diabetic foot emedicine

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DIABETIC FOOT emedicine

Introduction

Diabetic foot ulcers (DFUs) precede 85% of nontraumatic lower extremity amputations (LEAs).

Approximately 3-4% of individuals with diabetes currently have foot ulcers ordeep infections.

Semmes-Weinstein 5.07 (10 g) monofilament; the monofilament is applied to the high-risk areason the plantar surface of the foot (ie, toe pulps, metatarsal heads, heel). Patients who

cannot feel pressure from the monofilament have lost protective sensation and are at

risk of developing a diabetic foot ulcer.

Among persons with diabetes, 15% develop foot ulcers during their lifetime. Their risk of LEA

increases by a factor of 8 once an ulcer develops. At 2 years following transtibial amputation,

36% of these patients are known to have died.

Patient education

Patients should be provided the following information regarding daily foot care1

:

Wash feet every day with mild soap and warm water. Test the water temperature with

your hand first. Don't soak your feet. When drying them, pat each foot with a towel and

be careful between your toes.

Use quality lotion to keep the skin of your feet soft and moist, but don't put any lotion

between your toes.

Trim your toenails straight across. Avoid cutting the corners. Use a nail file or emery

board. If you find an ingrown toenail, see your doctor.

Don't use antiseptic solutions, drugstore medications, heating pads, or sharp instruments

on your feet. Don't put your feet on radiators or in front of the fireplace.

Always keep your feet warm. Wear loose socks to bed. Don't get your feet wet in snow or

rain. Wear warm socks and shoes in winter. Don't smoke or sit cross-legged. Both decrease blood supply to your feet.

Never walk barefoot or in sandals or thongs.

Choose and wear your shoes carefully. Buy new shoes late in the day when your feet are

larger. Buy shoes that are comfortable without a "breaking in" period. Check how your

shoe fits in width, length, back, bottom of heel, and sole. Avoid pointed-toe styles and

high heels. Try to get shoes made with leather upper material and deep toe boxes. Wear
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new shoes for only 2 hours or less at a time. Don't wear the same pair every day. Inspect

the inside of each shoe before putting it on. Don't lace your shoes too tightly or loosely.

Choose socks and stockings carefully. Wear clean, dry socks every day. Avoid socks with

holes or wrinkles. Thin cotton socks are more absorbent for summer wear. Square-toe

socks will not squeeze your toes. Avoid stockings with elastic tops.

Frequency

Among persons with diabetes, 15% develop diabetic foot ulcers (DFUs) during their lifetimes.

Currently, 3-4% of individuals with diabeteshave deep infections or DFUs.

Etiology

Peripheral neuropathy

Peripheral neuropathy affects sensory, motor, and autonomic pathways. Sensory neuropathy

deprives the patient of early warning signs of pain or pressure from footwear, from inadequate

soft-tissue padding, or from infection. This neuropathy appears in a stocking-glove distribution,with many patients complaining of burning or searing pain.2

Optimal control of blood glucose levels decreases the incidence of most diabetes-associated

organ system morbidity. The primary risk factor for the development of diabetic foot ulcers

(DFUs) is loss of protective sensation, best measured by insensitivity to the Semmes-Weinstein

5.07 (10 g) monofilament (see Image 1). Abnormal white blood cell (WBC) function and thepresence of peripheral vascular disease allow wounds to become contaminated and infected by

organisms that normally are nonpathogenic. This explains the identification of unusual bacteria

from the wounds of patients with diabetes.

Autonomic neuropathy produces chronic venous swelling. Motor peripheral neuropathy or

Charcot arthropathy can produce bony deformity, which, combined with the loss of protectivesensation, can result in skin ulceration from pressure or from shear forces. Associated factors are

a history of foot infection or ulceration and previous partial or whole-foot amputation.

Motor neuropathy leads to muscle weakness and intrinsic muscle atrophy in the hands and feet.

Patients with motor neuropathy can develop bunion, claw toe, and hammertoe deformities as a

result of muscle imbalance. They lose normal vascular tone and thermal regulation, often

developing severe venous swelling that can be managed only with compression hose. Severe

tissue swelling can lead to ulceration and infection. The patients develop dry, cracked skin as a

result of autonomic dysfunction, with the cracks allowing the entry of bacteria. Nail deformity or

pathologic proliferation may make the areas adjacent to the nails foci for skin breaks or for

infection.

