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COMBUSTIO/BURN/

LUKA BAKAR
COMBUSTIO
PENGERTIAN

 Vulnera/Luka adalah terjadinya gangguan kontinuitas suatu


jaringan sehingga terjadi pemisahan jaringan yang semula
normal

 Combustio/luka bakar adalah bentuk luka yang disebabkan oleh


trauma termis (bahan kimia, api, air panas dan aliran listrik0 yang
menimbulkan efek panas terhadap kulit, darah dan pembuluh
darah serta terhadap matabolisme secara umum.

 Secara umum luka terbagi manjadi dua, yaitu 1) Simplek, bila


hanya melibatkan kulut, 2) komplikatum, bila melibatkan kulit dan
jaringan di bawahnya.
TANDA-TANDA LUKA

Tanda-tanda umum :
1. Syok, akibat kegagalan sirkulasi perifer ditandai penurunan
tekanan darah, nadi kecil dan cepat, keringat dingin, lemah,
penurunan kesadaran

2. Syndroma remuk, terjadi akibat benyaknya daerah yang


hancur, misalnya otot-otot pada daerah luka sehingga
mioglobin turut hancur dan menumpuk di ginjal yang
mengakibatkan lower nephron nephrosis, ditandai urine
berwarna merah, oliguria hingga anuria, peningkatan ureum.
Tanda-tanda lokal :
 Rasa nyeri, akibat lesi pada sistem saraf

 Perdarahan
a. Perdarahan parenkimatosa, yang berasal dari dari
kapiler, tidak berbahaya kecuali organ-organ vital.
b. Perdarahan venosa, perdarahan yang berasal
dari
vena, tidak begitu berbahaya, kecuali pada
daerah
yang banyak mengandung varices.
c. Perdarahan arterial, perdarahan yang berasal dari
arteri
FAKTOR-FAKTOR YANG MEMPENGARUHI
PENANGANAN LUKA
 Lamanya luka
Rerata golden period luka adalah 6 jam, khusus pada daerah
dengan vaskularisasi baik (wajah, kepala) golden periodnya 8
jam. Tidak berlaku untuk luka kotor.
 Bentuk anatomi luka
luas, ada tidaknya under mining pada luka.
 Kebersihan luka
Luka kotor harussegera dibersihkan, ada tiaknya corpus alineum.
 Lokalisasi luka
Luka daerah thoraks, abdomen serta daerah yang mudah
digerakkan akan semakin sulit untuk disembuhkan
FASE LUKA BAKAR

 Fase awal, fase akut, fase syok


terjadi ganguan keseimbangan sirkulasi cairan dan elektrolit.
 Fase syok telah berakhir
akibat luka terbuka timbul berbagai masalah antara lain;
1. proses inflamasi
2. infeksi yang dapat menyebabkan sepsis
3. proeses penguapan cairan tubuh disertai panas atau energi
 Fase lanjut
Cedera luka bakar

Tek. Hidrostatika kapilker Respon Stress


Kerusakan kapiler

Permeabilitas kapiler Epineprin & norepineprin

Kehilangan plasma &


protein ke intertisial
Vasokosntriksi selektif
odema

tek. onkotik
Hemokonsentrasi
Tahanan perifer
Penurunan volume
darah Tek hidrostatik >
Tek onkotik
Afterload jantung
Curah jantung Odema umum
Sikap mental
positif kesehatan
Hygiene
baik

Istirahat &
Nutrisi
Latihan

Balutan f. Penyem
pengetahuan
sesuai buhan luka

Kontrol
usia
infeksi

inkontinensia nyeri
Penanganan
tepat
F. Psikologis
Takut, stress Kesehatan
Hygiene
Kurang baik

Kurang
Nutrisi
mobilisasi

Merokok f. Pengham Kondisi


Alkoholr bat luka langsung

Sirkulasi
usia
Kurang baik

Obat
nyeri
tertentu Penanganan
Tdk tepat
KLASIFIKASI KEDALAMAN LUKA BAKAR

 Derajat I
hanya mengenai epidermis dengan karakteristik : merah terang
sampai merah, edema minimal, tidak ada lepuh/never blisters, not
calculated in burn extent
 Derajat II
mengenai seluruh epidermis-dermis : kemerahan, lepuh, pink, moist,
painful, white, dry, less sensation
 Derajat III
sampai sub kutan (total epidermis dan dermis) warna bervariasi dari
putih-merah, coklat atau hitam, leathery, various colours
 Derajat IV
ADULT BURN CLASSIFICATION

