Chronic leg ulcer high critical topic for learning .ppt

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1. نمحرلا هللا مسب
ميحرلا

2. Chronic Leg Ulcers

Dr. Mohamed Taha
Mataria Teaching Hospital 2008
BY

3. What is a leg Ulcer?
Chronic leg ulcer is defined
as an open lesion between
the knee and the ankle joint
that remains unhealed for
at least four weeks.

4. BACKGROUND

5. Chronic leg ulcer is a major health problem in the
world, affecting principally the elderly.
The natural history of the disease is of a continuous
cycle of healing and breakdown over decades.
About 60-80% of chronic leg ulcers had a venous
component, 10-30% were associated with arterial
insufficiency and the other factors included diabetes
mellitus and rheumatoid disease.
Arterial and venous insufficiency combined in 10-
20% of cases

6. DIFFERENTIAL DIAGNOSIS
1.Venous ulcer - chronic venous insufficiency
2. Diabetic ulcer
3. Arterial ulcer – PVD
4. Vasculitis - RA, SLE, polyarteritis
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. Pressure ulcer
13. Other - pyoderma gangrenosum, inflammatory bowel disease

7. Venous Leg
Ulcers

8. Venous leg ulcers
Located in the gaiter area
70% medial 20% lateral 10% both
Shallow in appearance, sometimes with diffuse edges
Edema usually present
Often highly exuding wounds
30% of pts suffer with pain
Accompanied by Varicose Veins
Pulses can be palpated in the absence of edema
You may see ankle flare
Lipodermatosclerosis
Ulcers can be multiple or circumferential.
There can be eczema present, venous or gravitational.
Haemosidrin staining can be present (looks like rust)
There may also be atrophy blanche.
Approximately 50% of ulcers are venous.

9. 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

10. Gaiter area (2.5cm below malleoli to
lower third of calf)

14. Venous Ulcer – Classification
CEAP - American venous forum 1994
Clinical 1-6
reticular veins, varicose vein, edema
lipodermatosclerosis, healed ulcer, ulcer
Etiology
congenital© , primary(p), secondary(s)
Anatomical
superficial(s), deep(d)
Pathophysiologic
reflux®, obstruction(o)

15. MANAGEMENT
•It is widely accepted that sustained
compression provides the mainstay of
treatment in venous leg ulcers.
•This should be supported with adjunctive
medical and surgical therapy, appropriate
dressings and patient education.
•Multi-layer high compression bandaging
improves healing of venous leg ulcers when
compared with single layer.

16. Venous Ulcer - Management
1. Elevation of legs at rest
above the level of heart
reduce edema, exudate
accelerate regression of
skin changes.
2. Bed rest in severe cases
reduce venous pressure
12-15mmHg at ankle

17. 3. Graduated elastic compression
Heal up to 93% of venous ulcers
( Mayberry 1991)
(1) Compression bandage
Four layer compression bandage
heal 74% of ulcers at 12 weeks
orthopedic wool,
crepe bandages,
elastic bandages,
cohesive bandages.
- ankle pressure 40mmHg graduated to
18mmHg at knee

18. Johnson & Johnson DYNA-FLEX Multi-
Layer Compression System
FIRST LAYER
Padding is made of cool, breathable cotton compared to rayon,
polyester, or wool. The cotton is punched onto foam for added
strength and conformability.
SECOND LAYER
Compression bandage uses an innovative, patented visual cue to aid
proper application. Bandage is printed with a rectangular pattern that
turns to a square when correct level of stretch is achieved. This
ensures reproducible pressures from one application to the next even if
a different practitioner applies the bandage system.
THIRD LAYER
Cohesive compression bandage delivers additional pressure.

20. Smith & Nephew PROGUIDE
Multi-layer Compression
Bandage

21. Smith & Nephew PROFORE Lite Latex Free
Multi-Layer Compression Bandage System
Each Profore Lite Multi-Layer Compression Bandage System pack
contains the following:
One Profore WCL -- Sterile Wound Contact Layer -- helps protect the
wound site and help wick away exudate into the absorbent padding.
One Profore #1 absorbent padding bandage -- helps absorb exudate
and helps protect bony prominences.
 One Profore #2 light conformable bandage -- helps absorb exudate
and helps prepare and sculpt the leg for the application of the pressure
layers.
One Profore #4 cohesive compression bandage -- helps maintain
continuous compression and keeps the system in place for up to a full
week.

