All about Leg Ulcer

LEG ULCERSLEG ULCERSJulian ChoiJulian Choi

BACK GROUNDBACK GROUND

Leg Ulcers - major morbidityLeg ulcers present 3-4% of population > 65 years oldM:F 1:2 ratioChronicRecurrent

DIFFERENTIAL DIAGNOSISDIFFERENTIAL DIAGNOSIS1. Arterial ulcer - PVD2. Diabetic ulcer3. Venous ulcer - chronic venous insufficiency4. Pressure ulcer5. Neoplastic ulcers - MM, Marjolin ulcers6. Infectious ulcer - TB, syphilis, HIV7. Tropical ulcer - leishmaniasis, fungal8. Haematological ulcer- sickle cell, thalassaemia, leukaemia9. Nutritional/metabolic ulcer - vitamin def., uraemia10. Allergy - drugs, photosensitivity, chemical exposure11. Insect bite - white tail spider12. Vasculitis - RA, SLE, polyarteritis13. Other - pyoderma gangrenosum, inflammatory bowel disease

ARTERIAL ULCERARTERIAL ULCER

Chronic lower limb ischaemia presents:ClaudicationCritical limb ischaemia - rest pain, arterial ulceration,

gangrene of foot.

Definition of critical ischaemia -ankle systolic pressure < 30 - 50mmHg

Prognosis of Critical limb ischaemia is poor25% mortality within 1 yr; 50% within 5 yrs.

Arterial Ulcer Arterial Ulcer

1. General Assessment

1. Functional status2. Mobility

Arterial Ulcer Arterial Ulcer -- IxIx

2. Global vascular status1. Ankle brachial pressure index

ABPI < 0.9 PVDABPI 0.8 - 0.9 moderate PVDABPI 0.5 - 0.8 claudicationABPI < 0.5 critical ischaemia

2. Toe brachial pressure index - in diabetic

Arterial Ulcer Arterial Ulcer -- IxIx3. Disease localisation

1. Colour duplex scanningPeak velocity ratio > 2 - 50% stenosis

2. Digital subtraction angiography

3. CT angiography

Arterial Ulcer Arterial Ulcer -- RxRx

CLI significant financial burden.

Amputation can be more expensive than reconstruction in longer term.

If pt has a reasonable quality of life, attempt to revascularisation whenever possible.

Preoperative mobility and independence ADL -best predictor of post operative independence and mobility

after infrainguinal bypass for CLI.


Endovascular treatment

Endovascular Tx can be effective short term, first line treatment for arterial ulceration.

Applicable in 50 - 75% cases ( London 1995)

Aortoiliac disease to be treated first.

Subintimal angioplasty - used for SFA occlusion, femoro-popliteal disease.

Limb salvage rate between 50 - 89%.(Ray 1995, London 1995, Greenfield 1980)


Surgical Revasculisation

Suprainguinal BypassAortobifemoral Bypass

Femoro-femoral or Ileo-femoral bypass for unilateral Axillobifemoral bypass for bilateral

Infrainguinal BypassFemoropopliteal bypass

vein ( in situ/ reversed) graft vs PTFE graft


Surgical treatment

Infrainguinal BypassFemoropopliteal bypassFemorodistal ( tibial/ pedal) bypass

vein ( in situ/ reversed) graft vs PTFE graft

Primary patency ratesFemorodistal bypass - 60 -85% at 1yr

50-75% at 5 yrs


Non-surgical treatment

Pressure careSlow release opiate analgesiaProstacyclin analogues

Iloprost ( Feiessinger 1990)Meta-analysis of 6 RCTs( n - 700)Reduction in death and amputation at 6 months

( 35% vs 55%) Chemical sympathectomyDorsal column stimulation

DIABETIC ULCERDIABETIC ULCER

Incidence of diabetic foot ulcer - 3-7%

Aetiology - Purely neuropathic (45-60%), Ischaemic (10%),Mixed neuroischaemic origin (25-45%).

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Diabetic Ulcer Diabetic Ulcer -- AetiologyAetiology

1.Diabetic Neuropathy - sensory, motor, autonomic2.PVD3.Abnormal Microcirculation4.Biomechanical aspects - Increased plantar pressure, callus

altered foot shape5.Other - impaired vision, immobility, impaired neutrophil

function.

Diabetic Ulcer Diabetic Ulcer -- AetiologyAetiology

Diabetic neuropathy:

Hypothesis -

1. Microvascular disease causing nerve hypoxia2. Direct effect of hyperglycaemia on neuronal metabolism3. Abnormal NO metabolisim - perineural

vasoconstriction and neuronal damage.

