LEG ULCERS

Julian Choi
 BACK GROUND
Leg Ulcers - major morbidity
Leg ulcers present 3-4% of population > 65 years old
M:F 1:2 ratio
Chronic
Recurrent
 DIFFERENTIAL DIAGNOSIS
1. Arterial ulcer - PVD
2. Diabetic ulcer
3. Venous ulcer - chronic venous insufficiency
4. Pressure ulcer
5. Neoplastic ulcers - MM, Marjolin ulcers
6. Infectious ulcer - TB, syphilis, HIV
7. Tropical ulcer - leishmaniasis, fungal
8. Haematological ulcer- sickle cell, thalassaemia, leukaemia
9. Nutritional/metabolic ulcer - vitamin def., uraemia
10. Allergy - drugs, photosensitivity, chemical exposure
11. Insect bite - white tail spider
12. Vasculitis - RA, SLE, polyarteritis
13. Other - pyoderma gangrenosum, inflammatory bowel disease
 ARTERIAL ULCER

Chronic lower limb ischaemia presents:

Claudication
Critical limb ischaemia - rest pain, arterial ulceration,
gangrene of foot.

Definition of critical ischaemia -

ankle systolic pressure < 30 - 50mmHg

Prognosis of Critical limb ischaemia is poor

25% mortality within 1 yr; 50% within 5 yrs.
 Arterial Ulcer

1. General Assessment

1. Functional status
2. Mobility
 Arterial Ulcer - Ix

2. Global vascular status

1. Ankle brachial pressure index

ABPI < 0.9 PVD

ABPI 0.8 - 0.9 moderate PVD
ABPI 0.5 - 0.8 claudication
ABPI < 0.5 critical ischaemia

2. Toe brachial pressure index - in diabetic

 Arterial Ulcer - Ix
3. Disease localisation

1. Colour duplex scanning

Peak velocity ratio > 2 - 50% stenosis

2. Digital subtraction angiography

3. CT angiography
 Arterial Ulcer - Rx

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.
 Arterial Ulcer - Rx

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)
 Arterial Ulcer - Rx

Surgical Revasculisation

Suprainguinal Bypass
Aortobifemoral Bypass

Femoro-femoral or Ileo-femoral bypass for unilateral

Axillobifemoral bypass for bilateral

Infrainguinal Bypass
Femoropopliteal bypass
vein ( in situ/ reversed) graft vs PTFE graft
 Arterial Ulcer - Rx

Surgical treatment

Infrainguinal Bypass
Femoropopliteal bypass
Femorodistal ( tibial/ pedal) bypass
vein ( in situ/ reversed) graft vs PTFE graft

Primary patency rates

Femorodistal bypass - 60 -85% at 1yr
50-75% at 5 yrs
 Arterial Ulcer - Rx

Non-surgical treatment

Pressure care
Slow release opiate analgesia
Prostacyclin analogues
Iloprost ( Feiessinger 1990)
Meta-analysis of 6 RCTs( n - 700)
Reduction in death and amputation at 6 months
( 35% vs 55%)
Chemical sympathectomy
Dorsal column stimulation
 DIABETIC ULCER
Incidence of diabetic foot ulcer - 3-7%

Aetiology - Purely neuropathic (45-60%), Ischaemic (10%),

Mixed neuroischaemic origin (25-45%).

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

1.Diabetic Neuropathy - sensory, motor, autonomic

2.PVD
3.Abnormal Microcirculation
4.Biomechanical aspects - Increased plantar pressure, callus
altered foot shape
5.Other - impaired vision, immobility, impaired neutrophil
function.
 Diabetic Ulcer - Aetiology
Diabetic neuropathy:

Hypothesis -

1. Microvascular disease causing nerve hypoxia

2. Direct effect of hyperglycaemia on neuronal metabolism
3. Abnormal NO metabolisim - perineural
vasoconstriction and neuronal damage.
 Diabetic Ulcer - aetiology

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 - lead

to clawed toes, prominent MT heads.

3. Autonomic neuropathy - reduced sweating, AV shunt causing

increased blood flow - warm/bounding pulse with dry/cracked
skin prone for trauma and infection.
 Diabetic Ulcer - aetiology
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), doppler
wave form ( loss of triphasic wave form), pole test
 Diabetic Ulcer - Tx
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 Education

Malone 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 - Rx
Principles of Rx

5. Neuropathic ulcer

Pressure relief :
Appropriate footwear
Total contact cast - Mueller 90%(contact cast) healed
in 42d vs 67%(without cast) in 65 days.

Debridement of Callus
Prevent wound healing from the margin, hide
infection.
Weekly debridement/ review of shoes.
 Diabetic Ulcer -Rx
6. Ischemic ulcer

Prompt vascular assessment

Angiography

Aggressive Revasculisation when indicated

Local amputation for gangrene ( ray amp., transMT amp.)
Regular exercise (Ubels 1999)

ACEi (NEJM 2000)

Control other CVD risk factors - smoking

 Diabetic Ulcer - Rx
7. Rx of Infection

Bacterial colonisation is universal -

Superficial wound swab inadequate
Deep Bx( curetting of ulcer base, debridement)

Clinical signs of infection reliable (local erythema, swelling, pus)

systemic signs rare
abscess, crepitus (gangrene)

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

synergistic.

