Wound Care Update IMDA Quarterly Educational Session May 6, 2017 Jodie R. Harper, MD, CWS

What is a Chronic Wound? “An insult or injury that has failed to proceed through an orderly and timely repair process to produce anatomic and functional integrity” ‘To begin with, we need to define the playing field, so the first question is …’ Masoro and Austad, 2006

By the Numbers… …the Cost of “Success”? Chronic wounds affect 6.5 million Americans per year at a treatment cost of $25 billion per year Additional $39 billion in lost wages and medical care per year $15.3 billion estimated expense on wound care products in 2010 To answer this question, we simply need to do a little math… …the Cost of “Success”? Sen CK, Gordillo GM, Roy S, et al. Human Skin Wounds: A Major and Snowballing Threat to Public Health and the Economy. Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society. 2009;17(6):763-771. doi:10.1111/j.1524-475X.2009.00543.x.

Skin 101: Anatomy From an anatomic perspective the skin in composed of three layers, the epidermis -(‘trb’)-thin/avascular, regenerates every 4-6 wks, barrier to microbes and our environment. The dermis- (‘tf’)thicker/tensile strength, functional elements of skin (vessels, follicles, cells of regeneration (fibroblasts). The Sub q (‘mac’) major n/v/l, adipose and connective tissue Hess & Kirsner, 2003

Skin 101: Functions Protects Internal Structures Metabolism and Absorption Sensory Perception Immunologic Role Temperature and Fluid Regulation Social Communication Read …and its important in self esteem. If you don’t think so, keep in mind that there are an estimated 50k tanning salons in the US alone, with 5% of Americans as regular customers.

Skin 101: Physiology How Do Wounds Heal? First Day of injury: Hemostasis Vasoconstriction, platelet release, clot formation First Week: Inflammation Vasodilation Neutrophils/macrophages clean the wound and produce growth factors First Month: Proliferation Angiogenesis Collagen fiber synthesis by fibroblasts First Year: Maturation/Remodeling Shrinking and strengthening of the scar read

When Things Go Wrong… We need to become Wound Detectives History Location Size Appearance of the wound’s Edge Bed Periphery “However, when things go wrong and healing stops or fails to proceed accordingly, we need to become wound detectives…

Size DOES Matter Size Width Length Depth Tunneling Undermining And perhaps contrary to popular belief, size DOES matter in wound care at least. Wound Measurements are important in assessing the progress of wound closure , as well as helping us communicate effectively as wound care providers.

TIME Is Critical! …And we need to remember that in wound care, as in many other things, TIME is critical.

Take TIME to Assess the Wound Tissue viability Infection Moisture content Edge evaluation We need TIME to assess the wound. What is TIME you ask?...It s an acronym for a bedside tool help me evaluate wounds in systematic fashion in my clinic. Let’s look at some examples…

T = Tissue Viability Nonviable tissue in a wound bed is a deterrent to healing and must be removed…

I = Infection IS the wound infected? First, we need to remember that low levels of bacteria in the wound may actually be beneficial to healing by stimulating proteolytic enzymes and neutrophil release. Second, We need to distinguish between contaminated wounds (contain low #s of non replicating bacteria), colonized wounds (replicating bacteria without a host response) and infected wounds (high bacterial burden with a host response that delays healing including erythema, pain, and purulent discharge)

M = Moisture Balance A clean moist wound bed is critical for epithelial cell migration across its surface. While the old adage, ‘if its wet make it dry…isn't always true, it does convey the time-honored principle of dynamic moisture balance in effective wound healing. This is especially important, as we will see, in dressing selection.

E = Edge of Wound We need to look carefully at the wound edge. Hard, rolled, undermined edges are also a deterrent to epithelial cell migration across the wound bed and must be sharply excised.

Comprehensive PATIENT Assessment When we assess the wound, we need to remember to assess the patient beneath the wound. As its been said, we need to see the whole patient, rather than just the hole in the patient. To this end, we need to remember the Titanic Principle…

TITANIC Principle Diabetes Venous Hypertension Trauma Malignancy Peripheral Arterial Disease Psychosocial Issues It was the massive substructure of the ice beneath that caused the ship to founder. In the same way, if we try to heal the wound without addressing the underlying diabetes… then we are not likely to be successful.

