Книги по МРТ КТ на английском языке / Advanced Imaging of the Abdomen - Jovitas Skucas

LIVER

enhancement than in those with slow enhancement. Most hemangiomas increase in lesion- to-liver contrast on ferumoxides-enhanced T2-weighted MR images.

Scintigraphy

Both planar and SPECT Tc-99m–red blood cell imaging have high sensitivity and specificity in differentiating cavernous hemangiomas from other liver tumors and are often used as gold standards in comparison studies. Scintigraphy is especially useful with an atypical imaging appearance of a suspected hemangioma; SPECT detects smaller hemangiomas than planar images. Reported false positives include hepatocellular carcinoma, sarcoma, metastatic small cell lung carcinoma, and intrahepatic extramedullary hematopoiesis (11). Occasional false negatives are reported, often due to a lesion’s small size.

Early perfusion phase Tc-99m–red blood cell scintigraphy shows a focal photopenic defect that gradually fills in in a centripetal manner during the blood-pool phase. A perfusion/ blood-pool mismatch is the hallmark for hemangiomas. Technetium-99m–sulfur colloid and hepatobiliary scintigraphy simply reveal a filling defect. The increased activity seen on blood-pool images is absent if a thrombus has developed within a hemangioma.

If early liver images are obtained during prostate immunoscintigraphy with indium- 111–labeled antibodies, a hemangioma has an appearance similar to that seen with Tc- 99m–red blood cell imaging.

A marked increase in perfusion detected by scintigraphy should suggest arterioportal shunting.

Biopsy

Some radiologists hesitate to biopsy suspected hemangiomas for fear of complications, yet many have been biopsied without undue complication. This does not suggest that suspected hemangiomas should be biopsied; noninvasive protocols generally suffice for diagnosis. Rather, in an atypical and otherwise nondiagnostic suspected or even unsuspected hemangioma a biopsy can be a safe and diagnostic procedure. A bigger problem is in placing in proper perspective a biopsy that simply reveals blood cells.

Therapy

Many liver cavernous hemangiomas are managed simply by observation. Indications for surgery include an uncertain diagnosis, imaging showing enlargement, or a symptomatic tumor. An occasional one manifests acutely by bleeding or rupture, thus necessitating emergency surgery. They have been resected using a laparoscopic approach.

Palliation of symptomatic hemangiomas by transcatheter arterial embolization is an option. A rare symptomatic cavernous hemangioma is treated by radiofrequency ablation (75).

Orthotopic liver transplantation is an extreme option in patients with unresectable giant hemangiomas.

Infantile Hemangioma

Previously some hemangioendotheliomas, especially in infants, were lumped together with hemangiomas (hemangioendotheliomas are discussed later). In a setting of a vascular tumor in an infant, especially with clinical evidence of Kasabach-Merritt syndrome, a hemangioendothelioma rather than a hemangioma should be considered.

An infantile hemangioma is more common in girls and tends to be multiple. With age, these tumors tend to involute with few sequelae.

Large hemangiomas in infants are identified on T2-weighted MRI as hyperintense nodules containing fast flow and are seen as flow voids on SE images and hyperintense tumors on GRE images. One in an infant revealed an early rim enhancement after gadolinium, with progressive fill-in on delayed imaging (76). These tumors are fed by enlarged hepatic vessels; the proximal abdominal aorta is prominent, while distal to the feeding vessel takeoff it had a decreased caliber. These nodules regress after interferon-a-2a therapy and are replaced by normal-appearing liver parenchyma with no evident fat or fibrosis.

If necessary, embolization of the feeding vessels is performed to control congestive failure or treat other complications. A lobectomy is appropriate if a solitary hemangioma is confined to an anatomic lobe.

Some infants believed to have lifeor func- tion-threatening hemangiomas are treated with

radiation therapy (77); some of these infants have Kasabach-Merritt syndrome, and in these infants the hemangiomas regress and platelet counts increase after radiation therapy.

ADVANCED IMAGING OF THE ABDOMEN

A hypervascular metastasis, hemangioma and even an abscess are occasionally included in the differential diagnosis.

