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Portal vein thrombosis is an infrequent condition occurring in several different clinical scenarios. In the last years it has been increasingly recognised due to the broad use of radiological methods. In this review we underline the central role of imaging in diagnosing portal vein thrombosis, in clarifying its etiology, choosing the best therapeutic approach and screening possible complications. Special attention is given to the role of imaging to differentiate portal vein thrombosis from neoplastic invasion of the portal vein, and to new diagnostic methods available for clinical practice in this field.
Portal vein thrombosis (PVT) is the second most common cause of portal hypertension (PH) in the Western world and it is classically defined as the partial or complete obstruction of the portal vein lumen by a clot, or as the finding of its substitution by neo-formed tortuous vessels with hepatopetal flow termed “cavernoma”. Thrombosis in the portal venous system is increasingly recognised as the result of predisposing factors acting on one or more elements of the Virchow’s triad, namely hypercoagulability, endothelial dysfunction and stasis (Table 1) [
The presentation of PVT is very variable, and ranges from asymptomatic incidental findings to severe complications of portal hypertension, variceal bleeding in particular; the number of vessels involved (e.g. portal vein only vs. portal, splenic and mesenteric veins) and the degree of thrombosis (partial vs. complete) influence the clinical features, and the chance to respond to anticoagulation [
]. Additional complexity of PVT is due to the fact that it can occur in several different clinical scenarios, including cirrhosis, haematological diseases in non-cirrhotic subjects (mostly chronic myeloproliferative diseases), abdominal infections/surgery, central obesity [
]. In non-cirrhotic subjects, the term “PVT” should be replaced with the term “extrahepatic portal vein obstruction” (EPVHO), which does not include isolated splenic vein or mesenteric vein thrombosis [
Expanding consensus in portal hypertension: report of the Baveno VI consensus workshop: stratifying risk and individualizing care for portal hypertension.
]. In this complex scenario, the aim of this review is to describe how imaging methods can help the clinical hepatologist in all phases of the decision-making process related to PVT/EPVHO (in the review generally addressed as PVT).
2. The diagnosis of PVT: who should be suspected of PVT and how to investigate the presence of PVT and its severity
The diagnosis of PVT may occur in two major clinical scenarios: in asymptomatic and in symptomatic patients. If PVT is incidentally discovered the clinician will be asked to make a step backward and look for the risk factors leading to PVT, while in the case of symptomatic patients potentially at risk of carrying PVT the clinician will be asked to make a step forward and ask for the help of imaging to confirm or exclude the diagnosis of PVT. Even when a local risk factor is found or known, additional causes such as systemic prothrombotic conditions should be investigated [
The results of a recently published study suggest that the prognosis of incidentally detected splanchnic vein thrombosis is similar to that of clinically suspected splanchnic vein thrombosis suggesting that similar treatment strategies should be applied [
]. In all cases, after the diagnosis the clinician will need to carefully screen for complications of PVT and plan the most appropriate therapy and follow up.
The main clinical presentation of acute PVT is abdominal pain, especially if the superior mesenteric vein is involved. In chronic PVT the clinical presentation is related to the development of pre-hepatic portal hypertension (ascites, variceal bleeding, encephalopathy) or portal cholangiopathy (jaundice, abdominal pain, cholangitis).
When PVT is suspected ultrasound is the first line imaging method to be used (Fig. 1), since it holds an accuracy ranging 88–98% for the detection of PVT with a sensitivity and specificity of 80–100% in the majority of studies [
EFSUMB Education and Professional Standards Committee
Ultrasound in portal hypertension—part 2—and EFSUMB recommendations for the performance and reporting of ultrasound examinations in portal hypertension.
Ultraschall in der Medizin.2012; 33 (quiz 0–1): 8-32
In 2-D Gray-Scale ultrasonography a thrombus appears as a hypo/isoechoic material occupying part (partial thrombosis) or the entire vessel (complete thrombosis) (Fig. 2). The normal portal vein can be eventually replaced by multiple tortuous vessels with hepatopetal flow, a condition, named “cavernomatous transformation” or “cavernoma”, that can be also easily detected with Doppler-ultrasound (Fig. 2). Colour/power and pulsed Doppler should be mandatorily used to confirm whether the vessel has a remnant blood flow, so helping differentiating high degree partial thrombosis to complete thrombosis.
