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

2. 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

3. 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): doi: /j X x.

4. 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

5. 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.

6. 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

7. 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…

8. 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.

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

10. 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…

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

12. 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)

13. 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.

14. 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.

15. 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…

16. 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.

17. 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

18. Wound Etiologies

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

20. 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

21. Venous Ulcers
(mention ‘champagne bottle’ deformity)

22. 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

23. Lymphedema Before compression

24. Lymphedema After compression

25. 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)

26. 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

27. Arterial Ulcer

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

29. 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

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

31. 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, Atlanta, GA: US Department of Health and Human Services; 2014.

32. 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): doi: /j X x.

33. 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): doi: /dc

34. 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): doi: /dc

35. 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

36. 4. Pressure Ulcer

37. 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)

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

39. 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

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

41. 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

42. 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).

43. Stage II Pressure Ulcer

44. 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.

45. 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

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

47. Pressure Ulcer Stage III

48. 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

49. 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

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

51. Pressure Ulcer: Stage IV Right trochanter

52. 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

53. Pressure Ulcer: Unstageable

54. Pressure Ulcers Unable to Stage

55. Pressure Ulcer Unable to Stage

56. 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

57. Pressure Ulcer: Deep Tissue Injury

58. 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.

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

60. 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

61. 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

62. 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

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

64. Atypical Wounds: Autoimmune
RA, Sojourns
Pyoderma
Vasculitis

65. 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)

66. 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.

68. 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

69. 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.

70. 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

71. Sharp Debridement

72. Sharp Debridement

73. Sharp Debridement

74. Maintenance Debridement
Schultz,
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

75. 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

77. 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…

78. 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

79. 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.

80. 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

81. 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 ( ATA)
Typical treatment length is 90mins-2hrs

82. HBOT – Hyperbaric Oxygen Therapy

83. 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

84. 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…

85. 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.

86. 10 Days Later… Improved granular bed Viable tendon
No evidence of infection
Read

87. 30 Days Later… Significant depth reduction Tendon nearly covered
Ready for graft
Read

88. 45 Days Later… HEALED! Skin Grafted and
Healed… This patient was saved BKA amputation and all associated financial and personal costs.

89. 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

90. 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…

91. Questions?
Thank you.
THANK YOU