Approximately 15% of persons with diabetes will have an ulcer in their lifetime,[15,16] and 0.5% to 29.0% will have neuropathic joint changes.[17,18] Diabetes is the leading cause of nontraumatic amputations, amounting to 57,000 per year or 150 per day. One half to 80% of all amputations are diabetes-related.[16,19-21] It is postulated that 50% of these can be prevented through a comprehensive lower extremity amputation (LEA) prevention program,[22] which is part of the goals for Healthy People 2010 (Table 2).[23]

The cost of foot disease is astounding. Medicare records show that $1.5 billion was spent directly on diabetic foot ulcers from 1995 to 1996.[24] Almost three fourths of this was spent during inpatient treatment alone. Today, the annual cost of diabetic foot ulcer care is $5 billion in direct cost and $400 million in indirect cost.[25] Unfortunately, 70% of people with ulcers have little or no regular follow-up care, which is necessary to prevent progression.[25] In a study of inpatient ulcer care, only 1.6% had prescriptions for off-loading materials at discharge, and only 11.0% had arrangements for home health wound care.[26]
The sequelae of ulceration, including amputation, cost of prosthesis, and rehabilitation after amputation is enormous. The direct cost of LEA ranges from $20,000 to $60,000 per patient.[22,27-31] In 1992, the cost of rehabilitation was $14,500 to $21,500 per patient.[32] This does not include the cost of prosthesis.

Morbidity and Mortality

Among the patients having an estimated 57,000 to 125,000 LEAs per year,[33-35] 5% to 17% will die during the operation and 2% to 23% will die within 30 days of surgery.[36,37] Ipsilateral reamputation will be required in 8% to 22% of the survivors, and 26% to 44% will require a contralateral amputation within 4 years. Five-year survival is 40% overall, but only 25% in the very elderly (>80 years).[38] Despite surgical advances, these rates remain staggering.

In addition to the mortality of LEA, the morbidity is also considerable. After below-knee amputation, the work of walking increases, and amputees decrease their walking speed to maintain their rate of oxygen uptake (measured in milliliters per kilogram per minute). Above-knee amputees will have both decreased walking speed and increased rate of oxygen uptake.[39,40] A year-long study of amputees in a Texas hospital found that of the 97.3% admitted for amputation from home, 18.5% were discharged to a nursing home and 7.0% to a rehabilitation facility.[41] Not a single patient improved from their baseline functional activity. The extra weight-bearing load placed on the remaining extremity increases the contralateral risk for ulceration. This may explain why compliance with prosthesis declines over time and as few as 5% of amputees can walk safely outside of their home on uneven surfaces.[42,43]

Pathogenesis

Distal symmetric peripheral neuropathy affects up to 50% of diabetics within 15 years after diagnosis.[16] The etiology of this nerve damage is not well understood. The polylol theory postulates that biomechanical reactions related to hyperglycemia reduce blood glucose to sorbitol, which is thought to be toxic to tissues.[44,45] Another theory proposes that hyperglycemia damages the blood vessels supplying nerves and impairs neurotransmission.[15] Sensory neuropathy can be defined as loss of sensation as measured by the Semmes Weinstein 10 g monofilament, 4-question verbal neuropathy score, or vibration perception threshhold test[46] and is a major risk factor for ulceration. The ADA recommends the use of a 10 gram nylon Semmes Weinstein monofilament as an accurate and inexpensive way to evaluate sensory loss.[10,12,25,32,41,46,47] Disposable filaments and methods to screen and manage diabetic foot neuropathy can be obtained from the Lower Extremity Amputation Prevention (LEAP) Program of the Bureau of Primary Health Care (BPHC).*

