Cirrhosis and Portal Hypertension: Radiology and Imaging

Cirrhosis is the end stage of chronic liver injury, in which diffuse fibrosis and regenerative nodules distort the hepatic architecture. The stiff, scarred liver obstructs portal inflow, raising portal venous pressure and producing portal hypertension — splenomegaly, ascites, and portosystemic collaterals. This article covers the ultrasound, Doppler, CT, and MRI features of cirrhosis and portal hypertension, the normal reference measurements you need at the workstation, and the current Baveno VII criteria for diagnosing clinically significant portal hypertension.

Quiz

Which of the following is a feature of this pathology?

1. Caudate lobe atrophy
2. Right lobe hypertrophy
3. Caudate lobe hypertrophy

Key Imaging Features:

Ultrasound:

B mode:

• Surface nodularity.
• Coarse echotexture- pinhead echoes, inhomogenous in distribution, with no posterior shadows.
• Regenerative nodules.
• Caudate lobe hypertrophy (caudate / right lobe ratio > 0.65).
• Poor visualization of hepatic vessels.
• Splenomegaly (mid axillary length >13cm or largest cross sectional area through the hilum > 45 square cm).
• Gamna Gandy nodules: Multiple hyperechogenic nodules due to microbleed foci in the spleen and siderotic changes.
• Splenic interface sign: Linear hyperreflective channels in splenic parenchyma due to dilated intrasplenic venous sinuses with deposition of collagen in the walls.
• Increase in bowel wall and gallbladder wall thickness due to edema.

Color Doppler:

Alteration in normal doppler findings and spectral traces of portal vein, hepatic artery and hepatic vein.

• Visualization of collaterals and varices on color doppler. Following are a few schematic diagrams describing ultrasound and doppler features.

• Summarized list of features on doppler is as follows:

Contrast enhanced ultrasound:

•     Role of contrast enhanced ultrasound is described in the following chart.

Elastography:

• Transient elastography (TE) and acoustic radiation force impulse (ARFI) / shear-wave elastography are most commonly used.
• Liver stiffness < 10 kPa makes advanced chronic liver disease unlikely; 10–15 kPa is suggestive and > 15 kPa is highly suggestive of compensated advanced chronic liver disease (Baveno VII, 2022).
• Historic cutoffs of > 12.5–15 kPa for established cirrhosis remain broadly concordant; the dedicated diagnostic section below covers how stiffness now rules portal hypertension in and out.

CT:

Liver-

• Surface irregularity.
• Caudate to right lobe ratio increased > 0.65.

Easy to understand summary on calculation and interpretation of causate to right lobe ratio.

• Nodules –
  • Regenerative: Iso or hyperattenuating;
  • Siderotic: Hyperattenuating.
  • Malignant : Enhance in early arterial phase (20 seconds after contrast injection), show washout of contrast on delayed phase images.
• Confluent fibrosis appears hypoattenuating on non-contrast CT and isoattenuating or slightly hypoattenuating on contrast CT images.
• Splenomegaly.
• Ascites.
• Lymphadenopathy in advanced cases.
• Enlarged portal vein, splenic vein, superior mesenteric vein.
• Collaterals delineated on contrast CT and angiography images.

MRI-

• Morphological changes- Irregular contours, atrophy of right lobe of liver,hypertrophy of caudate lobe.
• Comma shaped intrahepatic varices seen on TOF images.
• Vascular anatomy seen with GRE images.
• Phase contrast MR Angiography sequence for direction of portal flow.
• MR Elastography : >4 kPa in fibrotic liver.
• Nodules: Regenerative, Dysplastic, Malignant nodules can be characterized.  A chart summarizing the common patterns on cross sectional imaging is as follows:

Normal vs. Portal Hypertension: Key Imaging Measurements

These are the quantitative thresholds most often needed at the ultrasound workstation. No single value is diagnostic in isolation — interpret them together with liver morphology and the presence of collaterals.

Diagnosing Portal Hypertension: HVPG and Baveno VII Non-Invasive Criteria

The hepatic venous pressure gradient (HVPG) is the reference standard for portal pressure. Clinically significant portal hypertension (CSPH) is defined as HVPG ≥ 10 mmHg — the threshold above which varices, ascites, and hepatic decompensation develop. Because HVPG is invasive, the 2022 Baveno VII consensus endorsed non-invasive, elastography-based criteria for everyday use.

