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Foot and Ankle Injuries in American Football
Foot and ankle injuries are common in American football, with injury rates significantly increasing over the past decade.1-5 Epidemiologic studies of collegiate football players have shown an annual incidence of foot and ankle injuries ranging from 9% to 39%,3,6 with as many as 72% of all collegiate players presenting to the National Football League (NFL) Combine with a history of a foot or ankle injury and 13% undergoing surgical treatment.5 Player position influences the rate and type of foot and ankle injury. Offensive and “skill position” players, including linemen, running backs, and wide receivers, are particularly susceptible to foot and ankle injuries due to high levels of force and torque placed on the distal extremity during running, cutting, and tackling. Shoe wear changes, playing field conditions, increasing player size and speed, and improved reporting of injuries are also contributing to increasing injury rates.
The interaction between player cleats and the playing surface is a central issue of foot and ankle injuries in football. Improved traction relates to performance, but increased subsequent torque on the lower extremity is associated with injury. While lateral ankle sprains are the most common foot and ankle injury experienced by football players,7 numerous other injuries can occur, including turf toe, Jones fractures, Lisfranc injuries, syndesmotic disruption, deltoid complex avulsion, and Achilles ruptures. It is important for physicians to be able to recognize, diagnose, and appropriately treat these injuries in players in order to expedite recovery, restore function, and help prevent future injury and long-term sequelae. This review focuses on updated treatment principles, surgical advances, and rehabilitation protocols for common football foot and ankle injuries.
Turf Toe
The term “turf toe” was first used in 1976 to refer to hyperextension injuries and plantar capsule-ligament sprains of the hallux metatarsophalangeal (MTP) joint that can lead to progressive cock-up deformity.8 While these injuries can occur on any surface and disrupt soft tissue balance with functional implications, predisposing factors include increasing playing surface hardness and decreasing shoe stiffness. In a classic scenario, the foot is fixed in equinus as an axial load is placed on the back of the heel, resulting in forced dorsiflexion of the hallux MTP joint.9 As the proximal phalanx extends, the sesamoids are drawn distally and the more dorsal portion of the metatarsal head articular surface bears the majority of the load, causing partial or complete tearing of the plantar plate with or without hallux MTP dislocation. Osteochondral lesions of the MTP joint and subchondral edema of the metatarsal head can occur concurrently as the proximal phalanx impacts or shears across the metatarsal head articular surface.
Clinical examination should focus on hallux swelling, alignment, and flexor hallucis longus (FHL) function along with vertical instability of the hallux MTP joint using a Lachman test. Radiographs should be evaluated for proximal migration of the sesamoids or diastasis (Figures W1A-W1C).
Indications for surgical intervention include loss of push-off strength, gross MTP instability, proximal migration of the sesamoids, and progressive hallux malalignment or clawing after immobilization. Cases can involve one or a combination of the following: (1) large capsular avulsion with unstable MTP joint; (2) diastasis of bipartite sesamoid; (3) diastasis of sesamoid fracture; (4) retraction of sesamoid; (5) traumatic hallux valgus deformity; (6) vertical instability (positive Lachman test); (7) loose body in MTP joint; or (8) chondral injury in MTP joint. The goal of surgery is the restoration of anatomy in order to restore normal function of the hallux MTP joint.
We have found that using dual medial and plantar incisions places less traction on the plantar medial cutaneous nerve, improves lateral exposure, and provides better wound healing. The medial capsulotomy extends from the metatarsal neck to the mid-phalanx to provide complete visualization of the sesamoid complex (Figures 1A-1F).
It is important to recognize that not all turf toe injuries involve pure hyperextension on artificial playing surfaces. In recent years, we have found an increasing rate of medial variant turf toe injuries in which a forceful valgus stress on the hallux leads to rupture of the medial collateral ligament, medial or plantar-medial capsule, and/or abductor halluces. Medial variant turf toe can lead to progressive hallux valgus and a traumatic bunion with a significant loss of push-off strength and difficulty with cutting maneuvers. Surgical treatment requires a modified McBride bunionectomy with adductor tenotomy and direct repair of the medial soft tissue defect.
Postoperative management is just as important as proper surgical technique for these injuries and involves a delicate balance between protecting the repair and starting early range of motion (ROM). Patients are immobilized non-weight-bearing (NWB) for 5 to 7 days maximum followed immediately with the initiation of passive hallux plantarflexion to keep the sesamoids moving. Active hallux plantarflexion is started at 4 weeks after surgery with active dorsiflexion from 6 to 8 weeks. Patients are transitioned to an accommodative shoe with stiff hallux insert 8 weeks postoperative with continued therapy focusing on hallux ROM. Running is initiated at 12 weeks and return to play (RTP) is typically allowed 4 months after surgery.
Jones Fractures
Jones fractures are fractures of the 5th metatarsal at the metaphyseal-diaphyseal junction, where there is a watershed area of decreased vascularity between the intramedullary nutrient and metaphyseal arteries. Current thought is that the rising rate of Jones fractures among football players is partially caused by the use of flexible, narrow cleats that do not provide enough stiffness and lateral support for the 5th metatarsal during running and cutting. Additionally, lateral overload from a baseline cavovarus foot posture with or without metatarsus adductus and/or skewfoot is thought to contribute to Jones fractures.10 Preoperative radiographs should be evaluated for fracture location, orientation, amount of cortical thickening, and overall geometry of the foot and 5th metatarsal. In elite athletes, the threshold for surgical intervention is decreasing in order to expedite healing and recovery and decrease re-fracture risk. This rationale is based on delayed union rates of 25% to 66%, nonunion rates of 7% to 28%,11 and re-fracture rates of up to 33% associated with nonoperative treatment.12 Nonoperative management is usually not feasible in the competitive athlete, as it typically involves a period of protected weight-bearing in a tall controlled ankle motion (CAM) boot for 6 to 8 weeks with serial radiographs to evaluate healing.
Our preference for surgical intervention involves percutaneous screw fixation with a “high and inside” starting point on fluoroscopy (Figures 2A-2D).
In career athletes, we augment the fracture site using a mixture of bone marrow aspirate concentrate (BMA) (Magellan, Arteriocyte Medical Systems) and demineralized bone matrix (DBM) (Mini Ignite, Wright Medical Technology) injected percutaneously in and around the fracture site under fluoroscopic guidance. Using this technique in a cohort of 25 NFL players treated operatively for Jones fractures, we found that 100% of athletes were able to RTP in the NFL in an average of 9.5 weeks.14 Two patients (7.5%) suffered re-fractures requiring revision surgery with iliac crest bone graft and repeat screw placement with a RTP after 15 weeks. We did not find an association between RTP and re-fracture rate.
The appropriate rehabilitation protocol for Jones fractures after surgery remains controversial and dependent on individual needs and abilities.15,16 For athletes in-season, we recommend a brief period of NWB for 1 to 2 weeks followed by toe-touch weight-bearing in a tall CAM boot for 2 to 4 weeks. After 4 weeks, patients begin gentle exercises on a stationary bike and pool therapy to reduce impact on the fracture site. Low-intensity pulsed ultrasound bone stimulators (Exogen, Bioventus) are frequently used directly over fracture site throughout the postoperative protocol as an adjuvant therapy. If clinically nontender over the fracture site, patients are allowed to begin running in modified protective shoe wear 4 weeks after surgery with an average RTP of 6 to 8 weeks. RTP is determined clinically, as radiographic union may not be evident for 12 to 16 weeks. Useful custom orthoses include turf toe plates with a cushioned lateral column and lateral heel wedge if hindfoot varus is present preoperatively.10 The solid intramedullary screw is left in place permanently.
In our experience, we have found the average re-fracture and nonunion rate to be approximately 8% across all athletes. Our observation that union rates do not appear to be related to RTP times suggests that underlying biology such as Vitamin D deficiency may play a larger role in union rates than previously thought. We have found that most Jones re-fractures occur in the first year after the initial injury, but can occur up to 2.5 years afterwards as well.14 For the management of symptomatic re-fractures and nonunions, the previous screw must be first removed. This can be difficult if the screw is bent or broken, and may require a lateral corticotomy of the metatarsal.
After hardware removal, we advocate open bone grafting of the fracture site using bone from the iliac crest retrieved with a small, percutaneous trephine. Re-fixation should be achieved using a larger, solid screw and postoperative adjuvants may include bone stimulators, Vitamin D and calcium supplemention, and possible teriparatide use (Forteo, Eli Lilly), depending on individual patient profile. In a cohort of 21 elite athletes treated for Jones fracture revision surgery with screw exchange and bone grafting, we found that 100% of patients had computed tomography (CT) evidence of union, with an average RTP of 12.3 weeks.17
Lisfranc Injuries
Lisfranc injuries include any bony or ligamentous damage that involves the tarsometatarsal (TMT) joints. While axial loading of a fixed, plantarflexed foot has traditionally been thought of as the most common mechanism of Lisfranc injury, we have found that noncontact twisting injuries leading to Lisfranc disruption are actually more common among NFL players. This mechanism is similar to noncontact turf toe and results in a purely ligamentous injury. We have found this to be particularly true in the case of defensive ends engaged with offensive linemen in which no axial loading or contact of the foot occurs. Clinically, patients often have painful weight-bearing, inability to perform a single limb heel rise, plantar ecchymosis, and swelling and point tenderness across the bases of the 1st and 2nd metatarsals.
It is critical to obtain comparison weight-bearing radiographs of both feet during initial work-up to look for evidence of instability. Subtle radiographic findings of Lisfranc injury include a bony “fleck” sign, compression fracture of the cuboid, and diastasis between the base of the 1st and 2nd metatarsals and/or medial and middle cuneiforms (Figures 3A, 3B).
The goal of surgical intervention is to obtain and maintain anatomic reduction of all unstable joints in order to restore a normal foot posture. One of the difficulties with Lisfranc injuries is that there are no exact diastasis parameters and individuals should be treated based on symptoms, functional needs, and degree of instability. It has been shown that 5 mm of displacement can have good long-term clinical results in select cases without surgery.18 For surgery, we recommend open reduction to remove interposed soft tissue debris and directly assess the articular surfaces (Figures 4A-4D).
Proximal-medial column Lisfranc injury variants are increasingly common among football players.20 In these injuries, the force of injury extends through the intercuneiform joint and exits out the naviculocuneiform joint, thus causing instability at multiple joints and an unstable 1st ray. Patients often have minimal clinical findings and normal radiographs and stress radiographs. MRI of the foot often reveals edema at the naviculocuneiform joint. Often patients fail to improve with nonoperative immobilization with continued inability to push off from the hallux. Unrecognized or untreated instability will lead to rapid deterioration of the naviculocuneiform joint. Surgical intervention requires a homerun screw and intercuneiform screw. We do not recommend primary arthrodesis in athletes due to significant risk of malunion and nonunion unless severe articular damage is present.
Patients are typically kept NWB in a splint for 2 weeks after surgery followed by NWB in a tall CAM from 3 to 4 weeks postoperative. Progressive weight-bearing and ROM exercises are initiated from 4 to 8 weeks, followed by return to accommodative shoe wear from 10 to 12 weeks. Hardware removal is performed 4 to 6 months after surgery, typically in the off-season to allow for 6 to 8 weeks or protected recovery afterwards. Premature hardware removal can lead to loss of reduction, particularly at the intercuneiform joints. All hardware crossing the TMT joints should be removed, while the homerun screw can be left in place in addition to the intercuneiform screw. RTP in football typically occurs 6 to 7 months after surgery. Final functional outcome is related to the adequacy of initial reduction and severity of the initial injury.21
Syndesmotic Disruption
Syndesmotic injuries comprise 1% to 18% of ankle sprains in the general population, but occur at much higher rates in football due to the increased rotation forces placed on the ankle during cutting and tackling. RTP after syndesmotic injury often takes twice as long when compared to isolated lateral ankle ligamentous injury.22 Missed injuries are common and if not treated properly can lead to chronic ankle instability and posttraumatic ankle arthritis.23 Syndesmotic injury can occur in isolation or with concomitant adjacent bony, cartilaginous, or ligamentous injuries. Therefore, clinical examination and imaging work-up are critical to successful management.
Syndesmotic injuries often result from an external rotation force applied to a hyperdorsiflexed ankle while the foot is planted. This mechanism causes the fibula to externally rotate while translating posteriorly and laterally, resulting in rupture of the anterior inferior tibiofibular ligament (AITFL) first, followed by the deep deltoid ligament, interosseous ligament (IOL), and lastly posterior talofibular ligament.24 Most syndesmotic injuries involve rupture of only the AITFL and IOL.25 Multiple clinical stress tests have been designed to assess syndesmotic stability, including the squeeze test, external rotation stress test, crossed-leg test, and fibula-translation test.26-29 However, no physical examination maneuver has been shown to reliably predict the presence or degree of syndesmotic injury and therefore imaging studies are necessary.30
Initial imaging should include standing radiographs of the affected ankle. An increase in the medial clear space between the medial malleolus and talus can occur with a combined syndesmotic and deltoid disruption. In the case of subtle syndesmotic injuries, contralateral comparison weight-bearing radiographs are recommended. CT and MRI can provide additional information, but these static imaging tests cannot identify instability. Fluoroscopic stress evaluation is beneficial but has a high false-negative rate in low-grade injuries and may not detect partial rupture of the AITFL and IOL.31 It has been shown that malrotation of as much as 30° of external rotation can occur if relying on intraoperative fluoroscopy alone.32 It has been our practice to recommend surgical reduction and stabilization for any syndesmotic injury with documented diastasis or instability seen on imaging and/or arthroscopy.
Nonoperative treatment is indicated for truly stable grade I syndesmotic injuries. This involves rest and immobilization followed by a progressive rehabilitation program consisting of stretching, strengthening, and proprioceptive exercises.33 After 1 week of protected weight-bearing in a cast or tall CAM boot, progression to full weight-bearing should occur over the following week. Active-assisted ankle ROM exercises and light proprioceptive training should then be initiated followed by sport-specific exercises 2 to 3 weeks after injury.
Arthroscopy can be a valuable diagnostic tool in the setting of subtle syndesmotic injury with negative radiographs, positive MRI for edema, and a protracted recovery course with vague pain (Figures W5A-W5E).
Implants are placed above the true syndesmotic joint (at least 15 mm above the tibial plafond) angled 30° posterior to anterior to follow the normal relationship of the fibula to the distal tibia in the incisura. Typically 2 suture-buttons are used, with the devices placed in a divergent fashion. We highly recommend the use of a fibular buttress plate with button placement in individuals returning to contact activity. This construct increases surface area distribution while preventing stress risers and the risk of fibula fractures. In a cadaver model with deliberate syndesmotic malreduction, suture-button stabilization resulted in decreased postoperative displacement as opposed to conventional screw fixation.34 Therefore, dynamic syndesmotic fixation may help to decrease the negative sequelae of iatrogenic clamp malreduction. Postoperative rehabilitation involves NWB in a cast or tall CAM boot for 4 weeks followed by ankle ROM exercises and progressive weight-bearing and physical therapy. Patients are transitioned to a lace-up ankle brace and athletic shoe from 6 to 12 weeks postoperative with increasing activity. Running and jumping is permitted 4 months after surgery with RTP typically at 6 to 7 months. Athletes who have had surgical stabilization for documented instability without any diastasis may engage in a more rapid recovery and RTP as symptoms and function allow.
Deltoid Complex Avulsion
Missed or neglected deltoid ligament injuries can lead to progressive chondral injury and joint degeneration. These injuries are often subtle and difficult to diagnose. An inability to perform a single limb heel rise, persistent pain with activity, and lack of normal functional improvement despite appropriate care are indicators of subtle ligament instability. These injuries often require an examination under anesthesia with combined ankle arthroscopy. Valgus stress testing of the ankle while directly visualizing the deltoid ligament from the anterolateral portal can reveal medial laxity in addition to potential osteochondral lesions along the anterolateral talar dome.
In American football players, we have observed that infolding and retraction of an avulsed superficial deltoid ligament complex after an ankle fracture, Maisonneuve injury, or severe high ankle sprain can be a source of persistent increased medial clear space, malreduction, and postoperative pain and medial instability. We have found that there is often complete avulsion of the superficial deltoid complex off the proximal aspect of the medial malleolus during high-energy ankle fractures in football players that is amenable to direct repair to bone (Figures W6A-W6E).
During surgical repair, an incision is made along the anterior aspect of the medial malleolus and the superficial deltoid ligament complex can often be found flipped and interposed in the medial gutter. A rongeur is used to create a bleeding cancellous bone surface for soft-tissue healing and 1 to 2 suture anchors are used to repair and imbricate the deltoid ligament complex back to the medial malleolus. The goal of these sutures is to repair the tibionavicular and tibial spring ligaments back to the medial malleolus. We believe that superficial deltoid complex avulsion during high-energy ankle fractures is a distinct injury pattern that should be recognized and may benefit from primary open repair.
We currently open explore every deltoid ligament complex in athletes with unstable syndesmotic injuries, as we believe that deltoid avulsion injuries are underrecognized and do not heal in an anatomic fashion if left alone. Postoperative recovery follows the same immobilization, progressive weight-bearing, and physical therapy protocol as that for syndesmotic disruption.
