| | Budd-Chiari syndrome: A review of imaging findingsReceived 16 October 2006; accepted 2 November 2006. Abstract Budd-Chiari syndrome is an uncommon, often fatal disorder resulting from an obstructed hepatic venous outflow tract. The obstructive lesion is situated in the main hepatic veins, in the inferior vena cava or in both. The nature, location and extention of the obstruction can be displayed on diagnostic imaging techniques. In addition to this direct evidence, the indirect findings of venous obstruction such as the presence of intra- and extrahepatic collateral veins, when combined with the altered morphology and enhancement pattern of the liver enables one to arrive at a confident diagnosis. In patients with suspected Budd-Chiari syndrome, gray-scale sonography with complementary support of color and pulsed Doppler examinations is the first step in approaching the diagnosis. It is followed by a contrast-enhanced cross-sectional technique, preferrentially by MR angiography. The patients with a high clinical suspicion of Budd-Chiari syndrome may undergo hepatic venography or venacavography directly so that a potential of recanalization (e.g. percutaneous transluminal angioplasty with or without stent placement or TIPS) of the obstructed segment under the guidance of these techniques would not be delayed. 1. Introduction  Budd-Chiari syndrome is a rare entity whose diagnosis is usually suspected during radiologic investigations. Imaging findings of this syndrome have an important role in directing the clinician to appropriate management algorithm. In this article, it is aimed to define an approach to the diagnosis of Budd-Chiari syndrome based on abnormal imaging findings. 2. Definition According to the European Group for the Study of Hepatic Vascular Diseases, Budd-Chiari syndrome is defined as hepatic venous outflow obstruction at any level from the small hepatic veins to the junction of the inferior vena cava and the right atrium, regardless of the cause of the obstruction. Cardiac etiologies of hepatic congestion or veno-occlusive disease (sinusoidal obstruction syndrome) are not included in this definition [1]. 3. Classification At present, no standardized classification is available for Budd-Chiari syndrome [1]. Several classifications have been proposed based on pathogenesis (primary or secondary), location of the venous occlusion (Types I–III), or clinical and morphologic features (fulminant, acute, subacute and chronic) [2], [3], [4]. Budd-Chiari syndrome is classified as primary when it is caused by an intrinsic luminal web or thrombus, and secondary when it is caused by an extraluminal compression or tumoral invasion [1], [2], [3], [4], [5]. 4. Pathogenesis and pathologic findings Membranous obstruction of suprahepatic inferior vena cava, which is also known as primary Budd-Chiari syndrome, is due to fibromuscular membrane (web) or an acquired lesion. Membrane or web arises from the wall of the vessel and may obliterate the lumen completely or partially [6]. This type of lesion is believed to be a sequela of long-standing thrombosis [7]. The etiology of the venous thrombosis is obviously an important consideration. Hematologic abnormalities such as myeloproliferative disorders, paroxymal nocturnal hemoglobinuria, the antiphospholipid syndrome, inherited deficiencies of protein C, protein S and antithrombin III, factor V Leiden mutation, prothrombin-gene mutation, methylenetetrahydrofolate reductase mutation are responsible for the majority of cases of Budd-Chiari syndrome [5], [8]. The other factors that contribute to the development of Budd-Chiari syndrome include pregnancy immediate postpartum period and use of oral contraceptives. The secondary Budd-Chiari syndrome is caused by an extraluminal compression of a space occupying lesion or luminal invasion of malignant tumor (renal cell carcinoma, hepatocellular carcinoma, adrenal carcinoma, hepatic metastasis, primary leiomyosarcoma of inferior vena cava) [5], [8]. In some instances, the cause is difficult to establish, and in others, multiple etiologic factors can play role in the development of the venous occlusion [5]. As the hepatic veins constitute the sole efferent vascular drainage of the liver, obstruction or increased pressure within these vessels or in their radicles result in an increased sinusoidal pressure. Regardless of the etiology, elevation of hepatic sinusoidal pressure leads delayed or reversed portal venous outflow. The portal venous stasis and congestion cause hypoxemic damage in adjacent hepatocytes. Afterwards centrilobular fibrosis, nodular regenerative hyperplasia, and ultimately cirrhosis occur. Main alterations in hepatic morphology include atrophy of peripheral regions and hypertrophy of the caudate lobe and central portions of the liver [8], [9]. Liver biopsy is an important procedure to confirm the diagnosis and assesses the degree of hepatocellular damage. Histopathologic clues of venous outflow obstruction are centrizonal congestion, hemorrhage and cell necrosis, sinusoidal dilatation with or without central vein obliteration and congestive pattern of cirrhosis [2]. 