Distal muscle atrophy is also common. Loss of motor nerve function causes weakening of the intrinsic foot muscles. This imbalance produces changes in foot structure and gait. The resulting deformity and limited range of motion contribute to increased mechanical stress on corresponding areas of the foot. Toe deformities can be easily recognized by the medical professional. Extension contracture at the metatarsophalangeal (MTP) joint with flexion contracture at the proximal interphalangeal (PIP) joint is commonly referred to as a hammer toe while hyperextension of the MTP and flexion of the PIP and distal interphalangeal (DIP) joint is termed a claw toe. Claw and hammer toes are a sign of distal muscle atrophy and neuropathy.[48] Claw toes increase pressure on the metatarsal heads and dorsal interphalangeal joints. Hammer toes can result in pressure at the distal ends of the toes. Pressure may lead to callus formation and ulceration.[49] Hallux rigidus, or limitation of dorsiflexion of the great toe, also predisposes to ulceration,[50] since the toe-off phase of gait requires 45° of metatarsophalangeal joint extension.[51]
* Bureau of Primary Health Care, Division of Programs for Special Populations, 4350 East West Highway, 9th Floor, Bethesda, MD 20814. Telephone: 1-888-275-4772.

Prevention

The best and most cost-effective way of preventing diabetic foot disease and amputation is to interrupt the pathway to amputation by preventing ulcer formation.[52]

Foot Screening

An annual foot screen by a health care provider is recommended for all diabetic patients. The foot screen presented in this paper was developed in the Carville and LSU Diabetic Foot Clinics (Figure). Health care professionals can easily learn how to identify a "high-risk" foot quickly and cost effectively.

Recurrence rate of an ulcer is 70%.[53] During the final stage of wound healing, scar tissue forms and there is a progressive increase in tissue strength due to cross-linking of collagen fibers along tension lines. A healed wound will gain 20% of its strength within 1 week and 60% in 4 to 6 weeks and will plateau somewhere between 70% and 90% over a period of 2 years.[54] The area of ulceration therefore will never be "normal" again and will be more vulnerable to injury and reulceration. The patient will automatically be placed into the highest risk category and should be referred to the appropriate wound and/or foot specialty clinic or supplier for protective footwear (Table 3).[55-57] The Medicare Therapeutic Shoe Bill pays for a portion of these services.

Toenails

Long, thick, or ingrown toenails can produce ulceration or infection. Regular and proper nail care is an important preventive measure in managing a patient with lower extremity neuropathy. Patient education regarding safe and effective nail care methods is critical. They should trim their nails parallel with the distal surface of the toe, and seek assistance from a professional if the nails are too thick to safely trim themselves.

Calluses

Localized callus formation on the plantar surface of the foot indicates an area of high mechanical stress and is a risk factor for ulceration.[58] Formation of an ulcer beneath a callus has been well documented. Discoloration beneath a callus or hemmorhage on the lateral border of a callus requires immediate debridement to prevent further complications.[59] Regular removal of calluses is an effective way to reduce pressure, thus decreasing the risk of ulceration.[60]

Protective Footwear

Appropriate footwear is integral to preventing ulcers.[61-64] Prescription footwear and custom fitted orthotics have been shown to prevent occurrence and recurrence of complications and increase patients' use of shoes outdoors.[61-65] One study compared a group of patients with history of ulceration or amputation wearing their own shoes versus patients who had custom footwear and orthotics. The group that wore their own shoes had more than double the rate of reulceration. However, this therapeutic modality is vastly underutilized. Findings from a random questionnaire sent to a group of eligible diabetics by the American Orthopedic Foot and Ankle Society suggested that only 12.2% wore prescription shoes and 15.4% wore custom foot orthoses.[66] Results of an effort to educate 43,000 Medicare beneficiaries with serious foot problems and their physicians about the Therapeutic Shoe Bill were disturbing.[67] Only 2% of the beneficiaries enrolled, and only 6% of the physicians notified enrolled any of their patients. Among the physicians who did enroll patients, only 26% were internists and 9% were family practitioners.[67] Another cohort of more than 60,000 Medicare beneficiaries showed that only 0.6% had therapeutic footwear.[68] The appropriate utilization of orthotics and footwear could greatly improve outcomes and decrease LEAs (Table 4).

