Critically ill surgical patients usually have a septic status combined with severe systemic inflammation and shock. Sepsis is commonly caused by a gastrointestinal tract perforation, bowel ischemia, or postoperative complications, such as, pneumonia, intra-abdominal infection, or anastomotic leakage. Severe systemic inflammation and sepsis can cause organ failure with high risk of mortality (4 ~ 15% vs. 1%). Sepsis affects about 18 million people annually, with a mortality rate of 25% for uncomplicated cases and 80% in patients developing multi-organ failure syndrome .
Prognostic markers like natriuretic peptide (NP), B-type natriuretic peptide (BNP), or pro-BNP are used to predict postoperative cardiac complications after cardiac or non-cardiac surgery, while procalcitonin is commonly used as prognostic marker and indicator of mortality and antibiotics usage in septic patients. In addition, lactate clearance was recently reported to be a useful indicator of resuscitation and prognosis in severe sepsis [2, 3]. Furthermore, some scoring systems, such as, the acute physiologic and chronic health evaluation (APACHE) II, the sequential organ failure assessment (SOFA), and multiple organ dysfunction score (MODS) systems, are also used to evaluate critically ill patient’s condition. However, no clinically adaptable markers, except lactate clearance and procalcitonin, are available for determining the outcomes of critically ill surgical patients with severe sepsis. Inflammatory processes after infection are known to involve cells, inflammatory mediators, cytokines, pro-inflammatory substances, nitric oxide, arachidonic acid metabolites, and oxygen free radicals. These mediate and induce organ injury leading to organ failure [4–10]. Recently, many reports have been issued on the roles of oxygen free radicals and antioxidants, such as, glutamine, zinc, and selenium, which act as cofactors of glutathione peroxidase [11, 12]. Oxygen free radicals (OFR) cause oxidative damage in cells, which lead to DNA damage and mitochondrial dysfunction culminates in cell death [13–15]. There is evidence that oxidative stress caused by reactive oxygen species(ROS) in sepsis is characterized by tissue ischemia reperfusion injury and intense systemic inflammatory response [16–19]. Furthermore, oxidative stress and OFR impair the microcirculation, which induce acute renal failure, and have been correlated with sepsis severity and sepsis-induced morbidity. In sepsis, the protective role of antioxidants against oxidative stress has been known for more than 15 years [20–22]. Supplementation with antioxidants, such as, glutamine, zinc, and selenium may decrease oxidative stress and increase antioxidant activity, but apparently, do not affect mortality [23–28]. Early recognition of oxidative damage in sepsis by assessment of oxidative stress biomarkers is an actual topic for future research [29, 30].