DR Mohammed Hussien, MD Lecturer of Hepatology and Gastroentrology at kafrelsheikh Unversity

1. DR/ MOHAMMED
HUSSIEN
LECTURER OF GASTROENTEROLOGY
& HEPATOLOGY
KAFRELSHEIK UNIVERSITY
MEMBERSHIP AT WORD ENDOSCOPY
ORGANIZATION (WEO)
MEMBERSHIP AT AMERICAN COLLAGE OF
GASTROENTEROLOGY (ACG)
MEMBERSHIP AT EGYPTIAN ASSOCIATION FOR
RESEARCH AND TRAINING IN
HEPATOGASTROENTROLOGY
MEMBERSHIP AT EGY-EUS ESIM

2. HOW TO APPROACH
BY
DR MOHAMMED HUSSIEN, MD

9. DIARRHEA

13. CongenitalPV. diseasesHepatic arterySinusoidal dis.HV. diseases.
Congenital
arteriovenous
malformations
(AVM)
Thrombosis of
the portal
venous axis
Hepatic artery
occlusion
Sinusoidal
obstruction
syndrome (SOS)
Budd-Chiari
Syndrome
Congenital
arterioportal
malformations
(APM)
Aneurysms of
the PV
Hepatic artery
aneurysms
Peliosis hepatisEndophlebitis
obliterans
hepatica
Congenital
portosystemic
shunts (PSS)
A-V fistulae in
the PV system
Hepatic
arterioportal
fistulae
Sinusoidal
dilatation
Liver
involvement by
HHT
HA lesions
following
orthotopic LT
Sinusoidal
fibrosis
Congenital
stenosis of the
portal vein
Sinusoidal
Infiltration

14. PVT
Two different entities, which
represent successive stages of the same disease and
share similar causes,
 but differ as to their management.
Acute PVT & Chronic PVT

15. PVTIN SPECIAL CLINICAL SITUATIONS
o In children,
o In cirrhosis,
o In liver transplant recipients
Their features and management
differ
from those in other groups.

16. PVT CAUSES
(RISK FACTORS)
oLocal (30%)
oGeneral (70%)
oCombination

17. LOCAL PVT RISK FACTORS.
Major causes:
o Malignant tumors within the portal venous territory (in the absence
of portal venous invasion or constriction), and
o Cirrhosis.
o In the rest of the patients, the most common local factor for PVT is
inflammatory foci in the abdomen.

18. LOCAL PVT RISK FACTORS.

19. LOCAL PVT RISK FACTORS.

20. GENERAL PVT RISK FACTORS.

21. FACTS TO REMEMBER
oA local factor for PVT is more frequently
recognized at the acute stage of PVT.
oIdentification of a local risk factor does not
exclude the possibility that a general risk
factor is present

22. ACUTE PVT:
CLINICAL AND LABORATORY FEATURES.
Occlusion can be complete or partial, Usually presents with
abdominal or lumbar pain of sudden Onset.
Rapid and complete obstruction of the PV or MVs, induces
intestinal congestion, manifested by severe continuous
colicky abdominal pain and occasionally non-bloody diarrhea.
When extensive thrombosis involves distal mesenteric veins,
intestinal ischemia & infarction occurs.

23. Liver function is preserved in patients with acute PVT.
Provided there is no extension of the thrombus to
mesenteric venous arches, all manifestations of acute PVT
are completely reversible, either by
recanalizationor cavernoma..

24. IMAGING FEATURES AND DIAGNOSIS
Sonography can show hyperechoic material in the vessel
lumen
Doppler imaging shows the absence of flow in part or all of
the lumen.
CT scan without contrast can show hyperattenuating material
in the PV. After injection of contrast agent, lack of luminal
enhancement, increased hepatic enhancement in the arterial
phase, and decreased hepatic enhancement in the portal
phase are shown.

26. For the assessment of thrombus extension within the portal
venous system, CT or MR angiography are more sensitive
techniques than Doppler sonography, because the mesenteric
veins are more difficult to visualize with ultrasound.

