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Burn and electrical injury
DR. MINSKY
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Epidemiology
USA
Incidence : 2,200,000/yr
Mortality : 5,500/yr
Admission : 60,000/yr
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Prognostic factor
Total Body Surface Area (TBSA) : Best known predictor
Critical for 2nd degree & 3rd degree burns
Assessed after initial debridement
Age : An independent predictor 2~40 yrs ; LA50 = 70~90 %
70yrs; LA50 = 30%
Inhalation injury : Most consistent factor that determines
survival
Obesity, Alcohol abuse, Neurologic impairment
Preexisting cardiac, liver and lung disease
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Total body surface area (TBSA)
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Criteria for admission / transfer to Burn
Centers
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Pathophysiology
Cause of burn
Thermal
Chemical
Electrical
Radiation
Friction
Scalding
1) Increased temp. kills cells
2) Denatures the surrounding
extracellular
matrix proteins (Zone of
necrosis)
3) Circulation ceases
4) Metabolically active state for a
while
5) Eventually circulation cease
again
6) Cell dies (Zone of stasis)
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Zone of
necrosis
Zone of stasis
Zone of hyperemia
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Pathophysiology(Local response)
Zone of coagulation (necrosis)
Heat Denature protein
Necrotic area
Irreversible change
Zone of hyperemia
Vasodilatation from the
inflammation
Surrounding the burn wound
Clearly viable tissue Healing process
No risk for further necrosis
Zone of stasis
Moderate degree of insult with
decreased tissue perfusion
Survive or go on to
coagulation necrosis (possible reversible),
associated with vascular
damage and vessel leakage
TXA2 present
High concentration - local
inhibitor : improve bloodcirculation
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Pathophysiology(Systemic response)
Systemic response
20% TBSA
Injuredtissue
Vasoactive
mediator
Complement,Coagulationsystem
Thrombosis,Vasodilatorrelease(Histamine,Bradykinin)
Capillary
leak,Interstitialedema
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Pathophysiology(Systemic response)
Systemic response
Interstitial edema, bacterialovergrowth
Proinflammatory cascade,antiinflammatory reaction
Immune dysfuction
Sepsis, Multi organ failure
Inflammatory mediator
Stress hormone
Hypermetabolic response
O2 demand
Skeletal m. catabolism,Immune deficiency, Lipolysis, Bone mineralizatio
n , Linear growth
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Burn depth
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Burn depth
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Healing process
Epidermis Regeneration Source = Keratinocyte stem cells
(The burge region of hair follicles)
Regeneration depends on.
The distance between sources of keratinocytes Depth
Supf. 2nd degree : 10~14 days
Deep 2nd, 3rd degree : months
Intervention Risk of infection (Death)
2nd degree : Topical antibiotic ointment
3rd degree : Deb. & skin graft / Keratinocyte placement
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Compartment syndrome
May happen to Full thickness circumferential burns
Collagen coagulation
leather-like (stretches little)
Tissue edema = Tourniquet effect
Pressure elevation
Necrosis of underlying muscles and nerves
Chest : Ventilation restriction Resp. failure
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Compartment syndrome
Treatment
Escharotomy
Longitudinal incisions of the
burn to relieve constriction
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Abdominal compartment syndrome
Pathophysiology Massive fluid resuscitation
Extreme tissue edema
Intra abdominal pressure
Venous congestion of kidney and gut
Limits thoracic expansion
Resp failure
Urine output
Intra Ab. Organs : ischemia
Diagnosis Bladderpressure > 30 mmHg (by Foley catheter)
Treatment Decompressive laparotomy
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Fluid resuscitation
In burn patients
Systemic inflammation
Leakage of fluid : intravascular space into the interstitium
Decreased perfusion to vital organs
Metabolic acidosis, Oliguria, Relative polycythemia
Hypovolemic shock
Organ failure
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Fluid resuscitation
Colloids : Restoration of
intravascular volume and
oncotic pressure
Leakage of albumin : first 14 ~
16 hours after injury but thenquickly subsides.
