Cirrhosis Overview and Causes

Cirrhosis: Overview

• Cirrhosis is the late stage of liver disease, marked by extensive liver cell damage.
• Fibrosis (scar tissue) and regenerative nodules replace healthy liver tissue in response to repair attempts.
• Cirrhosis typically develops over decades of chronic liver disease.

Etiology and Pathophysiology

• Various chronic liver diseases can lead to cirrhosis.
• Common causes in the US include chronic hepatitis C virus (HCV) infection, nonalcoholic steatohepatitis (NASH), and alcohol-induced liver disease.
• Alcohol-induced liver disease is exacerbated by malnutrition.
• Other causes include extreme dieting, malabsorption, and obesity.
• Environmental factors and genetics influence cirrhosis development.
• Chronic inflammation and cell necrosis from viral hepatitis cause progressive fibrosis and cirrhosis.
• Chronic hepatitis combined with alcohol use accelerates liver damage synergistically.
• Biliary issues such as primary biliary cholangitis (PBC) and primary sclerosing cholangitis (PSC) can contribute.
• Cardiac cirrhosis arises from severe, long-standing right-sided heart failure, causing hepatic congestion and damage.

Pathogenesis

• Liver cells attempt disorganized regeneration, affecting blood vessel and bile duct structures.
• Fibrous tissue overgrowth disrupts normal liver lobular structure, hindering blood flow.
• Disorganized regeneration, poor cell nutrition, and hypoxia (due to poor blood flow and scar tissue) decrease liver function.

Clinical Manifestations

Early Manifestations

• Often asymptomatic, or present with fatigue or an enlarged liver.
• Liver function tests might be normal (compensated cirrhosis).
• Diagnosis often occurs with more advanced symptoms.

Late Manifestations

• Results from liver failure and portal hypertension.
• Manifestations include jaundice, peripheral edema, ascites (fluid buildup), skin lesions, hematologic issues, endocrine problems, and peripheral neuropathy.
• Liver shrinks and becomes nodular with severe liver compromise.

Specific Manifestations

• Jaundice: Decreased bilirubin excretion due to bile duct compression.
• Skin lesions: Spider angiomas (dilated blood vessels) and palmar erythema (red palms) are due to elevated estrogen.
• Hematologic issues: Thrombocytopenia, leukopenia, anemia, and coagulation problems are linked to splenomegaly (enlarged spleen) resulting from portal hypertension.
• Coagulation problems: Liver's inability to produce clotting factors causes nosebleeds, purpura, bruising, and heavy menstruation.
• Endocrine problems: Increased estrogen causes gynecomastia, hair loss, testicular atrophy, and impotence in men, and amenorrhea in younger women and vaginal bleeding in older women. Low or irregular aldosterone metabolism can cause sodium and fluid retention.
• Peripheral neuropathy: A common finding in alcoholic cirrhosis, frequently related to thiamine, folic acid, and cobalamin deficiencies.

Complications

• Portal Hypertension: Increased blood pressure in the portal vein, leading to varices (enlarged veins).
• Esophageal and Gastric Varices: Enlarged veins in the esophagus and stomach, prone to bleeding (can be life-threatening). Causes melena or hematemesis.
• Peripheral Edema and Ascites: Fluid accumulation in the extremities and abdominal cavity, respectively, due to decreased albumin, portal hypertension, or hyperaldosteronism.
• Hepatic Encephalopathy: Neuropsychiatric syndrome linked to ammonia buildup when the liver's unable to process it. Causes confusion, coma, asterixis (flapping tremors).
• Hepatorenal Syndrome: Renal failure in cirrhosis linked to vasodilation, reduced arterial blood volume, renal vasoconstriction.

Diagnostic Studies

• Liver function tests (abnormal levels of enzymes, proteins, bilirubin)
• Liver biopsy (gold standard for diagnosis).
• Ultrasound (not reliable for cirrhosis detection), Fibroscan (non-invasive for liver fibrosis quantification).

Interprofessional Care

Ascites Management

• Sodium restriction (2 g/day max).
• Diuretics (e.g., spironolactone and furosemide).
• Paracentesis (fluid removal).
• TIPS (treat unresponsive ascites).

Varices Management

• Avoiding hepatotoxic substances.
• Upper endoscopy screening.
• Non-selective beta-blockers to reduce bleeding risk.
• Endoscopic ligation or sclerotherapy to prevent rebleeding.
• Balloon tamponade (used to control acute bleeding).
• Supportive measures (blood products, vitamin K, PPIs).

Hepatic Encephalopathy Management

• Reduce ammonia formation (lactulose, rifaximin).
• Treat risk factors (e.g., GI bleeding).

Nutrition Therapy

• High calorie, high carbohydrate, moderate-to-low fat diet for uncomplicated cirrhosis.
• Protein-calorie supplements for alcohol-related cirrhosis.
• Low sodium diet for ascites and edema.

Health Promotion and Acute Care

• Prevention focuses on reducing risk factors (alcohol use, malnutrition, viral hepatitis etc.).
• Encourage abstinence, support programs, adequate nutrition, and early treatment of hepatitis.
• Conserve energy, maintain muscle strength/tone, prevent complications, modify activity/rest schedule based on improvement.

Ambulatory Care

• Importance of ongoing care, appropriate lifestyle changes (diet, alcohol avoidance, hepatotoxic drug avoidance), and emotional support needed if required.

Evaluation

• Expected outcomes include adequate food/fluid intake, comfort relief, and minimal to no complications.