20 Wound Healing Flashcards by CABS Cabanela

Hemostasis

1º: Formation of platelet plug
2º: production of fibrin clot; intrinsic (8,9,10,12) and extrinsic (7) pathways-> common->coagulation phase

Intrinsic: APTT
Extrinsic: PT
Common: TT

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Inflammation cells

Neutrophils: first cells (24-48h), cytokines (TNF), proteases
Macrophage: activate and recruit other cells, chemoattractants, 48-96h
T lymph: bridge, strengthen scar formation (collagen), 1wk

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Proliferation

Day 4-12

Granulation tissue

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Proliferation important cells

Endothelial cells: mediated by TGFB, TNFa, VEGF; migrate and form new BV
Fibroblasts: ECM; mediated by PDGF

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Proliferation ECM

1 Structural proteins: collagen (type I [mature, 90%], type III [repair, 9%]; elastin
2 Proteoglycans: dermatan sulfate, chondroitin sulfate; forms ground substance, provide lattice for collagen
3 Adhesive proteins: fibronectin, laminin
4 Hyaluronic acid: fluid environment

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Reoganization

Type III -> I
ECM deposition (3 mo)

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Wound tensile strength

2 wk: 20%
3 wk: 30%
10-12 wk: 70-80% (max)

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Scar remodeling

12-18 mos

1-1.5 yrs = scar revision

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Epithelialization

Establish tissue integrity

Superficial = reepithelialization (24-48h, waterproof)

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Wound contraction

Contracture: inc contraction due to myofibroblasts
Myofibroblast: a-smooth muscle actin in thick bundles (stress fibers)

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Stratification of bacterial burden

Contamination (no multiply)
Colonization (multiply, no host response)
Infection (host response)

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Primary intention healing

Clean wounds
Mechanical apposition (sutures, tape glue, staples)

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Secondary intention healing

Reasons: infection, extensive tissue loss
More extensive healing (contracture)
Close spontaneously

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Tertiary intention healing

Potentially contaminated

Monitor for several days (clean, 3-5d)

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Systemic factors that affect wound healing

1 Age: physiologic changes, underlying diseases, medications
2 Nutrition: malnutrition (more infection, less collagen), vit C (no collagen, inc infection), vit A (inc inflammatory response), vit E, zinc (cofactor)
3 Metabolic disorders: DM (dec inflammation, angiogenesis, collagen; growth factors), uremia
4 Steroids: anti-inflammatory, prevents epithelialization and contraction
5 Chemo drugs: attenuates inflammation, delay 2 wks post-op
6 Smoking: vasoconstriction -> hypoxia

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Local factors affecting wound healing

1 Ionizing Radiation Therapy
2 Low Oxygen tension: hypoperfusion (low BV/cardiac failure; local causes), need for collagen synthesis; low BP = arterial insufficiency and vasoconstriction
3 Wound infections: >10^5 microorganisms per gram of tissue (high risk); staphcoccus

Class I: clean wounds

clean: no 3 tracts (respi, GI, GU),

Class ID: prosthetic devices

Class II: clean contaminated

entry into 3 tracts, done in elective procedures

Class III: contaminated

contaminated by not infected

no time to prepare patient

Class IV: dirty/infected

inflammatory reaction and frank infectious process

Antibiotic prophylaxis

Only in class 2 and 3
Must be given before surgery (30 mins)
Know the half-life of antibiotics or double the usual dose

Cefazolin

Acute wound (normal)

Predictable and result is well-healed wound

Standard inflammation, proliferation, remodeling

Chronic wound (impaired)

Does not heal for 4 wks
Due to local/systemic factors

Delayed wound: dec strength but gets same integrity as normal wound; cause by reversible factors
Impaired healing: no mechanical strength; pts with compromised immune system

Chronic wounds

Etiology: repeated trauma, excess inflammation, poor oxygen
Causes: GF breakdown, no synthesis of GFs

Ischemic arterial ulcer

Arterial stenosis -> obstruction -> peripheral vascular resistance (claudication) Diagnosis: distal portion of extremities, absent pulse, poor granulation, ankle-brachial index Treatment: revascularization -> wound care

Venous stasis ulcer

Aging -> venous stasis -> incompetent superficial/deep venous system -> ulceration Chronic: incompetence of deep venous system Diagnosis: shallow wound + lipodermatosclerosis (RBC leaks out) Treatment: compression therapy

Diabetic wounds

Neuropathy: sensory and motor loss = unrecognized injury, charcot foot Peripheral vascular disease Treatment: control DM

Pressure injury

Excess pressure -> capillary collapse, muscle wasting Supine: scarum Wheelchair: ischial tuberosity Treatment: prevention (turning schedule), wound care

Stages of pressure ulcers

``` 1 = intact skin 2 = partial thickness skin loss 3 = full thickness skin loss 4 = with fascia and bone unstageable = eschar ```

Hypertrophic scars

In confines of original wound 4 wks after trauma Occur when not following relaxed skin tension lines (Langer's lines)

Keloid scars

Extend beyond border Does not extend into subcutaneous Common: earlobe, deltoid, parasternal, upper back

Treatment of excess healing

intralesional corticosteroid injections: for younger scars, cannot remove scar just reduce; keloid > HTS; no systemic effects silicone sheets: 24h/day for 3 mos excision/surgery: HTS > keloid radiation: destroys fibroblasts, for older adults pressure: collagen maturation and flattening; for HTS after burns; pressure garment is worn 23-24 hrs for >1 yr