WOUND BIOBURDEN

(To fulfill the task of Wound Care subject )

Directed by:

GORY GOGENDRA

PIUS DAVID SUGIARTO

SIMUN DASA PUTRA

SUPERIOR PROGRAM OF INTERNATIONAL LEVEL

MAJOR OF NURSING

HEALTH POLYTECHNIC OF JAKARTA III

2010

PREFACE

Praise our Almighty GOD turning presence of His mercy and grace of Wound Care

paper entitled "Wound Bioburden" can be completed.

The author makes this paper in order to know how the provision of nursing care to

clients in the areas of community or family in the hospital.

In making this case we get the direction and guidance from various parties.

Therefore, the authors wish to thank:

1. Pramita Iriana,SKp.,M.Biomed

2. Parents who have prayed for the author

3. My friends who have given writer support.

The author realizes this paper are far from perfect. Therefore, criticisms and

suggestions are always waiting for the perfection of the authors of this paper. Hopefully

this paper can meet the expectations of all of us. Finally, the authors apologize if there are

errors in this paper.

Jakarta,September 2011

Writ

er

iii

CHAPTER I

INTRODUCTION

A. Background

Every human has skin and its covered whole part of the body. Sometime, skin

could be damaged by some agents or injury. So, being a nurse or nurse student, we

should understand how to treat client with skin damaged or injury. To understand

that materials, we should read and make a report or a paper that related on the skin,

including anatomy and physiology of the skin. So that’s the reason of the writer

makes this paper.

The integumentary system has a variety of functions; it may serve to waterproof,

cushion, and protect the deeper tissues, excrete wastes, and regulate temperature,

and is the attachment site for sensory receptors to detect pain, sensation, pressure,

and temperature. In most terrestrial vertebrates with significant exposure to

sunlight, the integumentary system also provides for vitamin D synthesis.

B. Purpose

The purpose to be achieved in this paper are to give the information to the reader

about the scope of wound Bioburden.

1. To inform the reader about The Anatomy of the skin

2. To inform the reader about Bioburden Wound

3. To inform the reader about wound infection

4. To inform the reader about method to identify wound infection

5. To inform the reader about wound culture and specimen

6. To inform the reader about analyzing wound culture and specimen

7. To inform the reader about managing wound bioburden

C. Writing Method

This paper was prepared by a way of search from books in the library and internet

literate related to Skin Anatomy and Physiology and also wound bioburden.

CHAPTER II

THEORETICAL

1. INTEGUMENT (Review

anatomy and physiologic

of integument)

The integumantary system

contains the largest organ in the

human body, the skin. It is also

comprised of such extensions of

the skin as hair and fingernails. The skin, however, is the most important of these. The skin

protects and cushions the body's delicate organs. It also provides the body a physical

barrier to keep out foreign materials and to prevent the body from drying out. The skin is

made of three separate layers, each with its own particular function.

The integumentary system has two major components: the cutaneous membrane or skin,

and the accessory structures.

1. The cutaneous membrane has two components; the epidermis or superficial

epithelium, and the dermis, an underlying area of connective tissues.

2. The accessory structures include hair, nails, and multicellular exocrine glands.

These structure are located primarily in the dermis and protrude through the

epidermis to the skin surface.

The general functions of the skin and subcutaneous layer include the following:

Protection of underlying tissues and organs against impact, abrasion, fluid loss, and

chemical attack.

Excretion of salts, water, and organic wastes by integumentary glands.

Maintenance of normal body temperature through either insulation or evaporative

cooling as needed.

Synthesis of vitamin D3, a steroid that is subsequently converted to calcitriol, a

hormone important to normal calcium metabolism.

Storage of lipids in adipocytes in the dermis and in adipose tissue in the

subcutaneous layer.

Detection of touch, pressure, pain, and temperature stimuli, and the relaying of that

information to the nervous system.

A. THE EPIDERMIS

The epidermis consist of a stratified squamous epithelium. The epidermis is

avascular, because there are no local blood vessels, the epidermal cells rely on the

diffusion of nutrients and oxygen from capillaries within the dermis.

