Influence of perioperative anaesthetic and analgesic interventions on oncological outcomes: a narrative review

Abstract

Surgery is an important treatment modality for the majority of solid organ cancers. Unfortunately, cancer recurrence following surgery of curative intent is common, and typically results in refractory disease and patient death. Surgery and other perioperative interventions induce a biological state conducive to the survival and growth of residual cancer cells released from the primary tumour intraoperatively, which may influence the risk of a subsequent metastatic disease. Evidence is accumulating that anaesthetic and analgesic interventions could affect many of these pathophysiological processes, influencing risk of cancer recurrence in either a beneficial or detrimental way. Much of this evidence is from experimental in vitro and in vivo models, with clinical evidence largely limited to retrospective observational studies or post hoc analysis of RCTs originally designed to evaluate non-cancer outcomes. This narrative review summarises the current state of evidence regarding the potential effect of perioperative anaesthetic and analgesic interventions on cancer biology and clinical outcomes. Proving a causal link will require data from prospective RCTs with oncological outcomes as primary endpoints, a number of which will report in the coming years. Until then, there is insufficient evidence to recommend any particular anaesthetic or analgesic technique for patients undergoing tumour resection surgery on the basis that it might alter the risk of recurrence or metastasis.

Keywords: anaesthesia, general; anaesthesia, inhalational; anaesthesia, intravenous; analgesia; cancer, recurrence; inflammation; opioid; stress response; surgery.

Fig. 1

Schematic representation of the pathophysiological mechanisms induced by surgery that promote survival and growth of metastatic deposits formed by circulating tumour cells (CTCs) released intraoperatively. COX-2, cyclo-oxygenase-2; HIF, hypoxia-inducible factor; HPA, hypothalamic–pituitary–adrenal axis; IL-6, interleukin 6; MMP, matrix metalloprotease; NF-κB, nuclear factor kappa B; NK, natural killer cell; Th2, Type 2 helper T cell; Treg, regulatory T cell; VEGF, vascular endothelial growth factor. Created with BioRender.