BURN PARTIAL FULL TICKNESS OTHER FACTORS


INJURY TICKNESS (DERAJAT III)
( DERAJAT
II)
Minor < 15 % <2% -

Moderate 15 – 25 % < 10 % -

Major > 25 % > 10 %  face, ears, eyes and


perineum
 inhalation injury,

electrical injury and


high risk patient
EXTENT OF BURN

 RULE OF NINE
1. Head and neck ……………… 9 %
2. Anterior trunk ………………..18 %
3. Posterior trunk ……………….18 %
4. Arms …………………… 2 X 9 %
5. Foots ………………….. 2 x 18 %
6. Perineum/genetalia ………….. 1 %
PASIEN YANG BERESIKO

 Lansia ---- resiko terjadi infeksi sangat tinggi

 Pasien dengan gangguan kardiovaskuler, paru-paru


dan ginjal ---- prognosisnya buruk

 Pasien dengan DM ---- penyembuhannya buruk/sulit


LOKASI LUKA BAKAR
 Muka dan leher ---- observasi pernapasan
mekaniknya

 Tangan, kaki, dan sendi ---- self care deficit

 Telinga, hidung dan daerah dengan poor blood


supply ---- potensial terjadi infeksi

 Genetalia & buttocks ---- potensial terjadi infeksi


WARNA DASAR LUKA

 Red – Yellow – Black / RYB

 Kemudahan sistem yang


diperkenalkan adalah
bersifat konsisten dan
mudah dimengerti serta
tepat guna dalam pemilihan
balutan
CAIRAN LUKA

Blood Inflammation

Chronic wound fluid Product of infection


Penanganan luka bakar
 Bersihkan luka dengan cairan savlon 1 % dan cukur rambut tumbuh
pada daerah luka bakar wajah, aksila, pubis dll.
 Lakukan nekrotomi atau debridemen jaringan nekrosis

 Lakukan escharotomy jaringan luka bakar melingkar dan eschar


menekan pembuluh darah
 Bula dibiarkan uth sampai hari ke 5 post op luka bakar

 Mandikan pasien tiap hari jika mungkin

 Jika banyak pus bersihkan dengan isodin cleaner

 Perhatikan ekspresi wajah dan KU pasien selama merawat luka.

 Bilas dengan savlon 1 % mengunaka cairan NaCl 0,9 %

 Keringkan dengan mengunakan kassa steril

 Beri salep silver Sulfadiansin setebal 0,5 cm pada seluruh luka bakar
(keculai wajah bila derajat III) dan jika luka bakar derajat I/II beri salep
antibiotika
 Tutup dengan kassa steril atau biarkan terbuka dengan cradle bed
PANDUAN IV LINE UNTUK LUKA BAKAR
 Terapi cairan untuk pasien LB > 20 %
- Cairan cristaloid : Rl, NaCl, D5W
- Cairan Coloid : Albumin, dextran

 Formula baxter :
4 ml RL/kgBB/% luas LB
- ½ total cairannya diberikan dalam 8 jam I
- ¼ total cairannya diberikan dalam 8 jam II
- ¼ total cairannya diberikan dalam 8 jam III

 Coloid bila 20 – 60 % dari voluma plasma

 D5W bila untuk mengembalikan kehilangan dari evaporasi.


STADIUM LUKA
BURN DEPTH

1ST DEGREE : epidermis 2nd DEGREE : epidermis and part of dermis


•SUPERFICIAL
•DEEP
skin appendages : sweat gland, sebacea
gland, hair follicle.

3rd DEGREE : epidermis and all dermis, could


reach deeper structure (muscle, bone)
1st degree 2nd degree 2nd degree deep 3rd degree
superficial

Sunburn Scald, fire Fire, electric Fire, electric,


chemical

Erythema, wet Erythema, wet Redness, mottled Charred black


Painful Blister pink and white brown or white,
Painful appearance, wet leathery
Blister (ESCHAR), dry
Painless thrombosed
vessels
No pain

Epithelization in 5 Epithelization in Granulates, Granulates


– 7 days 10 – 14 days scarring in 2 – 3
months

Scald : air mendidih, mottled : burik, leathery : kulit,


1st degree
2nd degree (superficial)
2nd degree (superficial)
2nd degree (deep)
2nd degree (deep)
3rd degree
3rd degree
BURN SIZE

Rules of nine For children and neonates


BURN SIZE

Lund Browder
PATHOPHYSIOLOGY

 Localeffect
 Systemic effect
LOCAL EFFECT

JACKSON (1947) :
 Zone of necrosis

 Zone of stasis

 Zone of hyperemia
SYSTEMIC EFFECT

1. Burn edema
 Superficial burn :
 Maksimal : setelah 12 jam, 90 % terjadi dalam 4 jam
 Peningakatan perfusi ke daerah injury
 Resorpsi : mullai 4 jam hingga 4 hari.

