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+ UPDATES IN WOUND MANAGEMENT Lisa M. Arello, MS, ANP-BC Plastic Surgery

UPDATES IN WOUND MANAGEMENT - bc.edu · A chronic wound does not does not progress through the normal stages of healing. ... Macrophages are transformed for cell repair and stimulation

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UPDATES IN WOUND

MANAGEMENT

Lisa M. Arello, MS, ANP-BC

Plastic Surgery

+

No Conflict of Interest

No Commercial Support

+Overview

Wound classification and types of wounds

Phases of healing

Factors affecting healing

Current treatment modalities

Topical Products/ Choosing a Dressing

Negative Pressure Options

Extracellular Matrix

Oxygen Therapies

Pulsed Irrigation

Electromagnetic/ Ultrasound Therapies

Growth Factors/Future Study

+Wound Classification

Why is this important?

Drives treatment plan and expected outcomes

Estimating the length of time to heal

Preventing and treating factors affecting the natural timely and

orderly progression of wound healing

A wound is a result of the disruption of the normal skin structure,

skin function and skin architecture. A chronic wound does not

does not progress through the normal stages of healing.

Atiyeh, BS. Et al. Management of acute ad chronic open wounds: the importance of moist

environment in optimal wound healing. Current Phamr. Biotechnology 2002,3:179.

+ACUTE VS. CHRONIC

Healthy

Identifiable mechanism of

injury, simple or complex

Adequate perfusion

Normal physiological events of

healing process

Orderly progression of stages

Time frame or injury longer

Poorly vascularized,

underlying co-morbidities

Normal phases of healing are

altered, slowed, stalled

Alteration in wound matrix and

typical pathway to healing

Estimated 1% of western

population:4 million people

ACUTE WOUND CHRONIC WOUND

+Chronic Wounds

+Chronic Wounds

Excessive and and aggressive levels of pro-inflammatory cytokines and proteases -> ECM degradation and chronic inflammatory phase of healing

Proliferative phase delay results in delayed granulation and epithelium, which means lack of healing

Excessive bioburden develops, stimulating a chronic inflammatory response, increase neutrophlis and macrophages and therefore, proteases

Bio-film replaces normal planktonic bacteria , have greater antibiotic resistance, are not detected on standard wound cultures

Estimates 60% of chronic wounds have biofilms

Lintzeris, D. etal. Effect of a new Purified Collagen matrix with PCMP on Recalcitrant Wounds of Various Etiologies, Case Study. Vol. 3, #3, 3/18.

+Acute wound

+Classification of Wounds

Clean

Clean contaminated

Uninfected; without inflammation; lack of involvement of the GI, respiratory, GU tract, genitals

Contaminated

Open, surgical or traumatic with inflammation; break in sterile technique, crush, drag injury

Infected

Old, traumatic, necrotic, purulent infection

Acute vs. chronic

Depth of injury: full vs. partial

Skin integrity of surrounding

tissues

Cause of injury ( intent)

Type of injury

Contusion, puncture,

laceration, incision,

pressure, abrasion, crush

Degree of Contamination Other Factors in Classification

+Classification of Decubitus Ulcers

Stage I: skin intact, pink

Stage II: injury to dermis, epidermis, blister

Stage III: injury into subcutaneous fat, full thickness

Stage IV: muscle and bone involvement, necrosis

USA: Un-staged eschar and Suspected deep tissue injury classifications

www.npuap.org/resources/educational-and-clinicalresources

+

Classification?Infected- necrotic, osteomyelitis

Chronic

Depth- Full thickness

Skin integrity- compromised

Cause- accidental

Type- frostbite

Treatment: partial amputation with flap closure, bone biopsy and referral to ID.

+Wound Healing Classification

Primary intention: All layers are closed, rapid healing time,

edges approximate.

Less scar, less risk of infection

Secondary intention: Closed deep layers, open superficial

layers.

Tissue loss, infection, increased scarring/ loss of cosmesis

Tertiary intention: open wound with delayed closure and

healing.

Moderate to high risks infection and scarring, loss of cosmesis

+Tertiary Intention

+Phases of Wound Healing

I. Inflammatory: Hemostasis and inflammation

Begins immediately and lasts up to 3 days, coagulation cascade,

vasoconstriction, platelets aggregate, fibrin clots.

