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Sunday, 2 October 2011

Shoulder Ultrasound

Anatomical review:

1. Patient seated faceing towards you. Arms resting on knees. Hands supinated.

2. AC joint:
 - Acromion and clavicle must be at the same level
 - AC joint space 2-4 mm normaly
 - Looking posteriorly, you can visualize the Supraspinatus muscle

3. Long head of the biceps tendon

Fluid surrounding the biceps tendon within the tendon sheath is a fairly sensitive indicator of glenohumeral pathology, though as this space communicates with the shoulder capsule, such pathology is not necessarily limited to the biceps tendon and may represent a sign of synovitis or adhesive capsulitis.

Medially find the Subscapularis muscle:

4. Subscapularis muscle

The subscapularis tendon is imaged in the same position as the biceps tendon, with the transducer placed more medially. Slight external rotation of the glenohumeral joint is helpful to elongate the tendon and allow more sensitive evaluation for tears. Images obtained during dynamic maneuvers in which the radiologist performs passive internal and external rotation of the shoulder with the elbow flexed 90 degrees helps to assess normal motion of the tendon, and allows further evaluation for tendon tears which will typically become more conspicuous with external rotation. Dislocation of the biceps tendon medially from the bicepital groove, indicative of full thickness tear of the transverse ligament of the supscapularis, may also be inapparent until passive external rotation.

Superiorly finde the supraspinatus muscle:

5. Supraspinatus muscle

These images are obtained in the modified Crass position, in which the patient extends and externally rotates the glenohumeral joint by placing the palm of his or her hand on the posterior aspect of the ipsilateral iliac wing and projects the flexed elbow joint posteriorly. This allows better visualization of the supraspinatus tendon, as in this position it will extend lateral to the acromion. Rotator cuff tears occur most commonly in this tendon, and are usually seen as hypoechoic defects in the contour of the tendon. Partial thickness tears can involve either the superficial (bursal) or deep (articular) surfaces of the tendon, and may be seen as either a mixed hypo- and hyperechoic focus or a solely hypoechoic focus extending to either tendon surface. Tears usually occur in the region of the critical zone, an area of relative avascularity within the tendon approximately 1 cm proximal to its insertion.

6. Infraspinatus muscle

Place the transducer over the posterior aspect of the glenohumeral joint with the arm in
the same position described at point-2 (or with the hand on the opposite shoulder) and
increase the depth to include the structures of the posterior fossa within the field-of-view
of the US image. Use the spine of the scapula as the landmark to distinguish the
supraspinous fossa (transducer shifted-up) from the infraspinous fossa (transducer
shifted-down) on sagittal planes.

Monday, 5 September 2011

Chest imaging sings

air bronchogram - indicates a parenchymal process, including non-obstructive

    atelectasis, as distinguished from pleural or mediastinal processes 
  • air crescent sign - indicates a lung cavity, often due to fungal infection 
  • deep sulcus sign on a supine radiograph - indicates pneumothorax  
  • continuous diaphragm sign - indicates pneumomediastinum 
  • ring around the artery sign (around pulmonary artery on lateral chest radiograph) 
    - indicates pneumomediastinum 
  • fallen lung sign - indicates a fractured bronchus 
  • flat waist sign- indicates left lower lobe collapse 
  • gloved finger sign - indicates bronchial impaction, which can be seen in allergic 
    bronchopulmonary aspergillosis 
  • Golden S sign - indicates lobar collapse with a central mass, suggesting an 
    obstructing bronchogenic carcinoma in an adult 
  • luftsichel sign - indicates upper lobe collapse, potentially due to an obstructing 
    bronchogenic carcinoma in an adult 
  • Hampton's hump - indicates a pulmonary infarct 
  • silhouette sign - loss of the contour of the heart or diaphragm used to localize a 
    parenchymal process (e.g. a process involving the medial segment of the right 
    middle lobe obscures the right heart border; a lingula process obscures the left 
    heart border; a basilar segmental lower lobe process obscures the diaphragm) 
  • cervicothoracic sign - a mediastinal opacity that projects above the clavicles is 
    retrotracheal and posteriorly situated while an opacity effaced along its superior 
    aspect and projecting at or below the clavicles is situated anteriorly  
  • tapered margins sign - a lesion in the chest wall, mediastinum or pleura will have 
    smooth tapered borders and obtuse angles with the chest wall or mediastinum 
    while parenchymal lesions usually form acute angles 
  • figure 3 sign - abnormal contour of the descending aorta, indicating coarctation 
    of the aorta 
  • fat pad sign or sandwich sign - indicates pericardial effusion on lateral chest 
  • scimitar sign - an abnormal pulmonary vein in venolobar syndrome 
  • double density sign - contour projecting over the right side of the heart, 
    indicating enlargement of the left atrium 
  • hilum overlay sign and hilum convergence sign -used to distinguish a hilar mass 
    from a non-hilar mass
Chest CT:
  • CT angiogram sign -  enhancing pulmonary vessels against a background of low 
    attenuation material in the lung 
  • halo sign -  suggesting invasive pulmonary aspergillosis in a leukemic patient 
  • split pleura sign - a sign of empyema


