By: 1 July 2008

The neuropathic foot is frequently associated with chronic medical conditions and it is not infrequent for individuals to be slaves to long-standing foot and ankle problems. Apart from ulcerations and deformities, loss of lifestyle and independence is profound. These problems cause immense emotional and financial losses and cause restriction of activity with loss of productivity.

Among individuals who are diagnosed with diabetes mellitus, the prevalence of foot ulcers is 4% to 10%, while the annual population-based incidence is 1.0% to 4.1%, and the lifetime incidence may be as high as 25%. Nonhealing ulcers lead to amputation 85% of the time. The key risk factors of diabetic foot ulceration and indeed for any non-healing ulcer includes a combination of neuropathy, deformity, and repetitive stress (trauma).

Causative Factors

A) Peripheral neuropathy
This is present to some degree in more than 50% of diabetic persons above the age of 60 years. Peripheral neuropathy must usually be profound before leading to loss of protective sensation. The consequent vulnerability to physical and thermal trauma increases the risk of foot ulceration by 7-fold. Diabetes is the commonest medical disorder causing peripheral neuropathy.

B) Excessive plantar pressure
This is related to both limited joint mobility (at the ankle, subtalar and first metatarsophalangeal joints) and to foot deformities. In one study of patients with peripheral neuropathy, 28% with high plantar pressure developed a foot ulcer during a 2.5-year follow-up as compared to none with normal pressure.

C) Repetitive physical unrecognised trauma such as extremes of temperature while bathing, injuring while paring of nails and ill-fitting and traumatic innerwear and footwear.

Contributory Factors

A) Atherosclerotic peripheral vascular disease is twice as common in persons with diabetes when compared to persons without diabetes and particularly affects the femoropopliteal and smaller vessels below the knee, while frequently sparing the pedal vessels.

B) Intrinsic wound-healing disturbances,
Immunohistological changes include impaired collagen cross-linking and matrix metalloproteinase function and poor polymorphonuclear leukocyte function

C) Higher rate of onychomycosis and toe-web fulminant and recurrent fungal infections that lead to skin disruption

Classification of the Diabetic Foot

A) International Working Group on the Diabetic Foot (IWGDF)

This group classifies patients based on presence of risk factors concurrent with neuropathic or vascular disease and eventual outcomes.

  • Group 0: patients without risk factors
  • Group 1: patients with neuropathy
  • Group 2: patients with neuropathy and a deformity of vascular disease
  • Group 3: patients with a history of ulcer or amputation

B) Texas Foot Risk Classification

  • Group 0 (no Peripheral Neuropathy, no Peripheral Arteriolar Occlusive Disease)
  • Group 1 (with Peripheral Neuropathy)
  • Group 2 (with Peripheral Arteriolar Occlusive Disease)
  • Group 3 (with current or past ulceration)
  • Group 4 (patient with an existing amputation)

Preventive Measures To Avoid Foot Ulcerations

I) General Preventive advice includes:

  • Regular foot examinations for redness, corns, callosity formations, fungal infections and developing deformities
  • Patients are advised to keep the feet clean and dry. The feet should be washed daily with lukewarm water. The water should be checked against extremes of temperatures. The dry foot should be liberally dusted with an antifungal powder.
  • Don't expose feet to extreme heat or cold. Always use closed footwear.
  • Never walk barefoot even at home.
  • Wear comfortable shoes. Shoes should be washed regularly with an antiseptic solution and should be completely dry before usage. Deformed feet may need customised or plastazote footwear.
  • Socks should fit properly. These should be ideally seamless and with out rough sewn or lumpy edges. A common recommendation is to wear the socks inside out to encourage the rough areas to face away from insensate skin.
  • Corn and callus should only be treated by a doctor or a qualified podi atrist. It is not advisable to pare the nails too close to the skin. This may give rise to ingrown toenails and predispose to chronic fungal infections and nail fold abscesses. Ingrown toenails should be trimmed straight across

II) Identification of at-risk populations.

Preventing foot complications also begins with identifying those at risk. These include:

  • Previous foot ulceration
  • Prior lower extremity amputation
  • Diabetes of more than 10 years duration
  • Poor glycemic control (glycosylated haemoglobin 9%)
  • Impaired vision (acuity20/40)
  • Examination of the feet for structural abnormalities (e.g. calluses, hammer or claw toes, flat feet, bunions), reduced joint mobility, dry or fissured skin, tinea, or onychomycosis, and also inspect footwear to ensure proper fit and comfort.

III) Screening for Loss of Protective Sensation

A) Monofilament Testing

The most frequently used instrument for detecting neuropathy is the nylon Semmes-Weinstein monofilament.

Testing for Large-fibre neuropathy.
Inability to perceive the 10 g of force from a 5.07 monofilament applied, is associated with clinically significant large-fibre neuropathy. In 3 prospective studies, the Semmes-Weinstein monofilament identified persons at increased risk of foot ulceration with a sensitivity of 66% to 91%, a specificity of 34% to 86%, a positive predictive value of 18% to 39%, and a negative predictive value of 94% to 95%. While authorities recommend testing 8 to 10 anatomic sites, testing just 4 plantar sites on the forefoot (great toe and bases of first, third and fifth metatarsals) identifies 90% of patients with an insensate site.

