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The medical and surgical management of foot disorders in the patient with diabetes should have as its basis a thorough understanding of the complications and metabolic consequences of diabetes mellitus. This is especially true in the patient who is undergoing a surgical procedure. Diabetes is rapidly increasing in prevalence worldwide and surgery in patients with diabetes is more common. Foot complications are already a major cause of admissions for diabetes, and comprise a disproportionately high number of hospital days because of increased surgical procedures and prolonged length of stay.

The global prevalence of diabetes is predicted to double by the year 2030 from 2.8% to 4.4% (). Of individuals with diabetes, a substantial number will develop lower extremity disease including peripheral neuropathy, foot ulcers, and peripheral arterial disease (PAD). In this chapter, the current epidemiology of lower extremity disease in individuals with diabetes is reviewed with a focus on foot ulcers. Population-based and hospital discharge survey data from several sources illustrate the magnitude of the problem in the United States. Analytic and experimental studies conducted in several countries, which used robust multivariable modeling techniques, are discussed to describe foot ulcer risk factors. The chapter concludes with information on the economic impact of lower extremity disease, primarily diabetic foot ulcers.

Man’s struggle to heal wounds is as old as history itself. As life forms evolved from single cell life to amphibian and finally mammal, the pristine ability to heal by regeneration was lost and thus repairs by inflammation and subsequent deposition of matrix protein (scar) evolved as the method of mammalian healing. This evolutionary change leading to scar (the deposition of collagen) seems to be the key to preventing regeneration. It is well known that when the point is reached on the ladder where regeneration on longer occurs, inflammation and collagen deposition are the difference. In fact, if one takes a form of life, which seems the first link between regeneration and scar formation and a collagen cross-linking inhibitor is fed to the animal, then regeneration will once again occur! If we could only bridge this gap, imagine how successful we could become in the management of diabetic wounds. Although uncertain regarding why this occurred in the evolutionary process, it is hypothesized that as mammals became sophisticated, they needed rapid healing to protect themselves from other predators and to eke out a physical survival in a very hostile environment. In early-recorded history, the Egyptians repaired wounds with primitive suture materials (such as insect claws) and used clean sheets on surgical fields to prevent “suppuration.”; The Greeks, led by Hippocrates, devised methods of treatment for primary wounds and chronic wounds. They used various gauze materials empirically which included wine, milk, honey, and other substances in open wounds similar to our treatment today. Today, one can assign scientific rationale to some of these ancient empirical choices. For example, the complex sugars of honey are known to suppress the growth of Gram-positive bacteria. Wine will suppress pseudomonas proliferation. Milk products may contain cytokines or serve as buffers to control wound pH. Although the ancients had no idea that pus was actually is made up of proteins and dead leukocytes, they understood that drainage of localized products of infection was a good sign (laudable pus). They understood that when signs opf inflammation could not be localized that death would inevitably follow. During the early Roman era, Celsius, unaware of the existence of bacteria, did recognize and describe the cardinal signs of clinical infection being (1) —erythema, (2) —swelling, (3) —pain, and (4) —heat.

Diabetes is on the rise in the United States and the rest of the world, and its complications are even more evident in the aging population. Among the most severe complications of diabetes are impaired circulation and wound healing. The former condition, together with peripheral neuropathy, contributes to an insensate, poorly vascularized lower extremity that is prone to the development of chronic wounds. Lack of sensation leads to aggravation of the injury, which can frequently lead to the spread of infection and the loss of all or part of the lower limb. The circulatory defects occur in both conducting vessels—which are prone to atherosclerosis—and the microcirculation, which shows signs of basement membrane thickening and diminished reparative capacity. Surgical intervention can sometimes alleviate the macrovascular defects, but grafting procedures cannot guarantee that tissue perfusion can be restored. With the exception of the retina, the poor growth of new capillary vessels in diabetes broadly diminishes the capacity to repair.

Acute or chronic injury to an organ is followed by a spontaneous healing process. Injury to the mammalian fetus is reversible during early stages of gestation; the spontaneous wound response is capable of restoring the structure and function of the original organ (regeneration). In contrast, the unimpaired response of adults to severe injury is an irreversible process leading to closure of the injured site by contraction and formation of scar, a nonphysiological tissue (repair). The consequences of irreversible healing at the organ scale are far reaching: they often result in an essentially nonfunctional organ.

Polyneuropathy is one of the commonest complications of the diabetes and the commonest form of neuropathy in the developed world. Diabetic polyneuropathy encompasses several neuropathic syndromes, the most common of which is distal symmetrical neuropathy, the main initiating factor for foot ulceration. The epidemiology of diabetic neuropathy has recently been reviewed in reasonable detail (). Several clinic- (,) and populationbased studies (,) show surprisingly similar prevalence rates for distal symmetrical neuropathy, affecting about 30% of all people with diabetes. The EURODIAB prospective complications study, which involved the examination of 3250 patient with type 1 from 16 European countries, found a prevalence rate of 28% for distal symmetrical neuropathy (). After excluding those with neuropathy at baseline, the study showed that over a 7-year period, about one-quarter of patients with type 1 diabetes developed distal symmetrical neuropathy; age, duration of diabetes, and poor glycemic control being major determinants (). The development of neuropathy was also associated with potentially modifiable cardiovascular risk factors such as serum lipids, hypertension, body mass index, and cigaret smoking (). Furthermore, cardiovascular disease at baseline carried a twofold risk of neuropathy, independent of cardiovascular risk factors (). Based on recent epidemiological studies, correlates of diabetic neuropathy include increasing age, increasing duration of diabetes, poor glycemic control, retinopathy, albuminuria, and vascular risk factors (,,,). The differing clinical presentation of the several neuropathic syndromes in diabetes suggests varied etiological factors.

