healing and wound care surgery 2
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Types of woundsWounding: disruption of tissue integrity
Insect bite:
Laceration:
Scalp avulsion:
Electrical burn: probably willsustain digital amputation
Burn
Foreign body reaction: fromsilicone injection. Picture thatfollows shows revisional surgery.
Subject: SURGERYTopic: Healing and Wound careLecturer: Dr. MarquinaDate of Lecture: June 22, 2011Transcriptionist: MopsterPages: 11 S
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2011-2
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General Objectives
At the end of the lecture, the studentsshould be able to discuss the basicconcepts of wound healing, as well as, thefundamental principles of woundmanagement.
Specific Objectives
At the end of the lecture, thestudents should be able to:o To discuss the bodys response
to injury and the sequence ofevents that follow during thecourse of normal woundhealing,
o To define the effects of local
and systemic factors on woundhealing
o To describe the steps in the
proper evaluation, care, andtreatment of the different typesof wounds
Course Outline
I. Historical backgroundII. Biology of normal wound healingA. Phases of wound healing
1. Inflammatory phase2. Proliferative phase3. Maturation and
remodeling phaseB. EpithelializationC. Wound ContractionD. Fetal wound healing
III. Factors affecting wound healingIV. Excessive healing/abnormal scars
V. Wound care and managementA. Classification of woundB. Types of wound closureC. Local wound careD. Dressings
Historical Background
Ancient timeso 2000 BC Sumerians
Incantations: probably inthe belief that the woundswere caused by evil spirits orthe gods.
Application of poultice likematerials
o 1650 BC: Egyptian papyrusdocuments
Infected vs. non infectedwounds
Used concoctions containing
Honey (antibacterialproperties
Lint (absorbentproperties)
Grease (barrier) fortreating wounds
o 2nd-3rd century AD
Greeks
Acute vs. chronic wounds
Practiced gentle tissuehandling, foreign bodyremoval, suturing skinedges, and protecting thewound with cleanmaterials
Galen, a doctor to Romangladiators
Emphasized theimportance of a moistwound environment to
ensure adequate healingo Present
Mid 1500: Ambroise Pare(French army doctor)
Rediscovered the value ofgentle methods of woundcare
Wounds healed rapidlywhen milder measureswere used.
1728 - 1793: John Hunter
Injury alone has in all
cases a tendency toproduce the depositionand the means toproduce a cure
1818-1865: Ignaz PhilippSemmelweiss (Hungarianobstetrician)
Introduced washing ofhands with soap andhypochlorite to decreasepuerperal infection.During those times, thestudents, sometimescoming from anatomydissections assisted withdeliveries, whichprobably led to manyinfections.
1822-1895: Louis Pasteur.
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Concept of germsentering the wound fromthe environment.
Used phenol to disinfectinstruments and ORwhich resulted in amarkedly reducedmortality rate
1876: Robert Johnson. Antiseptic dressing
(cotton gauzeimpregnated withiodoform)
1929: Howe, et al
3 classic phases of woundhealing
1962: Winter.
Proved scientifically thatepithelialization rateincreased by 50% in a
moist woundenvironment
Recent advances in research have notchanged our knowledge of the events ofwound healing but rather have addednew information on the methods by whichwound healing responses are controlled:
Inflammatory cytokines
Growth factors
Bioengineered tissues: for woundcoverage
Biology of Normal Wound Healing
Phases of Wound Healing1. Inflammatory (hemostasis and
inflammation)2. Proliferative (Fibroblastic phase)3. Maturation and Remodeling
There is overlap of the stages
Time Sequence of Classical WoundHealing
Note the overlap of the differentstages
Inflammatory Phase (Hemostasis andInflammation)
Inflammationo Vascular and cellular response
o Serves to clean the wound ofdevitalized tissue and foreignmaterial
Stimulus to inflammationo Physical injuryo Antigen antibody reactiono Infection
After the injury, initial changes are
vascular.o Within 5-10 minutes,
vasoconstriction occurs to slowblood flow
o Followed by active vasodilation
and increased permeabilityo Platelets, erythrocytes,
leukocytes line the vessel wallsand serum gains entry into thewound
Wounding disrupts tissue
integrityDivision of blood
vesselsDirect exposure of extracellularmatrix (collagen) to plateletsPlateletaggregation and
degranulationActivation of coagulationcascade
Platelet activation results in:
Release of wound activesubstanceso Platelet derived growth factor
(PDGF)o Transforming growth factor
(TGF)o Platelet activating factoro Fibronectino Serotonino Promote migration and
adhesion of neutrophils,monocytes, fibroblasts, andendothelial cells into the wound
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Activation of coagulation cascade
Culminates in the formation offibrin clot which serves asscaffolding for the migration ofPMNs, monocytes, and fibroblastsinto the wound
Cellular infiltration follows acharacteristic pattern:
Note: platelets come first, last toarrive are the fibroblasts andcapillaries.
