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РАДИОЛОГИЧЕСКАЯ БИБЛИОТЕКА

14.01.2011 КТ брюшной полости

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Интересные контрастируемые

Интересные контрастируемые "островки" в печени. Может это что-то связанное с артериями печени? Может мальформация какая. Хотя не похоже.

А что там по анализам?

 
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"Островки" такие часто бывают

"Островки" такие часто бывают при циррозах- вроде-бы связаны с "непортальным" кровотоком. Архитектоника сосудов там без грубых изменений.

Немного смущает вот это место (при опухолях тоже могут быть такие яркие  "хвосты" к периферии ,  но вроде в артериальную фазу оно тоже гиподенсивное (очаговый стеатоз?).

Хотелось бы крупно одно место рядом во все фазы :убедиться, что нет накопления, проходит ли через него артерия маленькая в первую фазу?

 Если сомнения остаются- можно порекомендовать кровь на онкомаркеры (кажется, эти пациенты с установленным циррозом и  так должны сдавать их периодически), но вообще-то на ГЦР (на фоне цирроза) не похоже.

А что конкретно не нравится "автору" исследования (если смотреть на рабочей станции)?

 

 
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ITA - опередила! По участкам

ITA - опередила! По участкам контрастирования в артериальную фазу - согласен, такое бывает при циррозах за счет особенности кровотока.
По поводу обозначенного выше очага - если на артериальной фазе там есть накопление, других вариантов кроме как ГЦР нет. Если в артериальную нет накопления - может быть регенеративный/диспластический узел.
Важно! При исследовании таких пациентов, не надо жалеть контраста (2 мл на 1 кг веса), можно запросто пропустить накопление в маленьком узле ГЦР в артериальную фазу. 

 

CT Imaging in Liver Cirrhosis:

 

Imaging studies, including ultrasonography, CT, and MRI, are used to assess liver size, the biliary tree, patency of hepatic vasculature, and sequelae of portal hypertension (e.g., ascites, varices, and splenomegaly) and to screen for HCC. Although the portosystemic pressure gradient may be directly measured via transjugular cannulation of the hepatic veins, this is invasive and often unnecessary because portal hypertension can be inferred by endoscopic findings of varices and sequelae of portal hypertension seen on imaging.

On cross-sectional imaging, the cirrhotic liver may demonstrate a nodular surface, widened fissures between lobes, and an increase in size of the hypertrophied caudate lobe relative to the atrophied right lobe (>0.6). Depending on the modality and imaging technique, fibrotic reticulations, fatty changes, and the presence of various hepatocellular nodules (RNs, DNs, HCC, FNH-like lesions) may be visible. The critical diagnostic distinction is between malignant nodules (e.g., HCC) and nonmalignant nodules (e.g., RNs, DNs, and FNH-like lesions).[22] Although DNs have higher rates of malignant transformation than RNs, the transformation rate is not sufficiently high to warrant ablation or other intervention, nor to increase imaging surveillance frequency or alter surveillance strategies.[23] The natural history of FNH-like lesions in cirrhosis is unknown, but these lesions are considered benign.[21] Simple hepatic cysts and hemangiomas are observed less frequently in the cirrhotic liver than in the noncirrhotic liver. These lesions are described elsewhere in this text. Peribiliary cysts are serous cysts that are hypothesized to represent obstructed periductal glands in patients who have severe liver disease. Recognition of these cysts on imaging helps radiologists to avoid the incorrect diagnosis of dilated bile ducts, abscesses, or cystic neoplasms.[24]

Classic vascular manifestations of cirrhosis include hepatic artery dilatation, tortuosity of hepatic arteries within the liver (“corkscrew” arteries, which may be observed with high-resolution, state-of-the-art CT and MRI), portal vein dilation in early portal hypertension, portal vein occlusion in late portal hypertension due to sluggish portal flow, and formation of shunts. Intrahepatic shunts (arterioportal and arteriovenous) may manifest on dynamic imaging studies as small (≤2 cm) hypervascular pseudolesions and may be mistaken for nodules.[25] Portosystemic shunts manifest as varices (e.g., esophagogastric and paraumbilical); these are usually located outside the liver, although intrahepatic varices also may occur. In addition to varices, other sequelae of portal hypertension (e.g., ascites, splenomegaly, peribiliary cysts, and Gamna-Gandy bodies) may be noted (Figs. 66-1 to 66-3).[26]

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▪ FIGURE 66-1  Hepatocellular carcinoma with invasion into the right portal vein. A, Axial CT image during hepatic arterial phase after injection of intravenous contrast agent demonstrates a large, encapsulated mass in the right lobe of the liver (black arrow). Note the irregular arteries coursing through the lesion center (white arrows), a finding suggestive of hepatocellular carcinoma. B, On a more inferior slice, the right portal vein is expanded and contains linear areas of arterial hypervascularity (arrow). These represent tumor vessels within a malignant thrombus.