Peliosis Hepatis

Clinical

Peliosis hepatis is a rare benign disorder of unknown etiology characterized by numerous blood-filled cavities in the liver. An association exists between peliosis hepatis and some drugs, including hormones. It has regressed in extent after cessation of oral contraceptive use. It can be congenital. Other associated conditions include malignant histiocytosis, myeloid metaplasia, and hemangiosarcoma. It has developed after liver transplantation. In AIDS patients, peliosis hepatis is associated with bacillary angiomatosis. It can be subclinical and be detected incidentally, when it is a source of diagnostic confusion.

These cavities range from single to diffuse, vary in size, and are lined by endothelial cells. Hepatic insufficiency develops if enough parenchyma is replaced by these vascular spaces. Rarely, peliosis hepatis ruptures spontaneously, and an intraperitoneal hemorrhage ensues.

Imaging

Rare liver calcifications are identified in patients with peliosis hepatis.

Postcontrast CT reveals well-marginated contrast collections in the liver. Some show delayed enhancement. Occasionally some of these cystic spaces do not opacify with contrast, presumably due to thrombosis. Some tumors have gradual centripetal CT contrast enhancement, thus mimicking a hemangioma (78). These tumors are hypoechoic or even anechoic with US. They are hyperintense with all MRI sequences and enhance postcontrast.

Angiography reveals numerous vascular spaces. Typically, contrast accumulates in the late arterial phase, which becomes more distinct during the venous phase. No communication exists with the portal venous system. Early feeding arteries and draining veins are not present in peliosis hepatis.

Hepatic scintigraphy with Tc-99m–sulfur colloid or gallium is normal.

Solitary (Fibrosing) Necrotic Nodule

Solitary nodules, initially described on the anterior aspect of the liver, consist of a necrotic center surrounded by a hyalinized fibrotic capsule containing elastic fibers. They are considered nonneoplastic, yet a number have been reported in patients with underlying neoplastic disease. Many are subcapsular and solitary; currently they are believed to be the final common pathway of a number of benign disorders.

They develop after microwave tissue coagulation and after various liver infections.

Focal Nodular Hyperplasia

Clinical

Focal nodular hyperplasia (FNH) is a development abnormality of unknown etiology and pathogenesis. Current thought is that it is a regenerative process; nodules appear related to a focal increase in arterial blood flow and resultant hyperplastic tissue response, and in that sense differ from adenomas, which are neoplastic. They are the second most common benign liver tumor in adults, after hemangioma. In distinction to a hepatic adenoma, FNH is not premalignant and is generally an incidental finding, but, similarly to adenomas, some of these tumors are associated with contraceptive use, and some regress after drug discontinuation. A high prevalence is found in women of childbearing age, with an occasional one encountered in infants and children.

Single nodules predominate. These are discrete tumors often having a characteristic central stellate scar containing blood vessels. Feeding vessels are of hepatic artery origin. Although vessels are prominent and the lesion contains typical hepatic structures, including hepatocytes, Kupffer cells, and proliferating bile ducts, the usual arrangement of portal tract vessels and bile ducts is not present. Histologically, anomalous arteries in fibrous septa connect to capillaries, which drain into sinusoids adjacent to fibrous septa, which in turn drain into veins located in the parenchyma.

LIVER

These findings suggest a focal arteriovenous malformation with growth of surrounding parenchyma as etiology for their formation. About 80% of FNHs have a typical histologic appearance; a minority reveal prominent vessels or, interestingly, show cellular atypia to the point of suggesting an adenoma.

A core biopsy reveals deranged architecture, a finding not appreciated with cytology.

Clinically, these lesions are usually an incidental finding and rarely present with bleeding, thus distinguishing them from adenomas. Their primary significance in most patients is that they mimic a more ominous tumor. With time they can increase, decrease, or remain constant in size.

Imaging

An occasional report describes fat within or adjacent to FNH, but fat is an uncharacteristic finding. Likewise, calcifications are uncommon. These calcifications are similar in appearance to those seen in some fibrolamellar hepatocellular carcinomas.

Although the specific pattern is different, FNH has a similar appearance with various imaging modalities. Most are solitary, subcapsular in location, are often lobulated and tend to be sharply marginated. Their usual homogeneous appearance reflects a lack of hemorrhage and necrosis, except in some larger ones. Majority are <5cm in diameter, with only a rare one being >10cm. An occasional one is exophytic. A central hypodense region, representing a central scar with radiating fibrosis, is found in larger tumors, although a scar is generally not visible in smaller ones. Presence of a central scar is not specific for FNH and a scar is occasionally found in other tumors, such as hepatocellular carcinomas, adenomas, intrahepatic cholangiocarcinomas, and some larger hemangiomas.

