Imaging diagnosis of portal hypertension | Radiología (English Edition)

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Esta sección ecográfica representa el signo del renacuajo. La dilatación de una vena gástrica izquierda >6mm (b) y la inversión del flujo, que es hepatófugo (c), nos indica la presencia de varices esofágicas." ] ] ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "M. Conangla-Planes, X. Serres, O. Persiva, S. Augustín" "autores" => array:4 [ 0 => array:2 [ "nombre" => "M." "apellidos" => "Conangla-Planes" ] 1 => array:2 [ "nombre" => "X." "apellidos" => "Serres" ] 2 => array:2 [ "nombre" => "O." "apellidos" => "Persiva" ] 3 => array:2 [ "nombre" => "S." 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Conangla-Planes, X. Serres, O. Persiva, S. Augustín" "autores" => array:4 [ 0 => array:4 [ "nombre" => "M." "apellidos" => "Conangla-Planes" "email" => array:1 [ 0 => "marina.conangla@gmail.com" ] "referencia" => array:2 [ 0 => array:2 [ "etiqueta" => "a" "identificador" => "aff0005" ] 1 => array:2 [ "etiqueta" => "*" "identificador" => "cor0005" ] ] ] 1 => array:3 [ "nombre" => "X." "apellidos" => "Serres" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "a" "identificador" => "aff0005" ] ] ] 2 => array:3 [ "nombre" => "O." "apellidos" => "Persiva" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "a" "identificador" => "aff0005" ] ] ] 3 => array:3 [ "nombre" => "S." "apellidos" => "Augustín" "referencia" => array:2 [ 0 => array:2 [ "etiqueta" => "b" "identificador" => "aff0010" ] 1 => array:2 [ "etiqueta" => "c" "identificador" => "aff0015" ] ] ] ] "afiliaciones" => array:3 [ 0 => array:3 [ "entidad" => "Servicio de Radiodiagnóstico, Hospital Universitari Vall d’Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain" "etiqueta" => "a" "identificador" => "aff0005" ] 1 => array:3 [ "entidad" => "Servicio de Medicina Interna, Hospital Universitari Vall d’Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain" "etiqueta" => "b" "identificador" => "aff0010" ] 2 => array:3 [ "entidad" => "Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBEREHD), Spain" "etiqueta" => "c" "identificador" => "aff0015" ] ] "correspondencia" => array:1 [ 0 => array:3 [ "identificador" => "cor0005" "etiqueta" => "⁎" "correspondencia" => "Corresponding author." ] ] ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Diagnóstico por imagen de la hipertensión portal" ] ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:7 [ "identificador" => "fig0015" "etiqueta" => "Figure 3" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr3.jpeg" "Alto" => 761 "Ancho" => 2000 "Tamanyo" => 119882 ] ] "descripcion" => array:1 [ "en" => "Left axilary sagittal ultrasound planes of one control ultrasound in a patient with hepatic cirrhosis and portal hypertension showing the left kidney (arrow) and a 17-cm splenomegaly (asterisk), with multiple hyperechogenic punctiformed images consistent with Gamna-Gandy bodies." ] ] ] "textoCompleto" => "IntroductionPortal hypertension (PHT) is a well-defined clinical condition consisting of hydrostatic pressure in the venous portal venous territory >5mmHg (normal pressures are between 1 and 5mmHg). It is not considered clinically significant until hydrostatic pressure reaches ≥10mmHg, a threshold from which associated clinical complications can occur: bleeding of esophageal varices, ascites, spontaneous bacterial peritonitis, hepatic encephalopathy, and hepatopulmonary or hepatorenal syndrome.<a class="elsevierStyleCrossRefs" href="#bib0355">1–4</a>The increased pressure in the portal venous system is initially due to increased intrahepatic vascular resistance, whether prehepatic or posthepatic, followed by increased splanchnic flow. All this determines the formation or restoration of a network of venous collateral blood vessels destined to decompress the system and redirect part of the portal flow toward systemic circulation while avoiding the liver.<a class="elsevierStyleCrossRefs" href="#bib0360">2,5</a>This increased pressure can have different causes, being hepatic cirrhosis the most common cause in our setting.<a class="elsevierStyleCrossRefs" href="#bib0380">6,7</a>This paper analyses various radiological findings, specially ultrasound findings, suggestive of the presence of PHT that allow us to define its etiology, severity, and possible complications.DiagnosisThe reference pattern to determine portal venous pressure is to measure the portal pressure gradient through the catheterization of suprahepatic veins (SHV). Its invasive nature and limited availability have led to the development of non-invasive alternatives for the diagnosis of PHT, among which we have the mention here the Doppler ultrasound, the elastography techniques, and certain analytical parameters.Thrombocytopenia is one of the analytical parameters that keeps a narrower correlation with the portal pressure gradient. Similarly, one model combining albumin, alanine aminotransferase, and the INR (International Normalized Ratio) has also proven effective to predict portal hypertension in compensated cirrhosis.<a class="elsevierStyleCrossRef" href="#bib0390">8</a>Today, elastography is a non-invasive method of great clinical utility. There are different techniques available today, such as Transient Elastography (TE) or Fibroscan, the Acoustic Radiation Force Impulse Imaging (ARFI), or the Real-time Shear Wave Elastography (SWE). These imaging modalities add structural information to the morphological properties that the ultrasound scan or the magnetic resonance imaging (MRI) provide by assessing hepatic elasticity, thus being the closest diagnostic alternative to hepatic biopsy for the diagnosis of patients with cirrhosis. Several studies have confirmed its excellent correlation with the portal pressure gradient.<a class="elsevierStyleCrossRefs" href="#bib0395">9–11</a> All this has made elastography an essential tool to be able to make decisions on the best therapeutic approach for the patient, including screening for hepatocellular carcinoma and esophageal varices.<a class="elsevierStyleCrossRefs" href="#bib0410">12,13</a>The B-mode Doppler ultrasound still plays a crucial role as a non-invasive alternative, since it can show the presence of PHT, define its etiology, severity, and possible complications. Also, it is useful for the follow-up of patients who have undergone transjugular intrahepatic portosystemic shunt (TIPS) procedures.<a class="elsevierStyleCrossRefs" href="#bib0420">14,15</a>Radiological findings in the diagnosis of portal hypertensionThe Doppler ultrasound is the most advanced imaging modality for the study of PHT due to its accessibility, safety and good cost-effectiveness ratio. Several ultrasound findings have been proposed as markers of PHT, both morphological and hemodynamic (<a class="elsevierStyleCrossRef" href="#tbl0005">Table 1</a> and <a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>). The utility of some of these findings has been put into question by different studies, mainly due to the high inter- and intraobserver variability of ultrasound measurements.<ul class="elsevierStyleList" id="lis0005"><li class="elsevierStyleListItem" id="lsti0005">•Portal caliber</li></ul><elsevierMultimedia ident="tbl0005"></elsevierMultimedia><elsevierMultimedia ident="fig0005"></elsevierMultimedia>Portal calibers >13mm suggest PHT with 100% specificity and an approximate 40% sensitivity<a class="elsevierStyleCrossRefs" href="#bib0425">15–18</a> due to cases of PHT with portosystemic collateral shunts. The main setback of this finding is the variations in the measurements of the portal caliber due to the patient's postural changes, breathing, or fasting.<a class="elsevierStyleCrossRefs" href="#bib0445">19,20</a> In an effort to achieve a good ultrasound determination of the diameter of the portal vein, it is advisable to place the transducer in the subxiphoid region, using the left lobe as an acoustic window in order to obtain an ultrasound section on the axis of the portal vein.<ul class="elsevierStyleList" id="lis0010"><li class="elsevierStyleListItem" id="lsti0010">•No changes in the caliber of the blood vessels of the portal system during breathing</li></ul>A reduced variation in the caliber of the blood vessels of the portal system (splenic vein and superior mesenteric vein) during breathing has been considered a specific, sensitive finding of PHT<a class="elsevierStyleCrossRef" href="#bib0430">16</a>; however, these data have not been confirmed in other studies.<a class="elsevierStyleCrossRef" href="#bib0440">18</a><ul class="elsevierStyleList" id="lis0015"><li class="elsevierStyleListItem" id="lsti0015">•Velocity and direction of portal flow</li></ul>On the Doppler study, portal velocity should be measured preferably with one insonation angle <60° between the ultrasound angle of incidence and the direction of flow (or Doppler angle). The insonation angle should always have a small value; if not we can end up taking measures that are not accurate, since the velocity of flow obtained is proportional to the cosine of the ultrasound angle of incidence over the direction of flow–a value that is close to 1 with lower angles.<a class="elsevierStyleCrossRefs" href="#bib0445">19,21–23</a> To better determine portal velocity, it is advisable to use the right intercostal approach. Similarly, to improve the visualization of the Doppler signal in depth we should reduce the frequency of emission of the Doppler signal to be able to detect slow flow velocities or increase such frequency for the detection of high flow velocities. The frequency of emission of the Doppler signal is a different parameter than the pulse repetition frequency. Traditionally, it has been said that portal velocity is significantly slower in patients with PHT compared to healthy individuals, and it is diagnostic when it reaches <15cm/s, with 88% sensitivity and 96% specificity.<a class="elsevierStyleCrossRef" href="#bib0470">24</a> However, some scientific journals put this premise into question and claim that portal velocity can vary in patients with similar portal pressures due to the significant variability of collateral and portosystemic patterns. For example, one repermeabilized paraumbilical vein can increase portal velocity, whereas one splenorenal or gastrorenal shunt procedure can reduce it.<a class="elsevierStyleCrossRef" href="#bib0425">15</a> In advanced fases, portal flow can alternate (becoming hepatopetal flow when breathing in and hepatofugal flow when breathing out), and even reverse (hepatofulgal flow). The latter is one specific finding of PHT.<a class="elsevierStyleCrossRefs" href="#bib0460">22,25</a><ul class="elsevierStyleList" id="lis0020"><li class="elsevierStyleListItem" id="lsti0020">•Thrombosis and portal hypertension</li></ul>Patients with PHT and hepatic cirrhosis have a greater risk of developing thrombosis of the portal vein compared to the general population due to a slower portal flow velocity and the underlying clotting disorder associated with the hepatopathy. Its prevalence in different studies is between 0.6 and 21%.<a class="elsevierStyleCrossRefs" href="#bib0480">26,27</a> Also, these patients have a higher incidence of hepatocellular carcinoma, which in turn increases their risk of thrombosis due to the possibility of compression or intravascular tumor invasion and prothrombotic state. The Doppler ultrasound is the initial imaging modality of choice for diagnostic purposes, although additional imaging modalities are usually needed (computed tomography angiography or magnetic resonance angiography) in order to assess the extension of the disease, map the portosystemic collaterals and rule out the tumor origin of thrombosis.<ul class="elsevierStyleList" id="lis0025"><li class="elsevierStyleListItem" id="lsti0025">•Portal cavernomatosis</li></ul>Portal thrombosis we be followed portal cavernomatosis (<a class="elsevierStyleCrossRef" href="#fig0010">Fig. 2</a>). It consists of one tortuous network of collateral blood vessels originated after the repermeabilization of the vasa vasorum of the portal vein.<a class="elsevierStyleCrossRefs" href="#bib0425">15,28</a> Portal cavernomatosis can cause the compression of the bile duct leading to a condition known as portal biliopathy.<a class="elsevierStyleCrossRef" href="#bib0495">29</a><ul class="elsevierStyleList" id="lis0030"><li class="elsevierStyleListItem" id="lsti0030">•Portal congestion index</li></ul><elsevierMultimedia ident="fig0010"></elsevierMultimedia>The portal congestion index is the ratio between the cross-sectional area (cm2) and the portal blood flow velocity (cm/s). In patients with PHT, this area is usually increased and portal velocity reduced, which is why in the presence of PHT, this index will be high.<a class="elsevierStyleCrossRef" href="#bib0500">30</a> Several studies show significant differences between the portal congestion index of patients with chronic hepatopathy and the portal congestion index of the normal population.<a class="elsevierStyleCrossRefs" href="#bib0505">31,32</a><ul class="elsevierStyleList" id="lis0035"><li class="elsevierStyleListItem" id="lsti0035">•Hepatic artery</li></ul>As the portal blood flow is reduced, the hepatic arterial flow is increased as a compensatory mechanism.