The epidermis is dominated by keratinocytes, the body’s most abundant epithelial

cells. These cells, which form several layers, contain large amounts of the protein

keratin. Thin skin, which covers most of the body surface, contains four layers of

keratinocytes, and is about as thick roughly 0.08 mm. Thick skin, which occurs on

the palms of the hands and the soles of the feet, contains five layers and roughly

0.5mm

B. LAYERS OF EPIDERMIS

The layers, in order from the basal lamina toward the free surface, are the stratum

germinavitum, the stratum spinosum, the stratum granulosum, the stratum lucidum,

and the stratum corneum.

1. stratum germinavitum, forms epidermal ridges. Large basal cells, or

germinative cells, dominate the stratum germinavitum.

2. stratum spinosum, which means “spiny layers,” refers to the fact the\at the

cells look like miniature pincushions in standard histological sections.

which consist of 8 to 10 layers of keratinocytes bound together by

desmosomes.

3. stratum granulosum, consist of five layers of keratinocytes displaced from

the stratum spinosum. Most have stopped dividing and have started making

large amounts of the proteins keratin and keratohyalin. Keratin, a tough,

fibrous protein, is the basic structural components of hair and nails in

humans.

4. stratum lucidum, covers the stratum granulosum. The cells in stratum

lucidum are flattened, densenly packed, and filled with keratin.

5. stratum corneum, contains of 15 to 30 layers of keratinizes cells. The

stratum corneum is water resistant, but not waterproof. Water from

interstitial fluid slowly penetrates the surface, to be evaporated into the

surrounding air. The process is called insensible perspiration, because

unable to see or feel the water loss, and very aware of the sensible

perspiration produced by active sweat glands.

C. THE DERMIS

The dermis has two major components: (1) a superficial papillary layer and (2) a

deeper reticular layer.

The papillary layer, which consist of areolar tissue, contains the capillaries,

lymphatics, and sensory neurons that supply the surface of the skin. The papillary

layer derives its name from the dermal papillae that project between the epidermal

ridges.

The reticular layer, deep to the papillary layer, consist of an interwoven meshwork

of dense irregular connective tissue containing both collagen and elastic fibers.

Collagen fibers of the reticular layer also extend superficially beyond the reticular

layer to blend into those of the papillary layer, so the boundary between the two

layers is indistinct.

Dermatitis is an inflammation of the skin that primarily involves the papillary layer.

The inflammation typically begins in a part of the skin exposed to infection or

irritated by chemicals, radiation, or mechanical stimuli. Dermatitis may cause no

discomfort, or it may produce an annoying itch, as in poison ivy. Other forms of the

condition can be quite painful, and inflammation can spread rapidly across the

entire integument.

Dermal Strength and Elasticity

The presence of two types of fibers--collagen fibers, which are very strong and

resist stretching but are easily bent or twisted, and elastic fibers, which permit

stretching but are easily bent or twisted, and elastic fibers, which permit stretching

and recoil to their original length, enables the dermis to tolerate limited stretching.

The elastic fibers provide flexibility, and the collagen fibers limit that flexibility to

prevent damage to the tissue.

The resulting damage to the dermis prevents it from recoiling to its original size

after delivery or weight loss. The skin then wrinkles and creases, creating a

network of stretch marks.

Tretinoin is a derivative of vitamin A that can be applied to the skin as a cream or

gel. This drug was originally developed to treat acne, but it also increases blood

flow to the dermis and stimulates dermal repair. The degree of improvement varies

among individuals.

Lines of cleavage

The resulting pattern of fibers bundles establishes lines of cleavage of the skin.

Lines of cleavage are clinically significant. A cut parallel to a cleavage are

clinically significant.

D. Accessory skin structures

The skin has the following appendages;

Skin

Appendage

Structure Function

Hair Hairs originate in the dermis and are

shafts of modified keratinized epithelium

which grow from the roots of hair

follicles.

Sensory role, retains heat of the

head and protects it from UV,

advertises sexual maturity and

disperses scents.

