1. 
   

   What clinical screening methods may detect the risk of potential foot problems in a diabetic patient?

   
   
2. 
   

   If a foot ulcer occurs, what treatment options are available?

   
   
3. 
   

   How are skin and soft tissue infections of the lower extremities classified and treated in diabetic patients?

   
   
4. 
   

   How is osteomyelitis diagnosed and treated in diabetic patients?

   
   
5. 
   

   How is the Charcot foot diagnosed and managed?

   
   
6. 
   

   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.

When an ulcer occurs, there may be initial bacterial colonization of the wound base. Subsequently, bacterial invasion of tissue may occur with development of overt infection, such as cellulitis, osteomyelitis, septic tenosynovitis, septic arthritis, or abscess. Rapid spread of infection along tissue planes may be facilitated by impaired immune function and poor vascularity. Therefore, a minor abrasion on a deformed toe that was caused by a poorly fitting shoe may rapidly evolve to a limb-threatening septic tenosynovitis, sometimes within one or two days.

Evaluation of the diabetic patient, with or without a foot lesion, includes the history and physical examination, with attention to the foot and ankle (Table 145-1). Guidelines for recommended frequency of screening evaluations and use of protective footwear are based on presence of neuropathy, history of ulcer, and foot deformity (Table 145-2).

History

History includes diabetes control and relevant diabetic complications such as neuropathy and vascular disease. Prior foot ulcers are associated with a high risk of a new foot ulcer or infection. Traumatic injury, even if minor, may cause tissue necrosis leading to an ulcer or initiate Charcot neuroarthropathy. The earliest indication of a diabetic foot infection may be a worsening of blood glucose control, which may precede fever, rigors, and local signs of sepsis.

Physical Examination

Physical examination includes inspection for ulcer, skin cracks, drainage, erythema, nail problems, and deformities (Table 145-3). Sensory neuropathy is confirmed by the absence of sensation upon contact with a 10 gram (Semmes-Weinstein) monofilament. Inspection between the toes may reveal maceration, ulcer, or purulent drainage, especially between the fourth and fifth toes. Erythema, swelling, and increased warmth may be early signs of Charcot neuroarthropathy, but presence of these signs with an ulcer or previous history of an ulcer will increase suspicion for presence of an associated infection. Erythema associated with infection persists during foot elevation, but erythema associated with Charcot neuroarthropathy may decrease when the foot is elevated. Palpable pulses do not exclude the presence of major microvascular disease.