Liver lesions

MRI for liver lesion characterisation - gadolinium preferred

Non-cirrhotic liver

• Cavernous haemangioma
  • Commonest hepatic lesion
    • Generally 30-50yo, F:M 3:1
    • Normal AFP
  • Benign - blood-filled spaces with slowly-moving blood
    • Subtype: giant haemangioma, which can show up with a central scar
    • Sclerosed - occurs after infarction. Capsular retraction, scarring.
    • Haemangiomatosis - rare - diffuse replacement of liver by haemangiomas
  • Features
    • USS
      • Hyperechoic, with no hypoechoic rim
      • No flow on doppler
      • USS contrast agents can be used to clinch the diagnosis
    • CT
      • Noncon: well-demarcated hypodense mass
      • Arterial: discontinuous, nodular peripheral enhancement
      • PV: progressive peripheral enhancement with more centripetal fill-in
      • Delayed: further irregular fill-in, therefore iso or hyper attenuating to liver parenchyma
      • Rim enhancement is NEVER a haemangioma
    • Edge often lobulated
    • Progressive infilling
    • MRI is the best test
      • Very high t2 signal
      • Follows blood pool in terms of contrast signal
• Focal nodular hyperplasia
  • Common, especially in young female adults (9:1 F:M, age 35-50)
  • Very rarely symptomatic
  • Hypoplastic result to vascular insult
  • Characteristic fibrous scar in centre of lesion
  • Findings
    • Central scar - 40-60% - high T2 signal
      • Beware the central scar!!! Not diagnostic of FNH
    • USS - often subtle
    • CT -
      • Noncon: hypo or isodense lesion with hypoattenuating centre
      • Arterial: avid uniform arterial enhancement, except for hypoattenuating central scar
      • PV: no washout (it FADES rather than WASHES OUT - that is, still brighter than normal liver on PV), microlobulated border. Usually slightly brighter than background normal liver in PV phase.
      • Delayed: mostly get enhancement of fibrotic scar
    • Invisible on pre-contrast, avid uniform arterial enhancement, slightly bright on PV, disappeared on late venous.
• Hepatocellular adenoma
  • True monoclonal neoplasms
    • Can progress to HCC
  • Less common than FNH
  • Age 20-40
  • Usually women (F:M 9:1)
  • 80% are single lesions
  • A/w:
    • Rupture
    • Growth in response to oestrogen/testosterone
    • Malignant transformation to HCC
    • Glycogen storage diseases
    • Metabolic syndrome
  • CT
    • Often look identical to FNH
    • Liver-specific contrast is necessary - these are usually dark in primovist phases
    • Noncon: well-demarcated, hypo or isodense lesion
    • Arterial: peripheral enhancement
    • PV: centripetal flow
    • Delayed: iso or hypodense
• Liver mets
  • CT/MRI
    • Rim enhancement on arterial phase, with early washout
    • PV: progressive enhancement of a thickened rind
    • Delayed: usually hypoattenuating (washout), but occasionally have delayed enhancement due to desmoplastic reaction
    • Dark on primovist phases (don't contain hepatocytes to take up the contrast)
    • Central necrosis common
  • Hypervascular mets
    • Neuroendocrine most common
    • RCC
    • Melanoma
    • Thyroid
    • Choriocarcinoma
  • Screening for liver mets - primovist MRI is best
• Intrahepatic cholangiocarcinoma
  • RFs:
    • Cirrhosis
    • HBV
    • HCV
  • CT
    • Noncon: homogenous hypoattenuating mass
    • Arterial: Rim type arterial phase hyperenhancement around a hypodense lesion
    • PV: progressive enhancement with centripetal filling
    • Delayed: iso or hypodense due to abundant fibrosis stroma
    • Capsular reaction
    • Satellite nodules
    • Delayed, cloud-like infilling of central stroma
• Hepatic angiomyolipoma
  • Seen in a/w tuberous sclerosis, or sporadically
• Fibrolamellar HCC
  • Very rare, usually adolescents or young adults, without cirrhosis
  • Large well-defined mass with large scar
  • Arterial enhancement with washout
  • Calcification common
• Epithelioid haemangioendothelioma
  • Multi-focal lesions
  • Geographical
  • Capsular retration
• Hydatid cyst
  • Parasitic infection with tapeworm
  • Hypodense lesion with hyperattenuating wall
  • Detachment of laminated membrane from pericyst can be visualised as linear areas of hyperattenuation
  • Daughter cysts are located peripherally within the mother cyst; they are usually at a lower density than the mother cyst
• Polycystic liver disease
• Biliary cystadenoma and cystadenocarcinoma
• Simple hepatic cysts
  • Homogenous hypoattenuation (0-10HU)
  • Imperceptible wall
  • No internal structures
  • No enhancement after IV contrast

Cirrhotic liver

• HCC
  • Can use LI-RADS to classify risk of HCC
  • CT
    • Non-con: hypodense lesion
    • Arterial: vivid non-rim arterial enhancement
      • But 10% of HCC are hypodense in arterial phase
      • Needs to be late arterial phase - allow enough time for contrast to get there
    • PV: rapid washout to become indistinct/hypodense, with enhancing capsule/pseudocapsule
    • Delayed: isodense with liver
    • Note that non-rim arterial hyperenhancement AND washout in PV phase have 100% specificity in HCC > 2cm, 90% in HCC 1-2cm (assuming the patient has correct pre-test probability of cirrhosis)
• Cirrhotic/regenerative nodules
  • Normal cirrhotic liver
• Macroregenerative lesions
  • Benign