Wound Care for the New Millenium - St. Vincent's …€¢TcPO2 increases in tissue after effective compression & edema reduction Roberts et al, Angiology 2002;53:451. Inflammatory

Wound Care for the New Millenium

Geoffrey L. Risley, MD, FACS

Cardiothoracic & Vascular Surgical Associates Medical Director St. Vincent’s Center for Limb Salvage, Advanced

Wound Care & Hyperbaric Therapy Medical Director Jacksonville Vein Center

Medical Director Vascular Access Center of Jacksonville

Disclosures

• Ev3

• C.S.I.

• Endologix

• Atheromed

• Cordis

Goals-Better Understanding

• Wound Healing Process

• Wound Classification/Evaluation

• Treatment Algorithm

• Advances in wound care technology

• How an aggressive integrated multi-disciplinary approach can lead to: • Reduced healing times • Reduced amputation

rates • Improved QOL

Overview Chronic Wounds

• 8 million people in US • 1.1-1.8 million new cases/yr • $25 Billion/year

• 25% DM develop DFU • Responsible for 600K admissions/yr • 12% DFUwill require amputation

• Prevalence VSU 600,000/yr • Loss 2 million wk-dys/yr

• Prevalence acute care pressure ulcer 14% • Occur in 9% of all hospitalized pts w/in 2 wks

Human Skin Wounds: A Major & Snowballing Threat to Public Health and the Economy. Wound Repair & Regeneration, 17:763-771, 2010.

1994

<4.5% Missing data 4.5 - 5.9% 6.0 - 7.4% 7.5 - 8.9% ≥9.0%

Age-adjusted Percentage of U.S. Adults Who Had Diagnosed Diabetes

CDC’s Division of Diabetes Translation. National Diabetes Surveillance System available at http://www.cdc.gov/diabetes/statistics

2000

<4.5% Missing data 4.5 - 5.9% 6.0 - 7.4% 7.5 - 8.9% ≥9.0%



2005

<4.5% Missing data 4.5 - 5.9% 6.0 - 7.4% 7.5 - 8.9% ≥9.0%



2009

<4.5% Missing data 4.5 - 5.9% 6.0 - 7.4% 7.5 - 8.9% ≥9.0%



2000

Obesity Trends* Among U.S. Adults BRFSS, 1990, 2000, 2010

(*BMI ≥30, or about 30 lbs. overweight for 5’4” person)

2010

1990

No Data <10% 10%–14% 15%–19% 20%–24% 25%–29% ≥30%

Aging Population

Source: US Census Bureau 2008

The Perfect Storm

Ageing population

Increasing DM Increasing Obesity

Increasing atherosclerosis

CHRONIC WOUNDS

CHRONIC WOUNDS

That’s GROSS DAD!!!!!!!

Wound Healing Process

• Stages • Coagulation • Inflammation • Proliferation • Maturation • Contraction

Chronic Wounds

• Senescent cells

• Hyperinflammatory

• Exudate

• Bacterial load

• Necrotic tissue

Chronic Wound Pathway Ischemia, Trauma, Infection, Necrotic Tissue

Prolonged Inflammatory State Excess PMNs, Macrophages

Excess Cytokines

MMPs/TIMPs Disturbance

Impaired Cell Migration,

Impaired Collagen Production, Growth Factor Destruction

Obstacles to Wound Healing

Extrinsic • Mechanical load • Wound bed

environment • Bacterial burden • Soft tissue/bone

infection • Devitalized tissue

Intrinsic • Systemic disease • Perfusion/oxygenation • Infection process • Nutrition/hydration • Medications


• Causes of inadequate perfusion • Atherosclerosis • Cardiac failure • Drug abuse • Microvascular disease • Radiation • Peripheral vasoconstriction • Smoking


• Diseases that interfere with wound healing • Diabetes Mellitus • Arteriosclerosis Obliterans • Collagen Vascular Diseases & Vasculitis • Venous Stasis • Malignancies

Wound Healing Time-line

CHRONIC WOUNDS FAIL TO PROGRESS!!

Where do we start??

