2004, Vol.23, Issues 1, Athletic Foot and Ankle Injuries

Clin Sports Med 23 (2004) xiii xiv
Preface
Athletic foot and ankle injuries
Shepard R. Hurwitz, MD Guest Editor
Nearly 10 years have passed since the Clinics in Sports Medicine published an issue that focused on foot and ankle injuries (Volume 13, Number 4, 1994). As many of this issues contributing authors comment in their opening paragraphs, the prevalence of athletic injuries of the ankle and foot is very high. More than 20,000 sports-related injuries of the ankle occur every day; even the small percentage that do not return to sport constitutes a large number of people. More complex injuries such as ankle fracture dislocation can be successfully treated until healed, but the athletes return to sport is a more daunting task than putting an office worker back on the job. There have been advances over the past 10 years in the recognition and treatment of sports injuries of the adult foot and ankle; many of these are presented in this issue. However, before going forward with what is new and improved, it is important to know that some of the old knowledge and principles are still valid. The human anatomy of the foot and ankle and our understanding of the physiology of the functional mechanics of the foot and ankle are not that different. The same is true of surgical anatomy. My opinion is the same as that of Dr. Phillip Kwong, the guest editor of volume 13, number 4, who stated: Successful treatment of the [foot and ankle] injuries depends on accurate data, sound clinical judgment, anatomic treatment and early functional rehabilitation. The authors of this issue were instructed to aim their message at general orthopedists and other physicians who treat athletes and to keep references focused on classic or current sources. Because it is impossible to cover all topics exhaustively without creating a large textbook, I selected several highly relevant topics concerning acute, chronic, and recurrent injuries of the foot and ankle in
0278-5919/04/$ see front matter D 2004 Elsevier Inc. All rights reserved. doi:10.1016/S0278-5919(03)00096-6
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S.R. Hurwitz / Clin Sports Med 23 (2004) xiiixiv
sports. The reader will benefit from the expert opinions regarding evaluation and management of problems including fractures, overuse syndromes, instability, pain, and dysfunctional residuals of injury. Each condition of the foot or ankle is presented with the appropriate references to anatomy, physical diagnosis, and biomechanics, so a separate article reviewing anatomy and biomechanics is not needed in this issue. Everyone involved with sports injuries knows that running is not fast walking, that jumping is a complex activity that requires strength and coordination, that footwear affects foot function, and that most athletes recover their competitive ability by using focused activity that mimics the sport itself. Though the intended audience of this issue is physicians, there is ample information here for other health care providers who evaluate and treat athletes. It may be helpful for the reader to use the references in each article for gaining more detail in the treatment techniques. There is no substitute for gathering history of the injury and performing a focused physical examination of the foot and ankle before undertaking treatment. Athletic trainers, physical therapists, sports physicians, and surgeons know that most diagnoses of sports injury are made without MRI, arthrograms, nerve conduction tests, and other tests. The evidence provided by mechanical testing devices and advanced imaging tools are very seductive. We need to (1) remind ourselves that we are confident in our examination of the patient, (2) confirm the diagnosis with tests, and (3) follow the progress (or lack of) of recovery again by questioning and examining the patient. The authors who contributed to this issue of the Clinics in Sports Medicine are recognized scholars in the field of foot and ankle surgery, physical therapy, physical medicine and athletic training. They are all clinicians with years of experience in caring for injured athletes and returning them to their respective sports. In essence, the authors share some of their experience and judgment in addition to basic knowledge of injury and repair. You, the reader, can learn something useful from each of the following articles that will help you treat foot and ankle problems in injured athletes. Shepard R. Hurwitz, MD Division of Foot and Ankle Surgery Department of Orthopedic Surgery University of Virginia Box 800159 Charlottesville, VA 22908-0159, USA E-mail address: srh5u@hscmail.mcc.virginia.edu
Clin Sports Med 23 (2004) xi
Foreword
Athletic foot and ankle injuries
Mark D. Miller, MD Consulting Editor
It is my extreme pleasure to introduce this issue of the Clinics in Sports Medicine. I invited my friend, mentor, and esteemed colleague Dr. Shep Hurwitz to serve as the Guest Editor for this issue, and, true to form, he exceeded my lofty expectations. As difficult (and sometimes distasteful) as it may be for some of us, foot and ankle injuries are very common in athletes. In fact, ankle sprains are the most common injury in sports. Although most of them get better, some do not which is why we need to read and understand this issue. Dr. Hurwitz has put together an impressive group of experts to discuss ankle sprains, subtalar injuries, tendinopathies, overuse injuries, plantar fasciitis, orthotics, arthroscopy, and a whole host of other sports-related foot and ankle problems. These are interesting and sometimes controversial topics, but here is the latest scoopI am proud to kick off this issue of the Clinics in Sports Medicine. Mark D. Miller, MD Department of Orthopedic Surgery University of Virginia Charlottesville, VA 22903-0753, USA E-mail address: mdm3p@hscmail.mcc.virginia.edu
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Clin Sports Med 23 (2004) 1 19
Acute ankle injury and chronic lateral instability in the athlete

Benedict F. DiGiovanni, MD*, George Partal, MD, Judith F. Baumhauer, MD
Department of Orthopaedics, University Of Rochester School of Medicine and Dentistry, 601 Elmwood Avenue, Rochester, NY 14642, USA
Acute ankle injuries Ankle sprains are the most common injuries in sports and recreational activity, accounting for 40% of all athletic injuries, especially in basketball, soccer, crosscountry running, dance, and ballet [1]. Ankle injuries make up 10% of all visits to the emergency room [2]. Ankle sprains account for 53% of injuries in basketball players and 29% of all extremity injuries in soccer players, and account for the most common trauma in modern dance and classical ballet [3,4]. In football, approximately 12% of all time lost to injuries is secondary to ankle injuries [5]. Three quarters of ankle sprains involve the lateral ligament process. Within specific sporting activities, the incidence is equal for males and females [5].
Ankle ligament anatomy and biomechanics Stability of the ankle depends on its passive or ligamentous supports as well as its muscular (peroneals) or active support. The ankle ligaments can be divided into three groups: lateral ligaments, medial ligaments, and the ligaments of the syndesmosis. The most common injuries involve the lateral ligaments. The lateral ligamentous complex consists of the anterior talofibular (ATFL), calcaneofibular (CFL), posterior talofibular (PTFL), and lateral talocalcaneal (LTCL) ligaments. The PTFL and LTCL are less commonly injured during
* Corresponding author. E-mail address: benedict_digiovanni@urmc.rochester.edu (B.F. DiGiovanni). 0278-5919/04/$ see front matter D 2004 Elsevier Inc. All rights reserved. doi:10.1016/S0278-5919(03)00095-4
B.F. DiGiovanni et al / Clin Sports Med 23 (2004) 119
Fig. 1. Lateral ankle ligaments. Detailed anatomy depicting the orientation of the anterior talofibular and calcaneofibular ligaments. (From Baumhauer J, OBrien T. Surgical considerations in the treatment of ankle instability. J Athl Train 2002:37(4)458 62; with permission.)
twisting injuries to the ankle and are of less clinical significance in chronic ankle instability. Anatomic variation in lateral ligament anatomy is common, but a general pattern is observed (Fig. 1). The anterior talofibular ligament is a thicker portion of the anterior ankle joint capsule, measuring 6 mm to 10 mm in width, 10 mm in length, and 2 mm in thickness [6]. It is contiguous with the joint capsule and is not easily defined in patients with recurrent ligament injury. The ATFL is the weakest of the lateral ankle ligaments [7]. It originates about 1 cm proximal to the tip of the lateral malleolus, and then inserts into the lateral talus just beyond the articular surface, at about 18 mm proximal to the subtalar joint. With the ankle is neutral position, the ATFL forms an angle of approximately 75 degrees with the floor from its fibular origin. The role of the ATFL is as the primary restraint against plantar flexion and internal rotation of the foot [8]. The calcanealfibular ligament is an extra-articular rounded ligament that crosses both the tibiotalar and subtalar joints. Measuring 20 mm to 25 mm in length and with a diameter of 6 mm to 8 mm, it runs obliquely downwards and backward to attach to the lateral surface of the calcaneus about 13 mm distal to the subtalar joint. The angle between the CFL and the fibula with the ankle in neutral position averages 133, but is variable, ranging from 113 to 150. It is in close association with the peroneal sheath, acting as the floor of the sheath. For this reason, a CFL injury is usually associated with a rupture of the peroneal sheath and occasionally a tear of the peroneal tendons and or of the peroneal retinaculum. The angle between the CFL and the ATFL is approximately 104, and this angle is an important detail during reconstructive procedures. From a relaxed position with the foot in neutral position, the CFL becomes more taut as the foot is brought into dorsiflexion. The CFL is the second weakest of the lateral ligaments.
Mechanism of injury The most common mechanism of injury to the lateral ankle ligaments occurs from a forced plantar flexion and inversion of the ankle, as the bodys center of gravity rolls over the ankle. First, the ATFL is injured, followed by the CFL. According to Attarian et al, the maximum load to failure for the CFL was 2 to 3.5 times greater than that for the ATFL (345.7 versus 139 newtons) [9]. Brostrom surgically explored 105 sprained ankles and found that two thirds of the cases had an isolated ATFL tear [10]. In this same study, the second most common injury was a combined rupture of the ATFL and CFL, which occurred in 25% of the cases. Medial or deltoid ligament tear is not as common, but does occur during an eversion injury when the bodys center of gravity rolls over the everted foot. The anterior portion of the deltoid ligament is most commonly injured. Most deltoid injuries are not isolated but do occur in conjunction with a fracture of the lateral malleolus [11]. High ankle sprainsisolated syndesmosis injuriesare uncommon. Fritschy reported only 12 cases of isolated syndesmosis rupture in a series of more than 400 ankle ligament ruptures [12]. These injuries are caused by a combination of forced external rotation, dorsiflexion, and axial loading of the ankle.
Diagnosis A careful history and physical can determine the severity of the injury and isolate the injured structures. For the first few days, an examination may be difficult to perform because of the acute pain and swelling that accompanies the injury. Van Dijks 1994 thesis in argues that the clinical examination has the greatest reliability and specificity 4 to 7 days after the injury [13]. History Most patients describe a rolling over of the ankle with an inversion, plantar flexion, or internal rotation mechanism. The major complaint is acute lateral ankle pain following an inversion injury to the ankle that is usually accompanied by a snap. Patients typically are seen early after injury in an emergency department or urgent care setting. They then present to the specialist within a week for further evaluation and treatment. Extent of ligament injury is related to information about initial swelling, ability to bear weight, and later ecchymosis. In general, the more extensive the ligament injury, the more difficult it is to bear weight, the more swelling noted acutely, and the more ecchymosis that develops over a few days. Physical examination Although the pain during the first hours after injury is often localized to the injured area, it soon becomes diffuse during the first few days. After a few days,
careful palpation will confirm which ligaments were most likely injured. In addition, a thorough examination is conducted to rule out other occult injuries. It is common for other injuries to be associated with an inversion injury to the lateral ligaments of the ankle. Most of the pain is usually localized over the area of the ATFL (the most commonly injured ligament) and is best evaluated 4 to 7 days after the injury; however, if the CFL is injured, most of the tenderness will be localized at the calcaneal insertion of the ligament. Funder et al in 1982 found that 52% of the patients with tenderness over the ATFL had a rupture of this ligament, and 72% of patients with tenderness over the CFL insertion had a rupture of the ligament [14]. The area of maximal swelling shows which ligament is disruptedmost frequently, the ATFL at its fibular insertion, followed by the CFL over its calcaneal insertion. Diagnostic studies Stiell and Greenbergs study in 1992 devised a set of clinical rules for the use of radiography in acute ankle injuries. These clinical guidelines for ordering ankle radiographs became known as the Ottawa ankle rules (OAR) [15]. These are listed in Box 1 below. Using the OAR has reduced cost in one emergency department by 3 million dollars per 100,000 patients, and the sensitivity for fractures remained nearly 100. When indicated, the radiographs should include anterior-posterior (AP), lateral, and mortise views. The mortise view is required to exclude distal fibular, tibial, and talar dome fracture, because the lateral malleolus is not overlapping the tibia, and the talus is equidistant from both malleoli. Stress radiographs are not usually indicated in an acute twisting ankle injury because they will not change the treatment protocol. Ultrasonography has recently been advocated for the evaluation of acute ankle ligament injuries, but it has yet to be accepted as a proven imaging technique for this condition. CT and MRI are typically not indicated in the majority of twisting ankle injuries. In select cases of acute lateral ankle sprains, however, MRI may be beneficial, especially in those suspected of having associated injuries. Differential diagnosis With an inversion injury to the ankle, the most common structures injured are the lateral ankle ligaments; however, associated injuries are not uncommon and
Box 1. Ottawa ankle rules. Radiographs only if ankle pain and one of the following: Bone tenderness at the base of the fifth metatarsal Inability to bear weight immediately after the injury and for four steps in the emergency department Bone tenderness at the tip or posterior edge of either malleolus
Box 2. Acute lateral ankle ligament injury: potential associated pathology Bony injuries: fractures of the ankle and foot Lateral, medial, posterior malleolus Proximal fibula Posterolateral process talus Lateral process talus Anterior process calcaneus Base of fifth metatarsal Navicular or other midtarsal bones Growth plate injuries in children (Salter Harris I distal fibula) Osteochondral fractures Anterolateral talus Posteromedial talus Distal tibia Ligamentous injuries Hindfoot sprain (calcaneocuboid, bifurcate, cervical, talocalcaneal) Midfoot sprain (tarsal-metatarsal, Lisfranc ligament complex) Tendon injury Peroneal brevis tear (most common) Peroneal longus tear Peroneal retinaculum injury (subluxation/dislocation peroneal tendons) Subluxation of dislocation of the peroneal Medial ankle tendons (posterior tibial [PT], flexor digitorum longus [FDL], flexor hallucis longus [FHL]) Nerve injury Superficial peroneal nerve
should be considered when evaluating patients with acute ankle injuries. Box 2 lists pathologies possibly associated with acute lateral ankle ligament injury. Frey et al [16] evaluated MRI findings in patients (15 cases) with acute lateral ankle sprains. High percentages of peroneal tendon pathology (brevis tear, 27%; longus tear, 13%; peroneal retinaculum injury, 27%) were noted. Surprisingly, medial ten-
don and deltoid ligament pathology were quite common after an acute inversion injury: deltoid ligament injury (6%), posterior tibialis tendonitis (53%), flexor hallucis tenosynovitis (13%), and flexor digitorum longus tenosynovitis (7%). Although the majority appear to resolve over time, persistent dysfunction may result if associated injuries are not properly diagnosed and treated in the acute setting. Grades of acute ankle injury Different classification systems exist for acute lateral ankle injuries, based on anatomy versus physical findings. Three anatomic grades of severity have traditionally classified lateral ankle ligament injuries [17]. A mild or Grade I sprain is mostly a ligament stretch rather than a tear. There is minimal swelling, mild tenderness, and no mechanical joint instability, which allows the patient to bear weight comfortably. A moderate or Grade II ligament sprain is defined as a torn ATFL with an intact CFL. There is moderate swelling and tenderness, and more difficulty with weight bearing. A severe or Grade III ankle sprain is a complete tear of both the ATFL and CFL. There is marked swelling and often more diffuse tenderness, ecchymosis over a few days, and inability to bear weight.
Prevention Prevention is always preferable to treating an injury. For this reason, sports medicine research has focused its attention on methods to reduce the incidence of ankle sprains. Rovere and Clarke [18] demonstrated in a retrospective study that a combination of a lace-up ankle brace and a low-top shoe significantly decreased the number of ankle sprains. Taping of the ankle improved proprioception before and after exercise, although taping is not without its limitations. Education of the athlete through injury awareness and proprioceptive training with a balance board can reduce the recurrence of acute ankle sprains. Prophylactic taping of the ankle joint combined with high-top shoes has been found to significantly decrease the number of ankle sprains [19]. The mechanism behind taping the ankle is not well understood. Although it provides an external splint to the ligaments, it only reduces range of motion for 2 to 3 hours of physical activity [20]. Ankle taping creates irritation and is rather expensive.
Treatment of acute lateral ligament injuries Balduinis functional conservative treatment for Grade I and II injury consists of three phases [1]. The initial rest, ice, compression, and elevation (RICE) treatment is followed by a short period of protection with supportive bandaging, taping, or bracing, and finally by early active range-of-motion exercises, proprioceptive training with a tilt-board, and strengthening exercise for the peroneus
muscle. It is important to keep the ankle in neutral or dorsiflexion, often by the use of ankle brace, as dorsiflexion was shown to reapproximate the fibers of the ATFL. In a study of the US cadets treated with this regimen, the average disability was 8 days for a Grade I injury and 15 days for a Grade II injury [21]. The treatment of Grade III lateral ligament tears is not as clear cut. Satisfactory subjective results have been obtained with either primary repair [22] or conservative treatment in several studies [23]. In a classic literature review by Kannus and Renstrom, 12 prospective randomized studies with a mean follow-up time of 6 months to 3.8 years compared acute repair versus cast immobilization versus early controlled mobilization. Return to work was two to four times faster in the functionally treated group compared with the patients treated by either surgery or cast immobilization [24]. No differences were observed in any study with regard to pain, swelling, or stiffness with activity. Incidence of chronic functional instability did not appear to be different between patients receiving functional treatment and those receiving surgical repair. Kaikkonen found that 87% of functionally treated patients had excellent to good results 9 months after injury, whereas only 60% of the surgically treated patients had those results. In summary, early controlled mobilization (functional treatment) proved to provide the quickest recovery in ankle mobility and an earlier return to work and physical activity without compromising the lateral mechanical stability of the ankle. Secondary surgical repair of the ruptured ankle ligaments (delayed anatomic repair) could be performed even years after the injury if necessary, with results that were comparable to those achieved with primary repair.
Functional rehabilitation program Biological background Four stages characterize the biology behind functional treatment of acute lateral ankle ligament tears: First, immediately after the injury the RICE program should be instituted to minimize hemorrhage, swelling, inflammation, and pain for best possible conditions for healing [25]. Second, the ligaments have to be protected during the following 1 to 3 weeks. This period is called the healing or proliferation phase. During this interval the fibroblasts invade the injured area and proliferate to form collagen fibers. Protection in the form of tape or brace should be used during this time. Vaes et al [26] found that the radiographic talar tilt in athletes with functional instability was decreased during an inversion moment in braced compared with unbraced ankles. Third, 3 weeks after the injury, the maturation phase begins, during which the collagen fibers mature and become scar tissue. Controlled stretching of muscles and movement of the joint not only encourage the orientation of the collagen fibers along the stress lines, but will also prevent the deleterious effects of immobilization on joint cartilage, bone, muscle, and tendons.
Fourth, after 6 to 8 weeks the new collagen fibers can withstand almost normal stress, and full return to activity is the goal. The entire maturation and remodeling of the injured ligaments lasts from 6 to 12 months. Treatment modalities Ankle mobilization. The early phases of treatment should begin with low resistance such as stationary cycling or swimming, with weight bearing as tolerated as soon as possible. Only once normal weight bearing and pain-free range of motion are achieved can muscle strengthening begin. Assisted eversion exercises should be performed in dorsiflexion to strengthen the peroneus brevis and tertius, and in plantar flexion to strengthen the peroneus longus. Proprioception. Once muscle strength has improved enough to support balance, then proprioception training begins, including the use of a tilt board. The goal of proprioception training is to improve balance and neuromuscular control. Additional forms of treatment. Of the different types of physical therapy modalities, only cryotherapy has been proven to be effective [27]. We do not recommend injection of cortisone into the ankle joint or ligaments. Nonsteroidal anti-inflammatory medications (NSAIDs) were found to be more effective than placebo in treating ankle tenderness and swelling during the first 2 weeks after the injury, but the differences were small and seemed to disappear during an extended follow-up [28]. Ointments and creams offer no benefit for ankle sprains. Aspiration of the ankle joint is of little value and carries an element of risk. When moist heat packs, warm whirlpool baths, electrogalvanic stimulation, and intermittent pneumatic compression (IPC) modalities were compared, only the IPC device was showed in randomized prospective studies to decrease swelling [28]. In the authors clinical practice, for severe or Grade III lateral ankle sprains we often use a fracture boot or short leg cast, full weight bearing, for the first 5 to 7 days. This allows the patient to eliminate the need for crutches and makes activities of daily living, including working and child care, much easier. In addition, we have found this tends to decrease the swelling and pain in a more rapid fashion. Surgery As mentioned above, no major difference has been found in the outcome of patients treated with primary repair of the torn ligaments compared with functional treatment. At this time, the orthopedist rarely performs acute repair of the lateral ligaments. Most authors agree that the preferred treatment in acute lateral ligament ankle injury is functional treatment. The authors have performed acute repair of torn ligaments in rare situations, one example being an open-ankle dislocation with gross disruption of the lateral ankle ligaments. Leach and Schepsis in 1990 argued that primary repair of torn ligaments should be undertaken in young athletes with a Grade III injury [29].
Chronic lateral ankle instability Presentation In cases of isolated chronic lateral ankle instability, the main complaint is intermittent giving out of the ankle. There is usually a history of at least two or three severe lateral ankle sprains. Patients have difficulty on uneven surfaces and are apprehensive about another giving-way episode that will cause pain and temporary dysfunction. These giving-way episodes are often associated with mild injury to the attenuated ligaments and short-term dysfunction (2 3 weeks). Between the giving-way episodes, patients are typically without pain and do not experience swelling, catching, or locking. Taping or an ankle brace usually helps to a certain degree; however, difficulties persist due to a combination of lateral ankle laxity, altered proprioception, and strength deficits. Physical examination Physical examination concentrates on the status of the lateral ankle ligaments through the use of ankle stability tests; however, a careful evaluation is performed to assess for potential contributing factors. Extremity alignment is noted, especially the association of possible hindfoot varus. If hindfoot varus malalignment is present, this will also need to be addressed if successful nonoperative or operative treatment is expected. Hindfoot motion is also evaluated to rule out potential existence of tarsal coalition, especially in the young athlete. The status of the peroneal muscles, which are often weak, are also assessed by manual muscle strength testing. In addition, signs of generalized ligamentous laxity are noted, because this also affects the results of nonoperative and operative treatment. Unless there is a history of a recent sprain, the ligaments are not typically tender to palpation or stress. Inspection and palpation of the ankle should also rule out unexpected bony or soft-tissue swelling or tenderness. Stability tests The two most common tests used to assess lateral ankle stability are the anterior drawer test and the talar tilt test. The anterior drawer test. The anterior drawer test is designed to indicate the amount of damage incurred to the ATFL, as indicated by the amount of anterior translation of the talus with respect to the tibia. The patient is seated with the knee flexed during the examination. The test is performed by holding the calcaneus with one hand while stabilizing the distal tibia with the other and translating the calcaneus forward. Positioning the ankle in 10 of plantar flexion was found to improve the sensitivity of the test. Increased translation indicates incompetence of the ATFL [30]. The amount of anterior translation is noted, as well as whether a solid end point is appreciated. The authors have found that placing the index finger and thumb in the anterior joint while the hypothenar eminence stabilizes the tibia
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allows for better appreciation of the anterior movement of the talus in relation to the tibia. This tactile sensation is felt to be more important than absolute radiographic parameters when assessing the status of the lateral ankle ligaments. In addition, the authors use the anterior drawer test to also learn more about the condition of the CFL. This is done by performing the anterior drawer test with the ankle in dorsiflexion, and thus placing the CFL under tension. Increased translation with a weak end point in plantar flexion that then produces a solid end point in ankle dorsiflexion is felt to represent an attenuated ATFL but a functioning CFL. This clinical scenario is felt to more likely represent functional instability rather than mechanical instability. Increased translation with a soft end point in both plantarflexion and dorsiflexion likely represents an incompetent CFL in addition to ATFL. The authors find the anterior drawer test to be a very helpful clinical test, especially when comparing a symptomatic with an asymptomatic contralateral ankle. Less emphasis is placed on radiographic numbers associated with an anterior drawer test, yet these stress radiographs are helpful in unclear clinical situations, and some authors find them very useful. Karlsson [31] defines normal anterior translation as between 2 mm and 9 mm. Abnormal laxity on the anterior drawer test is defined as an absolute anterior displacement of 10 mm, or 3 mm more than the contralateral side. The talar tilt test. The talar tilt test is used to help evaluate the status of the calcaneal-fibular ligament. First described by Faber in 1932, the talar tilt test is the angle formed during forceful inversion of the hindfoot between the talar dome and the tibial plafond. While the tibiotalar joint is held in a neutral position, one hand stabilizes the distal tibia and the other hand rotates the talus and calcaneus as a unit into inversion. During physical examination, it can be difficult to differentiate tibiotalar motion from subtalar motion; however, with stress radiographs each joint can be individually evaluated. The talar tilt test is more helpful as a radiographic stress test than as a physical examination technique. Incompetence of the ATFL and CFL each contribute to an increased talar tilt, but it is the CFL that is most directly evaluated. Controversy exists regarding how much talar tilt is physiologic, with normal values being reported by Cox as being between 5 and 23 [32]. For this reason, it is best to compare the injured side to the contralateral normal side. The authors view the talar tilt test as a diagnostic tool that is not depended on in routine cases, but can add valuable information when the diagnosis in unclear. Proprioception The feeling of giving way is an indication of a proprioceptive defect in the ankle. Studies have shown up to 86% peroneal and 83% tibial nerve injury due to stretch following Grade III ankle sprains, as diagnosed by electromyography [33]. Damage to the nerve can occur after as little as 6% stretch in the nerve. Proprioception is best assessed with a modified Romberg test, or stabilometry in the case of chronic ankle instability. The Romberg test is performed by asking the
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patient to stand first on the normal ankle with eyes open then closed, after which the process is repeated on the injured limb. Associated injuries As noted previously, patients with isolated chronic lateral ankle instability have pain that is intermittent and associated with specific inversion episodes. Although the lateral ligaments are the structures most frequently damaged with recurrent ankle inversion injuries, many structures have the potential for injury. These potential associated injuries are listed in Box 3. Patients suffering from associated injuries complain of ankle pain and disability between these instability episodes. Recent reports have noted that it is not uncommon for these patients with chronic lateral ankle instability to have additional injuries. In 2000, DiGiovanni et al reported on the type and frequency of associated injuries found at the time of surgery for chronic lateral ankle instability. At surgery, none of the 61 patients was found to have isolated lateral ligament injury. Fifteen different associated injuries were noted. The injuries found most often by direct inspection included: peroneal tenosynovitis, 47/61 patients (77%); anterolateral impingement lesion, 41/61 (67%); attenuated peroneal retinaculum, 33/61 (54%); and ankle synovitis, 30/61 (49%). Other less common but significant associated injuries included: intra-articular loose body, 16/61 (26%); peroneus brevis tear, 15/61 (25%); talus osteochondral lesion, 14/61 (23%); and medial ankle tendon tenosynovitis, 3/61 (5%) [34]. In 1999, Komenda and Ferkel reported on arthroscopic findings associated with ankle instability. Before lateral ankle reconstruction, ankle arthroscopy was performed on 54 patients with chronic ankle instability. At surgery, 51 ankles (93%) had intra-articular abnormalities, including loose bodies in 12 (22%), synovitis in 38 (70%), talus osteochondral lesions in 9 (17%), ossicles in 14 (26%), osteophytes in 6 (11%), adhesions in 8 (15%), and chondromalacia in 12 (22%) (12) [35]. Nonoperative management A functional treatment protocol, often using physical therapy, is the mainstay treatment for chronic lateral ankle instability. It has a high chance of success in patients with functional ankle instability, as well as those with mechanical instability who demonstrate peroneal muscle weakness and proprioception deficits. The length of treatment can vary widely and depends on the initial functional deficiency and the intensity of treatment. In general, a trial of at least 6 weeks of aggressive physical therapy is suggested before considering operative treatment. Contributing factors need to be considered and addressed as indicated. For patients with flexible hindfoot varus, an orthosis with a lateral heel wedge can be beneficial. A lateral flare to be added to an athletic shoe can be prescribed for
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Box 3. Potential associated injuries in patients with chronic lateral ankle ligament instability Nerve injury Superficial peroneal nerve dysfunction (most common) Sural nerve or tibial nerve dysfunction Soft tissue injury Anterolateral ankle impingement (proliferative synovitis and scar) Sinus tarsi syndrome Tendon injury Peroneus brevis tear Peroneal retinaculum attenuation (peroneal tendon instability) Peroneal longus tear Os peroneum syndrome Medial ankle tendons (PT, FDL, FHL) Osteochondral defects (OCD) Anterolateral talus Posteromedial talus Distal tibia Loose body in ankle joint Chondromalacia Ligament injury Subtalar instability Syndesmotic injury Bone injury Malleoli stress fracture Posterolateral process talus nonunion or os trigonum Lateral process talus nonunion Anterior process calcaneus nonunion Base fifth metatarsal nonunion Tibiotalar anterior bony impingement Tarsal coalition: bone/cartilage/fibrous
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patients with stiffness in hindfoot and a varus position. A heel lift may help decrease anterior impingement syndrome by opening the anterior tibiotalar joint. Taping of the ankle is beneficial initially; however, the initial support decreases by 50% after 10 minutes of exercise and provides no support after 1 hour of exercise [36]. An Air-Stirrup ankle brace (Aircast, Summit, New Jersey) has proven to significantly decrease inversion and eversion range of motion, and its effect did not decrease with exercise [37]. Operative treatment for chronic ankle instability The indication for lateral ligamentous reconstruction of the ankle includes persistent, symptomatic, mechanical instability that has failed a functional rehabilitation program. Contraindications to ligament reconstruction include pain with no instability, peripheral vascular disease, peripheral neuropathy, and inability to be compliant with postoperative management. As noted previously, associated injuries in patients with chronic lateral ankle instability are not uncommon and should be evaluated for. In patients suspected of having associated injuries, either intra-articular or extra-articular, the authors find ankle MRI very helpful. As noted by Komenda and Ferkel [35], ankle arthroscopy is useful to evaluate for potential intra-articular associated pathology; however, ankle arthroscopy is not mandatory because direct inspection of the joint is possible during the ligament procedure. More than 80 surgical procedures have been described. In general terms, they can be classified as either anatomic repair of the lateral ligaments or nonanatomic repair that involves tendon weaving procedure. The authors prefer an anatomic repair technique for the majority of patients, specifically using the BrostromGould technique. The Reconstructive tenodesis procedures preferred by the authors are the Brostrom-Evans and the Chrisman-Snook procedures. These are usually reserved for revision procedures or for patients with generalized ligamentous laxity, or heavy athletes such as football linemen. For almost all these procedures described in the literature, the reported success rate is greater than 80%. Brostrom-Gould anatomic lateral ligament repair In 1966, Brostrom reported on 60 patients who underwent direct late repair of the lateral ankle ligaments for chronic lateral instability (Fig. 2). The ATFL and CFL torn ends were shortened and repaired directly by midsubstance suturing [38]. Gould modified this procedure in 1980 by advancing the lateral aspect of the extensor retinaculum over the Brostrom repair [39]. This modification reinforces the repair, limits inversion, and helps to correct the subtalar component of the instability. The surgical procedure involves either of two approaches. If no extra-articular pathology is expected, an anterior approach along the anterior and distal border of the fibula is used. If peroneal tendon or peroneal retinacular pathology is present, however, then a more extensile posterior approach following the course of the peroneal tendons is used. The superficial peroneal nerve
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Fig. 2. Brostrom-Gould anatomic lateral ligament reconstruction. (A) Relationship between the sensory nerve branches and the incision (dotted lines) for the Brostrom-Gould anatomic repair. (B) Anterior talofibular ligament (ATFL) and calcaneofibular ligament (CFL) midsubstance tears. (C) Brostrom repair of the ATFL and CFL. (D) Mobilization of the proximal portion of the inferior extensor retincaculum to the fibula; the Gould modification of the Brostrom ligament repair. (From Baumhauer J, OBrien T. Surgical considerations in the treatment of ankle instability. J Athl Train 2002;37(4): 458 62; with permission.)
is identified and protected during exposure of the ankle capsule. The ATFL is divided midsubstance by making an anterolateral arthrotomy. The CF ligament is next identified under the peroneal tendons and also divided midsubstance. The ATFL and CFL are shortened by imbrication in a vest-over-pants fashion and repaired using two to three strands of 2-0 Ethibond. This technique of imbrication results in tightening and doubling the thickness of the lateral collateral ligaments. The CFL sutures are tightened with the ankle in plantar flexion and eversion,
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whereas the ATFL sutures are tied while the heel is hanging to avoid anterior subluxation of the talus. The Gould modification is then performed by advancing the extensor retinaculum and securing it to the fibula. At the procedures end, a plaster posterior splint with side struts (ankle stirrup) is applied and maintained for 2 weeks. A weight-bearing cast is then applied for 4 weeks, followed by an ankle brace, and a functional rehabilitation program is prescribed. The benefits of the procedure include maintaining normal ligamentous anatomy, avoiding need for tendon grafts, and most importantly preserving physiologic tibiotalar and subtalar motion. The disadvantage is that it relies on the quality of the tissue for a strong repair. This procedure has shown 95% goodto-excellent results in the hands of Hamilton et al in 1993 [40], and they noted it is particularly well suited for professional dancers or for those whose livelihood necessitates a full range of ankle motion. In 1988 Karlsson et al [41] found excellent or good results in 80% of the patients at a 6-year follow-up. The only poor results were found in patients who had prolonged instability, osteochondritis of the ankle, and generalized ligamentous instability. In the authors clinical practices, the Brostrom-Gould has become the workhorse procedure for chronic lateral ankle instability, with typically highly favorable results.
Fig. 3. The modified Brostrom-Evans procedure for chronic lateral ankle instability. End-to-end Brostrom anatomic repair (shortening with imbrications) of the anterior talofibular and calcaneofibular ligaments. This is followed by adding the Evans reconstructive lateral ankle tenodesis. The anterior half of the peroneus brevis tendon is harvested, maintaining distal attachment to the fibula. It is then routed anterior to posterior through a drill in the distal fibula and secured at entrance and exit sites. (From Gerard P. Clinical evaluation of the modified Brostrom-Evans procedure to restore ankle stability. Foot Ankle Int 1999;20:246 52; with permission.)
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Modified Brostrom-Evans procedure In 1953, Evans described releasing the peroneus brevis at the musculotendinous junction, rerouting it through the fibula, and reattaching it to its proximal stump [42]. This was later modified, suturing the tendon back to itself instead of reattaching it to the proximal stump [43]. In 1999, Girard et al reported on the results of a procedure that augments the Brostrom-Gould anatomic repair technique by using the anterior one third of the peroneus brevis in a tenodesis fashion. This procedure is referred to as the modified Brostrom-Evans procedure, and is outlined in Figs. 3 and 4 [44]. The postoperative protocol is similar to that following the Brostrom-Gould procedure. The main advantage of this procedure is that it adds static restraint without a significant sacrifice of dynamic peroneal restraint. This procedure has a role in heavy athletes such as football lineman, generalized ligament-laxity patients, or as revision surgery. Girard et al reported on the results of 21 patients with an average follow-up of 29.5 months [44]. They noted a significant loss of inversion compared with the uninjured contralateral side, but no change in range of motion and no significant loss of peroneal strength. Chrisman-Snook reconstruction The authors use this reconstructive tenodesis procedure primarily for revision surgeries. Of the various reconstructive tenodesis procedures, it is favored because it most closely parallels the native lateral ligament anatomy. Elmslie introduced a nonanatomic, lateral ligament reconstruction that passes a strip of
Fig. 4. Gould modification as the final step. The proximal portion of the inferior extensor retinaculum is advanced to the distal fibula to further stabilize both the tibiotalar and subtalar joints. (From Gerard P. Clinical evaluation of the modified Brostrom-Evans procedure to restore ankle stability. Foot Ankle Int 1999;20:246 52, with permission.)
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fascia lata through drill holes in the fibula and the calcaneus [45]. This was later modified in 1969 by Chrisman and Snook, using a split portion of the peroneus brevis instead of the strip of fascia lata [46]. The surgical approach involves making a posterior curvilinear incision from 4 cm to 5 cm proximal to the tip of the fibula to 2 cm proximal to the tip of the fifth metatarsal. Skin flaps are developed and the anterior slip of peroneus brevis is released from its musculotendinous junction. The anterior portion of the peroneus brevis tendon is passed through either the base of the ATFL or through a bone tunnel in the talus, followed by passing it through a bone tunnel through the fibula to recreate the insertion of the CFL tendon, and finally anchoring it into the calcaneal origin of the CFL tendon. In a 1985 long-term follow-up study, Snook et al found 79% excellent results and 14% fair results at an average 10-year follow-up [47]. Although it allows for a stable ankle joint, it does not allow for physiologic motion. It creates excessive restriction of the ankle and subtalar joint motion, and thus patients often find it difficult to adjust to uneven terrain. In our clinical experience, we have found that it is not uncommon to see patients 10 to 20 years after this procedure who have since developed significant degenerative joint disease (DJD) of subtalar joint, most likely secondary to nonphysiologic stresses on the joint over time.
References
[1] Balduini FC, Vegzo JJ, Torg JS, et al. Management and reahabilitation of ligamentous injuries to the ankle. Am J Sports Med 1987;4:364 80. [2] Barlet G, Anderson RB, Davis W. Chronic lateral ankle instability. Foot Ankle Clin 1999;4: 713 28. [3] Garrick JG, Requa RK. Role of external support in the prevention of ankle sprains. Med Sci Sports 1973;5:200 3. [4] Ekstrand J. Soccer injuries and their mechanisms: a prospective study. Med Sci Sports Exc 1983; 15:267 70. [5] Garric JG. The frequency of injury, mechanism of injury, and epidemiology of ankle sprains. Am J Sports Med 1977;5:241 2. [6] Brostrom L. Sprained ankles Ianatomic lesions in recent sprains. Acta Chir Scand 1964;128: 483 95. [7] Siegler S, Block J, Schneck CD. The mechanical characteristics of the collateral ligaments of the human ankle joint. Foot Ankle 1988;8:234 42. [8] Rasmussen O. Stability of the ankle joint. Acta Orthop Scand 1985;211:1 75. [9] Attarian DE, McCrackin HJ, Devito DP. Biomechanical characteristics of human ankle ligaments. Foot Ankle 1985;6:54 8. [10] Brostrom L. Sprained ankles IIIclinical observations in recent ligament ruptures. Acta Chir Scand 1965;130:560 9. [11] Brand RL, Collins MD. Operative management of ligamentous injuries to the ankle. Clin Sports Med 1982;1:119 30. [12] Fritschy D. An unusual ankle injury in top skiers. Am J Sports Med 1989;17:282 6. [13] Van Dijk CN. On diagnostic strategies in patients with severe ankle sprain [thesis]. Amsterdam (Netherlands): University of Amsterdam; 1994. [14] Funder V, Jorgensen JP, Andersen A, et al. Ruptures of the lateral ligaments of the ankle. Clinical diagnosis. Acta Orthop Scand 1982;53:997 1000.
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[15] Stiell J, Greenberg G. A study to develop clinical rules for the use of radiography in acute ankle injuries. Ann Emerg Med 1992;21:384 90. [16] Frey C, Bell J, Terassi L, et al. A comparison of MRI and clinical examinationination of acute lateral ankle sprains. Foot Ankle Int 1996;17(9):533 7. [17] Hamilton WG. Sprained ankles in ballet dancers. Foot Ankle 1982;3:99 102. [18] Rovere GD, Clarke TJ. Retrospective comparison of taping and ankle stabilizers in preventing ankle injuries. Am J Sports Med 1988;16:228 33. [19] Garrick JG, Requa RK. Role of external support in the prevention of ankle sprains. Med Sci Sports 1973;5:200 3. [20] Fiore RD, Leard JS. A functional approach in the rehabilitation of the ankle and rear foot. J Athl Train 1980;15:231 5. [21] Jackson DW, Ashley RL, Powell JW. Ankle sprains in young athletes. Relation of severity and diability. Clin Orthop 1974;101:201 15. [22] Jaskulka R, Fisher G, Schedl R. Injuries of the lateral ligaments of the ankle joint. Operative treatment and long-term results. Arch Orhop Trauma Surg 1988;107:217 21. [23] Drez D, Young JC, Waldman D, et al. Nonoperative treatment of double lateral ligament tears of the ankle. Am J Sports Med 1982;10:197 200. [24] Kannus P, Renstrom P. Current concepts review: treatment for acute tears of the lateral ligaments of the ankle. J Bone Joint Surg 1991;A73:305 12. [25] Jarvinen M. The effects of early mobilization and immobilization on the healing process following muscle injuries. Sports Med 1993;15:78 89. [26] Vaes P, Duquet W, Handelburg F. Objective roentgenologic measurements of the influence of ankle braces on pathologic joint mobility. A comparison of 9 braces. Acta Orthop Belg 1998; 64(2):201 9. [27] Dupont M, Beliveau P, Theriault G, et al. The efficacy of anti-inflammatory medication in the treatment of acutely sprained ankle. Am J Sports Med 1982;10:197 200. [28] Airaksinen O. Changes in posttraumatic ankle joint mobility, pain, and edema following intermittent pneumatic compression therapy. Arch Phys Med Rehabil 1989;70:341 4. [29] Leach RE, Schepsis AA. Acute injury to ligaments of the ankle. In: Evarts CM, editor. Surgery of the musculoskeletal system, vol. 4. New York: Churchill Livingstone; 1990. p. 3887 913. [30] Johannsen A. Radiological diagnosis of lateral ligament lesion of the ankle. Acta Orthop Scand 1978;49:295 301. [31] Karlsson J, Bergstan T, Lansinger O, et al. Surgical treatment of chronic lateral instability of the ankle joint. Am J Sports Med 1989;17:268 73. [32] Cox JS. Surgical and nonsurgical treatment of acute ankle sprains. Clin Orthop 1985;198:118 26. [33] Nitz AJ, Dobner JJ, Kersev V. Nerve injuries and Grades II and III ankle sprains. Am J Sports Med 1985;13:177 82. [34] DiGiovanni BF, Fraga CJ, Cohen BE, et al. Associated injuries found in chronic lateral ankle instability. Foot Ankle Int 2000;21(10):809 15. [35] Komenda GA, Ferkel RD. Arthroscopic findings associated with the unstable ankle. Foot Ankle Int 1999;20(11):708 13. [36] Myburg KH. The effects of ankle guards and taping on joint motion before, during, and after a squash match. Am J Sports Med 1984;12:441 6. [37] Gross MT. Effect of recurrent lateral ankle sprains on active and passive judgement of joint position. Phys Ther 1987;10:67 9. [38] Brostrom L. Sprained ankles IV: surgical treatment of chronic ligament ruptures. Acta Chir Scand 1966;132:551 65. [39] Gould N. Early and late repair of the lateral ligaments of the ankle. Foot Ankle Int 1980;1:84 9. [40] Hamilton WG, Thompson FM, Snow SW. Modified Brostrom procedure for lateral ankle instability. Foot Ankle 1993;14:1 7. [41] Karlsson J, Bergsten T, Lansinger O, et al. Reconstruction of the lateral ligaments of the ankle for chronic ankle instability. J Bone Joint Surg Am 1988;70:581 8.
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[42] Evans DL. Recurrent dislocations of the ankle: a method of surgical treatment. Proc R Soc Med 1953;46:343 8. [43] Ottson L. Lateral instability of the ankle treated with by a modified Evans procedure. Acta Orthop Scand 1978;49:302 5. [44] Girard P, Anderson RB, Davis WH. Clinical evaluation of the modified Brostrom-Evans procedure to restore ankle stability. Foot Ankle Int 1999;20:246 52. [45] Elmslie RC. Recurrent subluxations of the ankle joint. Ann Surg 1934;100:364 7. [46] Chrisman OD, Snook GA. Reconstruction of the lateral ligament tears of the ankle: an experimental study and clinical evaluation of seven patients treated by a new modification of the Elmslie procedure. J Bone Joint Surg Am 1969;51:904 12. [47] Snook GA, Chrisman OD, Wilson TC. Long-term results of the Chrisman-Snook operation for reconstruction of the lateral ligaments of the ankle. J Bone Joint Surg Am 1985;67:1 7.
Ankle pain and peroneal tendon pathology

