Diabetic Foot and Vascular Complications

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Chapter 29

Diabetic Foot and Vascular Complications

Despite numerous medical and surgical advances over the past decade, the “diabetic foot” continues to plague patients and providers across the entire spectrum of health care. Foot problems are the most common reason for hospitalization of a diabetic patient, with 15% of the nearly 21 million diabetic patients in the United States developing a foot complication severe enough to require hospitalization during their lifetime.1 Because this small group of people with diabetes (only 7% of the U.S. population) accounts for more than 60% of all nontraumatic lower-extremity amputations,2 public health initiatives have focused on aggressive treatment of the diabetic foot to halt the escalating number of amputations. However, the annual financial costs related to infection, ulceration, and amputation have increased to more than $1.5 billion nationwide despite these widespread efforts.3 Overall, the costs to society are enormous, medically, socially, and economically, and further dissemination of information is imperative to curtail the escalating vascular complications resulting from diabetes mellitus.

Research and clinical practice trends have eliminated many of the previously held misconceptions related to diabetes and vascular complications, and many care providers have successfully adopted the recommended multidisciplinary approach to handle diabetic patients within their institutions. Management of diabetic foot complications requires a thorough understanding of the pathophysiology of the underlying disease, as well as a familiarity with the wide range of therapeutic options currently available. The goal of this chapter is to delve into the current understanding of the diabetic foot and reinforce the most effective treatment strategies for both medical and surgical management.


The origin and physiology of diabetes mellitus were discussed in previous chapters, as were the major complications of retinopathy, neuropathy, and nephropathy. Similar mechanisms underlie complications stemming from the diabetic foot, including ulceration, gangrene, ischemia, and ultimately amputation. Although glycemic control is imperative in diabetes, it is not sufficient to eliminate unwanted complications of the diabetic foot. Furthermore, it is important for clinicians to be aware of the etiologic triad leading to diabetic foot complications (i.e., neuropathy, ischemia, and infection) and to recognize that these may occur in isolation but more frequently occur in combination with one another (Fig. 29-1).


The neuropathy stemming from diabetes mellitus has multiple manifestations within the diabetic foot because it encompasses sensory, motor, and autonomic fibers. Sensory neuropathy affects small-diameter pain and temperature fibers first, and susceptibility to injury is increased because these patients are less sensitive to pressure-related trauma and other minor skin injuries. Motor neuropathy affects the longer fibers that innervate the foot, including intrinsic foot muscles and leg muscles. Atrophy, or muscle wasting, in the intrinsic foot muscles allows the strong flexor muscles to draw up the toes in a “clawed” position, and new pressure points emerge at the tips of the toes and the prominent metatarsal heads. Limited joint mobility from glycation of scleral proteins exacerbates the situation by further changing the normal weight distribution on the foot. Last, autonomic neuropathy causes the skin to become dry through loss of sweat and oil gland function. This dry skin has a markedly increased susceptibility to skin breakdown and fissures, thus creating a portal of entry for bacteria. Additionally, diabetic patients experience a blunted neuroinflammatory response and thus are missing a crucial component of the body’s natural first-line defense against pathogens.4


Diabetic patients typically have an altered response to infectious processes owing to defects in their host immune defense system.5 Wound healing is delayed in diabetic patients as a result of abnormal cellular and inflammatory pathways involving fibroblasts, neutrophils, and advanced glycation end products (AGEs). Glycation is a nonenzymatic chemical reaction whereby sulfhydryl protein linkages are replaced by glucose, causing impairment in normal cellular and tissue functions.6 AGEs increase the stiffness of precapillary vessel walls and contribute to the development of diabetic microangiopathy.7 Furthermore, neuropathic and ischemic deficiencies in diabetic patients predispose them to infection and then unfortunately compound the problem by potentiating infection once a pathogen has been introduced.


Much progress has been made in identifying the cause of ischemia in the lower extremities of diabetic patients, and results have challenged long-standing misconceptions in the literature and in the medical community at large. It is imperative that practitioners continue to reject the “small-vessel disease” theory related to occlusions of the microcirculation, as espoused by a single histologic study in 1959,8 and instead embrace the notion that ischemia results from both atherosclerotic macrovascular disease and microcirculatory dysfunction.9 Diabetic patients typically suffer from tibial and peroneal arterial disease with sparing of the foot arteries, especially the dorsalis pedis and its branches (Fig. 29-2).

Research has shown that diabetes causes structural and functional changes within the arteriolar and capillary systems, notably thickening of the basement membrane. In spite of the thickened capillary basement membrane, no evidence reveals a decrease in capillary luminal diameter.10 A thickened membrane impairs the migration of leukocytes and hampers the normal hyperemic or vasodilatory response to injury, thus simultaneously increasing the susceptibility to injury while blunting the typical manifestations of such an injury.11 Overall, this dysfunction of the microcirculation in diabetic patients creates a functionally ischemic foot despite conditions that represent normal blood flow in healthy patients.