When faced with an overwhelming problem

start with a Differential Diagnosis

ARTERIAL ULCERS

Arterial Ulcer Appearance

• Areas trauma/pressure

• Dry, grey, necrotic

• “punched out”

• Minimal exudate

• Limb hair loss

• Absent/diminished pulses

• Pain worse with elevation

PAD

• 10-14% general population

• 20-30% population > 75

• 2.2% men > 50 claudicate

• 7.5% men >75 claudicate

• Symptomatic large vessel atherosclerosis have 10-15X increase in cardiac mortality

PAD Risk Factors

• Lipoproteins • HDL • LDL • Lpa

• Diet

• Smoking

• Hypertension

• Diabetes

• Systemic thrombogenic risk factors

• Obesity/Inactivity

• Genetic Factors

Arterial Supply = Tissue Oxygenation

Assessment • Pulse exam, ?bruit

• Doppler exam/waveform analysis/ratios

• ABI/Segmental Pressue/toe pressure

• PPG, oximetry, TcPO2

• Duplex Scan, Angiography, CTA, MRA

Aortogram CTA

MRA Duplex

PAD

Treatment Options

Risk Factor Modification Medical

Endovascular Surgical BPG

Hybrid Procedure

Bypass • GSV • PTFE • Heparin-coated PTFE • Cryovein • Bovine Artery

Angioplasty • Cryoplasty • Drug-eluting

Stent • Covered • Drug-eluting • Biodegradeable

Atherectomy • Orbital • Silverhawk • Laser

• Remote Endarterectomy

Always Consider PAD

• 10 – 20% 0f all LE ulcers will have PAD

• Only 25% of all Pts. with PAD are treated

• Intervention improves healing • ??? improves QOL and lifespan

VENOUS STASIS ULCERS

Venous Stasis Ulcers

• Caused by chronic venous insufficiency • 7 million suffer with CVI in US

• Responsible for 60-80% al LE Ulcers • 1.5 million new cases VSU/year

• World-wide prevalence of VSU 1-1.3%

What Causes VLUs?

• End result of venous hypertension • Elevation of ambulatory venous pressure

• Chronic Inflammatory up-regulation • Gradual skin scarring • Poor healing potential

Relationship Between Ambulatory Venous

Pressure (AVP) & Venous Stasis Ucleration

AVP (mmHg) Incidence VSU (%)

<45 0

45-49 5

50-59 15

60-69 50

70-79 75

>79 80

J. Vasc. Surg. ‘93; 17:414-9.

Why does CVI cause VSU?

• Prolonged venous hypertension causes “leaky capillaries” • RBC/Macromolecules

leak • Inflammatory

response recruits leukocytes into interstitial space

• ?Reduces o2 diffusion

VSU-what’s in all that fluid?

• Inflammatory mediators released by macrophage/neutrophils • Interleukins • TNF-alpha • Interferon-gamma • Alter MMP/TIMP ratio

• Anti-inflammatory cytokines down-regulated

• Results in unregulated tissue lysis phenotype

VSU are inflammatory ulcers

• Elevated Protease levels

• Elevated pro-inflammatory cytokines

• Healing is associated with reduction in the wound fluid components

What does this have to do with treating VSU?

• Have the correct diagnosis

• Eliminate venous hypertension

• Remove wound fluid from contact with skin & tissue due to the destructive proteins and enzymes in the fluid.

Why diagnose cause?

• Eliminate swelling & wound heals

• Etiology Swelling • CVI • Lymhedema • Morbid obesity • CHF • Renal failure

Diagnosing Venous Disease

Often PE is enough !



• Venous Duplex Scan

• Identify Reflux • Saphenous • Deep • Perforator

• Outflow Obstruction?

Treatment Options Eliminate Venous

Hypertension • Compression

• Eliminate Source of Reflux or Obstruction

COMPRESSION ABLATION/STRIPPING

Compression- What does it do?

• Prevents transmission of venous hypertension to skin & surrounding tissue. • Reduces per-wound inflammation

• May narrow veins to allow better function of the valves to prevent reflux.

• TcPO2 increases in tissue after effective compression & edema reduction

Roberts et al, Angiology 2002;53:451.