<a class="elsevierStyleCrossRefs" href="#bib0385">7,33</a><ul class="elsevierStyleList" id="lis0040"><li class="elsevierStyleListItem" id="lsti0040">•Increased resistance index</li></ul>Some studies have shown an increased resistance index (RI) of the hepatic artery in PHT. This index is independent from the Doppler angle and only shows the ratio between the peak systolic velocity and the end-diastolic velocity. In healthy people, the hepatic artery is one low-resistance artery (the liver requires continuous blood flow, even during the diastole), with pulse wave of pulsatile morphology. In general, the RI of low-resistance arteries is 0.55–0.7. High RIs are non-specific, since they can be present in cases of cirrhosis and chronic hepatitis, in postprandial states, and elderly patients. Low RIs can be due to stenoses or arteriovenous shunts due to severe cirrhosis, trauma or the Rendu-Osler-Weber syndrome.<a class="elsevierStyleCrossRef" href="#bib0460">22</a><ul class="elsevierStyleList" id="lis0045"><li class="elsevierStyleListItem" id="lsti0045">•Profile of suprahepatic veins</li></ul>The Doppler waveform of suprahepatic veins (SHV) in healthy patients has one triphasic morphology. This pattern is the consequence of the central venous pressure variations due to the cardiac cycle in such a way that the blood flow runs toward the heart during the atrial and ventricular diastole, and is briefly reversed during the atrial systole.<a class="elsevierStyleCrossRefs" href="#bib0520">34,35</a> The normal wave morphology is altered in 50% of the patients with PHT, thus reducing the amplitude of its oscillations or acquiring a sort of flattened morphology.<a class="elsevierStyleCrossRef" href="#bib0525">35</a> On the other hand, in patients with PHT due to hepatic cirrhosis we can have regional acceleration of flow resulting from focal compression due to regenerative nodules.<ul class="elsevierStyleList" id="lis0050"><li class="elsevierStyleListItem" id="lsti0050">•Spleen</li></ul>Splenomegaly is a common finding of PHT, but it is not an exclusive finding, because it can also be due to infiltrative diseases (lymphomas, amyloidosis) and certain hereditary disorders such as spherocytosis and thalassemia.<a class="elsevierStyleCrossRefs" href="#bib0355">1,36</a> It is important to bear in mind that the size of the spleen is related to the sex, height, and body weight of every individual.<a class="elsevierStyleCrossRef" href="#bib0535">37</a> The volumetric analysis of the spleen using CT scans or MRIs is the most objective imaging modality we have to assess it, although the measurement of the splenic cranial-caudal axis is the most widely used method (due to its simplicity) and it is considered enlarged when reaching >13cm.<a class="elsevierStyleCrossRef" href="#bib0540">38</a> Controlling its size allows us to conduct the prognostic staging of chirrotic patients, since size is closely related to the severity of cirrhosis and presence of esophageal varices and their degree.<a class="elsevierStyleCrossRef" href="#bib0545">39</a>Measuring splenic rigidity using elastography techniques has also proven useful when predicting the PHT.<a class="elsevierStyleCrossRef" href="#bib0550">40</a> Other findings relative to the spleen in patients with PHT are Gamna-Gandy bodies, millimetric siderotic nodules due to splenic microhemorrhages. The MRI is the imaging modality that best characterizes them, and they appear as low-signal intensity micronodules in all the sequences.<a class="elsevierStyleCrossRef" href="#bib0555">41</a> On the ultrasound they appear as small hyperechogenic foci without acoustic shadow (<a class="elsevierStyleCrossRef" href="#fig0015">Fig. 3</a>).<ul class="elsevierStyleList" id="lis0055"><li class="elsevierStyleListItem" id="lsti0055">•Ascites</li></ul><elsevierMultimedia ident="fig0015"></elsevierMultimedia>Ascites is a common finding of PHT, but it is not an exclusive finding, because it can also be due to pancreatitis, peritoneal carcinomatosis, nephrosis and other diseases.<a class="elsevierStyleCrossRef" href="#bib0560">42</a> Imaging modalities can help us identify the origin of the ascitic fluid.<ul class="elsevierStyleList" id="lis0060"><li class="elsevierStyleListItem" id="lsti0060">•Venous collateralse</li></ul>Portosystemic collaterality can be diagnosed using different imaging modalities being a direct, specific finding of PHT.<a class="elsevierStyleCrossRef" href="#bib0415">13</a> The formation of portosystemic collaterals is due to the re-opening of collapsed embryological channels, or blood flow reversion of existing adult veins with portal pressure gradients >10mmHg.<a class="elsevierStyleCrossRefs" href="#bib0565">43,44</a> Both the CT scan and the MRI with the administration of contrast are more sensitive than the ultrasound for the detection of collaterality and allow more comprehensive studies of the trajectory of blood vessels. Based on their drain site, they can be categorized into two (2) different groups<a class="elsevierStyleCrossRef" href="#bib0490">28</a>:They drain into the superior vena cava (SVC):<ul class="elsevierStyleList" id="lis0065"><li class="elsevierStyleListItem" id="lsti0065">-Coronary veins or left gastric veins. One coronary vein (left gastric vein) of over 5–6mm in diameter with an abnormal hepatofugal flow is an indicator of PHT.<a class="elsevierStyleCrossRef" href="#bib0490">28</a> There can be more than one coronary vein and different trajectories (<a class="elsevierStyleCrossRef" href="#fig0020">Fig. 4</a>). On the sagittal plane, at the epigastrial region, one section of a coronary vein through its axis with the transversal section of the portal or splenic veins looks like a tadpole (<a class="elsevierStyleCrossRef" href="#fig0025">Fig. 5</a>). From this same position, if we study the axial plane that runs through the bifurcation of the celiac trunk and looks like a water jet we will find the coronary vein running over such bifurcation in an image that reminds us of the ou com balla (tradition celebrated in Barcelona, Catalonya the day of the Corpus Christi and consisting of placing an empty egg on the water jet of a fountain at the cloister of the cathedral) (<a class="elsevierStyleCrossRef" href="#fig0030">Fig. 6</a>). The coronary veins divide into one anterior branch and one posterior branch supplying the esophageal and paraesophageal varices, respectively. There is a weak but positive correlation between the size of coronary veins (>6mm) and the risk of esophageal varices bleeding, and also between preserving hepatopetal flow and a lower risk of hemorrhace due to varices.<a class="elsevierStyleCrossRefs" href="#bib0570">44,45</a><elsevierMultimedia ident="fig0020"></elsevierMultimedia><elsevierMultimedia ident="fig0025"></elsevierMultimedia><elsevierMultimedia ident="fig0030"></elsevierMultimedia></li><li class="elsevierStyleListItem" id="lsti0070">-Esophageal varices. They are venous dilations of the esopaheal wall submucosa. They receive blood from the anterior branch of the coronary veins and drain into the azygos or hemiazygos system. Their prevalence among patients with cirrhosis is around 30–40%.<a class="elsevierStyleCrossRef" href="#bib0580">46</a> They are difficult to see using imaging modalities; on the CT scan or the MRI they can be identified by a certain thickening and intense enhancement of the esophageal wall after the administration of IV contrast. Today, if we are studying thecollateral circulation, we should also conduct one fibergastroscopy in order to rule out esophageal varices, since their diagnosis is of great clinical significance.<a class="elsevierStyleCrossRef" href="#bib0415">13</a> Esophageal varices are the cause of 70–90% of the hemorrhagic episodes described in these patients, and mortality rate is around 10–20% six (6) weeks after the bleeding.<a class="elsevierStyleCrossRefs" href="#bib0570">44,47–49</a></li><li class="elsevierStyleListItem" id="lsti0075">-Paraesophageal varices. Located outside the esophageal wall, they supply the posterior branch of coronary veins<a class="elsevierStyleCrossRef" href="#bib0570">44</a> (<a class="elsevierStyleCrossRef" href="#fig0035">Fig. 7</a>).<elsevierMultimedia ident="fig0035"></elsevierMultimedia></li><li class="elsevierStyleListItem" id="lsti0080">-Gastric varices. Network of tortuous blood vessels located at the level of the gastric fundus and splenic hilum.<a class="elsevierStyleCrossRef" href="#bib0565">43</a></li></ul><ul class="elsevierStyleList" id="lis0070"><li class="elsevierStyleListItem" id="lsti0085">1)They drain into the inferior vena cava (IVC):</li></ul><ul class="elsevierStyleList" id="lis0075"><li class="elsevierStyleListItem" id="lsti0090">-Splenorenal and gastrorenal shunts. They are tortuous blood vessels at the hilary region of the spleen and left kidney that are consistent with the collaterals found between the splenic vein or short gastric veins and the left renal vein. The asymmetrical increase of the left renal vein confirms its existence,<a class="elsevierStyleCrossRef" href="#bib0570">44</a> which should not be taken for a compression at the region of the aortomesenteric clamp.</li><li class="elsevierStyleListItem" id="lsti0095">-Paraumbilical varices. In healthy individuals, the umbilical vein persists as an obliterated fibrous remnant. In 10–32% of the cases of PHT, it can be redirected with the development of hepatofugal flow (<a class="elsevierStyleCrossRef" href="#fig0040">Fig. 8</a>). It runs from the left branch of the portal vein at the heart of the round ligament and connects to the periumbilical collaterals, to eventually drain into the inferior epigastrial veins and, less commonly, into the superior epigastrial veins. The dilation of such connections can originate venous viscosities that irradiate from the navel creating an image that is clinically known as “caput medusae”.<a class="elsevierStyleCrossRefs" href="#bib0490">28,44,50</a><elsevierMultimedia ident="fig0040"></elsevierMultimedia></li><li class="elsevierStyleListItem" id="lsti0100">-Gallbladder varices. They have been reported in 12% of the patients with PHT, being more common in patients with extrahepatic PHT. Their blood supply comes from the cystic branch–a branch of the right portal vein, and they drain into the SHV or into the intrahepatic portal vein. On the ultrasound they appear as cystic or tubular areas within the vesicular wall.</li><li class="elsevierStyleListItem" id="lsti0105">-Rectal varices. They connect the superior rectal veins that drain into the inferior mesenteric vein–tributary of the portal vein, with the middle and inferior rectal veins that drain into the internal iliac vein, tributary of the IVC.<a class="elsevierStyleCrossRef" href="#bib0565">43</a></li><li class="elsevierStyleListItem" id="lsti0110">-Retroperitoneal-paravertebral varices. Also known as the Veins of Retzius, they connect the mesenteric veins–tributary of the portal vein to the lumbar veins, tributary of the IVC.</li><li class="elsevierStyleListItem" id="lsti0115">-Omental varices. They can be found across the entire greater omentum and they are usually small yet numerous varices.<a class="elsevierStyleCrossRef" href="#bib0570">44</a></li></ul>Other less common portosystemic collaterals are the splenocaval shunt and the mesenteric-renal shunt (<a class="elsevierStyleCrossRef" href="#fig0045">Fig. 9</a>).<elsevierMultimedia ident="fig0045"></elsevierMultimedia>Other considerations in the imaging studies of portal hypertensionSeveral studies have assessed the utility of the ultrasound with IV contrast for the diagnosis or follow-up of patients with PHT. The transit-time analysis of the contrast bolus provides us with useful information on the cirrhotic patients’ hemodynamic changes, allowing us to distinguish them from healthy individuals.<a class="elsevierStyleCrossRefs" href="#bib0605">51,52</a> The MRI has also been studied as an alternative method to the ultrasound for the measurement of portal hemodynamic parameters. The MRI flow parameters, obtained from a comparative analysis of the intensity-time curves seen on the MRI after the administration of contrast, are closely related with the severity of cirrhosis and PHT.<a class="elsevierStyleCrossRef" href="#bib0615">53</a> Also, several predictive models of PHT have been proposed based on a combination of certain findings on the CT scan and MRI, such as the liver and spleen volumes, the presence of perihepatic ascites,<a class="elsevierStyleCrossRef" href="#bib0620">54</a> the number of varices, the degree of ascites, and the cranial-caudal length of the spleen.<a class="elsevierStyleCrossRef" href="#bib0625">55</a> One study showed that the velocity within the splenic artery and the T1 relaxation time of the hepatic tissue keep a close relation with the portal pressure gradient.<a class="elsevierStyleCrossRef" href="#bib0630">56</a>Etiological diagnosis of portal hypertensionThe increase of portal pressure can be due to different causes such as an increased vascular flow due to the presence of arterioportal fistulas, or an increase of flow resistance (<a class="elsevierStyleCrossRef" href="#tbl0010">Table 2</a>). The increase of flow resistance is categorized based on its anatomical location–intrahepatic or extrahepatic (posthepatic or prehepatic).<a class="elsevierStyleCrossRef" href="#bib0385">7</a> Intrahepatic PHT is the most common type in our setting due to the high prevalence of cirrhosis. Imaging modalities can help us determine if intrahepatic HPT is pre-sinusoidal, sinusoidal o post-sinusoidal.