5. Clinical findings The clinical presentation of Budd-Chiari syndrome depends on the extent and rapidity of the hepatic vein occlusion and on whether a venous collateral circulation has developed to decompress the hepatic sinusoids. Rapid onset of abdominal pain due to liver congestion and insidious onset of intractable ascites are major manifestations of acute form. The chronic form is manifested as complications of cirrhosis [2], [8]. Budd-Chiari syndrome may be quite indolent or even asymptpomatic in some patients [5]. 6. Radiologic procedures The diagnostic imaging is the starting point in the investigation for Budd-Chiari syndrome. The structural changes detected on imaging methods, when integrated with pertinent clinical findings and results of laboratory tests, enables one to arrive at a confident diagnosis. However, it should be noted that the imaging findings are usually overlooked despite they are rather typical. It is not unusual for patients with chronic forms of Budd-Chiari syndrome to be diagnosed with liver cirrhosis. Real time gray-scale sonography combined with color flow and duplex Doppler examination is considered by some to be the initial imaging technique [1], [8], [10], [11]. 6.1. Ultrasonography and color Doppler sonography The most important goal in patients who refers with the suspicion of having Budd-Chiari syndrome is assessment of the hepatic vein patency and size. The state of the inferior vena cava is also noteworthy. The obstructive process in the hepatic veins or in the inferior vena cava may have diverse appearances. The presence of echogenic material in the lumen indicates a thrombotic process. Color and pulsed Doppler techniques as the complementary of gray-scale sonography is very beneficial to confirm the diagnosis (Fig. 1). The sensitivity of pulsed Doppler examination in Budd-Chiari syndrome is 87.5% [12]. In a recent study, it is found that contrast-enhanced sonography is superior to gray-scale and color Doppler imaging for the detection and characterization of hepatic vein thrombosis [13]. Sonography has been used for the demonstration of webs since late 1980s [14]. Membrane or web is seen as an echogenic crescent-shaped focus constricting the lumen (Fig. 2). A tiny calcification presumably at the site of the web can be demonstrated. In segmental obstruction of inferior vena cava, a hyperechogenic cord-like structure is seen to obliterate the hepatic portion of the vessel [6]. Similar appearance in hepatic veins is seen in cases of chronic thrombosis (Fig. 3). Dilatation of one of the main hepatic veins may have a considerable importance in the diagnosis. Large hepatic vein can be either the indicator of a downstream stenosis usually involving the ostium of the hepatic veins or due to intrahepatic collateralization. A smaller caliber of a hepatic vein than normal while the other being considerably large should be a cautionary sign. In advanced disease, the calibers of one or more main hepatic veins are markedly reduced or even they may not be visualized [15], [16], [17]. Although non-visualization of hepatic veins is accepted as a hallmark of Budd-Chiari syndrome, patent hepatic veins may occasionally be obscured within the cirrhotic parenchyma even though they are patent. While imaging the patients with severe parenchymal changes, color Doppler imaging is useful to detect flow within hepatic venous branches that are inapparent on gray-scale images. Besides the main hepatic veins, inferior right hepatic vein and caudate vein are two vessels which should be examined during the sonographic evaluation of Budd-Chiari syndrome. Inferior right hepatic vein constitutes the main drainage vessel of the right postero-inferior area (segment 6) of the liver [18]. Actually it is present in 18% of normal population [19]. This vein is enlarged and