Judith F. Baumhauer, MDa,*, Deborah A. Nawoczenski, PT, PhDb, Benedict F. DiGiovanni, MDa, A. Samuel Flemistera
a
Division of Foot and Ankle Surgery, University of Rochester School of Medicine and Dentistry, 601 Elmwood Avenue, Rochester, NY 14642, USA b Department of Physical Therapy, Ithaca College, University of Rochester South Campus, 300 East River Road, Rochester, NY, 14623, USA
An estimated 50 million sports injuries occur each year in the United States. Eighty to ninety percent of these injuries include sprains, strains, and contusions [1 3]. The most common of all athletic injuries are ankle injuries [1,2,4], ranging from 17% to 20% of injuries in most sports [1,2,5 7]. Ankle injuries constitute 20% to 35% of total time lost to injury in every running or jumping sport [8]. Although ankle injuries are quite common, the complex etiologic factors leading to these injuries are unknown. Multiple components considered potential risk factors of injury have been divided into extrinsic and intrinsic variables. Extrinsic factors include the type of sport, playing time, level of competitions, equipment, and environmental conditions. Intrinsic factors consist of physical characteristics such as age, sex, fitness level, previous injury, strength, range of motion, joint laxity, and joint stability. The suspected multifactorial deficiencies related to ankle injury have remained elusive. The impact of loading on the foot and ankle and the study of ground reactive forces has been extensively studied [9 16]. These forces are altered by multiple factors including footwear (barefoot<shod) and velocity (walking, sprinting). The repetitive transmission of these forces to the foot and ankle have been linked with specific injuries [14,17 21].
Ankle joint anatomy The ankle joint is composed of an intricate relationship between bony and ligamentous support. The ankle joint is maintained by the cone-shaped talus and
* Corresponding author. E-mail address: Sue_Hauptman@URMC.Rochester.edu (J.F. Baumhauer). 0278-5919/04/$ see front matter D 2004 Elsevier Inc. All rights reserved. doi:10.1016/S0278-5919(03)00088-7
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its sculptured fit between the tibia and fibula [22]. In the neutral position of the ankle, there are strong osseous constraints. With increasing plantar flexion, the osseous constraints are removed and the soft tissues and ligaments maintain the joint stability. It is in this position that the ligamentous tissues are most susceptible to injury [23 26]. The soft tissue structure of the ankle is maintained by three groups of ligaments functioning as static stabilizers: the lateral ligaments, the deltoid ligament, and the syndesmosis complex. The dynamic stabilizers of the ankle joint consist of the muscles of the anterior, lateral, and posterior compartments of the leg. Muscle weakness and muscle imbalances have been implicated in persistent ankle pain and recurrent ankle sprains [27 31]. Five cutaneous nerves cross the ankle joint to supply the foot: (1) the tibial nerve, (2) the saphenous nerve, (3) the superficial peroneal nerve, (4) the deep
Box 1. Injury history Previous ankle injury Instability symptoms Taping or bracing practices Mechanism of injury Audible pop or snap at the time of injury Ambulation status initially and currently Initial treatment received Time delay in seeking care or follow-up Duration of symptoms Sports history Level of competition Training methods Mileage Timing surface Shoes/inserts Weather changes Medical history Generalized ligamentous laxity Limb alignment Personality traits Recent illnesses Other musculoskeletal injuries
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peroneal nerve, and (5) the sural nerve. Nerve entrapment syndromes have been implicated in the cause of chronic ankle pain in runners [32,33]. A careful history of the injury is imperative. Important considerations are listed in Box 1. The history will guide the physician toward the physical examination, and also potentially elucidate an etiologic factor for the injury occurrence, such as training error, a rapid increase in mileage, or new running shoes.
General physical examination A systematic approach to the palpation of the foot and ankle is important to identify the injured structures. Examination of the foot and proximal fibula rules out other possible injuries occurring concomitantly and masquerading as ankle pain. The areas of maximal tenderness are localized and recorded. Pain over the anatomic locations of the lateral or medial ligaments of the ankle are diagnostic of injury. An exception to this rule is pain posterior to the lateral malleolus in a congruous ankle joint. This may represent injury to the peroneal tendon complex rather than the posterior talofibular ligament. Pain in the anterior aspect of the ankle between the tibiofibular articulation may represent a syndesmosis ligament injury. This ligamentous complex can be further assessed by manual compression proximal of the fibula to the tibia, the squeeze test. Pain in the region of the syndesmosis with this maneuver suggests a syndesmotic ligament injury [34]. Routine range-of-motion and manual strength testing of the ankle should be performed to assess the degree of injury and may be used as a baseline during follow-up examinations. The nonspecific symptom of ankle pain has an extensive differential diagnosis, as outlined in Box 2. The differential diagnosis of ankle injuries includes intraarticular pathology, as well as acute fractures and stress fractures, musculotendinosis strains, retinacular tears, and nerve injuries. The most common causes of persistent ankle pain are described below.
Osteochondral lesions of the talus The misdiagnosis or delayed diagnosis of osteochondral (OCD) lesions of the talus occurs in up 81% of patients presenting with chronic ankle pain [35]. The symptoms of ankle pain, recurrent swelling, ankle instability, or the feeling of catching or locking of the ankle lead the clinician to the diagnosis. These lesions have been classically described as lateral or medial based on the cause [36 39], mechanism of injury [36,40 42], and propensity for healing [39,43]. Lateral lesions comprise 43% of osteochondral lesions and are wafer shaped, located in the anterior portion of the talar dome, and caused by a traumatic event such as an inversion ankle injury. Medial lesions (57%) are cup shaped, posterior in location, and the suspected etiology is osteochondrosis with associated degenerative cysts.
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Box 2. Differential diagnosis of ankle pain Soft tissue Ligament injury Ankle sprain Syndesmosis Injury Sinus tarsi syndrome Bassetts ligament Anterior tibiotalar impingement syndrome Tendon injury Achilles tendon Peroneal tendon Posterior tibial tendon Flexor hallucis longus Nerve entrapment syndromes Accessory musculature anomalies Cartilage/bone Osteochondral lesions of the talus Stress fractures Acute fractures Fracture nonunions Osteoarthritis Tumors
Both computed tomography (CT) and magnetic resonance imaging (MRI) have been recommended to better delineate these lesions. Berndt and Hardy described four stages of osteochondral lesions and related these stages to treatment options. Ferkel and Sgaglione described a computerized tomography staging system for these lesions, as described in Box 3 [35]. The current recommended treatment for Canale and Belding [37] Stages I, II and medial Stage III is a short leg non-weight bearing cast for 6 weeks. If symptoms persist after this treatment then ankle arthroscopy is indicated with excision, curettage, and drilling of small lesions. Larger lesions may be stabilized with
Box 3. Staging system for osteochondral fractures of the talus Stage I, compression of subchondral bone without break in cartilage Stage II, partial detached osteochondral fragment Stage III, totally detached osteochondral fragment remaining in crater Stage IV, displaced osteochondral ligament loose in joint.
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bioabsorbable or buried pins or screws. Lateral Stage III lesions and all Stage IV lesions are treated initially with excision of the small fragments, curettage, and drilling. Larger lesions, defined as more than one third of the articular surface, require pinning or screw fixation for stabilization [44]. Another option for treatment of large chronic OCD and an active area of research is osteocartilage allografts of the talar dome. Long-term results of this treatment with randomized prospective studies are needed.
Syndesmosis injuries The tibiofibular syndesmosis is composed of the anterior inferior and posterior inferior tibiofibular ligaments, the transverse ligament, and the interosseous membrane [45]. It maintains the relationship between the tibia and fibula and provides a lateral constraint to the talus within the ankle mortise. The inferior aspect of the syndesmosis also plays a pivotal role in maintaining the distal tibiofibular joint. The fibula rotates 3 laterally with dorsiflexion and 3 medially with plantar flexion [8]. With the ankle in plantar flexion and during the push-off phase of running, the fibula migrates distally in response to the contraction of the leg and foot musculature [46]. This distal descent deepens the ankle mortise, tightens the interosseous membrane, and therefore adds to the stability of the ankle. Syndesmosis ruptures are commonly associated with deltoid ligament injuries [45] and also with fractures [47,48]. Fifty percent of Weber B ankle fractures (fibula fracture occurring at the level of the tibial plafond) have corresponding syndesmosis disruptions [45,49]. Weber C ankle fractures (fibula fracture occurring above the level of the tibial plafond) often have a corresponding syndesmosis injury [45]. The mechanism of injury for syndesmosis disruption is a plantar flexion external rotation injury [50]. Fritschy reported the incidence of 12 cases of isolated syndesmosis injuries out of 400 ankle ligament ruptures. The athletes participated in a variety of sports including soccer, skiing, and skating [50]. Athletes with syndesmosis injuries complain of anterior lateral ankle pain in the region of the syndesmosis. The degree of swelling and pain associated with the injury can be significant. The patient will have difficulty bearing weight on the injured ankle. Palpation over the syndesmotic ligaments anteriorly causes pain, as does passive external rotation of the foot. Posterior palpation in the corresponding region of the syndesmosis causes less discomfort [50]. Provocative tests, in addition to passive external rotation of the foot, include the squeeze [34] and Cotton tests [45]. The squeeze test is performed by compressing the fibula and tibia together at the mid calf. A positive test produces pain at the distal tibiofibular articulation. The Cotton test is a lateral displacement assessment performed by grasping the heel and talus in one hand and the distal tibia in the other. The maneuver consists of attempting to move the talus laterally in the ankle mortise. Greater than 3 mm lateral displacement is considered a positive test of instability [45]. Comparison with the uninjured side is recommended.
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After an adequate ankle series (anterior/posterior, lateral, and mortise), a stress radiograph in plantar flexion and external rotation may demonstrate lateral diastasis [50]. Greater than 5 mm clear space medially indicates a syndesmosis disruption [45]. A variety of additional studies such as an MRI, CT scan, and a bone scan have been advocated in the establishment of the diagnosis [50 53]. The treatment of a complete rupture with loss of ankle joint congruity requires surgical intervention with stabilization of the syndesmosis. This can be accomplished through the use of syndesmotic screws, cerclage, or Kirshner wires [50,54]. Failure to maintain a congruous ankle joint can result in tibiotalar arthrosis [45,47]. A partial syndesmosis injury or strain can be treated with immobilization for a short period in the acute phase of injury to aid in pain control (7 to 10 days) [55]. The functional treatment is begun similar to an acute ankle sprain. The important difference is in the recovery time, with an acute ankle sprain ranging 3 to 6 weeks to return to activity and syndesmotic injuries taking an average of 3 months.
Anterior tibiotalar impingement syndrome Anterior tibiotalar impingement syndrome represents a group of pathologic conditions causing pain with ankle dorsiflexion secondary to bone or soft-tissue interposition. This was first described by Morris in soccer players with anterior ankle pain. The pain is brought on by dorsiflexion of the ankle. McMurray coined the phrase footballers ankle, noting its occurrence with soccer players [56]. Anterior tibial osteophytes and corresponding bone formation in the region of the talar neck causing dorsiflexion impingement at the tibiotalar joint was felt to be the pathology. It was hypothesized that forced plantar flexion of the ankle resulted in anterior capsular injury, leading to the laying down of bone in response to this trauma. ODonoghue later called the dorsal osteophytes impingement exostoses [57]. He and others felt these exostoses formed in any sport requiring rapid accelerations and decelerations at the extremes of ankle range of motion [43,58 63]. The symptoms consistent with impingement exostoses include pain at the extremes of motion, limited range of motion, and swelling. Objective findings include limited range of motion, particularly in dorsiflexion, and occasional palpable bony irregularities corresponding to the areas of pain. Radiographs demonstrate bony formation and the squaring of the anterior tibial lip. Bone is noted to fill in the area of the talar neck sulcus. Weight-bearing films in full dorsiflexion may demonstrate osteophyte contact anteriorly and posterior tibial talar joint widening. Conservative treatment consists of a heel lift, activity modification with limitation of dorsiflexion, rest and anti-inflammatory modalities. Bracing or taping directed toward the limitation of ankle dorsiflexion may be helpful; however this may provide only symptomatic relief with the impending return of pain upon discontinuance [55]. Surgical ostectomy can be performed either arthroscopically [59, 64,65] or through an open procedure [57,61], and is indicated when conservative management has failed to relieve the symptoms or upon the recurrence of pain.
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Soft-tissue lesions leading to tibiotalar impingement include Bassetts ligament [66] and meniscoid lesions [67 69]. Bassett, in 1990, reported on a prominent distal fascicle of the anterior inferior tibiofibular ligament as a cause of chronic ankle pain after an inversion ankle sprain [66]. He reported on a cadaveric study examining the anterior inferior talofibular ligament and found the distal fascicle contacted the talar dome in an average of 12 dorsiflexion. A parallel clinical study confirmed these results. The symptoms produced included anterolateral ankle pain, swelling, and ankle discomfort. He hypothesized that the loss of the anterior talofibular ligament integrity (after an inversion ankle injury) allowed the talus to subluxate anteriorly and subsequently make contact with the distal fascicle of the anterior inferior talofibular ligament, leading to tibial talar impingement. Five of seven clinical patients required chondroplasty of the anterolateral talar dome at the time of injury secondary to chondral abrasion from ligament irritation. Arthroscopic debridement of the distal fascicle of the anterior inferior tibiofibular ligament resulted in excellent long-term follow-up in five of seven patients and a good result in two of seven in one study. No instability upon resection was identified. Meniscoid lesions, defined as cartilaginous transformations of a ruptured anterior talofibular ligament, were first described by Wolin et al in 1950 [69]. They described the hyalinization of the anterior talofibular ligament in nine patients with chronic ankle pain and functional instability after an inversion ankle sprain. Surgical exploration of these ankles identified the meniscoid lesions at the anterolateral aspect of the ankle causing irritation in the lateral gutter of the ankle joint. McGinty et al felt the meniscoid lesions became interposed between the talus and the lateral malleolus, leading to pain, instability, swelling, and synovitis [68]. They advocated the arthroscopic removal of the lesion with resolution of the symptoms and signs. McCarroll similarly recommended surgical removal of the lesions with good results and return to prior level of activity [67]. A recent study disputed the hyalinized ligament theory resulting in the ankle joint symptoms and felt that generalized synovitis led to the ligament alterations [65]. The recommendations were to perform a complete synovectomy to relieve the symptoms. This resulted in a 75% excellent long-term outcome, with a 20% complication rate secondary to synovectomy consisting of sensory paresthesias, superficial infections, and a deep infection. Routine ankle functional rehabilitation protocol with ankle range of motion, subtalar range of motion, peroneal strengthening and ankle proprioception exercises is begun in the 4 to 6 week period after debridement of the ankle lesions (or synovectomy) and return to running and jumping activity may occur 1 to 2 months after rehabilitation initiation.
Nerve entrapment syndromes Heel and foot pain are common complaints among runners [33,70,71]. Although tarsal tunnel compression of the tibial nerve is a well-recognized nerve
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entrapment syndrome causing paresthesias in the plantar aspect of the foot, other lesser known peripheral nerve impingements occur causing ankle pain in runners. In a review article examining nerve entrapments of the foot and ankle in runners, 2 of 21 operative cases presented with dorsal ankle pain secondary to compression of the deep peroneal nerve at the superior talus [33]. Palpation of the maximal area of tenderness caused radiating paresthesias into the first web space of the foot. At surgery, a dorsal spur was present on the distal aspect of the talus causing the deep peroneal nerve compression. Other areas of deep peroneal nerve entrapment, also called anterior tarsal tunnel syndrome, include the distal aspect of the inferior extensor retinaculum, with or without associated compression of the extensor hallucis longus tendon [33]. Conservative treatment includes immobilization, local injections with lidocaine and cortisone, and nonsteroidal anti-inflammatories [70 75]. With resistant cases, surgical intervention consisting of the release of the nerve compression is successful. Preoperative nerve conduction studies or electromyographs (EMGs) are not felt to be necessary. The sensitivity and specificity of electrical diagnostic studies is poor. Postoperative, immobilization of the foot and ankle for 2 to 4 weeks is recommended. Mild jogging is begun at 8 weeks and full training at 12 weeks [33,73].
Peroneal tendon pathology Isolated peroneal pathology has been reported in a number of studies. The possible pathologic conditions include synovitis of the tendon sheath [76 78], longitudinal tendon tears [79 82], and peroneal retinacular attenuation with peroneal tendon subluxation or dislocation [83 86]. In cadaveric studies Sobel et al [87 89] concluded that incidental peroneus brevis splits are more common than previously recognized and range from 11% to 26% of cases. Complete rupture of either of the peroneal tendons is extremely rare, with the majority occurring with an inversion ankle injury [90 93]. The more common problem of peroneal tendinosis has been reported as a cause of chronic ankle pain in runners [79,94]. The largest series of longitudinal ruptures of the peroneal tendon in athletes was a retrospective study reported by Bassett and Speer [79]. Eight athletes were surgically found to have longitudinal tears of one of the peroneal tendons after a plantar flexion and inversion ankle injury. The athletes complained of persistent lateral ankle swelling, popping, and retrofibular pain after the initial injury. The ankles were stable to physical examination. Swelling was evident along the retrofibular area of the ankle. Active ankle circumduction revealed retrofibular popping. Passive motion did not recreate this finding. The peroneal tendons did not subluxate or dislocate with this maneuver. All plain radiographs of the ankle were normal. Peroneal tenograms were performed and found to be 100% sensitive but not specific for the degree of tendon disruption. Neither MRI nor CT was performed. Tenogram can demonstrate peroneal entrapment, adhesions, rupture, or tenosynovitis; however, it is an invasive ex-
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amination with possible complications. Each athlete completed his or her season with taping while wrapping and underwent surgical intervention at the conclusion of the season. Under local anesthesia, the retrofibular area was explored. The superior peroneal retinaculum was intact in all cases. The peroneus longus tendon was injured in five patients and peroneus brevis in three. The longitudinal tears ranged from 1 cm to 3 cm in size. With active circumduction of the ankle, the snapping appeared to be caused by one tendon moving over another with or without involvement of the longitudinal rent. The longitudinal defect was excised, as was any fusiform swelling, and the tendon was repaired longitudinally. Histologically the excised specimen demonstrated synovitis and focal myxoid degeneration with or without inflammatory cell invasion. The athletes made a full recovery with a gradual return to athletic activities after 3 to 4 weeks of immobilization. Surgery for longitudinal tears of the peroneus longus or brevis consists of debridement of the myxoid tendon margins and reapproximation of the longitudinal rent with a running absorbable suture. The limb is protected from active eversion in a removable walking boot for approximately 6 weeks. Passive inversion motion is encouraged to promote gliding of the tendons in the sheath. The ankle rehabilitationilitation protocol is begun at 6 weeks and return to running and jumping activity may occur at 10 to 12 weeks after surgery. Through a cadavaric study [79], Bassett found that with an inversion ankle injury and plantar flexion less than 15, the peroneal retinaculum will be injured, with resulting instability to the peroneal tendons. With plantar flexion in the range of 15 to 25, both peroneal tendons are perched along the distal fibula. With subsequent inversion motion, this causes tendon damage. With plantar flexion greater than 25, the peroneal tendons are well seated behind the fibula protecting them from injury. Peroneal tendon dislocation has been reported to be approximately 0.9% of lower extremity injuries in skiers [95]. This does occur to a lesser extent in other sport activities [76,85,91,96 104]. The etiology of this particular injury has initiated cadaveric studies examining the anatomic variations of the fibula and retrofibular sulcus. Edwards [99] examined 178 fibulas and found 82% had a definite sulcus involving the posterior aspect of the lateral malleolus, and 18% had either a flat groove or convex surface, which suggests a possible anatomic etiology to this problem. An inversion ankle sprain mechanism and related peroneal tendon dislocation have also been linked, though the most common mechanism is forced dorsiflexion with contraction of the peroneal tendons [33]. The classification of peroneal tendon dislocations has been described by Eckert and Davis. They classify the pathologic findings into three groups: Grade I retinacular separation of the anterior lip; Grade II peroneal retinacular tear; and Grade III avulsion of the lateral malleolus [84]. The diagnosis of a peroneal dislocation is made with patient history and characteristic swelling and tenderness occurring posterior and superior to the lateral malleolus. The patient with a peroneal dislocation usually reports a snapping sensation accompanied by pain in the posterolateral aspect of the ankle. Circum-
30
duction of the ankle with palpation over the peroneal tendons may elicit a dislocation or subluxation of the peroneal tendons. Treatment of this injury is controversial. Escalas [100] conservatively treated 38 patients with acute peroneal dislocation injuries using tendon reduction and compressive dressing. Twenty-eight patients went on to have recurrent dislocations. Eckert and Davis [84] treated seven acute injuries conservatively and six had persistent pain and recurrent dislocation. Of 73 patients with acute injuries treated with acute surgical repair, Eckert and Davis found that 76% had excellent results. Stover and Bryan [105] report on 17 acute peroneal dislocations. Seven were treated with non-weight bearing casts for 4 weeks. Six of these patients had excellent results. Eight patients went on to have conservative management with ankle strapping; 7 patients were unsuccessful with this treatment protocol. These 7 patients underwent surgical intervention. It is unclear whether or not these treatment failures were the result of unrecognized ankle instability concurrent with peroneal tendon dislocation, or peroneal tendinosis with longitudinal tears causing persistent pain, or recurrent dislocation. Chronic dislocations of the peroneal tendons are primarily treated surgically [83,85,96,102,106]. There are a number of procedures described, with variable success rates and follow-ups. The treatment options include periosteal reattachment procedures, groove deepening procedures, tenoplasty procedures, and bone block procedures. Immobilization of the ankle with a walking cast or boot is needed for approximately 6 weeks after surgical repair of an acute or chronic peroneal tendon dislocation. Ankle rehabilitationilitation is begun after this time for 6 additional weeks before return to sporting activities.
Summary Chronic ankle pain can be due to multiple causes. A thorough review of the patients history with a physical examination concentrating on anatomic structures surrounding the ankle is imperative. The most common of causes have been presented. The addition of provocative testing and radiographic examinations can aid in elucidating the pathology. After treatment of the injury, attention to training technique, shoe and insert usage as well as individual gait abnormalities are integrated into global patient education to decrease the incidence of injury recurrence.
References
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Arthroscopy for athletic foot and ankle injuries

