2018 CME-n-Ski

Wound Care for the Primary Care Provider

Marc Robins, DO, MPH, FUHMMedical Director

UVRMC Hyperbaric and Wound Clinic

2018 CME-n-Ski

Disclosures:

The author is on the Speaker’s

Bureau for AcelityTM but

otherwise has no affiliation or

financial interest with any

product or manufacturer

discussed or represented in

this presentation, and has

never actually endured a full

episode of Glee.

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Wound Care

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Objectives

• Chronic Wounds/Advanced wounds -when to refer

• Improve diagnostic acumen of the red and swollen lower extremity

• Treatment options

• What can be treated in the Primary Care office and what should be referred

• Team Approach to the evaluation and treatment of chronic wounds of the lower limb

• Role of HBO – when to refer

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Wound Care

* Traumatic wounds

* Burns, bites & stings

* Venous ulcers

* Diabetic ulcers

* Pressure ulcers

* Arterial ulcers

* Connective tissue disorders (RA, SLE, Scleroderma)

* Malignancy wounds (palliative)

* Some or all of the above

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Advanced Wound Care Clinic

• WC Team

• WC Specialist - Primary Care

• Surgeon (Plastic or General,

Vascular)

• Podiatrist

• WC Nurses (WOCN, CWCN, CWS)

• WC techs

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Acute Wounds in Normal Hosts

Most will heal no matter what you do in an unimpaired host, usually in days

to weeks. In impaired hosts… healing is measured in months, sometimes

years.

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Subcutaneous Hematoma

Drain, excise or compress?

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Hematoma

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Hematoma

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Hematoma

Post clot excision and VAC assisted closure

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*Normal Wound Healing

3. Proliferation phase - granulation

– (5-7 days-can last up to 4 weeks)

Fibroblast and collagen migration (new scar)

Angiogenesis (new blood)

Re-epithelialization (new skin)

4. Remodeling (weeks 3-12)

Maturation and contraction

Sequence of Events

1. Hemostasis (minutes)

Vasoconstriction, platelet adherence, thrombocyte clumping

2. Inflammation (first 6-8 hours)

Macrophages orchestrate

End result – clear area of infection, bring in substrate for rebuilding defect

Remodeling

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Why a wound won’t heal

Infection

Systemic vs Topical (Bioburden)

Poor Circulation

Venous vs arterial

Nutrition

Protein, Vitamin, proper caloric intake

Comorbidities

DM, tobacco, age, obesity, other

Compliance

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initial

attachment;

stage

irreversible

attachment;

stage

maturation I;

stage

maturation II;

stage dispersion

Planktonic vs Biofilm

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Biofilm

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Peripheral Vascular Disease

Arterial

Macro vs Micro

Venous

Macro vs Micro

Mixed

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Arterial or Venous Ulcer?

Dry, punched-out, deep

Absent or diminished

pulse

Wet, irregular, shallow

Indurated,

hyperpigmented

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Transcutaneous Oximetry (TCOM)

Non-invasive neonatal O2 monitor

Selection tool

HBO candidates

tissue hypoxia / responders to hyperoxia

Aids vascular assessment

Predict tx non-responders

Amputation level

Can be repeated in chamber

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Sensilase

•Reactive Hyperemia to measure Skin Perfusion Pressure (SPP)

•Impedance Flow Plethysmography to measure Pulse Volume Recording (PVR)

• Non invasive

• Not affected by calcification arteries, edema, heel and toe wounds

• Not operator dependent

Wound Healing is Oxygen Dependent

40 mmHg

0 mmHgAs the PO2 decreases below 40 mmHg the likelihood of

healing drops.

