SLIDE 1 Assessment and Treatment
Aimée D. Garcia, M.D.,CWS Assistant Professor, Baylor College of Medicine Director, Wound Care Clinic and Consult S ervice Michael E. DeBakey Houston VA Medical Center Houston, Texas
SLIDE 2
S peaker Disclosure
Dr. Garcia has disclosed that neither she nor
members of her immediate family have any actual or potential conflict of interest.
SLIDE 3 Obj ectives
- 1. Review wound types and risk factors.
- 2. Discuss management priorities and treatment
plans based on proper wound assessment.
SLIDE 4
Wound Repair Is a Complex Cellular and Biochemical Response to Inj ury
SLIDE 5
SLIDE 6
Wound Healing Physiology
Phases of Wound Healing
Hemostasis (0-3 hours) Inflammatory (0-3 days) Proliferative (3-21 days) Remodeling/Maturation (21 days-1.5 yrs.)
SLIDE 7 Factors that Impact Wound Healing
Nutrition Medications Infection Immobility Radiation Therapy Vascular Insufficiency Chronic Medical Diseases Aging
SLIDE 8 Nutrition in Wound Healing
CMS
and AHRQ specifically identify nutrition status as a significant risk factor for skin breakdown
Fibroblasts cannot synthesize collagen without
adequate nutrition
Wound contraction inhibited by malnutrition Protein deficiency poses greater risk for infection Muscle wasting increases risk for pressure inj ury
and wound trauma
SLIDE 9
Nutritional Assessment
Patient History Physical Exam Laboratory Testing Clinical Assessments
SLIDE 10 Assessment of Protein Metabolism
Visceral protein blood levels
S
erum albumin: 3.3-4.5 g/ dl
Transferrin: 200-400 mg/ dl Prealbumin: 20-40 mg/ dl
Total Lymphocyte counts
1500-3000 cells/ mm3
SLIDE 11 Nutritional S upport
Treatment Options
Oral nutritional support Enteral tube feeding Parenteral nutrition
Get a Nutrition consult early in the
management of chronic wounds if nutrition is a concern
SLIDE 12 Position of the Academy of Nutrition and Dietetics. J Acad Nut r Diet . 2019
SLIDE 13
Medications and Radiation
Compromised Wound Healing
S
teroids
Anti-inflammatory drugs Antimitotic drugs Radiation therapy
SLIDE 14 Wound Infection
Overgrowth of Microorganisms Resultant Tissue Destruction
Local symptoms
Wound deterioration Erythema, edema, drainage (purulent), tenderness,
warmth, induration and/ or crepitus S
ystemic symptoms
Fever, leukocytosis, confusion, tachycardia,
hypotension, malaise
SLIDE 15 https://doi.org/10.1111/j.1742-481X.2007.00388.x
SLIDE 16
SLIDE 17
Bacterial Burden and Wound Infection
Negative Impact on Wound Healing Prolongs the inflammatory stage Induces additional tissue destruction Delays collagen synthesis Prevents epithelialization
SLIDE 18 Colonization vs. Infection
Colonization
Bacteria in wound bed, not affecting the
environment Critical Colonization
Wounds with more than 100,000 organisms/ gram
will not heal
S
uspect bacterial burden if a clean wound shows no improvement after 14 DAYS
Infection
Invasion of the soft tissues
SLIDE 19 Wound Cultures
Traditional swab culture detects only surface
bacterial colonization/ contamination
May not reflect the invasive organism causing
infection Quantitative Wound Culture recommended for
determining infection
Documents bacterial burden Identifies bacteria actually invading wound tissue
SLIDE 20
Quantitative Wound Cultures
Tissue Biopsy Needle Aspiration Quantitative S
wab Technique
SLIDE 21
Antimicrobial Therapy
Determination of wound infection Identification of organism by culture or
gram stain prior to therapy
Do not use systemic therapy if infection is
local
Consideration of pharmacology and
toxicology
SLIDE 22
Aging S kin
Decrease dermal-epidermal turnover Decreased subcutaneous fat deposition Decreased elastin Decreased dermal blood flow Flattening of the rete ridges Thinning of the skin
SLIDE 23 Maj or Types of Wounds
Pressure Inj uries Vascular Ulcers
Arterial Ulcers Venous S
tasis Ulcers Neuropathic/ Diabetic Foot Ulcers Others
Pyoderma gangrenosum, malignancies,
calciphylaxis
SLIDE 24 Definition of Pressure Inj ury
A pressure inj ury is localized inj ury to the skin and/ or underlying tissue usually over a bony prominence, as a result of pressure, or pressure in combination with shear.
