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Electrolytic ablation is as effective as radiofrequency ablation in the treatment of artificial liver metastases in a pig model
Author(s) -
Hinz Sebastian,
Egberts JanHendrik,
Pauser Ursula,
Schafmayer Clemens,
Fändrich Fred,
Tepel Jürgen
Publication year - 2008
Publication title -
journal of surgical oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.201
H-Index - 111
eISSN - 1096-9098
pISSN - 0022-4790
DOI - 10.1002/jso.21088
Subject(s) - medicine , radiofrequency ablation , ablation , necrosis , lesion , radiology , surgery , pathology
Background The best treatment option for liver metastases is complete surgical resection. Unfortunately, at the time of diagnosis, not all patients are candidates for complete resection. Electrolytic therapy (ECT) is a novel non‐thermal method of tissue destruction. We evaluated its safety and effectiveness in comparison with radiofrequency ablation (RFA). Methods Tumor mimics were created by injecting a gel into the pig liver. The volume of the lesions was measured by ultrasound before treatment. The tumor mimics were treated with either RFA or electrolytic ablation. 48 h after treatment the liver was fixed in formalin and subjected to histological examination. Results Histological investigation confirmed that all lesions were completely surrounded by necrosis after treatment with either ECT or RFA. Two different types of necrosis were identified. After RFA the cell membranes disappeared but the nuclei were still intact, whereas after ECT these structures were completely disrupted. After ECT the necrosis was often surrounded by infiltrating lymphocytes. This inflammatory reaction was not apparent after RFA. Conclusion ECT produced predictable and reproducible necrosis in pig livers and was as effective as RFA at destroying a defined target lesion. A local inflammatory reaction after ECT may favour the development of a systemic immune response. Our results indicate that ECT is an alternative treatment option for irresectable liver metastases. J. Surg. Oncol. 2008;98:135–138. © 2008 Wiley‐Liss, Inc.