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Acute Complications of Cirrhosis Masterclass by Sarah Kessler, PharmD, BCPS, BCGP

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  • Increased structural resistance
    • Fibrous tissue
    • Vascular distortion
  • Intrahepatic vasoconstriction
    • Decreased nitric oxide bioavailability
  • Splanchnic arterial vasodilation
  • All leads to portosystemic collaterals
Image from http://www.surgicalcore.org

Predictive Models

Cirrhosis Severity

Child Pugh Classification

Includes: encephalopathy, ascites, INR, albumin, bilirubin
5-6A – least severe liver disease
7-9B – moderately severe liver disease
10-15C – most severe liver disease
Child pugh helps determine life expectancy as well as post-abdominal surgery mortality. Also used for medication drug dosing (DOACs)

Model for End Stage Liver Disease (MELD)

Includes: creatinine/need for dialysis, bilirubin, sodium, and INR
9-40Predicts 3-month mortality

Worsens with increasing score

Consider listing for transplant ~15-17

MELD: initially created to predict TIPS procedure survival, now typically used to determine transplant candidacy (Meld 15-17)

Clinical Presentation

  • Anorexia
  • Weight loss
  • Weakness
  • Fatigue
  • Osteoporosis
  • Jaundice
  • Pruritus
  • Gastrointestinal bleeding
  • Coagulopathy
  • Easy bruising
  • Increasing abdominal girth
  • Mental status changes

Physical Exam Findings

  • Decreased blood pressure
  • Spider angiomas
  • Palmar erythema
  • Sweet, pungent breath
  • Gynecomastia
  • Ascites
  • Peripheral edema
  • Hepatomegaly
  • Splenomegaly
  • Asterixis

Treatment Overview

  • As mentioned, cirrhosis is progressive and non-reversable
  • Treatment of cirrhosis is currently focused on mitigating complications that commonly arise