Dry skin, interdigital fissuring and forefoot plantar hyperkeratosis are all signs and symptoms that may predispose patients to forefoot ulcerations. A diabetic lower extremity examination may seem routine but documenting and addressing these seemingly small changes may deter the devastating effects of peripheral neuropathy. Moisture balance therapy, accommodative shoe gear and routine diabetic foot care remain important factors in the preventative care of the diabetic population.
Essential Principles In Treating Diabetic Forefoot Ulcers
In addition to emphasizing the correlation between gait abnormalities and diabetic forefoot ulcerations, these authors discuss the impact of equinus and motor sensory neuropathy, how diabetes affects wound healing and keys to successful offloading.
There are currently 24 million people in the United States who suffer from diabetes mellitus.1 A recent study estimates that one out of three American adults will be diagnosed with diabetes mellitus by the year 2050.1
With many well documented medical conditions associated with diabetes mellitus, peripheral neuropathy remains the most significant causal factor for complications of the diabetic lower extremity.2 The diabetic population in the United States contributes to the highest percentage of non-traumatic lower extremity amputations, many of which are directly associated with the presence of diabetic forefoot ulcerations.3 The diabetic foot ulcer is among the most destructive complications associated with diabetes mellitus because of the physical, social and economic strains placed upon the patient. Many of these patients experience a considerably decreased quality of life.4,5
The most documented locations of forefoot ulcerations include: the plantar surface of metatarsal heads, digital tufts of the hallux and lesser digits, the dorsomedial aspect of the first metatarsophalangeal joint, and the dorsal aspect of the interphalangeal joints of the lesser digits.6 We strongly believe the incidence and location of diabetic forefoot ulcerations are in direct correlation to the gait abnormalities that occur in patients with diabetes.
Neuropathic gait pattern changes include significantly slower walking speeds, prolonged stance phase, decreased joint movement of the lower extremity (hip, knee, ankle) and higher ground reactive forces, which are most costly in the sagittal and frontal planes.7 Without proper gait analysis and evaluation during the comprehensive patient assessment, ulcer recurrence and treatment failure become more prevalent.
For the purposes of surgical planning and intervention, the podiatric surgeon must address the pathomechanical transformations that occur with neuropathic gait patterns in the presence of plantar forefoot ulcerations.
Johnson and Christensen have described equinus as the “the most profound causal agent in foot pathomechanics and frequently linked to common foot pathology.”8 Ankle equinus is defined as less than +5 degrees of dorsiflexion of the ankle joint with the subtalar joint in neutral position and the midtarsal joint locked with the knee extended.9 Lavery and colleagues determined that non-enzymatic glycation and significant abnormalities of fibrillar density and fibrillar diameter of the Achilles tendon lead to shortening of the gastrocsoleus complex.10,11 These dynamic pathomechanical changes increase peak forefoot plantar pressure in the patient with diabetes three times more than that of non-diabetic patients.10,11 This ultimately leads to the tissue breakdown and ulcer formation. Therefore, addressing the equinus deformity is a crucial component of the algorithm in resolving and healing diabetic foot ulcerations.