Polymorphonuclear cells (PMNs)
Neutrophilso 1st infiltrating cellso Peak at 24-48 hours post
woundingo Phagocytosis of bacteria and
tissue debris (main task is toclean wound)
o Releases collagenases Matrix and ground substance
degradationo Do not appear to play a role
in collagen deposition oracquisition of mechanicalwound strength
Simpson and Ross inducedneutropenia in guinea pigs,
and noted that in theabsence of gross infection,wound repair proceededidentically to that of normalanimals
Macrophages
From monocytes
Peak at 48-96 hours post wounding Wound debridemnt via
phagocytosis
Contribute to microbial stasis byoxygen radial and nitric oxidesynthesis
Release cytokines and growthfactors that regulate fibroblastproliferation, matrix synthesis, andangiogenesis
Activated by:o IL-1
o TNFo TGFo VEGF (Vascular Endothelial
Growth Factor)o Insulin like Growth Factoro Epithelial Growth Factoro Lactate
Leibovich and Ross
Complete disappearance ofmacrophage from the wound byadministration of systemhydrocortisone and subcutaneousantimacrophage serum
Documented impairment ofphagocytosis, qualitative as well asquantitative decrease infibrinogenesis
T-Lymphocytes
Peak at 1 week post injuryo Produce lymphokineso Found to both inhibit and
stimulate fibroblast recruitmentand proliferation
Peterson, et al, have shown that:o Depletion of T lymphocytes
within 1 week after woundingresults in impaired collagensynthesis and deposition, anddecreased breaking strength ofthe wound
Proliferative Phase
Begins around 4th day and lasts 2-4
weeks post injury Fibroblasts (matrix synthesis) and
endothelial cells (angiogenesis):most important cells at this stage.
Culminates in the re-establishmentof tissue continuity
Fibroblastso Activated by cytokines and GFs
released by macrophages
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o Move along a framework offibrin fibers established duringthe initial hemostasis
o Responsible for matrix synthesis(glycosaminoglycans andfibrillar collagen)
Endothelial cellso Participate in angiognenesiso
Migrate and replicate form newcapillary tubules underinfluence of TNF, TGF, VEGF
Matrix synthesiso GAGS
Ground substance that playsa role in the subsequentaggregation of collagenfibers
An amorphous gel made upof a repeating disaccharideunits attached to a protein
core Chondroitin 4 sulfate
Dermatan sulfate
Heparan sulfate
Hyaluronic acido Collagen
Most abundant protein in thehuman body
18 types; 5 types are foundin human body
Type I (skin, tendon, and
bone) is 90% of all collagen Normal skin contains Type I
and III collagen in ratio of 4:1
Type and distribution ofcollagen (see below):
Collagen synthesiso Occurs intracellularly and
extracellularlyo Glycine Proline - Lysineo Protocollagen is translated from
mRNAo Hydroxylation
ProlineHydroxyproline
LysineHydroxylysine
o Prolyl hydroxylase requiresoxygen and iron as cofactors , ketoglutarate as cosubstrate,ascorbic acid (vitamin C) as anelectron donor
o Protocollagen is alsoglycosylated and assumes an -helical configuration
o 3 -helical chains form a righthanded superhelical structurecalled procollagen
o Excreted extracellularly,procollagen undergo polymerand cross - linking formingcollagen filaments
o ProtocollagenProcollagenCol
lagen filamentsCollagen
fibrilsCollagen fibers
Tensile Strength Tensile strength of the wound
o Measurement of its loadcapacity per unit area
o Constant
Breaking strength of the woundo The force required to break it
regardless of its dimension
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o Dependent of the thickness oftissues
o Collagen fibers are largelyresponsible for tensile strengthof wounds
o All wounds gain strength atapproximately the same rateduring first 14-21 days
o
In the skin, peak tensilestrength is achieved atapproximately 60 days afterinjury
o Tensile strength of a wound
reaches only about 80% of theoriginal unwounded skin
Maturation and Remodeling Phase
Begins approximately 3 weeks postinjury
Collagen synthesis and degradation
are accelerated no net increasein the wound collagen content
Reorganization of previouslysynthesized collageno More stable and permanent
cross links are establishedo Gain in tensile strength
Normal Type I: Type III collagenratio of 4:1 is achieved
Remodeling continues for 6 12months post - injury
Initially indurated, raised andpruritic scar becomes a maturescaro Large number of new capillaries
growing into wound regress anddisappear
o Water content of tissue returnto normal
o Avascular and acellular scar
Epithelialization
Proliferation and migration of
epithelial cells adjacent to thewound
Begins within 1 day of injury
Seen as thickening of theepidermis at the wound edge
Reepithelialization is complete inless than 48 hours in the case ofapproximated incised wound
In split thickness graft donor orsuperficial partial thickness burns,healing consists primarily of re epithelialization with minimal or no
fibroplasias and granulation tissueformation
Process:o Mobilization
Epithelial cells immediatelyadjacent to wound enlarge,flatten and detach fromneighboring cells and thebasement membrane
o Migration
Loss of contact inhibition, socell moves away from itsoriginal neighboring cells.
