Management of the Diabetic Foot: Preventing Amputation. (Featured CME Topic: Diabetes Mellitus).

OF THE MANY COMPLICATIONS of diabetes, amputation is the one most feared. This anxiety is valid in light of the fact that the number of lower extremity amputations performed on patients with diabetes is increasing annually in the United States. In 1979, the number of nontraumatic amputations in diabetic patients was 31,691. Despite efforts to reduce this number; it has gradually increased; by 1990, the number was 53,832. In 1996, the number had reached 85,530. (1,2) This number did not include approximately 3,000 amputations that occurred in Veterans Affairs hospitals.

Diabetes is the cause of 50% of all the nontraumatic amputations in the United States. This can be explained by the fact that the number of persons with diabetes is increasing rapidly, the diabetic population is aging, and a coding system enables the number of diabetic amputations to be accurately reported. Twenty-four percent of these amputations are of the toe, 5.8% are mid-foot, 38% are below the knee, and 21.4% are above the knee; the remaining 10% include the hip, pelvis, knee, and other sites. (3)

The loss of a lower extremity or even part of a lower extremity, significantly impacts quality of life (Table 1). Depression is common after amputation. Loss of a limb limits daily and leisure activities; it is difficult to play golf or tennis with a lower leg prosthesis. Worse still, loss of a limb frequently leads to early retirement and loss of income. In addition, "friends" often desert a person who has a disability.

Epidemiologic data indicate that most diabetic patients have foot problems after age 40 and that the incidence of these problems increases with age. (4) Amputation is more common in African Americans, (5) and there is a higher incidence of amputation in men than in women. (4,6)

Risk factors for lower extremity amputation vary from series to series. Most diabetic amputations, however; are due to peripheral arterial disease (PAD), peripheral neuropathy (PN), and infection. This triad .is the harbinger of the final pathologic events, gangrene and amputation. The various pathways leading to amputation are noted in the Figure. (7)

PERIPHERAL ARTERIAL DISEASE

The atherosclerotic plaques that occur in patients with diabetes are no different than those occurring in the nondiabetic; in both, such plaques are composed of deposits of cholesterol, calcium, lipids, smooth muscle cells, and macrophages. There are, however; some important differences in the characteristics of PAD in these two groups of patients; these differences are listed in Table 2.

Patients with diabetes should have a vascular examination at least once a year; while those who have evidence of PAD should be examined at least every 4 months. The most important steps in evaluating PAD are a medical history and a thorough vascular examination. In general, a history of intermittent claudication is one of the first symptoms of vascular insufficiency. Because of loss of sensation, however, diabetic patients may have ischemia without symptoms. Coldness of the foot and absence of pulses are hallmark clinical signs of PAD, as are shiny, atrophic skin and loss of hair.

When the medical history and physical examination reveal signs or symptoms of ischemia, the vascular laboratory can be of help. Patients with diabetes may have normal ankle pressures but significantly decreased toe pressures. It is extremely important, therefore, to measure toe pressures in patients with diabetes. Arterial waveforms as well as segmental pressures help to indicate areas of arterial narrowing.

Telling patients with PAD not to cross their legs is of little protective value. A study of diabetic patients with known PAD showed that crossing their legs did not decrease Doppler pressures. (8)

PERIPHERAL NEUROPATHY

Peripheral neuropathy with loss of sensation is the major cause of diabetic foot ulcers and amputation. Although the exact etiology of PN is unknown, it is probably the result of a combination of metabolic events, including the accumulation of glucose, sorbitol, and fructose in the nerve; a decrease in myo-inositol, which is important for nerve conduction; and ischemia due to narrowing of the vessels in the vasa nervorum.

Patients with diabetes should undergo examination of the peripheral nerves at least once a year. Loss of the Achilles tendon reflex and vibratory sensation are the earliest symptoms of PN. Although these symptoms usually occur together, they can occur independently.

The most important neurologic finding in PN is the loss of protective sensation. (9,10) The use of a pinprick to assess sensation is outdated. Sensation assessments are now carried out using the Semmes-Weinstein 5.07 monofilament. This simple device is pressed against the skin until it buckles; the amount of pressure is equal to 10 grams of linear strength. Inability to perceive pressure at this level indicates severe PN and puts the patient at high risk for the development of foot ulcers. This is a simple test that the patient can do at home, (9-11) and it is currently believed to be the most practical method of risk assessment for PN. (9,10)

The effectiveness of tight blood glucose control was shown in the Diabetes Control and Complications Trial. (11) To date, it is the only means of preventing neuropathy or slowing its progression.

Foot deformities are notoriously common in the diabetic patient with PN. Patients with diabetes are prone to having cocked-up toes, hammer toes, and/or claw toes. These deformities are frequently associated with thinning or shifting of the fat pad under the metatarsal heads. The areas at the top of the toes, the tips of the toes, and under the metatarsal heads are therefore vulnerable to ulceration, infection, and, subsequently, osteomyelitis, gangrene, and amputation. The ideal treatment is prophylactic surgery to straighten the toes while circulation is good. When surgery is not possible, the patient should wear a shoe with a large toe-box to accommodate the cocked-up toes and/or an in-depth shoe with a cushioned insole to reduce the pressure over the metatarsal heads and the tips of the toes. This will decrease the probability of ulceration in those areas.

