GIT Kurdistan Board GEH Journal club Lower PVT 2014.
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GIT Kurdistan Board GEH Journal club Lower PVT 2014.

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GIT Kurdistan Board GEH Journal club Lower PVT 2014.

GIT Kurdistan Board GEH Journal club Lower PVT 2014.

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GIT Kurdistan Board GEH Journal club Lower PVT 2014. GIT Kurdistan Board GEH Journal club Lower PVT 2014. Presentation Transcript

  • NATURE REVIEW GEH; MAY 2014 PVT: IMAGING IN CLINICAL DECISION-MAKING KURDISTAN BOARD GEH JOURNAL CLUB
  • PVT: ABSTRACT  A frequent & potentially life-threatening condition with various causes including liver cirrhosis, HCC, other solid tumours, abd septic foci, acute pancreatitis, haematological malignancies &congenital or acquired prothrombotic disorders. Clinical decision-making is a particularly complex process owing to the heterogeneity of the population affected by this condition & the lack of high-quality evidence from RCTs for anticoagulation therapy. A flowchart to use imaging in diagnosis based on current evidence is followed.
  • PVT: ABSTRACT Non-malignant causes: Liver cirrhosis  Abdominal septic foci  Acute pancreatitis Prothrombotic disorders (congenital or acquired).
  • PVT: ABSTRACT Malignant causes: HCC  Other solid tumours.  Haematological malignancies.
  • PVT: INTRODUCTION PVT indicates the presence of a clot in the PV lumen or a permanent obliteration of the portal vein as a result of prior thrombosis with replacement by numerous tortuous venous channels ( cavernoma). PVT can be located in the intrahepatic&/or the extrahepatic venous tracts & can extend to the splenic & superior mesenteric veins.  Thrombosis can also be restricted to the SV&/ or SMV& altogether these conditions are known as ‘thrombosis of the portal venous system’.
  • PVT: INTRODUCTION The prevalence of PVT in necropsy is 1%.  Rare in the general population .  > With pre-existing cirrhosis or neoplastic diseases, particularly HCC.  >60% of cases of non-cirrhotic, nonmalignant PVT are associated with congenital or acquired thrombophilic disorders, hypercoagulable states or prothrombotic diseases. in 30% of cases an additional known risk factor (namely, a local factor, such as a septic focus) can be identified. PVT prevalence in cirrhosis:10–25%,highest in advanced decomp cirrhosis. Risk factors for PVT in cirrhosis partially known& the result of a complex interaction between the 3 factors of the Virchow’s triad—stasis, hypercoagulability &endothelial dysfunction.
  • PVT: INTRODUCTION  PVT clinical presentation is extremely variable: Asymptomatic: identified during imaging for an alternative reason. To devastating episodes complicated by intestinal infarction. Acute PVT is often asymptomatic or paucisymptomatic in patients without underlying liver diseases  But can present as an acute process characterized by abdominal pain, fever &/or features of intestinal venous ischaemia.  In up to 30% of acute PVT cases, splenomegaly &minimal ascites are already present.
  • PVT: INTRODUCTION  The effect of PVT on the clinical outcome of patients with cirrhosis is controversial, but at least in some patients, it can result in worsening of pre-existing portal hypertension with development of ascites or variceal bleeding. It is an independent negative prognostic factor for post- transplantation survival in patients who are on a waiting list for liver transplantation. In patients with cirrhosis& HCC, the onset of malignant PVT indicates an advanced stage of the disease in which locoregional therapy is no longer indicated.
  • PVT: INTRODUCTION Anticoagulants are effective in recanalization in around 40% with acute PVT. Anticoagulants are safe in patients with a healthy liver & with cirrhosis. A prompt & accurate diagnosis of prothrombotic disorders is always required. Most patients with long-lasting chronic PVT, present with complications of portal hypertension (oeso varices, variceal bleeding&hypersplenism).  In these patients, surgical treatment or TIPS are often needed after meticulous evaluation by clinicians.
  • PVT: CIRRHOSIS VS NON U/S is the best method to assess whether PVT has taken place on the background of a healthy or a cirrhotic liver. The single most accurate sign of cirrhosis on U/S is liver surface nodularity, best by using high-frequency probes.  Changes in the morphology of the liver, such as caudate lobe hypertrophy & atrophy of the right liver lobe, can be seen by any of the 3( U/S, CT or MRI) ,but have poor specificity for cirrhosis, as they can be found in long-lasting no-ncirrhotic PVT as a consequence of lobar perfusion alterations&curling of hepatic veins cannot be considered specific for cirrhosis in patients with PVT.
  • PVT: CIRRHOSIS VS NON In unclear cases, more specific signs of altered liver morphology should be analysed using CT or MRI. The atrophy–hypertrophy complex (which includes atrophy of the right liver lobe &lateral segment of the left liver lobe, together with hypertrophy of the caudate lobe &the fourth liver segment) can be found in up to 91% of patients with non-cirrhotic cavernomatosis, usually absent in patients with cirrhosis.  Despite these different findings, long-lasting PVT, in particular that occurring in patients with idiopathic portal hypertension, is sometimes indistinguishable by standard imaging from the appearance of PVT in patients with cirrhosis.
