Oxidative Stress in the Critically Ill Polytrauma Patient

The critically ill patient with primary multiple traumas and having secondary complications, presents a complex challenge to the trauma team. The most commonly encountered primary injuries are traumatic brain, spinal cord, pulmonary and abdominal injuries or trauma to the pelvis and the extremities. Moreover, severe inflammations, infections, hyper-metabolism, as well as biochemical and physiological imbalances, lead to a significant increase in morbidity and mortality. Most recently, the role of free radicals has been a largely debated and reported topic. Once produced in excess, free radicals are responsible for inducing oxidative stress. The redox species known to have a destructive effect on cells include the superoxide anion, the hydroxyl radical, hydrogen peroxide, nitric oxide, peroxynitrite, lipid peroxyl and alkoxy lipid. Under normal conditions, free radicals are produced in the human body in small amounts, their activity being minimized by the body’s physiologically anti-oxidant systems which include superoxide dismutase, catalase, glutathione, glutathione peroxidase, peroxiredoxins, and glutaredoxins. In the critically ill patient, severe physiological and biochemical imbalances significantly reduce the body’s anti-oxidant capacity, disrupting the redox balance [1]. A series of biomarkers are in use, designed to quantify oxidative stress. These comprise interleukin 1 beta, interleukin 6, interleukin 10, tumor necrosis alpha, components of the complement, plasmatic levels of antioxidant enzymes and the microRNA species [2]. Oxidative stress in the polytrauma patient is produced shortly after the initial trauma. Subsequently, it transfers from the macroscopic level to the cellular level and thereafter to the molecular level. At this level, the oxidative stress is enhanced and self-sustained, generating a second wave of injury which is then responsible for a systemic inflammatory response syndrome (SIRS) and for the excessive biosynthesis of free radicals. In the critically ill patient with multiple traumas, these events are manifest by the patient becoming vulnerable to microbial grafting. The multiplication of pathogenic germs, immunosuppression and increased levels of pro-inflammatory molecules frequently leads to sepsis and despite intensive treatment, progresses to multiple organ dysfunction syndrome (MODS) and death. The implications of the oxidative stress in the critically ill polytrauma patient has been the subject of a number of recent reports. Hohl reported a statistically significant correlation between plasma levels of specific biomarkers for oxidative injury with a number of clinical variables, in their study on oxidative stress in patients with traumatic brain injury [3]. Nathens [4], in a similar study, reported a series of statistically significant correlations regarding oxidative stress in patients with pulmonary trauma. Moreover, the reduction of a systemic inflammatory response in these patients, following the administration of substances with high anti-oxidant capacity, was highlighted in these studies. A high percentage of the patients with multiple trauma present with haemorrhagic shock as a consequence of centralisation of the circulation in order to protect vital organs. Blockage in the micro-circulation ensues, followed by tissue hypo-oxygenation in organs with reduced blood flow [5-8]. Simultaneously, a systemic inflammatory response syndrome is triggered, modulated by trauma intensity and the genetic predisposition of each individual patient [9,10]. Crime [11] highlighted the decrease in required time on a mechanical ventilation and in mortality rates, in critically ill patients with multiple trauma who have