Management of Chronic Difficult
Wounds in the Long Term Care
Setting
Janice Locke, MS, GNP, BC
Nurse Practitioner
Erickson Health Medical Group –
Renaissance Gardens at Fox Run, Novi
Objectives
• At the completion of this session, participants will
be able to:
– Describe normal wound healing stages
– Identify what constitutes a chronic wound
– Describe which patients are at risk for developing
chronic wounds
– Identify goals for treating chronic wounds
– Describe treatment options for managing chronic
wounds
– Identify methods for evaluating wound healing
Disclosure and Disclaimer
• I have no financial relationships with any
wound product companies to disclose.
• Some “off-label” uses of products as well as
some anecdotal evidence will be presented.
• Attempts will be made to use generic terms
for wound care products however brand
names will be discussed and opinions
regarding specific products are my own.
Normal wound healing process
• Wound healing occurs as a cellular response
to tissue injury and involves activation of
several cell types.
• Acute wounds usually heal in an orderly and
efficient manner.
• Restoration of skin integrity following an acute
surgical wound in “normal” individuals is
usually complete within 2-4 weeks.
Normal wound healing
• Hemostasis – immediate response to injury
– Small vessels contract to provide some hemostasis
– Platelets aggregate to trigger clotting cascade and
release essential growth factors and cytokines
– Resulting fibrin matrix stabilizes the wound and
provides a provisional scaffold for the wound
healing process
Normal wound healing
• Inflammation
– Key components of this phase are increased vascular
permeability and cellular recruitment.
– Cells are recruited that will
• Create structural proteins
• Mediate vasodilation and cell migration
• Cause vessel permeability resulting in accumulation of
plasma and cellular elements (edema)
• Digest bacteria, foreign debris and necrotic tissue.
– This is usually the phase where chronic wounds
become arrested
Normal wound healing
• Epithelialization
– Proliferation and migration of epithelial cells until
individual cells are surrounded by cells of a similar
type.
– Challenged by wounds that are not closed by
primary intention.
– Presence of biofilm and senescent cells on wound
edge or base also challenges this stage.
Normal wound healing
• Fibroplasia
– Make the ground substance of the wound base
– Produce contractile proteins that work to pull the
edges of the wound together.
• Maturation
– Disorganized collagen is degraded and reformed
to enhance the tensile strength of the wound.
Chronic wounds
• A chronic wound is one that does not heal
within a “reasonable” time – usually 3
months.
• A “stalled wound” does not decrease in size by
30% in 3 weeks or by 50% in 4-5 weeks.
• A stalled wound isn’t necessarily going to be a
chronic wound – may just need a “kick start”
to resume healing process.
Chronic wounds
• Often stalled in the inflammatory phase
– The presence of necrotic tissue, foreign material,
and bacteria result in the abnormal production of
metallloproteases which alter the balance of
inflammation and impair the function of the
cytokines involved in initiation and progression of
wound healing (growth factors).
Factors associated with non-healing
wounds
• Intrinsic
– Impaired circulation
– Disease processes (inflammatory, metabolic,
malignancy)
– Malnutrition
– Age
– Obesity
– Infection
Factors associated with non-healing
wounds
• Extrinsic
– Mechanical forces (pressure, shear, friction)
– Pharmacology
– Foreign bodies
• Psychosocial
– Patient/family preferences, beliefs, goals,
expectations
– Caregiver/patient relationship
Factors associated with non-healing
wounds
• Access/implementation
– Availability of care
– Financial resources
– Ability to understand and perform care
Individual wound factors associated
with delayed healing
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Lack of acute “trigger” for healing
Extended inflammatory phase
Presence of matrix metalloproteases (MMPs)
Low levels of tissue inhibitors of proteases
(TIMPs)
• Deficiency of growth factor receptor sites and/or
growth factor destruction by MMPs
• Inefficient/senecent cells
• Biofilm
Who is at risk for non-healing wounds
• Patients with:
– Vascular impairment
– Impaired immune status
– Metastatic cancer
– Advanced age
– Diabetes
– Neuropathy/SCI
– Malnutrition
Identify goals of treatment
• Consistent with patient/family values and
lifestyle
• Cure/healing
• Palliation/comfort
Treatment options - Systemic
• Illness management
– Blood sugar control
– Management of oxygenation
• Circulation management
– Improve circulation to area
• Offloading
• Revascularization
• Edema management
Treatment options
• Reduce/eliminate causative factors
– Management of fecal and urinary incontinence
• Use of fecal bags/condom catheters or indwelling
catheters for short periods of time.