Monofilament Test for Light Touch Sensation
The 5.07 Semmes-Weinstein monofilament consists of a plastic handle supporting a nylon filament. The filament is placed perpendicular to the skin, and pressure is applied until the filament buckles. The filament is held in place for approximately 1 second, and then released. Testing 10 sites (as shown) evaluates all dermatomes of the foot and may improve the sensitivity and specificity compared with testing a single site.

B) Biothesiometer
A biothesiometer is a handheld device that assesses vibration perception threshold. A case-control study with 255 diabetic persons found that having either abnormal Semmes- Weinstein monofilament perception or a vibration-perception threshold of more than 25 V predicted foot ulceration with a sensitivity of 100% and a specificity of 77 %2

C) Tuning Fork
A tuning fork provides an easy and inexpensive test of vibratory sensation. With a conventional fork, an abnormal response occurs when the patient loses vibratory sensation while the examiner still perceives it.

D) Nerve conduction studies
These are considered the criterion standard for diagnosing peripheral neuropathy

IV) Screening for Patients With Elevated Plantar Pressure

Devices identifying high plantar pressure include

  • Mats to measure barefoot plantar load distribution
  • Transducers distributed in a removable shoe insole to measure pressure inside footwear

In case-control studies using the EMED pressure platform system (Novell, Minneapolis, Minn), a peak barefoot dynamic pressure of 70 Newton per Centimetre Square had a sensitivity of 70.0% and a specificity of 65.1%

V) Screening for Peripheral Vascular Disease

Peripheral vascular disease is most easily detected by the:

A) Ankle Brachial Pressure Index (ABPI)
It is the ratio of systolic blood pressure in the ankle to that of the brachial artery. An ABI of 0.90 or less suggests peripheral vascular disease, while higher than 1.1 may represent a falsely elevated pressure caused by medial arterial calcinosis. This test is easily performed, objective and reproducible

One large study found that the ABI was strongly related to the risk of foot ulceration (0.3 higher ABI is associated with an RR of 0.83)

B) Transcutaneous oximetry
Arterial oxygen supply can also be measured by transcutaneous oximetry. A transcutaneous oxygen tension higher than 30mmHg correlates with a high likelihood of wound healing. Transcutaneous oxygen tension is also inversely associated with the risk of foot ulceration (15mmHg higher dorsal foot transcutaneous oxygen tension is associated with an RR of 0.80).

Interventions to Prevent Foot Ulceration

A) Clinical Interventions to Prevent Foot Ulceration

  • Optimizing Glycemic Control
  • Smoking Cessation
  • Foot Examination by a Clinician
  • Custom Footwear and Orthotics Prescription shoes for high-risk patients should reduce areas of high plantar pressure and friction and accommodate foot deformities (e.g. with a deep, wide toe box and ample padding). Shoe inserts should cushion the plantar surface and redistribute pressure over a greater sur face area.
  • Debridement of Calluses Calluses (hyperkeratotic lesions) further increase pressure, which is a component cause of ulceration. Debriding hyperkeratoses can reduce peak plantar pressure by 26%
  • Foot Specialist and Multidisciplinary Team Care These include podiatrists, surgeons, district and community nurses, dieticians and social workers.
  • Prophylactic Foot Surgeries Clinical Interventions can also be staged or planned according to staging as follows:

B) Inflammatory stage
Localised warmth and swelling out of proportion to the injury. Radiographic findings may be normal in appearance have evidence of fracture, osteolysis and fragmentation of the bone. This will be followed by new bone formation then by subluxation and finally disorganisation of the joint. Bone scan is positive early before radiograph changes. Nerve conduction study shows prolonged sensory latency. Electromyogram shows fibrillation in muscle and reduction in motor unit action potential.

In the inflammatory stage the foot is immobilised in a nonweight bearing cast until all signs have settled.

C) Collapse deformity stage
Meta tarsophalangeal joints and tarsometatarsal joints are commonly involved and may cause Forefoot subluxation, Hind foot valgus, Plantar flexion of hind foot and talus or a contracted gastrosoleus.

In this stage the treatment options include:

  • Well padded non-weight bearing cast
  • Removal of prominent bony masses
  • Limited arthrodesis with autogenous bone grafting, rigid fixation and cast immobilisation
  • Amputations for advanced devascularisation.
  • Chopart amputation
    Tarsometatarsal amputation.

  • Tibiocalcaneal arthrodesis

Diabetic Ulcers
Multiple classifications are in vogue for classification of diabetic ulcers. The Wagner classification system is commonly used characterised by its simplicity and reproducibility. This is based on ulcer depth and the presence of osteomyelitis or gangrene.

