7. With muscle contraction, deep veins are compressed, one
way valves in deep system allow the high pressure flow to
move against gravity
One way valves in perforators close to prevent pressure
injury to the skin
In all patients with venous disease there is failure of these
one way valves
Worsened by impairment of leg muscle function or ankle
joint range of motion
8. Incompetent perforators and refluxIncompetent perforators and reflux
• Failure of venous valve (REFLUX)
and poor calf muscle function leads
to ambulatory venous hypertension
and sustained capillary hypertension
• 60% of venous ulcer patients have
isolated superficial vein insufficiency
9. PathogenesisPathogenesis
1. Capillary stasis: `Homans` postulated that stasis of venous
blood in post-thrombotic syndrome gave rise to anoxia and hence
venous ulcers
2. Fibrin cuff theory: `Browse and Bermand` postulated that
venous ulcer could be result of deposition of pericapillary fibrin due
to leakage of fibrinogen through pericapillary spaces. fibrinogen
polymerizes to form fibrin
Oxygen diffusion barrier
Increase in collagen IV in and around capillary
3. White cell trapping: `Coleridge and Smith` suggested that
leukocytes may become trapped in capillaries in static blood,
obstructing the flow
10. 4. Trapping growth factors: `Felanga and Eaglestein`
hypothesized that pericapillary fibrincuff , α-2 macroglobulin interfare
with growth factor transport
5. Multicausal model/ Maastricht model:
Elevated pressures on vascular side of capillaries lead to structural
changes in capillary wall
Interendothelial space broadens
Collagen IV layer disintegrates
Capillary wall becomes thicker
Water diffusion is effected- oedema
Larger molecules (fibrin ) escape- fibrin cuff formation
α-2 macroglobulin escapes and traps TGF-β
13. Signs and symptomsSigns and symptoms
• Usually preceded by patchy erythema or discoloration of an
intense bluish red colour (capillary congestion)
• Ischemia of the skin finally leads, to necrosis, often following
a minor episode of trauma (scratching, small knocks,
dermatitis)
• Ulcer is typically painless. Patients develop typical ischemic
pain on elevation of the ulcerated leg, which is edematous .
Associated with arterial disease can ( 1/3 of cases).
• Ulcer is covered with yellowish exudate over granulation
tissue
• Healing ulcers have a shallow sloping edge with healthy
granulation tissue in their base and little slough. Pink lip of
epithelium at the edge of ulcer is uniform and supplied by
relatively uncongested capillaries
14.
15.
16. • Signs:-
Signs of venous hypertension are present- LDS, varicose
veins, varicose eczema or oedema
An oedematous leg not responding to diuretics is a strong
clue to the diagnosis
18. DiagnosisDiagnosis
• Clinical:
Gaiter area
Signs of venous hypertension
Past history of venous thrombosis
Past history of treatment for varicose veins
Family history of venous disease
• Colour Doppler duplex USG: usually, after ulcer
heals
Confirm venous reflux, superficial venous incompitance
Confirm deep venous compliance
19. • Plethysmography:
To investigate calf muscle pump function when Colour
Duplex is normal
• Skin biopsy: not indicated in venous ulcer
Skin malignancy or vasculitis suspected
• Arterial disease must be excluded;
ABPI
Arterial duplex doppler scanning
arteriography
20. ManagementManagement
• Is done by the following means:-
1. CONSERVATIVE TREATMENT
2. SYSTEMIC MEDICATIONS
3. SURGICAL OPTIONS
• The goals of treatment are to reduce edema, improve ulcer
healing, and prevent recurrence.
21. COMPRESSION THERAPYCOMPRESSION THERAPY
• Compression therapy is the standard of care for venous ulcers
and chronic venous insufficiency
• Compression therapy reduces edema, improves venous reflux,
enhances healing of ulcers, and reduces pain.
• After an ulcer has healed, lifelong maintenance of compression
therapy may reduce the risk of recurrence
• Contraindications to compression therapy include clinically
significant arterial disease and uncompensated heart failure.
• Methods include
1. inelastic,
2. elastic,
3. intermittent pneumatic compression
22. 1. INELASTIC COMPRESSION :-
• Inelastic compression therapy provides high working pressure
during ambulation and muscle contraction, but no resting
pressure.