becomes the main drainage vessel of the right lobe in patients with right hepatic vein occlusion [18] (Fig. 4). The drainage of caudate lobe via caudate veins is preserved in Budd-Chiari syndrome. Caudate vein can be seen in 50% of patients with Budd-Chiari syndrome (Fig. 5). When US reveals a caudate vein equals to or larger than 3 mm in diameter in the appropriate clinical setting, one should questioned the presence of Budd-Chiari syndrome [20]. Intrahepatic collateral circulation is very useful indirect imaging finding for the diagnosis, being present in more than 90% of patients [21]. These intrahepatic collaterals connect the patent portion of the obliterated hepatic vein with a normal vein, with an accessory vein or with caudate lobe veins. They have quite characteristic configurations such as “hockey-stick” [15], “comma”, “undulated”, “h-shaped”, or “inverted U-shaped” and are easily recognized at both gray-scale and color Doppler imaging (Fig. 6). Because of their locations, the sonographic demonstration of the subcapsular collateral veins and the veins draining into suprahepatic portion of the inferior vena cava close to the right atrium may be difficult. In contrary to the flow in the portal vein branches, the triphasic nature of the hepatic vein flow in normal conditions, is advantageous for supporting the abnormal gray-scale sonography findings. The normal flow pattern in the hepatic veins is influenced by the pressure in the right atrium, compliance of the liver parenchyma and alterations in respiratory cycle. The normal flow direction is towards to the inferior vena cava. However, in Budd-Chiari syndrome, flow in the inferior vena cava, in the hepatic veins or in both changes from phasic to absent, continuous (flat), turbulent or reversed [11], [12], [15], [17] (Fig. 7). Neverthless, the absence of normal triphasic pattern in the hepatic veins is not a specific finding for Budd-Chiari syndrome. The continuous flow pattern is also seen patients with decreased hepatic parenchymal compliance as in cirrhosis of other etiologies. The ability to demonstrate the reversal of flow direction may be the most important superiority of Doppler imaging in comparison to contrast-enhanced cross-sectional methods (Fig. 8). The portal blood flow is affected in Budd-Chiari syndrome and is expected to be slowed [11]. Reversed flow direction in the main portal vein may be the consequence of synchronous occlusion in three main hepatic veins. In this circumstance, the portal vein becomes the draining vein of the liver and hepatofugal flow is detected in intrahepatic portal vein branches. Ascites and abnormal hepatic configuration are present in vast majority of the cases. Caudate lobe which has separate drainage into the inferior vena cava hypertrophies and may reach huge dimensions. In Budd-Chiari syndrome, the mean anteroposterior diameter of caudate lobe is greater than 35mm [20] (Fig. 9). The inferior vena cava may show narrowing due to compression by enlarged caudate lobe. Documentation of TIPS stent patency with a higher degree of accuracy is also an advantage of Doppler imaging [22] (Fig. 10). The limitations of sonography are restriction from body habitus, intestinal gas or excessive ascites, failure to detect fresh thrombus in veins, failure to demonstrate patent veins within congested or conversely, shrunken cirrhotic liver, failure to demonstrate retroperitoneal collaterals unless they are hugely dilated, and operator-dependency. In conclusion, despite of its limitations, sonography is usually the first imaging method of choice in Budd-Chiari syndrome. It offers characteristic imaging findings necessary for the diagnosis and provides objective hemodynamic datum when combined with Doppler technique. Moreover, it is relatively inexpensive, requires no contrast material and available in almost all institutions. 