Wound Healing
Tulane University
Division of Plastic & Reconstructive Surgery
Presentation Overview
Wound Healing
History
Phases
Factors Influencing
Adjuncts to Wound Healing
Fetal
Wound Care
Principles
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 Pare
Rediscovered gentle, clean wound handling during the battle of
Villaine
20th Century – Scientific Method
Phases of Wound Healing
Tissue Injury and Coagulation
Inflammation
Remove devitalized tissue and prevent infection
Early
Late
Fibroproliferative
Balance between scar formation and tissue
regeneration
Fibroblast migration
Collagen synthesis
Angiogenesis
Epithelialization
Maturation/Remodeling
Maximize strength and structural integrity
Contraction
Collagen Remodeling
Tissue Injury and Coagulation
Tissue Injury and Coagulation
INJURY (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 infiltration
24-48 hours
Stimulated by:
Complement components
(C5a)
Formyl-methionyl peptide
products from bacteria
Transforming Growth
Factor (TGF)-b
Early Inflammation
PMNS
Predominant cell type from 24-48 hours
Phagocytosis and debridement
Removal of PMNS does not alter wound healing
Late Inflammation
Macrophage
Most critical cell type
Predominates after 48-72 hours
Attracted by:
Growth factors (PDGF, TGF-b)
Complement
Clotting components
IgG
Collagen and elastin breakdown products
Leukotriene B4
Platelet factor IV
Late Inflammation
Macrophage Functions
Phagocytosis
Primary producer of Growth Factors (PDGF,
TGF-b)
Recruitment of fibroblasts (proliferative phase)
Proliferation of extracellular matrix by fibroblasts
Proliferation of endothelial cells (angiogenesis)
Proliferation of smooth muscle cells
This leads to the Fibroproliferative phase
Late Inflammation
Lymphocyte
Appears at 72 hours
Attracted by:
Interleukins
IgG
Complement products
Role yet to be determined
Fibroproliferative
Fibroblasts
Migrate into the wound via ECM
Predominant cell type by day 7
Collagen synthesis
Begins on days 5-7
Increases in linear fashion for 2 to 3 weeks
Angiogenesis
Promoted by macrophages (TNF-alpha, FGF, VEGF)
Epithelialization
Mitosis of epithelial cells after 48-72 hours
Modulated by growth factors (EGF, FGF, KGF)
Fibroproliferative
Extracellular Matrix
Forms a scaffold for cell migration and growth factor
sequestration (fibronectin, proteoglycans, collagen, etc.)
Proteoglycans and Glycosaminoglycans
Proteoglycans are proteins covalently linked to
Glycosaminoglycans
chondroitin sulfate
heparan sulfate
keratan sulfate
hyaluronic acid (1st to appear)
Proteoglycans
Create a charged and hydrated environment
Facilitates 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 1
Bones, skin, and tendons
90% of total body collagen
Found in all connective tissues except hyaline
cartilage and basement membranes
Type 2
Hyaline cartilage, cartilage-like tissues, and eye
tissue
Collagen Types
Type 3
Skin, arteries, uterus, abdominal wall, fetal tissue
Association with Type I collagen in varying ratios (remodeling
phase)
Type 4
Basement membranes only
Type 5
Basement membranes, cornea
Skin
Type 1 : Type 3 ratio is 4:1
Hypertrophic scars/immature scars ratio maybe as high as 2:1
Collagen Metabolism
Dynamic equilibrium
Synthesis (Fibrosis) vs. Degradation (collagenases)
Collagenase activity
Stimulated: PTH, Adrenal corticosteroids, colchicine
Inhibited: Alpha 2-macroglobulin, cysteine, progesterone
Healing wound
3-5 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 platelets
TGF-b and PDGF
PMN
Macrophages
TNF-alpha, FGF, VEGF
Angiogenesis
Endothelial Cell
Forms new blood vessels
VEGF (predominant chemotactic stimulator)
Move along the ECM created by fibroblast
Epithelialization
Repithelialization begins within hours of injury
Stimulated by
Loss 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
collagen
Enables migration between
dermis and fibrin eschar
Mitosis of epithelial cells 4872 hours after injury behind
leading edge
Maturation/Remodeling
Longest phase: 3 weeks – 1 year
Least understood phase
Wound Contraction and Collagen Remodeling
Wound Contraction
Myofibroblast
Fibroblasts with intracellular actin microfilaments
Uncertain if fibroblasts differentiate into, or if a separate
type of cell
Maturation/Remodeling
Collagen Remodeling
Type 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 Strength
Collagen 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 days
NEVER reaches pre-injury levels
Most optimal conditions  may reach up to
80%
Predominant Cell Types
Special Characteristics of Fetal