Achilles Ruptures
Acute midsubstance Achilles tendon ruptures are an increasingly common injury in patients 30 to 50 years of age, with more than 50% of all injuries occurring during basketball.36,37 Among NFL players, we have found that Achilles ruptures tend to occur at a higher rate during training camp, when athletes are deconditioned and quickly returning to explosive push-off activities. Physical examination should include a Thompson test, palpation of a gap within the tendon, and evaluation of resting ankle dorsiflexion in the affected extremity in the prone position with the knees bent. Lateral radiographs should be analyzed for the presence of a bony avulsion fragment indicative of an insertional avulsion injury or midsubstance calcium deposition reflecting chronic Achilles tendinosis, as both of these conditions will change surgical management. MRI is not recommended with acute midsubstance ruptures but may be helpful in the case of chronic ruptures or more proximal tears of the musculotendinous junction.
The management of acute midsubstance Achilles tendon ruptures is controversial, with no general consensus in the literature regarding nonoperative treatment, surgical repair, and ideal repair technique.36,38-42 American Academy of Orthopaedic Surgeons clinical practice guidelines report moderate evidence that nonoperative treatment of Achilles tendon ruptures has lower wound healing complications but higher rates of re-rupture.38,39 Additionally, limited incision approaches have been found to have fewer overall complications compared with traditional open repair. In an effort to reduce the incidence of postoperative wound complications while improving functional recovery, modern repair techniques focus on a limited incision repair using percutaneous suture insertion and management (PARS Achilles Jig System, Arthrex).36 The limited incision technique utilizes a 2-cm transverse incision and non-disposable jig with divergent needle passes and locking suture fixation options to secure and fixate both tendon ends with minimal dissection of skin, subcutaneous tissue, and paratenon. Limited incision repair is ideally performed within 2 weeks of the injury to ensure that both tendon ends are easy to identify, mobilize, and repair. An open repair is generally recommended for midsubstance ruptures more than 4 weeks old and cases of insertional rupture and Achilles tendinopathy.
In a cohort of 9 NFL players treated for midsubstance Achilles ruptures using the PARS technique, we found no re-ruptures, no wound complications, and no sural nerve issues after surgery.43 A comparative review of 270 cases of operatively treated Achilles tendon ruptures (101 PARS, 169 traditional open repair) showed that the PARS group had significantly shorter operative times and a higher number of patients able to return to baseline physical activities by 5 months compared to open repair.36 Although not statistically significant, the overall PARS complication rate was 5% while the open complication rate was 11%. The PARS group had no cases of sural neuritis or deep infection requiring reoperation. We currently use a limited incision technique for all acute midsubstance Achilles ruptures in athletes regardless of sport, patient size, or position played.
During surgery, a 2-cm transverse incision is made over the gap in the Achilles tendon and dissection is carried down to the rupture site with minimal manipulation of the skin (Figures 5A-5F).
A key aspect of postoperative recovery is avoiding excessive ankle dorsiflexion while the tendon is healing during the first 4 weeks after surgery, as this can lead to an elongated tendon with loss of push-off strength. Patients are kept in a plantarflexion splint NWB for 2 weeks after surgery. If the incision is healed at 2 weeks, sutures are removed and patients are transitioned into a NWB tall CAM boot for 2 weeks with gentle ankle ROM exercises. If there is any concern regarding wound healing status, sutures are maintained for an additional 1 to 2 weeks.
From 4 to 8 weeks after surgery, progressive weight-bearing with continued ankle ROM exercises is initiated with peel-away heel lifts (~2 cm thick total, 3 layers). Each layer of the heel lift is gradually removed as pain allows every 2 to 3 days with the goal of being full weight-bearing with the foot flat at 6 weeks postoperative. Physical therapy focusing on ankle ROM and gentle Achilles stretching and strengthening is also started 6 weeks after surgery. From 8 to 12 weeks postoperative, patients are transitioned out of the tall CAM boot into normal, accommodative shoe wear with full weight-bearing. We avoid ankle dorsiflexion past neutral until 12 weeks after surgery, as overlengthening of the Achilles complex and the subsequent loss of push-off power can be devastating to running athletes. Activity levels are increased as tolerated, with no running or jumping from 12 to 16 weeks with full release to all activities after 16 weeks. RTP often takes 5 to 6 months after surgery, depending on the position played.
Am J Orthop. 2016;45(6):358-367. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.
1. Canale ST, Cantler ED Jr, Sisk TD, Freeman BL 3rd. A chronicle of injuries of an American intercollegiate football team. Am J Sports Med. 1981;9(6):384-389.2. Robey JM, Blyth CS, Mueller FO. Athletic injuries. Application of epidemiologic methods. JAMA. 1971;217(2):184-189.
3. Saal JA. Common American football injuries. Sports Med. 1991;12(2):132-147.
4. Thompson N, Halpern B, Curl WW, et al. High school football injuries: evaluation. Am J Sports Med. 1987;15(2):117-124.
5. Kaplan LD, Jost PW, Honkamp N, Norwig J, West R, Bradley JP. Incidence and variance of foot and ankle injuries in elite college football players. Am J Orthop. 2011;40(1):40-44.
6. DeLee JC, Farney WC. Incidence of injury in Texas high school football. Am J Sports Med. 1992;20(5):575-580.
7. Brophy RH, Barnes R, Rodeo SA, Warren RF. Prevalence of musculoskeletal disorders at the NFL Combine--trends from 1987 to 2000. Med Sci Sports Exerc. 2007;39(1):22-27.
8. Bowers KD Jr, Martin RB. Turf-toe: a shoe-surface related football injury. Med Sci Sports. 1976;8(2):81-83.
9. McCormick JJ, Anderson RB. Turf toe: anatomy, diagnosis, and treatment. Sports Health. 2010;2(6):487-494.
10. Raikin SM, Slenker N, Ratigan B. The association of a varus hindfoot and fracture of the fifth metatarsal metaphyseal-diaphyseal junction: the Jones fracture. Am J Sports Med. 2008;36(7):1367-1372.
11. Title CI, Katchis SD. Traumatic foot and ankle injuries in the athlete. Orthop Clin North Am. 2002;33(3):587-598.
12. Quill GE Jr. Fractures of the proximal fifth metatarsal. Orthop Clin North Am. 1995;26(2):353-361.
13. Nunley JA, Glisson RR. A new option for intramedullary fixation of Jones fractures: the Charlotte Carolina Jones Fracture System. Foot Ankle Int. 2008;29(12):1216-1221.
14. Lareau CR, Hsu AR, Anderson RB. Return to play in National Football League players after operative Jones fracture treatment. Foot Ankle Int. 2016;37(1):8-16.
15. Larson CM, Almekinders LC, Taft TN, Garrett WE. Intramedullary screw fixation of Jones fractures. Analysis of failure. Am J Sports Med. 2002;30(1):55-60.
16. Portland G, Kelikian A, Kodros S. Acute surgical management of Jones’ fractures. Foot Ankle Int. 2003;24(11):829-833.
17. Hunt KJ, Anderson RB. Treatment of Jones fracture nonunions and refractures in the elite athlete: outcomes of intramedullary screw fixation with bone grafting. Am J Sports Med. 2011;39(9):1948-1954.
18. Nunley JA, Vertullo CJ. Classification, investigation, and management of midfoot sprains: Lisfranc injuries in the athlete. Am J Sports Med. 2002;30(6):871-878.
19. Alberta FG, Aronow MS, Barrero M, Diaz-Doran V, Sullivan RJ, Adams DJ. Ligamentous Lisfranc joint injuries: a biomechanical comparison of dorsal plate and transarticular screw fixation. Foot Ankle Int. 2005;26(6):462-473.
20. Ardoin GT, Anderson RB. Subtle Lisfranc injury. Tech Foot Ankle Surg. 2010;9(3):100-106.
21. Kuo RS, Tejwani NC, Digiovanni CW, et al. Outcome after open reduction and internal fixation of Lisfranc joint injuries. J Bone Joint Surg Am. 2000;82-A(11):1609-1618.
22. Wright RW, Barile RJ, Surprenant DA, Matava MJ. Ankle syndesmosis sprains in national hockey league players. Am J Sports Med. 2004;32(8):1941-1945.
23. Williams GN, Jones MH, Amendola A. Syndesmotic ankle sprains in athletes. Am J Sports Med. 2007;35(7):1197-1207.
24. Beumer A, Valstar ER, Garling EH, et al. Effects of ligament sectioning on the kinematics of the distal tibiofibular syndesmosis: a radiostereometric study of 10 cadaveric specimens based on presumed trauma mechanisms with suggestions for treatment. Acta Orthop. 2006;77(3):531-540.
25. McCollum GA, van den Bekerom MP, Kerkhoffs GM, Calder JD, van Dijk CN. Syndesmosis and deltoid ligament injuries in the athlete. Knee Surg Sports Traumatol Arthrosc. 2013;21(6):1328-1337.
26. Boytim MJ, Fischer DA, Neumann L. Syndesmotic ankle sprains. Am J Sports Med. 1991;19(3):294-298.
27. Nussbaum ED, Hosea TM, Sieler SD, Incremona BR, Kessler DE. Prospective evaluation of syndesmotic ankle sprains without diastasis. Am J Sports Med. 2001;29(1):31-35.
28. Kiter E, Bozkurt M. The crossed-leg test for examination of ankle syndesmosis injuries. Foot Ankle Int. 2005;26(2):187-188.
29. Beumer A, van Hemert WL, Swierstra BA, Jasper LE, Belkoff SM. A biomechanical evaluation of clinical stress tests for syndesmotic ankle instability. Foot Ankle Int. 2003;24(4):358-363.
30. Amendola A, Williams G, Foster D. Evidence-based approach to treatment of acute traumatic syndesmosis (high ankle) sprains. Sports Med Arthrosc. 2006;14(4):232-236.
31. Beumer A, Valstar ER, Garling EH, et al. External rotation stress imaging in syndesmotic injuries of the ankle: comparison of lateral radiography and radiostereometry in a cadaveric model. Acta Orthop Scand. 2003;74(2):201-205.
32. Marmor M, Hansen E, Han HK, Buckley J, Matityahu A. Limitations of standard fluoroscopy in detecting rotational malreduction of the syndesmosis in an ankle fracture model. Foot Ankle Int. 2011;32(6):616-622.
33. Williams GN, Allen EJ. Rehabilitation of syndesmotic (high) ankle sprains. Sports Health. 2010;2(6):460-470.
34. Westermann RW, Rungprai C, Goetz JE, Femino J, Amendola A, Phisitkul P. The effect of suture-button fixation on simulated syndesmotic malreduction: a cadaveric study. J Bone Joint Surg Am. 2014;96(20):1732-1738.
35. Hsu AR, Lareau CR, Anderson RB. Repair of acute superficial deltoid complex avulsion during ankle fracture fixation in National Football League players. Foot Ankle Int. 2015;36(11):1272-1278.
36. Hsu AR, Jones CP, Cohen BE, Davis WH, Ellington JK, Anderson RB. Clinical outcomes and complications of percutaneous Achilles repair system versus open technique for acute achilles tendon ruptures. Foot Ankle Int. 2015;36(11):1279-1286.
37. Raikin SM, Garras DN, Krapchev PV. Achilles tendon injuries in a United States population. Foot Ankle Int. 2013;34(4):475-480.
38. Chiodo CP, Glazebrook M, Bluman EM, et al. American Academy of Orthopaedic Surgeons clinical practice guideline on treatment of achilles tendon rupture. J Bone Joint Surg Am. 2010;92(14):2466-2468.
39. Chiodo CP, Glazebrook M, Bluman EM, et al. Diagnosis and treatment of acute achilles tendon rupture. J Am Acad Orthop Surg. 2010;18(8):503-510.
40. Khan RJ, Fick D, Keogh A, Crawford J, Brammar T, Parker M. Treatment of acute achilles tendon ruptures. A meta-analysis of randomized, controlled trials. J Bone Joint Surg Am. 2005;87(10):2202-2210.
41. Renninger CH, Kuhn K, Fellars T, Youngblood S, Bellamy J. Operative and nonoperative management of achilles tendon ruptures in active duty military population. Foot Ankle Int. 2016;37(3):269-273.
42. Khan RJ, Carey Smith RL. Surgical interventions for treating acute achilles tendon ruptures. Cochrane Database Syst Rev. 2010;(9):CD003674.
43. McCullough KA, Shaw CM, Anderson RB. Mini-open repair of achilles rupture in the national football league. J Surg Orthop Adv. 2014;23(4):179-183.
Foot and ankle injuries are common in American football, with injury rates significantly increasing over the past decade.1-5 Epidemiologic studies of collegiate football players have shown an annual incidence of foot and ankle injuries ranging from 9% to 39%,3,6 with as many as 72% of all collegiate players presenting to the National Football League (NFL) Combine with a history of a foot or ankle injury and 13% undergoing surgical treatment.5 Player position influences the rate and type of foot and ankle injury. Offensive and “skill position” players, including linemen, running backs, and wide receivers, are particularly susceptible to foot and ankle injuries due to high levels of force and torque placed on the distal extremity during running, cutting, and tackling. Shoe wear changes, playing field conditions, increasing player size and speed, and improved reporting of injuries are also contributing to increasing injury rates.
The interaction between player cleats and the playing surface is a central issue of foot and ankle injuries in football. Improved traction relates to performance, but increased subsequent torque on the lower extremity is associated with injury. While lateral ankle sprains are the most common foot and ankle injury experienced by football players,7 numerous other injuries can occur, including turf toe, Jones fractures, Lisfranc injuries, syndesmotic disruption, deltoid complex avulsion, and Achilles ruptures. It is important for physicians to be able to recognize, diagnose, and appropriately treat these injuries in players in order to expedite recovery, restore function, and help prevent future injury and long-term sequelae. This review focuses on updated treatment principles, surgical advances, and rehabilitation protocols for common football foot and ankle injuries.
Turf Toe
The term “turf toe” was first used in 1976 to refer to hyperextension injuries and plantar capsule-ligament sprains of the hallux metatarsophalangeal (MTP) joint that can lead to progressive cock-up deformity.8 While these injuries can occur on any surface and disrupt soft tissue balance with functional implications, predisposing factors include increasing playing surface hardness and decreasing shoe stiffness. In a classic scenario, the foot is fixed in equinus as an axial load is placed on the back of the heel, resulting in forced dorsiflexion of the hallux MTP joint.9 As the proximal phalanx extends, the sesamoids are drawn distally and the more dorsal portion of the metatarsal head articular surface bears the majority of the load, causing partial or complete tearing of the plantar plate with or without hallux MTP dislocation. Osteochondral lesions of the MTP joint and subchondral edema of the metatarsal head can occur concurrently as the proximal phalanx impacts or shears across the metatarsal head articular surface.
Clinical examination should focus on hallux swelling, alignment, and flexor hallucis longus (FHL) function along with vertical instability of the hallux MTP joint using a Lachman test. Radiographs should be evaluated for proximal migration of the sesamoids or diastasis (Figures W1A-W1C).
Indications for surgical intervention include loss of push-off strength, gross MTP instability, proximal migration of the sesamoids, and progressive hallux malalignment or clawing after immobilization. Cases can involve one or a combination of the following: (1) large capsular avulsion with unstable MTP joint; (2) diastasis of bipartite sesamoid; (3) diastasis of sesamoid fracture; (4) retraction of sesamoid; (5) traumatic hallux valgus deformity; (6) vertical instability (positive Lachman test); (7) loose body in MTP joint; or (8) chondral injury in MTP joint. The goal of surgery is the restoration of anatomy in order to restore normal function of the hallux MTP joint.
We have found that using dual medial and plantar incisions places less traction on the plantar medial cutaneous nerve, improves lateral exposure, and provides better wound healing. The medial capsulotomy extends from the metatarsal neck to the mid-phalanx to provide complete visualization of the sesamoid complex (Figures 1A-1F).
It is important to recognize that not all turf toe injuries involve pure hyperextension on artificial playing surfaces. In recent years, we have found an increasing rate of medial variant turf toe injuries in which a forceful valgus stress on the hallux leads to rupture of the medial collateral ligament, medial or plantar-medial capsule, and/or abductor halluces. Medial variant turf toe can lead to progressive hallux valgus and a traumatic bunion with a significant loss of push-off strength and difficulty with cutting maneuvers. Surgical treatment requires a modified McBride bunionectomy with adductor tenotomy and direct repair of the medial soft tissue defect.
Postoperative management is just as important as proper surgical technique for these injuries and involves a delicate balance between protecting the repair and starting early range of motion (ROM). Patients are immobilized non-weight-bearing (NWB) for 5 to 7 days maximum followed immediately with the initiation of passive hallux plantarflexion to keep the sesamoids moving. Active hallux plantarflexion is started at 4 weeks after surgery with active dorsiflexion from 6 to 8 weeks. Patients are transitioned to an accommodative shoe with stiff hallux insert 8 weeks postoperative with continued therapy focusing on hallux ROM. Running is initiated at 12 weeks and return to play (RTP) is typically allowed 4 months after surgery.