It has been nearly half a century since the concept of “small vessel disease”; was introduced as a unique entity in the microvasculature of the patient with diabetes. This misconception was arrived at through a retrospective histological study demonstrating the presence of periodic acid Schiff-positive material occluding the arterioles in amputated limb specimens of patients with diabetes (). From these observations, Goldenberg and his colleagues deduced that the deposits in the small and medium-sized arterioles were the hallmark of vascular disease in the patient with diabetes. Perpetuation of this erroneous idea led to the belief that preferential occlusion of the small vessels in the patient with diabetes produced a poorer prognosis with limited revascularization options.

Atherosclerotic peripheral vascular disease in patients with diabetes is a major factor in the progression of diabetic foot pathology. The rate of lower extremity amputation in the diabetic population is 15 times that seen in the nondiabetic population (). A number of factors conspire in the patient with diabetes, each of which synergistically contributes to this extremely high amputation rate. Peripheral neuropathy, infection, microvascular changes, and macrovascular changes all have complex interplay. Peripheral neuropathy leads to structural and sensory changes within the foot, making the limb injury-prone. In addition, once it occurs, that injury is often not easily detectable and heals slowly if at all. Microvascular changes are nonocclusive changes in the microcirculation that lead to impairment of normal cellular exchange, again preventing easy healing. Infection in patients with diabetes can often be aggressive and polymicrobial. Macrovascular disease, atherosclerosis of the peripheral arteries, contributes to poor perfusion of the extremities. Although the underlying pathogenesis of atherosclerotic disease in patients with diabetes is similar to that noted in patients without diabetes, there are some significant differences. It is important to realize that the diabetic foot is more susceptible to moderate changes in perfusion than the nondiabetic foot, resulting in a greater sensitivity to atherosclerotic occlusive disease. Compounding this scenario is the fact that patients with diabetes are noted to have a fourfold increase in the prevalence of atherosclerosis as well as a propensity for accelerated atherosclerosis. This chapter will review the pathobiology and anatomic distribution of occlusive disease in the patient with diabetes, the usual clinical presentation of peripheral vascular disease, and the various diagnostic modalities useful in planning treatment. It will conclude with a diagnostic and treatment protocol that can be used in patients presenting with this multifactorial disease process.

Several methods of measuring and reducing foot pressures including their advantages and limitations have been discussed. Extra-depth footwear, jogging shoes, hosiery, insoles, and orthoses have been shown to decrease plantar foot pressures. Furthermore, these devices can prevent the occurrence and recurrence of foot ulceration. However, when using orthoses or other inserts care must be taken not to increase pressures over another region of the foot.

In the last two decades, the development of intricate computerized systems has revolutionized diabetic foot pressure measurements and made their application possible for daily clinical practice. Foot pressure measurements obtained from out-of-shoe and inshoe methods may have far-reaching consequences for both research and clinical applications. Moreover, these systems can potentially identify at-risk patients and provide a basis for the implementation of either footwear modifications or surgical intervention. Foot pressure measurement systems are still being developed. Currently, research is in the initial phase of developing methods of measuring in-shoe shear forces. Piezoelectric transducers are currently being evaluated which may be able to measure both vertical and shear forces (). In the future, computer systems will hopefully become more widely available and may be employed routinely for diabetic foot management and a variety of foot conditions.

One of the principal functions of the foot is its shock-absorbing capability during heel strike and its adaptation to the uneven surface of the ground during gait. In this function the subtalar joint plays a basic role. The subtalar joint allows motion three planes and is described as pronation (a combination of eversion, abduction, and dorsiflexion) and supination (a combination of inversion, adduction, and plantar flexion) (,). The ankle joint is the major point for controlling sagittal plane movements of the leg relative to the foot, which is essential for bipedal ambulation over flat or uneven terrain (). The midtarsal joint, represents the functional articulation between the hindfoot and midfoot. The inter-relationship of the subtalar and midtarsal joint provides full pronation and supination motions throughout the foot. The first metatarsophalangeal joint (MTPJ) incorporates the first metatarsal head (MTH), the base of the proximal phalanx, and the superior surfaces of the medial and lateral sesamoid bones within a single joint capsule. The main motion of the first MTPJ and the lesser MTPJs is in the sagittal plane (dorsiflexion and plantar flexion). During propulsion the body weight is moving forward over the hallux creating relative dorsiflexion of the first MTPJ. This occurs with the hallux planted firmly on the ground and with the heel lifting for propulsion. The force acting across the first MTPJ approximates body weight, whereas the force across other MTPJs is considerably less (). Maximum loading of the first MTH and hallux is practically at the same time during stance in normal gait, highlighting the importance of the loadbearing function of both the hallux and first MTH.