Hepatology & Gastroenterology
Cirrhosis
Cirrhosis is the common end stage of most chronic liver diseases, defined histologically by extensive and diffuse fibrosis of the liver parenchyma with the formation of regenerative nodules that gradually replace the liver’s normal lobular architecture. This irreversible architectural remodeling results from the chronic activation of hepatic stellate cells (Ito cells) by fibrogenic stimuli—inflammation, oxidative stress, toxins—leading to excessive deposition of extracellular matrix (collagen) and progressive destruction of functional hepatocytes. Cirrhosis is a major public health disease: it affects approximately 1 to 2% of the global adult population and is the eleventh leading cause of death worldwide, with over 1.3 million annual deaths. In Canada, the main causes are alcoholic liver disease (40–50%), non-alcoholic steatohepatitis (NASH, rapidly increasing due to the obesity and type 2 diabetes epidemic), and chronic viral hepatitis (HCV—in sharp decline thanks to direct-acting antivirals, HBV). The natural course of cirrhosis distinguishes two clinical phases with radically different prognoses: compensated cirrhosis, during which the liver maintains sufficient function (preserved hepatic functional reserve) with a median survival exceeding 10 years; and decompensated cirrhosis, marked by the onset of complications—ascites, hepatic encephalopathy, bleeding from ruptured esophageal varices, spontaneous infection of ascites fluid (spontaneous bacterial peritonitis), hepatorenal syndrome—with a median survival that drops to 2 years and a 1-year mortality risk of 15 to 20%. While liver fibrosis was long considered irreversible, recent data have shown that partial regression of fibrosis is possible after treating the underlying cause (viral eradication of HCV with DAAs, alcohol withdrawal, significant weight loss in NASH)—though complete regression is not achieved in advanced cirrhosis. Liver transplantation remains the only curative treatment for decompensated cirrhosis that does not respond to medical therapy.
Main causes
| Etiology | Frequency (Western countries) | Key features |
|---|---|---|
| Alcoholic liver disease (ALD) | 40-50 % | Steatosis → alcoholic steatohepatitis → fibrosis → cirrhosis; risk threshold: > 30 g/day alcohol in men, > 20 g/day in women (1 standard drink = 14 g alcohol); aggravating factors: female sex (increased vulnerability), obesity, concomitant HCV; complete alcohol withdrawal - the only intervention that can stop progression and improve survival; severe acute alcoholic hepatitis (Maddrey score ≥ 32) treated with corticosteroids (prednisolone) |
| Non-alcoholic steatohepatitis (NASH) | 20–30 % and growing rapidly | NAFLD/MAFLD continuum: simple steatosis → steatohepatitis (NASH) → fibrosis → cirrhosis → HCC; strongly associated with metabolic syndrome (abdominal obesity, type 2 diabetes, dyslipidemia, hypertension); NASH-related cirrhosis is often diagnosed at an advanced stage because it is asymptomatic for a long time; notable feature: HCC can occur in a non-cirrhotic liver in 20–30% of cases; treatment: weight loss of ≥10% of body weight (demonstrated histological regression), regular physical activity, management of metabolic comorbidities |
| Chronic Hepatitis C (HCV) | 15–20 % (declining) | 25–30% of HCV-infected patients develop cirrhosis within 20–30 years; a risk accelerated by alcohol, diabetes, and age at the time of infection; viral eradication using direct-acting antivirals (sofosbuvir, glecaprevir/pibrentasvir — cure rate > 95% %) reduces the risk of decompensation and HCC by 70% % even in cases of established cirrhosis, but HCC surveillance must be maintained for life in cured cirrhotic patients |
| Chronic Hepatitis B (HBV) | 10-15 % | HBV can induce cirrhosis and HCC even without prior cirrhosis (genomic integration); antiviral treatment with nucleos(t)ide analogs (tenofovir, entecavir) lifelong reduces the risk of cirrhosis and HCC; universal HBV vaccination is the most effective preventive measure. |