• The most common method of inelastic compression therapy is
the Unna boot, a zinc oxide–impregnated, moist bandage that
hardens after application.
• Disadvantages:- because of its inelasticity, the Unna boot does
not conform to changes in leg size and may be uncomfortable to
wear.
• The Unna boot may lead to a foul smell from the accumulation
of exudate from the ulcer, requiring frequent reapplications
23.
24. 2. ELASTIC COMPRESSION :-
• Elastic compression therapy methods conform to changes in leg
size and sustain compression during both rest and activity
• Stockings or bandages can be used; however, elastic wraps are
not recommended because they do not provide enough pressure
• Compression stockings are removed at night, and should be
replaced every six months because they lose pressure with regular
washing
• Elastic bandages are alternatives to compression stockings
(multilayer bandages are more effective than single layer.)
Disadvantages:- multilayer compression bandages require skilled
application in the physician’s office one or two times per week,
depending on drainage.
25.
26.
27. 3. INTERMITTENT PNEUMATIC COMPRESSION:-
• comprises a pump that delivers air to inflatable and deflatable
sleeves that embrace extremities, providing intermittent
compression.
• generally reserved for bedridden patients who cannot tolerate
continuous compression therapy
Disadvantages :- expensive and requires immobilization of the
patient
28. LEG ELEVATION
• Leg elevation requires raising lower extremities above the level
of the heart, with the aim of reducing edema, improving
microcirculation and oxygen delivery, and hastening ulcer healing
DRESSINGS
• Dressings are often used under compression bandages to promote
faster healing and prevent adherence of the bandage to the ulcer
29. • Treatment of underlying cause of eczema:
Varicose
Contact allergy
Contact irritant
Emollients , Steroids if inflammed
• Cleansing and debridement:
1. Irrigation of ulcer with warm tap water, sterile saline
2. Debridement improves wound healing
30. Systemic therapySystemic therapy
• Antibiotics:- only used if there is clear evidence of
infection
• Pentoxyphylline:-
Fibrinolytic
Reduction in leukocyte adhesion
Dose of 400 to 800mgs TDS
• Ortal enteric coated aspirin:- 300mg
• Flavonoid drugs (e.g. oxerutins)
• Daflon 500
• Stanazolol:-androgenic steroid with fibrinolytic property.
Improves LDS
• Iloprost infusion (vasodilator that inhibits platelet
aggregation)
32. TYPES OF DEBRIDEMENT:
I. SHARP DEBRIDEMENT
II. MECHANICAL DEBRIDEMENT
III.AUTOLYTIC DEBRIDEMENT
IV.ENZYMATIC DEBRIEMENT
V. BIOLOGICAL DEBRIDEMENT
33. Dressing and topical therapiesDressing and topical therapies
Should keep ulcer moist not wet
Simple ,low adherent
Left undisturbed as long as possible
`strike through` of exudate to outside of the bandage is indication
for change
1. Knitted viscose primary dressings + superimposed
absorbent pad (secondary dressing)
2. Hydrocolloid dressing- dry sloughy wounds to reduce pain
3. Absorptive dressing (alginate, foam, hydrofibre) – highly
exuding wound
4. Zinc paste bandage (unna boot)
34.
35. Surgical treatmentSurgical treatment
• Between 50-70 % of ulcers heal at 3 months, 80-90% by
12 months
• 50% overall recurrence rate by 5-7 yrs , mostly in post-
thrombotic limbs
Surgical ligation of saphenous vein and incompetent
communicating veins is `no better than` stanozolol and
stockings in preventing ulcer
Various procedures used:
I. Ligation and stripping of saphenous veins
II. Compressive sclerotherapy
III.Complete extirpation of the communicating veins
`feeding` the ulcer
36. IV- deep vein bypass
V – valvuloplasty
VI- brachial valve transplant
Shave therapy:
•Excision of ulcer and surrounding LDS followed by meshed
split skin graft. Heals 88% of ulcers
Skin grafting
•Punch grafting
•Split skin grafts
•Mesh grafts
38. Lifelong:Lifelong: CompressionCompression
TherapyTherapy
• After healing of ulcer,
fit for custom stockings
• Remove and bathe each evening, apply
moisturizer
• Each morning put on
to prevent edema
• Pt should purchase in pairs of two,
replace every 6 months
39. Associations and Complication ofAssociations and Complication of
venous leg ulcervenous leg ulcer
1. General disease
1. Obesity
2. Hypertension
3. Cardiovascular diseases
2. Anaemia, hypoproteinemia
3. Depression
4. Inverted foot, equinus ,calf muscle atrophy
5. Zinc depletion
6. Infections: staph. aureus, groupA β- haemolytic
streptococci, pseudomonas, candida albicans
7. Contact dermatitis
8. haemorrage
45. CLINICAL FEATURES:-
1.Claudication-pain upon walking.
