Mr Blair Johnson¹, Mr Andrew Stevenson¹, Ms Fiona Wood^1,2, Mr Mark Fear¹, Mr Matthew Linden¹

¹University Of Western Australia, Crawley, Australia, ²Department of Health, Perth, Australia

Abstract:

It has been established that burn survivors are at a long-term increased risk of cardiovascular disease, with increased lengths of stay when hospitalised. However, the underlying pathology is poorly understood; this is compounded by a lack of research into non-severe burn injuries (NSBI), which comprise the majority of all burn cases in Australia (84%).

Platelets have an established role in the pathogenesis of cardiovascular diseases. During the acute burn injury circulating pro-thrombotic mediators increase susceptibility to venous thrombosis and pulmonary embolism. It has not been determined whether there is an association with NSBI and altered platelet reactivity that could drive a life-long risk of cardiovascular disease.

Platelet function was assessed in the post-acute period by flow cytometric analysis of platelet activation in mice and humans. Blood was collected from mouse models of NSBI (8% TBSA) and sham controls then incubated with a panel of canonical platelet agonists. Increased reactivity to stimulation of platelet collagen receptor was observed (1.2 fold change from sham). We then followed up in adult humans presenting with a NSBI, collecting blood samples at 2- and 6-weeks post-injury. An increase in circulating monocyte-platelet aggregates was observed without stimulation at 2 weeks, and expression of the fibrinogen-binding site upon stimulation with threshold doses of collagen-related peptide at 2 weeks. Platelet responsiveness to collagen-related peptide showed a trending increase across dosages and time points.

Platelet reactivity has been demonstrated to remain altered after the acute burn injury has resolved. Further research is recommended to establish a causative mechanism.

Biography:

Blair has just begun his PhD at the University of Western Australia investigating changes to immune profile and platelet function after burn injury.