LUKA (INJURY)

dr. Lauhil Mahfudz, Sp.B

Materi Kuliah Bedah, FK UNAYA
LUKA
TERPUTUSNYA KONTINUITAS JARINGAN LUNAK

Klasifikasi Luka :
• Luka Akut : luka baru, mendadak dan
penyembuhannya sesuai waktu yg diperkirakan :
Luka sayat, luka bakar, luka tusuk, crush injury

• Luka Kronis : luka gagal sembuh pd waktu yg

diperkirakan, tidak berespon baik thd terapi dan
punya tendensi untuk timbul kembali : Ulkus
dekubitus, ulkus diabetik, ulkus varicosum
Luka Akut

Luka Kronis
 Penyebab Luka
• Trauma
• Pembedahan
• Neuropatik
• Gangguan vaskuler
• Penekanan
• Keganasan
 MACAM – MACAM LUKA

I. LUKA TERTUTUP
II. LUKA TERBUKA
 KLASIFIKASI LUKA BARU

1. LUKA BERSIH ASEPTIK (Clean Wound)

2. LUKA BERSIH TERKONTAMINASI (Clean
Contaminated Wound)
3. LUKA INFEKSI (Infected Wound)
4. LUKA KOTOR (Dirty Wound)
 Anatomy & Physiology
• Layers of soft tissue
• Cutaneous layer
• Epidermis
• Dermis
• Subcutaneous layer
• Loose connective tissue
• Fat
• Deep Fascia
• Fibrous tissue
• Supportive & protective
 Anatomy & Physiology
• Functions of Soft Tissue
• Protection from Trauma
• Thermoregulation
• Sensory functions
• Pain, Touch, Temperature
• Protection from infection
• Fluid maintenance
Anatomi Kulit

5/28/2019 Faculty of Medicine - Gadjah Mada University 9

 Anatomy & Physiology
• Skin Tension Lines
• Static Tension
• constant force due to taut skin
• scar formation
• Dynamic Tension
• underlying muscle contraction
• scar formation
Relaxed Skin Lines

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Danger areas

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PENYEMBUHAN LUKA
UPAYA MEMPERBAIKI KERUSAKAN YANG TERJADI

• FASE I HEMOSTASIS, INFLAMASI :

VASOKONSTRIKSI, VASODILATASI, AKUMULASI PMN, FIBRIN,
MAKROFAG

• FASE II PROLIFERASI, FIBROPLASI :

GRANULASI, KOLAGENASI, EPITELIALISASI

• FASE III REMODELLING :

PEMATANGAN PARUT
 Mechanism of Healing

Tissue Injury

Wound
Healing

Tissue Repair Tissue Regeneration

Non Specific Specific

Scar Formation Original Tissue

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 Tissue Repair
Injury 3d 7d 3w 1-2y

Major Even Clot formation Growth factor Collagen deposition Collagen cross-linking
Hemostasis Elaboration
INFLAMMATORY
Repair phase
PROLIFERATION
REMODELING
Fibroblast
Cellular influx Lymphocytes
Macrophages

Vascular Neutrophils
response
Vasoconstriction
Vasodilatation
 Hemorrhagic

Injury

Hypovolemia:
Inadequate flow

Vasoconstriction
In spite of Ischemia Hypoxia
Clotting
formation
 • Fase Hemostasis & Inflamasi
- segera sampai 2-5 hari Platelet
- hemostasis : activation
• vasokonstriksi
• Agregasi platelet EGF
• thromboplastin  clot IGF-1
chemotactic
PDGF
- inflamasi TGF β
• vasodilatasi
• fagositosis recruitment

Neutrophil, macrophage,
Epithelial cells, mast cells
Endothelial cells, fibroblast

Tredget EE, 2002

Hemostasis Inflamasi
• Fase Proliferasi FIBROGENIC GF

- 2 hari sampai 3 minggu PDGF, IGF-1

TGF β, FGF
- granulasi
• Fibroblas sintesis kolagen
• Mengisi defek dan terbentuk kapiler baru
- Kontraksi
• Tarikan tepi luka yang akan mengurangi defek
- epitelialisasi
• Migrasi epitel dari tepi luka
• Fase Remodelling
- 3 minggu sampai 2 tahun
- Kolagen akan meningkatkan tensil strength luka
- Akhir proses terbentuk parut 80% kekuatan
jaringan semula
 Cytokine Cell of Origin Function

PDGF Platelets Cell chemotaxis

Macrophages Mitogenic for fibroblasts
Endothelial cells Stimulates angiogenesis
Stimulates wound contraction