 

▪ FIGURE 66-2  Extrahepatic manifestations of portal hypertension. A and B, Axial CT contrast-enhanced images show extensive intra-abdominal varices in a patient with long-standing portal venous thrombosis. Note pericholecystic (A, white arrow), peripancreatic, perisplenic (A, black arrow), and left gastric varices as well as cavernous transformation of the right portal vein (B, arrow). C, Coronal single-shot fast spin-echo T2W image in a different patient reveals varices along the anterior abdominal wall (arrow).

 

 

 

▪ FIGURE 66-3  Gamna-Gandy bodies (GGBs). A, On axial portal venous phase CT image, GGBs are difficult to visualize (arrow). B, On axial unenhanced gradient-recalled-echo MR image with ultrashort echo time (0.08 ms), a 1-cm GGB (arrow) and several subcentimeter GGBs are barely perceptible. C, On axial unenhanced co-localized gradient-recalled-echo MR image with echo time of 9 ms generated by the same radiofrequency excitation as in B, the 1-cm GGB (arrow) and several other GGBs are easily visible as focal hypointense lesions with associated blooming artifacts. Signal loss and blooming in GGBs are due to susceptibility from hemosiderin. As illustrated in this case, GGBs are more visible on MR images than on CT images, especially on T2*W gradient-recalled echo acquisitions.



Radiography

On plain radiographs, gynecomastia may be appreciated in males with cirrhosis; and on lateral films a recanalized umbilical vein may be noted as a round shadow in the fatty tissue anterior and inferior to the liver. Other possible findings include dilation of the azygos vein, a shrunken liver, and enlarged spleen. Barium esophagograms may depict large varices as serpentine-like defects at the inferior portion of the esophagus; these characteristically change in size in response to positional maneuvers. Esophagograms have limited sensitivity for small varices. Ultimately, however, radiography is an insufficient modality to assess cirrhosis or its complications.

Catheter angiography is used mainly for therapeutic purposes (e.g., transarterial chemoembolization and placement of TIPS). In some centers, it may be used for presurgical planning. It does not play a role in the routine imaging assessment of cirrhotic patients.[27]

CT Technical Considerations

The primary indications for performing multiphasic CT in patients with cirrhosis are the evaluation of disease progression, surveillance for HCC, and follow-up of known lesions. Contrast enhancement of vessels, liver, and other solid organs may be impaired in patients with cirrhosis owing to third spacing of fluid and leakage of contrast material into the pulmonary interstitium during passage through the right-sided circulation. For this reason, patients with cirrhosis may require higher rates and concentrations of contrast material than patients without cirrhosis. At our institution, iodinated contrast agents with a concentration of 0.5 mol/L are given at 4 to 5 mL/s. The critical phases for image acquisition are the late arterial (typically at 35 to 40 seconds), portal venous (at 60 to 80 seconds), and late venous (at 3 to 5 minutes).[27] Unenhanced images usually are recommended; cirrhotic nodules may be intrinsically hyperdense due to copper or iron deposition or high glycogen content and may appear hyperdense at hepatic arterial phase and be mistakenly characterized as hypervascular if unenhanced images are not acquired first. Some authors also advocate early arterial phase images (typically at 20 to 25 seconds) to detect very early enhancement of malignant lesions and permit more precise characterization of lesion enhancement features, but this strategy has not been proven to be superior for lesion diagnosis in large clinical trials. Owing to its radiation exposure, CT is not an optimal modality for use in children or pregnant women. CT hepatic artery angiography, CT portography, and CT after transarterial administration of iodized oil may be performed in select cases but are not utilized routinely in the assessment of cirrhotic patients and their discussion is beyond the scope of this chapter.

