Материал: Advanced Imaging of the Abdomen - Jovitas Skucas

moses. 3D gadolinium-enhanced MR readily identifies vascular complications detected by angiography or surgery, in one study reaching 100% sensitivity but only 74% specificity in detecting >50% hepatic artery stenoses (166).

Arterial Complications: The most common posttransplant vascular complication is hepatic artery thrombosis. Uncorrected, in most patients thrombosis leads to fulminant sepsis, liver infarction, necrosis, and graft loss. Patients with interposition of an allogeneic iliac graft or anastomosis to an aberrant right hepatic artery appear prone to develop hepatic artery thrombosis. Thrombosis can occur early or even as late as a year after transplantation. Clinically, some but not all these patients have elevated liver transaminases, sepsis, recurrent cholangitis, or gas within the liver. Transcapsular arterial collateral vessels tend to develop after hepatic artery occlusion.

Computed tomography detects most hepatic artery thromboses. Also, CT tends to identify an irregularly shaped hypodense region both preand postcontrast; some of these patients develop necrosis and biliary ischemia, findings not specific for hepatic artery thrombosis but they should suggest further investigative procedures. Although some studies have shown Doppler US and CT sensitivities and specificities to be roughly comparable, one problem with US is that the hepatic artery is often incompletely visualized. The combined use of color and power Doppler US are helpful. At times the lack of hepatic artery visualization, even after

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Levovist injection, is due to artery occlusion. Nevertheless, some authors have expressed caution on relying on US, with false-positive or -negative results being due to rejection, recurrent hepatitis, aberrant vascular anatomy, hypotension, presence of collaterals, and other reasons.

Color Doppler US detection of transcapsular collateral flow or hepatic artery flow in the wrong direction should raise suspicion for hepatic artery thrombosis.

An occasional patient with hepatic artery thrombosis and hepatic infarction does not undergo retransplantation. Ultrasonography in these patients shows hypoechoic regions with preservation of portal tracts; these changes either resolve or progress to infarction, seen as local hyperechoic regions. Eventually these patients develop biliary strictures, bilomas, abscesses, and calcifications.

Hepatic artery stenosis tends to be more insidious than thrombosis and is most common at the anastomosis; it results in an increase in flow velocity; at times turbulent flow is detected. Abnormal Doppler US values for both resistive indexes and systolic acceleration times are more accurate predictors of stenosis than either one alone as an independent parameter. Hepatic artery stenoses, either at the anastomosis or at other sites, are amenable to percutaneous transluminal balloon angioplasty (Figs.7.53 and 7.54). Complications of balloon angioplasty include artery spasm, pseudoaneurysm and rupture. An aortohepatic artery graft (Fig. 7.55) or

retransplantation are necessary if angioplasty is not successful.In a rare liver transplant ischemia develops secondary to an increased hepatic artery resistive index and increased splenic artery blood flow without evidence of a stenosis; some of these patients benefit from splenic artery embolization with coils.

Aneurysms occur at hepatic artery anastomoses. Aneurysm rupture leads to hemobilia, hemoperitoneum, or gastrointestinal tract bleeding. Ultrasonography reveals a cystic tumor. An aneurysm is suggested if this tumor communicates with the hepatic artery; otherwise the appearance mimics any other fluid collection. Doppler US is helpful in detecting internal blood flow, if present.

Splenic artery aneurysms are associated with portal hypertension. They are identified in about 15% of liver transplant patients.

Does hepatic arterial chemoembolization for hepatocellular carcinomas before orthotopic liver transplantation influence posttransplant hepatic arterial complications? Among 47 patients who underwent hepatic arterial chemoembolization pretransplantation, 13% developed hepatic arterial complications after transplantation (and an 8% prevalence of hepatic arterial thrombosis), while among controls 6% developed hepatic arterial complications (and 5% prevalence of hepatic arterial thrombosis) (167); the authors concluded that pretransplantation hepatic artery chemotherapy is not a risk factor for posttransplantation hepatic artery complications.

Venous Complications: The most common venous complication is portal vein thrombosis or stenosis and resultant extrahepatic portal hypertension. These patients develop ascites and variceal bleeding, at times life threatening.

The entire portal vein length needs to be visualized by real-time US to detect portal vein stenosis. Pressure gradients across a stenosis can be calculated from observed Doppler US velocities. Angiography verifies US findings. Transhepatic portal venography serves as a guide for balloon venoplasty of a stenotic segment. Occasionally an intravascular stent is necessary (Fig. 7.56). Surgical reconstruction is necessary only in a minority of these patients.

