Complete the 4 steps to earn your CE/CME credit:
CPME (Credits: 1)
PRESENT eLearning Systems, LLC is approved by the Council on Podiatric Medical Education as a provider of continuing education in podiatric medicine.
PRESENT eLearning Systems, LLC has approved this activity for a maximum of 1 continuing education contact hours.
Release Date: 03/16/2018 Expiration Date: 12/31/2020
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
To view Lectures online, the following specs are required:
It is the policy of PRESENT e-Learning Systems and it's accreditors to insure balance, independence, objectivity and scientific rigor in all its individually sponsored or jointly sponsored educational programs. All faculty participating in any PRESENT e-Learning Systems sponsored programs are expected to disclose to the program audience any real or apparent conflict(s) of interest that may have a direct bearing on the subject matter of the continuing education program. This pertains to relationships with pharmaceutical companies, biomedical device manufacturers, or other corporations whose products or services are related to the subject matter of the presentation topic. The intent of this policy is not to prevent a speaker with a potential conflict of interest from making a presentation. It is merely intended that any potential conflict should be identified openly so that the listeners may form their own judgments about the presentation with the full disclosure of the facts.---
Douglas Richie, Jr, has nothing to disclose
Male Speaker: Part 2 of this presentation will now focus on the clinical evaluation of patients presenting with adult acquired flatfoot deformity. Much of this evaluation process focuses on the detection of ligamentous insufficiency and its role in the staging of the adult acquired flatfoot. It’s interesting that today, most clinicians still rely on the classification of adult acquired flatfoot originally proposed by Johnson and Strom in 1986 and later modified by Myerson. This particular classification system was proposed and described long before any of these elegant cadaveric studies which have just now been presented to you, showing greater insight into the biomechanics, the pathomechanics and the pathoanatomy of this deformity, involving much more than just the posterior tibial tendon. Since this classification is so commonly used, we’re going to present it here and then expand upon it with better detailed classifications that have been proposed later. What a patient with Johnson and Strom stage I posterior tibial tendon dysfunction presents, the clinical presentation is really nothing more than a painful swollen tendon of the tibialis posterior on the medial aspect of the ankle. The deformity, so to speak, is poorly described in this classification but tends to be a flatfoot which is flexible and reproducible. A critical change occurs in stage II deformity, where now there’s visible difference between the right or left feet in the sense that this symptomatic foot shows visible collapse of the arch. The patient may show significant abduction of the forefoot and may not be able to perform the single foot heel-rise test. Johnson and Strom said that in stage II, there is actual attenuation or rupture of the posterior tibial tendon that led to these clinical findings. We will show you in a few minutes why this was shortsighted. It is emphasized that in stage II, the deformity is still flexible. In stage III deformity, there has now been a complete rupture of the posterior tibial tendon and deformity of the affected foot has worsened. The patient’s symptoms move from the medial aspect of the ankle to the lateral aspect, where compression of the subtalar joint or pressure of the calcaneus against the fibula creates lateral ankle pain. The critical differentiating feature of stage III compared to stage II is that stage III deformity is rigid. Myerson described a stage IV deformity where due to rupture of the deep deltoid ligament, a valgus rotation occurs within the talocrural joint, again, the deformity is rigid and nonreducible. The question is looking at a foot being flexible and reducible and determining stage II versus stage III is often difficult because patients present with variations of rigidity and flexibility. We actually need more objective criteria for staging deformity and making clinical decisions. More recently, a group of academic foot and ankle orthopedic surgeons gathered and proposed a classification system for adult acquired flatfoot that relied on more objective criteria, measurement and evaluation and breaking down the deformity into substages. This classification system begins with stage I, similar to Johnson and Strom, where there is tenosynovitis without deformity. This tenosynovitis can be due to autoimmune or inflammatory disease, not just due to mechanical overload. Patients may also present with a partial tear of the posterior tibial tendon, but have not undergone any type of visible deformation of the hindfoot.
