Portal thrombosis

Duodenal varices are rare. Consequently, their frequency is poorly documented. They are present predominantly in patients with prehepatic portal hypertension. Possible therapy options include banding and medication (terli-pressin, octreotide, later on P-blockers, etc.) or placement of a TIPS (provided there is no portal thrombosis). (63, 117)... 

Widman, A., Souza-de-Oliveira, I.R., Speranzini, M.B., Cerri, G.G., Saad, W.A., Gama-Rodrigues, X Portal thrombosis late postoperative prevalence in Mansoni s schistosomiasis. Hepato-Gastroenterol. 2003 50 1463-1466... 

Malkowski, R, Rawlak, J., Michalowicz, B., Szczerban, J., Wroblewski, T., Leowska, E., Krawczyk, M. Thrombolytic treatment of portal thrombosis. Hepato-Gastroenterol. 2003 50 2098 - 2100... 

Injection of ethanol into the liver to treat hepatocellular carcinoma commonly causes severe pain, fever, and hepatic dysfunction there can also be pleural effusion, pneumothorax, ascites, vasovagal reaction, transient hypotension, myoglobinuria, and portal thrombosis. Fatal massive hepatic necrosis distant from the injection site has also been attributed to this treatment (SEDA-18, 377). 

Performance of an acquisition during the portal phase of enhancement of a CT enables evaluation of portal and variceal anatomy and of portosystemic shunts without the need for an additional injection of contrast material. Three-dimensional reconstruction of portal-phase CT angiograms enhances the perception of the courses and anatomic relationships of varices and shunts, and the presence and extension of portal thrombosis (Henseler et al. 2001). SSD can be very useful for displaying variceal anatomy during the portal phase. Also, 3D-MR angiography can detect the presence and the extension of collateral vessel pathways. Patients with portal hypertension benefit from the use of MR angiog-... 

Fig.7.8a,b. Pyogenic abscess, a Pyogenic abscess in a 35-year old man status post laparoscopic right hepatectomy due to an hydatid cyst. Portal venous-phase contrast-enhanced CT scan shows a thick-walled cystic lesion with homogeneous low attenuation. b Pyogenic abscess with presence of gas within the lesion in a 52-year-old man with fever, head of pancreas neoplasia (not resectable due to superior mesenteric vein infiltration) and recent portal thrombosis. An axial portal phase CT scan shows an hypoattenuating lesion with non-homogeneous content and gas inside... 

Aspirin has been remarkably successful in the treatment of the pain and swelling of inflammatory disease and in fact, an estimated 45,000 tons of aspirin are still consumed each year. This success resulted in the syntheses of many other aspirin-like drugs , now referred to as NSAIDs. Aspirin, however, continues to have a unique use in the prevention of thrombosis. Since it produces irreversible inhibition of COX-1 by acetylation of serine at position 530 in the active site, a daily low dose of aspirin will cause a cumulative inhibition of COX-1 in platelets, in the portal circulation. A gradual inhibition of platelet aggregation occurs, reducing the possibility of occlusion of coronary or cerebral vessels by platelet thrombi. However, there are no systemic... 

Portal hypertension is a consequence of increased resistance to blood flow through the portal vein. Increased resistance is usually due to restructuring of intrahepatic tissue (sinusoidal damage) but may also be caused by presinusoidal damage such as portal vein occlusion from trauma, malignancy, or thrombosis. A third (and the least common) mechanism is outflow obstruction of the hepatic vein. This latter damage is posthepatic, and normal liver structure is maintained. This chapter will focus on portal hypertension caused by intrahepatic damage from cirrhosis. 

Twenty-five percent ofthrombophilic patients develop thrombosis at unusual sites resulting in cerebral venous thrombosis, mesenteric vein thrombosis, hepatic venous thrombosis, retinal vein thrombosis, purpura fulminans, splenic vein thrombosis, portal vein thrombosis, renal vein thrombosis, or axillary vein thrombosis. The thrombotic disorders may involve inflammatory factors that contribute to the vascular deficit. In addition, embolic events also play a role in the development of these thrombotic complications. 

