Approach and Management of all type of leg ulcer

1. APPROACH
TO
LEG ULCER

2. INTRODUCTION
• An ulcer can be defined as a break in the
epithelial continuity.
• Classified
– Non- specific
– Specific
– Malignant
• A leg ulcer is discontinuity of the squamous
epithelium of the skin usually around the ankle or
on the foot

3. • Leg ulcers are a common, chronic, recurring
condition
• Prevalence b/w 1.5 to 3 per 1000 and increases
with age.
• It’s estimated that up to 20 per 1000 people over
80 yrs will suffer from a leg ulcer
• Following healing, re-ulceration rates at one year
range from 26% - 69%

4. Classification of Chronic Leg Ulcers
VASCULAR
ARTERIAL
• Atherosclerosis
• Burger’s disease
• Vasuclitis
• Raynaud’s disease
VENOUS
• Chronic venous insufficiency
• Varicose vein
• Post sclerotherapy
LYMPHATIC
• Chronic lymphedema

5. • INFECTIVE
– Pyogenic
– Osteomyelitis
– Tuberculosis
– Syphillis
– Tropical disease
– Fungal disease
• TRAUMATIC
– Radiation
– Thermal burns
– Bites
– Decubitus
• NEOPLASTIC
– Melanoma
– SCC
– BCC
– Kapsoi’s sacroma

6. • SYSTEMIC METABOLIC
– Ulcerative colitis
– Diabetes
– Martolle’s ulcer
– Sickel cell disease
– Avitminosis
• NEUROPATHIC
– Cord lesion
– Pheripheral Neuropathies
– Trauma
– Diabetes
– Tabes dorsalis
– Alchoholism

7. Leg ulcer aetiology
Grey J.E et al. ABC Wound Healing BMJ 2006; 332: 347-50
• Venous insufficiency 80 - 85% (60 – 70 %)
• Arterial disease ( chronic lower limb ischemia) 20%
• Mixed arterial and venous disease
• Neuropathic Diabetic ulcer
• Rheumatoid arthritis - 7%
• Systemic vasculitis
• Lymphoedema
• Trauma
• Malignant ulcer (BCC, SCC, Malignant melanoma)
• Infective

8. CHRONIC VENOUS ULCER
• CVI- chronic venous insufficiency who have
developed irreversible skin damage as the
result of sustained ambulatory venous
hypertension
• CVU- chronic venous ulceration defined as a
break in the skin , present for more than 6
months , b/w the malleoli and tibial tuberosity
that is presumed to be wholly or partially due
to venous disease

9. CVI grade III is CVU
• Basle Classification ( widmer)
• CVI-I
– Corona phlebectatica ( venous, or malleolar, Flare)
• CVI-II
– Hyper or dipigemented areas ( lipodermatosclerosis,
atrophe blanche)
• CVI-III
– Open or healed ulceration

10. Others Classification
• SVS/ISCVS classification
– Clinical 0-3/ anatomical 0-7/ orgin 0- 2 /severity
– Clinical Class 3- ulceration
• CEAP classificaton
– Clincal class 5- healed ulceration
– Clinical class 6- active ulceration

11. Epidemiology of chronic venous ulcer
• At any point
– A third to a half will have trunk varicose veins
– 7% will have CVI- I
– 1-3%will have CVI- II
– 1% will have CVI- III
– Age – 3.6% over 65yrs
– M:F – 1:1
• Common association are
– Lower social class
– Occupation like prolong standing predisposes
– Inc BMI assoc with delayed CVU healing
– Fibre deficent diet n constipation aggravate
– Pregnancy n multiparity
– Caucasians

12. PATHOPHYSIOLOGY CVU
• CVI, culminating in CVU is the end result of
sustained ambulatory venous hypertension acting
upon a dermal microcirculation designed to
operate in the presences of low venous pressure
• Ambulatory venous pressure (AVP)
– Normal - < 25Hg
– >30 – inc incidence of CVU
• 31-40 mmHg- 15%
• >90mmHg- 100%

13. Pathophysiology contd…
Macrovascular
• Muscle pump dysfunction
– Ageing General debility/ MSK n neurological LL
pathologies ( fixed ankle, flat foot)
• Valvular reflux (90% in CVI)
– Primary alvular incompetence ( elastin/collagen)
– Secondary valvular incompetence (post phlebitic)
• Venous obstruction
• Valvular hypoplasia/ agenesis

