|ECR 2019 / C-2984|
|Imaging Findings, Diagnostic and Treatment Options of Post-transplant Non-occlusive Hepatic Artery Hypoperfusion (Splenic Steal) Syndrome|
Liver transplantation (LT) is the preferred curative treatment of irreversible chronic and acute end stage liver disease and selected cases of hepatocellular carcinoma.
Although the improvement of pre-transplant evaluation, patient selection, transplant procedure and technique extend the survival after LT, post-transplantation complications may still cause life threatening graft failure.
Potential complications: malignancy, graft rejection, biliary lesions and the most important: vascular complications
Venous complications are less frequent and less severe then the arterial ones:
- Portal vein thrombosis – incidence 1-2 %
- IVC stenosis/thrombosis - 1%
- Hepatic vein thrombosis - 1,5 %
Arterial complications are the most frequent and severe causes of morbidity and mortality after liver transplant:
- Thrombosis - 1,5-9%
- Stenosis – 5-10%
- Pseudoaneurysm - Rare
- Steal-syndromes – 5 % (probably underrecognized)
• Steal phenomenon is used to defined by the reduction of the arterial inflow in a vascular branch of a common artery, due to the increased flow in another branch of the same trunk.
• In the last two decades, steal syndromes arouse interest as a potential and probably underrecognized vascular complication after liver transplant (LT). It consists of a diminished flow in the hepatic artery (HA) caused by increased flow in other branches of the celiac trunk (most commonly in the splenic artery), leading to biliary duct ischemia and graft hypofunction. Splenic steal is described generally during the first 2 months after LT, with previous cirrhosis, portal hypertension and large splenomegaly. The first few POD (postoperative day) probably play a crucial role in the development of bile duct injury, thus in cases of late onset of symptoms, diagnosis may be questionable
• Gastroduodenal steal is less common and occurs due to a disorder of the splanchnic arterial perfusion with or without superior mesenteric artery (SMA) stenosis
• Recent studies propose that in steal syndromes the decreased HA flow is secondary to a dysregulation of the post-transplant haemodynamic changes: decreased portal resistance hyperperfusion in PV and a consequent HA vasoconstriction and arterial flow reduction
• Both effect may contribute to the insufficient arterial flow, hence non-occlusive hepatic artery hypoperfusion syndrome is a more appropriate denomination.
- Symptomatic steal-syndromes most frequently present with liver enzyme (aspartate aminotransferase and alanine aminotransferase) or total bilirubin level elevation, decreased liver function, persistent ascites and can lead to ischemic graft dysfunction, requiring re-LT.
- In the initial phases may be asymptomatic despite of characteristic radiologic findings. In these cases, treatment to increase hepatic arterial perfusion avoiding potential biliary ischemia is under debate, and further randomized studies are required
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