A Guide To Preventative Offloading Of Diabetic Foot Ulcers
- Volume 24 - Issue 12 - December 2011
- 10544 reads
- 1 comments
Given the repetitive microtrauma experienced by patients with diabetic peripheral neuropathy, proper offloading is critical to the prevention of diabetic foot ulcers. Accordingly, these authors explore the potential of total contact casts, Charcot restraint orthotic walkers and other offloading devices, and discuss key factors that affect patient adherence.
The diabetic foot ulcer (DFU) that podiatric physicians commonly treat today does not simply represent a local dermal interruption but a clinical manifestation of what is happening systemically among our diabetic population.
The most common causal pathway in the development of the diabetic foot ulcer is repetitive microtrauma.1 The clinical presentation of DFUs arises from unopposed repetitive microtrauma exacerbated by the systemic comorbidities associated with diabetes mellitus including peripheral neuropathy, structural changes and ischemia.2
In 1963, an early offloading publication established that providing equal distribution of plantar pressure throughout the sole of the foot was the principal factor in healing trophic ulcerations occurring in a neuropathic population.3 Yet nearly 50 years later, practical offloading of the diabetic foot ulcer still remains a critical challenge for podiatric physicians.
Up to 50 percent of people with diabetes eventually lose sensation in their feet, which is sufficient for them to injure themselves unknowingly. It is vital to offload these areas but due to patients’ inadequate sensation, they are unable to judge whether they have obtained pressure relief. Plantar pressure is a causative factor in the development of DFUs and ulceration is frequently a precursor to amputations and increases the mortality rate.4
Research indicates that there is a mechanical cause of diabetic ulcerations associated with foot slap secondary to progressive motor neuropathy, demonstrating an increased rate of tissue deformation. Landsman and colleagues show high rates of tissue deformation resulting in elevated intracellular calcium concentrations, leading to cellular death.5
Extrinsic mechanical factors such as abnormal plantar pressure distribution and high plantar pressure contribute to DFUs. Intrinsic factors such as calluses, foot deformities and peripheral neuropathy also play roles.
Skin breakdown occurs with increased plantar pressure and more specifically, peak plantar pressure. Repeated loading of high peak plantar pressure during walking has been associated with skin breakdown although there is no definite threshold that predicts ulceration. One must also consider the duration and repetition of pressures. The rate of spatial change in plantar pressure distribution and the peak pressure gradient may be other markers of skin trauma.6
Contact pressure on the plantar surface of the foot generates local internal forces that cause the subsurface tissue to deform. Breakdown occurs when the foot contacts the ground force, giving rise to distortion of the tissue and the formation of localized tissue damage. The maximum shear stress is vital in the mechanical failure criteria and may predict the tissue injury and skin breakdown.6