 Deep burns :
 Difference :
 Kerusakan vaskular kulit dan lymphatic plexus.
 Peningkatan kompliance intertisial jaringan ke ECF guna
penghancuran matrik molekul extracellular
 Free oxygen radicals from leukocytes : prolonged changes in
capillary permeability.
 The rate of tissue edema peaks later (maximal at 18 hours).
 Resorption is much delayed because of damage to the lymphatics.
2. Interstitial edema
Fluid mechanics of edema :

Starling Equation : Q = Kf (Pcap – Pi) +  (p - i)

 Increased hydraulic conductivity (Kf)


 Increased capillary hydrostatic pressure (Pcap)
 Reduced interstitial fluid hydrostatic pressure (Pi)
 Reduced reflection coefficient for the plasma proteins ()
 Reduced colloid osmotic pressure of plasma (p)
 Increased colloid osmotic pressure of interstitial fluid (i )
3. Intracellular edema :

 Response to a burn injury :“cellular shock” in burns greater than 30% TBSA.
 Systemic disturbances of sodium-potassium-ATPase pump in burned tissue
and unburned tissue
 Reduction in the transmembrane electrical potential (N:-90mV; become -
60mV : cell death).
 Marked increase in the intracellular sodium.
 Endothelial cells : swelling, become more spherical : the contracting
contiguous surfaces tend to pull away from adjacent surfaces of other
endothelial cells : openings between the cells : macromolecules can leak.
4. burn shock
 Fluid shifts into interstitial tissue (interstitial edema).
 Transmembrane decrease : intracellular edema.
 Myocardial depressant factor.
 Acute inflammatory process : production of cytokine : lead to
further tissue destruction, mediator production, and prolonged
changes in capillary permeability.
 Lymphatic transport capability.

Shift : pergeseran
SHOCK THERMALLY INJURED TISSUE

DECREASED SPLANCHNIC
RELEASE OF INFLAMMATORY CYTOKINE
CIRCULATION
: DAMAGE CELLS, NEUTROPHIL : TNF,
INTERLEUKIN
INTESTINAL VILLOUS ATROPHY,
DECREASED BOWEL MUCOSA
INTEGRITY ENTER THE CIRCULATION

BACTERIAL TRANSLOCATION : GI TRACT LUNG KIDNEY HEART


lumen of the gut into portal circulation

MULTIPLE ORGAN
SEPSIS
DYSFUNCTION (MOD) / SYSTEMIC INFLAMMATORY
FAILURE (MOF) RESPONSE SYNDROME (SIRS)
5. Inhalation injury
 Inhalation of noxious gas.

 Upper airway :
 Heat injury : absorbed by tongue and oropharynx.
 Rapid tissue swelling : narrowing.
 Tissue damage : denatured protein : release of histamine and other
vasoactive cytokines.

 Lower airway :
 Inhalation of heated vapors with a higher heat capacity.
 Toxins and particulate debris : induce rapid local vasodilation and
necrosis of the ciliated epithelial cell layer.
 Complete airway occlusion in medium and small-caliber airways :
 Protein-rich fluid leaks through the denuded mucosa.
 Necrotic slough of dead cellular components.
 Acute and chronic inflammatory cells.
EXAMINATION OF THE
PATIENT
HISTORY

 Etiology
 Time
 Suspicion of inhalation injury : closed area, loss of
consciousness ?
 Treatment to the wound
 Clothing material
 Age
 Underlying disease
 Another trauma : fall from
PHYSICAL EXAMINATION

 General examination : ABCD


 Inhalation injury
 Local examination :
 Burn size
 Burn depth
 Location : face, hand, external genitalia
 Circumferential burn : chest, extremity
 Electric : entry and exit wound
 Peripheral insufficiency due to eschar or compartment
syndrome
OTHER EXAMINATION

 Laboratory :
 Haemoglobin, haematocrit, leucocyte, trombocyte
 Urine examination
 Ureum, creatinin, SGOT, SGPT, blood glucose
 Blood gas analysis
 Chest X-ray
TREATMENT
AIRWAY

 Inhalation injury ?
 Burn in closed area
 Agitation, confused, loss of consciousness (hypoxia)
 Burn on face (nose, mouth)
 Singed eyebrow or nasal hair
 Carbonaceous sputum
 Oropharynx : edema, hyperemia, blister
 Hoarseness, stridor

