Wound Healing Tulane University Division of Plastic & Reconstructive Surgery.
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Transcript of Wound Healing Tulane University Division of Plastic & Reconstructive Surgery.
Wound HealingTulane University
Division of Plastic & Reconstructive Surgery
Presentation Overview
Wound HealingHistory
Phases
Factors Influencing
Adjuncts to Wound Healing
Fetal
Wound CarePrinciples
Dressings
Abnormal Scarring
Exotic Injuries
History of Wound Care
Smith papyrus (1700 B.C.)
7 of 48 case reports dealt with wound healing
Ancient Egypt, Greece, India, and Europe
Gentle wound handling
Foreign body removal
Approximating wound edges
Clean dressings
History of Wound Care
850 - Gunpowder (change in thought process)Boiling oil, hot cautery, scalding water
Worse outcomes
1500 - Ambroise PareRediscovered gentle, clean wound handling during the battle of Villaine
20th Century – Scientific Method
Phases of Wound Healing
Tissue Injury and Coagulation
InflammationRemove devitalized tissue and prevent infection
EarlyLate
FibroproliferativeBalance between scar formation and tissue regeneration
Fibroblast migrationCollagen synthesisAngiogenesisEpithelialization
Maturation/RemodelingMaximize strength and structural integrity
ContractionCollagen Remodeling
Tissue Injury and Coagulation
Tissue Injury and CoagulationINJURY (Physical, antigen-antibody reaction, or infection)
Transient (5-10 minute) vasoconstriction
Slows blood flow, aid in hemostasis
Histamine mediated vasodilation and permeability changes
Vessels become lined with leukocytes, platelets and erythrocytes
Leukocyte migration into the wound
Endothelial cells swell and pull away from each other -> allowing serum to enter the wound
Hemostatic factors from platelets, kinins, complement, and prostaglandins send signals to initiate the inflammatory phase
Fibrin, Fibronectin, and plasma help form a clot and stop bleeding
Early Inflammation
Complement Cascade Activation
PMN infiltration24-48 hours
Stimulated by:Complement components (C5a)
Formyl-methionyl peptide products from bacteria
Transforming Growth Factor (TGF)-b
Early InflammationPMNS
Predominant cell type from 24-48 hours
Phagocytosis and debridement
Removal of PMNS does not alter wound healing
Late InflammationMacrophage
Most critical cell type
Predominates after 48-72 hours
Attracted by:Growth factors (PDGF, TGF-b) ComplementClotting componentsIgGCollagen and elastin breakdown productsLeukotriene B4Platelet factor IV
Late InflammationMacrophage Functions
Phagocytosis
Primary producer of Growth Factors (PDGF, TGF-b)
Recruitment of fibroblasts (proliferative phase)Proliferation of extracellular matrix by fibroblastsProliferation of endothelial cells (angiogenesis)Proliferation of smooth muscle cells
This leads to the Fibroproliferative phase
Late InflammationLymphocyte
Appears at 72 hours
Attracted by: InterleukinsIgGComplement products
Role yet to be determined
Fibroproliferative
FibroblastsMigrate into the wound via ECM
Predominant cell type by day 7
Collagen synthesisBegins on days 5-7
Increases in linear fashion for 2 to 3 weeks
AngiogenesisPromoted by macrophages (TNF-alpha, FGF, VEGF)
EpithelializationMitosis of epithelial cells after 48-72 hours
Modulated by growth factors (EGF, FGF, KGF)
FibroproliferativeExtracellular Matrix
Forms a scaffold for cell migration and growth factor sequestration (fibronectin, proteoglycans, collagen, etc.)
