Wound healing Flashcards
Skin wound/damage: superficial thickness wound: how it gets damaged and how it regenerates
- shearing, friction
- healing by regeneration of epithelial cells
Partial thickness wounds where is the damage
- epidermis and uppermost dermis
- superficial and deep partial thickness wounds (deeper = not as painful because the nerve ending is gone
full thickness wounds
- extending all layers of the skin into subcutaneous tissue
if there is any slough or eschar = always full thickness
types of wound healing
primary intention/closure
- wound cleaned and edges approximated by sutures, staples or use of adhesives
- free from contamination; minimal tissue loss, heals in approximately two weeks
Types of wound healing
secondary intention/closure
- wound edges cannot be approximated
- granulation must be built to fill in wound
- once wounds become chronic/dehiscence you cannot close
Types of wound healing
delayed primary closure/teriary intention
- Dirty wound left open to allow cleaning then closed by surgeon via suturing, graft or flap placement
What are the phases of wound healing
- hemostasis/inflammation
- proliferation/epithelialization
- maturation and remodeling
Inflammatory phase of healing
1. when?
2. signs
3. what happens/goal
- typically 3-7 days
- changes: red, warmth, swelling, pain, loss of function
- vascular and cellular response
- cascade of activities including vasoconstriction and vasodilation
- goal: hemostasis and breakdown and removal of cellular, extracellular and pathogen debris to produce a clean wound
Hemostasis
what happens and clinical signs it has happened
- <1 hour
- clot formation - stop the bleeding, contain invader, begin attracting phagocytes
- clinical signs: clot formation/fibrous scab, hemostasis achieved, inflammation/edema
Hemostasis: vascular events
- transient arteriole constriction,
- fibrin from liver to form clot,
- vascular permeability increases after bleeding is contained
Hemostasis: cellular events
- clotting cascade:
- influx in neutrophils,
- platelet aggregation,
- release of platelets
inflammatory phase: vasoconstriction
- coagulation cause hypoxia that initiates the healing cascade of wound repair
- control hemorrhage/reduce blood loss
Inflammatory phase: vasodilation
- promotes increased perfusion and increased vessel permeability and increased temperature
Inflammatory phase: cellular response
platelet activiation
- initiates the clotting process and secretes cytokines and growth factors
Inflammatory phase: cellular response
neutrophils
primary cell for wound cleansing
Inflammatory phase: cellular response
mast cells
- secrete histamine
- improves vasodilation and permeability
- also promotes fibroblast recruitment
Inflammatory phase: cellular response
macrophages
- key in inflammatory and proliferation phases
- releases cytokines
- ingest debris, debride,
- initiate angiogensis
Inflammatory phase: cellular response
lymphocytes
- important for immunity
Inflammatory phase: cellular response
fibroblast
- a type of cell that synthesiszes the extracellular matrix and collagen
- responds to the signals from growth factors and cytokines that stimulate fibroblast proliferation differentiate into myofibroblasts (not inflammatory phase)
Cytokines and growth factors
cytokines are signaling molecules - peptide/protein
- proinflammatory cytokines: signal the system to mount an inflammatory response
- anti-inflammatory cytokines: inhibit the actions of inflammatory process
- cytokines/growth factors: respresent the intercellular signaling that orchestrates the complex sequence of cell migration, division, differentiation, and protein expression during wound healing
Proliferation phase
- few days post injury - 3 weeks
- angiogenesis:
- fibroplasia/collagen synthesis
- myofibroblast - wound contraction
- epithelialization: recover wound
wound dehiscence occurs most frequently during this phase - goal: fill in the wound with new tissue (granulation) nad restory integrity of skin
angiogenesis: need to see due to damage to vascular system to nourish and feed tissue
- fibroplasia: collage synthesis: fibroblasts come into area to depsoite collagen and elastin + some differentiate into myofibroblast
- myofibroblast - wound contraction
epithelialization: recover wound
Proliferation phase:
growth factors
what do these do during this phase of healing
- promote cell migration
Proliferation phase:
angiogensis
- restore vascular integrity
Proliferation phase:
fibroblasts
- heal by fibroplasia
- participate in biosyntehsis of collage to form ECM
Proliferation phase:
collagen
- type 3 in early wound healing
- later replaced by type 1 (most of the collagen in the body)
Proliferation phase:
myofibroblast
- wound contraction
- the process by which the edges of a wound are pulled together during the healing process
