Surgical Apgar Score predictive value for early postoperative organ dysfunction in cancer patients.

BACKGROUND: Surgical APGAR Score (SAS) is based only on intraoperative data and has the advantage of being easy to calculate. Low SAS was associated with an increased risk for postoperative complications, but its utility for specific outcomes prediction, such as postoperative cardiovascular, renal, or metabolic dysfunction is less investigated. Our study aimed to investigate SAS predictive value for early postoperative organ dysfunction in a surgical oncological population. METHODS: This is a prospective observational study that enrolled all consecutive patients submitted to oncologic surgery over 20-days. Registered parameters included demographics, comorbidities, diagnosis and surgery data, SAS score, postoperative complications, organ dysfunction and in-hospital mortality. SAS predictive value for postoperative organ dysfunction was assessed using logistic regression and ROC curves. RESULTS: The study included 205 oncological patients with a mean age (standard deviation) of 60 (12.8) years. SAS was between 8 and 10 in 60% of patients and between 0 and 7 in 40% of patients. Postoperative complications developed in 33 patients (16.1%) and organ dysfunction in 26 patients (12.7%). The rates of postoperative complications, organ dysfunction and mortality, were significantly higher in patients with a low SAS (0-7) than high SAS (8-10). SAS had a low discrimination capacity to distinguish between patients who will develop postoperative complications and those who will not (AUROC 0.65) but was more accurate in identifying surgical oncological patients at risk for cardiovascular and metabolic dysfunction (AUROC 0.83 and 0.85 respectively). CONCLUSION: SAS may be a useful tool to identify cancer surgery patients at risk for postoperative cardiovascular and metabolic dysfunction.

Sevoflurane Modulates AKT Isoforms in Triple Negative Breast Cancer Cells. An Experimental Study.

(1) Background: Triple negative breast cancer (TNBC) is a highly aggressive tumor, associated with high rates of early distant recurrence and short survival times, and treatment may require surgery, and thus anesthesia. The effects of anesthetic drugs on cancer progression are under scrutiny, but published data are controversial, and the involved mechanisms unclear. Anesthetic agents have been shown to modulate several molecular cascades, including PI3K/AKT/mTOR. AKT isoforms are frequently amplified in various malignant tumors and associated with malignant cell survival, proliferation and invasion. Their activation is often observed in human cancers and is associated with decreased survival rate. Certain anesthetics are known to affect hypoxia cell signaling mechanisms by upregulating hypoxia-inducible factors (HIFs). (2) Methods: MCF-10A and MDA-MB 231 cells were cultivated and CellTiter-Blue® Cell Viability assay, 2D and 3D matrigel assay, immunofluorescence assays and gene expressions assay were performed after exposure to different sevoflurane concentrations. (3) Results: Sevoflurane exposure of TNBC cells results in morphological and behavioral changes. Sevoflurane differently influences the AKT isoforms expression in a time-dependent manner, with an important early AKT3 upregulation. The most significant effects occur at 72 h after 2 mM sevoflurane treatment and consist in increased viability, proliferation and aggressiveness and increased vimentin and HIF expression. (4) Conclusions: Sevoflurane exposure during surgery may contribute to cancer recurrence via AKT3 induced epithelial-mesenchymal transition (EMT) and by all three AKT isoforms enhanced cancer cell survival and proliferation.