Neutrophils attack bacteria

Macrophages are transformed for cell repair and stimulation of

fibroblast division, collagen synthesis and angiogenesis

Key components of this phase include increased vascular

permeability and cellular recruitment, including secretion of

vimentin, as structural protein for wound healing.

Chronic wounds typically arrested in this stage due to abnormal

production of MMPs impairing function of cytokines to digest

bacteria and necrotic tissue. Armstonrg, etal. www. Uptodate.com, 2016

+Phase II: Proliferative

3 days to 6 weeks

Macrophages stimulate migration of fibroblasts into the

wound for secretion of collagen type III and elastin

Collagen needed for tensile strength

Formation of granulation tissue to replace fibrin/fibronectin

Extracellular matrix deposition and wound contraction

begins

Process impaired by biofilm and bacteria that promote

inflammation and impair epithelialization. www.uptodate.com 2016

+Phase III: Maturation

Week 3 up to year for scar remodeling

Fibroblasts continue to synthesize collagen and

proteoglycan for the wound bed to increase tensile strength.

Collagen III converts to collagen I which increases tensile

strength up to 80% by week 6.

Collagen cross-linking, remodeling, wound contraction and

re-pigmentation.

Fan, W., et al. Current Advances in Modern Wound Healing. Wounds UK, 2010, Vol. 6, No. 3,

22-36.

www.meddean.luc.edu/lumen/meded/surgery 2008 and www.uptodate.com 2016.

+Factors Affecting Wound Healing

Acute vs. Chronic

Infection

edema

Impaired circulation

Impaired mobility

Impaired nutrition

Infection

Smoking

Meddean, 2008.

Diabetes

Obesity

Chronic lung disease

Previous infection

Liver or kidney disease

Immunosepression

Drugs affecting inflammatory

or clotting response

+Hematoma and Osteomyelitis

+Acute Injury

+ Postop Shearing InjuryConsider pressure, contact, shearing

+

CHRONIC VENOUS

ULCERWounds that are do not heal in a timely or complete progression will have:

Increased inflammation

Increased pro-inflammatory cytokines

Increased proteases ( MMP: metalloproteins)

Decreased response of fibroblasts to

growth factors

EXAMPLES: diabetic ulcer, vascular ulcers, Decubitus ulcers

Ochs, D. et al. Evaluation of Mechanisms of Action of a Hydroconductive Dressing, Drawtex, in, Chronic Wounds. Wounds. 2012 September: 6-8.

+Goals of Wound Healing

Repair tissue in a timely manner

Restore function and anatomy

Prevent infection

Minimize inflammation and edema

Minimize pain

Best possible aesthetic outcome

+Basic Principles & Standards of wound

Management

Debride necrotic tissue

Remove excess wound exudate and/or provide moisture

Decrease bio-burden; all are colonized, but not all infected

Eliminate pressure

Control edema and inflammation

Prevent infection

Wound closure as quickly as possible

+First Stage of Healing A

Complicated Wound

+ Dog BiteContamination

Tissue loss

Mechanical function

cosmesis

+ Dog Bite RepairCleanse

Debride

Free flap

Bolster dressing

+Choosing the Best Dressing

Eliminate dead space

Control and/or absorb

exudate

Prevent buildup of biofilm and

bacteria

Maintain adequate moisture

without maceration

Prevent leakage onto healthy

tissues

Comfortable/reduce pain

Ease of application and removing/location

Control odor

Portable/orthotics/walkers

Length of wear time/moisture

Cost

Sensitivity and allergies

Dressing Goals Patient considerations

+The Perfect Dressing

Conforms to wound shape and

eliminates dead space

Pain free

Removes exudate and contains

drainage

Easy to apply and remove

Prevents and removes bacteria

Debrides necrotic tissue and

fibrinous slough

Low cost and available

Prevents maceration of wound edges

Does not leave material behind or shred within a tunnel

Does not require frequent changes

Provides compression where needed

Does not cause dermatitis

+

PERFECT DOES

NOT EXIST

There is not enough clinical evidence

to assist the provider in choosing one

dressing over another.

General accepted consensus based on

what products are available

Hydrogels for debridement stage

Foam and low-adherence dressings

during granulation stage

Hydrocolloid and low adherence

dressings for epithelial stage

Advanced therapies as individually

indicated and tolerated

Antimicrobials as needed; not

prophylactic

+Traditional Therapies: Updates

Hydrogels: promote autolytic debridement and hydration.