<elsevierMultimedia ident="tbl0010"></elsevierMultimedia>Cirrhosis is the end stage of different hepatopathies. Its main causes in Western countries are alcohol abuse, non-alcoholic fatty liver disease, and chronic viral hepatitis.<a class="elsevierStyleCrossRef" href="#bib0635">57</a> Its imaging diagnosis is based on the alterations of the structure and morphology of the liver, the presence of nodular contours, the heterogeneity of parenchyma, and the redistribution of lobe volumes, with right lobe atrophy, and left and caudate lobe hypertrophy.<a class="elsevierStyleCrossRefs" href="#bib0640">58–61</a> The importance of imaging modalities in individuals with cirrhosis lies in the creening of hepatocellular carcinoma, rather than in the diagnosis of the disease.Schistosomiasis, the deposit of eggs in the smallest portal venules leads to PHT and, in time, to the development of periportal fibrosis and hepatic cirrhosis.The toxic injury to hepatic sinusoids in the hepatic veno-occlusive disease determines the obstruction of hepatic venules leading to post-sinusoidal PHT. Today, the leading cause of hepatic veno-occlusive disease is the hematopoietic progenitors transplantation.<a class="elsevierStyleCrossRefs" href="#bib0450">20,62</a>Sarcoidosis is one non-caseating multisystemic granulomatous disease of unknown etiology that affects the lungs but in 70% of the cases we can also find liver damage.<a class="elsevierStyleCrossRefs" href="#bib0665">63–65</a>Myeloproliferative diseases are one heterogeneous group of hematological neoplasms whose most common characteristic is the uncontrolled proliferation of some of the spinal cord precursors. One of its complications is the appearance of prothrombotic disorders that can also lead to the development of PHT.In the long run, certain hepatotoxic substances (such as methotrexate, vitamin A, vinyl chloride and arsenic) can induce the development of cirrhosis and, eventually, PHT.<a class="elsevierStyleCrossRefs" href="#bib0355">1,66,67</a>Prehepatic PHT includes thrombosis and extrinsic compression or the stenosis of the splenoportal axis that can also be secondary to different processes such as vascular neoplastic infiltration due to hepatocellular carcinoma or pancreatic adenocarcinoma, pancreatitis or abdominal trauma.Post-hepatic causes include the Budd-Chiari syndrome and diseases causing the passive venonus congestion of the liver, such as constrictive pericarditis, restrictive cardiomyopathy and right heart failure.The Budd-Chiari syndrome includes one heterogeneous group of disorders characterized by the obstruction of the SHVs, IVC, or right atrium. Its appearance is commonly associated with states of hypercoagulability. Venous obstruction increases hepatic sinusoidal pressure leading to PHT, hepatic congestion, and reduced liver perfusion. The acute phase is characterized by hepatomegaly with lower attenuation on the CT scan images, reduced signal intensity on the T1-weighted MRI and heterogeneous signal increase on the T2-weighted images. The studies without IV contrast are used to identify the IVC and narrowed or hyperdense SHVs due to thrombosis. The administration of contrast provides a more intense and early enhancement of the central part of the liver. The Doppler findings can include the absence of flow in the SHVs or the IVC, the direct visualization of the thrombus, or the presence of retrograde monophasic flow.<a class="elsevierStyleCrossRefs" href="#bib0520">34,68,69</a>In the congestive hepatopathy (<a class="elsevierStyleCrossRef" href="#fig0050">Fig. 10</a>) we can see the following characteristic anomalies: dilation of the IVC and SHVs, hepatomegaly of the smooth edges, cardiomegaly, pleural effusion, ascites, contrast reflow toward the SHVs from the right atrium, heterogeneity of hepatic attenuation on the CT scan, loss of caliber variations in the IVC during breathing, and an increased flow pulsatility of the portal vein on the ultrasound.<a class="elsevierStyleCrossRefs" href="#bib0695">69,70</a><elsevierMultimedia ident="fig0050"></elsevierMultimedia>ConclusionThe findings of PHT or collateral circulation in patients with chronic hepatopathy are of great importance for diagnostic and therapeutic purposes. In these cases, imaging modalities are crucial for the management of these patients, they tell us what the best time is to conduct a fibergastroscopy or start screening for hepatocellular carcinoma. The role of elastography has become more and more relevant as a non-invasive modality. Similarly, imaging modalities allow us to obtain information on the type of PHT and its possible etiology.Authors<ul class="elsevierStyleList" id="lis0080"><li class="elsevierStyleListItem" id="lsti0120">1.Manager of the integrity of the study: MCP and XSC.</li><li class="elsevierStyleListItem" id="lsti0125">2.Study Idea: MCP and XSC.</li><li class="elsevierStyleListItem" id="lsti0130">3.Study Design: MCP and XSC.</li><li class="elsevierStyleListItem" id="lsti0135">4.Data Mining: MCP, XSC and OPM.</li><li class="elsevierStyleListItem" id="lsti0140">5.Data Analysis and Interpretation: MCP and XSC.</li><li class="elsevierStyleListItem" id="lsti0145">6.Statistical Analyses: N/A.</li><li class="elsevierStyleListItem" id="lsti0150">7.Reference MCP, XSC and SAR.</li><li class="elsevierStyleListItem" id="lsti0155">8.Writing: MCP and XSC.</li><li class="elsevierStyleListItem" id="lsti0160">9.Critical review of the manuscript with intellectually relevant remarks: MCP, XSC, OPM and SAR.</li><li class="elsevierStyleListItem" id="lsti0165">10.Approval of final version: MCP, XSC, OPM and SAR.</li></ul>Conflicts of interestsThe authors declare no conflict of interests associated with this article whatsoever." "textoCompletoSecciones" => array:1 [ "secciones" => array:10 [ 0 => array:3 [ "identificador" => "xres1060299" "titulo" => "Abstract" "secciones" => array:1 [ 0 => array:1 [ "identificador" => "abst0005" ] ] ] 1 => array:2 [ "identificador" => "xpalclavsec1009154" "titulo" => "Keywords" ] 2 => array:3 [ "identificador" => "xres1060300" "titulo" => "Resumen" "secciones" => array:1 [ 0 => array:1 [ "identificador" => "abst0010" ] ] ] 3 => array:2 [ "identificador" => "xpalclavsec1009153" "titulo" => "Palabras clave" ] 4 => array:2 [ "identificador" => "sec0005" "titulo" => "Introduction" ] 5 => array:3 [ "identificador" => "sec0010" "titulo" => "Diagnosis" "secciones" => array:3 [ 0 => array:2 [ "identificador" => "sec0015" "titulo" => "Radiological findings in the diagnosis of portal hypertension" ] 1 => array:2 [ "identificador" => "sec0020" "titulo" => "Other considerations in the imaging studies of portal hypertension" ] 2 => array:2 [ "identificador" => "sec0025" "titulo" => "Etiological diagnosis of portal hypertension" ] ] ] 6 => array:2 [ "identificador" => "sec0030" "titulo" => "Conclusion" ] 7 => array:2 [ "identificador" => "sec0035" "titulo" => "Authors" ] 8 => array:2 [ "identificador" => "sec0045" "titulo" => "Conflicts of interests" ] 9 => array:1 [ "titulo" => "References" ] ] ] "pdfFichero" => "main.pdf" "tienePdf" => true "fechaRecibido" => "2017-05-10" "fechaAceptado" => "2017-12-30" "PalabrasClave" => array:2 [ "en" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Keywords" "identificador" => "xpalclavsec1009154" "palabras" => array:4 [ 0 => "Portal hypertension" 1 => "Ultrasonography Doppler" 2 => "Collateral circulation" 3 => "Coronary veins" ] ] ] "es" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Palabras clave" "identificador" => "xpalclavsec1009153" "palabras" => array:4 [ 0 => "Hipertensión portal" 1 => "Ecografía Doppler" 2 => "Circulación colateral" 3 => "Venas coronarias" ] ] ] ] "tieneResumen" => true "resumen" => array:2 [ "en" => array:2 [ "titulo" => "Abstract" "resumen" => "Portal hypertension (PHT) is a clinical entity defined when hydrostatic pressure >5mm Hg in the portal venous territory, being clinically significant if it reaches ≥10mm Hg. At this threshold, complications can develop, such as the bleeding of esophageal varices, the appearance of ascites, or hepatic encephalopathy. Imaging modalities play an important role here as non-invasive methods to determining whether PHT is present or not. This article analyzes various imaging findings that can be suggestive of PHT and contributes to define its etiology, severity, and possible complications." ] "es" => array:2 [ "titulo" => "Resumen" "resumen" => "La hipertensión portal (HTP) es una condición clínica definida por una presión hidrostática >5mmHg en el territorio venoso portal, siendo clínicamente significativa cuando es ≥10mmHg. A partir de este umbral pueden desarrollarse complicaciones, como sangrado de varices esofágicas, aparición de ascitis o encefalopatía hepática. Las técnicas de imagen tienen un papel importante como método no invasivo para determinar la presencia de HTP. En este artículo se analizan varios hallazgos radiológicos que pueden sugerir HTP y contribuir a definir su etiología, gravedad y posibles complicaciones." ] ] "NotaPie" => array:1 [ 0 => array:2 [ "etiqueta" => "☆" "nota" => "Please cite this article as: Conangla-Planes M, Serres X, Persiva O, Augustín S. Diagnóstico por imagen de la hipertensión portal. Radiología. 2018;60:290–302." ] ] "multimedia" => array:12 [ 0 => array:7 [ "identificador" => "fig0005" "etiqueta" => "Figure 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 571 "Ancho" => 2333 "Tamanyo" => 138650 ] ] "descripcion" => array:1 [ "en" => "Seventy-three-year-old patient on ultrasound follow-up due to hepatic cirrhosis and portal hypertension. The ultrasound longitudinal plane on the portal vein (a) shows an increased portal caliber (16mm). The Doppler spectrum conducted at hepatic hilum level on one right intercostal plane (b) shows reduced portal velocity (14.6cm/s). Finally, one longitudinal plane on the spleen (c) shows one 16cm-splenomegaly." ] ] 1 => array:7 [ "identificador" => "fig0010" "etiqueta" => "Figure 2" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr2.jpeg" "Alto" => 791 "Ancho" => 2000 "Tamanyo" => 167612 ] ] "descripcion" => array:1 [ "en" => "Seventy-five-year-old patient on follow-up due to hepatic cirrhosis. The Doppler color ultrasound (left) and the gray-scale ultrasound (right) show one tangled network of collateral blood vessels at hepatic hilum level consistent with portal cavernomatosis (asterisk)." ] ] 2 => array:7 [ "identificador" => "fig0015" "etiqueta" => "Figure 3" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr3.jpeg" "Alto" => 761 "Ancho" => 2000 "Tamanyo" => 119882 ] ] "descripcion" => array:1 [ "en" => "Left axilary sagittal ultrasound planes of one control ultrasound in a patient with hepatic cirrhosis and portal hypertension showing the left kidney (arrow) and a 17-cm splenomegaly (asterisk), with multiple hyperechogenic punctiformed images consistent with Gamna-Gandy bodies." ] ] 3 => array:7 [ "identificador" => "fig0020" "etiqueta" => "Figure 4" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr4.jpeg" "Alto" => 523 "Ancho" => 1500 "Tamanyo" => 41909 ] ] "descripcion" => array:1 [ "en" => "Schematic representation of the outflow tract of the three left gastric veins (arrow) on a frontal plane at the upper edge of the portal vein, the confluence with the superior mesenteric vein, and the splenic vein. The dotted lines are indicative of the axial plane through the celiac trunk with respect to the position of each one of the coronary veins." ] ] 4 => array:7 [ "identificador" => "fig0025" "etiqueta" => "Figure 5" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr5.jpeg" "Alto" => 568 "Ancho" => 1750 "Tamanyo" => 145649 ] ] "descripcion" => array:1 [ "en" => "Sagittal ultrasound planes of the left gastric vein (asterisk) running underneath the common hepatic artery in a patient with portal pressures within normal ranges (a), and in a patient with portal hypertension (b and c). This ultrasound section shows the tadpole sign. The dilation of one left gastric vein >6mm (b) and the reversed hepatofugal flow (c) are indicative of the presence of esophageal varices." ] ] 5 => array:7 [ "identificador" => "fig0030" "etiqueta" => "Figure 6" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr6.jpeg" "Alto" => 1180 "Ancho" => 1750 "Tamanyo" => 177164 ] ] "descripcion" => array:1 [ "en" => "Correlation scheme for each one of the three nondilated left gastric veins with the corresponding ultrasound plane. There is one coronary vein that originates on the upper edge of the beginning of the portal vein and runs cranially underneath the common hepatic artery (arrow). The second coronary vein originates on the upper edge of the confluence of the superior mesenteric vein with the splenic vein and runs cranially above the celiac trunk. Finally, the third coronary vein originates on the upper distal edge of the splenic vein and runs cranially behind the splenic artery (asterisk)." ] ] 6 => array:7 [ "identificador" => "fig0035" "etiqueta" => "Figure 7" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr7.jpeg" "Alto" => 1564 "Ancho" => 2333 "Tamanyo" => 377127 ] ] "descripcion" => array:1 [ "en" => "Paraesophageal varices (arrow). Abdominal CT scan with IV contrast in venous phase requested for the post-chemoembolization control of one hepatocellular carcinoma in a 75-year-old patient with alcoholic liver cirrhosis and portal hypertension. The