Cells flow away from theadjoin cells until they meetcells from the opposite sideof the wound
o
Mitosis Fixed basal cells divide to
replace the migrating cellswhile the migrating cells, inturn, also divide and multiply
o Cellular differentiation
Upon reepithelialization, theorderly progression from thebasal mitotic cells throughlayers of differentiatedkeratinocytes to stratumcorneum is again established
Wound Contraction
Part of the repair process thatcloses a gap in soft tissue
The area of the wound is decreasedby this action (healing bysecondary intention)
In contrast to contracture which is:o Undesirable effect of wound
healingo Shortening of the scar that may
result in deformitieso May be due to contraction,
fibrosis, or other tissue damage
Myofibroblastso Cells postulated to be
responsible for woundcontraction (still controversial)
o Cytoskeletal structure (
smooth muscle actin)o Well formed intercellular
attachments such asdesmosomes and macula
adherens
Fetal Wound Healing
Lack of scar formation
More of a regenerative processwith minimal or no scar formation
Transition woundo Occurs at the beginning of the
3rd trimestero Scarless healing but there is a
loss of ability to generateappendages
Difference between adult and fetalwound healing
Wound environmento Fetus is bathed in sterile and
temperature stable fluidenvironment
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o Constituent of several enzymesessential for normal woundhealing
o Low serum levels impairepithelial and fibroblasticproliferation
o Studies have shown that zinc
enhances wound healing only
when there is a pre existingzinc deficiency state
Diabetes mellituso Results in reduced
inflammation, angiogenesis,and collagen synthesis
o Large and small vessel diseasescontributes to local hypoxemia
o Careful preoperative correctionof blood sugar levels improvesoutcome of wounds in pts.
o Insulin restores collagen
synthesis and granulation tissueformation to normal levels
Excessive Wound Healing/AbnormalScars
Widespread scars
Hypertrophic scars
KeloidsA preferred scar is one that has maturedrapidly without contracture or increase inwidth, and without forming more collagenthan necessary for its strength.
Wide spread scar
Typically flat, wide, and oftendepressed
Consequence of continued tensionin the dermis (covered byepidermis instead) and mobility ofthe wound
Hypertrophic scar
Elevated above skin surface butlimited to the initial boundaries ofthe injury
Tend to regress spontaneously
Responsive to treatment
Keloids
Extend beyond the border of theoriginal wound
Lack regression
Commonly in presternal, deltoids,back, and earlobes
Resistant to treatment, often worseafter surgery
Familiar predilection
Young age and dark skin color
Treatment modalities
Intralesional corticosteroindinjection
Silicone sheet/gel: shown to havesome positive effect on scarremodeling
Irradiation and pressure
Surgery (high recurrence rate)
Wound Care and ManagementClassification
Acute woundso Lacerations, tissue avulsions,
surgical woundo Heal in a predictable manner
and time tableo Result in a well healed wound
with few or no complications
Chronic woundso Wounds that have not healed in
3 monthso Risk factors include repeated
trauma, poor tissue perfusion,excessive inflammation
Ischemic arterial ulcers
Due to lack of bloodsupply
Symptoms of peripheralvascular disease like rest
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pain, intermittentclaudication, and colorchanges
On examination,diminished or absentpulses and poorformation of granulationtissue
Management isrevascularization oftissue and wound care
Venous stasis ulcers
Due to venous stasis andhydrostatic back pressure
Distention of dermal capsresult in leaking offibrinogen and theformation of perivascularfibrin cuffs that impedeoxygen delivery to tissue
Lipodermatosclerosis
Management iscompression and woundcare
Diabetic wounds
Neuropathy, footdeformity, and ischemia
Unrecognized injury from
ill fitting shoes, foreignbody, and trauma
Severe micro- andmacrovascularimpairment
Mangement includesadequate control of bloodglucose, control ofinfection by debridementand antibiotic
Decubitus/Pressure Ulcer
When soft tissue iscompressed betweenbony prominence andexternal surface
Excessive pressurecauses capillary collapseand impedes the deliveryof nutrients to tissues
Risk factors includeimmobility, chronicconditions, alteredmental status
Pressure ulcer at thetrochanteric area
Stages of Pressure Ulcer FormationI. Non blanching erythema of intact
skinII. Partial thickness kin lossIII. Full thickness skin loss but not thru
fasciaIV. Full thickness skin loss with
involvement of muscle and
boneMarjolins Ulcers:
Malignant transformation of long standing chronic ulcer
Squamous or basal carcinomas
Types of Wound Closure
Primary intention or primaryclosureo Wound edges are immediately
approximated using sutures,staples, or tapeo Delayed primary closure: in
contaminated wounds, woundedges are approximated after adelay of several days
Secondary Intention orSecondary Closureo Due to bacterial contamination
and tissue loss, the wound is
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left open to heal by granulationtissue formation and contraction
Tertiary Closureo Wound is closed by bringing
tissues from elsewhere in theform of graft or flap
See below: scar formation for thedifferent types of closure.
