Diabetic foot.pptx

management of diabetic foot ulcer

1. Diabetic foot BY: DR. MOHAMMAD MASOOM PARWEZ ACADEMIC RESIDENT, GENERAL SURGERY AIIMS BHOPAL

2. OUTLINE INTRODUCTION DEFINITION CLASSIFICATION & STAGING PATHOGENESIS CLINICAL FEATURES DIAGNOSIS AND EVALUATION MANAGEMENT PREVENTION GUIDELINES SUMMARY CONCLUSION REFERENCES

3. introduction

4. 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

5. definition

6. Definition Diabetic foot is 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)

7. classification

8. Classification and staging A standard classification is useful for: Assessing the etiology Designing appropriate Rx Predicting prognosis Monitoring course of disease process

9. Classification on basis of etiology NEUROPATHIC FOOT ISCHEMIC FOOT NEURO - ISCHEMIC FOOT

10. Classification on basis of 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)

11. Staging according to clinical 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

12. WAGNER’S classification (2001) Most widely used Grades diabetic foot on severity of ulcer penetration

13. Traditional MEGGITT - WAGNER’S classification (2001) Grade Physical Findings Description 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

14. Texas University wound classification system

15. Stages of Ulcer development

16. pathogenesis

17. Pathogenesis Development of diabetic foot is multi-factorial and complex First, it involves longstanding HYPERglycemia , contributing to: Neuropathy Angiopathy Immune dysfunction

18. 1(a). Neuropathy (Somatic Sensory ) 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

19. 1 (b). Neuropathy (Somatic Motor ) Weakness and decreased contraction of smooth muscles Muscle wasting/atrophy Foot Deformity Abnormal Gait Uneven pressure distribution Ulceration

20. Foot deformities predisposing to 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

21. 1 (c). Autonomic neuropathy Decreased sweat secretion Dry and brittle skin Easy cracks and fissures Infection Ulceration

22. Effect of diabetic peripheral neuropathy

23. Factors contributing to foot 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

24. 2. Angiopathy MACRO angiopathy Atherosclerosis of large arteries Increased peripheral resistance MICRO angiopathy Thickening of capillary basement membrane Decreased capillary permeability Decreased perfusion of foot structures Decreased immune cells infiltration and antibiotic effect Poor wound healing GANGRENE

25. 3. Immune dysfunction Impaired defenses against infections: Decreased Leucocyte migration Decreased Phagocytosis Decreased Intracellular killing Decreased Chemotaxis

26. Clinical features

27. The neuropathic foot Diminished sensation Invariably warm skin with intact, bounding pulses Ulcers Pressure points on plantar aspect Stress areas on dorsal aspect

28. 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

29. 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

30. The ischemic foot Gangrene may be present Critical ischemia – identification Characteristic pink Painful Pulseless Cold foot

31. Differentiating features Characteristics Neuropathic Ischemic 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

32. APPROACH

33. Nylon monofilament test

34. Management

35. Management includes 5 aspects: Metabolic control Effective blood sugar control, neuropathy Rx Mechanical control Reduce risk of trauma, treat deformities Vascular management Infection prophylaxis and treatment Patient education

36. Neuropathic foot Management of ulcer falls into 3 parts: Removal of callus Eradication of infection Reduction of weight bearing forces , often requiring bed rest with foot elevated

37. Neuropathic foot Excess keratin should be pared away with a scalpel blade to expose the floor of the ulcer and allow efficient drainage of the lesion

38. Neuropathic foot Radiograph – to assess the possibility of osteomyelitis A deep penetrating ulcer is present When lesions fail to heal Lesions continue to recur

39. Neuropathic foot A bacterial 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%)

40. Neuropathic foot Treatment should 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

41. Off loading

42. Neuropathic foot Cast should 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

43. Ischemic foot Ishemic foot 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

44. Ischemic foot Arterial imaging techniques include: Duplex scanning MRA Conventional arteriography Infrapopliteal angioplasty or distal bypass to tibial or peroneal vessels are important for limb salvage

45. Ischemic foot Amputation of 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

46. Rest pain in neuro-ischemic foot It can get relieved on successful revascularisation Paravertebral lumbar block Parenteral narcotics Last resort– below knee amputation

47. Urgent treatment Red flag/ Danger Signs : Redness/ swelling of foot Cellulitis/ discoloration and crepitus Pink, painful, pulseless foot even without gangrene– critical ischemic limb

48. Urgent treatment Bed rest Intravenous antibiotics Broad spectrum cover preferred Quadruple therapy comprising of: Amoxycillin Flucoxacillin Metronidazole Ceftazidime/Gentamicin

49. Urgent treatment Surgical debridement 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

50. 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

51. 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)

52. Neuropathic joint (Charcot) Radiographic hallmarks: Bony destruction, fragmentation Bony remodelling Joint destruction, subluxation and dislocation

53. Management Initial: Bed rest or 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

54. Long term care of 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

55. Prevention guidelines

56. 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

57. 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

58. Prevention guidelines Low risk foot : (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

59. Prevention guidelines High risk foot : (with ischemia, deformity, skin changes or previous ulcer) Three month follow up Intensified foot care education Rehabilitation for deformities/disability

60. summary

61. Management of Grade 1 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 300mg TDS X 2 weeks (75% ulcers heals in 2 weeks time)

62. Management of Grade 3 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

63. Management of grade 4 and 5 Urgent hospitalization and Surgical consultation Amputation is often needed

64. conclusion

65. CONCLUSION DF – pathological condition of foot in long standing diabetes Most costly complication of diabetes (WHO) Multi factorial 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

66. References WHO GUIDELINES ON 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)

67. THANK YOU