Wounds Flashcards
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
- Proliferation and repair
- Remodelling/ Maturation
Inflammation and debridement
- Characterized clincally by erythema and oedema of wound edges
- Immediate from time of tissue injury–> 1-3 days
- Haemorrhage
- Haemostatic and inflammatory mechanisms
- smooth muscle contraction- vasoconstriction
- wound enlargement
- primary haemostatic plug stabilized by fibrin
- activated platelet products
- vasodilation
- leukocyte migration
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
- Day 4-12
- End of lag (wound strength)
- Wound closure and tissue replacement- capillary ingrowth from surrounding existing vessels/ fibroblast proliferation and migration (fibroblasts produce collagen)
- collagen production: rapid gains in wound strength
Granulation Tissue
Appears between 3-6 days
- compose of fibroblasts, capillaries, macrophages and collagen with macrophages and granulocyte patrolling the surface
- Provides a mechanical barrier and biologic barrier against microbial infection to deep tissues
Wound contraction
Result of fibroblasts–> myofibroblasts
- extend feet which adhere to extracellular matrix, produce smooth muscle filaments, they contract
- no new skin is produced wound is just being pulled in- will continue until wound is closed unless there is too much tension in the other direction
- wound contraction commences about 5 days after wounding
- intussusceptive stretch in surrounding skin
Epithelialisation
- epithelial proliferation/ migration
- migrate across the wound surface
- stratification and thickening occurs
- only happens if granulation surface is okay. If poor, than migratory function doesn’t work very well
- ideally moist wound environment- otherwise dry slows the process down
- requires absence of infection
Maturation/ Remodelling
- Increases the strength and stability of the healed wound
- Type III collagen initially produced is remodelled
- Remodelling process- balance between collagen and synthesis and lysis
- never returns to normal strength- likely around 80% after about 3 months (1 week 3% wound strength; 3 weeks- 30%)
- process is ongoing- months to years
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?
- Cats only 50% as strong as dogs at day 7
- Slower granulation, slower epithelialisation, slower wound contraction
- therefore delay suture removal (despite healed appearance)
Impediments to wound healing- systemic factors
- Immunodeficiencies (ie. diabetes mellitus, obesity, malnutrition, hyperadrenocorticism)– because they affect white cell function)
- Neoplasia
- Age
- Hypoproteinaemia
- Therapeutic agents- corticosteroids, cytotoxic chemotherapy, radiation therapy
Impediments to wound healing- local factors
- Wound perfusion/ blood supply (O2 delivery)- surgeons need to preserve vasculature as much as possible near wounds
- Tissue viability
- Foreign material
- Fluid accumulation (Seroma, haematoma)- increases distance for diffusion (relative hypoxia) and cell migration; inhibits host immune response, medium for bacterial growth
- infection (prolongs and intensifies inflammatory phase of wound healing/ bacterial toxins and enzymative damage from the host response to tissues can be non-specific)
- mechanical factors
En-bloc debridement
Removing all of the tissue
Debridement
The process of removing nonliving tissue from pressure ulcers, burns, and other wounds.
Moist wound healing
- Cell proliferation and migration maximized
- Cell function in inflammatory and debridement phases maximized
- Leukocytes remain in wound- selective autolytic debridement
- Growth factors and cytokines preserved in wound fluid
Primary layer- dressing
Interacts with wound surface
Secondary layer- dressing
Absorbs wound fluid
Tertiary layer- dressing
fixes wound in place, pressure
Foam Dressings
More absorbent- highly exudative wounds, favourable moist wound environment, increased cost of dressings, less frequent dressing changes
Film dressings
Absorbent layer and 1 or 2 film layers, pores allow fluid and gas exchange, absorptive capabilities are limited (minimally exudative wounds or frequent bandage changes)
Alginates
Kelp extract, ion exchange forms gel, very absorbent, promotes haemostatisis and granulation, promote epithelialization, odour and purulent appearance
Hydroactive dressings
Insoluble polymers/ gels, hydrophilic and absorb wound exudates, autolytic debridement, preserve serum growth factors
Negative pressure wound therapy
- controlled sub-atmosphere pressure to wounds
- constant suction so they are less likely to pull their dressing off
- increases blood flow and O2 delivery to the tissues, exerts tension stress which upregulates cytokines and intracellular mechanisms that regulate cellular proliferation, it might remove more bacteria from the wound
- on the wound for maybe 3-5 days
- have to go back to surgery to dig the foam out
Timing wound closure
*assess tissue viability & degree of contamination
Tension lines
incisions parallel to tension lines, closure parallel to tension lines
Presuturing
2-3 days before surgery, mechanical creep
Undermining
Around the wound edges, deep to the panniculus carnosis muscle (present on trunk and head- not on the limbs) because of the vascular supply of dogs
Releasing incisions
Staggered parallel incisions about 1 cm long, relieves some tension
