Key Clinical Questions
What clinical screening methods may detect the risk of potential foot problems in a diabetic patient?
What treatment options are available for a foot ulcer?
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 treated?
What preventive measures may be taken to protect the diabetic foot?
During the past decade, the number of patients in the United States with known diabetes mellitus has increased by 38%, from 15.2 million people (2004) to 21 million people (2014). This rising prevalence is associated with 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% 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 2 years of diagnosis, and the lifetime cost of an amputation is approximately $50,000. Diabetic patients with foot ulcers are susceptible to amputation and death. Nonhealing ulcers precede 84% lower-extremity amputations in diabetic patients. The mortality rate of diabetic patients after lower-extremity amputation ranges from 11% to 41% within 1 year and 39% to 68% by 5 years.
Diabetic foot infections usually are caused by direct bacterial invasion from a skin ulcer or break in the skin barrier, such as from tinea pedis. Other contributing factors include oxidative stress, poor nutrition, impaired neutrophil function associated with hyperglycemia, and tissue ischemia from vascular insufficiency and inflammation.
Peripheral neuropathy in diabetic patients may cause sensory, motor, and autonomic disturbances that increase the risk of developing 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 leads to loss of protective sensation. Injuries, including repetitive minor trauma or persistent pressure from poorly fitting footwear, may go unnoticed and evolve into necrotic lesions. Motor neuropathy causes contracture of intrinsic muscles and secondary claw toe deformities, with the development of 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 may also contribute to ulcer development in diabetics. 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 osteopenia, resulting in increased susceptibility to fracture and joint injury. Damage to the bones and joints may collapse the longitudinal arch of the foot, leading to bony prominences, pressure points, and instability that may result in ulcer.