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infection and requires a therapeutic course ofantibiotics.
L. Smart1
1Murdoch University, College of Veterinary Medicine, Murdoch, Australia
Initial traumatic injury can be a combination of blunt force tissue injury, blood loss and hypoxia due to impaired pulmonary function. This talk will review the pathophysiology of the initial hours of traumatic injury and outline an up-to-date approach to managing traumatic shock in the first 6 hours.
Pathophysiology of traumatic shock
Blunt force trauma, caused by incidences such as motor vehicle accidents, dog bite injuries or falling from a height, is associated with changes in tissue perfusion and a cascade of pro-inflammatory mediator release. Lack of oxygen to the tissues leads to release of Danger- Associated Molecular Pattern molecules (DAMPs) that
act as chemo-attractants and activate immune cells, such as neutrophils and monocytes. Molecules such as high mobility group box-1 (HMGB1) and cell components, such as mitochondrial or cell-free DNA, are released early in trauma and can promote an acute inflammatory response.
Release of DAMPs is likely one of the key early steps to recruitment of neutrophils and monocytes to the site of injury but DAMPs are also probably one of the main instigators of distant organ injury as a part of a ‘second hit’.
In concert with the release of DAMPs, the innate immune system is promptly activated, including neutrophil recruitment and complement activation. Inflammatory cytokines are also quick to rise within hours of traumatic injury, including interleukin (IL)-6, IL-1β, IL-8, IL-10 and tumour necrosis factor-α (TNFα). They are joined
by a host of other pro-inflammatory and vasoactive mediators released from the endothelium, immune cells and damaged cells. These mediators are designed
to mediate tissue recovery and repair, and mitigate organism invasion, however, the response can be excessive, leading to Systemic Inflammatory Response Syndrome (SIRS) and, potentially, Multiple Organ Dysfunction Syndrome (MODS).
In addition to the inflammatory cascade that occurs, ischaemia due to hypovolaemia adds additional endothelial and tissue cell injury. After reperfusion, complement activation, production of reactive oxygen species, platelet activation and neutrophil margination prompt a cascade of pro-inflammatory events that can lead to distant organ injury. All of these responses can contribute to increased vascular permeability, loss of
· Do appropriately lavage and debride open wounds associated with fractures to reduce the amount of devitalized tissue andcontamination.
· Do use an appropriate method to close an open wound and minimize the need for ongoing open wound management. Closure should be with healthy well- vascularised soft tissue that is not undertension.
Don’ts of open fractures
· Do not use long-term antibiotics prophylactically. This will increase the likelihood of developing resistant bacteria. Only use long-term antibiotics therapeutically to treat
a confirmed bacterial infection. The choice
of antibiotic should be based on culture and sensitivity identification of a deep tissue sample or swab from the fracture site.
· Do not obtain superficial tissue or discharge samples for bacterial culture. They will not represent what, if any, bacteria are present at the fracturesite.
· Do not use ESFs for definitive treatment of open fractures unless the fracture will heal relatively quickly before the ESFs begin to fail. Most type III and many type II open fractures will not heal before the ESF fails, necessitating revision surgery. Owners should be advised prior to treatment that a 2-stage surgery with ESF and open wound management followed by further surgery with a bone plate etc may be necessary.
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