Arrector pili

muscles

Smooth muscle cells which extend from

the hair follicle to the papillary layer of

the dermis.

Cause the hair to stand on end -

"Goose Bumps".

Sweat glands There are two types; merocrine and

apocrine. They consist of coiled tubes

embedded in the dermis or hypodermis

and open out onto the skin surface.

Produce a watery substance to

cool the body, excretion of

wastes, excretion of body scents.

Nails The nail plate is composed of dead hard

keratinized cells which lie on top of a

nail bed and which grow from the nail

matrix under the skin.

Allows the tips of our fingers to

be soft and sensory. They serve as

tools to aid in the manipulation of

objects.

Sebaceous

glands

Flask shaped glands, located in the

dermis and open into the hair follicles.

Produce sebum, an oily secretion

which prevents the hair and skin

becoming dry.

2.WOUND BIOBURDEN

A. BIOBURDEN IN WOUND

The human body is in constant contact with multiple microorganisms originating from

both endogenous and exogenous sources. Usually these microorganisms are present

without any evidence of infection because a balance exist between host resistance and

microbial growth. Infections occurs when this equilibrium is upset, either because of

lowered host defenses or increased microorganisms quantity or virulence. Infection is

directly related to the number of organisms and to the virulence of the organisms, and

is inversely related to host resistance.

Skin provide a physical and chemical barrier to microorganisms. Many

microorganisms are able to survive on the skin and are known as skin colonizer, or

normal flora. Normal flora may actually inhibit the growth of more virulent

microorganisms and therefore, serve a protective function. This mutually beneficial

relationship between host and microorganism is referred to as a commensal

relationship.

Breaks in the skin allow microorganisms access to deeper tissue and structure where

they can more readily adhere and multiply.host response to microorganisms in the

wound is multiflected. Nonspecific host responses occur regardless of microbial

species. Specific host responses are triggered by specific microorganisms and involve

the immune system.Nonspecific responses include phagocytosis by polymorphonuclear

leukocytes ( PMSs) and macrophages and inflammation.thus the first phase of wound

healing is refered to as the inflammatory phase.

A. INFLAMMATION

Inflammation is integral to microbial resistance. Its triggered by both endogenous and

exogenous mediators.

1. Endogenous mediator such as cytokines and growth factors, arise from mast cells,

PMNs, macrophages, the complement system, and immune cells. These cells

release mediator in response to contact with microorganisms . endogenous

mediators are also released in response to tissue injury unrelated to microorganisms

such as injury caused by surgical procedure or trauma.

2. Exogenous mediators of inflammation are produced by microorganisms. Most

notable is endotoxin, which is produced by gram negative bacteria. If released into

blood, endotoxins activates all inflammatory mechanisms at once, resulting in

septic shock. Exotoxins are inflammatory mediators released by bacteria. Many

bacterial exotoxins attract leukocytes. However, many bacterial toxins don’t elicit

inflammatory directly. They directly elicit inflammation by activating mast cells

and macrophages when then produce inflammatory mediators.

The release of inflammatory mediators result in localized vasodilatation and

increased blood flow to the area of injury. It will promotes a rapid influx of

phagocyte cells, complement and antibody to the wound site. These physiological

responses to injury are expressed by the sign of inflammation, including erythema,

heat, edema, and pain.

Inflammation is characterized both of acute and chronic.

1. Acute inflammation is the initial response to injury and include pronounced

vascular change and the predominance of PMNs at the site of injury.

2. Chronic inflammation occurs if the injury of tissue isn’t resolved and persist

over a long period. The vascular responses become less pronounced during

chronic inflammation and the predominant leukocyte at the site of injury shift to

machrophages . proliferation of fibroblasts and scar tissue are the characteristic

of chronic inflammation.

B. INFECTION

Infection is the event when the host resistance fails to control the growth of

microorganisms. The persistence presence of microorganisms lead to the influx of

phagosytes, which release proteolytic enzymes, inflammatory mediators, and free

radicals. The accumulation of these substance in the wound is additional tissue injury

and wound deterioration. Moreover inflammatory mediators produce localized

thrombosis and vasoconstriction resulting in the hypoxic wound environtment. This

hypoxic environment promotes further bacterial proliferation establishing a destructive,

prolonged inflammatory cycle.