  • PVT: CIRRHOSIS VS NON In most patients in whom U/S & CT/ MRI cannot provide a conclusive answer regarding the presence of underlying cirrhosis, transient elastography can be successfully used.  New sonoelastography, which can be applied in real-time to both the liver & spleen (including acoustic radiation force-impulse imaging &shear wave elastography), might represent an important advance in the near future, but no study data are available so far. Liver biopsy remains the gold-standard technique in patients who cannot be classified by noninvasive methods&further investigation is needed to better define imaging surrogates of diagnosis.
  • PVT:PANCREATITIS & SEPTIC FOCI Pancreatitis cause PV system thrombosis in up to 2%. The patency of the portal, splenic & mesenteric veins should be assessed by imaging. Septic foci that increases the risks should be actively searched. CT & MRI are more accurate than U/S for assessing the presence of abd septic foci such as diverticulitis or abd abscesses. CT should be considered the method of choice in patients with fever or symptoms suggestive of infection.
  • PVT: HEPATIC & EXTRAHEPATIC CANCER U/S is the screening method of choice to identify potentially malignant nodules in cirrhosis. The presence of hepatic metastasis or extrahepatic malignancies (sp pancreatic cancer) causing direct invasion of the portal vein should be carefully evaluated during U/S performed for PVT. U/S alone is not accurate enough to characterize nodules in cirrhosis&is insufficiently sensitive to rule out intrahepatic metastasis or extrahepatic abdominal tumours in cases of negative findings.  CT or MRI should be used to accomplish a comprehensive abdominal assessment in patients with newly diagnosed PVT.
  • PVT: BENIGN VERSUS MALIGNANT THROMBOSIS IN HCC Malignant invasion of PV occurs in 12–30% with HCC. Nonmalignant PVT described in in HCC &cirrhosis. Presence of malignant PVT contraindicates locoregional therapies&liver transplantation,so an accurate, extensive imaging work-up is needed in any case of PVT arising in patients with cirrhosis& HCC, including those patients in whom the tumour has been treated by curative therapies.
  • PVT: BENIGN VERSUS MALIGNANT THROMBOSIS IN HCC Specific signs of malignant (neoplastic) PVT include:  Expansive (enlargement of PV due to mass-forming thrombus).  Disruption of the vessel’s walls. Intrathrombus arterial neovascularization , by CDUS or PWUS&much better by contrast-enhanced imaging. Hyperenhancement in the arterial phase & wash-out in the late phase are typical features of HCC & HCC-related PVT invasion on CEUS, CECT& CEMRI. Abnormal enhancement due to malignant thrombosis in HCC can also be identified by arteriography in early phases by thread &streak sign(thin linear or chainlike opacification in the portal vein after the injection of contrast, reflects neovessels within the tumour cast. Diffusion-weighted MRI & dual-energy CT is helpful to diff between benign& malignant thrombus. Finally biopsy of the thrombus should be considered for conclusive diagnosis.
  • PVT: THE EXTENT The chance of achieving recanalization by anticoagulant therapy in patients with acute noncirrhotic PVT decrease:  In patients who have complete PVT compared with those who have mural PVT. Involvement of >one vessel, or complete thrombosis of the whole portal venous system. The presence of abdominal fluid.
  • PVT: THE EXTENT In chronic PVT the extent of thrombosis is also central to planning treatment strategies to decompress the portal system in case of complications. Derivative surgery for portal hypertension & liver transplantation are only feasible if at least one of the main vessels of the portal venous system is patent; for example, PV or SMV in liver transplantation. U/S not accurate enough for excluding thrombosis extension to the SV or to the SMV ,so CECT or CEMRI is indicated to evaluate thrombosis extent after PVT diagnosed by U/S & the number, position, size of abdominal portosystemic collaterals.
  • PVT: THE EXTENT Common collaterals include those arising from left & short gastric veins usually feeding GE varices& spleno-renal collaterals& ectopic collaterals(outside the EGJ) Ectopic collaterals are more common in patients with PV system thrombosis(up to 40% ) &include vessels in the gallbladder wall, transparietal hepatic vessels, at site of biliary–enteric& entero- cutaneous surgical anastomosis. Collaterals can be of importance for planning effective trt programmes & large collaterals might be used in selected patients with a complete thrombosis of PVS to attempt surgical shunting or portal reconstruction on liver transplantation.
  • PVT: PORTAL HYPERTENSIVE BILIOPATHY Abno of biliary system&GB due to extrinsic vascular compression by collats ERCP or MRI show some degree of portal cholangiopathy in >80% with portal cavernoma. Few develop symptoms & labo tests are not useful to predict symptoms. MRC is the noninvasive procedure of choice &findings correlate with the risk of developing clinical symptoms, which are limited to patients showing dilatation of the biliary tree (grade 3 portal cholangiopathy). MRC should be performed at the time of diagnosis in chronic PVT & after 9–12 months of acute PVT if anticoagulants does not achieve recanalization to assess the presence of portal cholangiopathy at risk of later complications. if grade 3 portal cholangiopathy has not developed at the 12 month follow- up, no further MRC exam is needed, as no progression is expected to occur.