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A. Contributing Factors and Pathogenesis navigator

  1. Vascular Disease - Ischemia
    1. Arterial Insufficiency: atherosclerosis, vasculitis
    2. Transcutaneous oxygen pressure <30mmHg
    3. Usually associated with diabetes mellitus (DM)
  2. Sensory Neuropathy
    1. Primarily sensory neuropathy occurs in >80% of patients with ulcers
    2. Insensate to Semmes-Weinstein 5.07 monofilament
    3. May leads to reduced sense of pain and frequent trauma
    4. Motor and/or autonomic neuropathies may contribute
  3. Musculoskeletal Abnormalities
    1. Altered biomechanics
    2. Limited joint mobility
    3. Bony deformity (Charcot foot, claw toes, other)
    4. Severe pathologic changes in toenails
  4. DM is probably an independent risk factor (beyond vascular disease) [7]
  5. Previous trauma and/or infection predisposes to foot ulcer formation
  6. Pathogenesis
    1. Earliest changes include loss of sensation
    2. This leads to unnoticed foot trauma with skin breaks, damage
    3. Progression of open lesions to ulceration
    4. With vascular compromise, gangrene often follows
    5. Severe infection, tissue necrosis, poor wound healing often necessitate amputation

B. Foot Care in DM [3,4] navigator

  1. Foot infections are most common soft-tissue infections in diabetics
    1. Develop in ~15% of DM
    2. Leading cause of hospitalization for DM patients
  2. Exacerbating Factors in DM
    1. Peripheral neuropathy and trauma leading to deformity major initiating factors
    2. Impaired wound healing with poor peripheral circulation
    3. Impaired immune responses to infection
    4. Poor foot care
  3. Wagner Ulcer Classification System
    1. Grade 0: no open lesions, may have deformity or cellulitis
    2. Grade 1: superficial diabetic ulcer (partial or full thickness)
    3. Grade 2: ulcer extension to ligament, tendon, joint capsule, or deep facia
    4. Grade 3: deep ulcer with abscess, osteomyelitis, or joint sepsis
    5. Grade 4: gangrene localized to portion of forefoot or heel
    6. Grade 5: extensive gangrenous involvement of entire foot
    7. University of Texas system, more complex, has also been developed
    8. Grade and stage associated with prognosis
  4. Properly fitting shoes are absolutely crucial
  5. Patients with plantar foot ulcers should not walk on that foot
  6. Total-contact casts may be used also
  7. Consider referral to Podiatrist
  8. Note preventative measure below

C. Physical Findingsnavigator

  1. Callus or Blisters
  2. Bony prominences
  3. Erythema
  4. Pain is less common in DM due to peripheral neuropathy
  5. Suggestive of Infection
    1. Cellulitis: heat, cerpitation
    2. Sinus tract
    3. If bone can be seen or easily reached with probe, then osteomyelitis ~90% likely

D. Diagnosis navigator

  1. Distinguishing between ulcer colonization and true infection (cellulitis) is difficult [3]
    1. All skin wounds harbor microorganisms
    2. Swab cultures are not useful
    3. Deep tissue specimen for gram stain and culture should be obtained where possible
    4. Systemic signs of infection (fever, leukocytosis) may be present
    5. Local signs or symptoms of redness, warmth, induration, pain suggest infection
    6. Polymicrobial infections are common in DM and other immunosuppressed patients
  2. Osteomyelitis is a very frequent complication of DM foot ulcers (cellulitis)
    1. Therefore, ruling out osteomyelitis is essential in all evaluations
    2. White blood cell or gallium scan be helpful for distinguishing colonization and invasion
    3. Three-part bone scan can help in distinguishing cellulitis from osteomyelitis
  3. MRI Testing for Osteomyelitis
    1. Test of choice for diagnosis of osteomyelitis
    2. Probing bone in an infected ulcer makes osteomyelitis ~90% likely
    3. If bone is found, then treatment for osteomyelitis may be given without additional tests
  4. Limb Ischemia
    1. Often clinically silent
    2. Should be assessed by vascular surgeon
    3. Angioplasty, stenting or femorodistal bypass may be indicated
  5. Risk Factors for Non-Healing [8]
    1. Wound >2 months old
    2. Area larger than 2 square centimeters
    3. Grade 3 or higher (on Wagner scale, see above)