Inflammatory Mediators in VLU

EFFECT OF COMPRESSION

Optimal Amount Compression

• Overall goal is control of edema

• 40mmHg is optimal

• Accept less if improves compliance and still controls edema

Initial Treatment

• Unna’s Boot (Zinc oxide)/Dome Boot (Calamine lotion)

• Multi-layer compression

• Intermittent Pneumatic Compression

• Compression Hose

In Addition to AVP Correction (Compression)

• Manage Exudate

• Manage Biofilm

• Manage infection

Adjuvant Topical Therapies

• Skin Graft

• Bioengineered dermal substitutes • Apligraf • Dermagraf

• Non-living dermal substitutes • Oasis • Integra

• Growth factors

VLU recurrence after healing

• F/U data in 110 patients after healing

• Recurrent ulceration developed in: • 24% limbs w/in 1 year • 33% limbs w/in 2 years • 49% limbs w/in 5 years

Marston, et al, J. Vasc. Surg. ‘99; 30:491-8.

Prevention of recurrence ROLE OF COMPRESSION

Key Characteristics • Lifelong

• Daily

• Knee high

• 30-40mm Graduated optimal

• Whatever controls edema

Methods • Compression stocking

• Circ-Aide legging

• Short-stretch bandage

• Intermittent pneumatic compression

• No Effect on Ulcer healing rate or % healed

• Has a great effect on ulcer recurrence • 12% vs.28% recurrence @ 12mos comparing

surgery to compression alone

Lancet 2004: 363:1854-59

NEUROPATHIC ULCERS= DIABETIC FOOT ULCER

Diabetic effect on the foot

• Distal symmetrical polyneuropathy • Sensory • Motor

Diabetic foot abnormalities

• Claw/Hammer toe deformity

• Hallux Valgus/Bunion

• Charcot Foot

Correct the Mechanical Abnormality

• Foot reconstruction

• Orthotics

• Total Contact Casting

Promotion of Wound Healing

• Identify etiology(ies)- assessment

• Enact Pathway elements for specific etiologies

• Prepare the Wound Bed • Correct Wound-related Cause of Nonhealing

• Optimize the Patient • Treat Pt.-related Factors Preventing Healing

Normalize the Micro-environment

• Provide moist environment

• Debride necrotic tissue

• Manage exudate

• Control bio-burden

• Normalize systemic factors

Debridement A Mainstay of Modern Wound Care

• Removes dead tissue • Medium for bacterial growth • Senescent cells inhibit cell migration

• Removes Inflammatory mediators

• Removes biofilm • Improve antibacterial effectiveness • Improve tissue bacteriocidal ability

Types of Debridement • Surgical • Sharp debridement using surgical instrument • Fast & Selective • May be costly • Requires specialized training • Must address pain • Not everyone is a candidate

Types of Debridement • Autolytic • Enzymes in wound fluid dissolve debris • Slower than surgical but still selective • Less costly & painful • Maceration can be a problem • Inappropriate if infection present • Good if wound has several stages of healing at

the same time

Types of Debridement • Chemical • Prescription agent dissolves debris • Relatively selective if properly used • Slower than surgical but faster than autolytic • May cause local infection or burning pain • Should score eschar before applying • Helpful in pts. who cannot tolerate surgery

Types of Debridement • Mechanical • Wet to dry dressings, pulsatile lavage or

whirlpool • Nonselective & may injure healthy tissue • May be painful • Labor intensive in some cases • May be appropriate for initial removal of debris

from heavily contaminated wound but not for ongoing treatment

Types of Debridement

• Maggot Therapy • Secrete proteolytic

enzymes • Ingest liquified tissue • Stimulate serous

exudate from wound • Produce antimicrobial

factors

• 30 maggots consume 1 g of necrotic tissue daily

• Selective

Maintenance Debridement

• Ongoing removal of cellular burden and necrotic debris

• Periodic • Serial conservative sharp debridement • Alternating sharp and other types of debridement,

such as enzymes that don’t harm viable tissue

• Continuous • Enzymatic • Autolytic • Mechanical

Reducing Bioburden & Infection

Control • All chronic wounds are contaminated • Unless bioburden is severe, no harm done

