Cirrhosis and Ascites Pathophysiology

Cirrhosis Pathophysiology

• Cirrhosis is the end-stage of chronic liver disease, a leading cause of mortality.
• Frequent causes include viral hepatitis and alcohol-related liver damage (alcoholic hepatitis).
• Interference with local blood flow contributes to cell death, causing blood and bile to back up, leading to further injury and inflammation.
• This obstruction of blood flow through the portal circulation leads to widespread hepatocyte damage, fibrosis, and scarring.
• Ultimately, liver failure and death can result from these processes.

Common Complication: Ascites

• Ascites is the accumulation of fluid in the peritoneal cavity, a common complication of cirrhosis.
• Approximately 85% of ascites cases are related to cirrhosis.
• Cirrhosis causes fluid imbalance, with fluid loss to the third space, making it unavailable for use in the intracellular and extracellular fluids.

Ascites Pathophysiology

• Ascites arises from a combination of factors, including increased hydrostatic pressure due to hepatic vein obstruction and congestive heart failure.
• Decreased colloid osmotic pressure is also a contributing factor, resulting from malnutrition, nephrotic syndrome, increased capillary permeability, or malignancy, or bacterial peritoneal infection.

Cirrhosis Pathophysiology

• Chronic inflammation damages hepatocytes, leading to fibrosis and scarring.
• Obstructed liver sinusoids disrupt blood flow, causing increased hepatic (portal) pressure.
• Elevated pressure forces fluid out of capillaries, exceeding the lymphatic system's ability to return it, resulting in fluid accumulation (ascites).
• Increased vascular resistance triggers vasodilator release, initially increasing blood flow but ultimately contributing to decreased blood pressure due to compensating mechanisms, including sodium and water retention. This further exacerbates ascites.

Advanced Stage Cirrhosis

• In advanced stages, decreased albumin production reduces oncotic pressure, further contributing to fluid retention which is a major factor in developing ascites.
• Sodium and water retention due to the aforementioned mechanisms worsen the condition.

Renal Impairment in Cirrhosis

• Progressive cirrhosis can lead to impaired water excretion causing water retention.
• Dilutional hyponatremia and renal vasoconstriction can result, leading to a potentially life-threatening condition called hepatorenal syndrome, renal failure associated with severe renal vasoconstriction.

Cirrhosis Clinical Manifestations

• Clinical signs and symptoms of cirrhosis relate to ascites severity.
• Ascites volume ranges from moderate to large, with 500ml of fluid being detectable.
• Symptoms include moderate to severe abdominal discomfort, increased abdominal girth, and increased weight.
• Patients also experience severe sodium retention and dilutional hyponatremia from water retention, which can eventually lead to renal failure.

Cirrhosis Diagnostic Criteria

• Diagnosis involves history, physical exam, including body weight changes and abdominal circumference, and assessments of liver, kidney, and heart function.
• Laboratory tests include analysis of ascitic fluid to evaluate for conditions like portal hypertension or transudative ascites.
• Other tests include serum-ascetic albumin gradient (SAAG) to assess etiology, amylase for pancreatic origin, WBC for infection, or RBCs for malignancy.

Cirrhosis Treatment

• Treatment for cirrhosis primarily depends on the volume of ascites.
• Diuretics promote fluid loss, and sodium balance.
• Paracentesis is performed for severe ascites cases, where fluid is removed from the peritoneal cavity.
• Intravenous albumin may be used after paracentesis to help correct circulatory dysfunction.
• Preventing circulatory dysfunction and recurrence of ascites are also key aspects of treatment.