International NPUAP-EPUAP Pressure Ulcer Definition
SLIDE 25 Epidemiology
Pressure inj ury in vulnerable populations (elderly
and those with limited mobility) are common
Acute care – incidence ranges from 0.4%
to 38% with 2.5 million treated annually at cost of $11 billion/ year (1)
- 1. Pressure ulcers in America. Adv S
kin Wnd Care 2001;14(4): 208 - 215
SLIDE 26 Pressure Inj uries
Used to be:
Nursing issue only Physicians “ passive participants”
Currently:
Multidisciplinary: Dietitians Physical therapists Occupational therapists Physicians Nurses Physician Assistants/ Nurse Practitioners Patients Family members
- Wake. What clinicians need to know. The Permanent e Journal 2010
26
SLIDE 27 Pressure Inj uries – What Changed?
Cost
1996 – $64 billion(1.2%
2006 – $11 billion - hospital stays -PU as 1 or 2
dx(1)
$3500 – >$60,000/ person (depending on stage) (1)
CMS
Oct 2008 – withhold reimbursement for HAC
1HCUP 2008 data
27
SLIDE 28 CMS : Present on Admission for Acute Care
Pressure inj uries in acute care are “ reasonably
preventable”
One of eight original conditions selected as a
present on admission/ hospital-acquired condition (POA/ HAC)
October 1, 2008 – CMS
denied payment for HAPU
Hospitals took notice
SLIDE 29 CMS Regulations
Documentation requirements for care
settings
Influences
Reimbursement Citations and fines Public reporting
SLIDE 30 Present on Admission
S
tage 3 or 4 pressure inj uries
Location documented on admission by CMS
— defined professional legally responsible for making a medical diagnosis – are eligible for reimbursement
Physician MLP (nurse practitioner, clinical nurse specialist,
physician assistant)
SLIDE 31 CMS : Unavoidable Pressure Inj uries
CMS
revised guidance for health care surveyors for LTC
F Tag 314-pressure inj uries Identified pressure inj uries=s as most cited condition in
health quality checks (1)
Variances in survey findings between state and federal
surveyors
CMS
Goal –To provide more detailed and consistent guidance to surveyors
Added section on prevention and the definition of
unavoidable pressure ulcer for long-term care
- 1. Williamson, J Pressure’ s On. http:/ / mcknights.com/ pressures-on/ 107737/ . Pub 3/ 1/ 08
SLIDE 32 Unavoidable Pressure Inj ury
Pressure inj ury develops despite evaluation of
clinical condition and pressure ulcer risk factors
There needs to be definition and implementation
- f interventions consistent with needs, goals, and
recognized standards of practice
Must be monitoring and evaluation of the impact
Must be revision of the approaches to prevention
and treatment as appropriate
Ayello, Lyder, Research and Public Policy Context. Pressure ulcers: prevalence, incidence, an implication for the future. NPUAP , 2012
SLIDE 33
Pressure Inj ury S taging
CMS
requires S taging on their designated assessment forms in LTC and home care
SLIDE 34 CMS Mandated Assessment Instruments
Home Care – OAS
IS C (January 2010) requires documentation POA
Long-Term Care – Resident Assessment Instrument
(RAI) MDS 3.0 S ection M – (October 2010) requires documentation if S tage II,III, or IV or unstageable were POA
Inpatient Rehabilitation Facilities and Long-Term
Care Facilities – IRF-P AI (June 2012)
SLIDE 35 Common Sites of Pressure Injuries
Occiput (<1% ) Scapula (<1% ) Spine (<1% ) Elbow (<1% )
Sacrum & Coccyx (65%) Trochanter (9%)
Ischium (4% ) Knee (3% ) Tibia (2% )
Heel & Ankle (15%)
SLIDE 36
Wound S taging
Clinicians commonly describe pressure
inj uries using a six-stage classification