Fibrosis

On unenhanced images, the attenuation of normal liver is typically about 10 HU greater than that of the spleen. However, the density of the cirrhotic liver or of focal lesions may be reduced (e.g., by steatosis, fibrosis, or edema) or increased (e.g., by iron or copper deposition). Fibrosis typically is not visible on nonenhanced CT; if sufficiently severe, fibrosis may manifest as a diffuse lacework of hypoattenuating bands or as mottled areas of decreased density. Regions of confluent fibrosis are characterized as hypoattentuating wedge- or geographically shaped regions, radiating from the portal hilus and causing retraction of the overlying hepatic capsule (Fig. 66-4). Involvement of the medial segment of the left lobe or anterior segment of the right lobe is characteristic, but other segments may be involved as well. Confluent fibrosis is observed more commonly in alcoholic liver disease and primary sclerosing cholangitis than in viral and other liver diseases. On contrast-enhanced CT, fibrosis, especially if confluent, may show progressive enhancement and appear hyperattenuating on delayed images. Confluent fibrosis occasionally may be mass-like and cause diagnostic confusion. Differentiation from HCC is usually possible based on the characteristic capsular retraction, volume loss, and progressive enhancement pattern associated with confluent fibrosis. In difficult cases, follow-up imaging may be necessary: progressive volume loss, if observed, clinches the diagnosis of confluent fibrosis.[28]

 


 

▪ FIGURE 66-4  Confluent fibrosis. Coronal ultrasound (A), hepatic arterial phase contrast-enhanced CT (B), portal venous phase contrast-enhanced CT (C), and double-contrast–enhanced axial 2D spoiled gradient-echo (SGE) (D) images obtained at 3.0 T with echo time of 5.8 ms. A, On ultrasonography, individual regenerative nodules and reticulations of fibrotic tissue are difficult to delineate but the liver displays patchy areas of increased echogenicity (white arrow) suggesting increased fibrotic tissue in the liver. B and C, Unenhanced and contrast-enhanced CT images show confluent fibrosis as a hypoattenuating geographically shaped region radiating from the portal hilus and causing minimal contraction of the overlying hepatic capsule (white arrows). D, On the MR image, the fibrotic tissue takes up gadolinium and displays high signal intensity in the same geographically shaped formation that is seen on the CT images, while the surrounding regenerative tissue appears dark due to superparamagnetic iron oxide uptake.



Nodules

FNH-like lesions are small, ranging up to about 1 cm in diameter.[29] Isoattenuating on nonenhanced imaging, these lesions hyperenhance on the arterial phase and then fade to isoattenuation on more delayed images. On both nonenhanced and contrast-enhanced CT, RNs usually are isoattenuating relative to the surrounding hepatic parenchyma and are difficult to visualize (Figs. 66-5 and 66-6), although siderotic RNs may be hyperdense. On nonenhanced CT, large DNs are hyperattenuating relative to surrounding parenchyma due to the presence of increased iron and glycogen, whereas small DNs remain isoattenuating. Conversely, DNs enhance simultaneously with normal parenchyma on contrast-enhanced CT, appearing isoattenuated. With increased dedifferentiation, however, these DNs may appear hyperattenuating owing to increased vascularity and consequent increased contrast uptake.[25]

 


 

▪ FIGURE 66-5  Regenerative nodules (RNs). Axial unenhanced (A) and contrast-enhanced (B) arterial and portal venous phase (C) CT images. A-C, The liver parenchyma shows minimal heterogeneity, and discrete RNs are not confidently characterized. D, At the same level as the CT images, on axial 2D spoiled gradient-echo (SGE) MR image obtained at 3.0 T with echo time of 5.8 ms after SPIO administration, the RNs are visible as sharply demarcated hypointense nodules owing to phagocytic uptake of SPIO, which causes T2* shortening. E, On double-contrast–enhanced MR image after gadolinium administration, fibrotic reticulations display an increase in signal intensity owing to the extracellular accumulation of the low-molecular-weight contrast agent. Enhancement of fibrotic tissue further increases visibility of RNs (arrows). Note that this image shows innumerable RNs carpeting the liver. The two representative RNs as labeled for illustrative purposes are examples of SPIO-enhanced and double-contrast–enhanced MRI.