Charcot's foot is the classic diabetic foot deformity. Patients with this deformity frequently present with bounding pulses in a swollen, red, warm foot. The patient often gives a history of having sustained a sprain or minor injury to the ankle or foot a few days to a week before the development of swelling and erythema of the foot. These signs represent the acute onset of the Charcot foot. Despite these changes in the foot, there is only minimal discomfort. At this acute stage, the presence of cellulitis must be ruled out. Radiographs taken at this time usually reveal no abnormalities. The classic history of minor trauma, the absence of any portal of entry for infection, and the absence of other clinical signs or laboratory findings of infection are highly suggestive that the patient has an acute Charcot's foot, however.

The patient should be placed on non-weight-bearing status as soon as Charcot's foot is diagnosed. If the patient continues to walk, a variety of fractures will occur within a period of several weeks to months, particularly at the tarsometatarsal joint; fragmentation and dissolution of the bone are likely sequelae. If the patient is not casted and placed on non-weight-bearing status, the ankle joint will collapse, and the foot will take on a club-foot-like appearance and a rocker-bottom configuration. If the patient continues to walk without protection of the foot with a cast or special footwear, ulceration will occur on the mid-plantar surface of the foot. In some cases, surgical procedures can be performed to correct the deformity and/or stabilize the foot or joint. The deformed foot requires the use of a specially molded therapeutic shoe. (12-14)

Failure to recognize the acute stage of Charcot's foot is not uncommon. These patients frequently are treated for months with a variety of antibiotics until finally the foot collapses. At that time, the correct diagnosis is made, usually as a result of x-rays. The end result is a foot that is vulnerable to ulceration. Failure to diagnose the Charcot's foot in a timely fashion frequently leads to a malpractice suit for substandard care.

NEUROPATHIC ULCER

The plantar neuropathic ulcer is the condition that most commonly leads to amputation. (15) Foot ulcers are extremely common in patients with diabetes. Reiber et al, (5) in their review of diabetic foot ulcers in several populations, found a prevalence of 4.4% to 10.5%. Approximately 15% of all patients with diabetes will have foot ulcers during their lifetimes. (18)

Neuropathic foot ulcers result from repetitive stress on feet tendered insensitive by PN. This condition, which is the most important factor leading to ulceration, is present in more than 80% of diabetic patients with foot ulceration. (17,18) When stress persists, the foot develops "hot spots" and callus buildup.

Callus buildup can increase the foot pressure by as much as 30% (19); increased foot pressure contributes to plantar ulceration. Periodic reduction of calluses is, therefore, extremely important. Wearing cushioned shoes (20) and pressure-reducing hosiery (21) can also be beneficial in reducing the rate of callus build up. Patients should not go barefoot, not only because of possible trauma, but also because significantly more pressure is exerted on the feet when walking barefoot compared with walking on cushioned shoes. (22)

Calluses and ulceration occur most often at the site of maximum pressure, usually over the plantar surface of the metatarsal heads and on the plantar surface of the hallux. When ulceration occurs on the side of the foot, it is most likely due to ill-fitting shoes and ischemic pressure necrosis. When the ulceration is on the dorsum of the foot, it is usually the result of trauma.

MANAGEMENT OF THE NEUROPATHIC FOOT ULCER

Table 3 lists the steps in the management of diabetic foot ulcers, while Table 4 notes the impediments to wound healing in the diabetic patient, all of which must be considered in planning a management strategy. (7) The first step in management of the ulcer is to establish its size and depth; what appears to be a superficial ulceration may be only the tip of the iceberg. Penetration may extend deep into the tissues.

Radiographs are necessary to rule out osteomyelitis, gas formation, the presence of foreign objects, and asymptomatic fractures. Cavanagh et al (22) found that diabetic patients without neuropathy did not have excessive bone abnormalities. Diabetic patients with PN, however, and particularly those with a history of previous foot ulceration, had significantly more radiographic abnormalities. Previously unrecognized traumatic fractures were found in 22% of patients with neuropathic foot ulceration. (22) Radiographs should, therefore, be taken of any foot with ulceration or infection.

Neuropathic ulcers should be aggressively debrided by sharp dissection, with removal of all necrotic material and eschar. Not infrequently, there is infection beneath the eschar; the infection must be identified so that it can be treated. Removal of eschar in a patient with severe PAD should be done cautiously, since healing can be significantly impaired.

Debridement of a diabetic foot ulcer should be carried down to healthy, bleeding tissue. After debridement, the ulcer will probably be larger than it was at presentation. Whirlpool is not an effective method of debridement. Enzymatic debridement will be superficial. Debridement using maggots is an old form of treatment used for centuries by military surgeons. It was introduced to the civilian population in the 1930s, and recent reports have again suggested the effectiveness of maggots in cleansing wounds. (23,24)

When the foot is insensitive, minor sharp debridement can be carried out at the bedside. In many cases, however, the patient must be taken to the operating room for adequate debridement under anesthesia. Taylor and Porter (25) have reported that aggressive foot debridement and, when indicated, revascularization resulted in long-term salvage of threatened limbs, even in high-risk patients.

