PENYEMBUHAN LUKA, PRINSIP

PERAWATAN LUKA

KOLEGIUM BEDAH INDONESIA

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

Diegelmann, RF , Evans, MC , WOUND HEALING: AN OVERVIEW OF ACUTE, FIBROTIC AND DELAYED HEALING ,
Frontiers 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 & Perfusion Glucose Control Socio-economical Issues

Nutrition & Hydration Lipid Control Autoimmune Disease

Edema Control Infection/Inflammation Medications

Trauma ( Repetitive ) Psycho-social Issues

Chronicity Look a Likes

( Misdiagnosed/
Undiagnosed )
Hematological Everyday Care
abnormality
Smith AP.S., Etiology Of The Problem Wound
in Sheffield PJ, Fife CE, Wound Care Practice, 2nd ed, 2007 Rheumatologic Diseases
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

NONHEALING
WOUND
Warriner, 2003)
 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

NONHEALING
WOUND
( Warriner, 2003)
Identify Final Common
Pathways to Non Healing
• Infection
• Malperfusion and/or hypoxia
• Cellular failure
• Unrelieved pressure, repetitive
trauma
3 Components of the Initial
Problem Wound Evaluation
Identify Co-Morbidities Identify Wound Diagnosis
• Diabetes mellitus • Diabetic ulcer
•End stage renal disease, dialysis • Arterial insufficiency ulcer
•Cardiac disease, congestive heart failure • Venous leg ulcer
•Chronic arterial insufficiency • Pressure ulcer
(secondary) • Surgical wound dehiscence,
•Smoking failing flap or graft
•Pulmonary disease • Progressive soft tissue
• Vasculitis (secondary), Reynaud’s, other infection, osteomyelitis
collagen vascular disease
• Laceration, acute, traumatic
•Wound contamination continence
•Mobillity impairment, cerebral vascular
injury, crush injury
accident, spinal cord injury, other • Burn
musculoskeletal deformity • Abrasion, skin tear
•Steroid therapy, other chemotherapy • Contact dermatitis
•Distant malignancy • Dermatological condition,
•Malnutrition rash
•Psychosocial issue • Vasculitis ulcer
• Radiation wound
• Stoma wound
• Other
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 nutrition
 Enhancement of perfusion  Exudate control
 Resolution of edema  Odor control
 Relief of pressure  Pain control
 Ambulatory off-loading  Preservation of function
 Mechanical stabilization  Patient/caregiver
 Enhancement of tissue education
growth  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, Superficial  Deep
 No anasthesia or  General anasthesia
Local anasthesia  Good lightning for best
assessment & evaluation
 Control of hemostatic <  Control of hemostatic >
 Effectiveness <  Effectiveness >
 Low cost  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 Debridement

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.
 Waterproof Contaminants
Waterproof Contaminants
Modern Dressing

MoistEnvironment
Moist 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
The Choice of Wound Dressings
Scab Formation Necrosis Granulation Epithelialization

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 Layer

Tipis,
Semi permeable polyurethane film
Mencegah kontaminasi bakteri
Menjaga kelembaban luka
Absorptive Layer
Polyurethane foam
Daya Absorbsi tinggi
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

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