Terrence M. Philbin, DOa,b, Thomas H. Lee, MDb, Gregory C. Berlet, MDa,b,*
Department of Orthopaedic Surgery, The Ohio State University, 370 West 9th Avenue, Columbus, OH, 43210, USA b Orthopedic Foot and Ankle Center, 6200 Cleveland Avenue, Columbus, OH 43231, USA
a
Arthroscopic and endoscopic techniques used today have a long history of development. The earliest efforts involved instruments to view the urinary bladder. Professor Kenji Takagi of Tokyo University in Japan first applied endoscopic techniques to the knee joint in 1918 [1 4]. His initial goal was to diagnose and treat the stiffness of tuberculous arthritis, which caused serious social disabilities among Japanese citizens who were unable to kneel or squat. On July 6, 1932, he gave the first report of endoscopy of the knee to the Japanese Orthopedic Association [5]. Bircher, in 1921, placed the Jacobeus laparoscope into a knee and referred to the technique as artho-endoscopy [6,7]. Kreuscher published the first report describing arthroscopy in the US literature in 1925 [8]. He discussed the use of arthroscopy for the diagnosis and treatment of meniscal lesions. Unfortunately, World War II halted most of the advancements of arthroscopy until the 1950s. In 1955, Watanabe, a student of Professor Takagi, performed the first recorded arthroscopic surgical procedure [3,9,10]. During the late 1960s and 1970s, the teaching of arthroscopy grew rapidly in the United States. By the 1980s, arthroscopy was accepted as a minimally invasive diagnostic tool that was associated with few complications. This article describes recent arthroscopic techniques that are useful in diagnosing and treating athletic injuries of the foot and ankle.
Arthroscopy of the great toe In 1972, Watanabe described the first arthroscopy of the first metatarsophalangeal (MTP) joint [11]. Common indications for arthroscopy of the first
* Corresponding author. Orthopedic Foot and Ankle Center, 6200 Cleveland Avenue, Columbus, OH 43231. E-mail address: gberlet@aol.com (G.C. Berlet). 0278-5919/04/$ see front matter D 2004 Elsevier Inc. All rights reserved. doi:10.1016/S0278-5919(03)00093-0
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T.M. Philbin et al / Clin Sports Med 23 (2004) 3553
Table 1 Indications for first MTP arthroscopy Authors Davis and Saxby [12] van Dijk et al [13] Borton et al [14] Indications bone cyst of the proxmial phalanx meniscoid-like lesion painful sesamoid bones bacterial arthritis pigmented villonodular synovitis
MTP joint include osteophytes, hallux rigidus, chondromalacia, osteochondral dissecans, loose bodies, arthrofibrosis, and synovitis (Table 1 [12 14]). Dorsal osteophytes, hallux rigidus, and osteochondral lesions are common indications among athletes. Diagnostic first MTP arthroscopy may be indicated for patients who fail conservative treatment of recurrent edema, locking pain, and diminished range of motion [15]. Arthroscopic anatomy and portals The dorsal medial, dorsal lateral, and straight medial portals are used most commonly for arthroscopic evaluation and treatment of the first MTP joint (Fig. 1A,B). van Dijk et al reported that two portals are needed to visualize and treat disorders of the lateral sesamoidone in the first web space and another 4 cm proximal to the joint line between the short abductor and the flexor halluces
Fig. 1. (A,B) The dorsal medial, dorsal lateral, and straight medial portals. (Illustrations created by Peter Maurus, MD, Resident, Department of Orthopaedic Surgery, The Ohio State University, Columbus, OH.)
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brevis muscle [13]. When making portals, care must be taken to avoid injuring the branches of the deep peroneal nerve laterally, branches of the superficial nerve medially, and branches of the saphenous around the medial aspect of the first MTP joint. Technique The patient is placed in a supine position on the operating table with the heels resting on the end of the table. After appropriate anesthesia is administered, apply an ankle or thigh tourniquet (usually not inflated unless needed during the procedure). Routine sterile skin preparation and draping are performed. The joint can be visualized using manual traction or a sterile finger trap. Palpate the joint line either side of the extensor halluces longus (EHL), insert a 22-gauge spinal needle into the joint medial to the EHL, and inject 5 ml of normal saline to distend the joint. Make a longitudinal skin incision with a #15 blade and use a hemostat to spread the subcutaneous tissue to avoid trauma to the surrounding neurovascular bundles. A blunt trocar is inserted into the joint followed by the arthroscope. A 1.7 mm [15], 1.9 mm [12], and 2.7 [13] mm scope have all been used for first MTP arthroscopy. The dorsal lateral portal can be started once the joint is visualized. The spinal needle is then inserted to assist with appropriate placement of the dorsal lateral and straight medial portals. A 13-point, systematic examination of the first MTP, as described by Ferkel, proceeds as follows [16]: 1. Lateral gutter 2. Lateral corner of the metatarsal head 3. Central portion of the metatarsal 4. Medial corner of the metatarsal head 5. Medial gutter 6. Medial capsular reflection 7. Central bare area 8. Lateral capsular reflection 9. Medial portion of the proximal phalanx 10. Central portion of the proximal phalanx 11. Lateral potion of the proximal phalanx 12. Medial sesamoid 13. Lateral sesamoid Davies and Saxby list 10 equipment requirements for first MTP arthroscopy with finger trap distraction [17]: Thigh tourniquet Shoulder holder Sterile Chinese finger trap 1.9 mm, 30 arthroscope Small joint shaver
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2 mm probe 2 mm curette Small joint grasper Two 23-gauge needles 10 cc syringe Postoperative care and rehabilitation The small portals are approximated with interrupted nylon sutures and a bulky compressive dressing is applied for 1 week. The patient should remain nonweight bearing for the first week. After 1 week, a low-tide walker boot can be used until pain and swelling resolve. Range-of-motion exercises can be started 2 weeks postoperatively. Results There is a paucity of literature on the clinical results of first MTP arthroscopy. Ferkel and Van Buecken reported the results of 22 patients whose ages ranged from 18 to 70 years (mean age 40), with a mean follow-up of 54 months [18]. They reported a good outcome in 73% of the cases, fair outcome in 13.5%, and poor outcome in 13.5%. All patients in the fair and poor categories had degenerative joint disease and required a fusion later. van Dijk et al reported on 23 patients who underwent first MTP arthroscopy [13]. The patients averaged 33 years of age (range, 16 61 years) and the followup period averaged 2 years. They reported excellent or good results for 14 patients and fair or poor results for 9 patients. One patient experienced transient loss of medial hallux sensation and another experienced loss of lateral hallux sensation. The authors advocate sesamoid removal laterally with the scope but state that removing the medial sesamoid arthroscopically has not proven promising. Davies and Saxby performed first MTP arthroscopy on 11 patients ranging from 15 to 58 years of age (mean 30 years) with a mean follow-up of 19.3 months [17]. At the final follow-up, all the patients had no or minimal pain, decreased edema, and increased range of motion. One patient had a minor wound complication. Three patients required an arthrotomy during the surgery. In summary, first MTP arthroscopy is an evolving technique. The best indications are osteochondral lesions. Debridement of marked degenerative joint disease should be discouraged.
Subtalar arthroscopy In 1985, Parisien and Vangsness published the results of a cadaveric study of subtalar arthroscopy [19], followed by three case reports in 1988 [20]. The major potential advantages of the subtalar arthroscopy compared with subtalar arthrotomy include diminished morbidity and more rapid rehabilitation. Open subtalar arthrotomy often requires fat pad excision, extensor digitorum brevis
39
detachment, and cervical ligament transectionall of which can be avoided with subtalar arthroscopy. The indications for arthroscopy of the subtalar joint include chondromalacia, osteophytes, arthrofibrosis, synovitis, loose bodies, osteochondritis dissecans, painful os trigonum syndrome [21], and arthroscopic-assisted reduction in calcaneal fractures [22,23]. Subtalar arthroscopic anatomy and portals The most common primary portals used for subtalar arthroscopy are the anterior lateral, middle, and posterior lateral portals (Figs. 2 4). Cheng and Ferkel have described the accessory anterolateral and accessory posterolateral portals that are used for instrumentation [24]. Mekhail et al reported good subtalar joint visualization via a medial subtalar arthroscopic portal in a cadaveric study [25]. The bony anatomy and Achilles tendon should be outlined before surgery. The superficial peroneal nerve, sural nerve, and the dorsalis pedis neurovascular bundle should also be outlined. Establish the anterior lateral portal approximately 1 cm distal and 2 cm anterior to the tip of the fibula. The posterior lateral portal is positioned slightly proximal to the fibular tip and anterior to the Achilles tendon. Place the middle portal just anterior to the fibula and directly over the sinus tarsi. Frey et al reported the results of a cadaveric study evaluating subtalar arthroscopy portals and the structures at risk [26]. The posterior lateral portal posed the
Fig. 2. Sites are marked for creating the posterior lateral portal, middle portal, and anterolateral portal. (Courtesy of Christopher Hyer, MD, Columbus, OH.)
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Fig. 3. The arthroscope is placed in the anterior lateral portal and the shaver is placed in the middle portal. (Courtesy of Christopher Hyer, MD, Columbus, OH.)
greatest risk of nerve or vessel damage in the study. The sural nerve and lesser saphenous vein are at risk during posterior lateral portal placement. The middle portal was found to be without risk to the surrounding structures. The study showed that the dorsal intermediate cutaneous branch of the superficial nerve and a small branch of the lesser saphenous vein are at most risk with anterior lateral portal placement. Frey et al reported that the best portal combination for posterior facet visualization was placing the arthroscope in the anterior lateral portal and the instrumentation in the posterior lateral portal [26]. Technique The patient is placed in a lateral decubitus position with the operative extremity upward. After appropriate anesthesia is administered, a thigh tourniquet should be applied, as should a noninvasive distraction strap to assist with visualization. Following routine skin preparation and draping, the joint can be distracted by placing an 18-gauge needle into the anterior lateral portal, with the needle positioned away from the sinus tarsi upon entry to help prevent injury to the articular surface. Once the needle is in proper position, the joint is distended with fluid, and free backflow of fluid is used to help confirm intra-articular placement. The 2.7 mm arthroscope is then inserted into the joint and an outflow cannula is established with an 18-gauge needle in the posterior lateral portal. Care should be taken to avoid making the posterior lateral portal too proximal, which
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Fig. 4. The arthroscope is placed in the anterior lateral portal and the shaver is placed in the posterior lateral portal. (Courtesy of Christopher Hyer, MD, Columbus, OH.)
can prevent entering the posterior ankle joint. Visualization of the intra-articular needle helps to confirm proper positioning. The posterior lateral portal can be used for joint inspection or placement of instrumentation. Ferkel has recommended the following 13-point diagnostic subtalar exam [16]: 1. Deep interosseous ligament 2. Superficial interosseous ligament 3. Anterior posterior talocalcaneal joint 4. Anterolateral corner 5. Lateral talocalcaneal ligament 6. Calcaneofibular ligament 7. Central talocalcaneal joint 8. Posterolateral gutter 9. Posterolateral recess 10. Posterior gutter 11. Posteromedial recess 12. Posteromedial corner 13. Posterior talocalcaneal joint Numbers 1 through 8 should be visualized through the anterior lateral portal and numbers 9 through 13 can be seen through the posterior lateral portal.
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The authors recommend the following equipment for subtalar arthroscopy: 1.9 mm or 2.7 mm arthroscope Small joint shaver 18-gauge spinal needles Small joint probe and grasper Ring curets Small joint picks K-wires Noninvasive joint distracter Rarely, an ankle arthroscopy and subtalar arthroscopy may be required at the same operative setting. Should this occur, it is recommended that the subtalar arthroscopy be performed first, because after ankle arthroscopy, the fluid extravasation can prevent proper subtalar portal placement. Postoperative care and rehabilitation Following surgery, the small portals are approximated with interrupted nylon suture. The extremity is placed into a bulky dressing with a posterior splint. For the first week, patients are instructed to be non-weight bearing. At 1 week postoperatively, the extremity can be placed in a low-tide boot and walking may begin as pain and swelling allow. Range-of-motion exercises are commenced when wound healing is complete. Results There are few published reports of the results of arthroscopy of the subtalar joint. In 1994, Williams and Ferkel reported the results on 29 patients who had subtalar arthroscopy [27]. All the patients in the study underwent ankle arthroscopy followed by subtalar arthroscopy. With an average 32-month follow-up, 86% of the results were good-to-excellent and there were no major complications. Goldberger and Conti presented the clinical outcomes of 12 patients after subtalar arthroscopy [28]. Their mean age was 41 years and follow-up averaged 17.5 months. The mean preoperative American Orthopaedic Foot and Ankle Society (AOFAS) Ankle-Hindfoot Scale Score was 60, which improved to 71 postoperatively. Three patients improved their score by 10 or more points. Three of the 4 patients whose scores decreased scores later required subtalar fusion. The authors found subtalar arthroscopy to be a more accurate method of diagnosing subtalar articular injury than radiographs, bone scan, and magnetic resonance imaging. The therapeutic benefit in the treatment of early degenerative joint disease with subtalar arthroscopy was thought to be limited. Frey et al reported a retrospective study on 49 subtalar arthroscopies [29]. The average patient age was 35 years and the follow-up period averaged 54 months. Excellent-to-good results were achieved in 94% of the cases. The
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group had 90% good to excellent results. The authors believe that sinus tarsi syndrome is an inaccurate term and that subtalar arthroscopy is the proper tool to assist with accurate diagnosis of subtalar etiologies (14 of the patients had the preoperative diagnosis of sinus tarsi syndrome). After subtalar arthroscopy, all the diagnoses were changed. There were five minor complications resolved with nonoperative treatment; transient neuropraxia was the most common complication [29].
Anterior ankle impingement Anterior ankle impingement exostoses (footballers ankle) can decrease ankle dorsiflexion, cause anterior ankle pain, and can compromise ankle proprioception [30,31]. Anterior impingement lesions occur most commonly in the athletic population, particularly dancers and soccer players. Many etiological theories have been proposed, including anterior ankle capsular strain from forced plantarflexion with resultant calcific deposits along capsular lines, or repetitive dorsiflexion resulting in subchondral injury and new bone formation [31 33]. These spurs can occur coincidentally with degenerative joint disease, although there is no conclusive evidence that chronic ankle instability leads to degenerative joint disease [34]. Capsular strain likely represents the mechanism of anterior impingement lesions, which are found commonly in the chronically unstable ankle. Impingement can be classified according to the stages of Scranton and McDermott: Stage Ianterior tibial osteophytes less than 3 mm, Stage II osteophytes greater than 3 mm with osteochondral reaction, and Stage IIItibial and talar kissing lesions [35]. These lesions can be confirmed and staged with weight-bearing lateral radiographs in forced dorsiflexion. Using CT scanning for assessment of the axial malleolar distance, the mortise configuration has been proposed to influence the development of these spurs, as a more posteriorly positioned fibula increases the risk of lateral ankle instability and subsequent anterior impingement [36]. Berberian et al have shown that the talar spur peak lies medial to the midline, the tibial spur lies lateral to the midline, and the spurs typically do not overlap each other [37]. They also found that the tibial spur is wider than the talar spur, and the talar spur usually protrudes medially off the medial edge of the talar neck. The tibial spurs of impingement are anterior, whereas the degenerative spurs are more global [35]. Treatment considerations must include the association of lateral ankle instability and mechanical axis deviation as comorbid factors to the patients disability. Anterior ankle spurs can be removed arthroscopically or via open arthrotomy. It is the authors experience that arthroscopic intervention is successful in most cases, although the portals may need to be enlarged to accommodate large bony fragments. The spurs are best visualized with no distraction applied to the foot, because distraction tends to draw the anterior capsule close to the anterior bony structures. A 4.0 mm burr facilitates both the
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removal of the spur and adequate fluid flow to preserve visualization. A burr run on reverse has less potential for overly aggressive resection and can be useful for final smoothing or for less experienced arthroscopists. Degenerative spurs should be approached with caution, because the patients pain can be increased with improved ankle motion.
Posterior ankle arthroscopy Ankle arthroscopy has traditionally been performed using anterior ankle portals. At times, however, posterior pathology cannot be accessed through anterior portals. To facilitate posterior access, posterolateral, posteromedial, and transAchilles tendon portals can be used [38,39]. Pathology that may require posterior arthroscopic visualization includes posteromedial and posterolateral talar osteochondritis dissecans lesions, flexor halluces longus stenosing tenosynovitis, posterior ankle impingement, displaced fracture of the os trigonum, insertional Achilles tendinitis, and retrocalcaneal bursitis. Technique Although there are three portals described for posterior ankle arthroscopy, the majority of clinical research has focused on the posterolateral portal. The paraAchilles posterolateral portal is made at the level of or slightly above the tip of the lateral malleolus just lateral to the Achilles tendon. The portal is established by introducing a spinal needle at the posterolateral site, injecting the posterior ankle joint with saline to confirm placement, and then making a small vertical skin incision. Blunt dissection is carried down until bone is encountered and then a 30, 4.5 mm arthroscope shaft with a blunt trocar is introduced into the ankle joint. A coaxial portal placed directly posterior to the peroneal tendons can also be used. The para-Achilles portal should be created with the patient in the prone position, whereas the portal directly posterior to the peroneal tendons can be performed with the patient in the supine position. Results Drez et al reviewed 56 arthroscopies performed with a combination of anterior and posterior portals [40]. They found that the posterolateral portal allowed for a comprehensive view of the posterior recess and that the posteromedial portal was rarely needed. Ferkel et al likewise recommend the use of a posterolateral portal in routine ankle arthroscopy to confirm a complete visualization of the ankle joint [41]. The structures at risk with the posterolateral portal include the sural nerve and small saphenous vein. Sitler et al, in a cadaveric dissection study of the para-Achilles posterolateral portal, showed the average distance between the posterolateral portal and the sural nerve to be 3.2 mm and the average distance between the small saphenous vein and the portal to be 4.8 mm [39].
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Ferkel et al reported a neurological complication rate, using combination anterior and posterolateral portals, of 4.4% [41]. The posteromedial portal has been described being made in a para-Achilles location or in a true posteromedial location coursing between the posterior tibial tendon and flexor digitorum tendons [42 44]. The Achilles tendon posteromedial portal is made just medial to the Achilles tendon in the horizontal plane, at the same level as the posterolateral portal. A needle is inserted through the skin at the appropriate location, oriented toward the lateral aspect of the joint to ensure placement lateral to the flexor halluces longus tendon. The appropriate positioning of the needle can be confirmed via the arthroscope in the posterolateral portal before the posteromedial portal is created. The posteromedial portal is then established, with a short skin incision and blunt dissection to the posterior ankle joint following the course of the previous needle. The alternative posteromedial portal is made by developing the interval between the posterior tibial tendon and the flexor digitorum longus behind the medial malleolus. The blunt dissection is carried to the posterior ankle joint and the arthroscope introduced into the joint. Structures at risk with the posteromedial portal include the flexor halluces longus tendon and the posteromedial neurovascular bundle. Using the para-Achilles posteromedial portal, the average distance between the portal and the flexor halluces longus tendon was 2.7 mm, the average distance to the tibial nerve was 6.4 mm, and to the tibial artery 9.6 mm [39]. Using a posteromedial portal directly behind the medial malleolus adjacent to the posterior tibial tendon, the average distance from the cannula to the posterior tibial nerve was 5.7 mm and 6.4 mm to the tibial artery. The para-Achilles posteromedial portal is best used with the patient in the prone position, whereas the posteromedial portal may be used with the patient in the standard supine position.
Endoscopic calcaneal prominence resection The retrocalcaneal bursa and Achilles tendon can become compressed and irritated by a posterior-superior calcaneal prominence. When nonoperative treatment fails, the condition can be treated by open calcaneal resection, retrocalcaneal bursectomy, and Achilles debridement with repair when necessary. Recently, endoscopic calcaneoplasty has been described. The procedure is performed with the patient in a prone position, and posterior medial and posterior lateral portals are used. The portals are placed just medial and lateral to the Achilles tendon and just proximal to the superior aspect of the calcaneus. A 2.7 mm arthroscope and small joint equipment are recommended. To the authors knowledge, clinical results are yet to be published on endoscopic calcaneal resection. Extra-articular endoscopic decompression of the retrocalcaneal space can be useful for treating retrocalcaneal bursitis, Haglunds spur, and impingement. The arthroscopic approach may decrease postoperative recovery time and incisional complications. Using lateral and accessory medial portals, Leitze et al showed
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at an average of 22 months postoperatively, a comparable result to open retrocalcaneal decompression as measured by the AOFAS Ankle-Hindfoot Scale [45]. The study authors believe this technique is useful in minimizing wound complications and decreasing the postoperative recovery time.
Osteochondral lesions of the talus Osteochondral lesions of the talus (OLT) are most commonly attributed to trauma [46 54], and lateral talar dome lesions have a traumatic etiology more often than medial lesions [52,53]. The results of several biomechanical studies indicate that a repetitive overuse syndrome may be responsible for medial lesions, and support the belief that acute trauma causes lateral lesions [55 58]. The mechanism of injury of lateral lesions is inversion and dorsiflexion, in which the anterolateral aspect of the talus impacts the fibula. Medial lesions result from combined inversion, plantar flexion, and external rotational forces. The medial lesion is typically deep and cup-shaped, caused by the posteromedial talar dome impacting the tibial articular surface. Radiographic evaluation with the ankle in plantarflexion can show posteromedial lesions, and dorsiflexion can reveal anterolateral lesions. Magnetic resonance imaging is helpful in identifying injuries of the subchondral bone and cartilage. When an OLT is diagnosed, staging should follow according to one of several staging systems published previously [16,59 63]; however, studies correlating the stage of the lesion and outcome following treatment are lacking [49]. Treatment Arthroscopic treatment of OLT involves three principles: removing loose bodies, securing the OLT to the talar dome, and stimulating development of hyaline cartilage. Using a wide-angle, 2.7 mm arthroscope may provide more mobility than a 4 mm arthroscope, and noninvasive joint distraction enables visualization of the entire talar dome Microfracture The microfracture technique is relatively new in treating osteochondral defects of the talus, although the technique has been successful in treating chondral defects in the knee for several years [64,65]. Using awls, microfractures (perforations) are made approximately 3 mm to 4 mm apart in the subchondral bone while maintaining the integrity of the bone plate. The microfracture technique promotes new tissue formation by releasing substances such as mesenchymal stem cells, growth factors, and healing proteins [64]. Ultimately, cartilage-like cells form and fill the original defect. Steadman et al performed the microfracture technique in the knees of 25 professional football players between 1986 and 1997
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[66]. Players returning to the sport averaged 4.6 subsequent seasons of participation, and 9 players continued to play at the time of writing this article (April 2003). Thermann et al reported that early results show the technique is successful in improving function and restoring cartilage (as determined by MRI) in the talus [67].
Osteochondral autologous transfer system and mosaicplasty Osteochondral autologous transfer system (OATS) and mosaicplasty transplant either a single, large osteochondral plug into the talar defect, or multiple small plugs to cover the defect. The grafts are taken from the femoral trochlea or condyle. An advantage of the single-plug method is that fibrocartilage ingrowth is minimal, but a disadvantage is possible donor-site morbidity because of the large graft size. Mosaicplasty may reduce donor-site morbidity, but a disadvantage is that 20% to 40% of the defect can be filled with fibrocartilage because of the small size of the grafts [68]. Hangody et al [69] reported the results of mosaicplasty for large or unstable osteochondral lesions ( > 10 mm in diameter) in 36 patients. They used an average of three plugs, ranging from 3.5 mm to 6.5 mm. With follow-up ranging from 2 to 7 years, 94% of the patients had good-to-excellent results. There was no long-term ipsilateral knee donor site morbidity [69]. More recently, Hangody and Fules reported the results of autologous osteochondral mosaicplasty in 831 patients [70]. They reported good-to-excellent results in 94% of patients treated with talar procedures. Autologous chondrocyte implantation (ACI or Carticel, Genzyme Biosurgery, Cambridge, Massachusetts) is a process that grows the patients own cartilage cells, which are then implanted beneath a patch into the site of the defect. In one report of ACI in the knee, 79% of patients showed improvement 5 years postoperatively [71]. The researchers reported that ACI patients enjoyed greater improvement and higher levels of functioning than a control group treated with drilling, abrasionplasty, or microfracture techniques [71].
Arthroscopic repair of chronic ankle instability Ankle sprains are common injuries, occurring in an estimated 1/10,000 persons per day [72]. Although the majority of acute ankle sprains heal with physical therapy/ankle rehabilitation, approximately 29% to 42% of patients experience chronic functional ankle instability [73]. The anterior talofibular ligament (ATFL) is the most commonly injured ligament during ankle sprains. It serves as the primary restraint to inversion and translation at all angles of ankle flexion [74,75]. During an inversion ankle sprain, the anterolateral capsule is typically injured first, followed by the ATFL, calcaneal fibular ligament (CFL), and posterior talofibular ligament (PTFL).
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Thermal-assisted capsular modification Thermal-assisted capsular modification for chronic lateral ankle instability was introduced recently [76,77]. This technique has been successful in treating shoulder instability and early results in the ankle are encouraging. The concept is based on the fact that thermal energy between 65C and 70C shrinks collagen, which comprises more than 90% of joint capsules, ligaments, and tendons (TACS). Factors such as tissue properties themselves, variables related to the laser include the density, application time, and concentration area determine the amount of energy delivered to the tissue [78]. Pulsing the laser (alternating the beam on and off) can minimize tissue damage and control depth of penetration Our decision to use thermal capsular modification for lateral ligament reconstruction is influenced by the patients body habitus, activity pattern, and degree of ligament injury. Indications include patients with moderate build, intraligament stretching (not avulsed from bone), generalized ligamentous laxity with functional ankle instability, a commitment to adhere to the postoperative rehabilitation protocol, and no previous ankle ligament reconstructive surgery. Contraindications include muscle weakness, tendon tears and instability, proprioceptive disorders, subtalar instability, and tibiofibular joint instability. Preoperatively, each patient undergoes a focused physical examination assessing ankle instability, muscle weakness, tendon tears and tendon instability, proprioceptive disorders, subtalar instability, and tibiofibular joint instability. Radiographs of the affected ankle are obtained and MRI should be performed if peroneal tears and chondral injuries of the talus are suspected. Technique Following sterile preparation and drape of the ankle, a noninvasive ankle distractor strap is applied (Arthrex, Naples, Florida). Anteromedial and anterolateral portals are established. The surgeon should then perform a complete arthroscopic examination and treat any pathology encountered (eg, synovitis, osteochondral defects) accordingly. Impingement lesions in the anterolateral gutter are encountered frequently and should be debrided aggressively with an arthroscopic trimmer to allow adequate exposure of the anterolateral gutter. Once visualization of the anterolateral capsule and distal fibula is confirmed, introduce a thermal control wand through the lateral portal and release the distraction device when the thermal wand is in position. The anterior talofibular ligament can be identified consistently [79]. With maximum temperature set at 65C, the tissue of the anterolateral capsule (just distal and anterior to the distal fibula) and ATFL can be treated with the thermal wand by using a painting technique, starting deep in the lateral gutter and working anteriorly, avoiding repetitive treatment of a specific location. Thermal treatment is below the equator of the lateral arthroscopy portal to avoid creating an iatrogenic impingement lesion. The treated capsule will show a blushing following treatment. Surgeons familiar
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with shoulder thermal modification will note that there is a visual contraction of the shoulder capsule that occurs while working in the inferior glenohumeral pouch. There is much less visual confirmation of contraction in the ankle. Following adequate exposure to the thermal effects of the wand, the arthroscopic instrumentation can be removed. The ankle should be held in slight dorsiflexion and eversion as the portals are closed with suture and a well-padded posterior/ gutter splint (with cooling pack) is applied to the operative extremity. Results Between February 1999 and December 2001, the authors performed 42 arthroscopic thermal assisted capsular modifications of the anterolateral capsule and the ATFL [80]. The AOFAS hindfoot scores improved significantly: scores averaged 29.57 preoperatively (SD 15.6) and improved to 55.36 (SD 13.56) at an average follow-up of 14.1 months (P <.001). One patient had skin breakdown over the calf where the ankle distracter strap had been, which resolved with conservative wound care. There were no infections. Postoperatively, patients undergo physical examinations at 3-week intervals. Patients wear a non-weight bearing cast for the first 3 weeks, followed by a weight-bearing cast for 3 weeks, and then a weight-bearing boot walker for 3 weeks. Physical therapy ankle rehabilitation begins 9 weeks postoperatively. Favorable outcomes using thermal stabilization have been reported; however, no prospective studies have been published reporting the use of thermal modification for ankle instability [2,76,80 82]. The authors believe that select patients with chronic lateral instability who have failed a course of conservative treatment are good candidates for arthroscopic thermal capsular and ATFL shrinkage. Greater follow-up will be necessary to determine whether the ankle will remain stable over time. Longer-term followup will determine how the outcomes compare with traditional surgical methods (ie, modified Brostrom repair).
Acknowledgments Editorial assistance was provided by Janet L. Tremaine, Tremaine Medical Communications, Dublin, Ohio.
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T.M. Philbin et al / Clin Sports Med 23 (2004) 3553 mechanical and biochemical properties of cartilage from the human knee and ankle pairs. J Orthop Res 2000;18(5):739 48. Shepherd DE, Seedhom BB. Thickness of human articular cartilage in joints of the lower limb. Ann Rheum Dis 1999;58(1):27 34. Berndt AL, Harty M. Transchondral fractures (osteochondritis dissecans) of the talus. J Bone Joint Surg 1959;41-A:988 1020. Loomer R, Fisher C, Lloyd-Smith R, Sisler J, Cooney T. Osteochondral lesions of the talus. Am J Sports Med 1993;21:13 9. Dipaola JD, Nelson DW, Colville MR. Characterizing osteochondral lesions by magnetic resonance imaging. Arthroscopy 1991;7:101 4. Hepple S, Winson IG, Glew D. Osteochondral lesions of the talus: a revised classification. Foot Ankle Int 1999;20(12):789 93. Cheng MS, Ferkel RD, Applegate GR. Osteochondral lesions of the talus: a radiologic and surgical comparison. Abstract presented at the Annual Meeting of the American Academy of Orthopedic Surgeons. New Orleans, February 16 21, 1995. Steadman JR, Rodkey WG, Rodrigo JJ. Microfracture: surgical techcnique and rehabilitation to treat chondral defects. Clin Orthop 2001;391(Suppl):S362 9. Sledge SL. Microfracture techniques in the treatment of osteochondral injuries. Clin Sports Med 2001;20:365 77. Steadman JR, Miller BS, Karas SG, Schlegel TF, Briggs KK, Hawkins RJ. The microfracture technique in the treatment of full-thickness chondral lesions of the knee in National Football League players. J Knee Surg 2003;16:83 6. Thermann H, Becher C, Mueller S, Kilger R. The microfracture technique for the treatment of osteochondral and degenerative chondral lesions of the talus. Presented at the American Orthopaedic Foot and Ankle Society Summer Meeting. San Diego, July 19 21, 2001. Al-Shaikh RA, Chou LB, Mann JA, Dreeben SM, Prieskom D. Autologous osteochondral grafting for talar cartilage defects. Foot Ankle Int 2002;23(5):381 9. Hangody L, Kish G, Modis L, Szerb I, Gaspar L, Dioszegi Z, et al. Mosaicplasty for the treatment of osteochondritis dissecans of the talus: two to seven year results in 36 patients. Foot Ankle Int 2001;22(7):552 8. Hangody L, Fules P. Autologous osteochondral mosaicplasty for the treatment of full-thickness defects of weight-bearing joints: ten years of experimental and clinical experience. J Bone Joint Surg 2003;85-A(Suppl 2):25 32. Browne JE, Anderson AF, Micheli LJ, Erggelet C, Moseley JB, Fu F, et al. Five-year multicenter outcome of autologous chondrocyte implantation of the knee: results in the first 100 consecutive patients. Dallas (TX): American Academy of Orthopaedic Surgeons; 2002. Trevino SG, Davis P, Hecht PJ. Management of acute and chronic lateral ligament injuries of the ankle. Orthop Clin North Am 1994;25:1 16. Berlet GC, Anderson RB, Davis WH. Chronic lateral ankle instability. Foot Ankle Clin 1999; 4(4):713 28. Colville MR, Marder RA, Boyle JJ, Zaring B. Strain measurement in lateral ankle ligaments. Am J Sports Med 1990;18:196 200. Johnson EE, Markolf KL. The contribution of the anterior taalofibular ligament to ankle laxity. J Bone Joint Surg 1983;65:81 8. Ryan AH, Lee TH, Berlet GC. Arthroscopic thermal assisted capsular shrinkage in anterolateral ankle instability: a retrospective review of 13 patients. Presented at the AOFAS Annual Summer Meeting. Vail, CO, July 13 15, 2000. Myers JB, Lephart SM, Bradley JP, et al. Proprioception following thermal capsulorrhaphy. Presented at the AAOS Annual Meeting. San Francisco, February 28 March 4, 2001. Arnoczky SP, Aksan A. Thermal modification of connective tissues: basic science considerations and clinical implications. J Am Acad Orthop Surg 2000;8:305 13. Leyes M, Hersch J, Sferra J. Arthroscopic identification of the anterior talofibular ligament. Presented at the AOSSM Annual Meeting. Orlando, FL, June 30 July 2, 2002.
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[80] Berlet GC, Saar WE, Ryan A, Lee TH. Thermal-assisted capsular modification for functional ankle instability. Foot Ankle Clin 2002;7:567 76. [81] Orecchio A. Running Start, study reports heat shrinkage technique for ankle instability. BioMechanics 2000;April;14,5. [82] Berlet GC, Raissi A, Lee TH. Thermal capsular modification for chronic lateral ankle instability. Presented at the AOFAS Annual Summer Meeting. Traverse City, MI, July 12 14, 2002.
Overuse injuries: tendinopathies, stress fractures, compartment syndrome, and shin splints
Robert P. Wilder, MD, FACSM*, Shikha Sethi, MD
Department of Physical Medicine and Rehabilitation, The University of Virginia, 545 Ray C. Hunt Drive, Suite 240, P.O. Box 801004, Charlottesville, VA 22908-1004, USA
Approximately 50% of all sports injuries are secondary to overuse [1]. The frequency of overuse injuries evaluated in primary care sports medicine clinics is even greater, reportedly up to twice the frequency of acute injuries [2]. The majority of injuries evaluated in running injury clinics are related to overuse [3,4], and approximately half of these involve the lower leg (20%), ankle (15%), and foot (15%) [5,6]. Overuse injuries result from repetitive microtrauma that leads to local tissue damage in the form of cellular and extracellular degeneration, and are most likely to occur when an athlete changes the mode, intensity, or duration of training a phenomenon described as the principle of transition [7,8]. Physical training uses prescribed periods of intense activity to induce the desired goal of supercompensation or performance improvement. A mismatch between overload and recovery can lead to breakdown on a cellular, extracellular, or systemic level, however. At the cellular level, repetitive overload on tissues that fail to adapt to new or increased demands can lead to tissue breakdown and overuse injury. It is important to realize that, in theory, this subclinical tissue damage can accumulate for some time before the person experiences pain and becomes symptomatic. On the systemic level, rapid increases in training load without adequate recovery may cause a global overtraining syndrome. Strong predictors of overuse musculoskeletal injury include a previous history of injury as well as walking or running more than 20 miles per week [9]. Both intrinsic and extrinsic factors contribute to overuse injuries. Intrinsic factors are biomechanical abnormalities unique to a particular athlete and include such features as malalignments, muscle imbalance, inflexibility, weakness, and instability. High arches, for example, have been demonstrated to predispose to a
* Corresponding author. E-mail address: rpw4n@virginia.edu (R.P. Wilder). 0278-5919/04/$ see front matter D 2004 Elsevier Inc. All rights reserved. doi:10.1016/S0278-5919(03)00085-1
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R.P. Wilder, S. Sethi / Clin Sports Med 23 (2004) 5581
greater risk of musculoskeletal overuse injury than low arches (flat feet) in military recruits [10]. Extrinsic (avoidable) factors that commonly contribute to overload include poor technique, improper equipment, and improper changes in the duration or frequency of activity. These improper changes in activity duration/ frequency or training errors are the most common causes of overuse injuries in recreational athletes. Vulnerability to extrinsic overload varies with the intrinsic risk factors of an individual athlete [7]. Sports-acquired deficiencies, categorized as an extrinsic risk factor, actually represent the product of biomechanical abnormalities and training errors. Because sports activity can overload an athletes musculoskeletal system in predictable ways, athletic repetition without proper conditioning can propagate muscular imbalance and flexibility deficits. Injuries are often related to biomechanical abnormalities removed from the specific site of injury, underscoring the importance of evaluation of the entire kinetic chain [11]. Common overuse injuries of the lower leg, ankle, and foot include tendinopathies, stress fractures, chronic exertional compartment syndrome, and shin splints.
Tendinopathies Tendinopathies of the foot and ankle are relatively common and encompass a wide spectrum of maladies ranging from tendinitis (acute inflammation of the tendon) to tendinosis (chronic degeneration) to tenosynovitis (inflammation of tendon sheath) to partial and complete ruptures. Each one of these disorders is distinct, although they may be seen in combination. Four tendons in the foot and anklethe Achilles, posterior tibialis, peroneal brevis, and peroneal longus tendonsare most often involved. In contrast to acute traumatic tendinous injury, sport-related injuries most often involve repetitive submaximal loading of the tissues, resulting in repetitive microtrauma. An understanding of the anatomical pathophysiologic basis of these maladies is critical to their diagnosis and management. Histopathology The debate over the nomenclature of chronic tendon injury highlights some of the unresolved issues in the histopathology, etiology, and management of tendinopathies of the foot and ankle. Although the pathological label tendinosis has been in use for more than 25 years to describe collagen degeneration in tendinopathy [12], many clinicians still use the term tendinitis to describe painful chronic overuse injury, implying that the fundamental problem is inflammatory [13]. Maffulli, Khan, and Puddu advocate the use of the term tendinopathy as a generic descriptor of clinical conditions such as pain, swelling, and impaired performance in and around tendons arising from overuse, with the labels tendinosis and tendinitis most appropriately applied after histopathological examination [14].
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This nomenclature separates chronic degeneration of tendons from acute and mainly inflammatory processes, with implications for treatment and management. Tendinosis has been described as a failure of cell matrix adaptation to trauma because of an imbalance between matrix degeneration and synthesis [8]. The classic pathology is a loss of the normal collagenous architecture and replacement with an amorphous mucinous material that lacks the parallel, longitudinal architecture of normal tendon [15,16]. Histological examination reveals intratendinous collagen degeneration with fiber disorientation and thinning, hypercellularity, scattered vascular ingrowth, increases in the amount of ground substance and the proteoglycan concentration of ground substance, and a decrease in the ratio of Type I to Type III collagen [15,17,18]. Any inflammatory response or the presence of inflammatory cells is notably lacking in tissue samples of tendinopathy, differentiating tendinosis, or chronic overuse pathology from acute injury and tendinitis. Astrom and Rausing describe the major lesion in chronic Achilles tendinopathy as a degenerative process characterized by a curious absence of inflammatory cells and a poor healing response [18]. Similar histopathological findings in posterior tibial tendon dysfunction of a degenerative tendinosis with mucinous degeneration, fibroblast hypercellularity and neovascularization [19], and higher proportions of collagen Type III at the expense of collagen Type I [20] support the notion of a common disease process in overuse tendon injury, leading ultimately to tendon degeneration and an insufficient repair response. Functionally, whereas the healing response to an acute tendon injury involves an organized triphasic response of inflammation, proliferation, and maturation, the response to an overuse injury involves an inadequate, incomplete, and disorganized repair mechanism resulting in a substantially defective repaired tendon lacking in extracellular tissue organization, with decreased resistive strength and more vulnerability to further injury. Although the exact role of overuse in the pathogenesis of chronic tendon injuries and disorders is not completely understood, it is speculated that fatigued tendon loses its basal reparative ability with intensive repetitive activity, often eccentric in nature, leading to cumulative microtrauma that further weakens the collagen cross-linking and noncollagenous matrix and disturbs the micro- and macrovasculature of the tendon [21]. Ensuing local tissue hypoxia and impaired nutrition and energy metabolism likely play an important role in the sequence of events leading to tendon degeneration [13,21]. Leadbetter has called this the tendinosis cycle [8]. One of the first animal models of tendinopathy, developed by Soslowsky et al [22,23], has shown persistent microscopic changes of tendinosis in rat rotator-cuff supraspinatus tendon after exposure to multiple factors, including impingement and overuse [23]. Neither impingement alone nor overuse alone produced the same degree of changes, implying a multifactorial etiology for the pathologic effects of overuse on rotator cuff tendon. Current thinking supports the belief that a spontaneous tendon rupture is a typical end-state manifestation of degenerative processes in the tendon tissue [21], with partial macroscopic tears as a stage in the continuum of tendon degeneration [14]. Analysis of surgical specimens of Achilles tendons reveals that, although ruptured and tendinopathic tendons are histologically significantly more degen-
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erated than control tendons, the general pattern of degeneration seen is common to the ruptured and tendinopathic tendons, suggesting the possibility of a common, as yet unidentified, pathological mechanism acting on both tendon populations [24]. Laboratory and molecular analyses of tendinopathy have begun to reveal strategies that may guide future clinical management of overuse tendon injury. It has been hypothesized in the past that tendon degeneration may be preceded by acute and then chronic phases of inflammatory tendinitis [12,25,26]. Although no inflammatory infiltration has been observed in multiple studies of biopsy specimens of tendinopathic tendons, recent in-vitro work demonstrates that a molecular inflammation cascade mediated by IL-1 beta in human tendon cells can induce connective tissue cell expression of cytokines that further induces known matrix destructive enzymes such as matrix metalloproteinases (MMP-1 and MMP-3) [27]. Clinically, the activity of metalloproteinases in tendon destruction and degeneration is the target of the use of injectable aprotinin, a metalloproteinase inhibitor, in the setting of patellar and Achilles tendinopathy as an alternative to corticosteroid therapy [28,29]. Apoptosis, mediated by overuse-induced, stressactivated protein kinases, may also play a role in tendon degeneration and weakening, presenting another set of molecular targets for future therapies aimed at preventing or treating tendinopathy more effectively [16,30,31]. Achilles tendon disorders Commonly and inappropriately generalized as Achilles tendinitis by many clinicians, posterior heel pain in the setting of an overuse injury of the foot and ankle actually encompasses a spectrum of distinct and often coexistent pathological disorders with both inflammatory and degenerative etiologies [32]. The classification system set forth by Puddu et al separates degenerative conditions of the tendon itself (tendinosis with or without partial rupture) from inflammation of the paratenon (paratenonitis), inflammation of the tendon substance at its insertion (insertional tendonitis), and inflammation of the commonly afflicted bursa anterior to the insertion of the Achilles tendon on the calcaneus (retrocalcaneal bursitis) from complete tears caused by acute injury [12]. Puddu reserves a mixed category for paratenonitis with tendinosis including degeneration, partial tears, and calcification within the tendon [12], and Maffulli et al agree that clinically observed tendinopathy should include both of the histopathological entities peritendonitis and tendinosis [14]. According to Paavola et al, this suggestion has a sound basis because the clinical rationale to differentiate the histopathologic entities of Achilles peritendinitis and tendinosis is an uncertain one and there have been no randomized controlled studies comparing the outcomes of treatment or the natural history of these two conditions [25]. In clinical studies, the most common diagnosis of Achilles disorders was tendinopathy (55% 66%), followed by insertional problems (retrocalcaneal bursitis and insertional tendinopathy) (20% 25%) [25,33 36]. Achilles tendon disorders occur most often in athletes, and most often in those involved in running sports. An annual incidence of Achilles tendon disorders of 7%
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to 9% in top-level runners has been reported [6,37]. Kvist reviewed cases of 455 athletes with Achilles tendon disorders [33]. Eighty-nine percent of the athletes studied were men, with 53% involved in running sports and 11% involved in soccer. The rest of the patients were involved in other sports in which running was an important training means [13,33]. Interestingly, malalignment of the lower extremity was found in 60% of the athletes with Achilles tendon disorders [25,33,36]. Many intrinsic and extrinsic etiologic factors have been proposed to account for the development of Achilles tendon disorders. Common intrinsic etiologies invoked include various alignment and biomechanical faults, including hyperpronation of the foot, limited mobility of subtalar joints and limited range of motion of the ankle joint, leg-length discrepancy, varus deformity of the forefoot and increased hindfoot inversion, decreased ankle dorsiflexion with the knee in extension, poor vascularity, genetic makeup, and gender, age, endocrine, or metabolic factors [33,34,38 40]. Changes in training pattern, poor technique, monotonous, asymmetric, and specialized training, previous injuries, footwear, and environmental factors such as training on hard, slippery, or slanting surfaces have been cited by many authors as extrinsic factors which may predispose the athlete to tendinopathy. Training errors have been reported to be involved in 60% to 80% of runners who have tendon overuse injuries [25]. Training errors cited include running a distance that is too long, running at an intensity that is too high, increasing distance too greatly or intensity too rapidly, and performing too much uphill or downhill work [25,34,40,41]. Training errors, alignment, biomechanics, and extrinsic factors such as footwear and training surfaces can create microtrauma resulting from nonuniform stress within the Achilles tendon from different individual force contributions of the gastrocnemius and soleus, producing abnormal load concentrations within the tendon and frictional forces between the fibrils, and leading to localized fiber damage [13,42]. In this manner, excessive motion of the hindfoot in the frontal plane, especially a heel strike with excessive compensatory pronation, is thought to cause a whipping action on the Achilles tendon and predispose it to tendinopathy [13,43]. A complete discussion of the etiological factors of Achilles tendon disorders must include the caveat that the exact pathogenesis of Achilles tendinopathy and other disorders remains largely unknown [25]. In addition to the epidemiological studies showing Achilles tendon disorders in athletes, other studies have shown a significant incidence of Achilles tendinopathy in nonathletes and middle aged men with sedentary lifestyles [18,44]. In the absence of a true inflammatory reaction in chronic Achilles tendinopathy, the etiology of pain, the most limiting factor and usual chief complaint of patients with Achilles tendon disorders, is not well understood [45,46]. Puddu et al have shown that long-standing degeneration of the tendon can occur without clinical symptoms or pain, and yet tendinopathy can become symptomatic with the introduction of heavy training [12]. History and physical examination play a key role in the diagnosis of Achilles tendon injury. The onset of pain, its duration, and aggravating factors should be documented. A classic history involves an insidious and gradual increase in pain
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located 2 cm to 6 cm proximal to the insertion of the tendon and felt after exercise within days of a change in activity levels or training techniques. Rest often relieves symptoms, but return to activity reactivates the pain, generally within a few training sessions. In patients with advanced tendinopathy, pain may occur during exercise, and when severe, may interfere with the activities of daily living. Runners typically experience pain at the beginning and at the end of a training session, with a period of diminished discomfort in between. Clinical examination should start by the exposure of both legs from above the knees, and the patient should be examined standing and prone. Careful inspection should reveal malalignment, deformity, areas of swelling, obvious asymmetry in the size of the tendon, localized thickening, erythema, and any previous scars. Palpation should document contours of the tendons, tenderness, thickening, palpable tendon nodules or defects, crepitation, and warmth. Biomechanics of the foot, ankle, and leg during walking and running, including slow motion analysis, should be evaluated in athletes. All patients should be examined for evidence of ankle instability [25]. The painful arc sign may help to distinguish between lesions of the tendon and paratendon [47]. Whereas peritendinitis is characterized by crepitus, exquisite tenderness, and swelling that does not move with tendon action, chronic Achilles tendinopathy is notable for absence of crepitation and swelling, with focal tender nodules that move as the ankle is dorsiflexed and plantar flexed [47]. The VISA-A scale is a subjective, quantitative scale of symptoms and dysfunction in the Achilles tendon and may be a useful tool to assess and follow symptomatology over time [48]. Both ultrasound and magnetic resonance imaging (MRI) play a role in the diagnosis of Achilles tendon disorders. Ultrasonography provides an inexpensive, sensitive analysis of the pathology of the Achilles tendon, with data regarding tendon width, water content within the tendon and peritendon, and collagen integrity. Abnormal tendons may have increased tendon diameter, focal hypoechoic intratendinous areas (areas of increased water content which at surgery have been shown to be degenerated tissue), localized tendon swelling and thickening, collagen discontinuity, and tendon sheath swelling or calcifications [25]. In the acute phase, ultrasound examination may reveal fluid surrounding the tendon. In the chronic phase, thickening of the hypoechoic paratenon may be seen, although ultrasonography has not been shown to reliably differentiate focal tendinosis from partial rupture [49]. Abnormalities detected by ultrasonography in an asymptomatic Achilles tendon can accurately presage the development of Achilles tendinopathy [50]. Magnetic resonance imaging provides extensive information on the internal morphology of the tendon and the surrounding structures and is used often for evaluation before surgical intervention [32]. MRI can also help characterize retrocalcaneal bursitis and insertional tendinitis. In patients with chronic tendinopathy, MRI often reveals tendon thickening and increased signal within the Achilles tendon. Areas of mucoid degeneration are shown on MRI as a zone of high signal intensity on T1- and T2-weighted images. Two caveats on MRI interpretation in Achilles tendon disorders include the unreliability of MRI to demonstrate
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changes of paratenonitis [51] and the temptation of the clinician to mistake areas of increased signal on MRI for pathologic, clinically significant foci rather than asymptomatic areas of degeneration [32]. The goals of treatment in Achilles tendinopathy are threefold: (1) to minimize the pain, (2) to prevent further degeneration, and (3) to allow return to baseline activity. In athletes, an additional demand is that the recovery time should be as short as possible [25]. Initial conservative management aims to relieve symptoms and correct factors causing load imbalance and repetitive strain on the tendon and surrounding structures. This includes a combination of strategies aimed at controlling inflammation and correcting training errors, limb malalignment, decreased flexibility, and muscle weakness, and the use of appropriate equipment during sports [25,52]. The role of anti-inflammatory therapy such as oral nonsteroidal anti-inflammatory drugs (NSAIDS) or steroid pain relievers to control inflammation remains controversial. Although no inflammatory infiltrate has been documented in histological analyses of tendinopathic samples, anti-inflammatory medication does help to diminish pain and facilitate rehabilitation in cases of chronic tendinopathy and most certainly has a place in the management of retrocalcaneal bursitis and insertional tendinitis [17,53]. Cryotherapy has also been shown to be useful to help control inflammation and facilitate therapy in tendinopathy [54]. Occasionally, complete rest or cessation of the training that caused the symptoms may be required for a short time to settle severe symptoms. Because the repair and remodeling of collagen fibers are stimulated by loading of the tendon, only very short courses of complete rest should be prescribed. Heparin may be injected to prevent fibrin exudate in the paratenon region [17]. Recently, Ohberg and Alfredson have described successful ultrasound-guided injection of polidocanol, a sclerosing agent, to decrease the neovascularization and symptomotology of chronic midportion Achilles tendinosis [55]. Appropriate and progressive exercises using eccentric exercise programs targeting specific muscle hypertrophy, speed, strength, and endurance requirements represent the gold standard for Achilles tendon rehabilitation and appear to be effective in most athletes [56]. Mafi et al have shown prospectively that a program of eccentric calf muscle training was superior to concentric training in Achilles tendinosis [57]. Correction of biomechanical imperfections is clinically important, even if their effects on tendonitis are unclear. Interventions improving flexibility of the ankle joint, flexibility of calf muscles, amount or speed of foot pronation, and foot and ankle mechanics (with orthotics) have been implicated in ameliorating symptoms of tendinopathies. Operative treatment is recommended for patients who do not respond adequately to a 3- to 6-month trial of appropriate conservative treatment. To date, no prospective randomized controlled studies comparing operative and conservative treatment of Achilles tendinopathy have been published [25]. Surgery for overuse tendinopathies usually involves excision of fibrotic adhesions and degenerated nodules, or decompression of the tendon by longitudinal tenotomies. Reconstructive procedures may be necessary if large nodules and lesions are excised. Some authors have used open or percutaneous multiple longitudinal incisions of the
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tendon [58]. In most studies, satisfactory results in 75% to 100% of the patients have been reported after operative intervention of Achilles tendinopathy [25]. Generally, long-standing tendinopathies are associated with poorer surgical outcomes [51,58]. Recently, an overall complication rate of 11% was documented in a series of 432 consecutive patients [59]. Although much is known about Achilles tendon disorders, and much more is known about Achilles tendinopathies than about other tendinopathies of the foot and ankle, ample opportunity exists for better controlled studies to examine operative and conservative treatment regimens, postoperative rehabilitation protocols, and long-term follow-up of clinical interventions. In addition, further study of the etiologies of Achilles tendon disorders, the causative factors in the pain of chronic tendon injury, and the factors contributing to the histopathology of tendinopathy could help identify therapeutic targets for molecular medicine. Posterior tibial tendon dysfunction Posterior tibial tendon dysfunction (PTTD) is a common cause of painful acquired flatfoot deformity in adults and is associated with substantial functional problems resulting in significant morbidity. These patients typically have a loss of hindfoot inversion, inability to negotiate uneven ground, climb, and descend stairs [60]. As acquired flatfoot syndrome advances, progressive collapse of the medial longitudinal arch, hindfoot valgus, and forefoot abduction abnormalities are noted [19]. Shoe fitting is difficult. Pain and instability in the hindfoot have significant impact on daily routines [60]. Johnson and Strom [61] have described three distinct stages of posterior tibial tendon dysfunction. In Stage I, the patient has pain and swelling along the course of the tendon. Because the length of the tendon is normal, the patient is able to perform single heel raise. The flatfoot deformity is minimal, the alignment of the hindfootforefoot complex is normal and the subtalar joint remains flexible [19,62]. In Stage II, the patient is unable to perform a single heel raise because of attenuation or disruption of the posterior tibial tendon. The tendon is enlarged and elongated and functionally incompetent. The foot has adopted a pes planovalgus position with collapse of the medial longitudinal arch, hindfoot valgus and subtalar joint eversion, and forefoot abduction through the talonavicular joint. The subtalar joint remains flexible, and the hallmark of this stage is that with the ankle in equinus, the talonavicular joint can be reduced [19,62]. Stage III disease presents with the patient unable to perform a single heel raise and a more severe flatfoot deformity. In Stage III disease, the pes planovalgus deformity is fixed and the laterally subluxed navicular cannot be reduced [19,62]. The histopathology of PTTD reveals a degenerative intratendinous process similar to that seen in Achilles tendinopathy. Mosier et al studied 15 normal cadaveric tendons and 15 surgical specimens from patients with Stage II PTTD [63]. Four types of histopathology were present in the disease samples: (1) increased mucin content, (2) hypercellularity, (3) neovascularization, and (4) chondroid metaplasia. Disruption of the normal array of collagen bundles
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represented a degenerative tendinosis with a nonspecific reparative response to tissue injury [63]. Both ultrasound and magnetic resonance imaging can play a role in the diagnosis of PTTD. According to Perry et al, ultrasonography can positively identify peritendinitis and tendonitis. Tendon interruption, or inhomogeneity of tendon by MRI assessment, however, remains more sensitive than either clinical or ultrasound evaluation to evaluate for partial tears. In their study comparing clinical findings with those of magnetic resonance imaging and ultrasonography in 31 subjects, tendon dysfunction, as measured by heel raise, was not correlated with inhomogeneity by MRI [60]. They concluded that partial tears without painful sequelae may be missed by the clinician when doing tests to evaluate tendon function and resistance testing in an attempt to assess pain or dysfunction. Ultrasound to assess pain or dysfunction also may miss patients with partial tears. If ligamentous structures remain intact, they noted that there may be little change in the medial arch until the posterior tibial tendon finally tears, that pain on clinical palpation or resistance testing usually means inflammation is present, and that in these cases, the structure most likely to be affected is the tendon sheath [60]. Treatment of PTTD depends on many factors. During the time that the foot remains flexible, treatment is possible with a corrective orthosis such as the University of California Biomechanics Laboratory brace, molded ankle-foot orthosis, articulated molded ankle-foot orthosis, or Marzano brace [60]. The goal of nonoperative treatment in flexible flatfoot deformities is to control the progressive valgus of the calcaneus [62]. If a rigid deformity of the foot develops, then the orthosis should be accommodative to bony deformity and help prevent progression of the deformity. If nonoperative or conservative treatment fails, surgery is indicated because the progression of dysfunction may be rapid and disabling. When conservative treatment fails in the early stages of posterior tibial dysfunction, soft-tissue surgical procedures such as tenosynovectomy and tendon debridement may halt the progression of disease. Once flatfoot deformity develops, surgical procedures involving osteotomies and arthrodesis are necessary [60,62]. Many etiological factors have been proposed for PTTD including trauma, anatomic, mechanical, and ischemic processes [19]. None has been specifically proven to be a causative agent. Hypotheses on the association between pre-existing pes planus and PTTD suggest that the chronic stress placed on the posterior tibial tendon because of the flexible planovalgus foot and a tight heel cord could lead to an overuse injury, resulting in repetitive microtrauma and degeneration with time [19,64]. Further studies will be needed to more specifically identify risk factors and therapeutic targets in PTTD. Peroneal tendinopathies Peroneal tendon injuries are less common, and perhaps less commonly diagnosed, than corresponding injuries in the Achilles and posterior tibial tendons.
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Accordingly, there are fewer studies in the current literature on peroneal injury and peroneal tendinopathy. Case reports and case series document ruptures of the peroneus longus and peroneus brevis tendons in athletes and acute and chronic subluxation of peroneal tendon amenable to surgical correction [65 69]. In one series, Alanen et al reported on 38 operated cases of peroneal tendon injuries [70]. Eighty-two per cent of patients were competitive athletes. Of the 38 cases, there were 11 partial and 3 total ruptures of the peroneal brevis tendon, 2 partial and 2 total ruptures of the peroneus longus tendon, 9 cases of subluxation, 5 cases of chronic tendinitis, and 1 ganglion [70]. Peroneal injury including tendinopathy and partial tears of both the peroneus longus and brevis tendons has been linked to persistent lateral ankle pain and chronic lateral ankle instability [70 72]. Di Giovanni et al report on 61 patients who underwent a primary ankle ligament reconstruction for chronic instability [73]. Associated injuries found at surgery included 77% of patients with peroneal tenosynovitis, 54% with attenuated peroneal retinaculum, and 25% with peroneus brevis tear [73]. Based on their experiences, both Di Giovanni et al and Alanen et al suggest that peroneal tendon injuries may be an often overlooked cause of persistent lateral ankle pain and chronic ankle instability in settings of overuse and after acute trauma. In cases of primary peroneus longus tendinopathy without antecedent acute trauma, the specific anatomy of the peroneus longus tendon as it courses through three fibro-osseus tunnels and changes directions in the hindfoot is thought to play a role in the evolution of the disease process [74]. Brandes and Smith found that there was an association, although not a statistically significant one, between location and type of injury in peroneal tendinopathy [74]. Complete ruptures of the peroneus longus were all found at the cuboid notch, whereas 89% of the partial tears involved the region of the lateral calcaneal process. Eighty-two percent of patients presenting with peroneal tendinopathy had a cavo-varus hindfoot position with arch height in the ninetieth percentile for the general population [74]. Thirtythree percent of cases had associated peroneus brevis involvement [74]. Sammarco also found associated peroneus brevis pathology in 9 of 14 cases of acute and chronic peroneus longus tears [69]. Our understanding of the mechanisms involved in peroneal tendon injury, the histopathology of peroneal tendinopathy preceding partial and acute rupture, and the specific biomechanics and extrinsic factors contributing to development of disease is in its earliest stages. As more research is done on the etiology and evolution of tendinopathies of the foot and ankle, we hope that more will come to be known about accurate diagnosis, initial treatment, and prevention.
Stress fractures A stress fracture can be defined as a partial or complete bone fracture that results from repeated application of a stress lower than the stress required to fracture the bone in a single loading [75,76].
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Stress fractures develop when bone fails to adapt adequately to the mechanical load experienced during physical activity. Ground reaction forces and muscular contraction result in bone strain. Bone normally responds to strain by increasing the rate of remodeling. In this process, lamellar bone is resorbed by osteoclasts, creating resorption cavities, which are subsequently replaced with denser bone by osteoblasts. Because there is a lag between increased activity of the osteoclasts and osteoblasts, bone is weakened during this time. If sufficient recovery time is allowed, bone mass eventually increases. If loading continues, however, microdamage may accumulate at the weakened region. Remodeling is thought to repair normally occurring microdamage. The process of microdamage accumulation and bone remodeling, both resulting from bone strain, plays an important part in the development of stress fractures. If microdamage accumulates, repetitive loading continues, and remodeling cannot maintain the integrity of the bone; a stress fracture may result [77]. Stress fractures account for 0.7% to 20% of all injuries presenting to sports medicine clinics [78]. Track and field athletes have the highest incidence of stress fractures when compared with athletes in other sports such as football, basketball, soccer, and rowing [79]. Great variation exists in the absolute percentage of stress fractures reported at each bony site, but the most common sites seem to be the tibia, followed by the metatarsals and fibula [75]. The site of stress fractures also appears to vary from sport to sport. Among track athletes, navicular stress fractures predominate; tibial stress fractures are most common in distance runners; and metatarsal stress fractures predominate in dancers [75]. Although numerous risk factors for stress fractures have been proposed, research is needed to confirm anecdotal observations. Presently, most studies in athletes are case series, and are confined to injured groups only, or are crosssectional designs that do not allow the temporal relationship between risk factor and injury to be assessed. Results from large military epidemiological studies cannot be readily generalized to athletes, given important differences in training, fitness level, footwear, and services. These results may provide additional insight, however, especially given the deficiencies in the athletic literature [77]. One important risk factor is that of a history of a previous stress fracture. Low bone density is an identified risk factor in women, although this has not been as clearly studied in men [77,80]. Women in the military appear predisposed to stress fractures compared with their male counterparts, but this has not necessarily been confirmed in athletes. Overall training levels may influence this result [75]. Menstrual irregularity, in particular amenorrhea of longer than 6 months duration, is a risk factor [77,81]. A family history of osteoporosis is considered to be a risk factor for low bone density and osteoporosis in both females and males, but it is not clear that this necessarily predisposes to stress fractures in athletes [77,82,83]. Nutritional status, in particular low calcium intake, may contribute to stress fracture. Other dietary factors such as fiber, protein, alcohol, and caffeine intake may play a role but have not been as well studied [77]. Biomechanical factors may predispose to stress fractures by creating areas of stress concentration in bone or promoting muscle fatigue. High arches may
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predispose to increased risk for femoral and tibial stress fractures, whereas pes planus may predispose to metatarsal stress fractures [77,84 86]. Leg length inequality has been postulated as a risk factor. Friberg reported a higher incidence of tibial, metatarsal, and femoral fractures in the longer leg and a higher incidence of fibular stress fractures in the shorter leg in military recruits [87]. A leg-length discrepancy has also been reported to be associated with a higher incidence of stress fractures in athletes [77,88,89]. In particular, a leg-length inequality of greater than 0.5 cm was reported in 70% of women with stress fractures, compared with only 36% of women without stress fractures [89]. Other biomechanical variables linked to increase stress fracture risk have included hip external rotation of greater than 65 [90], greater forefoot varus, restricted ankle joint dorsiflexion, narrow transverse diameter of the tibial diaphysis, and smaller calf circumference measurement [79,90,91]. No studies have reported the effects of such physiological factors of muscle mass or muscle strength on predisposition to stress fracture [77]. Additionally, no consistent relationships have been observed between body size or composition and stress fracture risk. Anecdotal observation and clinical case series suggest that a transition in training, in particular increasing mileage, as well as a higher absolute volume of training can predispose to stress fractures in athletes, although little controlled research has examined this aspect [77]. Additionally, although no data exist on how stress fracture risk is specifically affected by training surface, it may be prudent to advise athletes to minimize the time they spend training on hard, uneven surfaces [75]. A higher incidence of stress fracture was reported in military recruits using older or worn running shoes [92]. It is unclear if this is a direct result of decreased shock absorption or perhaps decreased mechanical support [75]. Reports are conflicting about whether or not insoles can prevent stress fractures. From a practical standpoint it is important for individuals to train in shoes appropriate for their foot type. Athletes with high arched rigid feet should select cushioned shoes. Athletes with low arches should select shoes providing stability and motion control [75]. A patient with a stress fracture typically presents with a history of insidious onset of activity-related pain that progressively worsens over time. The most obvious physical examination feature is localized bony tenderness. Special clinical tests, such as the hop test for femoral stress fracture and spinal and hip extension used in diagnosis of pars stress fractures, may be helpful. Clinical reports have suggested that the application of ultrasound or a vibrating tuning fork may be helpful in the diagnosis of stress fractures by increasing pain at the fracture site; however, current literature neither supports nor refutes these commonly used clinical tools. Commonly used imaging studies include radiographs, bone scans, and MRIs. In approximately two thirds of symptomatic patients, radiographs are initially negative and only half ever develop positive radiograph findings [93]. The most common sign in early stress fracture is a region of focal periosteal bone formation. The gray cortex sign (a cortical area of decreased density) may also be seen [94,95]. In those cases where clinically indicated, advanced imaging such as a bone scan or
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MRI should be employed to confirm the diagnosis. Bone scans will confirm the diagnosis as early 2 to 8 days after the onset of symptoms [96]. MRI has shown promise in grading progressive stages of stress fractures severity. A four-stage grading system has been developed: grade 1 injuries demonstrate periosteal edema on the fat-suppressed images, grade 2 injuries demonstrate abnormal increased signal intensity on fat-suppressed T-2 weighted images, and in grade 3 injuries decreased signal intensity is seen on T-1 weighted images. In grade 4 injuries, an actual fracture line is present, typically visualized on both T-1 and T-2 weighted images [94,96]. Stress fractures can be generally classified as noncritical and critical. Noncritical stress fractures in the lower leg, foot, and ankle include the medial tibia, fibula, and metatarsals 2, 3, and 4. Treatment of these stress fractures requires relative rest. Athletes may benefit from a short period of immobilization in a walking boot (ie, 3 weeks), or in the case of metatarsal stress fractures, from a stiff sole shoe or steel insert. Return to full sport activity is generally achieved within 6 to 8 weeks. Critical stress fractures require special attention due to a higher rate of nonunion, and include the anterior tibia, medial malleolus, talus, navicular, fifth metatarsal, and sesamoids [75,77]. Medial tibia Stress fracture of the medial tibia present with medial shin pain aggravated by exercise. Tenderness is most commonly localized in the posteromedial border of the lower third, which is the most common site. Biomechanic examination may reveal either a rigid, high-arched foot that is incapable of absorbing load, or an excessively flat foot that causes muscle fatigue. Treatment involves relative rest until the pain resolves. Athletes may benefit from a short period use of either a walking boot or pneumatic brace (an air cast), which may be removed for nonimpact cross training. The air cast brace is believed to unload the tibia by compressing the lower leg, thus redistributing forces and decreasing the amount of tibial bowing [75,97 99]. Bony tenderness typically disappears between 4 to 8 weeks, after which the athlete may begin a gradual return to activity. Although the time to return to full activity varies considerably, the average period for full release to sport activity is 8 to 12 weeks. Anterior cortex of the tibia Stress fractures of the anterior cortex of the midshaft of the tibia are among the critical stress fractures because they are prone to delayed union, nonunion, and complete fracture. As with other stress fractures, in the acute phase plain radiographs are often normal and diagnosis may require bone scanning or MRI. In later stages, plain radiographs may demonstrate the dreaded black line. This appearance is due to bony resorption, and indicates nonunion. At this late stage, bone scanning will often be normal and patients may only have minimal symptoms and thus may be fully participating in sports. It is believed that the mid anterior cortex of the tibia is vulnerable to nonunion due to poor vascularity and increased
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tension because of morphologic bowing of the tibia [75]. Treatment programs have included prolonged periods of rest and immobilization (up to 4 to 6 months), bone stimulation, and surgery. Brukner recommends the use of a long pneumatic leg brace combined with electric stimulation for 10 hours per day for both the acute stress fracture and the established nonunion, as denoted by the presence of the dreaded black line on plain radiographs. Fracture healing is monitored both clinically and radiographically. Athletes do not return to activity until evidence exists of cortical bridging on radiography. If after 4 to 6 months there is no evidence of healing either clinically or radiologically, surgical intervention is indicated (drilling at the fracture site, bone grafting, or insertion of an intramedullary rod) [75]. Fibular stress fractures Because the fibula has a minimal role in weight bearing, it is believed that fibular stress fractures result from muscle traction and torsional forces. Although most stress fractures are in the distal third of the fibula, proximal stress fractures have been described. Patients are treated with weight bearing rest until bony tenderness resolves (usually 4 to 6 weeks). Athletes may benefit from a short period (ie, 3 weeks) in a walking boot. Sport activity is then gradually commenced. Soft tissue tightness should be corrected, as should biomechanical abnormalities such as excessive pronation or excessive supnation [75]. Medial malleolus Medial malleolar stress fractures generally present with a several-week history of mild discomfort followed by an acute episode that results in seeking medical attention. Although the fracture line is frequently vertical from the junction of the tibial plafond and the medial malleolus, it may run obliquely from the junction to the distal tibial metaphysis [75]. Excessive pronation and accompanying tibial rotation distributes excessive forces to the medial malleolus. Undisplaced or minimally displaced stress fractures of the medial malleolus are treated conservatively in a pneumatic leg brace for 6 weeks. A displaced fracture or a fracture that progresses to nonunion should be treated operatively. The talus Talar stress fractures most commonly involve the lateral body near the junction of the body with the lateral process of the talus. Talar neck stress fractures have been reported but are considered rare. Athletes may present with prolonged pain (for several months) following an ankle sprain despite rehabilitation. Excessive subtalar pronation is felt to predispose to talar stress fractures by allowing impingement of the lateral process of the calcaneus on the concave posterolateral corner of the talus. Treatment involves non-weight bearing rest for 6 weeks followed by rehabilitation. Orthotic control of pronation is recommended if present. Nonunion fractures respond well to surgical excision of the lateral process [75].
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The calcaneus Calcaneal stress fractures present with localized tenderness over the medial or lateral aspects of the calcaneus. The most common site is the upper posterior margin, just anterior to the apophyseal plate and at a right angle to the normal trabecular pattern. Plain radiographs may show a sclerotic appearance on lateral radiograph parallel to the posterior margin of the calcaneus. Bone scanning and MRI are more sensitive. Treatment is achieved with 6 to 8 weeks of weight-bearing rest with the use of a soft heel cushion. Joint mobilization and flexibility of the calf muscles are indicated when appropriate. Orthotics may be prescribed to control excessive pronation. Running is usually resumed after 6 weeks. The cuboid and cuneiforms Stress fractures of cuboid and cuneiform bones are rare. These are generally considered noncritical stress fractures that may be treated with weight-bearing rest until bony tenderness resolves, after which a gradual return to sport activity is commenced. As for other noncritical stress fractures, a short period in a walking boot may provide comfort. One report did propose a period of non-weight bearing on crutches for 4 weeks for a cuboid stress fracture, followed by progressive weight bearing and return to sport activity at 8 weeks [75,100]. The navicular Navicular stress fractures occur most commonly in the central third, which is believed to be susceptible to stress fracture and subsequent delayed union or nonunion because of relative avascularity and the presence of shear forces in this region. Pain is typically insidious in onset and somewhat nonspecific in location. Critical to clinical examination is palpation of the N spot in the proximal dorsal portion of the navicular. Plain radiography has low sensitivity and advanced imaging such as bone scan, computed tomography (CT), and MRI should be pursued early in suspected cases. Initial treatment requires 6 weeks of non-weight bearing immobilization. If at this point clinical tenderness remains, another 2 weeks may be required. Patient should then undergo a gradual return to activity coupled with physical therapy for joint mobilization, soft tissue work, muscle strengthening, and biomechanical correction. Patients that do not respond to the conservative treatment regimen undergo surgery (screw fixation with or without bone grafting of the established nonunion) [75,77,101]. Metatarsals Metatarsal stress fractures involving metatarsals 1, 3, 4, and the distal aspect of metatarsal 2 are usually uncomplicated and can be treated with relative rest. Patients may benefit from a walking boot or the use of a steel plate insert or counterforce arch brace. Once tenderness to palpation and pain with ambulation has resolved, a gradual return to running program is commenced. Fractures
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of the base of the second metatarsal and proximal fifth metatarsal require special consideration. Stress fractures at the base of the second metatarsal are most common among ballet dancers. Most of these fractures can be treated with weight-bearing rest but patients must refrain from training activity for 6 weeks. Three types of proximal fifth metatarsal stress fractures have been described: (1) the tuberosity avulsion fracture, (2) the Jones fracture at the junction of the metaphysis and diaphysis, and (3) the diaphysial stress fracture [75]. The most common fracture seen is a simple avulsion fracture of the tuberosity, usually caused by the contraction of the peroneus brevis tendon as a result of an acute inversion injury or the lateral band of the plantar aponeursis. This is usually an uncomplicated type of fracture that will respond to a short period of immobilization for pain relief, followed by progressive activity. The Jones and more distal diaphyseal stress fractures are critical stress fractures prone to nonunion and require 6 to 10 weeks of non-weight bearing rest. Athletes that fail to heal conservatively or those who require more rapid treatment undergo surgical fixation with placement of a fixation screw. Displaced fractures may require open reduction internal fixation. After screw fixation, progressive weight bearing is initiated at 2 weeks, with return to running in 7 weeks. When bone grafting is used, running activities are delayed for 12 weeks to allow for bony healing. The sesamoids The medial and lateral sesamoid bones at the first metatarsal phalangeal (MTP) joints act to increase mechanical advantage of the flexor hallucis brevis tendon and stabilize the first MTP joint in association with the plantar plate capsule. They also protect the flexor hallucis longus tendon and absorb weight-bearing stress on the medial forefoot. The medial sesamoid bone is more commonly affected. Radiographs are often negative and diagnosis may require advanced imaging. A bone scan or MRI is also useful in differentiating a bipartite sesamoid from a true stress fracture. Stress fractures of the sesamoid bones are prone to nonunion. Treatment involves non-weight bearing rest for 6 weeks. Weight bearing is commenced when bony tenderness is no longer present. Padding is used to distribute weight away from the sesamoid bones in the form of a sesamoid or dancer pad. If nonunion occurs, or if the bone is splintered, excision is recommended [75].
Exertional compartment syndrome Chronic exertional compartment syndrome is defined as reversible ischemia secondary to a noncompliant osseofascial compartment that is unresponsive to the expansion of muscle volume that occurs with exercise [102]. Most commonly seen in the lower leg, exertional compartment syndrome in athletes has also been described in the thigh and medial compartment of the foot [103 105]. It presents as recurrent episodes of leg discomfort experienced at a given distance or intensity of running. Though a characteristic history is highly suggestive of exertional
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compartment syndrome, no physical examination finding can firmly establish the diagnosis [102,106]. Diagnosis based solely on clinical presentation can lead to misdiagnosis and inappropriate therapy or delay of proper therapy [107]. An exercise challenge and documentation of elevated compartment pressure in one or more of the compartments of the leg confirms the diagnosis [102]. The characteristic presenting complaint of patients with chronic exertional compartment syndrome is recurrent exercise-induced leg discomfort that occurs at a well-defined and reproducible point in the run and increases if the training persists. The quality of pain is usually described as a tight, cramplike, or squeezing ache over a specific compartment of the leg. Athletes can reliably predict at what intensity or what distances the discomfort will occur as well as how long pain will last, depending on the intensity and distance run. Relief of symptoms only occurs with discontinuation of activity [108]. Examination may or may not demonstrate fascial hernias. In some cases, the classic exertional component is not as evident, and patients complain of pain at rest or with daily activities as well. Women may be more susceptible to chronic lower leg compartment syndrome than men, and women may also, for unclear reasons, respond less well than men to operative fasciotomy [109]. Chronic compartment syndrome, left untreated, can develop into an acute syndrome [110]. Several factors are believed to contribute to an increase in intracompartmental pressure during exercise [108,111]. These are enclosure of compartmental contents in an inelastic fascial sheath, increased volume of the skeletal muscle with exertion due to blood flow and edema, muscle hypertrophy as a response to exercise, and dynamic contraction factors due to the gait cycle. It has also been proposed that myofiber damage as a result of eccentric exercise causes a release of protein bound ions and a subsequent increase in osmotic pressure within the compartment. The increase in osmotic pressure increases capillary relaxation pressure, thus decreasing the blood flow [112]. Development of symptoms may be more common at the beginning of a running season due to muscle hypertrophy, which decreases the volume in the compartment [113]. Rapid increases in muscle size due to fluid retention are also believed to play a role in the development of chronic exertional compartment syndrome in athletes taking the popular supplement creatine monohydrate [108]. A neurologic and vascular examination should also be performed with reproduction of the symptoms [102]. Understanding the distribution of nerves and functions of muscles in relation to symptoms can help identify the affected compartment in cases where the pain is not well localized to one specific compartment, or it may help determine which compartments are more severely affected in cases where more than one compartment is involved [108]. There are four major compartments in the leg. Each is bound by bone and fascia, and each contains a major nerve. The anterior compartment contains the extensor hallucis longus, extensor digitorum longus, peroneus tertius, and anterior tibialis muscles, as well as the deep peroneal nerve. The lateral compartment contains the peroneus longus and brevis as well as the superficial peroneal nerve. Posteriorly there are two compartments: the superficial posterior and the deep posterior
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compartments. The superficial compartment contains the gastrocnemius and soleus muscles and the sural nerve. The deep posterior compartment contains the flexor hallucis longus, flexor digitorum longus, and posterior tibialis muscles, as well as the posterior tibial nerve. Some authors believe that the posterior tibialis should be considered a separate compartment, as it is surrounded by its own fascia [114]. Anterior compartment syndrome is most common (45%), followed by the deep posterior compartment (40%), lateral compartment (10%), and superficial posterior compartments (5%) [112]. If the anterior compartment is affected, the patient may display weakness of dorsiflexion or toe extension and paresthesias over the dorsum of the foot, numbness in the first web space, or even transient or persistent foot drop [102,113]. Paresthesias in the plantar aspect of the foot and weakness of toe flexion and foot inversion may be revealed when the deep posterior compartment is involved, whereas dorsolateral foot hypoesthesia and plantar flexion weakness may be present if the superficial posterior compartment is affected. Lateral compartment pressure elevation with compression of the superficial peroneal nerve can induce sensory changes over the anterolateral aspect of the leg and weakness of ankle eversion. An inversion as well as equinus deformity may also be present [102,115]. Several techniques have been described in the literature for measuring both static and dynamic intramuscular pressures. These techniques include the needle manometer [116], the wick catheter [117], slit catheter [118], continuous infusion [119], and a solid-state transducer intracompartmental catheter [120]. Each of these techniques offers several advantages and disadvantages. All are time-consuming, however, and require some degree of skill and experience to set up and perform [102,108]. Our preferred method for measurement of compartmental pressures is with a battery-operated, hand-held, digital fluid pressure monitor. The Stryker Intracompartmental Pressure Monitor (Stryker Corporation, Kalamazoo, Michigan) is a convenient and easy-to-use measuring device for use in the clinical setting [102,120]. This device has been found to be more accurate, versatile, convenient, and much less time-consuming to use than the needle manometer method [121]. Measurements were also found to be more reproducible among different examiners with the Stryker instrument [102]. The usefulness of pressure measurement and maintenance of patient safety with this invasive technique relies upon a thorough knowledge of the anatomy of the leg. Before attempting to measure compartment pressures, the physician should thoroughly study the anatomical structures in each compartment to avoid damaging neurovascular structures [102]. Generally accepted criteria for the diagnosis of chronic exertional compartment syndrome (CECS) are described by Pedowitz and colleagues [107]. One or more of the following pressure criteria must be met in addition to a history and physical examination that is consistent with the diagnosis of CECS: Pre-exercise pressure 15 mm Hg; 1 minute postexercise pressure 30 mm Hg; or 5 minutes postexercise pressure 20 mm Hg. Clinicians should also be aware that standard exercise protocols often used in the clinical setting may or may not be adequate to
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raise intracompartment pressure and diagnosis may require the sport-specific activity to induce symptoms and raise intracompartment pressure [122]. Recent interest has focused on the use of noninvasive tools in the diagnosis of chronic compartment syndrome: triple phase bone scan, MRI, near-infrared spectroscopy, and technetium-99m methoxyisobutyl isonitrile (MIBI) perfusion imaging [123 131]. The dynamic bone scan may support the diagnosis based on specific tracer uptake patterns. The characteristic appearance is that of decreased radionuclide concentration in the vicinity of the area of increased pressure, with increased softtissue concentration both superior and inferior to the abnormality. The area of decreased uptake is believed to be due to the increased pressure and decreased blood flow to the region [127]. On MRI imaging, exercise changes are characterized by swelling within a compartment, which manifests as intramuscular diffuse high signal intensity on T2-weighted images. Failure of the edematous muscle to return to baseline normal appearance by 25 minutes after completion of exercise is diagnostic [128]. The triple-phase bone scan and MRI offer alternatives to direct intracompartmental pressure measurements in cases in which the athlete is averse to repeated needle sticks or where the results of pressure monitoring may be borderline [102,129]. Near-infrared spectroscopy measures tissue deoxygenation of skeletal muscle caused by elevated intramuscular pressure during exercise [124]. MIBI perfusion imaging is a technique that assesses the uptake of an intravenously injected radiopharmaceutical, MIBI, by peripheral muscles. The uptake of the radiopharmaceutical is largely determined by muscle perfusion, but hypoxia also inhibits uptake of the MIBI, enhancing its potential for detecting muscle ischemia. Cases have been reported where visually detectable decreases in MIBI uptake in one or more compartments were noted during exercise when compared with studies taken at rest [125]. Treatment of chronic exertional compartment syndrome can include both conservative and surgical intervention. Conservative measures include relative rest (limiting activity to the level that avoids any more than minimal symptoms), anti-inflammatories, stretching and strengthening of the involved muscles, and orthotics (particularly in cases of excessive pronation). Some athletes will simply choose to refrain from the causative activity, which is a viable option provided they remain neurovascularly intact. In cases where symptoms persist despite 6 to 12 weeks of conservative care, or in cases of extreme pressure elevation, surgical remediation (fasciotomy of the involved compartments with or without fasciectomy) should be undertaken [132,133]. Single and double incision as well as endoscopic techniques have been described. Regardless of the technique, any fascial hernias must be included in the fascial incision. Due to a high rate of coexistence, some authors advocate release of the lateral compartment whenever a procedure for anterior compartment syndrome is performed. Others have stated that this dual release may not be necessary if clinical evaluation and compartment pressure testing fail to demonstrate lateral compart-
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ment involvement [134]. When performing a deep posterior compartment release, attention must be given to adequate decompression of the tibialis posterior [135]. Postoperatively, a compressive dressing is applied. Drains are not normally necessary. Crutches are used for comfort for a few days, but the patient begins active and passive motion immediately. Once the wound is healed, walking and bicycling are encouraged. Patients may begin a light jog in 2 weeks, and resume run training at 6 weeks. It usually takes 3 months for full rehabilitation, but patients with deep posterior compartment fasciotomies may need longer [114,136].
Shin splints Shin splints, or medial tibial stress syndrome, can be described as a clinical entity characterized by diffuse tenderness over the posteromedial aspect of the distal third of the tibia [137]. In mild cases, pain is present only with exercise; in more severe cases rest pain is present. Shin splints have been reported to account for 12% to 18% of running injuries [43,138 140] and to occur in 4% of all military recruits in basic training [141]. Women appear more frequently affected than men [138,142,143]. Medial tibial stress syndrome is to be differentiated from stress fracture and exertional compartment syndrome [144,145]. Although different entities, they may coexist. Plain films are negative (except in cases of previous or coexistent stress fracture). Bone scans will demonstrate characteristic vertical linear increased activity along the tibial periosteum, which differs from the more focal fusiform increased radiotracer uptake exhibited by stress fractures [123]. Medial tibial stress syndrome is felt by most to represent a periostalgia or tendinopathy along the tibial attachment of the tibialis posterior or soleus muscles [43,108,146,147]. Other proposed etiologies have included posterior compartment syndrome [148,149] and fascial inflammation [147]. Detmer proposed a classification scheme for medial tibial stress syndrome based on etiology. Type 1 included local stress fractures, type 2 periostitis/periostalgia, and type 3 was due to deep posterior compartment syndrome [150]. Increased valgus forces on the rear foot and excessive pronation that result in increased eccentric contraction of the soleus and posterior tibial muscles are often contributing causes [146]. Intrinsic factors that may increase valgus forces and pronation include femoral anteversion, genu varum, tibia or forefoot varus, and an excessive Q angle [137]. Other intrinsic factors linked to medial tibial stress syndrome include excessive planus or cavus, tarsal coalition, lower extremity length inequality, and muscle imbalances [151,152]. Extrinsic risk factors include improper shoe wear, a rapid transition in training, inadequate warm-up, running on uneven or hard surfaces, running in cold weather, and low calcium intake [137,153]. Treatment of medial tibial stress syndrome includes relative rest and the correction of any recent transition in training. Hill running and running on uneven surfaces should be avoided. Proper shoe wear is essential to minimize rear foot
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valgus and to correct excessive pronation, pes planus, or pes cavus. Orthotics are useful in cases that cannot be controlled by shoe wear alone. NSAIDS and anti-inflammatory modalities (ie, iontophoresis and ultrasound) can be useful adjuncts in the rehabilitation of medial tibial stress syndrome. A strengthening and flexibility program should be initiated with the goal of correcting any muscle imbalances. Flexibility of the gastrocsoleus should be emphasized, as well as strengthening (concentric and eccentric), including the foot intrinsics, dorsiflexors, plantarflexors, invertors, evertors, and gluteals. All deficits within the kinetic chain should be corrected [108]. A compressive sleeve may provide symptomatic relief. Operative therapy (posterior fasciotomy) has been described for the athlete with severe limitations of physical activity, frequent recurrence, or no response to available therapy [150,154]. Surgical treatment for periostalgia has not been uniformly successful and should be reserved for recalcitrant symptoms that have not responded to a well documented treatment program of at least 6 months [108].
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Bracing and rehabilitationwhats new

