Diabetes mellitus is among the leading causes of mortality and major morbidity in the United States. It continues to plague society with an additional 800 000 new cases diagnosed each year.1 Consequently, the cost of treating the associated complications such as cardiovascular death, end-stage renal failure, and major amputations has created a growing economic burden on U.S. health care systems. Fifty percent of diabetics will be affected by a manifestation of diabetic foot (neuropathy, ischemia, or infection) and 15% of diabetics will experience a foot ulcer in their lifetime.2,3 Diabetic foot problems are among the leading causes of hospitalization for diabetics; the cost of caring for diabetic foot ulcers is estimated as high as $13 billion annually, a figure that is approximately 27% of the total cost of diabetes care.4 Its seriousness cannot be overstated; 20% of those affected with a foot ulcer will progress to an amputation, a lower extremity amputation rate of 4.1 per 1000 diabetics per year.1,5 This confers an amputation relative risk 40 times greater for diabetics and a reamputation rate of more than 60% at 5 years.3,6
The pathophysiology of the diabetic foot is a multifactorial problem including neuropathy, ischemia, and infection. Treatment is based on a multidisciplined approach and requires control of infection, evaluation of ischemia, arterial reconstruction, and ultimate wound closure.
The diabetic foot is a result of the synergistic derangements affecting the peripheral nerves, peripheral vasculature, and host defenses. The contribution each makes to a particular clinical situation may vary, but the underlying changes in physiology and function of these three systems are chiefly responsible for the cascade of events that lead to an insensate foot, ulceration, bone and joint destruction, infection, ischemia, and possibly limb loss (Figure 42-1).7 An understanding of these primary processes is essential to treating a patient with diabetic foot.
Underlying mechanisms of diabetic foot ulceration. Sensorimotor neuropathy leads to diminished sensation and small muscle atrophy in foot, resulting in flexed metatarsals, metatarsal head prominence, and clawing of toes. Altered architecture of foot, coupled with ischemia and microvascular dysfunction, ultimately leads to ulceration.
Reproduced with permission from Akbari CM, LoGerfo FW. Diabetes and peripheral vascular disease. J Vasc Surg. 1999;30:373–384.
Diabetic Peripheral Neuropathy
An estimated 15% to 50% of diabetics have some degree of peripheral neuropathy.4 The importance of neuropathy as a contributory cause to foot ulceration was confirmed in a large multicenter study from Europe and North America that reported a 7% annual risk of ulceration in neuropathic patients. Previous evidence had suggested that the risk in non-neuropathic patients is less than 1%.8 Diabetic neuropathy is a result of segmental demyelination and axonal and neuronal degeneration. The ...