C. DEFINING INFECTION

Wound infection has been defined as the invasion and the multiplication of

microorganisms in wound tissue resulting in pathofisiologic effect or tissue injury.

Thus wound infection can be contrasted from, wound contamination and colonization.

Wound contamination is the presence of bacteria on wound surfaces with no

multiplication of bacteria. Wound colonization is characterized by the replication of

microorganisms on the wound surface without invasion of wound tissue and no host

immune response. some of these colonizers may be involved in a mutually beneficial

relationship with the host preventing the adherence of more virulent organisms I the

wound bed. These organisms include corynobacterium species, coagulase negative

staphylococci, and viridians streptococci.

The presence of microorganism on the wound surface doesn’t necessarily constitude

wound infection. Contamination and colonization with wound microorganisms is a

condition common to all wounds healing by secondary intention and in fact is a pre

requisite to the formation of granulation tissue.

The key element of wound infection are

1. Wound infection occurs in wound tissue, not on the surface of the wound bed

2. Wound infection occurs in viable wound tissue, it isn’t a phenomenon of necrotic

tissue, eschar or othe debris contained in the wound bed

3. Wound infection is caused by invasion and multiplication of microbes in the wound

4. Wound infection is manifested by host reaction or tissue injury

D. IDENTIFYING INFECTION

The identification and diagnosis of colonized wound Infection is wrought with

uncertainty in clinical practice .This is especially true for chronic wound which heal by

secondary intention. Conversely, the identification and diagnosis of localized infection

of acute wounds such as surgical incision is less equivocal because most of these

wound will display a clinically apparent ,inflammatory response. The normal time for

inflammation is 3 to 5 days if more could be called wound infection.

Identification of severe infection is the development of overt systemic sign and

symptom. For instance is extensive erythema , elevated body temperature, elevated

white count, and elevated blood sugar in people with diabetes are readily evident. a

wound that exposed bone or that can be probed to the bone with a sterile instrument

should be evaluated for osteomyelitis.

However, identifying milder, localized infection in chronic wounds is much more

problematic for a variety of reason.

1. Chronic wound by definition are slow to heal or don’t heal at all.

2. The manifestation of inflammation may be altered in chronic wounds because of

population specific factors.

3. The inflammatory response to bacteria may be influenced by age, diabetes, tissue

perfusion, and oxygenation and othe aspect of immune competence and anti

inflammtory drug use.finally, the factor that contribute to the confusion

surrounding identification of localized chronic wound infection, and operative

definition of wound infection can provide a foundation from which clinicians can

approach identification and diagnosis in a rational.

E. METHODE TO IDENTIFY WOUND INFECTION

In practice, wound infection is identified and diagnosed on clinical signs and symptoms

of infection. It could be detected by direct observation of the wound and periwound

area by the patients.the clinical signs and symptoms of wound can be devided into two,

they are:

1. Classic sign of infection

The classic sign and symptoms are erythema, heat, edema, pain and purulent

exudates.the first four of these signs , such as pain, erythema, edema,and heat are

also as the sign of inflammation. Purulent exudates is the result of bacterial

exotoxins recruiting white cells to the wound. These signs and symptoms are called

as reliable indicators of infection in acute wound such as surgical incision. Unlike

acute wound, the classic signs and symptoms don’t always present in the chronic

wounds with high wound bioburden.this may due to diminished systemic or local

inflammatory response among population with high prepalence of chronic wounds.

2. Sign and symptoms specific to secondary wound

. Sign and symptoms to secondary wounds include:

a. Serouse drainage with concurrent inflammation

b. Delayed healing

c. Dicolorization of granulation tissue

d. Pocketing at the base of the wound

e. Foul odor

f. Wound breakdown.

Many of these signs repreent disruption of the proliperative phase of wound healing.