Brent L. Arnold, PhD, ATCa,*, Carrie L. Docherty, PhD, ATCb,c
Sports Medicine Research Laboratory, Department of Exercise Science, Virginia Commonwealth University, PO Box 842037, Richmond, VA 23284-2037, USA b Smith Research Center, 2805 East Tenth Street, Bloomington, IN 47408, USA c Department of Kinesiology, Indiana University, 2805 East Tenth Street, Bloomington, IN 47408, USA
a
Ankle bracing/tape (supports) and rehabilitation are probably the two most common forms of ankle treatment. In recent years several new methods of evaluating ankle supports have been developed, and a variety of new rehabilitation treatments and concepts have been introduced. Thus, the purpose of this article is to review the current literature associated with both.
Ankle supports Athletic trainers and other practitioners typically use ankle supports (ie, tape or braces) to either prevent uninjured ankles from being sprained or reduce the chances of reinjury of an existing sprain. Although anecdotal reports by athletes and patients suggest at least a perceived improvement of joint stability, a specific mechanism for the improved stability has not been agreed upon. Several possible mechanisms have been studied, including taping/bracings effect on range of motion, kinesthesia, neuromuscular response, joint velocity, ground reaction forces, and postural control. Whether any of these are capable of protecting the joint is unclear. Thus, the primary purpose of this section is to review the current evidence for the role of these factors in preventing ankle sprains. Secondarily, we will address the effects of ankle supports on functional performance. To be effective, joint supports should provide joint stability; however, they cannot unduly affect the athletes ability to compete or the patients ability to engage in activities of daily living.
* Corresponding author. E-mail address: barnold@vcu.edu (B.L. Arnold). 0278-5919/04/$ see front matter D 2004 Elsevier Inc. All rights reserved. doi:10.1016/S0278-5919(03)00086-3
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B.L. Arnold, C.L. Docherty / Clin Sports Med 23 (2004) 8395
Range of motion Probably the most common mechanism proposed for the effectiveness of taping and bracing is limitation of joint motion. The majority of the literature has assessed range of motion passively. New dynamic techniques, including the use of simulated functional activities, have been developed, however. Each is described below. Non-weight bearing Historically, passive limitation of range of motion (ROM) has been the most frequently studied factor associated with ankle support effectiveness. For a complete historical review see Verhagen et al [1]. Recent research has used both roentgenography [2,3] and goniometry [4 6] to assess inversion range of motion. In all cases both taping and bracing were found to reduce talar tilt (Table 1) to 37% to 61% of the normal available inversion range. Although these restrictions would maintain talar tilt within normal (ie, uninjured) ranges, whether they are adequate to prevent injury is unclear. It should be emphasized that in all cases testing was performed passively to the limits of restriction. Loading of the joint was much lower than actually experienced during an inversion sprain. Thus, stressing the joint at loads typical for sprains may yield different results. Trap-door platform As an alternative to non-weight bearing assessment more dynamic tasks have been used. One method has been to use trap-door platforms These platforms have been designed with their axes of rotation aligned along the midsaggital plane of the foot to produce frontal plane rotation of the foot, or aligned along the subtalar axis to produce triplanar motion. The advantages of these platforms are that they include weight bearing and mimic the mechanism of a sprain; thus, restrictions on range of motion can be assessed during a more functional activity. The limitation of this
Table 1 Brace and tape restrictions during passive range of motion testing Pre exercise Post exercise
Normal range Restricted % Restricted Restricted % Restricted of motion (deg.) inversion (deg.) ROMa inversion (deg.) ROMa Eils et al [4] Lohrer et al [5] Vaes et al [2] Vaes et al [3] Yaggie & Kinzie [6] Mean
a b c
39 22 13.1 12.5 14.4c 18 23
14 22b 11 4.8 4.8 10.6b 10 12b 7.9
37 57b 50 37 37 78b 55 67b 43.5
14.5 6.3 3.3 4.5b -
66 48 52 88b -
Percentage of available range of motion. Lower values represent greater restriction. Ranges represent differences across multiple ankle support conditions. Range represents multiple baselines across the same group of subjects.
B.L. Arnold, C.L. Docherty / Clin Sports Med 23 (2004) 8395 Table 2 Brace and tape restrictions during trap door testing Pre exercise Post exercise
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Normal range Restricted % Restricted Restricted % Restricted of motion (deg.) inversion (deg.) ROMa inversion (deg.) ROMa Alt et al [8] Eils et al [4] Lohrer et al [5] Ricard et al [7] Vaes et al [2] Mean
a b c
28 30c 39 32 37.8 9.75 29.6
17 21b 19.89 18 26.2 27.4 6.4 14.8
27 42b 51 56 69 72 66 57.7
17 18b 21 23b 28.3 29.1 -
62 84b 66 72b 73 75 -
Percentage of available range of motion. Lower values represent greater restriction. Ranges represent differences across multiple ankle support conditions. Range represents multiple baselines of the same subjects.
method has been the restriction of tested ranges of motion and the fact that it is a static measure. For example, most studies have limited the range of motion to 30 to 50 [2,4,5,7,8]. This is short of the 63 of triplanar motion advocated by Vaes et al [9] to produce a sufficient inversion moment. Interestingly, the results between the non-weight bearing and trap-door platform studies are similar. In both cases taping and bracing significantly reduced inversion, but provided less restriction during the trap-door testing (Table 2). Specifically, supports restricted range of motion to 47% and 62% of the available range during non-weight bearing and trap-door testing, respectively. This difference is expected considering the weight-bearing aspect of trap-door testing. During the trap-door testing greater moments are placed on the ankle support, producing greater deformation. Thus, ROM restrictions that are provided under these conditions are probably closer to restrictions provided during activity. These joint loads are minimal compared with the loading that occurs during activities of daily living (ADL) and athletic activity, however. It should be noted that one recent study [10] did not show ROM restrictions with ankle supports. This may be due to at least two factors. First, the amount of tilt was limited to 10. This would account for only 32% of the average available inversion range as determined from the previously reported studiesless than the restrictions reported by others [2,4,5,7,8]. This suggests that the tilt may not have stressed the ankle support adequately. Second, subjects had both feet on the tilting portion of the platform, whereas subjects in all other studies had only one foot on the trap door. By having both feet on the platform, movement of the platform would have also resulted in some degree of frontal plane pelvic movement and may have resulted in knee flexion, both of which might have altered the kinematics of the ankle. Gait Probably the most functional approach to studying range of motion in supported ankles has been with gait analysis [11]. It has been determined that tape and lace-up style braces decrease the angle of supination at heel contact. In other words, the
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calcaneus was less inverted at the moment of contact. Theoretically, this change in the supination angle would require a greater amount of inversion to produce a sprain. Furthermore, the maximum pronation angle of the foot was increased with tape and the lace-up brace. Again, this indicates that the ankle under supported conditions was farther from inversion than under unsupported conditions. It should be noted that a semirigid brace did not produce the same effects. The reason for this is uncertain; however, it was suggested that because both the tape and the lace-up brace (RocketSoc, Smith & Nephew Donjoy, Inc., Carslbad, California) provided an eversion moment on the ankle via lateral strapping, this moment may have produced a relatively everted position of the foot. Finally, gait analysis provides a reasonable model for studying ankle motion during typical ADL, and thus, may help address the effectiveness of braces for average individuals with chronic ankle instability. Load on the joint and speed of movement during walking are much less than during running and typical athletic activities, however. Thus, extrapolation of these results to athletic activities should be avoided. Postexercise One of the well-recognized limitations of ankle supports is their tendency to loosen after activity. Table 1 and 2 also show the ROM restrictions provided by ankle supports after exercise. As can be seen, talar tilt increased following exercise, and these increases permitted 48% to 84% of the available talar tilt. These postexercise changes existed regardless of whether non-weight bearing or tilt platform methods were used and regardless of whether a brace or tape was used. It should be emphasized that despite the supports loosening, the inversion ROM remained less than the normal available ROM. Comparison among braces One of the difficulties in evaluating the current literature is the variety of braces and taping techniques studied. Thus, direct comparisons among studies are often impossible. Two recent studies [3,4], however, have studied multiple braces or taping techniques. From these studies three broad conclusions can be drawn. First, semirigid style braces (ie, those that combine fabric and rigid support) provided more support than soft (ie, fabric only) braces. Second, semirigid braces with a stirrup style rigid support (eg, the Air-Stirrup, Aircast, Summit, New Jersey) performed better than semi-rigid braces with other types of rigid support [4]. Third, tape performed similarly to semirigid style braces [3]. This latter finding suggests that bracing may be a preferred form of support because of convenience and cost. Sensorimotor changes Changes in the sensorimotor system following application of taping or bracing have also been proposed as mechanisms for ankle support effectiveness. Studies
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examining these factors can be divided into kinesthetic and neuormuscular response studies. Kinesthesia Recent studies in kinesthesia after bracing or taping have included a full range of findings. This is probably due to differing kinesthesia measurement techniques, differing bracing/taping techniques, and differing directions of tested motion. For example, taping produced no change in joint position sense for plantar/dorsiflexion [12]. In contrast, various ankle braces decreased the ability to detect inversion/ eversion movement [13]; however, semirigid bracing [14], but not taping or neoprene supports [15], increased the ability of subjects to reproduce target inversion/eversion angles. Clearly, more research is needed in this area with specific attention to the types of ankle support, direction of movements tested, and method of kinesthesia assessment. Neuromuscular response Ankle neuromuscular response studies can be divided into three areas: electromyography (EMG) latency studies, EMG amplitude studies, and H-reflex studies. The first two of these address the speed and adequacy of the muscle response to ankle perturbation. To accomplish this, investigators have used the previously described trap-door platforms to stimulate muscular reflex responses. In contrast, H-reflex studies examine the motor systems readiness for activity. Peroneal latency. Peroneal latency is defined as the interval of time between the onset of a perturbation (ie, movement of the trap door) to the point of the first recorded increase in EMG level. Injured ankles have been shown to have increased latencies (normal = 48 ms, injured = 59 ms) [16]. In other words, injured ankles have a slower response time to unexpected perturbations, and this may contribute to their susceptibility to reinjury. Ankle supports do not decrease this latency in injured or uninjured individuals [8,17,18]. It has been suggested, however, that even in normal individuals motor response times (time to meaningful muscular force) are too slow to protect the ankle joint [19]. Thus, even if ankle supports facilitated peroneal latency in injured ankles to normal levels, it is not likely to be fast enough to protect the joint. EMG amplitude. Motor latency to unexpected perturbation is only one part of the neuromuscular response. The vigorousness of that response as measured by its amplitude is also critical. It is generally accepted that the amplitude is related to force production; that is, increases in amplitude are associated with increased muscle force production. Interestingly, some studies examining EMG amplitudes following bracing [20] and taping [8] have shown decreases in amplitude. This suggests that ankle support is actually detrimental to the neuromuscular response. These studies, however, did not consider the EMG response relative to the smaller amount of motion available in the supported ankle. When the neuromuscular response was calculated as a ratio of EMG amplitude relative to the range of motion
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allowed by the ankle support, the EMG amplitude was 1.6 times greater in taped ankles [5]. In other words, the EMG response was increased despite a smaller stimulus (ie, decreased ROM). Viewed this way, taping actually has a potent facilitatory effect on EMG amplitude. H-reflex. The H-reflex is a useful method for assessing the excitability of the motor neuron pool. Increased excitability potentially increases the overall response to an unexpected perturbation. H-reflexes have been shown to be approximately 10% greater in individuals wearing semirigid ankle braces [21]. This is likely due to stimulation of proprioceptors in the ankle joint or ankle musculature with subsequent stimulation of the spinal motoneuron pool. This may explain the increase in EMG amplitude associated with ankle supports.
Velocity Decreased inversion velocity has been another proposed mechanism for ankle support effectiveness. Several studies have demonstrated that with either bracing or taping joint velocity decreases [2,22] and may decrease up to 25% to 40% [7,10]. This is important because damage to an unprotected ankle has been estimated to begin at 63 of supination [9] or 156 ms after unexpected perturbation. In contrast, the ability of the evertors to generate sufficient force to protect the joint has been estimated to be 176 ms [19]. Obviously, under unsupported conditions the neuromuscular response is too slow to protect the joint. By slowing the supination by 25% the time to injury would increase to 195 ms, potentially providing adequate time for the evertors to respond. It should be noted that these studies were conducted under controlled conditions with relatively slow joint velocities and low joint loads. Basketball rebounds have been reported to occur with three to six times body weight and with joint loading occurring in as little as 10 ms to 80 ms [23]. Thus, even with the longer time to injury produced by bracing, it is not likely to be long enough to allow protection from the evertors.
Ground reaction forces Ground reaction forces provide insight in to how a joint is loaded and what forces are being applied to the tissues. Because of ankle supports ability to restrict range of motion, it seems likely that ankle supports would decrease loads placed on the ankle, but this is not the case. Studies using gait [24], lateral shuffles [20], and drop jumps [25] have failed to show decreases in joint forces with bracing or taping. This suggests that supports are unable to protect the joint from increased loads. Additionally, decreases in time to peak forces have been found [25], and it has been suggested that this represents increased rigidity of the foot and ankle complex. If this is the case, increased rigidity might result in loads being transferred to the knee and hip. In other words, ankle supports may behave similarly to
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ski boots in providing protection to the ankle but increasing the risk of injury to the hip and knee. Postural control and balance Previous research has demonstrated that individuals with chronic ankle instability have increased postural sway and that this sway is predictive of future injury [26,27]. If ankle bracing could decrease this postural sway, then the risk of injury might be reduced. It has been shown that braces do decrease postural sway in individuals with functional ankle instability [28]; however, studies examining uninjured individuals have failed to demonstrate similar changes [29 31]. This suggests that braces may have a selective effect at the ankle. They may not be prophylactic for the uninjured ankle, but may improve postural stability and reduce the risk of injury for previously injured ankles. Functional testing As with any medical device, there is always the chance that ankle supports will have undesirable effects. The concern has been that taping and bracing would negatively affect functional performance. Ankle supports do not affect vertical jump [6]or isokinetic strength [32], however, and may actually improve shuttle run performance [33]. This latter finding may be indicative of an increased confidence during activity.
Rehabilitation Rehabilitation following an ankle sprain is an additional method of decreasing residual symptoms and preventing recurrent injuries. Significant research has been done on the effectiveness of a variety of protocols. These rehabilitation protocols typically consist of acute care, range of motion, strength, balance or proprioception, and functional exercises. The primary goal of this section is to review recent literature in each of these areas. Most rehabilitation exercises can occur independently at home or under the direct supervision of a health care provider in a clinic/athletic training room. Although the expertise of a clinician is often preferred, patients performing a home program can have the same strength and postural control improvements as patients who undergo supervised rehabilitation [34]. At 1-year follow-up, however, patients participating in supervised rehabilitation had significantly fewer subsequent injuries [34]. This indicates that rehabilitation with the assistance of a health care provider may reduce the risk of future injury. This may be due to the feedback provided by the athletic trainer or therapist during the exercise sessions, thus giving the patient a better understanding of how to properly perform the training protocol.
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Acute care Following an acute ankle injury, immediate care is taken to decrease pain and swelling of the joint. Traditional methods of reducing swelling are ice, compression, and elevation. Recently, hyperbaric oxygen therapy (HBO) has been used to assist with this process. HBO uses a pressurized chamber that administers oxygen above the atmospheric pressure to the patient. The goal is to increase oxygen delivery to damaged tissues [35]. A potential benefit to this treatment is decreased edema leading to earlier return to activity; however, an initial study using 100% oxygen at 2 atmospheres absolute pressure for three sessions (a 90-minute session and two 60-minute sessions) did not significantly improve range of motion, edema, function, and time to return-to-play over the placebo group [35]. Continued research is necessary to determine whether other combinations of treatments may be more effective. Immobilization and weight bearing assistance is often necessary following an acute traumatic injury. Proper immobilization following an initial ankle sprain has also been a topic of research in which a fine line exists between immobilizing the joint to prevent additional injury and loading the joint to facilitate healing. Current research recommends the combination of early weight bearing and immobilization. Immobilization boots and strapping have been shown to result in minimal residual symptoms or reinjury [36,37]. The boot or strapping provides the flexibility to allow early non-weight bearing exercises, but still protects the joint from further stress. Specifically, at 6 months postinjury, 70% of participants that performed early weight bearing were at their preinjury activity level, whereas only 36.8% of an immobilization group (plaster cast below the knee for 21 days) were at their preinjury levels [37]. Based on these results, the use of an immobilization boot in combination with early range of motion (eg, plantar flexion/dorsiflexion and inversion/eversion active range of motion; ankle alphabet) and strength exercises (eg, seated toe curls and pick-ups; plantar flexion/dorsiflexion and inversion/eversion elastic tubing exercises) appear to lead to decreased residual symptoms and an expedited recovery in the athletic population. Strength training Following an ankle injury many structures are damaged, including the muscles that cross the joint. After a period of inactivity or immobilization strength deficits or atrophy can occur. Exercises to improve strength can be done using therabands, free weights, manual resistance, or isokinetic machines. Many clinicians prefer the use of manual resistance for the early phases of strength training because it is perceived as less traumatic than other forms of exercise. Little research has been done comparing the effectiveness of the various methods and whether they impair joint healing, however. If aggravating the joint is a concern, exercising the contralateral ankle may be useful. Like other joints, training of one ankle can also facilitate improvements in the contralateral limb [38]. Although pain in the injured ankle may preclude strength training from being effective, training of the uninjured
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ankle could be initiated immediately. This early intervention may assist in decreasing atrophy that occurs with inactivity. Another advantage of strength training is that it appears to have a multimodal effect. Open kinetic chain strength training, such as plantar flexion, dorsiflexion, inversion, and eversion theraband training, not only results in strength improvements and but also produce proprioceptive/balance improvements [39,40]. What is unclear is whether closed kinetic and functional exercises might be more effective in producing multimodal effects. Balance (wobble board) training Deficits in static and dynamic balance can result following an ankle injury. If activity is resumed before accounting for these deficits, chance of reinjury may increase. Therefore, balance training is often performed on a variety of surfaces: firm, foam, tilt board, half disk, uneven walkway, minitrampoline, or Biomechanical Ankle Platform System (BAPS; Spectrum Therapy Products, Adrian, Michigan) board. Balance training typically occurs in 15- to 45-second bouts for a total of 10 to 15 minutes with a variety of different conditions to increase intensity [41 44]. Removing visual input, providing an external perturbation (theraband or manual), and concentrating on an alternate task (catching or throwing a ball, drawing numbers and letters in space with the contralateral foot) are all examples of progressively increasing balance training intensity. These balance training protocols have been found to improve postural sway [41,43] and ankle joint reposition sense [45]. Preventative balance training regimens can also prevent the frequency of future lower extremity injury [45,46]. Specifically, athletes that did not participate in preventative balance training were almost six times more likely to sustain an injury [46]. Conversely, in a prospective study using soccer athletes, balance training did not decrease the overall injury rate, but did decrease the incidence of severe injuries [42]. Daily unilateral balance training can also affect tibialis anterior muscle activation. Following 8 weeks of training the muscle activated faster in response to an unexpected perturbation [44]. Additionally, like much of the strength training research, a crossover effect has been reported with balance training. With unilateral balance training, onset latency decreased bilaterally [44]. This could also play a role in early intervention following an ankle sprain. Training could begin in the uninjured limb much earlier in the process, providing potential benefits to the injured limb as well. Despite these improvements in muscle reaction, it should be emphasized that much controversy still exists as to whether this muscle activation is fast enough to prevent an injury. A combination of proprioceptive and strength training is also effective in improving balance performance [39,47]. Because most clinicians use both types of exercises in rehabilitation protocols, this is potentially the most clinically applicable finding. Because time is often a factor in the amount the rehabilitation that can be provided, however, it is important to note that balance training and strength training alone also provided improvements in balance [39]. Continued
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research is needed to determine if strength training or proprioceptive training alone are also equally effective in total recovery measures such as frequency of recurrent injuries and overall function following rehabilitation.
Functional training Functional training is incorporated into the rehabilitation protocol during the final stages of this process. Examples of functional training include walking, forward hopping, lateral hopping, squats, lateral shuffles, slalom jumps, unilateral jumps, carioca, running, and cutting. These exercises can be done on the floor, treadmill, or agility ladder. With an emphasis on early exercise following an acute injury, an unloading technique in functional rehabilitation has recently been used [48]. With this procedure, all exercises are done by reducing the gravitational forces so the participant can perform in a pain-free range and still retain the benefits of activity. This can be achieved with a Total Gym (Engineering Fitness International, San Diego, California) by changing the incline angle for the squats and jumps or with a Zuni Incremental Weightbearing System (SOMA, Austin, Texas) that uses a harness and pulley system over a treadmill for walking, running, and shuffling. By limiting the gravitational forces, exercises can be done without further irritation to the joint. Potential benefits of this activity are increased range of motion, increased strength, and a shorter recovery period [48]. Unlike balance and strength training, 4 weeks of traditional agility training did not affect static single-limb postural sway [49]. This is probably due to the static testing measure used. If a semidynamic or dynamic balance testing procedure had been used, significant improvements might have been seen. A more dynamic test would also assist in determining readiness to return to play.
Summary Based on the recent evidence, ankle bracing and taping do appear to have positive effects on ankle support. For example, both bracing and taping restrict inversion range of motion, with tape and stirrup-style braces providing the best support. Although exercise reduces this restriction, the range remains consistent with levels considered to be within the normal range. Ankle supports also appear to improve the strength of the muscular response to perturbation, potentially providing a stronger muscular contraction. In contrast, ankle supports fail to improve the neuromuscular response time to unexpected perturbations. Thus, it appears that the stronger response may occur too slowly to protect the joint. This slowness of the neuromuscular response, however, may be offset by the supports ability to slow the inversion motion. The slowing of inversion appears to allow the neuromuscular system to respond at or before the point of ligament damage. Finally, ankle supports appear to improve balance only in individuals with previously injured ankles. This
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suggests that supports may have a selective effect in protecting injured but not uninjured individuals. Despite these positive effects, some cautions should be emphasized. First, most of the studies cited have been performed in the laboratory setting with joint velocities and loads much below what are encountered in the athletic and daily activities. Whether tape and braces can maintain their effectiveness under the more extreme conditions of functional activities remains unclear. Additionally, some evidence suggests that ankle supports may transfer loads to other joints putting them at risk for injury. Thus, further study is needed to determine the risk-to-benefit ratio of ankle supports. Finally, much of the research presented has been done only on uninjured ankles. Based on the current evidence, it seems possible that the effectiveness of ankle supports may differ depending on the population, and it seems clinically important to know whether we can expect the same results for injured and uninjured ankles. Proper and early rehabilitation is important in preventing residual ankle symptoms. Reports indicate that up to 73% of people who sustain a lateral ankle sprain have recurrent sprains [50], but it is unknown how many of these participants partake in rehabilitation. Proper immobilization and acute care of the injured ankle is imperative. An immobilization boot or strapping that can be removed during early non-weight bearing exercises seems to be most effective. Strength and balance training of the uninjured contralateral limb can be used to assist reaching full recovery in a shorter period of time. Functional exercises can also be performed earlier in the rehabilitation process by reducing the gravitational forces so patients can perform in a pain-free range and still receive the benefits of early activity. Evidence shows that daily ankle disk training assists in preventing ankle sprains, and is a relatively inexpensive and easy alternative to traditional rehabilitation protocols.
References
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[8] Alt W, Lohrer H, Gollhofer A. Functional properties of adhesive ankle taping: neuromuscular and mechanical effects before and after exercise. Foot Ankle Internat 1999;20(4):238 45. [9] Vaes P, Vam Gheluwe B, Duquet W. Control of acceleration during sudden ankle supination in people with unstable ankles. J Orthop Sports Phys Ther 2001;31(12):741 52. [10] Nishikawa T, Kurosaka M, Mizuno K, Grabiner M. Protection and performance effects of ankle bracing. Int Orthop 2000;24:285 8. [11] Nishikawa T, Kurosaka M, Yoshiya S, Lundin TM, Grabiner MD. Effects of prophylactic ankle supports on pronation during gait. Int Orthop 2002;26:381 5. [12] Refshauge KM, Kilbreath SL, Raymond J. The effect of recurrent ankle inversion sprain and taping on proprioception at the ankle. Med Sci Sports Exerc 2000;32:10 5. [13] Hubbard TJ, Kaminski TW. Kinesthesia is not affected by functional ankle instability status. J Athl Train 2002;37:481 6. [14] Hartsell HD. The effects of external bracing on joint positon sense awareness for the chronically unstable ankle. J Sport Rehabil 2000;9:279 89. [15] Kaminski TW, Gerlach TM. The effect of tape and neoprene ankle suports on ankle joint position sense. Phys Ther Sports 2001;2:132 40. [16] Vaes P, Van Gheluwe B, Duquet W. Control of acceleration during suddent ankle supination in people with unstable ankles. J Orthop Sports Phys Ther 2001;31(12):741 52. [17] Cordova ML, Ingersoll CD, LeBlanc MJ. Infuence of ankle support on joint range of motion before and after exercise: a meta-analysis. J Orthop Sports Phys Ther 2000;30(4):170 82. [18] Terranova AB, Zinder SM, Shultz SJ, Gansneder B. Athletic tape does not affect fibularis longus reflex latency in stable and unstable ankles. J Athl Train 2002;37:S-21. [19] Konradsen L, Voigt M, Hojsgaard C. Ankle inversion injuries. The role of the dynamic defense mechanism. Am J Sports Med 1997;25:54 8. [20] Cordova ML, Armstrong CW, Rankin JM, Yeasting RA. Ground reaction forces and EMG activity with ankle bracin during inversion stress. Med Sci Sports Exerc 1998;30:1363 70. [21] Nishikawa T, Grabiner MD. Peroneal motoneuron excitability increases immediately following application of a simirigid ankle brace. J Orthop Sports Phys Ther 1999;29(3):168 76. [22] McCaw S, Cerullo JF. Prophylactic ankle stabilizers affect akle joint kinematics during drop landings. Med Sci Sports Exerc 1999;31:702 7. [23] Ricard MD, Saret JJ, Schulthies SS. Comparison of the amount and rate of inversion between high top and low top shoes. J Athl Train 1997;32:S-13. [24] Spaulding SJ, Livingston LA, Hartsell HD. The influence of external orthotic support on the adaptive gait characteristics of individuals with chronically unstable ankles. Gait Posture 2003; 17:152 8. [25] Riemann BL, Schmitz RJ, Gale M, McCaw ST. Effect of ankle taping and bracing on vertical ground reaction forces during drop landings before and after treadmill jogging. J Orthop Sports Phys Ther 2002;32:628 35. [26] Tropp H, Ekstrand J, Gillquist J. Stabilometry in functional instability of the ankle and its value in predicting injury. Med Sci Sports Exerc 1984;16:64 6. [27] Tropp H, Odenrick P, Gillquist J. Stabilometry recordings in functional and mechanical instability of the ankle joint. Int J Sports Med 1985;6:180 2. [28] Baier M, Hopf T. Ankle rthoses effect on singl-limb balance in athletes with functional ankle instability. Arch Phys Med Rehabil 1998;79:939 44. [29] Palmieri RM, Ingersoll CD, Cordova ML, Kinzey SJ. The spectral qualities of postural control are unaffected by 4 days of ankle-brace application. J Athl Train 2002;37:269 74. [30] Barkoukis V, Sykaras E, Costa F, Tsorbatzoudis H. Effectiveness of taping and bracing in balance. Percept Mot Skills 2002;94:556 74. [31] Bentham SH, Hatcher J, Horsley I. The influence of an Aircast Sports Stirrup ankle brace on the ankle joint proprioception of professional soccer players. Sports Med Train and Rehabil 2001; 10:223 33. [32] Hartsell HD, Spaulding SJ. Effect of bracing on isokinetic torque for the chronically unstable ankle. J Sport Rehabil 1999;8:83 98.
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[33] Hals TV, Sitler MR, Mattacola CG. Effect of a semi-rigid ankle stabilizer on performance in persons with functional ankle instability. J Orthop Sports Phys Ther 2000;30(9):552 6. [34] Holme E, Magnusson SP, Becher K, Bieler T, Aagaard P, Kjaer M. The effect of supervised rehabilitation on strength, postural sway, position sense and re-injury risk after acute ankle ligament sprain. Scand J Med Sci Sports 1999;9(2):104 9. [35] Borromeo C, Ryan J, Marchetto P, Peterson R, Bove A. Hyperbaric oxygen therapy for acute ankle sprains. Am J Sports Med 1997;25(5):619 25. [36] Glasoe W, Allen M, Awtry B, Yack H. Weight-bearing immobilization and early exercise treatment following a Grade II lateral ankle sprain. J Orthop Sports Phys Ther 1999;29(7):394 9. [37] Ardevol J, Bolibar I, Belda V, Argilaga S. Treatment of complete rupture of the lateral ligaments of the ankle: a randomized clinical trial comparing cast immobilization with functional treatment. Knee Surg Sports Traumatol Arthrosc 2002;10:371 7. [38] Uh BS, Beynnon BD, Helie BV, Alosa DM, Renstrom PA. The benefit of a single-leg strength training program for the muscles around the untrained ankle. Am J Sports Med 2000;28(4): 568 73. [39] Blackburn T, Guskiewicz KM, Petschauer MA, Prentice WE. Balance and joint stability: the relative contributions of proprioception and muscular strength. J Sport Rehabil 2000;9:315 28. [40] Docherty CL, Moore JH, Arnold BL. Effects of strength training on strength development and joint position sense in functionally unstable ankles. J Athl Train 1998;33(4):3310 4. [41] Bernier JN, Perrin DH. Effect of coordination training on proprioception of the functionally unstable ankle. J Orthop Sports Phys Ther 1998;27(4):264 75. [42] Soderman K, Werner S, Pietila T, Engstrom B, Alfredson H. Balance board training: prevention of traumatic injuries of the lower extremities in female soccer players? A prospective randomized intervention study. Knee Surg Sports Traumatol Arthrosc 2000;8:356 63. [43] Matsusaka N, Yokoyama S, Tsurusaki T, Inkuchi S, Okita M. Effect of ankle disk training combined with tactile stimulation to the leg and foot on functional instability of the ankle. Am J Sports Med 2001;29(1):25 30. [44] Osborne M, Chou L, Laskowski E, Smith J, Kaufman K. The effect of ankle disk training on muscle reaction time in subjects with a history of ankle sprain. Am J Sports Med 2001;29(5): 627 32. [45] Eils E, Rosenbaum D. A multi-station proprioceptive exercise program in patients with ankle instability. Med Sci Sports Exerc 2001;33(12):1991 8. [46] Wedderkropp N, Kaltoft M, Lundgaard B, Rosendahl M, Froberg K. Prevention of injuries in young female players in European team handball. A prospective intervention study. Scand J Med Sci Sports 1999;9:41 7. [47] Mattacola CG, Lloyd JW. Effects of a 6-week strength and proprioceptioin training program on measures of dynamic balance: a single case design. J Athl Train 1997;32(2):127 35. [48] Kern-Steiner R, Washecheck H, Kelsey D. Strategy of exercise prescription using an unloading technique for functional rehabilitation of an athlete with an inversion ankle sprain. J Orthop Sports Phys Ther 1999;29(5):282 7. [49] Hess DA, Joyce CJ, Arnold BL, Gansneder BM. Effect of 4-week agility-training program on postural sway in the functionally unstable ankle. J Sport Rehabil 2001;10:24 35. [50] Yeung MS, Chan KM, So CH, Yuan WY. An epidemiological survey on ankle sprain. Br J Sports Med 1994;28(2):112 6.
Sprainsresidual instability of subtalar, Lisfranc joints, and turf toe