Other patients may show hindfoot valgus and a slight deformity, but generally there’s not a lot of asymmetry separating the right or left feet. In stage II adult acquired flatfoot, we realized many years looking at this progression of deformity that subclassification is necessary in this broad category of stage II. In stage II A, the patient has a reducible hindfoot valgus but there is no evidence of what we call forefoot supination. In this newer classification system, it is critical and important that the researchers proposed the importance of evaluating the forefoot supinatus or forefoot supination deformity that occurs as the adult acquired flatfoot progresses. Stage II B recognizes a flexible forefoot supination. As the hindfoot is moved from valgus to neutral, it becomes evident that the forefoot has a varus deformity, which is flexible. It is also known that as the ankle is plantarflexed in the off weightbearing position, the forefoot supination reduces and we’ll show you a picture of this in a few moments. In stage II C, this forefoot varus becomes fixed and nonreducible. Even though the hindfoot is corrected and the ankle is plantarflexed, we do not see forefoot supinatus reduced. In stage II D, a forefoot abduction deformity occurs usually in conjunction with a varus or supination deformity of the forefoot as well. This is primarily a radiographic finding, visible on either the anterior, posterior or lateral x-ray where we will see gapping at the joint surface of the first metatarsal medial cuneiform joint. A final stage II E subdivision is described where there is “medial ray instability.” In this particular phase of deformity, there is instability along the entire medial column at the various joints of the first ray, whether it’s at the first metatarsal medial cuneiform joint, the medial cuneiform navicular joint or even at the talonavicular joint. You will see sagittal plane breakdown across the entire medial column. Stage III deformity has been previously described and is generally described similar in this newer classification where there is a rigid nonreducible hindfoot valgus and certainly the presence of these forefoot deformities described in stage II. In stage IV deformity, there is a flexible ankle valgus or a rigid ankle valgus. But in either case, the detection of the ankle valgus deformity is radiographic. It is primarily the result of rupture of the deep deltoid ligament. Another interesting classification system was described in the Journal of Foot and Ankle Surgery in 2011, where a group of radiologists and orthopedic surgeons at Johns Hopkins University Medical School combined their insight and talents to use MR imaging detecting levels of ligamentous rupture in classifying the progression and staging of the adult acquired flatfoot. With proper MR imaging, we can pick up not only pathology within the posterior tibial tendon as shown in these images but we can also begin to detect pathology within the spring ligament as well as various other ligaments of the hindfoot and the ankle.
Based upon these four stage classification system, we will see a combination of clinical findings combined with MR findings and even treatment options that are proposed for the various stages. This is a very interesting article to review and read, not necessarily suggesting that we have to do MR imaging on all of our patients to stage the adult acquired flatfoot but more or less, reaffirming the importance of determining ligament instability or rupture and the role of ligament rupture in the progression of adult acquired flatfoot. We have found that there are certain clinical tests that are quite accurate, easy to perform, and will many times give us a very good assessment of ligamentous rupture and staging of the adult acquired flatfoot without the need for performing more expensive MR studies. These tests which are about to be described are well-known tests previously described in the medical literature but put together provide a nice paradigm or protocol for evaluating the patient who may present for the first time to the clinic complaining of a painful flatfoot deformity. The clinical examination of the patient with adult acquired flatfoot should actually begin in the weightbearing situation or in closed kinetic chain. As we first look at the patient standing in the clinic or in the hallway, we immediately see the typical presentation of unilateral deformity since this condition almost always presents unilateral. As we stand behind the patient, we see the accentuation of an everted calcaneus on the left foot which is the symptomatic foot. But we also see some other telltale signs. Look at the height of the medial malleolus of the left ankle compared to the right. The dropping of the medial malleolus as the hindfoot moves into valgus at not only the subtalar joint but at the ankle joint. Look at the forefoot relative on the left foot to the right foot. This is a classic presentation of the so-called too many toes sign, where on the symptomatic foot, significant abduction of the forefoot on the rearfoot reveals