Let’s Look Beneath the Wound… When did the wound occur? Who has taken care of the wound? What treatment has been successfully used in the past? What studies have been performed (i.e., arteriogram)? read

Wound Etiologies

Most common wound etiologies Venous Arterial Diabetic (DFU) Pressure Atypical

1. Venous Ulcer Location: midcalf to heel (Gaitor area) Appearance: shallow, irregular, exudate is common, +/- painful Origin: Venous valve incompetence Venous hypertension Extravascular blood loss/edema RBCs  hemosiderin staining WBCs  enzyme-mediated tissue destruction read

Venous Ulcers (mention ‘champagne bottle’ deformity)

Venous Ulcers: Treatment Eliminate swelling Leg Elevation 6 inches above heart Sodium Reduction <2000 mg daily Compression Therapy Multilayer Short stretch Prescription compression hose Pneumatic Compression Pumps

Lymphedema Before compression

Lymphedema After compression

Venous Ulcers: Treatment Debridement Appropriate dressings (moisture control) Alginates Antimicrobial dressings (Iodosorb®, Hydrofera Blue®, silver) Trental/Antibiotics Closure Skin graft Skin substitutes (Apligraf®/Dermagraft®) Endo-venous closure (laser ablation: ELVS)

2. Arterial Ulcer Location: Distal lower extremity Appearance: Distinct margin (cookie cutter), with central necrosis in setting of PAD: Cool extremity Diminished/absent pulses Shiny skin/hair loss read

Arterial Ulcer

Arterial Ulcers: Restore Blood Flow Large vessel bypass/endarterectomy/profundopl asty Endovascular procedures Balloon angioplasty (with or without stent) Laser ablation Atherectomy 28

Arterial Ulcers: Treatment Keep clean and dry Avoid pressure or trauma Including routine surgical debridement Pain control Nitropaste Apply to artery just proximal to wound

3. Diabetic Ulcer Location: Plantar aspect of the foot beneath a bony prominence Appearance: Ill-defined borders, prominent callus, and + / - palpable pulses ‘perfect storm’

with Diabetes Mellitus The Cost of Failure… 29.1 million Americans with Diabetes Mellitus Well if there is a cost to success, what is the cost of failure? Let’s consider the 26 million American diabetics… Centers for Disease Control and Prevention. National Diabetes Statistics Report: Estimates of Diabetes and Its Burden in the United States, 2014. Atlanta, GA: US Department of Health and Human Services; 2014.

Up to 25% of individuals with diabetes will develop a foot ulcer during their lifetime … 20 % of whom will develop a wound in there lifespan… 1. Wu SC, Driver VR, Wrobel JS, Armstrong DG. Foot ulcers in the diabetic patient, prevention and treatment. Vascular Health and Risk Management. 2007;3(1):65-76. 2. Sen CK, Gordillo GM, Roy S, et al. Human Skin Wounds: A Major and Snowballing Threat to Public Health and the Economy. Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society. 2009;17(6):763-771. doi:10.1111/j.1524-475X.2009.00543.x.

Foot wounds are now the most common diabetes-related cause of hospitalization and are a frequent precursor to amputation Lavery LA, Armstrong DG, Wunderlich RP, Mohler MJ, Wendel CS, Lipsky BA. Risk Factors for Foot Infections in Individuals With Diabetes. Diabetes Care. 2006;29(6):1288-1293. doi:10.2337/dc05-2425.

Individuals with diabetes have a 30-fold increased risk of undergoing a lower- extremity amputation Lavery LA, Armstrong DG, Wunderlich RP, Mohler MJ, Wendel CS, Lipsky BA. Risk Factors for Foot Infections in Individuals With Diabetes. Diabetes Care. 2006;29(6):1288-1293. doi:10.2337/dc05-2425.

