PENYEMBUHAN LUKA,

PRINSIP PERAWATAN LUKA

KOLEGIUM BEDAH
INDONESIA
 Introduction
Normal healing of acute skin wound :
- through 4 distinct, but overlapping phases

mann, RF , Evans, MC , WOUND HEALING: AN OVERVIEW OF ACUTE, FIBROTIC AND DELAYED

s in Bioscience 9, 283-289, January 1, 2004
 INFLAMMATORY PHASE
( lag phase or substrate phase ) 0-48 hrs
Clinical signs:
Rubor , Calor, Tumor, Dolor, Functio
Laesa
PROLIFERATIVE PHASE
(Fibroplasia phase) day 2 - ~
6 weeks
Clinical signs:
Disappearance of inflammatory signs,
Reduction of swelling,
Reduction of wound size (contraction),
itching

Key-elements:
Net collagen synthesis,
Increase in wound tensile strength,
Scar formation
PROLIFERATIVE PHASE
Wound Contraction
 “ Wounds heal from side to side but
contract from end to end ”
 Highest rate of contraction from days
10-21

Collagen Deposition
MATURATION AND RE-
MODELLING PHASE
3 weeks to 1-2 years
Type III collagen is replaced by type I collagen,
Duration of phase dependent upon :
patient age (decreased age - increased duration),
racial differences,
type of wound, body location
duration of inflammatory phase

Collagenases act to resorb necessary fibers

that have been deposited randomly - initially
collagen deposition = collagen resorption, but
eventually resorption is greater than deposition
WOUND HEALING
SUMMARIZED
A clot forms
Inflammatory cells debride injured tissue
during the inflammatory phase
Proliferative phase :
Epithelialization, fibroplasia & angiogenesis
Granulation tissue forms.
The wound begin to contract
Maturation phase :
Collagen forms tight cross links to other
collagen & with protein molecules  ↗ tensile
strength of the scar
Initial Insults :

1. Trauma
2. Surgery
3. Burn
4. Severe arterial insufficiency
5. Edema with venous insufficiency
6. Prolonged pressure
7. Intermittent trauma without protective
sensation &
poor perfusion
 WOUND HEALING &
PROBLEM
Most wounds heal through a normal healing
sequences,
regulated by integrated actions of chemokines,
cytokines, growth factors & proteases

Some develop into problem wounds :

- fail to heal normally
- undergo deterioration

Non healing chronic wounds utilize ± 80%

national ( USA ) health expenditure
Smith AP.S., Etiology Of The Problem Wound
in Sheffield PJ, Fife CE, Wound Care Practice, 2nd ed, 2007
 CHRONIC WOUND
Etiology Fail to heal :
1. Infection / inflammation
2. Recurrent trauma
3.Inadequate O2 & blood supply
4. Underlying chronic diseases
5. Inadequate medical care :
- socio-economic or psychosocial limitations
Chronic Wound :
- Arrest to heal
- Failure to progress normally over a 30 day
period

Smith AP.S., Etiology Of The Problem Wound

in Sheffield PJ, Fife CE, Wound Care Practice, 2nd ed, 2007
 ETIOLOGY OF PROBLEM
WOUND :
ONE GLITCH SAMPLER
Oxygen & Glucose Control Socio-economical
Perfusion Issues
Nutrition & Lipid Control Autoimmune
Hydration Disease
Edema Control Infection/Inflamm Medications
ation
Trauma Psycho-social
( Repetitive ) Issues
Chronicity Look a Likes
( Misdiagnosed/
Undiagnosed )
Smith AP.S., Etiology Of TheHematological
Problem Everyday Care
Wound
abnormality
in Sheffield PJ, Fife CE, Wound Care
WOUND ASSESSMENT :
COMMON TERMS
 Exudate :
material composed of serum, fibrin & WBC that escape from blood
vessels into superficial lession / inflammation area
 Necrosis :
- death of living tissue
 Slough :
- dead tissue that has separate from living tissue
 Fistula :
- abnormal tract from an abscess or hollow organ to body surface
 Sinus tract :
- elongated path from a focus of suppuration to the surface,
that often discharge pus
 Tunneling :
- tissue destruction underlying intact skin
Final Pathways to Wound Healing
Failure

Infection Malperfusion Cellular

Trauma
Hypoxia Failure

Synergy

PROBLEM
WOUND

( Warriner, 2003)
 Local Factors Affecting
Wound Healing

Infection Malperfusion Cellular Trauma

Colonization Hypoxia Failure Pressure
Foreign body Ishemia, Edema Inflammation,
Deformity
Invasive infection Radiation Injury, Local toxins,
Scarring Local malignancy,
Topical steroids,
Synergy Foreign body, Vasculitis,
Dermatological abnormalities