Vascular disease

Ischemicperipheral vascular disease is the second risk factor for developing diabetic foot ulcer

and infection. This disorder used to be considered a small vessel disease, but current research

links the vascular pathology to the basement membrane of the arterial wall. The characteristics of

the disease are similar in persons who are diabetic and those who are not, except that its

distribution is somewhat more scattered and geographic in persons who are not diabetic, as

opposed to being progressive in a distal direction in persons who are diabetic.
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Immune deficiency

The third major risk factor is related to the immune deficiency seen in persons with diabetes.

Glycosylated immune proteins lose efficiency, and granulocytes do not perform adequately,

leaving these patients prone to infection with organisms that would not affect a healthy host.

Each of these potential abnormalities make the diabetic foot susceptible to abnormal mechanical

stresses that can lead to a break in the normal soft-tissue envelope. This can initiate a foot

infection that cannot be resolved easily.

Pathophysiology

Pressure over a bony prominence has often been cited as the cause for skin breakdown in patients

with diabetes. Skin breakdown occurs at far lesser loads when the pressure is applied by shear

forces. The accompanying loss of protective sensation prevents the patient from being warnedthat intolerable loads have been applied. This leads to blister formation and full-thickness skin

loss. The process is heightened in the presence of severe venous swelling, which further lowers

the injury threshold. Shoes become tight due to swelling, thus increasing the direct pressure and

shear forces applied to skin overlying the bony prominence. Thickened, hypertrophic nails

increase pressure on the soft tissues surrounding the nails. The common result is tissue failure and

ulcer formation.

Once the skin barrier is broken, wound healing can be impaired by abnormally functioning

WBCs. Moreover, patients often are malnourished. Many have a marginal vascular supply, withless ability to achieve resolution of infection and wound healing.

Presentation

Classification of diabetic foot ulcers

Most experts use some variant of the classification system developed by Wagner and most

currently modified by Brodsky.3,4

Table 1. Depth-Ischemia Classification of Diabetic Foot Lesions*3

Depth

ClassificationDefinition Treatment

0 At-risk foot, no ulceration Patient education, accommodative footwear,

regular clinical examination

1 Superficial ulceration, not

infected

Offloading with total contact cast (TCC),

walking brace, or special footwear

2 Deep ulceration exposing

tendons or joints

Surgical debridement, wound care, offloading,

culture-specific antibiotics

3 Extensive ulceration or

abscess

Debridement or partial amputation, offloading,

culture-specific antibiotics

Ischemia

Classification

A Not ischemic
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B Ischemia without gangrene Noninvasive vascular testing, vascular

consultation if symptomatic

C Partial (forefoot) gangrene Vascular consultation

D Complete foot gangrene Major extremity amputation, vascular

consultation

*Adapted from Brodsky JW: The diabetic foot. In: Coughlin MJ, Mann RA, eds. Surgery of the

Foot and Ankle. St Louis, Mo: Mosby; 1999: 911.

Indications

From a practical standpoint, vascular surgery consultation is warranted only when the patient is

symptomatic with ischemic pain or a nonhealing ulcer. Ischemic ulcers generally require

angioplasty or vascular bypass surgery to achieve wound healing. Neuropathic ulcers require

debridement of nonviable or infected tissue, combined with local wound care and offloading.

Grade 3 ulcers require debridement of infected or gangrenous tissue. Partial foot amputation,

more complex offloading or non weight bearing, and culture-specific parenteral antibiotictherapy are necessary. Grade 4 ulcers require partial or whole foot amputation.

Contraindications

The 1 or 2 elective issues in this topic are clearly indicated within the text. Most of the substance

of this chapter is nonsurgical. Failure to follow the guidelines discussed here leads to deep

infection and amputation.

Workup

Imaging Studies

Imaging can often be useful in determining the treatment of patients with diabetic foot lesions.

Soft-tissue pathology, such as abscesses and sinus tracts, can be better defined through

ultrasonography, computed tomography (CT) scanning, and magnetic resonance imaging (MRI).

The most common use of imaging is for the detection of bone pathology and the confirmation

of the development ofosteomyelitis. Plain radiographs may at times be useful in confirming bone

infection if it reveals changes beneath an ulcer, but it is most likely to be sufficient for diagnosis

when the infection is already well established and when the bones of the forefoot or hindfoot are

involved. Withosteomyelitis, radiographic changes will accurately reflect the destructive process

but will lag at least 2 weeks behind the progress of the infection.

