Diabetic Foot Update 1996

Abstract

The Diabetic Foot update seminar is held yearly in San Antonio, Texas, and is sponsored by the Department of Orthopaedics at the University of Texas Health Science Center and the American Diabetes Association. The following is a summary of the topics presented at the 1996 seminar on December 13–15, 1996.

Mailing address: Department of Orthopaedics, 7703 Floyd Curl Dr, San Antonio, TX 78284-7776.

Diabetes Mellitus

Pathophysiology

An overview of the pathophysiology of diabetes mellitus provided by Ralph DeFronzo, MD, Chief of the Diabetic Division at the University of Texas Health Science Center at San Antonio, demonstrated that definition and redefinition of diabetes facilitate the understanding of the disease and disease process and allows for advances in the treatment of diabetes. The etiology of noninsulin-dependent diabetes mellitus has historically been thought of as resulting from decreased production of insulin from the beta pancreatic islet cells, thus necessitating the augmentation of this production with sulfonylureas or exogenous insulin. It has now been demonstrated that decreased insulin production does occur but usually is preceded by increased production of insulin because of relative insulin resistance by muscle and other cells of the body.

It is the identification of this insulin-resistant phase, the increased insulin-production phase, decreased glucose uptake, and decreased insulin output phase of noninsulin-dependent diabetes mellitus that has allowed the introduction of new medications for the treatment of the disease to reach the goal of glucose regulation. Depending on where pharmacotherapeutic intervention is instituted along the spectrum of noninsulin-dependent diabetes mellitus will dictate what type of medication will most likely help achieve regulation of glucose levels. Sulfonylureas act at the level of decreased insulin production to enhance production of insulin by the pancreatic beta cells. Glucophage lowers glucose output by the liver, decreases glucose absorption in the stomach, and enhances glucose uptake by muscle. Acarbose increases the absorption time of carbohydrates in the stomach. The glitazones have been shown to increase insulin sensitivity of fat, muscle, and liver. Exogenous insulin is still used to augment or substitute for insulin production.

Several studies have shown that intensive treatment of diabetes as outlined by the Diabetes Complication and Control Trials has had a significant effect on the prevention of the complications related to diabetes. Alteration in diet, activity level, and exercise, and institution of appropriate pharmacotherapy can help to achieve glucose regulation.

Prior to 1979, no standard classification of diabetes was present and, therefore, no guidelines for treatment could be established. A system of classification was then established placing patients with diabetes in either of two categories: noninsulin-dependent diabetes mellitus and insulin-dependent diabetes mellitus. However, this classification does not accurately reflect the pathophysiology of diabetes or allow for the appropriate guidelines for treatment. The consensus definition of diabetes has been developed with the help of physicians such as James Gavin III, MD, PhD, Chief Scientific Medical Officer at the Howard Hughes Institute, which is, “a metabolic disease characterized by hyperglycemia resulting from defects in insulin secretion, insulin action, or both. The chronic hyperglycemia of diabetes is associated with long-term damage, dysfunction, and failure of various organs especially the retina, kidney, nerves, and in addition an increased risk of cardiovascular disease.” A new classification system for the categorization of patients with diabetes is currently being designed to reflect the dynamic nature of diabetes. A consensus on a new classification at this juncture has only allowed for the following; 1) type I diabetes mellitus–autoimmune or idiopathic; and 2) type II diabetes mellitus–genetic defects, druginduced, endocrinopathies, infections.

The ideal fasting glucose is now classified as ≤ 105 mg/dL. If fasting plasma glucose is < 125 mg/dL with a 2-hr plasma glucose challenge of 140 to 199 mg/dL after a glucose challenge is referred to as impaired glucose tolerance. A fasting plasma glucose of ≥ 125 mg/dL or a 2-hr post-glucose challenge plasma glucose of 200 mg/dL suggests a diagnosis of diabetes mellitus. All values necessitate retesting to confirm the diagnosis of diabetes.