14. Microvascular
• Venous stasis n hypoxia
• Arteriovnous fistula ( stealing blood from skin)
• Peri-capillary fibrin cuff( Browse n Burnand)
• Leucocyte Migration (coleridge –smith)
• Capillary Proliferation

15. CVU as a failing wound
• Ulcer exduate inhibit keratinocyte migration and
fibroblast activity
• Increased proteolysis
• Upregulation of metaloproteinases- breakdown
important growth factor necessary for epithelialization
• Epithelial cells in CVI refractory to the normal signalling
process

16. ARTERIAL LEG ULCER
Chronic limb ischemia n Ulcer
Definition of CLI:
• Persistent rest pain that requires regular adequate
analgesia for at least 2 weeks, with resting ankle
pressure of < 50mmHg or a toe pressure of < 30
mmHg
• Presence of gangrene/ Ulcer of the foot/ toes with
the same resting pressure

17. • Arterial ulcers account for 10% - 15% of leg ulcers
• Major risk factors for Peripheral occlusive disease
– Men > 45 yrs
– Women >55 yrs or premature menopause
– Family history of premature atherosclerosis
– Smoking
– HDL < 35 mg/dl
– Hypertension
• Other risk factors
– DM
– Def antioxidant vitamins
– Elevated plasma fibrinogen level n homocysteine level
– Sedentary life style

18. Clinical categories of chronic limb ischemia
Grade Category Clinical description
0 0 Asymptomatic
1 Mild claudication
I 2 Moderated claudication
3 Severe claudication
II 4 Ischemic rest pain
III 5 Minor tissue loss- non healing ulcer, focal gangrene
with diffuse pedal edema
6 Major tissue loss- extending above TM level,
Functional foot no longer salvagable

19. Fontaine classification- severity of CLI
• Stage I- Asymptomatic
• Stage II- intermittent claudciation limiting lifestyle
• Stage III- Rest pain due to ischemia
• Stage IV- Ulcer/ Gangrene due to ischemia

20. Patho - physiology of Arterial ulcer
• Macrovascular
– Fatty streak
– Fibrous plaque
– Complicated lesion
• Ulcer
• Hemorrahage
• Calcification
• Necrosis
• Microvascular
– High blood viscosity
– Endothelial swelling
– Platelet/ RBC/ PMN plugging
– Inc permiability n tissue
edema
– Reduced n unevenly
distributed flow

21. Natural History of Atherosclesrosis
Macro n Microvascular changes
Chronic limb ischemia
Intermittent claudication ( 60% stabalise, 20 %improve)
(20%)Decrease claudication distance
Nocturnal ischemic pain
Rest pain
Progressive ischemia

22. Contd..
Tissue loss
Ulceration n gangrene
Minor trauma
Secondary infection
Ischemia n edema
Decrease perfusion
Thrombosis in microcirculation
Spread proximally to small arteries

23. DIABETIC FOOT ULCER
• 2% of whole population
• 10- 25% of all DM develop some foot problems
• 1 in 10 to 1 in 5 diabetic inpatient are due to foot
ulceration, infection or gangrene
• 5- 10% of all diabetic will require a lower extrimity
amputation (1% in UK)
• 45 % of all amputation are on diabetics
• Amputation on diabetics are 20 times higher than non-diabetic

24. Pathophysiology Diabetic foot ulcer
• Diabetic foot diseases is truly multifactorial
– Neuropathy
– Macrovascular ds
– Microvascular ds
– Infection
– Connective tissue abnormalities
– Haematological disturbances

25. Neuropathy
Ischemia
Ulcer
Infection
Trauma
SOMATIC SENSORY
SOMATIC MOTOR
VISCERAL SENSORY
AUTONOMIC

26. Classification of Diabetic foot ulcers
• 1981 Wagner FW: Wagner Classification
• 1996 Lavery & Armstrong: University of Texas
Diabetic Wound Classification System
• 1999 Macfarlane & Jeffcoate: S(AD)SAD
system

27. Wagner FW Classification
Gr O no obvious ulcer, but deformity, hyperkeratosis,
or bony abnormality
Gr 1 superficial ulcer, no infection sign
Gr 2 deep ulcer with infection, but no bony
involvement
Gr 3 deep ulcer with abscess & bony involvement
Gr 4 local gangrene (e.g., toe, forefoot)
Gr 5 whole foot gangrene

