wound care for the primary care provider
TRANSCRIPT
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2018 CME-n-Ski
Wound Care for the Primary Care Provider
Marc Robins, DO, MPH, FUHMMedical Director
UVRMC Hyperbaric and Wound Clinic
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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
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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
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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).
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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
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Bio-engineered tissue
Grafix®
All indications
EpiFix®
All indications
Amniotic membrane products
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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
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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?