressin — octreotide — emergency EGD — antibiotic prophylaxis — rescue TIPS — Sengstaken tube — prognosis |
Management of acute variceal bleeding — a major emergency: 6-week mortality: 10–20% even with optimal treatment → every hour of delay in treatment increases mortality → ABCs of resuscitation → hemodynamic stabilization: conservative fluid resuscitation (target Hb 70–80 g/L — restrictive transfusion) → avoid fluid overload (worsens portal pressure) → Villanueva 2013 — NEJM: restrictive transfusion (target Hb 70 g/L) vs. liberal (90 g/L) → reduced mortality at 6 weeks: 5 % vs. 9 % → reduced portal pressure (less blood dilution → lower pressure) → protect the airways if encephalopathy + correct coagulopathy (fresh frozen plasma if INR is very high + platelets if <50 × 10⁹/L + fibrinogen if <1 g/L) → patients with cirrhosis often have mixed coagulopathy → thromboelastogram (TEG/ROTEM) to guide transfusions; splanchnic vasoconstrictors (to be initiated as soon as suspected, BEFORE endoscopy): terlipressin (Glypressin) 2 mg IV every 4 hours × 5 days → vasopressin analog → splanchnic vasoconstriction → reduced portal flow + Ioannou 2003 — Gastroenterology: meta-analysis → terlipressin → the only vasoconstrictor shown to reduce mortality → 34% reduction in mortality (%) + reduced risk of recurrence → standard of care in Europe → adverse effects: coronary vasoconstriction + cardiomyopathy → ECG prior to treatment + contraindicated in ischemic heart disease + octreotide 50 µg IV bolus → then 25–50 µg/h as a continuous infusion × 5 days → somatostatin analog → inhibits glucagon secretion + splanchnic vasoconstriction → similar efficacy to terlipressin for bleeding + fewer cardiovascular effects + available in Canada (terlipressin less accessible) → vapreotide + somatostatin: alternatives; routine antibiotic prophylaxis (initiate upon admission — before endoscopy): norfloxacin 400 mg × 2/day × 7 days OR ceftriaxone 1 g/day IV × 7 days (preferred if advanced cirrhosis or bacterial colonization) → Bernard 1999 — NEJM: antibiotic prophylaxis in variceal bleeding → 32% reduction in bacterial infections + reduced mortality → standard of care → Fernández 2006 — Hepatology: ceftriaxone superior to norfloxacin in advanced cirrhosis (higher resistance to norfloxacin) → spontaneous bacterial peritonitis (SBP) and infections increase the risk of recurrent bleeding and mortality + emergency upper gastrointestinal endoscopy (UGIE): within 12 hours (or within 24 hours if stabilized) → endoscopic hemostasis: elastic ligation (banding): standard of care for esophageal varices + injection of N-butyl-2-cyanoacrylate (biological glue): gastric varices + sclerotherapy: discontinued (more adverse effects) → if endoscopic hemostasis is impossible → Sengstaken-Blakemore (SB): mechanical tamponade → bridge to TIPS → maintain balloon ≤24h → risk of esophageal necrosis if prolonged + covered self-expanding metal stent (SEMS): alternative to SB → endoscopic deployment → good control of bleeding → fewer adverse effects than SB → bridge to TIPS; Rescue TIPS: if bleeding is uncontrolled despite medical and endoscopic treatment → or early recurrence within 5 days → semi-emergency or emergency TIPS → reduction in portal pressure + control of bleeding in 90–95% of cases → Garcia-Pagan 2010 — NEJM: Early TIPS (≤72 h) in Child B patients with active bleeding + Child C <14 points → standard of care in this subgroup + post-TIPS encephalopathy: common complication (25–35% of cases) → lactulose + rifaximin | Villanueva 2013 — NEJM (RCT on restrictive transfusion, n=921): Target Hb 70 g/L → mortality 5 % vs. 9 % (target 90 g/L) → relative reduction 44 % → paradigm shift in emergency care + Ioannou 2003 — Gastroenterology (meta-analysis): terlipressin → only vasoconstrictor reducing mortality + 34% reduction in % → European standard of care + Bernard 1999 — NEJM: antibiotic prophylaxis → 32% reduction in infections with % + mortality reduction → absolute standard + Fernández 2006 — Hepatology: ceftriaxone superior to norfloxacin in advanced cirrhosis + Garcia-Pagan 2010 — NEJM (early TIPS RCT): mortality 14% % vs. 39% % → NNT = 4 → therapeutic breakthrough → EASL Guidelines 2022 (by Franchis — Journal of Hepatology): updated recommendations for the management of variceal bleeding → terlipressin + ceftriaxone + EOGD within 12 hours + early TIPS in high-risk groups + AASLD Practice Guidance 2021: North American recommendations + SOGC/CANACH guidelines |
