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Diabetic foot.pptx
- 1. DIABETIC FOOT BY: DR. MOHAMMADMASOOM PARWEZ ACADEMIC RESIDENT,GENERAL SURGERY AIIMS BHOPAL
- 3. OUTLINE • INTRODUCTION • DEFINITION •CLASSIFICATION & STAGING • PATHOGENESIS • CLINICAL FEATURES • DIAGNOSISAND EVALUATION • MANAGEMENT • PREVENTIONGUIDELINES • SUMMARY • CONCLUSION • REFERENCES
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- 6. Introduction • Diabetes –M/C/C of non traumatic amputation of lower limbs • Accounts for >70% of lower limb amputations • Leads to prolonged hospitalization, disability and impending socio economical and psychological impacts • Most common ulcer sites are toes (dorsal or plantar surface), followed by the plantar metatarsal heads • Diabetic foot ulcer conditions include chronic ulcers, superficial and deep infections of the foot, and osteomyelitis
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- 8. Definition • Diabetic footis a disease complex that can develop in skin, muscles and bones of the foot as a result of nerve damage, poor circulation and/or infections • Syndrome in which neuropathy, angiopathy and infection lead to tissue breakdown resulting in morbidity and possible amputation (WHO 1995) • Any foot pathology that results from diabetes or its long term results (Boulton 2002)
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- 11. Classification and staging •A standard classification is useful for: 1. Assessing the etiology 2. Designing appropriate Rx 3. Predicting prognosis 4. Monitoring course of disease process
- 12. Classification on basisof etiology • NEUROPATHIC FOOT • ISCHEMIC FOOT • NEURO-ISCHEMIC FOOT
- 13. Classification on basisof etiology • NEUROPATHIC FOOT • Due to peripheral POLYneuropathy i.e. “somatic + autonomic” both sensory and motor neuropathies • With/out CHARCOT joint disease (neuro-osteoarthropathy) • ISCHEMIC FOOT • Mainly MACROangiopathy i.e. PAD of LL • With/out infection • NEURO-ISCHEMIC FOOT (mixed)
- 15. Staging according toclinical condition (Edmond and Foster) Stage Clinical condition I NORMAL foot II HIGH RISK foot III ULCERATED foot IV CELLULITIC foot V NECROTIC foot VI MAJOR amputation
- 17. WAGNER’S classification (2001) •Most widely used • Grades diabetic foot on severity of ulcer penetration
- 18. Traditional MEGGITT -WAGNER’S classification(2001) Grade Physical Findings Description 0 INTACT SKIN NO ULCER (but HIGH RISK foot i.e. deformities, callus, insensitivity) 1 Superficial ULCER Only SKIN involvement 2 Deep ULCER Involves TENDONS and LIGAMENTS 3 Osteomyelitis BONE involvement 4 Partial GANGRENE TOES & FOREFOOT 5 Total GANGRENE Entire foot
- 20. Texas University woundclassification system
- 21. Stages of Ulcerdevelopment
- 22.
- 23. Pathogenesis • Development ofdiabetic foot is multi-factorial and complex • First, it involves longstanding HYPERglycemia, contributing to: 1. Neuropathy 2. Angiopathy 3. Immune dysfunction
- 24. 1(a). Neuropathy (SomaticSensory) Loss of pain sensation Unnoticed trauma (mechanical, thermal, chemical) Unchecked worsening of lesion Formation of callus Tissue damage and necrosis beneath the callus Development of cavity filled with serous fluid Cavity erupts to the surface Ulceration
- 26. 1 (b). Neuropathy(Somatic Motor) Weakness and decreased contraction of smooth muscles Muscle wasting/atrophy Foot Deformity Abnormal Gait Uneven pressure distribution Ulceration
- 27. Foot deformities predisposingto Ulceration • Clawed toes • Hammer toes • Pes cavus • Pes planus • Charcot joint • Talipes equinus (ankle joint rigidity) • Hallux valgus/varus/rigidus • Bunions (bony lump of hallux) • Nail deformities • Deformities from previous trauma/Sx
- 34. 1 (c). Autonomicneuropathy Decreased sweat secretion Dry and brittle skin Easy cracks and fissures Infection Ulceration
- 36. Effect of diabeticperipheral neuropathy
- 37. Factors contributing tofoot ulceration Intrinsic factors Extrinsic factors • Bony prominences • Walking barefoot • Limited joint mobility • Inappropriate footwear • Deformities • Falls and accidents • Callus formation • Mechanical pricks • Previous foot ulcer • Thermal injury • Charcot neuroarthropathy • Activity level
- 38. 2. Angiopathy • MACROangiopathy •Atherosclerosis of large arteries • Increased peripheral resistance • MICROangiopathy • Thickening of capillary basement membrane • Decreased capillary permeability Decreased perfusion of foot structures Decreased immune cells infiltration and antibiotic effect Poor wound healing GANGRENE