22. (2) Compression Stockings
Class 1 <25mmHg Mild VV, DVT
prophylaxis
Class 2 25 - 35
Marked VV, edema
Chronic venous insuf.
Class 3 35 - 45
Healed venous ulcer
Class 445-60
(ankle p)
Severe
lymphedema

23. (3) Mechanical devices
Sequential pneumatic compression
Flowtron boots
Foot pumps
4. 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

24. 5. 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.
Split skin graft
Effective for venous ulcer
50 - 70% complete healing of venous ulcer
Skin replacement graft

25. •Sustained compression
Any bandaging system providing sustained compression for at least
one week. (the first-line therapy for venous leg ulcers).
•Multi-layered (elastic) compression
Currently presented as 4-layer high compression bandaging
providing sustained, graduated compression.
•Multi-layered (inelastic) compression
Multi-layer inelastic bandaging
•Reduced compression
Compression of 15-25 mm Hg using a 1- or 2-bandage layer system
Reduced compression stockings are a valuable alternative.
•Compression stockings
Ideally, compression hosiery that provides compression of
35-45 mm Hg, but if not tolerated 25-35 mm Hg.
•Intermittent pneumatic compression
one of a number of devices which surround the leg and can be
inflated to provide short-term pressures up to a maximum of
100 mm Hg.
Definitions

26. Bandaging
4 Layer compression therapy is still the gold
standard in treatment of venous and mixed
ulceration.
It provides graduated compression, the highest
mmhg at the ankle, with approx ½ that at the
top of the calf.
Compression reduces the venous hypertension
within the vascular system by :-
1.Reducing the diameter of major blood
vessels,
thereby reducing the local blood volume.
2. Improving lymph drainage, by reducing
lymph in the tissues.
3. Reducing venous stasis
There are many different types of
compression that we can employ :-
1. 4 layer/ multilayer systems
2. Inelastic or short stretch
3. 3 layer tubigrip and shaped tubigrip
4. Highly elastic bandages, tensopress and
surepress.
Modified compression is used to achieve
compliance and remove edema when the
diagnosis is of mixed etiology, it also helps to
achieve pain control.
3 layer compression is not heavily dependant
on ankle size.

27. Arterial Ulcers

28. Arterial ulcers
Located on any part of the leg, most common on or below the ankle.
Small and punched out appearance.
Edema is generally localised to the wound.
Tendency to be dry wounds.
Slow capillary refill.
Usually very painful ulcers, mostly at night.
Leg can be shiny, tight, hairless and cold.
Pulses are reduced and/or absent.
You may see trophic changes to the nails
Rubor
Approximately 30% of leg ulcers are
arterial.

30. What are the other types
of
Leg Ulceration?

31. Rheumatoid Arthritis - Calcification of
blood vessels usually in the arterial tree
Diabetes Mellitus - Poor/ compromised peripheral
circulation

Malignancy - SCC, BCC, Melanoma & CTCL
Underlying Disease – Pyoderma
Gangrenosum, Mental Health (Artefact),
Eczema Craquele/dependant oedema,
Sickle Cell and thalassemia

32. Rheumatoid Arthritis
and
Systemic Vasculitis

33. Approximately 8% of patients with leg ulcer have
rheumatoid arthritis. These patients may have venous,
arterial or vasculitic ulcers. Those with vasculitic ulcers
will have clinical features of established disease.

They may be associated with systemic vasculitis, in which
case there will be evidence of vasculitic lesions
elsewhere, e.g. nail fold infarcts or splinter
haemorrhages. Rarely, ulceration will be due to
Felty.s syndrome or pyoderma gangrenosum.
Systemic vasculitis occurs as a feature of several collagen
vascular diseases when leg ulcers will usually be
multiple, necrotic, deep and have an atypical
distribution.

34. Leg ulceration in Rheumatoid
Arthritis
•The third most common cause of leg ulceration
is rheumatoid arthritis.
•RA is the third most common underlying
pathology, after venous disease and arterial
insufficiency.
•The etiology of such ulcers appears to be multi-
factorial – venous & arterial insufficiency,
trauma or pressure are factors commonly
involved

35. Factors affecting tissue
viability in RA
•Articular(joint) disease
•Extra-articular (systemic) disease – anaemia,
nodules, vasculitis, peripheral neuropathy
•Peripheral vascular disease
•Side effects of medication
•Reduced mobility and self care capacity
•Poor nutrition

36. Articular (joint) disease
•Synovitis
•Decreased mobility (dependent oedema)
•Foot & ankle deformity
increased plantar pressures
friction from ill-fitting footwear
loss of movement at the ankle
impairs the venous muscle pump,
increases venous pressure & may damage the veins

37. Extra-articular (systemic) disease
•Anaemia of chronic disease affects 33-60% of patients
•Nodules affect 15-39%
•Cutaneous vasculitis affects around 3.6%
•Neuropathy may be entrapment, distal sensory,
mononeuritis multiplex (3-58%) or sensorimotor

38. Peripheral vascular disease
•Link between RA and coronary heart disease;
frequency 4 times that of controls – Del Rincon (2001)
•Higher prevalence of carotid & peripheral
arterial disease than controls - Alkaabi et al (2003)
•Overall prevalence of PVD likely to be under-
estimated at 18% - Maradit-Kremers (2005)
•Impact of micro and macrovascular disease on
the lower limb in RA is poorly understood…

39. Diabetic
Ulcers

40. DIABETIC ULCERS
•Incidence of diabetic
foot ulcer - 3-7%
•Etiology - Purely
neuropathic (45-
60%), Ischemic
(10%),
•Mixed neuroischemic
origin (25-45%).

