Systemic release of prostaglandins following elective orthopedic surgery compared with fractures

Prostanoids are inflammatory mediators released from endothelial cells following (local) tissue damage. Bone fractures are associated with a discharge of high local energy, thus resulting in marked tissue trauma in the area of cavitation. Plasma levels of prostanoids therefore might be possible markers of the inflammatory response and the severity of trauma. The aim of this study was to elucidate the release of arachidonic acid (AA) metabolites following elective surgery (osteotomy) in comparison to long bone fractures of the lower extremity. 41 patients with osteotomy (group A) and 18 patients with bone damage (group B) were monitored perioperatively with regard to the release of prostacyclin (PGI(2)), thromboxane (TxA(2)), and prostaglandin (PG)F-2 alpha. All AA metabolites revealed a clear-cut release following trauma. Despite the longer lasting interval between trauma and the first blood sampling on hospital admission in group B there was a markedly pronounced release of prostanoids in patients with fractures compared to osteotomy. These results suggest that the damage to the soft tissue surrounding the fracture zone rather causes the systemic inflammatory response than the bone injury (fracture; osteotomy) itself. Our results support the empirical recommendation of external fracture fixation in large soft tissue injury and open fractures. The systemic release of prostanoids, thus influencing vascular permeability and resistance explain the likely impairment of pulmonal function often observed after long bone fractures.