Besides causing specific structural changes in the microcirculation, diabetes also causes a compromise in the overall biology of the foot. When compared with nondiabetic individuals with normal biology, diabetes causes an undesirable shift in the natural balance that exists between stress/ulceration and resistance to stress/ulceration. The diabetic foot thus is more prone to ulcerate under the stress of daily life. Additionally, the presence of neuropathy usually mandates revascularization under conditions of perfusion that would not require revascularization in the absence of neuropathy. In other words, the pathophysiology underlying diabetes creates situations whereby the compromised foot requires even more perfusion than usual to resist ulceration or respond appropriately to injury (Fig. 29-3).

Presentation and Diagnosis

All of the mechanisms described above place the diabetic patient at risk for foot complications, ranging from simple ulcers to severe life/limb-threatening infections or ischemic episodes. As with most diseases, patient education and access to health care are integral to the diagnosis and treatment of these complications. Patients who are aware of their foot care needs are more likely to seek help at the early stages of impending complications, and health care providers who regularly treat diabetic patients are more likely to catch a complication at its inception. To decrease the morbidity and mortality associated with diabetic foot complications, health care providers need to maintain heightened vigilance for these problems before they arise and similarly execute appropriate judgment when making the diagnoses in these patients.


The lifetime risk for acquiring foot ulcers has been estimated at 15% in diabetic patients, with an incidence of approximately 1.9% per year. Additionally, in more than 15% of diabetic patients, ulcers ultimately will lead to amputation.12 According to an American Diabetes Association consensus statement, the risk for foot ulcers is increased in diabetic patients who have had the disease for longer than 10 years, are male, have poor glycemic control, and already have other complications (cardiovascular, renal, or retinal).13 Many ulcers stem from the altered pressures created in the diabetic foot. These foot pressures are influenced by muscle atrophy, obesity, callous formation, other forms of local trauma (including improper footwear), and limited joint mobility. The presence of neuropathy, as was discussed previously, increases the risk for ulcer formation because diabetic patients might not be aware of the damage they are inflicting on their feet through their normal activities of daily living. Furthermore, impaired wound healing and blunted neuroinflammatory responses contribute to progression of the initial ulcer to a potentially more serious vascular complication.

Patients typically present with a wound that fails to heal or with pain at the site of a callus, pressure point, or other bony prominence. Important considerations for foot ulcers include the depth and extent of involvement, anatomic location, origin, presence of ischemia or infection, and clinical signs of systemic infection. Diagnosis of a foot ulcer stems from education and reliability on the part of both patient and physician. A patient must be instructed on the benefit of meticulous foot care and must seek treatment regularly from a health care provider who is familiar with the diabetic foot. Similarly, the health care provider must be learned in the field of diabetes management so as not to miss the sometimes confusing symptoms and signs of diabetic foot complications.


As was discussed earlier, diabetic patients have a blunted neuroinflammatory response and thus do not display the typical physiologic reactions to infection. In fact, the usual manifestations of infection (e.g., fever, tachycardia, elevated white blood cell count) are frequently absent in diabetic patients; therefore, these patients require extra vigilance so that providers do not overlook life-threatening conditions. Unexplained hyperglycemia should prompt an aggressive search for an infectious source in diabetic patients, because the elevated glucose might be the only sign of impending problems.14

Simple inspection of the diabetic foot or a patient’s history alone might not suffice to identify occult infection. Typically, patients will not recognize signs of infection until they smell a foul odor or notice drainage on a sock. At this point, the portal of entry for bacteria has already been well established, and a polymicrobial infection may have overcome the diabetic patient’s blunted host defense system. It is therefore imperative that all ulcers or calluses be carefully probed and inspected, followed by unroofing of superficial eschar to search for potential deep space abscesses. It is not uncommon for practitioners to find unexpected purulent material or necrotic tissue underneath an area of dry crust or dry gangrene. Again, it is important to emphasize that diabetic patients may lack the usual local signs of infection, such as erythema, rubor, cellulitis, or tenderness, and they similarly might not be capable of manifesting the usual systemic signs of infection.

Osteomyelitis occurs after the spread of superficial infection of the soft tissue to adjacent bone or marrow. Although numerous expensive radiologic techniques are currently available to assist clinicians, a simple metal probe usually will suffice. Grayson and coworkers revealed that if this sterile probe hits bone, then osteomyelitis can be diagnosed with a sensitivity of 66%, a specificity of 85%, and a positive predictive value of 89%.15

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