Biopsy should be considered when ulcers appear at an atypical location (not over the metatarsal heads or the plantar surface of the hallux), when they are unrelated to trauma, or when they are unresponsive to aggressive therapy. In a number of such cases, biopsies revealed primary and metastatic malignancies.

INFECTION

Infection is a common and serious complication of diabetic foot wounds. (26) Infection leads to formation of microthrombi, causing further ischemia, necrosis, and progressive gangrene. (27) Massive infection is the most common factor leading to amputation. Because infection in the diabetic foot can be complex, consultation with an expert in infectious disease may be beneficial.

Response to infection is often altered in the patient with diabetes. Infection-fighting capability is often diminished because of impaired leukocyte function. Impaired leukocyte function is significantly influenced by the degree of hyperglycemia; therefore, tight blood glucose control is extremely important when infection is present. In addition, patients with diabetes and severe foot infection often do not respond to the infection with elevation of body temperature and/or white blood cell (WBC) count. Leichter et al (28) have reviewed laboratory data in a large series of diabetic patients with serious pedal infections. Despite significantly elevated sedimentation rates, the mean WBC count was 9,700/[10.sup.2]/[mm.sup.3]. Gibbons and Eliopoulos (29) have also documented the absence of temperature elevation, chills, or leukocytosis in two thirds of the patients with limb-threatening infection, including abscesses and extensive soft tissue infection. Similarly, Eneroth et al (30) found that approximately 50% of patients with foot infection had temperatures under 37.8[degrees]C and WBC counts under 10,000/[10.sup.2]/[mm.sup.3]. (30) Given these findings, the clinician should not depend on elevated WBC counts and/or temperature elevation alone as indications of the severity of a diabetic foot infection.

Aerobic gram-positive staphylococci and streptococci usually are the cause of infection; however, gram-negative organisms are frequently present as well. Anaerobic infection is common. Leichter et al (28) found that the serious infections in their series were polymicrobial; 72% of organisms -cultured were gram-positive and 49 were ram-negative.

Culturing technique is extremely important in cases of diabetic foot infection. Simply swabbing the ulcer is not satisfactory and frequently produces inaccurate results. Specimens for culture should be obtained from tissue deep in the wound after debridement. (31) Cultures should be obtained anaerobically as well as aerobically.

Antibiotic therapy with a broad spectrum antibiotic should begin immediately after cultures have been obtained; the antibiotic can then be adjusted based upon the sensitivities of the causative organisms. Many diabetic foot infections contain gram-negative organisms; therefore, the initial antibiotic chosen should be effective against gram-negative as well as gram-positive organisms. Selection of an oral or a parenteral antibiotic for treatment of a diabetic foot infection must be based upon medical judgment.

If an oral antibiotic is selected, it is not advisable to simply instruct the patient to take the medication and return in a week. In the diabetic patient, infection can progress significantly in just 24 to 48 hours. The diabetic patient taking oral antibiotic therapy should therefore be seen within a few days after initiation of therapy. In addition, the patient must be instructed to notify the physician at once if any increase in redness or drainage or any evidence of lymphangitis is noted. While many of these patients have insensate feet, the development of pain is indicative of deep infection and requires immediate attention. The development of a foul odor also indicates worsening infection and may indicate the presence of anaerobes. It is important that diabetic patients with infection monitor their blood glucose levels closely, since rising blood glucose levels strongly suggest worsening infection, even when other signs and symptoms are absent.

The criteria for hospitalization and treatment with parenteral antibiotics include sepsis, leukocytosis, PAD, and uncontrolled diabetes. Another indication for immediate hospitalization is when what appears to be a minor infection on the plantar surface of the foot is accompanied by erythema and edema of the dorsum of the foot. When such signs are present even though the patient is not septic, there is a high probability that the infection has penetrated deep into the tissues and has spread to the dorsum of the foot. Such infections require incision, drainage of probable abscess, debridement, administration of parenteral antibiotics, and tight blood sugar control.

When infection fails to respond to aggressive treatment, the wound should be debrided and recultured, since the flora may have changed. Chronic, recurrent, or treatment-resistant infection suggests the presence of osteomyelitis.

Osteomyelitis is a frequent complication of diabetic foot ulcers and infection, but it may be difficult to detect on a clinical basis. In fact, Newman et al (32) found that only one third of biopsy-proven cases of osteomyelitis had been clinically suspected. If bone is visible or if the ulcer can be probed to the bone, the probability of osteomyelitis is high. (33) Scanning techniques for osteomyelitis are not always successful. The triple-phase scan with technetium lacks specificity, (34) but scanning with indium 111 is highly specific. (35) Magnetic resonance imaging (MRI) is a helpful technique. (36,37)

Although soaking of the feet has been a traditional approach to treatment, it is of no benefit; in fact, it can lead to maceration and worsening infection. Because the foot is insensitive, soaking may take place in water that is too hot, resulting in severe burns. Chemical soaks can result in chemical burns. Soaking the feet or using the whirlpool delays appropriate and aggressive therapy. (38)

Edema is frequently present and can contribute to vascular insufficiency by compressing the capillaries. Elevation of the feet to the thickness of one pillow can be beneficial, but higher elevation may impede circulation. Careful compression may be helpful.