Jones Fractures
Jones fractures are fractures of the 5th metatarsal at the metaphyseal-diaphyseal junction, where there is a watershed area of decreased vascularity between the intramedullary nutrient and metaphyseal arteries. Current thought is that the rising rate of Jones fractures among football players is partially caused by the use of flexible, narrow cleats that do not provide enough stiffness and lateral support for the 5th metatarsal during running and cutting. Additionally, lateral overload from a baseline cavovarus foot posture with or without metatarsus adductus and/or skewfoot is thought to contribute to Jones fractures.10 Preoperative radiographs should be evaluated for fracture location, orientation, amount of cortical thickening, and overall geometry of the foot and 5th metatarsal. In elite athletes, the threshold for surgical intervention is decreasing in order to expedite healing and recovery and decrease re-fracture risk. This rationale is based on delayed union rates of 25% to 66%, nonunion rates of 7% to 28%,11 and re-fracture rates of up to 33% associated with nonoperative treatment.12 Nonoperative management is usually not feasible in the competitive athlete, as it typically involves a period of protected weight-bearing in a tall controlled ankle motion (CAM) boot for 6 to 8 weeks with serial radiographs to evaluate healing.
Our preference for surgical intervention involves percutaneous screw fixation with a “high and inside” starting point on fluoroscopy (Figures 2A-2D).
In career athletes, we augment the fracture site using a mixture of bone marrow aspirate concentrate (BMA) (Magellan, Arteriocyte Medical Systems) and demineralized bone matrix (DBM) (Mini Ignite, Wright Medical Technology) injected percutaneously in and around the fracture site under fluoroscopic guidance. Using this technique in a cohort of 25 NFL players treated operatively for Jones fractures, we found that 100% of athletes were able to RTP in the NFL in an average of 9.5 weeks.14 Two patients (7.5%) suffered re-fractures requiring revision surgery with iliac crest bone graft and repeat screw placement with a RTP after 15 weeks. We did not find an association between RTP and re-fracture rate.
The appropriate rehabilitation protocol for Jones fractures after surgery remains controversial and dependent on individual needs and abilities.15,16 For athletes in-season, we recommend a brief period of NWB for 1 to 2 weeks followed by toe-touch weight-bearing in a tall CAM boot for 2 to 4 weeks. After 4 weeks, patients begin gentle exercises on a stationary bike and pool therapy to reduce impact on the fracture site. Low-intensity pulsed ultrasound bone stimulators (Exogen, Bioventus) are frequently used directly over fracture site throughout the postoperative protocol as an adjuvant therapy. If clinically nontender over the fracture site, patients are allowed to begin running in modified protective shoe wear 4 weeks after surgery with an average RTP of 6 to 8 weeks. RTP is determined clinically, as radiographic union may not be evident for 12 to 16 weeks. Useful custom orthoses include turf toe plates with a cushioned lateral column and lateral heel wedge if hindfoot varus is present preoperatively.10 The solid intramedullary screw is left in place permanently.
In our experience, we have found the average re-fracture and nonunion rate to be approximately 8% across all athletes. Our observation that union rates do not appear to be related to RTP times suggests that underlying biology such as Vitamin D deficiency may play a larger role in union rates than previously thought. We have found that most Jones re-fractures occur in the first year after the initial injury, but can occur up to 2.5 years afterwards as well.14 For the management of symptomatic re-fractures and nonunions, the previous screw must be first removed. This can be difficult if the screw is bent or broken, and may require a lateral corticotomy of the metatarsal.
After hardware removal, we advocate open bone grafting of the fracture site using bone from the iliac crest retrieved with a small, percutaneous trephine. Re-fixation should be achieved using a larger, solid screw and postoperative adjuvants may include bone stimulators, Vitamin D and calcium supplemention, and possible teriparatide use (Forteo, Eli Lilly), depending on individual patient profile. In a cohort of 21 elite athletes treated for Jones fracture revision surgery with screw exchange and bone grafting, we found that 100% of patients had computed tomography (CT) evidence of union, with an average RTP of 12.3 weeks.17
Lisfranc Injuries
Lisfranc injuries include any bony or ligamentous damage that involves the tarsometatarsal (TMT) joints. While axial loading of a fixed, plantarflexed foot has traditionally been thought of as the most common mechanism of Lisfranc injury, we have found that noncontact twisting injuries leading to Lisfranc disruption are actually more common among NFL players. This mechanism is similar to noncontact turf toe and results in a purely ligamentous injury. We have found this to be particularly true in the case of defensive ends engaged with offensive linemen in which no axial loading or contact of the foot occurs. Clinically, patients often have painful weight-bearing, inability to perform a single limb heel rise, plantar ecchymosis, and swelling and point tenderness across the bases of the 1st and 2nd metatarsals.
It is critical to obtain comparison weight-bearing radiographs of both feet during initial work-up to look for evidence of instability. Subtle radiographic findings of Lisfranc injury include a bony “fleck” sign, compression fracture of the cuboid, and diastasis between the base of the 1st and 2nd metatarsals and/or medial and middle cuneiforms (Figures 3A, 3B).
The goal of surgical intervention is to obtain and maintain anatomic reduction of all unstable joints in order to restore a normal foot posture. One of the difficulties with Lisfranc injuries is that there are no exact diastasis parameters and individuals should be treated based on symptoms, functional needs, and degree of instability. It has been shown that 5 mm of displacement can have good long-term clinical results in select cases without surgery.18 For surgery, we recommend open reduction to remove interposed soft tissue debris and directly assess the articular surfaces (Figures 4A-4D).
Proximal-medial column Lisfranc injury variants are increasingly common among football players.20 In these injuries, the force of injury extends through the intercuneiform joint and exits out the naviculocuneiform joint, thus causing instability at multiple joints and an unstable 1st ray. Patients often have minimal clinical findings and normal radiographs and stress radiographs. MRI of the foot often reveals edema at the naviculocuneiform joint. Often patients fail to improve with nonoperative immobilization with continued inability to push off from the hallux. Unrecognized or untreated instability will lead to rapid deterioration of the naviculocuneiform joint. Surgical intervention requires a homerun screw and intercuneiform screw. We do not recommend primary arthrodesis in athletes due to significant risk of malunion and nonunion unless severe articular damage is present.
Patients are typically kept NWB in a splint for 2 weeks after surgery followed by NWB in a tall CAM from 3 to 4 weeks postoperative. Progressive weight-bearing and ROM exercises are initiated from 4 to 8 weeks, followed by return to accommodative shoe wear from 10 to 12 weeks. Hardware removal is performed 4 to 6 months after surgery, typically in the off-season to allow for 6 to 8 weeks or protected recovery afterwards. Premature hardware removal can lead to loss of reduction, particularly at the intercuneiform joints. All hardware crossing the TMT joints should be removed, while the homerun screw can be left in place in addition to the intercuneiform screw. RTP in football typically occurs 6 to 7 months after surgery. Final functional outcome is related to the adequacy of initial reduction and severity of the initial injury.21
Syndesmotic Disruption
Syndesmotic injuries comprise 1% to 18% of ankle sprains in the general population, but occur at much higher rates in football due to the increased rotation forces placed on the ankle during cutting and tackling. RTP after syndesmotic injury often takes twice as long when compared to isolated lateral ankle ligamentous injury.22 Missed injuries are common and if not treated properly can lead to chronic ankle instability and posttraumatic ankle arthritis.23 Syndesmotic injury can occur in isolation or with concomitant adjacent bony, cartilaginous, or ligamentous injuries. Therefore, clinical examination and imaging work-up are critical to successful management.
Syndesmotic injuries often result from an external rotation force applied to a hyperdorsiflexed ankle while the foot is planted. This mechanism causes the fibula to externally rotate while translating posteriorly and laterally, resulting in rupture of the anterior inferior tibiofibular ligament (AITFL) first, followed by the deep deltoid ligament, interosseous ligament (IOL), and lastly posterior talofibular ligament.24 Most syndesmotic injuries involve rupture of only the AITFL and IOL.25 Multiple clinical stress tests have been designed to assess syndesmotic stability, including the squeeze test, external rotation stress test, crossed-leg test, and fibula-translation test.26-29 However, no physical examination maneuver has been shown to reliably predict the presence or degree of syndesmotic injury and therefore imaging studies are necessary.30
Initial imaging should include standing radiographs of the affected ankle. An increase in the medial clear space between the medial malleolus and talus can occur with a combined syndesmotic and deltoid disruption. In the case of subtle syndesmotic injuries, contralateral comparison weight-bearing radiographs are recommended. CT and MRI can provide additional information, but these static imaging tests cannot identify instability. Fluoroscopic stress evaluation is beneficial but has a high false-negative rate in low-grade injuries and may not detect partial rupture of the AITFL and IOL.31 It has been shown that malrotation of as much as 30° of external rotation can occur if relying on intraoperative fluoroscopy alone.32 It has been our practice to recommend surgical reduction and stabilization for any syndesmotic injury with documented diastasis or instability seen on imaging and/or arthroscopy.
Nonoperative treatment is indicated for truly stable grade I syndesmotic injuries. This involves rest and immobilization followed by a progressive rehabilitation program consisting of stretching, strengthening, and proprioceptive exercises.33 After 1 week of protected weight-bearing in a cast or tall CAM boot, progression to full weight-bearing should occur over the following week. Active-assisted ankle ROM exercises and light proprioceptive training should then be initiated followed by sport-specific exercises 2 to 3 weeks after injury.
Arthroscopy can be a valuable diagnostic tool in the setting of subtle syndesmotic injury with negative radiographs, positive MRI for edema, and a protracted recovery course with vague pain (Figures W5A-W5E).
Implants are placed above the true syndesmotic joint (at least 15 mm above the tibial plafond) angled 30° posterior to anterior to follow the normal relationship of the fibula to the distal tibia in the incisura. Typically 2 suture-buttons are used, with the devices placed in a divergent fashion. We highly recommend the use of a fibular buttress plate with button placement in individuals returning to contact activity. This construct increases surface area distribution while preventing stress risers and the risk of fibula fractures. In a cadaver model with deliberate syndesmotic malreduction, suture-button stabilization resulted in decreased postoperative displacement as opposed to conventional screw fixation.34 Therefore, dynamic syndesmotic fixation may help to decrease the negative sequelae of iatrogenic clamp malreduction. Postoperative rehabilitation involves NWB in a cast or tall CAM boot for 4 weeks followed by ankle ROM exercises and progressive weight-bearing and physical therapy. Patients are transitioned to a lace-up ankle brace and athletic shoe from 6 to 12 weeks postoperative with increasing activity. Running and jumping is permitted 4 months after surgery with RTP typically at 6 to 7 months. Athletes who have had surgical stabilization for documented instability without any diastasis may engage in a more rapid recovery and RTP as symptoms and function allow.
Deltoid Complex Avulsion
Missed or neglected deltoid ligament injuries can lead to progressive chondral injury and joint degeneration. These injuries are often subtle and difficult to diagnose. An inability to perform a single limb heel rise, persistent pain with activity, and lack of normal functional improvement despite appropriate care are indicators of subtle ligament instability. These injuries often require an examination under anesthesia with combined ankle arthroscopy. Valgus stress testing of the ankle while directly visualizing the deltoid ligament from the anterolateral portal can reveal medial laxity in addition to potential osteochondral lesions along the anterolateral talar dome.
In American football players, we have observed that infolding and retraction of an avulsed superficial deltoid ligament complex after an ankle fracture, Maisonneuve injury, or severe high ankle sprain can be a source of persistent increased medial clear space, malreduction, and postoperative pain and medial instability. We have found that there is often complete avulsion of the superficial deltoid complex off the proximal aspect of the medial malleolus during high-energy ankle fractures in football players that is amenable to direct repair to bone (Figures W6A-W6E).
During surgical repair, an incision is made along the anterior aspect of the medial malleolus and the superficial deltoid ligament complex can often be found flipped and interposed in the medial gutter. A rongeur is used to create a bleeding cancellous bone surface for soft-tissue healing and 1 to 2 suture anchors are used to repair and imbricate the deltoid ligament complex back to the medial malleolus. The goal of these sutures is to repair the tibionavicular and tibial spring ligaments back to the medial malleolus. We believe that superficial deltoid complex avulsion during high-energy ankle fractures is a distinct injury pattern that should be recognized and may benefit from primary open repair.
We currently open explore every deltoid ligament complex in athletes with unstable syndesmotic injuries, as we believe that deltoid avulsion injuries are underrecognized and do not heal in an anatomic fashion if left alone. Postoperative recovery follows the same immobilization, progressive weight-bearing, and physical therapy protocol as that for syndesmotic disruption.
Achilles Ruptures
Acute midsubstance Achilles tendon ruptures are an increasingly common injury in patients 30 to 50 years of age, with more than 50% of all injuries occurring during basketball.36,37 Among NFL players, we have found that Achilles ruptures tend to occur at a higher rate during training camp, when athletes are deconditioned and quickly returning to explosive push-off activities. Physical examination should include a Thompson test, palpation of a gap within the tendon, and evaluation of resting ankle dorsiflexion in the affected extremity in the prone position with the knees bent. Lateral radiographs should be analyzed for the presence of a bony avulsion fragment indicative of an insertional avulsion injury or midsubstance calcium deposition reflecting chronic Achilles tendinosis, as both of these conditions will change surgical management. MRI is not recommended with acute midsubstance ruptures but may be helpful in the case of chronic ruptures or more proximal tears of the musculotendinous junction.
The management of acute midsubstance Achilles tendon ruptures is controversial, with no general consensus in the literature regarding nonoperative treatment, surgical repair, and ideal repair technique.36,38-42 American Academy of Orthopaedic Surgeons clinical practice guidelines report moderate evidence that nonoperative treatment of Achilles tendon ruptures has lower wound healing complications but higher rates of re-rupture.38,39 Additionally, limited incision approaches have been found to have fewer overall complications compared with traditional open repair. In an effort to reduce the incidence of postoperative wound complications while improving functional recovery, modern repair techniques focus on a limited incision repair using percutaneous suture insertion and management (PARS Achilles Jig System, Arthrex).36 The limited incision technique utilizes a 2-cm transverse incision and non-disposable jig with divergent needle passes and locking suture fixation options to secure and fixate both tendon ends with minimal dissection of skin, subcutaneous tissue, and paratenon. Limited incision repair is ideally performed within 2 weeks of the injury to ensure that both tendon ends are easy to identify, mobilize, and repair. An open repair is generally recommended for midsubstance ruptures more than 4 weeks old and cases of insertional rupture and Achilles tendinopathy.
In a cohort of 9 NFL players treated for midsubstance Achilles ruptures using the PARS technique, we found no re-ruptures, no wound complications, and no sural nerve issues after surgery.43 A comparative review of 270 cases of operatively treated Achilles tendon ruptures (101 PARS, 169 traditional open repair) showed that the PARS group had significantly shorter operative times and a higher number of patients able to return to baseline physical activities by 5 months compared to open repair.36 Although not statistically significant, the overall PARS complication rate was 5% while the open complication rate was 11%. The PARS group had no cases of sural neuritis or deep infection requiring reoperation. We currently use a limited incision technique for all acute midsubstance Achilles ruptures in athletes regardless of sport, patient size, or position played.
During surgery, a 2-cm transverse incision is made over the gap in the Achilles tendon and dissection is carried down to the rupture site with minimal manipulation of the skin (Figures 5A-5F).
A key aspect of postoperative recovery is avoiding excessive ankle dorsiflexion while the tendon is healing during the first 4 weeks after surgery, as this can lead to an elongated tendon with loss of push-off strength. Patients are kept in a plantarflexion splint NWB for 2 weeks after surgery. If the incision is healed at 2 weeks, sutures are removed and patients are transitioned into a NWB tall CAM boot for 2 weeks with gentle ankle ROM exercises. If there is any concern regarding wound healing status, sutures are maintained for an additional 1 to 2 weeks.
From 4 to 8 weeks after surgery, progressive weight-bearing with continued ankle ROM exercises is initiated with peel-away heel lifts (~2 cm thick total, 3 layers). Each layer of the heel lift is gradually removed as pain allows every 2 to 3 days with the goal of being full weight-bearing with the foot flat at 6 weeks postoperative. Physical therapy focusing on ankle ROM and gentle Achilles stretching and strengthening is also started 6 weeks after surgery. From 8 to 12 weeks postoperative, patients are transitioned out of the tall CAM boot into normal, accommodative shoe wear with full weight-bearing. We avoid ankle dorsiflexion past neutral until 12 weeks after surgery, as overlengthening of the Achilles complex and the subsequent loss of push-off power can be devastating to running athletes. Activity levels are increased as tolerated, with no running or jumping from 12 to 16 weeks with full release to all activities after 16 weeks. RTP often takes 5 to 6 months after surgery, depending on the position played.
Am J Orthop. 2016;45(6):358-367. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.
Foot and ankle injuries are common in American football, with injury rates significantly increasing over the past decade.1-5 Epidemiologic studies of collegiate football players have shown an annual incidence of foot and ankle injuries ranging from 9% to 39%,3,6 with as many as 72% of all collegiate players presenting to the National Football League (NFL) Combine with a history of a foot or ankle injury and 13% undergoing surgical treatment.5 Player position influences the rate and type of foot and ankle injury. Offensive and “skill position” players, including linemen, running backs, and wide receivers, are particularly susceptible to foot and ankle injuries due to high levels of force and torque placed on the distal extremity during running, cutting, and tackling. Shoe wear changes, playing field conditions, increasing player size and speed, and improved reporting of injuries are also contributing to increasing injury rates.