Proteoglycans and GlycosaminoglycansProteoglycans are proteins covalently linked to Glycosaminoglycans
chondroitin sulfate
heparan sulfate
keratan sulfate
hyaluronic acid (1st to appear)Proteoglycans
Create a charged and hydrated environmentFacilitates cell mobility
Viscoelastic properties of normal connective tissue
Collagen
Principle building block of connective tissue
1/3 of total body protein content
3 polypeptide chains that wrap around each other to form a collagen unit (tropocollagen)
Filaments ->Fibrils -> Fibers
Collagen Types
Type 1Bones, skin, and tendons90% of total body collagen
Found in all connective tissues except hyaline cartilage and basement membranes
Type 2Hyaline cartilage, cartilage-like tissues, and eye tissue
Collagen Types
Type 3Skin, arteries, uterus, abdominal wall, fetal tissueAssociation with Type I collagen in varying ratios (remodeling phase)
Type 4Basement membranes only
Type 5Basement membranes, cornea
SkinType 1 : Type 3 ratio is 4:1Hypertrophic scars/immature scars ratio maybe as high as 2:1
Collagen Metabolism
Dynamic equilibriumSynthesis (Fibrosis) vs. Degradation (collagenases)
Collagenase activity
Stimulated: PTH, Adrenal corticosteroids, colchicine
Inhibited: Alpha 2-macroglobulin, cysteine, progesterone
Healing wound3-5 weeks equilibrium is reached between synthesis and degradation (no net change in quantity)
Angiogenesis
Formation of new blood vessels throughout inflammatory and proliferative phase of wound healing
Initiated by plateletsTGF-b and PDGF
PMN
Macrophages
TNF-alpha, FGF, VEGF
Angiogenesis
Endothelial CellForms new blood vessels
VEGF (predominant chemotactic stimulator)
Move along the ECM created by fibroblast
Epithelialization
Repithelialization begins within hours of injury
Stimulated byLoss of contact-inhibition
Growth factors
EGF (mitogenesis and chemotaxis)
KGF, FGF (proliferation)
Dissolution of hemidesmosomal links between epidermis and basement membrane allows lateral movement of epidermal cells
Expression of integrin receptors on epidermal cells allows interaction with ECM
Epithelialization
Epithelium advances across wound with leading edge cells becoming phagocytic
Collagenase (MMP)Degrades ECM proteins and collagenEnables migration between dermis and fibrin eschar
Mitosis of epithelial cells 48-72 hours after injury behind leading edge
Maturation/Remodeling
Longest phase: 3 weeks – 1 year
Least understood phase
Wound Contraction and Collagen Remodeling
Wound ContractionMyofibroblast
Fibroblasts with intracellular actin microfilaments
Uncertain if fibroblasts differentiate into, or if a separate type of cell
Maturation/Remodeling
Collagen RemodelingType 3 Collagen degraded and replaced with Type 1
Collagen degradation achieved by Matrix Metalloproteinase (MMP) activity (fibroblasts, PMNs, macrophages)Collagen reorientation
Larger bundles
Increased intermolecular crosslinks
Tensile StrengthCollagen is the main contributing factor
Load capacity per unit area(Breaking capacity- force required to break a wound regardless of its dimensions)
Rate of tensile strength increases in wounds vary greatly amongst species, tissues and individuals
All wounds begin to gain strength during the first 14-21 days (~20% strength), variable then after
Strength PEAKs @ 60 daysNEVER reaches pre-injury levels
Most optimal conditions may reach up to 80%
Predominant Cell Types
Special Characteristics of Fetal Wound Healing
Lack of inflammationAbsence of FGF and TGF-b
Regenerative process with minimal or no scar formation
Collagen deposition is more organized and rapidType 3 Collagen (No Type 1)
High in hyaluronic acid
Area of ongoing research
Factors That Influence Wound Healing
OxygenFibroblasts are oxygen-sensitive
Collagen synthesis cannot occur unless the PO2 >40mmHg
Deficiency is the most common cause for wound infection and breakdown
Hematocrit Mild to moderate anemia does not appear to have a negative influence wound healing (given sufficient oxygenation)
>50% decrease in HCT
some studies report a significant decrease in wound tensile strength
while other studies find no change
Factors That Influence Wound Healing
SmokingMultifactorial in limiting wound healing
Nicotine
Vasoconstrictive -> decreases proliferation of erythrocytes, macrophages, and fibroblasts
CO
Decreases the oxygen carrying capacity of Hgb
Hydrogen Cyanide
Inhibits oxidative enzymes
Increases blood viscosity, decrease collagen deposition and prostacyclin formation
A single cigarette may cause cutaneous vasoconstriction for up to 90 minutes
Factors That Influence Wound Healing
Mechanical StressAffects the quantity, aggregation, and orientation of collagen fibers
Abnormal tension -> blanching, necrosis, dermal rupture, and permanent stretching
Subcutaneous expansion produces stronger more organized scars
HydrationWell hydrated wounds epithelialize faster
Environmental TemperatureHealing is accelerated at temperatures of 30 C
Tensile strength decrease by 20% in 12C environment
Factors That Influence Wound Healing
DenervationNo direct effect on epithialization or contraction
Loss of sensation and high collagenase activities in skin -> prone to ulcerations
Foreign Bodies (including necrotic tissue)Delay healing and prolong the inflammatory phase
NutritionDelays increases in tensile strengthProlonged inflammatory phase and impaired fibroplasia