6.2. Computed tomography CT findings of Budd-Chiari syndrome have been established from clinical practice during the past 20 years [6], [23], [24]. CT shows a broad spectrum of morphologic and attenuation changes of the liver and of the hepatic vessels in obstruction of the inferior vena cava [24]. Non-visualization of the hepatic veins and fan-shaped enhancement of caudate lobe and central parts of the liver around the vena cava are two important findings [23]. The overall accuracy of CT for detecting hepatic venous thrombosis has been reported as 50% [4]. CT is not found to be useful in showing web in the inferior vena cava [6]. Heterogeneous patchy enhancenment (mottled appearance) is present due to stasis within hepatic sinusoids [23] (Fig. 11). Peripherally located linear, irregular or wedge-shaped hypoattenuated parenchymal areas can be seen [24] (Fig. 12). Parenchymal changes consistent with cirrhosis develop in the chronic stage. The presence of systemic collateral vessels; obliterated segment of the hepatic inferior vena cava, and rounded appearance of the infrahepatic inferior vena cava are the signs that help differentiation obstruction of the hepatic vena cava from posthepatitis cirrhosis [24]. CT angiography may be useful in demonstrating the vascular involvement and patency of TIPS shunt. The disadvantages of the method are exposing the patient to ionizing radiation or iodinated contrast material with the risk of allergic reaction and nephrotoxicity. 6.3. Magnetic resonance imaging MR imaging is preffered as a second line of investigation [1]. It is particularly beneficial in the evaluation of the patients with non-diagnostic ultrasonography. Its multiplanar capacity allows better anatomic orientation of the vessels. Particularly, the inferior vena cava can be visualized throughout its whole course on coronal images [15], [25], [26], [27]. Manifestations of MR imaging concerning the liver morphology and regional perfusional disorders are analogous to the features defined for contrast-enhanced CT [4], [28], [29]. However, some parenchymal lesions such as benign regeneration nodules, hemorrhagic necrosis and perfusion disorders can be characterized better with MR imaging. Benign regenerative nodules have been described in the literature in association with chronic Budd-Chiari syndrome [29], [30], [31], [32] (Fig. 13).The pathogenesis of benign regenerative nodules in Budd-Chiari syndrome is unclear. Hepatocellular growth factors and the disturbance of hepatic microcirculation may play role in their development [29], [30]. Surgical portocaval shunt can also be a risk factor in the pathogenesis of these nodules [30], [32]. Hepatic nodules in Budd-Chiari syndrome are typically multiple (>10), small (<4cm) and hypervascular [14], [29], [30], [31], [32]. On MR imaging, the benign hepatic nodules are often noted as hyperintense on T1-weighted images [29], [30], [31], [32] and iso-/hypointense on T2-weighted images [31], [32]. The nodules have an increased arterial supply corresponding to their dense enhancement on dynamic imaging. Number of such hepatic nodules progressively increase during the consecutive phases of MR angiography and their enhancement persists until the late venous phase [30], [33]. The patients with chronic end-stage liver disease are increased risk for development of hepatocellular carcinoma (HCC) [30], [31], [32] (Fig. 14). Thus, it is important to distinguish benign regenerative nodules from HCC. In general, the precontrast signal intensity characteristics and enhancement patterns of these two lesions permit their distinction. However, in some cases, the differentiation cannot be made on the basis of MR signal intensity [30]. An area of hemorrhagic necrosis can also simulate a neoplastic process [34]. Enhancement patterns between central and peripheral liver are found to be different for acute, subacute, and chronic Budd-Chiari syndromes [4]. In acute Budd-Chiari syndrome, both early and late gadolinium-enhanced MR images show diminished peripheral enhancement (Fig. 15). In subacute cases heterogeneously increased enhancement within the liver periphery is common finding. Enhancement differences throughout the hepatic parencyhma are minimal in chronic form of the disease. MR angiographic observations in patients with hepatic outflow obstruction support these enhancement patterns [35]. In chronic stage, atrophy of the right lobe of the liver (especially the peripheral regions), hypertrophy of the left lobe and the presence of regenerative nodules and contour irregularities show the progression to cirrhosis [23], [24], [36]. In about 40% of chronic cases the enhancement pattern of the liver is almost homogeneous [35]. Homogenity in enhancement may be the evidence of more stable hepatic perfusion that occurs after the formation of intra and extrahepatic collateral veins. In Budd-Chiari syndrome, hypertrophy of caudate lobe is found in 60–87% of all cases [6], [29], [35], [36] (Fig. 16). However, its size is not considered as a direct criterion to differentiate different stages of the disease. Multiphasic