Epithlelialization phase
what occurs
- restoring the wound surface
- funtion of keratinocytes to advance and resurface the open space
- stem from dermal appendages in partial thickness wounds or from wound edges in full thickness wounds
- begins within hours of injury
remodeling phase
- begins with formation of granulation tissue and can continue for 1-2 years
- matrix remodeling: takes time to become as strong as original tissue
- scar formation
- delicate equilibrium of collagen synthesis and lysis (scar changes from brigh red to pink to grey/white)
- causes scar/wound to heal (lysis)
goal: normotrophia or normal scaring
Intrinsic factors that can influnce healing
- age: changes in skin
- comorbidities
- vascular supply
- immunosuppression
- neurological impairment
- mental status: usually due to ability to take care of wounds
- nutrition: protein +hydration
- nature, size, location of injury
- condition of tissue prior to injury
extrinsic factors that can influence healing
- medication: blood thinners, NSAIDs, steriods
- nutritional status
- movement
- bioburden/infection
- psychophysiological stress
- lifestyle
iatrogenic factors that influence healing
- local ischemia
- inappropriate care
- tissue trauma
Where can wounds become chronic
- disrupted healing that can occur at any stage
chronic wounds: disrupted healing in
inflammatory phase
- inadequate perfusion
- ischemia
- decreased levels of cytokines and growth factors
chronic wounds: disrupted healing in
proliferation phase
- fibroblast senescence (process of deterioration)
- often have large tissue gaps or dead space
- chronic wound fluid that is inhibitory to cell regeneration
chronic wounds: disrupted healing in
epithelialization
- decreased keratinocyte migration
- lack of a moist, oxygen rich nutritious wound bed
- failure of cytokines to mediate the healing process
chronic wounds: disrupted healing in
remodeling phase
- imbalance of synthesis and lysis
What are the most common types of wounds (etiology)
Etiology of wounds
- venous (55%)
- diabetic/neuropathic (16%
- pressure (15%)
- other (9%)
- arterial (7%)
What are factors that are seen in all types of chronic wounds
- local tissue hypoxia: interventions should try to being blood
- bacterial colonization
- repetitive ischemia-reperfusion injury
- altered cellular and system stress
how does local tissue hypoxia vs ischemic distrupt healing and what should you consider
- ischemic wounds (poor perfusion or oxygenation) impair healing
- need to consider: atherosclerotic disease, edema (extracellular fluid = no perfusion) , pressure (usually causes hypoxia)
- ischemia = not getting to the area
- hypoxia = not getting O2 to the cells itself
- ischemia and tissue hypoxia are not the same
How can bacteria affect wounds
- an open wound becomes contaminated with bacteria from surrounding skin within 48 hours (quicker if more bacteria)
- inflammation is host immune response
fluid from chronic wounds demonstrates
- increased protease levels,
- increased pro-inflammatory factor levels
- reduced growth factor levels (fluid from chronic wounds)
ischemia-reperfusion injury
- pressure on a wound = ischemia
- adverse effects of molecular and cellular events following ischemia
- in chronic ounds events occur in repetitive fashion
- tissue damage evident in patients unable to avoid the cyclic dependent injury
impaired stress response
- chronic stress can cause cells to constantly replicate and enter replicative senescenece
- altered response in older adults to ischemic stress contributes to impaired healing response
- patients with more stress are 4x more likely to heal slower
- regular physical activity, sleep and nutrition increase wound healing
Assessment of healing status
-
- wound healing phase diagnosis is useful to demonstrate medical necessity for interventions
phases of healing overlap
- benchmarks may indicate multiple phases at the same time
- wound healing phase diagnosis is defined by the predominant phase appearance
Abnormal wound repsonses
- infection
- moisture
- wound edges
- hypergranulation
- necrotic/non-viable tissue
Assessment process
- wound tissue attributes
- peri wound skin attributes
- other tests and measures
assessment process: data collected to
- examine the severity of the lesion
- determine status of wound healing
- establish a baseline for wound
- prepare a plan of care
- report changes in wound over time
PT role in wound healing
- thorough evaluation: examination, comorbid conditions, mobility etc
- accurate assessment: medical condition, co-morbid conditions, mechanism of injury
- local wound care: cleansing, debridement, dressings
- exercise: to facilitate healing, health status and mobility
- education: wound care, positioning, safety