SilvaSorb gel: hydrophilic gel with ionic silver

Silvasorb sheet: up to 7 day dressing changes

TheraGuaze: polymer that will absorb or release moisture as needed

Wet to dry: alternative recommendations

TenderWet

Gentle autolytic debridement

Hydrogel dressing for cavities

+HYDROGEL?

+Traditional Therapies: Updates

Collagenase: dressing, ointment or powder

Santyl: 250 units/gram collagenase in petrolatum, enzymatic debridement

Promogran Matrix has 55% collagen, 45% ORC and can be used in exudating wounds

Promogran Prisma: 1% ORC added content for antimicrobial action.

Absorbs exudate

Binds to and inactivates MMPs which prevent wound healing ( biofilm)

Fibracol Plus: 90% collagenase and 10% alginate

Option for draining wound

+Necrotic Ulcer

+Collagenase Continued

Triple Helix by MPM Medical: 100% bovine collagen

Biodegradable in wound

Comes in powder form or sheets

Endoform: 90% collagen and 10% intact ECM components

that provide a broad spectrum reduction in MMPs in chronic

wounds.

Daily or Weekly application.

Not a prior authorization item, considered a dressing

+Autolytic Debridement

Resurgence of honey for autolytic debridement, re-hydration

and antimicrobial actions

High concentrations of sugar and high osmolarity result in

broad spectrum antimicrobial activity www.uptodate.com 2016

Careful for sensitivity reactions

Gel, strips, pads

Insufficient data to make scientific recommendations

+Autolytic Debridement Products

PMHB : polyhexamethylene biguande

Tielle foam

Hydrofera blue: ready or classic

PuraPly

Cadexomer idodine

Iodosorb

Iodoflex

+Traditional Therapies: Updates

Alginates: Thicker with better absorption

Reinforced, available with silver, rope for tunnels, not water

soluble

Foam dressings with silicone adhesive; more site conforming

options

Aquacel surgical hydrofiber dressing with flexible hydrocolloid

adhesive dressing; polyurethane film is waterproof with a

viral/bacterial barrier

Silvercel

Maxsorb

Restore

PolyMem

+Foam Dressings

Multiple brands and shapes

With and without silver

Two layer construction with an absorbing hydrophilic layer

and hydrophobic layer to prevent leakage and bacterial

entering the wound.

Silicone adhesive is skin friendly

Multiple day wear

Some pressure relief

+HydroActive Dressing

Newest synthetic dressings

Combines properties of a gel and a foam dressing

Selectively absorbs excess water/drainage and leaves

behind the needed growth factors and proteins to heal a

wound.

Can combine with enzymatic debriding agents

HydroTac

PermaFoam

Sorbact

Duoderm hydroactive dressing

+HydroConductive Dressing

Drawtex: 2011 on the market.

Non-adherent LevaFiber technology

Combines 2 types of absorbent, cross-action structures that facilitate the movement of large volumes of drainage and wound debris through the dressing. Couch KS. Discovering hydroconductive Dressings. Ostomy wound management, 2012; 58(4): 2-3.

Results: decrease bacterial level and nutrients for biofilm production, decrease MMPs and cytokines, facilitate wound bed preparation, minimize exudate

+Hydroconductive Dressing

Can be used in place of NPWT with skin grafts

Pilonidal sinus tracts

Burns

May double the layers for heavy drainage

Consider non-adherent dressing underneath superficial, but

draining wounds

+Diabetic Foot Ulcers:

Considerations

Neuropathy

Charcot foot or other deformity

Vascular status

Smoking

Edema

Offloading; contact casting

osteomyelitis

+Wagner Classification for DFU

Grade 0: no ulcer, but high risk

Grade 1: ulcer is full thickness of skin

Grade 2: Ulcer extends to ligaments, tendon

Grade 3: Cellulitis and/or abscess, osteomyelitis

Grade 4: gangrene locally

Grade 5: extensive gangrene of foot

+DFU Principles

Pressure relief

Control drainage, alginate

Control edema

Debridement, serial if needed

Re-vascularization

Improvements should be noted consistently or else surgical

intervention is warranted, don’t wait

+ DFU presentationSharp Debridement in office

Silvadene dressing

+ DFU: 1 weekDaily wash, Silvadene dressing and pressure

relief

Healed within 4 weeks

+Advanced Wound Therapies

+Extracellular Wound Matrix

Human extracellular matrix (ECM) is the structural complex

that surrounds cells and binds to tissue. In chronic wounds, the

body’s naturally occurring ECM is failing. In healthy skin, ECM

makes up the key components of the basement membrane that

anchors and replenishes epidermal cells, guides, stimulates

cell proliferation and migration to assist in modulation of

cellular response. Macneil S. What Role Does the ECM Service In Skin Grafting and

Wound healing? Burns. 1994; 20(supplement): S67-70.

