Understanding The Biomechanics Of The Transmetatarsal Amputation
Grant and colleagues studied the Achilles tendon specimens of patients with diabetes using electron microscopy and found several abnormalities. These abnormalities included an increased fibrillar density, irregularity of the four individual collagen fibrils, smaller fibril diameters and foci of collagen disruption and disorganization. This results in loss of tendinous elasticity and limited joint mobility.18 Given that intrinsic musculature and the plantar fascia are also sacrificed during a TMA, the foot loses its rigid lever effect during late midstance into propulsion. This causes increased pressures to exert at the distal aspect of the stump.17
Due to the muscular imbalance, decreased joint mobility, deformity and aforementioned gait alterations, many of the measurable gait parameters change and become pathologic. Researchers have hypothesized that the major difference in the gait cycle is an increase in the amount of time the foot contacts the ground during midstance and because of the decreased surface area of the plantar foot in the post-TMA patient, one should expect the total force exerting on the plantar foot to rise significantly.17
Garbalosa and colleagues demonstrated a statistically significant difference in peak mean plantar pressures during the gait cycle when comparing post-TMA feet with intact feet. There was a trend toward higher pressures in the forefoot in post-TMA feet and a frequency of peak pressures occurring mostly laterally and medially with none occurring at the heel.19
In studying patients with diabetes mellitus and TMA, Mueller and co-workers found that they displayed a decreased plantarflexion range of motion, took shorter steps, and walked slower in comparison to age-matched controls.20
Kelly and co-workers found that peak plantar pressures consistently occur at approximately 80 percent of the stance phase of the gait cycle in patients with diabetes and TMA. When it comes to this segment of the gait cycle in these patients, the study authors concluded that one should consider ambulation strategies and shoe gear options to help manage forefoot ulcers.21
Researchers have also shown that patients with triceps surae contractures will transfer pressure distribution from the hindfoot to the midfoot and forefoot, increasing the pressure on the latter by 38 percent and 59 percent respectively.22 The limited mobility at the ankle joint combined with increased peak plantar pressures puts the foot at a considerable risk for tissue breakdown and re-amputation.23 When the mobility of other pedal joints, such as the subtalar joint, are affected, the loss of the shock absorption mechanisms, such as pronation, become amplified.24,25 With continuous microtrauma to the forefoot in patients with peripheral neuropathy, the risk of tissue breakdown becomes a primary concern, particularly to the plantar lateral aspect of the stump.
To compensate for the equinus contracture, the body implements many mechanisms in the foot, knee and hip. When the foot cannot dorsiflex through the stance phase of gait, the tibia cannot move anteriorly over the talus. One mechanism of compensation occurs with early heel lift, which theoretically can induce toe walking.22 The hip flexors must now activate earlier and pull the leg forward during swing rather than rely on momentum that can no longer be generated, increasing energy expenditure.