TGF-alpha Macrophages Mitogenic for keratinocytes and fibroblasts

T lymphocytes Stimulates keratinocyte migration
Keratinocytes

TGF-beta Platelets Cell chemotaxis stimulates angiogenesis and fibroplasia

T lymphocytes
Macrophages
Endothelial cells
Keratinocytes

EGF Platelets Mitogenic for keratinocytes and fibroblasts

Macrophages Stimulates keratinocyte migration
Fibroblast Macrophages Chemotactic and mitogenic for fibroblasts and keratinocytes
growth factor Mast cells Stimulates angiogenesis
T lymphocytes
Endothelial cells
Keratinocyte Fibroblasts Stimulates keratinocyte migration, differentiation, and proliferation
growth factor
TNF Macrophages Activates macrophages
Mast cells Mitogenic for fibroblasts
T lymphocytes Stimulates angiogenesis
Interleukin Macrophages IL-1 - Induces fever and adrenocorticotropic hormone release,
(IL)–1, IL-2, IL- Mast cells enhances TNF-alpha and interferon (INF)–gamma, activates
6, and IL-8 Keratinocytes granulocytes and endothelial cells, and stimulates hematopoiesis
Lymphocytes IL-2 - Activates macrophages, T cells, natural killer cells, and
lymphokine-activated killer cells; stimulates differentiation of
activated B cells; stimulates proliferation of activated B and T cells;
and induces fever
IL-6 - Induces fever and enhances release of acute-phase reactants
by the liver
IL-8 - Enhances neutrophil adherence, chemotaxis, and granule
release
INFs (IFN- Lymphocytes Activate macrophages
alpha, -beta, Fibroblasts Inhibit fibroblast proliferation
and -delta)
Thromboxane Destroyed Potent vasoconstrictor
A2 wound cells
Masalah Luka :
• Jaringan nekrotik
• Bakteria
• Eksudat

Kegagalan Luka Sembuh Akibat :

• Hipoksia
• Infeksi
• Udem
• Abnormal metabolik
Factors Affecting Wound Healing
• Anatomic
• Location of the injury
• Skin Tension areas
• Pigmented skin
• Oily skin
Factors Affecting Wound Healing
• Drug Use
• Corticosteroids
• NSAIDs
• Penicillin
• Colchicine (used in gouty arthritis)
• Anticoagulants
• Antineoplastics
Factors Affecting Wound Healing
• Medical Conditions & Diseases
• Advanced age
• Alcoholism
• Acute uremia
• Hepatic failure
• Diabetes mellitus
• Hypoxia
• Severe anemia
• Malnutrition
• CVD & PVD
• Advanced cancer
High Risk Wounds
• Bites
• human
• animal
• Foreign Bodies
• Contaminated with organic matter
• Injection wounds
• Significant devitalized tissue
• Crush injury
• Immunocompromised patients
• Poor peripheral circulation
Factors Leading to Abnormal Scar Formation
• Keloid
• Excessive accumulation o scar tissue beyond original wound borders
• common in darkly pigmented
• common areas
• ears
• extremities
• sternum
Factors Leading to Abnormal Scar Formation
• Hypertrophic scar
• Excessive accumulation of scar tissue within the original wound borders
• Common in areas of high stress
• flexion creases across joints
Factors Leading to Abnormal Scar Formation
• Wounds Requiring Closure
• Cosmetic areas
• face, lip, eyebrow, etc
• Gaping Wounds
• Wounds over tension areas
• Degloving injuries
• Ring injuries
• Skin tearing injuries
Management of lacerations
• Primary intension
• Delayed primary intension

• If the wound is small enough, we can use physiological wound

contraction

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Timing for Wound Closure
• Principle governing: as soon as possible with minimal complication
• Traditional teaching:
• after 6 hours  secondary intention
• before 6 hours  primary intention
• Gradually 6 hours became 8 up to 12 hours

(Preuss, 2000)

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Techniques for Wound Closure
• Suturing

• Tape and adhesive • Staples

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Lack of Tissue
• If the wound is accompanied with skin loss or there is a lack of tissue

• Autograft (STSG / FTSG )

• Flap, if; nerve,tendon, big vessel or bone exposed

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ANATOMI KULIT
Eksisi + graft

Pre Eksisi Post eksisi + graft

Flap
Reconstructive Ladder

Fundamental principle in planning

closure of a defect from simple to
more complex.
(Place, 1997)

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Dressing
Should purpose:
• Protection
• Absorption
• Compression
• Immobilization
• Aesthetics
(Preuss, 2000)