| Primary Biliary Cirrhosis (PBC) and Primary Sclerosing Cholangitis (PSC) | 5-10 % | CBP: autoimmune disease of the small intrahepatic bile ducts; primarily affects women (90%); pathognomonic anti-mitochondrial antibodies (AMA-M2); treatment: ursodeoxycholic acid (UDCA) ± obeticholic acid; CSP: fibrosing inflammation of the intra- and extrahepatic bile ducts, strongly associated with chronic inflammatory bowel disease (IBD); lifetime risk of cholangiocarcinoma 10–15% (%); no effective medical treatment — liver transplantation |
| Hereditary hemochromatosis and other metabolic diseases | 5 % | Hemochromatosis (mutation Human Factors and Ergonomics C282Y) : iron overload → cirrhosis, diabetes, cardiomyopathy, arthropathy — treatment with regular phlebotomies; Wilson's disease (copper accumulation): treatment with D-penicillamine or trientine; alpha-1-antitrypsin deficiency (ZZ phenotype); hepatic glycogenoses |
Aggravating factors and cofactors of fibrogenesis
- Alcohol consumption in patients with pre-existing liver disease (HCV, NASH, PBC): supra-additive effect on fibrogenesis — alcohol consumption, even moderate, in patients with chronic hepatitis C or NASH multiplies the risk of progression to cirrhosis
- Obesity and metabolic syndrome: an aggravating cofactor for all chronic liver diseases — it accelerates fibrosis progression in viral hepatitis, hemochromatosis, and PBC
- Type 2 diabetes: independent risk factor for advanced liver fibrosis and hepatocellular carcinoma in all etiologies of cirrhosis
- HIV coinfection: Massively accelerates fibrosis progression in coinfected hepatitis C; HIV management (antiretrovirals) and HCV eradication have transformed the prognosis of these patients
- Cumulative drug hepatotoxicity: certain hepatotoxic drugs (long-term methotrexate, amiodarone, tamoxifen, prolonged corticosteroids in NASH) can worsen pre-existing liver fibrosis
Symptoms and complications
Compensated cirrhosis can remain asymptomatic for years. Symptoms appear gradually or suddenly during decompensation:
- Compensated phase: chronic fatigue, moderate anorexia, right upper quadrant discomfort; discrete physical signs: palmar erythema, spider angiomas, leukonychia (white nails), digital clubbing, splenomegaly, gynecomastia (male); abnormal liver function tests (moderate cytolysis, cholestasis, early hypoalbuminemia, prolonged PT); thrombocytopenia related to hypersplenism
- Ascites: accumulation of fluid in the abdominal cavity due to portal hypertension and hypoalbuminemia—the most common initial complication of decompensation (50% of cirrhotic patients at 10 years); treated with a strict salt-free diet, diuretics (spironolactone ± furosemide), and paracentesis with IV albumin infusion (8 g per liter of fluid removed) if refractory; transjugular intrahepatic portosystemic shunt (TIPS) for refractory ascites
- Gastrointestinal bleeding due to ruptured esophageal or gastric varices: a severe complication of portal hypertension; mortality of 10–20% per episode despite modern treatments; emergency treatment: IV terlipressin or octreotide + emergency endoscopic band ligation + antibiotic prophylaxis (norfloxacin or ceftriaxone); primary and secondary prevention with propranolol or nadolol (non-cardioselective beta-blockers)
- Hepatic encephalopathy (HE): reversible neuropsychiatric dysfunction due to accumulation of toxins (ammonia, mercaptans) not cleared by the cirrhotic liver; West Haven stages I (mild confusion, concentration difficulties) to IV (coma); precipitating factors: gastrointestinal bleeding, infection, constipation, hyponatremia, sedative medications, dehydration; treatment: lactulose (colonic acidification reducing ammonia production), rifaximin (non-absorbed antibiotic reducing ammonia-producing flora); correct precipitating factors.
