Definition

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

Etiology
1. Thermal Burn 2. Chemical Burn 3. Electrical Burn 4. Radiasi Injury 5. 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 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

Moderate burn wound

 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 (+)

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

2nd degree
Dermis and epidermis Erythema and moist, but still elastic Nerve viable pain (+) intact proprioseptif

Depth degree of the burn wound Differences 1st degree 2nd degree / Partial Thickness Burn 2nd degree / Superficial Partial Thickness Burn 3rd degree / Deep Partial Thickness Burn Epidermis-dermisdeeper layer (bone and muscle)

Location

Epidermis

Epidermis-1/3 dermis

Almost all layer of dermis

DERMALEPIDERMAL JUNCTION Color and appearance Pain Texture Skin Appendix (hair follicle, gland sweat, sebacea gland) Duration and healing time

(+)

Damage

Damage

Damage

Red

Red-sometimes pale-edematous & eksudatif; lepuh (+) Edema (bula)

Pink white White yellowish (thin escar) (+) Tebal

Pale or whiter OK eskar, black, or brown (-) Leathery

(+) Normal

(+)

(+)

Sebagian utuh

Damage

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 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) After shock end-phase/ post-shock / sub-acute SIRS + MODS because damage of the tissue (epitel, endotel) SIRS criteria (min.2) : o Body temperature > 38C or < 36C o HR > 90x/min o RR > 20x/min o PCO2 < 32 mmHg o Leukocytosis > 12.000/mm3 o Leukopenia < 4.000/mm3 o Leucocyte count N dgn > 10% shiftto-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 phase Late epitelization process & complication (hypertrophic scar,contracture, another deformity)

Damage tissue zone Coagulation/ NECROSIS

Direct contact Thermal trauma denaturation protein Necrosis (almost sure) immediately after contact

STASIS
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

HIPEREMIA
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)

Rules 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 Damage of the skin Increasing permeability Too much evaporation Too much fluid inflow to the bullae (2nd degree) Outflow fluid of the burn wound scab (3rd degree)

Following damage of the blood cell

Edema

Bullae

Anemia

Decreasing intravascular volume Loss of fluid

Be caught on fire in close room Burn wound on the face CO/gas poisoning Inhale the gas, smoke, hot steam

Stongly band the Hb

Damage of the airway mucose

Hb can not band the oxygen

Larynx oedema Mild Airway obstruction Enervate, confusion, dizzy, nausea, vomit Severe

Come

Shortness of breath

Takipneu

Stridor

Hoarse

Dark sputum

Pseudomonas aeruginosa infection Eksotoksin protease Sign : green color on the cover of burn wound

Non-invasive infection

Invasive infection Dry scab + changing od the tissue aound the outer side of scab (normal necrotic) Increase the degree of the wound

Easily loose scab Much pus

Septic burn wound Diagnose : Biopsy & culture of exudate found the germ & invasive germ around the tissue Spread by blood Septic shock

Langsung

Hot
Tidak langsung

Vascular coagulation

Arachidonate acid activation & kaskade komplemen 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 injury Cardiovascular 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-) These changes, coupled with fluid loss from the burn wound, result in systemic hypotension and end organ hypoperfusion hypovolemic shock Inflammatory mediators bronchoconstriction In severe burns, ARDS can occur BMR > 3x normal This, coupled with splanchnic hypoperfusion, necessitates early and aggressive enteral feeding to decrease catabolism and maintain gut integrity Non-specific down regulation of the immune response occurs, affecting both cell mediated and humoral pathways

Respiratory changes

Metabolic changes

Immunological changes

Systemic changes

PATOPHYSIOLOGI 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); INFLAMATION blockade serotonin > cardiac index, decrease pulmonary artery pulse, & EDEMA 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/ Curlings ulcer because stress + hiperasiditas gastric
Hipoxia & hipoxemia myocardial ischemic GIT ischemic stimulate release inflamation mediator (cytokines, TNF-), free radical, & myocardial depresant factor (MDF) OK neutrophile recruitment > decrease heart activity Hipoxia degradation glycoprotein of muscle mass activate urea cycle NO (vasodilator) > tissue damage (muscular system)

cardiac

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

Katekolamin : increase the availability of glucose via glukoneogenesis & glikogenolisis hepatik = the availability of fatty acid via lipolisis HIPERMETABOLISME/ perifer FLOW PHASE direct : via adrenergik - & - receptor (hepatocyte & lipocyte) indirect : via stimulate adrenergik receptor endocrine tissue (tachycardia, cardiac (pancreas) increase release glucose output >, elevated Glucocortikoid : neural stimulate hypothalamus-pituitary-adrenal energy expenditure, axis O2 consumption >, Glucagon : increase glucose hepatik production & lipolisis perifer via proteolisis & lipolisis, catecolamin stimulate indirect (receptor ) loss nitrogen) cortisol : induction insulin resistance catecolamin + glucagon & cortisol increase glucose release inflammation cell

