Hemorrhage and hemorrhagic shock instigate intestinal damage and inflammation. Multiple components of the innate immune response, including complement and neutrophil infiltration, are implicated in this pathology. To investigate the interaction of complement activation and other components of the innate immune response during hemorrhage, we treated mice post-hemorrhage with CR2-fH, a targeted inhibitor of the alternative complement pathway and assessed intestinal damage and inflammation 2 h after hemorrhage. In wildtype mice, CR2-fH attenuated hemorrhage-induced, mid-jejunal damage and inflammation as determined by decreased mucosal damage, macrophage infiltration, LTB4, IL-12p40, and TNF-α production. The critical nature of intestinal macrophage infiltration and activation in the response to hemorrhage was further determined using mice pre-treated with clodronate containing liposomes. The absence of either macrophages or IL-12p70 attenuated intestinal damage. These data suggest that complement activation and macrophage infiltration with IL-12p70 production are critical to hemorrhage induced mid-jejunal damage and inflammation.

With over half of the world population infected, Helicobacter infection is an important public health issue associated with gastrointestinal cancers and inflammatory bowel disease. Animal studies indicate that complement and oxidative stress play a role in Helicobacter infections. Hemorrhage induces tissue damage which is attenuated by blockade of either complement activation or oxidative stress products. Therefore, we hypothesized that chronic Helicobacter hepaticus infection would modulate hemorrhage-induced intestinal damage and inflammation. To test this hypothesis, we examined hemorrhage-induced jejunal damage and inflammation in uninfected and H. hepaticus infected mice. H. hepaticus infection increased hemorrhage-induced mid-jejunal mucosal damage despite attenuating complement activation. In addition, infection alone increased chemokine secretion, changing the hemorrhage-induced neutrophil infiltration to a macrophage-mediated inflammatory response. The hemorrhage-induced macrophage infiltration correlated with increased secretion of tumor necrosis factor-α (TNF-α3) and nitric oxide (NO) in the infected mice. Together these data indicate that Helicobacter infection modulates the mechanism of hemorrhage-induced intestinal damage and inflammation from a complement-mediated response to a macrophage response with elevated TNF-α and NO. These data indicate that chronic, low level infections change the response to trauma and should be considered when designing and administering therapeutics.

Thirty-day mortality and morbidity is, as expected, lower in the healthy surgical population. Age may be an indication to further risk stratify patients that are ASA PS 1 or 2 to better reflect perioperative risk.

Diabetes has been shown to be associated with postoperative infections; however, the association of haemoglobin A1c (HbA1c) with postoperative surgical site infections (SSI) is unclear. All HbA1c data from patients receiving general, vascular, or orthopaedic surgeries between 1 January 2014 and 1 December 2016 were identified from hospital records. The primary outcome was 30-day SSI. Multivariable logistic regression was performed to determine if HbA1c was associated with infection. The cohorts assessed were: (1) HbA1c < 6.5% (reference group); (2) greater than or equal to 6.5% and less than 8.0%; (3) greater than or equal to 8.0% and less than 10.0%; and (4) greater than or equal to 10.0%. There were 3064 patients included in the final analysis. The overall rate of 30-day SSI was 2.42%. After adjusting for confounders, when compared to the reference group, HbA1c ≥ 8.0% and less than 10.0% (OR 2.4, 95% CI 1.2–4.7, p =  0.015) and HbA1c ≥ 10.0% (OR 3.0, 95% CI 1.2–7.3, p =  0.016) had increased odds ratio for 30-day SSI. A HbA1c of 8.0% or higher significantly increased the odds ratio of developing postoperative SSI ( p <  0.05). This may aid in the development of guidelines for optimising diabetic patients.