Perioperative supplemental oxygen to reduce surgical site infection: too easy to be true.

To the Editor: The study by Stall et al. investigated the role of perioperative supplemental oxygen in reducing surgical site infection (SSI) after orthopedic surgery. This strategy has been widely studied, in recent years, in other surgical populations. Different type of surgery, same perplexities. Actually, reducing morbidity, hospital length of stay and costs associated with surgery, and even perioperative mortality, with such a simple, worldwide applicable, and considerably inexpensive intervention is a very attractive topic. The matter, however, is probably more complex. Of course, oxygen tension exerts a key role in both bacterial killing and tissue healing. However, it is not clear whether the reduction in SSI rates observed in some investigations (but not in others) is caused by the prevention of wound hypoxia rather than by systemic hyperoxia. Because optimizing cellular oxygen tension depends on both tissue perfusion and the oxygen gradient from capillary to cell, this implies oxygen delivery (DO2) optimization, administering supplemental oxygen being only one of the possible strategies to gain it, together with respiratory support; blood products, fluid, and inotropic therapy; adequate analgesia/ anesthesia; and temperature management. While very little about these variables has been reported in this as well as in other similar studies, the choice of an inspired oxygen fraction (FIO2) of 0.3 in the control group is very far from widespread clinical practice, accounting for an actual risk of low partial pressure of oxygen (PO2) if one relies only on pulse oximetry (especially with a lower limit of oxygen saturation of 92%). Moreover, any beneficial effect should be exerted by the PO2 reached with the FIO2 administered rather than by the FIO2 itself. Since the relation between these two variables depends on the patient’s clinical conditions, studies addressing the role of supplemental oxygen should focus on PO2 rather than FIO2. Remarkably, the only investigation based on blood gas analyses showed no correlation between PaO2 and SSI rate in 1,024 cardiac surgery patients. A possible explanation of the little differences (often not statistically significant, as in this case) in the SSI rates observed in some studies may be the prevention of unrecognized hypoxia at the time of surgery or in the early postoperative period, which in a minority of patients not receiving ‘‘supplemental’’ oxygen may contribute to both regional and systemic imbalance between oxygen supply and demand (that is what the term hypoxia rather implies). From this point of view, perioperative administration of supplemental oxygen may not mean giving more oxygen than needed to obtain some specific pharmacologic action but possibly (unawares) contributing to the so-called preemptive hemodynamic optimization. In this case, the key intervention to (significantly) reduce SSI should consist in the use of adequate monitoring to maintain appropriate DO2 rather than the indiscriminate increase in FIO2. Finally, despite the authors’ statement that this intervention is safe, some concerns exist. Accordingly, the recently published 2-year follow-up of the PROXI trial showed a significant mortality increase in the perioperative supplemental oxygen group that, beyond its statistical limitations, suggests caution. In light of these considerations, the study by Stall et al. represents yet another clue probably leading to exclude a clear beneficial effect of supplemental oxygen rather than an encouragement to further research.