Fig. 2Radiological images of portal vein thrombosis. A. Ultrasound image of an acute complete portal vein thrombosis (arrow). B. CECT image of a complete portal vein thrombosis (venous Phase) (arrow). C. Ultrasound image of a portal vein cavernoma (arrow). D. CEMRI image of a portal vein cavernoma (arrow).
The reliability of ultrasonography in the detection of PVT improves with the operator’s experience and whenever PVT is clinically suspected ultrasonography should be performed by experienced operators [
]. Ultrasonography suffers from other limitations, such as reduced visualisation in obese individuals and in case of abundant bowel gas and impossibility to assess bowel ischemia. This should be suspected in case of ascites and/or high blood lactate levels.
Ultrasound is sufficient to diagnose PVT in patients with a good acoustic window, but when ultrasonography is insufficient to clarify whether PVT is present or absent (for instance in patients with insufficient visualisation), a second line cross-sectional imaging method should be considered to confirm or exclude the diagnosis.
Contrast-enhanced 4 Phases (pre-contrast, arterial, portal and late) CT (CECT) and contrast-enhanced MRI (CEMRI) can be used, being CT preferred in unstable patients with acute abdominal symptoms. Advantages of MR and CT over US include the possibility of detecting bowel ischemia, septic foci, and intraabdominal malignancies, and higher sensitivity in the detection of thrombosis in the splenic and superior mesenteric vein (Table 2). The drawbacks of CT are well known and include exposure to ionizing radiation, the risk of allergic reactions and nephrotoxicity. CEMRI is also contraindicated in patients with acute renal failure for the risk of nephrogenic systemic fibrosis [
Non-contrast-enhanced MR portography with time-spatial labeling inversion pulses: comparison of imaging with three-dimensional half-fourier fast spin-echo and true steady-state free-precession sequences.
Journal of Magnetic Resonance Imaging.2009; 29: 1140-1146
Non-contrast-enhanced MR portography with balanced steady-state free-precession sequence and time-spatial labeling inversion pulses: comparison of imaging with flow-in and flow-out methods.
Journal of Magnetic Resonance Imaging.2014; 40: 583-587
Once PVT is diagnosed, CECT or CEMRI are mandatory to evaluate the extent of thrombosis and to allow a detailed mapping of porto-systemic collaterals (Fig. 1), crucial to the planning of interventions aimed at recanalising the PV system. It should be considered that clinical consequences of PVT mainly depend on the number of vessels completely occluded [
], as well on the degree of collateralization in chronic cases. Furthermore, the presence of ascites is a predictor of lack of response to anticoagulation, and should be reported [
]. Several classification/staging systems have been developed, but mostly rely upon anatomical considerations. The most commonly cited and used in clinical trials is the one proposed by Yerdel et al. [
At every new diagnosis of PVT the patency of the liver veins should also be assessed, since Budd–Chiari syndrome and EHPVO share the same risk factors.
2.1 Possible pitfalls of imaging methods: is this really a thrombosis?
When first detecting PVT the first important question to be answered is: “is this really a thrombosis?” US, CT and MR all suffer from possible pitfalls that can be at least partially avoided by increasing knowledge and awareness on their existence.
2.1.1 False positive findings
Ultrasound can give false positive findings leading to suspect/diagnose a thrombosis in the portal system in its absence; this can happen especially if blood flow velocity in the portal vein system is very low such as in case of decompensated cirrhosis. In these cases the scale of colour/power Doppler should be set low, with minimum possible pulse repetition frequency and the absence of flow should be confirmed by quantitative pulsed Doppler. Additionally, the use of contrast-enhanced ultrasonography (CEUS) is recommended to confirm or exclude the presence of a clot in doubtful cases [
Guidelines and good clinical practice recommendations for contrast enhanced ultrasound (CEUS) in the liver—update 2012: a WFUMB-EFSUMB initiative in cooperation with representatives of AFSUMB, AIUM, ASUM, FLAUS and ICUS.
