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Luka dan

Penanganannya
Definisi Luka

 Terputusnya kontinuitas jaringan tubuh


(Mansjoer,2000)
 Suatu gangguan dari kondisi normal pada
kulit (Taylor,1997)
 Kerusakan kontinuitas kulit,mukosa
membran dan tulang atau organ tubuh lain
(Kozier,1995)
Gambar anatomi Kulit

Frolich, Human Anatomy, Skin


Epidermis—a stratified epithelium

Frolich, Human Anatomy, Skin


Frolich, Human Anatomy, Skin
 Ketika luka timbul → efek yang muncul :
- Hilangnya seluruh atau sebagian fungsi
organ
- Respon stress simpatis
- Perdarahan dan Pembekuan darah
Wound Type
 Etiology : Trauma, Infection, Vascularisation
disorders, Neoplasm
 Time ; Acute and chronic
 Based on contamination grade : Clean
Wound, Clean-contamined Wounds,
Contamined Wounds, Dirty or Infected
Wounds
Phases of Wound Healing
 Hemostasis and Inflammation
 Proliferation
 Matrix Synthesis
 Maturation and Remodeling
 Epithelialization
 Contraction
Hemostasis and Inflammation
 Hemostasis releases chemotactic factors from
the wound site initiating inflammation
 Wounded tissue directly exposes the ECM to
platelets ->plt aggregation, degranulation,
activation of coagulation cascade
 Plt α granules – PDGF, TGF-β, PAF,
fibronectin, serotonin
Inflammation
 Fibrin clot- assists influx of PMNs/monocytes
 PMNs-1st to arrive, peak 24-48h,
  vasc permeability, chemoattractants (IL-1, TNF-α, TGF-β)
 Phagocytosis of bacteria/debris
 Secrete TNF-α which  angiogenesis & collagen synthesis
 Release proteases/collagenases which degrade
matrix/ground substance in early wound healing
 May delay epithelial closure
Inflammation
 Macrophages – peak 48-96h
 Phagocytosis, reactive oxygen species
 Wound debridement via collegenase, elastase
 Regulate cell proliferation, matrix synth,
angiogenesis (via TGF-β, VEGF, IGF, EGF)
Proliferation
 Days 4-12
 PDGF recruits fibroblasts which proliferate
 Assist in matrix/collagen synthesis and
remodeling
 Endothelial cells proliferate
 Migrate from nearby intact venules

 Angiogenesis of capillaries

 Regulated by cytokines/GFs (VEGF, TNF-α, TGF-β)


Maturation and Remodeling

 Wound strength depends upon the quality/quantitiy of deposited


collagen
 Early matrix – fibronectin and collagen type III
 Fibroplastic phase – reorganization of collagen
 Collagenolysis by collagenase a matrix metaloproteinase (MMPs)

 Second matrix – glycosaminoglycans/proteoglycans


 Final matrix – collagen type I
 Deposited over several wks, but tensile strength increases over mos

 Remodeling 6- 12 wks, Synth > lysis


 resulting scar is an acellular ECM
 Mechanical strength never reaches preinjury levels
Epithelialization
 Day 1 – proliferation and migration of epith
cells adjacent to wound
 Stimulated by ↓ contact inhibition, ECM
exposure, cytokines
 Marginal basal cells lose their dermal
attachment, enlarge, flatten, and migrate
across the matrix (leapfrog) to cover the
defect
 Fixed marginal basal cells undergo rapid
mitosis
 Once covered, epith cells become more
columnar, increase mitotic activity and
reestablish the layered epithelium
 Eventual keratinization
Wound Contraction
 All wounds contract
 Myofibroblasts contain α-smooth muscle
actin in thick bundles called stress fibers
 May be responsible for contraction
 Increases from day 7-21, fades after 4 wks
Classification of Healing
 Primary Intention
 Secondary
 Tertiary
Primary Intention
Wound is clean and sutured closed
Secondary
 Wound remains open to heal by granulation
tissue formation and scar retraction
 Chosen for bacterial contamination or tissue
loss
Tertiary
 Delayed primary closure after a few days of
open wound healing
Delayed Healing

 Normal healing – continual increase in mechanical


integrity/strength over time with an eventual
plateau
 Delayed – decrease in rate with eventual
achievement of normal plateau
 Nutritional deficiencies, infection, severe trauma

 Impaired/Chronic – failure to achieve normal


mechanical integrity/wound strength
 Immunocompromised, diabetes, chronic steroid
use, xrt damage
Anamnesis
 Lokasi ?
 Durasi ?
 Mekanisme injury?
 Nyeri spontan ?
 Nyeri induksi ?
 Nyeri posisional ?
 Manipulasi terhadap luka ?
 Eksudat ?
 Odor ?
 Riwayat radiasi, trauma ?
Pemeriksaan fisik
 Lokasi
 Warna
 Odor
 Fibrin
 Nekrosis
 Pembentukan sinus
 Ekspose jaringan
Penilaian suatu luka :
 Ins : jumlah, tipe, bentuk, kulit sekitar, corpus
alienum, tepi luka, jembatan jaringan,
perdarahan aktif, jaringan nekrotik,
pus
 Pal : Koordinat luka, ukuran luka, indurasi,
dasar luka, konsistensi
Regio plantar pedis dextra
 I : Tampak luka 1 buah,
laserasi, memanjang,
warna spt kulit sekitar,
corpus alienum (+)
berupa pasir, tepi luka
ireguler, jembatan
jaringan (+),
pendarahan aktif (-),
pus (-)
 Pal : luka 1 buah 4 cm
inferior dari maleolus
medialis, 3 cm anterior
dari calcaneus; uk 3 x1
x1 cm, dasar subkutis,
indurasi (-), konsistensi
kenyal
Pemeriksaan Penunjang
 Non Invasif : Termografi, Roentgenogram,
bone scan, MRI, USG Doppler, Vibration
testing, tes keringat

