DIABETIC FOOT ULCERATIONS
May 12th, 1995
Stuart E. Levine, MD, and Mark S. Myerson, MD
Abstract
In patients with diabetes, foot ulceration is a major cause of morbidity and hospitalization. Ulceration is a result of a peripheral neuropathy that produces abnormal weight-bearing and decreased sensation. Proper foot care will decrease the risk of ulceration. In the absence of infection and dysvascularity, most foot ulcers heal with nonoperative care involving total contact casting. Surgical intervention is occasionally required to remove infected tissue, improve blood flow, or decrease abnormal pressure distribution.
Introduction
When presented with a diabetic patient with a foot ulcer, the surgeon must establish the cause for the ulcer, determine the extent of the pathology, and devise a care plan that will produce a stable surface on the plantar foot. Although amputation may become necessary in certain cases of ischemia or infection, ablative surgery is rarely necessary for treatment of neuropathic ulceration and is to be avoided: decreased limb length correlates with increased energy expenditure for ambulation{2615} and amputation in a diabetic patient is associated with a 50{2602} to 66%{2599} incidence of contralateral amputation within five years. Therefore, appropriate diagnosis, treatment, and prevention of foot ulcers in the diabetic patient will preserve the patient's quality of life and functional status.
Pathogenesis
Neuropathic ulceration is due to local tissue trauma that results from abnormal distribution of load on the plantar foot surface.{2759, 4113} This abnormal loading results from multiple deformities related to the neuropathy and the decreased sensation that eliminates a patient's ability to perceive the mechanical irritation. Vascular insufficiency is not the cause of diabetic neuropathic ulceration, although ischemia may play a role if the ulcer does not heal despite appropriate care. Neuropathy, whether sensory, motor, or autonomic, plays an important role in the pathogenesis of diabetic foot ulcers,{4113} and 35% of diabetics will develop neuropathy substantial enough to be detected on gross physical examination.{4620}
Sensory neuropathy tends to occur in a stocking-glove distribution, with more distal aspects being more severely affected. The loss of protective sensation in the neuropathic foot allows abnormal stress, or even normal but repetitive stress, to continue to cause tissue injury, resulting in cell death and ulcer formation.{4620, 2610} It has been estimated that at least one half of patients who develop neuropathic ulcerations do so before they notice decreased sensation.{4620} Although decreased sensation plays an essential role in ulcer formation, it will not cause ulceration in the absence of abnormal pressure.
Autonomic neuropathy inhibits skin temperature regulation and prevents normal sweating.{4113} The skin becomes stiff and dry and splits easily, particularly in the stiff plantar calluses,{4389} resulting in fissures. These can propagate into the dermis and become infected.
Motor neuropathy results in intrinsic muscle atrophy, leading to an imbalance in extrinsic and intrinsic muscle control of the toes, causing fixed clawing of the lesser toes. The flexion contracture of the proximal interphalangeal joints can result in dorsal ulceration as the joint presses against the toe box. Hyperextension at the metatarsal phalangeal joint forces the metatarsal head plantarward, resulting in increased pressure and plantar ulceration in this region.{4113}
Increased pressure has been demonstrated under the metatarsal heads in patients with diabetic neuropathy.{2752} This increased pressure may be attributed to fixed claw toe deformity and fat pad atrophy. Often Achilles contracture and midfoot stiffness, particularly if associated with neuroarthropathy, will result in increased forefoot pressure. Correcting an underlying equinus deformity should decrease the abnormal forefoot pressures. Lee et al. (Lee,TH, Lin S, Wapner KL: Plantar ulceration with equinus deformity of the ankle in diabetes: the effect of Achilles lengthening and total contact casting. Unpublished data) have demonstrated a decrease in recurrence of forefoot ulcers with percutaneous tendoachilles lengthening.
Increased callus and corn formation is seen in diabetic patients. The etiology has not been well defined, but it may be due to changes in water absorption or failure of function of the sweat or sebaceous glands.{4619} This hyperkeratosis acts as a foreign body, damaging the dermis below and producing an ulcer.
Other factors, such as hyperglycemic inhibition of wound healing and decreased leukocyte mobilization, may play a role in ulcer propagation and subsequent infection.{4620}
Prevention
The cornerstone of the treatment for diabetic foot ulcers is prevention. On each visit, the clinician should review with the patient the nature of diabetic foot problems. The patient should also be encouraged to perform a visual foot inspection at the end of every day and to present immediately for any change, including blisters, ulcers, bruises, ingrown toenail, swelling, or increased warmth. The clinician should also advise the patient that wearing white socks will facilitate early detection of drainage, that barefoot walking should be avoided as it exposes the foot to direct trauma and imbedded foreign bodies, that insensate feet must not be placed near a radiato a)
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