- Spontaneous bacterial peritonitis (SBP): infection of ascitic fluid without a surgically identifiable cause; main agent: E. coli and Enterobacteriaceae (transluminal seeding from the digestive tract); diagnosed by ascitic fluid puncture (neutrophils > 250/mm³); therapeutic emergency — treatment with IV cefotaxime + IV albumin (renal protection); long-term norfloxacin for secondary prophylaxis
- Hepatorenal Syndrome (HRS): Severe functional renal failure due to intense renal vasoconstriction related to splanchnic vasodilation from portal hypertension; HRS type 1 (rapid deterioration in < 2 weeks) and type 2 (slowly progressing refractory ascites); treatment: terlipressin + IV albumin; TIPS; liver transplantation—the only curative treatment
- Hepatocellular carcinoma (HCC): a tumor-related complication of cirrhosis — annual incidence ranging from 1 to 8 per 100,000 depending on the etiology; biannual monitoring via ultrasound ± AFP is essential in all patients with Child-Pugh A or B cirrhosis
- Hepatopulmonary syndrome and portopulmonary hypertension: rare but serious pulmonary vascular complications, systematically evaluated before liver transplantation
Severity Assessment: Child-Pugh and MELD Scores
| Score / Class | Evaluated settings | Prognostic significance |
|---|---|---|
| Child-Pugh A (5–6 points) | Bilirubin, albumin, TP/INR, ascites, encephalopathy (each scored 1 to 3 based on severity) | Compensated cirrhosis; 1-year survival > 95% (%); 2-year survival 85% (%); typical candidates for liver surgery and HCC resection |
| Child-Pugh B (7–9 points) | Same | Moderately decompensated cirrhosis; 1-year survival rate: 80% (%); 2-year survival rate: 60% (%); surgical resection is risky; consider liver transplantation |
| Child-Pugh C (10–15 points) | Same | Severe decompensated cirrhosis; 1-year survival rate: 45% (%); 2-year survival rate: 35% (%); contraindicated for elective surgery; liver transplantation indicated if MELD score ≥ 15 |
| MELD Score (6 to 40) | Creatinine, bilirubin, INR (logarithmic formula) — assesses 3-month mortality without transplantation | MELD < 10: low short-term mortality; MELD 10–19: 6-month mortality 6 %; MELD 20–29: 20 %; MELD 30–39: 50 %; MELD ≥ 40: >70% 1-year survival; MELD-Na score (incorporating serum sodium levels) is more accurate; used by Transplant Québec to prioritize patients on the waiting list |
ℹ️
Cirrhosis is often diagnosed at an advanced stage because it is silent for years. Isolated thrombocytopenia, splenomegaly on imaging, or chronically abnormal liver function tests in a patient with risk factors (alcohol, obesity, diabetes, known viral infection) should lead to a comprehensive hepatological evaluation including liver elastography (Fibroscan®) — a non-invasive test that estimates liver fibrosis by measuring liver stiffness (kPa) without the need for biopsy in most cases.
Diagnosis
- Complete liver function tests: ALT, AST (cytolysis), GGT, ALP, total and direct bilirubin (cholestasis); albumin and PT/INR (hepatic synthetic function - prognostic markers); CBC with platelets (thrombocytopenia related to hypersplenism); creatinine and electrolytes (renal function, natremia); HBV and HCV serologies; ferritin and transferrin saturation index (hemochromatosis); copper and ceruloplasmin (Wilson's disease); AMA (primary biliary cirrhosis); ANA, anti-smooth muscle (autoimmune hepatitis)
- Élastographie hépatique par ultrason (Fibroscan® ou ARFI) : mesure non invasive de la rigidité hépatique en kilopascals (kPa) — corrélée au stade de fibrose (F0 à F4 selon METAVIR) ; seuil de cirrhose (F4) : > 12–14 kPa selon l'étiologie (plus élevé dans la maladie alcoolique) ; remplace la biopsie dans la grande majorité des cas pour le diagnostic et le suivi de la fibrose
- Échographie abdominale doppler : évalue la morphologie hépatique (foie dysmorphique, nodulaire, micronodulaire), la splénomégalie, l'ascite, la perméabilité et le flux de la veine porte (hypertension portale : flux portal ralenti ou hépatofuge, veine porte dilatée > 13 mm), les voies biliaires et dépiste le CHC ; examen de surveillance semestrielle chez tout patient cirrhotique
- Endoscopie digestive haute (fibroscopie œsogastroduodénale) : recherche et classifie les varices œsophagiennes (grade I à III) et gastriques (GOV1, GOV2, IGV) pour guider la prophylaxie hémorragique primaire (ligature endoscopique ou bêtabloquants)
- Biopsie hépatique transpariétale ou transjugulaire : gold standard historique pour le diagnostic de cirrhose et l'évaluation de l'étiologie en cas de doute ; réservée aux cas où les examens non invasifs sont discordants, insuffisants ou atypiques ; score METAVIR F4 = cirrhose ; voie transjugulaire si troubles de la coagulation sévères ou ascite volumineuse
- Scanner abdominal triphasique ou IRM hépatique : indiqués pour le bilan du CHC suspecté à l'échographie, l'évaluation préopératoire avant transplantation, et le diagnostic différentiel des nodules hépatiques
