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Douglas Richie, Jr, DPM
Clinical Associate Professor, Department of Biomechanics
California School of Podiatric Medicine
Clinical Associate Professor of Podiatric Medicine and Surgery
Western University of Health Sciences
Past President, American Academy of Podiatric Sports Medicine
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Dr. Doug Richie: Hello. I’m Dr. Doug Richie and I’m going to present a three-part lecture discussing one of the most challenging and if not fascinating pathologies which present to the podiatric physician. This three-part lecture will discuss the pathomechanics, the clinical evaluation and finally, the conservative treatment options available to treat the adult acquired flatfoot. One of the dilemmas clinicians face is determining whether a certain feet which appear flat and pronated are truly pathologic. This particular patient certainly shows severely pronated feet with a complete flattened arch. The assumption would be that this foot is pathologic but the reality is that this particular patient age 74 has completed over 50 marathon races and is relatively asymptomatic in his feet. The question is, how can a foot like this function normally while other feet which appear even less flat and deformed are truly symptomatic and pathologic? This first part of the lecture will explore this very question, why do some flatfeet function normal and actually remain pain free throughout life? The adult acquired flatfoot in terms of definition is no longer called posterior tibial tendon dysfunction. The true definition is that the adult acquired flatfoot is a condition resulting from loss of the dynamic and static supportive structures of the arch, the hindfoot and the ankle. If we look at these dynamic structures that support our arch, the first and most important is the plantar aponeurosis functioning through the windlass mechanism to stabilize and actually raise the arch during the propulsive phase of gait. The posterior tibial tendon dynamically contracts and stabilizes the arch. The plantar intrinsic muscles in the plantar surface of the foot are also thought to be important stabilizers of the arch. In static stance, other structures take over to hold up the arch or stabilize the arch. Beginning with the spring ligament complex, the superficial deltoid ligament, the long and short plantar ligaments and again the plantar aponeurosis functions both static and dynamic to stabilize the arch of the foot. All of these structures come into play in the progression of the adult acquired flatfoot. The reason we do not call this disorder posterior tibial tendon dysfunction anymore is the simple fact that rupture of the posterior tibial tendon by itself will not lead to a pathologic progressive flatfoot deformity. This has been shown in multiple studies where cadavers with normal arches have been studied to determine what is needed to make a normal arch go flat. Basically, in these cadaver studies when the posterior tibial tendon is cut by itself and no other structures are cut, a flatfoot deformity does not result. Deland and coworkers were among the first to show this phenomenon where normal cadaveric specimens with normal arches were studied to determine what it took to create a flatfoot deformity. Deland study showed that cutting the posterior tibial tendon by itself would not lead to visible collapse of the arch in the cadaveric specimens but only when these ligaments were cut and all of these ligaments were cut, did visibles change in the arch occur and the gradual movement of the foot into the posterior of an adult acquired flatfoot could actually be documented. The message here is, when a patient presents to clinical practice and reports that there’s been a visible change in the arch of their foot or a dropping of the arch or a flattening of their arch, one has to assume that these ligaments must have undergone attenuation or even rupture in order for the foot to have undergone an observed change.