more toes on the symptomatic foot than the asymptomatic foot. We can use radiographic evaluation to verify what we see clinically, the dramatic medial shifting of the talus over the calcaneus as the transverse plane part of the deformity becomes accentuated. But before we go into that, we’re going to look more at what we can see clinically. Often, we can get a better appreciation of the patient’s deformity by looking at the patient from the front or from the anterior view. As we look at this patient with what appears to be bilateral symmetrical flatfoot deformity, there is actually a difference between the right and left feet. The right foot is more symptomatic, in fact, it is the symptomatic foot. The difference then in feature is the lateral malleolus. Look at the marked difference between the positioning of the lateral malleolus on the right foot compared to the left foot and appreciate that the lateral malleolus is anteriorly displaced indicating a marked internal rotation of both the tibia and the fibula in the right foot compared to the left foot and the significant transverse plane deformity that results with internal rotation of the tibia and abduction of the forefoot, which is more accentuated in the right foot than the left foot. This patient shows a less accentuated positioning of the fibular malleolus but on her left foot. The lateral view or the lateral malleolus is more anteriorly displaced on the left foot than the right foot and there is certainly more bulging of the navicular and the talonavicular joint on the left foot compared to the right.
If we want to stage the deformity, we want to look for the ability of the clinician to reduce the deformity and determine the level of flexibility. This would differentiate a stage II from a stage III. To assess this, we have the patient stand and then with verbal command or with palpation, we invert the hindfoot. If we can invert the hindfoot and correct the subtalar joint to a neutral position, that deformity would be considered flexible and reducible, and therefore is a stage II and not a stage III or stage IV. While the patient is standing, the next clinical test is performed which is known as the Hubscher maneuver. In a healthy patient, the Hubscher maneuver activates the windlass mechanism and we will see the arch of the foot raised and we will see the tibia externally rotated. That same patient lifting the hallux, plantarflexes the first ray, raises the arch and we will note that the marker on the tibia has become more externally rotated. This was thought to be a test simply measuring and validating the effectiveness of the windlass mechanism and the integrity of the plantar aponeurosis. If we take a patient with adult acquired flatfoot on their asymptomatic left foot, we lift the hallux and an arch is established and the tibia externally rotates. When the Hubscher maneuver is attempted on the patient’s symptomatic contralateral foot, the hallux is difficult to raise off the ground manually and there is observed no change whatsoever in the height of the arch and there is no rotation of the tibia external. This is a Hubscher maneuver that has failed or unable to be performed on the patient’s symptomatic adult acquired flatfoot. The question arises, why do patients with stage II adult acquired flatfoot have a negative Hubscher test? Is it due to an attenuation or rupture of the plantar fascia? Because that’s what the Hubscher maneuver is thought to activate or verify. It’s interesting that studies done on patients with stage II and stage III adult acquired flatfoot actually do not show involvement of the plantar fascia. Of all the ligaments that appear to rupture in adult acquired flatfoot deformity, the plantar aponeurosis is probably the least likely to be involved, whereas the spring ligament, the long and short plantar ligaments are much more likely to be involved. As Deland pointed out, there are questions to be raised from biochemical models and previous studies that were shown in this presentation where the plantar fascia had to be released in order to simulate adult acquired flatfoot deformity. While we know other ligaments do rupture with adult acquired flatfoot, it does not appear that the plantar aponeurosis actually does rupture or attenuate. When we take a patient with stage II deformity as we see here and we try to lift the hallux off the ground, there is no raising of the arch and no external rotation of the tibia. This is not because the plantar fascia is ruptured, it is most likely because the spring ligament and perhaps the long and short plantar ligaments have ruptured and there is no ability of the windlass mechanism and the raising of the hallux to actually raise the arch of the foot. The next test that we are going to perform while the patient is standing on their feet in the clinic is probably the most recognized gold standard test for rupture of the posterior tibial tendon. Numerous authors have recommended performing what is known as the single foot heel-rise test to detect partial or complete rupture of the posterior tibial tendon.