The interaction between player cleats and the playing surface is a central issue of foot and ankle injuries in football. Improved traction relates to performance, but increased subsequent torque on the lower extremity is associated with injury. While lateral ankle sprains are the most common foot and ankle injury experienced by football players,7 numerous other injuries can occur, including turf toe, Jones fractures, Lisfranc injuries, syndesmotic disruption, deltoid complex avulsion, and Achilles ruptures. It is important for physicians to be able to recognize, diagnose, and appropriately treat these injuries in players in order to expedite recovery, restore function, and help prevent future injury and long-term sequelae. This review focuses on updated treatment principles, surgical advances, and rehabilitation protocols for common football foot and ankle injuries.
Turf Toe
The term “turf toe” was first used in 1976 to refer to hyperextension injuries and plantar capsule-ligament sprains of the hallux metatarsophalangeal (MTP) joint that can lead to progressive cock-up deformity.8 While these injuries can occur on any surface and disrupt soft tissue balance with functional implications, predisposing factors include increasing playing surface hardness and decreasing shoe stiffness. In a classic scenario, the foot is fixed in equinus as an axial load is placed on the back of the heel, resulting in forced dorsiflexion of the hallux MTP joint.9 As the proximal phalanx extends, the sesamoids are drawn distally and the more dorsal portion of the metatarsal head articular surface bears the majority of the load, causing partial or complete tearing of the plantar plate with or without hallux MTP dislocation. Osteochondral lesions of the MTP joint and subchondral edema of the metatarsal head can occur concurrently as the proximal phalanx impacts or shears across the metatarsal head articular surface.
Clinical examination should focus on hallux swelling, alignment, and flexor hallucis longus (FHL) function along with vertical instability of the hallux MTP joint using a Lachman test. Radiographs should be evaluated for proximal migration of the sesamoids or diastasis (Figures W1A-W1C).
Indications for surgical intervention include loss of push-off strength, gross MTP instability, proximal migration of the sesamoids, and progressive hallux malalignment or clawing after immobilization. Cases can involve one or a combination of the following: (1) large capsular avulsion with unstable MTP joint; (2) diastasis of bipartite sesamoid; (3) diastasis of sesamoid fracture; (4) retraction of sesamoid; (5) traumatic hallux valgus deformity; (6) vertical instability (positive Lachman test); (7) loose body in MTP joint; or (8) chondral injury in MTP joint. The goal of surgery is the restoration of anatomy in order to restore normal function of the hallux MTP joint.
We have found that using dual medial and plantar incisions places less traction on the plantar medial cutaneous nerve, improves lateral exposure, and provides better wound healing. The medial capsulotomy extends from the metatarsal neck to the mid-phalanx to provide complete visualization of the sesamoid complex (Figures 1A-1F).
It is important to recognize that not all turf toe injuries involve pure hyperextension on artificial playing surfaces. In recent years, we have found an increasing rate of medial variant turf toe injuries in which a forceful valgus stress on the hallux leads to rupture of the medial collateral ligament, medial or plantar-medial capsule, and/or abductor halluces. Medial variant turf toe can lead to progressive hallux valgus and a traumatic bunion with a significant loss of push-off strength and difficulty with cutting maneuvers. Surgical treatment requires a modified McBride bunionectomy with adductor tenotomy and direct repair of the medial soft tissue defect.
Postoperative management is just as important as proper surgical technique for these injuries and involves a delicate balance between protecting the repair and starting early range of motion (ROM). Patients are immobilized non-weight-bearing (NWB) for 5 to 7 days maximum followed immediately with the initiation of passive hallux plantarflexion to keep the sesamoids moving. Active hallux plantarflexion is started at 4 weeks after surgery with active dorsiflexion from 6 to 8 weeks. Patients are transitioned to an accommodative shoe with stiff hallux insert 8 weeks postoperative with continued therapy focusing on hallux ROM. Running is initiated at 12 weeks and return to play (RTP) is typically allowed 4 months after surgery.
Jones Fractures
Jones fractures are fractures of the 5th metatarsal at the metaphyseal-diaphyseal junction, where there is a watershed area of decreased vascularity between the intramedullary nutrient and metaphyseal arteries. Current thought is that the rising rate of Jones fractures among football players is partially caused by the use of flexible, narrow cleats that do not provide enough stiffness and lateral support for the 5th metatarsal during running and cutting. Additionally, lateral overload from a baseline cavovarus foot posture with or without metatarsus adductus and/or skewfoot is thought to contribute to Jones fractures.10 Preoperative radiographs should be evaluated for fracture location, orientation, amount of cortical thickening, and overall geometry of the foot and 5th metatarsal. In elite athletes, the threshold for surgical intervention is decreasing in order to expedite healing and recovery and decrease re-fracture risk. This rationale is based on delayed union rates of 25% to 66%, nonunion rates of 7% to 28%,11 and re-fracture rates of up to 33% associated with nonoperative treatment.12 Nonoperative management is usually not feasible in the competitive athlete, as it typically involves a period of protected weight-bearing in a tall controlled ankle motion (CAM) boot for 6 to 8 weeks with serial radiographs to evaluate healing.
Our preference for surgical intervention involves percutaneous screw fixation with a “high and inside” starting point on fluoroscopy (Figures 2A-2D).
In career athletes, we augment the fracture site using a mixture of bone marrow aspirate concentrate (BMA) (Magellan, Arteriocyte Medical Systems) and demineralized bone matrix (DBM) (Mini Ignite, Wright Medical Technology) injected percutaneously in and around the fracture site under fluoroscopic guidance. Using this technique in a cohort of 25 NFL players treated operatively for Jones fractures, we found that 100% of athletes were able to RTP in the NFL in an average of 9.5 weeks.14 Two patients (7.5%) suffered re-fractures requiring revision surgery with iliac crest bone graft and repeat screw placement with a RTP after 15 weeks. We did not find an association between RTP and re-fracture rate.
The appropriate rehabilitation protocol for Jones fractures after surgery remains controversial and dependent on individual needs and abilities.15,16 For athletes in-season, we recommend a brief period of NWB for 1 to 2 weeks followed by toe-touch weight-bearing in a tall CAM boot for 2 to 4 weeks. After 4 weeks, patients begin gentle exercises on a stationary bike and pool therapy to reduce impact on the fracture site. Low-intensity pulsed ultrasound bone stimulators (Exogen, Bioventus) are frequently used directly over fracture site throughout the postoperative protocol as an adjuvant therapy. If clinically nontender over the fracture site, patients are allowed to begin running in modified protective shoe wear 4 weeks after surgery with an average RTP of 6 to 8 weeks. RTP is determined clinically, as radiographic union may not be evident for 12 to 16 weeks. Useful custom orthoses include turf toe plates with a cushioned lateral column and lateral heel wedge if hindfoot varus is present preoperatively.10 The solid intramedullary screw is left in place permanently.
In our experience, we have found the average re-fracture and nonunion rate to be approximately 8% across all athletes. Our observation that union rates do not appear to be related to RTP times suggests that underlying biology such as Vitamin D deficiency may play a larger role in union rates than previously thought. We have found that most Jones re-fractures occur in the first year after the initial injury, but can occur up to 2.5 years afterwards as well.14 For the management of symptomatic re-fractures and nonunions, the previous screw must be first removed. This can be difficult if the screw is bent or broken, and may require a lateral corticotomy of the metatarsal.
After hardware removal, we advocate open bone grafting of the fracture site using bone from the iliac crest retrieved with a small, percutaneous trephine. Re-fixation should be achieved using a larger, solid screw and postoperative adjuvants may include bone stimulators, Vitamin D and calcium supplemention, and possible teriparatide use (Forteo, Eli Lilly), depending on individual patient profile. In a cohort of 21 elite athletes treated for Jones fracture revision surgery with screw exchange and bone grafting, we found that 100% of patients had computed tomography (CT) evidence of union, with an average RTP of 12.3 weeks.17
Lisfranc Injuries
Lisfranc injuries include any bony or ligamentous damage that involves the tarsometatarsal (TMT) joints. While axial loading of a fixed, plantarflexed foot has traditionally been thought of as the most common mechanism of Lisfranc injury, we have found that noncontact twisting injuries leading to Lisfranc disruption are actually more common among NFL players. This mechanism is similar to noncontact turf toe and results in a purely ligamentous injury. We have found this to be particularly true in the case of defensive ends engaged with offensive linemen in which no axial loading or contact of the foot occurs. Clinically, patients often have painful weight-bearing, inability to perform a single limb heel rise, plantar ecchymosis, and swelling and point tenderness across the bases of the 1st and 2nd metatarsals.
It is critical to obtain comparison weight-bearing radiographs of both feet during initial work-up to look for evidence of instability. Subtle radiographic findings of Lisfranc injury include a bony “fleck” sign, compression fracture of the cuboid, and diastasis between the base of the 1st and 2nd metatarsals and/or medial and middle cuneiforms (Figures 3A, 3B).
The goal of surgical intervention is to obtain and maintain anatomic reduction of all unstable joints in order to restore a normal foot posture. One of the difficulties with Lisfranc injuries is that there are no exact diastasis parameters and individuals should be treated based on symptoms, functional needs, and degree of instability. It has been shown that 5 mm of displacement can have good long-term clinical results in select cases without surgery.18 For surgery, we recommend open reduction to remove interposed soft tissue debris and directly assess the articular surfaces (Figures 4A-4D).
Proximal-medial column Lisfranc injury variants are increasingly common among football players.20 In these injuries, the force of injury extends through the intercuneiform joint and exits out the naviculocuneiform joint, thus causing instability at multiple joints and an unstable 1st ray. Patients often have minimal clinical findings and normal radiographs and stress radiographs. MRI of the foot often reveals edema at the naviculocuneiform joint. Often patients fail to improve with nonoperative immobilization with continued inability to push off from the hallux. Unrecognized or untreated instability will lead to rapid deterioration of the naviculocuneiform joint. Surgical intervention requires a homerun screw and intercuneiform screw. We do not recommend primary arthrodesis in athletes due to significant risk of malunion and nonunion unless severe articular damage is present.
Patients are typically kept NWB in a splint for 2 weeks after surgery followed by NWB in a tall CAM from 3 to 4 weeks postoperative. Progressive weight-bearing and ROM exercises are initiated from 4 to 8 weeks, followed by return to accommodative shoe wear from 10 to 12 weeks. Hardware removal is performed 4 to 6 months after surgery, typically in the off-season to allow for 6 to 8 weeks or protected recovery afterwards. Premature hardware removal can lead to loss of reduction, particularly at the intercuneiform joints. All hardware crossing the TMT joints should be removed, while the homerun screw can be left in place in addition to the intercuneiform screw. RTP in football typically occurs 6 to 7 months after surgery. Final functional outcome is related to the adequacy of initial reduction and severity of the initial injury.21
Syndesmotic Disruption
Syndesmotic injuries comprise 1% to 18% of ankle sprains in the general population, but occur at much higher rates in football due to the increased rotation forces placed on the ankle during cutting and tackling. RTP after syndesmotic injury often takes twice as long when compared to isolated lateral ankle ligamentous injury.22 Missed injuries are common and if not treated properly can lead to chronic ankle instability and posttraumatic ankle arthritis.23 Syndesmotic injury can occur in isolation or with concomitant adjacent bony, cartilaginous, or ligamentous injuries. Therefore, clinical examination and imaging work-up are critical to successful management.
Syndesmotic injuries often result from an external rotation force applied to a hyperdorsiflexed ankle while the foot is planted. This mechanism causes the fibula to externally rotate while translating posteriorly and laterally, resulting in rupture of the anterior inferior tibiofibular ligament (AITFL) first, followed by the deep deltoid ligament, interosseous ligament (IOL), and lastly posterior talofibular ligament.24 Most syndesmotic injuries involve rupture of only the AITFL and IOL.25 Multiple clinical stress tests have been designed to assess syndesmotic stability, including the squeeze test, external rotation stress test, crossed-leg test, and fibula-translation test.26-29 However, no physical examination maneuver has been shown to reliably predict the presence or degree of syndesmotic injury and therefore imaging studies are necessary.30
Initial imaging should include standing radiographs of the affected ankle. An increase in the medial clear space between the medial malleolus and talus can occur with a combined syndesmotic and deltoid disruption. In the case of subtle syndesmotic injuries, contralateral comparison weight-bearing radiographs are recommended. CT and MRI can provide additional information, but these static imaging tests cannot identify instability. Fluoroscopic stress evaluation is beneficial but has a high false-negative rate in low-grade injuries and may not detect partial rupture of the AITFL and IOL.31 It has been shown that malrotation of as much as 30° of external rotation can occur if relying on intraoperative fluoroscopy alone.32 It has been our practice to recommend surgical reduction and stabilization for any syndesmotic injury with documented diastasis or instability seen on imaging and/or arthroscopy.
Nonoperative treatment is indicated for truly stable grade I syndesmotic injuries. This involves rest and immobilization followed by a progressive rehabilitation program consisting of stretching, strengthening, and proprioceptive exercises.33 After 1 week of protected weight-bearing in a cast or tall CAM boot, progression to full weight-bearing should occur over the following week. Active-assisted ankle ROM exercises and light proprioceptive training should then be initiated followed by sport-specific exercises 2 to 3 weeks after injury.
Arthroscopy can be a valuable diagnostic tool in the setting of subtle syndesmotic injury with negative radiographs, positive MRI for edema, and a protracted recovery course with vague pain (Figures W5A-W5E).
Implants are placed above the true syndesmotic joint (at least 15 mm above the tibial plafond) angled 30° posterior to anterior to follow the normal relationship of the fibula to the distal tibia in the incisura. Typically 2 suture-buttons are used, with the devices placed in a divergent fashion. We highly recommend the use of a fibular buttress plate with button placement in individuals returning to contact activity. This construct increases surface area distribution while preventing stress risers and the risk of fibula fractures. In a cadaver model with deliberate syndesmotic malreduction, suture-button stabilization resulted in decreased postoperative displacement as opposed to conventional screw fixation.34 Therefore, dynamic syndesmotic fixation may help to decrease the negative sequelae of iatrogenic clamp malreduction. Postoperative rehabilitation involves NWB in a cast or tall CAM boot for 4 weeks followed by ankle ROM exercises and progressive weight-bearing and physical therapy. Patients are transitioned to a lace-up ankle brace and athletic shoe from 6 to 12 weeks postoperative with increasing activity. Running and jumping is permitted 4 months after surgery with RTP typically at 6 to 7 months. Athletes who have had surgical stabilization for documented instability without any diastasis may engage in a more rapid recovery and RTP as symptoms and function allow.
Deltoid Complex Avulsion
Missed or neglected deltoid ligament injuries can lead to progressive chondral injury and joint degeneration. These injuries are often subtle and difficult to diagnose. An inability to perform a single limb heel rise, persistent pain with activity, and lack of normal functional improvement despite appropriate care are indicators of subtle ligament instability. These injuries often require an examination under anesthesia with combined ankle arthroscopy. Valgus stress testing of the ankle while directly visualizing the deltoid ligament from the anterolateral portal can reveal medial laxity in addition to potential osteochondral lesions along the anterolateral talar dome.
In American football players, we have observed that infolding and retraction of an avulsed superficial deltoid ligament complex after an ankle fracture, Maisonneuve injury, or severe high ankle sprain can be a source of persistent increased medial clear space, malreduction, and postoperative pain and medial instability. We have found that there is often complete avulsion of the superficial deltoid complex off the proximal aspect of the medial malleolus during high-energy ankle fractures in football players that is amenable to direct repair to bone (Figures W6A-W6E).
During surgical repair, an incision is made along the anterior aspect of the medial malleolus and the superficial deltoid ligament complex can often be found flipped and interposed in the medial gutter. A rongeur is used to create a bleeding cancellous bone surface for soft-tissue healing and 1 to 2 suture anchors are used to repair and imbricate the deltoid ligament complex back to the medial malleolus. The goal of these sutures is to repair the tibionavicular and tibial spring ligaments back to the medial malleolus. We believe that superficial deltoid complex avulsion during high-energy ankle fractures is a distinct injury pattern that should be recognized and may benefit from primary open repair.
We currently open explore every deltoid ligament complex in athletes with unstable syndesmotic injuries, as we believe that deltoid avulsion injuries are underrecognized and do not heal in an anatomic fashion if left alone. Postoperative recovery follows the same immobilization, progressive weight-bearing, and physical therapy protocol as that for syndesmotic disruption.