Radionuclide scans have a limited role in diagnosis because inflammatory conditions may

enhance isotope uptake and diminish the specificity of the test. Leukocyte scans are more reliable

and can help to determine when an area of infection has subsided, but these tests still perform

poorly in the majority of evaluations. MRI has the highest diagnostic accuracy. When used by anexperienced radiologist, MRI can detect bone infection (characterized by an altered bone marrow

signal) with 90-100% sensitivity and specificity. Diagnosis can be complicated because changes

from acute Charcot arthropathy, fractures, and postoperative residues may be mistaken for

infection. Also, MRI findings can overestimate the extent of infection because of inflammatorychanges associated with surgery, fracture, neuroarthropathy, or septic arthritis.5
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Diagnostic Procedures

Qualitative and quantitative measures are used to assess the level of sensation. Qualitative

methods include light touch and pinprick sensation, 2-point discrimination, and proprioception.

These are often lowered in patients with sensory neuropathy, usually in a stocking-type pattern

below the knee. Quantitative methods offer more objective data. Most commonly, nylon

Semmes-Weinstein monofilaments of differing sizes are pressed into the skin perpendicularlyuntil they bend. The threshold of the patients sensation is the smallest filament that he/she can

feel. Protective sensation is assumed to be present if the patient can feel the 5.07 monofilament;

still, approximately 10% of patients with sensation at this level develop neuropathic joints orulcerations.

In addition, although a number of studies have utilized monofilaments for the assessment of

neuropathy, there are no substantive data that support any one standard method of application of

the monofilament.

Generally, testing is recommended at 8 to 10 anatomic sites, although a test of only 4 plantar sites

on the forefoot (the great toe and the base of the first through third metatarsals) can be used to

find 90% of patients with an insensate site.

The biothesiometer, an electrical device that delivers measurable stimulatory vibrations, has not

gained widespread use because of a lack of studies demonstrating its predictability and because

monofilaments are inexpensive and readily available. However, a prospective study of 103

patients suggested that the biothesiometer scored higher in sensitivity tests than did the 10 gmonofilament or its predecessor technology, the tuning fork.

Another case-control study, of 255 diabetic patients, found support for monofilament or

biothesiometer use. Foot ulceration was predicted with a specificity of 77% and a sensitivity of

100% based on either an abnormal Semmes-Weinstein monofilament perception or a vibration-

perception threshold of greater than 25 V.

The vascular examination will have the greatest effect on treatment choices. The qualitative

measurements include palpation of the pulses and determination of skin temperature, capillaryrefill, and hair and nail growth. Evidence of vascular disease is commonly gained through

palpating for the dorsalis pedis and posterior tibial pulses.

Qualitative methods focus on noninvasive measures of pressure, flow, and tissue oxygenation.

Doppler examination will yield pressure measurements at multiple levels of the leg, foot, and

ankle and depends on the compressibility of the vessels under study. The most common

measurement of peripheral vascular disease is the ankle-brachial index (ABI), the ratio of systolic

blood pressure in the ankle to that in the brachial artery. An ABI of 0.90 or less suggests the

presence of peripheral vascular disease. If the ABI is higher than 1.1, it should be considered

whether the measurement derives from a false elevation produced by medial arterial calcinosis.

Transcutaneous oxygen measurement requires expensive equipment, as well as a trained

technician and, thus, is not as widely used as a diagnostic tool. It is the most accurate method for

assessing local skin vascularity and healing potential. A transcutaneous oxygen tension of greater

than 30 mm Hg has been associated with a high likelihood that a wound will heal.

Treatment
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Medical Therapy

Preventive strategies

The major focus of current diabetic foot care is prevention. 12,13 Preventive strategies combine

patient education, prophylactic skin and nail care, and protective footwear. Foot-specific,

individualized patient education is the most important element of a comprehensive diabetic foot

program. Low-risk individuals must wear nonconstrictive shoes. Soft leather or athletic footwear

decreases the risk of tissue breakdown from direct pressure (see Image 2).

Depth-inlay, soft leather, laced shoe with a custom-made accommodative, pressure-

dissipating foot orthosis

Cushioned stockings are helpful, and white socks make identification of skin breakdown easier,

especially in individuals with impaired vision. Nails should be cut transversely to decrease the

risk of an ingrown toenail. Once a problem arises, the patient is instructed to seek medical

attention immediately. Often, the earliest sign of infection is slowly increasing blood sugars and

insulin requirement.