+ECM and Chronic Wounds

In chronic wounds, fibroblasts are unresponsive to growth

factors and other signals. These wounds lack the integrin

receptor for fibronectin binding and keratinocyte migration. Davin-Haraway,G. WWW.hpmcommunications.com

ECM triggers neovascularization and recruits cells that

differentiate into site specific tissues. When ECM allograft is

absorbed, it leaves functional tissue which becomes scar

tissue.

Le Chemiant, J and Fiel, C. Porcine Urinary Bladder Matrix: A Retrospective Study and

Establishment of Protocol. Journal of Wound Care, volume 21, no. 10, October 2012.

+ECM

Construct of collagen to act as a scaffold for growth of tissues

Complex, 3 dimensional, organized structure

Important to all stages of healing

Collagen types 1 & 3 are the structural proteins for strength and integrity of skin

Elastin protein provides elasticity

Cell adhesive glycoproteins are the modulators for growth factor activity by binding to surface integrin receptors

Matrix cellular proteins help regulate inflammatory response, keratinocyte migration for maturation and contraction of ECM.

+ECM Allografts

Multiple types and specific indications

Partial and full thickness wound, donor sites

Porcine, neonatal foreskin, amniotic membrane

Powder, sheets, multi-layers

Refrigeration or open storage

Require prior authorization and specific detailed application

notes

Absorbed and incorporated into the wound

+Common ECM Products

Epicel- cultured epidermis

Integra- 2 layered, bovine

collagen and outer silicone

AlloDerm- human cadaver

Biobrane- porcine collagen

and semipermeable silicone

membrane

Oasis- porcine

Puraply – Porcine, PHMB

Dermagraft- allogenic human

fibroblasts on bioabsorbale

scaffold

Apligraph & OrCell- allogenic

neonatal foreskin with

keratinocytes, fibroblasts,

bovine collagen

Acell- urinary bladder matrix

+ECM Application

Prepared wound bed

Type of wound

Edema

Amount of drainage

Documented failed standard wound treatments

Secondary dressing

Follow up/ multiple applications

Infection

Ovine, Porcine allergy or

kosher

Apligraph FDA approved for

diabetic and venous ulcers

Oasis and Acell indicated for

all wound types except 3rd

degree burns

Single use only

Clinical Considerations Contraindications

+ECM: Considerations for Treatment

Multiple, weekly applications

Control edema and drainage

Use of NPWT if needed

Control bio-burden and infection

Pressure relief and ambulation

Odor

Skilled dressing changes

Endpoint: wound closure, lack of progress

+ECM ready

+Negative pressure Therapy

Vacuum assisted wound closure

Continuous or intermittent -50 to-175mmhg sub-atmospheric pressure applied evenly to the wound surface

Used in tunnels, skin grafts post-op

Disposable, smaller models: PICO, SNAP

KCI: VERIFLOW, ACTIVAC AND VAC ULTA 4: TeleHealth

Fluid installation adjunct treatment

Fluid removal and negative pressure result in a reduction in healing in time with space compression and drawing edges together

Incisional NPWT…sutureless closure on the horizon

+Negative Pressure Therapy

Indications:

Slow, stagnant wounds that fail

conservative treatments

Heavy exudate

Tunneling

Require size reduction for

surgical closure

Skin grafts, 1 or 2 stage

Contraindications:

Malignancy

Untreated osteomyelitis

Necrotic tissue or eschar

Exposed vasculature, nerves,

organs, anastomotic sites,

unexplored fistulae

+NPWT Precautions

Friable, bleeding tissue

Exposed tendon, delicate fascia or ligaments

Enteric fistulae require special precautions

Bony fragments, infection, vascular anastomoses, spinal cord

injury

Henderson, V, etal. NPWT Made Easy in Everyday Practice.

Wounds International 2010; 1(15);

http://www.woundsinternational.com

+NPWT Treatment Benefits

Control exudate, increase blood flow

Reduce risk of infection

Reduce number of dressing changes

Reduced wound odor

Can be done in the home

May reduce pain

Prepare wound bed for surgical closure

+Foam or Gauze NPWT?

