Exam 1 - Wounds Flashcards
4 phases of wound healing
- inflammatory
- debridement
- proliferative
- maturation
What is the timeline of inflammatory phase?
0-6 hours
What kind of response occurs in the inflammatory phase?
vascular and cellular - immediate vasoconstriction to stop bleeding and capillary dilataion to bring cells in to area
What is the timeline of the debridement phase?
6-18 hours typically (may continue for days - depending on contamination of wound)
What effect does surgical incision have on debridement phase length and why?
Shortens length of debridement phase b/c the incision is clean
What is the timeline of the proliferative (repair) phase?
12+ hours
What are 4 processes that occur during the proliferative/repair phase?
collagen production, granulation tissue formation, wound contraction, re-epithelialization
what process characterize the maturation (remodeling) phase?
wound contraction and collagen remodeling
what is the timeline of the maturation/remodeling phase?
6 d - 2 yrs
during the maturation/remodeling phase, what causes the strength of the skin to increase?
the formation of of larger collagen bundles AND more intermolecular cross links btwn collagen bundles
Why will remodeled tissue not regain the same breaking strength as uninjured skin?
although the scar itself and the uninjured skin around it are strong, the interface btwn the two is not - this is where re injury most commonly occurs
What are the MAJOR cells involved in wound healing?
platelets and monocytes/macrophages
What are the primary cells involved in the inflammatory phase?
platelets and leukocytes
what is the role of platelets in the inflammatory phase?
hemostasis, provisional matrix, keep foreign material and debris out
what is the role of leukocytes in inflammatory phase?
control infection [mast cells] and remove foreign bodies and debris AND nerve sensitization
in addition to hemostasis, what other role do platelets play in inflammatory phase?
release chemo attractants and mitogens
what is a mitogen?
stimulate mitosis and lymphocyte transformation
what is a chemoattractant?
brings other cells to the party
what cells doe platelets attract to the wound?
monocytes and fibroblasts
what is MCP? and what secretes it?
monocyte chemoattractant protein - secreted by platelets
what is MIP and what secretes it?
macrophage inflammatory protein - secreted by platelets
what MAJOR cells are involved in debridement phase?
WBCs - NTs, lymphocytes, monos/macros, mast cells
what phases are NTs 1* involved in?
inflammatory and debridement
what is the function of NTs?
cleanse wound of foreign particles and bacT
when do NTs arrive?
day 1 [begin to leave on day 2 usually]
what processes occur during the proliferative/repair phase?
ECM deposition, angiogenesis, epithelialization
what are some cells involved in the proliferative/repair phase?
monos/macros, fibroblasts, epidermal cells, endothelial cells, T-lymphocytes, mast cells
without this cell, wound healing is very poor - this cell is THE MAJOR player in ALL wound healing
macrophages
what happens to macrophages after they arrive at the would site?
- adhere to ECM
- monocytes activated to be inflammatory OR repairative macrophages
what are 3 things that macrophage adherence stimulates the expression of?
colony stimulating factor 1
TNFalpha
PDGF
what is CSF-1?
cytokine necessary for survival of monocytes and macrophages
what is TNFa?
potent inflammatory cytokine
what is PDGF?
a potent chemoattractant and mitogen for fibroblasts
what do macrophages activate and release that is critical to wound healing?
growth factors (over 100) - to stimulate proliferation of mesenchymal cells, angiogenesis, ECM/granulation tissue production
when does graunlation tissue begin to develop
about 4 days post injury
what cells make up granulation tissue?
macros, fibroblasts, endothelial cells
what do macros provide for granulation tissue
growth factors
what do fibroblasts provide for granulation tissue
ECM
what do endothelial cells provide for granulation tissue?
form vessels to carry o2 and nutrients to the site
what type of healing dooes granulation tissue promote?
second intention healing
what bacT often grows on surface of granulation tissue?
pseudomonas
why does granulation tissue typically NOT get infected?
b/c it is highly vascular
4 benefits of granulation tissue
- surface for epithelial migrations
- resist infection
- essential for wound contraction
- collagaen production
what kind of surface do endothelial cells require to migrate?
smooth => NO hills/valleys
what do fibroblasts do?
- synthesis, deposition and remodeling of ECM
- produce GFs and MMPs - to replace provisional ECM with collagenous matrix
- wound contraction
what do macros, platelets, endo cells and epi cells secrete that stim fibroblasts to prod ECM?
TGFb
PDGF
FGF
what does TGFb1 do?
- stim fibroblasts to convert ECM to a more collagenous matrix
- converts fibroblasts to myofibroblasts
what do myofibroblasts do?
aid in wound contraction
what stimulates angiogenesis?
EGF (epi GF), PDGF (platelet derived GF), VEGf (vascular endothelial GF)
what stops angiogenesis?
programmed cell death when wound is filled w new granulation tissue
when does epithelialization begin?
about 12 hours post injury
what must be present for epithelial cells to migrate?
granulation tissue [if sutured, migration is immediate - if not, lag phase of 4-5 d]
is migration rate of epithelial cells slower on the upper body or distal limbs?
distal limbs (0.1 vs 0.2 mm/day)
when does epithelial cell proliferation begin?