Wound Healing
Lack of inflammation
Absence of FGF and TGF-b
Regenerative process with minimal or no scar formation
Collagen deposition is more organized and rapid
Type 3 Collagen (No Type 1)
High in hyaluronic acid
Area of ongoing research
Factors That Influence Wound
Healing
Oxygen
Fibroblasts 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
Smoking
Multifactorial 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 Stress
Affects the quantity, aggregation, and orientation of collagen fibers
Abnormal tension -> blanching, necrosis, dermal rupture, and
permanent stretching
Subcutaneous expansion produces stronger more organized scars
Hydration
Well hydrated wounds epithelialize faster
Environmental Temperature
Healing is accelerated at temperatures of 30 C
Tensile strength decrease by 20% in 12C environment
Factors That Influence Wound
Healing
Denervation
No 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
Nutrition
Delays increases in tensile strength
Prolonged inflammatory phase and impaired fibroplasia
Edema
May compromise tissue perfusion
Factors That Influence Wound
Healing
Lathyrogens
Inhibit the cross linking of collagen bundles
Ex. D-penacillamine
Oxygen Derived Free Radicals
Degrade Hyaluronic acid and collagen
Destroy cell and organelle membranes
Interfere with enzymatic functions
Age
Tensile strength and wound closure rates decrease with age
Factors That Influence Wound
Healing
Infection
Prolongs inflammatory phase, impairs epithiliazation and angiogenesis
Increased collagenolytic activity -> decreased wound strength and contracture
Bacterial counts > 105, b-hemolytic strep
Chemotherapy
Decreases fibroblast production and wound contraction
If started 10-14 days after injury, no significant long term problems, but short term
decreased tensile strength
Radiation
Stasis and occlusion of small blood vessels
Decreased tensile strength and collagen deposition
Systemic Diseases
DM
Glycosylated RBCs  Stiffened RBCs & Increased blood viscosity
Glycosylated WBCs  impaired immune function
Renal Dz
Factors That Influence Wound
Healing
Steroids
Inhibit wound macrophages
Interfere with fibrogenesis, angiogenesis, and wound
contraction
Vitamin A and Anabolic steroids can reverse the effects
Vitamin A
Stimulates collagen deposition and increase wound breaking
strength
Topical Vitamin A has been found to accelerate wound
reepithealization
Factors That Influence Wound
Healing
Vitamin C
Essential 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 E
Large doses inhibit wound healing
Decreased tensile strength
Less collagen accumulation
HOWEVER
Antioxidant 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
Zinc
Deficiency:
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
NSAIDs
Decrease collagen synthesis an average of 45% (ordinary
therapeutic doses)
Dose-dependent effect mediated through prostaglandins
Factors That Influence Wound
Healing
Fibrin-based tissue adhesives
Increase breaking strength, energy absorption, and elasticity in
healing wounds
Adjuncts to Wound Healing
Hydrotherapy
Whirlpool
Pulsed Lavage
Stimulates formation of granulation tissue
Clean non draining wounds with healthy granulation tissue should
NEVER be subjected to hydrotherapy
Water agitation damages fragile cells
Electrostimulation
Imitates the natural electrical current that occurs when skin is
injured
Increases migration of neutrophils and macrophages
Promotes fibroblasts
Increased collagen production and tensile strength
Adjuncts to Wound Healing
Ultrasound Therapy
Electrical 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 Oxygen
Increases 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 Coverage
14 Covered Areas (next slide)
~1/3 of claims are for problems not covered
Medicare Coverage of HBO
(1) Acute carbon monoxide
intoxication
(8) Acute peripheral arterial
insufficiency
(2) Decompression illness
(9) Preparation and preservation
of compromised skin grafts
(3) Gas embolism
(4) Gas gangrene
(5) Acute traumatic peripheral
ischemia
(6) Crush injuries
(7) Progressive necrotizing
infections
(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 Irrigation
Need at least 7psi to flush bacteria out of a wound
High pressure can damage wounds and should be reserved only
for heavily contaminated wounds
Debridement
Most 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
Enzymatic
Naturally occurring enzymes that selectively digest devitalized
tissue
Collagenase (Santyl), Papain-Urea (Accuzyme), etc.