Antimicrobial standard

Typically less painful and

easier to remove

Flat, round or channel drain

Easier and faster to apply and

remove

More “confident” removal in

tunnels

Silver foam must be requested

No drain choice, less fluid

removal

Less timely application and

caution in tunnels

Granulation adherence can

cause painful removal and

disrupt wound bed

Gauze Foam

+NPWT Treatment Considerations

Wound location; bridge

Tubing placement and pressure settings

Wound bed preparation

Size and number of wounds, frequency of changes

Patient expectations, mobility, cognitive and sensory

function, social environment and lifestyle

Installation: NS, 10-20 minutes then 2-6 hours NPWT

@125mmhg. Kim, et al. Negative Pressure Wound Therapy with Installation: Review of Evidence and

Recommendations, Suppl. Ostomy Wound Management, 2015.

+

Complex Wound

Consider co-morbidities

Difficult placement

Risks of infection and osteo

Nursing skill

+NPWT: Are We There Yet?

Patience with our patients

Uniform granulation and depth of wound

Stalling measurements

Bleeding

3 month “rule”…maybe

Pain or intolerance of the device

Drainage

+

NPWT ENDPOINTBeefy red granulation tissue

Cavity and tunnel filled in

Minimal drainage

No bony or tendon exposure

Wound bed prepared for skin grafting coverage…keep that NPWT

+

NPWT:

Suture-less closure

+

NPWT

Closing a large cavity,

Avoiding a first or second

surgery

+Closed Pulse Irrigation

Direct, localized hydrotherapy in a closed, contained system using a pulsatile pressurized stream of normal saline.

In place of sharp debridement

Not painful, minimal bleeding

Decreases bacteria

Ho, C. et al. Pulsatile Lavage for the Enhancement of Pressure Ulcer Healing: A Randomized Controlled Trial. Physical Therapy,1/2012, vol. 92,no 1, 38-48.

+Benefits of Pulsed Irrigation

Can be done daily, decreases pain, accelerates healing

Performed by nurses in the clinic, home or rehab setting

Use in conjunction with NPWT

Use in wound tunnels with special tips, 8-15 PSI

CPT codes 97597 ( up to 20 sq. cm) and 97598 used for

reimbursement by providers

Must use closed system to contain aerosols and infectious

disease risks: MDRO outbreak @ John’s Hopkins

+Pulsed irrigation with NPWT

+Biologically Active Wound Stimulation

Therapies

Electrical Stimulation

Bio-electric Dressing

Ultrasound Assisted Wound Therapy

Mist,

Electromagnetic Therapy, Diathermy

Modalities to reverse the current of injury; loss of the 40-80mV negative charge of the epidermis relative to the deeper tissues that carry a positive charge, when a full thickness injury occurs.

Moore, K. Electrical Stimulation of Chronic Wounds. Journal of Community Nursing, January 2007, volume 21, issue 1: 18-22.

+Basic Concepts of E-Stimulation

Loss of intact skin=change in charge gradient between the

skin and the deeper tissues

A micro-current will flow from the area of the intact skin into

the wound; voltage peaks and decreases as the wound heals.

In chronic wounds, the current flow is defective and healing

stalls.

E-Stim re-applies this current to stimulate healing via direct,

alternating or pulsed currents

+Bio-Electric Dressing

Woven polyester fabric surface with a matrix of bio-

compatible silver and zinc dots, 1 or 2mm

A secondary moist dressing is placed to maintain moisture

level and promote a micro-current of 0.6 to 0.7 volts

Human epithelial cells have an increased level of FGF-2, a

mediator that increases fibroblast proliferation needed for

wound healing through cellular membrane depolarization

that activates voltage dependent calcium channels.

Harding, A. etal. Efficacy of Bio-Electric Dressing in Healing Deep,

Partial Thickness Wounds Using a Porcine Model. Ostomy Wound

Management. 9/2012; 58(9):50-55.