Myerson’s group has also studied cadavers to determine what it takes to create an adult acquired flatfoot deformity. In these cadaveric specimens where physiologic load is applied to the various muscles of the lower extremity and axial load is applied to the leg of the cadaver. In order to create a flatfoot, multiple structures had to be cut, not just the posterior tibial tendon. The researcher showed that in order to create visible flattening, there is a need to cut the medial structures, including the spring ligament, the plantar ligament, such as the long and short plantar ligament and even the plantar fascia. Researchers in Seattle studied cadavers and created the adult acquired flatfoot model by cutting the posterior tibial tendon and also cutting essential ligaments. But in this study, they reattached the posterior tibial tendon and applied load to the tendon assuming that the flatfoot model would correct itself. Surprisingly, after reattaching the posterior tibial tendon, no improvement of alignment occurred. The researchers concluded that it’s the osteoligamentous structures that are essential in maintaining alignment of the arch and even after restoring function of the posterior tibial tendon, once these ligaments have been lost, you cannot reestablish alignment of the foot by simply reattaching or restoring function of the posterior tibial tendon. The researchers also pointed out that the posterior tibial tendon has its greatest influence on foot function during the heel-rise portion of gait or as we call it the propulsive phase of gait. And it’s during that phase that bracing should provide its essential support of the flatfoot. Other research performed at the hospital for special surgery looked at deltoid ligament strain and also found that it’s during the heel-rise portion of gait that the deltoid ligament undergoes its greatest strain, which seems to follow this function of the posterior tibial tendon where the medial structures are placed under their greatest load during heel-rise or during propulsion. If we look at the posterior tibial tendon and the tibialis posterior muscle, it is a unique muscle, different from the other ankle flexors in that this muscle undergoes two distinct contractions during the stance phase of gait. Early during the contact phase, the tibialis posterior undergoes a lengthening and an eccentric contraction to decelerate hindfoot pronation. The muscle then goes quiet during midstance and then undergoes a shortening or concentric contraction throughout the final portion of the stance phase of gait through propulsion. The shortening contraction of the tibialis posterior is peaking just before heel-rise causing the hindfoot to supinate or invert which allows a very important change to occur in the foot with contraction of the gastroc soleus. If we look at a patient in stage 2, adult acquired flatfoot, the left hand picture shows a hindfoot that is severely pronated and everted. At this point, as the gastroc soleus contracts for propulsion, this contraction of the gastroc soleus actually induces a further pronatory influence on the foot. With functional bracing in the right hand picture that same foot is now restored into proper alignment so that contraction of the gastroc soleus can actually impart a supinatory influence on the entire foot rather than a pronatory influence. Interesting studies have been performed on patients who have undergone transfer of the posterior tibial tendon for what is known as the Bridle procedure. This procedure is performed for patients with drop foot after injury to the common peroneal nerve. Transferring the posterior tibial tendon from the navicular to the dorsal aspect of the midfoot would presumably lead to flatfoot deformity but it actually does not.
In this first study looking at this very question, in a five-year followup, 17 patients who had the Bridle procedure performed did not develop clinical flatfoot and 82% of them could still perform a single foot heel-rise, a test thought to be diagnostic for rupture of the posterior tibial tendon. The question is, why would patients losing their posterior tibial tendon not develop a flatfoot deformity in this study? This research concluded as has been verified with other studies that the progression of adult acquired flatfoot or as they call it, tibialis posterior tendon dysfunction, has a lot to do with other structures in the arch of the foot, such as the ligaments and loss of the tibialis posterior tendon by itself did not lead to flatfoot deformity in these patients undergoing the Bridle procedure. But further evidence into this type of patient with a deficient common peroneal nerve has underscored the role of the peroneus brevis muscle and tendon, which in patients with common peroneal nerve injury there is no function of the peroneal musculature. When these patients undergo a Bridle procedure, they do not develop flatfoot possibly because they do not have the deforming force of the peroneus brevis. These researchers conclude that the pathologic condition associated with posterior tibial tendon insufficiency will not manifest itself if the peroneus brevis function is absent, such as those patients with common peroneal nerve injury. The role of the peroneus brevis is therefore thought to be a deforming force in the progression of the adult acquired flatfoot. Interestingly, researchers have actually proposed transferring the peroneus brevis tendon to remove its influence as a deforming force in the adult acquired flatfoot. If we want to look at the pathomechanics of the adult acquired flatfoot, the current literature and state of understanding follows the scheme of events. It is almost universally accepted that patients with symptomatic adult acquired flatfoot will tell you that they’ve had bad feet all of their life or have had flatfeet all of their life but then more recently something changed where one of their two feet became painful and became more deformed. It is thought that the preexisting flatfoot deformity throughout life causes as we call it increased gliding resistance to the posterior tibial tendon. The position of the hindfoot in a pronated or everted position throughout life unlocks the midtarsal joint during midstance, terminal stance and heel-rise. This unlocked position of the midtarsal joint leads to increased strain on the supportive ligaments as well as the tibialis posterior muscle. This leads to strain overload and eventual attenuation and rupture of the posterior tibial tendon. Once that tendon is lost and loses its protective influence, there is sequential rupture of the spring ligament, the superficial deltoid ligament as well as the interosseous talocalcaneal ligaments. Let’s explore the various steps of this mechanism. Many researchers have pointed out that historically patients with so-called posterior tibial tendon dysfunction have had flatfeet all of their life. Other research particularly, this landmark study published by Holmes and Mann way back in 1992, linked the fact that women are at much greater risk for development of adult acquired flatfoot than men. If you combine the risk factor of simply being a woman with obesity, hypertension and diabetes, you increase the risk or double the risk of adult acquired flatfoot.