Insertion of ETT atau tracheostomy


AIRWAY
AIRWAY
AIRWAY
BREATHING

Disturbance of ventilation
due to circumferential eschar
in chest

Eskarotomi
CIRCULATION
 Insertion of venous line, folley catether

 Resuscitation method :
 Amount : Baxter, actual fluid volume given should be titrated
to the physiologic response (urine output).
.
Jumlah cairan = 4 x luas luka bakar x BB (kg)
 ½ in the 1st 8 hours, the remaining in the next 16 hours.
 Lactat Ringer

 End point : urine output ? CVP ?


 Hypertonic saline (HTS = 7.5% NaCl) :
 Efficient intravascular volume resuscitation.
 Potential for expanding circulating volume by reabsorption
of fluid from the interstitial space.
 Significant modulation of SIRS secondary to reperfusion
injury.
 Colloid (Albumin, FFP, Dextran, HaES)
 Preservation of plasma osmotic pressure.
 More efficient plasma volume expansion.
 Decreased tissue and pulmonary edema.
 Bacterial translocation :
 Early enteral nutrition : prevent villi atrophy.
 High dose vitamin C
 Inotropic support
CIRCULATION

 Failure of resuscitation :

All resuscitation formulas are nothing more


than initial guidelines

 Inaccurate estimation of burn size.


 Undiagnosed inhalation injury.
 Frequently receive overly-aggressive resuscitation before arrival at
the burn center.
 Circumferential tourniquet-like eschar and/or compartment
syndromes.
 Cardiac dysfunction.
 Refractory shock.
WOUND TREATMENT

 Aspirasi adanya bulla/blister.


 Cuci luka dengan sabun, air keran (tap water).
 Dressing : moist dressing (NaCL 0,9%); outer layer : dry.
 Berikan Antimicrobial topikal.
 Anticontracture splint, night splint.
 Escharotomy : inflexible (kejur, keras) and circumferential
eschar (chest, extremity) :
 Mencegah gerakan dinding dada

 Impairment of distal tissue perfusion in extremity.


 Lakukan Debridemant pada jaringan yang mengalami
nekrosis
 Topical antibiotic dressings.
 Aggressive attempts (usaha) at wound closure
ESCHAROTOMY LINE
ESCHAROTOMY
ANTICONTRACTURE
FACIAL SCARRING AND NECK
CONTRACTURE
CONTRACTURE OF THE EXTREMITY
CONTRACTURE OF THE NECK
SKIN GRAFTING
SKIN GRAFTING OF THE FACE
ELECTRIC BURN

 UK : 3% of patients admitted to burn center;


2/3 : low voltage.

 Low voltage (< 1000 volts) : flash, direct contact

 High voltage (> 1000 volts) : flash, “true” high


tension (direct contact or arc (busar))

 vessels – nerve – muscle – bone – skin

 Entry wound

 Exit wound
ELECTRIC BURN
 Mechanism :
 Direct contact
 Arching (lengkungan)
 Flash

 Tissue damage :
 Voltage
 Current
 Resistance of tissue
 Area of contact
 Pathway of flow through the body

 Electroporation :
 Breakdown of cell membrane.
ELECTRIC BURN

ENTRY WOUND EXIT WOUND


ELECTRIC BURN
ELECTRIC BURN

 Fluid resuscitation :
 Resiko utama adalah gagal ginjal k kerusakan produksi
otot-ototnya (muscles product)

 Tujuan :
 Mempertahankan urine output : 50 – 75 ml/hr.

 Maintain clear myoglobin and haemoglobin from the


renal tubules; 100 ml/hr in the presence
myoglobinuria.
 Mannitol or hypertonic saline or high-volume infusions of
Ringer’s lactate.

 Monitor dengan EKG


ELECTRIC BURN

Fasciotomy
 Relieve (membebaskan)
pressure intracompartment
 5P:
 Pain

 Pallor

 Pulseless

 Parese

 paresthesia
FASCIOTOMY
SUMMARY
 Burn injury :
 Trauma yang menghancurkan (Devastating trauma).
 Mengganggu kondisi local and systemic
 Nyeri hebat dan psychologic impact.
 burn edema, burn shock, SIRS
 Diagnosis :
 Severity : burn size, depth, location, age, other trauma, previous disease.
 Inhalation injury.
 Management :
 ABCD
 Resuscitation : method only guidelines.
 Local treatment to prevent pain, deformity, and contracture.
THANK YOU