wound healing and the problem wound
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Wound Healing and the Problem Wound. Abigail E. Chaffin, M.D. Assistant Professor of Plastic Surgery Division of Plastic Surgery Tulane University School of Medicine. History of Wound Healing. 1700 BC Papyrus: Wound Healing 100 BC Egypt: Wound Healing Methods 1000 AD Gun Powder - PowerPoint PPT PresentationTRANSCRIPT
Abigail E. Chaffin, M.D.Assistant Professor of Plastic Surgery
Division of Plastic SurgeryTulane University School of Medicine
History of Wound Healing1700 BC Papyrus: Wound Healing100 BC Egypt: Wound Healing
Methods1000 AD Gun Powder1500 AD Hot Oil20th Century Scientific Method
WoundsCustomize
Shotgun approach not acceptable
No two patients OR wounds are identical
58y DM, Neuropathy: unaware of R foot gangrene
Wounds
Wounds
Reconstructive LadderSimple to
ComplexFormal Debridement, Elevation/ABI’sAppropriate IV ABX, Wound Vac, Skin Graft
Review of Wound HealingThree basic types of healing
PrimaryDelayed PrimarySecondary
PrimaryWound surfaces opposedHealing without complicationsMinimal new tissueResults optional
Delayed Primary
Left open initiallyEdges approximated 4-6 days later
SecondarySurfaces not approximatedDefect filled by granulationCovered with epitheliumLess functionalMore sensitive to thermal and mechanical
injury
Three Phases of Wound Three Phases of Wound HealingHealing
Inflammatory Phase Proliferative Phase Remodeling Phase
Three Phases of Wound HealingInflammatory PhaseProliferative Phase
Begins when wound is covered by epithelium
Production of collagen is hallmark7 days to 6 weeks
Remodeling Phase (Maturation Phase)
Inflammatory PhaseHemostasis and InflammationDays 4 - 6 Exposed collagen activates clotting
cascade and inflammatory phaseFibrin clot = scaffolding and
concentrate cytokines and growth factors
Inflammatory: Granulocytes
First 48 hoursAttracted by inflammatory mediators Oxygen-derived free radicals Non-specific
Inflammatory: MacrophagesMonocytes
attracted to area by complementActivated by:
fibrinforeign body material exposure to hypoxic and acidotic
environmentReached maximum after 24 hours Remain for weeks
Inflammatory: Macrophages Activated Macrophage:
Essential for progression onto Proliferative Phase
Mediate:Angiogenesis: FGF, PDGF, TGF-a&b
and TNF-aFibroplasia: IL’s, EGF and TNF
Synthesize NO Secrete collagenases
Three Phases of Wound HealingInflammatory PhaseProliferative PhaseRemodeling Phase
Proliferative PhaseEpithelization, Angiogenesis and
Provisional Matrix FormationBegins when wound is covered by
epitheliumDay 4 through 14Production of collagen is hallmark7 days to 6 weeks
EpithelializationEpithelialization Basal epithelial
cells at the wound margin flatten (mobilize) and migrate into the open wound
Basal cells at margin multiply (mitosis) in horizontal direction
Basal cells behind margin undergo vertical growth (differentiation))
Proliferative: FibroblastWork horse of wound repairProduce Granulation Tissue:
Main signals are PDGF and EGFCollagen type IIIGlycosaminoglycansFibronectin Elastin fibers
Tissue fibroblasts become myofibroblasts induced by TGF-b1
Wound ContractionActual contraction with pulling of edges
toward center making wounds smallerMyofibroblast: contractile propertiesSurrounding skin stretched, thinnedOriginal dermal thickness maintainedNo hair follicles, sweat glands
Epithelialization/ContractionEpithelialization/Contraction
EpithelializationEpithelialization
Collagen HomeostasisAfter Wounding (Optimal Healing)
Days 3 - 7 weekCollagen production begins
Days 7 – 42Synthesis with a net GAIN of collagenInitial increase in tensile strength due
to increase amount of collagenDays 42+
Remodeling with No net collagen gain
CollagenNormal Skin
collagen ratio 4 : 1 Type I/III
Hypertrophic Scarcollagen ratio 2 : 1 Type I/III