In this test, a healthy subject, with all of the weight on their healthy single foot, should be able to raise up on the ball of the foot, lifting the heel four to six inches off the floor. As the heel raises of the floor, the hindfoot, when viewed from behind, should be noted to invert or supinate during the heel-rise test. Now, it has been speculated that when the posterior tibial tendon is attenuated or ruptured, there is an inability to perform the single foot heel rise test. It raises a question really about what this test actually detects. If we look at the function of the tibialis posterior muscle and the tendon of the tibialis posterior, from a mechanical standpoint, we must ask, is it really a plantarflexor of the ankle or is it simply a supinator of the foot, or as shown earlier, a restraint to internal rotation of the tibia? Well, there have been several biomechanical studies that have looked at the role of the medial and posterior leg muscles and their role in normal standing and walking. In terms of the subtalar joint and the ability to supinate the subtalar joint, we can see that the tibialis posterior has the strongest supination moment arm of all of the muscles in the lower extremity and therefore, it is the most powerful supinator. It also has the shortest excursion range during contraction of all of the muscles of the lower leg. This is why just a few millimeters of stretch or attenuation in the tibialis posterior leads to significant loss of power and function compared to other muscles particularly the gastroc soleus. When it comes to ankle plantarflexion and extension, the tibialis posterior has the slowest moment arm for plantarflexion of the ankle. It is the weakest plantarflexor of the ankle. If we look from an anatomic standpoint and look at moment arm or lever arm, the distance of the tibialis posterior tendon to the ankle joint axis is relatively a few millimeters, whereas the lever arm for the tendo-Achilles is at least 10 to 15 centimeters. We clearly see from a mechanical standpoint that the posterior tibial tendon has no moment arm and no ability to actually plantarflex the ankle. Yet when it ruptures, patients cannot actively plantarflex their ankle and perform the single foot heel-rise test. Why is that? If we look at the single foot heel-rise test, it isn’t just a plantarflexion of the ankle in closed kinetic chain. If we look at the foot from the side during a single foot heel-rise, we appreciate that the ankle is plantarflexing and the entire foot as one rigid body is plantarflexing across the heads of the metatarsals, or the foot is plantarflexing across the metatarsophalangeal joints. This is made possible by the transfer of plantarflexion moment through the foot to the metatarsals. It is made possible because the foot itself is stable, the arch is stable, and there is relatively minimal movement across the multiple joints of the hindfoot and the midfoot. When we lose the posterior tibial tendon and we are unable to perform a single foot heel-rise, there are other events that have occurred that caused the patient to lose this ability. Certainly, the tibialis posterior must invert the hindfoot.