Although using clinical sign and symptoms of infection to monitor wounds for

infection is congruent with the definition of infection, the assessment of these

parameters is quite subjective. The Clinical Sign and Symptoms Checklist ( CSSC) was

developed to assess the presence of the clinical signs and symptoms of wound infection

in chronic wounds.. It provides a precise description for each of the clinical signs and

symptoms.

F. WOUND CULTURES and SPECIMENT

Like clinical signs and symptoms, the identification of wound infection based on

culture findings can be inconclusive. This problem has led many clinicians to abandon

wound cultures altogether, especially with respect to chronic wounds. The methods

presented here are limited to those most commonly used in practice.

Wound cultures can be conceptualized as consisting of two steps,The acquisition of a

specimen from the wound and The laboratory procedures used to grow, identify, and

quantify the microorganisms. Clinicians are directly responsible for the first part and

must be aware of laboratory processes included in the second to acquire an appropriate

wound specimen and effectively transport the specimen to the mcrobiology laboratory.

This requires close communication with the microbiologist and the microbiology

laboratory.

The three most common types of wound specimens are :

1. Wound tissue

The tissue biopsy method consists of aseptically removing a piece of viable wound

tissue with a scalpel or punch biopsy instrument. Wound tissue specimens are the

most congruent with the first two elements that define wound infection if the

specimens are samples from viable tissue rather than necrotic tissue. Among a

samples of 41 wounds of mixed etiology, the quantitative tissue biopsy method had

a sensitivity of 100%, a specificity of 93,5%, and as accuracy of 95.1% in

predicting the the success of delayed closure. Based on this and other data, the

tissue biopsy became the gold standard specimens for wound cultures are invasive,

skill-intensive (both from clinician and laboratory perspectives), and unavailable in

many settings. Therefore, they aren’t commonly used in practice but are often used

in research of wound microbiology.

2. Needle-aspirated wound fluid

Needle-asiration tachnique obtains fluid through multiple insertions of a 22G

needle into the tissue surrounding the wound. The needle is attached to a 10-cc

syringe. Although studies have compared needle aspiration technique with both

quantitative tissue biopsy and swab cultures, the sensitivity, specificity, and

accuracy of quantitative needle-aspiration remains unclear due to methodological

imitations. However, this may be the best technique for specimen collection when

focal collections of tissue fluid or abscess formation exist close to the wound.

3. Swabs.

The most practical and widely available method for obtaining wounfd specimens is

the swab culture. The usefulness of this method is extremely contentious. Since this

methods samples only wound surface organisms (as opposed to organisms with in

the tissue), many believe it’s ineffectual as a measure of infection because it can’t

distinguish between infection and contamination. In addition, it may be difficult to

recover anaerobic organisms from swab specimens. However, other defend the role

of swab cultures in monitoring infection, emphasizing its entrenchment in clinical

practice.

G. ANALIZING CULTURE and SPECIMENT

Laboratory procedures for the bacteriological analysis of wound specimens include

isolation and identification of the microorganisms alone or in combination with

quantification of the microorganisms isolated. When done alone, isolation and

identification is referred to as quantitative culture. Quantitative cultures provide

information regarding the type of organisms present in addition to the number of

organisms present, which is usually expressed as number per gram of tissue, milliliter

of fluid, swab. The number of organisms present provides information regarding the

rate of microorganism multiplication; therefore, quanttative cultures reflect the third

key element of wound infection more completely than quantitative cultures.

H. QUANTITATIVES CULTURE

The recovery, isolation, and identification of microorganisms gained importance in

identifying wound infection following the post-World War I (WWI) development of

organism-specific anti-microbials. According to the CDC, one sufficient criteria of

surgical site infection is as “organism isolated from an aseptically obtained culture of

fluid or tissue.” By this definition, an organism present in the tissue of the wound

indicates infection. It’s important to note that this CDC criterion implies that isolation

of organisms must be from within the tissue or tissue fluid, not isolation of organisms

from the wound surface. The CDC defines pressure ulcer infection as the presence of

two of the following clinical findings redness, tenderness, or swelling of wound edges

and organisms are isolated from a needle aspiration, tissue biopsy, or blood culture.

