Use of Transient Elastography (FibroScan®) to Assess Probability of Clinically Significant Portal Hypertension

Judith McLaughlin, MHealSc CNS Hepatology, Waitaha Canterbury. 027 538 3869

Clinically Significant Portal Hypertension

The development of clinically significant portal hypertension (CSPH) is an important prognostic event in the pathology of advanced chronic liver disease. CSPH is the most reliable predictor of decompensation and denotes a point of no return for some patients (Stedman, 2022).

CSPH occurs via two main mechanisms. The first is increased resistance to blood flow in the portal vein (early) from distortion of the liver structure and dysfunction of endothelial cells (decreased vasodilation and increased constriction). The second (later) is increased flow to the portal vein due to splanchnic vasodilation and cardiac output (Stedman, 2022).

Assessment of Clinically Significant Portal Hypertension

Until now, we have assessed for features of portal hypertension by examining ultrasound scan reports and/or performing gastroscopy surveillance for varices. Access to the gold standard of hepatic venous pressure gradient (HVPG) measurement is limited, and besides this is an invasive procedure not without risks.

Use of Liver Stiffness and Platelet Count to assess risk of CSPH

Transient elastography (TE), commonly using FibroScan®, has been shown to reliably identify risk of CSPH in those who have advanced fibrosis secondary to alcohol, viral hepatitis and non-obese (BMI<30)

Metabolic Associated Fatty Liver Disease (MAFLD) (De Franchis et al., 2022). In 2015, the Baveno Group produced consensus-based guidelines (Baveno VI) that used liver stiffness (LS) together with platelet count to rule in or rule out the likelihood of CSPH. If LS was <20kPa and platelet count >150x109/L, gastroscopy could be avoided (De Franchis, 2015).

Patients with a liver stiffness ≤20kPa & platelets ≥150x109/L have very low risk of having varices and gastroscopy can be avoided (De Franchis, 2015).

Rule of 5

In 2021 the Baveno VII workshop expanded the work on previous Baveno VI. Recognising that various stages of compensated advanced chronic liver disease (cACLD) are associated with different outcomes, they introduced a pragmatic approach to stratify risk based on liver stiffness using a rule of 5 (see Figure 1 below). LS <5 kPa has a high probability of being normal; LS <10 kPa, in the absence of other known clinical signs, rules out cACLD. Values between 10 and 15 kPa are suggestive of compensated advanced chronic liver disease but need further tests for confirmation. Values >15 kPa are highly suggestive of compensated advanced chronic liver disease. Values ≥20–25 kPa can rule in CSPH (De Franchis et al., 2022).

Figure 1

Algorithm for the non-invasive determination of cACLD and CSPH

Note. From “Baveno VII – Reviewing consensus in portal hypertension” by De Franchis et al., 2022, Journal of Hepatology, 76(4), p. 963.

A rule of 5 for liver stiffness measurement (LSM) by TE (10-15-20-25kPa) should be used to denote progressively higher relative risks of decompensation and liver related death independent of aetiology of liver disease (De Franchis et al., 2022).

Prevention of First Decompensation

Recent data have shown that identification and treatment of CSPH with a non-selective beta blocker (NSBB) can reduce the risk of decompensation, primarily through reducing the development of ascites (Villanueva et al., 2019). Professor Catherine Stedman delivered a presentation at the New Zealand Society of Gastroenterology/NZNO Gastroenterology Nurses’ College Annual Scientific Meeting in November last year titled “B blockers in cirrhosis – the shifting tides” in which she talked about the use of beta blockers. Carvedilol is now the preferred NSBB since it is more effective at reducing the HVPG, is better tolerated than traditional NSBB (e.g. nadolol) and has a greater benefit in preventing decompensation and improving survival (De Franchis et al., 2022).

Assessing Liver Stiffness Post Treatment

Another big change is that FibroScan® can be used both at diagnosis and during follow-up for assessment of CSPH. Many of us are not in the practice of performing FibroScan® post treatment/suppression of aetiology as risk of hepatocellular carcinoma remains, and it does not change our management. However, now it will determine whether or not patients are commenced on a beta blocker and the recommendation is that liver stiffness is assessed annually, particularly if there are ongoing risk factors (De Franchis et al., 2022).

How does this change my practice?

For me, this represents one of the biggest changes in the management of patients with advanced liver fibrosis that I have seen since the introduction of direct acting anti-viral medications to cure hepatitis C. It represents a big challenge and responsibility for those of us performing liver stiffness assessments and there are still some grey areas. In the Gastroenterology Department at Christchurch Hospital we are developing tools to aid our interpretation and I have included an example below of how we are now reporting liver stiffness and risk of CSPH. There is also a flow chart below that we use to aid our interpretation of LS and platelet count. It is important to note that this guideline only applies to viral hepatitis, alcohol related liver disease and MALFD (BMI<30). For other aetiologies such as PSC and PBC, gastroscopy every 2 years is recommended (De Franchis, 2015). For MAFLD (BMI>30) CSPH risk can be calculated using the ANTICIPATE-NASH nomogram (Rabiee et al., 2022). This is probably best covered in another issue as it is a little more complex and requires further validation.

Examples of Reporting of risk of CSPH

Patient A Pre-treatment (Old Guidelines) Post treatment (Baveno VII)

Hepatitis C (68y male)

18.4kPa (2012) 8.2kPa (2022)

Platelets 179x10(9)/L Platelets 230x10(9)/L

FibroScan® Comment Results consistent with cirrhosis. (Gastroscopy was arranged)

Patient B Pre-treatment (Baveno VII)

Hepatitis C (59y female)

Low risk of CSPH. No PHT follow-up required. Risk of HCC remains. (Gastroscopy not required)

27.3kPa (2022)

Platelets 165x10(9)/L

FibroScan® Comment Highly suggestive of advanced fibrosis and ≥90% risk of CSPH. Consider commencing NSBB. HCC surveillance recommended.

References

• De Franchis, R. (2015). Expanding consensus in portal hypertension: Report of the Baveno VI Consensus Workshop: Stratifying risk and individualising care for portal hypertension. Journal of Hepatology, 63(3), 743-752. https://doi.org/10.1016/j.jhep.2015.05.022

• De Franchis, R., Bosch, J., Garcia-Tsao, G., Reiberger, T., Ripoll, C., & Baveno VII Faculty. (2022). Baveno VII – Reviewing consensus in portal hypertension. Journal of Hepatology, 76(4), 959-974. https://doi. org/10.1016/j.jhep.2021.12.022

• Rabiee, A., Deng, Y., Ciarleglio, M., Chan, M., Chan, J., Pons, M., Genesca, J., Garcia-Tsao, G. (2022). Noninvasive predictors of clinically significant porta hypertension in NASH cirrhosis: Validation of ANTICIPATE models and development of a lab based model. Hepatology Communications, 6(12), 33243334. https://doi.org/10.1002/hep4.2091

• Stedman, C. (2022, November 23-25). B blockers in cirrhosis – the shifting tides [Conference presentation]. New Zealand Society of Gastroenterology/NZNO Gastroenterology Nurses’ College Annual Scientific Meeting, Auckland, New Zealand.