Achilles Ruptures
Acute midsubstance Achilles tendon ruptures are an increasingly common injury in patients 30 to 50 years of age, with more than 50% of all injuries occurring during basketball.36,37 Among NFL players, we have found that Achilles ruptures tend to occur at a higher rate during training camp, when athletes are deconditioned and quickly returning to explosive push-off activities. Physical examination should include a Thompson test, palpation of a gap within the tendon, and evaluation of resting ankle dorsiflexion in the affected extremity in the prone position with the knees bent. Lateral radiographs should be analyzed for the presence of a bony avulsion fragment indicative of an insertional avulsion injury or midsubstance calcium deposition reflecting chronic Achilles tendinosis, as both of these conditions will change surgical management. MRI is not recommended with acute midsubstance ruptures but may be helpful in the case of chronic ruptures or more proximal tears of the musculotendinous junction.
The management of acute midsubstance Achilles tendon ruptures is controversial, with no general consensus in the literature regarding nonoperative treatment, surgical repair, and ideal repair technique.36,38-42 American Academy of Orthopaedic Surgeons clinical practice guidelines report moderate evidence that nonoperative treatment of Achilles tendon ruptures has lower wound healing complications but higher rates of re-rupture.38,39 Additionally, limited incision approaches have been found to have fewer overall complications compared with traditional open repair. In an effort to reduce the incidence of postoperative wound complications while improving functional recovery, modern repair techniques focus on a limited incision repair using percutaneous suture insertion and management (PARS Achilles Jig System, Arthrex).36 The limited incision technique utilizes a 2-cm transverse incision and non-disposable jig with divergent needle passes and locking suture fixation options to secure and fixate both tendon ends with minimal dissection of skin, subcutaneous tissue, and paratenon. Limited incision repair is ideally performed within 2 weeks of the injury to ensure that both tendon ends are easy to identify, mobilize, and repair. An open repair is generally recommended for midsubstance ruptures more than 4 weeks old and cases of insertional rupture and Achilles tendinopathy.
In a cohort of 9 NFL players treated for midsubstance Achilles ruptures using the PARS technique, we found no re-ruptures, no wound complications, and no sural nerve issues after surgery.43 A comparative review of 270 cases of operatively treated Achilles tendon ruptures (101 PARS, 169 traditional open repair) showed that the PARS group had significantly shorter operative times and a higher number of patients able to return to baseline physical activities by 5 months compared to open repair.36 Although not statistically significant, the overall PARS complication rate was 5% while the open complication rate was 11%. The PARS group had no cases of sural neuritis or deep infection requiring reoperation. We currently use a limited incision technique for all acute midsubstance Achilles ruptures in athletes regardless of sport, patient size, or position played.
During surgery, a 2-cm transverse incision is made over the gap in the Achilles tendon and dissection is carried down to the rupture site with minimal manipulation of the skin (Figures 5A-5F).
A key aspect of postoperative recovery is avoiding excessive ankle dorsiflexion while the tendon is healing during the first 4 weeks after surgery, as this can lead to an elongated tendon with loss of push-off strength. Patients are kept in a plantarflexion splint NWB for 2 weeks after surgery. If the incision is healed at 2 weeks, sutures are removed and patients are transitioned into a NWB tall CAM boot for 2 weeks with gentle ankle ROM exercises. If there is any concern regarding wound healing status, sutures are maintained for an additional 1 to 2 weeks.
From 4 to 8 weeks after surgery, progressive weight-bearing with continued ankle ROM exercises is initiated with peel-away heel lifts (~2 cm thick total, 3 layers). Each layer of the heel lift is gradually removed as pain allows every 2 to 3 days with the goal of being full weight-bearing with the foot flat at 6 weeks postoperative. Physical therapy focusing on ankle ROM and gentle Achilles stretching and strengthening is also started 6 weeks after surgery. From 8 to 12 weeks postoperative, patients are transitioned out of the tall CAM boot into normal, accommodative shoe wear with full weight-bearing. We avoid ankle dorsiflexion past neutral until 12 weeks after surgery, as overlengthening of the Achilles complex and the subsequent loss of push-off power can be devastating to running athletes. Activity levels are increased as tolerated, with no running or jumping from 12 to 16 weeks with full release to all activities after 16 weeks. RTP often takes 5 to 6 months after surgery, depending on the position played.
Am J Orthop. 2016;45(6):358-367. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.
1. Canale ST, Cantler ED Jr, Sisk TD, Freeman BL 3rd. A chronicle of injuries of an American intercollegiate football team. Am J Sports Med. 1981;9(6):384-389.2. Robey JM, Blyth CS, Mueller FO. Athletic injuries. Application of epidemiologic methods. JAMA. 1971;217(2):184-189.
3. Saal JA. Common American football injuries. Sports Med. 1991;12(2):132-147.
4. Thompson N, Halpern B, Curl WW, et al. High school football injuries: evaluation. Am J Sports Med. 1987;15(2):117-124.
5. Kaplan LD, Jost PW, Honkamp N, Norwig J, West R, Bradley JP. Incidence and variance of foot and ankle injuries in elite college football players. Am J Orthop. 2011;40(1):40-44.
6. DeLee JC, Farney WC. Incidence of injury in Texas high school football. Am J Sports Med. 1992;20(5):575-580.
7. Brophy RH, Barnes R, Rodeo SA, Warren RF. Prevalence of musculoskeletal disorders at the NFL Combine--trends from 1987 to 2000. Med Sci Sports Exerc. 2007;39(1):22-27.
8. Bowers KD Jr, Martin RB. Turf-toe: a shoe-surface related football injury. Med Sci Sports. 1976;8(2):81-83.
9. McCormick JJ, Anderson RB. Turf toe: anatomy, diagnosis, and treatment. Sports Health. 2010;2(6):487-494.
10. Raikin SM, Slenker N, Ratigan B. The association of a varus hindfoot and fracture of the fifth metatarsal metaphyseal-diaphyseal junction: the Jones fracture. Am J Sports Med. 2008;36(7):1367-1372.
11. Title CI, Katchis SD. Traumatic foot and ankle injuries in the athlete. Orthop Clin North Am. 2002;33(3):587-598.
12. Quill GE Jr. Fractures of the proximal fifth metatarsal. Orthop Clin North Am. 1995;26(2):353-361.
13. Nunley JA, Glisson RR. A new option for intramedullary fixation of Jones fractures: the Charlotte Carolina Jones Fracture System. Foot Ankle Int. 2008;29(12):1216-1221.
14. Lareau CR, Hsu AR, Anderson RB. Return to play in National Football League players after operative Jones fracture treatment. Foot Ankle Int. 2016;37(1):8-16.
15. Larson CM, Almekinders LC, Taft TN, Garrett WE. Intramedullary screw fixation of Jones fractures. Analysis of failure. Am J Sports Med. 2002;30(1):55-60.
16. Portland G, Kelikian A, Kodros S. Acute surgical management of Jones’ fractures. Foot Ankle Int. 2003;24(11):829-833.
17. Hunt KJ, Anderson RB. Treatment of Jones fracture nonunions and refractures in the elite athlete: outcomes of intramedullary screw fixation with bone grafting. Am J Sports Med. 2011;39(9):1948-1954.
18. Nunley JA, Vertullo CJ. Classification, investigation, and management of midfoot sprains: Lisfranc injuries in the athlete. Am J Sports Med. 2002;30(6):871-878.
19. Alberta FG, Aronow MS, Barrero M, Diaz-Doran V, Sullivan RJ, Adams DJ. Ligamentous Lisfranc joint injuries: a biomechanical comparison of dorsal plate and transarticular screw fixation. Foot Ankle Int. 2005;26(6):462-473.
20. Ardoin GT, Anderson RB. Subtle Lisfranc injury. Tech Foot Ankle Surg. 2010;9(3):100-106.
21. Kuo RS, Tejwani NC, Digiovanni CW, et al. Outcome after open reduction and internal fixation of Lisfranc joint injuries. J Bone Joint Surg Am. 2000;82-A(11):1609-1618.
22. Wright RW, Barile RJ, Surprenant DA, Matava MJ. Ankle syndesmosis sprains in national hockey league players. Am J Sports Med. 2004;32(8):1941-1945.
23. Williams GN, Jones MH, Amendola A. Syndesmotic ankle sprains in athletes. Am J Sports Med. 2007;35(7):1197-1207.
24. Beumer A, Valstar ER, Garling EH, et al. Effects of ligament sectioning on the kinematics of the distal tibiofibular syndesmosis: a radiostereometric study of 10 cadaveric specimens based on presumed trauma mechanisms with suggestions for treatment. Acta Orthop. 2006;77(3):531-540.
25. McCollum GA, van den Bekerom MP, Kerkhoffs GM, Calder JD, van Dijk CN. Syndesmosis and deltoid ligament injuries in the athlete. Knee Surg Sports Traumatol Arthrosc. 2013;21(6):1328-1337.
26. Boytim MJ, Fischer DA, Neumann L. Syndesmotic ankle sprains. Am J Sports Med. 1991;19(3):294-298.
27. Nussbaum ED, Hosea TM, Sieler SD, Incremona BR, Kessler DE. Prospective evaluation of syndesmotic ankle sprains without diastasis. Am J Sports Med. 2001;29(1):31-35.
28. Kiter E, Bozkurt M. The crossed-leg test for examination of ankle syndesmosis injuries. Foot Ankle Int. 2005;26(2):187-188.
29. Beumer A, van Hemert WL, Swierstra BA, Jasper LE, Belkoff SM. A biomechanical evaluation of clinical stress tests for syndesmotic ankle instability. Foot Ankle Int. 2003;24(4):358-363.
30. Amendola A, Williams G, Foster D. Evidence-based approach to treatment of acute traumatic syndesmosis (high ankle) sprains. Sports Med Arthrosc. 2006;14(4):232-236.
31. Beumer A, Valstar ER, Garling EH, et al. External rotation stress imaging in syndesmotic injuries of the ankle: comparison of lateral radiography and radiostereometry in a cadaveric model. Acta Orthop Scand. 2003;74(2):201-205.
32. Marmor M, Hansen E, Han HK, Buckley J, Matityahu A. Limitations of standard fluoroscopy in detecting rotational malreduction of the syndesmosis in an ankle fracture model. Foot Ankle Int. 2011;32(6):616-622.
33. Williams GN, Allen EJ. Rehabilitation of syndesmotic (high) ankle sprains. Sports Health. 2010;2(6):460-470.
34. Westermann RW, Rungprai C, Goetz JE, Femino J, Amendola A, Phisitkul P. The effect of suture-button fixation on simulated syndesmotic malreduction: a cadaveric study. J Bone Joint Surg Am. 2014;96(20):1732-1738.
35. Hsu AR, Lareau CR, Anderson RB. Repair of acute superficial deltoid complex avulsion during ankle fracture fixation in National Football League players. Foot Ankle Int. 2015;36(11):1272-1278.
36. Hsu AR, Jones CP, Cohen BE, Davis WH, Ellington JK, Anderson RB. Clinical outcomes and complications of percutaneous Achilles repair system versus open technique for acute achilles tendon ruptures. Foot Ankle Int. 2015;36(11):1279-1286.
37. Raikin SM, Garras DN, Krapchev PV. Achilles tendon injuries in a United States population. Foot Ankle Int. 2013;34(4):475-480.
38. Chiodo CP, Glazebrook M, Bluman EM, et al. American Academy of Orthopaedic Surgeons clinical practice guideline on treatment of achilles tendon rupture. J Bone Joint Surg Am. 2010;92(14):2466-2468.
39. Chiodo CP, Glazebrook M, Bluman EM, et al. Diagnosis and treatment of acute achilles tendon rupture. J Am Acad Orthop Surg. 2010;18(8):503-510.
40. Khan RJ, Fick D, Keogh A, Crawford J, Brammar T, Parker M. Treatment of acute achilles tendon ruptures. A meta-analysis of randomized, controlled trials. J Bone Joint Surg Am. 2005;87(10):2202-2210.
41. Renninger CH, Kuhn K, Fellars T, Youngblood S, Bellamy J. Operative and nonoperative management of achilles tendon ruptures in active duty military population. Foot Ankle Int. 2016;37(3):269-273.
42. Khan RJ, Carey Smith RL. Surgical interventions for treating acute achilles tendon ruptures. Cochrane Database Syst Rev. 2010;(9):CD003674.
43. McCullough KA, Shaw CM, Anderson RB. Mini-open repair of achilles rupture in the national football league. J Surg Orthop Adv. 2014;23(4):179-183.
1. Canale ST, Cantler ED Jr, Sisk TD, Freeman BL 3rd. A chronicle of injuries of an American intercollegiate football team. Am J Sports Med. 1981;9(6):384-389.2. Robey JM, Blyth CS, Mueller FO. Athletic injuries. Application of epidemiologic methods. JAMA. 1971;217(2):184-189.
3. Saal JA. Common American football injuries. Sports Med. 1991;12(2):132-147.
4. Thompson N, Halpern B, Curl WW, et al. High school football injuries: evaluation. Am J Sports Med. 1987;15(2):117-124.
5. Kaplan LD, Jost PW, Honkamp N, Norwig J, West R, Bradley JP. Incidence and variance of foot and ankle injuries in elite college football players. Am J Orthop. 2011;40(1):40-44.
6. DeLee JC, Farney WC. Incidence of injury in Texas high school football. Am J Sports Med. 1992;20(5):575-580.
7. Brophy RH, Barnes R, Rodeo SA, Warren RF. Prevalence of musculoskeletal disorders at the NFL Combine--trends from 1987 to 2000. Med Sci Sports Exerc. 2007;39(1):22-27.
8. Bowers KD Jr, Martin RB. Turf-toe: a shoe-surface related football injury. Med Sci Sports. 1976;8(2):81-83.
9. McCormick JJ, Anderson RB. Turf toe: anatomy, diagnosis, and treatment. Sports Health. 2010;2(6):487-494.
10. Raikin SM, Slenker N, Ratigan B. The association of a varus hindfoot and fracture of the fifth metatarsal metaphyseal-diaphyseal junction: the Jones fracture. Am J Sports Med. 2008;36(7):1367-1372.
11. Title CI, Katchis SD. Traumatic foot and ankle injuries in the athlete. Orthop Clin North Am. 2002;33(3):587-598.
12. Quill GE Jr. Fractures of the proximal fifth metatarsal. Orthop Clin North Am. 1995;26(2):353-361.
13. Nunley JA, Glisson RR. A new option for intramedullary fixation of Jones fractures: the Charlotte Carolina Jones Fracture System. Foot Ankle Int. 2008;29(12):1216-1221.
14. Lareau CR, Hsu AR, Anderson RB. Return to play in National Football League players after operative Jones fracture treatment. Foot Ankle Int. 2016;37(1):8-16.
15. Larson CM, Almekinders LC, Taft TN, Garrett WE. Intramedullary screw fixation of Jones fractures. Analysis of failure. Am J Sports Med. 2002;30(1):55-60.
16. Portland G, Kelikian A, Kodros S. Acute surgical management of Jones’ fractures. Foot Ankle Int. 2003;24(11):829-833.
17. Hunt KJ, Anderson RB. Treatment of Jones fracture nonunions and refractures in the elite athlete: outcomes of intramedullary screw fixation with bone grafting. Am J Sports Med. 2011;39(9):1948-1954.
18. Nunley JA, Vertullo CJ. Classification, investigation, and management of midfoot sprains: Lisfranc injuries in the athlete. Am J Sports Med. 2002;30(6):871-878.
19. Alberta FG, Aronow MS, Barrero M, Diaz-Doran V, Sullivan RJ, Adams DJ. Ligamentous Lisfranc joint injuries: a biomechanical comparison of dorsal plate and transarticular screw fixation. Foot Ankle Int. 2005;26(6):462-473.
20. Ardoin GT, Anderson RB. Subtle Lisfranc injury. Tech Foot Ankle Surg. 2010;9(3):100-106.
21. Kuo RS, Tejwani NC, Digiovanni CW, et al. Outcome after open reduction and internal fixation of Lisfranc joint injuries. J Bone Joint Surg Am. 2000;82-A(11):1609-1618.
22. Wright RW, Barile RJ, Surprenant DA, Matava MJ. Ankle syndesmosis sprains in national hockey league players. Am J Sports Med. 2004;32(8):1941-1945.
23. Williams GN, Jones MH, Amendola A. Syndesmotic ankle sprains in athletes. Am J Sports Med. 2007;35(7):1197-1207.
24. Beumer A, Valstar ER, Garling EH, et al. Effects of ligament sectioning on the kinematics of the distal tibiofibular syndesmosis: a radiostereometric study of 10 cadaveric specimens based on presumed trauma mechanisms with suggestions for treatment. Acta Orthop. 2006;77(3):531-540.
25. McCollum GA, van den Bekerom MP, Kerkhoffs GM, Calder JD, van Dijk CN. Syndesmosis and deltoid ligament injuries in the athlete. Knee Surg Sports Traumatol Arthrosc. 2013;21(6):1328-1337.
26. Boytim MJ, Fischer DA, Neumann L. Syndesmotic ankle sprains. Am J Sports Med. 1991;19(3):294-298.
27. Nussbaum ED, Hosea TM, Sieler SD, Incremona BR, Kessler DE. Prospective evaluation of syndesmotic ankle sprains without diastasis. Am J Sports Med. 2001;29(1):31-35.
28. Kiter E, Bozkurt M. The crossed-leg test for examination of ankle syndesmosis injuries. Foot Ankle Int. 2005;26(2):187-188.