 

 

 

▪ FIGURE 66-6  Dynamic enhancement of fibrotic tissue in the cirrhotic liver. Dynamic contrast-enhanced (A), unenhanced portal venous phase (B), and delayed phase (C) CT images show the nodular liver surface diagnostic of cirrhosis. The liver parenchyma is homogeneous, with neither fibrotic reticulations nor RNs clearly identified. Dynamic gadolinium-enhanced axial gradient-recalled unenhanced (D), portal venous (E), and delayed (F) phase MR images obtained at the same level as the CT images show progressive enhancement of the fibrotic reticulations due to accumulation of the low-molecular-weight gadolinium. Dynamic MR images depict the enhancement of the fibrotic septa (arrows) with higher clarity than CT.

HCCs may have a varied appearance at CT depending on tumor size, vascularity, steatosis, cholestasis, hemorrhage, and necrosis. On nonenhanced CT, HCCs generally appear as hypoattenuating or heterogeneously attenuating lesions. Intralesional fat or blood products may be difficult to identify on CT; these features are more readily observed on MRI. After administration of contrast agents, HCCs become hyperattenuating or heterogeneously enhancing during the arterial phase, then fade to isoattenuation or wash out to hypoattenuation on venous and delayed phases. If a tumor capsule is present, it often enhances progressively and retains contrast material on delayed images. Vascular invasion, if present, is more easily appreciated on contrast-enhanced images.

Perfusional pseudolesions due to arteriovenous or arterioportal shunts enhance during the arterial phase and then fade to isoattenuation on images acquired during the portal venous and equilibrium phases. As opposed to true nodules, pseudolesions tend to have ill-defined or straight borders and may have blood vessels running through their center. In diagnostically challenging cases, longitudinal imaging is necessary. At follow-up, pseudolesions regress or are stable but rarely grow.

MRI Technical Considerations

Whereas MRI provides the best performance characteristics for the diagnosis of cirrhosis, it requires longer scan times than CT and is more costly. Therefore, it is generally employed when CT is not definitive or if further characterization of a lesion is required. Because of its lack of radiation, it is also used in lieu of CT in children when ultrasound findings raise further concerns.

There is controversy regarding which MR technique is optimal for evaluation of cirrhotic patients.[30] For T1-weighted (T1W) imaging, dual-phase in-phase and out-of-phase gradient-echo images are commonly acquired because these permit assessment of parenchymal and lesional fat content as well as provide characterization based on T1 relaxation. If a tissue contains no fat, it is also possible to infer qualitative T2* information from the dual-phase echoes: voxels with short T2* visibly lose signal on the later echo, whereas voxels with long T2* do not. Multiphase gradient-echo imaging, in which three or more gradient echoes are acquired after a single radiofrequency excitation, is now available on some scanners and permits more reliable characterization of fat content and T2* relaxation. T2-weighted (T2W) fast spin-echo imaging is useful for evaluating bile ducts, cysts, and fluid collections; single-shot fast spin-echo sequences are particularly useful for this purpose. T2W imaging also helps characterize RNs and DNs but has low sensitivity for detecting HCC. Diffusion-weighted imaging is another available technique and shows promise; HCCs tend to have restricted diffusion and appear bright on diffusion-weighted images.

The most common dynamic technique to evaluate the liver is MRI after a rapid bolus injection of gadolinium-based contrast agents at a rate of about 2 mL/s. The authors typically use the dose indicated in the product insert (0.1 mmol/kg). Because MRI has higher sensitivity to contrast agents than CT, the standard dose usually suffices and higher doses are rarely necessary. Patients with cirrhosis may develop acute renal failure due to hepatorenal syndrome and other mechanisms, which in theory increases their risk for developing nephrogenic systemic fibrosis after exposure to gadolinium-based contrast agents. For this reason, the American College of Radiology recommends assessment of the estimated glomerular filtration rate (eGFR) nearly contemporaneous with gadolinium exposure. If the eGFR exceeds 30 mL/min/1.73 m2, the risk of nephrogenic systemic fibrosis appears to be miniscule.[31],[32]

Volumetric 3D T1W fat-saturated spoiled gradient-echo acquisitions are usually utilized for dynamic imaging. The key phases are the hepatic arterial phase, in which the acquisition of the center of K space coincides with peak arterial perfusion of hepatic nodules, portal venous phase, acquired 60 to 80 seconds after gadolinium injection (see Fig. 66-6), and delayed venous phase image acquisitions (acquired 3 to 5 minutes after injection).[33-35] The delayed venous phase images help to assess venous wash out.