But as it inverts the hindfoot, it maintains the locking, so to speak, across the midtarsal joint. With loss of the tibialis posterior muscle and tendon, the midtarsal joint becomes unlocked and we have increased flexibility of the midtarsal joint. This has been described in multiple gait studies performed on patients with adult acquired flatfoot. Viewed from the side in measuring sagittal plane motion, we will see excessive plantarflexion of the hindfoot across the midfoot with observed lowering of the medial arch and dorsiflexion of the first ray. This is very elegantly demonstrated, whenever we look at a patient attempting to perform the single foot heel-rise test when viewed from the side and the patient attempts to rise up on the ball of the foot. If they have an unstable midtarsal joint, you will see a flexion occur across the talonavicular joint medially and dorsally as instability is illustrated with excessive plantarflexion of the rearfoot on the forefoot across the midtarsal joint. This locking mechanism, which is normally intact with healthy patients becomes an unlocking mechanism particularly when the tibialis posterior tendon has ruptured. We will see patients demonstrate this while they’re walking and we will see this when patients are observed during the single foot heel-rise test. The more unstable the midtarsal joint becomes, the more difficult for the patient to perform the single foot heel-rise test. As the rearfoot plantarflexes across the midtarsal joint, leverage is lost and the entire foot cannot lift off the ground. If we take the patient illustrated and demonstrated in my opening slides that had a severe flatfoot deformity, I mentioned that this patient had run over 50 marathons and had relatively pain-free feet. I asked if there was a difference between that patient’s foot and asymptomatic adult acquired flatfoot. If we look at this healthy patient performing a single foot heel-rise, we see that the patient has no difficulty whatsoever and there is no breakdown across the midtarsal joint. This patient has a flatfoot but it’s a stable flatfoot. He has a stable midtarsal joint with no sagittal plane instability. He is able to easily accomplish the single foot heel-rise and he is able to function normally in life with a good stable yet flatfoot deformity. We are now going to describe some tests that are done with the patient in the exam chair, off weightbearing. The first test we perform is a simple test for manual muscle testing to detect either weakness, attenuation, or rupture of the posterior tibial tendon. This test is almost as accurate as performing an MRI and it’s quick and easy to perform in the office setting if it’s performed properly. The patient is seated in the exam chair with the ankle hanging off the edge of the exam table. The examiner must carefully place their thumb against the medial half and plantar half of the first metatarsal head. At this point, the patient inverts their foot against resistance. Here is the patient with the foot hanging off the end of the exam table and an imaginary circle is drawn against the head of the first metatarsal. This allows us to choose the bottom half of the first metatarsal head, upon which to place the examiner thumb. The examiner pushes the thumb and pushes the patient’s foot into full range, end range eversion. At the end of this eversion, the patient is asked to push against the examiner’s thumb or to actively invert their foot. As the patient pushes with full strength against the examiner’s thumb, both the patient and the examiner will gain an appreciation for the strength of the patient to perform the test.
Do not perform the test with the foot supinated because if the test has begun in this direction or this alignment, you will see from the picture the bowstringing and activation of the tibialis anterior tendon. This adds a false grade of strength to the tibialis posterior and gives a false contribution of inversion strength not solely due to the tibialis posterior. When performing the test, you always compare to the contralateral foot and the patient and the examiner can usually easily determine a loss of even one grade of strength, indicating pathology in the tibialis posterior. To illustrate again the proper performance of the test, the patient sits with the foot hanging off the end of the table, the ankle is plantarflexed and the examiner pushes against the bottom half of the first metatarsal head moving the foot into end range eversion. At that point, the patient is asked to push their foot against the thumb of the examiner with all of their strength. The comparison is made to the contralateral foot. Another test which is interesting to perform both on and off weightbearing is known as the first metatarsal rise test, originally described by Hintermann in 1996. This test was found to be positive for detecting a rupture of the posterior tibial tendon in all 21 feet tested with both MR and first metatarsal rise. The test basically observes that in any healthy foot, when the foot itself is supinated in a weightbearing position, the first metatarsal always stays on the ground while the arch raises off the ground. But in an unhealthy foot, such as on the right hand side of the top picture and the right hand side of the bottom picture, as the foot is supinated, either by externally rotating the tibia or inverting the calcaneus, the first metatarsal does not stay on the ground but actually rises off the ground. Hintermann again found that this test was extremely accurate in detecting rupture of the posterior tibial tendon. Here we take a patient who has a flatfoot but when we externally rotate her tibia, the flatfoot has a slight arch and the first metatarsal stays on the ground. If we take their symptomatic ruptured posterior tibial tendon and externally rotate the tibia, indeed, there is no arch that is established and the first metatarsal rises off the ground. Often, you will see the hallux plantarflex or curl to the ground on the symptomatic foot during the first metatarsal rise. If we take another patient and instead of externally rotating the tibia, we invert the hindfoot, we note the first metatarsal rise detecting rupture of the posterior tibial tendon. Now we’ve later determined that this test is not just a rupture of the posterior tibial tendon but it’s really detecting the presence of a forefoot supination deformity. It’s an excellent detector and demonstration of that deformity. It helps us differentiate a flexible versus a fixed forefoot supination deformity, type B or C stage II adult acquired flatfoot. In this patient with symptomatic adult acquired flatfoot, when we correct the hindfoot to neutral, we see a forefoot varus or supination alignment. When we push down on the first ray, the deformity is reducible.