With unenhanced CT these nodules tend to be homogeneous and hypoto isodense. Precontrast FNHs tend to blend into surrounding parenchyma. Especially when small, they are identified mostly on immediate postcontrast images.

These lesions are supplied primarily by hepatic artery branches and thus arterial-phase CT reveals a transient but marked initial enhancement, which progresses to isodensity

during the parenchymal (portal) phase. Multiphasic CT in patients with FNH found all tumors to be hypervascular and hyperattenuating to the liver during arterial phase, and 92% were isodense on delayed scans (79); most enhanced homogeneously, and were smooth in outline and subcapsular in location. Single-level dynamic CT during hepatic arteriography of small FNH reveals centrifugal blood flow through a fibrous scar, drainage into adjacent dilated veins and then into a hepatic sinusoid in adjacent liver tissue (80).

Ultrasonography reveals FNHs tending toward a homogeneous and isoechoic appearance and often blending into normal adjacent parenchyma, although considerable variability exists. They tend to be well marginated. A central scar is either hypoechoic or not visualized. In some, color Doppler identifies vessels radiating in a central stellate pattern; the feeding artery shows a high diastolic flow rate and has a low pulsatility index. It has a high frequency and low resistance. Contrastenhanced US reveals intralesional flow, peripheral vascularity, and at times also a centripetal afferent vessel.

Magnetic resonance imaging appears more sensitive and specific than CT in detecting and characterizing FNH. On T1-weighted unenhanced MRI sequences, FNHs appear isoto hypointense compared to normal liver and isoto hyperintense on T2-weighted images (Fig. 7.22). Marked hyperintensity on T2-weighted

Figure 7.22. Extensive focal nodular hyperplasia. T1-weighted MRI identifies a hypointense tumor (arrows). (Courtesy of Algidas Basevicius, M.D., Kaunas Medical University, Kaunas, Lithuania.)

images is distinctly unusual and should suggest another diagnosis. A central scar, identified in over half of these tumors, tends to be hypointense on T1and hyperintense on T2weighted images, presumably due to prominent central vascularity. Although not encapsulated, compression of surrounding liver parenchyma often results in a hyperintense rim being evident on T2-weighted images,in distinction to the fibrotic hepatocellular carcinoma capsule which tends to be hypointense on both T1and T2-weighted images. Here also considerable variability exists and heterogeneity and a hyperintense signal is identified in some FNH on T1weighted images.

Postgadolinium MRI reflects their rich vascularity radiating in a stellate pattern. Similar to adenomas, an intense, uniform contrast enhancement is common during the arterial phase, becoming isodense during portal venous phase. A central scar is initially hypointense but gradually enhances on delayed images.

Because Kupffer cells are present in most FNH nodules, these tumors take up iron oxide contrast. Six FNH nodules showed a mean of 43% signal intensity loss on ferumoxidesenhanced T2-weighted images (81). A SPIOenhanced MR detects more tumors than a precontrast MR, but little difference in signal loss exists between FNH and adenomas.

Similar to adenomas, the presence of hepatocytes within the FNH results in Mn-DPDP (mangafodipir) uptake.

ADVANCED IMAGING OF THE ABDOMEN

Due to their Kupffer cell content, these tumors take up Tc-99m–sulfur colloid. Clearance of tracer from the tumor is delayed. A positive colloid scan is thus useful in differentiating these lesions from most hepatocellular carcinomas. A finding of decreased colloid uptake, on the other hand, is nonspecific. It should be kept in mind that some regenerating nodules, focal steatosis, and adenomas also take up sulfur colloid.

Iminodiacetic acid (IDA) hepatobiliary tracers accumulate within FNH, and most larger nodules appear as hot spots. Thus Tc-99m-IDA hepatobiliary scintigraphy shows increased tracer uptake on delayed scans in most larger tumors.