Percutaneous transhepatic balloon venoplasty was successful in 76% of children and adolescents with anastomotic portal vein stenoses in a setting of reduced-size hepatic

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transplantation (168); portal vein occlusion prevented portal vein access in the other 24%.

Inferior vena caval stenosis and hepatic vein stenosis is less common than portal vein involvement. It has led to Budd-Chiari syndrome. In some hands percutaneous transluminal angioplasty has had limited success, but others have found balloon angioplasty to be safe and effective in treating these chronic stenoses, and still others have achieved long-term angioplasty success only in combination with stenting (Fig. 7.57).

CT evaluates hepatic venous congestion after living donor liver transplantation; decreased contrast enhancement during CT portal venous phase correlates with severity of hepatic venous congestion and increased serum bilirubin level (169).

Postbiopsy

Complications of liver biopsy posttransplant include hemoperitoneum, hemothorax, pneumothorax, arterioportal fistula, and possible infection.

The overall prevalence of severe liver biopsy complications in posttransplant patients is similar to that found in patients without transplantation; posttransplant patients, however, are more prone to bleeding complications.

Malignancy/Lymphoproliferative Disorder

After liver transplantation and associated immunosuppression these patients are at increased risk for developing malignancies. In patients surviving more than several months posttransplantation, about 5% will develop a new tumor. Lymphoma is most common, at times being discovered within several months of transplantation. Of nonlymphoid cancers, skin cancer is the most common; other new tumors consist of a broad spectrum and include gastrointestinal adenocarcinomas, genitourinary cancers, laryngopharyngeal carcinomas, Kaposi’s sarcoma, and malignant melanoma. Some of these carcinomas grow rapidly after liver transplantation.

After orthotopic liver transplantation, a hepatocellular carcinoma recurs most often in lungs or in transplanted liver; it can be single or multiple. In these immunosuppressed patients CT is

more sensitive than serum tumor markers in detecting recurrence. Nevertheless, if a patient undergoes a liver transplant for a hepatocellular carcinoma and then develops a carcinoma in the allotransplanted liver, what is the origin of the second carcinoma? Generally recurrence of the original carcinoma is suspected, but proof can be obtained from carcinoma, transplanted liver, and recipient DNA to establish whether the carcinoma DNA is similar to or differs from the patient’s and donor liver DNA.

Computed tomography abnormalities are evident in most patients with proven posttransplantation lymphoproliferative disorder, with extranodal disease being more common than splenic involvement or adenopathy (170); extranodal involvement included liver (53%), small bowel (25%), kidney (17%), mesentery (14%), and to a lesser degree adrenal glands, abdominal wall, colon, stomach, and gallbladder. A poorly marginated periportal infiltrate can encase the adjacent bile ducts and blood vessels. Serologic evidence of exposure to Epstein-Barr virus is often evident in these patients.

Other Biliary Complications

Primary biliary cirrhosis recurs in some transplanted livers. It should be kept in mind that aside for recurrence of their disease these patients also develop other, similar appearing, complications. Thus chronic graft rejection can mimic recurrence of primary biliary cirrhosis.

Postoperative immunotherapy does not suppress underlying inflammatory bowel disease; in fact, reactivation of inflammatory bowel disease and growth of colon cancer have been reported after liver transplantation.

Reported recurrence of hepatitis C infection after orthotopic liver transplantation ranges from about 60% to almost universal, with varying clinical severity. Some patients develop severe cholestatic hepatitis. The long-term sequelae of recurrent infection include scarring and progression to end-stage liver disease. Interferon antiviral therapy appears of benefit. Posttransplantation diabetes occurs more often than expected in those patients who had hepatitis C before their transplantation.

A retrospective review of 4001 of orthotopic liver transplantations found 48 bowel obstruc-

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tions (171); etiology included adhesions, bowel ischemia, internal and external hernias, and volvulus. Obstructions due to internal hernias were transmesenteric or retroanastomotic and were related to choledochoenteric anastomoses. Neoplastic bowel obstruction included posttransplant lymphoproliferative disease and even an unsuspected colon carcinoma. Bowel obstruction tends to be difficult to diagnose in these patients mostly due to low suspicion and thus the lack of appropriate imaging studies.

Posttransplantation pancreatitis is uncommon.

These patients are prone to Candida liver abscesses, even years after liver transplantation. Hepatic abscesses are treatable by percutaneous drainage.

Pulmonary and soft tissue calcifications have developed in transplant patients with severe cytomegalovirus infection.