John E. Mullen, MDa, Martin J. OMalley, MDb,*
b
New Milford Hospital, 131 Kent Road, New Milford, CT 06776, USA Weill Medical College of Cornell University, Hospital for Special Surgery, 535 East 70th Street New York, NY 10021, USA
Although not as common as the lateral ankle sprain, athletic injuries of the hindfoot, midfoot, and forefoot can result in significant morbidity and loss of playing time. These injuries are often poorly understood and specific diagnoses are sometimes elusive. This article reviews the relevant anatomy, biomechanics, mechanism of injury, and treatment of these foot injuries to provide a guide for the treating clinician in assisting athletes in their return to competition.
Subtalar joint injuries Considerable attention has been given to the subtalar joint as an area of injury, yet these injuries remain poorly understood. Subtalar joint injuries vary from mild sprains to complete subtalar and talonavicular dislocations without fracture. Subtalar injuries occur commonly with lateral ankle sprains, and it is often difficult to separate the ankle from the subtalar joint as original site of injury and as the source of residual morbidity. The injury less frequently presents as an isolated subtalar injury that produces persistent pain. Subtalar joint anatomy The subtalar joint is a complex structure that gains its stability from the bony architecture and ligamentous structures. The joint has three articulating surfaces between the talus and the calcaneus. They are the anterior, middle, and posterior facets. These articulations allow for motion in three planes: inversion/eversion, flexion/extension, and abduction/adduction [1]. Failure of the hindfoot to move in these three planes reduces its effectiveness as a mechanical shock absorber and as a rigid lever necessary for normal gait [2].
* Corresponding author. E-mail address: omalleym@hss.edu (M.J. OMalley). 0278-5919/04/$ see front matter D 2004 Elsevier Inc. All rights reserved. doi:10.1016/S0278-5919(03)00089-9
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Fig. 1. (A,B) Coronal depiction of hindfoot ligamentous anatomy. Bands of inferior retinoculum: (a) lateral; (b) middle; (c) medial; (d) cervical ligament; (e) talocalcareal interosseous ligament. (Adapted from Harper MC. The lateral ligamentous support of the subtalar joint. Foot Ankle Int 1991;11:354 8; with permission.)
Several studies [3 5] confirm that the stability of the subtalar joint is largely due to three main ligamentous structures. They are the calaneofibular ligament, cervical ligament, and interosseous talocalcaneal ligament (Fig. 1). Cadaveric sectioning studies indicate that the calcaneofibular ligament appears to be the primary stabilizer. The calcaneofibular ligament has two major bands: a thin weak anterior band; and a wide, strong posterior band. Foot position dictates tautness of the ligament, with supination-dorsiflexion tightening the ligament and plantarflexion-eversion loosening it [6]. Secondary stability is provided by the cervical and interosseous talocalcaneal ligaments, with debate concerning which has a more important role. Subtalar instability: mechanism of injury Several mechanisms of injury have been proposed as the cause of a subtalar sprain. The most common cause is believed to be dorsiflexion and supination. This position places the calcaneofibular ligament in a position of maximal tightness. Further supination will lead to a rupture of the calcaneofibular ligament, followed by the cervical ligament and the interosseous talocalaneal ligament [7].
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Another theory proposed by Meyer et al [7] suggests that subtalar instability occurs as a progression of the classic inversion ankle sprain. In this case, the position of the ankle is plantarflexion and the force remains supination; the first ligament torn is the anterior talofibular ligament. This is followed by the calcaneofibular ligament, the lateral capsule, and then the interosseous talocalaneal ligament. It has been estimated that subtalar instability is seen in approximately 10% of cases of lateral ankle instability [8]. This supports the mechanism of plantarflexion and supination. In addition to these mechanisms, repetitive trauma to the interosseous talocalcaneal ligament has been proposed as a cause of chronic subtalar ankle instability [9]. A final factor that may predispose to subtalar instability is the posterior facet ankle of the talus. A lower facet angle may allow greater motion at the subtalar joint, which may increase the incidence of injury and instability [10]. Several authors have proposed that the athletes most at risk for subtalar injury are indoor cutting-and-jumping athletes[7,9]. Subtalar instability: clinical diagnosis Given the similar mechanisms of injury, subtalar instability is often difficult to distinguish from lateral ankle instability. The diagnosis is usually made after the patient has reached a chronic state. Patients will report recurrent inversion injuries to their foot or ankle, with the feeling that their ankle is going to give way. This is especially true when patients are running of walking on uneven ground. To compensate for their laxity and poor proprioception, patients will constantly look at the ground to avoid misstepping. An increased talar tilt is felt on examination, but it is difficult to determine whether the laxity is from the ankle or subtalar joint on exam alone. The other classic findings include swelling, stiffness, and pain [11]. The location of the pain is similar to that of sinus tarsi syndrome and it is often difficult to distinguish the two. The differential diagnosis for lateral foot pain, besides sinus tarsi syndrome, should include lateral ankle instability, osteochondral defect of the talus, superficial peroneal nerve entrapment, and neuropathic disorders [12]. Zwipp et al [12] proposed examining the hindfoot with the ankle fixed in dorsiflexion. With the talus locked within the ankle mortise, a varus stress is applied to the hindfoot and measurement of the rotation of the calcaneus in relation to the talus is made. An assessment of forward translation of the calcaneus beneath the talus can also be made. Subtalar instability: imaging The classic imaging study for diagnosing subtalar instability is the stress radiograph. The Brodens radiographic view is thought to best visualize the subtalar joint. This view is taken with the forefoot internally rotated approximately 40 and then the beam is angled cephalad from 10 to 40 (Fig. 2). At 30,
100 J.E. Mullen, M.J. OMalley / Clin Sports Med 23 (2004) 97121 Fig. 2. (A,B) Radiographic technique for Brodens view. (Adapted from Myerson M, editor. Foot and ankle disorders. Schematic of Brodens view. Philadelphia: Saunders; 2000. p. 1301; with permission.)
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the view is tangential to the posterior facet articulation and demonstrates instability of the joint complex [6]. In addition to stress radiographs, stress tomography has been described, but its value has not been clearly demonstrated [13,14]. With the use of subtalar stress radiography, there have been many different criteria put forth to define subtalar instability. Zwipp and Tscherne [15] used a talocalcaneal angle of more than 5, talocalcaneal tilt of more than 10, and a medial shift of the calcaneus with respect to the talus of more than 5 mm when compared with the uninjured side with the leg rotated 30 internally and the tube tilted 30 caudally. To define subtalar instability, Heilman et al [6] sequentially sectioned the calcaneofibular ligament and the interosseous talocalcaneal ligament. They measured the separation of the posterior facet of the talus and calcaneus during a stress Brodens view and found that they had less than 5 mm posterior facet opening, with isolated sectioning of the calcaneofibular ligament. With cutting both the calcaneofibular ligament and the interosseous talocalcaneal ligament and application of a varus stress, the posterior facet opened 7 mm or more. This gap is their definition of subtalar instability. Laurin et al [16] also used sequential sectioning of cadaveric lateral hindfeet to radiographically define subtalar instability. Their criterion for ligamentous injury and instability was any loss of parallelism of the posterior facet on a stress Brodens view (Fig. 3). In addition to stress radiography and tomography, several other tools have been described. Zell et al [17] used stress fluoroscopy of the posterior and middle facets both pre- and intraoperatively to define subtalar instability, and to judge the adequacy of the repair. Meyer and Lagier [18] used arthrograms to confirm that cases of subtalar instability dye leaks through the lateral posterior capsule and into the sinus tarsi were correlated operatively with tears in the lateral talocalcaneal ligament and the interosseous ligament. Jarde et al [19] used magnetic resonance imaging (MRI) very effectively to view pathology in the structures of the lateral ankle and the subtalar joint. All 46 patients with hindfoot instability in their study demonstrated capsuloligamentous pathology. This high sensitivity, noninvasiveness, and increasing availability make MRI an appealing study for subtalar instability. We routinely use MRI for the severe hindfoot sprains in athletes and feel they provide important information on the extent and severity of the injury. Subtalar instability: treatment There is little literature concerning the treatment of acute subtalar injuries, as most patients will suffer a concomitant ankle sprain that precludes a definitive diagnosis. When identified acutely, an isolated subtalar sprain can be treated similarly to an ankle sprain with a standard protocol of rest, ice, compression, and elevation. Immobilization and protected weight bearing may be implemented also based on the severity of the injury. High grade subtalar sprains (as determined by examination and imaging studies) are treated with 2 weeks non-weight bearing in a below-knee cast followed by 4 weeks in a commercial walker boot.
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Fig. 3. Stress Brodens view. (Adapted from Heilman AE, Braly G, Bishop JO, et al. An anatomic study of subtalar instability. Foot Ankle Int 1990;10:226; with permission.)
Chronic subtalar instability may be initially treated with physical therapy and bracing. Therapy should focus on Achilles stretching, peroneal strengthening, and proprioceptive training. These have all been found helpful in avoiding malposition of the hind foot [20]. There are a significant number of different braces available today, yet the braces that provide adequate stability have been criticized for being too bulky and cumbersome for athletics [21]. Failure of these conservative measures to allow the athlete to return to sports is an indication for surgical treatment. Surgical treatment of chronic subtalar insufficiency was initially a duplication of those procedures to stabilize the lateral ankle by reconstructing the anterior talofibular (ATFL) and calcaneofibular (CFL). In general two categories of procedures were used: tendon transfer procedures, or anatomic repairs. One of the initial procedures was described by Elmslie [22]. He wove fascia lata graph through drill holes in the calcaneus, distal fibula, and talus to reconstruct the calcaneofibular ligament and the anterior talofibular ligament. Chrisman and Snook [23] modified this by using a split peroneus brevis graft rather than the fascia lata. The split peroneus brevis graft is run retrograde through the distal fibula and then back antegrade through a tunnel in the calcaneus. The graft is
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Fig. 4. Modified Brostrom procedure. (A) ATFL and CFL shortened and repaired. (B) Inferior retinaculum attached to distal fibula.
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then sewn back upon the insertion of the peroneus brevis at the base of the fifth metatarsal. Brostrom [24] described an anatomic repair of the attenuated anterior talofibular ligament and the calcaneofibular ligament. This shortened the lax ligaments, but was not effective in treating subtalar instability. The procedure was subsequently modified by Gould et al [25]; they mobilized the lateral portion of the extensor retinaculum and sutured it to the tip of the lateral malleolus over the repaired ligaments (Fig. 4). This was found to reinforce the repair and correct the subtalar component to the instability, as the inferior retinaculum reinforces the support of the calcaneofibular ligament. More recently, triligamentous repairs (anterior talofibular, calcaneofibular, and cervical ligaments) using the peroneus brevis has been advocated by Schon et al (Fig. 5). We believe that the surgical procedure for subtalar instability must be individualized for each patient, but in general we perform the Brostrum-Gould procedure and feel it effectively addresses both lateral ankle and subtalar instability, which are frequently both present, and allows the most normal range of motion. Tendon transfer procedures using the peroneus brevis via tunnels across the subtalar joint will certainly provide good stability, but one can expect a longer recovery, higher complication rate, and more postoperative stiffness than with extra-articular reconstructions.
Fig. 5. Schon Triligamentous reconstruction with peroneus brevis. Peroneus brevis runs from calcaneus to talus to fibula to calcaneus to talus. (Adapted from Schon LC, Clanton TO, Baxter DE. Reconstruction for subtalar instability: a review. Foot Ankle 1991;11:323; with permission.)
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Subtalar injury: return to play Very little has been written on the specifics of returning to play after a subtalar injury. The timing of this should be based on the patients symptoms. After the pain and swelling has resolved, a program of walking and running activities is initiated, followed by a monitored sport-specific program. Once this has been mastered, competition is allowed. A supportive device such as a brace or ankle sleeve may hasten a patients return to play. These criteria and this protocol also apply to patients after surgical treatment. In our experience with professional ballet dancers return to full activity after a Brostrom-Gould procedure usually occurs around the 12-week mark.
Lisfranc (tarsometatarsal) injuries Injuries to the Lisfranc joint complex are often associated with high-energy motor vehicle accidents, but lower-velocity Lisfranc injuries can occur during athletic competition.
Fig. 6. Ligamentous attachments of tarsometatarsal joints. (Adapted from Wiley JJ. The mechanism of tarsometatarsal joint injuries. J Bone and Joint Surg 1971;53B:474; with permission.)
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Lisfranc joint anatomy The tarsometatarsal (Lisfranc) articulation is a complex osseous and capsuloligamentous structure. The cuneiforms, cuboid, and the corresponding metatarsal bases form a series of self-locking wedges, which make up the transverse arch. The keystone to this arch is the base of the second metatarsal. It has a triangular shape and is recessed between the surrounding cuneiforms. The tarsometatarsal articulation is restricted to motion in a plantar direction with flexion and extension. Because of this, displacement in any other direction is a clear sign that there has been a fracture of the second metatarsal base or a disruption of the stabilizing ligaments [26]. A significant amount of stability of the tarsometatarsal articulation comes from the capsuloligamentous structures (Fig. 6). A strong intermetatarsal ligament runs between the bases of the second through the fifth metatarsals. There is no intermetatarsal ligament from the base of the first metatarsal to the second
Fig. 7. Normal radiographs of Lisfranc joint. (A) AP view of the foot. The medial border of the second metatarsal aligns with the medial border of the middle cuneiform. (B) Medial border of the 4th metatarsal aligns with the medial border of the cuboid.
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metatarsal; rather the strong Lisfranc ligament runs between the medial cuneiform and the base of the second metatarsal. This ligament is the largest of the tarsometatarsal articulation and runs in a plantar direction to stabilize the second metatarsal into its mortise. The Lisfranc ligament and the plantar ligaments are significantly stiffer and stronger than the dorsal ligaments, which makes the dorsal ligamentous complex a weak point [27]. Lisfranc sprain: mechanism of injury The majority of published reports on Lisfranc injuries indicate that a preponderance of these injuries occur during high-energy trauma, such as motor vehicle accidents and falls [28 30]. Over the past ten years several studies have looked at lower-velocity, twisting type injuries that occur during athletics [26,31,32]. The most commonly described mechanism of injury is an axial load
Fig. 7 (continued).
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applied to a plantar flexed and slightly rotated foot. Football, basketball, and running are the sports that frequently cause this injury [31]. Another mechanism described is when the hindfoot is placed in plantarflexion with a fixed forefoot forced into abduction. This occurs in sports where the forefoot is fixed in position, such as when a foot is caught in a stirrup during an equestrian accident. The same mechanism has been described in windsurfers [31]. Regardless of the exact mechanism, there seems to be a consensus that these forces cause a disruption of the dorsal ligament complex of the tarsometatarsal joint [26,28 32]. Lisfranc injury: imaging The initial radiographic study usually done for Lisfranc injuries consists of the standing anteroposterior, oblique, and lateral radiographs of the foot. The radiographs should reveal that the medial border of the second metatarsal lines up with the medial border of the middle cuneiform, and the medial border of the fourth metatarsal lines up with the medial border of the cuboid on the anterior-posterior and oblique radiographs (Fig. 7). In addition, comparison standing radiographs are quite often obtained for suspected Lisfranc injuries. Several studies have reported the importance of weight-bearing radiographs of the foot [32 34]. In Nunley and Vertullos series [32], 50% of their patients with diastasis of the first and second metatarsals bones had normal non-weight bearing anteroposterior radiographs (Fig. 8). Faciszewski et al [34] stressed the importance of lateral weight-bearing radiographs to differentiate a simple sprain from a complex ligamentous disruption. This was done by noting the distance, on the lateral weight-bearing radiograph, from the plantar aspect of the base of the fifth metatarsal to the plantar medial cuneiform (Fig. 9). Several authors [31,35] have
Fig. 8. (A,B) Nonweight bearing and weight bearing views demonstrate diastasis with weightbearing. (Adapted from Bloome DM, Clanton TO. Treatment of lisfranc injuries in the athlete. Techniques in Foot and Ankle Surgery 2002;1(2):94 101; with permission.)
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Fig. 9. Method for measuring the distance from the plantar aspect of the base of the 5th metatarsal to the medial cuneiform. (A) Normal relationship has a positive value. (B) Flattening of the foot. The medial cuneiform is plantar to the fifth metatarsal (negative value). (Adapted from Faciszewski T, Burks RT, Manaster ST. Subtle injuries of lisfranc joint. JBJS 1990;72A:1520; with permission.)
advocated the use of stress fluoroscopy with the patient under anesthesia. Nunley and Vertullo [32] questioned the use of stress radiography, citing the limited force that can be exerted on the tarsometatarsal joint complex compared with weight bearing and the lack of a standardized criteria. Bone scintigraphy is another tool available for diagnosing occult midfoot pathology. A number of authors [32,36,37] have touted its sensitivity, availability, ease of interpretation, and relative low cost. In addition, bone scintigraphy can remain positive in midfoot injuries that are over a year old. Magnetic resonance imaging and computed axial tomography are excellent modalities for better visualizing the soft tissue and osseous structures respectively. MRI [38 41] has become especially effective in diagnosing Lisfranc sprains with normal bony anatomy (Fig. 10). Lisfranc injury: clinical diagnosis Patients with Lisfranc injuries will present with complaints of midfoot pain. They may or may not recall the specific event in which they were injured, depending on the severity of the injury. Because in athletics these injuries tend to be lower-velocity, twisting-type injuries, the physical findings may be subtle. Early physical signs include midfoot swelling and tenderness, which may be followed by plantar ecchymosis. Some authors [26,34] stress the importance of evaluating the functional status of the foot. Assessing the patients gait, medial longitudinal arch, and ability to bear weight on the toes does this. Curtis et al [31] proposed a passive pronation-abduction test, which should elicit tenderness across the midfoot. It was noted that this test is limited in the early, acute phase of an injury.
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Fig. 11. Nunley and Vertulla classification of Lisfranc injuries. (Adapted from Nunley J, Vertullo CJ. Classification, investigation, and management of midfoot sprains. Am J Sports Med 2002;30:872; with permission.)
Several classification systems have been proposed for Lisfranc injuries, but none are universally accepted. Nunley and Vertullo [32] recently proposed a grading system that is based on clinical findings, weight-bearing radiography, and bone scintigraphy results. A Stage I sprain to the midfoot has no diastasis or arch height loss on weight-bearing radiographs, but does have increased uptake on bone scintigraphy. With Stage II sprains there is a 2 mm to 5 mm diastasis between the first and second metatarsals, but no loss of arch height. Stage III sprains have a diastasis between the first and second metatarsal greater than 5 mm, and in addition have a loss of arch height. This is seen as a decrease in the distance between the plantar aspect of the fifth metatarsal bone and the plantar aspect of the medial cuneiform bone on a weight-bearing lateral radiograph (Fig. 11). Treatment type was based on the stage of the sprain. Lisfranc injury: treatment Treatment of Lisfranc complex injuries is largely based on the amount of diastasis between the first and the second metatarsals and the relationship of the
Fig. 10. (A) Normal MRI of Lisfranc ligament. (B) MRI showing rupture of Lisfranc ligament with bony avulsion.
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medial cuneiform and fifth metatarsal on lateral weight-bearing radiographs. These radiographic findings are a direct indication of the amount of instability that is present in the midfoot. A number of studies [26,31,32] have shown that Stage I injuries can be reliably treated with cast immobilization and protected weight bearing with excellent results. These results were obtained in patients were symptoms had gone undiagnosed for up to 8 months. The duration of the treatment varied between the studies, but most recommended 4 to 6 weeks. The length of the treatment should be based on the patients symptoms. There is varying approaches to the treatment of Stage II injuries. Wippula [42] reviewed 26 patients with Lisfranc injuries who had been treated either nonoperatively or operatively. He evaluated function as it correlated with first-second metatarsal diastasis. Gaps of less than 5 mm were found to have the best results regardless of treatment type, whereas those with separation greater than 10 mm did poorly. Based on these results, closed treatment of first-second metatarsal gaps of 5 mm or less was recommended. Faciszewski et al [34] reviewed 15 patients with subtle Lisfranc injuries (2 mm 5 mm of diastasis) and found no correlation between first-second metatarsal diastasis size and pain. Rather they found that in six of the seven patients with persistent pain there was a reversal of the normal medial cuneiform-fifth metatarsal relationship on the lateral weight-bearing radiographs. The authors therefore recommended cast immobilization and non-weight bearing for Stage II injuries, and open reduction and internal fixation for Stage III injuries. Nunley and Vertullo [32] also reported on 15 athletes with Lisfranc injuries. They performed early closed reduction and internal fixation on 6 patients with early Stage II injuries and late open reduction and internal fixation on 2 patients with chronic Stage II injuries. All of their patients had excellent results, with the exception of one of the chronic Stage II patients who went 10 months before having surgery. Although there were no Stage III injuries in their study, they postulated that these would have a poorer prognosis and should have early anatomic reduction and fixation. Curtis et al [31] performed a retrospective review of 19 athletes with tarsometatarsal joint injuries. Three of these patients had third-degree sprains, which were defined as any diastasis between the first and second metatarsals. There was no evaluation of the medial cuneiform-fifth metatarsal relationship on lateral weight-bearing radiographs. Two of the three were treated with open reduction and internal fixation with good to excellent results. The third patient had initially been managed with a cast and had done poorly, requiring a tarsometatarsal fusion. They recommended open reduction and internal fixation for all patients with diastasis, regardless of degree. We advocate early open reduction internal fixation for all grade 2 and 3 sprains in athletes (Fig. 12). Our rationale is that stable anatomic bony alignment will most likely lead to ligamentous healing and subsequent healing of the capsuloligamentous support of the arch. Although we acknowledge that screws placed across these joints could lead to arthrosis, we believe the tarsometarsal joints
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Fig. 12. Typical internal fixation pattern for Lisfranc ORIF.
function better with more stiffness than with laxity, as their main job is to form a rigid lever to propel the athletes body weight forward. More recently, we have been performing some primary fusions of the first and second tarsometarsal joints for Lisfranc injuries with severe intra-articular damage (Fig. 13). The use of absorbable screws for these injuries is a theoretical advantage, but no study exists to compare absorbable versus standard internal fixation, and thus there is no basis on which to make a recommendation. Lisfranc injury: return to play With Lisfranc injuries, activity can be advanced as the patients pain and inflammation diminish. After an initial period of protected weight bearing,
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Fig. 13. 33 year old NBA basketball player 8 months after untreated Lisfranc sprain. (A) Lateral weightbearing radiograph reveals flattening of the longitudinal arch with loss of distance from the base of the 5th metatarsal to cuneiform. (B) Restoration of the arch following 1st and 2nd tarsometarasal fusion. The player returned to professional basketball. (Adapted from Rodeo SA, OBrien S, Warren RF, et al. Turf-toe: an analysis of metatarsophalangeal joint sprains in professional football players. Am J Sports Med 1990;18(3):280; with permission.)
patients are slowly advanced from walking to running to cutting activities. A patients final task is to complete sport-specific drills. Once this is accomplished, play can resume, usually with the aid of a custom orthotic. Nunley et al [32] found they had a 15.4-week interval before return to play in their operative patients, which compared favorably to the 15-week period seen in their nonoperative patients. In the series by Curtis et al [31], the return to play interval was varied, ranging from 6 weeks to 9 months. In addition, three of their patients did not return to playing sports.
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The great toe Metatarsophalangeal joint injuries in athletics have become an ever-increasing source of forefoot pain and dysfunction. The most common injury is to the plantar plate (turf toe), alone or in combination with sesamoid and collateral ligament injuries. Turf toe anatomy The first metatarsophalangeal joint derives most of its stability from the surrounding capsuloligamentous complex (Fig. 14). A minimal amount of
Fig. 14. Capsular-ligamentous-sesamoid complex of the hallux. (A) Medial view. (B) Plantar view. (Copyright CMC, 1999.)
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stability comes from the condyloid architecture of the biconvex metatarsal head and the shallow socket of the proximal phalanx. The joint has approximately 30 of flexion and 80 of extension with active motion of the joint [43]. There is very little medial to lateral motion at this joint. The joint capsule is reinforced on the plantar surface by the plantar plate, a thick fibrous structure that is firmly anchored to the base of the proximal phalanx and loosely attached to the plantar neck of the metatarsal. The distal attachment on the proximal phalanx is stronger than the metatarsal attachment [44]. The volar plate contains the two sesamoid bones, which have several structures that insert onto them. The abductor hallucis tendon contributes to the capsule as it inserts onto the medial sesamoid, and the adductor hallucis does the same to the lateral sesamoid [45]. The sesamoids are enveloped within the double tendon of the flexor hallucis brevis, and they function as a fulcrum to increase the mechanical advantage of the tendon. The metatarsophalangeal joint is supported by strong collateral ligaments that limit medial-to-lateral motion of the joint [44]. Turf toe: mechanism of injury There are several different mechanisms of injury that have been described for turf toe [44 46]. The most common mechanism of injury is a hyperextension force to the first metatarsalphalangeal joint with a concomitant axial load applied to the heel (Fig 15). This results in a tear of the capsule at its insertion onto the metatarsal neck and a compression injury to the dorsal articular surface of the metatarsal head. This injury typically occurs in football players when the forefoot is fixed on the ground with the heel elevated and another player lands on the back of the foot, causing a hyperextension injury.
Fig. 15. Mechanism of turf toe injury. (Copyright CMC, 1999.)
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In addition to hyperflexion, valgus and varus mechanism have been described [44 46]. The hyperflexion injury occurs when a forward force is applied to the knee of a player with his foot plantarflexed. The valgus injury is seen when players such as offensive linemen push off from a stance [44]. This usually occurs in conjunction with additional forces such as hyperextension. A varus mechanism of injury, which is quite uncommon, occurs when an external rotation force is applied to a fixed forefoot [47]. Several other factors have been linked to the occurrence of turf toe, specifically artificial turf and shoe wear. Studies have looked at the hardness of artificial turf as well as the increased surface friction. Bowers and Martin [48] showed that as artificial turf ages it loses its ability to absorb force. Despite this, Clanton et al [49] were unable to show a change in the incidence of turf toe when a newer turf was installed. Nigg and Segesser [50] saw increased incidence of turf toe on artificial turf and postulated that this was due to increased surface friction and a fixed forefoot. As the overall national trend is back toward natural playing surfaces, we would expect a decreased incidence of this injury. Shoe stiffness has also been identified as a risk factor. Turf shoes, although providing excellent friction, are light and have a flexible forefoot, which allows increased motion of the metatarsophalangeal joint. This provides less resistance to hyperextension forces. Newer shoes with a stiffened forefoot have decreased the incidence of injury [49].
Turf toe: clinical diagnosis Patients will present with a history of a single acute or multiple episodes of forefoot trauma. Clinically, the metatarsophalangeal joint will be tender, swollen, red, and painful with motion. With chronic cases, patients can develop hammering, angulation, and subluxation. Clanton and Ford [45] have proposed a grading system to aid in assessment and treatment. A grade 1 sprain is a stretch injury to the capsuloligamentous complex of the first metatarsalphalangeal joint. Symptoms are generally minimal. A grade 2 sprain is a partial tear of the capsuloligamentous complex of the first metatarsalphalangeal joint. Symptoms will include eccymosis moderate restriction of motion, and pain with weight bearing. A grade 3 sprain is a complete tear of the capsuloligamentous complex, with disruption of the plantar plate from the metatarsal neck. With this grade of injury, the symptoms include severe pain, tenderness, swelling, eccymosis, and marked restriction of motion. The patient is unable to bear weight normally.
Turf toe: imaging Plain radiographs in anterior-posterior, lateral, and oblique planes should be taken in all cases of suspected turf toe. The position of the sesamoids should be noted and comparison views of the opposite foot should be obtained if it appears the sesamoids have migrated proximally (Fig. 16). In addition, plain radiographs
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Fig. 16. AP radiograph demonstarting proximal migration of the sesamoids following plantar plate rupture.
can rule out a capsular avulsion, sesamoid fracture, impaction injuries, or separation of a bipartite sesamoid [44,51]. MRI is recommended for any patient with radiographic abnormalities, as well as all grade 2 and 3 sprains (Fig. 17). This study best evaluates the degree of softtissue damage as well as osseous and articular cartilage status. We agree with Anderson that MRI can assist in grading these injuries and formulating a treatment plan in the athlete [52].
Fig. 17. Abductor hallucis tendon mobilized and rerouted to plantar aspect of joint. (Adapted from Watson TS, Anderson RB, Davis WH. Periarticular injuries to the hallux metatarsophalangeal joint in athletes. Foot and Ankle Clinics 2000;5(3):703; with permission.)
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Turf toe: treatment Initial treatment for acute turf toe consists of the standard protocol of rest, ice, compression, and elevation. Further treatment can be based upon the grade of the sprain, with grade 1 requiring toe taping and a stiff insole, but usually no loss of playing time. Grade 2 injuries can often require up to 2 weeks of rest, and grade 3 injuries may need protected weight bearing and prolonged rest [45]. Operative treatment for turf toes should be considered for large capsular avulsions with an unstable joint, diastasis of a bipartite or sesamoid fracture, traumatic bunion, retraction of sesamoids, or loose body [52]. Coker et al [46] discuss capsular repair in both the acute and chronic settings for turf toe. Anderson uses the abductor hallucis in cases where primary repair is not possible to reinforce the plantar plate (Fig. 17). This technique is also used in cases where medial sesamoid excision is performed for fracture. We have used this technique with good success and recommend it for those cases of turf toe that do not heal with conservative care. Turf toe injury: return to play Return to play for turf toe follows a logical sequence of events. Initially, weight bearing will be protected as the pain and swelling subside. Walking is progressed to running, followed by cutting and sport-specific activities. Once this is completed, sports may be resumed with the aid of an orthotic with a stiff forefoot. Anderson [52] found return to play dependent on a players position, level of discomfort, and healing potential. He felt this correlated with painless dorsiflexion of 50 to 60 of the first metatarsophalangeal joint. Clanton and Ford [45] found that the period of recovery usually lasts 4 weeks regardless of the degree of the sprain.
Summary Sprains of the hindfoot, midfoot and forefoot are being diagnosed with more regularity in athletes. Each of these injuries can go on to develop chronic instability with associated disability. With early diagnosis and appropriate treatment significant morbidity and loss of playing time can be avoided. Knowledge of the relevant anatomy, mechanism of injury, and available diagnostic tools is essential for making the proper diagnosis. Once the correct diagnosis is made, proper treatment can be implemented to avoid long term complications of instability.
References
[1] Perry J. Anatomy and biomechanics of the hindfoot. Clin Orthop 1983;177:9 15. [2] Wright DG, Deai SM, Henderson WH. Action of the subtalar and ankle joint complex during the stance phase of walking. J Bone Joint Surg 1964;46A:361 82.
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[3] Ruth CJ. The surgical treatment of injuries of the fibular collateral ligaments of the ankle. J Bone Joint Surg 1961;43A:229 39. [4] Harper MC. The lateral ligamentous supportof the subtalar joint. Foot Ankle Int 1991;11(6): 354 8. [5] Kjaersgaard-Andersen P, Wethelund JO, Neilsen S. Lateral talocalcaneal instability following section of the calcaneofibular ligament: a kinesiologic study. Foot Ankle 1987;7:355 61. [6] Heilman AE, Braly WG, Bishop JO, Noble PC, Tullos HS. An anatomic study of subtalar instability. Foot Ankle 1990;10:224 8. [7] Meyer JM, Garcia J, Hoffmeyer P, Fritschy D. The subtalar sprain: a Roentgenographic study. Clin Orthop 1988;226:169 73. [8] Renstro m PA. Persistently painful sprained ankle. J Am Acad Orthop Surg 1994;2:270 80. [9] Pisani G. Chronic laxity of the subtalar joint. Orthop 1996;19:431 7. [10] Kato T. The diagnosis and treatment of instability of the subtalar joint. J Bone Joint Surg 1995; 77B:400 6. [11] Keefe DT, Haddad SL. Subtalar instability: etiology, diagnosis, and management. Foot Ankle Clin 2002;7:577 609. [12] Zwipp H, Rammelt S, Grass R. Ligamentous injuries about the ankle and subtalar joints. Clin Podiatr Med Surg 2002;19:195 229. [13] Brantigan JW, Pedegana LR, Lippert FG. Instability of the subtalar joint. Diagnosis by stress tomography in three cases. J Bone Joint Surg 1977;59A(3):321 4. [14] Rubin G, Whitten M. The subtalar joint and symptoms of turning over on the ankle: a method of evaluation utilizing tomography. Am J Orthop 1962;4:16 9. [15] Zwipp H, Tscherne H. Die radiologische diagnostik der rotationsinstabilita t im hinteren unteren sprunggelenk. Unfallheilkunde 1982;85:494. [16] Laurin CA, Oulette R, St. Jacques R. Talar and subtalar tilt: an experimental investigation. Can J Surg 1968;11:270 9. [17] Zell BK, Shereff MJ, Greenspan A, Liebowitz S. Combined ankle and subtalar instability. Bull Hosp Jt Dis Orthop Inst 1986;46:37 45. [18] Meyer JM, Lagier R. Post-traumatic sinus tarsi syndrome: an anatomic and radiological study. Acta Orthop Scand 1977;48:121 8. [19] Jarde O, Duboille G, Abi-Raad G, Boulu G, Massy S. Ankle instability with involvement of the subtalar joint demonstrated by MRI. Results with the Castaing procedure in 45 cases. Acta Orthop Belg 2002;68:515 28. [20] Clanton TO. Instability of the subtalar joint. Orthop Clin North Am 1989;20:583 92. [21] Mann RA. Athletic injuries to the soft tissue of the foot and ankle. In: Mann RA, Coughlin MJ, editors. Surgery of the foot and ankle. 7th edition. St. Louis (MO): Mosby; 1999. p. 1153 65. [22] Elmslie RC. Recurrent subluxation of the ankle joint. Ann Surg 1934;100:364 7. [23] Chrisman OD, Snook G. Reconstruction of lateral ligament tears of the ankle: an experimental study and clinical evaluation of seven patients treated by a new modification of the Elmslie procedure. J Bone Joint Surg 1969;51A:904 12. [24] Brostrom L. Sprained ankles, IV: surgical treatment of chronic ligament ruptures. Acta Chir Scand 1966;132:551 65. [25] Gould N, Selligson D, Gassman J. Early and late repair of the lateral ligaments of the ankle. Foot Ankle 1980;1:84 9. [26] Mantas JP, Burks RT. Lisfranc injuries in the athlete. Clin Sports Med 1994;13:719 30. [27] Solan MC, Moorman 3rd CT, Miyamoto RG, Jasper LE, Belkoff SM. Ligamentous restraints of the second tarsometatarsal joint: a biomechanical evaluation. Foot Ankle Int 2001;22:637 41. [28] Aitken AP, Poulson D. Dislocations of the tarsometatarsal joint. J Bone Joint Surg 1963;45: 246 60. [29] Wilson DW. Injuries of the tarsometatarsal joints: etiology, classification and results of treatment. J Bone Joint Surg 1972;54:677 86. [30] Richter M, Wipperman B, Krettek C, Schratt HE, Hufner T, Therman H. Fractures and fracture
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dislocations of the midfoot: occurrence, causes and long-term results. Foot Ankle Int 2001;22: 392 8. Curtis MJ, Meyerson M, Szura B. Tarsometatarsal joint injuries in the athlete. Am J Sports Med 1993;21:497 502. Nunley JA, Vertullo CJ. Classification, investigation and management of midfoot sprains. Am J Sports Med 2002;30:871 8. Shapiro MS, Wascher DC, Finerman GA. Rupture of Lisfrancs ligament in athletes. Am J Sports Med 1994;22:687 91. Faciszewski T, Burks RT, Manaster BJ. Subtle injuries of the Lisfranc joint. J Bone Joint Surg Am 1990;72(10):1519 22. Myerson M. The diagnosis and treatment of injuries to the Lisfranc joint complex. Orthop Clin North Am 1989;20(4):655 64. Groshar D, Alperson M, Mendes DG, Barsky V, Liberson A. Bone scintigraphy findings in Lisfranc joint injury. Foot Ankle Int 1995;16(11):710 1. Meyer SA, Callaghan JJ, Albright JP, Crowley ET, Powell JW. Midfoot sprains in collegiate football players. Am J Sports Med 1994;22(3):392 401. Preidler KW, Brossman J, Daenen B, Goodwin D, Schweitzer M, Resnick D. MR imaging of the tarsometatarsal joint: analysis of injuries in 11 patients. AJR Am J Roentgenol 1996;167(5): 1217 22. Preidler KW, Wang YC, Brossman J, Trudell D, Daenen B, Resnick D. Tarsometatarsal joint: anatomic detail on MR images. Radiology 1996;199:733 6. Preidler KW, Peicha G, Lajtai G, Seibert FJ, Fock C, Szolar DM, et al. Conventional radiography, CT, and MR imaging in patients with hyperflexion injuries of the foot: diagnostic accuracy in the detection of bony and ligamentous changes. AJR Am J Roentgenol 1999;173(6):1673 7. Goiney RC, Connell DG, Nichols DM. CT evaluation of tarsometatarsal fracture-dislocation injuries. AJR Am J Roentgenol 1985;144(5):985 90. Wippula E. Tarsometatarsal fracture-dislocation: late results in 26 patients. Acta Orthop Scand 1972;44:335 45. Clanton TO. Etiology of injury to the foot and ankle. In: Delee JC, Drez D, Miller M, editors. Orthopedic sports medicine: principles and practice. Philadelphia: WB Saunders; 2003. p. 2504 11. Rodeo SA, OBrien S, Warren RF, Barnes R, Wickiewicz TL, Dillingham MF. Turf-toe: an analysis of metatarsophalangeal joint sprains in professional football players. Am J Sports Med 1990;18(3):280 5. Clanton TO, Ford JJ. Turf toe injury. Clin Sports Med 1994;13(4):731 41. Coker TP, Arnold JA, Weber DL. Traumatic lesions of the metatarsophalangeal joint of the great toe in athletes. Am J Sports Med 1978;6(6):326 34. Mullis DL, Miller WE. A disabling sports injury of the great toe. Foot Ankle 1980;1(1):22 5. Bowers Jr KD, Martin RB. Impact absorption, new and old Astroturf at West Virginia University. Med Sci Sports 1974;6(3):217 21. Clanton TO, Butler JE, Eggert A. Injuries to the metatarsophalangeal joints in athletes. Foot Ankle 1986;7(3):162 76. Nigg BM, Segesser B. The influence of playing surfaces on the load on the locomotor system and on football and tennis injuries. Sports Med 1988;5(6):375 85. Rodeo SA, Warren RF, OBrien SJ, Pavlov H, Barnes R, Hanks GA. Diastasis of bipartite sesamoids of the first metatarsophalangeal joint. Foot Ankle 1993;14(8):425 34. Anderson RB. Turf toe injuries of the hallux metatarsophalangeal joint. Techniques in Foot and Ankle Surg 2002;1(2):102 11.
Clin Sports Med 23 (2004) 123 144
Heel painplantar fasciitis and Achilles enthesopathy