EdemaMay compromise tissue perfusion
Factors That Influence Wound Healing
LathyrogensInhibit the cross linking of collagen bundles
Ex. D-penacillamine
Oxygen Derived Free RadicalsDegrade Hyaluronic acid and collagen
Destroy cell and organelle membranes
Interfere with enzymatic functions
AgeTensile strength and wound closure rates decrease with age
Factors That Influence Wound Healing
InfectionProlongs inflammatory phase, impairs epithiliazation and angiogenesisIncreased collagenolytic activity -> decreased wound strength and contractureBacterial counts > 105, b-hemolytic strep
ChemotherapyDecreases fibroblast production and wound contractionIf started 10-14 days after injury, no significant long term problems, but short term decreased tensile strength
RadiationStasis and occlusion of small blood vesselsDecreased tensile strength and collagen deposition
Systemic DiseasesDM
Glycosylated RBCs Stiffened RBCs & Increased blood viscosityGlycosylated WBCs impaired immune function
Renal Dz
Factors That Influence Wound Healing
SteroidsInhibit wound macrophages
Interfere with fibrogenesis, angiogenesis, and wound contraction
Vitamin A and Anabolic steroids can reverse the effects
Vitamin AStimulates collagen deposition and increase wound breaking strength
Topical Vitamin A has been found to accelerate wound reepithealization
Factors That Influence Wound Healing
Vitamin CEssential cofactor in the synthesis of collagen
Deficiency is associated with immune dysfunction and failed wound healing (Scurvy)
Immature fibroblasts and extracellular material
Decreased Alkaline phosphatase
Defective capillary formation -> local hemorrhages
High concentrations do not accelerate healing
Factors That Influence Wound Healing
Vitamin ELarge doses inhibit wound healing
Decreased tensile strength
Less collagen accumulation
HOWEVERAntioxidant that neutralizes lipid peroxidation caused by radiation Decreasing levels of free radicals and peroxidases increases the breaking strength of wounds exposed to preoperative radiation
Factors That Influence Wound Healing
ZincDeficiency:
Impairs epithelial and fibroblast proliferation
Decreases B and T cell activity
Only accelerates healing when there is a preexisting deficiency
Factors That Influence Wound Healing
NSAIDsDecrease collagen synthesis an average of 45% (ordinary therapeutic doses)
Dose-dependent effect mediated through prostaglandins
Factors That Influence Wound Healing
Fibrin-based tissue adhesivesIncrease breaking strength, energy absorption, and elasticity in healing wounds
Adjuncts to Wound Healing
HydrotherapyWhirlpool
Pulsed LavageStimulates formation of granulation tissue
Clean non draining wounds with healthy granulation tissue should NEVER be subjected to hydrotherapy
Water agitation damages fragile cells
ElectrostimulationImitates the natural electrical current that occurs when skin is injured
Increases migration of neutrophils and macrophages
Promotes fibroblastsIncreased collagen production and tensile strength
Adjuncts to Wound Healing
Ultrasound TherapyElectrical energy converted to sound waves
Thermal component -> improves scar outcome
Nonthermal component -> cavitation
In animal models
Changes in cell membrane permeability, increase cellular recruitment, collagen synthesis, tensile strength, angiogenesis, wound contraction, fibrinolysis, and stimulates fibroblast and macrophage production
Clinically results are equivocal
LED (Light-emitting diode)Produces light at multiple wave lengths
Larger area than lasers
Studied by NASA in weightless environments (space station, submarines)
Improved wound healing alone or in combination with hyperbaric oxygen
Adjuncts to Wound Healing
Hyperbaric OxygenIncreases levels of O2 and NO to the wound
Benefit: Amputations, osteoradionecrosis, surgical flaps, skin grafts
None to minimal benefit with necrotizing soft-tissue infections
Wounds require adequate perfusion
Many off-label uses (Benefit? Financial?)Acne, Migraines, Lupus, Stroke, MS, and many more
Medicare Coverage14 Covered Areas (next slide)
~1/3 of claims are for problems not covered
Medicare Coverage of HBO
(1) Acute carbon monoxide intoxication
(2) Decompression illness
(3) Gas embolism
(4) Gas gangrene
(5) Acute traumatic peripheral ischemia
(6) Crush injuries
(7) Progressive necrotizing infections
(8) Acute peripheral arterial insufficiency
(9) Preparation and preservation of compromised skin grafts
(10) Chronic refractory osteomyelitis
(11) Osteoradionecrosis (ORN)
(12) Soft tissue radionecrosis (STRN)
(13) Cyanide poisoning
(14) Actinomycosis
Adjuncts to Wound Healing
Lasers “Biostimulation”Excites physiologic processes and increases cellular activity in wounded skin
Accelerates healing of hypoxic and infected wounds when combined with hyperbaric oxygen
Low energy -> promote epithelialization
Different wave-lengths (multiple treatments)
VAC
Bioengineered Matrices
Adjuncts to Wound Healing
Wound Care General Principles
Cleaning and IrrigationNeed at least 7psi to flush bacteria out of a wound
High pressure can damage wounds and should be reserved only for heavily contaminated wounds
DebridementMost critical step to produce a wound that will heal rapidly without infection
Non-selective: WTD, DTD, WTW, Hydrogen Peroxide, etc.