Clnical signs and symptoms of infection mst be present along with isolation of an

organism known to cause disease.

Acute wounds often contain skin flora, such as staphylococci and diptheroids. Chronic

wounds, with their distinctive environment, often contain larger numbers and types of

microorganisms than acute wounds. These wounds have large amounts of exudate,

necrotic tissue and eschar, large surface areas, and deep cracks and crevices suitable for

a variety of microbial species. Chronic wounds have been associated with anaerobes

and multiple types of organisms. Common organisms isolated from chronic wound are

Proteus mirabilis, Escherichia coli, and Streptococcus, Staphylococcus, Pseudomonas,

Corynebacteria, and Bacteriodes species. Limitated data indicate that the presence of

proteus mirabilis, Pseudomonas aeroginosa, and Bacteriodes, and anaerobe, deter

chronic wound healng. Nonhealing chronic wounds were also associated with the

presence of E. Coli, group D Streptococci, and other anaerobic cocci. Although the

presence of methicillin-resistant Staphylococcus aureus (MRSA) in chronic wounds

prsents a problem for infection control in health care settings, the association between

colonization with MRSA and subsequent infection or bacteremia is unclear. Only the

presence of B-hemolytic Streptococcus is considered to be a notable threat in the

chronic wound at levels less than 105 organisms per gram of tissue. Nonetheless,

qualitative cultures have a role in the monitoring of wounds and in guiding antibiotic

selection for infected wounds. Qualitative cultures are accomplished by plating wound

specimens on solid media, identifying isolates using standard microbiological

procedures, and testing for antibiotic sensitivity.

In summary, the identification of wound infection remains ambiguous and uncertain.

Monitoring wunds for the clinical signs and symptoms of infection is an important

component of wound assessment. Indicators of inflammation are especially important

markers in acute wounds, such as SSIs. However, the signs and symptoms associated

with inflammation may not be present in some petients with acute wounds or in

patients with chronic wounds. The signs specific to secondary wounds may be useful in

these cases and should be incorporated into clinical assessment. Wounds suspected of

infection, especially those with delayed healing, are often cultured cultured to confirm

the diagnosis. While qualitative cultures provide useful information in wounds that are

demonstrating obvious clinical signs of infection, they may not be as useful in

diagnosing infection in the absense of signs and symptoms unless certain pathogens are

isolated. In the absence of clinical signs and symptoms, quantitative cultures are the

gold standard method for diagnosing localized wound infection.

I. MANAGING WOUND BIOBURDEN

Controlling wound bioburden requires a multifaceted approach consisting of one or

more of the following:

1. Correction of the host factors that contributed to the infection

2. Removal of devitalized tissue and foreign debris

3. Initation of antimicrobial therapy

While not all of these interventions will be indicated in every case of wound infection,

they each have a role to play in either reducing the number of microorganisms or

enhancing host resistance.

The presence of host factors that reduce resistance to infection are often overlooked in

management of wound bioburden. Judicious attention to restoration of adequate blood

supply, provision of nutritional support, maintenance of glycemic control, reduction of

edema, and protection from mechanical forces on the wounded tissue will aid in

restoring the balance between host resistance and microorganisms. Failure to address

these host factors may contribute to continued proliferation of microorganisms despite

initation of other treatment modalities.

Removal of devitalized tissue and debris is an essential step in treating wound

infection, since necrotictissue provides an excellent media for growth of

microorganisms. When devitalized tissue is adherent to the wound bed, wound

debridement is indicated.

J. WOUND CLEANING

The presence of foreign debris and contaminants on the surface of the wound can

harbor microorganisms or provide nutrients for their growth. Wound cleaning is a

process that removes these less adherent inflammatory contaminants from the wound

surface and renders the wound less condusive to microbial growth. However, the

process of wound cleaning can create tissue trauma. Effective wound cleaning requires

selection of methods that minimize chemical and mechanical trauma to wound tissue

while removing surface debris and contaminants. Although definitive research is

lacking to guide selection of wound cleaning methods, the available practice evidence

suggests using a nontoxic cleaning solution in combination with a delivery device that

will create sufficient mechanical forces to remove the surface debris while limiting

tissue injury.