Monday, 15 August 2011


An anatomic map of metastatic pathways


Some of the most common cancer types, including breast cancer, prostate cancer, and lung cancer, show a predilection to metastasize to bone.

Effects of bone metastasis:
severe pain, bone fractures, spinal cord compression, hypercalcemia, anemia, spinal instability, decreased mobility.


- Renal cell
- Thyroid
- Multiple myeloma
- Breast


- Prostate
- Breast
- Colonic carcinoma
- Melanoma
- Bladder carcinoma
- Soft-tissue sarcoma.

The findings of sclerotic metastases virtually exclude an untreated renal tumor or hepatocellular carcinoma.

Bone metastases may be osteolytic, sclerotic, or mixed on radiographs. Lesions usually appear in the medullary cavity, spread to destroy the medullary bone, and then involve the cortex. Osteolytic metastases are encountered most frequently, especially in breast and lung carcinomas . The specific appearance of bone metastases is often useful in suggesting the nature of the underlying primary malignancy.

Metastases from certain primary sites (eg, renal cell or thyroid carcinomas) are almost always osteolytic, whereas those from other sites (eg, prostatic carcinoma) are predominantly sclerotic.
Other malignancies associated with sclerotic metastases include breast carcinoma, colonic carcinoma, melanoma, bladder carcinoma, and soft-tissue sarcoma. The findings of sclerotic metastases virtually exclude an untreated renal tumor or hepatocellular carcinoma.

In vertebrae, clues to metastatic involvement include pedicular destruction, an associated soft-tissue mass, and an angular or irregular deformity of the vertebral endplates.

Healing process:
The initial manifestation of healing in an osteolytic metastatic lesion is a sclerotic rim of reactive bone. With progressive healing, sclerosis increases and advances from periphery of the lesion to its center: The lesion shrinks and eventually resolves. For a mixed osteolytic-sclerotic lesion, a healing response to therapy is demonstrated as uniform lesional sclerosis, whereas increasing osteolysis indicates disease progression.

Purely sclerotic lesions are more difficult to assess. A sclerotic lesion that shrinks or completely disappears after therapy signifies disease regression, whereas one that grows and causes destruction implies progression.

Osteolytic metastases can mimic osteoarthritis both clinically and radiographically; for example, they can mimic subchondral cysts and Schmorl nodes in the spine. Osteolytic foci may resemble amyloidosis, cystic angiomatosis, and infiltrative bone marrow lesions.
metastases may be difficult to distinguish from other sclerotic bone lesions such as bone islands, tuberous sclerosis, mastocytosis, and osteopoikilosis.

Role of nuclear medicine:

Technetium-99m (99m Tc) bone scintiscanning (ie, radionuclide bone scanning) is widely regarded as the most cost-effective and available whole-body screening test for the assessment of bone metastases. Conventional radiography is the best modality for characterizing lesions that are depicted on bone scintiscans. Combined analysis and reporting of findings on radiographs and99m Tc bone scintiscans improve the diagnostic accuracy in detecting bone metastases and assessing the response to therapy.

Indications for bone scintiscanning include staging in asymptomatic patients, evaluating persistent pain in the presence of equivocal or negative radiographic findings, determining the extent of bone metastases in patients with positive radiograph findings, differentiating metastatic from traumatic fractures by assessing the pattern of involvement, and determining the therapeutic response to metastases.

PET scanning can help in identifying bone metastases at an early stage of growth, before host reactions to the osteoblasts occur. FDG-PET scanning depicts early malignant bone-marrow infiltration because of the early increased glucose metabolism in neoplastic cells.

Isotopic imaging methods depict bone metastatic lesions as areas of increased tracer uptake. The classic pattern appears as the presence of multiple randomly distributed focal lesions throughout the skeleton. Findings of a solitary scintigraphic abnormality or just a few lesions may present special problems in the interpretation of findings.

The differential diagnosis of multiple scintigraphic abnormalities includes metabolic problems (eg, Cushing syndrome), osteomalacia, trauma, arthritis, osteomyelitis, Paget disease, and infarctions. Some metastases may produce normal scintiscan findings. Cold or photopenic metastases may be found in association with lesions of highly aggressive anaplastic carcinomas. In diffuse metastatic disease, isotopic accumulation may be sufficiently uniform to produce a false-negative impression.


