Definition

• caused by the contact with heat, flame, chemicals, electricity, radiation and frost bite on the skin and subcutaneous tissue.

Etiology

1. Thermal Burn2. Chemical Burn3. Electrical Burn4. Radiasi Injury5. Frost Bite

Classification of the burn wound

• Caused by:– Flame – Hot water– Chemical (strong acid and strong base)– Radiation– Electricity and lighting

• By the depth of the wound :– 1st degree– 2nd degree – 3rd degree

• By the severity of the wound :– Minor burn wound

• 1st and 2nd degree with <15% area of the wound in adult• 1st and 2nd degree with <10% area of the wound in children• 3rd degree wound with <20% area of the wound• Patient need home care

– Moderate burn wound• 2nd degree with 15-25% area of the wound in adult• 2nd degree with 10-20% area of the wound in children• 3rd degree with <30% area of the wound• Patient needs hospitalization

– Severe burn wound• 2nd degree with >25% area of the wound in adult• 2nd degree with >20% area of the wound in children• 3rd degree with >10% area of the wound• The wound are on the hands, face, eyes, ears, feet,

genital, joint around the armpit• All the patient with the inhalation burn wound

complication with the severe trauma, and high risk burn wound

• Patient needs hospitalization

Traditional Classification

• 1st degree– Epidermis– Erythema (+), pain (+)

sun burn– Bullae (+)

• 2nd degree– Dermis and epidermis– Erythema and moist, but

still elastic– Nerve viable pain (+)

intact proprioseptif

• 3rd degree– All skin layers– Burn dermis, non-elastic– Nerve damage pain (-)

Differences

Depth degree of the burn wound

1st degree 2nd degree / Partial Thickness Burn

2nd degree / Superficial Partial

Thickness Burn

3rd degree / Deep Partial Thickness

Burn

Location Epidermis Epidermis-1/3 dermis

Almost all layer of dermis

Epidermis-dermis-deeper layer (bone

and muscle)

DERMAL-EPIDERMAL JUNCTION

(+) Damage Damage Damage

Color and appearance Red

Red-sometimes pale-edematous &

eksudatif; lepuh

• Pink – white • White yellowish

(thin escar)

Pale or whiterOK eskar, black, or

brown

Pain (+) (+) (+) (-)

Texture Normal Edema (bula) Tebal Leathery

Skin Appendix (hair follicle, gland sweat, sebacea gland)

(+) (+) Sebagian utuh Damage

Duration and healing time

5-7 days without scar 10-14 days +/- scar 25-60 days + thick

scar #

1st degree / superficial 2nd degree / dermis 3red degree

Burn wound

3rd degree burn wound

Burn wound phase

Early phase/ acute / shock After shock end-phase/ post-shock / sub-acute Late phase

•G3 Airway (asupan O2) : inhalation trauma& 3 breathing mechanical

•G3 Breathing because of eskar round on the thorax wall delay the expand movement of thorax or the multiple trauma in thoraxic cavity

•G3 Circulation (O2 distribution) the cells can normally functioning

↓G3 systemic (electrolyte, carbohydrate metabolism,

fat, protein; balance)

•SIRS + MODS because damage of the tissue (epitel, endotel)

•SIRS criteria (min.2) :o Body temperature > 38C or < 36CoHR > 90x/mino RR > 20x/mino PCO2 < 32 mmHgo Leukocytosis > 12.000/mm3o Leukopenia < 4.000/mm3o Leucocyte count N dgn > 10% shift-

to-the-left; patient need to be infected to be SIRS

•MODS : interference of the organ functiong 2 or more (acute) homeotasis cannot be maintained without intervention

•Late epitelization process & complication (hypertrophic scar,contracture, another deformity)

Damage tissue zone

Coagulation/ NECROSIS STASIS HIPEREMIA

•Direct contact•Thermal trauma denaturation protein

•Necrosis (almost sure) immediately after contact

•location : outside or around and direct connection with coagulation zone

•Transformation of vascular endotel, trombocyte, leucocyte, + transformation od capillary permeability, trombosis, and local inflammation response trouble od perfusion (no flow phenomena)

•Damage of the vascular and tearing of the vascular; tromboksan A2 (poten vasoconstrictor) ↑

•Duration : 12-24 hour post-trauma•Healed : Tissue necrosis

•Location : outside of stasis zone

•There are vasodilatation reaction but no cell reaction involved

•Spontaneous healing, or becoming stasis zone or even necrotic zone (wound degradation changing of wound degree become worse)