Using the hepatocyte receptor Tc-99m- neoglycoalbumin (NGA), scintigraphy showed normal to increased uptake in FNH, thus differentiating these tumors from most malignancies, which have very low to no uptake.

A characteristic arteriographic finding is a single artery feeding a hypervascular tumor that contains intense venous staining (Fig. 7.23). Although arteriography readily detects FNH, it lacks specificity in differentiating it from other focal hypervascular tumors, and angiography is rarely employed in the workup of these tumors.

The use of imaging techniques is illustrated by a report of a 17-year-old girl with a 2-cm- diameter left lobe tumor detected incidentally by US (82); CT and MRI confirmed the tumor,

LIVER

and postcontrast CT and CO2-enhanced US demonstrated early central enhancement with gradual enhancement spreading to the periphery. Color Doppler flow imaging detected a central color spot, shown by pulsed Doppler spectrum analysis to represent an artery. The lesion was not detected by hepatic arteriography. Biopsy confirmed the FNH.

In summary, no pathognomonic imaging finding exists for FNH. A fibrolamellar hepatocellular carcinoma has a very similar CT and US appearance. Likewise, overlap exists with some large hemangiomas, adenomas, and metastases. In a cancer patient findings suggesting a FNH should be confirmed by biopsy.

Nodular Regenerative Hyperplasia

Nodular regenerative hyperplasia (at times simply called regenerative nodules) is a specific nonneoplastic entity consisting of multiple nodules surrounded by liver atrophy. It differs from regenerating nodules seen in cirrhosis (discussed in a later section). This uncommon condition occurs in noncirrhotic livers. About half the patients have portal hypertension. The etiology is unknown, and pathogenesis appears to be multifactorial, with focal ischemia postulated by some. It is associated with collagen vascular diseases, rheumatoid arthritis, Felty’s syndrome, some myeloproliferative disorders, and some drug therapy.A rare association exists with CREST syndrome (calcinosis cutis, Raynaud’s phenomenon, esophageal dysfunction, sclerodactyly, and telangiectasia) and primary biliary cirrhosis.

Histologically, numerous hyperplastic nodules varying in size are diffusely scattered throughout the liver. No significant fibrosis is evident, thus distinguishing this condition from cirrhosis and focal nodular hyperplasia; the exception is if long-standing portal hypertension has developed, when fibrosis with portal venous obliteration develop; whether portal venous obliteration precedes portal hypertension or vice versa is unknown. Histologically,this condition mimics an adenoma,but the latter is usually single, while nodular regenerative hyperplasia is diffuse throughout the liver.

Computed tomography reveals multiple hypodense nodules that do not enhance postcontrast. Associated hemorrhage modifies the

imaging appearance. Nodule rupture is a rare complication, with the resultant appearance mimicking an adenoma.

Ultrasonography is generally noncontributory.

The T1-weighted MR appearance is variable; most nodules are hypoto isointense on T2weighted images.

These regenerating nodules contain Kupffer cells and take up Tc-99m–sulfur colloid.

Inflammatory Tumor

Inflammatory tumors (pseudotumors) are rare in the liver. Some are discovered incidentally. Their etiology is unknown; although some probably represent an atypical inflammatory reaction to infection, others appear to be a variant of Castleman’s disease (These tumors are discussed in more detail in Chapter 14). Some progress in size and are multifocal. Resection establishes the diagnosis, although at times even then a diagnosis is not definitive. At times immunohistochemistry is useful to exclude a malignancy.

Computed tomography and US usually reveal a poorly defined heterogeneous hypovascular tumor mimicking a neoplasm. Magnetic resonance contrast enhancement is variable, at times with rapid wash-out of contrast. Gadolinium enhanced gradient-echo MR of one tumor revealed an early, intense peripheral enhancement followed by homogeneous enhancement (83); no uptake was evident with ferumoxides nor mangafodipir. Some of these tumors are surrounded by a hyperintense capsule. In general, imaging suggests a malignancy.

Regenerating Nodules in Cirrhosis

Cirrhotic livers develop small nodules, called regenerating or regenerative nodules and siderotic nodules, histologically consisting of either foci of regeneration or dysplasia (or both), together with supporting stroma. They contain hepatocytes, bile ducts, Kupffer cells, and fibrosis, and often contain increased iron. The reason for their formation is unknown, but they appear to represent a response to growth factors. These regenerating nodules tend to be small and scattered throughout the liver.

