Wound Care Management

By:
dr. Agil Salim Sp. B (k) Trauma FICS, FINACS
Tujuan Covering

Membantu proses penyembuhan luka

pada semua fase (imflamasi/eksudasi,
granulasi, epthelialisasi)
Faktor-faktor yang Berperan
dalam Penyembuhan Luka
1. Eksudat
2. Kelembaban
3. Calcium
4. Absorpsi
5. Bentuk gel
6. Efek anti mikroba
7. Rasa nyaman
8. Ekonomis
9. Covering
10. Aplikasi mudah & tidak allergi
11. Efek autolysis debridement
I. Physiolgy Of Wound Healing
Skin Constitution

Epidermis
Corium of Dermis
Subcutis

The total skin area of adult humans

covers approx. 1 to 2 meters
Skin & Role of Epithelial Cells

Two layers :
1. Dermis
2. Epidermis
Keratin
Lucidum
Granulosum
Spinosum
Basal layer
Basal layers main source of
epithelial cells
 Disruption dermal layers more
effort, energy, & longer time of healing
Wound < 1 cm heal in 1 week
 Basal layer migrate slowly and
shortly
Sources of epithelial cells skin
appendages i.e hair follisle, sweet
glands, and sebaceous glands
Blood

Composition of the Blood

1. Serum
2. Blood cells
a. Erythrocytes
b. Monocytes
c. Eosinophil
d. Lympocytes
e. Platelets
Function of the Blood

Supply of oxygen and nutrients

Transport of endogenous messenger
substances and enzymes
Contains cells of the defence system
Contains componens of the
coagulation system for rapid wound
closure.
Why is it important

Understanding Normal Healing

Enables recognition of
abnormal healing
 Recognition
the phases of healing

Assist w/ planning,
implementation, & evaluation
of wound management
Inflammatory Phase

Starts : immediately to 4 6 days

Goal : removed devitalized tissue &
prevent invasive infection.
Characterized
Vascular
Permeability & secretion
of chemotactic cytokines
 Wound clothing cascade (intrinsic & extrinsic
pathway)
Culminates : fibrin clot/ provisional matric &
hemostasis
Fibrin clot :
Neutrophils
Monocytes
Fibroblast
Endothelial cells
Cytokines
Growth factors
Cytokines & growth factors released by platelest,
thrombin, and fibronectin
 Neutrophil
First responder
Clearing the invading bacteria & cellular debris
Monocytes
48 to 72-96 hours after injury
Phagocytose debris & bacteria
Orchestrated productions of growth factors
extracellulers matrix & angiogenesis
Transition to proliferative phase
Proliferation Phase

Starts : 4 to 14 -21 days after injury

Goals :
Formation of granulation tissue
Composed of new capillary network,
fibrobalst, and macrophages
Closed wound
 Fibroblas Migation
Stimulated by PDGF & EGF from
platelets & Macraphages
Synthesize colagen & prolerate at wound
site
 Epithelialization
Starts immediately
KGF-1, KGF-2, & II-6 keratinocytes
migration to wound area, proliferate &
differentiate in the epidermis.
Characterized by replication & migration
of epithelial cells across the skin edges
Maturation/ remodelling Phase

Starts : 8 to 21 days 1 year

Goal : newly formed epithelial layer
& wound tensile strength.
Characterized : remodelling of
collagen deposit & scar contraction
 Final Phase balancing deposition &
degradation of collagen
Wond Closure

Goal : closed healing wound with

functional and aesthetically
satisfactory scar
Wound closure :
Primary intention
Secondary intention
Teritary intention
Primary Wound Healing
Without loss of tissue
The union of two closely opposing edges
Short inflammatory and granulation phases.
Complete epithelialisation takes approx. 10 -
14 days
Minimal scar tissue fades quickly from pink
to white.
Maturation phase takes place over several
months
Secondary Wound Healing

With loss of tissue

Wounds heal by formation of new
capillaries and collagen.
Granulation phase may take weeks or
months depending on the amount of
tissue loss and underlying disease
Scar tissue may be evident.
II. Factors Influencing Wound
Healing
 Local
Factors

Wound
Healing
Process

Systemic
Factors
Systemic factors :
Malnutrition Cancer Jaundice
Diabetes melitus Uremia Geriatric age
Systemic Chemotherapy Smoking
corticosteroids
Alcoholism Obesity Etc.