Rule’s of Nine

Lund & Browder Chart

http://www.medstudentlc.com/uploaded_images/Lund%20Browder%20Rakel.gif

Burn Severity

http://emcrit.org/030-064/056-thermal.burn.htm

Pathophysiology

Burn Wound(high temperature)

Damage of the capillary

Following damage of the

blood cell

Anemia

Increasing permeability

Edema Bullae

Decreasing intravascular volume

Damage of the skin

•Too much evaporation•Too much fluid inflow to the bullae (2nd degree)•Outflow fluid of the burn wound scab (3rd degree)

Loss of fluid

•Be caught on fire in close room•Burn wound on the face

Inhale the gas, smoke, hot steam

Damage of the airway mucose

Larynx oedema

Airway obstruction

Shortness of breath Takipneu Stridor Hoarse Dark sputum

CO/gas poisoning

Stongly band the Hb

Hb can not band the oxygen

Mild Severe

Enervate, confusion, dizzy, nausea, vomit

Come

Pseudomonas aeruginosa infection

Eksotoksin protease

Sign : green color on the cover of burn wound

Non-invasive infection Invasive infection

•Easily loose scab•Much pus

Dry scab + changing od the tissue aound the outer side of scab (normal necrotic)

Increase the degree of the wound

Septic burn wound

Spread by blood

Septic shock

Diagnose :Biopsy & culture of exudate found the germ & invasive germ around the tissue

Langsung Tidak langsungHot

Arachidonate acid activation & kaskade komplemenVascular coagulation

Mediator releasing

Vasoconstriction ↑ capillary permeability

Netrofil migrate to the intertitium

Tissue oedema

Worse perfusion

PATOFISIOLOGI MODS

SYSTEMIC RESPONSE Due to the release of cytokines and other inflammatory mediators at the site of injuryCardiovascular changes

• Capillary permeability ↑ loss of intravascular proteins and fluids into the interstitial compartment

• Peripheral and splanchnic vasoconstriction occurs• Myocardial contractility is << (due to release of TNF-α)• These changes, coupled with fluid loss from the burn wound, result in

systemic hypotension and end organ hypoperfusion hypovolemic shock

Respiratory changes • Inflammatory mediators bronchoconstriction• In severe burns, ARDS can occur

Metabolic changes • BMR ↑ > 3x normal• This, coupled with splanchnic hypoperfusion, necessitates early and

aggressive enteral feeding to decrease catabolism and maintain gut integrity

Immunological changes

• Non-specific down regulation of the immune response occurs, affecting both cell mediated and humoral pathways

Systemic changes PATOPHYSIOLOGI

INFLAMATION & EDEMA

•Mast cell inflamation mediator (histamin, bradikinin, amin vasoaktif, PG, leukotriene, katekolamin, komplemen yg teraktivasi) Artery dan capillary vasodilatation capillary permeability ↑ fluid (and protein) flow to interstisiel tissue edema

•agregation platelet produces serotonin increase pulmonary vascular resistance (direct) & worsening effect of amin vasoaktif (indirect); blockade serotonin > cardiac index, decrease pulmonary artery pulse, decrease O2 consumption after burn wound

•Tromboksan A2 (potent vasoconstrictor) vasokonstriksi & platelet agregation (wound) zone stasis expansion

•Microvasculare changes cardiopulmoner changes (loss of plasma volume, increase perifer vascular resistance, decrease cardiac output)

RENAL•Blood volume & cardic output < renal blood flow & GFR <•mediator (angiotensin, aldosteron, vasopresin) ↓ renal blood flow < oliguria # th/ necrosis of tubuler acute & renal failure

Systemic changes PATOPHYSIOLOGI

GIT

•Mucosa atrofi : apoptosis, vesikulasi mikrovili, damage filamen aktin tissue because decrease blood flow splangnikus circulation

•Absorpsi disruption : decrease glucose & amino acid, decrease fatty acid absorption, brush border lipase activity <; N 48-72 jam after damage

•Permeabilitas intestinal > : increase apoptosis; pd polietilen 3350, laktulosa, manitol expand burn wound; decrease intestine blood flow (5 hours after burn wound)

•Hepar : hipoxemia metabolic disorder, synthesis, & detoxication; decrease [ ] SGOT & SGPT, fosfatase alkali, gamma globulim transferase & bilirubin; shock hipometabolic; circulation back to normal increase hepar activity (metabolic disorder dysfunction >> liver failure

•Stress ulcer/ Curling’s ulcer because stress + hiperasiditas gastric

cardiac

•Hipoxia & hipoxemia myocardial ischemic•GIT ischemic stimulate release inflamation mediator (cytokines, TNF-α), free radical, & myocardial depresant factor (MDF) OK neutrophile recruitment > decrease heart activity

