1. Managing Complications of Cirrhosis
Marion Peters MD
University of California San Francisco

2. Natural History of ESLD
Increasing liver fibrosis
Development of HCC
Chronic liver disease
Compensated cirrhosis
Decompensated cirrhosis
Death or
transplant
Alcohol
Hepatitis C/B
NASH
Cholestatic
Autoimmune
PSC
Variceal hemorrhage
Ascites
Encephalopathy
Jaundice
HCC, hepatocellular carcinoma; NASH, nonalcoholic steacohepatitis
Garcia Tsao CCO Hepatitis.com 2008

3. Natural History of ESLD
Increasing liver fibrosis
Development of HCC
Chronic liver disease
Compensated cirrhosis
Decompensated cirrhosis
Death or
transplant
Alcohol
Hepatitis C/B
NASH
Cholestatic
Autoimmune
PSC
Variceal hemorrhage
Ascites
Encephalopathy
Jaundice
HCC, hepatocellular carcinoma; NASH, nonalcoholic steacohepatitis
Garcia Tsao CCO Hepatitis.com 2008

4. How to diagnose Cirrhosis
Clinically- only useful in late stages
Cirrhosis with portal hypertension
Low platelets, spider nevi, splenomegaly, ascites
Liver Biopsy
Imaging
Ultrasound- only of value in cirrhosis with portal hypertension
Elastography
Serum markers

5. METHODS TO STAGE FIBROSIS
Liver Biopsy with Histologic Evaluation
Percutaneous
Laparoscopic
Transjugular
Elastography
Transient elastography- FibroScan
Acoustic Radiation Force Impulse (ARFI)
MRI
Serum Biomarkers
Common Tests
Laboratory/ Commercial tests

6. Transient Elastography

7. TRANSIENT ELASTOGRAPHY
Measures elasticity using sound waves
Stiffness determined by multiple factors
Degree of Fibrosis
Degree of Inflammation- not good for acute hepatitis
Degree of Steatosis
Not effective in morbidly obese patients >3.5cm
Approved in U.S
now have XL probes
J Gastrointestin Liver Dis Jun;17(2):

8. Elastography: HCV Fibroscan
2.5 kPa
Cholestasis F kPa
Affected by weight, access of probe (2 cm), steatosis

9. Natural history of ESLD
Transition to decompensated cirrhosis: 5% to 7% of patients per year.
Best predictor of decompensation: hepatic venous pressure gradient (HVPG) > 10 mm Hg
HCC
can trigger decompensation
Tools for predicting disease severity and death in decompensated cirrhosis
Child-Turcotte-Pugh (CTP) score
Model for End-Stage Liver Disease (MELD) score
D’Amico 2006

10. Child-Pugh-Turcotte Score
Points
1 (normal) 2 3
Hepatic encephalopathy
None
1-2
3-4
Ascites
slight
mod
Bilirubin
<2
2-3
>3
Albumin
>3.5
<2.8 PT
<4 secs 
4-6 secs
>6 secs
or INR
<1.7
>2.3
A: 5-6; B: 7-9; C: > 9

11. MELD: Model for End-Stage Liver Disease
Bilirubin
INR
Creatinine
MELD

12. Complications of cirrhosis
Portal hypertension
Variceal hemorrhage
Ascites
Encephalopathy
Jaundice

13. Portal Hypertension
An increase in the blood pressure around the liver called the portal venous system. Veins coming from the stomach, intestine, spleen, and pancreas merge into the portal vein, which then branches into smaller vessels and travels through the liver

16. Complications of cirrhosis
Variceal hemorrhage
Ascites
Encephalopathy
Jaundice

17. Risk of Bleeding from Esophageal Varices
Cirrhosis
25%-40%
Prevalence
35%-80%
50%-70%
30%-50%
Survive
Die
70%
Rebleed 17

18. Variceal Surveillance
All cirrhotics require Esophagogastroduodenoscopy
No varices
Small varices (< 5 mm), Child B/C
Medium or large varices
Repeat endoscopy in years (well compensated); in 1 year if decompensated
No beta-blocker prophylaxis
Child Class A, no red wales: beta blockers
Child class B/C, red wales: beta blockers or band ligation
Nonselective Beta-blocker prophylaxis
Garcia-Tsao G, et al. Hepatology. 2007;46: 18

19. Complications of cirrhosis
Variceal hemorrhage
Ascites
Encephalopathy
Jaundice

20. Stages of ascites Diuretic-responsive ascites Refractory ascites
Hyponatremia
Hepatorenal syndrome (HRS)
Each stage reflects a more deranged circulatory state.

