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), and determination of lesion location can be critical if surgical resection is being considered. Each segment has portal veins, hepatic arteries, and bile ducts, and each drains into individual lobar hepatic veins (Table 6-1). The middle hepatic vein divides the liver into right and left lobes. The left lobe is then further subdivided by the left hepatic vein into medial (segment IV—sometimes further subdivided into segments IVa and IVb) and lateral components (segments II and III) (Figs. 6-1 and 6-2). Segments II and III are in turn separated by the left portal vein, with segment II above and segment III below (Figs. 6-1 and 6-2). The right hepatic vein subdivides the right lobe into anterior and posterior segments with the right portal vein further dividing these into upper and lower segments (Figs. 6-1 and 6-2). Segment VIII is upper anterior, segment VII is upper posterior, segment V is lower anterior, and segment VI is lower posterior. Segment I, or the caudate lobe, is posterior.

Figure 6-1 Schematic representation of hepatic Couinaud segments.

Table 6-1

Couinaud Liver Segments

Structure Right Lobe
Middle hepatic vein Divides right and left lobes
Right hepatic vein Separates right lobe into anterior (segments VIII and V) and posterior (segments VII and VI)
Right portal vein Separates right lobe into superior (segments VII and VIII) and inferior (segments V and VI)
Left hepatic vein Divides left lobe into medial (segment IVa and IVb) and lateral (segments II and III)
Left portal vein Separates segment II (above) and segment III (below)
Caudate lobe Segment I (posterior)
Falciform ligament Divides medial and lateral segments of left lobe (segment IV from II and III)
Ligamentum venosum Obliterated umbilical vein: extends from falciform ligament to umbilicus
Figure 6-2 A through D, Axial contrast-enhanced images of hepatic segments. LHV, Left hepatic vein; LPV, left portal vein; RHV, right hepatic vein; RPV, right portal vein.
The liver has a dual blood supply, with approximately 80% supplied from the portal vein and 20% from the hepatic artery, and blood freely circulates into the extravascular spaces. An understanding of this paradigm is important in planning appropriate contrast-enhanced imaging protocols because different diseases have different enhancement characteristics depending on the source of their primary blood supply.

Imaging Methods

All imaging methods, from plain radiograph to positron emission tomography (PET), have a role in hepatic imaging. However, the majority of hepatic abnormalities are not only detected, but also characterized, by means of cross-sectional imaging.

Plain Radiograph and Fluoroscopy

Although infrequently used as a primary imaging tool, the plain radiograph is still useful to assess prosthetic positioning, intrahepatic gas, and occasionally calcification and hepatomegaly. Conventional fluoroscopy is still the primary method of choice for performing most interventional hepatic therapeutic procedures.


Hepatic evaluation by ultrasound (US) is now considered less optimal than CT or magnetic resonance imaging (MRI), particularly in the United States, although the use of Doppler harmonic and US contrast imaging has shown some advantages. However, these are not in wide clinical use. US still has a critical role in the evaluation of cirrhosis and infiltrative disease, some specific liver lesions, and some interventional procedures. US is highly operator dependent and requires extensive training, and perhaps for these reasons CT and MRI have often superseded it in clinical practice, at least in the United States. This should not deter the radiologist from using US in the appropriate setting, however, given that it is less expensive, relatively easily available, and quick, produces no ionizing radiation, and in the right hands, provides substantial opportunities for liver lesion characterization.

Computed Tomography

Multidetector CT (MDCT) is the workhorse for hepatic imaging because of its excellent spatial and contrast resolution, speed, ease of use, reproducibility, use of intravenous (IV) contrast agents, and ability to postprocess images into multiplanar formats (particularly with the newer higher detector arrays). Imaging can be tailored to coincide with maximal parenchymal, lesion, or vascular enhancement after administration of IV contrast agents, depending on the disease in question. CT provides excellent morphologic information about both the disease and its relationship to normal anatomy. Dual-energy hardware offers further opportunity to evaluate and quantify disease. Perhaps because CT is so ubiquitous and clinically useful, some have raised concerns about overuse, mainly because of cost and radiation dose. Whether less expensive and more nonionizing radiation techniques will supersede the current demand for CT remains to be determined.
The density of the unenhanced normal liver at CT typically ranges between 55 and 65 HU. Unenhanced CT is useful for the evaluation of depositional disease (e.g., hepatic steatosis, hemochromatosis), liver calcifications, hemorrhage, and some high-contrast embolic material used for therapeutic procedures. Most patients, however, are imaged after the administration of IV iodinated contrast medium. Because of the dual blood supply to the liver, the liver can be imaged during multiple phases. Early imaging during the arterial phase (typically a scan delay of approximately 20 seconds from the start of IV contrast injection), when most of the hepatic normal parenchyma is not yet enhanced, visualizes the arterial structures and offers the opportunity to evaluate disease that is supplied primarily with an arterial blood supply (Table 6-2 and Fig. 6-3). Maximal opacification of the portal vein occurs at approximately 40 seconds after the initiation of IV injection, and the hepatic parenchyma is subsequently maximally enhanced during the portal or hepatic venous phase, usually at approximately 60 seconds. Most hepatic lesions are hypodense during this phase, in contrast to the relatively hyperdense liver parenchyma (Fig. 6-4). A number of lesions can be further characterized with delayed imaging (either because they retain contrast material or because they are more conspicuous against the normal liver background), usually at approximately 120 to 180 seconds after initiation of the injection (Fig. 6-5). Scan times are optimized through automatic bolus tracking techniques, which trigger scanning to coincide with the optimal arterial or portal venous phase (PVP). A fundamental understanding of these vascular dynamics is required to optimize MDCT scan protocols for the disease in question. Some diseases are best imaged with one phase, some with two phases, or some even with three phases. By the addition of a noncontrast CT, the lesions can potentially be evaluated with four phases, although because of the radiation burden this should be avoided unless clinically necessary.

Table 6-2

Phase of CT Imaging in Hepatic Disease


CT, Computed tomography; FNH, focal nodular hyperplasia; HCC, hepatocellular carcinoma; NCCT, noncontrast CT scan; PVP, portal venous phase.

Figure 6-3 

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