28. LEG ULCERATION IN RA
• Leg ulceration is often poorly defined in research
• Surprisingly little is known about the prevalence
and aetiology
• The validated overall prevalence of leg ulceration
in 324 in-patients was over 8%
(Wilkinson & Kirk, 1965)
• A postal survey of 250 RA patients taken from a
diagnostic register found a validated overall
prevalence of 9%
(Thurtle & Cawley, 1983)

29. 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

31. Figure 2

32. LEG ULCER IN VASCULITIS
• Inflammation with destruction of the vascular wall.
• Cutaneous vasculitis is more common than systemic
• Clinical presentation ranges from reticulated erythema to
widespread purpura and finally necrosis leading to ulceration.
Common caueses of vasculitis are
• Infection,
– Meningococcus/mycobacterium leprae/ rickettsia/ spirochetes
• Immunoloigcal
– Connective tissue disorder
– Cryoglobuinemia
– Goodpasture syndrome
– Drugs ( antibiotics n NSAID)
• Idiopathic
– PAN/ giant cell arteritis/ Takayasu diseases

33. Pathophysiology
• Immune complexes- deposited in wall of blood vessles
• This often starts in the legs because of the high hydrostatic
pressure in the post-capillary venules due to gravity.
• activates the complement system, causing the chemotaxis
of neutrophil
• Activated neutrophil release proteolytic enzymes
• Inflammation n vessel wall destruction

34. LEG ULCER IN LYMPHEDEMA
Chronic oedema –
defined as oedema that
has been present for
more than 3 months and
does not go down
overnight
(Moffatt et al 2003, Williams 2003)

35. Aeitology
• Primary lymphoedema
– aplasia/hypoplasia/valvular incompetence
• Secondary lymphoedema
– Cancer treatment
– Recurrent infection
– Trauma
– Parasitic infection
– Obstruction by tumor
– Immobility
• Lymphovenous oedema due to CVI or traditional venous
ulcer bandaging systems

36. Pathophysiology
• Although chronic oedema is not directly responsible for
ulcer development, it will affect wound healing
(Mortimer and Browse, 2003).
• This is due to the reduced oxygenation of the tissues
resulting from the presence of edema (Casley- Smith,
1997).
• As such, skin damage to an edematous limb may lead to
ulceration.
•
• Ulceration can also follow superficial infection

37. EVALUATION OF LEG ULCER
• HISTORY
• EXAMINATION OF ULCER N SURROUNDING
• EXAMINATION OF VASCULAR INSUFFICENCY
• EXAMINATON OF NERVE LESION

38. The history of an ulcer
History
– Mode of onset /Precipitating event
– Duration
– Symptoms (pain/ discharge/
– Systemic features
– Risk factors
– Peripheral ischemic symptoms
– Previous interventions
– Treatment

39. The history of an ulcer
Venous
– Varicose veins
– DVT/thrombophlebitis
– Previous ulceration
– Previous treatments
– Sclerotic changes
– Oedema
– Painless
– Precipating factors (age, occupation, BMI, low socioeconomic)
– Coexsistence
• PVD (20%), DM (5%), RA (8%)

40. The history of an ulcer
Arterial
• Intermittent Claudication
• rest pain
Risk factors
• HTN, smoking,
hyperlipidemia, sedentary
• Previous arterial
intervention
Vasculitis
– History of autoimmune
disease
– Painful
– Lack chronic arterial
occlusive symptoms
– Systemic symptoms of
autoimmune disease

41. The history of an ulcer
• Infective
– Exposures
– Associated cellulitis
– Systemic symptoms
– Exudate
– Spreading
– Foul smell
• Neoplastic
– Chronicity
– Previous malignancy
– Risks
• Exposures
• UV radiation
• Ionising radiation

42. CLINICAL ASSESSMENT OF LEG ULCER
FEATURES VENOUS ARTERIAL NEUROTROPHIC TRAUMATIC MALIGNANT
SITE
gaiter area 70%,
lateral 20%,
circumferential
5%
malleoli,
heel,
metatarsal
heads,
5 MT base
pressure area
site of
trauma
face, lips,
toungue
SIZE/SHAPE
large shallow
,vertically oval,
small deep variable variable variable
MARGIN irregular regular regular
EDGE sloping punched out sloping
everted/roll
ed
FLOOR granulation
slough/
necrotic
slough variable black mass