Useful in wounds with heavy contamination
When starts to granulate, start selective
Selective: sharp, enzymatic, autolytic, or biologic
Selective Debridement
EnzymaticNaturally occurring enzymes that selectively digest devitalized tissue
Collagenase (Santyl), Papain-Urea (Accuzyme), etc.
AutolyticUses the body’s own enzymes and moisture to breakdown necrotic tissue
7-10 days under semi occlusive and occlusive dressings
Ineffective in malnourished patients
BiologicMaggots
Calcium salts and bactericidal peptides
Separate necrotic from living tissue making surgical debridement easier
Wound Care General Principles
Fundamentals of Surgical Wound ClosureIncision should follow tension lines and natural folds in the skin
Gentle tissue handling
Complete hemostasis
Eliminate tension
Fine sutures and early removal
Evert wound edges
Allow scars to mature before repeat intervention (2 weeks to 2 months scar appearance is the worst)
Scar appearance depends more on type of injury than method of closure
Technical factors of suture placement and removal are more critical than type of suture used
Immobilization of wounds to prevent disruptions and excessive scarring (Adhesive strips after suture removal)
Wound Dressings
Over 2,000 commercially available
Red-Yellow-Black ClassificationCreated to help choose appropriate dressings in wounds healing by secondary intention
Treat worse colors first Black -> Yellow -> Red
Dressing Types
AlginatesWounds with heavy exudates (dry the wound)
Converts in a sodium salt -> hydrophilic gel occlusive environment
Change when begins to weep exudate
CreamsOpaque, soft solid or thick liquids with a slight drying effect
Wounds with moist weeping lesions
OintmentsSemisolids that melt at body temperature
Aid in rehydration and topical application of drugs
Dressing Types
FoamsHydrophobic polyurethane sheets with a non absorbent adhesive occlusive cover (very absorbent and nonadherent)
Absorb environmental water and slow epitheliaztion
FilmsTransparent polyurethane membranes with water-resistant adhesives
Conform well, semipermeable to moisture and oxygen, impermeable to bacteria
Promote autolytic debridement
Good for wound monitoring
Can lead to maceration in wounds with a heavy exudate and can tear skin
Dressing Types
GauzeHighly permeable to air and allow rapid moisture evaporation
Stick to granulation tissue and damage the wound with removal
Painful removal
Lint can harbor bacteria
HydrocolloidsCompletely impermeable
Avoid in anaerobic infections
Comfortable and adhere well (good for high-friction areas)
Good at absorbing exudate
HydrogelsStarch and water polymers in gels, sheets, or impregnated gauze
Rehydrate wounds (poor for absorbing exudate)
Dressing Types
VAC DressingSub atmospheric pressure dressing to convert an open wound to a controlled closed wound
Decreases interstitial fluid/edema
Improves tissue oxygenation
Removes inflammatory mediators
Increase speed of granulation tissue formation
Reduces bacterial counts
Silver-impregnated (Acticoat, Arglaes, Silveron)Antibacterial (effective against MRSA, VRE, yeast, and fungi)
Moist environment
Wound Matrix (Alloderm, Oasis, Apligraft, Dermagraft, Integra)
Alloderm
Acellular dermal matrix derived from donated human skin
Epidermis and all dermal cellular components are removed
Oasis
Thin (0.15mm), translucent layer of porcine small intestinal submucosa (SIS)
Primarily made of a collagen-based ECM
Biologically important components of the ECM remain active
Glycosaminoglycans (hyaluronic acid), proteoglycans, fibronectin, and growth factors such as FGF and TGF
Application:
Clean wound base
Cut to size slightly larger than wound, apply directly, moisten with saline
Dress with standard dressings: moist, compressive, etc.