It is thought that the tendon of the tibialis posterior is at risk for rupture and unique from all other tendons in the hindfoot simply because a zone of hypovascularity exists from the tip of the medial malleolus distally to the insertion on the navicular. This zone of hypovascularity is a risk factor for rupture. This has been cited many times in studies and reports and evaluation of posterior tibial tendon dysfunction. It was based upon this paper published in 1990 by Frey, et al., where they studied the blood supply of the posterior tibial tendon and found this so-called hypovascular zone. But more recent modern methods of studying the vasculature of tendons has actually disproved the previous Frey study. This study published in 2006, a group of researchers using a more accurate technique to study the vascularization of the posterior tibial tendon, concluded that there is not an area of decreased vascularity as previously described in this tendon. This leads to another theory of why the posterior tibial tendon ruptures and that’s the theory of increased gliding resistance. This has been studied in various cadaveric specimens where a flatfoot model has been created and the friction or gliding resistance has actually been measured in the posterior tibial tendon and it has been shown that as the foot progressively flattens and pronates, load and friction on the posterior tibial tendon increases. The posterior tibial tendon is unique in its location against the distal tibia and medial malleolus. It seems to have a natural friction point at the pulley of the medial malleolus different than the flexor digitorum longus, which is slightly medial and posterior and somewhat protected from friction and gliding resistance. This may be why only the posterior tibial tendon increases gliding resistance as the flatfoot deformity increases. This study verified that notion, published in 2009, looking at the other tendons or the medial tendons of the ankle and determining that increased gliding resistance only hurts in the posterior tibial tendon, not in the flexor digitorum longus and not in the flexor hallucis longus. So if we look at this unique tibialis posterior tendon, we have to appreciate the fact that the insertion of this tendon extends far beyond just the navicular tuberosity, that there are multiple insertions distal to the navicular that may actually be more important. Sarafian shows all of these insertions distal to the navicular, including the peroneus longus tendon and the insertions on the base of metatarsals two, three and four acting as a restraint or a stabilizer of the midtarsal joint. The proximal area of the tibialis posterior muscle has also been studied and it’s quite interesting. This is a bipennate muscle and it’s designed to contract under a very short range and the muscle itself originates from both the fibula and the tibia. If we look closer, researchers have shown that this multipennate origin from the fibula is stronger and more important than the tibial origin. And that the orientation of the muscle itself originating primarily from the fibula allows it a better lever arm to control transverse plane rotation of the tibiofibular unit. The orientation of the fibers are almost transverse rather than linear leading these researchers to speculate that the primary role of the tibialis posterior muscle is to control internal rotation of the tibia.