21. Treatment of ascites Diuretic-responsive ascites Refractory ascites
Sodium restriction- you have normal amount of Na- too much water
Spironolactone ( mg) and furosemide (20-40 mg)
Refractory ascites
Large volume paracentesis with 25% albumin (50 cc/L)
For symptom management
TIPS- higher transplant free survival but higher PSE (confusion)

22. Ascites: LVP Albumin
Albumin infusion after large-volume paracentesis (LVP)
Meta-analysis of 17 trials involving 1,225 patients showed that albumin improved survival
Albumin infusion is recommended when more than 4 Liters of ascitic fluid are removed
Albumin infusion may not be necessary for a single paracentesis of less than 4 L (AASLD guidelines)
(Bernardi Hepatology 2012)

23. Hepatorenal syndrome (HRS)
Acute renal failure occurs in 14% to 25% of hospitalized patients with cirrhosis
Most common form of prerenal failure (accounting for 60% to 80% of the cases)

24. Hepatorenal syndrome
results from vasodilatation and marked reduction in effective arterial blood volume leading to renal vasoconstriction
occurs in patients with unresponsive or refractory ascites and/or low sodium (hyponatremia)

25. HRS treatment OLT Midodrine and octreotide
HRS due to extreme splanchnic and systemic vasodilatation
Drugs  vasoconstriction
Albumin to increase intravascular volume

26. Spontaneous bacterial peritonitis (SBP)
Most common type of bacterial infection in hospitalized cirrhotic patients
Clinical suspicion:
unexplained encephalopathy, jaundice
worsening renal failure
<50%: fever, abdominal pain or tenderness, and leukocytosis
Diagnose: tap ascites: WCC>500, PMN > 250 cells/mm3
Place ascites in blood culture bottles
Start treatment immediately before culture results

27. Complications of cirrhosis
Variceal hemorrhage
Ascites
Encephalopathy
Jaundice

28. Hepatic Encephalopathy
Confusion resulting from the liver not processing toxins from the gut
Precipitants
Infection- especially SBP or UTI
Bleeding
Electrolyte imbalance
Portal vein thrombosis
Worsening liver disease
HCC

29. Hepatic Encephalopathy
Treatment aims to reduce production of ammonia from the colon through
nonabsorbable disaccharides
lactulose, lactitol, and lactose
Induce diarrhea
Change gut bacteria to sugar from protein
nonabsorbable antibiotics
neomycin, rifaximin

30. Hepatic Encephalopathy
Protein restriction promotes protein degradation and, if maintained for long periods, worsens nutritional status and decreases muscle mass
No longer recommended
Night- time snacks

31. Indications for Liver Transplantation
Development of decompensation (liver dysfunction, MELD >12, ascites, variceal bleed, encephalopathy) in patients with cirrhosis
HCC that is confined to the liver by Milan criteria: 1 lesion <5 cm or 3 lesions < 3 cm
UCSF criteria <6.5 cm total
Adherent, no drug use, alcohol, adequate support
No extrahepatic disease

32. Liver Transplantation
MELD
Serum sodium
Underestimated
chronic encephalopathy- confusion
hepatic hydrothorax- fluid around the lung
hepatopulmonary syndrome- low oxygen
portopulmonary hypertension- high pressure
Recurrent cholangitis- infection

33. MELD: Model for End-Stage Liver Disease
Bilirubin
INR
Creatinine
MELD

34. Managing complications of cirrhosis
Portal hypertension
elastography can be used to assess severity of fibrosis/cirrhosis
Can measure Portal hypertension
Variceal hemorrhage
monitor varices with endoscopy

35. Managing complications of cirrhosis
Ascites
Need to decrease fluid in body not salt
Low salt diet
LVP treats symptoms
TIPS decreases pressure around liver but increases risk of confusion

36. Managing complications of cirrhosis
Encephalopathy
Monitor closely may be subtle
Treat infection aggressively
Nutrition different in cirrhosis
Consider OLT when first liver decompensation occurs