• When
    London (GMT 0:00)
  • About
    We usually consider wounds as cutaneous lesions with a breach in the integrity of the skin. These wounds may be minor as in local tissue damage caused by an infected cut or insect bite, a deliberate (incisional) wound made at the time of surgery, or extensive tissue destruction due to physical trauma, for example following burn injury. However, wounds can occur with the skin intact typically by some form of blunt trauma, a bruise being an example of damage to small capillaries and blood vessels with blood pooling in a discrete area of the body. However, closed injuries can also result in damage to underlying muscle and bone, which may not be obvious without imaging the injured area. A major complication of road traffic accidents or falls is closed head injury; the skin of the head is intact but damage to the vault and cerebrum can present a major risk to survival. It is often forgotten that wounds do occur in brain. We cannot ‘see’ intracerebral bruising (haematoma) nor the destruction of neurological tissue and structures directly.

    Irrespective of site, tissue damage initiates an acute phase response which ‘drives’ biochemical, endocrine, metabolic and inflammatory cascades soon after the wound is created. Duration to healing may extend from hours to days to weeks depending upon the extent of tissue destruction and presence of infection or sepsis. The size of the wound is typically determined by the initial insult and wound requirements for repair begin immediately with the inflammatory response. In closed wounds, skin epithelium can be replaced within days but for open wounds, granulation tissue will form and with it the mix of newly formed blood vessels and immune cells increasing the demand for oxygen, nutrients, and minerals. The size of the wound gives some indication as to the demands the wound is going to make upon the body; in essence the mass of the wound, primarily composed of granulation tissue, acts as a ‘new organ’ added on to the body, with both ‘pull’ (tissue demand) and ‘push’ (wound metabolites, cytokine release) effects on the body.

    In this lecture, the metabolic response to wounds will be presented to illustrate the perturbations arising from the creation of a range of wound types, the interplay between the newly created wound and its effects on the host and eventual clinical interventions required to ‘satisfy’ demands for calories, nutrients, and oxygen. The potentially life-threatening consequences of infection and sepsis, together with the impact of delayed healing on metabolic responses, will be considered within the context of antimicrobial resistance.
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  • Language
    Anyone with the event link can attend
  • Dial-in available
    (listen only)
    Not available.