Plastic And Reconstructive Surgery Flashcards
Time of injury until 3-4 days after injury
Hemostasis and inflammation-sterilization phase
Inflammation
Platelet aggregation and release of vasoconstrictive factors (TXA, Factor V) Proinflammatory cytokine (PDGF, TGFB, IGF1, fibrinogen)
Leading to PMN recruitment
Hemostasis
Cell recruitment
Neutrophil -> Mac -> Fibroblast -> Lymphocyte
Matrix synthesis 1st to last
Fibronectin
Collagen III
Collagen I (stays)
Wound breaking strength
PMNs induce vasodilation and recruitment of mac, lymphocyte, fibroblast
Superoxide and collagenase sterilize and degrade devitalized tissue
Inflammation-sterilization
Major chemoattractant for fibroblast during proliferation phase
PDGF
Wounds only reach this percentage of overall healed strength by 30 days
80%
3-7 days after injury
Initial collagen matrix is laid down
Macrophage infiltrate and release cytokines
Inc vascular permeability and angiogenesis
Lymphocyte activation -> fibroblast response and epithelial cell migration
Proliferation
Fibroblast activated by macrophage via EGF and IGF1
platelets via PDGF lay down disorganized collagen matrix (Type I, II, III)
Fibroplasia
Collagen network provides scaffolding for vascular framework
Granulation
Epidermal cells activated and migrate over the granulating field to close defect
Initial framework comprises developing membrane
Epithelialization
Lasts 1 year after injury
Involves collagen remodelling and crosslinking -> inc wound strength dec vascularity
Maximum wound strength is achieved by
Remodelling and maturation
1 year
Scars are dense collagen matrixes that lack
Dermal appendages such as hair follicle or sweat gland
Tensile strength 70-80% original tissue
6th day, myofibroblast contract and persist for 4-6 weeks in wound
Final crosslinking contributes to final scar
Contracture
Source: Mac, T cell
Target cell: fibroblast, mac
Activates mac, PMN, fibroblast
Induces collagenase activity
IFNy
Source: Mac, fibroblast
Target: keratinocyte, endothelial cell, fibroblast
Triggers mitosis of fibroblast and keratinocyte
Induces collagen production, inc vascular permeability
IGF-1
Source: PMNs, mac
Target cell: Fibroblasts, keratinocyte
Recruits fibroblast, keratinocyte
Induces collagen synthesis
IL1alpha
IL1beta
Source: T cell
Target cell: Fibroblast
Recruits and triggers mitosis in fibroblast
IL2
Source: Mac, Platelet, endothelial cell
Target: PMN, Mac, fibroblast, endothelial cell
Recruit PMN, mac, fibroblast
Stimulates angiogenesis
Inc vascular permeability
PDGF
Source: mac, platelet, fibroblast
Target: fibroblast, keratinocyte, endothelial cell
Induces mitosis in fibroblast, keratinocyte
Promotes angiogenesis, matrix production
TGFB
Source: PMNs
Target cell: Mac, fibroblast
Activates immune cells
Recruits mac
Induces cytotoxicity
TNFalpha
Source: Mac, keratinocyte
Target: keratinocyte, endothelial cell
Stimulates angiogenesis
Induces inc vascular endothelial permeability
VEGF
Most susceptible to radiation injury
fibroblast
keratinocyte
basal epithelial cell
endothelial cell damage creates
hypoxic wound bed and severe inhibition of angiogenesis
If patient presents with radiation-induced ulceration
Confirm that ulceration is
not tumor recurrence
Tx: complete excision of radiated bed with regional flap or flee flap reconstruction necessary for closure of complex wounds and revascularization of wound bed
If pedicle flap is used donor vessel from
nonirradiated tissue bed is preferred to minimize risk of flap necrosis
Wounds with this content of bacteria will not close and cannot support skin graft
> 10 to the fifth bacteria/g
Oxygenases require minimum oxygen tension to function properly
20mmHg
Presence of this organism prevents wound healing
Beta hemolytic Streptococcus
Cytotoxic
Inhibitor of angiogenesis
Poorly vascularized fibrotic wound and inhibited fibroblast activity
Radiation
Congested wound with heavy drainage and poor immune cell/fibroblast wound localization
Can lead to hypoxic tissue
Venous inssuficiency
Involved in crosslinking glycine residues from differing collagen bundles
Involved in collagen synthesis
Vitamin C
Deficiency results in scurvy
Involved in bone growth and vision
Deficiency impairs monocyte activation
cell localization and cell adhesion resulting in night blindness, xeropthalmia, keratomalacis
vitamin A
retinol
Promotes catabolic state and inhibits immune cell localization (PMN supressed)
Corticosteroid use
Impairment of wound healing by corticosteroid use is mitigated with
Topical Vitamin A administration
Antiangiogenesis therapy
bevacizumab
Associated with relative upregulation of MMP 2 and MMP 9
Dec collagen synthesis
Aging
Skin bones tendon
Ehlers Danlos
Osteogenesis imperfecta
Scurvy
Primary form in healed wound
Type I
Cartilage
Chondrodysplasia
Type II