Post on 04-Apr-2018
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Dr.Khalid Al.Zahrani
Assistant professor and consultant plastic surgeon
King Khalid University Hospital.
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Inflammatory response to injury to restore tissue function
Eradicate invading microorganisms
Local- limited duration, restores function Major
overwhelming inflammatory response
Potential multi-organ failure
Adversely impacts patient survival
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Endocraine.
Metabolic.
Immunologic.
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Activated by: Injured tissue:
Mediators: TNF alpha
Neural.
Intravascular volume depletion.
2 main types: Hypothalamic-pituitary control.
Autonomic nervous system.
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Pain, Fear, Anxiety Mediators from IT Nociceptors Baroreceptor
HypothalamicPituitary Axes
AutonomicAxes
ACTHCortisolAldesterone
TSHGHProlactinEndo-OpiodsADH
AD/NAAldesteroneInsulinGlucagon
Target Organ
Cell SurfaceReceptors
IntracellularReceptors
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Hormone classifications polypeptide (cytokine, insulin)
amino acid (epinephrine, serotonin, or histamine)
fatty acid (cortisol, leukotrienes)
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Synthesized anterior pituitary
Regulated by circadian signals
Pattern is dramatically altered in injured patients
Elevation is proportional to injury severity Released by: pain, anxiety, vasopressin,
angiotensin II, cholecystokinin, catecholamines, and pro-inflammatory cytokines
ACTH signals increase glucocorticoid production
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Cortisol elevated following injury, duration of elevation depends on severity of injury
Potentiates hyperglycemia
Hepatic gluconeogenesis Muscle and adipose tissue > induces insulin resistance
Skeletal m.> protein degradation, lactate release
Adipose -> reduces release of TG, FFA, glycerol
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GH: Protein synthesis.
Fat mobilization.
Hyperglycemia.
Immunostimulatory.
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During stress -> protein synth, fat mobilization, andskeletal cartilage growth
2 to release of insulin-like growth factor (IGF1)
Injury reduces IGF1 levels IGF1 inhibited by pro-inflammatory cytokines
TNF-, IL-1, IL-6
GH admin to pediatric burn patients shows
improvement in their clinical course
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Catecholamines.
Aldosterone.
Renin-angiotensin.
Insuline. Glucagon.
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Severe injury activates the adrenergic system Norepi and Epi immed. increase 3-4 fold and remain
elevated 24-48hrs after injury
Epinephrine hepatic glycogenolysis, gluconeogenesis, lipolysis, and
ketogenesis Decreases insulin and glucagon secretion Peripheral- lipolysis, insulin resistance in skeletal m.
= stress induced hyperglycemia
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Synthesized, stored, released from the adrenal zonaglomerulosa
Maintains intravascular volume
Conserves sodium Eliminates potassium and hydrogen ions
Acts on the early distal convoluted tubules
Deficiency- hypotension, hyperkalemia
Excess- edema, HTN, hypokalemia, metab alkalosis
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Stress inhibited release + peripheral insulin resistance= hyperglycemia
Injury has 2 phases of insulin release Within hours- release is suppressed Later- normal/xs insulin production with peripheral
insulin resistance
Activated lymphocytes have insulin receptors ->enhanced Tcell proliferation and cytotoxicity
Tight control of glucose levels esp. in diabeticssignificantly reduces mortality after injury
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EbbPhase Flow Phase
Injury
Catabolism
Anabolism
Death
Minutes
Hours DaysWeeks
Energy
Temperature
O2 Consumption
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Energy balance: Increased energy expenditure and oxygen consumption.
Lipid metabolism: Lipolysis.
Carbohydrates: Hyperglycemia.
Protein and AA:
Increased break down.
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Wound: a disruption of normal anatomic relations as aresult of injury intentional or unintentional.Regardless of causation or tissue type, wound healingpresents with identical biochemical and physiologic
processes, though wound healing may vary in timingand intensity.
