LIVER CIRRHOSIS

 Liver Cirrhosis

Cirrhosis of the liver is permanent scarring that damages your liver and interferes with its functioning. Alcohol and drugs, viruses and metabolic factors are the most common causes. Cirrhosis remains a leading cause of morbidity and mortality, with increasing prevalence due to rising rates of non-alcoholic fatty liver disease (NAFLD) and viral hepatitis (Hepatitis B, Hepatitis C)

Etiology of Liver Cirrhosis

Cirrhosis is a histological diagnosis caused by a wide spectrum of chronic liver insults. The most common etiologies are:

1. Alcoholic Liver Disease (ALD)

Chronic excessive alcohol consumption results in progressive hepatic steatosis, alcoholic hepatitis, and ultimately cirrhosis. It remains one of the most frequent causes of liver-related deaths.

2. Viral Hepatitis (HBV and HCV)

• Chronic Hepatitis B Virus (HBV): Prevalence remains high across the world, particularly in Asia and sub-Saharan Africa.

• Chronic Hepatitis C Virus (HCV): Although curable with DAAs, untreated chronic infection causes cirrhosis in 20–30% of patients after decades.

3. Non-Alcoholic Steatohepatitis (NASH)

The advanced, progressive form of NAFLD, NASH, is highly linked to obesity, insulin resistance, metabolic syndrome, and type 2 diabetes. It is a rapidly becoming leading indication for liver transplantation in the West.

4. Autoimmune Hepatitis (AIH)

A T-cell-mediated inflammatory state where immune dysregulation causes chronic liver injury. Needs immunosuppressive therapy to halt fibrosis progression.

5. Metabolic and Genetic Disorders

•Hemochromatosis (HFE mutation): Iron overload causes hepatic tissue damage.

•Wilson's Disease: Copper deposition secondary to ATP7B mutation.

•Alpha-1 Antitrypsin Deficiency: Misfolding of proteins causes hepatocellular damage.

6. Cholestatic Liver Diseases

• Primary Biliary Cholangitis (PBC) and

• Primary Sclerosing Cholangitis (PSC): Chronic biliary obstruction and inflammation may lead to cirrhosis in the long term.

 Pathogenesis and Histology

Cirrhosis follows chronic hepatocyte injury, followed by inflammation, hepatic stellate cell activation, and collagen deposition. Fibrotic remodeling results in portal hypertension and deranged synthetic and detoxifying capacity.

Cirrhosis histologically is divided into compensated and decompensated forms, the latter being characterized by variceal bleeding, ascites, hepatic encephalopathy, and jaundice.

Clinical Presentation

Early (Compensated) Cirrhosis

• Usually asymptomatic

• Mild fatigue, loss of appetite, right upper abdominal pain.

Decompensated Cirrhosis

• Ascites.

• Esophageal or gastric variceal bleeding

• Hepatic encephalopathy

• Jaundice

• Coagulopathy

• Muscle wasting (sarcopenia)

  Physical Signs

• Spider angiomas

• Palmar erythema

• Gynecomastia

• Splenomegaly

• Caput medusae (Dilated tortuous superficial epigastric veins is seen in patients with severe portal hypertension)

Complications of Cirrhosis

• Portal Hypertension: Leads to varices, ascites, and hypersplenism.

• Hepatocellular Carcinoma (HCC): Regular surveillance is critical.

• Hepatorenal Syndrome (HRS): Functional renal failure in advanced disease.

• Spontaneous Bacterial Peritonitis (SBP)

• Hepatic Encephalopathy: Altered mentation due to ammonia accumulation.

 Diagnosis

Laboratory Findings

• Elevated liver enzymes (AST > ALT in ALD)

• Hyperbilirubinemia

• Hypoalbuminemia

• Prolonged PT/INR

• Thrombocytopenia (from splenic sequestration)

Imaging

• Ultrasound with Doppler: First-line modality

• Transient Elastography (FibroScan): Non-invasive fibrosis assessment

• CT/MRI: Evaluate nodularity, portal hypertension, and HCC screening

  Liver Biopsy

Still the gold standard for staging, but more and more being replaced by non-invasive techniques.

Management of Cirrhosis

1. Treat Underlying Cause

• Alcohol cessation: Decreases mortality; supportive care or pharmacotherapy for withdrawal.

• Antivirals: DAAs for HCV; NUCs for HBV.

• Weight loss and glycemic control: In NAFLD/NASH.

• Immunosuppressants: Prednisone and azathioprine for AIH.

2. Prevent and Manage Complications

• Ascites: Sodium restriction, diuretics (spironolactone/furosemide), therapeutic paracentesis.

• Variceal Bleeding: Non-selective beta-blockers (NSBBs), endoscopic band ligation.

• Encephalopathy: Lactulose and rifaximin.

• SBP: Empiric antibiotics, albumin, high-risk prophylaxis.

• Renal protection: No nephrotoxic drugs; albumin in high-risk environments.

3. Monitoring and Surveillance

• HCC screening: Abdominal ultrasound + AFP every 6 months.

• Endoscopy: For variceal detection.

• Liver function tests: Regular follow-up.

4. Nutritional Support

• High-protein diet except if encephalopathy is uncontrolled.

• Correct vitamin and mineral deficiencies (most importantly zinc, vitamins A, D, E, K).

5. Liver Transplantation

Definitive management for end-stage liver disease. Indications are MELD score ≥15, refractory complications, or HCC fulfilling Milan criteria.

Prognosis

• Compensated cirrhosis: Median survival >10 years.

• Decompensated cirrhosis: 1-year survival ~60%; much lower with ongoing complications.

• MELD and Child-Pugh scores are utilized for prognostication and transplant suitability.

Conclusion

Liver cirrhosis is a multifactorial, progressive, and complicated disease. Early diagnosis, risk factor modification, and prompt treatment of complications are crucial to enhance outcomes. With increasing NAFLD burden, preventive care and early screening are crucial. Liver transplantation continues to be the gold standard for patients with end-stage liver disease and those with suitable hepatocellular carcinoma.