2.Rest pain-in advanced disease. Limb is kept in a dependent position.
3.Peripheral pulses are poor/absent.
4.Color changes in the limbs with alteration of position indicating
ischemia.
5.Site:over a bony prominence-toes , ankle.
46. Clinical featuresClinical features
• Ulcer: typically round with sharply demarcated borders.
• Base-dry &covered with necrotic debris.
• No granulation tissue is seen.
• Exposure of tendons/deep tissues.
• Surrounding skin-normal /
dry, cold, shiny &hair less.
• Lossof S/C tissue; Muscle wasting & atrophic skin of
lower calf and foot.
• Toe nails-thickened.
• Severe pain is present.
• Audible bruits present.
49. MANAGEMENT:
• Aim is to establish adequate arterial supply.
• General-Low cholesterol diet;
Reduction of smoking;
weight reduction;
Control of HTN; DM; Hyperlipidemia.
• Drugs:
• Lipid lowering drugs-HMG-COA Reductase inhibitors.
• Antiplatelet drugs-Aspirin.
Clopidogrel
Cilastozol
• Others-Exercise-dev.of collateral circulation.
Elevation of head of bed
Adequate pain control
Keeping the limbs warm.
50. TreatmentTreatment
Treatment:-assess by arterial duplex USG or Angiography
Condition is often indolent, healing only when blood supply
is improved + ulcer base is excised and grafted
i.ABPI <0.5 :-immediate revascularization
ii.ABPI >0.5 but <0.85 :-modified compression, short stretch
bandages with low resting pressures, intermittent pneumatic
compression ?
Revascularization should be considered in ulcer that do not
heal
Amputation
54. b)Autonomic neuropathy hypohydrosis of
foot fissures
& calluses ulceration
c)Atherosclerotic changes in LL vessels
thickening of capillary BM & endothelial gapsinc.vascular
permeabilityulcer.
55. C/F:
• Burning,numbness,itching,paresthesias of distal extremeties.
• claudication history present.
• Location –at pressure sites.
a.Plantar surface overlying the I & V metatarsal heads.
b.Plantar surface of great toe& the heel.
• Ulcer-”punched out” with thick rim of callus surrounding the
ulcer.
• Dryness &fissuring of surrounding skin.
62. Hypertensive ulcer/martorell`s ulcerHypertensive ulcer/martorell`s ulcer
• Associated with longstanding, poorly controlled
hypertension
• Female to male preponderance
• Often initiated by trauma and ischemia, failure to meet
demand of repair
• CLINICAL FEATURES
Preceded by small macular cyanotic lesion
Bilateral superficial ulcerations over ant. aspect of leg b/w
middle and lower 1/3. livid edge is characteristic
Extremely painful, alleviated by holding leg in dependent
position
Normal peripheral pulses
63. • Pain and ulceration with livid reticulate edge but no LDS.