studies with MR angiography have an advantage over conventional angiography that; not only the hepatic veins and inferior vena cava but also hepatic arterial and portal venous system are examined with one injection of contrast material [37], [38]. Narrowing, stretching or distortions of arterial and portal vessels on MR angiography are indirect signs of severe structural changes in parenchyma (Fig. 17). In portal venous phase (second phase) of MR angiography, venous outflow obstruction can be inferred from the patchy enhancement of the liver. Because hepatic circulation is slow in Budd-Chiari syndrome, late venous phase imaging is necessary to visualize the patent hepatic veins and intrahepatic venous collaterals on contrast-enhanced MR angiography. Hepatic veins with sluggish flow may be missed if inadequate delay time is used. Besides this, in later phases of examination, intraluminal contrast material is diluted and the contrast difference between the vessels and parenchyma progressively diminishes. Thus thin collaterals seen on sonography may be inconspicuous at MR angiography. Thrombosis and structural abnormalities including a web in the hepatic veins or in the inferior vena cava can be demonstrated. The nature of obstruction (intrinsic or extrinsic in origin) as well as the condition of the surrounding tissues and both proximal and distal portions of the obstruction can be depicted by MR angiography (Fig. 18, Fig. 19) [37], [38]. The stenosis of the inferior vena cava due to external compression of the caudate lobe is seen as a smooth narrowing (Fig. 20) and is differentiated from the other types of stenosis by evaluating the vessel in various planes. Intrahepatic collateral veins are identified by their typical configuration or tortuous course (Fig. 21). The locations of extrahepatic collateral veins in Budd-Chiari syndrome are usually different from those seen in cirrhosis. Extrahepatic systemic venous collateral routes in Budd-Chiari syndrome can be evaluated in four groups and mainly develop in the retroperitoneum [39]. Deep and central tributaries of the systemic circulation (i.e., ascending lumber veins, vertabral venous plexus, azygos and hemiazygos veins) are the most frequent collateralized routes (Fig. 22). These vessels can be observed on MR angiography and CT in 36% and 32% of the cases, respectively [15], [29]. Unless they are hugely dilated retroperitoneal collaterals are not detectable on Doppler sonography. The other collateral vessels commonly seen in this entity are the left renal-hemiazygos pathway and inferior phrenic-pericardiophrenic veins (Fig. 23). The superficial tributaries of the systemic circulation (i.e, veins in the abdominal wall) may also function as a collateral. Although collateralized abdominal wall veins can be seen even at physical examination of the patients, they may not be displayed on MR angiograms if they remain outside the selected imaging volume. The accurate delineation of the portal system is particularly important when assessing the possible management options like portosystemic shunt creation. MR angiography is useful not only in evaluating treatment options but also in assessing therapeutic effects in follow-up period [40], [41], [42] (Fig. 24). The patency and caliber changes of surgical shunts can be displayed by MR angiography several days after operation when the large bandages on the patient's abdomen do not allow even a small sonographic window. In contrary, difficulties are present in evaluating TIPS patency. TIPS stents due to their metallic contents cause localized magnetic field distortions and signal loss, so that the flow in their lumen could not be detected with MR angiography even if they were patent. Neverthless, MR angiography can be used to demonstrate the complications of TIPS such as arterioportal fistula (Fig. 25). The main advantages of contrast-enhanced 3D MR angiography over Doppler sonography include, no restriction from body habitus and intestinal gas; short examination time; no operator-dependency; better anatomic orientation, and easy documentation of surgical portacaval shunt patency and portal venous system. It also offers the possibility to evaluate the enhancement patterns of liver parenchyma. 