Seth K. Williams, MD*, Michael Brage, MD
Department of Orthopaedic Surgery, University of California, San Diego, 200 West Arbor Drive, #8894, San Diego, CA 92103, USA
Plantar fasciitis and Achilles enthesopathy are two of the most common causes of posterior heel pain. In the vast majority of cases, non-surgical treatment methods are effective. In recalcitrant cases, surgery has been shown to be generally effective. There are a variety of described endoscopic and open techniques for both conditions.
Plantar fasciitis Plantar fascia: anatomy, pathophysiology, and function The plantar fascia is comprised primarily of a substantial central longitudinal component, the plantar aponeurosis, as well as medial and lateral components. The thick central portion is narrowest at its origin at the anteromedial process of the calcaneal tuberosity. Dorsal to the plantar fascia lies the flexor digitorum brevis muscle, and more dorsal still lie the abductor hallucis and quadratus plantae muscles. A branch of the lateral plantar nerve divides from the tibial nerve medially and runs between the fascia of the flexor digitorum brevis and quadratus plantae muscles, very near to the muscular and fascial origins at the anteromedial process, to innervate the abductor digiti minimi. The fascia broadens and thins as it traverses the arch of the foot and, distally, divides near the metatarsal heads into five digital slips, one for each toe. As these digital slips course distally, the fibers further separate and insert into dorsally oriented fibers that form arches with the flexor sheaths for the flexor tendons, into
* Corresponding author. E-mail address: swilliams@ucsd.edu (S.K. Williams). 0278-5919/04/$ see front matter D 2004 Elsevier Inc. All rights reserved. doi:10.1016/S0278-5919(03)00094-2
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transversely-oriented fibers that augment the transverse metatarsal ligaments, and into interdigitations with the integument. The thinner lateral and medial components of the plantar fascia support the abductor digiti minimi and abductor hallucis muscles, respectively [1,2]. Biopsy of pathologic plantar fascia has revealed various patterns of collagen degeneration and repair, angiogenesis, chondroid metaplasia, microtears, and matrix calcification. These findings are most consistent with the various phases of injury to the tissues and cause inadequate healing, chronic inflammation, and fatigue failure [3]. These pathophysiologic findings support the theory that plantar fasciitis is a result of chronic overload of the plantar fascia. The plantar fascia provides an intimate attachment to the overlying skin and functions to provide protection to the underlying muscles, tendons, arteries, and nerves. The fascia assists in the maintenance of the foot arch and keeps the foot in relative supination through the push-off phase of ambulation. This is illustrated by the windlass mechanism, a combination of deepening of the arch, foot supination, and external rotation of the leg resulting from tightening of the plantar fascia produced by passive dorsiflexion of the toes [4]. During heel strike, the plantar fascia remains supple and allows the foot to adjust to the ground surface and absorb shock. Then, during the toe-off phase of ambulation, the plantar fascia becomes taut and thereby renders the foot a rigid lever, thus facilitating forward movement [3,5]. Plantar fasciitis: definition and differential diagnosis Plantar fasciitis indicates inflammation of the plantar fascia and is the pathophysiological name given to a characteristic inferior heel pain pattern. Nevertheless, plantar, or inferior, heel pain may have traumatic, vascular, neurologic, arthritic, infectious, autoimmune, or mechanical causes. The term plantar fasciitis is often used interchangeably with these various causes of heel pain. A case in point is that mechanical causes of heel pain are generally synonymous with plantar fasciitis. Lastly, some cases are enigmatic in etiology and are deemed idiopathic. Historically, insertional pain at the medial calcaneal tubercle was called painful heel by Lapidus and Guidotti, avoiding the propensity to use terms such as plantar fasciitis, heel spur syndrome, or calcaneal periostitis [6]. This name was deliberately used because of its vagueness, indicating that there are many causes of inferior heel pain. Since that time, the term plantar fasciitis has become equated with inferior heel pain. Tuberculosis and gonorrhea are primarily of historical value as systemic conditions associated with inferior heel pain, having given way to rheumatoid arthritis, ankylosing spondylitis, Reiter syndrome, and other seronegative arthropathies. These diagnoses must be entertained in the appropriate age group and gender, especially when the pain is bilateral. Infection must be considered in the diabetic or otherwise immunocompromised individual. Osteoarthrosis may involve multiple joints throughout the body, or may be post-traumatic and therefore focal. Traumatic causes, if chronic in nature, are mainly limited to
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calcaneal stress fractures. Vascular insufficiency produces a characteristic pain pattern that is almost exactly opposite in provocative and palliative factors when compared with plantar fasciitis. Nerve entrapment syndromes, such as compression of the first branch of the lateral plantar nerve or tarsal tunnel syndrome, may be an isolated cause of heel pain, or may overlap with plantar fasciitis. Heel spurs, calcaneal bursitis, inappropriate shoe wear, and fat pad atrophy are other potential causes of heel pain. Clinical presentation and diagnosis A history, physical examination, and plain radiographs are usually sufficient to make the diagnosis of plantar fasciitis. In so doing, the other less common, but perhaps more foreboding, causes of plantar heel pain are eliminated from consideration. The typical individual stricken with plantar fasciitis is most afflicted upon initiation of ambulation, after rising from sleep or other sedentary respite. The pain subsides with each subsequent step, but often returns insidiously as the day progresses and more time is spent on the feet. The pain is reliably alleviated with rest [7]. On physical examination, there is often tenderness to palpation over the calcaneal origin of the plantar fascia. In the senior authors experience, pain with forced dorsiflexion of the toes, which is a reproduction of the windlass mechanism, is rarely found. Radiographs may show a spur (enthesyte) on the leading edge of the calcaneal inferior surface, but this radiographic finding is not pathognomonic of the condition, nor is it necessary for diagnosis (Fig. 1). Rubin and Witten studied radiographs of 425 patients without arthritis, and found plantar calcaneal spurs in 125, only 10% of which were deemed symptomatic [8]. The other causes of plantar heel pain usually are associated with characteristics that are not at all typical of idiopathic plantar fasciitis. Patients with systemic conditions and those with potential infection will have other areas of involvement, or at least a history of diabetes, chemotherapy, or retroviral infection. As rare as these causes of plantar heel pain are, it is even rarer that the heel pain is the presenting symptom of the condition. Osteoarthrosis is diagnosed based on history of a traumatic event or other joint involvement, and is strongly correlated with radiographic findings. In patients with stress fractures of the calcaneus, often the entire posterior heel tuber is tender to palpation. At times, however, calcaneal stress fractures may be somewhat difficult to separate from plantar fasciitis, but if suspected despite negative plain radiographs, they will be readily diagnosed with magnetic resonance imaging or nuclear bone scan. Vascular insufficiency is associated with diminished or absent pulses, lack of hair distally, and trophic skin changes. The role of nerve entrapment in painful heel syndrome deserves special attention. It is difficult to rule out nerve entrapment in the face of plantar fasciitis signs and symptoms, and some authors feel that the two conditions are intimately related. The branch of the lateral plantar nerve serving the abductor digiti minimi runs in a transverse fashion along the plantar fascia, in the area of the typical calcaneal spur [9,10]. Treatment modalities aimed at decreasing inflammation of
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Fig. 1. Lateral radiograph of the hindfoot showing both plantar and posterior spurs, often associated with plantar fasciitis and Achilles enthesopathy, respectively.
the plantar fascia may also decompress this nerve, as would surgical plantar fascial release or release of the fascia of the abductor hallucis and quadratus plantae. Nerve conduction studies do not lead to a reliable diagnosis of nerve entrapment, so it usually cannot be said with certainty that a particular case of heel pain is due solely to plantar fasciitis or nerve entrapment. Indeed it is plausible that the plantar fasciitis causes the nerve entrapment, and so in treating the former the latter is rendered asymptomatic, and a cure is effected. The diagnosis of isolated nerve entrapment is made on clinical characteristics. Usually the pain occurs after activity rather than upon the first steps in the morning, and the maximal point of tenderness to palpation is at the site of compression between the taut abductor hallucis fascia and the medial margin of the quadratus plantae muscle. Risk factors for development of heel pain Plantar fasciitis has been reported to occur primarily in athletic individuals and military personnel, as well as those with sedentary lifestyles [11]. These are seemingly disparate groups, but may have in common a chronic overload of the plantar fascia insertion into the calcaneus. This causes painful microtrauma at the insertional site of the plantar fascia. Riddle et al used a matched case-control study methodology to determine the risk factors for developing plantar fasciitis. Fifty consecutive patients with a
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clinical diagnosis of unilateral plantar fasciitis were matched with asymptomatic individuals. Ankle dorsiflexion was compared with the contralateral uninvolved extremity. The amount of time spent on the feet at work was elucidated. The authors concluded that the risk of plantar fasciitis increases as the range of ankle dorsiflexion decreases, the body mass index or obesity increases, and the amount of workday spent on the feet increases. The authors postulate that increased tensile loads on the plantar fascia is the biologic basis for plantar fasciitis. Limited ankle dorsiflexion during ambulation forces the forefoot to compensate with dorsiflexion and pronation, thus placing repetitive longitudinal stress on the plantar fascia. Obesity and prolonged ambulation cause similar such repetitive stressing of the plantar fascia [12]. The correlation of obesity and heel pain was supported by a prospective study by Rano et al [13]. Treatment methods: nonsurgical Treatment of plantar fasciitis is often initiated by the patient, perhaps by changing foot wear, altering activities, or by the use of inserts. If unsuccessful, the assistance of a physician is sought, and the mainstay of treatment remains nonsurgical. Good outcomes are expected with nonsurgical treatment, and only a small percentage will go on to require surgical management [14 16]. Modification of daily activities and habits is a seemingly simple measure that is not often easily applied. Runners may be reluctant to alter their training, and workers who spend time on their feet as part of their job may not be able to easily modify their duties. Overweight people often have difficulty losing weight. Nevertheless, lifestyle modification is successful in some patients, who then may be able to resume their previous activities once the plantar fascia has healed. To prevent recurrence, they should employ such strategies as maintenance of weight loss for the obese, shoe modification, or stretching as described later. Shoe modification, strapping or taping the foot, or the use of orthoses may be done concomitantly with activity modification. The underlying principle of these treatments is to support the arch of the foot, prevent relative pronation, and thus unload the plantar fascia. Additional goals should be absorption of shock, so well-padded shoes or orthoses are beneficial. Tension on the plantar fascia may be reduced by a rigid shank, which limits the excursion of the windlass mechanism. A deep heel cup that holds the heel in relative varus and prevents the heel from lifting off the insole further protects the plantar fascia from excessive forces. Mizel et al used shoe modification consisting of a steel shank and anterior rocker bottom as a part of an effective treatment protocol [17]. Pfeffer et al found that both prefabricated and custom inserts were effective in the treatment of plantar fasciitis, with prefabricated inserts somewhat superior [18]. Short leg casting is a more extreme version of shoe modification that prevents the windlass mechanism from stretching beyond neutral, but may be poorly tolerated and has other negative aspects, such as atrophy and the inability to perform concomitant stretching exercises. A rigid, removable cast boot may be a worthy compromise in the recalcitrant case.
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DiGiovanni et al showed in a prospective, randomized fashion that non-weight bearing stretching exercises specific to the plantar fascia are superior to weightbearing Achilles tendon stretching exercises for the treatment of proximal plantar fasciitis [19]. During the toe-off phase of ambulation, a tight Achilles tendon will prevent optimal dorsiflexion, and to maintain normal gait mechanics, the windlass mechanism is increased, and the plantar fascia may become pathologically stretched. The theory behind dorsiflexion splinting and stretching of the Achilles tendon and plantar fascia is to provide for supple ankle and forefoot motion through the phases of ambulation without placing undue stress on the plantar fascia itself. Dorsiflexion night splints and ankle-foot orthoses, as well as stretching exercises, have been used successfully to treat plantar fasciitis. Night splinting and ankle-foot orthoses hold the plantar fascia and Achilles tendon in an elongated position, thereby preventing nocturnal contracture. Therefore this modality of treatment may show particular benefit in preventing the severe pain that often comes with the first steps in the morning upon awakening. Additional benefit is presumed to be a result of a broader range of dorsiflexion obtained from Achilles tendon stretching. A full range of dorsiflexion through the ankle spares the plantar fascia from excess tension during ambulation. As previously mentioned, Riddle et al showed an association between decreased ankle dorsiflexion and plantar fasciitis [20]. Probe et al showed improvement in 68% of patients with oral anti-inflammatory medications, Achilles stretching exercises, and shoe recommendations, but did not find any further benefit from addition of a dorsiflexion night splint to the protocol [21]. Powell et al demonstrated effective treatment of recalcitrant plantar fasciitis in a group of overweight patients with dorsiflexion night splints [22]. Barry et al used a retrospective study design to compare stretching exercises to night splinting, and concluded that night splinting was superior [23]. Iontophoresis is the use of an electric current to introduce the ions of a medication into tissues. Bipolar electrodes are placed on the skin, and an ionizable material in solution, such as a steroid, are carried through the skin toward the oppositely-charged electrode. Gudeman et al used a randomized, placebo-controlled study to demonstrate the effectiveness of this treatment modality in the treatment of plantar fasciitis [24]. Based on their results, they recommend the iontophoresis of dexamethasone when more immediate results are desired, such as in performance athletes and active patients. Shock wave therapy was introduced to clinical medicine as lithotripsy, used to treat kidney stones. Since that time, the use has expanded to the treatment of many musculoskeletal conditions, including calcific shoulder tendinitis and delayed unions of fractures. Shock waves are sound waves emitted at such a velocity and amplitude as to produce a mechanical effect. The mechanisms by which shock waves induce healing within the musculoskeletal system are not completely understood. The observed effects of shock waves are known to cause microtrauma to target tissues, which in turn elicits a healing response [25]. The degree of microtrauma depends on the energy and duration of the applied shock
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wave. Depending on the technology used, the generated shock wave is generally considered high energy or low energy. Ogden et al evaluated the use of highenergy shock wave therapy for chronic proximal plantar fasciitis in over 300 patients, and after 3 months of follow up, deemed the technique safe and effective. Fifty-six percent more of the treated patients experienced a satisfactory improvement in symptoms than patients in the placebo group [26]. Based on this study, the Food and Drug Administration approved the use of shock waves for the treatment of proximal plantar fasciitis. High-energy shock wave treatment is painful and is typically performed under regional anesthesia. Low-energy shock wave treatment is less painful, and in some patients may be applied without anesthesia; however, Rompe et al reported that all patients who underwent low-energy shock wave treatment found the treatment uncomfortable [27,28]. The theoretical risks of shock wave therapy are analogous to blunt trauma to the heel, which could produce pain, ecchymoses, damage to fascia, nerves, blood vessels, or muscles, and fractures. Ikeda et al studied the application of high-energy shock wave therapy to bone in an animal model, and found that periosteal elevation and small fractures of the inner surface of the cortex occurred [29]. Rompe et al demonstrated dose-dependent changes in rabbit tendon and paratenon, and cautioned against the use of high-energy shock waves until further studies could be performed. The authors supported their findings with reports of kidney, liver, and lung damage secondary to high-energy shock wave application for lithotripsy and in animal models [30]. Theoretically, because shock waves produce microtrauma to the tissues, excessive application could weaken the plantar fascia to the point of delayed rupture. This has not been reported clinically to our knowledge, and the recent literature supports the use of both high-energy and low-energy shock wave treatment as a safe and effective treatment for plantar fasciitis [31 33]. The efficacy is still controversial, however, and a recent report by Speed et al found no difference between patients treated with medium-energy shock wave therapy or sham therapy [34]. Steroid injections are commonly used in primary care, rheumatology, and orthopedic surgery practice to treat painful conditions such as rotator cuff tendonitis, lateral epicondylitis, and osteoarthrosis. The use of steroid injections in the treatment of plantar fasciitis has been used since the 1950s [35]. Crawford et al injected either prednisolone, or local anesthetic, or a combination of both, into the proximal plantar fascia region, and assessed the degree of heel pain reduction at 1, 3, and 6 months [36]. They found benefit of steroid injection over local anesthetic alone at 1 month, but no difference amongst the groups at 3 and 6 months. Kane et al reported four cases of plantar fasciitis unresponsive to steroid injection at the point of maximum tenderness who received relief of symptoms after undergoing ultrasound-guided injection [37]. Ultrasound allows for confirmation of the diagnosis of plantar fasciitis, and injection is then performed into the area of the plantar fascia that appears to be most edematous. The main concern with the use of steroid injections is delayed rupture of the plantar fascia. Leach et al were the first to report on the spontaneous rupture of
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the plantar fascia after steroid injection [38]. Acevedo and Beskin reported 44 ruptures of the plantar fascia in 765 patients who had undergone local steroid injection for plantar fasciitis [39]. The rupture was acute in 68% of patients and more insidious in nature in 32% of patients, and was typically associated with resolution of the plantar fasciitis symptoms. More than 50% of these patients went on to develop long-term sequelae such as longitudinal arch strain, lateral plantar nerve dysfunction, stress fracture, and development of hammertoe deformity, however. The biomechanical consequences of plantar fascia sectioning have been described [40]. It has been suggested that the importance of the plantar fascia in maintaining longitudinal arch stability may lead to serious adverse effects after sectioning of the plantar fascia. This may help explain the residual symptoms in those patients who sustained plantar fascia rupture after steroid injection; however, it does not explain why surgical plantar fasciectomy has been generally reported to lead to good outcomes in the treatment of recalcitrant plantar fasciitis. Treatment methods: surgical A small percentage of patients do not improve with nonsurgical treatment, and if all such modalities have been exhausted and the symptoms of plantar fasciitis are disabling, surgical treatment is appropriate. There are several surgical techniques, including plantar fasciectomy or fasciotomy, heel spur excision, neu-
Fig. 2. Incision site for open partial plantar fascia release marked on the plantar-medial foot.
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Fig. 3. Plantar fascia exposed for open partial plantar fascia release.
rolysis, and calcaneal osteotomy. Success has been reported with all such techniques [41]. Release of the plantar fascia does alter the mechanics of the foot, creating a less stable arch. Patients may walk less energetically on the involved side and place less force on the heel [42,43]. Partial fasciotomy produces measurable but less profound effects [44]. The most common procedures are open and endoscopic partial plantar fascia release. There are many different techniques described in the literature (Figs. 2 4). With the open procedure, some techniques include a dedicated decompression of the first branch of the lateral plantar nerve in addition to partial fascia release. Endoscopically, the nerve is not directly decompressed. All such procedures may have in common decompression of the nerve, however, either directly or indirectly. The potential benefits of endoscopic release are a quicker recovery time and improved cosmesis. Davies et al reported on 43 patients who underwent partial plantar fascia release with decompression of the nerve to the abductor digiti minimi for intractable plantar fasciitis [45]. They used the surgical technique as outlined by Singh et al [46]. At follow-up, 75% of heels were pain-free or only mildly painful. Overall, fewer than 50% of patients were totally satisfied with the outcome. Recovery from surgery averaged 7.85 months. The authors felt that surgery should be considered only after exhaustion of all nonoperative measures over a 12 to 18-month time course, and that patients should be carefully counseled about the prolonged recovery period and inconsistent patient satisfaction. The lateral
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Fig. 4. Plantar fascia released in open partial plantar fascia release.
plantar nerve was addressed because the authors believe that the successful outcomes with the variety of described surgical techniques are due at least in part to direct or indirect nerve decompression. Benton-Weil et al described a percutaneous technique for plantar fasciotomy [47]. The procedure was performed under local anesthetic, using a beaver-type blade to partially release the fascia from the anterior and inferior junction of the medial calcaneal tuberosity. Follow-up was obtained on 35 patients, 83% of whom felt the procedure met or exceeded their expectations. Complications included a self-limited case of peroneal tendonitis and two self-limited cases of calcaneocuboid joint pain. Recovery time was not addressed. Boyle and Slater reported the results of endoscopic plantar fascia release in 17 patients, with an average follow-up of sixteen months [48]. All patients were totally satisfied or satisfied with only minor restrictions; 82.4% reported mild or no pain. There were various minor complications described, including a case of perioperative sural nerve entrapment, but all complications apparently resolved within 6 months. Leitze et al stopped using the lateral portal after one case of sural neuropathy, and found a single medial portal technically feasible [49]. OMalley et al reported 20 cases of endoscopic release, 4 of which were bilateral [50]. Nine feet became asymptomatic, nine feet were improved, and two feet (bilateral case) were not improved. Time to return to full activity averaged 3.7 months in the unilateral cases and 7.8 months in the bilateral cases. There
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were no complications. Reeve et al performed a cross-sectional anatomic study to determine the structures at risk during endoscopic plantar fascia release [51]. They found that the average distance from the cannula margin to the lateral plantar nerve was 6 mm at the medial border of the plantar fascia. The nerve was not damaged on any of the specimens, but was felt to be closer to the cannula than previously described.
Achilles enthesopathy Achilles tendinopathy: tendonitis and tendinosis and enthesopathy The insertion of the Achilles tendon into the calcaneus bears great load and is a site of localized posterior heel pain. Achilles tendonitis is the general term commonly used to describe pain about the Achilles tendon. Achilles tendinopathy may be a more appropriate term, because there are several distinct Achilles tendon disorders with different clinical presentations and underlying pathophysiology. It is usually possible to discern insertional from noninsertional Achilles disorders. Noninsertional Achilles tendinosis usually presents as pain about the tendon belly, whereas insertional Achilles tendonitis manifests as pos-
Fig. 5. A rather large example of Haglunds deformity on the postero-lateral aspect of the heel.
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terior heel pain, in the distalmost region of the tendon. Enthesopathy describes a disease process specifically involving the enthesis, which is the insertion of tendon, ligament, fascia, muscle, or articular capsule into bone [52]. Enthesopathy can be differentiated from tendonitis, which is inflammation of the tendon alone. Therefore Achilles enthosopathy is another term for insertional Achilles tendonitis. Both insertional and noninsertional Achilles tendinopathy are processes that usually respond to nonoperative management; however, the underlying pathological changes are different. Those areas of painful tendon that would lead to a clinical diagnosis of Achilles tendonitis are histologically characterized by a degenerative noninflammatory process, and so should be termed Achilles tendinosis. In contradistinction, insertional Achilles tendonitis specimens demonstrate an inflammatory process histologically [53]. It is important to differentiate between insertional and noninsertional Achilles tendon disorders; this distinction becomes critical when the condition is managed surgically. Achilles enthesopathy and tendinosis are generally considered syndromes of overuse. Noninsertional tendinosis is the most common Achilles disorder, followed by enthesopathy [54].
Achilles tendon: anatomy and function The triceps surae complex begins proximally at the medial and lateral femoral condyles as the two heads of the gastrocnemius muscle, which cross the knee and
Fig. 6. Clinical photograph of a patient with Achilles enthesopathy, showing swelling over the Achilles insertion.
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combine with the soleus muscle. The function is primarily to dorsiflex the foot, but it also flexes across the knee. As muscle becomes tendon, the tendon rotates 90 and inserts into the middle third of the posterior calcaneal tuberosity, with the retrocalcaneal bursa deep and the pretendinous bursa superficial with respect to the tendon [55]. The Achilles tendon is stronger than any other tendon in the body, routinely withstanding forces eight times body weight or more during running activities [56,57]. Achilles tendinopathy: differential diagnosis Patients with insertional Achilles tendonitis typically describe an insidious onset of chronic posterior heel pain and swelling. The diagnosis then requires differentiation amongst retrocalcaneal bursitis, Haglunds deformity, insertional Achilles tendonitis, inflammation of the peritenon or peritendonitis, and the rare systemic or local conditions that may mimic these clinical findings. Retrocalcaneal bursitis produces posterior heel pain and tenderness to palpation with application of digital medial and lateral pressure anterosuperior to the Achilles tendon insertion, with relative sparing of the Achilles tendon and insertion site. Haglunds deformity is a prominence of the posterosuperior lateral aspect of the calcaneus, with irritation of the superficial bursa. This prominence is located
Fig. 7. Posterior calcaneal spur associated with Achilles enthesopathy, same patient as in Fig. 6.
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more toward the lateral side of the Achilles insertion, and although often asymptomatic, may be tender to palpation (Fig. 5). Symptoms are exacerbated by rigid shoe wear, such as with high-heeled shoes. Usually the afflicted individual is younger and more active than those with retrocalcaneal bursitis [53,57]. Patients with bilateral involvement, other joint or regional symptoms, or constitutional complaints should be evaluated for rheumatoid arthritis and the seronegative arthropathies. Tumors and trauma are other causes of localized unilateral heel pain, and are best diagnosed with imaging modalities. Fluoroquinolone antibiotics are well known for their effectiveness against certain gram-negative pathogens, and are generally well tolerated, but have gained some notoriety for causing Achilles tendon disorders. Movin et al and Van der Linden et al reported cases of Achilles tendonitis and rupture after the use of fluoroquinolones [58,59]. The association is rare but should be considered in the appropriate setting. Clinical presentation and diagnosis The diagnosis of Achilles enthesopathy is generally clinical. Only rarely are imaging studies necessary, although plain radiographs should be obtained. Ten-
Fig. 8. MRI showing thickened insertion of the Achilles tendon in Achilles enthesopathy, same patient as in Fig. 6.
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derness to palpation directly over the distalmost aspect of the tendon is highly suggestive of Achilles enthesopathy (Fig. 6). Though sedentary individuals are afflicted, athletes also are a common demographic afflicted, and indeed the symptoms are typically worsened with prolonged exercise. The condition is thought to be caused by overuse and repetitive microtrauma. Passive heel stretch reproduces symptoms, and loss of passive dorsiflexion is typical [53,56,57]. It is not uncommon for a patient with posterior heel pain to possess variable components of noninsertional Achilles tendinosis, insertional Achilles tendonitis, retrocalcaneal bursitis, and Haglunds deformity concomitantly. The diagnoses often overlap. Radiographs of the foot in a patient with Achilles enthesopathy may show a spur off the posterior part of the calcaneus (Fig. 7). Plain radiographs often underestimate the true size of the spur because of its broad width in the coronal plane [57]. Chao et al demonstrated that the insertion of the Achilles tendon occurs between the spur and the posterior wall of the calcaneus, rather than onto the tip of the spur [55]. The bone spur may be present in the asymptomatic foot or absent in the symptomatic foot, and so is neither necessary for diagnosis nor pathognomonic of Achilles enthesopathy. Magnetic resonance imaging and ultrasound are other imaging modalities that have been used in the diagnosis of insertional Achilles tendonitis (Fig. 8). Kamel et al found ultrasound more sensitive than MRI in detecting early changes of heel enthesitis, consisting of
Fig. 9. Achilles tendon in a patient with Achilles enthesopathy exposed, with pathologic tissue marked for debridement.
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fatty degeneration and calcific changes [52]. MRI shows thickening of the tendon at its insertion with loss of concavity at the anterior margin [60]. MRI is most useful in tumor and stress fracture diagnosis and in differentiating amongst overlapping conditions in the patient with indistinct symptoms and signs, such as may occur with peritendonitis, insertional Achilles tendinosis, Achilles enthesopathy, and retrocalcaneal bursitis.
Treatment methods: nonsurgical Nonsurgical treatment is usually effective for Achilles enthesopathy. Initial treatment consists of ice, activity modification, nonsteroidal anti-inflammatory medications, heel lifts and heel cups, and stretching and strengthening exercises. Pads may be fashioned to unload the Achilles insertion, and changes in shoe wear may be beneficial. For those patients who are more active, such as the recreational or competitive athlete, alteration of the training schedule may be poorly received initially, but ultimately necessary if complete resolution of symptoms is desired. Night splinting is tried if these modalities are unsuccessful. The final step of conservative therapy is a period of immobilization in a cam walker or cast. Steroid injection into the region is not advised because of the risk of delayed Achilles tendon rupture.
Fig. 10. Achilles tendon debrided and hole drilled in calcaneus to accept Achilles allograft.
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Treatment methods: surgical Surgery is reserved for the patient who has exhausted all nonsurgical treatment options over a prolonged period. Operative treatment is directed at excision of the diseased area of tendon as well as the calcaneal spur [61]. Choice of surgical approach depends upon the site of maximal tenderness, with consideration of MRI findings if the study is obtained, and so may be central, lateral, or medial. The central portion of the tendon is most commonly diseased [57]. McGarvey et al performed a central tendon splitting approach and found central tendon involvement in 21 of 22 cases, with isolated lateral involvement in the remaining patient. The patients underwent tendon debridement, retrocalcaneal bursectomy, and removal of the osteophyte. The remaining tendon was reapproximated, and augmented with suture anchors or plantaris tendon transfer when more than 50% of the insertion was diseased. The authors reported an 82% satisfaction rate [61]. Watson et al compared the results of retrocalcaneal decompression in the treatment of either retrocalcaneal bursitis or insertional Achilles tendinosis. They performed a posterolateral approach, elevation of the lateral aspect of the Achilles tendon, retrocalcaneal bursectomy, and calcaneal debridement. Suture anchors were used if necessary. The ankle was immobilized in equinus for 2 weeks, followed by a 4-week period in a walking cast. The authors found that both groups benefited from the surgery, but the insertional Achilles tendinosis patients
Fig. 11. Achilles tendon allograft with attached calcaneal bone plug, sized to match the drilled defect in the calcaneus.
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took longer to recover, were somewhat less satisfied, and were more likely to have restrictions on their shoe wear [62]. Yodlowski et al reported 35 surgical cases of insertional Achilles tendinosis in athletes. The authors performed a lateral approach, excised the bursa, fat pad, and scar tissue, osteotomized the calcaneal tuberosity, and then resected that part of the Achilles tendon that was calcified. In one case, suture anchors were used to reattach part of the Achilles tendon to the calcaneus, but otherwise augmentation was not necessary. All patients returned to their previous level of athletic participation [63]. Wilcox et al described flexor hallucis longus (FHL) tendon transfer in the treatment of chronic Achilles tendon disorders. The authors felt that the morbidity of harvesting the FHL was minimal, and based on their clinical results, recommended FHL tendon transfer and augmentation in the surgical treatment of Achilles tendinopathy [64]. These described techniques involve some degree of tendon resection, theoretically leaving the patient at risk for Achilles tendon rupture. Kolodziej et al used cadaveric specimens, and released the Achilles tendon from its insertion in 25% increments and loaded the tendon with body weight. Based on their results, they felt that 50% of the Achilles tendon insertion could be safely resected without risking rupture during routine activities [65]. When the amount of diseased tendon exceeds 50%, augmentation with allograft is another option. A fresh-frozen Achilles tendon is cut to match the
Fig. 12. Achilles tendon allograft in place, sewn into native tendon.
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Fig. 13. Lateral radiograph showing placement of the interference screw to hold in place the allograft
defect after debridement of diseased tendon, with a distal bone plug at the insertion site. A reciprocal hole is drilled into the posterosuperior aspect of the calcaneus, and the bone plug held in place with an interference screw. The allograft is then oversewn into the native tendon (Figs. 9 13).
Summary Plantar fasciitis and Achilles enthesopathy are two of the most common causes of posterior heel pain. In the vast majority of cases, nonsurgical treatment methods are effective. In recalcitrant cases, surgery has been shown to be generally effective. There are a variety of described techniques for both conditions. Endoscopic treatment of plantar fasciitis leads to slightly enhanced recovery times compared with the traditional open release, but in the long term the results seem to be equivalent. Open debridement of the retrocalcaneal bursa, calcaneal osteophyte, and diseased tendon is the underlying principle behind surgical treatment of Achilles enthesopathy. This can be performed through a variety of approaches, and augmentation with suture anchors, tendon transfers, or allograft may be necessary when more than 50% of the tendon is excised.
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Clin Sports Med 23 (2004) 145 155
Complex regional pain syndrome (ref lex sympathetic dystrophy)

