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LUKA BAKAR
COMBUSTIO
PENGERTIAN
Tanda-tanda umum :
1. Syok, akibat kegagalan sirkulasi perifer ditandai penurunan
tekanan darah, nadi kecil dan cepat, keringat dingin, lemah,
penurunan kesadaran
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
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
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
Moderate 15 – 25 % < 10 % -
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
Blood Inflammation
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
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 :
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
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
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
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
Failure of resuscitation :
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
Fluid resuscitation :
Resiko utama adalah gagal ginjal k kerusakan produksi
otot-ototnya (muscles product)
Tujuan :
Mempertahankan urine output : 50 – 75 ml/hr.
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.
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