Current Concepts In Offloading Diabetic Foot Ulcers
- Volume 22 - Issue 9 - September 2009
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As the prevalence of diabetes mellitus increases worldwide, there will be a concomitant increase in the development of the lower extremity manifestations of the disease process. In the United States alone, there are currently an estimated 24 million patients living with diabetes.1,2 Given the reported 15 percent lifetime incidence for the development of lower extremity ulcerations in this patient population, this equates to approximately 3.6 million diabetic foot ulcers (DFUs).3
Obviously, podiatrists are on the frontlines when it comes to treating ulcerations in these complex patients. It is important for the physician involved in lower extremity limb preservation to be well versed in both the surgical and conservative methods of treatment.
The morbidity and mortality associated with the development of lower extremity ulcerations has been well established, and it is important for the clinician to recognize that greater than 80 percent of all non-traumatic lower extremity amputations are diabetes related.3,4 Those patients undergoing major amputation have a significantly diminished life expectancy. In fact, recent research has demonstrated that the morbidity and mortality associated with major limb amputation are greater than most cancers.5
Assessing The Impact Of Pressure In The Development Of Wounds
Often patients with diabetes present with significant systemic and local factors that lead to the development and progression of lower extremity wounds. A triad of pathology exists whereby vasculopathy, neuropathy and musculoskeletal deformity in the context of increased pressures forces combine in the development of DFUs.6,7
The literature demonstrates that diabetic neuropathy affects up to 50 percent of patients and that neuropathic ulcerations are a primary risk factor for the development of non-traumatic LEA.8,9 Patients with diabetic neuropathy commonly present with a diffuse somatic neuropathy of the distal symmetric sensorimotor type. These patients can present with mixed sensorimotor deficits, pain, paresthesia, hyperesthesia and dysesthesias. These patients often demonstrate proprioceptive deficits, autonomic dysregulation and muscle atrophy. These neurological deficits can combine to contribute to wound development in the context of increased shear and vertical forces.8,10
In addition to neuropathy, the hyperkeratotic wound margins can increase plantar pressures due to what has been termed the “edge effect.”11 When this occurs, the wound margins roll inward, limiting migration toward the center of the wound while simultaneously creating increased pressure forces along the wound periphery. These developments lead to further tissue breakdown.
During ambulation, ground reactive forces (GRF) exert significant force through the lower extremity. These forces can be perpendicular to the foot (vertical stress) or they can be parallel to the foot (shear stress). When working together, vertical loading and shear forces can cause repetitive stress to the tissues and lead to ulceration. This is of particular concern in those patients who suffer from diabetic neuropathy and have lost the “gift of pain.”12
When considering the transmission of forces in the lower extremity, one must consider the gait cycle.13 During the gait cycle, research has demonstrated that the pressure imparted through one foot can be 1.2 to 1.5 times the patient’s body weight.14
When a skeletal deformity exists, pressure can also be higher due to the development of boney prominences. Commonly, this skeletal deformity is a consequence of intrinsic muscle atrophy due to peripheral motor neuropathy.15 Often, these foot deformities present prior to the development of sensory neuropathy symptoms in what were previously described as “low-risk” patients. In fact, the American Diabetes Association (ADA) has now included foot deformity as a risk factor in its Foot Risk Classification system.3