43. FEATURES VENOUS ARTERIAL NEURO TRAUMA MALIGNANT
BASE fix /no induration no no no indurated
deep up to
DEPTH shallow deep
bone
variable shallow
DISCh
serous/
pureulent/ sero-sanguineous/
gree
nish/bloody
TENDER painless painful painless painful painless
SKIN
edema/eczema/
pigmentation/
atrophie blanche/
varicose vein
Thin skin/ dec
hair growth/
loss of sc fat/
loss of
shininess/
brittle nails
callus/ loss of
sensation
cellulitis
fix to
underlying
str
LYPMH
NODE
absent absent absent
present
except BCC

44. Uncommon variants of leg ulcer
• Marjolin’s ulcer
• Gummatous ulcer
• Meleney’s ulcer
• Erythrocyanoid ulcer
• Martorell’s ulcer

45. DISTINGUISHING FEATURES OF ARTERIAL AND VENOUS ULCERS
C/F ARTERIAL ULCER VENOUS ULCER
Gender M>F F>M
Age >60yrs 40 -60 yrs
Risk Factors Smkn, HTN, DM, Hyperlipidemia DVT,Thromphophilia, Varicose vein
Past History peripheral, coronary, Cerebrovascular DVT,Long bone #
Symptoms severe pain except DM neuropathy 3rd have slight pain
Site
malleoli, heel, metatarsal heads,
5 th MT base
Medial (70%), Lateral (20%) or both
and gaiter area
Edge Regular,Punched out, Indolent irrregular wit neo epithelium
Base
deep , green (soughy) or black
(necrotic) with no granulation tissue,
may comprise major tendon, bone n jt
pink n granulating but may be
covered in yellow green slough
Surrounding skin features of severe limb ishemia
LDS, Varicose eczema, atrophie
blanche
Veins empty full
Swelling usually absent often present

46. EVALUATION OF VASCULAR INSUFFICENCY
• Signs of ischemia
– Thinning of skin/diminished
hair growth/loss of
subcutaneous fat/ loss of
shininess/ brittle nails/ ulcer
in pressure areas/ coldness
• Burger’s postural test/
Burger’s angle
– angle of 30 degree indicates
severe ishemia
• Capillary filling time- 20- 30
sec
• Crossed leg test (Fuschsig’s
test)- detect popliteal
pulsation
• Palpation of Blood vessles
• ABPI
• Bordie-Terendelenburg test
– To determine the
incompetency of the
saphenofemoral valve and
other communicating systems
• Tourniquet test
• Perthes’s test-
– Cramping pain in DVT
• Schwartz test-
• Pratt’s test- position of leg
perforators
• Fegan method-
• Homan’s sign
• Moses’s sign

47. ANKLE BRACHIAL PRESSURE INDEX
(ABPI)
ABPI < 0.9 ABPI 0.9 – 1.1 ABPI >1.1
Palpable foot
pulse
PVD possible ,
assess furtther
PVD likely Calcification
• An ABPI of < 0.8 at rest indicates haemodynamically
significant lower limb arterial disease
• 0.7- claudication
• 0.4- rest pain
• < 0.3 suggests imminent necrosis
present- PVF
possible,
assess further
No palpable
foot pulse
PVD probable,
assess further
PVD likely
assess further
Calcification
present- PVD
probable,
assess further

48. PULSES OF LOWER LIMB
• The four pulses are:
– femoral
– popliteal
– posterior tibial
– dosalis pedis

49. Locate the superior border of the pubis
in the mid line of the body; this is the
uppermost part of the pubic symphysis.
Feel the anterior limit of the iliac crest.
The femoral pulse can be found
midway between these two bony points
(the mid-inguinal point)

50. Popliteal pulse
Ask the subject to bend the knee so that it is
flexed to about 90 degrees. Sit on the right
hand edge of the bed close to the subject
right foot. As before gently clasp the sides of
the knee (of either limb) and press the pulps
of your fingers into the popliteal fossa.

51. Locate the medial malleolus. 2-3cm below and
behind it you should find the posterior tibial
pulse. when taking the pulse on your own foot
it is easier to use the thumb. In clinical practice
the pulse is palpated using the pulps of the
index and middle fingers. The artery is slightly
deeper placed than the dorsalis pedis and
therefore more concentration is often required
to feel its pulsations
Place your fingers half way down the
dorsum of the foot on the bony area in
the line between the first and second
toes. The bones you can feel are the
dorsal aspect of the navicular and the
intermediate cuneiform bones. The
pulse is palpated where the artery
passes over this area.