Data provided by Anne Peters, MD, Associate Professor of Medicine at the University of California School of Medicine in Los Angeles, showed that approximately 6% of the population has diabetes requiring 15% of total health care dollars. An average patient with diabetes costs the health care system approximately $9,500 a year compared with someone without diabetes who costs the system approximately $2,600. Most of the cost comes from the treatment of the chronic complications related to diabetes. The quality of care provided to diabetic patients has not approached the standards set forth by the American Diabetes Association in regard to preventive and management therapies, mostly because of the expense of providing quality care in a managed care environment. The cost of treating patients with diabetes is increased initially in order to provide the intensive therapy required to gain glucose regulation and slow the rate of onset of the complications related to diabetes, which will save health care dollars in the long term. Treatment protocols are being developed to help facilitate quality of care with managed costs and ultimately lead to a disease-management model.

Education

Davida Kruger, RN, CDE, Endocrinology and Metabolism Department at Henry Ford Hospital in Detroit, showed that there are 16 million people with diabetes with 8 million persons having yet been diagnosed with the disease. Approximately 650,000 people will be diagnosed with diabetes this year. By the time these patients are diagnosed, they will have had diabetes for a minimum of 5 to 7 years. Diabetes is the leading cause of blindness with 12,000 to 24,000 new cases diagnosed each year. Only 50% of diabetics receive an annual eye examination with an average of 70 people losing their vision because of diabetes-related complications that could have been prevented with routine eye examinations. Approximately 54,000 lower extremity amputations are performed annually with an underlying neuropathy as a major contributing factor. Less than 30% of patients with diabetes ever receive a foot examination that could have prevented an amputation. There are 19,000 new cases of kidney disease annually with most patients not receiving a kidney examination. Cardiovascular disease is present in 75% of all diabetesrelated deaths. Long-term heart disease could be reduced with early and continued control of diabetes.

Appropriate education of patients as well as the health care personnel who provide their care will help to prevent these long-term complications. Glucose regulation is the most important factor in the prevention of long-term complications. A glycosated hemoglobin value of 8% has been shown to be associated with the increased occurrence of diabetes-related complications. With the initial introduction of intensive therapy to reduce the patient’s glycosated hemoglobin, a degree of weight gain caused by alterations in metabolism will result, which may be offset with the appropriate nutrition counseling. A development of a treatment program between the health care provider and the patient will hopefully lead to better compliance and glucose control. An understanding of the patient’s lifestyle and responsibilities will help with the generation of an effective treatment program.

Perioperative Management of the Patient With Diabetes

The average patient with diabetes spends 30% to 50% more time in the hospital following a surgical procedure compared with nondiabetics. The perioperative mortality is higher compared with the nondiabetic patient. Patients older than 50 years of age usually have some diminished renal function that requires monitoring in regard to drug clearance. Hyperglycemia decreases wound healing and immunologic response. Perioperative stress may also produce hyperglycemia. The release of catecholamines, growth hormones, glucagon, and cortisol act as counterregulatory agents to insulin. This may have antagonistic effects to glucose regulation in the perioperative period.

Patients with type I diabetes usually do not respond well to withholding of insulin preoperatively. They must be maintained on insulin during the perioperative period with appropriate adjustments. Type II diabetics can have their hyperglycemic agent withheld preoperatively while remaining “nothing per mouth” with appropriate monitoring with little risk of complications.

The average patient with diabetes is on four to five medications and needs to be assessed preoperatively in order to anticipate adjustments perioperatively.

All sulfonylureas should be withheld 24 hr prior to any surgical procedure except for chlorpropamide, which should be withheld 3 to 5 days prior to any surgical procedure. The most common cause of hypoglycemia on the surgical ward is caused by inappropriate management of chlorpropamide. Patients with type I diabetes can be managed best perioperatively with a continuous insulin infusion. Only 50% of the morning neutral protamine hagedorn insulin should be given with regular insulin withheld altogether.

Glucophage carries a serious risk of lactic acidosis perioperatively and therefore should be withheld preoperatively. There is a 30% mortality rate because of lactic acidosis associated with glucophage, which inhibits excretion of lactate. Tissue injury resulting from hypoxemia may generate increased plasma lactate and cause lactic acidosis. Acarbose should also be discontinued preoperatively and resumed postoperatively when the patient is tolerating meals.