K. CLEANING AGENT

The usefulness of specific agents depends on a balance between their antibacterial

properties and their cytotoxicity to wound healing cells, such as white blood cells

(WBCs) and fibroblasts. For the majority of wounds, isotonic saline is adequate to

clean the wound surface. Water, although not isotonic, is a suitable alternative, as long

as it’s free of any potential contaminants. Since the fluid has only brief contact with the

wound surface, it isn’t crucial that the solution be isotonic (0,9% sodium chloride). An

inexpensive salin

L. CLEANING DEVICES

The effectiveness of wound cleaning is influenced by the type of cleaning device used

to deliver the solution to the wound surface. It’s essential that the method used provide

sufficient force to remove surface contaminants and debris ehile minimizing trauma to

the wound. A variety of scrubbing cloths, sponges, and brushes are available for

wound cleaning. Alhough evidence related to their efficacy is limited, it has been

demonstrated that wound cleaned with coarse sponges were significantly more

suceptible to infection than those scrubbled with a smoother sponge. Furthermore,

when compared to saline, wound cleaners containing surfactant were found to

decrease the coeficient of friction between the scrubbing device and wound tissue.

Wound irrigation promotes wound cleaning by screating hydraulic forces generated by

the fluid stream. In order for irrigation stream must be greater than the adhesion forces

that hold the debris to the surface of the wound.

When irrigationis delivered with a mechanical irrigation device, such as those used for

dental hygiene, grather pressures are attainable than with other methods.

Although high pressure optimizes wound cleaning, the risk of dispersing fluid into

adjacent wound tissue or along tissue planes is increased when higher pressures are

used for irrigation. The magnitude of this dispersion is related to the amount of fluid

stream pressure.

While high pressures should be avoided in performing wound irrigation, it’s also

necessary to create sufficient hydraulic forces with the fluid stream to overcome the

adhesion forces holding debris to the wound surface.

A significant decrease was observed in both wound inflammation and wound infection

in those wound cleaned with the syringe and needle compared with the bulb syringe.

A variety of needle and syringe combinations can be used to achieve the desired range

of irrigation pressure. The size of the syringe and the needle gauge determine the

amount of pressure of the fluid stream. The opposite effect occurs by increasing the

size of the needle. Since the larger the lumen of the needle, the greater will be the flow

of fluids, needles of 25-, 21-, and 19G will create pressures of 4, 6, and 8 psi,

respectively, when used with a 35-cc syringe.

In addition to varying the amount of pressure used for wound irrigaation, the fluid

steam can be delivered in either pulsatile or continous flow pattern. The bennefit of

delivering wound irrigation with a pulsatile as compared to a continous fluid stream

has not has been substatinated in experimental studies.

An alternate approach to wound irrigation is the whirlpool bath. It cleans the wound

by exposing the entire wound bed and surrounding skin to agitating water generated

by jets in the side of the whirlpool tub. Only two studies have investigated the cleaning

effectiveness of whirlpool and these are methodologically confounded with wound

irrigation, which was provided at the end of the whirlpool theraphy. The benefit of

whirlpool is thught to be derrived from the prolonged exposure of the wound to water,

which softens wound of the wound debris and makes it more amendable to removal.

M. ANTIMICROBIAL THERAPY

When removal of necrotic tissue doesnt reduce bacterial burden to a level compatible

with healing, additional interventions that act directly on the bacteria indicated. The

clinical used of antibiotics to control bacterial burden in chronic woundds has been

characterized by misonceptions and controvery. As a result, antibiotics have frequently

been used too extensively or for too long a time. Research evidenced has documented

that systemic antibiotics are of no value in reducing bacterial counts in chronic,

granulating wounds, furthermore, the presence of purulent exudate, a recognized sign

of infection in an accute wound, is not a suficient indicator of the need to initiate

antibiotic therapy to threat chronic wound. Give the current state of ambiguity

regarding valid clinical sign and symptom of chronic wound infection, the decission to

initiateantimicrobial therapy is best guided by failure of a wound to make progress

toward healing, despite the absence of devitalized tissue.