NONHEALIN
G
Warriner, 2003) WOUND
 Systemic Factors Affecting
Wound Healing

Infection Malperfusion Cellular

Trauma
Immune disorders Hypoxia
Failure Tobacco use, Diabetes,
Nutrition,
Vascular disease, Hereditary, Renal failure,
Arterial, Venous Alcohol use, Malignancy,
Connective tissue disease,
Synergy Drug effects
NONHEALIN
G
WOUND ( Warriner, 2003)
Identify Final Identify Co-Morbidities Identify Wound
Common Pathways Diagnosis
to Non Healing
• Infection • Diabetes mellitus • Diabetic ulcer
• Malperfusion and/or •End stage renal disease, • Arterial insufficiency
hypoxia dialysis ulcer
• Cellular failure •Cardiac disease, congestive • Venous leg ulcer
• Unrelieved pressure, heart failure • Pressure ulcer
repetitive trauma •Chronic arterial insufficiency • Surgical wound
(secondary) dehiscence, failing
•Smoking flap or graft
•Pulmonary disease
• Progressive soft
• Vasculitis (secondary),
tissue infection,
Reynaud’s, other collagen
vascular disease osteomyelitis
•Wound contamination • Laceration, acute,
continence traumatic injury,
•Mobillity impairment, crush injury
cerebral vascular accident, • Burn
spinal cord injury, other • Abrasion, skin tear
musculoskeletal deformity • Contact dermatitis
3 Components of the •Steroid therapy, other
chemotherapy
• Dermatological
condition, rash
Initial •Distant malignancy
•Malnutrition
• Vasculitis ulcer
• Radiation wound
Problem Wound •Psychosocial issue • Stoma wound
Setting Key Therapeutic
Goals

Not all of the steps of evaluation are

required for every wound & wound patient
Identify nature of the wound
 more focused evaluation
Identify final common pathway components
of wound healing failure & co-morbidities

 Effective Treatment Plan

KEY THERAPEUTIC GOALS
Resolution of infection Enhancement of
Enhancement of nutrition
perfusion Exudate control
Resolution of edema
Odor control
Relief of pressure
Ambulatory off-loading
Pain control
Mechanical Preservation of
stabilization function
Enhancement of tissue Patient/caregiver
growth education
Patient compliance
MONITORING THE RESPONSE TO
TREATMENT
Regular, periodic wound assessment :
- by any trained healthcare provider
- periodic reevaluation by the physician
Determined by :
• nature & seriousness of the wound
• condition of the patient
• early respons to treatment
Completeness or otherwise of wound
healing depends upon :
Reparative abilities of the tissue

Type of damage
Local
Factors
Extent of damage

General state of health Systemic

Factors
Ideal Local Conditions
Prasetyono TOH. General concept of wound healing: revisited.
Med J Indones.2009; 19(.)

Tissue is viable No Foreign Bodies

Normal Healing Process

Free From Excessive Bacterial Contamination

Types of Wound Healing
1. Primary intention

2. Secondary intention

3. Tertiary intention
Primary intention
involves epidermis and dermis without total
penetration of dermis healing by process of
epithelialization
When wound edges are brought together so that
they are adjacent to each other (re-approximated)
Minimizes scarring
Most surgical wounds heal by primary intention
healing
Wound closure is performed with sutures (stitches),
staples, or adhesive tape
Examples: well-repaired lacerations,well reduced
bone fractures,healing after flap surgery
Secondary intention
The wound is allowed to granulate
Surgeon may pack the wound with a gauze or
use a drainage system
Granulation results in a broader scar
Healing process can be slow due to presence
of drainage from infection
Wound care must be performed daily to
encourage wound debris removal to allow for
granulation tissue formation
Examples:gingivectomy,gingivoplasty,tooth
extraction sockets, poorly reduced fractures.
Tertiary intention
(Delayed primary closure or secondary
suture):
The wound is initially cleaned, debrided
and observed, typically 4 or 5 days before
closure.
The wound is purposely left open
Examples:healing of wounds by use of
tissue grafts.
GENERAL PRINCIPLES OF
WOUND CARE
Local Bioburden Management / Infection
Control
Wound Debridement
Surgical / sharp debridement
Mechanical Debridement
Chemical or Enzymatic Debridement
Autolytic Debridement
Concept of Wound Bed
Preparation
Debridement of nonviable tissue and
denatured extracellular matrix (ECM),

Control of bacterial burden and

inflammation,

Establishing optimal moisture balance,

Stimulation of epidermal cell migration at

the wound edge.
Wound Bed Preparation
Aim :
 Optimal Wound Healing
Environment :
Well vascularized Wound Bed
Stable Wound Bed
Minimal Exudate

Structured & Systematic Approach :

Removal of Barriers
Wound Problems =
Barriers

1. Necrotic tissue  Debridement

2. Bacterial Infection  Bacterial Load

Management

3. Exudate  Moisture Control

1. Wound Debridement

Wound debridement is the cornerstone

of treament for acute & chronic wound

Types of debridement :
Surgical / sharp debridement
Mechanical Debridement
Chemical or Enzymatic Debridement
Autolytic Debridement
Surgical Debridement
Sharp debridement uses a scalpel, scissor or
other instrument to cut devitalized tissue

The fast & most efficient method

The preffered method in rapidly developing

inflammation of the body’s connective tissue
& general infection ( Sepsis )

Carried out by physician :

 Bedsite or in Operating theatre
Surgical Debridement :
General Consideration
Bedside Operating theatre
Minor sized, Deep
Superficial General anasthesia
No anasthesia or
Good lightning for
Local anasthesia
best assessment &
Control of hemostatic
evaluation
< Control of
Effectiveness < hemostatic >
Low cost Effectiveness >
High cost
Mechanical Debridement
Saline-moistened dressing is allowed to dry
overnight and adhere to the dead tissue.
As the dressing is removed, the devitalized
tissue is pulled away.