If we push down on the first ray and it will not move back down to the floor, that’s known as a rigid or nonreducible supination deformity. It is thought that the forefoot supination deformity can be visualized in the exam chair with the patient seated supine. If we carefully orient the hindfoot into neutral, we can see an inverted plane of metatarsals 1 through 5. As we plantarflex the ankle, the deformity reduces. This is detecting the reducibility of deformity in the exam chair rather than in a standing position. This is a photograph of a patient standing with bilateral pronated subtalar joints and supinated midtarsal joints. Yes, if we look at these feet from behind, the entire foot looks pronated but we must appreciate that there are certain movements within the foot that have occurred in this compensated position of the subtalar joint fully pronated to end range eversion. Off weightbearing, when the foot is moved to full pronation at the subtalar joint, the heel and the forefoot move equally in the direction of eversion. But when that foot is placed on the ground and the subtalar joint pronates and everts, in order for the forefoot to remain on the ground, the forefoot must supinate to an equal and opposite direction of inversion while the heel is moving into eversion, or the subtalar joint is moving into eversion. Otherwise, that foot placed on the ground would have the lateral column, the fourth and fifth metatarsals everted off of the ground. In order to see a foot where all the metatarsals are balanced on the ground and bearing weight, an everted rearfoot must have an inverted forefoot. That is the compensatory supination of the forefoot that occurs when there is a pronated flatfoot deformity. This reciprocal pronation of the rearfoot and supination of the forefoot is an observation that was actually made many years ago. Forefoot supinatus or supination deformity is an acquired forefoot varus. It is not a congenital deformity of forefoot varus which we have been taught from Root biomechanics theory. It is an acquired deformity that occurs after rupture of the posterior tibial tendon. It was Steindler back in 1929 in the Journal of Bone and Joint Surgery that described this supinatory, compensatory torsion that occurs in the forefoot and seen in a pes valgus or flatfoot deformity. Steindler talks about this supinatory position, which is really a counter pressure balancing of the forefoot when the rearfoot moves in to eversion and the forefoot remains balanced on the ground and accepting weight equally across all five metatarsals. Detecting or measuring the degree of forefoot supination or supinatus deformity is not always that easy. But if we look at this lateral weightbearing radiograph of a patient with adult acquired flatfoot, we can see the breakdown of the medial column or the dorsiflexion of the first ray relative to the talus. This is actually depicting a supination deformity of the forefoot on the rearfoot. Because as the first ray dorsiflexes, it does so as part of the supination compensation or inversion of the forefoot on the rearfoot as the hindfoot everts progressively during stance and during gait.