Reserch studies have suggested the potential utility antibiotics in reducing bacterial

burden in chronic wounds. In a randomized controlled trial of 31 pressure ulcers, all

ulcers treated with topical genamicin cream and standard treatment consisting of

debridement, cleaning, pressure reducting and nutritional support demonstrated

significant improvement, while only three of the nine given standard treatment alone

improved. Serial bacteriological and pathological observasions made over a 1- to 4-

week treatment period showed a rapid reduction in bacterial counts to level less than

106 per ml in all ulcers treated with gentamicin.

The efficacy of topical antibiotics in reducing bacterial burden in chonic wounds was

substantiated further in randomized trial of 45 patients with a sigle infected pressure

ulcer that were randomly assigned to receive silver sulfadiazine cream, povidone-

iodine solution, or saline gauze dressing.

Recent advances in technology have oroduce dressing that incorporate silver directly

into the dressing material, thus eliminating the necessity of applying and removing the

silver sulfadiazine cream. While such dressing would appear to possess the same

antibacterial benefits as direct application of the cream, this has not substantiated in

controlled clinical studies. These tyoes of dressing are designed to provide an

antimicrobial barrier and have not been demonstrated to reduce bacterial levels in

chronic wounds.

Although clinical studies provide evidence supporting the utility of topical antibiotics

in reducing bacterial burden in chronic wounds, these agents can cause adverse

reaction in some patients. Reports of permanent hearing loss with topical 1 %

neomycin solution and accute anaphylactic reactions with topically applied Bacitracin

suggest that careful monitoring is indicated when using these agents. Additionally,

since there’s a risk of selecting out ressistent strains of bacteria, antibiotics that are

used to treat infections systematically should not be used in a topical form on chronic

wounds.

While topical antibiotics have demonstrated effectiveness in reducing bacterial burden

when the area of involvement, such as advancing cellulitis. In these instance, systemic

antibiotic therpy is indicated. Since the type of organisms and degree of invasiveness

will vary, the choice of antimicrobial therapy will need to be individualized.

Unfortunately, little resarch evidence exists to guide selection of antibiotics to treat

chronic wound infections. Generally. Chronic wound infections are treated impirically

with broad-spectrum antibiotics administered orally. Parenteral therapy may be

indicated when the infection involves deeper tissue and is accompanied by sistemic

signs, such as fever, chiils, and elevated WBC count. Regardless of the route, the

effectiveness of any sistemic antibiotic in reducing bacterial burden will be dependent

on the adequacy of the patient’s peripheral circulation. In those instance where

peripheral vascular disease compromises the blood flow to the infected tissue,

systemic antimicrobial therapy may produce no clinical improvement in the wound.

CHAPTER III

SUMMARY

A. SUMMARY

Most of our understanding of wound infection has been derived from the study of

acute wounds. As wound healing science has evolved, it has become clear that

chronic wounds are distinctly different environments where host resistance has

been overwhelmed by bacterial burden. The classic sign and symptoms of infection

are well recognized. However, they’re based on assessment made of acute wound

and aren’t valid in the chronic wound. While indicators of chronic wound infection

remain ambiguous, substantial evidence exists showing that necrotic tissue harbors

microorganisms. Therefore, debridement of necrotic tissue in the wound bed is an

essential first step to reducing bacterial burden. Regular wound cleaning with a

noncytotoxic solution, using sufficient force to remove surface contaminants. In

those instances where these measures aren’t sufficient to restore a balance between

host resistance and bacterial burden, antimicrobial that act directly on the bacteria

are indicated.

REFFERENCES

During the arrangement of this paper, writer using some references to find

materials and to collect various data from any sources, namely:

http://en.wikipedia.org/wiki/Integumentary_system

http://www.anatomy.tv/StudyGuides/StudyGuide.aspx?

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