One of the oldest methods of debridement.

Painful since the dressing adhered to non-vital

as well as vital tissue.

Not selective: good and bad tissue

 an unacceptable debridement method for
clean
wounds where a new layer of healing cells is
already developing.
 Vapor Gauze

Scab
Exudate Epidermis
Dry dead skin
Dermis

Fat

Gauze Epithelial cell

Detaching Detached with
Gauze
dressing
Epithelial cell
Moving below
dry skin
Chemical Debridement
 The use of certain enzymes and other compounds
to dissolve necrotic tissue.
 More selective than mechanical debridement.
 The body makes its own enzyme, collagenase, to
break down collagen, one of the major building
blocks of skin.
 A pharmaceutical version of collagenase is highly
effective as a debridement agent.
 The area first is flushed with saline.
Any crust of dead tissue is etched in a cross-
hatched pattern to allow the enzyme to penetrate.
 Moist dressing is then placed over the wound.
Enzymatic Debridemen

Traditional Collagenase :

- Bromelain : nanas
- Papain : papaya
- Maggots
Maggots Therapy
Autolytic Debridement
Autolytic debridement takes advantage of the
body's own ability to dissolve dead tissue.
The key to the technique is keeping the
wound moist,
which can be accomplished with a variety of
dressings. These dressings help to trap wound
fluid that contains growth factors, enzymes, and
immune cells that promote wound healing.
Autolytic debridement is more selective than
any other debridement method, takes the
longest time to work.
Inappropriate for wounds that have become
infected.
2. Bacterial Load
Management
Antibiotic ?
Antiseptic ?
Bacterial burden in the wound bed (Melhuish 1994)

Systemic
antibiotics and
local antimicrobial
No antimicrobial treatment - Local
treatment
standard MWH antimicrobial
treatment

No host reaction Observed

Bacterial count
Critically colonised
Contaminated Colonised Infected

Bacterial count rising = signs of

infection increase
3. Moisture Control
• Moist wound healing is twice as fast as
dry wound healing
1962 Winter - on pigs

1963 Hinman and Maibach confirmed

Winter's work on human beings.

 Waterpro Contaminants
of
Waterproof Contaminants
Modern Dressing

Moist
Moist
Environment
Environment

WOUND HEALING’S
CONCEPT
TYPES OF WOUNDS &
COLOUR’S SYMBOLS
Necrotic tissue
Black

Slough
Yellow

Infection
Green

Granulation
Red

Epithelialization
Pink
INDICATIONS OF MODERN
DRESSINGS
Kinds & Properties of Wound Dressing
e Choice of Wound Dressings
Scab Necrosis Granulation Epithelialization
Formation
Red → Black Yellow Red Pink
Degree I

Degree II

Degree III

Degree IV

Hydrocolloid, Thin Polyurethane Foam

Polyurethane Film
Alginate, Polymer Bead, Cavity Filler
Hydrogel
Polyurethane
Foam
Product Information

(N=Normal)
Tipis,
Semi permeable
polyurethane film
Mencegah kontaminasi
bakteri
Menjaga kelembaban luka
Protective Layer

Absorptive Layer
Polyurethane foam
Daya Absorbsi tinggi
Mampu menampung eksudat secara
optimal
Product Information

Indikasi
Untuk penyembuhan luka basah/ normal (luka
gores, luka trauma, luka bernanah akut &kronik,
luka borok, leg ulcer, luka diabetes, luka bedah,
luka bakar tingkat I & II, luka ganas )

Penggunaan
1x pakai, dapat di potong sesuai ukuran luka
Product Information

(B=Based)

Absorptive Layer
Polyurethane foam
Daya Absorbsi tinggi
Mampu menampung eksudat
secara optimal
Product Information

Indikasi
Untuk penyembuhan luka sangat basah/ parah (luka bernanah kronis &
akut, luka borok, leg ulcer, luka diabetes, luka ganas, luka bakar
tingkat III)

Penggunaan
1x pakai, dapat di potong sesuai ukuran
Product Information

(F=Film)

Low allergetic
Waterproof
Mudah digunakan

Adhesive Film
Layer

Protective Film
Absorptive Layer
Tipis, Layer
Semi permeable polyurethane film Polyurethane foam
Mencegah kontaminasi bakteri Daya Absorbsi tinggi
Menjaga kelembaban luka Mampu menampung eksudat secara
optimal
Product Information

Indikasi
Untuk penyembuhan luka dengan luas luka kecil & ringan

Penggunaan
1x pakai , langsung ditempel pada luka.
 TERIMA KASIH

56