Autolytic
Uses the body’s own enzymes and moisture to breakdown necrotic
tissue
7-10 days under semi occlusive and occlusive dressings
Ineffective in malnourished patients
Biologic
Maggots
Calcium salts and bactericidal peptides
Separate necrotic from living tissue making surgical debridement easier
Wound Care General Principles
Fundamentals of Surgical Wound Closure
Incision 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 Classification
Created to help choose appropriate dressings in wounds healing
by secondary intention
Treat worse colors first
Black -> Yellow -> Red
Dressing Types
Alginates
Wounds with heavy exudates (dry the wound)
Converts in a sodium salt -> hydrophilic gel occlusive
environment
Change when begins to weep exudate
Creams
Opaque, soft solid or thick liquids with a slight drying effect
Wounds with moist weeping lesions
Ointments
Semisolids that melt at body temperature
Aid in rehydration and topical application of drugs
Dressing Types
Foams
Hydrophobic polyurethane sheets with a non absorbent adhesive
occlusive cover (very absorbent and nonadherent)
Absorb environmental water and slow epitheliaztion
Films
Transparent 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
Gauze
Highly permeable to air and allow rapid moisture evaporation
Stick to granulation tissue and damage the wound with
removal
Painful removal
Lint can harbor bacteria
Hydrocolloids
Completely impermeable
Avoid in anaerobic infections
Comfortable and adhere well (good for high-friction areas)
Good at absorbing exudate
Hydrogels
Starch and water polymers in gels, sheets, or impregnated
gauze
Rehydrate wounds (poor for absorbing exudate)
Dressing Types
VAC Dressing
Sub 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 semipermeable 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 therapy
Often 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 Low familial incidence
predilection
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 rate
Excision with early postoperative radiation (~25% reoccurrence rate)
Excision with corticosteroids (50-70% reoccurrence rate)
Pressure- increase collagenase activity
24-30mm 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- intralesional
Decreases 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
Cryotherapy
Found to be helpful in early vascularized lesions
Keloid Treatment
Radiation
Most effective when given post operatively
No 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 Treatments
Antitumor/Immunosuppressive
Agents
5-FU
Reports 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
Bleomycin
Limited studies to date suggesting effectiveness
Interferon
Some 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 transference
Free radicals form causing intracellular and molecular damage
Main targets: Cellular and Nuclear Membranes, DNA
Rapidly dividing cells are the most sensitive
Skin, bone marrow, GI
Morbidity
Dose received
Time
Volume of tissue
Type of radiation
Cellular changes
Low dose -> apoptosis
High dose-> direct cellular necrosis
Radiation Injury
Injury with Time
1st 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 Principles
Establish a diagnosis
Rule out malignancy
Determine extent of injury
Often 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 Liquor
Warm 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
Cement
Injuries 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 Phosphorus
Insecticides and Fertilizers
Yellow burn with a garlic-like scent
Tx:
Copious irrigation and neutralization with a dilute Copper Sulfate
solution
Specific Chemical Burns
Chromic Acid
Used in alloy and dye production
Coagulative necrosis
Possible 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 Acid
Rubber, Textile Tanning, Descaling Agent
Causes a systemic acidosis- IV hydration, HCO3, dialysis
Burns treated with irrigation
Hydrofluoric Acid
Industrial 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 year
8,000 are venomous
Majority from Pit Vipers
~15 deaths annually
General Treatment
Incision 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
Neurotoxin
20-30 minutes -> cramps, abdominal pain, restlessness,
perspiration, possible convulsions and shock
Treatment
Calcium 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