When applied to diabetic populations, the above strategies have been shown to markedly decrease

the rates of diabetic foot ulcer (DFU) and lower extremity amputation(LEA). Patient education

materials are available through the American Orthopaedic Foot and Ankle Society, theAmerican

Diabetes Association, the American Podiatric Medical Association, and the National Institutes of

Health (NIH) web site Feet Can Last a Lifetime.

When individuals progress to a higher degree of risk, they require accommodative footwear and

prophylactic skin and nail care. Depth-inlay, soft leather, Oxford-laced shoes with

accommodative pressure and custom-made shear-dissipating foot orthoses (insoles) have been

shown to appreciably decrease the development of DFUs. The complexity and individualized

nature of the shoes and custom-made foot orthoses vary with the magnitude of deformity and loss

of protective sensation. Calluses should be pared to decrease the incidence of shear-mediated

ulcer formation. Trained professionals should perform skin and nail care in these individuals.

Ulcer treatment

The first step in the treatment of a patient with diabetes who has a foot ulcer is medical

management of the systemic diabetes. Many individuals with diabetes are malnourished due to
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chronic renal disease or chronic infection. Many are also immunocompromised. Once the

systemic condition of the patient is optimized, specific attention can be directed to the foot

ulcer.14,15,16

Ulcers can be neuropathic or ischemic. Neuropathic ulcers are caused by pressure or by shear

forces. Once the ulcer is unroofed and the necrotic tissue is debrided, the soft-tissue base reveals

healthy granulation tissue. If the ulcer is unroofed and the tissue at the base is necrotic, the ulceris likely to be ischemic. A vascular surgeon should evaluate patients with ischemic ulcers to

determine if the limb can be salvaged. A risk-benefit analysis then can then be performed to

determine whether treatment should entail limb salvage, amputation, or a combination of both. Ifthe ulcer is neuropathic, noninvasive vascular testing is in order in the absence of palpable pedal

pulses.

From a practical standpoint, vascular surgery consultation is warranted only when the patient is

symptomatic with ischemic pain or a nonhealing ulcer. Ischemic ulcers generally require

angioplasty or vascular bypass surgery to achieve wound healing. Neuropathic ulcers require

debridement of nonviable or infected tissue, combined with local wound care and offloading.

Wet-to-dry wound care does not promote wound healing because dry wounds desiccate. This

allows potential wound-healing cells to die and opportunistic infection to propagate. Dry wounds

should be kept moist with saline-soaked dressings or hydrocolloid gels. Wounds that produce

massive quantities of exudative material should be treated with absorbent materials (calcium

alginate) and dressings while the wound is kept moist. Growth factor gels have been shown to

promote wound healing in wounds with reasonable wound-healing potential.17,18

Offloading distributes weight-bearing pressure over a larger surface area and provides an

interface to decrease shear forces. Elimination of weight bearing is generally not required. The

optimal offloading device is the total contact cast (TCC). 19,20This device acts to dissipate weight-

bearing and shearing loads by eliminating foot or ankle motion, using an interface material to

distribute pressure and shear forces. Venous swelling is lessened by the compression effect of the

cast. When the ulcer shows appreciable improvement, foot care can be simplified with

prefabricated walking braces that have a plantar weight-bearing surface lined with Plastazote or

other pressure-dissipating materials (see Image 3). When the swelling decreases or when ankleimmobilization is not necessary, healing shoes can be used (see Image 4).

Removable walking boot with a Plastazote-

lined weight-bearing surface

Healing shoe.
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The grade 0 foot has no ulcers but is at risk. Treatment involves foot-specific patient education

and appropriate footwear. Prefabricated, pressure-dissipating insoles are appropriate.

Occasionally, a bony prominence or deformity (eg, bunion, hammertoe) cannot be accommodated

by therapeutic footwear. In this situation, removal of the bony prominence (exostectomy) orcorrection of the deformity is advised to prevent ulceration. As ulcers increase in grade, they

require additional treatment.

o Grade 1 ulcers require debridement of nonviable or infected tissue, local wound care, and

offloading.

o Grade 2 ulcers require debridement, culture-specific antibiotics, local wound care, and

more extensive offloading techniques.

o Grade 3 ulcers require debridement of infected or gangrenous tissue. Partial foot

amputation, more complex offloading or nonweight-bearing strategies, and culture-

specific parenteral antibiotic therapy are necessary.

o Grade 4 ulcers require partial or whole foot amputation.

