This document discusses different types of leg ulcers including venous, arterial, diabetic neuropathic, and hypertensive ulcers. It provides information on: 1. The causes, risk factors, signs and symptoms, investigations and management for each type of ulcer. 2. Venous ulcers are the most common type, caused by venous insufficiency and reflux, and are typically treated with compression therapy and dressings. 3. Arterial ulcers are caused by peripheral arterial disease and present with dry necrotic wounds, often over bony prominences of the feet. Revascularization may be required for healing. 4. Diabetic and neuropathic ulcers occur due to loss of sensation from

1. LEG ULCERSLEG ULCERS
Dr Y SRI HARSHA

2. WHAT IS AN ULCER??WHAT IS AN ULCER??

3. Causes of lower limb ulcerationCauses of lower limb ulceration
1. Venous insufficiency (45 -60%)
2. Arterial insufficiency (10 -20%)
3. Diabetes (15 -25%)
4. Vasculitis
5. Haematological dissease
6. Infections
7. Trauma
8. Drugs/therapy:-hydroxy urea
9. Skin conditions:- pyoderma gangrenosum, necrobiosis lipoidica
10. malignancies
11. Genetic :-prolidase deficiency, klinefelter`s syndrome

4. Venous Leg UlcersVenous Leg Ulcers

5. • Ulcers caused due to venous insufficiency
• Often at medial lower aspect of leg `gaiter region`
• With or without visible varicose veins

6. NORMAL PHYSIOLOGYNORMAL PHYSIOLOGY

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

11. Causes of venous ulcerCauses of venous ulcer

12. Risk factorsRisk factors

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

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

17. Complications:
1)Infection- >105
/cm2
tissue.
S.aureus;GAB Hemolytic
streptococcus; Candida
2)Haemorrhage
3)Lymphoedema
4)Malignant change
5)Subcutaneous calcification
6)Bone changes.

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

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.

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)

31. • Sodium dobesilate:- 500 mgs BD

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)

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

37. • Subfascial endoscopic perforator
surgery (SEPS)
• Improves healing rates, and reoccurence

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

40. 9. Lymphoedema
10.Malignant change
11.Sub cutaneous calfication
12.Bone changes

41. Arterial ulceration

42. ARTERIAL ULCERSARTERIAL ULCERS
• Common in age gp. >40yrs.
• Risk factors- smoking;DM;Hyperlipidemia;
hyperhomocystenemia;
male gender; sedentarylifestyle.
• Associated with-Buerger’s disease; Erythromelalgia etc.
Pathogenesis: progressive narrowing of arterial lumen
obstruction to blood flow
Tissue ischemia,necrosis &ulceration.

43. EtiologyEtiology

44. Risk factorsRisk factors

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.

48. INVESTIGATIONSINVESTIGATIONS
• Routine blood count-anemia / polycythemia
S.Electrolytes; RFT; ECG; CXR; S.Cholesterol &
triglycerides.
• Bacterial C/S
• Deep wedge biopsy
• Measurement of Ankle-Brachial doppler pressure index.
ABI: 0.5-0.9=Claudication
< 0.5 =ischemia
• Transcutaneous PO2-using a heated (clarke’s electrode.)

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

53. NEUROPATHIC ULCERSNEUROPATHIC ULCERS
• Common are Diabetic ulcers; Leprosy .
DIABETIC ULCERS :
• Neuropathy &peripheral vascular disease are
imp.etiological factors.
• Pathogenesis:
a)Neuropathy->lossof protective pain sensation
&motor dysfunction
repetitive trauma
ulceration.
.

54. b)Autonomic neuropathy hypohydrosis of
foot fissures
& calluses  ulceration
c)Atherosclerotic changes in LL vessels
thickening of capillary BM & endothelial gapsinc.vascular
permeabilityulcer.

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.

58. Investigations:
• Routine hemogram; Blood sugar levels;
• Hemoglobin AIc- glycated Hb levels-
3-6% normal
7-8%  well controlled diabetes
> 9% neuropathy
& nephropathy.
• Contrast Arteriography.
• MRA &Contrast Tomographic angiography.

59. Management:
• Aggressive debridement-
mechanical/enzymatic.
• Treatment of associated arterial diseases.
• Restoration of circulation to the lower extremity.
• Calluses-debridement &sterile dressings.
• Dry necrotic ulcers-Hydrocolloid dressing &Hydrogels.
• Orthotic devices-decrease pressure at the site.
• Becaplermin gel-topical application.

61. Hypertensive ulcer

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

68. TreatmentTreatment
• Conservative management
• Immunosuppressive therapy:- Persistent or progressive
ulceration due to histologically confirmed vasculitis

69. Rheumatoid DiseaseRheumatoid Disease
• CAUSES
• Poor joint movement- impairs calf muscle pump/ imobility
increases risk of DVT
• True ``Rheumatoid Ulcer`` because of rheumatoid arteritis
• Ulceration of rheumatoid nodule
• CLINICAL FEATURES
• Ulcer in gaiter region, sloughy base with poor granulation
tissue
• D/D venous ulcer:-
• No surrounding LDS and other signs of venous ulcer
• Positive RF
• Normal Doppler pressure and venous duplex studies

70. OTHER AUTOIMMUNE DISEASES:-
•Lupus erythematosus
•Felty`s syndrome- associated with skin ulcers
1. Rheumatoid arthritis
2. Splenomegaly
3. neutropenia
•Still`s disease
•Polyostotic fibrous dysplasia
•s/c or muscular fibrosis
SARCOIDOSIS

71. • LIVEDO RETICULARIS
• Fixed but broken pattern of mottling
1. Vasculitis
2. Intravascular thrombosis
1. Cryoproteniemia
2. Antiphospholipid syndrome
3. Sneddon`s syndrome

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

75. CausesCauses
• Gastrointestinal- ulcerative colitis, crohns, collagenous
colitis,gastritis, gastroduodenal ulcer
• Arthritides:- Rheumatoid arthritis, Seronegative arthritis,
osteoarthritis
• Haematological:- Leukaemias, myelofibrosis,
myelodysplastic syndromes,
paraprotenemia,waldenstrom`s macroglobulinemia
• Hepatic:- chronic active hepatitis ,PBC, sclerosing
cholingitis
• Other vasculitides, collagen vascular and related
disorders

76. • Acne and related disorders
• Autoimmune:- thyroid disease, DM
• Drugs:- CSF, gefinib, interferon, PTU, isotretinoin
• Solid organ tumors:- colon pancreas, breast, bronchus,
carcinoid
• Miscellaneous:- sarcoidosis, HIV, hep. C, chorinic lung
disease

77. Diagnostic criteriaDiagnostic criteria

78. DiagnosisDiagnosis

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%) ,

81. • Treatment: steroids, aspirin, topical retenoids ,
topical PUVA,fumaric acid esters,
cyclosporine, surgical
excision

82. tumorstumors

83. Marjolin`s ulcerMarjolin`s ulcer

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

89. INFECTIONSINFECTIONS
1. Primary uncomplicated pyococcal ulceration
2. Meleney`s ulcer
3. Tuberculous ulcer
4. Other mycobacterial infections
5. Leprosy
6. Tertiary syphilis
7. Yaws
8. `desert` or `veldt` sore
9. Tropical ulcer
10. Leishmaniasis
11. Glanders, tularemia, brucellosis, cat scratch fever

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

93. • Management
• Rest, limb elevation
• Treatment of underlying cause, malnutrition
• Penicillins and/or metronidazole

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