الفهرس 
AnatomyOnly 14 pages are availabe for public view
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Abstract
Liver resection is in many cases the only option for longterm survival for patients with primary or secondary liver malignancies. One of the major reasons for unresectability of the liver is that the remnant liver volume is insufficient to support postoperative liver function. Liver insufficiency after hepatectomy is one of the most serious complications in patients undergoing major hepatic resection for hepatobiliary diseases. It has been shown that liver failure is directly related to the functional volume of the liver remnant. Transcatheter portal vein embolization is performed widely for inducing atrophy of the lobe to be resected and compensatory hypertrophy of the contralateral lobe. This procedure is considered to reduce the risks of patients who are potential candidates for major hepatic resection. For unresectable HCC, preoperative intervention with transcatheter arterial chemoembolization (TACE), portal vein embolization (PVE), or percutaneous RFA could control tumor progression and invasion, downstage tumor status, increase remnant liver volume, and decrease tumor recurrence rate, thus making hepatectomy possible.
Portal vein embolization is an increasingly common and useful procedure that helps to increase the future liver remnant volume and thereby improve the chances of surgical resection in patients with liver malignancies, who might otherwise not be considered for surgery. This procedure is based on the concept that the liver has the unique ability to regenerate after injury. PVE has a high technical and clinicalrate. The complication rate is low, but local tumor progression after PVE is an imminent cause of unresectablilty.
PVE functions not only to increase the volume and function of the FLR but also to dissociate the impact of portal flow diversion from the impact of surgical stress to the small liver remnant. PVE minimizes the sudden elevation in portal pressure at resection that can result in hepatocellular damage in the residual liver.This change in portal pressure, in combination with surgical manipulation, may result in hepatic congestion and post-resection dysfunction.
Both normal and diseased livers can grow in response to PVE, and the degree of hypertrophy appears to be an important predictor of outcome after hepatectomy performed after PVE. Cirrhotic livers regenerate at a slower rate and to a lesser extent than normal livers; other clinical factors, including diabetes and steatohepatitis, also negatively affect the rate and possibly degree of liver hypertrophy.
In patients with normal liver, the plateau in regeneration occurs 3-4 weeks after PVE, thus measurement of post-PVE volume before 3 weeks may underestimate the actual regeneration capacity. In patients with cirrhosis and possibly in patients with diabetes, post-PVE volume may need to be assessed even later (e.g., 6 to 8 weeks after PVE) to provide a more accurate estimate of the true growth capacity.
Anatomic variations of the portal vein (PV) are relatively common. PV variations play a critical role in evaluations before surgical interventions, transplantation, and interventional procedures of the liver. Lack of knowledge of these variations might prove to be dangerous during these procedures, whereas awareness of them might help in reducing complications.