E. Infected Foot Ulcers [1,3,4,9] navigator

  1. High suspicion for highly virulent organisms
  2. Evaluation of all DM foot ulcers should include rule out osteomyelitis
  3. Treatment Overview
    1. Good debridement is critical for ulcers ± osteomyelitis (wound cultures should be done)
    2. Sharp surgical debridement, removal of callus, has been best studied and most reliable
    3. Antibiotics must cover mixed infections (Gram positive, negative and anaerobes)
    4. Assess for fungal colonization; consider treatment with topical antifungal agents
    5. In some (diabetic) patients, fungi may be primarily responsible for slowing healing
    6. Alleviation of mechanical load ("off-loading") is paramount to allow infection cure
  4. Antibiotic Coverage
    1. Suggest ticarcillin-clavulanate (Timentin®) or piperacillin-sulbactam (Zosyn®)
    2. Carbapenams (imipenem-cilistatin, meropenam, ertapenem) very effective
    3. Piperacillin/tazobactam (Zosyn®) and ertapenem (Invanz®) have similar efficacy in diabetic foot infections [10]
    4. Avoid long-term aminoglycosides
    5. Antibiotics are to cure infection, and not necessarily heal the wound
  5. Growth Factors
    1. Platelet derived growth factor (PGDF) 0.01% gel (becaplermin, Regranex®) accelerates healing of diabetic foot ulcers [5]
    2. G-CSF (filgrastim, Neupogen®) improves healing and reduces hospitalization duration [6]
  6. Skin Grafts [3]
    1. Skin graft, such as Dermagraft cultured skin, may permit closure of deep ulcers
    2. A variety of other skin graft materials (Apligraf®, others) are now available
    3. Mainly used for resistant wounds which do not heal
    4. Improved efficacy over standard care for osteomyelitis
  7. Surgery
    1. May be required, especially if osteomyelitis is present
    2. Excellent debridement is absolutely required to permit healing
    3. Diabetes is most common cause of above and below knee amputations
    4. Surgery may include tenotomy, tendon lengthening, removal of bony prominences
  8. Recurrences are common and patient education critical to reduce these
  9. Long term prevention of pressure ulcers, particularly in DM, is critical to reduce morbidity

G. Principles of Foot Ulcer Prevention [1,7,9]navigator

  1. Patient Education
    1. Careful attention to foot care
    2. Self-assessment of peripheral sensation
    3. Frequent examination of lower extremities for problems
  2. Podiatric Care [7]
    1. Regular visits, examinations, and foot care
    2. Risk assessment
    3. Early detection and aggressive treatment of new lesions
    4. Semmes-Weinstein monofilament (SWM) test for protective sensation
    5. SWM 5.07 consists of plastic handle supporting nylon filament
    6. Filament is placed perpendicular to skin and pressure applied until filament buckles
    7. Hold filament in place for ~1 second, then release
    8. Inability to perceive this ~1gm force indicates clinically significant large fiber neuropathy
    9. Testing 10 sites with SWM on the foot may improve sensitivity and specificity
  3. Distal Pulse Examination
    1. Evaluation for claudication and pain at rest
    2. Asessment of foot pulses by exam
    3. Non-invasive ultrasound vascular testing when indicated
  4. Protective Shoes
    1. Well cushioned, room to protect feet from injury
    2. Walking sneakers, custom molded shoes
    3. Special modifications as necessary
  5. Pressure Reduction
    1. Pressure measurements
    2. Cushioned insoles, custom orthoses, padded hosiery
  6. Prophylactic Surgery
    1. Correction of structural deformities: hammer toes, bunions, Charcot's Foot
    2. Prevention of recurrent ulcers over deformities
    3. Intervention early in course
  7. Prevention Education
    1. Patient education: daily inspection and early intervention
    2. Physician: close physical exam, above concepts of foot management
  8. American Diabetes Association Link: www.diabetes.org

References navigator

  1. Jeffcoate WJ and Harding KG. 2003. Lancet. 361(9368):1545 abstract
  2. Sumpio BE. 2000. NEJM. 343(11):787 abstract
  3. Boulton AJM, Kirsner RS, Vileikyte L. 2004. NEJM. 351(1):48 abstract
  4. Frykberg RG. 2002. Am Fam Phys. 66(9):1655 abstract
  5. Becaplermin (PGDF). 1998. Med Let. 40(1031):73 abstract
  6. Gough A, Clapperton M, Rolando N, et al. 1997. Lancet. 350(9081):855 abstract
  7. Singh N, Armstrong DG, Lipsky BA. 2005. JAMA. 293(2):217 abstract
  8. Margolis DJ, Allen-Taylor L, Hoffstad O, Berlin JA. 2003. Am J Med. 115(8):627 abstract
  9. Cavanagh PR, Lipsky BA, Bradbury AW, Botek G. 2005. Lancet. 366(9498):1725 abstract
  10. Lipsky BA, Armstrong DG, Citron DM, et al. 2005. Lancet. 366(9498):1695 abstract