], since the sensitivity of this method is very high, exceeding 95%. As for CECT, if the images are acquired during the late arterial phase the “portal” phase will not be representative and PVT may be falsely diagnosed. The same pitfall may occur in case of reduced portal flow velocity and in case of delayed arrival of contrast material from one of the vessels composing the portal vein system. In order to obtain a good quality portal phase it is advised to acquire the images 60–70 s after contrast injection [
A “thrombosed” portal vein is a frequent finding in patients with hepatocellular (or intrahepatic cholangiocellular) carcinoma (HCC/ICC). These patients can develop bland thrombosis as a consequence of more severe cirrhosis or paraneoplastic thrombophilia but a neoplastic/tumour invasion of the portal vein is also frequent (12–30%) [
]. The term “malignant portal vein thrombosis” has been often used to address neoplastic invasion of the PV and led to confusion in this field. For instance, in autopsy-based studies, PVT had a prevalence of 1.0% [
], but neoplastic invasion was included in the definition. In our opinion the term “malignant thrombosis” should be avoided since it can be misleading, and neoplastic or tumour invasion should be used to define the presence of neoplastic tissue within the portal vein lumen. Given the major prognostic and therapeutic consequences of diagnosing a neoplastic PV invasion (e.g. advanced stage of HCC with clear contraindication to liver transplantation; no indication to anticoagulation), imaging should report in detail all the possible related signs. At every new diagnosis of PVT, in particular in patients with a history of HCC or other malignancies (e.g. pancreas carcinoma), neoplastic PV invasion should be carefully ruled-out. It should not be forgot that neoplastic invasion of the PV can be the first presentation of a else not evident HCC [
Signs of neoplastic invasion of the PV on ultrasound include an expansive aspect of the mass inside the lumen, with heterogenous aspect and disruption of the portal vein walls. Colour/power-Doppler ultrasound typically shows signs of arterial neovascularization within the mass, and pulsed Doppler confirms arterial flow with high resistance index at this level. CEUS is the most sensitive imaging method to confirm neoplastic invasion, and it can be applied right after the ultrasound detection of a new PVT with small additional costs [
]. In contrast to bland PVT which remains unenhanced in all phases, an intraluminal neoplastic invasion mass shows the same contrast-behavior as HCC, namely a rapid wash-in (hyper-perfusion in comparison to the surrounding liver parenchyma) in the arterial phase, and a wash-out (hypo-perfusion in comparison to the surrounding liver parenchyma) in the portal/late phase (Fig. 3). CEUS holds a high sensitivity (88–100%) and specificity (94–96%) for the differential diagnosis between bland PVT and neoplastic portal vein invasion in patients with HCC [
Diagnosis of benign and malignant portal vein thrombosis in cirrhotic patients with hepatocellular carcinoma: color Doppler US, contrast-enhanced US, and fine-needle biopsy.
Contrast-enhanced us: a simple, quick and sensitive tool in the differential diagnosis of benign and malignant portal vein thrombosis in cirrhotic patients with hepatocellular carcinoma.
Contrast-enhanced ultrasonography and spiral computed tomography in the detection and characterization of portal vein thrombosis complicating hepatocellular carcinoma.
]. CT performance in the differentiation between PVT and neoplastic invasion may be improved by software-based texture analysis (in patients with and without HCC) [
Characterization of portal vein thrombosis (neoplastic versus bland) on CT images using software-based texture analysis and thrombus density (Hounsfield units).
AJR American Journal of Roentgenology.2016; : W1-W7
Dual-energy CT with iodine quantification in distinguishing between bland and neoplastic portal vein thrombosis in patients with hepatocellular carcinoma.
]. Susceptibility-weighted MR imaging seems to have a higher sensitivity and specificity as compared to CT, but further data are needed before its use in clinical practice [
Differentiation of bland from neoplastic thrombus of the portal vein in patients with hepatocellular carcinoma: application of susceptibility-weighted MR imaging.
