Lower Extremity Ulcer

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    LowerExtremity

    UlcerBagus Andi PramonoSupervisors:

    dr. Hariadi Hariawan, SpPD, SpJPK

    Dr. dr. Budi Yuli Setianto, SpPDK, SpJPK

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    Background

    Chronic ulceration of the lower leg is a frequent condition,with a prevalence of 35% in the population over 65 years ofage.

    The incidence of ulceration is rising as a result of the ageingpopulation and increased risk factors for atheroscleroticocclusion such as smoking, obesity and diabetes.

    A leg ulcer is a loss of skin below the knee in the leg or foot which takesmore than 4 - 6 weeks to heal

    Mekkes et al., 2003

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    Background An appreciation of evidence-based treatment pathways

    and an understanding of the pathophysiology of chronicwounds are important elements in the management ofpatients with chronic wounds

    Vascular contribution in ulcer pathogenesis

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    Common causes Venous insufficiency (post-thrombotic syndrome)

    Peripheral arterial disease (arteriosclerosis)

    Diabetes (neuropathy and or arterial occlusion)

    Decubitus (pressure) Infection (mostly Streptococcus haemolyticus)

    Vasculitis (small vessel leucocytoclastic vasculitis)

    Mekkes et al., 2003

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    Leg ulcers Causes Poor circulation, often caused by arteriosclerosis

    Venous insufficiency (a failure of the valves in the veins of the leg that

    causes congestion and slowing of blood circulation in the veins)

    Other disorders of clotting and circulation that may or may not be related

    to atherosclerosis

    Diabetes

    Renal (kidney) failure

    Hypertension (treated or untreated)

    Lymphedema (a buildup of fluid that causes swelling in the legs or feet)

    Inflammatory diseases including vasculitis, lupus, scleroderma or other

    rheumatological conditions

    Other medical conditions such as high cholesterol, heart disease, high

    blood pressure, sickle cell anemia, bowel disorders History of smoking (either current or past)

    Pressure caused by lying in one position for too long

    Genetics (ulcers may be hereditary)

    A malignancy (tumor or cancerous mass)

    Infections

    Certain medications

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    Percentage

    81%

    10%

    7%

    1%

    1%1%

    Causes

    VenousArterial

    Mixed

    Diabetic

    Malignancy

    Rheumatoid

    O Brien et al., 2000

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    Philips et al, 1991

    Venous ulcers

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    Venous ulcer

    History of venous diseaseDVTs

    Recurrent Painless Signs of venous hypertension

    Haemosiderin Lipodermatoclerosis Eczema Flares/spider nevi

    Note : Normal ABIs Painless

    Tierney, 2009

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    Commonly noted in the"gaiter" region of the legs.

    Larger but shallower Moist granulating base,

    irregular border. This base oozes venous

    blood when manipulated. The tissue surrounding these

    ulcers may exhibit signs of

    stasis dermatitis. mild pain that is relieved by

    elevation.

    Venous ulcers

    Gabriel, 2012

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    Arterial ulcers

    Atherosclerosis

    Skin crack

    Arterial embolization

    Inadequateperfusion

    Ulcer

    Ischemia

    Necrotic tissue

    Mekkes et al., 2003

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    Arterial

    History of intermittent claudication

    Pain

    Absent pulses

    Reduced ABIs

    Beware

    Colour

    Temperature

    Capillary filling unreliable

    Tierney, 2009

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    Located distally and on the dorsum of the foot or

    toes. Irregular edgesa better-defined appearance.