Superparamagnetic iron oxides (SPIOs) may be given to evaluate phagocytic function of hepatic Kupffer cells. The agent is administered as a slow infusion, typically over 30 minutes. Uptake of SPIOs results in T2 and T2* shortening.[36] Lesions with Kupffer cells (most RNs and DNs) lose signal intensity on SPIO-enhanced T2W and T2*W images, whereas lesions deficient in Kupffer cells (most HCCs and cirrhotic scars) do not lose signal intensity and appear relatively hyperintense. There is controversy regarding whether spin-echo or gradient-echo techniques are most well suited for evaluating SPIO uptake.[37] We prefer gradient-echo images, but other institutions may prefer spin-echo images.

In select centers, double-contrast–enhanced imaging, in which SPIO followed by gadolinium are administered sequentially in the same examination, is performed. The sequential administration of two agents theoretically improves the characterization of cirrhotic nodules by permitting the assessment of two complementary biologic features (phagocytic activity of Kupffer cells and vascularity).[30]

Fibrosis

Fibrosis in the cirrhotic liver has low signal intensity on unenhanced T1W images and high signal on T2W images. Similar to its appearance on CT, confluent fibrosis tends to have straight borders and is associated with progressive volume loss over time at follow-up imaging. When gadolinium is administered, fibrotic tissue slowly enhances in the arterial phase and retains contrast on portal venous and delayed images. As a result, fibrosis has relatively high signal on delayed gadolinium-enhanced images (see Figs. 66-4 and 66-5). Fibrosis, which lacks Kupffer cells, also has relatively high signal intensity on T2W and T2*W images after SPIO administration. Double-contrast–enhanced gradient-echo images show the reticulations and bands of liver fibrosis to greatest advantage; the fibrotic tissue appears hyperintense due to gadolinium accumulation while the background liver parenchyma appears hypointense due to SPIO accumulation. Such images also show other features of cirrhosis, including capsular thickening (Fig. 66-7) and nonuniform distribution of fibrosis (Fig. 66-8).

 


 

▪ FIGURE 66-7  Hepatic capsular thickening. On this axial double-contrast–enhanced MR image, the hepatic capsule can be seen retaining gadolinium and has high signal intensity similar to the fibrotic reticulations distributed throughout the liver. As illustrated in this case, the fibrotic thickening of the liver capsule (arrows) is a frequent manifestation of cirrhosis but it is not always observed on imaging.

 


 

▪ FIGURE 66-8  Nonuniform distribution of fibrosis. A, On this axial arterial-phase contrast-enhanced CT image the liver has an unusual contour and there is relative hypertrophy of the posterior portion of the lateral segment of the left lobe (black arrow). The liver parenchyma is relatively heterogeneous with areas of hyperattenuation and hypoattenuation (white arrows). B, The axial double-contrast–enhanced MR image shows to better advantage the nonuniform distribution of fibrosis within this cirrhotic liver. Note that areas of atrophy and volume loss are associated with a higher density of fibrotic tissue (black arrow) than areas of hypertrophy (white arrows).

Nodules

FNH-like lesions are typically isointense on both T1W and T2*W imaging. Similar to their appearance on contrast-enhanced CT, these lesions enhance during the hepatic arterial phase after injection of gadolinium-based agents and then fade to isointensity on more delayed phases. RNs have a variable appearance at unenhanced T1W imaging and may be hypointense, isointense, or hyperintense. Some RNs are steatotic and lose signal intensity on out-of-phase compared with in-phase imaging (Fig. 66-9). Most RNs are isointense and not detectable at T2W and T2*W imaging, whereas some RNs, particularly those with high iron concentration, are hypointense at T2W and T2*W imaging.[38],[39] High signal intensity on T2W and T2*W images is distinctly unusual for RNs; marked T2 hyperintensity suggests a simple cyst, whereas mild to moderate T2 hyperintensity raises suspicion for HCC. On administration of gadolinium, RNs enhance to a similar degree as surrounding parenchyma and appear isointense. When SPIOs are administered, RNs take up the iron particles and, due to superparamagnetic effects, appear hypointense on T2W and T2*W images (see Fig. 66-5). DNs, like RNs, have variable signal intensity on unenhanced T1W images and appear isointense or hypointense on T2W images. On gadolinium and SPIO-enhanced imaging, low-grade DNs typically are difficult to distinguish from RNs, whereas high-grade dysplastic nodules may resemble well-differentiated HCCs.