Avoidance of weight bearing is essential. These patients have insensate feet and, because the ulcers are not painful, they continue to walk. The result is an increase in pressure necrosis that not only delays healing, but also can result in enlargement of the ulcer. How can non-weight-bearing status best be achieved? Prolonged bed rest is impractical and potentially dangerous because of the risk of venous thrombosis and pulmonary emboli. The use of crutches is difficult and can be dangerous, since many of these patients have some degree of ataxia due to neuropathy. A wheelchair is seldom successful in achieving total avoidance of weight bearing. For consistent weight-bearing avoidance, in the appropriately selected patient the best choice is the contact cast. A contact cast is contraindicated in patients who have severe PAD or are ataxic, blind, or pathologically Obese. (39) By decreasing pressure on the ulcerated area, the contact cast allows the patient to be ambulatory but essentially non-weight bearing. (39) A recent article has reported the improved effectiveness and safety of a non-removable fiberglass off-weight-bearing cast. (40) In that study of the treatment of neuropathic foot ulcers, there was 50% healing in 30 days in patients using the fiberglass cast, compared with 20% healing in 30 days in those using a therapeutic shoe. There was a high rate of patient compliance in the study.

The incidence of immunosuppresion is increasing in patients with diabetes because of the increasing frequency of kidney and pancreas transplants. Immunosuppression markedly impairs healing of foot ulcers and eradication of infection, and immunosuppressed patients have a higher amputation rate. (41) Limb amputation occurs in the short term for at least 15% of diabetic patients who have had kidney transplants, and it becomes necessary for approximately 33% of 10-year survivors. (42)

The worst impediment to wound healing or clearing of infection in the diabetic patient is vascular insufficiency. When an ulcer does not heal despite good metabolic control, adequate debridement, parenteral antibiotic therapy, and avoidance of weight bearing, vascular insufficiency should be suspected as the reason. In a study conducted by Mills et at, (43) all appropriately treated neuropathic ulcers and forefoot infections healed in patients with palpable pedal pulses. When foot pulses were absent and arteriography confirmed significant stenosis, foot lesions and infections healed with revascularization. Ankle/brachial indices of less than 0.50 and transcutaneous oxygen pressures of less than 30 mm Hg are highly predictive of infections that will not resolve and ulcers that will not heal. Vascular surgery should be considered in these cases. LoGerfo et al (44) illustrated the importance of peripheral arterial reconstruction. In 2,883 cases of extreme-distal arterial reconstruction, they found a statisticall y significant decrease in every category of amputation, and that decrease correlated precisely with an increasing rate of dorsalis pedis artery bypass.

Finally, managed care can be an impediment to wound healing. Managed care limits the time the clinician can spend with the patient, making it impossible to take a comprehensive history, perform a thorough examination, adequately treat the wound, and instruct the patient in wound care. The clinician who must see another patient every 15 minutes cannot adhere to standards of care; furthermore, in some situations managed care delays appropriate consultations and hospitalization. (45)

ADJUNCTIVE THERAPIES

A variety of adjunctive treatments have been proposed for accelerating wound healing (Table 5). To be successful, all of the basic wound-healing techniques listed in Table 3 should be used. The adjunctive therapies of electrical stimulation (46) and ultrasonography (47) require additional studies in controlle trials to establish their efficacies

The use of hyperbaric oxygen (HBO) (48) is encouraging; however; a criticism regarding HBO is that, with one exception, (49) there have been no randomized controlled trials. (50) Certainly more trials are needed. (51) Using HBO for treatment of diabetic foot ulcers should not be considered the primary treatment HBO should be used only after all of the standard treatments described herein have been done. In addition, patients with severe vascular insufficiency are not candidates for HBO.

The use of growth factors to stimulate wound healing is gaining greater acceptance. Procuren (52) (Curative Health Services Inc, Hauppauge, NY), autologous growth factors made from the patient's own platelets, came into use in the early 1990s but has not been approved by the Food and Drug Administration (FDA). A recombinant platelet-derived growth factor, Regranex, (Ortho-McNeil Pharmaceuticals Inc, Raritan, NJ) is FDA-approved and is now widely used. (53) Living tissue equivalents have been shown to accelerate wound healing. (54,55) Apligraf (Organogenesis Inc, Canton, Mass), a bilayereci living skin equivalent, is FDA-approved. Dermagraft (Advanced Tissue Sciences Inc, LaJolla, Calif), another living skin equivalent, is awaiting FDA approval. (55) The administration of a granulo-cyte-stimulating factor appears to be potentially helpful by stimulating white blood cell production to fight infection, and it has been reported to accelerate wound healing. (56)

POSTTREATMENT MANAGEMENT OF HEALED FOOT ULCERS

Because the recurrence of a healed ulcer is so common, the management of the healed ulcer is important. The chance of recurrence is high because the underlying etiologies responsible for a foot ulcer--PN, PAD, calluses, increased pressure, and foot deformities--are still present. Moreover, scar tissue from healed ulcers is not strong and is vulnerable to the shearing forces of walking.