DFU: Management Principles “Its about MECHANICS, not MEDICINE… It’s more important what you TAKE OFF the wound than what you PUT ON” Off-loading… off-loading… off-loading… Debridement/dressing selection (clean, moist wound bed) Evaluate and correct ischemia/osteomyelitis Adjunctive therapy Skin substitutes (Apligraf®/Dermagraft®) HBOT

4. Pressure Ulcer

Pressure Ulcer Definition Localized injury to the skin and/or underlying tissue usually over a bony prominence, as a result of pressure, or pressure in combination with shear and/or friction. A number of contributing or confounding factors are also associated with pressure ulcers; the significance of these factors is yet to be elucidated. Staging system based on degree of anatomical tissue loss (NPUAP)

Pressure Ulcer Stages Stage I Stage II Stage III Stage IV Unstageable DEEP TISSUE INJURY (DTI) We will discuss DTI in more detail.

Pressure Ulcer: Stages Stage I: Nonblanchable redness of intact skin. Darkly pigmented skin may not have visible blanching; its color may differ from the surrounding area Area may be painful, firm, soft, warmer or cooler as compared to adjacent tissue May be difficult to detect in dark skin tones

Pressure Ulcer: Stage I Stage I pressure ulcer: Intact skin with nonblanchable erythema, typically the first sign of deep tissue injury (DTI)

Pressure Ulcer: Stages Stage II: Partial thickness loss of dermis presenting as a shallow open ulcer with a red or pink wound bed, without slough or bruising. Intact or open / ruptured serum-filled blister Should NOT be used to describe skin tears, tape burns, perineal dermatitis, maceration or excoriation

Pressure Ulcer: Stage II Stage II pressure ulcer: Partial-thickness skin loss into the dermis. May also present as an intact or ruptured serum-filled blister (NPUAP, 2007).

Stage II Pressure Ulcer

Pressure Ulcer: Stages Stage III: Full thickness tissue loss. Subcutaneous fat may be visible but bone, tendon or muscle are not exposed. Slough may be present but does not obscure depth of tissue loss May include undermining or tunneling Depth varies on anatomical location.

Ulcer: Stages Stage III: Further description: The depth of a stage III pressure ulcer varies by anatomical location. The bridge of the nose, ear, occiput and malleolus do not have subcutaneous tissue and stage III ulcers can be shallow. In contrast, areas of significant adiposity can develop extremely deep stage III pressure ulcers. Bone/tendon is not visible or directly palpable. 45 45

Pressure Ulcer: Stage III Stage III pressure ulcer: Full-thickness tissue loss into subcutaneous fat.

Pressure Ulcer Stage III

Pressure Ulcer: Stages Stage IV: Full thickness tissue loss with exposed bone, tendon or muscle. Slough or eschar may be present on some parts of the wound Depth varies depending on anatomical location Often include undermining and tunneling Exposed bone / tendon is visible or directly palpable

Stage IV Further Description: The depth of a stage IV pressure ulcer varies by anatomical location. The bridge of the nose, ear, occiput and malleolus do not have subcutaneous tissue and these ulcers can be shallow. Stage IV ulcers can extend into muscle and/or supporting structures (e.g., fascia, tendon or joint capsule) making osteomyelitis possible. Exposed bone/tendon is visible or directly palpable. 49 49

Pressure Ulcer: Stage IV Stage IV pressure ulcer: Full-thickness tissue loss with exposed bone, tendon, or muscle.

Pressure Ulcer: Stage IV Right trochanter

Unstageable: Full thickness tissue loss in which the base of the ulcer is covered by slough (yellow, tan, gray, green or brown) and/or eschar (tan, brown or black) in the wound bed. Until enough slough and/or eschar is removed to expose the base of the wound, the true depth, and therefore stage, cannot be determined. 52 52

Pressure Ulcer: Unstageable

Pressure Ulcers Unable to Stage

Pressure Ulcer Unable to Stage

Pressure Ulcer: Stages Suspected Deep Tissue Injury Purple or maroon localized area of discolored intact skin or blood- filled blister due to damage of underlying soft tissue from pressure and / or shear. Area may be preceded by tissue that is painful, firm, mushy, boggy, warmer or cooler as compared to adjacent tissue

Pressure Ulcer: Deep Tissue Injury

Suspected Deep Tissue Injury Deep tissue injury may be difficult to detect in individuals with dark skin tones. Evolution may include a thin blister over a dark wound bed. The wound may further evolve and become covered by thin eschar. Evolution may be rapid exposing additional layers of tissue even with optimal treatment.