41. Etiology of Diabetic Ulcers
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.

42. Diabetic neuropathy
1. Microvascular disease causing nerve
hypoxia
2. Direct effect of hyperglycemia on
neuronal metabolism
3. Abnormal NO metabolisim - perineural
vasoconstriction and neuronal damage.

43. Diabetic neuropathy
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.

44. 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, Toe brachial pressure
index.

45. Diabetic Ulcer
Principles of Management
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

46. Types of ulcers in diabetic patients
Neuropathic ulcer
Ischemic ulcer
Infection
Osteomyelitis

47. Pressure Ulcers
 heel, malleoli, sacral & trochanter
 hospitalized pt.
Common in paralysed, debilitated, unconscious patients.
 additional risk factors:
incontinence, bad nutritional state,
increased body temperature,
diabetes, peripheral arterial diseases, age

48. Pressure ulcers
4 stages according to the tissue damage
stage I : nonblanchable erythema
stage II : partial thickness loss of skin
layers (blister, abrasion)
stage III : full thickness loss exposing
subcutaneous fat(superficial ulcer)
stage IV : exposed muscle or bone(deep
ulcer or necrosis)

49. 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 and surgical debridement.

50. Felty syndrome
Triad of

①
rheumatoid arthritis

②
splenomegaly

③
neutropenia

52. Hematological disorders
Anemias associated with lower leg ulceration
 sickle cell disease
 thalassemia
 hereditary spherocytosis
 glucose-6-phosphate dehydrogenase deficiency

53. Other hematological conditions
 essential thrombocythemia
 thrombotic thrombocytopenic purpura
 polycythemia
 leukemia
 dysproteinemia

54. Clotting disorders
Hereditary or acquired conditions
predisposing to thrombosis ↑
 antiphospholipid syndrome
 deficiency of antithrombin III, protein C or protein S
 abnormal clotting factors (factor V Leiden)

55. Hydroxyurea Ulcer

56. Antiphospholipid Syndromes
♦ Triad

①
increased risk for venous thrombosis


②
thrombocytopenia

③
habitual abortion
♦ Two most frequently found antibodies

①
lupus anticoagulant

②
anticardiolipin

58. Antiphospholipid Syndromes
Cutaneous Symptoms
ulceration
livedo reticularis,
acrocyanosis
Raynaud phenomenon
capillaritis
thrombophlebitis
vascular thrombosis

59. Antiphospholipid Syndromes
autoimmune diseases
SLE, autoimmune thrombocytic purpura, hemolytic anemia,
rheumatoid arthritis, Sjogren synd, giant cell arthritis
malignancies
hematological disorders
myelofibrosis, von Willebrand disease, paraproteinemia
infections
tuberculosis, mycoplasma, HIV, hepatitis
-neurological disorders
myasthenia gravis, multiple sclerosis

60. Malignancies
♦ Two most frequent ulcerating tumors
basal cell carcinoma
squamous cell carcinoma
♦ Malignancies developing secondarily
in chronic leg ulcers:
squamous cell carcinoma
fibrosarcoma

61. Diagnostic approach in patients
with leg ulcer
Vasculitis
irregular border, black necrosis,
erythema or bluish or purple
discoloration of adjacent skin

62. Laboratory screening tests for
Vasculitis
Urine analysis for proteinuria, haematuria, cylindruria
Routine and immunohistopathology of skin biopsies
Erythrocyte sedimentation rate, hemoglobin, differential
blood count, kidney and liver function
Antinuclear antibodies, rheumatoid factor
Complement C4, circulating immune complexes
Paraproteins, immunoglobulin fractions
Antineutrophil cytoplasmic antibodies
Serological tests and cultures for underlying infections

63. 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

64. Evidence based
Recommendations

65. Measurement of ankle brachial pressure ratio (index)
(ABPI) by hand-held Doppler is essential in the
assessment of chronic leg ulcers.
Patients with an ABPI <0.8 should be assumed to have
arterial disease.
The surface area of the ulcer should be measured serially
over time.
A non-healing or atypical leg ulcer should be referred for
biopsy.
Leg ulcer patients with associated dermatitis should be
referred for patch-testing. Standard series patch-
testing is inadequate: a leg ulcer series is
recommended.

66. Ulcerated legs should be washed normally in tap water
and carefully dried.
 Simple non adherent dressings are recommended in
the treatment of venous ulcers, as no specific dressing
has been shown to improve healing rates.
 Hydrocolloid or foam dressings may be of value in
painful ulcers.
 Antibiotics should be reserved for evidence of cellulitis
or active infection before grafting.
 Topical antibiotics are frequent sensitisers and should
be avoided.
 Systemic therapy in the treatment of leg ulcers is not
recommended.
 Venous surgery followed by graduated compression
should be considered in patients with chronic
venous ulceration.

67. REASSESSMENT
Formal reassessment should be carried out
12 weeks after the start of treatment and
thereafter at 12-week intervals.
SECONDARY PREVENTION
Correctly fitted graduated compression
hosiery should be prescribed for at least
five years for all patients who have
successfully healed their venous leg ulcer.

68. Thanks for Listening!

69. Questions?

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