Monday, 25 July 2011

The Knee Joint

The knee joint is a hinge-type joint, which is capable of flexion and extension motions. Flexion and extension are not the only motions of the knee, it has been discovered that the knee performs slight rotational movement. It is this rotational component that accounts for the frequency of knee injuries. The distal femur articulates with the tibia and the patella. The distal femur is broadly adapted for articulation with the tibia. The articulation with the tibia is through its large prominent condyles that project posteriorly. A large intercondylar notch seen posteriorly separates the medial and lateral condyles of the femur. On the anterior surface the condyles are separated by a slight groove called the patellar surface over which the patella (kneecap) glides during flexion and extension of the knee joint. The patella is a sesamoid bone developed within the tendon of the quadriceps femoris tendon. The patella is triangular shaped having a broad base and an inferiorly pointed apex. The articular surfaces on the posterior aspect of the patella articulate with the medial and lateral condyles of the femur. The two primary functions of the patella are to strengthen the tendon of the quadriceps femoris muscle, and to protect the knee joint. The patella strengthens the quadriceps muscle by increasing its leverage as it extends (straightens) the knee joint. Essentially, the role of the patella is to aid in changing the direction of forces from the quadriceps muscle as they pass through the knee joint and are applied to the tibia.

Soft tissue injury can manifest as swelling about the knee, inability to bear weight, loss of function such as bending or straightening of the joint, or other clinical indicators. Radiographically, soft tissue surrounding the knee must be demonstrated when imaging for trauma. Fractures that involve the upper fourth of the tibia, may or may not involve the knee joint, and may be limited to ligaments supporting the joint. Fractures that enter the knee joint often render the joint defective and the once smooth joint surface made irregular. Additionally, fractures resulting in improper limb alignment may contribute to long-term morbidity like arthritis, instability, and functional loss of motion.

The proximal fibula also contributes to lateral stability of the knee joint by providing supportive attachment for the lateral collateral ligament of the knee. Ligaments within the knee joint also support the knee. These ligaments may be injured with trauma sparing bone.

The stabilizing ligaments of the knee include the medial collateral ligament (MCL) and lateral collateral ligament (LCL), and are located outside the knee joint proper; the anterior cruciate ligament (ACL) and posterior cruciate ligament (PCL) are stabilizer ligaments located within the knee joint. The patellar ligament is located outside the knee joint; it also provides support for the knee by shielding it, and strengthening the actions of the quadriceps femoris muscle. Because the patella is integrated into the extensor knee apparatus it contains both passive and active elements. The patellar ligament is one of the passive elements of the knee. It originates at the apex of the patella and extends to the tibial tuberosity. The role of the patellar ligament is to limit proximal patellar ascent.

The knee contains two semi-lunar C-shaped menisci composed of fibrocartilage. The two menisci lie on the tibial plateaus along the lateral peripheries of the joint. The function of the meniscus is to provide shock absorption to the knee during the stress of weight-bearing and movement. The youthful healthy meniscus is only partially supplied with blood and is stronger than older cartilage. With age the meniscus deteriorates and can easily tear. A damaged torn meniscus can seed torn pieces into the joint (meniscal fragment) causing pain, swelling, and loss of function. The reason meniscal fragments are released is that the majority of the meniscus has no blood supply and does not properly heal when damaged. Instead, deteriorated portions of the meniscus tend to tear off and enter the joint space between the bones. A surgical procedure called arthroscopic surgery may be indicated to remove some types meniscal fragments or flaps.

Other soft tissue structures that are critical to proper knee function include the medial collateral ligament (MCL), lateral collateral ligament (LCL), anterior cruciate ligament (ACL), posterior cruciate ligament (PCL), articular cartilage, joint capsule and synovial fluid, and bursa. The collateral ligaments resist widening of the knee joint. The cruciate ligaments, which are within the knee joint proper, resist hyperflexion and hyper extension and also slight rotational movements of the knee. Articular cartilage is bathed by synovial fluid that lubricates the knee joint.

There are two collateral ligaments of the knee, the medial collateral ligament (MCL) and lateral collateral ligament (LCL). The MCL spans from the medial femoral condyle to the top of the lateral tibia (shin bone) and had multidirectional fibers on the inside of the knee joint too. The medial collateral ligament resists medial widening of the joint that would 'open-up' the knee. The LCL spans from the lateral condyle of the femur to the lateral portions of the fibula. Its main function is to resist lateral widening of the knee joint.

