Burn and electrical injury

8/7/2019 Burn and electrical injury

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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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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


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.

Burn and electrical injury

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