Local Wound Care
Obtain a history of eventssurrounding injury
Examine the wound to assess itsdepth and configuration, extent ofnon-viable tissues as well as thepresence of FB and contaminants
Irrigation and debridement of theedges of the wound under localanesthesiao High pressure (70 PSI) irrigation
with normal salineo Gentle handling of tissues
o Marginally viable flap of skinand tissues should be resectedor revascularized before woundrepair
o Use of povidone iodine,hydrogen peroxide impairwound healing
Antibiotic administrationo Must appropriate for organism
o Must be given at proper time, inproper dose, via proper route
Eg, elective surgery,contaminated, traumaticwounds
Tetanus prophylaxis
Planning the type and timing ofwound repair
Dressing
Mimics the barrier role ofepithelium
Primary dressing vs. secondarydressingo Primary dressing
Placed directly on the wound
Absorption of secretions,prevent dessication,infection and adhesion ofsecondary dressings
o Secondary dressing Placed over the primary
dressing
Provide compression andocclusion and form a barrier
Absorbent dressingo Cotton, wool, and spongeo Should absorb without getting
soaked through, as this wouldpermit entrance of bacteriafrom the outside
Non adherent dressingso Impregnated with paraffin,
petroleum jelly, water solublejelly
o Used as primary dressing
Medicated dressingso Used as a drug delivery systemo May contain benzoyl peroxide,
zinc oxide, neomycin,bacitracin, and chlorhexidine
o Shown to increase
epithelializaton by 28%
Skin Replacements
Conventional skin graftso Split or partial thickness
skin grafts
Epidermis and part of dermis
Donor site heals byepithelialization
Lower rate of primarycontraction (contractionafter harvesting) but higherrate of secondary
contraction (contracture) Contraction:centripetal
movement of the wholethickness of surrounding skinreducing scar
Contracture: the physicalconstriction or limitation offunction as the result ofContraction (scars acrossjoints, mouth, eyelid)
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o Full thickness skin grafts
Entire epidermis and dermis
Higher rate of contraction
(contraction afterharvesting) but lower rate ofsecondary contraction(contracture
Best coverage of lesion onthe face and over jts.
Donor site should be closedprimarily, but size is limited
Sources of Grafts
Autograft: from same individual
Isograft: from a twin Allograft/homograft: from the
same species. Eg, from non identical donor or cadaver
Xenograft/heterograft: fromanother species. Eg, porcine
Skin substitutes
Provide coverage for extensivewounds with limited availability ofautografts
Product of tissue engineering;novel materials are combined withliving cells
Disadvantages include limitedsurvival, high cost, and the needfor multiple applications
Types:o Cultured epithelial
autografts
Keratinocytes harvestedfrom a biopsy of patientsskin are cultured withfibroblasts and growthfactors, and grown intosheets.
o Cultured allogenic
keratinocyte graft
From cadavers andunrelated donors
o Cultured bilayer skinequivalent
Acellular (collagen orsynthetic materials)elements that act asscaffolding for cell growthand migration and cellularelements to reestablish losttissue.
Eg, Biobrane
Important points1. Regardless of the cause of injury,the body responds in a predictablesequence of events
2. An understanding of the biology ofnormal wound healing guides thephysician in the care of wounds.
3. Several local and systemic factorsaffect wound healing; controllingthese factors will ensure that thenormal processes of wound healingshall proceed efficiently
4. In the care of wounds, thephysician must remember thebasic surgical principles: gentlehandling of tissues, maintenance ofaseptic technique, ensuring tissueviability, and avoidance of tension.
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End of transcriptionIn all these things we have complete
victory through him who loved us.
Romans 8:37-39