Selective hepatic vascular exclusion versus Pringle manoeuvre in liver resection for tumours encroaching on major hepatic veins.
Summary of "Selective hepatic vascular exclusion versus Pringle manoeuvre in liver resection for tumours encroaching on major hepatic veins."
Control of bleeding is crucial during liver resection, and several techniques have been developed to achieve this. This study compared the safety and efficacy of selective hepatic vascular exclusion (SHVE) and Pringle manoeuvre in partial hepatectomy for liver tumours compressing or involving major hepatic veins.
All patients undergoing liver resection between January 2003 and December 2010 for liver tumours compressing or involving one or more major hepatic veins were identified retrospectively from a prospective institutional database. Either SHVE or Pringle manoeuvre was used to minimize blood loss during hepatectomy. Data on demographics and the intraoperative and postoperative course were analysed.
From the database of 3900 patients, 1420 were identified who underwent liver resection for tumours encroaching on major hepatic veins using either SHVE (550) or the Pringle manoeuvre (870). Intraoperative blood loss (mean(s.d.) 480(210) versus 830(340) ml; P = 0·007) and transfusion requirements (mean(s.d.) 1·3(0·6) versus 2·9(1·4) units; P = 0·008) were significantly less in the SHVE group. In the Pringle group, hepatic vein injury resulted in major intraoperative bleeding of over 1000 ml in 65 patients (7·5 per cent) and air embolism in 14 (1·6 per cent), and three patients (0·3 per cent) died during surgery, whereas there was no major bleeding, air embolism or intraoperative death in the SHVE group. Postoperative liver failure, multiple organ failure and in-hospital death were significantly more common in the Pringle group (P = 0·019, P = 0·032 and P = 0·004 respectively).
SHVE was more efficacious than the Pringle manoeuvre in minimizing intraoperative bleeding and air embolism during partial hepatectomy for tumours encroaching on major hepatic veins, and decreased the postoperative liver failure rate. Copyright © 2012 British Journal of Surgery Society Ltd. Published by John Wiley & Sons, Ltd.
Third Department of Hepatic Surgery, Eastern Hepatobiliary Surgery Hospital, Second Military Medical University, Shanghai, China.
This article was published in the following journal.
Name: The British journal of surgery
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Medical and Biotech [MESH] Definitions
A form of rapid-onset LIVER FAILURE, also known as fulminant hepatic failure, caused by severe liver injury or massive loss of HEPATOCYTES. It is characterized by sudden development of liver dysfunction and JAUNDICE. Acute liver failure may progress to exhibit cerebral dysfunction even HEPATIC COMA depending on the etiology that includes hepatic ISCHEMIA, drug toxicity, malignant infiltration, and viral hepatitis such as post-transfusion HEPATITIS B and HEPATITIS C.
Conditions in which the LIVER functions fall below the normal ranges. Severe hepatic insufficiency may cause LIVER FAILURE or DEATH. Treatment may include LIVER TRANSPLANTATION.
Liver disease in which the normal microcirculation, the gross vascular anatomy, and the hepatic architecture have been variably destroyed and altered with fibrous septa surrounding regenerated or regenerating parenchymal nodules.
Passages within the liver for the conveyance of bile. Includes right and left hepatic ducts even though these may join outside the liver to form the common hepatic duct.
A group of metabolic diseases due to deficiency of one of a number of LIVER enzymes in the biosynthetic pathway of HEME. They are characterized by the accumulation and increased excretion of PORPHYRINS or its precursors. Clinical features include neurological symptoms (PORPHYRIA, ACUTE INTERMITTENT), cutaneous lesions due to photosensitivity (PORPHYRIA CUTANEA TARDA), or both (HEREDITARY COPROPORPHYRIA). Hepatic porphyrias can be hereditary or acquired as a result of toxicity to the hepatic tissues.