]. It should be noted that the majority of the published imaging studies was performed in patients with known HCC (who have a high pre-test probability for neoplastic portal vein invasion), and that their performance in patients without known HCC is yet to be determined. Therefore, it should be stressed that when a clear-cut differentiation between bland PVT and neoplastic invasion cannot be achieved through imaging methods a biopsy of the thrombus/intraluminal mass should be considered [
Fig. 3Radiological images in case of neoplastic invasion of the portal vein. A. In Grey scale (B-mode) expansive aspect of the “thrombus” with disruption of the wall (arrow). B. Signs of arterial vascularization at Colour-Doppler. C. CEUS (arterial phase): hyperenhancement of the portal vein content (wash in) (arrow). D. CEUS (late phase): hypoenhancement in the late phase (wash out) (arrow).
3. After ascertaining the diagnosis: clinically relevant aspects to be investigated by imaging
Once the diagnosis of PVT has been made and the possible pitfalls are excluded the clinician should perform further investigations in order to plan therapy. A series of relevant questions should be addressed as they can affect patient management and follow up.
3.1 Has the patient liver cirrhosis?
Since cirrhosis is per se a factor determining a severe prognosis, its presence or absence should be actively investigated. Imaging can provide reliable information regarding the presence or absence of cirrhosis. Ultrasound signs include liver surface nodularity (best assessed with high frequency linear probe), heterogeneity of liver echotexture, hypertrophy of the left and caudate lobe, splenomegaly and other signs of portal hypertension [
EFSUMB Education and Professional Standards Committee
Ultrasound in portal hypertension—part 2—and EFSUMB recommendations for the performance and reporting of ultrasound examinations in portal hypertension.
Ultraschall in der Medizin.2012; 33 (quiz 0–1): 8-32
]. Although hypertrophy of the left and caudate lobe has been described as a typical sign of cirrhosis, it has also been reported in the absence of cirrhosis in patients with cavernous transformation of the portal vein and/or Budd–Chiari syndrome [
]. Therefore, this sign is not specific enough in patients with PVT to diagnose cirrhosis. The liver can undergo morphological changes following a long-lasting PVT. Atrophy–hypertrophy complex (atrophy of the right lobe and lateral segment of the left lobe, with hypertrophy of the forth segment and caudate lobe) can be found in up to 91% of patients with cavernous transformation of the portal vein while it is usually absent in cirrhosis. However, overlap between these changes can be found, and caution is needed on images interpretation [
In the last years ultrasound and magnetic resonance elastography techniques have been developed to estimate the stiffness of the liver and spleen tissue, a physical property which is proportional to the presence and severity of liver fibrosis in the liver, and to the severity of portal hypertension in the spleen [
Role of hepatic vein catheterisation and transient elastography in the diagnosis of idiopathic portal hypertension.
Digestive and Liver Disease: Official Journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver.2012; 44: 855-860
] so allowing differentiating cirrhotic and non-cirrhotic livers in the presence of indeterminate imaging signs. However, liver stiffness (by any method) can be increased by food ingestion, acute inflammation, biliary obstruction, passive hepatic congestion and neoplastic infiltration of the liver independent of fibrosis, and should therefore interpreted taking into account its possible confounders [
]. Interestingly, spleen stiffness correlates with the size of gastroesophageal varices and seems to provide data regarding the bleeding risk in patients with EHPVO [
]. Hence, it would be important to date the thrombotic process. The presence/absence of abdominal symptoms cannot be the only parameter to consider when distinguishing acute from chronic PVT, since despite that abdominal pain is common in acute thrombosis [
], this may also be present in case of re-thrombotic episodes in the contest of chronic PVT. On the other hand, in many cases acute PVT may be asymptomatic or pauci-symptomatic. In this context, imaging can be of help in some instances, but there is no gold-standard method able to exactly estimate the age of the thrombosis and this is a field for future investigations.
3.2.1 What are the imaging-signs indicating an acute thrombosis?
Typical features of an acute thrombosis include the presence of a hypoechogenic/hypodense/hypointense thrombus in US/CT/MR, while later on the aspect of the thrombus tends to be iso/hyperechogenic/-dense/-intense. On ultrasound the portal vein may appear dilated; although this presentation should prompt further investigation to exclude neoplastic invasion in patients with known hepatocellular or cholangiocellular carcinoma, the diameter of the PV in bland thrombosis does not usually exceed 2 cm [
]. The absence of porto-systemic collaterals or splenomegaly (signs of PH) usually indicates an acute thrombosis. On the other hand, the presence of these signs does not automatically indicate chronic thrombosis, since splenomegaly can also be presents in cirrhosis and in myeloproliferative disorders, and porto-systemic collaterals may have formed in patients with cirrhosis due to sinusoidal portal hypertension.