The anterior and posterior cruciate ligaments are located within the center of the knee joint. The PCL originates in a fan-shaped fashion from the anterolateral aspect of the medial femoral condyle near the intercondylar notch. It courses posteroinferomedially to insert on the backside of the tibial plateau. It functions to reduce internal rotational movements of the knee, and to prevent the tibia from sliding backwards on the femur. In other words, the PCL prevents hyperflexion of the knee joint. The ACL arises from the posterior part of the medial surface of the lateral condyle and courses anteroinferiorly and medially to the anterior plateau just posterior to a rather prominent synovial fold. It then inserts in a fossa in front of and lateral to the anterior intercondylar eminence of the tibia. It should be noted that the ACL lies within an intra-articular compartment of the knee joint, but is extrasynovial. The functions of the anterior cruciate ligament are to resist rotational motion of the knee and prevent the femur from translating backwards on the tibia. In other words, it limits hyperflexion of the knee joint. The most common mechanism of ACL injury is internal rotation of the femur when the knee is in full extension. A damaged ACL or PCL will result in instability of the knee when the foot is planted causing the knee to give way or to buckle.

Synovial joints are found where there is extensive movement of bone on bone such as the femur and tibia of the knee. Synovial joints are also classified as diarthroses, or freely movable joints. At the point of bone articulation there is a thin covering of hyaline cartilage covering the ends of bone called articular cartilage. This cartilage is maintained in apposition by ligaments of the knee and the surrounding joint capsule. Articular cartilage of the knee is found on the articular surfaces of the femur, tibia, and underside of the patella. Articular cartilage is void of blood vessels (avascular) and depends on diffusion of nutrients from synovial fluid that bathes it. The capsule of the knee joint is a sac that encloses the joint cavity. It is perhaps better thought of as a cavity rather a simple membrane. It completely surrounds the knee joint having compartments that surround the patella and the knee joint. The capsule is firmly attached to bone and is composed of a tough fibrous outer membrane and an inner synovial membrane. It is the inner layer of the synovial membrane that produces synovial fluid that bathes structures within the knee joint proper. Four bursa are found in the knee are found near tendons to provide smoothening of motions of their muscles. Like all bursa those of the knee are also subject to inflammation (bursitis) and to inflammatory reaction from trauma.



Sunday, 3 July 2011

Contrast enhanced ultrasound - CEUS

Second-generation” blood pool ultrasonographic (US) contrast media are filled with gases other than air and allow continuous real-time assessment of liver lesions at low acoustic pressure (low mechanical index).

Older Air-filled agents (first-generation US contrast media), on the other hand, can be used only with high-mechanical-index intermittent technologies because micro-bubble rupture is necessary to obtain an adequate echo signal.

1- The arterial (early) phase (15–35 seconds after injection),
2- the portal (venous) phase (35–90 seconds),
3- the sinusoidal (parenchymal or late vascular) phase (90–240 seconds).

What do we see afte injection?
Contrast medium is seen arriving in the hepatic artery and rapidly spreading through its branches. Liver parenchymal echogenicity increases consistently from the arterial to the portal phase and then decreases slightly during the sinusoidal phase. Enhancement of the branches of the hepatic artery and portal vein is readily visualized, without flow signals “bleeding” outside the vessel lumina (as happens with Doppler US). Cirrhotic liver may exhibit slightly delayed and less intense parenchymal enhancement during the portal phase.

How to describe what we see?
Echogenicity is defined with respect to the surrounding parenchymal echo levels at the same imaging time and depth. In addition, lesions can be compared with the blood pool, being hypervascular when demonstrating the same echogenicity as contrast material–enhanced vessels and hypovascular when demonstrating a lower echogenicity.


Lesion conspicuity depends on the lesion-to-parenchyma echogenicity gradient; in this case, HCC has greater conspicuity during the arterial phase and appears hyperechoic. During the portal and sinusoidal phases, the lesion is first slightly and then clearly hypoechoic relative to the surrounding parenchyma.

Enhancement may be absent (eg, cyst, small hemangioma, dysplastic nodule, or early HCC) or
may be diffuse homogeneous or diffuse heterogeneous (eg, hypervascular metastasis or atypical CCC, lymphoma, FNH).
Rim pattern manifests as peripheral, irregular but continuous arterial phase enhancement (eg, metastasis, CCC).
The globular pattern consists of discontinuous peripheral arterial phase enhancement with discrete echoic globules (eg, cavernous hemangioma). The spokelike pattern seen during the arterial phase is due to discrete arteries radiating to the periphery (eg, FNH).
The stippled pattern seen during this phase consists of discrete arteries with a chaotic distribution (eg, HCC).
The arterial phase “basket” pattern, usually seen in combination with a stippled appearance, consists of a feeding artery branching around and then within a nodule (eg, HCC).