• Increased bioburden can lead to local infection • Only symptom may be failure to progress • May have increased exudate, odor, exuberant

granulation tissue, bridging of nonviable epidermis

Biofilm

• Dentistry’s role in chronic wounds

• Dental plaque is a biofilm

• Dental health relies on elimination of biofilm

• Is a protective mechanism of the bacteria

Reducing Bioburden & Infection Control

• Local Infection may have periwound edema, warmth, erythema, purulence, pain • Debride to reduce bioburden • Culture cleansed wound bed


• May try topical antimicrobials till cx. back • Caution- may be cytotoxic, sensitizers, promote

growth of resistant strains

• May try new antimicrobial dressings • Not cytotoxic but may be allergenic

• Handwashing!!!


• Positive Cultures or Systemic Infection • Treat based on culture results • Tissue, post debridement swab, needle

aspiration • May need blood tests, radiology, or MRI


• Use systemic antibiotics • Poor GI absorption may require parenteral

antibiotics. • Poor peripheral circulation may impair

effectiveness • May need excision or amputation

Microbial Identification

• 99% of chronic wounds are polymicrobial, with high abundance.

• Less than 5% of known wound microbes can be readily grown in traditional culture.

• 97% of chronic wounds contain these “easily grown” microbes at less than 1% !

• The limitations and inadequacies of traditional culture routinely lead to empirical therapy, largely ineffective for the microbial reality.

• PathoGenius® is a PCR technique to ID the bacteria in wound

Clinical Pathway for Wound Healing

Advanced Wound Care Practices at St . Vincent’s Center for Advanced Wound Healing

• Comprehensive wound care evaluation utilizing non-invasive diagnostic testing, including our Vascular Lab, Radiology, MRI, Doppler studies, etc.

• Multidisciplinary physician involvement in each and every

case (i.e. Internal Medicine, Vascular Surgeons, Plastic Surgeons, Infectious Disease, and Podiatry)

• Surgical intervention (i.e. debridement, by-pass)

Advanced Techniques (cont)

• Coordination of follow-up wound care and post wound care protocol

• Hyperbaric Oxygen Therapy • Use of advanced wound care products and

techniques: • Apligraf/Dermagraft • Wound Vac • OASIS Matrix

• Off-loading devices and nutritional support

ADJUNCTIVE ROLE OF HYPERBARIC OXYGEN THERAPY

IN WOUND HEALING

HBO Effect - Hyperoxygenation

Breathing pure oxygen at increased atmospheric pressure causes oxygen to be dissolved in plasma, as much as a 10-15 fold increase (2200 mmHg @ 3atm abs) By having plasma in addition to hemoglobin carry oxygen, more oxygen is delivered to compromised tissue.

Oxygen is transported further in poorly vascularized tissue. The oxygen diffusion distance through tissue can be increased 2 to four times that of normal atmospheric pressure.

Tissue oxygen tensions remain elevated for 2 to 4 hours following treatment.

1.

2.

3.

Dr. I. Boerma LIFE WITHOUT BLOOD

• Exsanguinated a pig

• Replaced Blood with plasma only

• Exposed to 100% O2 @ 3ATM x 24hrs

• Resuscitate with blood

• No problems

WE DON’T NEED NO STINKING BLOOD!!!!!

HBO Treatment

High dose oxygen inhalation in which a patient

breathes 100% oxygen under greater than

atmospheric pressure in a full body hyperbaric

chamber

HBO Mechanisms

Immunologic Increases killing by PMNs

Lethal to some anaerobes

Inhibits toxin formation by some anaerobes

Oxygen free radicals

Enhances bactericidal activity of antibiotics

Microcirculatory Increases flexibility of RBCs

Promotes growth of capillaries (neovascularization)

