In addition to today’s resource, please review:
How to approach elevated liver enzymes? from the Liver Fellow Network of the American Association For The Study Of Liver Diseases.
Today, I review, link to, and excerpt from StatPearls‘ “Liver Imaging”. Shahrzad Azizaddini; Nisha Mani. Last Update: February 20, 2023.
All that follows is from the above resource.
- Continuing Education Activity
- Introduction
- Anatomy
- Plain Films
- Computed Tomography
- Magnetic Resonance
- Ultrasonography
- Nuclear Medicine
- Angiography
- Patient Positioning
- Clinical Significance
- Review Questions
- References
Introduction
Liver lesions have a broad spectrum of pathologies, ranging from benign lesions such as hemangiomas to malignant lesions such as primary hepatocellular carcinoma and metastasis. Imaging is a crucial step in diagnosing these conditions, as liver enzymes can be elevated in up to 9% of individuals in the USA.[1][2] A combination of medical history, serologic, and radiologic investigations can provide a diagnosis in most cases.[3] Liver lesions can be categorized into focal and diffuse liver lesions.
Focal liver lesions generally fall into 3 main clinical categories.
Diffuse liver lesions can be categorized into vascular, inflammatory, and storage diseases.
Benign liver lesions can be classified into 3 categories based on their tissue origin:
Liver ultrasonography (US), computed tomography (CT), and magnetic resonance imaging (MRI) are the primary imaging modalities to diagnose liver lesions. Postcontrast imaging can help distinguish lesions depending on their degree of vascularity and composition. Postcontrast hepatic imaging falls into 3 distinct phases: the arterial phase, the portal venous phase, and the delayed venous phase.[4] Ultrasound can be a method of choice as a screening modality, and contrast-enhanced multidetector CT (MDCT) is a modality of choice in most hepatic imaging.[5] MRI plays a role in better-characterizing lesions with equivocal features on US and CT.
Anatomy
The most widely used anatomic classification of hepatic segments is the Couinaud classification, which describes 8 functionally independent liver segments based on vascularization, bile duct distribution, and lymphatic drainage.[6] Each segment is wedge-shaped, with the apex directed towards the hepatic hilum with some variability.[7] A single branch of the hepatic artery, portal vein, and bile duct enters through the apex into the hepatic segments. The hepatic vein runs between 2 adjacent segments and drains into the inferior vena cava (IVC). The middle hepatic vein runs from the inferior vena cava to the gallbladder fossa and divides the liver into the right and left lobes.[8] The right hepatic vein divides the right lobe into the anterior and posterior segments, and the falciform ligament divides the left lobe into medial and lateral segments. The portal vein divides segments horizontally into superior and inferior segments. Segment I is the unique caudate lobe, which can receive dual blood supply from the right and left portal vein and drains directly into IVC. Segments II, III, and IV are left hepatic lobe sections. Segments V, VI, VII, and VIII constitute the right lobe hepatic sections.[9]
The hepatic blood supply is from the portal vein (about two-thirds), and the rest is from the hepatic artery; thus, maximum enhancement of the liver is attained during the portal venous phase, which is 60 to 120 seconds after arterial phase enhancement.[10] Tumors supplied from the hepatic artery enhance during the arterial phase, the principle in transarterial chemoembolization and chemoembolization.[11] Arterial embolization and treatment target tumors rather than normal hepatic cells.[12] The hepatic veins enter the inferior vena cava. They can be seen as anechoic tubes with thin walls on ultrasound (see Image. Color Doppler Ultrasound, Hepatic Veins With Hepatic Venous Waveforms). The portal triad, which includes the portal veins, hepatic arteries, and bile ducts surrounded by fibrofatty tissue, can be seen as echogenic foci throughout the liver.[13]
The portal vein forms from the junction of the superior mesenteric artery and splenic veins behind the neck of the pancreas.[14] Inferior mesenteric, gastric, and cystic veins drain into the portal vein. It divides into the right hepatic vein and porta hepatis. Although the portal vein provides 75% of the liver’s blood supply, it provides 50% of its oxygen supply.[15] Portal hypertension or hepatic venous pressure gradient is a portosystemic pressure gradient. Different pathologies can cause portal hypertension, including portal vein thrombosis, cirrhosis, viral hepatitis, Budd-Chiari syndrome, and congestive heart failure.[16] Ultrasound manifestations of portal hypertension are a dilated portal vein (>13 mm), a dilation of the splenic and superior mesenteric veins, the presence of collateral vessels between the portal and systemic pathways, splenomegaly, ascites, and the presence of biphasic or reversed flow (hepatofugal flow) on Doppler US which is diagnostic and pathognomonic for portal hypertension.[17] Portal hypertension can be appreciated in CT and MRI with similar manifestations on ultrasound and the presence of contrast in the paraumbilical vein, which is pathognomonic.
Hepatomegaly and liver cirrhosis are 2 main pathologies that distort the liver anatomy. Cardiac disease, including congestive heart failure, restrictive cardiomyopathy, and right-sided valvular disease, can cause hepatomegaly and dilation of hepatic veins, called passive hepatic congestion.[18] It is due to hepatic venous drainage impairment and stasis of blood in hepatic parenchyma. Ultrasound manifestations of passive hepatic congestion are right hepatic lobe enlargement, inferior vena cava dilatation, and hepatic vein enlargement.[19] Changes in the hepatic vein and IVC velocity pattern can be appreciated in color Doppler ultrasound with loss of normal triphasic flow and flattening of the waveform in hepatic veins.[20] Congestive right heart failure also can cause painless, diffuse wall thickening of the gallbladder.[21][22] The most common etiologies of cirrhosis are alcohol, followed by viral hepatitis, cryptogenic infection, vascular pathologies, and metabolic disorders.[23] The most common ultrasound changes in cirrhosis are a nodular appearance on the surface, heterogeneous echotexture, relative enlargement of the caudate lobe compared to the right lobe, and atrophy of the medial segment of the left lobe. The presence of portal hypertension imaging changes increases the sensitivity and specificity of cirrhosis based on the ultrasound changes, but these usually happen in the advanced and late stages of cirrhosis.[3]