Special measures are therefore necessary to protect the vulnerable sites of previous ulceration. Patients should be taught to take shorter steps when walking and to decrease their overall walking. Patients whose jobs require standing or walking may need to change jobs.

THERAPEUTIC SHOES

The use of therapeutic shoes is critical in preventing ulceration or recurrence. Patients who have cocked-Lip toes require a shoe with a bigger toe box. In addition, an in-depth shoe with an insole of a plastic-like material is frequently required to redistribute the weight away from the previously ulcerated site and thus prevent recurrence. The patient with a marked deformity, such as Charcot's foot, needs a molded shoe.

The importance of wearing therapeutic shoes has been clearly shown. A study at King's College (57) in London showed that while patients who wore therapeutic shoes had an ulcer recurrence rate of only 17%, those who returned to wearing regular shoes had an recurrence rate.

A recent demonstration study (58) that supplied therapeutic shoes to diabetic patients with selected foot problems showed no increased cost to Medicare. Medicare now provides partial payment for therapeutic shoe for diabetic patients with specific foot problems. For proper fit of therapeutic shoes and selection of appropriate insoles, a podiatrist and/or certified pedorthist should be consulted. (59,60)

TEAMWORK

Because wound healing and prevention of foot problems is complex, the expertise of many disciplines is necessary (Table 6). All of the team members should have a special interest and expertise in diabetic foot problems and wound healing. The success of the team approach in reducing amputations has been well documented. (61) Even with the best care, amputation may become necessary; should this unfortunate event occur, the involvement of a skilled rehabilitation team will also be required. (62,63)

PATIENT EDUCATION

Patient education in foot care and foot inspection is the most important factor in preventing amputation. Patients should be taught to inspect their feet on a daily basis, and shoes and socks must be removed for foot inspection during every office visit. The nurse and/or physician should inspect the patient's feet and review the "dos and don'ts" of foot care (Table 7). A successful foot-care education program cannot be accomplished by simply handing the patient a list of instructions. Instead, the list of instructions should be reviewed with and explained to the patient and questions should be encouraged. Foot-care instructions should be reviewed with the patient at least once a year and preferably more often. The effectiveness of educational programs in reducing amputation has been well documented. (64,65)

One of the most important factors in saving the foot of the diabetic patient is inspection of the foot at each office visit, including checking between the toes; unfortunately, this simple examination is frequently omitted. In one series, only 61% of the patients had their feet inspected at least once. (66) In one managed care program, examination of the feet was not noted in 94% of the patients' records. (67) A percentage of these patients may have had their feet examined but not documented; however an often-quoted caveat is that if it was not recorded, it was not done.

Diabetic patients with loss of sensation in their feet and previous ulcers and foot deformities should not do weight-bearing exercises such as jogging, walking on a treadmill, prolonged walking, or step exercises. Exercises that are acceptable for the diabetic patient with loss of sensation include swimming, bicycling, rowing, chair exercises, and arm exercises.

LEGAL ISSUES

This review would not be complete without mention of the frequency with which lawsuits follow amputations. Some of the most common complaints leading to litigation are listed in Table 8. No health care provider is immune to such litigation. The steps for avoiding litigation when managing diabetic foot problems have been outlined. (69) A poor outcome does not necessarily mean deviation from the standards of care. When the standards of care are not met and an amputation results, however, the likelihood of a successful defense are markedly diminished.

CONCLUSION

Foot lesions, especially ulcerations, are common in patients with diabetes. If treatment is delayed or inappropriate treatment is rendered, the lesion can become infected, resulting in gangrene and/or amputation. Physicians, clinics, and wound-healing centers that follow a rigid protocol, including aggressive therapy, revascularizaton when indicated, therapeutic shoes when indicated, a team approach, and repeated education of the patient in foot care, have reduced amputation rates by 50% or more. (70)

(*.) Presented at the Fourth Annual conference on Diabetes, Southern Medical Association, Destin, Fla, October 5-7, 2001.