The liver-enhancing effect of the blood pool contrast agent SonoVue (Bracco, Milan, Italy) lasts 3–5 minutes; more than 5 minutes after contrast material injection, most lesions become undetectable or have the same echogenicity as on baseline images.

Imaging techniques:
Can be divided into two main groups:(a) high-mechanical-index modalities, which allow static, intermittent imaging, and (b) low-mechanical-index modalities, which allow dynamic, continuous acquisition and require second-generation contrast media.

SonoVue: A sulfur hexafluoride–based contrast medium. This agent comes as a sterile, nonpyrogenic, lyophilized powder. A white milky suspension is obtained by adding 5 mL of 0.9% normal saline solution with an aseptic technique and vigorously shaking the mixture for 10 seconds. The reconstituted product provides 8 μL/mL of SF6 micro-bubbles, which is then administered either in its entirety (4.8 mL) or as a half dose (2.4 mL). The half dose is usually sufficient, but injecting the entire volume may be desirable in cases of liver steatosis or chronic hepatitis.

It is usually administered as a single rapid bolus injection into an antecubital vein. US is started immediately and lasts 4–5 minutes.



Liver hemangioma is a hypervascular lesion consisting of a network of vascular spaces with slow or, less commonly, rapid flow. The distribution of small arterial branches, venous lakes, and fibrosis varies. Arterial inflow is present, whereas portal afference is absent or minimal, and there is no arteriovenous fistula.

Small (<1-cm) hemangiomas are usually iso-vascular relative to the surrounding parenchyma during the arterial phase. Less commonly, a subtle, diffuse enhancement (homogeneous or heterogeneous) is seen. Larger hemangiomas (>1 cm) usually demonstrate peripheral globular pooling of contrast medium, with hyperechoic globules (nodules) becoming progressively larger and more numerous (puddle enhancement). Contrast material uptake can be fast or slow depending on intralesional circulation speed. Uncommonly, contrast material enhancement is rapid and homogeneous, simulating that of hypervascular metastases. Rarely, peripheral rimlike enhancement or diffuse homogeneous enhancement is seen (small, hypervascular hemangioma). Discrete intralesional arteries are usually not seen in hemangiomas.

(a) Baseline US image shows two homogeneously hyperechoic lesions (arrowheads) contiguous with a portal branch (arrow).

Early portal phase US image obtained 35 seconds after contrast material injection demonstrates lesion isoechogenicity. Arrow indicates an enhanced vein.

(c) Parenchymal phase US image obtained 121 seconds after injection demonstrates persistent lesion isoechogenicity.


(a) Baseline US image shows a heterogeneously hypoechoic lesion (arrow).

(b) Arterial phase US image obtained 22 seconds after contrast material injection demonstrates peripheral globular enhancement (large arrow) and a perilesional vessel (small arrow).

(c) Portal phase US image obtained 93 seconds after injection demonstrates centripetal (albeit incomplete) lesion enhancement (large arrow), which is clearly hyperechoic relative to the surrounding parenchyma. Small arrow indicates the perilesional vessel.

(d) Portal phase computed tomographic (CT) scan shows a hyperattenuating lesion with small central areas of poor enhancement (arrow).

Isovascularity persists throughout the portal and sinusoidal phases in small hemangiomas. In contrast, larger hemangiomas show progressive centripetal enlargement of peripheral hyperechoic globules with progressive filling. As the globules enlarge, they create “bridges” to the opposite side of the lesion. Centripetal filling may be absent in smaller lesions, but real-time images usually allow identification of this finding even in small, rapidly enhancing hemangiomas. Persistent strong intralesional enhancement (hyperechogenicity) is typical, although a central area or sac of persistent poor enhancement due to fibrosis may be seen in larger hemangiomas; owing to the blood pool nature of US contrast media, incomplete centripetal filling is more common at US than at CT or magnetic resonance (MR) imaging. Rarely, hemangioma shows heterogeneous hypoechogenicity (thrombosis)

Early portal phase US image obtained 43 seconds after contrast material injection shows multiple peripheral enhancing globules (large arrows) and thin enhancing septa centrally (small arrows). Although most of the lesion is hypoechoic, and was even on delayed images (not shown), the globular pattern allowed characterization.



Adenoma is a hypervascular lesion without portal tracts. Large, subcapsular tributary arteries are typical, whereas necrotic and hemorrhagic changes are frequently seen in larger masses.