52. MANAGEMENT
PRINCIPLE:
• Determine etiology
• Accurate assessment of ulcer
• Identify n correct co morbid factors
• Treat underlying causes
• Adequate drainage and desloughing
• Avoid adherent dressing

53. The Investigation of a Leg Ulcer
General Investigations
Haematological FBC
U&E, LFT’s
Blood Glucose
Lipid profile
CRP
Other ECG
X Ray
Swab C&S (remember TB)

54. The Investigation of a Leg Ulcer
Arterial
ABI’s
Doppler USG
Duplex USG
Arteropraphy
Digital substraction
angiogram (DSA)
CTA
MRA
Plethysmography
Transcutaneous oxygen tension
Isotope blood flow
Venous
Doppler USG
Duplex USG
Ambulatory Venous Pressure
(AVP) measurement
Phlebography (Ascending/
Descending)
Photoplethysmography
Vacricography
CT/MR Venography
Other
wound swab c/s
Biopsy
RF, ANA DNA binding
Compliment Levels

55. Doppler USG
• A standard Doppler probe emits a sound when blood
flows past the transmitting and receiving crystals.
• It may be uniphasic or biphasic
• Minimum level of investigation
• Quick/ Easy/ Non-invasive/ Inexpensive
• Useful in
– Patency of vein
– Venous reflux (SFJ > SPJ)
– Exclude arterial diseases
• ‘Doppler signal’ indicates moving blood, not viablility

56. Duplex Ultasonography
• Generates 3 types of image information based on
• Grey scale B mode ultrasound/ Color flow (triplex)/
Pulsed Doppler spectral analysis
• Uses
– blood velocity n valve closure time
– Detailed analysis of anatomy n physiology
– Valvular reflux / incompetnecy
• Red in color map flow
– Infrainguinal DVT
– Origin of varicose vein n venous ulceration
– Preoperative marking of LSV for FP bypas
– Post operative surveillence of vein grafts
– Arterial stenosis
• 100% peak systolic volume rise compared with a normal area

57. Limitation of duplex
• Cannot reliable distinguish deep venous incompetence due
to primary from secondary
• Cannot reliably deterimine the presence of functional
severity of venous outflow obstruction
• Unreliable in suprainguinal venous system
• Time consuming and operator dependent
• Oversensetive to clinically insignificant degrees of reflux

58. Phlebography
• Replaced by combination of
duplex and plethysmograpy
• Anatomy of deep venous
system
• Presence of residual thrombus
• Extent of recanalisation
• Distriution of collaterals
• Functional phlebography
enable to detect the site of
phlebography Venogram showing post-thrombotic
venous occlusions with collateral
pathways.

59. Varicography

60. Plethysmography
• Amount of blood in dermal circulation is
measured by the amount of light absorbed and
reflected
• Screening test
• Mesures the refilling time(RT) in dermal
circulation
• RT > 20 sec is normal
• Incompetency is indicated by short RT
• Little practical use in arterial disease

61. CT n MR venography
• Ideal for imaging for
large central vein
• Not widely used for
peripheral venous
disease

62. Ambulatory Venous Pressure
• Direct method has little practical use
• Measurement
– Stand motionless- 90 mmHg
– Walking (10 tip toe mov)- 15-30 mmHg
– Again stand still- RT 90 is 18- 40 sec
• Close relationship b/w AVP and ulcer
– <30 mmHg- none
– 41-50 mmHg- 22%
– 61- 70 mmHg- 57%
– >80mmHg- 73%

63. Transcutaneous oxygen tension
measurement
• Metabolic state of tissue
• Dorsum of the foot/ calf/ thigh
• Testing tcpo2 is 60 mmHg
• Useful in determining the site of amputation

64. Arteriography
• Gold standard for assessment
of LL
• DSA is more advance method
and provide the image of
contrast within the lumen of
the artery without the
surrounding tissues
• Site- Femoral/ Brachial/
Common femoral vein
• RF n INR should be normal
• Stop oral-hypoglycemic and
anticoagulant

65. lymphangiogram

66. Overveiw of TREATMENT of Leg Ulcer
• MEDICAL MANAGEMENT n LIFESTYLE
• DRESSING n TOPICAL AGENTS
• PHARMACOTHERAPY
• PHYSICAL THERAPIES
• SURGICAL MANAGEMENT

67. SELF CARE GUIDELINES
• Keep mobile with regular walking if possible
• Elevate legs when immobile
• Use emollient and examine legs regularly for
broken skin, blisters, swelling or redness
• Lose weight if appropriate
• Stop smoking