Muscular system•Hipoxia degradation glycoprotein of muscle mass activate urea cycle NO (vasodilator) > tissue damage (muscular system)

IMMUNE SYSTEM•Macrofag production < (48-72 hours after burn wound) : Elaborate spontaneous negatif regulator myeloid (+ endotoxin & G-CSF atau inhibisi PGE2 therapy)

•Netrofil < (48-72 hours after burn wound) : def aktivity p47-phox after stimulate inflammation & mechanical damage that relates response motil netrofil

•Limfosit B & T < : polarization IL-2 & INF cytokine according to TH1 response TH2 (IL4 &-10 production)

•Activity disorder of CD8+ : increase risk of infection (function & virus); early burn excision increase T sitotoksik cell activity

HIPOMETABOLISME /early phase

•Hipovolemia, BP < curah jantung <, body temperature <, O2 consumption <; duration: a few minute - 48-72 hour pasca trauma

HIPERMETABOLISME/FLOW PHASE

(tachycardia, cardiac output >, elevated energy expenditure, O2 consumption >, proteolisis & lipolisis, loss nitrogen)

•Katekolamin : increase the availability of glucose via glukoneogenesis & glikogenolisis hepatik = the availability of fatty acid via lipolisis perifer

direct : via adrenergik -α & -β receptor (hepatocyte & lipocyte)indirect : via stimulate adrenergik receptor endocrine tissue (pancreas) increase release glucose

•Glucocortikoid : neural stimulate hypothalamus-pituitary-adrenal axis

•Glucagon : increase glucose hepatik production & lipolisis perifer via catecolamin stimulate indirect (receptor α)

•cortisol : induction insulin resistance •catecolamin + glucagon & cortisol increase glucose release inflammation cell

Changes Hipovolemic Diuretic

mechanism impact Mechanism impact

Extracellular fluid

Vasculare interstitial

Hemoconcentration, edema burn wound

Interstitial vascular

Hemodilution

Renal function Decrease blood flow to renal

Oliguria Increase renal blood flow

Diuresis

Sodium level Na+ is absorbed by the renal, but the loss of Na+ and smothered by exudate in liquid edema

Sodium deficit loss Na+ caused by diuresis (back to normal after 1 week)

Sodium deficit

Potassium level Damage tissue release K+, decrease excretion because decrease renal function

Hipercalemi K+ move back into the cell, K+ wasted through diuresis (4-5 days after burn wound).

Hipocalemia

Changes Hipovolemic Diuretic

mechanism impact mechanism impact

protein level Protein loss into tissue due to increase in permeability

Hipoproteinemia The ongoing loss of protein catabolism

Hipoproteinemia

nitrogen balance Catabolism tissue, loss of protein in tissue, a lot more to loss than input

Negative nitrogen balance

Catabolism tissue, loss of protein in tissue, immobility.

Negative nitrogen balance

Acid-base balance

Anaerob metabolic an increase of acid end products, renal function↓, serum bicarbonate loss

Metabolic acidosis

Loss of sodium bicarbonate through diuresis, hipermetabolic, increase end products

Metabolic acidosis

Changes Hipovolemic Diuretic

mechanism impact mechanism impact

Stress response

trauma, increase cortison production

Decrease renal blood flow

Occur due to the nature of the injury lasts along time and threatened personal psychology

Stress caused by wound

Eritrocyte Occur due to heat broke

Anemia Does not happen on first day

Hemoconcentrate

gastric Gastric ulcus, bleeding, pain

Stimulation of hipothalamus and increase cortison

Dilatation acute and gut paralysis

Increase cortison

cardiac MDF ↑ 2x toxic glicoprotein produced by burn wound

Cardiac disfunction

↑ MDF (miokard depresant factor) -26 unit, septic shock

Decrease CO

Emergency Burn Trauma

1. Electric Burn Wound2. Burn Wound with Inhalation Trauma3. Chemical Burn Wound4. Burn Wound with Preganancy

Electrical BurnsCellular Damage Due To Electrical CurrentHigh vs. Low Tension Injuries

AC & DC

• High-voltage direct current (DC) :– single muscle spasm often throwing the victim

from the source a shorter duration of exposure but the likelihood of traumatic blunt injury.

