Pathophysiology & Risk Factors

Fibrosis of the cirrhotic liver backs blood up into the portal venous system, raising portal pressure above the normal 5-10 mmHg. This single mechanism of portal hypertension drives nearly every major complication: collateral vessels dilate into varices, splanchnic vasodilation and low oncotic pressure third-space fluid as ascites, and splenic congestion lowers platelets.

Portal hypertension cascade

Portal hypertensionfrom cirrhotic fibrosis
Esophageal/gastric varicescollateral vessels rupture -> massive GI bleed
Ascites+ hypoalbuminemia + hyperaldosteronism
Spontaneous bacterial peritonitisinfection of ascitic fluid
Hepatic encephalopathyammonia accumulation
Hepatorenal syndromesplanchnic vasodilation -> renal vasoconstriction

Signs & Symptoms

EarlyProgresses →

Increasing abdominal girth

ascites; positive fluid wave

Peripheral edema

Late / Severe

Asterixis Hallmark

motor sign of hepatic encephalopathy

Confusion

neurocognitive decline from rising ammonia

Other findings

Jaundice

Spider angiomata

Palmar erythema

Caput medusae

distended periumbilical veins from portal hypertension

Easy bruising

ecchymoses from coagulopathy

Diagnostics & Labs

Diagnostic

Low serum albumin

reduced hepatic synthesis

Prolonged PT/INR

impaired clotting factor synthesis

Thrombocytopenia

splenic sequestration

Ascitic fluid neutrophils >= 250 cells/mm3 Hallmark

diagnostic criterion for SBP

Urine sodium < 10 mEq/L

hepatorenal syndrome; avid sodium retention

Monitor

Hyponatremia

dilutional from water retention

Rising serum creatinine

HRS; unresponsive to volume

Elevated serum ammonia

hepatic encephalopathy

Interventions & Priorities

Assess for active variceal bleeding

most immediately lethal complication

Institute bleeding precautions

electric razor, soft-bristled toothbrush

Extended pressure to puncture sites

standard 2-minute hold insufficient

Sodium restriction for ascites

Daily weight and abdominal girth

cap diuresis at 0.5 kg/day without edema

Monitor for worsening mental status

asterixis signals encephalopathy

Monitor urine output and creatinine

detect hepatorenal syndrome

Treatments & Medications

Spironolactone

first-line diuretic; antagonizes hyperaldosteronism

Furosemide

adjunct when spironolactone alone inadequate

IV albumin after large-volume paracentesis

prevents circulatory dysfunction

Therapeutic paracentesis

void before; voiding prevents bladder puncture

Patient Teaching

Avoid alcohol

Avoid NSAIDs

nephrotoxic; increase bleeding risk

Restrict dietary sodium

limits ascites fluid retention

Use electric razor and soft toothbrush

prevent lacerations and gingival bleeding

Report increasing abdominal girth

Report black or bloody stools

melena signals GI bleed

Complications

Esophageal varices

rupture is most immediately lethal

Ascites

Spontaneous bacterial peritonitis

infected ascites without surgical source

Hepatic encephalopathy

ammonia-driven altered mentation

Hepatorenal syndrome

functional renal failure; structurally normal kidneys

Thrombocytopenia

from splenomegaly

Report Nowescalate immediately

Hematemesis

variceal bleed; even a single episode warrants escalation

Melena

upper GI hemorrhage

Fever with new abdominal tenderness

SBP in a client with ascites

New or worsening asterixis

worsening hepatic encephalopathy

Worsening confusion

rising ammonia

Oliguria with rising creatinine

hepatorenal syndrome; does not respond to fluids

Clinical Pearl

Picture portal hypertension as a backed-up highway: varices are the dangerous detours that bleed, ascites is the flooding, and SBP is infection in the floodwater.

Cirrhosis Complications