Change dressings with standard frequency
Apligraf
Living bilayered skin substitute (epidermis and dermis)
Dermis is devoid of Langerhans cells, melanocytes, macrophages, lymphocytes, hair or blood vessels
Includes: PDGF, TNF, VEGF, FGF
Has shown improved healing in Diabetic and Venous stasis ulcers
Dermagraft
Derived from newborn foreskin tissue
Cryopreserved human fibroblast-derived dermal substitute
Composed of fibroblasts, ECM, and a bioabsorbable scaffold
Fibroblast are seeded into the scaffold and secrete collagen, matrix proteins, growth factors and cytokines to create a human dermal substitute containing living cells
Multiple studies showing higher percentage of healed diabetic foot ulcers versus controls
Integra
Outer layer of a semi-permeable silicone membrane
Inner layer is a porous matrix of fibers of cross-linked bovine tendon and glycosaminoglycans, that allows dermal ingrowth
After dermal ingrowth the silicone film is removed and a STSG is placed (~3 weeks)
Abnormal Scarring
Hypertrophic Scars
Keloids
Widespread Scar
Comparison of Abnormal Scars
Keloid Hypertrophic Scar
Widespread Scar
Borders Outgrows wound borders Remains within wound borders
Wide, flat, depressed
Natural History
Appears months after injury, rarely regresses
Appears soon after injury, regresses with time
Appears within 6 months of injury
Location Mostly face, earlobes, chest(Never eyelids or mucosa)
Flexor surfaces Arms, legs, abdomen
Etiologic Factors
Possible autoimmune, endocrine (puberty, pregnancy)
Tension Tension and mobility of wound edges
Treatment Intralesional steroids, compression therapy, silicone gel sheeting, radiation therapyOften worse after surgery alone
Same as Keloids but outcome usually more successful
Scar excision/layered closure
Comparison of Abnormal Scars
Keloid Hypertrophic Scar Widespread Scar
Genetics
Significant familial predilection
Low familial incidence
No inheritance pattern
Race African > Caucasian
Low racial incidence Not related to race
Sex Females > Males(Equal)
Equal Unknown
Age Most commonly 10-30 years
Any age, mostly less than 20 years
Any Age
Hypertrophic Scar
Keloids
Keloid: Treatments
No universally effective treatment, usually a combination of treatment types
Case by Case basis
Prevention (the best therapy)Avoid non essential surgery, minimal tension, use cuticular monofilament synthetic sutures, avoid wound-lengthening techniques, and avoid incisions across joints
Keloids: Treatments
Surgery: Alone 50-80% reoccurrence rateExcision with early postoperative radiation (~25% reoccurrence rate)
Excision with corticosteroids (50-70% reoccurrence rate)
Pressure- increase collagenase activity24-30mm Hg, 18-24h/day for 4-6 months
Silicone gel sheeting- mechanism unclear (decrease movement/tension)80-100% -improvement in hypertrophic scars
35%- improvement in keloids
Corticosteroids- intralesionalDecreases collagen synthesis- unclear mechanism
Maybe used in conjunction with surgical excision
Complications- hypopigmentation, skin atrophy, telangiectasias
Lack of randomized control trials to determine site specific dosages
CryotherapyFound to be helpful in early vascularized lesions
Keloid TreatmentRadiation
Most effective when given post operativelyNo advantage if given preoperatively
~25% reoccurrence rate when combined with excision
15-20 Gy administered over several doses (5-6)
Guix et al: Bracytherapy is more effective than externally supplied
Keloid TreatmentsAntitumor/Immunosuppressive Agents
5-FUReports of effectiveness
Uppal et al.: 50% improvement in Keloid Score
Haurani et al.: 19% reoccurrence rate after intralesion injection after surgery at 1 year
Literature still in debate over appropriate dosage
BleomycinLimited studies to date suggesting effectiveness
InterferonSome reports showing effectiveness others showing none
Ongoing study needed
Exotic Wounds
Radiation Injury
Chemical burns
Aquatic animal wounds
Bites (snakes, spiders)
Radiation Injury
Damage caused by energy transferenceFree radicals form causing intracellular and molecular damage
Main targets: Cellular and Nuclear Membranes, DNA