Wound Healing Process

Local factors :
Insfection Venus insufficiency
Foreign bodies Local toxin
Hypoxia/iscemia Scars/previous
trauma
Radiation damage
Malnutrion
Glucose as Arginine & Methionine
the main fuel needed for matrix depo,
for collagen syntesis cell prolif, angiogen

Glutamine Mg, Mn, Co, Ca, Fe

Enhances actions Co Factor in
of PMN collagen production

Vit C influences
collagen
modification

Wound Healing
 Glycine, arginine, Zn influences
methionine to control reepithealization
imflammation & collagen depo

Zn, Vit. C, Se, Co L-arghinine for

For immune endothelial func,
Function Metabolic func,
Synthesis NO

Oncotic pressure
To prevent edema

Wound Healing
Obesity (BMI > 30,0 39, 9 & Morbid Obesity, BMI > 40

Related to higher complication rate in

surgery
Donor site complication
Flap loss
infection

?
Poor Tissue Healing
 Cardiovascular Disease

Impaired
Tissue
Hypoxemia Wound
Hypoxia
Healing
 Respiratory Disease

Impaired
Tissue
Hypoxemia Wound
Hypoxia
Healing
Smoking
Multifactor

Nicotine
+ Hydrogen
Cyanide + CO

Increases platelet aggretion

Decreases collagen deposition
Decreases prostacyclin formation

Especially on Graft and flap failure :

Not a transient vasoconstriction
 Renal Failure

Impaired
Uremic Metabolic
Dialysis Immune System
Toxin Acidosis

Insfection Suspecttibility
Hepatic Failure

Clotting Factors

Low Plasma Protein

Failure of glucose regulation

Critical illness
Critical illness

Stresses on acute illness

Immense demand of cellular activity

for wound healing

Higher demand of oxygen supply

Malignancy
Steroid
Medication

Radiation Cytotoxic Potent

Treatment Medication Antimetabolic tx

MALIGNANCY

Ectopic hormone Hematological

production compromise

Specific organ
Poor Nutrition Severe pain
compromise
Metabolic / Endocrine Disease
Hypothyroidism

Decrease solube hydroxyprolin

Collagen Production
Diabetes Melitus
Infection

Impaired
Metabolic Vascular Neuropatic
Pathway Patheway Patheway Wound
Healing
Ideal Local Condition

Tissue is Viable No Foreign Bodies

Normal Healing Process

Free from excessive bacterial contamination

Ideal Condition

Non viable tissue

Energy drifted into autolysis the necrotic
tissue
Wound more vulnerable to interuption
e.g by infection & local systemic
metabolic disorders
Example : traumatic crush oe degloving
injury on lower extremity
Main enemy ischemia tissue
 No Foreign Bodies
Tissue is Viable
Although bacterial colonization
of all wounds is almost guaranteed,
Normal healing usually can occur.

Must be free from infection to avoid

metabolic load imposed by bacteria
(bacterial bioburden)

Free from critical bacterial contamination

III. Wound Bed Preparation
Aim of Wound Bed
Preparation
Stable
Wound Bed

Well
Minimal
Vascularized
exudate
Wound Bed

Optimal
Wound
Healing
Environment
The Barriers

Necrosis

Energy is drifted to autolysis the necrotic

tissue.
Necrotic tissue nourishes bacteria and
retarding in inflammatory phase
 Bacterial Load

Metabolic Load

Bacterial bioburden
 Chronic Wound Exudate

Slow down or prevent wound healing

and can reflect changes in bacterial load
What Do We Do In
Wound Bed Preapration ?
 Bacterial
Debridement Load
Management

