For U.S. Healthcare Professionals

Cirrhosis impacts Cirrhosis impacts

Hepatic encephalopathy (HE)
is a challenging condition.

The first step in managing HE is understanding it.

Chronic liver disease (CLD) can progress to cirrhosis and cause complications like HE,
which requires prompt attention to manage HE episodes1-3

CLD arrow

Early Screening for Severe Liver Damage Can Help Identify Cirrhosis Before Complications Emerge4,5

Liver damagesLiver damages horiline horiline
  • NORMAL
  • FIBROSIS
  • arrowarrow
  • CIRRHOSIS

~4.5

million

US adults have liver disease (2018 data)6

By 2030,

~2.5 million

adults are estimated to have cirrhosis7

Who is most at risk for cirrhosis and its complications?

Who has a high risk of MASLD/MASH? Those diagnosed with type 2 diabetes (or prediabetes), obesity (or metabolic syndrome), hepatic steatosis (on imaging), or persistently elevated liver enzymes (AST or ALT >30 IU/L for >6 months)

Who has a high risk of ALD? Those with a history of heavy alcohol use (or binge drinking), including alcohol use disorder

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See valuable data and clinician insights into
CLD and cirrhosis

Liver Health Trends Report Download icon

How can I uncover cirrhosis in my patients?

  • Cirrhosis is often not diagnosed until complications from decompensation present9
  • Noninvasive tools like FIB-4 can be used to stratify fibrosis/cirrhosis risk5
  • Higher FIB-4 scores correlate with development of cirrhosis and future decompensation4,5
    • This may signal the need for liver specialist involvement and secondary testing (elastography, ELF)

Medical history and physical exam alone are often insufficient to detect cirrhosis10

Up to

40%

of patients with cirrhosis are asymptomatic11

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Learn more about FIB-4 stratification and
access a FIB-4 calculator

FIB-4 Brochure Download icon
FIB-4 Calculator External icon

How does decompensated cirrhosis develop?

  • Cirrhosis alters the gut-liver-brain axis and can lead to organ involvement beyond the liver12-14:
    • Gut barrier instability, inflammation, reduced pathogen control, and increased bacterial toxin production
  • Portal hypertension and hepatic insufficiency from progressive cirrhosis can cause1,2:
    • Portosystemic shunting, bypassing blood flow through the liver
    • Collateral vessels and varices
    • Impaired metabolism of byproducts and toxins
Portal hypertension diagram

Median survival

decreases from

>12
years to <2
years

after progression from
compensated to decompensated
cirrhosis1,2

pdf

Explore an enhanced learning experience about
cirrhosis and its progression

Interactive PDF: Cirrhosis Progression Download icon

How does decompensated cirrhosis present?

  • The most common complications of decompensated cirrhosis are15:

    • HE can be either covert (with subtle/mild cognitive, behavioral, and/or neurologic symptoms) or overt (with pronounced psychiatric and/or neurologic symptoms)16

    • Variceal hemorrhage
    • Ascites
  • Patients at risk for decompensation should be screened for cirrhosis progression and potential complications as part of guideline-based care15

In one study,

50%

of patients (n=238/476) had ≥1 decompensating event when diagnosed with cirrhosis9

Data from a retrospective study that included patients (N=476) diagnosed with liver cirrhosis at a non-transplant hospital in Vienna from January 2015 to March 2020. Etiology of cirrhosis, sex, weight, height, presence of ascites or HE, medication, diabetes, endoscopy reports of varices, and imaging reports were assessed at baseline.9

In patients with MASLD, HE is the most common first decompensating event17

ALD, alcohol-associated liver disease; ALT, alanine aminotransferase; AST, aspartate aminotransferase; CLD, chronic liver disease; ELF, enhanced liver fibrosis; FIB-4, fibrosis-4 index; MASH, metabolic dysfunction–associated steatohepatitis; MASLD, metabolic dysfunction–associated steatotic liver disease.

References

1. Garcia-Tsao G. In: Goldman L et al, eds: Goldman-Cecil Medicine. 26th ed. Elsevier; 2016:990-8.e3. 2. Poordad FF. Curr Med Res Opin. 2015;31(5):925-937. 3. Shawcross DL et al. Eur J Gastroenterol Hepatol. 2016;28(2):146-152. 4. Rinella ME et al. Hepatology. 2023;77(5):1797-1835. 5. Cusi K et al. Endocr Pract. 2022;28(5):528-562. 6. CDC, National Center for Health Statistics. Summary Health Statistics: National Health Interview Survey, 2018. Accessed December 14, 2024. https://ftp.cdc.gov/pub/Health_Statistics/NCHS/NHIS/SHS/2018_SHS_Table_A-4.pdf 7. Wong RJ et al. Clin Transl Gastroenterol. 2025;16(5):e00823. 8. Jophlin LL et al. Am J Gastroenterol. 2024;119(1):30-54. 9. Schwarz M et al. PLoS One. 2023;18(8):e0290352. 10. de Bruyn G, Graviss EA. BMC Med Inform Decis Mak. 2001;1:6. 11. Heidelbaugh JJ, Bruderly M. Am Fam Physician. 2006;74(5):756-762. 12. Liu Y et al. BMC Gastroenterol. 2025;25(1):16. 13. Bajaj JS et al. J Hepatol. 2014;60(5):940-947. 14. Wu Z et al. Front Cell Infect Microbiol. 2023;13:1218552. 15. Garcia-Tsao G et al. Hepatology. 2017;65(1):310-335. 16. Vilstrup H et al. Hepatology. 2014;60(2):715-735. 17. Sanyal AJ et al. N Engl J Med. 2021;385(17):1559-1569.