axial planes (a and b) and MIP reconstructions on the coronal (c) and sagittal planes (d) show a network of tortuous blood vessels located at the level of the distal esophagus that connect to the portal vein through the left gastric vein." ] ] 7 => array:7 [ "identificador" => "fig0040" "etiqueta" => "Figure 8" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr8.jpeg" "Alto" => 1292 "Ancho" => 2333 "Tamanyo" => 363259 ] ] "descripcion" => array:1 [ "en" => "CT images with IV contrast with MIP reconstructions on the axial (a and b) and sagittal planes(c) and ultrasound (d y e) of the same patient. In both imaging modalities we can see findings of advanced chronic hepatopathy with a small, heterogeneous liver with nodular edges and signs of portal hypertension, a significant amount of ascitic fluid (asterisk) and the repermeabilization of the umbilical vein (arrow)." ] ] 8 => array:7 [ "identificador" => "fig0045" "etiqueta" => "Figure 9" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr9.jpeg" "Alto" => 1756 "Ancho" => 2333 "Tamanyo" => 588815 ] ] "descripcion" => array:1 [ "en" => "Eighty-year-old patient with hepatic cirrhosis and known hepatocellular carcinoma. The Doppler color ultrasound with IV contrast (a-c) shows a network of tortuous blood vessels of subhepatic location that on the CT scan with IV contrast (d-f) are consistent with one portocaval shunt through the communication of the superior mesenteric vein with the right renal vein (arrow)." ] ] 9 => array:7 [ "identificador" => "fig0050" "etiqueta" => "Figure 10" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr10.jpeg" "Alto" => 643 "Ancho" => 2000 "Tamanyo" => 119365 ] ] "descripcion" => array:1 [ "en" => "Follow-up ultrasound study of a patient with congestive hepatopathy due to heart disease. The right, subcostal, obliquous, transverse plane with cranial inclination toward the superior hepatic segments (a) shows where the three suprahepatic veins meet with the significantly dilated inferior vena cava (diameter >1cm in the segment where it drains into the inferior vena cava)–secondary findings of a difficult venous return. The Doppler spectrum (b) shows waving portal flow." ] ] 10 => array:8 [ "identificador" => "tbl0005" "etiqueta" => "Table 1" "tipo" => "MULTIMEDIATABLA" "mostrarFloat" => true "mostrarDisplay" => false "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at1" "detalle" => "Table " "rol" => "short" ] ] "tabla" => array:1 [ "tablatextoimagen" => array:1 [ 0 => array:2 [ "tabla" => array:1 [ 0 => """ <table border="0" frame="\n \t\t\t\t\tvoid\n \t\t\t\t" class=""><tbody title="tbody"><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Portal caliber >13mm \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Splenomegaly \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Doppler US: \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Reduced portal velocity (<15cm/s) or hepatofugal flow \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Increased arterial RI (>0.7) \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Portosystemic collaterality \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Ascites \t\t\t\t\t\t\n \t\t\t\t</td></tr></tbody></table> """ ] "imagenFichero" => array:1 [ 0 => "xTab1804555.png" ] ] ] ] "descripcion" => array:1 [ "en" => "Radiological findings of portal hypertension." ] ] 11 => array:8 [ "identificador" => "tbl0010" "etiqueta" => "Table 2" "tipo" => "MULTIMEDIATABLA" "mostrarFloat" => true "mostrarDisplay" => false "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at2" "detalle" => "Table " "rol" => "short" ] ] "tabla" => array:1 [ "tablatextoimagen" => array:1 [ 0 => array:2 [ "tabla" => array:1 [ 0 => """ <table border="0" frame="\n \t\t\t\t\tvoid\n \t\t\t\t" class=""><thead title="thead"><tr title="table-row"><th class="td" title="table-head " colspan="2" align="center" valign="top" scope="col" style="border-bottom: 2px solid black">Increased blood flow resistance</th></tr></thead><tbody title="tbody"><tr title="table-row"><td class="td" title="table-entry " colspan="2" align="left" valign="top">Intrahepatic</td></tr><tr title="table-row"><td class="td" title="table-entry " rowspan="6" align="left" valign="top">Pre-sinusoidal</td><td class="td" title="table-entry " align="left" valign="top">Schistosomiasis \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Sarcoidosis \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Myeloproliferative diseases \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Congenital hepatic fibrosis \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Idiopathic portal hypertension \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Hepatotoxicity due to vinyl chloride, arsenic, azathioprine, etc. \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="table-entry " rowspan="3" align="left" valign="top">Sinusoidal</td><td class="td" title="table-entry " align="left" valign="top">Cirrhosis \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Methotrexate \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Hypervitaminosis A \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Post-sinusoidal \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top">Veno-occlusive disease \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="table-entry " colspan="2" align="left" valign="top"></td></tr><tr title="table-row"><td class="td" title="table-entry " colspan="2" align="left" valign="top">Extrahepatic</td></tr><tr title="table-row"><td class="td" title="table-entry " rowspan="3" align="left" valign="top">Prehepatic</td><td class="td" title="table-entry " align="left" valign="top">Portal vein/splenic vein thrombosis \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Portal stenosis \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">External compression of the portal vein \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="table-entry " rowspan="4" align="left" valign="top">Post-hepatic</td><td class="td" title="table-entry " align="left" valign="top">Obstruction or thrombosis o the inferior vena cava \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Budd-Chiari syndrome \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Constrictive pericarditis or restrictive cardiomyopathy \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Tricuspid valve disease or right heart failure \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="table-entry " colspan="2" align="left" valign="top"></td></tr><tr title="table-row"><td class="td" title="table-entry " colspan="2" align="left" valign="top">Increased vascular flow</td></tr><tr title="table-row"><td class="td" title="table-entry " align="" valign="top"> \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top">Arterioportal fistulas (splanchnic, intrahepatic, intrasplenic) \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="table-entry " align="" valign="top"> \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top">Arteriovenous malformations \t\t\t\t\t\t\n \t\t\t\t</td></tr></tbody></table> """ ] "imagenFichero" => array:1 [ 0 => "xTab1804554.png" ] ] ] ] "descripcion" => array:1 [ "en" => "Main causes of portal hypertension." ] ] ] "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0015" "bibliografiaReferencia" => array:70 [ 0 => array:3 [ "identificador" => "bib0355" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Harrison's principles of internal medicine" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:6 [ 0 => "D.L. 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Update in Radiology

Imaging diagnosis of portal hypertension

Diagnóstico por imagen de la hipertensión portal

M. Conangla-Planesa,

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marina.conangla@gmail.com

Corresponding author.

, X. Serresa, O. Persivaa, S. Augustínb,c

a Servicio de Radiodiagnóstico, Hospital Universitari Vall d’Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain

b Servicio de Medicina Interna, Hospital Universitari Vall d’Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain

c Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBEREHD), Spain

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    "textoCompleto" => "<span class="elsevierStyleSections"><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0025">Introduction</span><p id="par0005" class="elsevierStylePara elsevierViewall">Portal hypertension &#40;PHT&#41; is a well-defined clinical condition consisting of hydrostatic pressure in the venous portal venous territory &#62;5<span class="elsevierStyleHsp" style=""></span>mmHg &#40;normal pressures are between 1 and 5<span class="elsevierStyleHsp" style=""></span>mmHg&#41;&#46; It is not considered clinically significant until hydrostatic pressure reaches &#8805;10<span class="elsevierStyleHsp" style=""></span>mmHg&#44; a threshold from which associated clinical complications can occur&#58; bleeding of esophageal varices&#44; ascites&#44; spontaneous bacterial peritonitis&#44; hepatic encephalopathy&#44; and hepatopulmonary or hepatorenal syndrome&#46;<a class="elsevierStyleCrossRefs" href="#bib0355"><span class="elsevierStyleSup">1&#8211;4</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">The increased pressure in the portal venous system is initially due to increased intrahepatic vascular resistance&#44; whether prehepatic or posthepatic&#44; followed by increased splanchnic flow&#46; All this determines the formation or restoration of a network of venous collateral blood vessels destined to decompress the system and redirect part of the portal flow toward systemic circulation while avoiding the liver&#46;<a class="elsevierStyleCrossRefs" href="#bib0360"><span class="elsevierStyleSup">2&#44;5</span></a></p><p id="par0015" class="elsevierStylePara elsevierViewall">This increased pressure can have different causes&#44; being hepatic cirrhosis the most common cause in our setting&#46;<a class="elsevierStyleCrossRefs" href="#bib0380"><span class="elsevierStyleSup">6&#44;7</span></a></p><p id="par0020" class="elsevierStylePara elsevierViewall">This paper analyses various radiological findings&#44; specially ultrasound findings&#44; suggestive of the presence of PHT that allow us to define its etiology&#44; severity&#44; and possible complications&#46;</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0030">Diagnosis</span><p id="par0025" class="elsevierStylePara elsevierViewall">The reference pattern to determine portal venous pressure is to measure the portal pressure gradient through the catheterization of suprahepatic veins &#40;SHV&#41;&#46; Its invasive nature and limited availability have led to the development of non-invasive alternatives for the diagnosis of PHT&#44; among which we have the mention here the Doppler ultrasound&#44; the elastography techniques&#44; and certain analytical parameters&#46;</p><p id="par0030" class="elsevierStylePara elsevierViewall">Thrombocytopenia is one of the analytical parameters that keeps a narrower correlation with the portal pressure gradient&#46; Similarly&#44; one model combining albumin&#44; alanine aminotransferase&#44; and the INR &#40;International Normalized Ratio&#41; has also proven effective to predict portal hypertension in compensated cirrhosis&#46;<a class="elsevierStyleCrossRef" href="#bib0390"><span class="elsevierStyleSup">8</span></a></p><p id="par0035" class="elsevierStylePara elsevierViewall">Today&#44; elastography is a non-invasive method of great clinical utility&#46; There are different techniques available today&#44; such as Transient Elastography &#40;TE&#41; or Fibroscan&#44; the Acoustic Radiation Force Impulse Imaging &#40;ARFI&#41;&#44; or the Real-time Shear Wave Elastography &#40;SWE&#41;&#46; These imaging modalities add structural information to the morphological properties that the ultrasound scan or the magnetic resonance imaging &#40;MRI&#41; provide by assessing hepatic elasticity&#44; thus being the closest diagnostic alternative to hepatic biopsy for the diagnosis of patients with cirrhosis&#46; Several studies have confirmed its excellent correlation with the portal pressure gradient&#46;<a class="elsevierStyleCrossRefs" href="#bib0395"><span class="elsevierStyleSup">9&#8211;11</span></a> All this has made elastography an essential tool to be able to make decisions on the best therapeutic approach for the patient&#44; including screening for hepatocellular carcinoma and esophageal varices&#46;<a class="elsevierStyleCrossRefs" href="#bib0410"><span class="elsevierStyleSup">12&#44;13</span></a></p><p id="par0040" class="elsevierStylePara elsevierViewall">The B-mode Doppler ultrasound still plays a crucial role as a non-invasive alternative&#44; since it can show the presence of PHT&#44; define its etiology&#44; severity&#44; and possible complications&#46; Also&#44; it is useful for the follow-up of patients who have undergone transjugular intrahepatic portosystemic shunt &#40;TIPS&#41; procedures&#46;<a class="elsevierStyleCrossRefs" href="#bib0420"><span class="elsevierStyleSup">14&#44;15</span></a></p><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0035">Radiological findings in the diagnosis of portal hypertension</span><p id="par0045" class="elsevierStylePara elsevierViewall">The Doppler ultrasound is the most advanced imaging modality for the study of PHT due to its accessibility&#44; safety and good cost-effectiveness ratio&#46; Several