• Alternating current (AC):– 3x > dangerous than DC (same voltage)– continuous muscle contraction, or tetany occurs

when the muscle fibers are stimulated at 40-110x/ second

http://ehs.okstate.edu/modules/electric/Emergency.htm

http://www.uic.edu/labs/lightninginjury/treatment.html

Electrical Burns - Acute Care

A - Airway B - Breathing C - Circulation D - Disability E - Expose The Patient

Managementafter Injury

Managementafter Injury

Compication

http://www.uic.edu/labs/lightninginjury/treatment.html

Lightening Injuries

Pathofisiology

– Primary Survey– Assess Injury

• History (Other Trauma, Cardiac Arrest)• Physical Exam (Include Thorough Neurologic Exam)

– Maintain Airway– Cardiac Monitoring

• ECG On Admission• Continuous Cardiac Monitor For 24 Hours

Management Lightening Injury

– Resuscitation• Increased Fluid Requirements Due To Underlying

Muscle Damage• Foley Catheter• Analyze Urine For Myoglobin

– Maintenance Of Peripheral Circulation• Frequent Monitoring• Decompress With Escharotomy Or Fasciotomy

Complication• Low Voltage Common

– Usually Minimal Cutaneous Injury– No Muscle Damage

• Injuries To Oral Commissure– Look Worse Than They Really Are– No Immediate Debridement– Watch For Delayed Bleed With Eschar Separation

Chemical Burn Trauma

• First Aid :– Remove clothing– Flush with cold water– The exception, if exposed to water :

• HCL acid : give NaOH soapy water• Fenol or phosfor : disolve with oil

Complication1. Shock (Loss of liquid)2. Sepsis / toxication3. Acute renal failure4. Pneumonia

PROGNOSA :• Depending on the degrees of burn• Depending on the surface of area• Affected area perineum, armpit, neck and hand • age and patient healthy

Burn and pregnancy

wound 60 % / > spontaneous termination of pregnancyManagement:1. Immediately perform the stabilization of airway. Hipoksia can

occur to mother and fetus2. Hipoksia breathing distress uterus vascular resistent, < uterus

blood flow fetus oksigen3. Fetus monitoring4. Consulting with the obstretic and ginecologComplication 1., Hipoksia with fluid and electrolyte disorder

Termination of pregnancy due to hipotension2. Premature birth3. The death of fetus intrauterine

MANAGEMENT

PrehospitalA. History

• Time of incident• Open/ close area• Etiology fire, hot water,

chemical, explosion.• Duration of exposure• Toxic substance : sianida

plastic• Mechanism of trauma:

vehicle, drop, jump• Amount of IV fluids that be

given

Prehospital

B. PERAWATAN DITEMPAT•Move the patient from the incident place•Check if the trauma threaten to death•Clear the wound with the water•Bandage with sterile dry gauze•Give Oxygen and protect the airway• Immediately transport to hospital

Primary Survey

Airway and breathingwatch if there stridor (snoring), hoarse, black sputum, breathing failure, burnt nostrils hair, face oedem.

Burn wound around oropharinx and neck need intubation (apply the airway tube to trachea/ rod throat) to keep the adequate airway and open.

Circulationo should do assessment of the state of the fluid.o Make sure the burn area for the calculation of the fluid.o Given by IV if the area of the burn wound >10%. If less give the

fluid through the mouth. o The IV fluid is Crystaloid (ringer laktat, NaCl 0,9%/normal Saline).

Crystaloid with dekstrose (sugar) for baby with the burn wound.

Penatalaksanaan

Hospitalization Indication

1. 2nd degree > 15% in adult and > 10% in children.

2. 2nd degree on the face, hand, feet and perineum.

3. 3rd degree > 2 % in adult and every 3rd degree burn wound in children.

4. Burn wound with vicera trauma, bone and airway.

5. Burn wound on the eyes

6. Inhalation trauma

Management Description

Wound treatment • Pencucian luka dengan larutan detergen encer • Kulit compang camping dibuang• Bila luka utuh > 5 cm cairan dihisap, < 5 cm dibiarkan• Luka dikeringkan, diolesi mercurochrom atau Silver Sulfa Diazine (SSD)• Perawatan terbuka atau tertutup dengan balutan• Pasien dipindahkan ke ruang steril

Perawatan di ruangan • Perawatan terbuka dengan krim SSD obat yang dapat menembus eskar• Mandi 2x sehari dengan air mengalir• Eskarotomi dilakukan bila ada penakanan saraf/ pembuluh darah• Eskarotomi di ruanagan lain bila eskar mulai melunak• “Skin Graft” dilakukan setelah mulai ada granulasi

Antibiotics • AB pilihan : cephalosporin generasi I (cefazolin, cephapirin, cephalotin), generasi III (ceftazidim) • Aminoglikosida pseudomonas

