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