29. PVT CLASSIFICATIONS

30. TREATMENT OF ACUTE PVT
 Anticoagulation therapy for at least 3 months to all patients.
 Start with LMW heparin in order to achieve rapid
anticoagulation. Shift to oral anticoagulation as soon as the
patient’s condition has stabilized,
 Consider permanent anticoagulation in,
Non correctable prothrombotic disorder
or
SMV currently or previously involved

31. The reported experience with other treatment
modalities (surgical thrombectomy, systemic or in situ
thrombolysis, or [TIPS]) in the treatment of acute PVT
is extremely limited.
In intestinal infarction, emergency laparotomy
for (resection).
+
Surgical thrombectomy can be performed at
the same time.

32. CHRONIC PVT
(PORTAL CAVERNOMA)Definitions.
The obstructed portal vein is replaced by a network of
hepatopetal collateral veins connecting the patent portion of
the vein upstream from the thrombus to the patent portion
downstream.
Complete occlusion of the portal vein trunk, or of its two main
branches is virtually always associated with portal
hypertension and the development of portosystemic
collaterals.

33. CLINICAL AND LABORATORY MANIFESTATIONS IN
CHRONIC PVT
o Hypersplenism
o Portal hypertension.
o Ascites and encephalopathy are uncommon.
o Liver tests are typically normal
o Portal cholangiopathy .. rarely.

34. IMAGING FEATURES AND DIAGNOSIS
Absence of a visible normal portal vein
and
its replacement with serpiginous veins.
+
Hepatic arteries are usually enlarged.

35. TREATMENT OF CHRONIC PVT
• Prevention and Treatment of Gastrointestinal Bleeding.
(medical, endoscopic and surgical “limited data”)
• Prevention of Recurrent Thrombosis : An expert panel
recommended that anticoagulation therapy be considered
only in patients with a documented permanent
prothrombotic condition.
 Treatment of Portal Cholangiopathy. insertion of a biliary
endoprosthesis after endoscopic extraction of secondary
stones

36. PVT IN PATIENTS WITH CIRRHOSIS
PVT is most common in patients with pre-existing cirrhosis.
The prevalence of PVT increases with the severity of the
cirrhosis, being less than 1% in patients with compensated
cirrhosis but 8%-25% in candidates for liver transplantation.

37. WHY PVT IN LC !?
A. In patients with cirrhosis, portal venous obstruction is
commonly related to invasion by HCC.
Neoplastic obstruction should be considered, when:
serum alpha fetoprotein levels are increased,
when the portal vein is larger than 23 mm in diameter,
when endoluminal material enhances during the arterial
phase of contrast injection,
or when an arterial-like pulsatile flow is seen on Doppler
ultrasound

38. B. Otherwise, even in compensated cirrhosis, an underlying
prothrombotic condition is difficult to detect because of a
nonspecific decrease in the plasma levels of coagulation
inhibitors.
In cirrhotic patients with PVT, compared with those without
PVT, however, molecular testing shows an increased
prevalence of the factor V Leiden, and prothrombin gene
mutations, the latter being particularly common.

39. PELIOSIS HEPATIS
Peliosis hepatis is characterized by the presence of multiple
blood-filled cavities distributed randomly throughout
the liver. The cavities range in size from a few millimeters to
3 cm across and usually are seen in association with dilated
hepatic sinusoids.
In the parenchymal type, blood-filled cavities are lined
by hepatocytes, and hemorrhagic parenchymal necrosis and
congestion usually are present. In the phlebectatic type,
the cavities are lined by endothelial cells associated with
aneurysmal dilatation of the central vein.

40. HISTOPATHOLOGIC FEATURES OF PELIOSIS HEPATIS. NOTE THE PRESENCE OF THREE BLOOD-FILLED CYSTS WITHOUT LINING
CELLS AND AN ADJACENT PORTAL TRACT. SINUSOIDAL DILATATION IS ALSO PRESENT. (COURTESY OF EDWARD LEE, MD,
WASHINGTON, DC.). SLIESINGER 2007.

41. ASSOCIATIONS
• association with renal transplantation and the acquired
immunodeficiency syndrome (AIDS) have increased clinical
awareness of this syndrome.
• anabolic steroids, oral contraceptives, tamoxifen, danazol,
vitamin A, glucocorticoids, 6-thioguanine, and azathioprine and
exposure to urethane, vinyl chloride, and thorium dioxide.
• Bacillary peliosis is caused by the bacterium responsible for
cat-scratch disease, in the genus Bartonella.
• The pathogenesis of peliosis hepatis is unknown