- 42. 3. Immune dysfunction •Impaired defenses against infections: • Decreased Leucocyte migration • Decreased Phagocytosis • Decreased Intracellular killing • Decreased Chemotaxis
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- 45. The neuropathic foot •Diminished sensation • Invariably warm skin with intact, bounding pulses • Ulcers Pressure points on plantar aspect Stress areas on dorsal aspect
- 46. The neuropathic foot •Ulcer often preceded by callus formation • Secondary infected ulcers • Progresses rapidly to cellulitis, abscess formation and osteomyelitis • Sepsis may complicate resulting in gangrene
- 47. The ischemic foot •Foot pulses are absent indicating ischemia • Foot is NOT warm • Lesions on the margins of the foot/ tips of toes • Absence of callus – characteristic feature
- 48. The ischemic foot •Gangrene may be present • Critical ischemia – identification • Characteristic pink • Painful • Pulseless • Cold foot
- 49. Differentiating features Characteristics NeuropathicIschemic Skin temperature Warm Cold Color Not altered Pink Cyanotic Pulse Bounding pulse Diminished Pulseless Sensation Painless Painful Skin Dry, thick, fissured Atrophic, thin Callus Present at pressure points Usually absent Ulceration On pressure points On toe tips, heels, foot margins Complication Charcot foot Gangrene
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- 65. Management includes 5aspects: • Metabolic control • Effective blood sugar control, neuropathy Rx • Mechanical control • Reduce risk of trauma, treat deformities • Vascular management • Infection prophylaxis and treatment • Patient education
- 66. Neuropathic foot • Managementof ulcer falls into 3 parts: • Removal of callus • Eradication of infection • Reduction of weight bearing forces, often requiring bed rest with foot elevated
- 67. Neuropathic foot • Excesskeratin should be pared away with a scalpel blade to expose the floor of the ulcer and allow efficient drainage of the lesion
- 68. Neuropathic foot • Radiograph– to assess the possibility of osteomyelitis • A deep penetrating ulcer is present • When lesions fail to heal • Lesions continue to recur
- 69. Neuropathic foot • Abacterial swab should be taken from floor of the ulcer • Culture of excised tissue • Superficial ulcer treated on OPD basis • Oral antibiotics as per culture reports • Most likely organisms to infect superficial ulcers are: • Staphylococci (89%) • Streptococci (42%) • Anaerobes (17%)
- 70. Neuropathic foot • Treatmentshould be started with amoxycillin, flucloxacillin, and metronidazole • Antibiotic adjusted as per the culture sensitivity reports • Simple non adherent dressing should be applied after cleaning the ulcer with normal saline • Deep indolent ulcer requires off loading - with total contact plaster cast
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- 72. Neuropathic foot • Castshould conform to the contours of the foot, thereby reducing shear forces on the plantar surface • Foot lesions not responding to treatment in one month duration requires further investigations and a different approach altogether
- 73. Ischemic foot • Ishemicfoot does NOT respond to medical treatment and requires vascular investigations • Doppler studies to measure pressure index (ABPI): PI 1.2 Indicates RIGID/CALCIFIED vessels or both PI 1.0 Normal (or calcified) PI 0.9 Indicates presence of ISCHEMIA PI 0.6 Indicates severe ISCHEMIA
- 74. Ischemic foot • Arterialimaging techniques include: • Duplex scanning • MRA • Conventional arteriography • Infrapopliteal angioplasty or distal bypass to tibial or peroneal vessels are important for limb salvage
- 75. Ischemic foot • Amputationof the toe is usually unsuccessful unless revascularisation procedures are carried out • If this is not possible, the dry necrotic toe should be allowed to auto-amputate • After attempts to control infection, Below Knee Amputation is indicated in those with extensive tissue destruction
- 77. Rest pain inneuro-ischemic foot • It can get relieved on successful revascularisation • Paravertebral lumbar block • Parenteral narcotics • Last resort– below knee amputation
- 78. Urgent treatment Red flag/Danger Signs: • Redness/ swelling of foot • Cellulitis/ discoloration and crepitus • Pink, painful, pulseless foot even without gangrene– critical ischemic limb
- 79. Urgent treatment • Bedrest • Intravenous antibiotics • Broad spectrum cover preferred • Quadruple therapy comprising of: • Amoxycillin • Flucoxacillin • Metronidazole • Ceftazidime/Gentamicin