Following wound healing, patients should use offloading permanently. The plantigrade foot can

be managed with depth-inlay, soft leather, Oxford-laced shoes and custom-made accommodative

foot orthoses. When plantigrade alignment cannot be obtained, an ankle-foot orthosis or surgical

reconstruction or stabilization is required.

Persistent or recurrent ulceration

Ulcers that do not heal or that recur in appropriate footwear require careful evaluation. Heel

impact or increased forefoot loading can be lessened with a cushioned heel and/or rocker solemodification of the shoe. Consider surgery when accommodative methods are unsuccessful.Increased forefoot loading or ankle equinus (static or dynamic) can be treated with percutaneous

Achilles tendon lengthening, followed by immobilization in a below-knee walking cast for 4-6

weeks. Plastic surgery intervention with rotational flaps or free tissue transfer occasionally is

indicated. The key to success in these patients is patient education, accommodative pedorthic

footwear, and careful monitoring.

Prescription footwear

The Medicare Therapeutic Shoe Bill of 1993 provides financial support for 1 pair of appropriate

inlay-depth shoes and 3 pairs of custom-made foot orthoses yearly for individuals with diabetes.

Most insurance carriers have followed their lead with similar guidelines. They have realized thatpreventive strategies are cost-effective compared with amputation. The certified pedorthist is an

essential consultant in providing these devices. The bill requires that both the clinician treating

the diabetes and the orthopedic surgeon or podiatrist treating the foot sign the prescription.

Charcot foot

Charcot foot is a hypertrophic osteoarthropathy currently seen primarily in patients with diabetes

who have peripheral neuropathy. The etiology is neurotraumatic or neurovascular. The traumatic
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etiology implies fracture or stress fracture without protective sensation. The hypertropic response

results from the inherent motion applied to a nonimmobilized fracture. The vascular etiology

implies an abnormal vascular inflow producing bony resorption, bony weakening, and a similar

result. Eichenholtz stage 1 is the proliferative phase of the disease. The foot is very swollen, and

radiographs are negative for fracture or dislocation. Stage 2 is the period of periarticular fractureor dislocation. Stage 3 is the phase of consolidation or healing.

Treatment historically has been anecdotal, with only recent attempts at a scientific approach. 21

The foot with active disease is immobilized in a non-weight-bearing fashion in a total contact cast

(TCC) or other prefabricated device. When the process has consolidated, treatment has beenaccommodative, including with a specialized type of ankle-foot orthosis, the Charcot restraint

orthotic walker (CROW). Surgery is advised for bony infection, nonhealing ulcers, or a deformity

that cannot be accommodated with a custom orthosis. There has been a trend toward attempted

joint fusion in stages 2 and 3 to prevent deformity that would be difficult to accommodate with a

shoe-orthotic construct.

Surgical Therapy

Amputation

Any discussion of the diabetic foot requires introduction of the concept of function-preserving

amputation surgery.22Partial and whole foot amputations frequently are necessary as treatment for

infection or gangrene. The goal of treatment is the preservation of function, not just the

preservation of tissue. Amputation surgery should be the first step in the rehabilitation of the

patient. Because most of these individuals are ambulatory, surgical planning should be directed at

the creation of a load-bearing terminal end organ that can interface most easily with

accommodative footwear, a prosthesis, or a combination of both (ie, prosthosis). The principles

that direct construction of a residual limb for weight bearing with a prosthesis should be

employed when performing debridement or partial foot amputation.

The major value of partial foot amputation is the potential for the retention of plantar load-

bearing tissues, which are uniquely capable of tolerating the forces involved in weight bearing.23

The soft-tissue envelope should be capable of minimizing these forces. Avoid the use of split-

thickness skin grafts in load-bearing areas. Deformity should be avoided as much as possible.

Tendo-Achilles lengthening should be used to avoid equinus deformity and increased loading of

the residual forefoot in partial foot amputations. Retention of a deformed foot with exposed bony

prominence leads only to decreased walking ability and recurrent ulceration.

Complications

Failure to follow the above prevention and treatment guidelines leads to deep infection and

amputation.

Outcome and Prognosis

Individuals who develop foot ulcers have a significant health-related decrease in their quality of

life and consume a large quantity of health care resources. At 2 years following transtibial

amputation, 36% of these patients are known to have died, which means that preventive programsare extremely important. Preventive programs have been shown to markedly decrease the rates of

DFU and LEA in diabetic populations.
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