• Usually more proximal than venous ulcer
64. • BIOPSY:-
• Increased thickness of arteriolar wall with luminal
narrowing by subendothelial hyaline degeneration
• Smooth muscle hyperplasia, most marked in media. Later
replaced by collagen fibers
• TREATMENT:-
• Anti-hypertensives (ß-blockers avoided)
• Firm non-elastic (short-stretch) support bandage
• Leg should be placed in position to prevent oedema, not so
high to promote ischemia
• smoking is to be stopped
• Excision of ulcer area with grafting advised
65. VASCULITIS/VASCULVASCULITIS/VASCUL
OPATHYOPATHY
Mostly acute, sometimes subacute and chronic
Usually multiple
Palpable purpura is characteristic, may be
polymorphous, even pustular
An irregular border, black necrosis, erythema,
bluish or purple discoloration of adjacent skin are
suggestive of vasculitis
66. Cutaneous ulcerations is usually caused by medium sized
to small vessel leucocytoclastic vasculitis
Small vessel vasculitis include
I. Cutaneous small vessel vasculitis
II. HSP
III. Wegener`s granulomatosis
IV. Essential mixed cryoglobulinemia
V. Rheumatoid nodules
Medium vessel vasculitis include
I. Classical PAN
I. Cutaneous form
II. Kawasaki disease
67. Lab screening tests for vasculitisLab screening tests for vasculitis
i. Urine routine for proteinuria, haematuria, cylindruria
ii. Routine and immunohistopathology of skin
iii. ESR, haemoglobin, differential blood count, LFT, RFT
iv. ANA, RF
v. Complement C4, circulating immune complexes
vi. Paraproteins, immunoglobulin fractions
vii. ANCA
viii. Serological tests and cultures for underlying infections
72. LIVEDOID VASCULOPATHYLIVEDOID VASCULOPATHY
• Occlusive vasculopathy limited to gaiter region extending
down to the dorsum of foot
• Hyalinization and thrombosis of the microvasculature with
scarce inflammatory infiltrate
• Ulcers are small painful, heal with ivory white scars
(Atrophie Blanche)
• TREATMENT
• Immunosupression not effective, treatment of
hypercoagulable state
73. Pyoderma gangrenosumPyoderma gangrenosum
• Rare, non infectious, neutrophilic dermatosis commonly
associated with underlying disease
• Classic/Ulcerative PG variant usually presents with painful
ulcers ,commonly on legs (70%)
• Clinical features:
presents as solitory or multiple small, tender, red-blue
papules, plaques or pustules that evolve into painful ulcers
with charesteristic violaceous undermined edges
There may be granulation tissue, necrosis or purulent
exudate at the ulcer base
Pathergy occurs in 25%
Healing usually occurs with atrophic cribriform scar
79. treatmenttreatment
For early or mild lesions:-
Wet compresses, hydrophilic occlusive dressings, antimicrobial agents
and topical corticosteroid
Topical tacrolimus- mild early lesions
Intralesional corticosteroids
Benzoyl peroxide, 5-aminosalicylic acid, nitrogen mustard,
cromoglycate, PDGF, intralesional ciclosporin
For more severe/resistant to topical therapy
Corticosteroids are mainstay of treatment
Dapsone , low dose colchicine
Ciclosporine, cyclophosphamide, chlorambucil, intravenous
tacrolimus, mycophenolate mofetil and thalidomide
TNF-α inhibitors:- etanercept, adalimumab, infliximab
Plasmapharesis, IVIg
80. Necrobiosis lipoidicaNecrobiosis lipoidica
• Age of onset is around 30 years, women three times more
cases
• Prevalence of 0.3 to 3.0 % in patients with diabetes
• Other than Diabetes (75%) and GA other reported
associations include rheumatologic, endocrine, and
haematologic disorders
• Presents as one to several sharply demarcated yellow-
brown plaques on the anterior pretibial region, have
violaceous, irregular border that may be raised and
indurated.