– Pressure redistribution/reduction
– Control friction/shear
Treatment - Nutrition
• Complex issue – lots of conflicting data and
lack of strong (level A and B evidence) to
support specific recommendations for
supplementation
• Albumin, Total Protein, Total Lymphocyte
Count, Pre- albumin, Transferrin levels.
Treatment - Nutrition
• Protein requirements
– Healthy adult = 0.8gm protein/Kg/24 hours
– 1.5-2.1 gm/Kg or more could be required
depending on individual metabolic and clinical
condition
• Micronutrients
– Zinc, Copper, Iron, Vitamin A, Vitamin C, Vitamin E,
Arginine, Glutamine
• Consult RD
Infection
• Cultures –
– Swab cultures most frequently used – they reflect the
surface colonization rather than infection. AHQR Guideline
recommends against using swab cultures to define
microbiology of a pressure ulcer.
– For infection control practices, a swab culture may be
useful in identifying patients colonized with MRSA or other
resistant bacteria.
– Blood culture or deep tissue biopsy culture is more
clinically significant.
– Culturing deep tissue specimens from a surgically cleaned
and debrided ulcer is the gold standard for wound culture.
Colonization vs Infection
• Both can delay/impair healing
• Superficial infection is localized without
systemic signs, non-healing ulcer
– Local wound care
• Debridement of necrotic tissue
• Moist wound dressing
• Nutritional support and pressure reduction
– Trial of topical antibiotic to reduce local bacterial
counts
Topical antimicrobial agents
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Silver sulfadiazine 1% cream
Combination antibiotic ointments
Silver-containing dressings
Avoid cytotoxic agents
– Hydrogen peroxide
– Povidone-iodine
• AHQR recommends 2 week trial of topical abx
for clean wounds that fail to heal after 2-4
weeks of optimal care.
Deep infection
• Cellulitis – patients with neuropathy may not
have pain. Leukocytosis and fever may or may
not be present.
• Osteomyelitis – has been reported in 17-34%
of patients
• Bacteremia
• Base treatment on bacterial cultures
whenever possible
Local Care of the wound
• TIME
• T = tissue (nonviable/deficient).
– Debridement – episodic or continuous
• I = Infection or Inflammation
– Topical and/or systemic antibiotics
• M = moisture imbalance
– Apply moisture balancing dressings
• E = edge
– Evaluate and correct impediments to epithelial
migration
Cleansing
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pH balanced cleansers
Normal saline
Soap and water
Psi
Debridement
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Enzymatic
Sharp/surgical
Mechanical
Biologic
Debridement
Post-debridement
Debridement
The image above is a copyrighted product of AACW (www.aawconline.org) and
has been reproduced with permission
Moisture control
• Maintaining appropriate amount of moisture
in wound bed is critical.
– too moist = maceration/denuding, increased
breakdown
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Hydrofibers
Calcium alginates
Foams
Combination products
Moisture control
• Too dry = dessication. Dry wounds lack wound
fluids that provide the tissue growth factors to
facilitate reepithelialization
– Saline moistened gauze
– Transparent films
– Hydrocolloids
– Hydrogels
Moisture control
Edges
• Examine edges of the wound
• Epibole = the upper edges of the epidermis
roll to envelop the basement membrane or
lower edges of the epidermis so that epithelial
migration does not occur at wound edges.
• The edges curl under and epithelial migration
stops.
Epibole
Topical treatments
• Dressings
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Films
Foams
Hydrocolloids
Hydrogels
Hydrofibers
Composites
• Other topicals
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Collagen Matrix
Growth factor
Xenaderm
Barrier creams
Silver products
Honey
Topical Treatments
• Film dressings –
– will not manage excess moisture. Avoid using if
there is any drainage from the wound.
– Do use if the wound is too dry.
– Can combine with Santyl ointment to help soften
eschar
– Also, can apply over eschar that has been
crosshatched.
Use of film dressing for autolytic
debridement
The image above is a copyrighted product of AAWC (www.aawconlin.org) and has
been reproduced with permission.
Foams and Hydrofibers
• Use with wounds that are more heavily
exudating to help with management of wound
fluid.