Neuropathic Fracture

A neuropathic (Charcot) fracture is one resulting from chronic destruction of the bones and joints of the foot. The etiology of neuroarthropathy is poorly understood,[69,70] but it may involve a combination of sensorimotor neuropathy, minor trauma, autonomic neuroarthropathy with increased blood flow to the bone, corticosteroid-induced osteoporosis, and metabolic abnormalities that weaken the bone.[70]

Early recognition and management of an acute Charcot fracture is essential to minimize bone destruction. Charcot's arthropathy is diagnosed in 1% to 2% of the general diabetic population, while 13% to 29% of patients evaluated in specialty foot clinics are found to have Charcot joint changes.[17,18] This may be partly explained by referral bias but also likely represents underdiagnosis. Minor or unperceived trauma often precipitates the fracture.[71,72] Signs of fracture include redness, swelling, and more than 2°C skin temperature difference when compared with the contralateral foot. Dorsalis pedis pulses are often bounding.[73] The patient is afebrile unless a systemic infection is present. Elevation and rest of the extremity results in an immediate decrease in swelling. During the dissolution (inflammatory) phase, immobilization is required for a period of 3 to 9 months with total contact cast or healing boots. Non-weight-bearing is needed with modified gait and an assistive device.[18,69,71,72,74] Bisphosphonates may be of benefit.[75] The coalescence (healing) phase should show radiographic evidence of consolidation of bony fragments and should be treated with protected weight-bearing, a removable cast or a walker, ankle-foot orthosis, or pressure relief ankle-foot orthosis. At resolution (remodeling), therapeutic shoes and inserts are beneficial to prevent recurrence.[18,69,71,72,74] Surgery is indicated for unstable, malaligned, or nonreducible fractures.[69] Often confusing is the absence of pain. The majority of people who have a Charcot fracture have lost protective sensation, so that pain is no longer a reliable indicator. Osteomyelitis may occasionally be confused with a Charcot fracture but will usually have an overlying ulcer. However, a person with an ulcer can have a neuropathic fracture. Magnetic resonance imaging (MRI), radionucleotide bone scan, scintigraphy, or bone biopsy may be required to differentiate the two in difficult cases.[76,77]

Patient-Related Factors

Patients who have loss of vision, mobility, or flexibility may be impeded from doing a daily foot examination. A hand-held mirror placed on the floor or a wall mirror may assist patients with hip or knee problems. A family member may need to examine the feet daily if the patient has visual defects. Diabetics who live alone may be at a higher risk for ulceration because of the inability to perform daily self-care, though this has not been documented in the literature.

Conclusion

Multiple studies have documented the ability of preventive diabetic foot care to reduce complications and costs.[78-80] Patout et a[80] compared patient outcomes before and after 1 year of enrollment in a comprehensive LEAP program. The results showed a dramatic reduction in foot-related complications (Table 5). Armstrong and Harkless[78] have also shown that a multidisciplinary diabetes care team can result in fewer foot complications. Over a period of 3 years, their clinic had an average of only 1.1/1,000 amputations per year, compared with 11/1,000 amputations per year in the general diabetic population.[24] A model developed to estimate the expected incidence and cost of amputation showed that the economic benefits (discounted at 5%) using strategies of education, multidisciplinary care referral, and therapeutic shoes totaled $2 million to $3 million for a cohort of 10,000 diabetic patients.[81]
In summary, a strategy of yearly comprehensive foot examinations and education with appropriate interventions and risk reduction can be a cost-effective means of improving both the quality and duration of life in those with diabetes mellitus.

 Sidebar: Keypoints

• Yearly foot examinations should assess skin, neurologic, vascular, and biomechanical status.
  
• Distal symmetric peripheral neuropathy affects 50% of diabetics 15 years after diagnosis, is best screened for by using a monofilament and may lead to muscle atrophy and deformity.
  
• Long, thick ingrown toenails and callus formation are risk factors for ulceration and should be trimmed.
  
• Prescription footwear and custom orthotics have been shown to prevent occurrence and recurrence of foot-related complications.
  
• Charcot (or neuropathic) fractures can be recognized by redness, swelling, warmth, bounding dorsalis pedis pulses, and absence or presence of pain. These fractures require immediate immobilization.

Send reprint requests to Bryan T. Green, MD, Duke University Medical Center, Division of Gastroenterology, Durham, NC 27710.

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Melissa F. Green, PT, Zarrintaj Aliabadi, PhD, PA-C, Bryan T. Green, MD, Department of Internal Medicine and the Comprehensive Diabetic Foot Clinic, University of South Alabama, Mobile South Med J 95(1):95-101, 2002. © 2002 Southern Medical Association