plastic surgery - wound healing Flashcards
1
Q
open wounds categories
A
- Laceration- Ragged tears and cuts
- Puncture- Sharp penetration
- Abrasion- Superficial layer of the skin is removed
- Avulsion- Sections of skin torn off either in part or completely
- Amputation- Nonsurgical removal of limb from the body
2
Q
wounds intro
A
- Violation of live tissue integrity
- Largest organ in the body (skin)
- Wounding will affect normal function
- Historically wounding most primitive challenge to survival
- Thus injury eliminatd the unfit
3
Q
general techniques of wound rx - primary intention
A
Primary Intention - all tissues closed with suture material
4
Q
general techniques of wound rx - secondary intention
A
Secondary Intention - Wound left open and closes naturally
5
Q
general techniques of wound rx - tertiary intention
A
Tertiary Intention - Wound left open for a number of days and then closed when clean
6
Q
phases of wound healing stages
A
- hemostasis (sec-min)- blood clot
- inflammatory (day 3-5) - scab, fibroblast, macrophage, blood vessel
- proliferative (day 4-21) - fibroblast proliferating, subcutaneous fat
- remodelling (> day 21) - freshly healed epidermis & dermis
7
Q
phases of wound healing - haemostasis
A
- seconds to minutes
- Immediate response to injury is vasoconstriction
- Caused by release of Thromboxane and Prostaglandins
- Platelets adhere to exposed collagen and release
contents of their granules - Tissue Factor activates both platelets and the coagulation cascades
- Results in a platelet matrix
- Controls hemorrhage, concentrates growth factors and serves as the scaffold of the wound
8
Q
phases of wound healing - inflammation
A
- 3 to 5 days
- Begins immediately following tissue injury
- Functional priorities are removal of devitalized tissues and prevention of colonization & invasive infection by microbial pathogens
- Prostaglandins, histamine, serotonin, kinins, and bacterial products cause vasodilatation and capillary permeability, resulting in edema
- Variety of factors and cytokines attract granulocytes to the wound
- Neutrophils enter and remove dead tissue by phagocytosis & prevent infection
- Absence does not affect wound healing
- Monocytes/ Macrophages predominant cell by day 3
post wounding - Phagocyte debris and bacteria
- Also critical in production of growth factors vital for production of ECM by Fibroblasts & new blood vessel production
- Lymphocytes enter wound day 5–7, role not clear
9
Q
cytokines in wound healing (inflammatory)
A
- epidermal growth factor
- transforming growth factor alpha and beta
- fibroblast growth factor
- keratinocyte growth factor
- tumor necrosis factor
- interleukin 1, 2, 6, 8
- platelet derived growth factor
- vascular endothelial growth factor
- endothelium derived growth factor (nitric oxide)
10
Q
phases of wound healing - proliferation
A
- day 4 - 21
- Functional priority is balance between scar formation and tissue regeneration
- Scar formation predominates
- In foetal wound healing regeneration possible
- Phase characterized by reepithelialization
- Relies on the migration of epithelial cells from the wound margins and from any remaining adnexal structures in the dermis, such as hair follicles, sebaceous glands, and sweat glands.
- Provisional fibrin matrix replaced by granulation tissue (new platform for migration) & thinner type III collagen
11
Q
Granulation tissue composed of 3 cell types
A
(proliferation phase)
1. Fibroblast – produce ECM that fills the healing scar &
provides scaffold for keratinocyte migration
2. Macrophages – continue to produce growth factors that induce fibroblast to proliferate, migrate & deposit ECM as well as stimulate endothelial cells
3. Endothelial cells – form new blood vessels through angiogenesis and vasculogenesis
12
Q
phases of wound healing - remodelling
A
- Longest phase, lasts from 21 days up to a year
- Begins after wound filled in with granulation tissue and
keratinocyte migration has reepithelialized it - Characterized by wound contraction and collagen remodeling
- Wound contraction produced by wound myofibroblast (fibroblasts with intracellular actin microfilaments)
- Collagen remodeling of type III to type I collagen
- Mediated by Matrix Metalloproteinases
- Class of enzymes secreted by granulation tissue
13
Q
foetal wound healing
A
- Scarless regenerative healing
- Dependent on size and timing (<24 weeks gestation)
14
Q
foetal vs adult wound healing
A
- Cellular differences – foetal fibroblast secrete more type III & I V collagen, higher gene expression of MMP
- Wound repair differences – foetal faster collagen synthesis, rate of epithelialization, reduced inflammatory cellular infiltrates
- Growth factor expression – foetal upregulated VEGF
- Gene expression – foetal increased gene ass with development (e.g homeobox gene)
- Matrix composition – foetal wound matrix composed of more hyaluronic acid
15
Q
factors affecting wound healing
A
- local
- systematic
16
Q
local factors affecting wound healing
A
- Infection
- Foreign bodies
- Ischemia
- Edema
- Idiopathic manipulation (e.g. rough handling, tight sutures)
