management of diabetic foot ulcer

1. DIABETIC FOOT
BY:
DR. MOHAMMAD MASOOM PARWEZ
ACADEMIC RESIDENT,GENERAL SURGERY
AIIMS BHOPAL

3. OUTLINE
• INTRODUCTION
• DEFINITION
• CLASSIFICATION & STAGING
• PATHOGENESIS
• CLINICAL FEATURES
• DIAGNOSISAND EVALUATION
• MANAGEMENT
• PREVENTIONGUIDELINES
• SUMMARY
• CONCLUSION
• REFERENCES

5. INTRODUCTION

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

7. DEFINITION

8. 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)

10. CLASSIFICATION

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 basis of etiology
• NEUROPATHIC FOOT
• ISCHEMIC FOOT
• NEURO-ISCHEMIC FOOT

13. 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)

15. 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

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 wound classification
system

21. Stages of Ulcer development

22. PATHOGENESIS

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

24. 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

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 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

34. 1 (c). Autonomic neuropathy
Decreased sweat secretion
Dry and brittle skin
Easy cracks and fissures
Infection
Ulceration

36. Effect of diabetic peripheral neuropathy

37. 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

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

44. CLINICAL FEATURES

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 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

50. APPROACH

63. Nylon monofilament test

64. MANAGEMENT

65. 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

66. 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

67. 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

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
• 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%)

70. 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

71. Off loading

72. 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

73. 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

74. 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

75. 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

77. Rest pain in neuro-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
• Bed rest
• Intravenous antibiotics
• Broad spectrum cover preferred
• Quadruple therapy comprising of:
• Amoxycillin
• Flucoxacillin
• Metronidazole
• Ceftazidime/Gentamicin

80. 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

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)
Radiographic hallmarks:
• Bony destruction,
fragmentation
• Bony remodelling
• Joint destruction,
subluxation and dislocation

85. 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

86. 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

87. PREVENTION
GUIDELINES

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 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

91. 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

92. SUMMARY

93. 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 300mgTDS X 2 weeks (75%
ulcers heals in 2 weeks time)

94. 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

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

96. CONCLUSION

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 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)

99. THANK YOU