Autonomic dysfunction will impact the patient’s ability to tolerate anesthesia. Postural hypotension, persistent tachycardia, inability to appropriately increase or decrease heart rate in response to stresses, hypersensitivity to catecholamines that may be used during surgery, and painless angina are all abnormalities affecting the heart in the presence of autonomic dysfunction.

Coronary artery disease accounts for as much as 80% of diabetic deaths. There is a twofold to fourfold increased risk of cardiac complications in patients with diabetes as compared with nondiabetic patients. Diabetics usually carry multiple risk factors for accelerated coronary artery disease.

Perioperative hydration is important to prevent metabolic decompensation especially in type I diabetics. Diabetic ketoacidosis can occur in type I as well as type II diabetics under stressful situations and can result in a 10% mortality rate. The diagnostic criteria for diabetic ketoacidosis include hypoglycemia, presence of ketones in the serum, and an anion gap metabolic acidosis with a serum bicarbonate less than 15. Rehydration, insulin therapy, potassium and bicarbonate repletion, and removal of causative factor is the treatment for diabetic ketoacidosis.

Lower Extremity Complications

Neuropathy

Distal symmetric polyneuropathy, as discussed by Michael Pfeifer, MD, Director of the Diabetes Research and Treatment Center at Southern Illinois University School of Medicine in Springfield, has been shown to be present in up to 40% to 60% in both type I and type II diabetic patients. The etiology involves effects of abnormal vaso nervorum blood flow, insulin deficiency causing abnormal fatty acid metabolism, increased plasma glucose causing changes within the polyol pathway, decreased myo-inositol, and increased glycosylation of neural proteins can lead to decreased nerve function. Increased plasma glucose has been shown to precipitate distal symmetric polyneuropathy and that with glucose regulation, nerve conduction velocity has been improved. Following the Diabetes Complication and Control Trials’ protocols, the development of clinical distal symmetric polyneuropathy has been shown to be decreased by 60% as well as a slowing of the progression of neuropathy. While metabolic causes of distal symmetric polyneuropathy may be considered reversible, there are structural causes of distal symmetric polyneuropathy that remain irreversible. Concentrating on controlling the reversible causes of neuropathy will help decrease the complications because of neuropathy.

Chronic painful neuropathy can be classified into dysesthesia, paresthesia, and muscle pain. The symptoms of each of these are different as are the treatments. Dysesthesia, characterized by burning or tingling, is caused from the firing of damaged nociceptive fibers in the cutaneous or subcutaneous nerves. Capsaicin cream and gabapentin can be used to alleviate these symptoms. Paresthesia is characterized by sharp, electrical, numb, aching, or lancinating pain and is caused by loss of segmental inhibition of large, myelinated and unmyelinated nerve fibers, ectopic impulses generated from demyelinated paths of myelinated axons, and increased firing caused by stimulation of endings of nociceptive afferent fibers that innervate nerve sheaths. Treatment includes the use of tricyclic antidepressants such as mexiletine, carbamazepine, phenytoin, or imipramine. Muscle pain secondary to injury to motor nerves or reflex loops is characterized by cramps, spasms, or deep aches and can be treated with stretching exercises, appropriate shoes, short-term skeletal muscle relaxants such as metaxalone, or nonsteroidal anti-inflammatory medicines. Therapy should be directed toward the type of chronic pain that is present, keeping in mind that they may occur singularly or in combination with periodic reevaluations to determine the efficacy of treatment.

Ulceration

The etiology of pedal ulceration among patients with diabetes is usually multifactorial. An understanding of the risk factors for ulceration and appropriate intervention to prevent pedal ulceration is basic to the treatment of the diabetic foot. An interrelationship between physiologic risk factors such as neuropathy, vascular disease, deformity, and limited joint mobility, history of previous ulceration, retinopathy or impaired visual acuity, age and duration of diabetes, and inappropriate footwear have been shown to be associated with diabetic foot complications. Socioeconomic risk factors such as lower income and access to health care, knowledge of disease process, compliance, appropriate footwear availability, and social interaction have also been shown to play a role in the increased risk of pedal complications related to diabetes such as ulceration. Aggressive preventive care in the diabetic foot with an understanding of the association of these risk factors will lead to a greater success in the management of patients with diabetes.

