GIT Kurdistan Board GEH Journal club Lower PVT 2014.

1. NATURE REVIEW GEH; MAY 2014
PVT: IMAGING IN CLINICAL
DECISION-MAKING
KURDISTAN BOARD GEH JOURNAL CLUB

2. 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.

3. PVT: ABSTRACT
Non-malignant causes:
Liver cirrhosis
 Abdominal septic foci
 Acute pancreatitis
Prothrombotic disorders (congenital or acquired).

4. PVT: ABSTRACT
Malignant causes:
HCC
 Other solid tumours.
 Haematological malignancies.

5. 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’.

6. 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.

7. 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.

8. 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.

9. 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.

10. 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.

11. 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.

12. 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.

13. 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.

14. 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.

15. 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.

16. 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.

17. 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.

18. 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.

19. 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.

20. 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.