Intense, rapid or slow contrast material enhancement is seen during the arterial phase. Discrete, perilesional feeding arteries manifest as enhancement around the tumor capsule; such enhancement is never seen in HCC. Heterogeneous enhancement with perfusion defects corresponding to hemorrhagic areas is present in larger masses.

More or less rapid washout is seen during the portal and sinusoidal phases, with initial hypervascularity followed by isovascularity; a hypoechoic appearance is never seen. A heterogeneous texture is seen in larger masses, with internal hypoechoic regions.

(a) Baseline US image shows a subtle hyperechoic area (arrow).

(b) Arterial phase US image obtained 21 seconds after contrast material injection demonstrates early, marked lesion enhancement (arrow). K = kidney.

(c) Portal phase US image obtained 55 seconds after injection demonstrates subtle but persistent enhancement (arrow). K = kidney.


Focal Nodular Hyperplasia - FNH

FNH is a hypervascular, hyperplastic lesion caused by preexisting vascular malformation. Patients are typically women with a history of oral contraception. FNH is not seen in patients with cirrhosis. There is usually a peripheral pseudo-capsule and a central or eccentric fibrous scar radiating to the periphery and containing arteries.

During the arterial phase, FNH manifests as a tortuous feeding artery and a central artery with very early centrifugal stellate branching (“wheel spoke” or “central spider” pattern). Immediately thereafter, during the full arterial phase, the lesion demonstrates homogeneous, intense, and very rapid contrast material enhancement. A hypoechoic central scar may be present.

(a) Baseline US image shows a slightly hypoechoic lesion (arrows).

(b) Very early arterial phase US image obtained 15 seconds after contrast material injection demonstrates rapid lesion enhancement (arrows) with discrete intralesional and perilesional arteries.

(c) Later arterial phase US image obtained 29 seconds after injection demonstrates marked homogeneous lesion enhancement (arrows).

(d) Portal phase US image obtained 49 seconds after injection demonstrates lesion isoechogenicity (arrows).

During the portal and sinusoidal phases, there is slow or, less commonly, rapid washout, with initial hypervascularity followed by isovascularity (isoechoic or hyperechoic appearance). A homogeneous texture with possible central stellate hypoechogenicity is characteristic.


(a) Baseline US image shows a homogeneous, well-defined mass (arrows) depending from the right hepatic lobe.

(b) Arterial phase US image obtained 22 seconds after contrast material injection demonstrates multiple radiating arteries within the mass (arrows).

(c) Portal phase US image obtained 56 seconds after injection demonstrates marked enhancement of the mass (white arrows), with a hypoechoic central scar (black arrow).

(d) Late arterial phase CT scan shows a markedly enhancing mass (white arrows) with central scarring (black arrow) (cf c).

The overall appearance of FNH usually allows differentiation from fibrolamellar HCC, an uncommon lesion that also contains a central scar. Fibrolamellar HCC is usually heterogeneous because of necrosis, shows internal calcification, and is hypoechoic on portal phase images.


Dysplastic Nodules and Early HCC

Dysplastic nodules are premalignant lesions within a cirrhotic liver that develop small arteries and exhibit portal tracts. Early HCC is usually a small, well-differentiated nodule with increased arterialization and gradual loss of portal vessels.

During the arterial phase, dysplastic nodules and early HCC are usually substantially isovascular with no arterial enhancement. Nevertheless, high-grade dysplastic nodules can sometimes demonstrate marked enhancement.

Dysplastic nodules and early HCC have an isoechoic or subtly hypoechogenic appearance throughout the portal and sinusoidal phases.

(a) Baseline US image shows a small, hypoechoic nodule (arrow).

(b) Arterial phase US image obtained 25 seconds after contrast material injection fails to depict any lesion.


Advanced HCC

Small to medium-sized HCC (1–5 cm) is a hypervascular lesion, with neoangiogenesis. There is little or no portal supply.
In arterial phase, advanced HCC demonstrates hyperperfusion starting immediately after enhancement of the hepatic artery. Smaller HCCs usually enhance slightly faster than larger ones.

(nem másoltam ki a képeket)

One or more hypertrophic feeding arteries are seen reaching lesion poles and branching intralesionally (basket pattern).

Discrete peri- and intranodular vessels are also recognizable at US, usually being dysmorphic, chaotic, and randomly stippled and having a corkscrew-shaped distribution.

Uncommon hypovascular HCC demonstrates isoperfusion or even hypoperfusion relative to the surrounding parenchyma and hence is difficult to characterize.

Areas of fatty degeneration with increased echogenicity, within the HCC do not show enhancement. Large lesions (“big” HCC) demonstrate peripheral enhancement, central hypovascular necrotic areas, and vascular lakes with hyperechoic contrast agent pooling.