References

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(37.) Fisher AJ, Gilula LA, McEnery KW: Imaging of the diabetic foot. Levin and O'Neal's The Diabetic Foot. Bowker JH, Pfeifer MA (eds). St. Louis, CV Mosby, 6th Ed, 2001, pp 333-354

(38.) Levin ME, Spratt IL: To soak or not to soak, Clin Diab 1986; 4:44-45

(39.) Sinacore DR, Mueller MJ: Total-contact casting in the treatment of neuropathic ulcers. Levin and O'Neal's The Diabetic Foot. Bowker JH, Pfeifer MA (eds). St. Louis, CV Mosby, 6th Ed, 2001, pp 301-320

(40.) Garavaggi C, Fagflia E, DeGiglio R, et al: Effectiveness and safety of a nonremovable fiberglass off-bearing cast versus a therapeutic shoe in the treatment of neuropathic foot ulcers. Diabetes Care 2000; 23:1746-1751

(41.) Fletcher F, Ain M, Jacobs R: Healing of foot ulcers in immunosuppressed renal transplant patients. Clin Orthop 1993; 296:37-42

(42.) Friedman EA: Diabetic renal disease. Ellenberg and Rifkin's Diabetes Mellitus: Theory and Practice. Rifkin H, Porte D (eds). New York, Elsevier, 4th Ed, 1990, pp 684-709

(43.) Mills JL, Beckett WC, Taylor SM: The diabetic foot: consequences of delayed treatment and referral. South Med J 1991; 84:970-974

(44.) LoGerfo FW, Gibbons OW, Pomposelli FB Jr: Trends in the care of the diabetic foot expanded role of arterial reconstruction. Arch Surg 1992; 127:617-621

(45.) Levin ME: Managed care and diabetes: the best of times or the worst of times. BioMechanics 1997; 4:67-70

(46.) Baker LL, Chambers R, DeMuth SK, et al: Effects of electrical stimulation on wound healing in patients with diabetic ulcers. Diabetes Care 1997; 20:405-412

(47.) McCulloch J: Physical modalities in wound management: ultrasound, vasopneumatic devices and hydrotherapy. Ostomy/Wound Management 1995; 41:30-32, 36-37

(48.) Cianci P, Hunt TK: Adjunctive hyperbaric therapy in the treatment of diabetic foot wounds. Levin and O'Neal's The Diabetic Foot. Bowker JH, Pfeifer MA (eds). St. Louis, CV Mosby, 6th Ed, 2001, pp 404-421

(49.) Faglia F, Favales F, Aldeghi A, et al: Adjunctive systemic hyperbaric oxygen therapy in treatment of severe prevalently ischemic diabetic foot ulcer: a randomized study. Diabetes Care 1996; 19:1338-1343

(50.) Tibbles PM, Edelsberg JS: Hyperbaric-oxygen therapy. NEnglJMed 1996; 334:1642-1648

(51.) Wunderlich RP, Peters EJG, Lavery LA: Systemic hyperbaric oxygen therapy: lower-extremity wound healing and the diabetic foot. Diabetes Care 2000; 23:1551-1555

(52.) Holloway GA, Steed DL, DeMarco MJ, et al: A randomized, controlled dose-response trial of activated platelet supernatant, topical CT-102 in chronic, non-healing, diabetic wounds. Wounds 1993; 5:198-206

(53.) Steed D: The diabetic ulcer study group: clinical evaluation of recombinant human platelet-derived growth factor for the treatment of lower extremity diabetic ulcers. J Vasc Surg 1995; 1:7-81

(54.) Brem H, Balledux J, Bloom T, et al: Healing of diabetic foot ulcers and pressure ulcers with human skin equivalent: a new paradigm in wound healing. Arch Surg 2000; 135:627-634

(55.) Gentzkow GD, Iwasaki SD, Hershon KS, et al: Use of Dermagraft, a cultured human dermis, to treat foot ulcers. Diabetes Care 1996; 19:350-354

(56.) Gough A, Clapperton M, Rolando N, et al: Randomised placebo-controlled trial of granulocyte-colony stimulating factor in diabetic foot infection. Lancet 1997; 350:855-859

(57.) Edmonds ME, Blundell MP, Morris ME, et al: Improved survival of the diabetic foot: the role of a specialized foot clinic. QJ Med 1986; 60:763-771

(58.) Wooldridge J, Bergeron J, Thomton C: Preventing diabetic foot disease: lessons from the Medicare therapeutic shoe demonstration. AmJPublic Health 1996; 86:935-938

(59.) Coleman WC: Footwear for injury prevention: correlation with risk category. Levin and O'Neal's The Diabetic Foot. Bowker JH, Pfeifer MA (eds). St. Louis, CV Mosby, 6th Ed, 2001, pp 422-438

(60.) Janisse DJ: Pedorthic care of the diabetic foot. Lenin and O'Neal's The Diabetic Foot. Bowker JH, Pfeifer MA (eds). St. Louis, CV Mosby, 6th Ed, 2001, pp 700-726

(61.) Larsson J, Apelqvist J, Agardh CD, et al: Decreasing incidence of major amputation in diabetic patients: a consequence of a multidisciplinary foot care team approach? Diabetic Med 1995; 12:770-776

(62.) Helm PA, Kowalske KJ: Rehabilitation. The Diabetic Foot. Levin ME, O'Neal LW, Bowker JH (eds). St. Louis, CV Mosby, 5th Ed, 1993, pp 493-505