3.2.2 What are the imaging signs of a chronic thrombosis?
A completely absent (fibrotic) portal vein and the presence of a cavernoma are signs suggesting chronic PVT. However, a study conducted on 9 patients with acute portal vein thrombosis followed-up by ultrasound demonstrated that the formation of a cavernoma can already take place 6–20 days after the acute event [
]. Therefore, the definition of “chronic PVT” probably encompasses a wide temporal spectrum, ranging from few-days to years.
Massive signs of portal hypertension (such as extensive porto-systemic collaterals) in the absence of cirrhosis or other concomitant causes of PH usually indicate a chronic PVT.
The presence of wall/thrombus calcifications is a pathognomonic sign of chronic PVT, and if the perfusion of the vessel has been restored, a history of thrombosis [
]. Calcification appear hyperdense in CT and as hyperechogenic in ultrasound while they cannot be visualised on MRI.
In candidates for liver transplantation the presence of PV calcifications should be actively investigated since they imply a more fragile vessel and may complicate surgical procedure [
3.3 Has the patient developed PVT-related complications?
3.3.1 Portal hypertension
Since PVT causes pre-hepatic portal hypertension, the clinical features of portal hypertension constitute a common presentation of PVT both in the cirrhotic and non-cirrhotic population. A recent study on 178 patients with chronic EHPVO showed that more than two third of the subjects (71%) had gastro-esophageal varices (GOV) at screening endoscopy [
]. This figure supports the Baveno VI recommendations stating that it is mandatory to perform screening endoscopy in all patients on diagnosis of chronic PVT and within 6 months from the acute episode if a complete recanalization of thrombosis is not achieved [
Expanding consensus in portal hypertension: report of the Baveno VI consensus workshop: stratifying risk and individualizing care for portal hypertension.
Expanding consensus in portal hypertension: report of the Baveno VI consensus workshop: stratifying risk and individualizing care for portal hypertension.
], and PVT should be investigated in all patients with cirrhosis presenting with variceal bleeding, since it can worsen portal hypertension in this population; sudden worsening of ascites should also prompt PVT screening [
EFSUMB Education and Professional Standards Committee
Ultrasound in portal hypertension—part 2—and EFSUMB recommendations for the performance and reporting of ultrasound examinations in portal hypertension.
Ultraschall in der Medizin.2012; 33 (quiz 0–1): 8-32
As regards to the primary prevention of bleeding, no randomised controlled trial compared the effectiveness of non-selective beta-blockers vs. endoscopic band ligation in EPVHO/PVT. In this scenario, as well as in the context of the acute bleeding and of secondary prophylaxis, Baveno VI recommends to follow the guidelines regarding PH in cirrhosis [
Expanding consensus in portal hypertension: report of the Baveno VI consensus workshop: stratifying risk and individualizing care for portal hypertension.
]. Whenever a patient with PVT bleeds from varices, CECT or CEMRI should be performed to evaluate possible new episodes of thrombosis and map the patent vessels and porto-systemic collaterals (often ectopic, and relatively often source of difficult to control bleedings) in order to assess whether intravascular procedures (e.g. TIPS; embolization of collaterals) or shunt surgery are potentially feasible.
