As someone who teaches and writes a great deal about biomechanics, orthopedic and pediatric podiatric medicine, I often discuss equinus influences as among the most destructive on the foot in gait. This critical sagittal plane pathology can occur at any age and comes in congenital and acquired forms. As bipedal locomotion is essentially a sagittal plane event as we move the body forward on a horizontal surface, limitations in sagittal plane motion can lead to destructive compensations that ultimately precipitate pathology.
The most common form of equinus we see is gastroc-soleus equinus with shortening in the muscles that form the conjoined Achilles tendinous insertion into the retrocalcaneal bone. There is a required minimum of 5 degrees of dorsiflexion at the ankle with the knee extended for normal gait and we identify many patients with tightness at this critical juncture.
However, we must remember to evaluate our patients for equinus influences at other levels. These may be proximal to the ankle in the superstructure as well as distal to the ankle within the foot. Hamstring and iliopsoas tightness are examples of equinus influences in the superstructure. Anterior cavus and forefoot plantarflexion deformities are examples of distal equinus. Any sagittal plane limitation or increase in demand for dorsiflexion — similar to what a plantarflexed forefoot creates — leads to compensations in the lower extremity to meet the demands of moving the body over the planted foot to complete a step in gait.
In biomechanics, we teach that joints such as the hip, knee, midtarsal, first ray and first metatarsophalangeal joints (MPJs) are all prime sites for compensation for equinus influences because they all have dominant sagittal plane ranges of motion. This means that our examination of patients should include attempts to identify these influences throughout the kinetic chain and identify compensations in any of these primary sites that may be occurring as a result of these limitations.
Once we identify equinus influences and trace them to compensation sites within the lower extremity, we face a dual mission as clinicians. The first mission is to help our patients make an effort to increase the sagittal plane motion at the site or sites where it is limited by the equinus deformity. This may include shortened stride length, structured stretching regimens, rehab medicine referrals, cross-training and careful shoe gear selection. Patients with more severe conditions may require surgical lengthening of the shortened area.
However, one must make the patient understand that this is an essential part of helping him or her with the chief complaint, even if that complaint is located remotely from the site of the muscle in need of increased motion. The patient may have to learn to avoid certain heel heights and shoe styles that may be contributing to further shortening of soft tissue. A lifetime of wearing high-heeled pumps may be the reason an ankle equinus has developed and continued use of those shoes may work against any effort to stretch that muscle.
The second mission is to identify sites of compensation for the equinus and reduce abnormal positions and motions that may be contributing to symptoms associated with that motion. The classical example of this is plantar fascia complaints associated with excessive midtarsal joint motion as a result of equinus.
We must limit that compensatory motion at these sites through the use of straps, braces, orthoses and shoes to allow an injured part to heal. When we limit the compensatory motions occurring to accommodate equinus, we need to take care to help the patient reduce the strain being placed on the injured part while it heals. This may require the use of heel lifts and careful selection of heel height in shoes (real heel height is the difference in height from the heel to the forefoot) to accompany your efforts to reduce the compensatory motions in the foot that are leading to symptoms. A patient with foot complaints resulting from compensation for equinus would be unwise to walk around in flat flip-flops.
If we fail to do these two missions, then our efforts to control untoward motions occurring in the foot may be met with new symptoms resulting from efforts to fight control of these distal joints as the body requires the necessary sagittal plane motion to complete a step in gait. Failure to “accommodate” the equinus influence while controlling compensatory motions in the foot often leads to failure of those necessary efforts to control the foot. The foot control is required to relieve the symptoms but the patient must be able to tolerate the control or the therapy is doomed to fail.
When I teach on this subject, I am often asked if we are not making the equinus “worse” by prescribing lifts or higher heel heights. My answer is that we must accommodate the tight structures with these measures or our efforts to control the foot will fail. I emphasize that patients should concurrently stretch the tight structures (provided it is not exacerbating symptoms) to relieve the tightness. This takes time and concerted effort on the part of the patient.
Until stretching has yielded results, this combined approach of accommodating tightness while limiting untoward foot compensations causing symptoms is required to successfully manage an acute complaint. The astute clinician gradually manages the precipitating equinus etiology as the primary complaint eases with the use of this combined approach to patient management.