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Venous Stasis Ulcer

Ulceration -spontaneous or traumatic • elevated ambulatory venous pressure (venous hypertension and

reflux) without other primary etiology

Diagnosis - clinical history and examination• anatomic/physiologic data to confirm venous etiology

• rule out other causes (arterial insufficiency)

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Normal Venous Anatomy

Deep Vein System

Superficial Vein System

Perforator System

Directs flow superficial to deep

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Venous Insufficiency

Calf muscle pump failure

Usually secondary to valve incompetence

Increasing vein pressures cause edema leading to ulcer

Venous hypertension

History

DVT, family history, obesity, pregnancy, mixed venous and arterial disease

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Abnormal Anatomy: The Source of the Problem

Venous valvular incompetence

Retrograde blood flow

Venous hypertension

Edema and RBC/ WBC extravasation

Acute and chronic inflammation

Tissue injury Wound

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Calf Muscle Pump Failure

Muscle failure

polio

muscular dystrophy

fixed ankle (equinus)

Valve Failure

Venous obstruction

Venous Hypertension

Increased hydrostatic pressure

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Stasis Ulcers

Irregular shape

Well -defined borders

Dermal Fibrosis and erythema are common

Copious yellow fibrin exudate

Usually malleolar (“gaiter” area)

“Ache” relieved on elevation

Edema almost always present

PAD in 10-25% of patients

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Fibrin Cuff Theory Leading to “Leukocyte Trapping”

Venous hypertension and limb dependency

fibrinogen and fibrin cuffs

extravasation and activation of WBCs

Edema

hypoxic endothelial cells stimulate adherence of WC

Activate WC release O2 radicals, collagenases, elastases, MMPs and TNF which injure surrounding tissue

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Lipodermatosclerosis

‘FAT + SKIN +

HARD’

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Lipodermatosclerosis

Atrophie Blanche

Lividoid vasculopathy

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VSU – differential Diagnosis

Arterial insufficiency ulcers

Bacterial infection (cellulitis)

Primary dermatologic conditions (pyoderma, necrobiosis)

Primary or metastatic neoplasms or malignant transformation

Factitious

Drug reaction, contact dermatitis

Vasculitis (rheumatoid, SLE, scleroderma)

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Lividoid Vasculopathy

AKA:

Lividoid Vasculitis

Livedo Reticularis

Atrophie Blanche

Segmental Hyalinizing Vasculitis

Primary (Idiopathic)

Young – middle age women

Secondary (chronic)

Venous Hypertension/varicosities

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Progression of Vasculopathy

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Progression of Vasculopathy

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Progression of Vasculopathy

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Progression of Vasculopathy

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Progression of Vasculopathy

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Progression of Vasculopathy

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Venous Dermatitis

Violaceous, exudative, weeping

patches and plaques

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Pyoderma Gangrenosum

Auto-immune?

(Neutrophil dysfunction?)

Often associated with chronic inflammatory diseases

Difficult diagnosis

Treatment: steroids, cyclosporine

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Work Up

Clinically significant arterial disease should be ruled out by establishing that pedal pulses are present on physical examination and/or that the ABI is > 0.8. (may also consider toe pressures, PtcO2, IFP) (Level I)

Evaluate for sickle cell disease if suspected (Level II)

Apparent venous ulcers without signs of healing for 3 months or no response after 6 weeks of treatment should be biopsied for histological diagnosis. (Level III)

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Essential Steps in Healing Enhance perfusion and oxygenation

Remove nonviable tissue

Resolve infection, maintain microbial balance

Resolve inflammation

Resolve edema

Optimize wound bed moisture balance and exudate/ odor control

Enhance of tissue growth

Relieve pressure, provide effective offloading, protection, injury prevention, preserve function and activity

Control and diminish pain

Optimize host factors

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Compression

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2 layer wrap

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Compression in the Face of Undiagnosed Arterial Disease

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Clinical Course

• 30-75% initial ulcer healing with

compression

• 16-20 weeks average time to heal • >70% recurrence rate

• Traditional surgical interventions

(‘stripping and ligation’)• poor long-term results

Pentoxifylline and VSU ( Level 1 Evidence/WHS)

Improves perfusion in impaired circulation of peripheral and cerebral vascular beds

