Imaging Pearls ❯ Liver ❯ Liver Infarction
-- OR -- |
|
- "Hepatic infarction is defined as areas of coagulation necrosis from hepatocyte cell death caused by local ischemia, which in turn results from the obstruction of circulation to the affected area, most commonly by a thrombus or embolus. Hepatic infarction is uncommon because of the dual blood supply from the hepatic artery and portal vein, as well as extensive collateral vessels. In most cases, hepatic infarction results from either insult to the hepatic artery or portal vein thrombosis superimposed on hepatic arterial occlusion."
CT of Nonneoplastic Hepatic Vascular and Perfusion Disorders
Maha Torabi et al.
RadioGraphics 2008; 28:1967–1982 - "Hepatic infarction may be iatrogenic (occurring after hepatobiliary surgery, intrahepatic chemoembolization, or a transjugular intrahepatic portosystemic shunt procedure) or posttraumatic (occurring after hepatic artery or portal vein laceration)."
CT of Nonneoplastic Hepatic Vascular and Perfusion Disorders
Maha Torabi et al.
RadioGraphics 2008; 28:1967–1982 - "It may occur as a complication of hepatic artery stenosis or thrombosis after liver transplantation, or it may be secondary to hypercoagulability (in sickle cell disease or antiphospholipid antibody syndrome), vasculitis (in polyarteritis nodosa or systemic lupus erythematosus), or infection (in sepsis and shock or rare "emphysematous hepatitis")."
CT of Nonneoplastic Hepatic Vascular and Perfusion Disorders
Maha Torabi et al.
RadioGraphics 2008; 28:1967–1982 - "Hepatic infarction is uncommon, occurring at any age, without sex predilection. Hepatic artery thrombosis leading to infarction most often occurs after hepatic transplantation and has been reported in 3% of adult transplant recipients and 12% of pediatric transplant recipients."
CT of Nonneoplastic Hepatic Vascular and Perfusion Disorders
Maha Torabi et al.
RadioGraphics 2008; 28:1967–1982 - "Gas formation has been described in sterile infarcts as well as infected ones. Sterile gas is related to the release of intracellular gas from necrotic tissue, an origin similar to that of gas bubbles in hepatic tumors after embolization therapy or radiofrequency ablation."
CT of Nonneoplastic Hepatic Vascular and Perfusion Disorders
Maha Torabi et al.
RadioGraphics 2008; 28:1967–1982 - "Infarction is a serious complication of liver transplantation that results in significant morbidity and mortality and often requires repeat transplantation. Preservation of portal tracts is a feature worthy of emphasis because it helps differentiate infarction from other causes of hypoattenuating foci in transplanted livers (eg, abscess, biloma, and postbiopsy hematoma)."
CT of Nonneoplastic Hepatic Vascular and Perfusion Disorders
Maha Torabi et al.
RadioGraphics 2008; 28:1967–1982 - "Focal steatosis may mimic hepatic infarction; however, steatosis tends to occur in characteristic locations, and the enhancement of vessels in focal regions of steatosis is preserved, with enhancement approaching that of normal liver parenchyma. Hepatic abscess, which also is included in the differential diagnosis, often has a cluster-of-grapes appearance with rimlike peripheral enhancement and a nonenhancing central pyogenic component."
CT of Nonneoplastic Hepatic Vascular and Perfusion Disorders
Maha Torabi et al.
RadioGraphics 2008; 28:1967–1982
- “Hepatic infarction is defined as areas of coagulation necrosis from hepatocyte cell death caused by local ischemia, which in turn results from the obstruction of circulation to the affected area, most commonly by a thrombus or embolus. Hepatic infarction is uncommon because of the dual blood supply from the hepatic artery and portal vein, as well as extensive collateral vessels. In most cases, hepatic infarction results from either insult to the hepatic artery or portal vein thrombosis superimposed on hepatic arterial occlusion.”
CT of Nonneoplastic Hepatic Vascular and Perfusion Disorders Torabi et al. RadioGraphics Vol. 28, No. 7: 1967-1982 - “Hepatic infarction may be iatrogenic (occurring after hepatobiliary surgery, intrahepatic chemoembolization, or a transjugular intrahepatic portosystemic shunt procedure) or posttraumatic (occurring after hepatic artery or portal vein laceration). It may occur as a complication of hepatic artery stenosis or thrombosis after liver transplantation, or it may be secondary to hypercoagulability (in sickle cell disease or antiphospholipid antibody syndrome), vasculitis (in polyarteritis nodosa or systemic lupus erythematosus), or infection (in sepsis and shock or rare “emphysematous hepatitis”).”
CT of Nonneoplastic Hepatic Vascular and Perfusion Disorders Torabi et al. RadioGraphics Vol. 28, No. 7: 1967-1982 - “Infarction is a serious complication of liver transplantation that results in significant morbidity and mortality and often requires repeat transplantation. Preservation of portal tracts is a feature worthy of emphasis because it helps differentiate infarction from other causes of hypoattenuating foci in transplanted livers (eg, abscess, biloma, and postbiopsy hematoma). Focal steatosis may mimic hepatic infarction; however, steatosis tends to occur in characteristic locations, and the enhancement of vessels in focal regions of steatosis is preserved, with enhancement approaching that of normal liver parenchyma. Hepatic abscess, which also is included in the differential diagnosis, often has a cluster-of-grapes appearance with rimlike peripheral enhancement and a nonenhancing central pyogenic component.”
CT of Nonneoplastic Hepatic Vascular and Perfusion Disorders Torabi et al. RadioGraphics Vol. 28, No. 7: 1967-1982