ultrasound findings have been proposed as markers of PHT&#44; both morphological and hemodynamic &#40;<a class="elsevierStyleCrossRef" href="#tbl0005">Table 1</a> and <a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>&#41;&#46; The utility of some of these findings has been put into question by different studies&#44; mainly due to the high inter- and intraobserver variability of ultrasound measurements&#46;<ul class="elsevierStyleList" id="lis0005"><li class="elsevierStyleListItem" id="lsti0005"><span class="elsevierStyleLabel">&#8226;</span><p id="par0050" class="elsevierStylePara elsevierViewall">Portal caliber</p></li></ul></p><elsevierMultimedia ident="tbl0005"></elsevierMultimedia><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0055" class="elsevierStylePara elsevierViewall">Portal calibers &#62;13<span class="elsevierStyleHsp" style=""></span>mm suggest PHT with 100&#37; specificity and an approximate 40&#37; sensitivity<a class="elsevierStyleCrossRefs" href="#bib0425"><span class="elsevierStyleSup">15&#8211;18</span></a> due to cases of PHT with portosystemic collateral shunts&#46; The main setback of this finding is the variations in the measurements of the portal caliber due to the patient&#39;s postural changes&#44; breathing&#44; or fasting&#46;<a class="elsevierStyleCrossRefs" href="#bib0445"><span class="elsevierStyleSup">19&#44;20</span></a> In an effort to achieve a good ultrasound determination of the diameter of the portal vein&#44; it is advisable to place the transducer in the subxiphoid region&#44; using the left lobe as an acoustic window in order to obtain an ultrasound section on the axis of the portal vein&#46;<ul class="elsevierStyleList" id="lis0010"><li class="elsevierStyleListItem" id="lsti0010"><span class="elsevierStyleLabel">&#8226;</span><p id="par0060" class="elsevierStylePara elsevierViewall">No changes in the caliber of the blood vessels of the portal system during breathing</p></li></ul></p><p id="par0065" class="elsevierStylePara elsevierViewall">A reduced variation in the caliber of the blood vessels of the portal system &#40;splenic vein and superior mesenteric vein&#41; during breathing has been considered a specific&#44; sensitive finding of PHT<a class="elsevierStyleCrossRef" href="#bib0430"><span class="elsevierStyleSup">16</span></a>&#59; however&#44; these data have not been confirmed in other studies&#46;<a class="elsevierStyleCrossRef" href="#bib0440"><span class="elsevierStyleSup">18</span></a><ul class="elsevierStyleList" id="lis0015"><li class="elsevierStyleListItem" id="lsti0015"><span class="elsevierStyleLabel">&#8226;</span><p id="par0070" class="elsevierStylePara elsevierViewall">Velocity and direction of portal flow</p></li></ul></p><p id="par0075" class="elsevierStylePara elsevierViewall">On the Doppler study&#44; portal velocity should be measured preferably with one insonation angle &#60;60&#176; between the ultrasound angle of incidence and the direction of flow &#40;or Doppler angle&#41;&#46; The insonation angle should always have a small value&#59; if not we can end up taking measures that are not accurate&#44; since the velocity of flow obtained is proportional to the cosine of the ultrasound angle of incidence over the direction of flow&#8211;a value that is close to 1 with lower angles&#46;<a class="elsevierStyleCrossRefs" href="#bib0445"><span class="elsevierStyleSup">19&#44;21&#8211;23</span></a> To better determine portal velocity&#44; it is advisable to use the right intercostal approach&#46; Similarly&#44; to improve the visualization of the Doppler signal in depth we should reduce the frequency of emission of the Doppler signal to be able to detect slow flow velocities or increase such frequency for the detection of high flow velocities&#46; The frequency of emission of the Doppler signal is a different parameter than the pulse repetition frequency&#46; Traditionally&#44; it has been said that portal velocity is significantly slower in patients with PHT compared to healthy individuals&#44; and it is diagnostic when it reaches &#60;15<span class="elsevierStyleHsp" style=""></span>cm&#47;s&#44; with 88&#37; sensitivity and 96&#37; specificity&#46;<a class="elsevierStyleCrossRef" href="#bib0470"><span class="elsevierStyleSup">24</span></a> However&#44; some scientific journals put this premise into question and claim that portal velocity can vary in patients with similar portal pressures due to the significant variability of collateral and portosystemic patterns&#46; For example&#44; one repermeabilized paraumbilical vein can increase portal velocity&#44; whereas one splenorenal or gastrorenal shunt procedure can reduce it&#46;<a class="elsevierStyleCrossRef" href="#bib0425"><span class="elsevierStyleSup">15</span></a> In advanced fases&#44; portal flow can alternate &#40;becoming hepatopetal flow when breathing in and hepatofugal flow when breathing out&#41;&#44; and even reverse &#40;hepatofulgal flow&#41;&#46; The latter is one specific finding of PHT&#46;<a class="elsevierStyleCrossRefs" href="#bib0460"><span class="elsevierStyleSup">22&#44;25</span></a><ul class="elsevierStyleList" id="lis0020"><li class="elsevierStyleListItem" id="lsti0020"><span class="elsevierStyleLabel">&#8226;</span><p id="par0080" class="elsevierStylePara elsevierViewall">Thrombosis and portal hypertension</p></li></ul></p><p id="par0085" class="elsevierStylePara elsevierViewall">Patients with PHT and hepatic cirrhosis have a greater risk of developing thrombosis of the portal vein compared to the general population due to a slower portal flow velocity and the underlying clotting disorder associated with the hepatopathy&#46; Its prevalence in different studies is between 0&#46;6 and 21&#37;&#46;<a class="elsevierStyleCrossRefs" href="#bib0480"><span class="elsevierStyleSup">26&#44;27</span></a> Also&#44; these patients have a higher incidence of hepatocellular carcinoma&#44; which in turn increases their risk of thrombosis due to the possibility of compression or intravascular tumor invasion and prothrombotic state&#46; The Doppler ultrasound is the initial imaging modality of choice for diagnostic purposes&#44; although additional imaging modalities are usually needed &#40;computed tomography angiography or magnetic resonance angiography&#41; in order to assess the extension of the disease&#44; map the portosystemic collaterals and rule out the tumor origin of thrombosis&#46;<ul class="elsevierStyleList" id="lis0025"><li class="elsevierStyleListItem" id="lsti0025"><span class="elsevierStyleLabel">&#8226;</span><p id="par0090" class="elsevierStylePara elsevierViewall">Portal cavernomatosis</p></li></ul></p><p id="par0095" class="elsevierStylePara elsevierViewall">Portal thrombosis we be followed portal cavernomatosis &#40;<a class="elsevierStyleCrossRef" href="#fig0010">Fig&#46; 2</a>&#41;&#46; It consists of one tortuous network of collateral blood vessels originated after the repermeabilization of the vasa vasorum of the portal vein&#46;<a class="elsevierStyleCrossRefs" href="#bib0425"><span class="elsevierStyleSup">15&#44;28</span></a> Portal cavernomatosis can cause the compression of the bile duct leading to a condition known as portal biliopathy&#46;<a class="elsevierStyleCrossRef" href="#bib0495"><span class="elsevierStyleSup">29</span></a><ul class="elsevierStyleList" id="lis0030"><li class="elsevierStyleListItem" id="lsti0030"><span class="elsevierStyleLabel">&#8226;</span><p id="par0100" class="elsevierStylePara elsevierViewall">Portal congestion index</p></li></ul></p><elsevierMultimedia ident="fig0010"></elsevierMultimedia><p id="par0105" class="elsevierStylePara elsevierViewall">The portal congestion index is the ratio between the cross-sectional area &#40;cm<span class="elsevierStyleSup">2</span>&#41; and the portal blood flow velocity &#40;cm&#47;s&#41;&#46; In patients with PHT&#44; this area is usually increased and portal velocity reduced&#44; which is why in the presence of PHT&#44; this index will be high&#46;<a class="elsevierStyleCrossRef" href="#bib0500"><span class="elsevierStyleSup">30</span></a> Several studies show significant differences between the portal congestion index of patients with chronic hepatopathy and the portal congestion index of the normal population&#46;<a class="elsevierStyleCrossRefs" href="#bib0505"><span class="elsevierStyleSup">31&#44;32</span></a><ul class="elsevierStyleList" id="lis0035"><li class="elsevierStyleListItem" id="lsti0035"><span class="elsevierStyleLabel">&#8226;</span><p id="par0110" class="elsevierStylePara elsevierViewall">Hepatic artery</p></li></ul></p><p id="par0115" class="elsevierStylePara elsevierViewall">As the portal blood flow is reduced&#44; the hepatic arterial flow is increased as a compensatory mechanism&#46;<a class="elsevierStyleCrossRefs" href="#bib0385"><span class="elsevierStyleSup">7&#44;33</span></a><ul class="elsevierStyleList" id="lis0040"><li class="elsevierStyleListItem" id="lsti0040"><span class="elsevierStyleLabel">&#8226;</span><p id="par0120" class="elsevierStylePara elsevierViewall">Increased resistance index</p></li></ul></p><p id="par0125" class="elsevierStylePara elsevierViewall">Some studies have shown an increased resistance index &#40;RI&#41; of the hepatic artery in PHT&#46; This index is independent from the Doppler angle and only shows the ratio between the peak systolic velocity and the end-diastolic velocity&#46; In healthy people&#44; the hepatic artery is one low-resistance artery &#40;the liver requires continuous blood flow&#44; even during the diastole&#41;&#44; with pulse wave of pulsatile morphology&#46; In general&#44; the RI of low-resistance arteries is 0&#46;55&#8211;0&#46;7&#46; High RIs are non-specific&#44; since they can be present in cases of cirrhosis and chronic hepatitis&#44; in postprandial states&#44; and elderly patients&#46; Low RIs can be due to stenoses or arteriovenous shunts due to severe cirrhosis&#44; trauma or the Rendu-Osler-Weber syndrome&#46;<a class="elsevierStyleCrossRef" href="#bib0460"><span class="elsevierStyleSup">22</span></a><ul class="elsevierStyleList" id="lis0045"><li class="elsevierStyleListItem" id="lsti0045"><span class="elsevierStyleLabel">&#8226;</span><p id="par0130" class="elsevierStylePara elsevierViewall">Profile of suprahepatic veins</p></li></ul></p><p id="par0135" class="elsevierStylePara elsevierViewall">The Doppler waveform of suprahepatic veins &#40;SHV&#41; in healthy patients has one triphasic morphology&#46; This pattern is the consequence of the central venous pressure variations due to the cardiac cycle in such a way that the blood flow runs toward the heart during the atrial and ventricular diastole&#44; and is briefly reversed during the atrial systole&#46;<a class="elsevierStyleCrossRefs" href="#bib0520"><span class="elsevierStyleSup">34&#44;35</span></a> The normal wave morphology is altered in 50&#37; of the patients with PHT&#44; thus reducing the amplitude of its oscillations or acquiring a sort of flattened morphology&#46;<a class="elsevierStyleCrossRef" href="#bib0525"><span class="elsevierStyleSup">35</span></a> On the other hand&#44; in patients with PHT due to hepatic cirrhosis we can have regional acceleration of flow resulting from focal compression due to regenerative nodules&#46;<ul class="elsevierStyleList" id="lis0050"><li class="elsevierStyleListItem" id="lsti0050"><span class="elsevierStyleLabel">&#8226;</span><p id="par0140" class="elsevierStylePara elsevierViewall">Spleen</p></li></ul></p><p id="par0145" class="elsevierStylePara elsevierViewall">Splenomegaly is a common finding of PHT&#44; but it is not an exclusive finding&#44; because it can also be due to infiltrative diseases &#40;lymphomas&#44; amyloidosis&#41; and certain hereditary disorders such as spherocytosis and thalassemia&#46;<a class="elsevierStyleCrossRefs" href="#bib0355"><span class="elsevierStyleSup">1&#44;36</span></a> It is important to bear in mind that the size of the spleen is related to the sex&#44; height&#44; and body weight of every individual&#46;<a class="elsevierStyleCrossRef" href="#bib0535"><span class="elsevierStyleSup">37</span></a> The volumetric analysis of the spleen using CT scans or MRIs is the most objective imaging modality we have to assess it&#44; although the measurement of the splenic cranial-caudal axis is the most widely used method &#40;due to its simplicity&#41; and it is considered enlarged when reaching &#62;13<span class="elsevierStyleHsp" style=""></span>cm&#46;<a class="elsevierStyleCrossRef" href="#bib0540"><span class="elsevierStyleSup">38</span></a> Controlling its size allows us to conduct the prognostic staging of chirrotic patients&#44; since size is closely related to the severity of cirrhosis and presence of esophageal varices and their degree&#46;<a class="elsevierStyleCrossRef" href="#bib0545"><span class="elsevierStyleSup">39</span></a></p><p id="par0150" class="elsevierStylePara elsevierViewall">Measuring splenic rigidity using elastography techniques has also proven useful when predicting the PHT&#46;<a class="elsevierStyleCrossRef" href="#bib0550"><span class="elsevierStyleSup">40</span></a> Other findings relative to the spleen in patients with PHT are Gamna-Gandy bodies&#44; millimetric siderotic nodules due to splenic microhemorrhages&#46; The MRI is the imaging modality that best characterizes them&#44; and they appear as low-signal intensity