Deep Tissue Injury Tell story of Sherry and ET tube and tongue

Avoidable Resident developed a pressure ulcer Facility did NOT do one or more of the following: Evaluate clinical condition and risk factors Define and implement interventions Monitor and evaluate the interventions Revise as appropriate

Unavoidable Resident developed a pressure ulcer despite Evaluate clinical condition and risk factors Define and implement interventions Monitor and evaluate the interventions Revise as appropriate

Pressure Ulcer: Management Principles HIGH PRESSURE Pressure avoidance Frequent repositioning Pressure reducing surface Nutrition: Ensure proper intake and monitor Continence and moisture control (when possible) Wound care Debridement Dressing selection Infection surveillance/control

5. Atypical Wounds Depend upon causative factors Examples: Brown Recluse spider bite Post radiation treatment Malignancy Autoimmune process

Atypical Wounds: Autoimmune RA, Sojourns Pyoderma Vasculitis

Make the Diagnosis Malignant Melanoma (Stage 4) 35 y/o golf pro with heel wound that just wouldn’t heal…bx stage 4 melanoma Malignant Melanoma (Stage 4)

The Necrotic Wound Eschar Dead, avascular tissue White/gray to yellow or tan and finally to black or brown Tissue consistency changes as the tissues dry Slough Dead cellular debris on wound surface Yellow/yellow-white Mucunous, stringy  firm It is not possible to stage a wound with necrotic tissue. Once the nonviable tissue is removed and the wound bed has granulation tissue, it is then possible to stage or classify the wound and identify the amount of tissue damage.

Why Debride? Necrotic tissue prolongs the inflammatory phase and delays wound healing Necrotic tissue is a medium for bacterial growth Facilitates visualization of wound base Interrupts the cycle of the chronic wound Debridement reduces the bio-burden of the wound and controls and potentially prevents wound infection in the deteriorating wound. Debridement facilitates visualization of the wound wall and base. With necrotic tissue present, it is not possible to asses viable tissue. Debridement Interrupts the cycle of the chronic wound so that protease and cytokine levels approximate the acute wound. Advances in Skin and Wound Care. Vol14, No 2

Debridement Contraindications Ischemic wound covered with dry eschar, no signs/symptoms of infection Heel ulcer covered with dry eschar, no signs/symptoms of infection Wounds with dry gangrene Ischemic wounds: goal is maintenance of closed wound to prevent infection, as there is not enough blood supply to support wound healing. Heel ulcer: Leave eschar intact and closely monitor for infection.

Types of Debridement Surgical – excision/wide resection of necrotic tissue ± viable tissue (surgeons) Sharp – removal of dead tissue above viable tissue Mechanical (irrigation, wet-to-dry dressings) Autolytic (phagocytic cells, proteolytic enzymes) Enzymatic (collagenase Santyl®) Biological (maggot therapy) Select the method most appropriate for the patients condition and goals

Sharp Debridement

Sharp Debridement

Sharp Debridement

Maintenance Debridement Schultz, 200310 Continuous removal of necrotic burden throughout the life of the wound Difficult to fully remove all debris with single debridement Necrotic burden continues to accumulate Temporary improvement  deterioration Stimulates the “stunned” wound

Granulation Tissue Desired healing process for wounds which involves the growth of small blood vessels and connective tissue Healthy: firm, moist, red, shiny Unhealthy: dark red/blue vs. pale, dehydrated, dull, friable Read slide

Appropriate Dressings Meet specific requirements of the wound (clean, moist wound bed) Goals and objectives of treatment Comfort for the patient Provide balance between cost and benefit We would all like to use appropriate dressings in the care of our patients. These are the ones that meet…

Inappropriate Dressings Compromise peri-wound integrity Maceration Tape injury Contact dermatitis Delay wound healing Wound bed injury Hypergranulation Dehydration Increase Pain Increase risk of Infection

Dressing Decision Tree So with this in mind…Here is an example of a dressing decision tree we use in our clinic (apologize for the print). The concept is that one size doesn’t fit all, and that dressings are selected based on the unique presentation of the wound and patient. For example, if the wound is highly exudative, we are going to want to absorb that drainage in order to avoid tissue maceration. So in this case, we might select a hydrofiber or calcium alginate.