68. DRESSING n TOPICAL AGENT
IDEAL DRESSING
• Control (absorb) odour, exudates and or bleeding
• Exclude pathogenic bacteria and minimize colonization
• Relieve pain
• Ehance the would environment to speed up healing
• Protect the wound from further environmental injury
• Main the wound at body temperature
• Reduce excessive scarring and or recurrence
• Hide the wound form sight

69. Venous leg Ulcer – treatment
• There is no proven role of antiseptics
• Irrigate the wound with warm tap water or saline, then dry.
•
• Remove slough or necrotic tissue by gentle washing
• potassium permanganate 0.01% soak if the ulcer is malodorous
• For uncomplicated, non-infected ulcers apply a simple low-adherent
dressing like paraffin emollients n gauge and Zinc & replace weekly.
• Other dressings may be used if needed - pain (hydrocolloid), heavy
exudate (alginate) or slough (hydrogel)
• Biological dressing provide growth factors n scaffold for the ulcer
healing n is more promising

70. Venous leg ulcer - treating infection
• All chronic wounds are colonised with bacteria
• Antibiotics should be used only if there is evidence of cellulitis
or active infection (e.g. pyrexia, increasing pain, enlarging
ulcer)
• If there are clinical signs of infection present, clean ulcer with
warm tap water or saline before taking a swab
• Start immediate empiric treatment with an anti-staphylococcal
antibiotic i.e. flucloxacillin or erythromycin 500mg qds for
seven days
• Change dressing daily or alternate days to assess if infection is
improving
• Do not use antimicrobial dressings
• Do not start compression therapy if ulcer is infected

71. Physical therapies
• Elevation n Bed rest will eventually heal virtually all CVU
• Regular exercise will improve AVP
• Compression therapy has been the main stay of treatment for CVI
• Elastic bandage has better healing rates
• For moderate to sever CVI class III (34-45 mmHg) n IV( >45mmHg)
• Commence at metatarsal head terminate at tibial tuberosity
• Multilayer has advantages over single layer
– Charing cross four-layered bandage ( 42 at ankle n 17 below
knee)
• In mixed ulcer 3 layered compression bandage is used
• Compression is contraindicated if the ABPI < 0.6
• Replace every 6 months
• Graduated compression stockings should be used for at least 5 years
after ulcer healing

72. Surgery- varicose ulcer
• Varicose vein – SFJ / SPJ ligation , GSV stripping , Avulsion of
varicosities .
• Open perforator surgery
• Sub fascial perforator surgery
• Deep vein reconstruction
– Vein valve repair
– Vein valve transplantation
– Vein diameter reduction
– Veno-venous bypass ( palma porcedure)
• Skin Graft
– SSG
– Pinch graft
• Amputation

73. TREATMENT OF ARTERIAL ULCER
• Infection can cause rapid deterioration of an arterial ulcer
• It is not appropriate to debride arterial ulcers as this may produce
further ischaemia and formation of a larger ulcer
• Compression bandaging should not be applied
• Choice of dressing is dictated by the nature of the wound
• Treatment options include
– Risk factor modification
– Pharmacotherapy
– Lumbar sympathectomy
– Angioplasty
– Graft
– Amputation
• To relieve pain n remove a life threatining ischemic
• Below knee have great advantage of rehabilitation
• Above knee have better wound healing

74. TREATMENT OF NEUROPATHIC ULCER
• GENERAL ISSUES
– Good well fitting shoes with sufficient depth
– Look n feel before putting shoe
– Careful toe nail cutting
– Never to attempt trimming calluses
• Chiropody (nail, callus, padding)
• orthotics
• Surgery- excision of prominent bone
• Eradication of infection
• Dressing
• Surgical debridement and or amputation for neuroischemic
or ishcemic ulcer

75. Treatment option for Rheumatoid leg ulcer
• Treat the etiology
• Relieve the pain
• Local support n dressing
• Bed rest n Elevation
• Anti inflammatory agent
– Colchicine (1.5mg daily)
– Dapsone (100mg daily)
– Prednisolone 20-40mg daily
– Triamcinolone acetate (Kenalog 10mg/ml) 0.75-1ml for
ulcer of 5cm diameter
• Topical growth factor
• Surgical option- SSG

76. Approach to vasculitic leg ulcer

77. Approach to lymphedema n ulcer

78. THANK YOU