Rapidly dividing cells are the most sensitiveSkin, bone marrow, GI
MorbidityDose received
Time
Volume of tissue
Type of radiation
Cellular changesLow dose -> apoptosis
High dose-> direct cellular necrosis
Radiation Injury
Injury with Time1st week: faint erythema, hair loss, dryness
3rd/4th week: localized erythema, edema, warmth, tenderness
5th week:30G: dry desquamation, pruritus, scaling, increase pigmentation -> brown pigmentation at 2 months
>40G: moist desquamation, bullous formation, may rupture -> ulcers (tendency to heal and recur)
1 year: thin semi translucent skin, dry, easily seen vessels, lack of hair follicles and sebaceous glands -> fibrosis, induration
Radiation Injury
Delayed:
Eccentric vessel proliferation -> thrombosis -> ischemic changes within the skin -> ulceration
Hard to heal, painful, easily traumatized and infected
Radiation Injury
Surgical PrinciplesEstablish a diagnosis
Rule out malignancy
Determine extent of injuryOften boundaries exceed what is seen grossly
Debride all nonviable tissue and foreign material (in stages if needed)
Transfer as much tissue as possible to permit resection of additional tissue in the periphery of questionable wounds
Replace with well vascularized tissue (all neurovascular bundles, bone tendon, prosthetic material, etc. – need coverage)
Better to base pedicle flaps on non irradiated pedicle
Free flaps should utilize non irradiated recipient vessels
Plan for complications and other reconstructive options
Specific Chemical Burns
Black LiquorWarm alkaline solution used to convert wood chips to pulp
Tx:
Water irrigation
Silvadene and normal saline occlusive dressings BID
May require debridement and skin grafting
Specific Chemical Burns
CementInjuries related to alkaline nature or heat related
Initial contact is initially painless and allows progression
Redness ->Purple-Blue -> Blistering and Ulceration
Tx:Removal of the cement and copious irrigation
White PhosphorusInsecticides and Fertilizers
Yellow burn with a garlic-like scent
Tx:Copious irrigation and neutralization with a dilute Copper Sulfate solution
Specific Chemical Burns
Chromic AcidUsed in alloy and dye production
Coagulative necrosisPossible systemic toxicity (require dialysis, exchange transfusion)
GI hemorrhage, n/v, diarrhea, renal, hepatic, CNS, coagulopathies
Tx:
Burns <2% calcium EDTA dressings
Burns >2% immediate excision and STSG
Specific Chemical Burns
Formic AcidRubber, Textile Tanning, Descaling Agent
Causes a systemic acidosis- IV hydration, HCO3, dialysis
Burns treated with irrigation
Hydrofluoric AcidIndustrial and cleaning industries
Initial injury may be subtle, deep penetration of fluoride ion leads to liquefactive necrosis of soft tissue and decalcification and corrosion of bone
Cardiac and Respiratory complications
Irrigation and treatment with calcium gluconate gel
Wounds by Aquatic Animals
Easily become infected, should allow to heal by secondary intention
Snake Bites
45,000 snakebites per year8,000 are venomous
Majority from Pit Vipers
~15 deaths annually
General TreatmentIncision and drainage through a linear incision through skin across the fang marks and slightly beyond
Only works in the first 45 minutes
Loose tourniquet if over an hour from the time of the bite and a delay in transport is anticipated can decrease venom dissemination by 50%
Antibiotics and Tetanus
Debridement of necrotic tissue
Fashiotomy if evidence of compartment syndrome
Antivenin if indicated
Spider Bites
Black Widow Females only carry enough venom
Neurotoxin20-30 minutes -> cramps, abdominal pain, restlessness, perspiration, possible convulsions and shock
TreatmentCalcium gluconate 10ml of 10% solution over 20 minutes for pain control
Muscle relaxants- robaxin, valium
Black widow antivenin- 2.5 ml vial (Lyovac) in severe cases
Spider Bites
Brown Recluse
Proteolytic enzymes
Several hours- erythema, blistering (pale halo)
Progressing to ulceration, extensive tissue destruction, occasional limb loss
System symptoms include hemolytic anemia, thrombocytopenia, and DIC
Treatment- (Controversial)
Dapsone 100-200 mg po qd x 10-25 days
Surgical excision
Thank You