Original article Selective portal clamping to minimize hepatic ischaemia–reperfusion damage and avoid accelerated outgrowth of experimental colorectal liver metastases J. D. W. van der Bilt, O. Kranenburg, A. Verheem, R. van Hillegersberg and I. H. M. Borel Rinkes Department of Surgery, University Medical Center Utrecht, Utrecht, The Netherlands Correspondence to: Professor I. H. M. Borel Rinkes, Department of Surgery (G04.228), PO Box 85500, 3508 GA Utrecht, The Netherlands (e-mail: i.h.m.borelrinkes@umcutrecht.nl) Background: Temporary vascular clamping during local ablation for colorectal liver metastases increases destruction volumes. However, it also causes ischaemia–reperfusion (IR) injury to the liver parenchyma and accelerates the outgrowth of microscopic tumour deposits. The aim of this study was to investigate the effects of selective portal clamping on hepatocellular damage and tumour growth. Methods: Mice carrying pre-established hepatic colorectal micrometastases underwent either simultaneous clamping of both the portal vein and the hepatic artery or selective clamping of the portal vein to the median and left liver lobes for 45 min. Sham-operated mice served as controls. Hepatic injury and tumour growth were assessed over time. Results: Standard inflow occlusion resulted in a rise in liver enzymes, a local inflammatory response and hepatocellular necrosis. The outgrowth of pre-established micrometastases was accelerated three- to fourfold in clamped compared with non-clamped liver lobes (27·4 versus 7·8 per cent, P < 0·010). Conversely, selective portal clamping induced minimal liver injury, tissue inflammation or hepatocellular necrosis, and completely stopped the accelerated outgrowth of micrometastases. Conclusion: Selective portal clamping does not induce liver tissue damage or accelerate micrometastasis outgrowth and may therefore be the preferable clamping method during local ablative treatment of hepatic metastases. Presented to a meeting of the American Association for Cancer Research, Anaheim, California, USA, April 2005, and in part as a poster to a meeting of the European Hepato-Pancreato-Biliary Association, Heidelberg, Germany, May 2005, and published in abstract form as Eur J Gastroenterol Hepatol 2006; 18: A3 Paper accepted 9 February 2006 Published online 31 May 2006 in Wiley InterScience (www.bjs.co.uk). DOI: 10.1002/bjs.5382 Introduction Colorectal cancer is one of the most prevalent malignan- cies in the western world and is the third leading cause of cancer-related deaths 1 . Mortality is strongly associated with the development of liver metastases, which eventually occurs in 50 – 70 per cent of patients with colorectal cancer. Once liver metastases have developed, the natural course of the disease is associated with poor survival rates 2–4 . Partial liver resection remains the only hope for cure, offering 5-year survival rates of 30–40 per cent; however, only 15–20 per cent of patients are eligible for curative resection 5–8 . For non-resectable liver metastases, local ablative techniques such as radiofrequency ablation and laser-induced thermotherapy may provide local control and increase life expectancy 9–11 . In these patients, the tumour is destroyed by heat from energy-transmitting sources, resulting in coagulative necrosis 12 . Unfortunately, even after an apparently complete destruction, most patients will have tumour recurrence in the liver within 2 years 13,14 . Several mechanisms may underlie tumour recurrence 12–14 . First, new regional intrahepatic recurrences may develop from previously undetected micrometastases, as reported in 60–90 per cent of patients 10,14,15 . Second, local recur- rences in and around the primary lesion occur in 10–68 per cent of cases and are the result of incom- plete heat-destruction of tumour tissue, or from the out- growth of previously undetected microsatellite lesions 16 . Copyright  2006 British Journal of Surgery Society Ltd British Journal of Surgery 2006; 93: 1015–1022 Published by John Wiley & Sons Ltd