Three Phases of Wound HealingInflammatory PhaseProliferative PhaseRemodeling Phase
Maturation PhaseRandom to organized
fibrils Day 8 through yearsType III replaced by type IWound may increase in
strength for up to 2 years after injuryCollagen organizationCross linking of
collagen
Impaired Wound Healing
Wound HealingTo treat the wound, you have to treat
the patientOptimize the patient
CirculatoryPulmonaryNutritionAssociated diseases or conditions
Oxygen
Fibroblasts are oxygen-sensitivePO2 < 40 mmHg collagen synthesis
cannot take place Decreased PO2: most common cause of
wound infectionHealing is Energy DependentProliferative Phase has greatly
increased metabolism and protein synthesis
Hypoxia:
Endothelium responds with vasodilation
Capillary leakFibrin depositionTNF-a induction and apoptosis
Edema
Increased tissue pressureCompromise perfusionCell death and tissue ulceration
Infection
Decreased tissue PO2 and prolongs the inflammatory phase
Impaired angiogenesis and epithelialization
Increased collagenase activity
NutritionLow protein levels prolonged inflammatory phase impaired fibroplasiaOf the essential amino
Methionine is critical
Hydration A well hydrated wound will epithelialize faster
than a dry oneOcclusive wound dressings hasten epithelial
repair and control the proliferation of granulation tissue
TemperatureWound healing is accelerated at
environmental temperatures of 30°CTensile strength decreases by 20% in
a cold (12°C) wound environment
DenervationDenervation has no effect on either
wound contraction or epithelialization
Diabetes MellitusLarger arteries, rather than the arterioles,
are typically affected Sorbitol accumulationIncreased dermal vascular permeability
and pericapillary albumin depositionImpaired oxygen and nutrient delivery
Stiffened red blood cells and increased blood viscosity
affinity of glycosylated hemoglobin for oxygen contributing to low O2 delivery
impaired phagocytosis and bacterial killingneuropathy
Radiation TherapyAcute radiation injury
stasis and occlusion of small vesselsfibrosis and necrosis of capillariesdecrease in wound tensile strengthdirect, permanent, adverse effect on
fibroblast may be progressivefibroblast defects are the central problem
in the healing of chronic radiation injury
MedicationsSteroids
Stabilize lysosomes and arrest of inflammation response
inhibit both macrophages and neutrophilsinterferes with fibrogenesis, angiogenesis,
and wound contractionAlso direct effect on Fibroblasts
Minimal endoplasmic reticulumvitamin A
oral ingestion of 25,000 IU per day pre op and 3d post op (not to pregnant women)
Restores inflammatory response and promotes epithelializaton
Does not reverse detrimental effects on contraction and infection
Nutritional Supplements
Vitamin C ( Ascorbic Acid) is an essential cofactor in the
synthesis of collagenexcessive concentrations of ascorbic
acid do not promote supranormal healing
Vitamin Etherapeutic efficacy and indications
remain to be definedlarge doses of vitamin E inhibit
healingincrease the breaking strength of
wounds exposed to preoperative irradiation
Nutritional SupplementsGlutamine
Enhance actions of lymphocytes, macrophages and neutrophils
GlycineInhibitory effect on leukocytes, might reduce
inflammation related tissue injuryZinc
common constituent of dozens of enzymesInfluences B and T cell activityepithelial and fibroblastic proliferation is
impaired in patients with low serum zinc levels
Factors in Wound HealingSmoking
1ppd = 3x freq of flap necrosis2ppd = 6x freq of flap necrosisNicotine acts via the sympathetic system
vasoconstriction and limit distal perfusion1 cigarette = vasoconstriction > 90 min
Decrease proliferation of erythrocytes, macrophages and fibroblasts
Smoke contains high levels of carbon monoxide shifts the oxygen-hemoglobin curve to the left decreased tissue oxygen delivery
Syndromes Associated with Abnormal Wound HealingCutis Laxa