During the portal and sinusoidal phases, advanced HCC demonstrates rapid washout (faster than with FNH or adenoma) and has an isovascular or, less commonly, hypovascular appearance. Transient isoechogenicity is seen on full portal phase images, eventually followed by moderate hypoechogenicity on delayed images.


Cholangiocellular Carcinoma

CCC can be hypovascular or, less commonly, hypervascular on arterial phase images, with portal phase vascularity usually being limited.

CCC demonstrates peripheral rimlike enhancement or heterogeneous enhancement during the arterial phase. Poor heterogeneous enhancement is possible, with an overall isoechoic or hypoechoic appearance.

CCC usually has a hypoechoic appearance on portal and sinusoidal phase images. Persistent subtle rim enhancement is possible. Conspicuity increases progressively, and necrotic areas with more marked hypoechogenicity may be seen. Satellite lesions may also be encountered.



Liver metastasis can be hypo- or, less commonly, hypervascular on arterial phase images depending on the organ of origin. All metastases show some degree of arterial neoangiogenesis (peripheral macrovessels and central microvessels) and lack at least a portion of the portal supply.

During the arterial phase, liver metastasis shows peripheral rimlike enhancement of varying thickness and uniformity, with an eventual target-like appearance.

There is always some kind of arterial inflow peripherally, even if subtle and heterogeneous, whereas most of the lesion is isoechoic relative to the surrounding parenchyma. Perilesional hyperemia with arterial phase–dependent enhancement of normal tissue is possible, and few discrete perilesional arteries can be found. Macroscopic arteries are usually not seen within the lesion.

There is no centripetal filling during the portal and sinusoidal phases. Subtle rim enhancement may persist. Washout is rapid; lesions are seen as filling defects that progressively increase in conspicuity relative to normal parenchymal enhancement (black holes on a bright background).

Metastases have a heterogeneously hypoechoic appearance with internal echo pollution due to microbubbles and haphazard movement within abnormal small tumor vessels (microcirculation).

Markedly hypoechoic areas within larger lesions are due to necrosis. Less commonly, hypervascular metastases may become isoechoic (undetectable) during this phase.



Primary and secondary liver lymphomas are hypercellular lesions with some degree of arterial neoangiogenesis and a poor portal supply.

Like metastasis, lymphoma demonstrates peripheral rimlike enhancement of varying thickness and uniformity during the arterial phase, with an eventual targetlike appearance. Intense, diffuse heterogeneous enhancement is rarely noted.

Like metastasis, lymphoma demonstrates no centripetal filling during the portal and sinusoidal phase. Washout is rapid, and lymphoma has a heterogeneous hypoechoic appearance with internal echo pollution (microcirculation) that progressively increases in conspicuity.



Pyogenic and amoebic liver abscesses have a variable degree of liquefaction and loculation. Their vascularity depends on the evolution stage.

Liver abscesses, especially pyogenic abscesses, have an overall coalescent appearance with a sharply defined necrotic cavity. Rim enhancement is typical. Discrete arteries are noted running along lesion margins and internal septa, with persistent enhancement of the septa. Internal enhancement is absent, and there is no microcirculation within fluid or necrotic components. Perilesional hyperemia with arterial phase–dependent enhancement of normal tissue can be seen.

During the portal and sinusoidal phases, abscesses demonstrate rapid (or sometimes slower) washout, an overall hypoechoic appearance, and marked necrotic and fluid areas internally.


Peliosis Hepatis

Peliosis hepatis is characterized by multiple blood-filled spaces ranging from 1 mm to 4–5 cm within the hepatic parenchyma.

During the arterial phase, peliosis hepatis shows a transient “fast surge” central echo enhancement that is synchronous with vessel enhancement.

During the portal and sinusoidal phases, peliosis hepatis demonstrates isoechogenicity or hypoechogenicity with no contrast material pooling or centripetal filling, allowing differentiation of this entity from hemangiomatosis.


Focal Steatosis

Focal areas of fatty infiltration may have a round, lesionlike appearance and are hyperechoic on conventional US images. Vascularity is normal.

During the arterial phase, focal steatosis demonstrates substantial isovascularity but no arterial enhancement, with normal vessels traversing the pseudolesion without mass effect.

Isovascularity persists during the portal and sinusoidal phases, with normal vessels still traversing the pseudolesion without mass effect.


Skip Area in Fatty Liver

Focal regions of spared normal parenchyma within a heterogeneously distributed steatosis may have a round, pseudolesional appearance and are hypoechoic at baseline US. The vascularity of these spared areas is normal.