| Ascites and hepatorenal syndrome Paracentesis — spironolactone — furosemide — IV albumin — TIPS — transplant — SHR — terlipressin — norepinephrine — midodrine — octreotide |
Pathophysiology of ascites in cirrhosis: splanchnic vasodilation → reduction in effective blood volume → activation of the RAAS + ADH + SNS → water and sodium retention → expansion of extracellular volume → accumulation in the peritoneal cavity + portal hypertension → increased hydrostatic pressure in the sinusoids → filtration into the peritoneal cavityperitoneal cavity + hypoalbuminemia → reduced oncotic pressure → exacerbates accumulation → diagnosis of ascites: diagnostic puncture (paracentesis): SASG (Serum-Ascites Albumin Gradient) = serum albumin − ascites fluid albumin → SASG ≥11 g/L → PHT (cirrhosis + HF + PBS + Budd-Chiari syndrome) → SASG <11 g/L → no PHT (tuberculosis + peritoneal carcinomatosis + prerenal SHR) + cell count + albumin + fluid protein + cytology if neoplasia is suspected + bacterial culture (PBS if PNN >250/mm³); treatment of ascites based on severity: grade 1 ascites (mild — detectable only by ultrasound): low-sodium diet (<2 g NaCl/day = <88 mmol/day) alone → grade 2 ascites (moderate): spironolactone 100 mg/day + furosemide 40 mg/day → gradual increase (100/40 mg) if insufficient → up to 400 mg/day spironolactone + 160 mg/day furosemide → weight control (-500 g/day if no edema + up to -1 kg/day if edema) + urinary NaCl assessment (target natriuresis >78 mmol/day) → Bernardi 2012 — Alimentary Pharmacology and Therapeutics: spironolactone superior to furosemide alone as a first-line diuretic → refractory ascites (grade 3 — recurrent or refractory to diuretics): large-volume therapeutic paracentesis (LVP) → >5 L removed → replacement with IV albumin at 8 g/L of ascites removed → Moore 1994 — Gastroenterology: LVP paracentesis + albumin vs. paracentesis alone → reduction in SHR and mortality with albumin → essential if >5 L → Serra 2010 — Hepatology: IV albumin in cirrhosis → multiple benefits (anti-inflammatory + vasoactive + antioxidant) → TIPS in refractory ascites: ascites control in 70–80% of patients → improved survival in certain subgroups → Salerno 2007 — Hepatology + Narahara 2011 — Journal of Gastroenterology: TIPS vs. repeated paracentesis → better survival without transplantation + better ascites control → contraindications for TIPS: refractory encephalopathy + disseminated intravascular coagulation + severe heart disease + active infection + bilirubin >50 µmol/L; spontaneous bacterial peritonitis (SBP): major infectious complication of ascites → PNN in ascites ≥250/mm³ or positive culture → mortality 30–40% within 1–3 months without treatment → treatment: ceftriaxone 2 g/day IV × 5 days (or norfloxacin 400 mg × 2/day PO × 7 days if outpatient) + IV albumin 1.5 g/kg on Day 1 + 1 g/kg on Day 3 → Sort 1999 — NEJM: albumin in PBS → reduced SHR (SHR risk reduced by 60% in %) + reduced in-hospital mortality → absolute standard → secondary prophylaxis of PBS: norfloxacin 400 mg/day indefinitely → or trimethoprim-sulfamethoxazole 1 tablet/day; hepatorenal syndrome (HRS): major complication of decompensated cirrhosis → HRS-AKI (type 1: rapid deterioration — creatinine × 2 in 2 weeks → >221 µmol/L) + HRS-CKD (type 2: progressive deterioration) → mechanism: severe renal vasoconstriction (response to splanchnic vasodilation) → oliguria + AKI without iatrogenic or structural cause (diagnosis by exclusion) → treatment: terlipressin 0.5–1 mg IV every 4–6 hours + IV albumin 1 g/kg/day × 48 hours → then 20–40 g/day + Martín-Llahí 2008 — Gastroenterology + Sanyal 2008 — NEJM (RELIEF trial): terlipressin → reversal of SHR in 40–50% of patients vs. 8–13% of placebo patients → reduced mortality → FDA approval in 2022 (Terlivaz) for SHR-AKI → alternative if terlipressin is unavailable: norepinephrine 0.5–3 mg/h IV in the ICU + or midodrine 7.5 mg × 3/day + octreotide 200 µg × 3/day SC + IV albumin → less effective but available in Canada | 1999 — NEJM: IV albumin in acute liver failure → 60% reduction in SHR (3-month survival rate) + reduction in in-hospital mortality → gold standard + Moore 1994 — Gastroenterology: IV albumin + LVP paracentesis → reduction in SHR + mortality → essential if >5 L removed + Salerno 2007 — Hepatology + Narahara 2011 — Journal of Gastroenterology: TIPS vs. paracentesis → better survival without transplantation + Martín-Llahí 2008 — Gastroenterology: terlipressin + SHR → reversal of 40–50% % + Sanyal 2008 — NEJM (RELIEF): terlipressin + albumin vs. placebo + albumin → SHR-AKI → reversal 32 % vs. 17 % → FDA approval 2022 + Bernardi 2012 — APT: spironolactone superior to furosemide alone as first-line diuretic + Serra 2010 — Hepatology: IV albumin in cirrhosis → multiple benefits + EASL 2018 Clinical Practice Guidelines: ascites + PBS + SHR → gold standard recommendations + AASLD 2021 + Canadian SOGC guidelines |
| Hepatic encephalopathy and other complications Encephalopathy - lactulose - rifaximin - ammonemia - West Haven - TIPS - hepatopulmonary syndrome - cirrhotic cardiomyopathy - transplantation |
Hepatic encephalopathy (HE) — pathophysiology and treatment: pathophysiology: accumulation of nitrogenous toxins (ammonia + mercaptans + short-chain fatty acids) → hepatic detoxification failure + portosystemic shunts → entry into the systemic circulation → neuroinflammation + astrocyte dysfunction → cerebral edema + disruption of neurotransmitters (GABA + glutamate + histamine) → clinical manifestations: West Haven classification: Grade 0: cryptic (detectable by neuropsychological testing) → Grade 1: impaired attention + euphoria or anxiety + early-onset flapping tremor → Grade 2: lethargy + inappropriate behavior + flapping tremor → Grade 3: severe confusion + disorientation + unintelligible speech → Grade 4: coma → precipitating factors to be identified (TIPS mnemonic): Thrombosis + Infection (PBS + sepsis) + PBS + Gastrointestinal bleeding → gastrointestinal hemorrhage (proteins in the intestine → ammonia) → Sedative medications + Constipation + Hyponatremia + dehydration + urinary retention; treatment of acute EH: lactulose 20–30 mL PO × 2–4/day → goal 2–3 loose stools/day → mechanism: colonic acidification → reduced ammonia absorption (captured NH₄⁺) + catharsis → Prasad 2007 — Alimentary Pharmacology and Therapeutics: lactulose → reduction in EH → but insufficient data on mortality + rifaximin (Xifaxan) 550 mg × 2/day: non-absorbable antibiotic → reduction in bacterial ammonia production in the colon → Bass 2010 — NEJM (RCT n=299): rifaximin + lactulose → 57% reduction in the risk of EH recurrence % + reduced mortality + reduced hospitalizations → standard of care for secondary prevention of EH + zinc: supplementation 220 mg × 2/day → enzymatic cofactor in the urea cycle → limited data but well tolerated → BCAAs (branched-chain amino acids): IV in severe acute HEP → neurological improvement → expensive + L-ornithine L-aspartate (LOLA): stimulates the urea cycle → reduction in ammonia → positive data → not available in Canada + secondary prevention of HEP: rifaximin + lactulose → standard of care according to EASL 2014 + treat precipitating factors; Hepatopulmonary syndrome (HPS): intrapulmonary vascular dilation → right-to-left shunt → hypoxemia → evaluation by contrast-enhanced echocardiography (microbubbles) + calculation of AaPO₂ → definitive treatment: liver transplantation (resolution of HPS in most cases after transplant) + cirrhogenic cardiomyopathy: diastolic dysfunction (often subclinical) + impaired chronotropic and inotropic response → QT prolongation → risk factor during TIPS placement or transplantation + portopulmonary hypertension (PPH): elevated pulmonary arterial pressure (mean PAP >25 mmHg) due to HTP → high PVR → evaluation: echocardiography + right heart catheterization + treatment: pulmonary vasodilators (ambrisentan + macitentan + riociguat) → transplantation is contraindicated if mean PAP >35 mmHg (very high morbidity); orthotopic liver transplantation (OLT): definitive treatment for decompensated cirrhosis + PHT → primary indication: MELD ≥15 (Model for End-Stage Liver Disease) → criteria: decompensated cirrhosis (ascites + hepatic encephalopathy + variceal bleeding) + or MELD ≥15 → contraindications: active uncontrolled sepsis + extrahepatic carcinoma (with exceptions) + active alcohol addiction without treatment + severe portal hypertension (mean PAP >35 mmHg) + severe cardiomyopathy → MELD score: 3.78 × log(bilirubin μmol/L/17.1) + 11.2 × log(INR) + 9.57 × log(creatinine μmol/L/88.4) + 6.43 → MELD >15 → benefit of transplantation vs. waiting list → data: 1-year post-transplant survival: 85–90% % + 5-year survival: 70–80% % → Kim 2008 — Gastroenterology: MELD + graft allocation → reduced mortality on the waiting list | Bass 2010 — NEJM (RCT, n=299): rifaximin + lactulose → reduced recurrence of HE in 57% of patients (%) + reduced mortality and hospitalizations → standard of care + Prasad 2007 — APT: lactulose in HE → beneficial data but mortality insufficiently documented + EASL 2014 Clinical Practice Guidelines on Hepatic Encephalopathy: rifaximin + lactulose for secondary prevention → Level A recommendation + EASL 2022 Clinical Practice Guidelines for Decompensated Cirrhosis: comprehensive recommendations + Kim 2008 — Gastroenterology: MELD and organ allocation → Villanueva 2013 — NEJM: restrictive transfusion → 44% reduction in mortality in % + Garcia-Pagan 2010 — NEJM: early TIPS → NNT = 4 in high-risk subgroups → all major interventions in HTP → EASL 2018 CPG ascites + EASL 2022 CPG decompensated cirrhosis: European reference guidelines + AASLD 2021 + SOGC/CASL 2022: Canadian recommendations |
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Variceal bleeding is a life-threatening emergency—management must begin immediately with three simultaneous measures even before endoscopy: As soon as a variceal hemorrhage is suspected, a splanchnic vasoconstrictor (terlipressin or octreotide), antibiotic prophylaxis (ceftriaxone 1 g IV) must be initiated without delay, and upper gastrointestinal endoscopy should be planned within 12 hours. Transfusion is restrictive (target Hb 70–80 g/L) — overly liberal transfusion worsens portal pressure and favors recurrence. Early TIPS (within 72 hours) in Child B patients with active bleeding or Child C <14 should be considered from the outset, as it reduces mortality by 61 %.
Situations requiring a 911 call or urgent care
Hematemesis (vomiting red blood or coffee grounds) + melena + hypotension + tachycardia + pallor in a patient with cirrhosis or a history of alcoholism → Probable variceal hemorrhage → Call 911 → Resuscitation (2 IV lines + careful fluid resuscitation → goal Hb 70-80 g/L) → IV terlipressin or IV octreotide → 1g IV ceftriaxone → Endoscopy within 12 hours → TIPS if not controlled → DO NOT transfuse beyond Hb 80 g/L.
Cirrhotic patient with ascites + fever + abdominal pain + general deterioration → Spontaneous bacterial peritonitis until proven otherwise → medical emergency → emergency diagnostic paracentesis → if ANC ≥250/mm³ → ceftriaxone 2 g/day IV × 5 days + IV albumin 1.5 g/kg on D1 + 1 g/kg on D3 → without albumin → high risk of HRS.
Cirrhotic patient with progressive oliguria + creatinine doubled in 48h + ascites + no iatrogenic or obstructive cause → Hepatorenal syndrome (HRS-AKI) → medical emergencies → IV terlipressin + IV albumin 1 g/kg/day × 48 hours → aim for resolution of HRS → if no response → evaluation for liver transplantation → without treatment → mortality >80% at 30 days.
Cirrhotic patient with confusion + agitation + disorientation + flapping tremor + no other obvious diagnosis Hepatic encephalopathy → look for and treat the precipitating factor (bleeding + SBP + constipation + sedatives) → lactulose + rifaximin → if grade 3-4 → hospitalization + airway protection → do not use benzodiazepines (worsen HE).
Consult at Clinique Omicron
Clinique Omicron's physicians provide follow-up care for patients with compensated cirrhosis and portal hypertension, prescribe non-selective beta-blockers for primary prophylaxis, manage outpatient complications (mild ascites, mild encephalopathy, diuretic treatment), and refer patients to hepatologists and specialized gastroenterologists for endoscopies, interventional procedures (TIPS), and transplant evaluation. Consultations are available at several service locations in Quebec and via telemedicine. To make an appointment, visit cliniqueomicron.ca.
The content of this page is for informational purposes only and does not replace the advice of a doctor or a specialized hepatologist. Portal hypertension is a serious condition requiring structured medical monitoring and multidisciplinary management.
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