 Invasif : Arteriografi, Venografi,


limfangiografi, biopsi kultur, kultur swab,
Konduksi saraf, elektromiografi
Diagnosis
 Tipe Luka
 Lokasi
 Derajat
 Penyebab
 Snake bite gr I r/
pedis dekstra
 Vulnus sclopetorum r/
femur dekstra e.c
senapan angin
Rencana Awal terapi
 Informed consent
 Wound toilet
 Hecting
 Debridement
Prinsip penyembuhan luka

Non bedah
Pembedahan
Fase penyembuhan Jahit primer
luka
Mekanisme Skin graft
penyembuhan luka
Flap lokal
Wound toilet
Flap jauh
Wound dressing Free flap

Repair support
Growth Factor Therapy
• PDGF-BB is FDA approved for treatment of
diabetic foot ulcers
– Recombinant human GF in a gel suspension
– Increases healing, decreases healing time
Dressings
• Mimics epithelial barrier, protection of site
• Compression provides hemostasis, decreases edema
• Occlusion controls hydration and allows for
oxygenation/gaseous diffusion
• Occlusion stimulates collagen synth and epith cell
migration
• Primary- directly on wound
• Secondary- placed on a primary dressing
PENJAHITAN LUKA
• Dasar penjahitan luka :
Gentle handling
Tajam
Tidak boleh tegang
Siap alat
PERAWATAN SESUDAH OPERASI

• DARAH SEPUTAR LUKA DIBERSIHKAN DENGAN


LARUTAN STERIL/ SALIN
• LUKA DIKERINGKAN DENGAN TAMPON
• PENUTUPAN LUKA
• OBSERVASI LUKA DAN PASIEN
• PENCEGAHAN MUTILASI SENDIRI (LUKA DIGIGIT)
• PENGAMBILAN JAHITAN
MONITORING POST OPERASI

• AMATI :
EKSUDAT : PURULEN -INFEKSI
ERITHEMA : TAMBAH BANYAK/ SEDIKIT
EDEMA : BERAT/ TIDAK
HEMATOMA : TAMBAH BANYAK/ SEDIKIT
RASA SAKIT : ADA/ TIDAK-PARAH/TIDAK
BAU : TIDAK BERBAU ATAU BERBAU
MANAJEMEN LUKA SEKUNDER
• PENUTUPAN LUKA :
ABSORPSI EKSUDAT
ANALGESIA
PROTEKSI LUKA
PENCEGAHAN INFEKSI
MEMACU KESEMBUHAN
• PRYMARY LAYER (MATERIAL YG DITEMPATKAN
LANGSUNG PD LUKA)
• TREATMENT TOPIKAL : SALEP SULFADIAZIN
• SECONDARY LAYER : MEMPERKUAT YANG-1
• TERTIARY LAYER : MENCEGAH MUTILASI, BIASANYA
BERSIFAT ELASTIS
• Menggunakan
Hyperbarik oksigen 100%
Oksigen
Therapy dengan tekanan
2.4 ATM

Support
repair
• Menggunakan
Vacuum alat berupa
Assisted
Closure vacum dengan
Therapy memberikan
tekanan negative
Terapi Hyperbaric ↑ tekanan atm =2.4
Oksigen dan ATM dan
memberikan
Vacuum Therapy tekanan negatif

Meningkatkan
gradien konsentrasi Hb menjadi
oksigen jenuh  darah
hiperoksigenasi • Hemostatis
melebur o2 • Menghilangkan
agen infeksius
• Respon inflamasi
• ↑ matrik jaringan
fibroblast proliferasi + sintesis ikat
kolagen
• Angiogenesis
Stimulasi growth Factor
↑ intracellular leukosit
• Menutup luka
Hyperbarik Oxygen Therapy
(HBOT)
Radiation
Crush
tissue
Injury
damage

Keracunan Thermal
CO2 burn

Necrosing
Emboli
gas Indikasi soft tissue
infection
Hyperbaric
Oxygen
Therapy

Dengan memberikan oksigen 100% via masker dan


peningkatan tekanan atm = 2.4 ATM selama 60-90 menit
Vaccum Assisted
Closure Therapy

Dengan memberikan tekanan negative sebesar -125


sampai dengan -75 mmHg.
Bisa dilakukan secara konstan atau intermiten
selama 15 menit.
Potong
dressing
seukuran luka

Tempelkan busa
dg ditutup
membran
adesive
transparan

•Ujung pipa distal


dihubungkan dg
vacum

Setelah vacum
dihidupkan udara
akan terhisap
keluar.
TERIMA KASIH

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