In a broader context, regeneration is a common feature after hepatocyte damage,

regardless of etiology. Regenerative activity among liver cells and their nuclei is mild in a setting of primary biliary cirrhosis, more so in alcoholic cirrhosis, and most prominent in posthepatitic cirrhosis (HBV related); thus patients with posthepatitic cirrhosis are at greater risk for carcinoma than those with other types of cirrhosis.

Histologic differentiation of a dysplastic nodule from a regenerating nodule in a cirrhotic liver tends to be difficult from small biopsy specimens.

Neither CT nor US detects smaller nodules. Precontrast, detectable nodules are isoto hyperdense, depending on their iron content and, in fact, are better identified precontrast than postcontrast. In distinction to most liver tumors, the blood supply to regenerating nodules is mostly portal venous, and they are thus isodense during portal phase imaging. Because of their mostly portal blood supply, these nodules do not enhance much on postcontrast arterial phase CT. In distinction to hepatocellular carcinomas,which derive most of their blood from an arterial supply, a regenerating or dysplastic nodule should be suspected if dynamic CT suggests a mostly portal venous blood supply to a nodule. One should keep in mind, however, that a dual blood supply is normal, and in actual practice this blood supply differentiation is difficult to apply to small tumors.

ADVANCED IMAGING OF THE ABDOMEN

Computed tomography arterial portography performed prior to partial liver resection for hepatocellular carcinoma in cirrhotic patients revealed regenerative nodules as enhancing 3- to 10-mm tumors surrounded by lower density fibrous septa (84) (Fig. 7.24); CT hepatic arteriography identified regenerative nodules as nonenhancing tumors, similar in size to those seen with arterial portography, surrounded by enhancing fibrous septa. Tumor conspicuity is determined to a large degree by surrounding fibrosis. Nevertheless, CT hepatic arteriography detects more nodules and is more sensitive than CT arterial portography.

With US, regenerating nodules range from hypoechoic to hyperechoic compared to normal liver parenchyma.

Magnetic resonance imaging is more sensitive in detecting regenerating nodules than CT or US. Most regenerating nodules are isoto hypointense on T1and hypointense on T2weighted images. Surrounding inflammation and fibrous septa tend to be hypointense on T1and isoor hyperintense on T2-weighted images. Their hypointensity on T2-weighted sequences is secondary to a paramagnetic effect from their increased iron and, in part, to surrounding fibrous septa. More complex nodules are inhomogeneous and contain discrete foci of iron (siderotic nodules),and T2-weighted MR in these reveals a hypointense focus due to the iron within a larger hyperintense iron-poor nodule.

LIVER

Regenerating nodules enhance with MR contrast similar to liver parenchyma and thus are difficult to identify postcontrast.

An occasional regenerating nodule infarcts and resembles a hypovascular hepatocellular carcinoma or a metastasis on CT and MR imaging.

Dysplastic Nodules

The currently accepted term dysplastic nodule was preceded by a varied nomenclature, including adenomatous hyperplasia, adenomatoid hyperplasia, macroregenerative nodule, hepatocellular pseudotumor, and regenerative and dysplastic nodules. Whether dysplastic nodules are neoplastic or hyperplastic in origin is not settled, although a number of authors believe they represent a transition in eventual hepatocellular carcinoma development and thus should be considered premalignant, keeping in mind that some cancers appear to bypass a dysplastic stage.

A distinct nodule containing dysplastic cells without histologic evidence for malignancy is the hallmark of dysplastic nodules, although not uncommonly a pathologist identifies a small focus of hepatocellular carcinoma. From a clinical and imaging viewpoint, dysplastic nodules are often considered to represent one end of a continuous spectrum from benign to malignant tumors. Nevertheless, whether carcinogenesis involves a stepwise progression from a regener-

ative nodule to a dysplastic nodule and an eventual carcinoma is conjecture; some cancers appear to bypass a dysplastic stage.

Dysplastic nodules develop earlier in the course of cirrhosis in patients with chronic hepatitis than in those with an alcohol cause. Also, these nodules are more common in a setting of several congenital conditions such as a1- antitrypsin deficiency and Wilson’s disease.