The team approach to the management of the diabetic foot is of primary importance for the overall preservation of the lower extremity. Lower extremity bypass surgery has increased the chances of limb salvage in the presence of macrovascular disease. Distal dorsalis pedis bypass grafts performed at the Beth Israel New England Deaconess Hospital have proven to be effective procedures in lower extremity preservation with a 5-year primary patency rate of 90%. Secondary patency rates have been shown to be just below 70%. Overall limb salvage has increased to approximately 95%.

Foot ulceration accounts for more hospital days than any other diabetes-related complication. Structural deformities and dynamic deformities in the neuropathic foot need to be accommodated with appropriate shoes or corrected surgically to decrease plantar pressures and reduce the risk of ulceration. Callus formation is an important indicator of underlying deformity and increased plantar pressure, which can lead to ulceration in the neuropathic foot. When present, the underlying etiology must be identified and addressed with the appropriate treatment modalities.

When ulceration is present, adequate vascular supply, absence of spreading infection, good metabolic control, and ability to off-load the area are required in order to successfully treat the ulceration. Probing the ulcer with a sterile instrument to assess the involvement of contiguous bone is important and helps guide therapy. Debridement of the marginal hyperkeratosis is an important part of local wound care. Off-loading techniques using modalities such as total contact casting, felted foam inlays, healing sandals, and walkers are currently being used and evaluated as to the effectiveness in reducing plantar peak pressures and healing of ulcers. When maceration is present, excessive weightbearing is usually the etiology and can be useful in evaluating the success of the off-loading modality.

Infection

Evaluation and management of diabetic foot infections are still based on established protocols including the use of initial empiric antibiotic therapy with subsequent use of therapeutic antibiotics based on accurate culture and sensitivity results. Group A Streptococcus infections have become more prevalent within the past decade because of increases in the strains that produce proteases, which are more destructive to tissues. Necrotizing fasciitis, toxic shock syndrome, and secondary bacteremia have been associated with group A Streptococcus infections. Penicillin is still the drug of choice for treating infection with group A Streptococcus; however, the addition of clindamycin may be added because of its protein synthesis inhibition properties in the presence of an invasive infection.

Microvascular Disease

Wound healing can be considered the body’s attempt to restore tissue continuity and tissue homeostasis in the face of injury. Microvascular function is intimately involved in the process of wound healing by providing nutrients and substrates for repair. In the presence of lowered oxygen tension, wound healing is impaired. Wound healing in the presence of diabetes and peripheral vascular disease, has been shown experimentally to be less mature with the presence of increased numbers of neutrophils and macrophages compared with control wounds. In the presence of TcPO₂ of more than 20 mmHg, wounds matured much more readily.

The functional microcirculation is generally a poorly understood component of peripheral vascular disease. John Tooke, MD, of the Royal Devon & Exeter Hospital in Exeter, United Kingdom, is one of the leading researchers in the area of microvascular disease affecting diabetics. He has demonstrated that in the presence of diabetes, endothelial cell function is impaired through reduced anticoagulant potential, reduced release of platelet inhibitors, relative increase in the release of vasoconstrictors, altered expression of cell-adhesion molecules, and increased production of basement membrane. The endothelial cell is the most significant cell when discussing microvascular disease. It is involved in the limitation of coagulation and clot lysis, the escape of white blood cells from vessels into the wounded area, growth of new blood vessels, regulation of blood flow to the area, provides the fibronectin skeleton, which allows new blood vessels to grow into an area of granulation tissue, and basement membrane formation.