(63.) Gailey RS Jr, Clark CR: Rehabilitation of the diabetic amputee. Lenin and O'Neal's The Diabetic Foot. Bowker JH, Pfeifer MA (eds). St. Louis, CV Mosby, 6th Ed, 2001, pp 636-653

(64.) Litzelman DK, Slemenda CW, Langefeld CD, et al: Reduction of lower extremity clinical abnormalities in patients with non-insulin dependent diabetes mellitus. Ann Intern Med 1993; 119:36-41

(65.) Faglia E, Favales F, Morabito A: New ulceration, new major amputation, and survival rates in diabetic subjects hospitalized for foot ulceration from 1990 to 1993: a 6.5 year followup. Diabetes Care 2001; 24:78-83

(66.) Beckles GLA, Engelgau MM, Narayan KMV, et al: Population based assessment of the level of care among adults with diabetes in the US. Diabetes Care 1998; 21:1432-1438

(67.) Peters AL, Legorreta AP, Ossorio RC, et al: Quality of Outpatient care provided to diabetic patients: a health maintenance organization experience. Diabetes Care 1996; 19:601-606

(68.) Levin ME: The diabetic foot. The Health Professional's Guide to Diabetes and Exercise. Ruderman N, Devlin JT (eds). Alexandria, Va, American Diabetes Association Inc, 1995, pp 137-141

(69.) Frank JJ, Frank JA: Medicolegal aspects of care and treatment of the diabetic foot. Levin and O'Neal's The Diabetic Foot. Bowker JH, Pfeifer MA (eds). St. Louis, CV Mosby, 6th Ed, 2001, pp 757-765

(70.) Gibbons GW, Marcaccio E Jr, Burgess AM, et al: Improved quality of diabetic foot care. 1984 vs 1990: reduced length of stay and costs, insufficient reimbursement. Arch Surg 1993; 128:576-581

TABLE 1.

Some Effects of Amputation on Quality of Life

* Limitation of daily activities
* Impairment of physical activity
* Depression
* Early retirement
* Decreased income
* Loss of social contacts
* Impairment of sexual activity
TABLE 2.

Differences in Diabetic and Nondiabetic Peripheral Artery Disease

                               Diabetic

Clinical                       More common
                               Younger patient
                               More rapid
Male/female ratio              Male = female
Occlusion                      Multisegmental
Vessels adjacent to occlusion  Involved
Collateral vessels             Involved
Lower extremities              Bilateral involvement
Vessels involved               Tibial artery
                               Peroneal artery
                               Small vessels
                               Arterioles

                               Nondiabetic

Clinical                       Less common
                               Older patient
                               Less rapid
Male/female ratio              Male >> female
Occlusion                      Single segment
Vessels adjacent to occlusion  Not involved
Collateral vessels             Usually normal
Lower extremities              Unilateral involvement
Vessels involved               Aortic artery
                               Iliac artery
                               Femoral artery


Adapted from Levin and O'Neal's The Diabetic Foot(7)
Table 3.

Treatment of Foot Ulcers

 1. Evaluation:
       Clinical appearance
       Establish for depth
       X-ray for:
                  Osteomyelitis
                  Foreign objects
                  Subcutaneous air
       Biopsy if indicated
 2. Metabolic control
 3. Debridement, sharp radical
 4. Bacterial cultures (aerobic, anaerobic)
 5. Antibiotics:
       Oral
       Parenteral
 6. Do not soak the feet
 7. Do not use whirlpool
 8. Non-weight-bearing
       Bed rest
       Crutches
       Walkers
       Contact casting
       Special shoes

 9. Improve circulation (vascular surgery)

10. Consultation

Adapted from Levin and O'Neal's The Diabetic Foot. (7)
TABLE 4.

Impediments to Wound Healing

1. Vascular
     Atherosclerosis
     Increased viscosity

2. Neurologic:
     Insensate foot

3. Infection:
     Inadequate debridement
     Poor blood supply
     Microthrombi
     Hyperglycemia
     Decreased neutropil function
     Polymicrobial infection
     Changing bacterial flora
     Osteomyelitis

4. Immunosuppression

5. Mechanical
     Edema
     Weight hearing

6. Poor nutrition:
     Low serum albumin

7. Poor patient compliance

8. Delayed treatment and referral

9. Managed care

Adapted from Levin and O'Neal's The Diabetic Foot. (7)
TABLE 5.

Adjunct Therapies for the Treatment of Diabetic Foot Wounds

* Living skin equivalents
* Autologous growth factors growth factors
* Recombinant growth factors
* Hyperbaric oxygen
* Electrical stimulation
* Ultrasound stimulation
* Granulocyte-stimulating factor
TABLE 6.

Team Members Involved in the Care of the Diabetic Foot

 1. Primary physician

 2. Endocrinologist

 3. Diabetologist

 4. Podiatrist

 5. Nurse-educator

 6. Physician assistant

 7. Enterostomal nurse

 8. Infectious disease specialist

 9. Neurologist

10. Radiologist

11. Specialist in hyperbaric medicine

12. Surgeon
       Vascular
       Orthopedic
       Plastic

13. Physiatrist

14. Physical therapist

15. Pedorthist

16. Orthotist

17. Prosthetist

18. Social worker

19. Home care nurse

20. Sex therapist
TABLE 7.

Patient Instructions for the Care of the Diabetic Foot

 1. Inspect the feet daily for blisters, cuts, scratches, and reddened
    areas. The use of a mirror can aid in seeing the bottom of the foot.
    Always check between the toes.

