Chapter 115 - Wound care Flashcards
Phases of wound healing
1) inflammatory 2) proliferation 3) remodeling
Inflammatory phase key points
1) mast cells, neutrophil and macrophages 2) 24 hrs to 2 weeks 3) cytokine: TNF alpha, TFN delta and ILs 4) fibroblast and epithelial cell recruitment 5) MMPs from neutrophil –> break down collagen, gelatin and elastin
MMPs corresponding to the breaking down of collagen, gelatin and elastin
Collagen: MMP-1 and 8 Gelatin: MMP-2 and 9 Elastin: elastase
MMP activity controlled by
Tissue inhibitor of MMP (TIMPs) produced by macrophages
Proliferative phase key points
1) macrophages make PDGF, TGF beta and VEGF 2) fibroblast recruitment and synthesize collagen and proteoglycan –> granulation 3) VEGF, TGF beta and HIF1 (hypoxia-inducible factor) –> capillary growth and network 4) MMP –> breakdown old capillary
Remodeling/epithelialization phase key points
1) epithelial GF and keratinocyte GF –> epithelialization 2) epithelial cell migrate into wound by secreting MMP to degrade non-viable tissue (controlled by TIMPs) 3) type III collagen replaced by mature type I collagen
Chronic disorders that cause unchecked proinflammatory state and reduce healing
1) venous HTN 2) chronic pressure 3) bacterial colonization 4) inadequate tissue perfusion 5) cellular senescence
Prolonged inflammation results in
1) upregulation of proinflammatory cytokines and MMPs (2 and 9) low levels of TIMPs 2) inhibit DNA synthesis and mitotic activity of normal cells 3) upregulation of TNF alpha, IL1, IL6
MMP levels after compression therapy in venous disease
decrease wounds with high MMPs show better response to compression therapy
Cell senescence key points
1) reduced activity of cells from chronic ulcers 2) worse with higher CEAP class
Etiology of wounds various possible causes
1) infection 2) malignancy 3) macrovascular arterial insufficiency 4) vasculitis/vasculopathy (microvascular) 5) venous insufficiency 6) lymphatic obstruction 7) hematologic abnormalities 8) collagen vascular disorders 9) excessive pressure
Distribution of venous refluex in deep, superficial and perforator or combination
TABLE 115.2
Marjolin’s ulcer
squamous cell malignancy = Squamous transformation from preexisting benign chronic wound
Wagner grading system and associated 1 year amputation risk
For diabetic foot ulcers TABLE 115.3
ways to debride a wound
1) surgical debridement 2) chemical debridement: collagenase) not effective against thick tissue 3) larval therapy: faster debridement; higher pain score; no difference in healing or QOL 4) ultrasound/hydro: better wound healing but lack clear evidence
Dressing type: Gauze pro/con/example uses
Pro: mechanical debridement permeable to gas fills dead space Con: damage granulation on removal dehydrate wound frequent changes Kling, sof-wick use in infected or draining wounds
Dressing type: film pro/con/example uses
Pro: semipermeable, waterproof, retain moisture, visualization con: cannot use in infection tegaderm post-op wounds, partial thickness wounds
Dressing type: hydrogel pro/con/example uses
Pro: rehydrate wound, extended time between dressing change Con: maceration possible, minimal absorption NU-GEL, curasol, hypergel use on dry wounds, DFU
Dressing type: hydrocolloid pro/con/example uses
pro: impermeable to bacteria, autolytic debridement, water resistant, self adhesive con: cannot use on infected wound with heavy exudate Restore use on partial thickness low exudate pressure sore
dressing type: foam pro/con/example use
Pro: absorptive, nonadherent, protect from trauma con: mascerate, cannot use on dry exchar Allevyn, hydrofera blue use in exudative wound, venous ulcer under comperssion
Dressing type: alginate pro/con/example use
Pro: moist gel in wound, absorptive, control exudate Con: cannot use in dry wound, dehydrates bed Kaltostat, algisite use in heavy exudative deep wound, venous ulcer under compression, tunnelling wounds
Benefit of including silver in dressing care for wounds
no clear evidence by Cochrane analysis
Adjunctive strategies to treat venous ulcers besides surgery
1) compresion 2) pharmacologic agents: pentoxifylline, flavonoids, anticoagulants 3) skin graft 4) human skin equivalents
Pentoxifylline in venous ulcer
higher healing rate in venous ulcer than placebo
Flavonoid what is it and does it help venous ulcer
plant-derived compound with antiinflammatory and antioxidant properties benefit in venous ulcer healing
Anticoagulation in venous ulcer
LMWH 1 year accelerated venous wound healing 83.8% vs 60.6% without cost and complication not suitable for all patients but select patients yes
Venous strippling for venous ulcer
1) when there’s superficial reflux 30-50% of the time 2) reduces ulcer recurrence 31% vs 56% at 4 years
Rate of healing venous ulcer with just compression alone
60-70% after 4-6 months
STSG and free flap in venous leg ulcer
may help to reduce wound burden but Cochrane no clear evidence
Apligraf what is it
Cultured bilayer cellular construct (BLCC) from neonatal foreskin bovine collagen lattice at base Cytokines released include FGF, VEGF, PDGF, TGF-beta, ILs
When can human skin equivalents be used
1) well-grandulated 2) no exudative and bacteria
Types of synthetic skin
1) Apligraf 2) porcine small intestine submucosa
Evidence of synthetic skin
not clear and not cost effective maybe in chronic wounds
Adjunctive therapy in DFU healing
1) vitamin D 2) PDGF (Becaplermin) topical 3) Apligraf 4) Dermagraft (neonatal foreskin) 5) integra
Black box warning of becaplermin
increase death from cancer
Integra what is it
Acellular dermal matrix product Integra dermal regeneration template 1) acellular bilayer matrix 2) bottom: 3D matrix collagen and chondroitin-6-sulfate (glycosaminoglycan 3) top layer = silicone (temporary)
Benefit of integra in DFU
complete healing 51% vs 32% without Improved pain and physical function
Prostaglandin in ischemic ulcers
1) not FDA approved 2) needs IV infusion 3) side effect headache and dizziness
Pentoxifylline and cilostazol in ischemic ulcers
no clear evidence for either
IPC in ischemic ulcer key points
1) improves circulation 2) increases vasodilator activity 3) improves wound healing 4) long lasting effect even after termination of therapy 5) synchronized vs not synchronized no clear difference
Managing ischemic wounds after arterial intervention
IPC may decrease swelling eschar can be taken or left alone
Hyperbaric oxygen therapy key points
1) treat patient with 100% 2) higher atmospheric pressure 3) 1-2 treatments/day for 20-40 treatments 4) oxygen stimulate angiogenesis, enhance fibroblast and leukocyte function and normalize cutaneous microvascular reflexes
Side effect of hyperbaric oxygen chamber
1) barotraumatic otitis 2) hyperoxic seizure 3) pneumothorax all rare
Grafix what is it
cryopreserved living cells from placental membrane seeded into 3D cell matrix then apply to wound