Early hypothesis of hemodynamic abnormalities in the microvasculature in diabetics identified a paradoxical increased pressure and flow that injured the lining endothelium, resulting in excessive formation of extracellular matrix proteins and basement membrane thickening. Using micropuncture of the nail fold capillaries of the hand to evaluate the pressure directly among patients with insulin-dependent diabetes mellitus showed a small but significant increase in the capillary pressure that confirmed this hypothesis. This same process was repeated using the nail fold capillaries in the foot revealing a marked increase in pressure as compared with the hand. This was attributed to a postural vasoconstrictor response abnormality in patients with diabetes. This abnormal postural vasoconstrictive response has been shown to be similar among children with and without diabetes; however, once these children reach adolescence, this response was found to be impaired among young adults with diabetes.

This suggests that there is a limitation of flow reserve that occurs with increasing age. The microvascular blood flow response is impaired with mild injury to the skin, resulting in a reduced hyperemic response. This has been shown to occur in patients without macrovascular disease or neuropathy indicating a microvascular abnormality.

In an evaluation of patients who have noninsulindependent diabetes mellitus at the time of diagnosis, the degree of impairment of this microvascular response observed was equivalent to the impairment seen in patients with insulin-dependent diabetes mellitus for 18 years. This is considered to be related to the development of this impaired vasoconstriction response simultaneously with impaired glucose tolerance, which precedes a diagnosis of diabetes mellitus.

The etiology of this microvascular impairment may be related to basement membrane thickening, which has been shown to be greater among patients with diabetes leading to an inverse relationship between basement membrane thickening and hyperemic response. The role of endothelial cells’ dysfunction has been shown to be impaired by studying the degree of endothelial cell-dependent relaxation of small blood vessels with exposure to acetylcholine in a dose-response relationship as compared with nondiabetic controls.

Neuropathy has been shown to affect the resting capillary pressure in those patients with diabetes. Patients had a higher capillary pressure at rest and a smaller fall in pressure when standing, supporting the hypothesis of capillary hypertension with impaired postural vasoconstriction.

Capillary pressure has been shown to be directly related to glycosylated hemoglobin, although it has been shown that those patients with nephropathy and increased capillary pressures exhibited similar glycemic control as compared with patients without microangiopathy.

Using laser Doppler flowmetry, evaluation of the changes within capillary hemodynamics with glucose regulation showed that as glycosylated hemoglobin values decreased, the vasodilatory reserve was improved over a 12-month period. This was presumed to be caused by basement membrane remodeling and removal of advanced glycosylation end-products. Permeability of the microvasculature has been shown to be increased with diabetes. With better glucose regulation, capillary permeability was shown to improve with the normalization of endothelial adhesion molecules. Continuous insulin infusion for acute glucose regulation has also been shown to increase capillary flow velocity, indicating improvement of microvascular flow with glucose regulation.

Interventional Radiology

The use of interventional radiography has increased the overall understanding of macrovascular disease among patients with diabetes. Carlos Encarnacion, MD, Associate Professor of Radiology, along with Julio Palmaz, MD, Distinguished Professor of Radiology at the University of Texas Health Science Center at San Antonio, have found that there is a similar prevalence of femoral and popliteal vascular disease between diabetic and nondiabetic patients. The tibioperoneal vessels are usually affected in patients with diabetes with the sparing of at least one pedal vessel. The technical success of tibioperoneal angioplasty is 83% to 97% with a clinical success of 83% to 95% for 2-year limb salvage. Iliac stenting using the Palmaz Stent (Johnson and Johnson, New Brunswick, NJ) can be used with failure of angioplasty and tibioperoneal disease with concomitant iliac inflow disease. The clinical success of iliac stenting has been found to be 98.9% immediately, and 86.2% at 48 months. Long-term success was 73% in diabetic patients versus 93% in nondiabetic patients because of the presence of poor outflow.

