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 CellStechjk@ufl.edu

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 Officecowan@ufl.edu

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