system to define the depth of tissue involved
SLIDE 37
Wound S taging
The basis for:
Developing treatment protocols S
electing reduction support surface
Obtaining reimbursement for a variety of
wound– related products
SLIDE 38 Rules of S taging
Only used for pressure inj uries S
tage all pressure inj uries at the deepest level of damage
Once a pressure inj uries is staged, it remains at that
stage
Reverse-staging/ back-staging* should never be used
to describe the healing of a pressure inj uries
SLIDE 39
CLASSIFICATIONS S tage 1 – Non-blanchable erythema of intact skin
SLIDE 40
S tage 2 – Partial thickness skin loss with exposed dermis
SLIDE 41
SLIDE 42 S tage 3 – Full-thickness loss of skin, in which adipose (fat)
is visible in the ulcer and granulation tissue and epibole (rolled wound edges) are often present. S lough and/ or eschar may be visible.
SLIDE 43
S tage 3 Pressure Inj ury
SLIDE 44 S tage 4 – Full-thickness skin and tissue loss with exposed or
directly palpable fascia, muscle, tendon, ligament, cartilage or bone in the ulcer. S lough and/ or eschar may be visible.
SLIDE 45
SLIDE 46 Deep Tissue – Inj ury-Intact or non-intact skin with
localized area of persistent non-blanchable deep red, maroon, purple discoloration or epidermal separation revealing a dark wound bed or blood-filled blister.
SLIDE 47
SLIDE 48 Unstageable – Full-thickness skin and tissue loss in
which the extent of tissue damage within the ulcer cannot be confirmed because it is obscured by slough or eschar.
SLIDE 49
SLIDE 50 Arterial Insufficiency
Peripheral arteriosclerotic occlusive disease is
the most common disorder associated with associated compromised wound healing
Resultant insufficient arterial perfusion to an
extremity
Complete or partial arterial blockage may lead to
tissue necrosis and or ulceration
SLIDE 51 Arterial Insufficiency/ Ulceration
Risk Factors:
Peripheral Vascular Disease (PVD) Diabetes Mellitus Hypertension Advanced age S
moking
SLIDE 52
Arterial Ulcer Location
Distal toes Heel Pretibial area Lateral malleolus
SLIDE 53
Arterial Ulcer Characteristics
Painful ulceration Pale wound bed lacking granulation Minimal drainage – desiccated and dry Appearance – “ punched out” May be necrotic Peri-wound skin pale
SLIDE 54
SLIDE 55 Arterial Assessment
Clinical Assessment:
Weak/ absent pulses Pain and Claudication Dependent rubor Elevation pallor Absence of leg hair S
kin shiny, dry, pale
Thickened nails
Vascular Assessment:
ABI <0.8 TCOM CT angio if symptomatic Referral for intervention- IR, Cardiology, Vascular surgery
SLIDE 56 Arterial Ulcer Management
Maximize blood flow and tissue perfusion
Refer early if symptomatic
Treatment Options:
S
urgical revascularization
Angioplasty Pharmacotherapy agents Lifestyle changes
SLIDE 57 Arterial Ulcer Management Optimize the
Wound Environment
Topical dressings
If dry, keep dry If wet/ unstable, moist dressings
Autolytic debridement Moist wound healing
Observe for infection
If poor blood flow, antibiotic usefulness may be limited Topical antimicrobial therapy if no s/ s of infection
Judicious debridement
May not have vascular ability to support healing
No sharp debridement Other types of debridement can be used if wound bed is
unstable May potentiate the tissue ischemia
SLIDE 58 Venous Insufficiency
1%
3.5%
- f persons over 65 yr of age
Recurrence rate of 70% Venous ulcers account for 90%
- f all chronic wounds
- n the lower leg
Result from disorders of the
deep venous system
SLIDE 59 Venous Ulcers
Predisposing factors:
Thrombophlebitis Deep Vein Thrombosis (DVT) Prior pregnancy Leg trauma Cardiac disease Poor nutrition Absence of/ or poor calf muscle pumps
SLIDE 60 Venous Ulcer
Location/ Characteristics
Most common location
Medial aspect of leg superior to medial malleolus
Exudation varies Degree of pain varies greatly from painless to
extremely painful
Irregular wound margins Granulation tissue usually present
SLIDE 61
Venous Ulcer Assessment
Edema Hemosiderin deposits Pulses present “ Ankle Flaring” Lipodermatosclerosis Dermatitis S
carring from previous ulcer
SLIDE 62 Venous Ulcer Management
Goal:
Reduce venous hypertension and improve venous
return Treatment Options
Elevation of legs Topical Management/ Dressings Compression therapy S
urgical ligation of incompetent perforators
SLIDE 63 Venous Ulcer Management
Optimize Wound Environment
Compression therapy
Increases interstitial tissue
pressure, which eliminates the leakage of fluid from capillaries into tissues and supports reabsorption of fluid back into blood stream
SLIDE 64 Diabetic Foot Ulcers
Plantar ulcers (metatarsal heads) caused by
combination of neuropathy and small vessel vascular insufficiency, leading to ischemia in the soft tissues compressed against bone
Hyperglycemia impairs leukocyte function and
collagen synthesis
SLIDE 65 Diabetic Foot Ulcer
Affect more than 1 million patients at some
point in their lifetime
Diabetic patients form the single largest
group of non-traumatic amputations in the United S tates
50%
- f patients with amputation of a leg
due to Diabetes will have the other leg amputated within 2 years.
SLIDE 66 Diabetic Foot Ulcer
Predisposing Factors
Peripheral vascular disease Peripheral neuropathy
Altered or complete loss of sensation in foot/ leg Lose all sharp-dull discrimination Cuts or trauma can go unnoticed
SLIDE 67
Diabetic Ulcer Characteristics
Painless Even wound margins with propensity to
form callous
Deep wound bed Granular tissue
SLIDE 68 Diabetic Ulcer Assessment
Neuropathy
Diminished or no sensation in foot
Foot deformities Arterial evaluation
SLIDE 69 Charcot Foot Deformity
Arterial vascular compromise and bone infarcts
leading to midfoot micro fractures result in collapse of normal boney architecture
Disfigurement, swelling, and abnormal bony
prominences Plantar ulcerations with necrosis and infection
SLIDE 70 Diabetic Ulcer Management
Control serum glucose levels Offloading & Orthotics Absorb drainage Maintain a moist wound
environment
Monitor for infection Debride necrotic tissue and
hyperkeratotic rim
SLIDE 71 Documentation
Must take systematic approach
Ulcer measured from head-to-toe Length X Width X Depth in centimeters Assess periwound tissues, wound bed and level
and type of exudate
Evaluate undermining Cannot “ backstage”
SLIDE 72
UNDERMINING
Dead S
pace
Appropriate dressing Risk of infection
SLIDE 73
General Principles of Wound Management
Reduce/ eliminate the cause Provide systemic support Appropriate topical therapy
SLIDE 74
Reduce/ Eliminate the Cause
Pressure S
hear
Friction Moisture Circulatory impairment Neuropathy
SLIDE 75
Provide S ystemic S upport
S
upport fluid and nutritional intake
Gain control of systemic factors affecting
wound healing
SLIDE 76 S ibbald G, et al. Adv S kin Wound Care. 2007 Jul; 20(7):390-405
SLIDE 77
Conclusion
Identification of the type of wound guides
management
Good documentation is important for
communication
Wound bed preparation is the cornerstone of
wound healing