Moisture
Control

Facilitate the Healing

Debridement

The process of removing

Dead (necrotic) tissue
Exudate
Metabolic debris

Help stimulate a non advancing wound

margin.
Mechanical Debridement
Types
Surgery

Wet to dry dressing

Hydrotherapy treatments

Pulse lavage instruments

Moisture Control

Exudate Management

Maintaining moist
Environtment
Always Exudate

Venous ulcer
Artenal ulcer
Diabetic
Chronic gangrene
Wound Pressure sore
Exudate

A result of vasolidation under the

influence of inflammatory mediators
(histamine and bradykinin)
Serous fluid in the wound bed (part of
normal wound healing in acute
wounds)
 Exudate
Component Functions
Fibrin Clotting
Platelets Clotting
Polymorphonuclearcytes (PNNS Immune defence, production of growth factors
Lymphocites Immune defence, production of growth factors
Macrophages
Plasma proteins Maintain asmotic pressure, immunity
Albumin, Globulin, fibrinogen Transport of macromolecules
Lactic acid Product of cellular metabolism and indicating hypoxia
Glucose Cellular energy source
Inorganics salts Buffering, pH hydrogen in concentration
Growth factors Proteins controlling factors specific healing activities
Proteoliytic enzymes Enzymes degrading proteins (serine, cysteine, NMPs)
NMPs Matrix matalloproteinases, endopeptidases, involved
In e.g cell proliferation, migration, differentiation, apoptosis
TIMPs Controlled inhibition of NMPs
Microorganism Exogenous factors
Wound debris / dead cells No function
 In chronic wound, exudate

Changes quantiatively and qualitatively

Contain proteolytic enzymes and

other components not seen in acute wounds

Has the capacity to degrade growth factors

And peri-wound skin, and predispose to imflammation
 Differences between Acute
and Chronic Exudate
Acute Exudate Chronic Exudate

Fluids supports cell proliferation Fluid doesnt support cell

proliferation
Fluids does not damage peri Fluids damages peri wound skin
wound skin
Fibronectin intact Fibronectin degraded

Neutrophil elastase serine and Neutrophil elastase serine and

NMP levels normal MMP level high
Normal fibroblast lifespan Altered fibroblast lifespan
IV. Use Of Antiseptic, Antibiotics,
and Topical Antimicrobes
Wound Microbiology

Wounds prone to potential infection,

but not always infected.
Stages of condition related to the
existance of microbes.
1. Contaminated
2. Colonized
3. Infected

Chronic wound is always contaminated.

 Infection is tissue destructive and
prevents wound healing.
Infection depends on

a. Numbers (close) of bacteria (

enterococcus and candida need to be
many, but other solitare specific
bacteria will be dangerous.
b. Potential (virulensi) (those product
hylaluronidase, toxin)
c. Host resistance (depends on local
and systemic factors)
Sign Of Local Infection

1. Excessive amount of exudate.

2. Sign of imflammation (rubor, kalor,
dolor, edema, nyeri)
 Spesimen mikrobiologis akan lebih
baik diambil melalui pengambilan
sampel jaringan.
Four Basic Principles For
Dressing

1. Desiccated wounds need hydration

2. Exudative wounds need absorption
3. Necrotic wounds need debridement
4. Infected wounds need antimicrobial
agent /device.
Proper & Adequate dressing

Able to keep wound moist

Effective in absorbing exudate
Effective in managing colonization and
infection
Mechanism of Action

1. Remove edema and chronic wound

exudates
2. Enhance angiogenesis
3. Reduce bacterial colonization
4. Enhance granulation tissue formation
V. Rational Decision On
Dressing Material
Four Basic Principles For
Dressing

1. Desiccated wounds need hydration

2. Exudative wounds need absorption
3. Necrotic wounds need debridement
4. Infected wounds need antimicrobial
agent /device.
Take home points

Ideal Dressing
Creates a moist environment
Removes excess exudate
Prevents dessication
Allow for gaseous exchange
Immpermeable to microorganism
Thermally insulating
 Prevents particulate contamination
Nontoxic to beneficial host cells
Provides mechanical protection
Nontraumatic
Easy to use
Cost effective
BURNAZIN PLUS

PT.Darya Varia Laboratoria

Outlines

Introduction
What is Silver Sulfadiazine used for?

Hyaluronic Acid and its role in tissue repair

BURNAZIN PLUS : The way to Heal Acute & Chronic

Wound

Summary
 Introduction
The overall aim of wound management is to promote wound healing.

Both patients and health There are many reasons why

professionals, for different implementation of effective
reasons, want wound closure to wound care practice is so
occur as quickly as possible. variable.
Wound Healing Phases
Wound healing process
Time Concept
Wound Bed Preparation
TIME to prepare for optimal healing
Outlines

Introduction

What is Silver Sulfadiazine used for?