29. Beumer A, van Hemert WL, Swierstra BA, Jasper LE, Belkoff SM. A biomechanical evaluation of clinical stress tests for syndesmotic ankle instability. Foot Ankle Int. 2003;24(4):358-363.
30. Amendola A, Williams G, Foster D. Evidence-based approach to treatment of acute traumatic syndesmosis (high ankle) sprains. Sports Med Arthrosc. 2006;14(4):232-236.
31. Beumer A, Valstar ER, Garling EH, et al. External rotation stress imaging in syndesmotic injuries of the ankle: comparison of lateral radiography and radiostereometry in a cadaveric model. Acta Orthop Scand. 2003;74(2):201-205.
32. Marmor M, Hansen E, Han HK, Buckley J, Matityahu A. Limitations of standard fluoroscopy in detecting rotational malreduction of the syndesmosis in an ankle fracture model. Foot Ankle Int. 2011;32(6):616-622.
33. Williams GN, Allen EJ. Rehabilitation of syndesmotic (high) ankle sprains. Sports Health. 2010;2(6):460-470.
34. Westermann RW, Rungprai C, Goetz JE, Femino J, Amendola A, Phisitkul P. The effect of suture-button fixation on simulated syndesmotic malreduction: a cadaveric study. J Bone Joint Surg Am. 2014;96(20):1732-1738.
35. Hsu AR, Lareau CR, Anderson RB. Repair of acute superficial deltoid complex avulsion during ankle fracture fixation in National Football League players. Foot Ankle Int. 2015;36(11):1272-1278.
36. Hsu AR, Jones CP, Cohen BE, Davis WH, Ellington JK, Anderson RB. Clinical outcomes and complications of percutaneous Achilles repair system versus open technique for acute achilles tendon ruptures. Foot Ankle Int. 2015;36(11):1279-1286.
37. Raikin SM, Garras DN, Krapchev PV. Achilles tendon injuries in a United States population. Foot Ankle Int. 2013;34(4):475-480.
38. Chiodo CP, Glazebrook M, Bluman EM, et al. American Academy of Orthopaedic Surgeons clinical practice guideline on treatment of achilles tendon rupture. J Bone Joint Surg Am. 2010;92(14):2466-2468.
39. Chiodo CP, Glazebrook M, Bluman EM, et al. Diagnosis and treatment of acute achilles tendon rupture. J Am Acad Orthop Surg. 2010;18(8):503-510.
40. Khan RJ, Fick D, Keogh A, Crawford J, Brammar T, Parker M. Treatment of acute achilles tendon ruptures. A meta-analysis of randomized, controlled trials. J Bone Joint Surg Am. 2005;87(10):2202-2210.
41. Renninger CH, Kuhn K, Fellars T, Youngblood S, Bellamy J. Operative and nonoperative management of achilles tendon ruptures in active duty military population. Foot Ankle Int. 2016;37(3):269-273.
42. Khan RJ, Carey Smith RL. Surgical interventions for treating acute achilles tendon ruptures. Cochrane Database Syst Rev. 2010;(9):CD003674.
43. McCullough KA, Shaw CM, Anderson RB. Mini-open repair of achilles rupture in the national football league. J Surg Orthop Adv. 2014;23(4):179-183.
Concussions in American Football
Football is an important component of American culture, with approximately 3 million youth athletes, 1.1 million high school athletes, and 100,000 college athletes participating each year.1 Participation in football provides athletes with physical, social, psychological, and academic benefits. Despite these benefits, widespread focus has been placed on the safety of football due to the risk for sport-related concussion (SRC) and potentially long-term effects; however, little recognition has been given to the advancements in concussion management across time and occurrence of concussions during most life activities. Although it is reasonable for concerns to be presented, it is important to better understand SRC and the current factors leading to prolonged recoveries, increased risk for injury, and potentially long-term effects.
What Is a Concussion?
Concussions occur after sustaining direct or indirect injury to the head or other parts of the body, as long as the injury force is transmitted to the head. Athletes often experience physical, cognitive, emotional, and sleep-related symptoms post-concussion secondary to an “energy crisis” within the brain.2 The energy crisis occurs as the result of transient neurological dysfunction triggered by changes in the brain (eg, release of neurotransmitters, impaired axonal function).2,3 Concussion is undetectable with traditional imaging; however, advanced imaging techniques (eg, diffuse tensor imaging) have shown progress in assessing axonal injury.3 Symptom duration post-concussion is highly variable due to individual differences; a recent study showed recovery took 3 to 4 weeks for memory and symptoms.4,5
Previous Concussion Management
Identification techniques and return-to-play guidelines for concussion have significantly changed across time. In the past, concussion grading scales were utilized for diagnosis and return to play was possible within the same contest.6,7 It has since been recognized that initial concussion severity makes it difficult to predict recovery.3 For example, research revealed memory decline and increased symptoms 36 hours post-injury for athletes with a grade 1 concussion (ie, transient confusion, no loss of consciousness, concussion symptoms or mental status changes that resolve within 15 minutes of injury) compared to baseline.7 Another study found duration of mental status changes to be related to slower symptom resolution and memory impairment 36 hours to 7 days post-injury.6 Consequently, return to play within the same contest was likely too liberal. Guidelines today recommend immediate removal from play with suspected SRC. Nevertheless, the “play through pain” culture has led athletes to continue playing after SRC, contributing to prolonged recoveries and potentially long-term effects.
Current Concussion Management: Continued Concerns and Areas of Improvement
Despite increased awareness of concussions, recent estimates revealed high rates (ie, 27:1 ratio for general players) of underreporting in college football, particularly amongst offensive linemen.8 Researchers have studied recovery implications for remaining in play, with one study revealing a 2.2 times greater risk for prolonged recovery in college athletes with delayed vs immediate removal.9 Another similar study discovered an 8.8 times greater risk for prolonged recovery in adolescent and young adult athletes not removed vs removed from play.10 Further analysis found remaining in play to be the greatest risk factor for prolonged recovery compared to other previously studied risk factors (eg, age, sex, posttraumatic migraine).10 Additionally, significant differences in neurocognitive data were seen between the “removed” and “not removed” groups for verbal memory, visual memory, processing speed, and reaction time at 1 to 7 days and 8 to 30 days.10 The recovery implications of remaining in play and the additional risk for second impact syndrome (SIS), or repeat concussion when recovering from another injury, emphasizes the need for further education efforts amongst athletes to encourage immediate reporting of injury.11
Sideline Assessment
Sideline assessment has become a vital component of concussion management to rule out concussion and/or significant injury other than concussion. Assessment should include observation, cognitive/balance testing, neurologic examination, and possible exertion testing to ensure a comprehensive evaluation of all areas of potential dysfunction.12 Indications for emergency department evaluation include suspicion for cervical spine injury, intracranial hemorrhage, or skull fracture as well as prolonged loss of consciousness, high-risk mechanisms, posttraumatic seizure(s), and/or significant worsening of symptoms.12
Observation
On the sideline, it is important to identify any immediate signs of injury (ie, loss of consciousness, anterograde/retrograde amnesia, and disorientation/confusion). Since immediate signs are not always present, it is important to be aware of the most commonly reported symptoms, including headache, difficulty concentrating, fatigue, drowsiness, and dizziness.13 If symptoms are not reported by the athlete, balance problems, lack of coordination, increased emotionality, and difficulty following instructions may be observed during play.12
On-Field Assessment
Cognitive and balance testing are essential in determining if an athlete has sustained a concussion. Immediate declines in memory, concentration abilities, and balance abilities are common. Given limitations in administering long testing batteries on the sideline, brief standardized tests such as the Standardized Assessment of Concussion (SAC), Balance Error Scoring System (BESS), and Sport Concussion Assessment Tool (SCAT) are commonly utilized. Identification of cognitive and/or balance abnormalities can help the athlete recognize deficits following injury.12 Balance problems are experienced due to abnormalities in sensory organization and generally resolve during the acute recovery period.14,15 Cognitive difficulties typically persist longer than balance problems, though duration varies widely.
Neurologic Evaluation
A neurologic evaluation including cranial nerve testing and evaluation of motor-sensory function (ie, assessment for the strength and sensation of upper and lower extremities) is important to identify focal deficits (ie, sensation changes, loss of fine motor control) indicative of serious intracranial pathology.12 Additionally, clinicians have suggested inclusion of vestibular and oculomotor assessments due to frequent dysfunction post-concussion.12,15,16 Examination of the vestibular/oculomotor systems through tools such as the Vestibular/Ocular Motor Screening (VOMS) assessment (assesses both the vestibular and oculomotor systems) and King-Devick Test (primarily assesses saccadic eye movements) can elicit symptoms that may not present immediately. If assessment appears normal, exertion testing can be utilized to determine if symptoms are provoked through physical exercise that should include cardio, dynamic, and sport-specific activities to stress the vestibular system.12
Risk Factors for Injury and Prolonged Recovery
Medical professionals must consider the presence of risk factors when managing concussion in order to make appropriate treatment recommendations and return-to-play decisions. Research has demonstrated the role of female gender, learning disability, attention-deficit/hyperactivity disorder, psychiatric history, young age, motion sickness, sleep problems, somatization, concussion history, on-field dizziness, posttraumatic migraine, and fogginess in increased risk for injury and/or prolonged recovery.17-25 Additionally, athletes with ongoing symptoms from a previous injury are at risk for sustaining another injury.
Acute Home Concussion Management
Although strict rest has been recommended post-concussion, recent research evaluating strict rest vs usual care for adolescents revealed greater symptom reports and longer recovery periods for the strict rest group.26 Based on these findings and emphasis for regulation within the migraine literature (due to the common pathophysiology between migraine and concussion27), we recommend that athletes follow a regulated daily schedule post-concussion including: 1) regular sleep-wake schedule with avoidance of naps, 2) regular meals, 3) adequate fluid hydration, 4) light noncontact physical activity (ie, walking, with progressions recommended by a physician), and 5) stress management techniques. Use of these strategies immediately can help in preventing against increased symptoms and stress, and decreases the need for medication in select cases. Additionally, over-the-counter medications should be limited to 2 to 3 doses per week to avoid rebound headaches.28
In-Office Concussion Management
Athletes diagnosed with SRC will experience different symptoms based on the injury mechanism, risk factors, and management approach. Comprehensive evaluation should include assessment of risk factors, injury details, symptoms, neurocognitive functioning, vestibular/oculomotor dysfunction, tolerance of physical exertion, balance functioning, and cervical spine integrity (if necessary).29,30 Due to individual differences and the heterogeneous symptom profiles, concussion management must move beyond a “one size fits all” approach to avoid nonspecific treatment strategies and consequently prolonged recoveries.29 Clinicians and researchers at University of Pittsburgh Medical Center have identified 6 concussion clinical profiles (ie, vestibular, ocular, posttraumatic migraine, cervical, anxiety/mood, and cognitive/fatigue) that are generally identifiable 48 hours after injury.29,30 Identification of the clinical profile(s) through a comprehensive evaluation guides the development of individualized treatment plans and targeted rehabilitation strategies.29,30
Vestibular. The vestibular system is responsible for stabilizing vision while the head moves and balance control.15 Athletes can experience central and/or peripheral vestibular dysfunction to include benign paroxysmal positional vertigo (BPPV), visual motion sensitivity, vestibular ocular reflex impairment, and balance impairment.30,31 Symptoms typically include dizziness, impaired balance, blurry vision, difficulty focusing, and environmental sensitivity.15,29,30 Potential treatment options include vestibular rehabilitation, exertion therapy, and school/work accommodations.
Ocular. The oculomotor system is responsible for control of eye movements. Athletes can experience many different posttraumatic vision changes, including convergence problems, eye-tracking difficulties, refractive error, difficulty with pursuits/saccades, and accommodation insufficiency. Symptoms typically include light sensitivity, blurred vision, double vision, headaches, fatigue, and memory difficulties.15,29,30 Potential treatment options include vision therapy, vestibular rehabilitation, and school/work accommodations.32
Posttraumatic Migraine. Headache, the most common post-concussion symptom, can persist and meet criteria for posttraumatic migraine (ie, unilateral headache with accompanying nausea and/or photophobia and phonophobia).29,30,33 Implementation of a routine schedule, daily physical activity, exertion therapy, pharmacologic intervention, and school/work accommodations are potential treatment options.
Cervical. The cervical spine can be injured during whiplash-type injuries. Therefore, determining the location, onset, and typical exacerbations of pain can be helpful in identifying cervical involvement.29,30 Symptoms typically include headaches, neck pain, numbness, and tingling. Evaluation and therapy by a certified physical therapist and pharmacologic intervention (eg, muscle relaxants) are potential treatment options. 29,30
Anxiety/Mood. Anxiety, or worry and fear about everyday situations, is common post-concussion and can sometimes be related to ongoing vestibular impairment. Symptoms typically include ruminative thoughts, avoidance of specific situations, hypervigilance, feelings of being overwhelmed, and difficulty falling asleep.29,30 Potential treatment options include implementation of a routine schedule, exposure to provocative situations, psychotherapy, pharmacologic intervention, and school/work accommodations.34
Cognitive/Fatigue. A global concussion factor (including cognitive, fatigue, and migraine symptoms) has been identified within 1 to 7 days of injury. Although this factor of symptoms generally resolves during the acute recovery period, it persists in select cases.13 Symptoms typically include fatigue, decreased energy levels, nonspecific headaches, potential sleep disruption, increased symptoms towards the end of the day, difficulty concentrating, and increased headache with cognitive activities.29,30,35 Routine schedule, daily physical activity, exertion therapy, pharmacologic intervention (eg, amantadine), and school/work accommodations are potential treatment options.30
Conclusion
Advancements in SRC management warrant change in the conversations regarding concussion in football. Specifically, conversations should address the current understanding of concussion and improvements in the safety of football through stricter concussion guidelines, detailed sideline evaluations, recognition of risk factors, improved acute management, and identification of concussion profiles that help to direct individualized treatment plans and targeted rehabilitation strategies. The biggest concerns related to concussions in football include underreporting of injury, premature return to play, and receiving routine rather than individualized treatment. Therefore, to further improve the safety of football and management of concussion it is essential that future efforts focus on the following 6 areas:
Education: Improved understanding of concussion is imperative to reducing poor outcomes and widespread concerns.
Immediate reporting: Reporting of concussion must be expected and encouraged through consistent responses by coaches to reduce underreporting and fear of reporting in athletes.
Prevention techniques: Athletes must be taught proper form and playing techniques to reduce the risk for concussion. Proper form and technique should be incentivized.
Targeted treatment: Individualized treatment plans and targeted rehabilitation strategies must be developed based on the identified clinical profile(s) to avoid nonspecific treatment recommendations.
Multidisciplinary treatment teams: Given the heterogeneous symptoms profiles and need for care provided by different medical specialties, multidisciplinary teams are essential.
Remain current: With the progress in understanding concussion, providers must remain vigilant of future advances in concussion management to further improve the safety of football.
Am J Orthop. 2016;45(6):352-356. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.
1. Dompier TP, Kerr ZY, Marshall SW, et al. Incidence of concussion during practice and games in youth, high school, and collegiate American football players. JAMA Pediatrics. 2015;169(7):659-665.
2. Giza C, Hovda D. The new neurometabolic cascade of concussion
3. Barkhoudarian G, Hovda DA, Giza CC. The molecular pathophysiology of concussive brain injury - an update. Phys Med Rehabil Clin N Am. 2016;27:373-393.
4. Henry L, Elbin R, Collins M, Marchetti G, Kontos A. Examining recovery trajectories after sport-related concussion with a multimodal clinical assessment approach. Neurosurgery. 2016;78(2):232-241.
5. McCrory P, Meeuwisse WH, Aubry M, et al. Consensus statement on concussion in sport: the 4th International Conference on Concussion in Sport held in Zurich, November 2012. Brit J Sports Med. 2013;47(5):250-258.
6. Lovell MR, Collins MW, Iverson GL, et al. Recovery from mild concussion in high school athletes. J Neurosurg. 2003;98(2):296-301.
7. Lovell MR, Collins MW, Iverson GL, Johnston KM, Bradley JP. Grade 1 or “ding” concussions in high school athletes. Am J Sports Med. 2004;32(1):47-54.
8. Baugh CM, Kroshus E, Daneshvar DH, Filali NA, Hiscox MJ, Glantz LH. Concussion management in United States college sports: compliance with National Collegiate Athletic Association concussion policy and areas for improvement. Am J Sports Med. 2015;43(1):47-56.
9. Asken BM, McCrea MA, Clugston JR, Snyder AR, Houck ZM, Bauer RM. “Playing through it”: Delayed reporting and removal from athletic activity after concussion predicts prolonged recovery. J Athl Train. 2016;51(4):329-335.
10. Elbin RJ, Sufrinko A, Schatz P, et al. Athletes that continue to play with concussion demonstrate worse recovery outcomes than athletes immediately removed from play. J Pediatr. In press.
11. Signoretti S, Lazzarino G, Tavazzi B, Vagnozzi R. The pathophysiology of concussion. PM R. 2011;3(10 Suppl 2):S359-S368.