Diabetic Ulcer Diabetic Ulcer -- aetiologyaetiology

1. Sensory neuropathy - distal, symmetrical sensory loss (pain, T, vibration, absent ankle reflex), burning, paraesthesiae, shooting pain nocturnal exacerbation, lack of relationship to exercise.

2. Motor neuropathy - wasting of intrinsic muscles of foot - leadto clawed toes, prominent MT heads.

3. Autonomic neuropathy - reduced sweating, AV shunt causing increased blood flow - warm/bounding pulse with dry/crackedskin prone for trauma and infection.

Diabetic Ulcer Diabetic Ulcer -- aetiologyaetiology

PVD

PVD x 20 times more common in DM.

More distal disease.

Clinical features - painful ulcers in end of toes, absent pedal pulses,ABI < 0.9 ( beware of hard DM vessels), dopplerwave form ( loss of triphasic wave form), pole test

Diabetic Ulcer Diabetic Ulcer -- TxTx

Principles of Tx

1. Multidisciplinary team -endocrinologist, surgeon, podiatrist,orthotist, diabetic educator, vascular/ orthopaedic surgeon.

2. Annual screening of ‘at risk’ foot - semmes-weinstein monofilaments screening for PN, ABI, PVS examination.

3. Foot Care EducationMalone et al. 2/3 reduction in amputation and ulceration Rate with 1 h educational session.

4. Tight control of BSL - aim for normoglycaemia

Diabetic Ulcer Diabetic Ulcer -- RxRx

Principles of Rx

5. Neuropathic ulcer

Pressure relief : Appropriate footwearTotal contact cast - Mueller 90%(contact cast) healed

in 42d vs 67%(without cast) in 65 days.

Debridement of CallusPrevent wound healing from the margin, hide

infection.Weekly debridement/ review of shoes.

Diabetic Ulcer Diabetic Ulcer --RxRx

6. Ischemic ulcer

Prompt vascular assessment

Angiography

Aggressive Revasculisation when indicatedLocal amputation for gangrene ( ray amp., transMT amp.)

Regular exercise (Ubels 1999)

ACEi (NEJM 2000)

Control other CVD risk factors - smoking

Diabetic Ulcer Diabetic Ulcer -- RxRx7. Rx of Infection

Bacterial colonisation is universal -Superficial wound swab inadequateDeep Bx( curetting of ulcer base, debridement)

Clinical signs of infection reliable (local erythema, swelling, pus)systemic signs rareabscess, crepitus (gangrene)

Polymicrobial infection ( G+v, G-v, Anaerobes, MRSA) & synergistic.

Broad spectrum antibiotics

Diabetic Ulcer Diabetic Ulcer -- RxRx8. Osteomyelitis

Suspected in deep DM ulcer

Clinical evidence - ability to probe bone with a instrument atthe base of ulcer - useful test of OM( Grayson 1996, sensitivity 66%, specificity 89%)

Diabetic Ulcer Diabetic Ulcer -- RxRxOsteomyelitis

Imaging1. Xray - 2 wk lag, sensitivity/specificity 70%,

may need > 50% bony destruction to detect OM.

2. Bone scan

3. White cell Scan or combination of both ( >90% sens/spec)

4. MRI - valuable differentiating Charcot neuropathy

Infected bone must be debrided.

Diabetic UlcerDiabetic Ulcer

7. Other Rx Appropriate dressing, bed rest

BecaplerminPDGF - improves diabetic ulcer healing

Living dermal replacement ( skin substitue)

Hyperbaric oxygen therapy (esp. PVD)

VENOUS ULCERVENOUS ULCER

VENOUS ULCERVENOUS ULCER

80% of leg ulcers are venous ulcers, 10-25% have mixed venous and arterial disease.

Prevalence - 2-9% or 1.48 - 1.8/1000 to 3.3-3.8/1000 over 60 y.o.

50% venous ulcers present> 12 months, 72% recurrent.

Venous UlcerVenous Ulcer

Clinical features of chronic venous insufficiency

1. Swelling2. Varicose eczema ( dry, scaly skin), pruritis, pigmentation,

fibrosis - lipodermatosclerosis.3. Venous ulcers - minor trauma, medial aspect of lower leg4. Varicose veins ( not always visible)5. DVT6. General ache7. Venous claudication

Venous Ulcer Venous Ulcer -- aetiologyaetiology

1. Venous hypertension

1. Superficial venous reflux - long and/or short saphenous reflux.2. Deep venous reflux - primary or secondary (DVT)3. Deep venous occlusion4. Perforating vein reflux5. Abnormal calf pump

Venous Ulcer Venous Ulcer -- aetiologyaetiology

2. Microcirculation? venous hypertension - lipodermatosclerosis - ulcer pathway not fully understood.

1. White cell trappingBlockage of capillaries by white cells - damage the capillaries.

2. Fibrin Cuff theoryDefective interstitial fibrinolytic system w/I lower limb - accumulation of fibrin - barrier to oxygen-local ischaemia.