Contrast-enhanced US has an 89% sensitivity and a 100% specificity in the diagnosis of hemangioma. The capability of this modality to characterize hemangiomas is approximately equal to that of MR imaging, even in small lesions. Peripheral globular enhancement with centripetal filling indicates a hemangioma, even if central enhancement is subtle or absent on portal and sinusoidal phase images. Centripetal filling is not seen in malignancies. Peripheral enhancement followed by centripetal enhancement has a 100% specificity but only an 18% sensitivity for hemangioma. Globular peripheral enhancement is found in 70%–92% of hemangiomas, rimlike peripheral enhancement in 10%–25%, and diffuse homogeneous enhancement in 5% . Peripheral nodular enhancement with contrast material filling and absence of intralesional arteries has showed an 88% sensitivity and a 99% specificity for hemangioma. Peripheral or diffuse contrast material pooling is typical for hemangioma, with a 76.5% sensitivity and a 100% specificity.

Contrast-enhanced US has a 94% sensitivity and a 93% specificity in the diagnosis of HCC and has proved sensitive in demonstrating HCC vascularity. In one series, contrast-enhanced US demonstrated vascularity in 91% of HCC nodules, CT in 93%, and angiography in 88%. Contrast-enhanced US is more sensitive than Doppler US in this setting. In one study, color Doppler US demonstrated blood flow in 87% of HCC nodules that were hypervascular at contrast-enhanced US; in another series, power Doppler US demonstrated vascularity in 69% of HCC nodules that were identified at angiography-assisted CT, whereas contrast-enhanced US showed vascularity in 96%.

HCC is typically hypervascular on arterial phase images but never exhibits rim or globular enhancement. Enhancement is homogeneous in 50% of cases and heterogeneous in 50%. Diffuse lesion enhancement on early arterial phase images indicates HCC, especially when followed by rapid washout. If a diffuse or mosaic-like arterial phase enhancement pattern or a reticular parenchymal phase enhancement pattern is regarded as indicating HCC, contrast-enhanced US has a 92% sensitivity and a 96% specificity for this entity. The presence of intratumoral vessels on arterial phase images combined with homogeneous or heterogeneous enhancement on portal phase images has a 95% sensitivity and a 94% specificity for HCC. The presence of arteries spreading into the lesion together with homogeneous hyperechoic tumor enhancement has an 83% sensitivity and a 94% specificity for HCC.

Arterial phase enhancement with slow deenhancement suggests adenoma or FNH instead of HCC. HCC and FNH can be distinguished on the basis of several distinctive morphologic features. FNH is homogeneous, even when large, whereas HCC tends to develop necrotic areas. Moreover, FNH is usually hyperechoic during the portal phase of enhancement, whereas HCC becomes iso- or hypoechoic. Central stellate enhancement has a specificity of 100% but a sensitivity of only 67% for FNH.

Contrast-enhanced US has a sensitivity of 77% and a specificity of 93% in the diagnosis of metastases. This modality is more sensitive than conventional US in detecting liver metastasis and almost as sensitive as CT or MR imaging. In one series, conventional US helped detect 59% of liver metastases seen at CT, whereas contrast-enhanced US helped detect 97%. In another study, the number of lesions detected rose from nine to 19 when contrast-enhanced US was used in addition to conventional US; contrast-enhanced US in particular allowed detection of small metastases. Contrast-enhanced US has been shown to help detect 90% of liver metastases that are visualized at ferumoxides-enhanced MR imaging.

Peripheral rim enhancement strongly suggests metastasis, especially if it is not followed by lesion filling and is not combined with a finding of intralesional vessels. Rim enhancement has been observed in 48%–70% of liver metastases. Rim enhancement, a clear parenchymal phase defect, or both can be used to diagnose metastasis or CCC with a 90% sensitivity and a 95% specificity. Of course, hypervascular metastases overlap with other benign and especially malignant hypervascular lesions, although general context and a clearly hypoechoic appearance during the portal phase generally allow differentiation.

Aside from its arterial phase appearance, a homogeneously hypoechoic lesion on portal or sinusoidal phase images should be considered malignant until proved otherwise, since benign lesions are iso- or hyperechoic during these phases. A clearly hypoechoic lesion on portal or sinusoidal phase images is usually considered to represent metastasis. The differential diagnosis of enhancement defects includes lesions such as lymphoma, CCC, HCC, dysplastic nodules in chronic liver disease (rarely), and abscess. The constellation of contrast-enhanced US findings in pyogenic abscess has been shown to be effective in differentiating this benign entity from metastasis.

In itself, the arrival time of contrast medium cannot be used to distinguish between benign and malignant lesions; early arrival is only 67% sensitive and 60% specific for malignancy.