Hydrogels and Hydrocolloids
• Useful in promoting autolytic debridement
and adding moisture to a wound
The image above is a copyrighted product of AAWC (www.aawconline.org) and has
been reproduced with permission.
Pain Control in chronic wounds
• Two types of pain associated with open
wounds:
– Nociceptive pain from the tissue damage creating
the wound
– Neuropathic pain from damaged peripheral
nerves at the site of the wound
Pain assessment
• The “usual” pain assessment will help
determine the most appropriate treatment
– Location
– Timing
– Severity
– Aggravating/alleviating factors
– Quality
Topical treatment of pain
• Dressing choice – avoid dressings that adhere
to the wound bed and in essence do
mechanical debridement with every dressing
change a cause pain.
– Protect skin surrounding the wound
– Premedicate with systemic pain med prior to
dressing changes
Topical Treatments for pain
• Topical medication prior to debridement
– EMLA (Eutetic Mixture of Local Anesthetics, 2.5%
lidocaine and 2.5% prilocaine, AstraZeneca,
Wilmington, Del)
– 2% Lidocaine gel
Topical treatments for pain
• Topical opioids:
– Morphine in a water-based gel
– Methadone in an inert wound powder
– The usual concentration in the studies is 1%
concentration of the opioid.
– Use of powder or gel depends on the condition of
the wound.
• Foam/Ibuprofen combination dressings.
Other treatment modalities
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NPWT
Hyperbaric Oxygen treatments
Compression
E stimulation
Ultrasound
Contact casting/offloading
Maggot therapy
The above images are copyrighted products of AAWC (www.aawconline.org) and
are reproduced with permission.
Complementary, alternative and
integrative therapy
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Accupuncture
Yoga/meditation
Biofeedback
Guided imagery
Massage
Therapeutic touch
• Herbs/dietary
supplements
• Aroma therapy
• Exercise
• Emotional health/stress
management
• Spiritual health
Managing the hard to heal wound
• Assessment
– Missed diagnosis?
– Cofactors contributing to the lack of healing
• Wound factors
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Edges
Base
Biofilm
Local treatment – appropriate choice, being done
appropriately?
Managing hard to heal wounds
• Patient factors
– Cooperating/participating in care? (“compliant”)
– Illness progression
– Mental health/social/spiritual
• Establish goals for care
– Healing
– Maintenance/palliation
– Symptom control
Treatment of hard to heal wounds
• Address etiology and cofactors affecting
healing based on goals of treatment
– Debride/cauterize edges of wound if epibole
present
– Treat hypergranulation/exuberant granulation
– Treat/manage biofilm in wound bed
– Treat/manage local and systemic infection
– Treat/manage systemic illness as able.
Hypergranulation
Image above is a copyrighted product of AAWC (aawconline.org) and has been
reproduced with permission
Managing local infection/biofilm
• Topical agents
– Silver sulfadiazine
– Topical antibiotics
– Topical silver – hydrofiber, gels
– Flagyl 500mg tab crushed, mixed in Santyl
ointment and applied daily to twice daily for 7
days *
* Note: this is an “off label use” of Flagyl. Works well in wounds with foul odor
indicating high local bacterial count in wound bed
Diphenyl hydantoin sodium (phenytoin)
• Capacity to accelerate ulcer healing was
reported over 40 years ago and has been used
in many different kinds of wounds.
• Possible mechanisms of action:
– Decrease in serum corticosteriod
– Acceleration of assembly and presence of collagen
and fibrin in the ulcer area
– Stimulation of alkaline phosphatase secretion
Other treatment options under study
• Oral Pentoxifylline along with compression to
treating venous ulcers
• Effects of stress response (epinepherine) and
the impact on wound healing = A new use for
Beta blocker therapy?
Assess for healing
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Pressure Ulcer Scale for Healing (PUSH)
Pressure Sore Status Tool (PSST)
Sessing Scale
Wound Healing Scale.
Pressure Ulcer Scale for Healing
(PUSH)
• Length x Width (in cm2) = score of 0-10 (0 cm2
- >24 cm2)
• Exudate amount = score of 0-3 (none, light,
moderate, heavy)
• Tissue type = score of 0-4 (closed, epithelial
tissue, granulation tissue, slough, necrotic
tissue)
• Total the 3 sub-scores. If the total score goes
down over time, the wound is healing.
Wound still not healing?
• Reassess goals of care
• Change the local treatment
• Refer to wound care clinic, vascular surgeon,
infectious disease specialist