Hyaluronic Acid and its role in tissue repair

BURNAZIN PLUS : The way to Heal Acute & Chronic

Wound

Summary
 Mechanism of Silver

Bind to the DNA of bacteria and bacterial spores reducing

their ability to replicate (Ballard 2002; Cooper 2004)

Binds to the cell membranes causing significant damage

(Ballard 2002)
 Sulfadiazine
Sulfonamide antibiotic

It eliminates bacteria that cause infections by stopping

the production of folate inside the bacterial cell
 Silver Sulfadiazine

The most broadly

The application of
used treatment
SSD on chronic
for the prevention Increase the rate of
wounds can yield a
of infection in neovascularization
faster healing
patients with burn
time.
wounds
sulfadiazine

Kjolseth D, Frank JM, Barker JH, et al. Comparison of the effects of commonly used wound agents on epithelialization and neovascularization. J Am College Surgeons 1994
Sept;179:305-12.
Role of Silver Sulfadiazine
Outlines

Introduction

What is Silver Sulfadiazine used for?

Hyaluronic Acid and its role in tissue repair

BURNAZIN PLUS : The way to Heal Acute & Chronic
Wound

Summary
 HYALURONIC ACID (HA)
DISCOVERY
1934 - Karl Meyer and his assistant John Palmer isolated
new glykoaminoglycane from the vitreous humour of
bovine eyes

vitreous humour
bovine
 Hyaluronic Acid

Is a polysaccharide An extracellular
matrix component, Synthesized in the plasma
is a membrane of fibroblasts
glycosaminoglycan and other cells
Regulation of its
biosynthesis is not well
understood; however,
many inflammatory
mediators and growths
factors activate HA
synthesis
 Hyaluronic Acid in the Body

On the skin, HA is the main reservoir

 HYALURONIC ACID (HA)

Dahiya P, Kamal R. Hyaluronic acid: A boon in periodontal therapy. North Am J Med Sci 2013;5:309-15
 HYALURONIC ACID (HA)
IN WOUND REPAIR

Hyaluronic acid binds through 3 major classes of surface receptors involved

in the modulation of tissue repair and in various other functions :

CD44 Migration, Proliferation, and Cell activation (keratinocytes)

RHAMM Fibroblast migration

ICAM-1 Control of inflammation and neo-angiogenesis

HA in Wound Repair
HA in Wound Repair

REMODELING
 HA PLAYS A ROLE
IN ALL PHASES OF TISSUE REPAIR

Initial Hyaluronic Acid accumulates at the lesion site

phase

Hyaluronic Acid recruits MACROPHAGES and

Inflammation modulates the inflammatory response (also
exerting scavenger activity)

Hyaluronic Acid contributes the granulation tissue

Proliferation formation and NEO-Angiogenesis

Hyaluronic Acid favors RE-EPITHELIALIZATION

Remodeling
and orderly deposition of collagen fibers.
Outlines

Introduction

What is Silver Sulfadiazine used for?

Hyaluronic Acid and its role in tissue repair

BURNAZIN PLUS : The way to Heal Acute &

Chronic Wound
Summary
BURNAZIN PLUS
 BURNAZIN PLUS
Burnazin PLUS cream is a bioactive
association containing Hyaluronic Acid
(HA) and SSD, Ideal for infected wounds.

Compositions:
0.2 % Hyaluronic acid

1 % Silver Sulfadiazine

Indications :
Management of skin lesions, especially those at high risk of infection. It is intended to cover acute and
chronic wounds (first and second degree burns, vascular and metabolic ulcers and pressure sores) and to
provide a moist microba-free wound environment.

Burnazin PLUS can be used on non-infected wounds to help prevent infection and following
successful treatment of infected wounds, to help prevent recurrence of infection.
 BURNAZIN PLUS
Hyaluronic Acid 0,2 %

Creates a moist environtment for optimal tissue repair

Increases keratinocytes and fibroblasts proliferation and promotes

angiogenesis

Mediates production of the antimicrobial peptide 2-Defensin by wound

keratinocytes

Silver Sulfadiazine 1 %
Wide spectrum antibacterial action

Effective against many species of fungi

Include in the WHO Model list of Essential Medicines

Gold Standard for the topical treatments of burns

 CLINICAL CASES

Promotion of healing and prevention of infection

Female patient, 79 years old, with atrial fibrillation and senile dementia. The patient has a
multiple venous ulcer in the internal malleolar area. The wounds are slightly exuding, with a
fibrous bed and edematous margins.

Baseline
After disinfection with 0.05% chlorexidine, BURNAZIN Plus was applied and
covered with a medium stretch compression bandage to treat edema. The
dressing was changed daily.

After 25 days
The size of the two major wounds decreased, with less edematous wound
margins and development of granulation tissue. The small wound in the lower
area is completely healed. The dressing was changed daily to prevent infection.