Changes

Hipovolemic mechanism impact Hemoconcentrati on, edema burn wound Oliguria Sodium deficit

Diuretic Mechanism Interstitial vascular Increase renal blood flow impact Hemodilution

Extracellular fluid Renal function Sodium level

Vasculare interstitial Decrease blood flow to renal Na+ is absorbed by the renal, but the loss of Na+ and smothered by exudate in liquid edema Damage tissue release K+, decrease excretion because decrease renal function

Diuresis

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

Potassium level

Hipercalemi

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

Hipocalemia

Changes

Hipovolemic mechanism impact Hipoproteinemia mechanism

Diuretic impact Hipoproteinemia

protein level

Protein loss into tissue due to increase in permeability

The ongoing loss of protein catabolism Catabolism tissue, loss of protein in tissue, immobility. Loss of sodium bicarbonate through diuresis, hipermetabolic, increase end products

nitrogen balance

Catabolism Negative tissue, loss of nitrogen balance protein in tissue, a lot more to loss than input Anaerob metabolic an increase of acid end products, renal function, serum bicarbonate loss Metabolic acidosis

Negative nitrogen balance

Acid-base balance

Metabolic acidosis

Changes

Hipovolemic mechanism impact Decrease renal blood flow mechanism

Diuretic impact Stress caused by wound

Stress response

trauma, increase cortison production

Occur due to the nature of the injury lasts along time and threatened personal psychology Does not happen on first day

Eritrocyte

Occur due to heat broke

Anemia

Hemoconcentrat e

gastric

Gastric ulcus, bleeding, pain

Stimulation of hipothalamus and increase cortison

Cardiac disfunction

Dilatation acute and gut paralysis

Increase cortison

cardiac

MDF 2x toxic glicoprotein produced by burn wound

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

Emergency Burn Trauma

1. Electric Burn Wound 2. Burn Wound with Inhalation Trauma 3. Chemical Burn Wound 4. Burn Wound with Preganancy

Electrical Burns
Cellular Damage Due To Electrical Current High 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

Management after Injury

Management after Injury

Compication

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

Lightening Injuries

Pathofisiology

Management Lightening Injury

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

 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

Complication 1. Shock (Loss of liquid) 2. Sepsis / toxication 3. Acute renal failure 4. 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 pregnancy Management: 1. Immediately perform the stabilization of airway. Hipoksia can occur to mother and fetus 2. Hipoksia breathing distress uterus vascular resistent, < uterus blood flow fetus oksigen 3. Fetus monitoring 4. Consulting with the obstretic and ginecolog Complication 1., Hipoksia with fluid and electrolyte disorder Termination of pregnancy due to hipotension 2. Premature birth 3. The death of fetus intrauterine

MANAGEMENT

Prehospital
A. 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 breathing
watch 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.

Circulation
o 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 Wound treatment

Description 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 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

Perawatan di ruangan

Antibiotics

AB pilihan : cephalosporin generasi I (cefazolin, cephapirin, cephalotin), generasi III (ceftazidim) Aminoglikosida pseudomonas
Untuk pencegahan tukak stres & pada suhu tinggi 2500 3500 calories sehari dengan kadar protein tinggi Latihan pernafasan dan gerakan otot sendi

Antasida & antipiretik Nutrition Fisioterapi

Fluid Therapy
A. Goal : fix the circulation and presserve B. Indication : Children: area of 2nd or 3rd degree burn wound 20 % Adult : area of 2nd or 3rd degree burn wound 30%

Terapi Cairan
C. 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, 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
40%

Extra Cellular Fluid

15% 5% Dextrose 5% RL NaCl 0,9% Koloid Protein plasma Blood

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 monitoring urine plasma volume output 30 ml/ hour 50% fluid volume at the first 24 hour + 2000 ml D5W 50% fluid volume at the first 24 hour

Evans (Yowler, Saline fluid 1 2000) ml/kg/%LB, 2000 ml D5W*, and colloid 1 ml/ kg / %LB Slater (Yowler, RL 2 L/24 hours + 2000) 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 Saline solution , monitor urine output 1 U fresh frozen plasma for each littre from solution of saline + D5W for hipoglycemy.

Monafo hypertonic Demling

250 mEq/L 1/3 Saline saline monitor solution, monitor urine output 30 urine output. 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.

Formula Evans-Brooke
Formula Evans
1ml/kgBB/ %LB colloid (blood) lml/kgBB / %LB saline solution (electrolyte) 2000ml glucose Monitor : Diuresis (>50 ml/hour)

Forrnula Brooke
0.5ml/ kgBB/ %LB colloid (blood) 1.5ml/kgBB/ %LB saline solution (electrolyte) 2000ml glucose Monitor : 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) Neurogenic 2. Airway failure
Inhale hot air oedema larynx, laryngospasm asphyxia

3. 4. 5. 6.

CO toxic Ulcus curling Infection Pseudomonas, sepsis, pneumonia 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)