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Soft Tissue Injuries
• Contusion
• epidermis intact
• vessels in dermis are torn
• swelling & pain
• blood accumulation results in ecchymosis
• Hematoma
• collection of blood beneath skin
• larger amount of tissue damage
• larger vessels are damaged
Soft Tissue Injuries
• Abrasion
• superficial injury
• outermost skin damaged by shearing forces
• painful in proportion to degree of injury
• no bleeding or minor bleeding
• contamination is primary concern
Soft Tissue Injuries
• Laceration
• Skin disruption with greater depth than abrasion
• jagged wound ends bleed easily
• may involve other soft tissue injuries
• caused by forceful impact with sharp object
• bleeding may be severe
Soft Tissue Injuries
• Incisions
• Skin disruption with greater depth than abrasion
• similar to laceration except wound ends are smooth and even
• tend to heal better than lacerations
• caused by very sharp objects
Soft Tissue Injuries
• Avulsion
• flap of skin or tissue torn loose or pulled completely off
• avulsed tissue may or may not be viable
• Amputation
• involves extremities or body parts
• jagged skin and/or bone edges at site
• three types
• complete, partial, degloving
Crush Injury & Compartment Syndrome
• Crush Injuries
• caused by a crushing (compressive) force
• may result in organ injury
• often associated with severe fractures
• overlying skin may be intact
• causes
• collapse of structure onto body area
• compressive trauma to body area
• prolonged compression in a chronic situation
Crush Injury & Compartment Syndrome
• Crush Syndrome
• may be painful, swollen, deformed
• little or no external bleeding
• internal bleeding may be severe
• reperfusion phenomenon
• systemic effects occur after the issue is reperfused
• oxygen free radicals result in muscle injury
• high intracellular calcium
Crush Injury & Compartment Syndrome
• Rhabdomyolysis - Pathophysiology
• muscle destroyed
• extracellular fluid moves into muscle cells
• increased H20, NaCl, Calcium
• Fluid from muscle move into extracellular fluid
• Lactic acid
• Myoglobin
• Potassium, Phosphate
• Thromboplastin, Creatine kinase & Creatinine
Crush Injury & Compartment Syndrome
• Rhabdomyolysis - Potential Complications
• Hypovolemia
• Hypocalcemia  Cardiotoxicity
• Hyperkalemia
• Metabolic acidosis
• Hyperuricemia
• Hyperphosphatemia
• Possible DIC
Crush Injury & Compartment Syndrome
• Compartment Syndrome
• local evidence of muscle ischemia
• results from compressive forces in a closed space
• e.g. within fascia
Crush Injury & Compartment Syndrome
• Compartment Syndrome
• Tissue pressure > capillary hydrostatic pressure
• Results in ischemia to muscle
• Muscle cell edema begins
• Prolonged ischemia (>6-8 hrs) leads to tissue hypoxia and cell death
• Direct soft tissue trauma also adds to edema and ischemia
Crush Injury & Compartment Syndrome
• Compartment Syndrome
• Renal failure
• hypovolemia
• renal tubules become obstructed
• nephrotoxic agents present
Crush Injury & Compartment Syndrome
• Compartment Syndrome
• Early signs of crush syndrome
• paralysis and sensory loss to injured area
• rigor of joint distal to the injured muscles
• pain, swelling, sensory changes, weakness
• may have pulses present and warm skin
• Later signs indicating compartment syndrome
• 5 Ps
• pain, paresthesia, pallor, pressure, pulselessness
• some include “polar”
Soft Tissue Injury Management
• General Principles
• Control Bleeding
• Apply Dressing
• Method dependent on location of injury
• Immobilization
• Bandaging
• Antibacterial ointment
• Consider need for further Evaluation
Soft Tissue Injury Management
• Need for Further Evaluation
• Treat and Release
• Treat and Refer
• Treat and Transport
Soft Tissue Injury Management
• Wounds Requiring Transport for Evaluation
• Neural compromise
• Vascular compromise
• Muscular compromise
• Tendon/Ligament compromise
• Heavy contamination or High Risk Wounds
• Cosmetic complications
• Foreign body complications
Soft Tissue Injury Management
• Other Considerations
• Tetanus vaccine
• Caused by Clostridium tetani
• anaerobic bacteria
• Initial vaccine
• Booster
• q 10 years
• q 5 years for high risk persons
• Potential for allergic reaction
Soft Tissue Injury Management
• Other Considerations
• Potential Risk of Infection
• Common complication
• Risk factors
• Microflora common on skin surface
• Source on wound mechanism
• Patient immunocompromised
• Infection Minimization
• minimize contamination
• clean wound soon after injury
• Protect

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