micronodules in all the sequences&#46;<a class="elsevierStyleCrossRef" href="#bib0555"><span class="elsevierStyleSup">41</span></a> On the ultrasound they appear as small hyperechogenic foci without acoustic shadow &#40;<a class="elsevierStyleCrossRef" href="#fig0015">Fig&#46; 3</a>&#41;&#46;<ul class="elsevierStyleList" id="lis0055"><li class="elsevierStyleListItem" id="lsti0055"><span class="elsevierStyleLabel">&#8226;</span><p id="par0155" class="elsevierStylePara elsevierViewall">Ascites</p></li></ul></p><elsevierMultimedia ident="fig0015"></elsevierMultimedia><p id="par0160" class="elsevierStylePara elsevierViewall">Ascites is a common finding of PHT&#44; but it is not an exclusive finding&#44; because it can also be due to pancreatitis&#44; peritoneal carcinomatosis&#44; nephrosis and other diseases&#46;<a class="elsevierStyleCrossRef" href="#bib0560"><span class="elsevierStyleSup">42</span></a> Imaging modalities can help us identify the origin of the ascitic fluid&#46;<ul class="elsevierStyleList" id="lis0060"><li class="elsevierStyleListItem" id="lsti0060"><span class="elsevierStyleLabel">&#8226;</span><p id="par0165" class="elsevierStylePara elsevierViewall">Venous collateralse</p></li></ul></p><p id="par0170" class="elsevierStylePara elsevierViewall">Portosystemic collaterality can be diagnosed using different imaging modalities being a direct&#44; specific finding of PHT&#46;<a class="elsevierStyleCrossRef" href="#bib0415"><span class="elsevierStyleSup">13</span></a> The formation of portosystemic collaterals is due to the re-opening of collapsed embryological channels&#44; or blood flow reversion of existing adult veins with portal pressure gradients &#62;10<span class="elsevierStyleHsp" style=""></span>mmHg&#46;<a class="elsevierStyleCrossRefs" href="#bib0565"><span class="elsevierStyleSup">43&#44;44</span></a> Both the CT scan and the MRI with the administration of contrast are more sensitive than the ultrasound for the detection of collaterality and allow more comprehensive studies of the trajectory of blood vessels&#46; Based on their drain site&#44; they can be categorized into two &#40;2&#41; different groups<a class="elsevierStyleCrossRef" href="#bib0490"><span class="elsevierStyleSup">28</span></a>&#58;</p><p id="par0175" class="elsevierStylePara elsevierViewall">They drain into the superior vena cava &#40;SVC&#41;&#58;<ul class="elsevierStyleList" id="lis0065"><li class="elsevierStyleListItem" id="lsti0065"><span class="elsevierStyleLabel">-</span><p id="par0180" class="elsevierStylePara elsevierViewall">Coronary veins or left gastric veins&#46; One coronary vein &#40;left gastric vein&#41; of over 5&#8211;6<span class="elsevierStyleHsp" style=""></span>mm in diameter with an abnormal hepatofugal flow is an indicator of PHT&#46;<a class="elsevierStyleCrossRef" href="#bib0490"><span class="elsevierStyleSup">28</span></a> There can be more than one coronary vein and different trajectories &#40;<a class="elsevierStyleCrossRef" href="#fig0020">Fig&#46; 4</a>&#41;&#46; On the sagittal plane&#44; at the epigastrial region&#44; one section of a coronary vein through its axis with the transversal section of the portal or splenic veins looks like a tadpole &#40;<a class="elsevierStyleCrossRef" href="#fig0025">Fig&#46; 5</a>&#41;&#46; From this same position&#44; if we study the axial plane that runs through the bifurcation of the celiac trunk and looks like a water jet we will find the coronary vein running over such bifurcation in an image that reminds us of the <span class="elsevierStyleItalic">ou com balla</span> &#40;tradition celebrated in Barcelona&#44; Catalonya the day of the Corpus Christi and consisting of placing an empty egg on the water jet of a fountain at the cloister of the cathedral&#41; &#40;<a class="elsevierStyleCrossRef" href="#fig0030">Fig&#46; 6</a>&#41;&#46; The coronary veins divide into one anterior branch and one posterior branch supplying the esophageal and paraesophageal varices&#44; respectively&#46; There is a weak but positive correlation between the size of coronary veins &#40;&#62;6<span class="elsevierStyleHsp" style=""></span>mm&#41; and the risk of esophageal varices bleeding&#44; and also between preserving hepatopetal flow and a lower risk of hemorrhace due to varices&#46;<a class="elsevierStyleCrossRefs" href="#bib0570"><span class="elsevierStyleSup">44&#44;45</span></a></p><elsevierMultimedia ident="fig0020"></elsevierMultimedia><elsevierMultimedia ident="fig0025"></elsevierMultimedia><elsevierMultimedia ident="fig0030"></elsevierMultimedia></li><li class="elsevierStyleListItem" id="lsti0070"><span class="elsevierStyleLabel">-</span><p id="par0185" class="elsevierStylePara elsevierViewall">Esophageal varices&#46; They are venous dilations of the esopaheal wall submucosa&#46; They receive blood from the anterior branch of the coronary veins and drain into the azygos or hemiazygos system&#46; Their prevalence among patients with cirrhosis is around 30&#8211;40&#37;&#46;<a class="elsevierStyleCrossRef" href="#bib0580"><span class="elsevierStyleSup">46</span></a> They are difficult to see using imaging modalities&#59; on the CT scan or the MRI they can be identified by a certain thickening and intense enhancement of the esophageal wall after the administration of IV contrast&#46; Today&#44; if we are studying thecollateral circulation&#44; we should also conduct one fibergastroscopy in order to rule out esophageal varices&#44; since their diagnosis is of great clinical significance&#46;<a class="elsevierStyleCrossRef" href="#bib0415"><span class="elsevierStyleSup">13</span></a> Esophageal varices are the cause of 70&#8211;90&#37; of the hemorrhagic episodes described in these patients&#44; and mortality rate is around 10&#8211;20&#37; six &#40;6&#41; weeks after the bleeding&#46;<a class="elsevierStyleCrossRefs" href="#bib0570"><span class="elsevierStyleSup">44&#44;47&#8211;49</span></a></p></li><li class="elsevierStyleListItem" id="lsti0075"><span class="elsevierStyleLabel">-</span><p id="par0190" class="elsevierStylePara elsevierViewall">Paraesophageal varices&#46; Located outside the esophageal wall&#44; they supply the posterior branch of coronary veins<a class="elsevierStyleCrossRef" href="#bib0570"><span class="elsevierStyleSup">44</span></a> &#40;<a class="elsevierStyleCrossRef" href="#fig0035">Fig&#46; 7</a>&#41;&#46;</p><elsevierMultimedia ident="fig0035"></elsevierMultimedia></li><li class="elsevierStyleListItem" id="lsti0080"><span class="elsevierStyleLabel">-</span><p id="par0195" class="elsevierStylePara elsevierViewall">Gastric varices&#46; Network of tortuous blood vessels located at the level of the gastric fundus and splenic hilum&#46;<a class="elsevierStyleCrossRef" href="#bib0565"><span class="elsevierStyleSup">43</span></a></p></li></ul></p><p id="par0200" class="elsevierStylePara elsevierViewall"><ul class="elsevierStyleList" id="lis0070"><li class="elsevierStyleListItem" id="lsti0085"><span class="elsevierStyleLabel">1&#41;</span><p id="par0205" class="elsevierStylePara elsevierViewall">They drain into the inferior vena cava &#40;IVC&#41;&#58;</p></li></ul><ul class="elsevierStyleList" id="lis0075"><li class="elsevierStyleListItem" id="lsti0090"><span class="elsevierStyleLabel">-</span><p id="par0210" class="elsevierStylePara elsevierViewall">Splenorenal and gastrorenal shunts&#46; They are tortuous blood vessels at the hilary region of the spleen and left kidney that are consistent with the collaterals found between the splenic vein or short gastric veins and the left renal vein&#46; The asymmetrical increase of the left renal vein confirms its existence&#44;<a class="elsevierStyleCrossRef" href="#bib0570"><span class="elsevierStyleSup">44</span></a> which should not be taken for a compression at the region of the aortomesenteric clamp&#46;</p></li><li class="elsevierStyleListItem" id="lsti0095"><span class="elsevierStyleLabel">-</span><p id="par0215" class="elsevierStylePara elsevierViewall">Paraumbilical varices&#46; In healthy individuals&#44; the umbilical vein persists as an obliterated fibrous remnant&#46; In 10&#8211;32&#37; of the cases of PHT&#44; it can be redirected with the development of hepatofugal flow &#40;<a class="elsevierStyleCrossRef" href="#fig0040">Fig&#46; 8</a>&#41;&#46; It runs from the left branch of the portal vein at the heart of the round ligament and connects to the periumbilical collaterals&#44; to eventually drain into the inferior epigastrial veins and&#44; less commonly&#44; into the superior epigastrial veins&#46; The dilation of such connections can originate venous viscosities that irradiate from the navel creating an image that is clinically known as &#8220;caput medusae&#8221;&#46;<a class="elsevierStyleCrossRefs" href="#bib0490"><span class="elsevierStyleSup">28&#44;44&#44;50</span></a></p><elsevierMultimedia ident="fig0040"></elsevierMultimedia></li><li class="elsevierStyleListItem" id="lsti0100"><span class="elsevierStyleLabel">-</span><p id="par0220" class="elsevierStylePara elsevierViewall">Gallbladder varices&#46; They have been reported in 12&#37; of the patients with PHT&#44; being more common in patients with extrahepatic PHT&#46; Their blood supply comes from the cystic branch&#8211;a branch of the right portal vein&#44; and they drain into the SHV or into the intrahepatic portal vein&#46; On the ultrasound they appear as cystic or tubular areas within the vesicular wall&#46;</p></li><li class="elsevierStyleListItem" id="lsti0105"><span class="elsevierStyleLabel">-</span><p id="par0225" class="elsevierStylePara elsevierViewall">Rectal varices&#46; They connect the superior rectal veins that drain into the inferior mesenteric vein&#8211;tributary of the portal vein&#44; with the middle and inferior rectal veins that drain into the internal iliac vein&#44; tributary of the IVC&#46;<a class="elsevierStyleCrossRef" href="#bib0565"><span class="elsevierStyleSup">43</span></a></p></li><li class="elsevierStyleListItem" id="lsti0110"><span class="elsevierStyleLabel">-</span><p id="par0230" class="elsevierStylePara elsevierViewall">Retroperitoneal-paravertebral varices&#46; Also known as the Veins of Retzius&#44; they connect the mesenteric veins&#8211;tributary of the portal vein to the lumbar veins&#44; tributary of the IVC&#46;</p></li><li class="elsevierStyleListItem" id="lsti0115"><span class="elsevierStyleLabel">-</span><p id="par0235" class="elsevierStylePara elsevierViewall">Omental varices&#46; They can be found across the entire greater omentum and they are usually small yet numerous varices&#46;<a class="elsevierStyleCrossRef" href="#bib0570"><span class="elsevierStyleSup">44</span></a></p></li></ul></p><p id="par0240" class="elsevierStylePara elsevierViewall">Other less common portosystemic collaterals are the splenocaval shunt and the mesenteric-renal shunt &#40;<a class="elsevierStyleCrossRef" href="#fig0045">Fig&#46; 9</a>&#41;&#46;</p><elsevierMultimedia ident="fig0045"></elsevierMultimedia></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0040">Other considerations in the imaging studies of portal hypertension</span><p id="par0245" class="elsevierStylePara elsevierViewall">Several studies have assessed the utility of the ultrasound with IV contrast for the diagnosis or follow-up of patients with PHT&#46; The transit-time analysis of the contrast bolus provides us with useful information on the cirrhotic patients&#8217; hemodynamic changes&#44; allowing us to distinguish them from healthy individuals&#46;<a class="elsevierStyleCrossRefs" href="#bib0605"><span class="elsevierStyleSup">51&#44;52</span></a> The MRI has also been studied as an alternative method to the ultrasound for the measurement of portal hemodynamic parameters&#46; The MRI flow parameters&#44; obtained from a comparative analysis of the intensity-time curves seen on the MRI after the administration of contrast&#44; are closely related with the severity of cirrhosis and PHT&#46;<a class="elsevierStyleCrossRef" href="#bib0615"><span class="elsevierStyleSup">53</span></a> Also&#44; several predictive models of PHT have been proposed based on a combination of certain findings on the CT scan and MRI&#44; such as the liver and spleen volumes&#44; the presence of perihepatic ascites&#44;<a class="elsevierStyleCrossRef" href="#bib0620"><span class="elsevierStyleSup">54</span></a> the number of varices&#44; the degree of ascites&#44; and the cranial-caudal length of the spleen&#46;<a class="elsevierStyleCrossRef" href="#bib0625"><span class="elsevierStyleSup">55</span></a> One study showed that the velocity within the splenic artery and the T1 relaxation time of the hepatic tissue keep a close relation with the portal pressure gradient&#46;<a class="elsevierStyleCrossRef" href="#bib0630"><span class="elsevierStyleSup">56</span></a></p></span><span id="sec0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0045">Etiological diagnosis of portal hypertension</span><p id="par0250" class="elsevierStylePara elsevierViewall">The increase of portal pressure can be due to different causes such as an increased vascular flow due to the presence of arterioportal fistulas&#44; or an increase of flow resistance &#40;<a class="elsevierStyleCrossRef" href="#tbl0010">Table 2</a>&#41;&#46; The increase of flow resistance is categorized based on its anatomical location&#8211;intrahepatic or extrahepatic &#40;posthepatic or