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Surgical site infection is still one of the most frequent postoperative complications, and can be costly and disabling. Multiple methods have emerged to try and prevent it, but despite our best efforts, most wound infections can not be predicted in elective surgery.
Recently, the pathogenesis of wound infection has been studied in detail, focusing on wound environment as capable of activating, through local signaling, a more pathogenic phenotype of present bacteria, which become virulent enough to overcome the host defense mechanisms and cause infection.
In normal conditions, there is a balance between the host (the patient) and the microbiome (the bacteria). There are factors (i.e. surgery, fasting, antibiotics) that cause a change in the host toward a more hostile environment, with fewer available nutrients. On the other hand, bacteria detect this new atmosphere and adapt by means of quorum sensing. Those bacteria that have a more aggressive phenotype can survive. The host provides the microbiome with nutrients and bacteria process them into metabolites which the host utilizes. As long as this fair trade functions, peace will prevail in the system.
Ideally, minimally invasive surgery, prophylactic antibiotic only and early oral intake should be the norm. This translates into a healthy refaunation of the gastrointestinal microbiome that allows for the exclusion of any transient pathobiota which may have bloomed. When the surgical process and physiological stress are too severe, the microbiota becomes depleted and the quiescence of the system turns into confrontation. Prolonged antibiotic use and restricted oral intake allow for a pathogenic microbiota to bloom, causing complications such as surgical site infection, ileus, anastomotic leaks and sepsis.
It is important to remember that surgical site infection can occur in the absence of translocation or bacterial dissemination. A possible explanation is an inflamed wound environment acting as a chemoattractant for bacteria that are already present. The Trojan Horse theory explains how neutrophils can engulf MRSA and transport it to the surgical site. This shows that SSI can happen in a previously sterile wound, invaded by GI pathogenic bacteria.
Many guidelines have been published on the prevention of surgical site infection. They reference many point measures involving the patient, the OR and the surgeon. To this day, no universal and definitive protocol has been established.
One of the main aspects to take into consideration is the type of surgery. In recent decades, minimally invasive surgery has allowed for smaller and fewer incisions. Less surgical stress correlates to a lower SSI rate.
Studies have been performed to test several local antibiotics in different presentations, none of which have proven effective. Pressure irrigation or simple irrigation did not yield any benefit either. To this day, there is no solid evidence on local measures that can help reduce SSI rates.
It is known that hypoxia, or, more accurately, hypoperfusion, correlates to higher SSI rates as a result of an ischemic wound. There are clinical studies that propose 80% oxygenation during the procedure and the immediate postoperative period as a way of preventing SSI with good results, but there is no definitive conclusion on this matter.
Lastly, no opioids. The effects of opioids on intestinal motility have been well established. The disruption in normal functionality results in dysbiosis. Since the introduction of the ERAS protocol, there has been a significant reduction in opioid use in postoperative analgesia worldwide.
In conclusion, good surgical principles have helped reduce the SSI rate, but recognizing bacterial virulence as a key pathogenic factor in SSI may allow for the discovery of new measures to prevent it and also to reduce antibiotic resistance.
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