Pathologists distinguish low-grade from high-grade dysplasia by the degree of cytologic atypia. Lack of invasion distinguishes highgrade dysplasia from malignancy. In distinction to hepatocellular carcinoma, immunohistochemical staining reveals no a-fetoprotein expression in dysplastic nodules. A confident diagnosis of dysplasia is problematic from a small needle biopsy, and often a resected specimen is necessary to exclude malignancy. Also, a biopsy finding of dysplasia does not exclude an adjacent malignancy.

Dynamic CT achieves a low sensitivity in detecting dysplastic nodules when subsequent orthotopic liver transplantation is used as a gold standard. Computed tomography arterial portography and CT hepatic arteriography confirm a variable and inconsistent portal and arterial blood supply (85) (Fig. 7.25).

Dysplastic nodules vary in their MR appearance, although they are rarely hyperintense on T2-weighted images, and such a finding helps differentiate them from mostly hyperintense hepatocellular carcinomas. Dysplastic nodules

tend to have a mostly portal venous blood supply and, in distinction to hepatocellular carcinomas, do not enhance as intensely during the arterial phase. Nevertheless, dysplastic nodules are believed to be capable of inducing angioneogenesis, and some do contain enough of an arterial blood supply to make arterial-phase differentiation difficult. A hepatocellular carcinoma developing in a dysplastic nodule tends to be hyperintense within a hypointense tumor on T2-weighted images, although the presence of cirrhosis makes MR differentiation difficult. Pretransplantation MRI in cirrhotic patients detects only a minority of dysplastic nodules.

Adding confusion to this issue, some nondysplastic nodules in cirrhotic livers are hyperintense on T1-weighted gradient-echo MRI and do not lose signal intensity on opposed-phase imaging (86); they also do not enhance during the arterial phase.

Because dysplastic nodules contain Kupffer cells, on post-SPIO contrast these nodules range from isoto hypointense. The contrast ratios between dysplastic nodules and their surrounding liver parenchyma during SPIO-enhanced T2-weighted fast spin echo (FSE) MRI was zero or nearly zero (87); histopathologically, essentially no difference was evident in the number of Kupffer cells in these dysplastic nodules and surrounding parenchyma.

The risk of cancer in a cirrhotic liver containing dysplastic nodules makes nodule resection a rarely viable option. Liver transplantation is considered in these patients.

Extramedullary Hematopoiesis

Intrahepatic extramedullary hematopoiesis develops in some congenital hematologic disorders and hematologic malignancies. Hematopoiesis ranges from focal tumors to a rare extensive diffuse involvement. It can mimic fatty infiltration.

Intrahepatic Spleen

Splenic tissue located outside Glisson’s capsule usually represents splenosis after implantation of splenic tissue due to prior splenic trauma.

Intrahepatic spleens are uncommon. Most present as a focal tumor. Splenic tissue partly embedded into liver should represent hyperpla-

ADVANCED IMAGING OF THE ABDOMEN

sia of congenitally ectopic splenic tissue rather than splenosis as long as it is beneath a common capsule, even in a patient postsplenectomy.

Teratoma

A teratoma is a developmental anomaly, arising from embryonal totipotential cells and containing ectoderm, mesoderm, and endoderm tissue. It is rare in the liver. It occurs primarily in infants. Some are associated with an elevated serum a-fetoprotein level and thus are confused with a hepatoblastoma.

Cystic Lesions

The differential diagnosis for an intrahepatic cyst is rather extensive. Rare cystic metastases to the liver include neuroendocrine and ovarian neoplasms. Primary cystic neoplasms are mostly of bile duct origin and are discussed in Chapter 8.

Liver and renal cysts develop in a setting of Ehlers-Danlos syndrome. The origin of some intrahepatic cysts is difficult to determine and histologic examination not only of the cyst content but also of the cyst wall is often helpful. Pathologists distinguish between true cysts (i.e., those containing an epithelial lining) and other cystic structures. A need to establish a specific diagnosis also influences therapy. Thus while percutaneous aspiration and ethanol sclerotherapy is therapeutic for some cysts, cystectomy, cyst unroofing, or fenestration provide access to a larger cyst wall specimen.