 2. Wash feet daily. Dry carefully, especially between the toes.

 3. Avoid extreme temperatures. Test water with hand or elbow before
    bathing.

 4. If feet feel cold at night, wear socks. Do not apply a hot water
    bottle, electric blanket, or heating pad.

 5. Do not walk on hot surfaces, such as sandy beaches or the cement
    around swimming pools.

 6. Do not walk barefoot.

 7. Do not cut corns. Do not use chemical agents for removal of corns
    and calluses. Do not use corn plasters. Do not use strong antiseptic
    solutions on your feet.

 8. Do not use adhesive tape on your feet.

 9. Inspect the inside of shoes daily for foreign objects, nail points,
    torn linings, and rough areas.

10. If your vision is impaired, have a family member inspect feet daily,
    trim nails, and buff down calluses.

11.     Do not soak your feet unless specifically instructed.

12. For dry skin, use a very thin coat of a lubricating oil or cream.
    Apply after bathing. Do not put the oil or cream between toes.
    Consult physician for type of lubricant and detailed instructions.

13. Wear stockings that fit properly. Do not wear mended stockings.
    Avoid stockings with seams. Change stockings daily. Do not wear
    garters.

14. Shoes should be comfortable at the time of purchase. Purchase
    shoes in the afternoon when feet tend to be the largest. Do not
    depend on them to stretch. Shoes should be made of leather.
    Running or walking shoes may be worn after checking with the
    physician.

15. Inform your shoe salesperson that you are diabetic.

16. Do not wear shoes without stockings.

17. Do not wear sandals with thongs between the toes.

18. Ask about therapeutic shoes if you have a foot deformity, such as
    bunions or claw toes, or if you have had a previous ulcer.

19. Take special precautions in the winter. Wear wool socks and
    protective footgear, such as fleece-lined boots.

20. Cut nails straight across or follow the curve of the nail.

21. Do not cut corns and calluses. Follow special instructions from
    your physician or podiatrist. If the nails are thick or
    difficult to cut, have a family member, physician, or podiatrist
    do it.

22. See your physician regularly and be sure that your feet, including
    between the toes, are examined at each visit.

23. Do not smoke.

24. Notify your physician or podiatrist at once should you develop a
    blister or sore on your foot.

25. Be sure to inform your podiatrist that you are diabetic.

Adapted from Levin and O'Neel's The Diabetic Foot. (7)
TABLE 8.

Most Common Omissions Leading to Litigation

 1. Failure to educate the patient about proper foot care

 2. Failure to perform a neurologic or vascular examination

 3. Failure to control blood glucose level

 4. Failure to adequately debride ulcer

 5. Failure to culture the wound for aerobes and anaerobes

 6. Failure to x-ray

 7. Failure to recognize worsening infection

 8. Failure to inform patient of the signs and symptoms of worsening
    infection

 9. Failure to prescribe non-weight bearing

10. Failure to hospitalize or delayed hospitalization in the face
    of worsening infection

11. Failure to obtain consultation or delay in doing so

RELATED ARTICLE: EPIDEMIOLOGY OF DIABETIC FOOT ULCER

* 16 million diabetics

* 15% have foot ulcers

* 6% require hospitalization

FOOT PROBLEMS

Causative factors include:

* Neuropathy

* Ischemia

* Infection

CHANCE OF AMPUTATION OF OPPOSITE LEG AFTER FIRST AMPUTATION


1-3 years  3-5 years
42%        56%

WOUND DEBRIDEMENT MODERN APPROACH

* Radical, aggressive debridement is mandatory

* Goal -> Healthy, noninfected, bleeding tissue

WOUND DEBRIDEMENT PROBLEMS WITH CONSERVATIVE TREATMENT

All necrotic tissue is not excised

Sinus tracts -> necrotic tissue -> anaerobic environment

Infected bone and tendon remain -> reinfection Bacteria produce glycocalyx

DEBRIDEMENT EFFECTS

* Removes foreign bodies, necrotic tissue

* Decreases bacterial load

* Cleans ulcer bed

* Increases platelets/growth factors at ulcer site

* Allows better visual assessment of ulcer area

Adapted from Steed et al, 1998.

DIABETIC FOOT CONDITIONS LIMITING EXERCISE

* Insensate foot

* Deformed foot

Cocked-up toes

Charcot's foot

* Foot ulcer

* Previous ulcer

EXERCISES FOR DIABETICS WITH PERIPHERAL NEUROPATHY

* Non-weight-bearing exercise

* Swimming

* Chair exercise

* Cycling

* Rowing

CONTRAINDICATED EXERCISES

* Treadmill

* Prolonged walking

* Jogging

* Stairmaster