- 80. Urgent treatment • Surgicaldebridement • To drain pus/ abscess cavities • To remove all necrotic and infected tissues • To remove all devitalised bone in osteomyelitis • Necrosis in digit: Amputation • Skin grafting after development of granulation tissue accelerates wound healing process
- 81. Neuropathic joint (Charcot) •Loss of pain sensation and rarefaction of bones • Abnormal mechanical stresses (usually prevented by pain) damages the susceptible bones by relatively minor trauma Presentation: • Hot swollen foot (sometimes aching) – mistaken for infection • Injury may have occured days/weeks earlier -- unnoticed
- 82. Neuropathic joint (Charcot) •Destructive process stops after definite period of time (weeks/months) Bony changes most often seen at: • Ankle joint • Tarso-metatarsal region of foot (TMT) • Metatarso-phalangeal region (MTP)
- 83. Neuropathic joint (Charcot) Radiographichallmarks: • Bony destruction, fragmentation • Bony remodelling • Joint destruction, subluxation and dislocation
- 85. Management Initial: • Bed restor use of non weight bearing crutches (until edema subsides) • Alternatively, foot immobilisation in well moulded total contact plaster cast • Immobilisation done until bony repair is complete (2-3 months) • Bisphosphonates- promising results Long term: • Special shoes and Insoles fitted to accommodate deformity and prevent ulceration
- 86. Long term careof wound Footwear: • For redistribution of weight bearing forces from vulnerable parts of the foot • Moulded insoles made from plastazote or microcellular rubber are suitable for long term use • Failure to wear appropriate shoes-- recurrence
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- 88. Screening and prevention •Foot must be examined thoroughly at the onset of diabetes and annually thereafter • Identification of critically ischemic foot is necessary • Patient awareness about the need for appropriate footwear • Test for sensations in the foot (inability to detect stimulus– risk of ulceration) • Nylon monofilament test
- 89. Screening and prevention •Examination of distal pulses in the lower limb and comparing with the other limb • Active lesions should be sought and treated immediately (lesions in obscured areas) • Early detection of skin cracks, callosities, discoloration and deformities
- 90. Prevention guidelines Low riskfoot: (With normal sensations and palpable pulses) • Individual foot care education At risk foot: (neuropathy/absent pulses/ others) • Enhance foot care education • Feet examination every 6 months
- 91. Prevention guidelines High riskfoot: (with ischemia, deformity, skin changes or previous ulcer) • Three month follow up • Intensified foot care education • Rehabilitation for deformities/disability
- 92.
- 93. Management of Grade1 and 2 lesions • Extensive Debridement • Good local wound care • Relief of pressure from ulcer (off- loading) • Close monitoring • In non healing ulcers, hospitalization for bed rest and parenteral antibiotics • Culture from ulcer bed • Oral/IV antibiotics as per severity and culture reports • Usually, oral Cephalexin 500mg QID or Clindamycin 300mgTDS X 2 weeks (75% ulcers heals in 2 weeks time)
- 94. Management of Grade3 lesions • Evaluation of PAD • Evaluation for bony involvement: • Osteomyelitis is likely if--- • Bone seen at floor of deep ulcer • Detected on probing the ulcer • Ulcer depth > 3mm • ESR > 40mm/hr • Surgical Debridement • Culture from ulcer bed and bone biopsy • Prolonged course of parenteral antibiotics (10-12 weeks) as per sensitivity reports • Oral antibiotic therapy after discharge
- 95. Management of grade4 and 5 • Urgent hospitalization and Surgical consultation • Amputation is often needed
- 96.
- 97. CONCLUSION • DF –pathological condition of foot in long standing diabetes • Most costly complication of diabetes (WHO) • Multifactorial pathogenesis • Management is case dependent • Close coordination b/w physician, nurse, surgeons, orthopaedic, physiotherapist, psychotherapist and the patient is vital • Most foot problems are preventable • Patient education and awareness is of utmost importance
- 98. References • WHO GUIDELINESON DIABETES • NATIONAL CLINICAL GUIDELINES FOR MANAGEMNET OF DM, MOHFW • MANAGEMENT OF DIABETIC FOOT, Sunil Gupta, MEDICINE UPDATE 2012 • THE DIABETIC FOOT- MEDICAL AND SURGICAL MANAGEMENT • GOOGLE.CO.IN (IMAGES)
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