1. Imaging of cirrhosis Valérie Vilgrain Service de Radiologie
Hôpital Beaujon
France

2. Cirrhosis Extensive fibrosis and regenerative nodules
Main causes alcohol ingestion
chronic hepatitis C
chronic hepatitis B
hemochromatosis
Wilson disease
Micronodular nodules < 3 mm
Macronodular larger nodules

3. Diagnosis
Liver diseases mimicking cirrhosis
Prognosis
Non invasive diagnosis of fibrosis

4. Diagnosis of cirrhosis
Nodularity of the liver surface
Nodular internal architecture
Changes of hepatic morphology
Vascular changes
Portal hypertension

5. Nodularity of the liver surface Nodular internal architecture
Correlate with the gross appearance of cirrhosis
Surface
. Initially described with high frequency transducer
. Seen with US, CT and MR
Internal architecture
. Best seen with US and MR
. Regenerative nodules hypoechoic - hypointense
. Septa hyperechoic - hyperintense
Dilelio, Radiology 1989

6. Cirrhosis Surface nodularity
Se Sp Accuracy
Di Lelio
Richard
Ferral
Ladenheim
Colli 54 95
Radiology 1989
J. Radiol 1985
Gastrointest 1992
Radiology 1992
Radiology 2003

8. Hepatic morphologic changes

9. Hepatic morphologic changes Quantitative results (1)
Caudate lobe
Caudate-right lobe ratio (> 0.65)
Modified caudate-right lobe ratio (> 0.90)
Harbin, Radiology 1980
Awaya, Radiology 2002

10. Hepatic morphologic changes Quantitative results (2)
Segment 4
Control group 43 ± 8 mm
Cirrhosis ± 9 mm
Cutoff: 30 mm
Limit: measurement obtained at US
Lafortune, Radiology 1998

11. Hepatic morphologic changes Other signs
Expanded gallbladder fossa
Specificity and PPV of 98%
Associated with atrophy of the segment 4
Enlargment of hilar periportal space
Seen in 98% in early cirrhosis
Cutoff of 10 mm
. Control group: 5.3 mm
. Cirrhosis: mm
Ito, Radiology 1999
Ito, JMRI 2000

12. Vascular changes Hepatic veins Normally triphasic Cirrhosis
decreased diameter
altered waveform in 50%
correlated with the severity
reduced transit time (contrast US)
Bolondi, Radiology 1991
Colli, AJR 1994
Albrecht, Lancet 1999

13. Vascular changes Hepatic artery HA diastolic velocity > PV velocity
Increased HA diameter
Increased RI and PI of the hepatic artery
Portal vein velocity
Liver vascular index =
Hepatic artery PI
< 12 cm/sec
Iwao, Am J Gastroenterol 1997

14. Portal hypertension Increased pressure > 15 mm Hg
Portocaval gradient > 5 mm Hg
Portal hemodynamics
Collaterals
Ascites
Splenomegaly

15. Diagnosis of PHT Splanchnic veins
Enlargment of splanchnic veins
Lack of caliber variations of SMV
Reversed flow SMV 2.1%
splenic vein 3.1%
Alpern, Radiology 1987
Bolondi, Radiology 1982

16. Diagnosis of PHT Diameter of the portal vein > 13 mm Se 40%
Alterations of portal blood flow abs of end-diastolic
arterialized flow
bidirectional flow
reversed flow 1%
Bolondi, Radiology 1982
Vilgrain, Gastrointest Radiol 1990
Lafortune 1990
Gaiani, Gastroenterology 1991

17. Diagnosis of PHT Left gastric vein
Diameter > 6 mm 26%
Hepatofugal flow 78%
Wachsberg, AJR 1994

18. Diagnosis of PHT Gastroesophageal veins

20. Diagnosis of PHT Paraumbilical vein

21. Diagnosis of PHT Splenorenal veins

23. Diagnosis of PHT Other collaterals
Retroperitoneal veins
Omental veins
Rectal varices
Gallbladder varices

24. Diagnosis of PHT Mean portal velocity Mean portal blood flow
cm/sec ml/min
controls cirrhosis controls cirrhosis
Gaiani et al 19     625
Moriyasu et al 15.3     289
Zoli et al 16     46
Ohnishi et al 17     258
Gaiani, Hepatology 1989
Moriyasu, AJR 1986
Zoli, J Ultrasound Med 1985
Ohnishi, Gastroenterology 1985

25. Cirrhosis Ultrasound-Score
Accuracy
Surface nodularity
+ mean portal velocity 82%
Spleen length 84%
+ mean portal velocity
Spleen length 89%
+mean portal velocity
+hepatic venous spectrum
Gaiani, J Hepatol 1997
Aubé, J Hepatol 1999
Aubé, Eur J Gastroentrol 2004

26. Liver diseases mimicking cirrhosis
Common findings
Morphologic changes of the liver
May give signs of PHT
Generally vascular or biliary diseases
But
Rarely cause nodularity of the liver surface
Rarely have nodular regeneration

27. Primary sclerosing cholangitis
Lobular contour 73%
Caudate hypertrophy 98%
Lateral segment atrophy 58%
Posterior segment atrophy 36%
Dilated ducts 67%
End stage disease
Dodd, Radiology 1999

28. Congenital hepatic fibrosis
Mean age 39 years
Liver morphologic abnormalities 89%
Splenomegaly 83%
Varices 78%
Renal abnormalities 56%
Ductal plate malformation 50%
Zeitoun, Radiology 2004

29. Congenital hepatic fibrosis
Hypertrophy of the left lateral
Normal or hypertrophy of the segment 4
Atrophy of the right lobe
Zeitoun, Radiology 2004

30. Budd-Chiari disease Hypertrophy of the caudate lobe > 50%
Lobar atrophy/hypertrophy
Abnormal hepatic veins
Hepatic venous collaterals

31. Portal cavernoma
Central vs peripheral zone
Vilgrain, Radiology 2006

32. Imaging in assessing prognosis?
Comparison between compensated and uncompensated cirrhosis
Serial imaging
Stability and functional reserve
. Hypertrophy and increasing of the caudate lobe 1, 2, 3
. High caudate to right lobe ratio 1
. Increasing lateral segment 2
Clinical progression
. Progressive atrophy of the right lobe and medial segment 2
. Spleen enlargment 3
. Varices 3
1. Watanabe, Dig Dis Sci 1999
2. Ito, Radiology 1998
3. Ito, AJR 1997

33. Limitations of non invasive imaging
Most signs seen in advanced cirrhosis
No specific signs associated with fibrosis
=> Need to find other criteria
other imaging

34. Diagnosis of fibrosis Blood tests: Fibrotest Elastrography
Liver MR diffusion
Liver perfusion

35. Fibrotest Alpha 2 macroglobulin Haptoglobin Apolipoprotein 1
Total bilirubin
GGT
ALT
Probability of fibrosis < 10%
Liver biopsy recommended
Probability of fibrosis > 90%
Imbert-Bismuth, Lancet 2001

36. Elastography (Fibroscan)
Ultrasound (5MHz) and low frequency
(50 Hz) elastic waves
Propagation velocity is related to elasticity

37. Liver MR diffusion
Reduced ADC in cirrhosis
Taouli, Radiology 2003

38. Liver perfusion
Van Beers, AJR 2001

39. CONCLUSION
Today, non invasive imaging is crucial for diagnosing cirrhosis and its complications.
Tomorrow, the challenge of imaging will be to detect early stages of fibrosis and cirrhosis and to demonstrate therapeutic response.