Antasida & antipiretik • Untuk pencegahan tukak stres & pada suhu tinggi

Nutrition • 2500 – 3500 calories sehari dengan kadar protein tinggi

Fisioterapi • Latihan pernafasan dan gerakan otot sendi

Fluid Therapy

A. Goal : fix the circulation and presserveB. Indication :

Children: area of 2nd or 3rd degree burn wound ≥ 20 %Adult : area of 2nd or 3rd degree burn wound ≥ 30%

Terapi CairanC. Giving way :

1. Children : first day :- subtitution plasma = bb x % lb x 1 ml- electrolyte/ ringer laktat = bb x %lb x 1 ml- glukose 5% : NaCl 0,9% = 3 : 1 (Insensible Water Loss/IWL)

bb < 10 kg : 100 ml/kgbb 10-20 kg : 50 ml/kgbb

> 20 kg : 20 ml/kgbb

Th next day :- Half each Plasma and electrolyte from the day one.- IWL still given with the same amount.

2. Adult :same with children, but for IWL is given glukose 5% for 2000 ml

Note : • During the first day, ½ amount of fluid has to be given in the first 8

hours, and the rest of it in the next 16 hours.• IWL Subtituiton fluid is given after recovery of peripheral circulation

(urine product > 1 ml/kgbb/hour)• For the next day the liquid divided equally for 24 hours• For children with weight < 15 kg, the maximal amount of fluid is as

muchas calculated of the burn wound 30 %, even though if the area of burn wound > 30 %

• For children with weight > 15 kg and adult, the maximum limit 50 %• If the patient arrives too late, give fluid as the accordance with the

way of overcoming shock.• for monitoring, apply dauer catheter to measure the urine

production.

Fluid Resuscitation

Intra Cellular Fluid Extra Cellular Fluid

40% 15% 5% Dextrose 5%

RLNaCl 0,9%

KoloidProtein plasmaBlood

Formula The first 24 hour fluid

Crystalloid at the second 24 hour

Colloid at the second 24 hour

Parkland RL 4 ml / kg / %LB 20-60% estimate plasma volume

monitoring urine output 30 ml/ hour

Evans (Yowler, 2000)

Saline fluid 1 ml/kg/%LB, 2000 ml D5W*, and colloid 1 ml/ kg / %LB

50% fluid volume at the first 24 hour + 2000 ml D5W

50% fluid volume at the first 24 hour

Slater (Yowler, 2000)

RL 2 L/24 hours + fresh frozen plasma 75 ml/kg/24 hour

Brooke (Yowler, 2000)

RL 1.5 ml / kg / %LB, colloid 0.5 ml / kg/ %LB, and 2000 ml D5W

50% fluid volume at the first 24 hour + 2000 ml D5W

50% fluid volume at the first 24 hour

Modified Brooke RL 2 ml / kg / %LB

MetroHealth (Cleveland)

RL + 50 mEq sodium bicarbonate per liter, 4 ml / kg / %LB

½ Saline solution , monitor urine output

1 U fresh frozen plasma for each littre from ½ solution of saline + D5W for hipoglycemy.

Monafo hypertonic Demling

250 mEq/L saline monitor urine output 30 ml/hour, dextran 40 in saline solution 2 ml/kg/hour for 8 hours, RL monitor urine output 30 ml/hour, and fresh frozen plasma 0.5 ml/hour for 18 hours begin 8 hours after burning.

1/3 Saline solution, monitor urine output.

Formula Evans-Brooke

Formula Evans Forrnula Brooke

1ml/kgBB/ %LB colloid (blood)lml/kgBB / %LB saline solution(electrolyte)2000ml glucoseMonitor :

Diuresis (>50 ml/hour)

0.5ml/ kgBB/ %LB colloid (blood)1.5ml/kgBB/ %LB saline solution(electrolyte)2000ml glucoseMonitor : Diuresis (30-50 ml/hour)

Nutrition level

• Drink given to the burn wound patient :– Immediately as soon as the peristaltic become normal– 25 ml/kgBB/day– Until the minimal urine production 30 ml/jam

• Feeding by oral:– Immediately as soon as the patient can drink normally– 2500 calories/day– Contain 100-150 gr protein/day

• Additional nutrition given everyday:– Vitamin A, B, and D– Vitamin C 500 mg– Fe sulfat 500 mg– antasida

Death causes on burn wound

1. Shock hipovolemic (fluid body disorder) Neurogenic2. Airway failure

• Inhale hot air oedema larynx, laryngospasm asphyxia

3. CO toxic4. Ulcus curling5. Infection Pseudomonas, sepsis, pneumonia6. Acute renal failure

• Dehidration hemoconsentration glomerulus vascularisation disorder renal ischemic irreversible

• damage of the renal tubules myoglobin cumulation (massive muscle necrosis) and hemoglobin pigmen (hemolisis eritrocyte)