Charcot Neuroarthropathy

Diabetic neuroarthropathy as seen on plain film radiography is composed of two forms: atrophic and hypertrophic. Atrophic neuroarthropathy is characterized by areas of osteolysis around joints. Hypertrophic neuroarthropathy is characterized by areas of progressive degenerative joint disease, sclerosis, and osteophytosis. Mark Myerson, Director of Foot and Ankle Services at Baltimore’s Union Memorial Hospital, demonstrated that a staging approach in the treatment of the Charcot foot or ankle will increase the overall successful management of the patient. In an acute neuroarthropathy, the treatment is usually nonoperative in nature with prolonged immobilization as the mainstay of the treatment regimen. The goal of treatment is to obtain and maintain a plantigrade foot with an 8-week course of immobilization, which is usually adequate to arrest the acute neuroarthropathic process following a fracture or dislocation. Midfoot neuroarthropathy usually requires 4 to 6 months of immobilization following surgical reconstruction to stabilize. This is evaluated clinically by monitoring skin temperatures with comparison with the contralateral limb to indicate progression to a stable state. Once a chronic stable state is reached, weightbearing can be resumed.

In an acute dislocation, an open reduction and internal fixation with arthrodesis is indicated to stabilize the foot and obtain a plantigrade foot. While primary arthrodesis may be unsuccessful, a fibrous ankylosis is acceptable as long as the joints are stable and the foot remains plantigrade. Eminent skin problems such as ischemia or necrosis are also an indication for surgical stabilization of the acute neuroarthropathic foot. Neuropathic patients with non-Charcot-related ankle fractures should be immobilized for longer periods of time because these patients are susceptible to post-traumatic Charcot episodes. Subacute Charcot feet may possess an equinus deformity. Dorsiflexion of the foot can occur mostly through the unstable midfoot instead of the ankle joint which, in time, may produce a rocker-bottom foot. These feet may require a tendo Achillis lengthening and a midfoot stabilization procedure to produce a plantigrade foot.

The chronic neuroarthropathic foot can be treated effectively with bracing to support the ankle and foot with the aid of walkers or ankle-foot orthoses. Palliative surgery to remove prominences should be performed judiciously in order to avoid precipitation of an acute Charcot event. Skin temperature mapping using a dermal thermometry device can be used as a sensitive clinical indicator of an impending neuropathic ulceration, effectiveness of accommodative shoes and inlay, or to follow the process of Charcot neuroarthropathy. A difference of 3° to 3.5° from the corresponding contralateral site should be considered significant with appropriate off-loading therapy instituted. It is important to understand the arthrodesis rate does not equal limb-salvage rates. Limb salvage is the preferred goal.

Amputations in the Diabetic Foot

The goal is a plantigrade foot. Tendon balancing must be considered with proximal midfoot amputations. Amputation level should be chosen on the basis of likelihood of healing at the most distal aspect of the limb. The transmetatarsal amputation is typically a stable level with usually no need for tendon balancing. Achilles tendon-lengthening procedures may be needed if the foot cannot dorsiflex adequately at the ankle. Short transmetatarsal amputations, Lisfranc’s joint amputations, or Chopart’s joint amputations may require a tendo Achillis tenotomy to maintain a plantigrade foot. With amputation at the Lisfranc’s joint level, the base of the fifth metatarsal can be maintained to preserve the attachment of the peroneus brevis and tertius to inhibit varus deformities.

Equinus and equinovarus deformities may be a long-term result from an amputation at Chopart’s joint because of residual soft tissue investments of the posterior tibial tendon.

High-top shoes with ankle-foot orthoses can be used effectively to accommodate Chopart’s amputations.

Conservative Care of the Diabetic Foot

Insole Materials

Michael Mueller, PT, PhD, Assistant Professor at Washington University’s School of Medicine, St Louis, MO, reviewed off-loading modalities and physical therapy strategies to decrease peak plantar pressures in the diabetic foot. Cyclic loading, heat, and moisture cause changes within the molecular structure of the material and subsequently, the viscoelastic properties. The selection of insole material must incorporate the activity level of the patient, peak pressures developed by the patient, and the service-life expectancy of the material itself. By matching the appropriate durometer and desired characteristic of the insole material with the desired accommodation, plantar peak pressures can be reduced effectively.

To accommodate increased plantar peak pressures, gait-training strategies can be a useful adjunct to reduce the force subjected to the plantar foot. Hipstrategy gait patterns, a step-to-gait pattern, or shuffling gait can be useful in reducing plantar pressures as much as 50% in the place of a normal heel-to-toe gait pattern.