Robert D. Teasdall, MD*, Beth Paterson Smith, PhD, L. Andrew Koman, MD
Wake Forest University School of Medicine, Medical Center Boulevard, Winston-Salem, NC 27157, USA
Chronic pain from complex regional pain syndrome (CRPS) or reflex sympathetic dystrophy (RSD) of the foot and ankle presents a myriad of diagnostic and therapeutic challenges to the foot and ankle surgeon. The disease involves multiple organ systems, including neural, vascular, bony, and soft tissue structures [1 5]. CRPS is a descriptive term defining a complex disorder or group of disorders that may develop as a consequence of trauma affecting the limbs, with or without an identifiable nerve lesion. To differentiate the presence or absence of nerve trauma, the two categories of CRPS type 1, with no identifiable nerve injury, and CRPS type 2, with identifiable nerve injury, have been proposed. CRPS consists of pain and related sensory abnormalities, abnormal blood flow and sweating, abnormalities in the motor system, changes in structure in both superficial and deep tissues (trophic changes), or functional impairment. It does not exist in the absence of pain. CRPS may be sympathetically independent (SIP) or sympathetically maintained (SMP) [6,7]. Sympathetically maintained pain is defined as significant pain decreased or relief after sympathetic intervention by oral medications (eg, amytriptylene) or parenteral intervention (eg, IV phentolamine, stellate ganglion block). SMP is more completely characterized than SIP, is more responsive to treatment, and has a better prognosis. A hallmark feature of SMP is thermoregulatory and vasomotor instability responding to sympatholytic intervention. A mechanical or neural precipitating or exacerbating event is termed nociceptive.
* Corresponding author. E-mail address: teasdall@wfubmc.edu (R.D. Teasdall). 0278-5919/04/$ see front matter D 2004 Elsevier Inc. All rights reserved. doi:10.1016/S0278-5919(03)00090-5
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Because the single best prediction of success in the management of CRPS is early treatment, the prompt diagnosis of CRPS, identification of the nociceptive focus, determination of physiologic staging (hot/cold, SMP versus SIP), and prompt treatment provide palliation and allow recovery.
Anatomic/physiologic considerations Perception of pain is complex and is dependent upon the initiating event, afferent input, efferent modulation, and cortical interpretation. Nociceptive or painful events secondary to cellular damage produce a secondary inflammatory cascade, which includes the activation of polymodal afferent neurons (pain receptors) that input through the dorsal horn of the spinal cord to higher cortical centers (Fig. 1). If nociceptive signals are inappropriately intense or ineffectively modulated by descending pathways, symptoms may escalate beyond the magnitude of the cellular insult. In the extremity, increased receptor-neurotransmitter activity potentiates sympathetically maintained pain through one or more of the following: microvascular control, direct neural input, or central sensitization [8 11]. Following trauma, lower-extremity physiology is altered by the magnitude of the insult, subsequent internal responses, and external occurrences. How
Fig. 1. Nociceptive (painful) information is relayed through the dorsal horn of the spinal cord for processing and modulation before cortical evaluation. (From Koman LA, editor. Bowman Gray orthopaedic manual 1996. Winston-Salem [NC]: Orthopaedic Press; 1996; with permission.)
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Fig. 2. Abnormal extremity physiology is an expected occurrence following trauma. Prolonged or persistent abnormal physiology may characterize a dystrophic response. Over time, irreversible events may occur. (From Koman LA, editor. Bowman Gray orthopaedic Manual 1996. Winston-Salem [NC]: Orthopaedic Press; 1996; with permission.)
an individual perceives pain depends upon a complex interplay of physiological occurrences and psychological adaptations. In the majority of cases, return to normal, or a premorbid functional steady state, occurs in a predictable manner [1,12]. The persistence of abnormal extremity physiology beyond normal time frames, with concomitant pain and functional impairment, is pathologic. The presence of transient dystrophic pain is normal, but the abnormally prolonged persistence of that dystrophic pain is pathologic and is termed causalgia, reflex sympathetic dystrophy, algodystrophy, or complex regional pain syndrome (Fig. 2). Persistence of pathologic responses can result in permanent structural or functional damage within the extremity, the central nervous system, or both. Because of individual variability in the natural history of the dystrophic process, time frames for staging CRPS often are inappropriate. Physiologic responses are influenced by the magnitude of damage from the initiating injury, the structures damaged, variability in premorbid physiology, existing extremity adaptability, and the effects of partial treatment [1,12 16].
Clinical definition Reflex sympathetic dystrophy, a series of complex physiologic events, must include pain in combination with impaired function, trophic change, and auto-
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nomic dysfunction [17]. The distinction between sympathetically maintained pain and sympathetically independent pain is important [7,10,11]. Because early recognition and treatment of RSD is the single most important predictor of functional recovery and pain relief, objective techniques to diagnose the syndrome are crucial [12,18]. Pain Pain is manifest in a variety of presentations. Hyperalgesia, increased intensity of pain, is common and may be primary, affecting the area of injury, or secondary, affecting nontraumatized surrounding regions. Allodynia, pain produced by normally nonpainful stimuli, is frequently a characteristic of SMP. The use of standardized questionnaires or scales such as the Visual Analog Scale [19], the McGill Pain Questionnaire [20], the Rand Corporation short form (SF-36) [21 23], or a self-administered questionnaire for assessment of symptom severity and functional status are useful tests for conversion of subjective complaints of pain into objective scores [19]. Trophic changes Trophic changes are common in the dystrophic process and include stiffness, edema, osteopenia, and atrophy of hair, nails, and skin. Edema may be followed with volumetric studies; however, most trophic changes are difficult to qualify. Osteopenia, unless severe, may not be documented by plain roentgenograms and, for quantitative analysis, must be analyzed by dual photon absorptiometry or quantitative scintigraphy [24,25]. Endurance testing using computerized equipment may detect subtle functional changes that may reflex extremity stiffness or atrophy [12,18]. Autonomic dysfunction Autonomic function controls sweating, piloerection, and microvascular perfusion in the digits. It may be evaluated by an assessment of: (1) total digital blood flow, which is composed of both thermoregulatory and nutritional components; and (2) sudomotor activity (sweating). Total digital perfusion and its components can be analyzed by indirect measures such as temperature, laser Doppler fluxmetry, and plethysmography, and by direct techniques such as vital capillaroscopy (Figs. 3, 4) [26]. Sweating may be analyzed by changes in galvanic skin response, which measures skin resistance using Ag/AgCl (silver/ silver chloride) electrodes. Changes in electrical conductance/resistance (galvanic skin response) are related to the rate of sweating, which in turn is under sympathetic control [12,20]. Quantitative analysis of thermoregulatory and nutritional microvascular flow allows physiologic staging of RSD and provides a mechanism to evaluate the effects of interventions and time upon the process (see Figs. 3, 4) [12,15,18,26 28]. Use of physiologic stress in some form is a
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Fig. 3. Cold stress testing using digital temperature and laser Doppler fluxmetry provides a physiologic assessment of autonomic function in patients with reflex sympathetic dystrophy. The effects of exposure to a mild thermal challenge (cold) can be observed and digital temperatures (above right) and laser Doppler fluxmetry (below right) can be analyzed from computer-generated plots before, during, and after stress. (From Koman LA, editor. Bowman Gray orthopaedic manual 1996. Winston-Salem [NC]: Orthopaedic Press; 1996; with permission.)
necessary component of extremity testing for reproducible analysis of dynamic physiologic events [12,15].
Physiologic staging The inability to classify or stage CRPS with consistency has been a problem. CRPS may progress rapidly or slowly, so chronologic staging may confound the clinical picture. By using existing objective instruments and tests, it is possible to stage pain patients using physiologic and functional criteria. The following discussion assumes that patients fulfill the clinical criteria for CRPS as defined previously.
Sympathetically maintained pain versus sympathetically independent pain Differentiation of SIP from SMP is important diagnostically. The former implies a more central process, often with irreversible end-organ adaptations and the presence of central pain. Prognosis for recovery in SIP is guarded. SMP is diagnosed in patients who experience an improvement during or after treatment with sympathetic medications. Classically, SMP must respond to a epidural, intrathecal, or lumbar plexus block or peripheral nerve block. Rapid response to such blocks supports the concept of receptor-mediated CRPS and has led to the suggestion that pain relief following intravenous phentolamine, a mixed
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Fig. 4. Vital capillaroscopy allows the direct evaluation of the cutaneous nutritional papillary capillaries and a direct measure of nutritional blood flowa component of total digital blood flow. The presence of abnormal capillary morphology associated with post-traumatic events or systemic disease may be diagnostic. (From Koman LA, editor. Bowman Gray orthopaedic manual 1996. Winston-Salem [NC]: Orthopedic Press; 1996; with permission.)
a1 and a 2 antagonist, is pathognomonic for SMP [29,30]. Not all patients with clinical SMP who respond to other forms of sympathetic intervention report relief with phentolamine, however. Although clinical signs and symptoms of RSD and pain relief following pharmacologic interventions that affect sympathetic controls can combine to support the diagnosis of SMP, it must be stressed that there is no single pathognomonic test for SMP. Once a sympathetic component of pain is verified, it is important to determine the presence or absence of a mechanical or a neurologic focal trigger or nociceptive event. If an identifiable focus can be corrected, surgical treatment should be performed once optimal nonoperative relief has been obtained (Fig. 5). In the foot, ankle, and lower extremity, posterior tibial nerve entrapment or compression, contusion of superficial sensory nerves in the dorsum of the foot, peroneal nerve entrapment, or injury to the intrapatellar branch of the saphenous nerve are common nerve irritants. Mechanical nociceptive conditions include entrapment of the peroneal tendons, intra-articular abnormalities such as cartilage flaps, arthrofibrosis, and others. In general, these conditions require pharmacologic palliation preoperatively and pharmacologic protection postoperatively. Identifiable peripheral nerve lesions include neuroma, neuroma-in-continuity, and compression neuropathy. Neural involvement may have been primary (ie, part of an initiating injury), or secondary (ie, caused by altered extremity physiology). In either situation, the compromised and irritated nerve serves as a nociceptive focus. Surgical intervention is indicated if symptoms persist after nonoperative
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Fig. 5. Symptoms and function in a dystrophic patient following carpal tunnel surgery may be followed objectively using appropriate instruments (Levine). In the carpal tunnel instrument, 11 questions regarding symptoms (rated from none, 1, to severe, 5) and 8 questions related to function (rated from no difficulty, 1, to cannot do, 5) are scored. Numerical scores that reflect symptoms and function can then be followed over time and the effects of various interventions analyzed. (From Koman LA, editor. Bowman Gray orthopaedic manual 1996. Winston-Salem [NC]: Orthopaedic Press; 1996; with permission.)
intervention. Although surgery can precipitate a dystrophic flare, it still can be performed safely in patients with active or latent RSD [12,18,31]. Two major microvascularly mediated pathophysiologic stages associated with lower extremity CRPS are identifiable (Table 1): (1) the hot swollen stage increased total flow with decreased nutritional flow, and (2) the cold-stiff
Table 1 Two states of microvascular perfusion associated with reflex sympathetic dystrophy Increased total flow, decreased nutritional flow Symptoms Signs Pain Hot, swollen Edema Increased sweating Pain with hyperalgesia without hyperalgesia with cold intolerance without cold tolerance Decreased total flow, decreased nutritional flow Cold, stiff Atrophic Pain Hyperalgesia Cold intolerance
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stagedecreased total flow with decreased nutritional flow [8]. In addition, the presence or absence of edema, with or without hyperalgesia, provides two clinical subgroups within the increased total flow group. Treatment modalities can be selected based on specific physiologic states and the overall clinical condition. In general, the more simple techniques and drugs should be used before trying more complex modalities.
Management Management alternatives of patients with CRPS include physical therapy, medication, and surgery. Therapeutic interventions Physical therapy is important in the management of patients with SMP. Motion of the lower extremity is crucial to provide cartilage nutrition and periarticular circulation to joints in order to decrease hypersensitivity and to prevent contractures. It is important for the therapy to involve the entire limb, because decreased ankle motion is a common complication in patients with CRPS of the knee. In addition, active and passive range of motion is recommended. Transcutaneous nerve stimulator (TENS), contrast baths, hydrotherapy, and continuous passive motion also may be helpful. It is theorized that the use of a TENS unit decreases symptoms by increasing nutritional flow and inhibiting smaller nociceptive fibers [32 34]. The use of contrast bathsalternating hot and cold therapycan provide clinical palliation by overloading nonpainful larger fibers, and thereby blocking painful sensations. Oral and parenteral pharmacologic treatment The prompt use of pharmacologic management is integral to optimal outcome. Narcotic medications are less effective in managing dystrophic symptoms than sympatholytic interventions that: (1) decrease nerve hyperexcitability (eg, membrane stabilizers such as steroids or anticonvulsives); (2) diminish receptor upregulations (eg, phentolamines, a2 agonists, tricyclic antidepressants); (3) block or decrease neural transmission (eg, peripheral nerve blocks, intrathecal medications); or (4) improve nutritional flow (eg, calcium channel blockers). Oral medications should be initiated early in the presence of burning, tearing, or searing pain that does not respond to analgesic medications (non-narcotic or narcotic). First-line agents include nonsteroidal anti-inflammatory drugs (NSAIDS), tricyclic antidepressants, (eg, low-dose amytriptyline), anticonvulsant (eg, phenytoin or gabapentin), or steroids. Because of concerns over the development of avascular necrosis, steroids are often avoided by orthopaedic surgeons but are commonly employed by internists. The judicious use of steroids is appropriate.
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Surgery If identifiable and manageable by surgery, dystrophic foci should be corrected after optimal pharmacologic protection has been obtained. Injury to peripheral nerves is the most common source of nociceptive (dystrophic) irritation; it may be associated with osseous and nonosseous derangements. Nerves may require neurolysis, neurorrhaphy, neuroma resection, and if necessary, environmental modification of the nerve bed [12,31]. When CRPS is suspected, a combination of NSAIDS may be combined with combination sympatholetics. For example, burning dysesthetic hyperpathic foot pain after a sprain associated with swelling would be treated with physical therapy, contrast baths, COX-2 nonsteroidal medication, low dose amytriptyline (25 mg tid or 50 gtts); and either phenytoin (100 mg tid) or gabapentin (starting at 100 mg tid), or a calcium channel blocker (eg, Norvasc at 5mg qd) may be employed. Drugs are tapered or actively increased depending on the patients response. If symptoms are not alleviated, a short course of high-dose steroid or continuous blocks should be considered. In the presence of edema and localized hyperalgesia, an alpha2 agonist (eg, clonidine, 0.1 mg patch) may be applied to the hyperalgesic area. If the extremity is painful, cool, and early trophic changes are present, physical therapy, physical modalities (eg, contrast baths), a tricyclic antidepressant, and a calcium channel blocker may be effective. If the patient shows no appropriate response, intermittent or continuous autonomic blocks should be considered. We prefer continuous epidural blocks for 5 to 7 days, combined with outpatient therapy. Optimal management of CRPS Box 1. Oral and parenteral drugs used in treatment of CRPS Oral Nonsteroidal anti-inflammatory Steroids Antidepressants Tricylclic Serotonin reuptake inhibitors Anticonvulsants Calcium channel blockers Alpha2 agonists
Parenteral Bretylium Steroids Alpha2 agonists
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in the lower extremity is multimodal and requires titration of interventions and drugs, modifications of intervention based upon response, and art as well as science. General principles of treatment include: (1) use of physical modalities such as range of motion, intermittent stress (eg, weight bearing, impact), or contrast baths (should be initiated early); (2) oral medications based upon staging (hot/cold, edema/trophic) and adjusted depending on response; (3) use of the least invasive, least expensive, and safest interventions first, with an increase in complexity of treatment until adequate response occurs; (4) identification of any nociceptive foci and surgical intervention if necessary; and (5) the use of pain consultants for intermittent or continuous autonomic blocks in refractory patients. Oral and parenteral drugs used in treatment of CRPS are listed in Box 1.
Summary The management of CRPS can be approached using objective criteria in a logical and systematic fashion. Frustration during treatment is common because: (1) the pathophysiology of CRPS is incompletely understood, (2) there is significant variation in presentation due to disparate premorbid anatomy and physiology, and (3) the natural history may be affected by incomplete treatment. Therapeutic efforts that should be effective may fail, and a trial-and-error approach to treatment is often mandatory. Early recognition of CRPS and prompt intervention, however, provide the best opportunity for clinical improvement.
References
[1] Pollock Jr FE, Koman LA, Smith BP, Poehling GG. Patterns of microvascular response associated with reflex sympathetic dystrophy of the hand and wrist. J Hand Surg Am 1993;18(5): 847 52. [2] Hendler N. Reflex sympathetic dystrophy and causalgia. In: Tollison CD, editor. Handbook of chronic pain management. Baltimore: Williams and Wilkins; 1989. p. 444 54. [3] Nathan PW. Pain and the sympathetic system. J Auton Nerv Syst 1983;7(3 4):363 70. [4] Kozin F, McCarty DJ, Sims J, Genant H. The reflex sympathetic dystrophy syndrome. I. Clinical and histologic studies: evidence for bilaterality, response to corticosteroids and articular involvement. Am J Med 1976;60(3):321 31. [5] Kozin F, Ryan LM, Carerra GF, Soin JS, Wortmann RL. The reflex sympathetic dystrophy syndrome (RSDS). III. Scintigraphic studies, further evidence for the therapeutic efficacy of systemic corticosteroids, and proposed diagnostic criteria. Am J Med 1981;70(1):23 30. [6] Czop C, Smith TL, Rauck R, Koman LA. The pharmacologic approach to the painful hand. Hand Clin 1996;12(4):633 42. [7] Amadio PC, Mackinnon SE, Merritt WH, Brody GS, Terzis JK. Reflex sympathetic dystrophy syndrome: consensus report of an ad hoc committee of the American Association for Hand Surgery on the definition of reflex sympathetic dystrophy syndrome. Plast Reconstr Surg 1991;87(2):371 5. [8] Koman LA, Smith TL, Smith BP, Li Z. The painful hand. Hand Clin 1996;12(4):757 64. [9] Arnold JM, Teasell RW, MacLeod AP, Brown JE, Carruthers SG. Increased venous alphaadrenoceptor responsiveness in patients with reflex sympathetic dystrophy. Ann Intern Med 1993;118(8):619 21.
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[10] Raja SN, Davis KD, Campbell JN. The adrenergic pharmacology of sympathetically-maintained pain. J Reconstr Microsurg 1992;8(1):63 9. [11] Raja SN, Meyer RA, Campbell JN. Peripheral mechanisms of somatic pain. Anesthesiology 1988;68(4):571 90. [12] Koman LA, Smith TL, Smith BP. Reflex sympathetic and other dystrophies. Surgery of the hand and upper extremity. New York: McGraw Hill; 1996. [13] Bonica JJ. Causalgia and other reflex sympathetic dystrophies. Postgrad Med 1973;53(6):143 8. [14] Bonica JJ. Causalgia and other reflex sympathetic dystrophies. Adv Pain Res Ther 1979;3:141. [15] Koman LA, Barden A, Smith BP, Pollock Jr FE, Sinal S, Poehling GG. Reflex sympathetic dystrophy in an adolescent. Foot Ankle 1993;14(5):273 7. [16] Veldman PH, Reynen HM, Arntz IE, Goris RJ. Signs and symptoms of reflex sympathetic dystrophy: prospective study of 829 patients. Lancet 1993;342(8878):1012 6. [17] Merskey H, editor. Classification of chronic pain: descriptions of chronic pain syndromes and definitions of pain terms. Pain 1986;26(S29). [18] Koman LA, Poehling GG. Reflex sympathetic dystrophy. In: Gelberman RH, editor. Operative nerve repair and reconstruction. Philadelphia: JB Lippincott; 1991. p. 1497. [19] Huskisson EC. Measurement of pain. Lancet 1974;2(7889):1127 31. [20] Kellogg Jr DL, Johnson JM, Kosiba WA. Competition between cutaneous active vasoconstriction and active vasodilation during exercise in humans. Am J Physiol 1991;261(4 Pt 2): H1184 9. [21] Stewart AL, Ware Jr JE, Brook RH. Advances in the measurement of functional status: construction of aggregate indexes. Med Care 1981;19(5):473 88. [22] Stewart AL, Greenfield S, Hays RD, Wells K, Rogers WH, Berry SD, et al. Functional status and well-being of patients with chronic conditions. Results from the Medical Outcomes Study. JAMA 1989;262(7):907 13. [23] Ware Jr JE, Sherbourne CD. The MOS 36-item short-form health survey (SF-36). I. Conceptual framework and item selection. Med Care 1992;30(6):473 83. [24] Atkins RM, Tindale W, Bickerstaff D, Kanis JA. Quantitative bone scintigraphy in reflex sympathetic dystrophy. Br J Rheumatol 1993;32(1):41 5. [25] Bickerstaff DR, Charlesworth D, Kanis JA. Changes in cortical and trabecular bone in algodystrophy. Br J Rheumatol 1993;32(1):46 51. [26] Koman LA, Smith BP, Smith TL. Stress testing in the evaluation of upper-extremity perfusion. Hand Clin 1993;9(1):59 83. [27] Daemen M, Kurvers H, Slaff D, et al. Reflex sympathetic dystrophy: microcirculatory observations in humans. In: Slaff DW, editor. Amsterdam: Elsevier; 1995. p. 105. [28] Koman LA, Smith TL, Poehling GG, et al. Reflex sympathetic dystrophy. Curr Opin Orthop 1993;4:85. [29] Liu S, Kopacz DJ, Carpenter RL. Quantitative assessment of differential sensory nerve block after lidocaine spinal anesthesia. Anesthesiology 1995;82(1):60 3. [30] Raja SN, Treede RD, Davis KD, Campbell JN. Systemic alpha-adrenergic blockade with phentolamine: a diagnostic test for sympathetically maintained pain. Anesthesiology 1991;74(4): 691 8. [31] Jupiter JB, Seiler III JG, Zienowicz R. Sympathetic maintained pain (causalgia) associated with a demonstrable peripheral-nerve lesion. Operative treatment. J Bone Joint Surg Am 1994; 76(9):1376 84. [32] Long DM. Electrical stimulation for relief of pain from chronic nerve injury. J Neurosurg 1973; 39(6):718 22. [33] Melzack R. Prolonged relief of pain by brief, intense transcutaneous somatic stimulation. Pain 1975;1(4):357 73. [34] Richlin DM, Carron H, Rowlingson JC, Sussman MD, Baugher WH, Goldner RD. Reflex sympathetic dystrophy: successful treatment by transcutaneous nerve stimulation. J Pediatr 1978:93(1):84 6.
Clin Sports Med 23 (2004) 157 167
Foot orthoses in rehabilitationwhats new

