Cirrhosis

Also known as: Liver cirrhosis

End-stage result of chronic liver injury characterized by diffuse hepatic fibrosis and regenerative nodule formation, causing distortion of normal hepatic architecture and vasculature, leading to portal hypertension and progressive loss of synthetic/metabolic liver function. Represents the final common pathway of most chronic liver diseases.

Major etiologies:

Alcohol-related liver disease
Metabolic dysfunction-associated steatotic liver disease (MASLD, formerly NAFLD/NASH) — increasingly common cause globally
Chronic viral hepatitis (HBV, HCV)
Autoimmune hepatitis
Cholestatic: primary biliary cholangitis (PBC), primary sclerosing cholangitis (PSC)
Metabolic/genetic: hemochromatosis, Wilson's disease, alpha-1 antitrypsin deficiency
Vascular: Budd-Chiari syndrome, chronic right heart failure (cardiac cirrhosis)
Drug-induced (methotrexate, amiodarone)

Classified by:

Compensated: asymptomatic or mild non-specific symptoms, no major complications
Decompensated: development of ascites, variceal hemorrhage, hepatic encephalopathy, or jaundice — marks major prognostic transition, median survival drops from ~12 years (compensated) to ~2 years (decompensated)
Severity/prognostic scoring: Child-Pugh (A/B/C) and MELD/MELD-Na scores — guide transplant listing and prognosis

Compensated (may be asymptomatic, found incidentally):

Fatigue, anorexia, weight loss, nausea
Signs of chronic liver disease: spider angiomata, palmar erythema, gynecomastia, testicular atrophy, Dupuytren's contracture, caput medusae, leukonychia, clubbing
Hepatomegaly (may become small/shrunken in advanced disease) ± splenomegaly (portal hypertension)

Decompensated:

Ascites: abdominal distension, shifting dullness, fluid thrill — most common decompensation event
Variceal hemorrhage: hematemesis, melena — from esophageal/gastric varices due to portal hypertension
Hepatic encephalopathy: confusion, asterixis (flapping tremor), altered sleep-wake cycle, progressing to stupor/coma (West Haven grading I–IV)
Jaundice: scleral icterus, generalized jaundice — reflects impaired bilirubin conjugation/excretion
Coagulopathy: easy bruising, bleeding (reduced synthesis of clotting factors)
Peripheral edema (hypoalbuminemia)
Muscle wasting/sarcopenia
Fetor hepaticus (sweet, musty breath odor)

Complications to actively screen for: hepatocellular carcinoma (HCC), spontaneous bacterial peritonitis (SBP), hepatorenal syndrome, hepatopulmonary syndrome, portal vein thrombosis.

Labs:
LFTs — may be normal in burnt-out cirrhosis; AST/ALT ratio >1 suggestive of alcohol-related disease
Synthetic function: low albumin, prolonged PT/INR
FBC: thrombocytopenia (earliest lab clue — portal hypertension/hypersplenism), anemia
U&E/creatinine: baseline renal function (hepatorenal syndrome risk)
Non-invasive fibrosis assessment (first-line, replacing biopsy in most cases):
Transient elastography (FibroScan): liver stiffness measurement in kPa — values vary by etiology, generally >12–15 kPa suggestive of cirrhosis
Serum fibrosis markers/scores: FIB-4 index, APRI score — screening tools, especially in MASLD
MR elastography: more accurate, less available
Liver biopsy: gold standard but reserved for diagnostic uncertainty or when etiology unclear despite non-invasive workup
Imaging: ultrasound — nodular liver contour, coarse echotexture, splenomegaly, ascites; also used for HCC surveillance
Etiology workup: viral hepatitis serology (HBsAg, anti-HCV), autoimmune markers (ANA, ASMA, anti-LKM, immunoglobulins), ferritin/transferrin saturation (hemochromatosis), ceruloplasmin (Wilson's, if young), alpha-1 antitrypsin level, lipid profile/HbA1c (MASLD risk factors)
Endoscopy (OGD): screening for esophageal/gastric varices at diagnosis of cirrhosis, repeated per surveillance interval based on findings
HCC surveillance: ultrasound ± AFP every 6 months in all cirrhotic patients

Differentials for decompensation presentations: other causes of ascites (malignancy, TB peritonitis, cardiac), other causes of encephalopathy (sepsis, uremia, drugs, intracranial pathology), other causes of UGIB (peptic ulcer).

General/etiology-specific:

Treat underlying cause: antiviral therapy (HBV — tenofovir/entecavir; HCV — direct-acting antivirals, near-100% cure rates), alcohol cessation (+ addiction support), weight loss/metabolic control for MASLD, immunosuppression for autoimmune hepatitis, venesection for hemochromatosis
Avoid hepatotoxic drugs, NSAIDs (renal risk in cirrhosis), sedatives (precipitate encephalopathy)
Vaccination: hepatitis A/B (if not immune), pneumococcal, influenza, COVID-19
Nutrition: adequate protein intake (1.2–1.5g/kg/day — do NOT protein-restrict, worsens sarcopenia), avoid prolonged fasting, late-evening snack recommended (reduces overnight catabolism)

Ascites management:

Sodium restriction (<2g/day)
Diuretics: spironolactone 100mg od (up titrate to max 400mg/day) ± furosemide 40mg od (up titrate to max 160mg/day), typical ratio 100:40 — monitor renal function/electrolytes closely
Large-volume paracentesis for tense/refractory ascites — albumin replacement 6–8g per liter removed if >5L drained (prevents post-paracentesis circulatory dysfunction)
Refractory ascites: consider TIPS (transjugular intrahepatic portosystemic shunt) or liver transplant referral