12. Bloom J, Blount JG. Sideline evaluation of concussion. UpToDate. 2016. http://www.uptodate.com/contents/sideline-evaluation-of-concussion. Accessed July 13, 2016.
13. Kontos AP, Elbin RJ, Schatz P, et al. A revised factor structure for the post-concussion symptom scale: baseline and postconcussion factors. Am J Sports Med. 2012;40(10):2375-2384.
14. Guskiewicz KM, Ross SE, Marshall SW. Postural stability and neuropsychological deficits after concussion in collegiate athletes. J Athl Train. 2001;36(3):263.
15. Mucha A, Collins MW, Elbin R, et al. A brief Vestibular/Ocular Motor Screening (VOMS) assessment to evaluate concussions preliminary findings. Am J Sports Med. 2014;42(10):2479-2486.
16. Bloom J. Vestibular and ocular motor assessments: Important pieces to the concussion puzzle. Athletic Training and Sports Health Care. 2013;5(6):246-248.
17. Covassin T, Elbin R, Harris W, Parker T, Kontos A. The role of age and sex in symptoms, neurocognitive performance, and postural stability in athletes after concussion. Am J Sports Med. 2012;40(6):1303-1312.
18. Kontos A, Sufrinko A, Elbin R, Puskar A, Collins M. Reliability and associated risk factors for performance on the Vestibular/Ocular Motor Screening (VOMS) tool in healthy collegiate athletes. Am J Sports Med. 2016;44(6):1400-1406.
19. Guskiewicz KM, McCrea M, Marshall SW, et al. Cumulative effects associated with recurrent concussion in collegiate football players: the NCAA Concussion Study. JAMA. 2003;290(19):2549-2555.
20. Lau B, Lovell MR, Collins MW, Pardini J. Neurocognitive and symptom predictors of recovery in high school athletes. Clin J Sport Med. 2009;19(3):216-221.
21. Lau BC, Kontos AP, Collins MW, Mucha A, Lovell MR. Which on-field signs/symptoms predict protracted recovery from sport-related concussion among high school football players? Am J Sports Med. 2011;39(11):2311-2318.
22. Mihalik JP, Register-Mihalik J, Kerr ZY, Marshall SW, McCrea MC, Guskiewicz KM. Recovery of posttraumatic migraine characteristics in patients after mild traumatic brain injury. Am J Sports Med. 2013;41(7):1490-1496.
23. Covassin T, Moran R, Elbin RJ. Sex differences in reported concussion injury rates and time loss from participation: An update of the National Collegiate Athletic Association injury surveillance program from 2004-2005 through 2008-2009. J Athl Train. 2016;51(3):189-194.
24. Root JM, Zuckerbraun NS, Wang L, et al. History of somatization is associated with prolonged recovery from concussion. J Pediatr. 2016;174:39-44.
25. Sufrinko A, Pearce K, Elbin RJ, et al. The effect of preinjury sleep difficulties on neurocognitive impairment and symptoms after sport-related concussion. Am J Sports Med. 2015;43(4):830-838.
26. Thomas DG, Apps JN, Hoffmann RG, McCrea M, Hammeke T. Benefits of strict rest after acute concussion: a randomized controlled trial. Pediatrics. 2015;135(2):213-223.
27. Choe M, Blume H. Pediatric posttraumatic Headache: a review. J Child Neurol. 2016;31(1):76-85.
28. Tepper SJ, Tepper DE. Breaking the cycle of medication overuse. Cleve Clin J Med. 2010;77(4):236-242.
29. Collins M, Kontos A, Reynolds E, Murawski C, Fu F. A comprehensive, targeted approach to the clinical care of athletes following sport-related concussion. Knee Surg Sports Traumatol Arthrosc. 2014;22(2):235-246.
30. Reynolds E, Collins MW, Mucha A, Troutman-Ensecki C. Establishing a clinical service for the management of sports-related concussions. Neurosurgery. 2014;75 Suppl 4:S71-S81.
31. Broglio SP, Collins MW, Williams RM, Mucha A, Kontos AP. Current and emerging rehabilitation for concussion: a review of the evidence. Clin Sports Med. 2015;34(2):213-231.
32. Master C, Scheiman M, Gallaway M, et al. Vision diagnoses are common after concussion in adolescents. Clin Pediatr (Phila). 2016;55(3):260-267.
33. Headache Classification Committee of the International Headache Society (IHS). The international classification of headache disorders, 3rd edition (beta version). Cephalalgia. 2013;33(9):629-808.
34. Kontos A, Deitrick JM, Reynolds E. Mental health implication and consequences following sport-related concussion. Brit J Sports Med. 2016;50(3):139-140.
35. Kontos AP, Covassin T, Elbin R, Parker T. Depression and neurocognitive performance after concussion among male and female high school and collegiate athletes. Arch Phys Med Rehabil. 2012;93(10):1751-1756.
Football is an important component of American culture, with approximately 3 million youth athletes, 1.1 million high school athletes, and 100,000 college athletes participating each year.1 Participation in football provides athletes with physical, social, psychological, and academic benefits. Despite these benefits, widespread focus has been placed on the safety of football due to the risk for sport-related concussion (SRC) and potentially long-term effects; however, little recognition has been given to the advancements in concussion management across time and occurrence of concussions during most life activities. Although it is reasonable for concerns to be presented, it is important to better understand SRC and the current factors leading to prolonged recoveries, increased risk for injury, and potentially long-term effects.
What Is a Concussion?
Concussions occur after sustaining direct or indirect injury to the head or other parts of the body, as long as the injury force is transmitted to the head. Athletes often experience physical, cognitive, emotional, and sleep-related symptoms post-concussion secondary to an “energy crisis” within the brain.2 The energy crisis occurs as the result of transient neurological dysfunction triggered by changes in the brain (eg, release of neurotransmitters, impaired axonal function).2,3 Concussion is undetectable with traditional imaging; however, advanced imaging techniques (eg, diffuse tensor imaging) have shown progress in assessing axonal injury.3 Symptom duration post-concussion is highly variable due to individual differences; a recent study showed recovery took 3 to 4 weeks for memory and symptoms.4,5
Previous Concussion Management
Identification techniques and return-to-play guidelines for concussion have significantly changed across time. In the past, concussion grading scales were utilized for diagnosis and return to play was possible within the same contest.6,7 It has since been recognized that initial concussion severity makes it difficult to predict recovery.3 For example, research revealed memory decline and increased symptoms 36 hours post-injury for athletes with a grade 1 concussion (ie, transient confusion, no loss of consciousness, concussion symptoms or mental status changes that resolve within 15 minutes of injury) compared to baseline.7 Another study found duration of mental status changes to be related to slower symptom resolution and memory impairment 36 hours to 7 days post-injury.6 Consequently, return to play within the same contest was likely too liberal. Guidelines today recommend immediate removal from play with suspected SRC. Nevertheless, the “play through pain” culture has led athletes to continue playing after SRC, contributing to prolonged recoveries and potentially long-term effects.
Current Concussion Management: Continued Concerns and Areas of Improvement
Despite increased awareness of concussions, recent estimates revealed high rates (ie, 27:1 ratio for general players) of underreporting in college football, particularly amongst offensive linemen.8 Researchers have studied recovery implications for remaining in play, with one study revealing a 2.2 times greater risk for prolonged recovery in college athletes with delayed vs immediate removal.9 Another similar study discovered an 8.8 times greater risk for prolonged recovery in adolescent and young adult athletes not removed vs removed from play.10 Further analysis found remaining in play to be the greatest risk factor for prolonged recovery compared to other previously studied risk factors (eg, age, sex, posttraumatic migraine).10 Additionally, significant differences in neurocognitive data were seen between the “removed” and “not removed” groups for verbal memory, visual memory, processing speed, and reaction time at 1 to 7 days and 8 to 30 days.10 The recovery implications of remaining in play and the additional risk for second impact syndrome (SIS), or repeat concussion when recovering from another injury, emphasizes the need for further education efforts amongst athletes to encourage immediate reporting of injury.11
Sideline Assessment
Sideline assessment has become a vital component of concussion management to rule out concussion and/or significant injury other than concussion. Assessment should include observation, cognitive/balance testing, neurologic examination, and possible exertion testing to ensure a comprehensive evaluation of all areas of potential dysfunction.12 Indications for emergency department evaluation include suspicion for cervical spine injury, intracranial hemorrhage, or skull fracture as well as prolonged loss of consciousness, high-risk mechanisms, posttraumatic seizure(s), and/or significant worsening of symptoms.12
Observation
On the sideline, it is important to identify any immediate signs of injury (ie, loss of consciousness, anterograde/retrograde amnesia, and disorientation/confusion). Since immediate signs are not always present, it is important to be aware of the most commonly reported symptoms, including headache, difficulty concentrating, fatigue, drowsiness, and dizziness.13 If symptoms are not reported by the athlete, balance problems, lack of coordination, increased emotionality, and difficulty following instructions may be observed during play.12
On-Field Assessment
Cognitive and balance testing are essential in determining if an athlete has sustained a concussion. Immediate declines in memory, concentration abilities, and balance abilities are common. Given limitations in administering long testing batteries on the sideline, brief standardized tests such as the Standardized Assessment of Concussion (SAC), Balance Error Scoring System (BESS), and Sport Concussion Assessment Tool (SCAT) are commonly utilized. Identification of cognitive and/or balance abnormalities can help the athlete recognize deficits following injury.12 Balance problems are experienced due to abnormalities in sensory organization and generally resolve during the acute recovery period.14,15 Cognitive difficulties typically persist longer than balance problems, though duration varies widely.
Neurologic Evaluation
A neurologic evaluation including cranial nerve testing and evaluation of motor-sensory function (ie, assessment for the strength and sensation of upper and lower extremities) is important to identify focal deficits (ie, sensation changes, loss of fine motor control) indicative of serious intracranial pathology.12 Additionally, clinicians have suggested inclusion of vestibular and oculomotor assessments due to frequent dysfunction post-concussion.12,15,16 Examination of the vestibular/oculomotor systems through tools such as the Vestibular/Ocular Motor Screening (VOMS) assessment (assesses both the vestibular and oculomotor systems) and King-Devick Test (primarily assesses saccadic eye movements) can elicit symptoms that may not present immediately. If assessment appears normal, exertion testing can be utilized to determine if symptoms are provoked through physical exercise that should include cardio, dynamic, and sport-specific activities to stress the vestibular system.12
Risk Factors for Injury and Prolonged Recovery
Medical professionals must consider the presence of risk factors when managing concussion in order to make appropriate treatment recommendations and return-to-play decisions. Research has demonstrated the role of female gender, learning disability, attention-deficit/hyperactivity disorder, psychiatric history, young age, motion sickness, sleep problems, somatization, concussion history, on-field dizziness, posttraumatic migraine, and fogginess in increased risk for injury and/or prolonged recovery.17-25 Additionally, athletes with ongoing symptoms from a previous injury are at risk for sustaining another injury.
Acute Home Concussion Management
Although strict rest has been recommended post-concussion, recent research evaluating strict rest vs usual care for adolescents revealed greater symptom reports and longer recovery periods for the strict rest group.26 Based on these findings and emphasis for regulation within the migraine literature (due to the common pathophysiology between migraine and concussion27), we recommend that athletes follow a regulated daily schedule post-concussion including: 1) regular sleep-wake schedule with avoidance of naps, 2) regular meals, 3) adequate fluid hydration, 4) light noncontact physical activity (ie, walking, with progressions recommended by a physician), and 5) stress management techniques. Use of these strategies immediately can help in preventing against increased symptoms and stress, and decreases the need for medication in select cases. Additionally, over-the-counter medications should be limited to 2 to 3 doses per week to avoid rebound headaches.28
In-Office Concussion Management
Athletes diagnosed with SRC will experience different symptoms based on the injury mechanism, risk factors, and management approach. Comprehensive evaluation should include assessment of risk factors, injury details, symptoms, neurocognitive functioning, vestibular/oculomotor dysfunction, tolerance of physical exertion, balance functioning, and cervical spine integrity (if necessary).29,30 Due to individual differences and the heterogeneous symptom profiles, concussion management must move beyond a “one size fits all” approach to avoid nonspecific treatment strategies and consequently prolonged recoveries.29 Clinicians and researchers at University of Pittsburgh Medical Center have identified 6 concussion clinical profiles (ie, vestibular, ocular, posttraumatic migraine, cervical, anxiety/mood, and cognitive/fatigue) that are generally identifiable 48 hours after injury.29,30 Identification of the clinical profile(s) through a comprehensive evaluation guides the development of individualized treatment plans and targeted rehabilitation strategies.29,30
Vestibular. The vestibular system is responsible for stabilizing vision while the head moves and balance control.15 Athletes can experience central and/or peripheral vestibular dysfunction to include benign paroxysmal positional vertigo (BPPV), visual motion sensitivity, vestibular ocular reflex impairment, and balance impairment.30,31 Symptoms typically include dizziness, impaired balance, blurry vision, difficulty focusing, and environmental sensitivity.15,29,30 Potential treatment options include vestibular rehabilitation, exertion therapy, and school/work accommodations.
Ocular. The oculomotor system is responsible for control of eye movements. Athletes can experience many different posttraumatic vision changes, including convergence problems, eye-tracking difficulties, refractive error, difficulty with pursuits/saccades, and accommodation insufficiency. Symptoms typically include light sensitivity, blurred vision, double vision, headaches, fatigue, and memory difficulties.15,29,30 Potential treatment options include vision therapy, vestibular rehabilitation, and school/work accommodations.32
Posttraumatic Migraine. Headache, the most common post-concussion symptom, can persist and meet criteria for posttraumatic migraine (ie, unilateral headache with accompanying nausea and/or photophobia and phonophobia).29,30,33 Implementation of a routine schedule, daily physical activity, exertion therapy, pharmacologic intervention, and school/work accommodations are potential treatment options.
Cervical. The cervical spine can be injured during whiplash-type injuries. Therefore, determining the location, onset, and typical exacerbations of pain can be helpful in identifying cervical involvement.29,30 Symptoms typically include headaches, neck pain, numbness, and tingling. Evaluation and therapy by a certified physical therapist and pharmacologic intervention (eg, muscle relaxants) are potential treatment options. 29,30
Anxiety/Mood. Anxiety, or worry and fear about everyday situations, is common post-concussion and can sometimes be related to ongoing vestibular impairment. Symptoms typically include ruminative thoughts, avoidance of specific situations, hypervigilance, feelings of being overwhelmed, and difficulty falling asleep.29,30 Potential treatment options include implementation of a routine schedule, exposure to provocative situations, psychotherapy, pharmacologic intervention, and school/work accommodations.34
Cognitive/Fatigue. A global concussion factor (including cognitive, fatigue, and migraine symptoms) has been identified within 1 to 7 days of injury. Although this factor of symptoms generally resolves during the acute recovery period, it persists in select cases.13 Symptoms typically include fatigue, decreased energy levels, nonspecific headaches, potential sleep disruption, increased symptoms towards the end of the day, difficulty concentrating, and increased headache with cognitive activities.29,30,35 Routine schedule, daily physical activity, exertion therapy, pharmacologic intervention (eg, amantadine), and school/work accommodations are potential treatment options.30
Conclusion
Advancements in SRC management warrant change in the conversations regarding concussion in football. Specifically, conversations should address the current understanding of concussion and improvements in the safety of football through stricter concussion guidelines, detailed sideline evaluations, recognition of risk factors, improved acute management, and identification of concussion profiles that help to direct individualized treatment plans and targeted rehabilitation strategies. The biggest concerns related to concussions in football include underreporting of injury, premature return to play, and receiving routine rather than individualized treatment. Therefore, to further improve the safety of football and management of concussion it is essential that future efforts focus on the following 6 areas:
Education: Improved understanding of concussion is imperative to reducing poor outcomes and widespread concerns.
Immediate reporting: Reporting of concussion must be expected and encouraged through consistent responses by coaches to reduce underreporting and fear of reporting in athletes.
Prevention techniques: Athletes must be taught proper form and playing techniques to reduce the risk for concussion. Proper form and technique should be incentivized.
Targeted treatment: Individualized treatment plans and targeted rehabilitation strategies must be developed based on the identified clinical profile(s) to avoid nonspecific treatment recommendations.
Multidisciplinary treatment teams: Given the heterogeneous symptoms profiles and need for care provided by different medical specialties, multidisciplinary teams are essential.
Remain current: With the progress in understanding concussion, providers must remain vigilant of future advances in concussion management to further improve the safety of football.
Am J Orthop. 2016;45(6):352-356. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.
Football is an important component of American culture, with approximately 3 million youth athletes, 1.1 million high school athletes, and 100,000 college athletes participating each year.1 Participation in football provides athletes with physical, social, psychological, and academic benefits. Despite these benefits, widespread focus has been placed on the safety of football due to the risk for sport-related concussion (SRC) and potentially long-term effects; however, little recognition has been given to the advancements in concussion management across time and occurrence of concussions during most life activities. Although it is reasonable for concerns to be presented, it is important to better understand SRC and the current factors leading to prolonged recoveries, increased risk for injury, and potentially long-term effects.
What Is a Concussion?