 


 

▪ FIGURE 66-9  Fatty regenerative nodules (RNs). On axial unenhanced MR in-phase (A) and out-of-phase (B) images, regenerative nodules can be appreciated (arrows). The regenerative nodules lose signal, as evidenced by the decrease in signal intensity on out-of-phase images, indicating the presence of intralesional fat. Innumerable nodules are present in the images.



HCCs display variable signal intensity on unenhanced T1W imaging. They characteristically appear hyperintense at T2W imaging, but T2W imaging has limited sensitivity for HCCs and may render them invisible or mildly hypointense. After administration of gadolinium, hypervascular HCCs enhance rapidly to high signal intensity on arterial phase images and then become hypointense on portal venous and delayed images. Compared with RNs and DNs, HCCs tend to have a reduced concentration of Kupffer cells and diminished phagocytic capacity. Hence, when SPIOs are administered, HCCs do not take up the particles and have high signal intensity relative to the adjacent non-neoplastic parenchyma. Focal areas of fibrosis also have high signal on such images and may be mistaken for HCCs on low-resolution SPIO-enhanced images. High-resolution SPIO-enhanced imaging usually permits differentiation of fibrosis (reticulated morphology) from HCC (nodular morphology). In challenging cases, gadolinium administration or follow-up imaging is necessary.

Perfusional pseudolesions may be indistinguishable from FNH-like lesions; similar to FNH-like lesions, the pseudolesions hyperenhance during the arterial phase and then fade to isointensity. Differentiation is not clinically important, however, because both FNH-like lesions and perfusional pseudolesions are benign. If these entities are suspected, follow-up imaging rather than intervention is recommended.

Ultrasonography Technical Considerations

Because of its low cost and lack of radiation, ultrasonography is typically the initial imaging modality performed in patients with cirrhosis. It provides information about liver size and shape and, if high-frequency transducers are used, may detect subtle nodularity along the liver surface to establish the diagnosis of cirrhosis in clinically equivocal cases. In patients with established cirrhosis, ultrasonography plays an important role in assessing sequelae of portal hypertension (e.g., splenomegaly and ascites). On gray-scale images, features suggestive of portal hypertension include dilation of the portal vein to greater than 13 mm, splenic vein to greater than 11 mm, and superior mesenteric vein to greater than 12 mm. Color Doppler tracings can be utilized to further characterize portal vein patency and direction of flow. Portal hypertension is associated with increased pulsatility of the portal vein Doppler tracing and loss of the normal triphasic hepatic vein Doppler tracing. When portal flow is hepatofugal, the liver has progressed to end-stage disease and shunt placement or liver transplantation may be required. Color Doppler tracings can also be used to monitor shunt patency as well as patency of vascular anastomoses after transplantation.

In Europe, Asia, and select centers in North America, microbubble-based contrast agents may be administered intravenously to assess lesion vascularity using ultrasonography. Similar to CT and MRI, multiple phases are acquired: arterial phase (15 to 30 seconds after injection), portal phase (30 to 60 seconds after injection), and sinusoidal (or blood pool) phase (60 to 240 seconds after injection).[25]

Nodules

Ultrasonography has limited sensitivity for cirrhosis-associated nodules. Discrete RNs are rarely identified even if they are obvious on other imaging modalities. Coarsening and heterogeneity of the liver echotexture may suggest the presence of RNs, but this finding is neither sensitive nor specific and the liver parenchyma may appear normal even if cirrhosis is advanced (see Figs. 66-4 and 66-10). Another indirect clue to the presence of RNs includes nodularity of the liver surface, most reliably appreciated if high-resolution transducers are used; in this setting, the RNs themselves are usually not visible and their presence is inferred by the bulging of the liver capsule.

 


 

▪ FIGURE 66-10  Ultrasound (A), CT (B), and MR (C) images of the liver of a male patient with cirrhosis. On the ultrasound image the liver has increased echogenicity and heterogeneity, although specific reticulations are difficult to identify. On the axial CT image, reticulations are again difficult to appreciate. However, on the double-contrast–enhanced MR image the fibrotic tissue forms honeycomb-like reticulations of high signal intensity surrounding the low signal regenerative nodules. Of the three modalities, the extent and degree of fibrosis are more easily appreciated with MRI.