Treatment
- Traitement étiologique : sevrage alcoolique complet et définitif (alcoolisme) — accompagnement addictologique indispensable ; antiviraux à action directe (VHC) — guérison virologique dans > 95 % des cas, réduction de la progression ; analogues nucléos(t)idiques à vie (VHB — ténofovir, entécavir) ; perte de poids ≥ 10 % et activité physique (NASH) — seule intervention ayant démontré une régression histologique significative ; phlébotomies régulières (hémochromatose) ; D-pénicillamine ou trientine (Wilson) ; AUDC ± acide obéticholique (CBP)
- Prise en charge de l'hypertension portale : bêtabloquants non cardiosélectifs (propranolol ou nadolol) en prophylaxie primaire des varices à haut risque de saignement (grade II–III ou varices avec signes rouges) ; ligature par bandes élastiques (band ligation) endoscopique si contre-indication aux bêtabloquants ou après hémorragie ; TIPS (Transjugular Intrahepatic Portosystemic Shunt) pour l'ascite réfractaire et les hémorragies récidivantes
- Traitement de l'ascite : régime hyposodé strict (< 2 g de sel par jour) ; spironolactone 100–400 mg/jour ± furosémide 40–160 mg/jour ; paracentèse évacuatrice pour les ascites volumineuses avec injection d'albumine humaine IV (8 g par litre retiré) pour prévenir le syndrome de dysfonction circulatoire post-paracentèse
- Prévention et traitement de l'encéphalopathie hépatique : lactulose 30–60 mL 2–3 fois par jour (selles molles 2–3 fois par jour comme objectif) ; rifaximine 550 mg 2 fois par jour en prévention des récidives ; correction systématique des facteurs précipitants ; zinc oral (carence fréquente dans la cirrhose)
- Prophylaxie des infections : norfloxacine 400 mg/jour au long cours après un premier épisode de PBS ; prophylaxie antibiotique péri-procédurale ; vaccination antigrippale, antipneumococcique, anti-VHA et anti-VHB si non immunisé
- Transplantation hépatique : seul traitement curatif de la cirrhose décompensée — indiquée si MELD ≥ 15 ou complications réfractaires (ascite réfractaire, encéphalopathie récidivante, SHR, PBS répétées) ; contre-indications : alcoolisme actif (sevrage > 6 mois requis), cancer extra-hépatique, infection non contrôlée, comorbidités cardiovasculaires sévères ; survie à 5 ans post-transplantation : 70–80 % ; évaluation par le centre de transplantation (CHUM, MUHC au Québec)
- Surveillance du carcinome hépatocellulaire : échographie abdominale + AFP semestrielles chez tous les cirrhotiques Child-Pugh A et B — programme de surveillance permettant un diagnostic à un stade curatif (résection, transplantation, ablation)
- Nutrition et supplémentation : dénutrition fréquente dans la cirrhose avancée — apport protéique suffisant (1,2–1,5 g/kg/jour), collation nocturne recommandée (améliore le bilan azoté) ; supplémentation en vitamines (B1, B6, B12, acide folique, vitamine D) et zinc ; alimentation entérale ou parentérale si dénutrition sévère
Signs requiring urgent consultation or 911
Dial 911 ou rendez-vous immédiatement à l'urgence si un patient cirrhotique connu présente : une hémorragie digestive (hématémèse, méléna — sang noir dans les selles), une confusion ou une somnolence inexpliquée (encéphalopathie hépatique), une fièvre avec douleurs abdominales (péritonite bactérienne spontanée), une augmentation rapide et douloureuse de l'ascite, une détresse respiratoire ou une hypotension. Ces complications engagent le pronostic vital et requièrent une prise en charge hospitalière urgente. Tout patient avec des facteurs de risque de cirrhose présentant pour la première fois un ictère, une ascite ou des signes d'encéphalopathie doit également être évalué sans délai.
Pour une évaluation hépatologique, un Fibroscan, un bilan d'hépatite chronique ou une orientation vers un hépatologue, Clinique Omicron offre des consultations dans nos succursales au Québec ainsi qu'en télémédecine. Pour prendre rendez-vous, visitez cliniqueomicron.ca.
Consult at Clinique Omicron
Les médecins de Clinique Omicron évaluent les patients présentant des facteurs de risque ou des anomalies biologiques évocatrices de maladie hépatique chronique, prescrivent le bilan hépatologique complet et orientent vers les hépatologues et les centres de transplantation selon la sévérité. Des consultations sont disponibles dans nos succursales au Québec ainsi qu'en télémédecine pour l'ensemble de la province. Pour prendre rendez-vous, visitez cliniqueomicron.ca.
Le contenu de cette page est fourni à titre informatif uniquement et ne remplace pas l'avis d'un professionnel de santé qualifié. La cirrhose et ses complications nécessitent une prise en charge spécialisée en hépatologie dans un centre hospitalier disposant des expertises en gastro-entérologie, hépatologie interventionnelle et chirurgie de transplantation.
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