Adjunctive Modalities Electrical stimulation Meta-analysis shows provides significant healing in many wound etiologies23 Negative Pressure Wound Therapy Wound V.A.C.® Anodyne® Therapy System MIRE (monochromatic infrared energy) MIST TherapyTM System HBOT

What is HBOT? Breathing 100% Oxygen at increased atmospheric pressure The patient is enclosed in a clear, acrylic chamber Pressure within the chamber is gradually increased (2.0-2.5ATA) Typical treatment length is 90mins-2hrs

HBOT – Hyperbaric Oxygen Therapy

UHMS Approved Indications Cms approved indications Air or gas embolism Carbon monoxide poisoning Clostridial myositis and myonecrosis (gas gangrene) Crush injury, compartment syndrome, and other acute traumatic ischemias Decompression sickness Arterial insufficiencies Severe anemia Intracranial abscess Necrotizing soft tissue infections Osteomyelitis (refractory) Delayed radiation injury (soft tissues and bony necrosis) Comprised skin grafts and flaps Acute thermal burn injury Idiopathic sudden sensorineural hearing loss Acute carbon monoxide intoxication Decompression illness Gas embolism Gas gangrene Acute traumatic peripheral ischemia Crush injuries and suturing of severed limbs Progressive necrotizing infections (necrotizing fasciitis) Acute peripheral arterial insufficiency Preparation and preservation of compromised skin grafts Chronic refractory osteomyelitis Osteoradionecrosis Soft tissue radionecrosis Cyanide poisoning Actinomycosis Diabetic wounds of the lower extremities CRAO Enhancement of healing in selected problem wounds read

The Four Mechanisms of HBOT Mechanical 2. Oxygen delivery 3. Antimicrobial effect 4. Poison Antidote Alters the size of gas bubbles Supplies O2 to ischemic tissues/ cell signaler Bacteriostatic/cidal Reverse effects of CO and Cyanide through gas exchange We talked about the science of HBO, now I want to look at the 4 main mechanisms that benefit our patients with this therapy. For the purposes of our discussion today, lets focus on the two that are most pertinent to wound care…

A Case in Point… Day 1: Dusky appearance Dry tendon No signs of healing HBOT Initiated  This patient stepped on a nail, developed an abscess and presented to the WHC with a large area of necrotic tissue. His wound was surgically debrided and treated with standard wound care with no improvement. The wound is dusky, the tendon is dry, and few signs of healing are noted. TCOM was completed determining tissue hypoxia and a vascular consult was obtained to rule out a corrective surgical measure. HBOT was recommended.

10 Days Later… Improved granular bed Viable tendon No evidence of infection Read

30 Days Later… Significant depth reduction Tendon nearly covered Ready for graft Read

45 Days Later… HEALED! Skin Grafted and Healed… This patient was saved BKA amputation and all associated financial and personal costs.

Putting the Pieces Together Normal Healing Evaluate Wounds and Patients Common Wounds So in summary, who benefits from this process? Dressing Selection Hyperbaric Oxygen Therapy

What Can You Do? Recognize who is at RISK for chronic wounds Perform an accurate assessment of the WOUND and the PATIENT Implement PREVENTATIVE measures Nutritional support Surface offloading/skin protection Choose appropriate DRESSINGS Make prompt REFERRALS for wound care, vascular specialists …but let me remind you of some things you can do to benefit these ‘challenging’ patients. As caregivers, we have to…

Questions? Thank you. THANK YOU