Nodules sufficiently large or anomalous to be visible in the cirrhotic liver on ultrasound evaluation are likely to be HCCs. If visible on ultrasonography, HCCs tend to be hypoechoic or have mixed echogenicity. Unenhanced ultrasonography has limited sensitivity for HCC, however, and most HCCs are not visible unless large or associated with vascular invasion. If microbubbles are administered, HCCs typically hyperenhance and become vividly hyperechoic on arterial phase and then wash out to become hypoechoic on the portal and sinusoidal phases.

Fibrosis

Similar to cirrhotic nodules, ultrasonography has low sensitivity for fibrosis. Advanced fibrosis associated with cirrhosis may manifest as diffuse increase in echogenicity, with poor visualization of coursing liver vessels. Findings overlap with those of simple steatosis, and it is common for cirrhosis to be misdiagnosed as fatty liver on the basis of ultrasound findings.

Nuclear Medicine

Nuclear medicine imaging of the cirrhotic liver is limited by poor performance characteristics and is no longer utilized in standard clinical practice. Historically, the primary hepatic radionuclide study was radiocolloid liver scintigraphy or, more commonly, the liver-spleen scan. Liver-spleen scintigraphy is based on the principle that radiolabeled colloid particles are phagocytosed and localized to the reticuloendothelial system of the liver, spleen, and bone marrow after intravenous injection. The radiopharmaceutical agent most commonly used for liver-spleen scanning is technetium-99m sulfur colloid (99mTc-SC). The radionuclide has a relatively short half-life of 6 hours, does not release beta radiation, and discharges gamma photons at 140 keV/m.[27] Imaging is performed 15 to 20 minutes after intravenous injection of 3 to 8 mCi of 99mTc-SC. The normal liver demonstrates greater uptake of radiocolloid than the spleen. In advanced cirrhosis, hepatic uptake may be reduced, leading to relatively greater uptake in the spleen (“colloid shift”). Other scintigraphic findings of advanced cirrhosis include morphologic alterations of the liver (e.g., enlargement of the left lobe and caudate with atrophy of the right lobe) and reduced activity in the distribution of the left portal vein if there is shunting into a recanalized umbilical vein. Splenomegaly may be evident. Ascites may be inferred if there is separation of the liver from the abdominal wall or if a photopenic rim is seen around the liver. Dynamic flow images may be acquired immediately after injection to assess vascularity of hepatic lesions, although this is less accurate than the dynamic images acquired at CT or MRI.

Imaging Algorithm

The most appropriate method for assessing cirrhosis and screening for HCC through imaging is complicated and controversial. The American Association for the Study of Liver Diseases recommends ultrasonographic screening every 6 to 12 months, but ultrasonography has low sensitivity and may fail to detect HCC until advanced stages when it is no longer curable.[40] Therefore, many centers use CT for initial screening, with contrast-enhanced MRI reserved for further characterization of known lesions. Although MRI offers higher sensitivity to contrast agents, higher tissue contrast, and a larger variety of contrast agents with different biologic properties, MR costs and time preclude it from being utilized as a screening modality in most centers. Even so, some academic centers primarily utilize MRI for screening purposes because of its perceived benefits (Table 66-1).

 

Classic Signs of Cirrhosis

       Classic signs for the diagnosis of cirrhosis include morphologic and textural alterations.
       The most definitive morphologic alteration is surface nodularity, which is due to the presence of regenerative nodules subjacent to the liver capsule. The presence of surface nodularity is highly specific for cirrhosis in the right clinical setting but has low sensitivity for early cirrhosis, in which the liver surface may be smooth.
       Another morphologic alteration is atrophy of certain segments with relative enlargement of others. Characteristically, the right lobe atrophies, often in association with surface notching at the junction of the caudate and segment 6. The left lobe atrophies less and appears large by comparison. Alternatively, there may be atrophy of the central segments (4, 5, and 8), with or without enlargement of other segments.
       As certain portions of the liver atrophy, the hepatic fissures (falciform, venosum), gallbladder fossa, and porta hepatis may widen, and the anterior liver surface may withdraw from the anterior abdominal wall. Focal areas of surface retraction may develop due to confluent fibrosis. Unless advanced, however, these global contour alterations are nonspecific and there is considerable overlap in the overall shape of the normal and diseased liver.
       Textural alterations consist of meshwork fibrotic reticulations surrounding regenerative nodules. Unlike the morphologic alterations, which may be identified with similar confidence at CT, MRI, and ultrasonography, visualization of textural alterations is technique dependent. These textural alterations tend to be invisible at CT unless disease is markedly advanced, in which case CT may depict nonspecific parenchymal heterogeneity.
       Direct CT visualization of fibrosis or regenerative nodules is relatively uncommon.
       Ultrasonography shows nonspecific coarsening of liver echotexture but, as with CT, rarely permits direct visualization of fibrosis or nodules.
       MRI, by comparison, may show fibrosis and regenerative nodules with exquisite detail, particularly if contrast-enhanced or double-contrast–enhanced techniques are used.

