Hepatic thrombosis

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. 

The most common adverse events reported with sirolimus are leukopenia (20%), thrombocytopenia (13% to 30%), and hyperlipidemia (38% to 57%).11,31 Other adverse effects include delayed wound healing, anemia, diarrhea, arthralgias, rash, and mouth ulcers. Sirolimus has an FDA black-box warning in newly transplanted liver and lung recipients.11 In liver transplant recipients, use of sirolimus immediately after transplant is associated with an increased risk of hepatic artery thrombosis, graft loss, and death. In lung transplant... 

Gallbladder disease, hepatic adenoma, pancreatitis, thrombosis of abdominal artery or vein Endometrial, cervical, or vaginal cancer Deep vein thrombosis... 

Initial dosage in HIT or heparin-induced thrombocytopenia and thrombosis syndrome (HITTS) Before administering argatroban, discontinue heparin therapy and obtain a baseline activated partial thromboplastin time (aPTT). The recommended initial dose of argatroban for adults without hepatic impairment is 2 mcg/kg/min administered as a continuous infusion (see table). 

Increased susceptibility to infection and the possible development of lymphoma may result from immunosuppression. Only physicians experienced in immunosuppressive therapy and management of renal transplant patients should use sirolimus. Manage patients receiving the drug in facilities equipped and staffed with adequate laboratory and supportive medical resources. The physician responsible for maintenance therapy should have complete information needed for the follow-up of the patient. Liver transplantation-excess mortality, graft loss, and hepatic artery thrombosis (HAT) The use of sirolimus in combination with tacrolimus was associated with excess mortality and graft loss in a study in de novo liver transplant recipients. Many of these patients had evidence of infection at or near the time of death. 

Hepatic artery thrombosis In de novo liver transplant recipients, the use of sirolimus in combination with cyclosporine or tacrolimus was associated with an increase in P.1153... 

Drug abusers have never bothered about hepatitis, overdoses, choking to death on their own vomit, thrombosis, gangrene or heroin cut with strychnine—so why should they worry about AIDS The fact that more and more drug abusers are being identified as HIV-positive is unlikely to influence them. 

It also appears that the incidence of hepatic adenomas is increased in women taking oral contraceptives. Ischemic bowel disease secondary to thrombosis of the celiac and superior and inferior mesenteric arteries and veins has also been reported in women using these drugs. 

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. 

It was noted that she had gram-negative rods on her blood smear her blood culture grew penicillin-sensitive Streptococcus pneumoniae, in 6 hours. At autopsy, she was noted to have Streptococcus pneumoniae endocarditis of the right ventricle, focal ischemia of the left ventricle, bilateral pleural effusions, hepatic congestion with thrombosis, renal congestion, bilateral adrenal hemorrhage, and necrosis. Death was due to septic shock from Streptococcus pneumoniae. 

Young (<50 years) and no other cause found past history or family history of venous thrombosis, especially if unusual site (cerebral, mesenteric, hepatic veins) recurrent miscarriage thrombocytopenia cardiac valve vegetations livedo reticularis raised ESR malaise positive syphilis serology... 

Thrombophilia personal or family history of thrombosis (usually venous, particularly in unusual sites such as hepatic vein) at unusually young age... 

Outside the liver the common hepatic duct is joined by the cystic duct of the gallbladder and becomes the common bile duct (CBD). The extrahepatic and intrahepatic ducts are supplied with blood by a fine network of tiny arterial branches that originate from the hepatic and gastroduodenal arteries. As it has no other blood supply, the biliary tree is particularly susceptible to ischaemic injury, such as hepatic artery thrombosis or injury to the biliary plexus during laparoscopic surgery. This can result in extrahepatic and complex hilar and perihilar ischaemic strictures of the biliary tree. 

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