Venous Ulcer Venous Ulcer -- classificationclassification

CEAP - American venous forum 1994

Clinical 1-6reticular vein, varicose vein, oedemalipodermatosclerosis, healed ulcer, ulcer

Aetiology congenital©, primary(p), secondary(s)

Anatomicalsuperficial(s), deep(d)

Pathophysiologicreflux®, obstruction(o)

Venous Ulcer Venous Ulcer -- InvestigationInvestigation

Duplex scanning - gold standard

B-mode grey scale with Doppler

Venous Ulcer Venous Ulcer -- RxRx

1. Elevation of legs at rest above the level of heartreduce oedema, exudate accelerate regression of skin changes.

2. Bed rest - in severe casereduce venous pressure12-15mmHg at ankle


3. Graduated elastic compression

Heal upto 93% of venous ulcers ( Mayberry 1991)

1. Compression bandage Four layer compression bandage heal 74% of

ulcers at 12 weeks- wool, crepe, elastic bandages, coban- ankle pressure 40mmHg graduated to 18mmHg

at knee


2. Compression Stockings

Severe lymphodemaSevere lymphodema4545--60 60 (ankle p)(ankle p)

Class 4Class 4

Healed venous ulcerHealed venous ulcer3535--4545Class 3Class 3

Marked VV, oedemaMarked VV, oedema

Chronic venous insuf.Chronic venous insuf.

2525--3535Class 2Class 2

Mild VV, DVT Mild VV, DVT prophylaxisprophylaxis

<25mmHg<25mmHgClass 1Class 1


3. Mechanical devices

Sequential pneumatic compressionFlowtron bootsFoot pumps


5. Dressings

Wide range of topic dressings available.Lack of evidence what’s best dressing.Role of occlusive dressings

a. reduction of infectionb. autolytic debridementc. reduction of wound paind. stimulation of granulation tissue

Typesfilms, hydrocolloids, foams, alginates, hydrogels


6. Surgery

Role of surgery in healing venous ulcers is controversial.

Surgery justified if ulcer fails to heal or recur despite adequateconservative treatment.

Superficial venous surgery indicated if isolated superficial refluxor predominantly superficial disease.

High saphenous ligation/ stripping of LSV/Multiple avulsion

Role of deep venous reconstruction is limitied.


Split skin graft

Effective for venous ulcer50 - 70% complete healing of venous ulcer

Skin replacement graft

Venous Ulcer Venous Ulcer --RxRx

6. Mixed arterial and venous disease

Combined arterial and venous disease in 13%.

In severe PVD ( ABI<0.5), PVD to be Rx first.

If ABI > 0.85, ulcer can be treated with compression withoutarterial intervention.

Use of 3 layer bandage.

Pressure UlcerPressure Ulcer

Common in paralysed, debilitated, unconscious patients.

Prevention strategy1. Identification of high risk patients2. Frequent assessment of pressure areas3. Preventive measures such as regular repositioning,

pressure relief bedding, moisture barriers, adequate diet.

Therapeutic measurespressure relief, moist wound care, infection controlsurgical debridement.

V.A.C V.A.C -- Vacuum assisted Vacuum assisted closureclosure

V.A.C. therapy system

applies controlled, localised sub-atmospheric pressure to helpdraw wounds closed

removes interstitial fluid allowing tissue decompression and enhanced blood flow

promotes granulation tissue formation

removes infectious material

closed, moist wound healing environment

V.A.C V.A.C -- Vacuum assisted closureVacuum assisted closure



POLYARTERITIS NODOSAPOLYARTERITIS NODOSA

PYODERMA GANGRENOSUMPYODERMA GANGRENOSUM

POLYARTERITIS NODOSAPOLYARTERITIS NODOSA

LICHEN PLANUSLICHEN PLANUS

CRYOGLOBULINEMIACRYOGLOBULINEMIA

White Tail Spider biteWhite Tail Spider bite

QuickTime™ and a TIFF (Uncompressed) decompressor are needed to see this picture.QuickTime™ and a TIFF (Uncompressed) decompressor are needed to see this picture.

SummarySummary

Management of Chronic Leg Ulcer

1. Careful history and examination2. Accurate diagnosis - diabetic, venous, arterial, mixed, others3. Treat underlying cause/ specific treatment - revasculisation4. Local wound management

1. Appropriate dressings2. Control sepsis3. Debridement4. V.A.C / SSG

• Consider alternative diagnosis - biopsy lesion when in doubt

All about Leg Ulcer

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