TABLE 66-1   -- Accuracy, Limitations, and Pitfalls of the Modalities Used in Imaging of Cirrhosis
Modality
Accuracy
Pitfalls
Limitations
CT

     Detects morphologic alterations of cirrhosis, which have high specificity but low sensitivity for cirrhosis
     Low sensitivity for RNs and DNs

     Most cirrhosis-associated hepatocellular nodules are not visible.
     The liver parenchyma may appear normal even if cirrhosis is advanced.

 

     Exposes patient to ionizing radiation.
     Less intrinsic soft tissue contrast and less sensitivity to contrast agents compared with MRI
     Vascular and parenchymal enhancement may be suboptimal.
     Higher contrast agent concentrations and rates may be necessary.
     Does not assess vascular flow direction
MRI

     Like CT, detects morphologic alterations of cirrhosis
     Sensitivity and specificity for cirrhosis may be improved by using double-contrast techniques.
     Depending on the imaging technique, hepatocellular nodules (RNs, DNs, and HCC) may be visible with high clarity.
Imaging features of nonmalignant lesions (RNs, DNs, perfusional pseudolesions, confluent fibrosis) may overlap with those of HCC.

     More time consuming and expensive than CT
     Prone to imaging artifacts, especially in uncooperative patients and those with severe ascites
     Using standard techniques, does not assess vascular flow direction
Ultrasonography

     Using high-resolution transducers, can detect subtle nodularity along cirrhotic liver surface
     Low sensitivity for all cirrhosis-associated hepatocellular nodules (RNs, DNs, HCC)
     High accuracy for detecting vascular flow direction

     Most cirrhosis-associated hepatocellular nodules are not visible.
     The liver parenchyma may appear normal even if cirrhosis is advanced.
     If abnormal, the parenchymal findings are nonspecific and ultrasonography does not reliably distinguish fibrosis from steatosis.

     Operator dependent
     Limited evaluation of liver parenchyma

RNs, regenerative nodules; DNs, dysplastic nodules; HCC, hepatocellular carcinoma.

 
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Dr.Mario, почему-то не видны

Dr.Mario, почему-то не видны картинки в Ваших очень нужных информационных материалах. Или это только уменя так? По ссылке тоже открывается только сайт Амазон.

 

 
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Картинки должны отображаться.

Картинки должны отображаться.

 
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Вверху ссылка на сайт Amazon

Вверху ссылка на сайт Amazon - верно, эта ссылка на книгу откуда была взята информация.

Насчёт картинок - я постараюсь исправить.

 
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Смутило больше всего что

Смутило больше всего что воротрная вена контрастирована то этого участка (я понимаю, без дайкома не разобраться, домой не взял)

 

 

 
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Я тоже обратил внимание, но

Я тоже обратил внимание, но очень мало срезов. Тромбоз портальной вены указывает на высокую вероятность ГЦР.

 
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Dr.Mario, теперь все видно.

Dr.Mario, теперь все видно. Спасибо огромное!

 
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ГЦР можно заподозрить уже по

ГЦР можно заподозрить уже по первым картинкам - гиперваскулярный фокус в паренхиме и похожее  усиление  тромботических масс портальнй вены быстрое вымывание контраста на следующих сканах подтверждает мысль о карциноме на фоне цирроза.

 
 

Новый опрос

Кто подскажет как попасть в DropBox для загрузки видео в свой каталог? Не могу нигде найти.
Ссылка не работает
60%
Нет нигде закладки
40%
Total votes: 10

RADIOGRAPHIA и FACEBOOK

МЦ "Тигренок"