Gilbert’s syndrome and transplantation of a liver containing an inborn error of metabolism should be suspected if unconjugated bilirubin levels remain elevated in the face of normal liver enzymes.

In Children

In children, biliary complications consisting of biliary obstruction or leak occur during the first several weeks after transplantation. Ascites is not uncommon in children after liver transplantation.

The prevalence of vascular complications appears to be greater in children than in adults. Hepatic artery thrombosis is the most serious complication in children, occurring in almost 10%; portal vein thrombosis is less common. Surgical edema has led to an increase in intraabdominal pressure to the point of hepatic artery or portal vein compression or occlusion.Various biliary complications are similar to those seen in adults.

Children are typically initially followed with daily Doppler US. As in adults, Doppler US evaluates vascular patency; a sensitivity of over 90% is achieved in showing a patent hepatic artery and portal vein. Computed tomography serves to detect suspected liver parenchymal ischemia and abscesses.

LIVER

Rare posttransplant leiomyosarcomas appear to be more common in pediatric hepatic allograft patients than in adults.

Liver Cell Transplantation

Transplanted hepatocytes remain viable and function on a long-term basis. Preliminary studies suggest that such transplantation is useful for some familial hyperbilirubinemia conditions, but little clinical data is available.

Bone Marrow Transplantation

Liver veno-occlusive disease is an ominous complication after bone marrow transplantation, usually developing shortly after transplantation. Among 100 patients receiving total body irradiation or busulfan therapy followed by hematopoietic stem cell transplantation, 25% developed hepatic veno-occlusive disease and 9% died (172).

A hepatic artery resistive index below 0.55 suggests liver dysfunction in children undergoing bone marrow transplantation, but whether duplex US is sufficiently accurate in diagnosing veno-occlusive disease is not clear.

Hepatectomy/Embolization

The ability of the liver to regenerate was already known to ancient Greeks. In response to injury and influenced by a number of factors, the most important being hepatocyte growth factor, hepatocytes have an ability to divide and grow. Regeneration is a rapid process, peaking within several weeks and then gradually slowing. Such regeneration is most obvious after a partial hepatectomy, but also occurs after segmental portal vein obstruction and atrophy of involved segments. This phenomenon can be used to advantage prior to major resection by performing portal vein embolization; atrophy of embolized segments induces enlargement of remaining nondiseased segments. Such portal vein embolization is most often performed if initial residual nondiseased liver tissue is deemed to be insufficient to permit a major resection. Either a percutaneous transhepatic approach or surgical cannulation of a portal vein branch, such as the superior mesenteric vein, is used. Coils, iodized oil, and other agents

serve as embolic agents. Portal blood flow to noninvolved liver, measured by Doppler US, increases markedly after embolization and then approaches baseline within 2 weeks or so; parenchymal enlargement is directly related to increased portal blood flow.

The amount of liver tissue necessary for survival after a partial hepatectomy is not established, but it varies with the degree of underlying liver disease.

Examination Complications

Vascular Procedures

Patients with atherosclerosis undergoing vascular surgery or arterial catheterization procedures are at risk for cholesterol crystal embolization. In the liver such embolization has led to focal necrosis. Usually multiple organs are involved.

Thorotrastosis

Clinical

The use of radioactive a-emitting colloid thorium dioxide (Thorotrast) as a contrast agent during the 1930s to 1950s is associated with numerous malignancies, including angiosarcoma, cholangiocarcinoma, and hepatocellular carcinoma. Synchronous cancers have developed. In addition, a-emissions cause extensive liver and spleen fibrosis and liver cirrhosis. Thorium 232 has a half-life of 1.4 ¥ 1010 years and after intravascular injection is stored in reticuloendothelial cells.

A German Thorotrast study group was started in 1968 and includes 2326 Thorotrast patients (173); through 1999, 454 primary liver cancers have been registered, compared to three in a control group. A correlation exists between mean accumulated liver dose and risk of liver cancer, being about 600 per 10,000 persons for a liver exposure of 1Gy.

Imaging

Thorotrast liver and spleen deposits are readily visualized with conventional radiography. Computed tomography shows Thorotrast as highdensity collections in the liver, spleen, and, at

times, in lymph nodes. Ultrasonography reveals a heterogeneous echo pattern.

With MRI, the spleen contrast-to-noise ratio on T1-weighted images is lower than normal. Actual Thorotrast deposits are not seen on MRI, but MRI is useful in detecting Thorotrastinduced liver and biliary tumors.

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