- Radiation therapy
17
Q
systemic factors affecting wound healing
A
- Age
- Malnutrition
- Drugs (e.g. steroids)
- Smoking
- Chemotherapy
- Systematic conditions (e.g. DM, Obesity, CVD, COPD, renal, hepatic, endocrine, small vessel dx, Ca)
18
Q
factors affecting wound healing - age
A
- Wound healing is the function of age
- Age affects rate of multiplication of cells
- Tensile strength and wound closure rates decrease with age
- Phases of healing are protracted
- Therefore events begin later, proceed more slowly, and often do not reach the same level
19
Q
factors affecting wound healing - infection
A
- Prolongs inflammatory phase of healing
- Increased bacterial counts or presence beta-hemolytic streptococcus inhibits healing
- Prolongs the inflammatory phase and interferes with epithelialization, contraction, and collagen deposition
- Bacterial endotoxins decrease tissue PO2 and stimulate phagocytosis and release of collagenase and reactive oxygen species
- Further degrades collagen and contribute to the destruction of normal adjacent tissue
20
Q
Biofilm
A
- Bacteria encased in their own polymeric matrix
- Moves from planktonic to sessile state
- Makes it difficult for antibiotics to penetrate
21
Q
factors affecting wound healing - smoking
A
- Mechanism multifactorial
- Nicotine is a vasoconstrictive substance that decreases proliferation of erythrocytes, macrophages, and fibroblasts
- Hydrogen cyanide inhibits oxidative enzymes
- Carbon monoxide decreases the oxygen-carrying capacity of hb by competitively inhibiting oxygen binding
- increases platelet aggregation,
- Increases blood viscosity
- Decreases collagen deposition
- Decreases prostacyclin formation
22
Q
factors affecting wound healing - DM
A
- Affects healing via metabolic, vascular and neuropathic pathways
- Neuropathy consequence of chronically elevated glucose
- Production of glucose by product called sorbitol leads to nerve damage
- Unregulated glucose leads elevated advanced glycosylated end products
- Induce microvascular injury
- Compounded by stiffened red blood cells and increased blood viscosity
- Hyperglycaemia affects body’s ability to fight infection (diminish PMN, macrophage, lymphocytes ability to fight infection)
- Ability to coat bacteria with antibiotic diminished
23
Q
factors affecting wound healing - steroids
A
- Have a direct inhibitory effect on macrophages, leukocytes, and fibroblasts
- Greatly decreases the inflammatory reaction to injury
- Results in decreased collagen deposition, impaired angiogenesis, delayed epithelialization, decreased wound contraction, and increased infection
- Effects can be partially reversed with Vit A 25 000 IU daily 3/7
24
Q
factors affecting wound healing - DXT
A
- Acute radiation injury causes stasis and occlusion of small vessels
- Leads to decrease in wound tensile strength and total collagen deposition
- Also causes damage to fibroblasts
- Injury irreversible and progressive
25
Q
fundamentals of wound care
A
- Optimize systemic parameters (nutrition, glucose control, smoking cessation)
- Debride nonviable tissue
- Reduce wound bioburden
- Optimize blood flow (warmth, hydration, surgical revasc)
- Reduce edema (elevation, compression)
- Use appropriate dressings (moist wound healing, exudate removal, avoidance of trauma to wound or patient)
- Use pharmacologic therapy when necessary
- Close wound surgically with grafts or flaps as indicated
26
Q
wound bed preparation
A
TIME
T – Removal of devitalized and unhealthy tissue
I – Control of infection and reduction of bacterial load
M – Maintenance of moisture balance at the wound surface
E – Epidermal margin or advancing wound edge
27
Q
wound dressing (red, yellow, black) classification
A
- Narrowed mystery in choosing dressing
- Useful in wounds healing by secondary intention
- Based on balance of healthy granulation tissue and necrotic tissue
- Treat worse problem (color) first i.e. black before yellow before red
28
Q
red, yellow, black wound dressing classification - black
A
- Remove eschar & devitalize dtissue
- Use Sharp/ Surgical debridement
- Other options include enzymatic debridement, autolytic debridement, biological debridement, occlusive or moisture returning dressings to promote autolysis
29
Q
red, yellow, black wound dressing classification - yellow
A
- In absence of infection, actively remove exudate & debris
- If infected add antibiotics
- Use hydrotherapy, wet to damp dressings, VAC
- To promote Autolysis – transparent films, hydrocolloids, hydrogels
- Exudate absorbers – copolymers, starches, foams, alignates, enzymatic debridement
30
Q
red, yellow, black wound dressing classification - red
A
- Provide moist wound environment
- Use nonadherent & impregnated gauzes, transparent films, hydrocolloids, hydrogels
31
Q
wound dressings classification
A
- biological (cellular/ cell free)
- deriding agents (chemical/ enzymatic)
- non biological (occlusive/ non-occlusive)
cellular: apigraf, dermagraf, laserskin, transitie
cell free: alloderm, biobrane, integra
chemical: hydrogen peroxide, aserbine, milton, eusol
enzymatic: iruxol, varidase