The degree of supination deformity actually dictates our treatment options, not only in the nonsurgical but the surgical correction of the adult acquired flatfoot. If we go back to the classification system presented earlier, which is an updated revision of the previous Johnson and Strom classification, we are reminded that stage II flexible, reducible adult acquired flatfoot is now broken down into various stages depending on whether the degree of supination is flexible as in a IIB deformity, or whether it is a fixed or rigid supination deformity. A flexible supination deformity would be corrected with a soft tissue balancing surgical procedure or perhaps a plantarflectory osteotomy of the medial column. A fixed forefoot supination deformity would be more appropriately addressed with an arthrodesis procedure of the medial column. To look at fixed versus reducible, we place the patient with adult acquired flatfoot into a neutral position in the weightbearing position and we see if we can, first of all, detect that inverted or supinated appearance of the forefoot, and then see if we can manually reduce it as we can here. This would be a stage IIB flexible forefoot supination deformity. If the patient has a reducible supination deformity of the forefoot, we should reduce it when we’re performing impression casting for a custom foot orthosis or for a custom ankle foot orthosis. Because correcting the deformity, as we see in the right hand picture, takes the foot back to its native shape before it compensated and broke down across the medial column. If we can shape an orthosis more accurately to the corrected position of the foot on the right hand picture, we will get a much better clinical result with our foot orthosis or with our AFO device. If you cannot correct the deformity manually, if it is not flexible, you’re going to have to actually realign the joints of the medial column and perform various levels of arthrodesis to achieve full correction. The deformity seen in stage II and stage III adult acquired flatfoot can be very dramatically demonstrated to both the clinician and the patient by having them perform a simple test in the clinic known as supination lag. In this test, the patient is seated on the exam table with their feet literally hanging off the edge of the table, the knees can be bent slightly but the feet are not touching the table but are actually hanging in space. From this position, the patient is given the instruction to supinate their feet or a better description is, ask the patient to bring the soles of the feet together. Here is a patient with stage II adult acquired flatfoot deformity on their right foot. When asked to supinate their feet with their feet hanging off the edge of the exam table, there’s quite a dramatic difference between the appearance of the two feet. The healthy left foot can supinate their foot past the midline or they can invert the foot medial to a bisection of the anterior crest of the tibia. On the right foot, because the tibialis posterior tendon has been ruptured, the patient is unable to move their foot past the midline. Looking down at the two feet, it becomes quite apparent that there’s been a tendon rupture which can easily be demonstrated to the patient. We can use supination lag to actually somewhat stage the progression of the deformity.
Because in a rigid nonreducible stage III adult acquired flatfoot, there will be no movement at all of the foot in the direction of supination. Whereas in a stage II more flexible deformity, we’ll see some evidence of movement of the foot but it will still be asymmetrical compared to the healthy foot. Here’s an example of a stage II deformity where the patient’s left foot is in stage II and it can slightly invert past the midline so there’s some motion of supination. But the right foot is far superior in terms of the degree of supination motion available. This is a patient whose right foot is in stage III or a more rigid deformity. Here, the right foot does not move at all past the midline whereas the left foot will move past the midline because the posterior tibial tendon is still intact. Again, this is quite a dramatic appearance for the patient to look down and appreciate as well as the clinician examiner. Contraction of the gastrocnemius can be measured with the Silfverskiold test, where ankle joint dorsiflexion is measured with a goniometer with the knee flexed and then compared to the knee extended. When there’s a significant difference in ankle joint dorsiflexion, specifically when there is less dorsiflexion with the knee extended in this picture, we detect a significant contracture of the gastrocnemius which may necessitate a gastrocnemius recession surgical procedure as an adjunct to other procedures performed in the correction of adult acquired flatfoot. To summarize what we’ve discussed in part I and part II of this lecture series, we can look at this gait study, looking at the kinematics of patients with posterior tibial tendon dysfunction or adult acquired flatfoot. Clinically, besides just seeing palpable tenderness of the posterior tibial tendon, we’re going to just actually visualize swelling along the distal sheath of the posterior tibial tendon. We will perform various tests among which probably the most dramatic weightbearing test is the inability to perform the single foot heel-rise. As we have them stand, we see a visible valgus deformity of the hindfoot which may be flexible in stage II or rigid in stage III. When they walk, we will see this dominant transverse plane deformity where the forefoot is carried abducted particularly evident during swing phase but also visible in static stance as well. Going back to the more archaic Johnson and Strom classification system, which is still very popular today, we can see that the assessment of the adult acquired flatfoot on that system was very subjective and really looked at only a few measurement techniques to classify stage I, II, III or IV. With today’s lecture and multiple clinical tests, we can give a much more accurate assessment of the presence of spring ligament rupture and the degree of forefoot supinatus deformity, all of which are very important criteria for determining treatment options both conservatively and with surgical intervention.