Broad spectrum antibiotics

 Diabetic Ulcer - Rx
8. Osteomyelitis

Suspected in deep DM ulcer

Clinical evidence - ability to probe bone with a instrument at

the base of ulcer - useful test of OM
( Grayson 1996, sensitivity 66%, specificity 89%)
 Diabetic Ulcer - Rx
Osteomyelitis

Imaging
1. 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 Ulcer
7. Other Rx
Appropriate dressing, bed rest

Becaplermin
PDGF - improves diabetic ulcer healing

Living dermal replacement ( skin substitue)

Hyperbaric oxygen therapy (esp. PVD)

VENOUS ULCER
 VENOUS 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 Ulcer
Clinical features of chronic venous insufficiency

1. Swelling
2. Varicose eczema ( dry, scaly skin), pruritis, pigmentation,
fibrosis - lipodermatosclerosis.
3. Venous ulcers - minor trauma, medial aspect of lower leg
4. Varicose veins ( not always visible)
5. DVT
6. General ache
7. Venous claudication
 Venous Ulcer - aetiology

1. Venous hypertension

1. Superficial venous reflux - long and/or short saphenous reflux.

2. Deep venous reflux - primary or secondary (DVT)
3. Deep venous occlusion
4. Perforating vein reflux
5. Abnormal calf pump
 Venous Ulcer - aetiology
2. Microcirculation
? venous hypertension - lipodermatosclerosis - ulcer
pathway not fully understood.

1. White cell trapping

Blockage of capillaries by white cells - damage
the capillaries.

2. Fibrin Cuff theory

Defective interstitial fibrinolytic system w/I lower
limb - accumulation of fibrin - barrier to oxygen-
local ischaemia.
Venous Ulcer - classification
CEAP - American venous forum 1994

Clinical 1-6
reticular vein, varicose vein, oedema
lipodermatosclerosis, healed ulcer, ulcer
Aetiology
congenital©, primary(p), secondary(s)

Anatomical
superficial(s), deep(d)

Pathophysiologic
reflux®, obstruction(o)
Venous Ulcer - Investigation

Duplex scanning - gold standard

B-mode grey scale with Doppler

 Venous Ulcer - Rx

1. Elevation of legs at rest above the level of heart

reduce oedema, exudate accelerate regression of skin
changes.

2. Bed rest - in severe case

reduce venous pressure
12-15mmHg at ankle
 Venous Ulcer - Rx

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
Venous Ulcer - Rx
 Venous Ulcer - Rx

2. Compression Stockings

Class 1 <25mmHg Mild VV, DVT

prophylaxis
Class 2 25-35 Marked VV, oedema
Chronic venous insuf.
Class 3 35-45 Healed venous ulcer

Class 4 45-60 Severe lymphodema

(ankle p)
 Venous Ulcer - Rx

3. Mechanical devices

Sequential pneumatic compression

Flowtron boots
Foot pumps
 Venous Ulcer - Rx

5. Dressings

Wide range of topic dressings available.

Lack of evidence what’s best dressing.
Role of occlusive dressings
a. reduction of infection
b. autolytic debridement
c. reduction of wound pain
d. stimulation of granulation tissue
Types
films, hydrocolloids, foams, alginates, hydrogels
 Venous Ulcer - Rx

6. Surgery

Role of surgery in healing venous ulcers is controversial.

Surgery justified if ulcer fails to heal or recur despite adequate

conservative treatment.

Superficial venous surgery indicated if isolated superficial reflux

or predominantly superficial disease.
High saphenous ligation/ stripping of LSV/
Multiple avulsion
Role of deep venous reconstruction is limitied.
 Venous Ulcer - Rx
Split skin graft

Effective for venous ulcer

50 - 70% complete healing of venous ulcer

Skin replacement graft

 Venous Ulcer -Rx

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 without

arterial intervention.

Use of 3 layer bandage.

 Pressure Ulcer
Common in paralysed, debilitated, unconscious patients.

Prevention strategy
1. Identification of high risk patients
2. Frequent assessment of pressure areas
3. Preventive measures such as regular repositioning,
pressure relief bedding, moisture barriers,
adequate diet.

Therapeutic measures
pressure relief, moist wound care, infection control
surgical debridement.
 V.A.C - Vacuum assisted
closure
V.A.C. therapy system

applies controlled, localised sub-atmospheric pressure to help

draw 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 - Vacuum assisted closure

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

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POLYARTERITIS NODOSA
PYODERMA GANGRENOSUM
POLYARTERITIS NODOSA
LICHEN PLANUS
CRYOGLOBULINEMIA
 White Tail Spider bite

QuickTime™ and a TIFF (Uncompressed) decompressor are needed to see this picture.
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 Summary
Management of Chronic Leg Ulcer

1. Careful history and examination

2. Accurate diagnosis - diabetic, venous, arterial, mixed, others
3. Treat underlying cause/ specific treatment - revasculisation
4. Local wound management
1. Appropriate dressings
2. Control sepsis
3. Debridement
4. V.A.C / SSG
• Consider alternative diagnosis - biopsy lesion when in doubt