Enhances fibrolysis and causes overall improvement of hemorrheological characteristics such as erythrocyte deformability, platelet aggregation and blood viscosity (Renton 1999). [i]

Trophic skin changes associated with venous leg ulcers may be secondary to capillary and endothelial cell dysfunction arising from increased endothelial permeability, leukocyte adherence and transendothelial migration (Bauersachs et al. 1996;[ii] Leach 2004[iii

[i] Renton EJ (1999) Pharmacological treatments for venous leg ulcers. J Wound Care. 8 (4) 195197

[ii] Bauersachs J, Fleming I, Busse R (1996) Pathophysiology of chronic venous insufficiency. Phlebology. 11 1 16-22

[iii] Leach MJ (2004) Making sense of the venous leg ulcer debate: a literature review. Journal of Wound Care. 13 (2) 52-56

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Interventions

Subfascial Endoscopic Perforator Surgery (SEPS)

Endovenous Closure

Injection sclerotherapy

Micro-phlebectomy

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Long Term Prevention of Recurrence of Ulcers

Well- measured and fitted compression garments

Patient education

Regular vascular assessment

Maintenance of healthy skin

Regular examination and replacement of compression garments

Rapid access to clinic following recurrence

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Flaps and Grafts

Epidermal skin graft

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Dermal Substitutes

Supportive Role to cell and vessel recovery

Dermal template or scaffold

Promotes guided regeneration

Reduced scar hyperplasia

Improved remodeling

Stimulation of growth factors in senescent cells

Yannas IV. Studies on the biological activity of the dermal regeneration template. Wound Repair Regen.1998;6:518–523. [PubMed]

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Derived Growth Factors

Regranex®

recombinant platelet-derived growth factor (PDGF)

Platelet Derived Growth Factors (PDGF)

Platelet-rich Plasma (PRP)

Insulin like growth factor (IGF) Vascular endothelial growth factor (VEGF) Platelet derived angiogenic factor (PDAF) Transforming growth factor beta (TGF-β).

Xenografts

• Oasis®

– Porcine small intestine submucosa

• OrthAdapt® -(Tendon repair)

– Equine type I collagen from tendon

• CuffPatch®

– Porcine small intestine submuscosal type I collagen

• Restore®

– Porcine small intestine submuscosal type I collagen

• PuraPly ®

– Porcine small intestine submuscosal type I collagen + PHMB

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Synthetic Tissue

Integra®

Marlex®

All indications

Bilayer bovine tendon/silicone matrix

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Bio-engineered tissue

Apligraf®

DFU

VS

Dermagraft®DFU

Cultured Tissues

Bio-engineered tissue

Grafix®

All indications

EpiFix®

All indications

Amniotic membrane products

Bio-engineered tissue

AlloDerm®

DermaPure®

Primatrix®

GraftJacket®

hMatrix®

DermaSpan®

TheraSkin®

All indications

Acellular Dermal Matrix Graft (ADMG)

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Hyperbaric Oxygen Therapy

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Monoplace Chambers

Elevates PO2

(supersaturation)

1. Reverses Hypoxia

2. Enhances WBC killingEnzyme

regulation and

oxygen signaling

O2 diffusion

gradient

ROS

Decreased Leukocyte adhesion:

harmful inflammation suppressed,

changes in enzyme activity and

gene expression; angiogenesis,

stimulates Growth Factors

Effects of HBO

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What Do We Treat?

Carbon Monoxide Poisoning

Decompression Illness

Arterial Gas Embolism

Gas Gangrene

Deep Necrotizing Infections

Includes Necrotizing Fasciitis and Fournier’s Gangrene

Compromised skin flaps or grafts

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What Do We Treat?

Delayed Effects of Radiation

Acute Peripheral Arterial Insufficiency

Acute traumatic peripheral ischemias

Crush injuries, compartment syndromes, reattachment of severed limbs (post op), etc.

Diabetic Foot Ulcers

Wagner Grade 3 or worse

Chronic Refractory Osteomyelitis

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Questions?