When it comes to diagnosing and treating lower extremity issues in patients with diabetes, a thorough biomechanical evaluation is at the top of the list. More often than not, a current ulcer began as a superficial hyperkeratosis, which unfortunately developed in a patient whose ability to perceive the pain normally associated with such a lesion in a timely manner was compromised due to neuropathy. Progression of the disease not only destroys the protective response but ultimately has an adverse impact on the deep proprioceptors that surround the joints, which may lead to the development of a Charcot deformity.
While we can certainly treat the diabetic foot ulcer, as podiatrists, we also need to be more proactive in working up the patient with diabetes who has not yet developed an actual tissue defect.
Diabetes impacts a patient’s neurovascular status in a significant manner. Specifically, peripheral neuropathy in patients with diabetes mellitus increases the risk of foot ulceration sevenfold and, in turn, contributes to considerable morbidity.1,2 Patients with diabetic neuropathy may have large fiber or small fiber neuropathy. According to Kanji and colleagues, large-fiber peripheral neuropathy often occurs in the insensate foot and patients may be unaware of their condition.3 This is the neuropathy of concern when evaluating gait as it is related to loss of pain and proprioception.
Various researchers have attempted to discover the pathophysiology behind the development of diabetic neuropathy. Multiple studies have concluded that neuropathy is the result of vascular endothelial dysfunction. LaFontaine and co-workers noted that in diabetes, compromised endothelial function has been implicated in microthrombus formation, ischemia, neuropathy, an increased risk of atherosclerosis and hypertension.4
The concept of a hyperkeratotic lesion eventually breaking down into an ulceration due to neuropathy has been well documented. However, in addition to performing a neurovascular exam, analyzing a patient’s gait is critical to understanding the reason behind the callus formation and patterns. According to Lavery and colleagues, pressure sites exposed to repetitive trauma produced during normal walking are predisposed to injury and ulceration.5 A study by Mueller and co-workers showed that analysis of the walking patterns of patients with diabetes may lead to a better understanding of the mechanics of gait and to treatments to reduce the number of injuries in this patient population.6
Key Clues That Signify A Loss Of Proprioception
Proprioception is the sense of the position of parts of the body relative to other neighboring parts of the body. Proprioception signals are carried from stretch and tension sensors in the muscles through the nerves to the brain, and can be interrupted in patients with poorly controlled diabetes.
Patients with diabetes who have a loss of proprioception may have symptoms of falling down while walking. Often, one may find these patients focusing on a distant object for balance or looking down at their feet for visual cues during walking to compensate for their loss of proprioception.
According to Levin and O’Neal, the widely agreed upon role of sensory feedback in gait does not apply to the patient with diabetes.7 Richardson and colleagues found that patients with diabetic neuropathy exhibited increased variability in step width and other gait parameters in poorly illuminated settings.8 They have also demonstrated that challenging environments (irregular surfaces and low lighting) magnify gait differences between older women with and without peripheral neuropathy that are correlated with the severity of peripheral neuropathy.9
Why A Widened Base Of Gait May Be A Warning Sign
Another parameter to consider in patients with diabetes is the base of gait. Brach and colleagues as well as Petrofsky and co-workers noted that patients with diabetes exhibit a wider base of stance in their gait in comparison to non-diabetic individuals.10,11 The base of gait is defined as the distance between the center of the left and right heel during gait, specifically at heel strike of the stance phase perpendicular to the line of progression. The exact increase in the base of gait for patients with diabetes varies with Brach and colleagues reporting an approximate 14 percent increase while Petrofsky and co-workers report a 13.49 percent increase.10,11
Although the exact pathophysiology as to why the base of gait widens in patients with diabetes is not definitively known, it is believed to increase stability and balance during ambulation.10,11 One may see an extension of a widened base of gait whereby the ambulating patient with diabetes begins to abduct both the arms and legs. Children beginning to walk also exhibit these same features, a widened base of gait and abducted arms, in an attempt to increase stability and balance. As their motor skills and nervous system mature and develop, these features typically disappear. The presence of these symptoms in the patient with diabetes should be a warning that his or her diabetic condition is progressing, and warrants increased attention not only from the podiatrist but other members of the multidisciplinary team.
A distinct finding of a widened base of gait is an increased lateral or frontal plane sway when walking. This may be referred to as weight shifting. This sway begins during toe off, occurs initially toward the support limb and then falls back to the swing limb as it becomes ready for heel strike. One may envision it as an excessive push off from the toes but it is a secondary effect of the widened base of gait. Clinicians may experience this phenomenon themselves just by walking with their feet exaggeratedly wide apart.
Why Are There More Diabetic Wounds In The Forefoot And Lesser MPJs? A Closer Look At Biomechanical Factors
So what are some key points that podiatrists should include as part of any screening exam? If one were to look at the percentage of where a majority of diabetic wounds develop, there is clearly an increased incidence of these wounds developing in the forefoot. Furthermore, the wounds also seem to have a predilection for the lesser metatarsophalangeal joints (MPJs).12-14
This is not by accident. The biomechanical changes that occur during the gait cycle convert the foot temporarily into a very efficient shock absorber. Unfortunately, persistent abnormal pronation of the foot leaves the forefoot susceptible to the reactive force of the ground and this can have serious implications for patients with diabetes. This particularly affects the integrity of the first and fifth rays, which are unable to resist the upward force that develops. As these two segments are loaded, the fifth ray is forced into a dorsiflexed, everted and abducted position, and the first ray, having its own axis, is forced into a dorsiflexed and inverted position. What is the result? The development of hyperkeratosis plantar to the second, third and fourth MPJs due to increased pressures.
Propulsive phase pronation in conjunction with feet that demonstrate a high degree of a congenital forefoot adductus often leads to transverse plane deformities of the first MPJ in the way of a hallux abducto valgus deformity. The relatively abducted malalignment of the digits to their respective metatarsals changes the vector of the muscles that collectively are responsible for lesser digit stability, resulting in hammertoe conditions and the like.
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.
Ms. Goldman, Mr. Poonai and Ms. Kamal are third-year students at the New York College of Podiatric Medicine.
Dr. Khan is an Assistant Professor within the Department of Medical Sciences at the New York College of Podiatric Medicine.
Dr. Steinberg is an Associate Professor in the Department of Plastic Surgery at the Georgetown University School of Medicine in Washington, D.C. He is a Fellow of the American College of Foot and Ankle Surgeons.
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