3.3.2 Portal cholangiopathy
Portal cholangiopathy is characterised by abnormalities of the biliary system and gallbladder in the setting of EHPVO. The pathogenesis of portal cholangiopathy can be summarised as (I) ischemia at the time of portal vein thrombosis and (II) local ischemia due to prolonged local wall compression by the peribiliary collaterals [
]. It has been reported that >80% of patients with portal cavernoma develop some degree of portal cholangiopathy, but just a minority of them develops symptoms during the follow up (right abdominal pain, pruritus, jaundice, gallbladder stones and cholangitis) [
]. The gold standard for the diagnosis of portal cholangiopathy used to be conventional cholangiography which can display one or more of these features: extrahepatic strictures, intrahepatic biliary dilatation, caliber irregularity, ductal ectasia, indentations, displacement and angulations of ducts, clustering and pruning of intrahepatic ducts, filling defects in intra and extrahepatic biliary system. This invasive technique is now reserved for interventional purposes and the first line diagnostic method for portal cholangiopathy is now considered magnetic resonance cholangiopancreatography (MRCP) [
]. MRCP allows also a classification of biliary tree abnormality with clinical correlates: (I) minimal irregularities or angulation of the biliary tree; (II) indentations or strictures without dilatation of the biliary tree; (III) strictures with dilatation (intrahepatic duct >4 mm or extrahepatic duct >7 mm) [
A study on 67 patients with PVT showed that portal cholangiopathy might be an early event in the natural history of EHPVO and that after its onset it may not progress. In the same study only patients with severe biliary tree abnormalities (Grade III) showed cholangiopathy related symptoms during follow up [
]. These results still need to be validated in independent series but based on these initial findings it has been suggested that MRCP should be performed at every new diagnosis of chronic PVT and 9–12 months after acute PVT if recanalization has not been achieved [
A mocking finding: portal cavernoma mimicking neoplastic mass: first sign of myeloproliferative disorder in a patient with Janus kinase2 V617F mutation.
European Journal of Gastroenterology & Hepatology.2009; 21: 233-236
Ideally, the goal of therapy is to recanalise the thrombosis, as well as to avoid its extension and clinical complications. However, little is known about the natural history of PVT, and there is no randomised controlled trial assessing the best therapeutic option in this population. Imaging should then assist the clinician in tailoring therapy on presentation and follow-up.
Currently, in adults, two major approaches to PVT are possible, namely anticoagulation (with heparin/low molecular weight heparin or with oral anticoagulants) and transjugular intrahepatic porto-systemic shunt (TIPS) in selected cases. In this context the BAVENO VI recommendations are generally based on a low level of evidence, and differentiate between patients with and without cirrhosis. Major attention is paid to the concept of “transplantability” of patients with cirrhosis, since PVT complicates the surgical procedure; in these patients anticoagulation is suggested and if a choice of not anticoagulating is made, a strict trimestral imaging follow-up should be performed to detect extension of the thrombotic process and begin anticoagulation if needed. In patients with cirrhosis not candidate to liver transplantation anticoagulation may be considered if superior mesenteric vein is involved or if the patient carries a known prothrombotic condition [
Expanding consensus in portal hypertension: report of the Baveno VI consensus workshop: stratifying risk and individualizing care for portal hypertension.
In non-cirrhotic acute EHPVO anticoagulant therapy with low molecular weight heparin followed by oral anticoagulation is recommended for at least six months and long term anticoagulation should be considered if a persistent prothrombotic state is documented [
Expanding consensus in portal hypertension: report of the Baveno VI consensus workshop: stratifying risk and individualizing care for portal hypertension.
]. Imaging should be used to identify patients who achieve a successful recanalization during anticoagulant therapy and to monitor the persistence of patency once therapy is stopped. Despite there is no recommendation regarding the timing of controls and the imaging method to be used, our practice is to do a first control after 3–6 months of therapy using the same cross-sectional imaging method used on diagnosis, and then use ultrasound in patients with optimal visualization of the PV system thereafter (minimum every 6 months). In patients who are not good candidates to ultrasound, CEMR/CECT should be used according to the expertise of the center and patients’ characteristics.
TIPS is increasingly used as an option to access and attempt a recanalization of the PV system both in cirrhosis and in EHPVO. The success likelihood is higher when a remnant of the PV can be visualised on imaging [
EFSUMB Education and Professional Standards Committee
Ultrasound in portal hypertension—part 2—and EFSUMB recommendations for the performance and reporting of ultrasound examinations in portal hypertension.
Ultraschall in der Medizin.2012; 33 (quiz 0–1): 8-32
]. In selected cases surgical shunts (meso-cava; spleno-renal, etc.) are the only option to correct severe cases of PH secondary to EHPVO, and again imaging is crucial to plan the best surgical approach and on follow-up.