    Grayish, unhealthy-appearing granulation tissue. Debridingbleed very little or not at all. Characteristic pain

    Characteristic findings of chronic ischemia(hairlessness, pale skin, and absent pulses)

    Gabriel, 2012

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    Anders et al., 2010

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    Wong, 2014

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    Chadwick et al.,2013

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    Pressure

    Neuropathic

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    Chadwick et al.,2013

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    Management

    Debridement

    Pressure control

    Infection control

    Exudate management

    Mustoe et al., 2006

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    TIME framework

    issue debridement

    Inflammation and infection control

    Moisture balance (optimal dressing selection)

    Epithelial edge advancement

    Chadwick et al.,2013

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    Debridement

    Methods of debridement used including surgical/sharp, larval,autolytic and, more recently, hydrosurgery and ultrasonic

    The requirement for further debridement should be determined ateach dressing change.

    No one debridement method has been shown to be more effectivein achieving complete ulcer healing

    Removes necrotic/sloughy tissue and callus

    Reduces pressure, allows full inspection of the underlying tissues Helps drainage of secretions or pus

    Helps optimise the effectiveness of topical preparations Stimulates healing

    Chadwick et al.,2013

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    Pressure control

    The key to the successful healing of chronic venous ulcers will be tocorrect the underlying venous hypertension using graduatedcompression therapy

    Education for patients regarding the need for life long support ofthe veins in their legs is paramount and should be emphasised fromthe beginning of treatment.

    Several different types of bandaging systems are available, each of

    which may have advantages over the others for particularapplications.

    EWMA, 2003; Moffatt, 2007

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    Infection control

    Start empiric oral antibiotic therapy targeted at Staphylococcusaureus and -haemolytic Streptococcus

    Change to an alternate antibiotic if the culture results indicate amore appropriate antibiotic

    Obtain another optimum specimen for culture if the wound does

    not respond to treatment.

    Topical antimicrobials benefit in: Concerns regarding reduced antibiotic tissue penetration

    poor vascular supply clinical suspicion of increased bacterial bioburden

    Chadwick et al.,2013

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    Common topical antimicrobial agents

    Silverdressings containing silver (elemental, inorganiccompound or organic complex) or silver sulphadiazine cream/dressings

    Polyhexamethylene biguanide (PHMB)solution, gel or

    impregnated dressings Iodinepovidone iodine (impregnated dressing) or cadexomer

    iodine (ointment, beads or impregnated dressings) Medical-grade honeygel, ointment or impregnated dressings

    Topical antimicrobial agents should not be used alone in those withclinical signs of infection

    Chadwick et al.,2013

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    Exudate management

    Dressings that can help to manage wound exudate optimally andpromote a balanced environment are key to improving outcomes

    Consider :

    Location of the wound Extent (size/depth) of the wound Amount and type of exudate The predominant tissue type on the wound surface Condition of the periwound skin Compatibility with other therapies (eg contact casts)

    Wound bioburden and risk of infection Avoidance of pain and trauma at dressing changes Quality of life and patient wellbeing

    Chadwick et al.,2013

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    The best dressing

    There is no consensus about the best agent. The method of debridement chosen may depend on the status of

    the wound, the capability of the healthcare provider and theoverall condition of the patient.

    It is common to combine methods of debridement in order to maximize the healing rates.

    Barbul, 2007

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    Adjunctive therapy

    Considered when needed and available

    Ulcers not healed with conventional therapy

    Growth factor (PDGF, GCSF)

    Negative pressure wound therapy Biological dressing

    Bioenginered skin equivalent

    Hyperbaric oxygen therapy Platelet rich plasma

    Greer, 2012

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    Conclusions Knowledge about etiology and pathophysiology of

    the lower extremity ulcers is needed to managepatients with ulcer in lower extremity;

    Vascular contribution plays major role in the ulcer of

    the lower extremity;

    Three important components of ulcer management: treat the causes, treat persons related complaints,

    treat the wound

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    Chadwick et al.,2013

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    Gist, 2009

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    Stages of chronic venous

    insufficiency(Expert meeting in Moscow, 2000.)

    0 - no symptoms;

    1 - heavy feet syndrome;

    2 - intermittent edema;

    3 - persistent edema, hyper- or

    hypopigmentation, lipodermatosclerosis,eczema;

    4 - venous ulcer.

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