+Electrical Stimulation

Treatment

Pressure ulcers, leg ulcers

High or low voltage

45 minutes 3-5 days per week

Angiogenesis is enhanced by

improving capillary dermal

formation

Effect on Healing

Inhibit bacterial growth and

disrupts biofilm

Increases keratinocyte

migration

Increases fibroblast protein

synthesis, collagen production

and organization of collagen

fibers

+Biologically Stimulating Irrigation

Techniques

Combine pressurized water irrigation with ultrasound

Portable for clinic use

Multiple tips for varying pressure and area treated

Minimal collateral tissue damage

No nerve damage if done properly

Consider storage, sterilizing, reimbursement

+Misonix Sonic One Plus System

+Misonix System

+

MIST ULTRASOUND

THERAPY

Saline is converted to fine

particles released into

wound by sound waves to

remove dead tissue and

promote healing

+MIST ULTRASOUND

Painless, non-contact, low

frequency ultrasound

Delivered through a saline

mist that acts as a conduit from

the US to the treatment site

Stimulates cells in and below

the wound bed to accelerate

the healing process by

reducing bacteria and biofilm,

decreases MMP-9 and

sustained inflammation

Increases vasodilation and

angiogenesis leading to

release of growth factors and

collagen deposition.

Used in wounds related to

vascular insufficiency, trauma,

ischemia, neuropathy and

chronic wounds

Limited evidence, more

studies needed

Keltie, K. etal, www.alliqua.com,

www.nchi.nlm.nih.gov/pubmed/190

18197

+MIST THERAPY

CONTRAINDICATIONS

Malignancy

Pregnancy

Pacemaker or other electronic implanted devices

Acute gangrene

Acute ischemia

+Ultrasound Assisted Wound Healing

First appeared in the literature in 1949

Therapeutic ultrasound delivers energy in the form of sound waves from mechanical vibrations; similar to diagnostic imaging waves

Primary effects related to inflammatory and repair phases of muscle and soft tissue healing.

Low frequency, provides non-thermal effects of cavitation and acoustic streaming

The shock waves will liquefy necrotic tissue, wound debris and biofilm without injury to healthy tissue with greater tensile strength.

With or without water irrigation

+Ultrasound Assisted Wound Therapy

Wound Indications

Local infection, not systemic

Vascular disease

Pressure ulcers

Diabetic foot and LE ulcers

Wounds needing debridement

Contraindications

Systemic infection

Advancing cellulitis

Joint replacement or local

hardware

Implanted electronic devices

within the treatment field

www.todayswoundclinic.com

+Electromagnetic Therapy: Sub-thermal

PSWT

Pulsed shortwaves produce electromagnetic fields believed to enhance healing; electric or magnetic field

Most research has been done with magnetic field effects

Pulsed wave energy is absorbed in wet, ionic, less dense tissues: muscle and nerves

Diminishes inflammation and increases repair of musculoskeletal and soft tissues through increased membrane transportation that restores ionic balance with energy absorbed

Can be high or radio electromagnetic short wave therapy, but most literature focuses on short wave magnetic

+PSWT

Pulse duration are short resulting in less “on” energy time

than “off” time, resulting in mean power delivery as relatively

low, but up to 150-200 watts of peak power.

Control to vary the mean power delivered and the pulsing

parameters

Most evidence indicates that the combination of pulse

repetition rate and pulse duration is the critical parameter

for energy delivered for tissue heating

Cells in the inflammatory phase have reduced cell

membrane potential, ionic imbalance, altered osmotic action

http://www.linkedin.com/pub/tim-watson/34/351/666

+PSWT

Increased white cells and

fibroblasts =decreased

inflammation

Promote fibrin and collagen

deposition and layering

Increases protein and nerve

growth factors

Restored ionic balance and

membrane transport

Pacemakers

Pregnant females

Bleeding tissues

Malignancy

Active TB

Ischemia or thrombosis

Radiated tissue

Primary Effects on Wound Healing Contraindications

+Wound Stimulation Therapy Limitations

Multiple machines

Multiple energy outputs

Lack of treatment parameters: dosage, timing

Lack of research studies

Use manufacturers guidelines, least amount of energy

needed for therapeutic result

+Oxygen Therapies

Transdermal/continuous diffusion oxygen (CDO), topical

hyperbaric (THO) , hyperbaric oxygen (HBOT)

Therapeutic and technologically differences

HBOT oldest and most accepted form

CDO newest approach with growing evidence, less reported

risks and side effects, due to lower flow rates and lack of

pressure.

www.uptodate.com2016, principles of wound management.