In children an additional option is sometimes possible, namely Meso-Rex bypass, which allows the restoration of a physiological flow to the liver, with improvement of clinical outcomes [
While wedged portography is needed to identify a patent Rex recessus, ultrasound-Doppler is the best technique to follow-up patients after the procedure [
Imaging helps and guides the clinician in all the phases of patient’s management in the field of PVT. A multidisciplinary approach based on a good cooperation between hepatologists, diagnostic and interventional radiologists, and liver surgeons is needed to offer to patients the best possible care. Identifying imaging biomarkers useful to stratify the risk of patients, namely to select those who have a high likelihood to resolve PVT with anticoagulation alone, and those who would require a more aggressive interventional approach is among the prioritaire unmet needs in this field. Validation studies will be needed to assess the diagnostic potential of CEUS and CECT/CEMRI in the differential diagnosis of PVT from neoplastic invasion on first imaging assessment of new cases of PVT, and of unenhanced magnetic resonance portography for the study of the entire portal vein system in patients with contraindications to iodine or gadolinium-based contrast material.
Finally, a shared classification system based on radiological and clinical features will represent a major step forward in order to standardise clinical trials and tailor therapeutic decisions for PVT.
Conflicts of interest
None declared.
References
Plessier A.
Darwish-Murad S.
Hernandez-Guerra M.
et al.
Acute portal vein thrombosis unrelated to cirrhosis: a prospective multicenter follow-up study.
Expanding consensus in portal hypertension: report of the Baveno VI consensus workshop: stratifying risk and individualizing care for portal hypertension.
EFSUMB Education and Professional Standards Committee
Ultrasound in portal hypertension—part 2—and EFSUMB recommendations for the performance and reporting of ultrasound examinations in portal hypertension.
Ultraschall in der Medizin.2012; 33 (quiz 0–1): 8-32
Non-contrast-enhanced MR portography with time-spatial labeling inversion pulses: comparison of imaging with three-dimensional half-fourier fast spin-echo and true steady-state free-precession sequences.
Journal of Magnetic Resonance Imaging.2009; 29: 1140-1146
Non-contrast-enhanced MR portography with balanced steady-state free-precession sequence and time-spatial labeling inversion pulses: comparison of imaging with flow-in and flow-out methods.
Journal of Magnetic Resonance Imaging.2014; 40: 583-587
Guidelines and good clinical practice recommendations for contrast enhanced ultrasound (CEUS) in the liver—update 2012: a WFUMB-EFSUMB initiative in cooperation with representatives of AFSUMB, AIUM, ASUM, FLAUS and ICUS.
Diagnosis of benign and malignant portal vein thrombosis in cirrhotic patients with hepatocellular carcinoma: color Doppler US, contrast-enhanced US, and fine-needle biopsy.
Contrast-enhanced us: a simple, quick and sensitive tool in the differential diagnosis of benign and malignant portal vein thrombosis in cirrhotic patients with hepatocellular carcinoma.
Contrast-enhanced ultrasonography and spiral computed tomography in the detection and characterization of portal vein thrombosis complicating hepatocellular carcinoma.
Characterization of portal vein thrombosis (neoplastic versus bland) on CT images using software-based texture analysis and thrombus density (Hounsfield units).
AJR American Journal of Roentgenology.2016; : W1-W7
Dual-energy CT with iodine quantification in distinguishing between bland and neoplastic portal vein thrombosis in patients with hepatocellular carcinoma.
Differentiation of bland from neoplastic thrombus of the portal vein in patients with hepatocellular carcinoma: application of susceptibility-weighted MR imaging.
Role of hepatic vein catheterisation and transient elastography in the diagnosis of idiopathic portal hypertension.
Digestive and Liver Disease: Official Journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver.2012; 44: 855-860
A mocking finding: portal cavernoma mimicking neoplastic mass: first sign of myeloproliferative disorder in a patient with Janus kinase2 V617F mutation.
European Journal of Gastroenterology & Hepatology.2009; 21: 233-236
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