Hepatic venous thrombosis, also known as Budd-Chiari syndrome, is caused by hypercoagulable disorders precipitated by pregnancy, infection, and birth control medication. An acute painful abdomen, sudden enlargement of the liver, and the presence of ascites make up a triad of clinical symptoms that are important in the diagnosis of this syndrome. Myeloproliferative disorders such as polycythemia vera and paroxysmal nocturnal dyspnea were previously thought to be responsible. Factor V Leiden and prothrombin 20210 mutations are also known to be responsible, Other intraabdominal thromboses include portal vein thrombosis, mesenteric vein thrombosis and renal vein thrombosis. 

Amitrano L, Brancacio V Guardascione MA, et al. Inherited coagulation disorder in cirrhotic patients with portal vein thrombosis. Hepatology 2000 3 I (2) 345-348. 

A review of 253 cases of Budd-Chiari syndrome found COC use to be the presumed cause in 9% of patients [29]. There appears to be a correlation between the development of BCS and the oestrogenic component of COCs [12]. Obstruction of the hepatic and portal veins has been documented and has been attributed to the thrombotic effects of the COCs however, the affected women may have had an underlying coagulation defect [16]. Budd-Chiari patients should be advised not to use COCs, as such patients have a demonstrated haematological tendency to form thrombi, and oestrogen-containing contraceptives may increase the risk of recurrent thrombosis [2]. 

Collateral hepatic circulation (cirrhosis, portal vein thrombosis, occlusion of hepatic vein, etc)... 

Portal vein thrombosis (see chapter 39.3.3) with gradual or incomplete obstruction merely produces anastomoses and develops asymptomatically. After complete obstruction, ultrasonography will showparaportal, angiomatous anastomoses, predominantly in the porta hepatis (= cavernous transformation). (95) Splenomegaly is evidenced with a normal-sized liver. The portal vein is not detectable. Colour Doppler sonography has become of paramount importance in portal vein system diagnostics. 

Fig. 8.10 DifTuse metastazation in pancreatic carcinoma ( ) numerous focus-Uke signs of aerobilia (f) thrombosis of the left portal vein (A)...

Percutaneous transhepatic hepatophlebography involves a typical puncture of the liver with a needle from the right midaxillary line to enter a hepatic vein. Pressure measurement and CM injection ensure that the position of the needle or the catheter is correct. Thrombosis of the portal vein is an absolute contraindication, which is why indirect splenoportography must be carried out prior to percutaneous hepatophlebography. Serious complications occur in 1.5-4.0% of cases. 

Tc-DTPA Arterial perfusion accounts for 20%-40% of the circulation in portal hypertension, cirrhosis causes arterial perfusion to increase to over 60%. In portal vein thrombosis, only an arterial curve is visible. Liver metastasis usually displays relatively high arterial perfusion. In (rare) occlusions of the hepatic artery, only a portal venous curve is visible. When a bolus injection of 400 MBq "Tc-diethylenetriamine pentaacetic acid (DTPA) is applied, scintigraphy is able to reveal a bi-phasic time-activity curve. The initial increase of activity is produced by the arterial influence and the second peak by the portal venous inflow. Both curves can be evaluated quantitatively. (36) Perfusion scintigraphy may be useful in the case of liver trauma, TIPS, hyper-vascularized hepatic tumours and partial liver resection as well as after liver transplantation. 

Liver cirrhosis (37), liver tumours, liver echinococcosis, portal vein thrombosis, thrombosis of the splenic vein, right heart failure, Budd-Chiari syndrome, peliosis hepatis (39), etc. 

Compression or thrombosis of the splenic vein = segmental portal hypertension... 

Thrombosis of small portal veins due to bacterial cholangitis with pericholangitis or to malignant and subsequently thrombotic processes can cause an increase in presinusoidal resistance. 

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