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THE LIVER IN HEART FAILURE
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Shock liver, or ischemic hepatopathy, results from an acute fall in cardiac output due, for example, to acute myocardial infarction or arrhythmia, usually in a patient with passive congestion of the liver Clinical hypotension may be absent (or unwitnessed) In some cases, the precipitating event is arterial hypoxemia due to respiratory failure, septic shock, severe anemia, heat stroke, carbon monoxide poisoning, cocaine use, or bacterial endocarditis The hallmark is a rapid and striking elevation of serum aminotransferase levels (often > 5000 units/L); an early rapid rise in the serum lactate dehydrogenase level is also typical, but elevations of serum alkaline phosphatase and bilirubin are usually mild The prothrombin time may be prolonged, and encephalopathy or hepatopulmonary syndrome may develop The mortality rate due to the underlying disease is high, but in patients who recover, the aminotransferase levels return to normal quickly, usually within 1 week in contrast to viral hepatitis In patients with passive congestion of the liver due to right-sided heart failure, the serum bilirubin level may be elevated, occasionally as high as 40 mg/dL, due in part to hypoxia of perivenular hepatocytes Serum alkaline phosphatase levels are normal or slightly elevated Hepatojugular reflux is present, and with tricuspid regurgitation the liver may be pulsatile Ascites may be out of proportion to peripheral edema, with a high serum ascites-albumin gradient (> 11) and a protein content of more than 25 g/dL In severe cases, signs of encephalopathy may develop
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Ebert EC Hypoxic liver injury Mayo Clin Proc 2006 Sep;81(9): 1232 6 [PMID: 16970220]
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(portal vein thrombosis often with cavernous transformation), splenic vein obstruction (presenting as gastric varices without esophageal varices), schistosomiasis, noncirrhotic portal fibrosis, nodular regenerative hyperplasia, or arterial-portal vein fistula Acute portal vein thrombosis usually causes abdominal pain Aside from splenomegaly, the physical findings are not remarkable, although hepatic decompensation can follow severe gastrointestinal bleeding or a concurrent hepatic disorder, and intestinal infarction may occur when portal vein thrombosis is associated with mesenteric venous thrombosis Minimal hepatic encephalopathy is reported to be common in patients with noncirrhotic portal vein thrombosis Endoscopy shows esophageal or gastric varices The liver tests are usually normal, but there may be findings of hypersplenism Color Doppler ultrasound and contrast-enhanced CT are usually the initial diagnostic tests for portal vein thrombosis Magnetic resonance angiography (MRA) of the portal system is generally confirmatory Endoscopic ultrasound may be helpful in some cases In patients with jaundice, magnetic resonance cholangiography may demonstrate compression of the bile duct by a large portal cavernoma Needle biopsy of the liver may be indicated to diagnose schistosomiasis and noncirrhotic intrahepatic portal sclerosis and may demonstrate sinusoidal dilatation An underlying hypercoagulable state is found in many patients with portal vein thrombosis; this includes myeloproliferative disorders (often associated with a specific mutation [V617F] in the gene coding for JAK2 tyrosine kinase), mutation G20210A of prothrombin, factor V Leiden mutation, protein C and S deficiency, antiphospholipid syndrome, mutation TT677 of methylenetetrahydrofolate reductase, elevated factor VIII levels, and hyperhomocysteinemia It is possible, however, that deficiency of protein C and S as well as of antithrombin is a secondary phenomenon due to portosystemic shunting and reduced hepatic blood flow Portal vein thrombosis may occur in up to 15% of patients with cirrhosis and may be associated with hepatocellular carcinoma Splenic vein thrombosis may complicate pancreatitis or pancreatic cancer Pylephlebitis (septic thrombophlebitis of the portal vein) may complicate intra-abdominal inflammatory disorders such as appendicitis or diverticulitis, particularly when anaerobic organisms are involved If splenic vein thrombosis is the cause of variceal bleeding, splenectomy is curative For other causes, band ligation or sclerotherapy followed by -blockers to reduce portal pressure is initiated for variceal bleeding, and portosystemic shunting (including TIPS) is reserved for failures of endoscopic therapy; rarely progressive liver dysfunction requires liver transplantation Anticoagulation or thrombolytic therapy may be indicated for isolated acute portal vein thrombosis if a hypercoagulable disorder is identified
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Primignani M et al Role of the JAK2 mutation in the diagnosis of chronic myeloproliferative disorders in splanchnic vein thrombosis Hepatology 2006 Dec;44(6):1528 34 [PMID: 17133457] Sarin SK et al Noncirrhotic portal hypertension Clin Liver Dis 2006 Aug;10(3):627 51 [PMID: 17162232]
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