Deborah A. Nawoczenski, PT, PhDa,*, Dennis J. Janisse, Cpedb
a
Department of Physical Therapy, Ithaca College, University of Rochester South Campus, 300 East River Road, Suite 1-102, Rochester, NY, 14623, USA b Department of Physical Medicine and Rehabilitation, Medical College of Wisconsin, 8701 Watertown Plank Road, Milwaukee, WI 53226, USA
Overuse injuries are common sequelae of exercise and sporting activities in general, and of running in particular. As a means of treatment and prevention of further injury, foot orthoses and shoe modifications are widely prescribed, with the primary goal of altering lower extremity joint alignment and patterns of movement. From a biomechanical perspective, if foot orthoses place the foot and lower extremity in a more advantageous position, applied stresses to the active and passive soft tissues of the foot and lower limb may be minimized [1 3]. Ample evidence exists, based on subjective pain relief, symptom resolution, and patient satisfaction [4 6], to support the continued use of these devices, particularly in runners. The biomechanical mechanisms through which we believe the clinical benefits are derived, however, are comparatively limited and not fully understood. This article presents the evidence that may support or refute the use of orthotic intervention as an adjunct to the athletes rehabilitation program. Alternative mechanisms of foot orthoses action that may be linked to their effectiveness, as well as the direction for future investigations, are discussed. Options for orthotic intervention for specific sports-related injuries complete the article.
Evidence and contradictions Advances in motion analysis technology have improved our understanding of foot orthoses and shoe design effects on foot and lower extremity movement. Comparative studies of orthotic effectiveness are often confusing, however: it appears that for every investigation showing a positive response for some bio-
* Corresponding author. E-mail address: dnawoczenski@ithaca.edu (D.A. Nawoczenski). 0278-5919/04/$ see front matter D 2004 Elsevier Inc. All rights reserved. doi:10.1016/S0278-5919(03)00087-5
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D.A. Nawoczenski, D.J. Janisse / Clin Sports Med 23 (2004) 157167
mechanical parameter, another study may show no change. Discrepancies among the studies may be due to a number of factors, including the anatomical variability in the subjects foot structures, differences in orthotic fabrication, materials, and posting locations, variations in footwear and testing conditions, and lack of statistical power. It is also important to recognize that there may be various solutions or movement strategies with respect to the magnitude of rotations and peak moments between the segments of the lower extremity that an individual may adopt for a given activity [7,8]. Changes in rotation patterns as a result of the orthotic intervention may be subtle, and not large enough to demonstrate statistical differences, particularly when considering the sample sizes of many studies. Few investigations have shown consistent systematic trends with foot orthoses; rather, changes were highly subject-specific, and frequently correlated with a reduction in symptoms [3,8]. Nevertheless, even a small change in angular or kinetic variables may reduce the risk of injury [9 14]. It is not presently known how large such a difference needs to be to have a positive outcome. Although their use extends across various sporting activities, orthotic effectiveness has been primarily assessed in runners. Several factors have been suggested to increase a runners risk for injuries, including excessive pronation or rearfoot eversion, high eversion velocity, increase internal tibial rotation, increased impact and loading rate of vertical ground reaction force, increased ankle inversion moments, and increased knee abduction and external rotation moments [7,8,15 17]. To date, the majority of studies have focused on kinematic alterations; foot orthoses have been used to reduce symptoms by purportedly affecting these factors. Kinematic changes are often small and not consistently significant [10]. Recent investigations have speculated that modifications in the maximal vertical loading rate and vertical force impact peak [18] and reduction of ankle or knee joint moments [3,7,17] may be equally important functions of foot orthoses.
Alternative mechanisms of foot orthoses action To date, the majority of clinical studies have assessed orthotic effectiveness on changing the biomechanical parameters of lower extremity movement patterns. The multifactorial nature of many athletic injuries, and intrinsic biomechanical abnormalities (training techniques, training terrain, equipment, footwear, previous injury history, etc) make it difficult to draw clear conclusions on the specific etiological factors contributing to a particular injury. Orthotic intervention may be appropriate for those injuries resulting from identifiable abnormal biomechanics, however. Orthoses may also derive their benefit by altering muscle activation [19] and proprioceptive mechanisms involved in regulating muscle function [8,20]. Investigators have proposed that foot orthoses may increase the afferent feedback from cutaneous receptors, which may positively alter the muscles response to stabilize joint motion [8,12,17,20]. A positive response would be classified as a
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reduction in muscle activation and fatigue. Damping soft-tissue vibrations through various material properties of the orthoses has also been proposed as a strategy for reducing muscle activity [20]. Based on these assumptions, performance should improve with an optimal orthotic. Further experimental work is needed to support this concept. In summary, subject responses to orthotic intervention have been highly variable and individualized. Kinematic studies have reported small changes in foot and lower extremity rotation patterns that may initially seem inconsequential, but when considered over time and repetition, even these small changes may have a positive impact. Continued investigations to explore afferent feedback changes through orthotic intervention and its impact on muscle activation, as well as alterations in joint moments, are needed to understand and validate the recommended use of orthoses.
Specific sports-related injuries and orthotic applications Though not exhaustive, the following section provides examples of common conditions of the forefoot, midfoot, and rearfoot that may benefit from foot orthoses and external shoe modifications [21]. In many cases, premade or generic over-the-counter orthoses are adequate and are significantly less expensive than custom-made designs. The over-the-counter orthoses are available in a variety of materials and, in general, are designed to provide shock absorption, increased support, or both in specific areas of the foot, or across the entire foot. Examples include heel cushions, arch supports, or full-length insoles. For the athlete with more complicated foot problems, a custom made orthosis may be necessary. The total contact orthoses (TCO) is a custom-made orthosis that is fabricated from a model or impression of the patients foot, thereby achieving total contact with the plantar aspect of the foot. The TCO consists of a shell, the layer of material that is next to the foot and in total contact with the plantar surface; and the posting, or the material that fills the space between the shell and the shoe. The specific designs and materials vary according to the needs of the patient. To provide more control or shock absorption/cushioning, the TCO can be further customized by adding small amounts of additional materials to specific areas of the orthoses, such as viscoelastic polymer under the metatarsal heads or heel. Though the focus is on the orthoses, it is essential that footwear be considered concurrently with the orthotic recommendation. Shoes are the essential foundation for effective orthotic intervention. Outsole, midsole, and insole features, as well as heel counter and shoe toe box/upper design can all be used to maximize the benefits of foot orthoses. In many situations, choosing a shoe that has been designed for the athletes particular sport, that is appropriate for that individuals foot alignment, and that fits properly may be the only adaptation that is necessary; this should be the first consideration in the management of foot-related musculoskeletal problems.
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Fitness footwear can also be modified to accommodate various patient diagnoses and various foot structures. External shoe modifications most commonly prescribed for the athlete include rocker soles, extended steel shanks, solid ankle cushion heels (or SACH), and flares. The reader is referred to resources available in the literature that describe these external shoe modifications in detail [21 23]. In the following section, solutions for specific sports-related injuries and conditions of the forefoot, midfoot, and rearfoot are presented. Each condition is presented by the clinical diagnosis, followed by the desired goal or function of the orthoses, and the specific footwear modification or recommendation. Many of the modifications have been derived through an understanding of the biomechanical mechanisms underlying the specific pathology, in combination with knowledge of the athletes foot structure and the requirements of the sporting activity. Specific modifications and control will differ in each persons case and alterations may be needed during the course of treatment. Forefoot Turf toe and hallux rigidus The objectives for treating turf toe or hallux rigidus are to limit dorsiflexion of the great toe, relieve dorsal or plantar pressures that may be present at the first metatarsophalangeal joint, and decrease abnormal pronation of the foot, if it is present. A TCO with a built-in plate made of lightweight carbon fiber material may be effective in limiting hallux dorsiflexion. Footwear may need to be modified with a
Fig. 1. Shoe with extended steel shank and an example of a carbon fiber plate.
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rocker sole and an extended steel shank placed between the layers of the shoe sole. This footwear design allows a smooth transition, or rocking, between heel contact and toe off, while at the same time limiting hallux dorsiflexion (Fig. 1). Mortons toe (elongated second metatarsal) The goal of orthotic intervention for Mortons toe is to relieve excessive plantar pressure beneath the second metatarsal head. It may be necessary to transfer some of the pressure onto the first metatarsal head. A TCO with a metatarsal pad placed proximal to the second and possibly the third metatarsal head can help to relieve pressure in this region. It may also be necessary to increase the pressure on the first metatarsal head. A Mortons extension that consists of posting material placed under the first metatarsal shaft and head may increase the pressure on the first metatarsal head, thereby relieving the second and third metatarsal heads (Fig. 2). It is important to remember that with any type of shoe selection, with or without insoles modification, the shoes need to fit properly. In many cases, shoes are fit to length of the great toe when the second toe should be used as the reference. Bunion deformity Any excessive pressure created by the medial prominence associated with a bunion deformity must be relieved. This includes relief of dorsal pressure over the first metatarsal as well. Adequate shoe room, especially in the toe box of the shoe, is essential with a bunion deformity. Shoes may need to be stretched to accommodate the medial prominence. If excessive foot pronation accompanies the deformity, a TCO with medial posting may be helpful in minimizing the
Fig. 2. Total contact orthosis (TCO) with Mortons extension.
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abnormal mechanics associated with the excessive pronation [8,10,11,13, 14,16,24]. Interdigital neuroma (Mortons neuroma) and sesamoiditis The goals of orthotic intervention are to increase shock absorption and relieve plantar pressure on the metatarsal heads, sesamoids, or both. A built-in metatarsal relief or metatarsal pad can be applied to over-the-counter orthoses just proximal to the involved web space. In more severe cases, or in the presence of an underlying biomechanical foot deviation, a custom molded TCO with an added metatarsal pad may be helpful. For Mortons neuroma, the metatarsal pad may increase dorsiflexion of the metatarsals, resulting in relative plantarflexion of the proximal phalanx. This in turn may decrease the angulation of the digital nerves as they course underneath the intermetatarsal ligament. At highly sensitive areas, viscoelastic polymer may be added to the TCO under the sesamoids. Shoe modification with a full-length steel shank and anterior rocker bottom may also be helpful in minimizing the bending moment at the metatarsophalangeal joints [25]. Metatarsal stress fracture The primary function of orthoses and footwear after a metatarsal stress fracture are to promote healing by limiting motion. A TCO reinforced with firm posting material, such as cork, can provide support and limit excessive foot motion. Foot motion can be further limited with the use of a rocker sole shoe with an extended steel shank. Midfoot and rearfoot Pes cavus This high-arch or supinated foot type tends to be a more rigid foot structure. The objectives for orthotic intervention are to provide shock absorption, especially at heel strike, and plantar pressure relief under the prominent metatarsal heads. Over-the-counter insoles with good shock absorption, together with added metatarsal relief under the first, fifth, or both metatarsal heads may be adequate. In cases that do not respond to the inexpensive approaches, an accommodative, shock-absorbing TCO that is molded from an impression of the foot may be required. Additional posting on the lateral aspect of the forefoot (in cases of a forefoot valgus) may help prevent excessive heel varus and subtalar joint supination. Curved-last footwear with good shock absorption may be modified with a lateral flare to decrease excessive supination. Pes planus The majority of investigations on orthotic effectiveness have focused on the pes planus, or excessively pronated foot type (the reader is referred to selected references at the end of this article for a comprehensive review of the literature on orthotic effectiveness in clinical trials [26 28]). This foot type tends to be more
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flexible, and orthoses and footwear need to focus on support or control of excessive pronation. Over-the-counter, full-length insoles with added medial support under rearfoot and arch areas or medial rearfoot and forefoot regions may be adequate for most athletes. If custom orthoses are prescribed, they should consist of firmer, more rigid materials that are posted medially to help minimize excessive pronation. Straight-last footwear with motion control features such as a reinforced heel counter and medial midsole reinforcement should be recommended for this foot type. Posterior tibial tendinitis The primary objective for posterior tibial tendinitis is to minimize the excessive pronation that frequently precipitates and exacerbates this condition. Over-thecounter full length insoles modified with medial posting in rearfoot, arch, or forefoot locations, or in some cases just an arch support, may help to minimize tendon stress due to excessive subtalar or midtarsal pronation. Pressure relief for any associated tenderness in the area of the navicular tuberosity may also be necessary. More severe cases may require a TCO with firm posting material in the medial rearfoot, arch, or forefoot. Viscoelastic polymer material, silicon, or polyurethane may be added to the TCO along the course of the posterior tibial tendon and under the navicular. The shoe recommendation for the pes planus foot type is also appropriate for posterior tibial tendinitis, and should include a reinforced heel counter and medial midsole; a medial flare may also be added. Peroneal tendinitis With peroneal tendinitis, the objectives are to balance the foot to decrease pressure on the affected tendon and, in most cases, to relieve excessive supination. Pressure relief may also be necessary for any tenderness at the base of the fifth metatarsal. An over-the-counter insole with lateral support in the midfoot and rearfoot may be helpful. As stated previously, if the premade insole is not effective, a TCO posted laterally in the heel and possibly the forefoot can be used. Viscoelastic polymer, silicon, or polyurethane can also be added to the TCO for extra pressure relief along the course of the tendon and under the fifth metatarsal. The addition of a lateral flare to a shoe with a strong lateral heel counter may assist in further reduction of supination (Fig. 3). In some cases, peroneal tendinitis and associated tenderness at the tip of the lateral malleolus may be a result of the tendons being pinched between the lateral calcaneus and tip of the fibula as a result of rearfoot valgus or excessive pronation. Orthoses and footwear management would be similar to that described previously for a pes planus foot. Plantar fasciitis The primary objective when treating plantar fasciitis is to minimize the abnormal mechanical factors associated with irritation of the plantar fascia, particularly in the region of the medial calcaneal tubercle. Because plantar fasciitis can be associated with both the pes cavus and pes planus foot structures, orthoses
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Fig. 3. Lateral flare on athletic shoe.
and footwear modifications aimed at minimizing the abnormal supination or pronation associated with these foot types may also be effective in reducing stress on the plantar fascia. Variable success has been reported using over-the-counter heel wedges, heel cups, arch supports, and full length insoles [29,30]. Custom orthoses may also incorporate a viscoelastic polymer-filled relief at the tender area of the medial calcaneal tubercle. In some cases, a SACH modification to the shoe may offer additional pressure relief (Fig. 4).
Fig. 4. An example of how an athletic shoe can be modified with a SACH heel.
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Achilles tendinitis The primary objective in treating Achilles tendinitis is to reduce tension on the Achilles tendon. This reduction can be accomplished using a firm heel cushion that actually lifts the heel. Heel elevation can also be placed in the shoe to minimize the strain on the Achilles tendon. In more chronic cases, or when the tendinitis is associated with excessive pronation or an equinus deformity, a custom orthoses with the medial posting modifications previously described for the pes planus foot, in combination with a deep heel cup or cradle, may also be helpful in reducing symptoms. Haglunds deformity and retrocalcaneal bursitis The goal for Haglunds deformity and retrocalcaneal bursitis is simply to relieve pressure on the resulting bony prominence or inflamed bursa. A shoe with a heavily padded heel counter that will disperse the pressures may be adequate, or it may be necessary to cut out a portion of the heel counter to provide relief for the irritated area. Severs disease Severs disease occurs in adolescents, usually as the result of running on hard surfaces or using footwear with poor shock absorption. Tenderness is experienced at the heel and with stretching of the Achilles tendon. Over-the-counter insoles with a good arch support and shock absorption is often adequate when used with footwear that provides heel control and a shock-absorbing sole.
Summary Foot orthoses have been effective in the treatment of a variety of sport-related foot conditions. Although their use is well-established in clinical practice, many of the orthoses have not been evaluated in experimental conditions. Of the clinical studies that have examined the biomechanical changes associated with their use, many do not have predictable results. The failure of some studies to find trends for a particular variable does not preclude this variable being affected by the orthoses in an individual patient; rather, it may speak to the highly subject-specific responses with orthotic use. It is important to recognize that foot orthoses cannot be considered independent of a rehabilitation protocol that includes stretching and strengtheningspecific therapies, as well as a consideration of training surfaces and training regimes. Additionally, foot orthoses must be considered in concert with the footwear recommendation.
References
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2004, Vol.23, Issues 1, Athletic Foot and Ankle Injuries

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2004, Vol.23, Issues 1, Athletic Foot and Ankle Injuries

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Clin Sports Med 23 (2004) xiii xiv

Athletic foot and ankle injuries

Shepard R. Hurwitz, MD Guest Editor

S.R. Hurwitz / Clin Sports Med 23 (2004) xiiixiv

Clin Sports Med 23 (2004) xi

Athletic foot and ankle injuries

Mark D. Miller, MD Consulting Editor

Clin Sports Med 23 (2004) 1 19

Acute ankle injury and chronic lateral instability in the athlete

B.F. DiGiovanni et al / Clin Sports Med 23 (2004) 119

B.F. DiGiovanni et al / Clin Sports Med 23 (2004) 119

B.F. DiGiovanni et al / Clin Sports Med 23 (2004) 119

B.F. DiGiovanni et al / Clin Sports Med 23 (2004) 119

B.F. DiGiovanni et al / Clin Sports Med 23 (2004) 119

B.F. DiGiovanni et al / Clin Sports Med 23 (2004) 119

B.F. DiGiovanni et al / Clin Sports Med 23 (2004) 119

B.F. DiGiovanni et al / Clin Sports Med 23 (2004) 119

B.F. DiGiovanni et al / Clin Sports Med 23 (2004) 119

B.F. DiGiovanni et al / Clin Sports Med 23 (2004) 119

B.F. DiGiovanni et al / Clin Sports Med 23 (2004) 119

B.F. DiGiovanni et al / Clin Sports Med 23 (2004) 119

B.F. DiGiovanni et al / Clin Sports Med 23 (2004) 119

B.F. DiGiovanni et al / Clin Sports Med 23 (2004) 119

B.F. DiGiovanni et al / Clin Sports Med 23 (2004) 119

B.F. DiGiovanni et al / Clin Sports Med 23 (2004) 119

B.F. DiGiovanni et al / Clin Sports Med 23 (2004) 119

B.F. DiGiovanni et al / Clin Sports Med 23 (2004) 119

Clin Sports Med 23 (2004) 21 34

Ankle pain and peroneal tendon pathology

J.F. Baumhauer et al / Clin Sports Med 23 (2004) 2134

J.F. Baumhauer et al / Clin Sports Med 23 (2004) 2134

J.F. Baumhauer et al / Clin Sports Med 23 (2004) 2134

J.F. Baumhauer et al / Clin Sports Med 23 (2004) 2134

J.F. Baumhauer et al / Clin Sports Med 23 (2004) 2134

J.F. Baumhauer et al / Clin Sports Med 23 (2004) 2134

J.F. Baumhauer et al / Clin Sports Med 23 (2004) 2134

J.F. Baumhauer et al / Clin Sports Med 23 (2004) 2134

J.F. Baumhauer et al / Clin Sports Med 23 (2004) 2134

J.F. Baumhauer et al / Clin Sports Med 23 (2004) 2134

J.F. Baumhauer et al / Clin Sports Med 23 (2004) 2134

J.F. Baumhauer et al / Clin Sports Med 23 (2004) 2134

J.F. Baumhauer et al / Clin Sports Med 23 (2004) 2134

Clin Sports Med 23 (2004) 35 53

Arthroscopy for athletic foot and ankle injuries

T.M. Philbin et al / Clin Sports Med 23 (2004) 3553

T.M. Philbin et al / Clin Sports Med 23 (2004) 3553

T.M. Philbin et al / Clin Sports Med 23 (2004) 3553

T.M. Philbin et al / Clin Sports Med 23 (2004) 3553

T.M. Philbin et al / Clin Sports Med 23 (2004) 3553

T.M. Philbin et al / Clin Sports Med 23 (2004) 3553

T.M. Philbin et al / Clin Sports Med 23 (2004) 3553

T.M. Philbin et al / Clin Sports Med 23 (2004) 3553

T.M. Philbin et al / Clin Sports Med 23 (2004) 3553

T.M. Philbin et al / Clin Sports Med 23 (2004) 3553

T.M. Philbin et al / Clin Sports Med 23 (2004) 3553

T.M. Philbin et al / Clin Sports Med 23 (2004) 3553

T.M. Philbin et al / Clin Sports Med 23 (2004) 3553

T.M. Philbin et al / Clin Sports Med 23 (2004) 3553

T.M. Philbin et al / Clin Sports Med 23 (2004) 3553

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T.M. Philbin et al / Clin Sports Med 23 (2004) 3553