occlusive: VAC, films, honey, hydrogel, hydrocolloids, hydropolymers, hydrocellular
non-occlisive: gauze, absorbent, dry, acticoat
32
Q
abnormal wound healing
A
- Useful to consider the balance between attempts to replace tissue defects with new, substitute tissue (scar formation) against the recreation of the original tissue in situ (regeneration)
- Classify into 4 categories
33
Q
abnormal wound healing categories
A
- inadequate regeneration
- inadequate scar formation
- excessive regeneration
- excessive scar formation
34
Q
abnormal wound healing categories - inadequate regeneration
A
- Response to injury characterized by no restoration or recovery
- Classic example is found in CNS
35
Q
abnormal wound healing categories - inadequate scar formation
A
- Examples include diabetic foot ulcers, sacral decubitus and venous stasis ulcers
- In these conditions stable scar tissue would be sufficient to restore cutaneous integrity and eliminate pathology
36
Q
abnormal wound healing categories - excessive regeneration
A
- In these cases pathways of tissue regeneration lead to the recreation of the absent tissue, but there are functional problems reintegrating the tissue into the systemic physiology
- Occurs in peripheral nerve tissue e.g. neuroma
37
Q
abnormal wound healing categories - excessive scar formation
A
- Abnormal scarring classified as either hypertrophic scarring or keloid formation
- Both due to overexuberant scarring
- Etiology and Pathophysiology unknown
- Theories proposed include mechanical strain, inflammation, bacterial colonization, and foreign body reaction
- Modalities for treatments include steroid injection, pressure therapy with silicone sheeting, and external beam radiation
- Recurrence remain high (approach 75%)
38
Q
hypertrophic scar VS keloids
A
clinical distinction
- hypertrophic
* More common
* Not associated with race
* Preceded by injury
* No anatomical association
* Confined to original injury
* Most resolves spontaneously
* No recurrence post op
* Associated with contracture formation - keloids
* Less common
* Associated with race
* Not preceded by injury
* Occurs commonly on ears, deltoid, presternal area
* Extends to surrounding tissues
* doesn’t resolve spontaneously
* Yes, recurrence post op
* not associated with contracture formation
39
Q
adjuncts to wound healing (in addition to help healing)
A
- Negative Pressure Therapy (V.A.C)
- Hyperbaric Oxygen (HBO)
- LASER
- Ultrasound
- Growth Factors
- Bioengineered Skin
40
Q
V.A.C / Negative Pressure Therapy
A
- Use of sub atmospheric pressure dressing to convert open wound to closed controlled wound
- Gives surgeon time to transform hostile wound to manageable wound
- Relieves interstitial fluid and edema
- Removes inflammatory mediators that suppress normal
progression of healing - Reduces bacterial count
- Speeds up formation of granulation
41
Q
hyperbaric oxygen / HBO
A
- Dividing cells in a wound require a minimum oxygen tension of 30mmHg
- Normal oxygen tension ranges between 30 – 50mmHg
- Wounds with poor show oxygen values of 5–20mmHg
- When subjected to hyperbaric chambers at pressures of 2.4ATA, tissue oxygen tension rises to 800–1100mmHg
- Increases expression of NO
- Requires patent vascular system to be effective
- Beneficial in amputations, ORN, surgical flaps and skin graft
42
Q
laser
A
- Low energy LASER beneficial
- Termed biostimulation
- Excites physiologic processes and results in increased cellular activity in wounded skin.
- Mechanism believed to be stimulation of ascorbic acid uptake by cells, stimulation of photoreceptors in the mitochondria, changes in cellular ATP, and cell membrane stabilization.
- Accelerate healing of ischemic, hypoxic, and infected wounds
- Promote epithelialization for wound closure and better tissue
healing. - Most common type used is Helium-Neon LASER and Gallium- Arsenide( or infrared) Laser
43
Q
ultrasound
A
- Result of electrical energy that is converted to sound waves
- Sound waves transmitted to tissues through a hydrated medium between the tissue and the transducer
- Therapeutic effect stems from thermal and non-thermal effect
- Thermal effect improves scar
- Non thermal effect cause changes in cell membrane permeability, increase cellular recruitment, collagen synthesis, tensile strength, angiogenesis, wound con- traction, fibrinolysis, and stimulate fibroblast and macrophage production
44
Q
growth factors
A
- Agent that promote cell proliferation
- Induce migration of cells
- Regranex only growth factor approved by the FDA
- It is a recombinant platelet derived growth factor
- increase the rate of wound healing in chronic wounds, pressure ulcers, and diabetic foot wounds
- High mortality rate when used in malignancy
45
Q
bioengineered skin
A
- Provides living supply of growth factors, cytokines & collagen matrix
- Acts is a template for wound to build on
- Most commonly used in our setting is Integra
- Composed of bovine collagen and shark chondroitin- 6- sulfate covered by silicone membrane
- Matrix becomes vascularized
- Wound can then be grafted
- Initially used for burns
- Use expanded to wounds with exposed bone or tendon