• Clinical course is indolent spontaneous remission in 20%
• Ulceration is most severe complication (13 to 35%) ,
84. • Marjolin's ulcer is a rare and often aggressive cutaneous
malignancy (scc 75-96%) that arises in previously
traumatized or chronically inflamed skin, particularly after
burns
• Several theories including the toxin, chronic irritation,
traumatic epithelial elements implantation, heredity,
immunologic privileged site, co-carcinogen, ultraviolet
rays, initiation and promotion and environmental and
genetic interaction theories have been reported to explain
the malignant transformation
• The latency period from the time of injury to the onset of
malignant transformation averages 36 years
85. • Marjolin's ulcers are very aggressive tumors that necessitate
a well thought out treatment plan to optimize care and
assure patient survival. Early diagnosis and prompt surgical
intervention is mandatory
86. HAEMATOLOGICAL DISORDERSHAEMATOLOGICAL DISORDERS
• CAUSES
o Sickle cell anaemia
o Hereditary spherocytosis
o Other haemolytic diseases
o Myloproliferative diseases
o Cell size compromises capillary perfusion
o If thrombosis develops
o Treatment (hydroxycarbamide)
87. HYDROXYCARBAMIDEHYDROXYCARBAMIDE
• Leg ulceration was reported in 9% of patients taking this
drug in a prospective study
• Indicated for CML, CLL , polycythemia vera, essential
thrombocythaemia, sickle cell anemia
• Ulcers develop after at least 1 year of treatment in dose
dependent fashion
• Ulcers are located on or near the malleoli in ¾ of cases. Are
very painful, resemble atrophie blanche
• Treatment:- after withdrawal of hydroxycarbamide 85% of
ulcers heal spontaneously in 1-9 months
• Debridement, f/b split skin graft in non-healing ulcers
88. STEROID ULCERSTEROID ULCER
CAUSES:-
• I/L steroid injections particularly over areas with
impoverished blood supply
• Strong topical corticosteroid applied to venous or other
ulcer of lower leg
CLINICAL FEATURE:-
• Indolent ulcer with characteristic
greyish slough
90. Primary pyococcal ulcerationPrimary pyococcal ulceration
• Some microorganisms like β-haemolytic Streptococcus
pyogens can cause tissue necrosis
• Causes wide range of clinical symptoms
• erysipelas
• punched out ulcers (Ecthyma)
• Deep cellulitis
• Fascitis necroticans, sepsis and multiorgan failure
• Treatment:-
• Immediate high dose antibiotics
• Special attention to possibility of combined infection with Staph.
aureus and anaerobic species
91. Bazin`s disease/Tuberculous ulcerBazin`s disease/Tuberculous ulcer
• Usually present as subcutaneous nodules and plaques on
calves in young adult female
• Gradually involve overlying skin, often with ulceration
Ulcer has irregular bluish and friable undermined edges.
Generally multiple ,bilaterally symmetrical
• There is generally evidence of pulmonary or skeletal
tuberculosis
• Develop in cold weather initially
• TREATMENT:-
• ATT
92. Tropical/phagedenic ulcerTropical/phagedenic ulcer
• Synergistic bacterial infection by at least two organisms
fusobacterium species (F. ulcerans) and spirochete or some
anaerobe
• Common in hot and humid tropical regions, clustering of
cases
CLINICAL FEATURES
• Most lesions follow minor trauma on exposed parts such
as legs
• Papule rapidly breaks down to form sharply defined ulcer,
most often with undermined edges
• Painful , constitutional symptoms are usual
• No lymphadenopathy
94. PROLIDASE DEFICIENCYPROLIDASE DEFICIENCY
• Autosomal Recessive condition caused by defect in
prolidase gene on chromosome. 19q13.11
• Prolidase/iminodipeptidase degrades collagen .
• Cleaves dipeptides with hydroxyproline/proline at C-
terminus
• Deficiency results in impaired recycling of proline residues
CLINICAL FEATURES:-
• Presents before 12yrs, multisystem disorder, primarily
involves skin (85%)
95. • Recurrent, multiple ulcers of
lower extremities are seen in over 50%
• Fragility of skin, easy breakdown, usually
preceded by purpura or bruising
• Fine scarring, telangiectasis and
eczematous lesions may be feature
96. • Characteristic facies:- hypertelorism, saddle nose in
mentally retarded
• Other associations: dental caries, splenomegaly,
hyperextensibility of ligaments, osteoporosis, respiratory
infections, corneal opacities, amblyopia and optic atrophy
DIAGNOSIS:
Iminodipeptiduria >5 mmol/24 hour
Decreased prolidase activity in blood
Thrombocytopenia, hypergammaglobulinemia, iron
deficiency anaemia
97. TREATMENT:
Refractory to all forms of treatment, including graft
rejection
Oral and intravenous antibiotics in case of secondary
infection
Ascorbic acid and manganese (cofactors of prolidase)
Diphenylhydantoin
5% glycine and 5% proline ointment
Apheresis exchange
Topical and systemic growth hormone