HBO Mechanisms

Other

Decrease tissue edema

Stimulates fibroblast growth

Increases collagen formation & deposition

HBO Covered Indications

1. Air or Gas Embolism

2. Carbon Monoxide Poisoning Carbon Monoxide Poisoning Complicated by Cyanide Poisoning

3. Clostridial Myositis and Myonecrosis (Gas Gangrene)

4. Crush Injury, Compartment Syndrome, and other Acute Traumatic Ischemias

5. Decompression Sickness

6. Enhancement of Healing in Selected Problem Wounds

7. Exceptional Blood Loss (Anemia)

HBO Covered Indications 8. Intracranial Abscess

9. Necrotizing Soft Tissue Infections

10. Osteomyelitis (Refractory)

11. Delayed Radiation Injury (Soft Tissue and Bony Necrosis)

12. Skin Grafts & Flaps (Compromised)

13. Actinomycosis

14. Diabetic wounds of LE (Wagner III or higher) unresponsive to conventional wound care

Source: Hyperbaric Oxygen Therapy Committee of the Undersea and Hyperbaric Medical Society (UHMS).

April 2003

HBO Indications by Specialty

• Plastic Surgeon – compromised flap or preservation of graft

• Vascular, General, OB GYN – necrotizing infection, failed flap/graft

• Orthopedics – chronic osteomyelitis

• Podiatry – diabetic wounds LE, chronic osteo, acute aterial insufficiency, gas gangrene

• Oral Surgeons – osteoradionecrosis [Marx Protocol]

HBO Treatment • Monoplace (1 person) or multiplace

(> 2 person) chamber

• Patient(s) placed entirely within the chamber

• Breathes 100% oxygen

• Chamber pressure is increased to >2 atm abs

• Monitored ability to equalize inner ear pressures - chamber pressure adjusted accordingly

**Breathing 100% oxygen at 1 atm abs (sea level) or exposing isolated parts of body to 100% oxygen does not constitute HBO therapy

Today’s Monoplace Chamber

HBO Treatment

• Approximately 30 treatments – 1-2 hr each

• Treatments 5-6 days / wk over 5-6 wks

• Some require shorter treatment interval

• Some may undergo a longer or a repeat series of

treatments in the setting of recurrent or refractory

problems

HBO Treatment Not a substitute for:

Local wound care

Antibiotic therapy

Vascular intervention

Biomechanical considerations

**Hyperbaric oxygen therapy is a catalyst that hastens the healing process

Multi-specialty Group of Collaborating Physician

Physician Panel

• Geoff Risley, MD • Medical Director • Vascular Surgery

• Carol Bowen-Wells, MD • General Surgery

• Ed Chisholm, MD • General Surgery

• Brad Herbst, DPM • Podiatry

• Ronnie Bateh, DPM • Podiatry

• Gene Ruckh, DPM • Podiatry

• Reginald Sykes, MD • Internal Medicine

• Lenka Zachar, MD • General Surgery

Case Studies

Debridement Compression

Apligraf

Vascular Referral

Re-occurring ulcer for the last 5 years. Diabetes, PVD, DVT, Superficial venous insufficiency, MO

Healed in 6 weeks

History of diabetes, burns to bilateral plantar foot after

walking on the beach in August

HBO Treatment

•55 y.o. male IDDM •Penetrating wound •Polymicrobial •S/P debridement

HBO Treatment

•S/P 15 HBO Tx’s •IV Abx •Wound care •Glucose control

HBO Treatment

•S/P 45 hbo tx •Went on to closure

HBO Treatment

•78 y.o. male IDDM •2 wks S/P resection bone •Con’t drainage

HBO Treatment

•S/P 20 HBO Tx’s

HBO Treatment

•Healed •S/P 30 HBO Tx’s

In Summary, the St. Vincent’s New Wound Care

Program Offers:

• Assessment

• Vascular studies

• Revascularization

• Infection control

• Wound excision

• Remodeling

• Growth factor therapy

• HBO

• Skin grafting & bio-engineered skin products

• Nutritional Support

• Protection devices

• Patient education

• Referrals

• Communication

Questions

Documents

Wound Care for the New Millenium - St. Vincent's …€¢TcPO2 increases in tissue after effective compression & edema reduction Roberts et al, Angiology 2002;53:451. Inflammatory