Concussions occur after sustaining direct or indirect injury to the head or other parts of the body, as long as the injury force is transmitted to the head. Athletes often experience physical, cognitive, emotional, and sleep-related symptoms post-concussion secondary to an “energy crisis” within the brain.2 The energy crisis occurs as the result of transient neurological dysfunction triggered by changes in the brain (eg, release of neurotransmitters, impaired axonal function).2,3 Concussion is undetectable with traditional imaging; however, advanced imaging techniques (eg, diffuse tensor imaging) have shown progress in assessing axonal injury.3 Symptom duration post-concussion is highly variable due to individual differences; a recent study showed recovery took 3 to 4 weeks for memory and symptoms.4,5
Previous Concussion Management
Identification techniques and return-to-play guidelines for concussion have significantly changed across time. In the past, concussion grading scales were utilized for diagnosis and return to play was possible within the same contest.6,7 It has since been recognized that initial concussion severity makes it difficult to predict recovery.3 For example, research revealed memory decline and increased symptoms 36 hours post-injury for athletes with a grade 1 concussion (ie, transient confusion, no loss of consciousness, concussion symptoms or mental status changes that resolve within 15 minutes of injury) compared to baseline.7 Another study found duration of mental status changes to be related to slower symptom resolution and memory impairment 36 hours to 7 days post-injury.6 Consequently, return to play within the same contest was likely too liberal. Guidelines today recommend immediate removal from play with suspected SRC. Nevertheless, the “play through pain” culture has led athletes to continue playing after SRC, contributing to prolonged recoveries and potentially long-term effects.
Current Concussion Management: Continued Concerns and Areas of Improvement
Despite increased awareness of concussions, recent estimates revealed high rates (ie, 27:1 ratio for general players) of underreporting in college football, particularly amongst offensive linemen.8 Researchers have studied recovery implications for remaining in play, with one study revealing a 2.2 times greater risk for prolonged recovery in college athletes with delayed vs immediate removal.9 Another similar study discovered an 8.8 times greater risk for prolonged recovery in adolescent and young adult athletes not removed vs removed from play.10 Further analysis found remaining in play to be the greatest risk factor for prolonged recovery compared to other previously studied risk factors (eg, age, sex, posttraumatic migraine).10 Additionally, significant differences in neurocognitive data were seen between the “removed” and “not removed” groups for verbal memory, visual memory, processing speed, and reaction time at 1 to 7 days and 8 to 30 days.10 The recovery implications of remaining in play and the additional risk for second impact syndrome (SIS), or repeat concussion when recovering from another injury, emphasizes the need for further education efforts amongst athletes to encourage immediate reporting of injury.11
Sideline Assessment
Sideline assessment has become a vital component of concussion management to rule out concussion and/or significant injury other than concussion. Assessment should include observation, cognitive/balance testing, neurologic examination, and possible exertion testing to ensure a comprehensive evaluation of all areas of potential dysfunction.12 Indications for emergency department evaluation include suspicion for cervical spine injury, intracranial hemorrhage, or skull fracture as well as prolonged loss of consciousness, high-risk mechanisms, posttraumatic seizure(s), and/or significant worsening of symptoms.12
Observation
On the sideline, it is important to identify any immediate signs of injury (ie, loss of consciousness, anterograde/retrograde amnesia, and disorientation/confusion). Since immediate signs are not always present, it is important to be aware of the most commonly reported symptoms, including headache, difficulty concentrating, fatigue, drowsiness, and dizziness.13 If symptoms are not reported by the athlete, balance problems, lack of coordination, increased emotionality, and difficulty following instructions may be observed during play.12
On-Field Assessment
Cognitive and balance testing are essential in determining if an athlete has sustained a concussion. Immediate declines in memory, concentration abilities, and balance abilities are common. Given limitations in administering long testing batteries on the sideline, brief standardized tests such as the Standardized Assessment of Concussion (SAC), Balance Error Scoring System (BESS), and Sport Concussion Assessment Tool (SCAT) are commonly utilized. Identification of cognitive and/or balance abnormalities can help the athlete recognize deficits following injury.12 Balance problems are experienced due to abnormalities in sensory organization and generally resolve during the acute recovery period.14,15 Cognitive difficulties typically persist longer than balance problems, though duration varies widely.
Neurologic Evaluation
A neurologic evaluation including cranial nerve testing and evaluation of motor-sensory function (ie, assessment for the strength and sensation of upper and lower extremities) is important to identify focal deficits (ie, sensation changes, loss of fine motor control) indicative of serious intracranial pathology.12 Additionally, clinicians have suggested inclusion of vestibular and oculomotor assessments due to frequent dysfunction post-concussion.12,15,16 Examination of the vestibular/oculomotor systems through tools such as the Vestibular/Ocular Motor Screening (VOMS) assessment (assesses both the vestibular and oculomotor systems) and King-Devick Test (primarily assesses saccadic eye movements) can elicit symptoms that may not present immediately. If assessment appears normal, exertion testing can be utilized to determine if symptoms are provoked through physical exercise that should include cardio, dynamic, and sport-specific activities to stress the vestibular system.12
Risk Factors for Injury and Prolonged Recovery
Medical professionals must consider the presence of risk factors when managing concussion in order to make appropriate treatment recommendations and return-to-play decisions. Research has demonstrated the role of female gender, learning disability, attention-deficit/hyperactivity disorder, psychiatric history, young age, motion sickness, sleep problems, somatization, concussion history, on-field dizziness, posttraumatic migraine, and fogginess in increased risk for injury and/or prolonged recovery.17-25 Additionally, athletes with ongoing symptoms from a previous injury are at risk for sustaining another injury.
Acute Home Concussion Management
Although strict rest has been recommended post-concussion, recent research evaluating strict rest vs usual care for adolescents revealed greater symptom reports and longer recovery periods for the strict rest group.26 Based on these findings and emphasis for regulation within the migraine literature (due to the common pathophysiology between migraine and concussion27), we recommend that athletes follow a regulated daily schedule post-concussion including: 1) regular sleep-wake schedule with avoidance of naps, 2) regular meals, 3) adequate fluid hydration, 4) light noncontact physical activity (ie, walking, with progressions recommended by a physician), and 5) stress management techniques. Use of these strategies immediately can help in preventing against increased symptoms and stress, and decreases the need for medication in select cases. Additionally, over-the-counter medications should be limited to 2 to 3 doses per week to avoid rebound headaches.28
In-Office Concussion Management
Athletes diagnosed with SRC will experience different symptoms based on the injury mechanism, risk factors, and management approach. Comprehensive evaluation should include assessment of risk factors, injury details, symptoms, neurocognitive functioning, vestibular/oculomotor dysfunction, tolerance of physical exertion, balance functioning, and cervical spine integrity (if necessary).29,30 Due to individual differences and the heterogeneous symptom profiles, concussion management must move beyond a “one size fits all” approach to avoid nonspecific treatment strategies and consequently prolonged recoveries.29 Clinicians and researchers at University of Pittsburgh Medical Center have identified 6 concussion clinical profiles (ie, vestibular, ocular, posttraumatic migraine, cervical, anxiety/mood, and cognitive/fatigue) that are generally identifiable 48 hours after injury.29,30 Identification of the clinical profile(s) through a comprehensive evaluation guides the development of individualized treatment plans and targeted rehabilitation strategies.29,30
Vestibular. The vestibular system is responsible for stabilizing vision while the head moves and balance control.15 Athletes can experience central and/or peripheral vestibular dysfunction to include benign paroxysmal positional vertigo (BPPV), visual motion sensitivity, vestibular ocular reflex impairment, and balance impairment.30,31 Symptoms typically include dizziness, impaired balance, blurry vision, difficulty focusing, and environmental sensitivity.15,29,30 Potential treatment options include vestibular rehabilitation, exertion therapy, and school/work accommodations.
Ocular. The oculomotor system is responsible for control of eye movements. Athletes can experience many different posttraumatic vision changes, including convergence problems, eye-tracking difficulties, refractive error, difficulty with pursuits/saccades, and accommodation insufficiency. Symptoms typically include light sensitivity, blurred vision, double vision, headaches, fatigue, and memory difficulties.15,29,30 Potential treatment options include vision therapy, vestibular rehabilitation, and school/work accommodations.32
Posttraumatic Migraine. Headache, the most common post-concussion symptom, can persist and meet criteria for posttraumatic migraine (ie, unilateral headache with accompanying nausea and/or photophobia and phonophobia).29,30,33 Implementation of a routine schedule, daily physical activity, exertion therapy, pharmacologic intervention, and school/work accommodations are potential treatment options.
Cervical. The cervical spine can be injured during whiplash-type injuries. Therefore, determining the location, onset, and typical exacerbations of pain can be helpful in identifying cervical involvement.29,30 Symptoms typically include headaches, neck pain, numbness, and tingling. Evaluation and therapy by a certified physical therapist and pharmacologic intervention (eg, muscle relaxants) are potential treatment options. 29,30
Anxiety/Mood. Anxiety, or worry and fear about everyday situations, is common post-concussion and can sometimes be related to ongoing vestibular impairment. Symptoms typically include ruminative thoughts, avoidance of specific situations, hypervigilance, feelings of being overwhelmed, and difficulty falling asleep.29,30 Potential treatment options include implementation of a routine schedule, exposure to provocative situations, psychotherapy, pharmacologic intervention, and school/work accommodations.34
Cognitive/Fatigue. A global concussion factor (including cognitive, fatigue, and migraine symptoms) has been identified within 1 to 7 days of injury. Although this factor of symptoms generally resolves during the acute recovery period, it persists in select cases.13 Symptoms typically include fatigue, decreased energy levels, nonspecific headaches, potential sleep disruption, increased symptoms towards the end of the day, difficulty concentrating, and increased headache with cognitive activities.29,30,35 Routine schedule, daily physical activity, exertion therapy, pharmacologic intervention (eg, amantadine), and school/work accommodations are potential treatment options.30
Conclusion
Advancements in SRC management warrant change in the conversations regarding concussion in football. Specifically, conversations should address the current understanding of concussion and improvements in the safety of football through stricter concussion guidelines, detailed sideline evaluations, recognition of risk factors, improved acute management, and identification of concussion profiles that help to direct individualized treatment plans and targeted rehabilitation strategies. The biggest concerns related to concussions in football include underreporting of injury, premature return to play, and receiving routine rather than individualized treatment. Therefore, to further improve the safety of football and management of concussion it is essential that future efforts focus on the following 6 areas:
Education: Improved understanding of concussion is imperative to reducing poor outcomes and widespread concerns.
Immediate reporting: Reporting of concussion must be expected and encouraged through consistent responses by coaches to reduce underreporting and fear of reporting in athletes.
Prevention techniques: Athletes must be taught proper form and playing techniques to reduce the risk for concussion. Proper form and technique should be incentivized.
Targeted treatment: Individualized treatment plans and targeted rehabilitation strategies must be developed based on the identified clinical profile(s) to avoid nonspecific treatment recommendations.
Multidisciplinary treatment teams: Given the heterogeneous symptoms profiles and need for care provided by different medical specialties, multidisciplinary teams are essential.
Remain current: With the progress in understanding concussion, providers must remain vigilant of future advances in concussion management to further improve the safety of football.
Am J Orthop. 2016;45(6):352-356. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.
1. Dompier TP, Kerr ZY, Marshall SW, et al. Incidence of concussion during practice and games in youth, high school, and collegiate American football players. JAMA Pediatrics. 2015;169(7):659-665.
2. Giza C, Hovda D. The new neurometabolic cascade of concussion
3. Barkhoudarian G, Hovda DA, Giza CC. The molecular pathophysiology of concussive brain injury - an update. Phys Med Rehabil Clin N Am. 2016;27:373-393.
4. Henry L, Elbin R, Collins M, Marchetti G, Kontos A. Examining recovery trajectories after sport-related concussion with a multimodal clinical assessment approach. Neurosurgery. 2016;78(2):232-241.
5. McCrory P, Meeuwisse WH, Aubry M, et al. Consensus statement on concussion in sport: the 4th International Conference on Concussion in Sport held in Zurich, November 2012. Brit J Sports Med. 2013;47(5):250-258.
6. Lovell MR, Collins MW, Iverson GL, et al. Recovery from mild concussion in high school athletes. J Neurosurg. 2003;98(2):296-301.
7. Lovell MR, Collins MW, Iverson GL, Johnston KM, Bradley JP. Grade 1 or “ding” concussions in high school athletes. Am J Sports Med. 2004;32(1):47-54.
8. Baugh CM, Kroshus E, Daneshvar DH, Filali NA, Hiscox MJ, Glantz LH. Concussion management in United States college sports: compliance with National Collegiate Athletic Association concussion policy and areas for improvement. Am J Sports Med. 2015;43(1):47-56.
9. Asken BM, McCrea MA, Clugston JR, Snyder AR, Houck ZM, Bauer RM. “Playing through it”: Delayed reporting and removal from athletic activity after concussion predicts prolonged recovery. J Athl Train. 2016;51(4):329-335.
10. Elbin RJ, Sufrinko A, Schatz P, et al. Athletes that continue to play with concussion demonstrate worse recovery outcomes than athletes immediately removed from play. J Pediatr. In press.
11. Signoretti S, Lazzarino G, Tavazzi B, Vagnozzi R. The pathophysiology of concussion. PM R. 2011;3(10 Suppl 2):S359-S368.
12. Bloom J, Blount JG. Sideline evaluation of concussion. UpToDate. 2016. http://www.uptodate.com/contents/sideline-evaluation-of-concussion. Accessed July 13, 2016.
13. Kontos AP, Elbin RJ, Schatz P, et al. A revised factor structure for the post-concussion symptom scale: baseline and postconcussion factors. Am J Sports Med. 2012;40(10):2375-2384.
14. Guskiewicz KM, Ross SE, Marshall SW. Postural stability and neuropsychological deficits after concussion in collegiate athletes. J Athl Train. 2001;36(3):263.
15. Mucha A, Collins MW, Elbin R, et al. A brief Vestibular/Ocular Motor Screening (VOMS) assessment to evaluate concussions preliminary findings. Am J Sports Med. 2014;42(10):2479-2486.
16. Bloom J. Vestibular and ocular motor assessments: Important pieces to the concussion puzzle. Athletic Training and Sports Health Care. 2013;5(6):246-248.
17. Covassin T, Elbin R, Harris W, Parker T, Kontos A. The role of age and sex in symptoms, neurocognitive performance, and postural stability in athletes after concussion. Am J Sports Med. 2012;40(6):1303-1312.
18. Kontos A, Sufrinko A, Elbin R, Puskar A, Collins M. Reliability and associated risk factors for performance on the Vestibular/Ocular Motor Screening (VOMS) tool in healthy collegiate athletes. Am J Sports Med. 2016;44(6):1400-1406.
19. Guskiewicz KM, McCrea M, Marshall SW, et al. Cumulative effects associated with recurrent concussion in collegiate football players: the NCAA Concussion Study. JAMA. 2003;290(19):2549-2555.
20. Lau B, Lovell MR, Collins MW, Pardini J. Neurocognitive and symptom predictors of recovery in high school athletes. Clin J Sport Med. 2009;19(3):216-221.
21. Lau BC, Kontos AP, Collins MW, Mucha A, Lovell MR. Which on-field signs/symptoms predict protracted recovery from sport-related concussion among high school football players? Am J Sports Med. 2011;39(11):2311-2318.
22. Mihalik JP, Register-Mihalik J, Kerr ZY, Marshall SW, McCrea MC, Guskiewicz KM. Recovery of posttraumatic migraine characteristics in patients after mild traumatic brain injury. Am J Sports Med. 2013;41(7):1490-1496.
23. Covassin T, Moran R, Elbin RJ. Sex differences in reported concussion injury rates and time loss from participation: An update of the National Collegiate Athletic Association injury surveillance program from 2004-2005 through 2008-2009. J Athl Train. 2016;51(3):189-194.
24. Root JM, Zuckerbraun NS, Wang L, et al. History of somatization is associated with prolonged recovery from concussion. J Pediatr. 2016;174:39-44.
25. Sufrinko A, Pearce K, Elbin RJ, et al. The effect of preinjury sleep difficulties on neurocognitive impairment and symptoms after sport-related concussion. Am J Sports Med. 2015;43(4):830-838.
26. Thomas DG, Apps JN, Hoffmann RG, McCrea M, Hammeke T. Benefits of strict rest after acute concussion: a randomized controlled trial. Pediatrics. 2015;135(2):213-223.
27. Choe M, Blume H. Pediatric posttraumatic Headache: a review. J Child Neurol. 2016;31(1):76-85.
28. Tepper SJ, Tepper DE. Breaking the cycle of medication overuse. Cleve Clin J Med. 2010;77(4):236-242.
29. Collins M, Kontos A, Reynolds E, Murawski C, Fu F. A comprehensive, targeted approach to the clinical care of athletes following sport-related concussion. Knee Surg Sports Traumatol Arthrosc. 2014;22(2):235-246.
30. Reynolds E, Collins MW, Mucha A, Troutman-Ensecki C. Establishing a clinical service for the management of sports-related concussions. Neurosurgery. 2014;75 Suppl 4:S71-S81.
31. Broglio SP, Collins MW, Williams RM, Mucha A, Kontos AP. