chronic leg ulcers
TRANSCRIPT
Chronic Leg Ulcers
Joyce K. Stechmiller PhD, ARNP, FAANLinda J. Cowan, PhD, APRN, FNP-BC-CWS
Disclosures
Joyce K. StechmillerTitle: Associate ProfessorDept: Biobehavioral Nursing Science, College of NursingContact info: 352-263-6394 Office352-273-6536 Fax352-284-1801 [email protected]
We have no relevant financial relationships or commercial interests to disclose regarding the content of this presentation.
Linda J. CowanCourtesy Associate Clinical Professor, UF College of MedicineAssociate Chief, Nursing Service Research & Associate Director, VISN 8 Patient Safety Center of InquiryJames A. Haley Veteran’s Hospital & Clinics, Tampa, FL 813-558-3932 [email protected]
OBJECTIVES
• Define types of chronic leg ulcers
• Identify common leg ulcer pathophysiology (venous, arterial, diabetic leg ulcers)
• Discuss venous versus lymph edema
• Describe common impediments to wound healing
• List common complications associated with chronic lower extremity wounds
• Describe required elements of clinical assessment
• Summarize evidence-based wound care management
CHRONIC ULCER
• “Chronic” leg ulcer commonly considered an
ulceration of more than 4-6 weeks duration
• Chronic ulcers results when sequel of repair is
disturbed at one or more stages of inflammation,
proliferation, re-epithelialization, remodelling
• Not following expected pathway to healing
• Staph aureus, Strep pyogens, Strep fecalis, E. coli
are common organisms colonizing lower
extremity ulcers
• Biofilm structures commonly identified
ETIOLOGY OF LEG ULCERS
• Venous
• Arterial
• Mixed – arterial / venous / neuropathic
• Diabetic foot ulcers
• Other:– Connective tissue disorders- vasculitis
– Malignancy
– Trauma (surgical, accident, injury, bite/sting, self-inflicted)
CASE DISCUSSION - MRS. JONES*
*Names used for cases are ficticious
MRS. JONES
• 75 years old, Ht 5’2” Weight 160 lbs
• VS today: BP 140/75; P 76; R 20; T 98.4
• Widow, lives alone
• Diabetes type II x 15 years, well controlled;
borderline hypertension
What else do you want to know about Mrs. Jones?
Why?
ASSESSMENT OF LE ULCERS• Evaluate patient’s description of wound etiology, significant past medical
history/comorbidies, location of wound, duration of wound
• Has patient had any vascular consult/diagnostic testing past 12 months?
• Evaluate / examine: Peripheral pulses Dorsalis Pedis / Popliteal;
Extremity skin color, temperature, edema of surrounding skin / extremity:
Warm / Cool to touch;
• Wound size, wound bed appearance (presence of viable/nonviable tissue),
exudates, odor, tunneling, undermining, periwound skin
• Evaluate patient’s need for debridement & patient’s level of pain in wound
• Evaluate S/S of active infection / potential infection: Superficial high
bioburden; Local / cellulitis; Deep / osteomyelitis; Systemic
• Determine appropriate diagnostic needs: ABI; Doppler; TCPO2; X-ray,
MRI, bone scan, etc.; Labs (culture, biopsy, WBC, Hgb/Hct, pre-albumin,
serum zinc, vit. D; other nutritional markers)
TEMPLATES
DIAGNOSTIC & TREATMENT GUIDELINES AND ALGORITHMS
• WOCN – Wound, Ostomy, Continence Nurses Society
– www.wocn.org
• AAWC – Association for the Advancement o Wound Care
– www.aawconline.org
• SIGN – Scottish Intercollegiate Network
– Mobile app
VENOUS LEG ULCERS
• Venous leg ulcers (VLU’s) account for 70-90% of leg
ulcers
• Affect 500,000 to 2 million persons annually
– 2-4% of the population at any given time will have
ulcers due to venous disease – increased as more
people are living longer
– 4% of people over 65 years of age
• Average age of VLU patients 70 years
• Women twice as likely to be affected than men
• Cost: In the US, $2.5 billion per year; as much as 1%
of healthcare costs
• Gross arterial disease should be ruled out
• Elevation of ambulatory venous pressure (venous hypertension) is most common cause
• Venous hypertension
– Blood backflows or pools in deep veins
– Varicosities when superficial veins stretch
• Capillary hypertension
– Results in edema, fibrin cuffs, hemosiderin
staining (also called hyperpigmentation)
VENOUS ULCERS
WHY VLU DEVELOP?• Chronic Venous Insufficience (CVI) most common
cause of VLU
• Venous hypertension, or abnormally sustained
elevation of venous pressure on walking
• vein valve reflux, outflow problems or both
• Venous outflow issues
• Venous obstruction
• Poor function of calf muscle pump impairs ability
to return venous blood to heart
• Ankle movement limitations contribute to calf
muscle pump failure
VENOUS ANATOMY
Courtesy of Norma Stordahl, ARNP, CWS, 2006
VENOUS INSUFFICIENCY
Courtesy of Norma Stordahl, 2006
DIAGNOSIS
• Clinical history
• Physical exam
• Diagnostic procedures
• Differential diagnoses of leg ulcers
COMMON VLU HISTORY• Age over 55 years
• 50% have a history of leg injury
• Obesity / higher Body Mass Index (BMI)
• Family history of varicose veins / CVI / ankle ulcers
• Prolonged standing
• History of pulmonary embolism / DVT or Phlebitis
• Varicose vein surgery
• Lower extremities skeletal or joint disease
• Increased number of pregnancies
• Physical inactivity
PHYSICAL FINDINGS OF CVI • Swelling and aching of legs, worse at end of day and
improved by leg elevation (exacerbated by dependency)
• Dependent edema, varicose veins, reddish-brown
pigmentation, purpura, subsequent hemosiderin deposition
• Eczematous changes with redness, scaling, pruritus
• Smooth, ivory-white, stellate atrophic plaques of sclerosis
(atrophie blanche)
• History of ulcer recurrence, particularly at same location
• Chronic CVI leads to lipodermatosclerosis (LDS) –
scarring/fibrosis of skin and fat (painful)
CHRONIC VENOUS INSUFFICIENCY
EDEMA• Excessive fluid in interstitium
• Hallmark of venous insufficiency
• Inflammatory response to injury—
– histamine release
– vasodilation
– increased vascular permeability
• Limb dependency, venous hypertension
• Considerations:
– Congestive heart failure
– Lymphedema
LYMPHEDEMA VS. VENOUS INSUFFICIENCY
• Firmer than
hydrostatic
edema
• Involvement of
toes
• Stemmer’s sign
• Peau d’orange• More difficult
to treat
• Chronic
infection
CVI VS LYMPHEDEMA
LYMPHEDEMA STAGES• Stage 0 – new classification, latent or preclinical stage, no edema present.
Studies indicate through use of bioimpedance, is possible to identify
changes in limb at risk, before symptoms become visible.
• Stage 1 – Swollen tissues soft, pitting edema. Lmphedema treatment
should be begun as soon as early signs are detected. Waiting for swelling to
increase, or for infection to develop, only makes condition more difficult to
treat. Prompt treatment can control it and may prevent it from becoming
more severe.
• Stage II – Elevation of limb does not reduce swelling, no pitting, tissues just
starting to become firm, can usually be improved with intense treatment
• Stage III - Tissue increasingly fibrotic (hardened) - Lymphostatic
elephantiasis. With intense therapy, Stage III lymphedema may improve and
potentially be prevented from becoming worse; however, rarely reversed to
an earlier stage.
RESOURCE
• The Diagnosis and Treatment of Peripheral
Lymphedema. 2009 Consensus Document of the
International Society of Lymphology. Lymphology 42,
June 2009, pages 53-54.
WOCN CLINICAL GUIDE
Venous insufficiency vs.
Arterial insufficiency vs.
Peripheral neuropathy
ARTERIAL VS. VENOUS ULCERSArterial:
• Progressive pain: intermediate claudication with less activity finally rest pain indicates 90% occlusion
• Pain usually lessens with dependent position
• Elevation pallor, dependent rubor
• Thin shiny skin; leg hair loss
• Reduced ABI (<.6 vascular surgeon consult)
• Punched out appearance
• Dry, pale wound bed
• Weak or absent pulses
Venous:
• Superficial
• Edema, erythema, scaling and weeping of lower leg
• Aching Pain worse toward end of day & relieved by elevating legs
• Ulcer edges usually irregular
• Ulcer base ruddy in color and exudative/wet appearing
• Needs Compression but always rule out arterial involvement first
PREVENTING VLU• Aggressive control of reversible risk factors
• Management of relevant comorbid conditions (CHF,
PVD)
• Healthy diet, weight control
• Exercise
• Management of hypercoagulable state
• Stockings: at least 20-30 mm Hg pressure
• use highest level of compression tolerable up to
45mm Hg
• Surgical venous ablation
EDEMA CONTROL
• Elevation
• Compression therapy with garment, pneumatic
compression and layered wrap systems
• Classes of compression
1. Class 1: 15-20 mmHg
2. Class 2: 21-30 mmHg
3. Class 3: 31-40 mmHg
4. Class 4: 41-50 mmHg
MULTI-LAYER COMPRESSION DRESSINGS—ACHIEVING CLASS 3 COMPRESSION 30-40MMHG
STRETCH BANDAGES ALONE - NOT EFFECTIVEEberhard Rabe, Hugo
Partsch, Juerg Hafner, et al.
(2018). Indications for
medical compression
stockings in venous and
lymphatic disorders: An
evidence-based consensus
statement. Phlebology, Vol.
33(3) 163–184
CLASS III COMPRESSION GARMENT-30-40MMHG-DISTAL TO PROXIMAL
COMPRESSION PUMPS
Pneumatic compression
• often prescribed for
overnight use
• single chamber or
sequential
HOW LONG SHOULD CLINICIANS PRESCRIBE COMPRESSION THERAPY?• Continue until ulcer heals and continue
indefinitely after healing to prevent recurrence
• Instruct how to put on stockings
– Ensure proper measurement and fit
– On first thing in morning and off at bedtime
– Assistive devices for arthritic, obese, elderly patients
– Replace stockings at least every 6 months
– Helpful to have 2 pairs (wear one, pair wash one)
– Hand wash, not machine wash/dry; mild detergent
ROLE OF EXERCISE/PHYSICAL THERAPY FOR CVI, VLU & LYMPHEDEMA• Aim: to improve range of ankle movement and calf
muscle pump function
• May enhance ulcer healing
CONSIDER REFERRAL
• Prognostic factors associated with slower healing
– Large wound area (>5 cm2) and long duration (>6 months)
– Ulcer history, BMI >33 kg/m, physical inactivity
– Prolonged venous filling time, deep venous insufficiency
– Severe lymphedema / mixed etiologies
– Ulcer depth >2 cm, atypical ulcer location (posterior calf)
• Refer to (wound) specialist when wounds fail to
decrease in size during first month of treatment
– Expertise may be found in a variety of specialties
– Vascular medicine and surgery, podiatry, dermatology,
infectious disease, etc.
MANAGING INFECTION -ROLE OF ANTIBIOTICS
• Bacteria can secondarily colonize the wound and
general tendency is to over treat
• Not necessarily indicate infection
• Wound bacteria may be transient and may not be
detected on random swabs
• Fever / erythema /swelling / increased pain /
leucocytosis
• Frequent fungal involvement
• Consider other pathologies (pyoderma gangrenosum)
VLU PATIENT AND CAREGIVER EDUCATION
• Encourage patients to adhere to compression
therapy
• Provide educational materials on pathophysiology,
management, and prevention (“teach back”)
• Consider video-based educational interventions
to teach patients about the disease
• Consider patient support groups for education
on self-management
VLU TREATMENT
Goals: reduce edema, reduce pain, heal ulcer, prevent
recurrence
Maintenance:
Moist wound bed and regular debridement
Infection control
Compression with elastic multilayer bandages
If no improvement in 4 weeks: consider referral to
wound expert and adjuvant therapies
Prevent recurrence: indefinite use of compression
stockings and vascular intervention
ARTERIAL INVOLVEMENT• All patients with lower extremity ulcers should
be evaluated for arterial disease
• 20% who have venous also have arterial disease
• Common Symptoms:
– Claudication
– Rest pain
– Dry, cool skin
– Distal atrophy and alopecia
– Dependent rubor, elevation pallor
– Absent pedal and proximal pulses
ARTERIAL INSUFFICIENCY ULCER
ARTERIAL OCCLUSION
• Indicate the presence of severe occlusive disease
Atherosclerosis, vasospasm, inflammatory
vascular disease
• Loss of nutrients and oxygen lead to tissue break
down
• Common locations: between toes, tips of toes,
ankles
CLINICAL SIGNS OF ARTERIAL DISEASE
• Claudication
• Rest pain- distal limb
• Dry, cool skin
• Distal atrophy and alopecia
• Dependent rubor, elevation pallor
• Absent pedal and proximal pulses
PREVENTION
• Vigilance in high risk population
• Education and interdisciplinary approach
• Monitor for critical limb ischemia ABI <0.40
• Smoking cessation
• Physical activity to induce collateral vessels
• Protective Footwear
• Control systemic conditions (diabetes, hypertension,
hyperlipidemia)
ARTERIAL ULCERSCLINICAL CHARACTERISTICS
• Deep punched out appearance
• Scant granulation in wound bed
• Location between toes, on toe tips, outer ankle
• Dry gangrene (vs. wet gangrene)
ARTERIAL INSUFFICIENCY
PAD RISK FACTORS
• Smoking
• Diabetes
• Hypertension
• Obesity
• Hypothyroidism
• Age >65
MR. SMITH
What do you suspect? What do you want to know?
NON INVASIVE STUDIES
• Ankle-Brachial Index (ABI)
• Color Doppler
• TcPO2
• TBI (toe)
ABI TECHNIQUE
• Patient recumbent for five minutes
• Obtain resting systolic blood pressures:
Average of both arms= brachial reading (denominator)
Each individual L & R ankle systolic BP (numerators)
• ABI= L or R ankle pressure / average arm pressure
• For ABI < 0.9, recommend to do comparative ABI
following exercise
• For diabetic, measure great toe pressure for TBI
NON-INVASIVE RESULTS• ABI 0.9 to 1.2= normal
• ABI 0.6-0.9 = PAD (possibly intermittent
claudication)
• ABI <0.6 = severe disease, likely leg pain at rest
• ABI < 0.4 = limb threatening PAD/critical ischemia
• ABI > 1.2 = arterial disease: DM, kidney disease
Consider vascular surgery consult if:
• ABI < 0.8 or > 1.2
• TBI <0.75 for diabetic non-compressible vessels
• TcPO2 on periwound <40mmHg
MR. SMITH
• Ruled out lymphedema
• ABI 0.8
• Dependant edema, worse at night
• Suspect both venous and arterial components
• No complaints of pain at rest
• Would you use compression?
• Would you recommend walking exercise?
• What other recommendations would you have?
DIABETES – FACTS • 16 million diabetics: 15% develop foot ulcers
• 30% of hospitalizations related to foot problems
• Amputations on the rise - 85% of LE amputations
preceded by diabetic foot ulcer (DFU)
• 35% recurrence rate in first year, 70% recurrence
rate in 5 years
• 50% develop contra lateral foot problems and 50%
again will have amputations
• 3 year mortality is approximately 50%
• 5 year mortality is approximately 70% after
amputation
DIABETIC ULCERS
DIABETIC FOOT ULCER RISK FACTORS
• Abnormal ABI
• Peripheral or autonomic neuropathy (abnormal
monofilament testing 10g)
• Abnormal hemoglobin A1c
• Lack of routine foot care
DIABETES
• Hyper glycemia leads to increase in glucose content in the tissues which binds to proteins leading to cellular damage
• Increase sorbitol and fructose in cells leads to accumulation of water in the cells
• Increased sorbitol leads to decreased myoinositol in cells also postulated for the cellular damge
• Neutrophil dysfunction and phagocytosis
DIABETIC ULCERS WITH HAMMER TOES
DIAGNOSIS
• Location of ulcer
• Clinical history—footwear, trauma
• Rule out arterial insufficiency—present in 50%
• Presence of neuropathy—up to 60%
DIABETIC NEUROPATHY
• Neuropathy with abnormal pressure points,
particularly on the plantar aspect of the foot
- Sensory - diminished sensation to touch, pain or
temperature
- Autonomic - absence of sweating, loss of skin temp
regulation, abnormal blood flow to soles of the feet
(xerosis, fissures, cracked skin on soles of feet)
• Untreated, leads to musculoskeletal foot
deformity (hammertoes, hallux valgus, bunions,
Charcot foot)
EXAMINATION / ASSESSMENT• Deformities
hammer toes, bunion (hallux valgus), foot drop, Charcot,
fracture, neuromas, tissue loss (previous amputation or
trauma), heel spurs
• Appearance
ROM, strength, pain, edema, toenails; vascular status
• Sensation
Semmes-Weinstein 10g, vibration (tuning fork)
• Skin Description
temperature, color/discoloration, dry, callus, cracks, fissures,
ulceration
Ms. Wilson
MS. WILSON
• What do you want to know?
• What do you consider for orders?
• What do you recommend?
• What are the 3 most important factors of her
treatment plan?
DIABETIC ULCER CHARACTERISTICS
• Location
– plantar midfoot
– Metatarsal pads
– Heel
– Site repetitive trauma
• Wound Appearance
– Well defined margins, variable depth, granulation
frequently present, macerated perimeter
• Surrounding Skin
– Erythema (cellulitis), induration, callus
OFF-LOADING TO MINIMIZE REPETITIVE INJURY• Reverse detrimental effects of neuropathy and
deformity to decrease morbidity
• Acceptable methods of offloading include crutches,
wheelchairs, custom shoes, custom inserts, diabetic
boots, forefoot and heel relief shoes, total contact
casts, knee-walkers
OTHER CAUSES OF LOWER LEG ULCERS
• Malignancy
• Trauma
• Osteomyelitis
• Vasculitis
• Pyoderma Gangrenosum
WOUND HEALING
SYSTEMIC FACTORS THAT IMPAIR WOUND HEALING
Age:
Decreased rate of
cellular proliferation,
Angiogenesis,
Contraction, Collagen
formation & remodeling;
Increased rate of
dryness & desiccation
Hypoxia:
Severe
anemia,
Insufficient
volume,
Cold/pain,
Shock
Psychological:
Stress,
depression,
sleep disorders
LOCAL FACTORS THAT IMPAIR WOUND HEALING
Devitalized
Tissue
Presence of
bacteria/fungi
Edema
Reduced
collagen
production
Infection Decreased
perfusion: pain,
cold, meds, SNS
stimulation
LOCAL FACTORS THAT IMPAIR WOUND HEALING
Wound
dressings
Example:
wet-to-dry
(lack of
evidence,
disruption of
viable ECM,
fibroblasts,
etc.)
Cytotoxic
Wound
Cleansers
or mechanical
injury
Drying out
wound bed:
epithelialization
50% faster in
moist
environment
SYSTEMIC FACTORS THAT IMPAIR WOUND HEALING- Nutrition:
Deficiency of
protein, calories,
vitamins, trace
minerals (ZN, CU)
- Hydration
Weight
Extremes:
Obesity
(BMI>30)
Under wt
(BMI <18.5)
CoMorbid cond:
COPD, DM,
CVD, SCI,
Cancer,
Connective
tissue disorders,
autoimmune dz
Medications:
NSAIDS, steroids,
chemo, antibx,
heparin/coumadin
Radiation Immune
suppression
WOUND MANAGEMENT(ADDRESS ETIOLOGY)
IDEAL DRESSING AGENT
• Protect from bacterial invasion
• Maintain optimum humidity, temperature,
moisture
• Absorb excess exudate from wound site
• Protect granulation tissue
• Reduce pain
• Wet-to-dry dressings are not evidence-
based wound care!
GOALS FOR THERAPY • What does patient want?
• Healing
– Sheehan et al. (2003). Percent Change in Wound Area of
Diabetic Foot Ulcers Over a 4-Week Period Is a Robust
Predictor of Complete Healing in a 12-Week Prospective
Trial. Diabetes Care, 26(6), 1879-1882.
• Palliative
• Treat/prevent infection
• Pain control
• Odor control
• Prevent recurrence
DOCUMENT & EDUCATE
• Document, document, document
• Educate, educate, educate
• Document again – Follow up!
HAPPY WOUND HEALING
QUESTIONS?
ADDITIONAL REFERENCES• Bryant, R. A., & Nix, D. P. (2015). Acute & Chronic Wounds: Current Management
Concepts. St. Louis, Mo: Elsevier Mosby.
• Cowan, L., Phillips, P., Stechmiller, J., Yang, Q., Wolcott, R., Schultz, G. (2013). Chapter 4:
Antibiofilm strategies and antiseptics (Chapter 4). In Antiseptics in Surgery – update 2013.
Christian Willy (Editor). Ulm, Germany: Lindqvist Book Publishing.
• Cowan, L. (2013). Wound Series Part 1: Assessing and Diagnosing Chronic Wounds of the
Lower Extremity. CEUFAST,
http://www.ceufast.com/courses/viewcourse.asp?id=257&nurse-ce-course-
title=Wound+Series+Part+1%3A+Assessing+and+Diagnosing+Chronic+Wounds+of+the+L
ower+Extremity
• Lower Extremity Wounds: A Problem-Based Learning Approach. (2009). First Edition. Edited
by Karen Ousey and Caroline McIntosh. London, England: Wiley Publishers.
• Phillips, P., Wolcott, R., Cowan, L. & Schultz, G. (2016) Functional Biomaterials: Biofilms in
Wound dressings (Chapter 3). In: Wound Healing Biomaterials, Volume II, Edited by Magnus
S. Ågren, Copenhagen Wound Healing Center, Denmark, pp.55-78. DOI 10.1016/B978-1-
78242-456-7.00003-9.
• White-Chu, E.F., and Conner-Kerr, T.A. (2014). Overview of guidelines for the prevention
and treatment of venous leg ulcers: a US perspective. Journal of Multidisciplinary Healthcare
7:111-117. doi:10.2147/JMDH.S38616 PMID: 24596466