Cirrhosis of the Liver: A Comprehensive Guide

Introduction

Cirrhosis is a chronic, progressive liver disease defined by irreversible fibrosis with regenerative nodules that distort hepatic architecture. It represents the end stage of sustained liver injury from causes such as viral hepatitis, alcohol-associated liver disease, and metabolic dysfunction–associated steatotic liver disease (MASLD, formerly NAFLD). This guide summarizes the history, common clinical features, core pathology, mechanisms, diagnostic approaches, and current management strategies.

History

Descriptions consistent with advanced liver disease date to Hippocratic texts. The term “cirrhosis” derives from the Greek kirrhos (“tawny”), reflecting the orange-brown appearance of a cirrhotic liver. Modern advances—liver function testing, ultrasound/CT/MRI, elastography, and percutaneous/transjugular biopsy—have refined diagnosis, staging, and complication risk assessment.

Pathophysiology

Altered Liver Function

Fibrosis and nodule formation disrupt hepatic microanatomy, reducing capacity for toxin clearance, protein/albumin/coagulation factor synthesis, and hormone/vitamin regulation.

Portal Hypertension

Fibrotic remodeling elevates portal venous resistance, driving varices and ascites. Splanchnic vasodilation and hyperdynamic circulation further increase portal inflow.

Systemic Consequences

Extrahepatic dysfunction can include renal failure (hepatorenal syndrome) and neurocognitive changes (hepatic encephalopathy).

Diagnostic Workup

• Blood tests: Liver enzymes, bilirubin, INR, albumin; etiology labs (e.g., viral hepatitis serologies, autoimmune markers, iron studies).
• Imaging: Ultrasound ± Doppler; CT/MRI for morphology and HCC surveillance when indicated.
• Elastography: Noninvasive fibrosis assessment (e.g., transient elastography).
• Liver biopsy: When diagnosis remains uncertain or to clarify etiology/stage.

Treatment

Core principles: treat the cause, prevent decompensation, and manage complications.

• Lifestyle: Alcohol cessation; vaccination; nutrition with adequate protein; sodium restriction for ascites.
• Diuretics: For ascites (e.g., spironolactone ± loop diuretic) with monitoring.
• Antibiotics: Treat infections promptly; SBP prophylaxis when appropriate.
• Portal HTN: Nonselective beta-blockers and endoscopic band ligation for variceal prevention/management.
• Transplant: Curative option for end-stage disease; referral based on severity criteria (e.g., MELD).

References

1. Bataller R, Brenner DA. Liver fibrosis. J Clin Invest. 2005;115(2):209-218.
2. Schuppan D, Afdhal NH. Liver cirrhosis. Lancet. 2008;371(9615):838-851.
3. Garcia-Tsao G, Lim JK. Management of cirrhosis and portal hypertension. Am J Gastroenterol. 2009;104(7):1802-1829.
4. Tsochatzis EA, Bosch J, Burroughs AK. Liver cirrhosis. Lancet. 2014;383(9930):1749-1761.

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