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
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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
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3
Q

general techniques of wound rx - primary intention

A

Primary Intention - all tissues closed with suture material

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4
Q

general techniques of wound rx - secondary intention

A

Secondary Intention - Wound left open and closes naturally

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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

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6
Q

phases of wound healing stages

A
  1. hemostasis (sec-min)- blood clot
  2. inflammatory (day 3-5) - scab, fibroblast, macrophage, blood vessel
  3. proliferative (day 4-21) - fibroblast proliferating, subcutaneous fat
  4. remodelling (> day 21) - freshly healed epidermis & dermis
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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
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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
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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)
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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
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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

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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
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13
Q

foetal wound healing

A
  • Scarless regenerative healing
  • Dependent on size and timing (<24 weeks gestation)
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14
Q

foetal vs adult wound healing

A
  1. Cellular differences – foetal fibroblast secrete more type III & I V collagen, higher gene expression of MMP
  2. Wound repair differences – foetal faster collagen synthesis, rate of epithelialization, reduced inflammatory cellular infiltrates
  3. Growth factor expression – foetal upregulated VEGF
  4. Gene expression – foetal increased gene ass with development (e.g homeobox gene)
  5. Matrix composition – foetal wound matrix composed of more hyaluronic acid
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15
Q

factors affecting wound healing

A
  • local
  • systematic
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16
Q

local factors affecting wound healing

A
  • Infection
  • Foreign bodies
  • Ischemia
  • Edema
  • Idiopathic manipulation (e.g. rough handling, tight sutures)
  • Radiation therapy
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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)
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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
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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
  1. inadequate regeneration
  2. inadequate scar formation
  3. excessive regeneration
  4. 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

  1. 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
  2. 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