Variceal hemorrhage:

Primary prophylaxis (known varices, not yet bled): non-selective beta-blocker (propranolol, carvedilol) or endoscopic variceal band ligation
Acute bleed: resuscitation, restrictive transfusion strategy (target Hb ~7–8g/dL), IV terlipressin or octreotide (splanchnic vasoconstriction), prophylactic antibiotics (ceftriaxone 1g IV od — reduces mortality, prevents SBP/rebleeding), urgent endoscopy within 12 hours for band ligation/sclerotherapy
Secondary prophylaxis: combination beta-blocker + band ligation program

Hepatic encephalopathy:

Identify/correct precipitant (infection, GI bleed, constipation, electrolyte imbalance, sedatives, dehydration)
Lactulose 30mL PO tds-qds, titrate to 2–3 soft stools/day (traps ammonia as ammonium, laxative effect)
Rifaximin 550mg PO bd — add-on for recurrent episodes despite lactulose (reduces ammonia-producing gut flora)

Spontaneous bacterial peritonitis (SBP): diagnostic paracentesis if new/worsening ascites, fever, abdominal pain, or encephalopathy — ascitic fluid neutrophil count >250 cells/mm³ diagnostic; treat with IV cefotaxime/ceftriaxone + IV albumin (1.5g/kg day 1, 1g/kg day 3 — reduces hepatorenal syndrome risk); secondary prophylaxis with norfloxacin/ciprofloxacin after first episode

HCC: surveillance ultrasound ± AFP 6-monthly; management per BCLC staging (resection, ablation, TACE, systemic therapy, or transplant depending on stage)

Liver transplant referral: decompensated cirrhosis, MELD-Na ≥15, refractory complications (ascites, encephalopathy, recurrent variceal bleeding), HCC within transplant criteria (Milan criteria), or synthetic dysfunction (Child-Pugh C).

Clinical toolsCalculators

BMI GCS EDD Parkland Formula

Corrected Sodium Corrected Calcium Anion Gap Creatinine Clearance Insulin Calculations qSOFA Wells PE Wells DVT CHA₂DS₂-VASc HAS-BLED CURB-65 Centor/McIsaac

Hepatic Encephalopathy

Reversible neuropsychiatric syndrome resulting from liver dysfunction and portosystemic shunting, allowing gut derived neurotoxins, principally ammonia, to bypass hepatic clearance and reach the brain, causing astrocyte swelling and altered neurotransmission.

Occurs in acute liver failure (see separate entry) and, more commonly in everyday practice, as a complication of decompensated cirrhosis.

Classified by the West Haven criteria: Grade I (subtle changes, mild confusion, altered sleep pattern, shortened attention span), Grade II (lethargy, disorientation, personality change, asterixis present), Grade III (marked confusion, somnolence but rousable, gross disorientation), and Grade IV (coma, unresponsive to stimuli).

Cognitive and personality change (often noticed first by family rather than the patient), altered sleep wake cycle (day night reversal), asterixis (flapping tremor on wrist extension, present from Grade II onward), fetor hepaticus, and, in advanced grades, progressive obtundation to coma.

Precipitants must always be actively sought: gastrointestinal bleeding (increased protein and blood load to the gut), infection (particularly spontaneous bacterial peritonitis), constipation, electrolyte disturbance (particularly hyponatremia and hypokalemia), dehydration or diuretic overuse, sedative or opioid use, and progression of underlying liver disease or a new portosystemic shunt (spontaneous or TIPS related).

Primarily clinical, based on the presence of known liver disease plus a compatible mental state change, ideally with a precipitant identified.

Ammonia level supports the diagnosis but correlates poorly with grade and is not required to make the diagnosis in a typical clinical picture.

Investigation is directed at finding the precipitant: FBC and CRP (infection), U&E (electrolytes, renal function), stool for occult blood or overt melena history, ascitic tap if ascites is present (neutrophil count above 250 cells per mm3 diagnostic of spontaneous bacterial peritonitis), and a careful medication review.

CT head is reserved for atypical presentations, focal neurological signs, or a history of trauma, to exclude intracranial hemorrhage, which cirrhotic patients are predisposed to given coagulopathy and thrombocytopenia.

Differentials include intracranial hemorrhage, other metabolic encephalopathies (uremia, hypoglycemia, hyponatremia), alcohol intoxication or withdrawal, Wernicke's encephalopathy, sepsis associated encephalopathy, and primary psychiatric illness.

Identify and treat the precipitant, this is often the single most important intervention.
Lactulose is first-line, titrated to achieve two to three soft stools per day; it works by acidifying the colon, trapping ammonia as ammonium and providing a laxative effect that reduces colonic transit time and bacterial ammonia production.
Rifaximin is added for recurrent episodes despite adequate lactulose, reducing ammonia producing gut flora.
Correct electrolyte disturbances, particularly hypokalemia and hyponatremia, both of which worsen encephalopathy independently.
Nutritional support with adequate protein intake (protein restriction is no longer recommended, since it worsens muscle wasting and does not improve outcomes) should continue throughout.
Airway protection is required in Grade III to IV encephalopathy given aspiration risk.
Address underlying liver disease progression and consider whether the episode signals a need for transplant assessment in appropriate candidates.

Referral: hepatology for recurrent or refractory encephalopathy, or for transplant assessment if episodes reflect progressive decompensation.

Cirrhosis

Overview

Clinical Features

Diagnosis

Management

Overview

Clinical Features

Diagnosis

Management