Emphasizing Proactive Gait Assessment In Patients With Diabetes
- Volume 24 - Issue 4 - April 2011
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While Root identified and thoroughly discussed the classic signs of abnormal propulsive phase pronation of the subtalar joint, the importance of the midtarsal joint and its contribution to the integrity of the longitudinal arch cannot be overly emphasized.15 This becomes extremely important in the case of the patient who has begun to demonstrate signs of a loss of protective sensation since the so-called “compensated equinus” foot deformity ultimately leads to a “rocker bottom” deformity. In this instance, the foot will commonly break down either plantar to the calcaneocuboid or talonavicular joints, both of which collectively form the midtarsal joint.
While “intra-pedal” compensation for an equinus is often employed as a neutralization technique, patients often will alter their gait pattern as another means to offset the lack of sufficient mobility at the ankle to permit normal progression of the body across the foot during mid-stance. Specifically, patients develop an external or abducted gait relative to the forward line of progression. Mechanically, this has the effect of shortening the lever arm of the ankle and the patient will merely “walk over” the medial side of his or her foot.
Unfortunately, one cannot utilize an abducted or markedly, externally rotated gait without consequences. An abducted gait will indeed enable the patient to move his or her trunk forward across the foot. However, this also places the entire medial column of the foot in serious jeopardy since the upward reactive force of the ground is concentrated along an area of the foot that we have previously identified as being innately unstable.
What is the result? An elevatus of the first ray, which in turn affects the ability of the first ray to remain plantarflexed against the ground. As we know, this plantarflexion is crucial since it facilitates a dorsal and posterior shift in the axis of the first metatarsophalangeal joint, which ultimately enables the joint to work smoothly. Any inhibition of this mechanism will result in a blockade of hallux dorsiflexion, known as hallux limitus.
Mechanically, the rotational axis of the first MPJ is then transferred distally to the interphalangeal joint (IPJ) of the hallux. Unfortunately, anatomically, the IPJ was never intended to permit dorsiflexion and, as a result, a shearing force occurs along the medial aspect of the joint. Initially, this results in the development of hyperkeratotic tissue. In the patient with diabetes who has lost the ability to react to the pain associated with this chronic buildup of tissue, this hyperkeratotic tissue can lead to the subsequent emergence of another commonly seen and often difficult to resolve wound.
Although it may be easy to view the patient with diabetes returning for treatment of a painful callus as nothing more than routine foot care, one should never overlook the potentially damaging consequences.
A passive analysis of the patient with diabetes walking from the waiting area to his or her treatment room — and even how he or she progresses into the treatment chair — can reveal subtle yet powerful clues about the stage of one’s diabetes, particularly when it comes to those with long-term or uncontrolled diabetes.
The appearance of an orthopedic deformity should also remind the clinician to look for accompanying biomechanical pathology in the patient as a further exam can reveal previously unnoticed malfunctioning of the foot and ankle. Performing a thorough biomechanical evaluation including a gait exam can connect the abnormal functioning of the foot with the hyperkeratotic lesion pattern. This allows podiatric physicians to understand why the callus is present in the first place and take preemptive steps to prevent any worsening of the condition and hopefully prevent the patient from going down the road of ulcerations and amputations.