+Hyperbaric Oxygen

Since 1600’s, systemic application 5-7 days per week for 90

minutes in a chamber, intermittent

Adjunct to wound healing therapies

100% O2 delivered under increased atmospheric pressure

greater than 1 atmosphere, up to 3

Goal: raise the O2 levels within the wound bed to correct

hypoxia in chronic wounds

New standards developing for acute burns, surgical flaps and

grafts

+Hyperbaric Oxygen: Therapeutic

Effects

Reverse local tissue hypoxia

Increase stimulation of collagen synthesis

Improved rate of bacterial killing

Diminish inflammatory signals

Issue: Few controlled trials, different wound types and

outcome parameters, but overall, demonstrated improvement

in healing

Eskes, A. et al. Hyperbaric Oxygen Therapy: Solution for Difficult to

Heal Acute Wounds? Systematic Review. World Journal of

Surgery(2011) 35:535-542

+

Approved Wounds

for HBOTDiabetic lower limb ulcers

Chronic, refractory osteomyelitis

Necrotizing fasciitis

Acute peripheral arterial insufficiency

Compromised surgical flaps and skin grafts

Actinomycosis

Soft tissue radionecrosis and osteoradionecrosis

Crush injury/ acute traumatic peripheral ischemia

+Complications of Hyperbaric

Therapy

Middle ear trauma and effusions

Sinus barotrauma (sneeze)

Reversible myopia

Pulmonary toxicity

seizures

+Topical Hyperbaric Oxygen

Since 1960’s

Affected area in a boot, bag or extremity chamber which is

sealed and filled with O2 at high flow rate for O2 rich

environment

5-7 days per week for 90 minutes to 4 hours, intermittent

Low pressures and therefore lower risk of side effects

Requires an open wound surface, not used for necrotic or

sinus tracts

Noted to increase angiogenesis and wound closure rates

+Continuous Diffusion of Oxygen

Therapy

Newest class

Provide continuous O2 delivery at lowest flow rates

Portable, smaller, increase access, lower cost

Also called low-flow or transcutaneous O2, , continuous

7 days per week, 24 hours, 3-12 ml/hr O2 delivery

Not applicable in wounds with eschar or sinus tracts

Improves granulation tissue, increased collagen and

epitheliazation

+Topical Growth Factors

Becaplermin ( Regranex): platelet derived growth factor gel that promotes cellular angiogenesis to improve wound healing.

Approved for diabetic foot ulcers and chronic wounds

Black box warning for malignancy, noted to be with increased use

GM-CSF: granulocyte-macrophage colony stimulating factor is and intradermal injection to promote healing in chronic leg ulcers. Being studied in chronic wounds.

Epidermal Growth Factor: studies on treating chronic venous ulcers

+Future Studies

Growth factors

platelet derived (PDGF-BB)

VGF: vascular endothelial derived

basic fibroblast

granulocyte-macrophage colony stimulating factors

Drugs to improve vasodilation and blood flow

Stem cell therapy

bone marrow

Adipose tissue

muscle tissue

Gene therapy

Specific genes to target specific cells

Improve, alter or negate a cell function and genetic coding once the gene is incorporated into the cell

Includes growth factors, receptors, adhesion molecules and protease inhibitors.

Gene activated matrix

Wii-ping, Linda Fan, 2010

+References

Atiyeh,BS, et al. Management of acute & Chronic open wounds: the importance of moist environment in optimal wound

healing. Curr Pharm Biotech 2002:3, 179.

Beita, J & Rijswijk, L. Content Validation of Algorithms to Guide Negative Pressure Wound Therapy in Adults with Acute or

Chronic Wounds: A Cross Sectional Study. Ostomy Wound Management. 2012, vol. 58, no. 9: 32-39.

Chester, H. et al. Pulsatile Lavage for the Enhancement of Pressure Ulcer Healing; A Randomized Controlled Trial. Physical

Therapy. 1/2012, vol. 92. no. 1: 38-48

Conlan, W. and Weir, D. Ultrasound Assisted Wound Therapy: An Exceptional Adjunct to Wound Bed Preparation.

www.todayswoundclinic.com

Eskes, A. et al. Hyperbaric Oxygen Therapy: solution for Difficult to Heal Acute Wounds? Systematic Review. Would

Journal of Surgery. 2100, vol.35: 535-542.

Flegg, J. et al. Mathematical Model of Hyperbaric Oxygen Therapy Applied to Chronic Diabetic Wounds. Bulletin of

Mathematical Biology. 20120, vol. 72: 1867-1891.

www.guideline.gov/content/aspx: Agency for Healthcare Research and Quality Guideline for Management of Wounds in

Patients with Lower Extremity Venous ulcers.

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