Final visit (55 days)

All lesions are completely healed with formation of repair tissue.
For prevention of recurrence, class 1 compression stockings
are prescribed.
 CLINICAL CASE (1)

Female patient, 79 years old, IRC, atrial fibrillation and senile dementia. The patient has a multiple
venous wound on the internal malleolar zone of her right leg. The wound appeared in April
2009 and the patient came to the center on 10 August 2009. The wound is slightly exuding, with a
slightly fibrous bed, not very vital margins and edematous skin around the wound.

13 August 2009
The wound is cleansed with physiological solution and then Amukine Med 0.05 is
applied as an antiseptic. Decision to apply BURNAZIN Plus gauzes impregnated with
hyaluronic acid and silver sulfadiazine to stimulate the healing processes and prevent
infection, covered with a medium stretch compression bandage to treat the edema.
Medication change every 3 days.

7 September 2009
The size of the wound is smaller, the bed is cleaner with signs of granulation. Slightly
improved margins, but still partly edematous. The wound is cleansed with physiological
solution, Amukine Med 0.05 is applied as antiseptic, followed by BURNAZIN PLUS to
stimulate healing process and prevent infection. The wound is then covered with a
medium stretch compression bandage to treat edema. The dressing is changed every
3 days.

6 October 2009
The wound is completely healed and closed. Excellent repair result. Fisian cream is
applied to the leg, and a Gloria fix AD knee sock and class 1 compression stocking is
prescribed.
 CLINICAL CASE (2)
Female patient, 66 years old, resident in RSA, affected by serious mental retardation, type II
diabetes, and venous insufficiency in her lower limbs. On admission the patient has an
extensive mixed wound on the front of her left leg, moderate exudation and bleeding.

13 November 2010
Decision to apply BURNAZIN PLUS to stimulate healing process and prevent
infection.

16 December 2010
The size of the wound has reduced drastically (95%) with extensive re-
epithelialization. Treatment continues with BURNAZIN PLUS to further stimulate
healing and prevent infection.

14 January 2011
The wound healed in 61 days, with excellent results.
 CLINICAL CASE (3)
Male patient, 61 years old, former smoker, with chronic cerebral vascular insufficiency,
underwent femoral aorta bypass due to critical ischemia in the right leg. De-ambulation deficit. On
admittance, the patient has trophic wounds on his right knee and tibia. Here, we consider the
wound on the right knee.
14 June 2011
The wound shows medium exudation, fibrin in the wound bed and inflamed, fragile
skin around the wound. The patient complains of very intense pain (score of 9 on the
VAS). The wound is cleansed with physiological solution followed by application of
BURNAZIN Plus to stimulate healing and prevent infection. A non-adherent gauze is
used as secondary medication along with an elastic bandage to secure it in place.
The dressing is changed twice weekly.

15 July 2011
The wound shows advanced re-epithelialization, with no signs of inflammation and
correct healing structure. There is a reduction in the amount of self-reported pain
patient (score of 4 on the VAS).

20 July 2011
On discharge, the wound is completely healed, except for a very small zone of
approx. 0.5 x 0.3 cm with imperfect re-epithelialization, in line with the patella
(probably due to mechanical traction of the anatomical zone). The patient is
prescribed home medication, with a check-up after 2 weeks.
 How to Use

Clean the wound Apply a 2 mm layer Cover with Non Apply a bandage to
using Physiological of Burnazin Plus stick medication, ensure the
solutions Control Cream once such as non necessary contact
a day. adherent dressing
A sterile spatula
can be used for
easier application

102
Outlines

Introduction

What is Silver Sulfadiazine used for?

Hyaluronic Acid and its role in tissue repair

BURNAZIN PLUS : The way to Heal Acute & Chronic

Wound

Summary
 Summary
Silver sulfadiazine has been THE GOLD STANDARD for topical burn therapy

SSD cream in modern wound treatment besides being indicated for burn

wound treatment will be very beneficial for preparation of chronic wound beds

from any cause

HA is commonly used as a therapeutic in a wide range of applications,

including osteoarthritis, ophthalmic surgery, cosmetic application and tissue

engineering.

HA extracts are safe and efficacious products to be used in skin repair

Hyaluronic acid combined with silver sulfadiazine (BURNAZIN PLUS) is

effective as wound infection control & repair tissue management

104
Thank You