We must appreciate that the talus is firmly locked inside the ankle mortise and that internal rotation of the tibia drives internal rotation of the talus, which really is the dominant level of the adult acquired flatfoot deformity. If we look carefully at this patient who presents with bilateral flatfeet, we realize that the key difference in the right and left feet is the position of the fibular malleolus on the patient’s right foot demonstrating the marked internal rotation of the tibiofibular unit which is the dominant difference and dominant part of the adult acquired flatfoot deformity differentiating the patient’s right foot which is symptomatic from the left foot which is asymptomatic. Indeed, the adult acquired flatfoot deformity is primarily a transverse plane deformity wherein the transverse plane, the tibia and the fibula shift medially and internally rotate on the calcaneus. Kinematic studies of patients with stage 2 and stage 3 adult acquired flatfoot deformity point out that the access of motion moves into a more vertical orientation leading to marked increased abduction of the forefoot on a range of approximately 20 degrees compared to normal subjects. This underscores the importance of the transverse plane deformity in adult acquired flatfoot. Indeed, gait studies in our own visual evaluation of patients with adult acquired flatfoot shows even during swing phase the marked carriage of the foot into abduction because of a deficient tibialis posterior muscle tendon unit and the right hand picture underscores the power of functional bracing to correct that transverse plane deformity. Next, we’re going to explore the role of the supportive ligaments of the ankle and the hindfoot and how progressive rupture leads to progressive deformity and allows us to stage the deformity in clinical evaluation. The most important ligament is probably the spring ligament as we evaluate the pathology of the adult acquired flatfoot. From an anatomic standpoint, this may be one of the more misunderstood structures in the hindfoot and certainly in adult acquired flatfoot. An excellent reference for all students and surgeons to look at when they do surgery and evaluate adult acquired flatfoot is this article by Davis, et al. published in 1996 where they took 38 fresh frozen cadaver specimens and they performed dissection and they ultimately described very intimate detailed description of the ligament components of the spring ligament and more importantly talked about this relationship between the posterior tibial tendon and its critical role in actually supporting and protecting the spring ligament. Now the spring ligament originally if we look at Grey’s Anatomy was the structure shown in this diagram called the inferior calcaneonavicular ligament. As Davis and coworkers point out in their study, this ligament, the inferior calcaneonavicular ligament probably is the least important structure in supporting the talonavicular joint simply because it does not have any type of contact with the head of the talus at all. The more important structure is what we now call the superomedial calcaneonavicular ligament which lies immediately adjacent to the inferior calcaneonavicular ligament. It is this superomedial calcaneonavicular ligament that has such a key role in restraining the talus, the head of the talus and providing plantar and medial support to the talonavicular joint.
This superomedial calcaneonavicular ligament originates on the sustentaculum tali and it actually has a facet that articulates with the head of the talus. It inserts on the navicular and it has a little sheet of cartilage that cradles the head of the talus. It acts as a sling for the head of the talus during load bearing and during normal function of the foot during gait. So here’s an artist’s drawing from that article from Davis showing the origin of the superomedial calcaneonavicular ligament primarily from the middle facet of the subtalar joint and extending to the navicular with this articular cartilage upon which rest the head of the talus. Notice again how lateral the inferior calcaneonavicular ligament the older so-called spring ligament and its lack of real location and ability to support the head of the talus. This posterior tibial tendon has two attachments superior and inferior literally reinforcing the role of the superomedial calcaneonavicular ligament. Just above it is the superficial deltoid ligament and that too helps restrain the head of the talus and should be considered part of what we called the spring ligament complex and it too becomes attenuated and ruptures in stage 2 adult acquired flatfoot deformity. The superficial deltoid ligament inserts along the entire length of the superomedial calcaneonavicular ligament, helping form a concavity around the head of the talus. The overall function of this complex, which contains four components, creates an acetabulum for the head of the talus. It restrains the head of the talus in both medial and plantar direction. Histopathologic study of these ligament sections showed no elastin and no actual spring in the ligament itself. It should be thought of as an articular sling for the head of the talus but by itself, it cannot hold up the arch alone. Other ligaments contribute greatly to the stability of the human arch. How important is the spring ligament in the progression of adult acquired flatfoot? Several papers and this is one example from Deland performed MR imaging of groups of patients with stage 2 and stage 3 adult acquired flatfoot and they found as we see in this conclusion that ligament involvement is extensive and posterior tibial tendon insufficiency and the spring ligament complex is the most frequently affected. In fact we see spring ligament pathology almost as common as posterior tibial tendon pathology when we performed MRI studies of patients in stage 2 deformity. A similar study published in Journal of Foot and Ankle Surgery in 2014 shows again that with MRI studies of patients with adult acquired flatfoot, pathology within the spring ligament complex is found with equal importance to posterior tibial tendon dysfunction. This almost raises the question instead of using the term posterior tibial tendon dysfunction, should we add the term or substitute the term spring ligament dysfunction? Ligament insufficiency is a big part of the pathomechanics of the adult acquired flatfoot. In part 2 of this presentation, we will explore how we can perform certain clinical test to determine the extent of ligament insufficiency so that we can make proper treatment decisions for our patients with this disorder.