Immune depression in musculoskeletal trauma

Abstract

The immune responses after musculoskeletal trauma are physiological reactions of the organism to restore homeostasis. An imbalance between the early systemic inflammatory response syndrome and the later compensatory anti-inflammatory response syndrome may be responsible for organ dysfunction and increased susceptibility to infections. Cytokines are known to be integral components of the immune response, and the balance or imbalance of the different cytokines partly controls the clinical course in the patients. The major pro-inflammatory cytokines include tumor necrosis factor-alpha (TNF-a), interleukin-1beta (IL-1b), IL-6, and IL-8. These cytokines are predominantly produced by monocytes and macrophages, they mediate overlapping effects, and their actions can be additive. TNF-a and IL-1b are early regulators of the immune response, and both induce the release of secondary pro-inflammatory cytokines. IL-10 is an anti-inflammatory cytokine which reduces the synthesis of pro-inflammatory mediators. The extent of traumatic damage correlates with the immunological changes and determines a graded depression of leucocytes to express cytokines on edotoxin exposure. Correspondingly, it has become clinically evident that in unstable traumatised patients, the recommendation today is damage control orthopaedics, i.e. initial stabilisation of long bone fractures by external fixation followed by definitive stabilisation at about 1 week.

Cytokine Levels (IL-4, IL-6, IL-8 and TGFβ) as Potential Biomarkers of Systemic Inflammatory Response in Trauma Patients

“…In patients with severe injuries this increase may persist longer [2,3]. In such patients the "secondary hit" inflammatory reaction, following ETC procedures, may aggravate the acute systemic inflammatory reaction syndrome (SIRS), and may lead to development of acute respiratory distress syndrome (ARDS) and multiple organ failure (MOF) with a relatively high morbidity and mortality [2,[9][10][11][12].…”

Influence of Propofol, Isoflurane and Enflurance on Levels of Serum Interleukin-8 and Interleukin-10 in Cancer Patients

“…Multiple studies found that anesthetic agents had significant influence on serum cytokines in patients who underwent surgeries (Dermitzaki et al, 2009;Reikerås et al, 2010). Propofol, as one of the anesthetic agents commonly used in clinic, has favorable sedation, anti-inflammatory responses and anti-oxidation characteristics (Cavalca et al, 2008;Gonzalez-Correa et al, 2008).…”

Biomechanics of Musculoskeletal Injury

“…They affect a wide www.intechopen.com variety of cells to induce fever, production of cytokines, endothelial gene regulation, chemotaxis, leukocyte adherence, and activation of fibroblasts. They are responsible for the systemic effects of inflammation, such as loss of appetite and tachycardia (Reikeras, 2010). IL-6 is another cytokine that appears to be critical in the inflammatory cascade in the setting of trauma.…”

“…IL-6 levels are elevated 60 minutes after trauma (or surgery) and decline over days 2 to 5 after trauma. Importantly, the magnitude of IL-6 elevation after mechanical trauma can be used as a reliable marker for the magnitude of systemic inflammation and correlates with the risk of post-injury complications (Reikeras, 2010;Biffl et al, 1996;. IL-6 appears to be responsible for regulating the acute phase response (Reikeras, 2010).…”

“…Careful consideration of timing is critical in the care of the trauma patients since further surgical intervention can worsen the inflammatory response. In severe polytrauma patients, it is often preferable to perform limited fracture stabilization, rather than definitive orthopaedic repair immediately, since surgery can function as a second traumatic event with a second wave of inflammatory cytokine release, which can augment the initial systemic inflammatory response to the trauma with increased potential to cause systemic disease including SIRS and ARDS (Second hit theory) (Reikeras, 2010;Sears et al, 2009). Hauser et al reports that SIRS is universal after traumatic injury and that the clinical presentation differs only in intensity .…”