Foot ulcers are the major risk factor for amputation among people with diabetes. Fifteen percent of people with diabetes will experience a foot ulcer. In this particular patient population, 14 to 24 percent will require lower extremity amputation.1 Loss of protective sensation and repetitive mechanical trauma (high foot pressures) are the major causes of diabetic foot ulceration.2,3
As per the ADA consensus report, the plantar forefoot is the most common location for foot ulcers.1 The underlying source of forefoot ulceration is increased forefoot pressure that results from pathologic gait patterns and structural deformity.4,5
So when it comes to prophylaxis of foot complications in the non-ulcerated neuropathic foot and for the cure in the ulcerated foot that cannot be appropriately accommodated externally by shoes and or braces, the goal is to control the foot deformity internally via reconstruction or amputation and accommodation.
The trend in recent years for any elective or non-elective foot surgery has been to focus upon osseous structures in order to maintain the correction. It is well known that soft tissue correction, such as tendon lengthening or transfer as an isolated procedure, will have a high rate of failure due to progressive contracture postoperatively. While osseous procedures are generally required for rigid deformity, it is also true that isolated osseous procedures that do not address soft tissue contractures in diabetic foot surgery will also lead to overall failure.5
While there are tendon balancing procedures that are recommended for the neurologically intact foot as well as the insensate foot, it’s important to have a strong understanding of the role of muscle imbalances as they relate to diabetic foot pathology.
How Muscle Imbalances Come Into Play
Diabetic polyneuropathy is a frequently encountered complication in the lower extremities.6 Polyneuropathy has sensory, autonomic and motor components. Anterior leg weakness and intrinsic muscle atrophy of the foot are the result of motor neuropathy. When peroneal nerve atrophy is present, be aware that is a contributing factor in allowing the posterior muscle groups to gain a mechanical advantage over the weak anterior muscles.7 You may also attribute gait and balance disturbances to the degradation of muscle proprioception.8 Van Gils, et. al., offer an in-depth discussion of the pathological biomechanics associated with the diabetic foot.7
Non-enzymatic glycosylation of soft tissues has also been implicated in diabetic complications, although this was not necessarily limited to the lower extremity.9-11 When researchers examined collagen fibers under electron microscopy, they found that the fibers had increased packing density, decreased diameter of fibers and abnormal morphology of fibrils in the Achilles tendons of diabetics who had concomitant gastroc-soleus equinus. These factors all contribute to tightening and contracture of the Achilles tendon.12 Glycosylation of the flexor tendons of the foot was reported by Ramirez, et. al.13
Cheiroarthropathy, a syndrome of limited joint mobility associated with diabetes, has been observed as a frequent and early complication of diabetes.7 This condition, which is more common in the upper extremities, has been described in the lower extremities as well.14-16 This syndrome has been associated with the other well-known complications of diabetes, including cardiovascular disease, retinopathy and nephropathy.17 Long-term glycemic control, as measured by hemoglobin A1C (HbA1C), demonstrates close correlation with limited joint syndrome. The risk of cheiroarthropathy increases by 250 percent for each 1 percent increase in HbA1C over 8 percent.18
While complications in the diabetic foot may be attributed to different tendinous and bony pathology, equinus and equinovarus foot position are two of the most important and commonly encountered pre- and post-surgical foot deformities. (See “Understanding The Impact Of Equinus And Equinovarus Deformities” on page 66)