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Substrate or reactive phase, immediatetypicallydays 1-10
Response to limit and prevent further injury,inflammation, hemostasis, sealing surface,removing necrotic tissue and debris,migration of cells into wound by chemotaxis,cytokines, and growth factors
Initial intense localvasoconstriction of arteriolesand capillaries followed by vasodilation and
vascular permeability
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Tissue injury & blood vessel damage
exposure ofsubendothelial collagento platelets andvWF activatesthe coagulation pathway
Plugging: Platelet and fibrinProvisional matrix:platelets, fibrin, and fibronectinPlatelet aggregation:Thromboxane (vasoconstrict),
thrombin, platelet factor 4
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Alpha granules contain:
-platelet factor 4: aggregation-Beta-thrombomodulin: binds
thrombin
-PDGF: chemoattractant-TGF-beta: key component tissue repair
Dense granules containvasoactive substances:adenosine, serotonin, and calcium
Other factors released: TXA, Platelet activatefactor, Transform. growth factor alpha, Fibroblast
growth factor, Beta lysin (antimicrobial), PGE2
and PGI2 (vasodilate) and PGF2 (vasoconstrict).
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Chemotaxins attract after extravasation
Migrate through the ECM by transientinteraction with integrins
PMNs scavenge, present antigens,
provide cytotoxicity-free radicals (H2O2)Migration PMNs stops with woundcontamination control usually a few days
Persistant contaminant: continuous influxPMNs and tissue destruction, necrosis,abscess, & systemic infection
PMNs are not essential to wound healing
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Monocytes migrate &
activate: Macrophages
Appear when PMNsdisappear 24-48 hr
Do the same activities as PMNsPlus orchestrate release of enzymes(collagenase, elastase), PGEs,
cytokines (IL-1, TNF alpha,IFN ), growth factors (TGF& PDGF), and fibronectin
(scaffold/anchor for fibroblasts)Activate Fibroblasts, endothelial andepithelial cells to form Gran. Tissue
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Fibroblasts
differentiatefrom restingmesenchymalcells in connective
tissue
3-5 days migrate fromwoundedge
Fibroplasia: Fibroblasts
proliferate replace
fibronectin-fibrinwith
collagen contribute ECM
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I(80%
skin)
Most Common: skin,
bone, tendon.
Primary type in
wound healing.
II Cartilage
III(20 %skin)
Increased Ratio inhealing wound, also
blood vessels and skin
IV Basement Membrane
V Widespread,
particularly in the
cornea
Type III predominant collagensynthesis days 1-2Type I days3-4Type III replaced by Type I in3
weeks
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6 Week = 60% original,80% final strength
8 Week-1year 80%
original (Max)Net Collagen = 6 weeksamount stays thesame but cont.
crosslink increasestrength = maturation
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Remodeling of wound3 week-1+year
Type I replaces Type III Collagen: net amount doesntchange after 6 weeks, organization & crosslinking
Decreased vascularity, less fibroblasts & hyaluronicacid
Peripheral nerves regenerate @ 1mm/day
Accelerated Wound Healing: reopening results inquicker healing 2nd time around
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Contraction: centripetalmovement of the wholethickness of surrounding skin
reducing scarMyofibroblasts: specialFibroblasts express smoothmuscle and bundles of actin
connected through cellularfibronexus to ECM fibronectin,communicate viagap junctionstopull edges of the wound
Contracture: the physicalconstriction or limitation offunction as the result ofContraction (scars across
joints, mouth, eyelid)
Burn/Keloid causingcontracture
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Excess Deposition ofCollagen Causes Scar
Growth Beyond theBorder of theOriginal wound
Tx: XRT, steroids, silicone sheeting, pressure,excise. often Refractory toTx & not preventable
Autosomal Dominant,Darker Pigment, Often
above clavicle but notalwa s
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Excess collagen deposit causingraised scar remains within theoriginal wound confines
Darker pigmented skin & flexorsurfaces of upper torso
Often occurs in burns or woundsthat take a long time to heal,sometimes preventable
Can regress spontaneously
Tx: steroids, silicone, pressuregarments
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Diabetes: impedes the early phase
response
Malnurishment:Albumin
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Osteogenesis Imperfecta: Type I Collagen defectEhler-Danlos syndrome: Collagen disorder, 10 types
Marfan Syndrome: fibrillin defect (collagen)
Epidermolysis Bullosa: Excess fibroblasts Tx:phenytoinScurvy:Vit C req. for proline hydroxylation
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Thank you