A Guide To Offloading The Diabetic Foot

By Nick Martin, DPM, Tim Oldani, DPM, and Matthew J. Claxton, DPM

   Increased plantar foot pressure is a leading cause of ulceration in the diabetic population.1 Healing these ulcers requires adequate blood supply, control of infection, excellent wound care and offloading or pressure redistribution of the ulcerative area.2-16 Out of all these factors, offloading presents a particularly unique challenge in treating chronic wounds. As diabetic foot care has evolved over the years, podiatrists have used numerous approaches including complete bed rest, cutout felt pads and total contact casting to offload these wounds.3,15,17    However, in order to select an appropriate offloading modality, it is important to be aware of the potential causes of increased plantar pressure in the diabetic foot.    Ground reactive forces (GRF) impact the plantar foot during weightbearing activities in all ambulatory individuals. The difference in response for diabetic versus non-diabetic individuals is our primary concern as limb salvage specialists. Ground reactive forces can be perpendicular to the foot (known as vertical stress) or they can work parallel to the foot (known as shear stress). When these forces work together in a repetitive fashion, ulcers may form on the plantar foot in people with diabetes due to the inability to appreciate the increased stress on the foot.18    When people stand, each foot takes on 50 percent of the body weight. However, when people walk, they transfer all of the body weight from one foot to the other.19 During the stance phase of the gait cycle, the entire foot is only on the ground (foot flat) 23 percent of the time.20,21 The heel is in contact with the ground the first 64 percent of the phase while the forefoot is in contact the last 59 percent of the phase. This means all of the body weight is on one heel or one forefoot a significant period of time. This pressure can equal 1.2 to 1.5 times the body weight depending on the walking speed.19    When a deformity is present, there is increased pressure on the foot. Researchers have shown that diabetes causes a decrease in conduction speed in the tibial and peroneal nerves.22 This correlates to increased lower extremity muscle weakness.22 Muscle weakness may lead to foot deformity and subsequently cause areas of increased pressure.    Greenman, et. al., have shown that small muscle atrophy occurs in the diabetic foot before clinical peripheral neuropathy is detected.23 Using MRI to look at the cross-sectional anatomy of the foot, they compared the muscle area to total area in non-diabetic controls, diabetic patients without sensory neuropathy and diabetic patients with sensory neuropathy.    The diabetic group with no sensory neuropathy developed muscle atrophy before clinical sensory loss. Therefore, structural changes may occur with this early muscle weakness before protective sensation becomes diminished. This muscle atrophy may lead to increased plantar foot pressure even in the “low-risk,” sensate diabetic foot. When coupled with the insensate foot, increased pressure patterns typically lead to foot ulceration.

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