The goal of therapeutic footwear is mainly twofold: protect the foot from injury and maximize functional mobility. Following a transmetatarsal amputation, the accommodation of the residuum becomes difficult in a regular shoe. The lever arm between the shoe and the residuum is unequal allowing rotation of the residuum within the shoe, the heel tends to slip out of the heel counter, and there appears to be increased sheer forces at the distal aspect of the residuum creating the potential for skin breakdown. A total contact insert reduces peak plantar pressure effectively and can be used in a regular length shoe with a rocker bottom placed proximal to the end of the residuum to increase mobility.

Diabetic Footwear

Alan Darby, CPed, presented an overview of diabetic footwear. Proper fitting footwear is essential for the prevention of ulceration. The average step is 26 inches; there are then 2,437 steps to a mile; 12,185 steps in a 5-mile day; a person weighing 160 pounds has exerted 974 tons of pressure on his feet. A parallelism would be a steel hammer weighing 160 pounds pounding the ground at that rate for 4 months would have to be replaced each day and eventually would have to be dug out of the deepest hole on earth at the end of 4 months. Shoes have the right to wear out.

Extra-depth shoes can be made to accommodate a total contact insert by varying the material during manufacture to improve the cosmetic appearance. These types of shoes are expensive without commensurate insurance reimbursement. Rocker soles can be incorporated to reduce pressures at the metatarsal heads. The type of rocker sole should be matched with the type of foot and footwear goal that the patient needs.

Sole flaring can be used to stabilize inversion or eversion excess during gait. Stabilizers can be used to increase the base of support within the shoe with hyperpronation, posterior tendon dysfunction or ruptures, or to increase toe force along the longitudinal or medial aspect of the midfoot. An extended shank is incorporated between the layers of the sole of the shoe and is used in addition to a rocker sole to replace the normal dynamic range of motion required from the metatarsophalangeal joints during gait with a static range of motion from the shoe. A solid angle cushioned heel helps to decrease the force at heel strike.

Sensory Substitution

A digital, electronic gait trainer can be used as a substitute replacement for lost protective sensation. By using auditory signals indicating excessive plantar peak pressure through the use of digital sensors embedded into insoles, the patient with diabetes will be able to detect potentially damaging forces to the feet. With retraining of the patient to rely on substitutional sensory input, alterations in gait can be made to prevent excessive plantar pressures. With continued use, the patient may also be able to identify that portion of the gait cycle that produces increased plantar peak pressure and be able to anticipate a signal and modify his or her gait pattern before it actually occurs.

Hyperbaric Medicine

Oxygen is the controlling factor in wound healing with respect to collagen deposition and neovascularization. In regard to infection control, hypoxic leukocytes will become prematurely activated and have altered priming causing reduced superoxide manufacturing to kill bacteria as well as impaired diapedesis. Despite a completely normal arterial oxygen supply, wound oxygen tensions may be severely diminished because of microvascular disease. Through manipulation of the partial pressure gradient of oxygen between microvasculature and tissue with hyperbaric oxygen therapy, tissue oxygen demands for wound healing can be met. Indications for hyperbaric oxygen therapy include acute or chronic wounds with local tissue hypoxia in a normobaric oxygen environment, a TcPO₂ of less than 40 mmHg, or if the TcPO₂ cannot be elevated above 30 mmHg in an environment of 100% O₂.

Conclusion

The comprehensive team approach to the care of the diabetic foot assumes that the patient is the central figure essential to the reduction of lower extremity complication and attaining the St. Vincent’s Declaration of a 50% reduction in amputations. With the differentiation between vascular disease and neuropathy as the associated factor with pedal ulceration, neuropathy has been shown to be the permissive factor in more than 50% of pedal ulcerations, which means they can be prevented. With the increasing influence of managed care on the overall care of the diabetic patient, chronic disease management models are needed to demonstrate long-term therapy outcomes. These models will ensure the establishment of appropriate care guidelines of the diabetic foot with economic responsibility.

Education is the most powerful tool in the prevention of complications with the feet of patients with diabetes. Identifying risk factors for complications with appropriate intervention and prevention of complications is the basis of appropriate care of the diabetic foot.