6.4. Venography Hepatic venography and inferior venocavography are classical diagnostic techniques for Budd-Chiari syndrome. Currently these imaging methods are usually performed to provide a guidance for interventional therapeutic approaches. The determinants that influence the diagnostic efficacy of the venographic methods include type of venous access, site of catheter, amount and injection pressure of administrated contrast material, direction of blood in the inferior vena cava and presence of collateral vessels. Because of these factors, there may be considerable discrepancies between the real hemodynamics of the patients and informational content of the venographic images. Thus, it is necessary to complement venography with Doppler sonography [11]. Venographic examinations demonstrate the level and extent of the hepatic venous or caval obstruction and offers the oppurtunity for measuring the luminal pressure neccesary to determine the effect of the therapeutic approach. This modality also allows concurrent liver biopsy with transvenous approach [1]. The spider web appearance on hepatic venography is characteristic for hepatic venous occlusion. This pattern is a result of the numerous small interconnecting collaterals which develop after the main hepatic veins are occluded. Due to hypertrophy of the caudate lobe, the inferior vena cava may be compressed in its retrohepatic portion. Inhomogeneous prolonged intense hepatogram with fine mottling can also be seen [23]. 7. Management and interventional radiologic procedures Various algorithms for management of Budd-Chiari syndrome are suggested [1], [43]. Medical management of the Budd-Chiari syndrome includes efforts to control the further development of ascites with diuretics and paracentesis, the use of anticoagulants to prevent further extension of the venous thrombosis, and the treatment of detectable underlying causes [8]. At present, interventional radiology techniques are more frequently used for reliefing of hepatic venous outflow obstruction. Depending on the etiology of Budd-Chiari syndrome, two main techniques are used: transjugular intrahepatic portosystemic shunt (TIPS) and percutaneous transluminal angioplasty (PTA) of the stenosed hepatic veins or inferior vena cava (Fig. 26). The short segment occlusion or stenosis of the hepatic veins can be recanalized by transvenous or combined percutaneous–transvenous approach [44]. PTA and stent placements proved a safe and effective treatment in Budd-Chiari syndrome and had a good long-term outcome [45]. Locally administrated thrombolysis in conjunction with angioplasty may have additional benefits. Another treatment modality for patients with progressive Budd-Chiari syndrome is a surgical portosystemic shunt. In patients with fulminant hepatic failure and the ineffective portosystemic shunt are considered for liver transplantation [8]. The current 10-year survival rate in Budd-Chiari syndrome is about 75% [46]. 8. Conclusion The patients with Budd-Chiari syndrome may present with either no symptoms and signs or entirely non-specific ones. Thus the radiologic imaging represents the focal point in the diagnosis of the majority of cases. Gray-scale sonography combined with Doppler techniques, given their wide avaliability are used as the initial imaging method in the evaluation of patients with Budd-Chiari syndrome and is the preffered first-line modality for follow-up of the TIPS and surgical shunts. Hepatic veins should always evaluated in respect of their visibility and caliber. If a drainage impairment of the liver is suspected according to the sonographic findings, a contrast-enhanced cross-sectional examination method for confirmation the diagnosis and evaluation of the extent of the disease would be suitable. Before selecting a treatment modality, the MR angiography as a contrast-enhanced method is advantageous over the other techniques. This method provides the demonstration of vascular structures both in the liver and the upper abdomen in various planes and also yields information concerning the parenchymal status. Prominent advances in cross-sectional imaging have resulted in contraction of the role of venography in Budd-Chiari syndrome. Pertaining to the radiologic methods and depending on the etiology of Budd-Chiari syndrome, the step after MR angiography is interventional therapeutic procedures (e.g. transluminal balon angioplasty with or without stent placement, TIPS) under hepatic venography or inferior venacavography guidance. References [1]. 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PII: S0720-048X(06)00444-X doi:10.1016/j.ejrad.2006.11.004 © 2006 Published by Elsevier Inc. | |
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