1-2 days post injury
describe epithelial cell proliferation through wound
- begin at wound margin, behind migrating cells
- migrate or restratify to restore the original epidermis to close wound
some limiting factors to epithelialization
infection excess granulation tissue repeated dressing changes extreme hypothermia desiccation of wound surface reduced o2 tension
1* cells involved in remodeling/maturation phase ?
macros, fibroblasts/myofibroblasts, epidermal and endothelial cells
process during remodeling/maturation phase?
wound contraction
collagen remodeling
inc wound strength
when does wound contraction begin to occur?
3-4 days post injury [independent of epithelialization]
what cell is responsible for movement of tissue during wound contraction?
myofibroblasts
upper body wounds heal primarily by wound contraction or epithelialization?
and distal limb wounds?
upper body: contraction
distal limb: epithelialization
when does collagen remodeling begin?
5 days post injury
these collagen fiber types are replaced by these fiber types
type 1 [mature] collagen => type 3 collagen
how long does collagen accumulation continue for? what happens after that?
3 weeks - after that, synthesis is balanced by degradation
2 main goals of traumatic wound treatment:
preserve life
prevent infection
goals of debridement:
remove damaged tissue, foreign bodies and bacT
obtain fresh skin edge for 1* closur
light debridement vs surgical debridement:
light = wet to dry wraps surgical = removing fat, fascia and muscles
how to facilitate autolytic debridement:
maintain warm, moist environment - bandage wound to accomplish this
benefits of keeping exudate around wound?
rich in endogenous enz, GFs, cytokines - stim migration of fibroblasts, epithelial cells, vascular tissues, NTs, macros
what is an Acemannan hydrogel used for?
prod from aloe vera leaves - facilitates autolytic debridement - promotes collagenase prod - nonadherent and occlusive
how does Calcium Alginate product work?
a dry 3D fabrick that absorbs exudate to form gel like substance - hemostasis and bioabsorbable
2 ideal lavage fluids?
saline or LRS
goals for wound closure - to minimize what 3 things?
skin loss
tension
infection or contamination
4 types of wound closures?
primary
delayed primary
secondary
none (2nd intention)
what is the window for delayed primary closure?
up to 5 days post injury
describe secondary closure
after granulation tissue appears - about 5-6 days post injury
process of second intention healing?
granulation tissue formation, wound contraction, epithelialization
indications for 2nd intention healing?
contaminated or infected wound, extensive tissue loss, excessive skin tension
common issues with lower limb wounds that make healing difficult:
tight skin, lack of supporting deep tissues, wound contraction limited, reduced rate of epithelialization, predisposes to proud flesh
what is proud flesh?
exuberant granulation tissue
what makes up proud flesh?
1* fibroblasts and capillaries
where does proud flesh commonly occur?
distal limb
why does proud flesh occur?
- infection / chronic inflammation
- collagen metabolism imbalance
- lack of muscle/soft tissue
- poor blood supply
Tx of granulation tissue?
surgical excision, corticosteroids +/- abx, equine amnion, chemical debridement
benefits of bandages?
- protect from contamination
- absorbs exudate
- px (prevent) swelling
- stabilize wound margins
- control granulation tissue
- maintain moist environment
how do occlusive dressings work?
- retain wound exudate and px opportunistic bacT infections
- impermeable so dec o2 tension in wound
how do non occlusive dressing work?
allow wounds to drain and breathe
how are bandage casts applied?
applied over half limb or full limb bandage, set then split either front and back or medial and lateral
how does vacuum assisted closure work?
sub atmospheric pressure creates mild suction to pull wound together - keep margins from expanding - continuously removing excess fluid - inc local blood flow and tissue oxygenation by dec pressure on small vessels
benefits of VAC?
dec edema, dec bacT counts, remove inflammatory mediators, promote formation of granulation tissue, promote angiogenesis, dec need for bandage changes, dec need for maintaining intact skin
what is hyperbaric o2 therapy?
intermittently administered 100% o2 at pressure greater than atmospheric pressure
when is hyperbaric o2 therapy good?
if blood flow diminished, o2 supply compromised, anaerobic infections
when is skin grafting used?
defect greater than ability to epithelialize and contract, large lower limb wounds, defect under neoplasm
what is necessary for acceptance of graft?
ability to establish arterial/venous network w/in graft
why do grafts fail?
poor revascularization due to: -blood/serum accumulation -insufficient immobilization baccT infection b/c: - slow cell migration - cell destruction - destroys fibrin film
inadequate recipient bed [fat, tendon, bone, infection, old granulation tissue, etc]
how to stimulate granulation tissue?
hydrotherapy, wet saline bandages, dilute povidone-iodine dressings, waater soluble antimicrobial ointments
ideal granulation tissue is?
smooth, slightly convex, immobile
chronic granulation tissue appearance?
grey/red, edametous, exudate, fibrotic,, less vasacular
advantages to pinch graft?
local anesthesia, minimal trauma, physiologic covering, no bandaging
pinch graft dis advantages?
cobblestone appearance, poor quality healing of skin w tendency to bleed and crack
punch graft advantages?
easy revascularization, resistant to motion, resists infection
punch graft dis advantages?
multi directional growth, needs bandage, graft may come off with bandage removal