Early administration of colloids
may not be useful for
minimizing edema
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Fluid resuscitation
Monitoring
Hourly urine output
Neurologic function
Mean blood pressure
Central venous pressure Serum base deficit
End point
Urine output 0.5~1mL/kg/hr
Maintain
Blood pressure
Urine output Normalize ABGA
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Nutrition
Basal metabolic rate 50% to 100% increase
Glucose production
Insulin resistance
Muscle protein catabolism Adequate nutritional support
Enteral feeding : preferred
Clinical response: best indicator
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All wound eventually heal if left alone unless
there is infection, lack of blood flow(ischemia),
inadequate nutritional intake
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Wound care
Debridement
Healthy bed for the migration of keratinocytes.
Coverage
Moist, antibacterial covering,
Minimize fluid loss, painful stimuli
Maximize skin regeneration
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Wound care Topical dressing
Silver sulfadiazine (Silvadene)
Intermediate wound
penetration
Good antibacterial spectrum :
8~10 hr activity Cx. : Transient leukopenia
switch and restart
Mafenide acetate (Sulfamylon)
E
xcellent escharp
enetration Bacteriostatic action
Cx. : Painful
Dakin solution (0.25% sodium
hypochlorite)
Wet to dry dressing for minor
debridement of the wound
surface, esp. if graft looks
infected
Silver nitrate
Excellent antibacterial
Cx. : discoloration Acticoat;
no discoloration
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Wound care Surgical treatment
Main goals of surgical treatment Debridement of the burn (1day to 3 weeks after injury)
Placement of stable permanent skin coverage
Tangential debridement Cutting the skin tissue at the depth of the dermal and subcutaneouscapillary network
1 cm2 1mL of blood loss
In adults, 1% of TBSA burn , average 100mL of bleeding
Each debridement session : less than 10~20% TBSA for blood losscontrol
Autologous split-thickness skin graft The gold standard for burn wounds if enough donor sites are
available
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Wound care Wound coverage
Permanent coverage
Autologous STSG: BEST!!
Cultured Epidermal Autograft (CEA): debrided full-thickness burnsthat lack of any dermal elements motion, poor function, reopening
Dermal replacement better functional results
prevent extensive scarring
Integra : undenatured bovine collagen and shark chondroitin sulfate,a proteoglycan
long time from excision to final epithelial coverage
Alloderm : freeze-dried human dermis from cadaveric split-thicknessskin
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Complication
Infection Wounds, venous access sites, lungs
>10% TBSA
Tx : re-establish the barrier function of the gut and skin
Do not use prophylactic antibiotics, but empirical antibiotics are used ifinfection is suspected
Gastrointestinal ulcers Mucosal ischemia due to burn injury Curlings Ulcers
>40% TBSA
Tx. : antacids, H2 blockers, enteral feeding
Heterotopic Ossification Calcium deposit in joint restriction of motion
Hypertropic scar : Early skin grafting of deep wounds
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Special injury
Electrical injury
>500 volts
Skin necrosis at the entry points, exit point
Muscle, nerve, bone
Compartment syndrome
Myonecrosis with severe myoglobinemia : ARF
Cardiac injury, fatal arrythmia Monitor for 24hrs at least.
Tar Deep 2nd or 3rd degree burn
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Special injury
Smoke inhalation
Upper airway(supraglottic) : thermal injury by flame or hot gases
Rarely subglottic.
Lower airways & lung parenchyme: inflammation by toxins and
particulate matters in smoke.
Facial burns
Carboxyhemoglobin level, direct laryngoscopy or bronchoscopy
Conservative care
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Reference
Chap. 29 Burn and Electrical Injury. Vol. 1 Mathes PlasticSurgery Second Edition
Adam J. Singer, MD, Department ofEmergency Medicine,
State University of New York at Stony Brook, Stony Brook,NY. : Thermal Burns: Rapid Assessment And Treatment.Emergency Medicine Practice. September. 2000
Dennis P. Orgill, M.D., Ph.D. Division ofPlastic andReconstructive Surgery, Brigham and Women's Hospital,
Boston. : Excision and Skin Grafting of Thermal Burns. N EnglJ Med 2009; 360:893-901February 26, 2009
Tiffany B. Grunwald, M.D.,M.Ed.Warren L. Garner,M.D.LosAngeles, Calif. Plast. Reconstr. Surg.121: 311e, 2008.
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