Uncomplicated cysts are hypointense on T1and hyperintense on T2-weighted images. They do not enhance on postgadolinium arterialphase T1-weighted SGE images; they appear hypointense during portal venous phase, and continue to maintain their lack of enhancement during the even later hepatic venous phase.

Peribiliary Cysts

Peribiliary cysts are believed to be secondary to obstruction and dilation of peribiliary glands; these cysts are distinct from congenital simple cysts. They are more common in a cirrhotic liver.

These cysts tend to be multiple, tubular, <1.5cm in diameter, and are located either close to the hilum or along larger portal tracts. Some

LIVER

enlarging cysts obstruct adjacent bile ducts. If extensive, a string-of-beads appearance is evident. A peribiliary cyst is also suggested if CT or US reveals water-density cysts around secondto fourth-order intrahepatic portal vein branches.

On T2-weighted MR images these cysts are similar in appearance to dilated intrahepatic bile ducts.

Simple Cysts

Simple liver cysts are common entities. They are lined by epithelium similar to that in bile ducts but they do not communicate with bile ducts. They are more common in women and increase in number with age. Some are congenital and probably originate from dilated aberrant bile ducts that did not connect with the biliary tree.

Most simple cysts are asymptomatic and are discovered as an incidental finding. An occasional one becomes huge and compresses adjacent structures. Some are complicated by bleeding or infection. Hemorrhage often leads to pain. Spontaneous rupture also occurs, at times into the peritoneal cavity.

Most simple cysts are unilocular with no internal structures. Occasionally cyst wall calcifications develop.

These cysts range in CT density between 0 and 10HU. The cyst wall is thin or not visible, a finding not seen with most intrahepatic abscesses. A thin wall is seen, however, with cystadenomas and cystocarcinomas. A simple cyst reveals no contrast enhancement. Computed tomography of most simple cysts is diagnostic. Hemorrhage into a cyst increases the CT attenuation by 20HU or so, seen with MRI as increased signal intensity.

Ultrasonography of a simple cyst reveals an anechoic lumen, increased throughtransmission, and a thin, well-defined wall. Increased echogenicity generally is secondary to hemorrhage.

Simple cysts are very hypointense on T1and markedly hyperintense on T2-weighted MR images, an appearance similar to a hemangioma and an occasional metastasis. Contrastenhanced MRI distinguishes an enhancing hemangioma from a nonenhancing cyst.

Cytology, a-fetoprotein, CA 19.9, CEA, fluid culture, and lack of communication between the

cyst and intrahepatic bile ducts shown by cholangiography aid in excluding other, more ominous diagnoses. Especially with hemorrhage into these cysts, the differential diagnosis includes a cystic or necrotic metastasis and a primary hepatobiliary cystic neoplasm.

Because these cysts are lined by epithelium, they recur after simple aspiration. They are amenable to laparoscopic fenestration and percutaneous ablation therapy. The simplest initial therapy for patients with symptomatic cysts is US-guided percutaneous aspiration and ethanol sclerotherapy. Few complications are encountered.

Ciliated (Foregut) Cysts

The presence of ciliated epithelium within a liver cyst should suggest a hepatic foregut cyst. These rare, congenital lesions are usually less than several centimeters in size, well defined, unilocular, isolated, and subcapsular in location. Some bulge beyond the liver outline and a thin cyst wall is evident. They tend to be hypodense on precontrast CT and hypoto anechoic on US. They have a variable signal intensity on T1and are strongly hyperintense on T2weighted MR images. These cysts do not enhance postcontrast, but at times the cyst wall will enhance. They tend to be filled with bloody mucinous fluid and their hyperintensity on T1weighted images depends on the amount of mucin and blood within the cyst.

Although a foregut cyst can be strongly suspected from its MR appearance, occasionally a cystic metastasis has a similar appearance.

Lymphangioma

The classification of lymphangiomas varies. They are related to hemangiomas in their histologic appearance and, when generalized, the term systemic cystic angiomatosis is often used. In the liver they range from solitary to multiple, but are rare. These cystic nonepithelial tumors are lined by endothelial cells and are filled with serous fluid or chyle. Most are solitary.

Imaging reveals complex cysts containing thin septa.

Intrahepatic Pseudocysts

Intrahepatic pseudocysts in a setting of pancreatitis are rare. Computed tomography reveals