Abrasion
Partial thickness epithelial injuries secondary to shear forces. Rapid healing is expected via re-epithelialisation.
Puncture wounds
Sharp force penetrating injury. Deep tissue injury and contamination occurs and usually involves a much larger area or volume than initial wound appearance suggests e.g. bit wounds, penetrating trauma, gunshot/ other projectiles
Laceration
Sharply incised wounds involving epidermis, dermis +/- deeper tissues including muscles and tendons. Depending on the nature of the wounding object, some potential for necrosis of wound edges exists. Some authors include incisions as lacerations or separate them into a separate group.
Degloving injuries
Anatomic or physiologic. Anatomic degloves result in the loss of skin at the time of trauma. In physiologic degloves, the skin is initially intact but deprived of the underlying vascular supply resulting in necrosis and dehiscence (wound ruptures along surgical suture) which may only become apparent after 5-7 days. These injuries result from shear forces and may induce large amount of soft tissue and bone loss either directly or indirectly secondary to loss of vascular supply.
What are the phases of wound healing?
Inflammation and debridement
Neutrophil function
kill bacterial species via the release of active oxygen species to phagocytose them. Process requires sufficient partial pressure of oxygen within the wound and is impaired by wound hypoxia. Neutrophils also breakdown and phagocytosis of ECM via proteolytic enzymes and cytokine production prolonging inflammatory phase
Clean
Wound does not enter a hollow viscous or lumen of the body e.g. fresh laceration
Clean- contaminated
Wound enters or penetrates into a colonized viscous or cavity of the body, but under elective and controlled circumstances (e.g. ovariohysterectomy; enterotomy without spillage of luminal content)
Contaminated
Gross contamination is present at the surgical site in the absence of obvious infection e.g. penetrating injury to the abdominal cavity with intestinal perforation. Wound should never be closed
Dirty
Active infection is already present e.g. long-standing open wounds > 6 hours, abscess). Wound should never be closed.
Chemokine
Cytokines mediating chemotaxis
Cytokines and chemokines
Initiate, mediate, and sustain activity within the healing wound
* are ligands for cell surface receptors stimulating intracellular signalling mechanisms
Macrophage function
Phagocytosis (neutrophils, bacteria, ECM)
Cytokine production- the controllers of wound healing
Proliferation/ Repair
Granulation Tissue
Appears between 3-6 days
Wound contraction
Result of fibroblasts–> myofibroblasts
Epithelialisation
Maturation/ Remodelling
Sutured wounds
Idential mechanisms occur- process occurs more rapidly- less distance, optimised wound environment (after debridement), wound contraction not required
Differences with cat wound healing?
Impediments to wound healing- systemic factors
Impediments to wound healing- local factors
En-bloc debridement
Removing all of the tissue