A) Wagner Grading

  • Grade 0 (pre-or post-ulcerative lesion)
  • Grade 1 (partial/full thickness ulcer)
  • Grade 2 (probing to tendon or capsule)
  • Grade 3 (deep with osteitis)
  • Grade 4 (partial foot gangrene)
  • Grade 5 (whole foot gangrene)

B) University of Texas System

This system assesses ulcer depth, the presence of wound infection, and the presence of clinical signs of lower-extremity ischemia.

  • Grade 0 (pre-or post-ulcerative site that has healed)
  • Grade 1 (superficial wound not involving tendon, capsule, or bone)
  • Grade 2 (wound penetrating to tendon or capsule)
  • Grade 3 (wound penetrating bone or joint)

Within each wound grade there are four stages:

  • Stage A: Clean wounds
  • Stage B: Non-ischemic infected wounds
  • Stage C: Ischemic non-infected wounds
  • Stage D: Ischemic infected wounds

Successful treatment in diabetic foot ulcers requires the following basic issues

Ulcer Evaluation

  • Documentation of wound's location, size, shape, depth, base and border
  • Probe for sinus tract, and check if wound probes to tendon, joint, or bone
  • Signs and types of infection to be documented
  • Obtain culture reports
  • Establish a differential diagnosis from the physical findings Debridement
  • Complete removal of necrotic tissue, callous formation and foreign bodies.
  • Copius saline irrigation.
  • Various dressing materials used.


  • Use of a wheelchair or crutches to stop weight bearing on the affected foot
  • Total contact plaster (TCP) casts reduce pressure on wounds and helps in the healing process
  • Removable cast walkers are preferred since they allow for wound inspection, dressing changes and early detection of infection

Infection Control

  • Mild to moderate infections are controlled by oral broad-spectrum antibiotics after initial culture
  • Limb-threatening infection patients should be hospitalised
  • Intravenous antibiotics which cover both gram positive and gram negative organisms should be administered

Appropriate foot wear
Specific measures to be followed once the ulcers are healed are listed below

  • Moulded insoles
  • Extra deep shoes
  • Rocker-bottom soles
  • Polymer insole material shoe
  • Custom made foot wear
  • Ankle foot orthosis or double upright brace with limited ankle joint motion

Treatment of fixed deformities
These surgical procedures used include:

  • Correction of claw toes
  • Arthrodesis of IP joint of the hallux
  • Resection of head of metatarsals
  • Lengthening of tendocalcaneus
  • Treatments for Ulcer Healing

Wound Dressings

  • Initially Betadine or Dakin's solution is applied to the woundWhen the wounds are clean and granulating the following dressing are advised which increases epithelisation:
  • Normal Saline
  • Petrolatum gauze-impregnated dressing
  • Hydrophilic dressing for desiccated wounds
  • Calcium alginate dressings for moist wounds
  • Large wounds can be covered with the help of Xeroform gauze, artificial skin substitutes or homograft
  • Silvadene is considered to be an effective adjunct to most wounds in the healing process
  • There are different types of dressings available such as hydro gels, foams, calcium alginates, absorbent polymers, growth factors, and skin replacements
  • Ulcers, which do not heal with standard dressings, should be treated with Becaplermin. Becaplermin contains the beta chain platelet derived growth factors.

Wound closure
In a recent study, comparison of negative pressure wound therapy using vacuum-assisted closure versus advanced moist wound therapy in the treatment of diabetic foot ulcers was performed. The study was a multicenter randomised controlled trial that enrolled 342 patients with a mean age of 58 years; 79% were male patients. Patients were randomly assigned to either NPWT (vacuum-assisted closure) or AMWT (predominately hydrogels and alginates) and received standard off-loading therapy as needed. A greater proportion of foot ulcers achieved complete ulcer closure with NPWT (73 of 169, 43.2%) than with AMWT (48 of 166, 28.9%) within the 112-day active treatment phase (P = 0.007). The authors have concluded that NPWT appears to be as safe as and more efficacious than AMWT for the treatment of diabetic foot ulcers

Management of foot problems in the neuropathic foot requires treatment of not only the affected extremity but also a consolidated plan for systemic management and damage control. This needs a thorough understanding of the pathophysiology of the underlying disease. Treatment of neuropathy is directed at pressure relief and prevention of deformity. Infection is addressed with antibiotics, debridement, and improvement of the vascularity and oxygenation of the tissues. Amputation should be viewed, not as evidence of treatment failure, but as a reconstructive procedure, the goal of which is to regain energy-efficient ambulation. The orthopaedic surgeon can play a critical role in the team approach to the care of the diabetic patient with foot problems only with team effort and multidisciplinary management.

Recommended Reading

  1. Lavery LA, Armstrong DG, Wunderlich Tredwell JL, Boulton AJM. Predictive value of foot pressure assessment as part of a population-based diabetes disease management program. Diabetes Care. 2003; 26:1069-1073.
  2. Ince P, Abbas Z G, Lutale J K Use of the SINBAD Classification System and Score in Comparing Outcome of Foot Ulcer Management on Three Continents. Diabetes Care 31: 964-967; published online before print as 10.2337/dc07-2367
  3. Ghanassia E, Villon L, Dieudonn