prehepatic&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0385"><span class="elsevierStyleSup">7</span></a> Intrahepatic PHT is the most common type in our setting due to the high prevalence of cirrhosis&#46; Imaging modalities can help us determine if intrahepatic HPT is pre-sinusoidal&#44; sinusoidal o post-sinusoidal&#46;</p><elsevierMultimedia ident="tbl0010"></elsevierMultimedia><p id="par0255" class="elsevierStylePara elsevierViewall">Cirrhosis is the end stage of different hepatopathies&#46; Its main causes in Western countries are alcohol abuse&#44; non-alcoholic fatty liver disease&#44; and chronic viral hepatitis&#46;<a class="elsevierStyleCrossRef" href="#bib0635"><span class="elsevierStyleSup">57</span></a> Its imaging diagnosis is based on the alterations of the structure and morphology of the liver&#44; the presence of nodular contours&#44; the heterogeneity of parenchyma&#44; and the redistribution of lobe volumes&#44; with right lobe atrophy&#44; and left and caudate lobe hypertrophy&#46;<a class="elsevierStyleCrossRefs" href="#bib0640"><span class="elsevierStyleSup">58&#8211;61</span></a> The importance of imaging modalities in individuals with cirrhosis lies in the creening of hepatocellular carcinoma&#44; rather than in the diagnosis of the disease&#46;</p><p id="par0260" class="elsevierStylePara elsevierViewall">Schistosomiasis&#44; the deposit of eggs in the smallest portal venules leads to PHT and&#44; in time&#44; to the development of periportal fibrosis and hepatic cirrhosis&#46;</p><p id="par0265" class="elsevierStylePara elsevierViewall">The toxic injury to hepatic sinusoids in the hepatic veno-occlusive disease determines the obstruction of hepatic venules leading to post-sinusoidal PHT&#46; Today&#44; the leading cause of hepatic veno-occlusive disease is the hematopoietic progenitors transplantation&#46;<a class="elsevierStyleCrossRefs" href="#bib0450"><span class="elsevierStyleSup">20&#44;62</span></a></p><p id="par0270" class="elsevierStylePara elsevierViewall">Sarcoidosis is one non-caseating multisystemic granulomatous disease of unknown etiology that affects the lungs but in 70&#37; of the cases we can also find liver damage&#46;<a class="elsevierStyleCrossRefs" href="#bib0665"><span class="elsevierStyleSup">63&#8211;65</span></a></p><p id="par0275" class="elsevierStylePara elsevierViewall">Myeloproliferative diseases are one heterogeneous group of hematological neoplasms whose most common characteristic is the uncontrolled proliferation of some of the spinal cord precursors&#46; One of its complications is the appearance of prothrombotic disorders that can also lead to the development of PHT&#46;</p><p id="par0280" class="elsevierStylePara elsevierViewall">In the long run&#44; certain hepatotoxic substances &#40;such as methotrexate&#44; vitamin A&#44; vinyl chloride and arsenic&#41; can induce the development of cirrhosis and&#44; eventually&#44; PHT&#46;<a class="elsevierStyleCrossRefs" href="#bib0355"><span class="elsevierStyleSup">1&#44;66&#44;67</span></a></p><p id="par0285" class="elsevierStylePara elsevierViewall">Prehepatic PHT includes thrombosis and extrinsic compression or the stenosis of the splenoportal axis that can also be secondary to different processes such as vascular neoplastic infiltration due to hepatocellular carcinoma or pancreatic adenocarcinoma&#44; pancreatitis or abdominal trauma&#46;</p><p id="par0290" class="elsevierStylePara elsevierViewall">Post-hepatic causes include the Budd-Chiari syndrome and diseases causing the passive venonus congestion of the liver&#44; such as constrictive pericarditis&#44; restrictive cardiomyopathy and right heart failure&#46;</p><p id="par0295" class="elsevierStylePara elsevierViewall">The Budd-Chiari syndrome includes one heterogeneous group of disorders characterized by the obstruction of the SHVs&#44; IVC&#44; or right atrium&#46; Its appearance is commonly associated with states of hypercoagulability&#46; Venous obstruction increases hepatic sinusoidal pressure leading to PHT&#44; hepatic congestion&#44; and reduced liver perfusion&#46; The acute phase is characterized by hepatomegaly with lower attenuation on the CT scan images&#44; reduced signal intensity on the T1-weighted MRI and heterogeneous signal increase on the T2-weighted images&#46; The studies without IV contrast are used to identify the IVC and narrowed or hyperdense SHVs due to thrombosis&#46; The administration of contrast provides a more intense and early enhancement of the central part of the liver&#46; The Doppler findings can include the absence of flow in the SHVs or the IVC&#44; the direct visualization of the thrombus&#44; or the presence of retrograde monophasic flow&#46;<a class="elsevierStyleCrossRefs" href="#bib0520"><span class="elsevierStyleSup">34&#44;68&#44;69</span></a></p><p id="par0300" class="elsevierStylePara elsevierViewall">In the congestive hepatopathy &#40;<a class="elsevierStyleCrossRef" href="#fig0050">Fig&#46; 10</a>&#41; we can see the following characteristic anomalies&#58; dilation of the IVC and SHVs&#44; hepatomegaly of the smooth edges&#44; cardiomegaly&#44; pleural effusion&#44; ascites&#44; contrast reflow toward the SHVs from the right atrium&#44; heterogeneity of hepatic attenuation on the CT scan&#44; loss of caliber variations in the IVC during breathing&#44; and an increased flow pulsatility of the portal vein on the ultrasound&#46;<a class="elsevierStyleCrossRefs" href="#bib0695"><span class="elsevierStyleSup">69&#44;70</span></a></p><elsevierMultimedia ident="fig0050"></elsevierMultimedia></span></span><span id="sec0030" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0050">Conclusion</span><p id="par0305" class="elsevierStylePara elsevierViewall">The findings of PHT or collateral circulation in patients with chronic hepatopathy are of great importance for diagnostic and therapeutic purposes&#46; In these cases&#44; imaging modalities are crucial for the management of these patients&#44; they tell us what the best time is to conduct a fibergastroscopy or start screening for hepatocellular carcinoma&#46; The role of elastography has become more and more relevant as a non-invasive modality&#46; Similarly&#44; imaging modalities allow us to obtain information on the type of PHT and its possible etiology&#46;</p></span><span id="sec0035" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0055">Authors</span><p id="par0310" class="elsevierStylePara elsevierViewall"><ul class="elsevierStyleList" id="lis0080"><li class="elsevierStyleListItem" id="lsti0120"><span class="elsevierStyleLabel">1&#46;</span><p id="par0315" class="elsevierStylePara elsevierViewall">Manager of the integrity of the study&#58; MCP and XSC&#46;</p></li><li class="elsevierStyleListItem" id="lsti0125"><span class="elsevierStyleLabel">2&#46;</span><p id="par0320" class="elsevierStylePara elsevierViewall">Study Idea&#58; MCP and XSC&#46;</p></li><li class="elsevierStyleListItem" id="lsti0130"><span class="elsevierStyleLabel">3&#46;</span><p id="par0325" class="elsevierStylePara elsevierViewall">Study Design&#58; MCP and XSC&#46;</p></li><li class="elsevierStyleListItem" id="lsti0135"><span class="elsevierStyleLabel">4&#46;</span><p id="par0330" class="elsevierStylePara elsevierViewall">Data Mining&#58; MCP&#44; XSC and OPM&#46;</p></li><li class="elsevierStyleListItem" id="lsti0140"><span class="elsevierStyleLabel">5&#46;</span><p id="par0335" class="elsevierStylePara elsevierViewall">Data Analysis and Interpretation&#58; MCP and XSC&#46;</p></li><li class="elsevierStyleListItem" id="lsti0145"><span class="elsevierStyleLabel">6&#46;</span><p id="par0340" class="elsevierStylePara elsevierViewall">Statistical Analyses&#58; N&#47;A&#46;</p></li><li class="elsevierStyleListItem" id="lsti0150"><span class="elsevierStyleLabel">7&#46;</span><p id="par0345" class="elsevierStylePara elsevierViewall">Reference MCP&#44; XSC and SAR&#46;</p></li><li class="elsevierStyleListItem" id="lsti0155"><span class="elsevierStyleLabel">8&#46;</span><p id="par0350" class="elsevierStylePara elsevierViewall">Writing&#58; MCP and XSC&#46;</p></li><li class="elsevierStyleListItem" id="lsti0160"><span class="elsevierStyleLabel">9&#46;</span><p id="par0355" class="elsevierStylePara elsevierViewall">Critical review of the manuscript with intellectually relevant remarks&#58; MCP&#44; XSC&#44; OPM and SAR&#46;</p></li><li class="elsevierStyleListItem" id="lsti0165"><span class="elsevierStyleLabel">10&#46;</span><p id="par0360" class="elsevierStylePara elsevierViewall">Approval of final version&#58; MCP&#44; XSC&#44; OPM and SAR&#46;</p></li></ul></p></span><span id="sec0045" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0065">Conflicts of interests</span><p id="par0670" class="elsevierStylePara elsevierViewall">The authors declare no conflict of interests associated with this article whatsoever&#46;</p></span></span>"
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          "identificador" => "xres1060299"
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              "identificador" => "abst0005"
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        1 => array:2 [
          "identificador" => "xpalclavsec1009154"
          "titulo" => "Keywords"
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          "identificador" => "sec0005"
          "titulo" => "Introduction"
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          "titulo" => "Diagnosis"
          "secciones" => array:3 [
            0 => array:2 [
              "identificador" => "sec0015"
              "titulo" => "Radiological findings in the diagnosis of portal hypertension"
            ]
            1 => array:2 [
              "identificador" => "sec0020"
              "titulo" => "Other considerations in the imaging studies of portal hypertension"
            ]
            2 => array:2 [
              "identificador" => "sec0025"
              "titulo" => "Etiological diagnosis of portal hypertension"
            ]
          ]
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          "titulo" => "References"
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      ]
    ]
    "pdfFichero" => "main.pdf"
    "tienePdf" => true
    "fechaRecibido" => "2017-05-10"
    "fechaAceptado" => "2017-12-30"
    "PalabrasClave" => array:2 [
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        0 => array:4 [
          "clase" => "keyword"
          "titulo" => "Keywords"
          "identificador" => "xpalclavsec1009154"
          "palabras" => array:4 [
            0 => "Portal hypertension"
            1 => "Ultrasonography Doppler"
            2 => "Collateral circulation"
            3 => "Coronary veins"
          ]
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        0 => array:4 [
          "clase" => "keyword"
          "titulo" => "Palabras clave"
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          "palabras" => array:4 [
            0 => "Hipertensi&#243;n portal"
            1 => "Ecograf&#237;a Doppler"
            2 => "Circulaci&#243;n colateral"
            3 => "Venas coronarias"
          ]
        ]
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        "titulo" => "Abstract"
        "resumen" => "<span id="abst0005" class="elsevierStyleSection elsevierViewall"><p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Portal hypertension &#40;PHT&#41; is a clinical entity defined when hydrostatic pressure &#62;5<span class="elsevierStyleHsp" style=""></span>mm Hg in the portal venous territory&#44; being clinically significant if it reaches &#8805;10<span class="elsevierStyleHsp" style=""></span>mm Hg&#46; At this threshold&#44; complications can develop&#44; such as the bleeding of esophageal varices&#44; the appearance of ascites&#44; or hepatic encephalopathy&#46; Imaging modalities play an important role here as non-invasive methods to determining whether PHT is present or not&#46; This article analyzes various imaging findings that can be suggestive of PHT and contributes to define its etiology&#44; severity&#44; and possible complications&#46;</p></span>"
      ]
      "es" => array:2 [
        "titulo" => "Resumen"
        "resumen" => "<span id="abst0010" class="elsevierStyleSection elsevierViewall"><p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">La hipertensi&#243;n portal &#40;HTP&#41; es una condici&#243;n cl&#237;nica definida por una presi&#243;n hidrost&#225;tica &#62;5<span class="elsevierStyleHsp" style=""></span>mmHg en el territorio venoso portal&#44; siendo cl&#237;nicamente significativa cuando es &#8805;10<span class="elsevierStyleHsp" style=""></span>mmHg&#46; A partir de este umbral pueden desarrollarse complicaciones&#44; como sangrado de varices esof&#225;gicas&#44; aparici&#243;n de ascitis o encefalopat&#237;a hep&#225;tica&#46; Las t&#233;cnicas de imagen tienen un papel importante como m&#233;todo no invasivo para determinar la presencia de HTP&#46; En este art&#237;culo se analizan varios hallazgos radiol&#243;gicos que pueden sugerir HTP y contribuir a definir su etiolog&#237;a&#44; gravedad y posibles complicaciones&#46;</p></span>"
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        "etiqueta" => "&#9734;"
        "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as&#58; Conangla-Planes M&#44; Serres X&#44; Persiva O&#44; August&#237;n S&#46; Diagn&#243;stico por imagen de la hipertensi&#243;n portal&#46; Radiolog&#237;a&#46; 2018&#59;60&#58;290&#8211;302&#46;</p>"
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          "en" => "<p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">Seventy-three-year-old patient on ultrasound follow-up due to hepatic cirrhosis and portal hypertension&#46; The ultrasound longitudinal plane on the portal vein &#40;a&#41; shows an increased portal caliber &#40;16<span class="elsevierStyleHsp" style=""></span>mm&#41;&#46; The Doppler spectrum conducted at hepatic hilum level on one right intercostal plane &#40;b&#41; shows reduced portal velocity &#40;14&#46;6<span class="elsevierStyleHsp" style=""></span>cm&#47;s&#41;&#46; Finally&#44; one longitudinal plane on the spleen &#40;c&#41; shows one 16<span class="elsevierStyleHsp" style=""></span>cm-splenomegaly&#46;</p>"
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          "en" => "<p id="spar0020" class="elsevierStyleSimplePara elsevierViewall">Seventy-five-year-old patient on follow-up due to hepatic cirrhosis&#46; The Doppler color ultrasound &#40;left&#41; and the gray-scale ultrasound &#40;right&#41; show one tangled network of collateral blood vessels at hepatic hilum level consistent with portal cavernomatosis &#40;asterisk&#41;&#46;</p>"
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          "en" => "<p id="spar0025" class="elsevierStyleSimplePara elsevierViewall">Left axilary sagittal ultrasound planes of one control ultrasound in a patient with hepatic cirrhosis and portal hypertension showing the left kidney &#40;arrow&#41; and a 17-cm splenomegaly &#40;asterisk&#41;&#44; with multiple hyperechogenic punctiformed images consistent with Gamna-Gandy bodies&#46;</p>"
        ]
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      3 => array:7 [
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        "mostrarFloat" => true
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          "en" => "<p id="spar0030" class="elsevierStyleSimplePara elsevierViewall">Schematic representation of the outflow tract of the three left gastric veins &#40;arrow&#41; on a frontal plane at the upper edge of the portal vein&#44; the confluence with the superior mesenteric vein&#44; and the splenic vein&#46; The dotted lines are indicative of the axial plane through the celiac trunk with respect to the position of each one of the coronary veins&#46;</p>"
        ]
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          "en" => "<p id="spar0035" class="elsevierStyleSimplePara elsevierViewall">Sagittal ultrasound planes of the left gastric vein &#40;asterisk&#41; running underneath the common hepatic artery in a patient with portal pressures within normal ranges &#40;a&#41;&#44; and in a patient with portal hypertension &#40;b and c&#41;&#46; This ultrasound section shows the tadpole sign&#46; The dilation of one left gastric vein &#62;6<span class="elsevierStyleHsp" style=""></span>mm &#40;b&#41; and the reversed hepatofugal flow &#40;c&#41; are indicative of the presence of esophageal varices&#46;</p>"
        ]
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        "identificador" => "fig0030"
        "etiqueta" => "Figure 6"
        "tipo" => "MULTIMEDIAFIGURA"
        "mostrarFloat" => true
        "mostrarDisplay" => false
        "figura" => array:1 [
          0 => array:4 [
            "imagen" => "gr6.jpeg"
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        "descripcion" => array:1 [
          "en" => "<p id="spar0040" class="elsevierStyleSimplePara elsevierViewall">Correlation scheme for each one of the three nondilated left gastric veins with the corresponding ultrasound plane&#46; There is one coronary vein that originates on the upper edge of the beginning of the portal vein and runs cranially underneath the common hepatic artery &#40;arrow&#41;&#46; The second coronary vein originates on the upper edge of the confluence of the superior mesenteric vein with the splenic vein and runs cranially above the celiac trunk&#46; Finally&#44; the third coronary vein originates on the upper distal edge of the splenic vein and runs cranially behind the splenic artery &#40;asterisk&#41;&#46;</p>"
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        "identificador" => "fig0035"
        "etiqueta" => "Figure 7"
        "tipo" => "MULTIMEDIAFIGURA"
        "mostrarFloat" => true
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          0 => array:4 [
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        "descripcion" => array:1 [
          "en" => "<p id="spar0045" class="elsevierStyleSimplePara elsevierViewall">Paraesophageal varices &#40;arrow&#41;&#46; Abdominal CT scan with IV contrast in venous phase requested for the post-chemoembolization control of one hepatocellular carcinoma in a 75-year-old patient with alcoholic liver cirrhosis and portal hypertension&#46; The axial planes &#40;a and b&#41; and MIP reconstructions on the coronal &#40;c&#41; and sagittal planes &#40;d&#41; show a network of tortuous blood vessels located at the level of the distal esophagus that connect to the portal vein through the left gastric vein&#46;</p>"
        ]
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        "identificador" => "fig0040"
        "etiqueta" => "Figure 8"
        "tipo" => "MULTIMEDIAFIGURA"
        "mostrarFloat" => true
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        "figura" => array:1 [
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            "imagen" => "gr8.jpeg"
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            "Tamanyo" => 363259
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        "descripcion" => array:1 [
          "en" => "<p id="spar0050" class="elsevierStyleSimplePara elsevierViewall">CT images with IV contrast with MIP reconstructions on the axial &#40;a and b&#41; and sagittal planes&#40;c&#41; and ultrasound &#40;d y e&#41; of the same patient&#46; In both imaging modalities we can see findings of advanced chronic hepatopathy with a small&#44; heterogeneous liver with nodular edges and signs of portal hypertension&#44; a significant amount of ascitic fluid &#40;asterisk&#41; and the repermeabilization of the umbilical vein &#40;arrow&#41;&#46;</p>"
        ]
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        "identificador" => "fig0045"
        "etiqueta" => "Figure 9"
        "tipo" => "MULTIMEDIAFIGURA"
        "mostrarFloat" => true
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        "figura" => array:1 [
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        "descripcion" => array:1 [
          "en" => "<p id="spar0055" class="elsevierStyleSimplePara elsevierViewall">Eighty-year-old patient with hepatic cirrhosis and known hepatocellular carcinoma&#46; The Doppler color ultrasound with IV contrast &#40;a-c&#41; shows a network of tortuous blood vessels of subhepatic location that on the CT scan with IV contrast &#40;d-f&#41; are consistent with one portocaval shunt through the communication of the superior mesenteric vein with the right renal vein &#40;arrow&#41;&#46;</p>"
        ]
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        "etiqueta" => "Figure 10"
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        "descripcion" => array:1 [
          "en" => "<p id="spar0060" class="elsevierStyleSimplePara elsevierViewall">Follow-up ultrasound study of a patient with congestive hepatopathy due to heart disease&#46; The right&#44; subcostal&#44; obliquous&#44; transverse plane with cranial inclination toward the superior hepatic segments &#40;a&#41; shows where the three suprahepatic veins meet with the significantly dilated inferior vena cava &#40;diameter &#62;1<span class="elsevierStyleHsp" style=""></span>cm in the segment where it drains into the inferior vena cava&#41;&#8211;secondary findings of a difficult venous return&#46; The Doppler spectrum &#40;b&#41; shows waving portal flow&#46;</p>"
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                  \t\t\t\t\tvoid\n
                  \t\t\t\t" class=""><tbody title="tbody"><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Portal caliber &#62;13<span class="elsevierStyleHsp" style=""></span>mm&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Splenomegaly&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Doppler US&#58;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Reduced portal velocity &#40;&#60;15<span class="elsevierStyleHsp" style=""></span>cm&#47;s&#41; or hepatofugal flow&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Increased arterial RI &#40;&#62;0&#46;7&#41;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Portosystemic collaterality&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Ascites&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr></tbody></table>
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        "descripcion" => array:1 [
          "en" => "<p id="spar0065" class="elsevierStyleSimplePara elsevierViewall">Radiological findings of portal hypertension&#46;</p>"
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                  \t\t\t\t\tvoid\n
                  \t\t\t\t" class=""><thead title="thead"><tr title="table-row"><th class="td" title="table-head  " colspan="2" align="center" valign="top" scope="col" style="border-bottom: 2px solid black">Increased blood flow resistance</th></tr></thead><tbody title="tbody"><tr title="table-row"><td class="td" title="table-entry  " colspan="2" align="left" valign="top"><span class="elsevierStyleItalic">Intrahepatic</span></td></tr><tr title="table-row"><td class="td" title="table-entry  " rowspan="6" align="left" valign="top"><span class="elsevierStyleHsp" style=""></span>Pre-sinusoidal</td><td class="td" title="table-entry  " align="left" valign="top">Schistosomiasis&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Sarcoidosis&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Myeloproliferative diseases&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Congenital hepatic fibrosis&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Idiopathic portal hypertension&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Hepatotoxicity due to vinyl chloride&#44; arsenic&#44; azathioprine&#44; etc&#46;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="table-entry  " rowspan="3" align="left" valign="top"><span class="elsevierStyleHsp" style=""></span>Sinusoidal</td><td class="td" title="table-entry  " align="left" valign="top">Cirrhosis&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Methotrexate&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Hypervitaminosis A&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top"><span class="elsevierStyleHsp" style=""></span>Post-sinusoidal&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Veno-occlusive disease&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="table-entry  " colspan="2" align="left" valign="top"><span class="elsevierStyleVsp" style="height:0.5px"></span></td></tr><tr title="table-row"><td class="td" title="table-entry  " colspan="2" align="left" valign="top"><span class="elsevierStyleItalic">Extrahepatic</span></td></tr><tr title="table-row"><td class="td" title="table-entry  " rowspan="3" align="left" valign="top"><span class="elsevierStyleHsp" style=""></span>Prehepatic</td><td class="td" title="table-entry  " align="left" valign="top">Portal vein&#47;splenic vein thrombosis&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Portal stenosis&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">External compression of the portal vein&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="table-entry  " rowspan="4" align="left" valign="top"><span class="elsevierStyleHsp" style=""></span>Post-hepatic</td><td class="td" title="table-entry  " align="left" valign="top">Obstruction or thrombosis o the inferior vena cava&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Budd-Chiari syndrome&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Constrictive pericarditis or restrictive cardiomyopathy&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Tricuspid valve disease or right heart failure&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="table-entry  " colspan="2" align="left" valign="top"><span class="elsevierStyleVsp" style="height:0.5px"></span></td></tr><tr title="table-row"><td class="td" title="table-entry  " colspan="2" align="left" valign="top"><span class="elsevierStyleItalic">Increased vascular flow</span></td></tr><tr title="table-row"><td class="td" title="table-entry  " align="" valign="top">&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Arterioportal fistulas &#40;splanchnic&#44; intrahepatic&#44; intrasplenic&#41;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="table-entry  " align="" valign="top">&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Arteriovenous malformations&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr></tbody></table>
                  """
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          "en" => "<p id="spar0070" class="elsevierStyleSimplePara elsevierViewall">Main causes of portal hypertension&#46;</p>"
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Article information

ISSN: 21735107
Original language: English

DOI:10.1016/j.rxeng.2018.04.004

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