What clinical screening methods may detect the risk of potential foot problems in a diabetic patient?
If a foot ulcer occurs, what treatment options are available?
How are skin and soft tissue infections of the lower extremities classified and treated in diabetic patients?
How is osteomyelitis diagnosed and treated in diabetic patients?
How is the Charcot foot diagnosed and managed?
What preventive measures may be taken to protect the diabetic foot?
During the past decade, the number of patients in the United States with diabetes mellitus has increased by 50%, from 15.7 million people to 23.6 million people. This rising prevalence is associated with the soaring numbers of the overweight and elderly in the population. Patients with diabetes mellitus are susceptible to peripheral neuropathy, peripheral vascular disease, and foot and ankle ulcers. Approximately 15% of diabetics develop a foot ulcer during their lifetime. Ulcers may heal or may be complicated by cellulitis, abscess formation, osteomyelitis, gangrene, and amputation. The financial burden of a foot ulcer is approximately $28,000 within two years of diagnosis, and the lifetime cost of an amputation is approximately $50,000. Nonhealing ulcers precede amputation in 84% of lower extremity amputations in diabetic patients. The mortality rate of diabetic patients after lower extremity amputation ranges from 11–41% within one year and 39–68% by five years.
Diabetic foot infections usually are caused by direct bacterial invasion from a skin ulcer or a break in the skin barrier, such as from tinea pedis. Other contributing factors include oxidative stress, poor nutritional condition, immunocompromised status, impaired neutrophil function associated with hyperglycemia, and tissue ischemia from vascular insufficiency and inflammation. These factors may contribute to polymicrobial infection commonly noted in the diabetic foot.
Peripheral neuropathy in diabetic patients may cause sensory, motor, and autonomic disturbances that may contribute to the development of foot ulcers. In individuals with normal sensation in their feet, minor injuries cause pain, leading to rest and treatment that promote healing. However, diabetic sensory neuropathy may cause loss of protective sensation. Injuries, including repetitive minor trauma or persistent pressure from poorly fitting footwear, may go unnoticed and evolve to a necrotic lesion. Motor neuropathy causes contracture of intrinsic muscles and secondary claw toe deformities, with increased pressure points on the toes or metatarsal heads. Autonomic neuropathy may cause skin dryness and cracking, allowing bacteria to invade and destroy the subcutaneous tissues.
Charcot neuroarthropathy is another complication of diabetic neuropathy that may contribute to ulcer development. Charcot neuroarthropathy arises from repetitive microtrauma in the absence of protective sensation, leading to macroscopic fracture and joint injury. Furthermore, arteriovenous shunting associated with autonomic neuropathy may contribute to abnormal bone vascularity and associated osteopenia, resulting in increased susceptibility to fracture and joint injury. Damage to the bones and joints may cause collapse of the longitudinal arch of the foot or other foot deformity, resulting in bony prominence, points of pressure, and instability that may result in ulcer.