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Leg ulcers

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leg ulcers seen commonly

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Leg ulcers

  1. 1. LEG ULCERSLEG ULCERS Dr Y SRI HARSHA
  2. 2. WHAT IS AN ULCER??WHAT IS AN ULCER??
  3. 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. 4. Venous Leg UlcersVenous Leg Ulcers
  5. 5. • Ulcers caused due to venous insufficiency • Often at medial lower aspect of leg `gaiter region` • With or without visible varicose veins
  6. 6. NORMAL PHYSIOLOGYNORMAL PHYSIOLOGY
  7. 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. 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. 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. 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. 11. Causes of venous ulcerCauses of venous ulcer
  12. 12. Risk factorsRisk factors
  13. 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. 14. • 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
  15. 15. 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.
  16. 16. 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
  17. 17. • 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
  18. 18. 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.
  19. 19. 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
  20. 20. 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
  21. 21. 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.
  22. 22. 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
  23. 23. 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
  24. 24. • 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
  25. 25. 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)
  26. 26. • Sodium dobesilate:- 500 mgs BD
  27. 27.  TYPES OF DEBRIDEMENT: I. SHARP DEBRIDEMENT II. MECHANICAL DEBRIDEMENT III.AUTOLYTIC DEBRIDEMENT IV.ENZYMATIC DEBRIEMENT V. BIOLOGICAL DEBRIDEMENT
  28. 28. 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)
  29. 29. 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
  30. 30. 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
  31. 31. • Subfascial endoscopic perforator surgery (SEPS) • Improves healing rates, and reoccurence
  32. 32. 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
  33. 33. 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
  34. 34. 9. Lymphoedema 10.Malignant change 11.Sub cutaneous calfication 12.Bone changes
  35. 35. Arterial ulceration
  36. 36. 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.
  37. 37. EtiologyEtiology
  38. 38. Risk factorsRisk factors
  39. 39. 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.
  40. 40. 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.
  41. 41. 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.)
  42. 42. 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.
  43. 43. 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
  44. 44. 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. .
  45. 45. 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.
  46. 46. 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.
  47. 47. 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.
  48. 48. 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.
  49. 49. Hypertensive ulcer
  50. 50. 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
  51. 51. • Pain and ulceration with livid reticulate edge but no LDS. • Usually more proximal than venous ulcer
  52. 52. • 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
  53. 53. 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
  54. 54.  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
  55. 55. 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
  56. 56. TreatmentTreatment • Conservative management • Immunosuppressive therapy:- Persistent or progressive ulceration due to histologically confirmed vasculitis
  57. 57. 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
  58. 58. 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
  59. 59. • LIVEDO RETICULARIS • Fixed but broken pattern of mottling 1. Vasculitis 2. Intravascular thrombosis 1. Cryoproteniemia 2. Antiphospholipid syndrome 3. Sneddon`s syndrome
  60. 60. 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
  61. 61. 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
  62. 62. 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
  63. 63. • 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
  64. 64. Diagnostic criteriaDiagnostic criteria
  65. 65. DiagnosisDiagnosis
  66. 66. 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
  67. 67. 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%) ,
  68. 68. • Treatment: steroids, aspirin, topical retenoids , topical PUVA,fumaric acid esters, cyclosporine, surgical excision
  69. 69. tumorstumors
  70. 70. Marjolin`s ulcerMarjolin`s ulcer
  71. 71. • 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
  72. 72. • 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
  73. 73. 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)
  74. 74. 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
  75. 75. 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
  76. 76. 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
  77. 77. 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
  78. 78. 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
  79. 79. 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
  80. 80. • Management • Rest, limb elevation • Treatment of underlying cause, malnutrition • Penicillins and/or metronidazole
  81. 81. 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%)
  82. 82. • 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
  83. 83. • 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
  84. 84. 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

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