Cirrhosis Complications
Portal hypertension silently rewires abdominal circulation, creating life-threatening detours. Knowing which complication kills fastest changes how you prioritize your assessment.
Core Concept
As the cirrhotic liver becomes fibrotic, blood backs up into the portal venous system, raising portal pressure above the normal 5–10 mmHg. This single mechanism drives most major complications. Esophageal varices form as collateral vessels dilate under pressure; rupture causes massive upper GI hemorrhage — the most immediately lethal complication. Ascites develops when portal hypertension combines with low albumin (reduced oncotic pressure) and sodium/water retention from secondary hyperaldosteronism. Third-spacing of fluid into the peritoneum can exceed several liters. Spontaneous bacterial peritonitis (SBP) occurs when ascitic fluid becomes infected without a surgical source; suspect it when a client with ascites develops fever, abdominal pain, or worsening mental status. Paracentesis fluid with an absolute neutrophil count ≥250 cells/mm³ confirms SBP. Hepatorenal syndrome is progressive renal failure triggered by severe splanchnic vasodilation; urine output drops despite adequate volume, and it carries high mortality. Splenomegaly from portal congestion causes thrombocytopenia, increasing bleeding risk beyond what coagulopathy alone explains.
Watch Out For
Don't confuse variceal bleeding (painless, massive hematemesis from portal hypertension) with peptic ulcer bleeding (epigastric pain, smaller volume). Students mix up SBP (infection of existing ascites, neutrophils ≥250) with secondary peritonitis (surgical perforation, multiple organisms). Hepatorenal syndrome looks like prerenal failure on labs but does not respond to fluid resuscitation — that distinction is highly testable.
Clinical Pearl
Think of portal hypertension as a backed-up highway: varices are the dangerous detours, ascites is the flooding, and SBP is infection in the floodwater.
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