What causes swelling in cirrhosis?

Why Cirrhosis Causes Swelling

Cirrhosis causes swelling through two fundamental mechanisms: portal hypertension (elevated pressure in the liver's blood vessels) and renal sodium/water retention triggered by splanchnic arterial vasodilation, which together lead to fluid accumulation in the abdomen (ascites) and peripheral tissues (edema). 1

Primary Pathophysiologic Mechanisms

Portal Hypertension as the Essential Trigger

• Portal pressure must exceed 8 mm Hg for ascites to develop—below this threshold, fluid accumulation does not occur regardless of other factors. 1
• Architectural changes from advanced fibrosis create the primary mechanism: progressive collagen deposition and nodule formation distort the liver's normal vascular architecture, increasing resistance to portal blood flow. 1
• Activated hepatic stellate cells become contractile and recruit around newly formed sinusoidal vessels, further increasing vascular resistance (accounting for approximately 25% of increased intrahepatic resistance). 1
• Reduced nitric oxide production/bioavailability in the cirrhotic liver additionally raises vascular tone within the liver. 1

The Splanchnic Vasodilation Cascade

• Portal hypertension triggers overproduction of nitric oxide, prostacyclin, and endocannabinoids in the splanchnic (intestinal) circulation, causing profound arterial vasodilation. 1, 2
• This splanchnic vasodilation creates a state of "effective hypovolaemia"—the body perceives inadequate blood volume despite actual hypervolemia because blood pools in the dilated splanchnic vessels. 1
• The perceived hypovolemia activates compensatory mechanisms: the sympathetic nervous system, renin-angiotensin-aldosterone system, and non-osmotic arginine-vasopressin release. 1, 2
• These systems stimulate aggressive sodium reabsorption throughout the nephron (proximal tubule, distal tubule, loop of Henle, and collecting duct), leading to sodium and water retention. 1

The Compartmentalization Effect

• Portal hypertension acts as a "compartmentalizing factor"—it determines where the retained fluid accumulates by increasing hydrostatic pressure in hepatic sinusoids and splanchnic capillaries. 1
• Elevated hydrostatic pressure in splanchnic capillaries causes excessive lymph production that overwhelms lymphatic return capacity. 3
• Lymph leakage from the liver surface and other splanchnic organs is the direct mechanism of fluid accumulation in the abdominal cavity (ascites). 3
• Peripheral edema develops when the extracellular fluid volume expansion extends beyond the peritoneal cavity. 1

Additional Contributing Factors

Systemic Inflammation

• Bacterial translocation associated with portal hypertension activates innate immune responses through pathogen-associated molecular patterns. 1
• This systemic inflammation releases proinflammatory cytokines and reactive oxygen/nitrogen species, contributing to further vasodilation and organ dysfunction. 1
• Inflammation-induced renal function abnormalities play an increasingly important role in advanced cirrhosis stages. 1

Hepatic Insufficiency

• Reduced albumin synthesis by the failing liver decreases oncotic pressure, facilitating fluid transudation from vessels into tissues. 4
• Impaired hepatic clearance of vasodilators allows their systemic accumulation, perpetuating the circulatory dysfunction. 3

Clinical Significance

• Ascites development marks a critical milestone: 5-year survival drops from approximately 80% in compensated cirrhosis to 30% in decompensated cirrhosis with ascites. 1
• About 20% of cirrhosis patients present with ascites at initial diagnosis, and 20% of those with new-onset ascites die within the first year. 1
• The swelling impairs quality of life, often necessitates hospitalization, and directly causes complications including spontaneous bacterial peritonitis, restrictive ventilatory dysfunction, and abdominal hernias. 1

Common Pitfalls to Recognize

• Presinusoidal portal hypertension without cirrhosis (e.g., isolated portal vein thrombosis) rarely causes ascites—both portal hypertension AND hepatic dysfunction are typically required. 1
• Postsinusoidal portal hypertension (e.g., acute hepatic vein thrombosis) usually causes ascites because it affects sinusoidal pressure directly. 1
• The hyperdynamic circulation with low blood pressure complicates management, as treatments like beta-blockers must be used cautiously to avoid worsening hypotension. 2
• Excessive fluid administration attempting to correct perceived hypovolemia paradoxically worsens ascites and can precipitate pulmonary edema. 2