Liver stiffness (LSM by transient elastography)

• Compensated advanced chronic liver disease (cACLD): LSM < 10 kPa rules out cACLD; 10–15 kPa is suggestive; > 15 kPa is highly suggestive.
• Rule of 5 (10-15-20-25 kPa): each 5-kPa step marks a progressively higher risk of decompensation and liver-related death, independent of aetiology.
• Ruling CSPH in and out: LSM ≥ 25 kPa alone is sufficient to diagnose CSPH; LSM ≤ 15 kPa with a platelet count ≥ 150 × 10⁹/L rules CSPH out.

Spleen stiffness (SSM)

Spleen stiffness tracks portal pressure more directly than liver stiffness. In viral cACLD, SSM < 21 kPa rules CSPH out and SSM > 50 kPa rules it in. An SSM ≤ 40 kPa helps identify patients at low probability of high-risk varices, in whom screening endoscopy may be avoided.

Cross-sectional imaging supports the diagnosis when it shows portosystemic collaterals (paraumbilical, gastro-oesophageal, or splenorenal), a recanalised paraumbilical vein, splenomegaly, or ascites — any of which is independently diagnostic of CSPH.

Pathophysiology

As the liver becomes too stiff due to fibrosis, it cannot effectively drain blood via the hepatic veins into the inferior vena cava. The pressure builds up in the portal vessels and flow reverses away from the liver. Collateral circulation becomes active to bypass the liver in draining blood to the heart.

The next two images show line diagrams of normal portal and systemic blood flows, and altered portosystemic shunts.

Imaging Recommendation:

Routine surveillance for malignancy, usually with 6 monthly ultrasound, or earlier as per case scenario.

Top 3 Differential Diagnosis:

Summary on few top differential diagnosis for cirrhosis are as follows:

Clinical Features:

• Symptoms –

• Age/Sex predilection: Variable

• Risk factors: Hepatitis B,C,D infections, excessive Alcohol consumption, underlying pathologies like alpha antitrypsin deficiency. Refer Etiological Classification for summarized list.

Child–Pugh and MELD remain the mainstays of severity grading. Since 2023, U.S. transplant allocation uses MELD 3.0, which refines the score by adding serum albumin and a sex correction (women were historically disadvantaged) to creatinine, bilirubin, INR, and sodium.

Etymology and synonyms :

The Greek word ‘kirros’ means yellowish and tawny. Adding ‘osis’ a common medical suffix to it, formed the word Cirrhosis, first described in this way by French physician Laennec.

Treatment :

Frequently Asked Questions

What is the normal portal vein velocity?

Normal main portal vein mean velocity is about 16–40 cm/s, with hepatopetal (toward-liver) flow and a gently undulating waveform. A mean velocity below 16 cm/s, loss of undulation, or reversed (hepatofugal) flow suggests portal hypertension.

What is a normal portal vein diameter?

The main portal vein normally measures ≤ 13 mm at quiet respiration. A diameter > 13 mm is highly specific for portal hypertension but has low sensitivity, because the vein can normalise once collaterals decompress the system.

What is the caudate-to-right-lobe ratio in cirrhosis?

The caudate-to-right-lobe (C/RL) ratio compares the width of the caudate lobe to that of the right lobe. A ratio ≥ 0.65 reflects the caudate hypertrophy and right-lobe atrophy typical of cirrhosis and is a useful, though not fully sensitive, morphological sign.

What HVPG defines clinically significant portal hypertension?

Hepatic venous pressure gradient (HVPG) is normally 1–5 mmHg. A gradient of 6–9 mmHg is subclinical portal hypertension; ≥ 10 mmHg defines clinically significant portal hypertension (CSPH); and ≥ 12 mmHg carries the risk of variceal bleeding.

How is portal hypertension diagnosed non-invasively?

Per Baveno VII, liver stiffness ≥ 25 kPa on transient elastography is enough to diagnose CSPH, while ≤ 15 kPa plus a platelet count ≥ 150 × 10⁹/L rules it out. Spleen stiffness and imaging evidence of portosystemic collaterals or splenomegaly further support the diagnosis.

References:

Single best review article:

Owen, C. and Meyers, P. (2006) ‘Sonographic evaluation of the portal and Hepatic Systems’, Journal of Diagnostic Medical Sonography, 22(5), pp. 317–328. doi:10.1177/8756479306293101.

Other references:

Case co-authored by TeamGyan Member  Dr. Bhargavi Sovani

Illustrations by Dr Bhargavi Sovani.

 

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