Think defective elastin fibersCongenital
AD, recessive or X-linked recessiveAcquired
Drug, neoplasms or inflammatory skin conditions
Ehlers-Danlos SyndromeThink defective collagen metabolismAD and recessive patters10 phenotypes
Syndromes Associated with Abnormal Wound HealingEhlers-Danlos Syndrome
Connective tissue abnormalities due to defects:Inherent strengthElasticityIntegrityHealing properties
Syndromes Associated with Abnormal Wound HealingEhlers-Danlos Syndrome
Four major clinical featuresSkin hyper-extensibilityJoint hyper-mobilityTissue fragilityPoor wound healing
Electrostimulation
Electrical current applied to woundsIncreases migration of cells109% increase in collagen40% increase in tensile strength1 to 50 mA direct or pulsed based on
wound
Hyperbaric Oxygen
Developed 1662 by Henshaw: DomicilliumAtmospheric pressure at sea level = 1
ATA = 1.5ml O2/dLNormal SubQ O2 tension is 30-50 mmHg.SubQ O2 tension < 30 mmHg = chronic
wound
Excessive Healing
Hypertrophic ScarsKeloids
KeloidsExtends beyond original boundsRaised and firmRarely occur distal to wrist or kneePredilection for sternum, mandible and
deltoidRate of collagen synthesis increased Water content higherIncreased glycosaminoglycans
Keloid TreatmentTriamcinolone injections3-4 weeksCross linking modulatedInjections continued until no excess
abnormal collagenExcisePrevention during healing – pressure and
injection
Keloid
Keloid
Questions
The proliferative phase of wound healing occurs how long after the injury?
A. 1 dayB. 2 daysC. 7 daysD. 14 days
Which type of collagen is most important in wound healing?
A. Type IIIB. Type VC. Type VIID. Type XI
The tensile strength of a wound reaches normal (pre-injury) levels:
A. 10 days after injuryB. 3 months after injuryC. 1 year after injuryD. never
Which of the following is commonly seen in Ehlers-Danlos syndrome?
A. Small bowel obstructionsB. Spontaneous thrombosisC. Direct hernia in childrenD. Abnormal scarring of the hands with
contractures.
Steroids impair wound healing by:
A. Decreasing angiogenesis and macrophage migration
B. Decreasing platelet plug integrityC. Increasing release of lysosomal enzymesD. Increasing fibrinolysis
Supplementation of which of the following micronutrients improves wound healing in patients without micronutrient deficiency?
A. Vitamin CB. Vitamin AC. SeleniumD. Zinc
Signs of malignant transformation in a chronic wound include:
A. Persistent granulation tissue with bleedingB. Overturned wound edgesC. Non-healing after 2 weeks of therapyD. Distal edema
The treatment of choices for keloids is:
A. Excision aloneB. Excision with adjuvant therapy (e.g. radiation)C. Pressure treatmentD. Intralesional injection of steroids
The major cause of impaired wound healing is:
A. AnemiaB. Diabetes mellitusC. Local tissue infectionD. Malnutrition
Bradykinin, serotonin, and histamine in wounds are released from:
A. LymphocytesB. Mast cellsC. Polymorphonuclear leukocytesD. Platelets
Platelets in the wound form a hemostatic clot and release clotting factors to produce:
A. FibrinB. FibrinogenC. ThrombinD. Thromboplastin
In a healing wound, metalloproteinases are responsible for:
A. Establishing collagen cross-linkB. Glycosylation of collagen moleculesC. Incorporation of hydroxyproline into the
collagen chainD. Initiating collagen degradation
Severe cases of hidradenitis suppurativa in the groin area are best managed by excision of the involved area and?
A. Closure by secondary intensionB. Delayed primary closureC. Primary closureD. Split thickness skin grafting
All of the following statements about keloids are true except?
A. Keloids do not regress spontaneouslyB. Keloids extend beyond the boundaries of the
original woundC. Keloids or hypertrophic scars are best managed
by excision and careful reapproximation of the wound
D. Keloid tissue contains an abnormally large amount of collagen.
Thank You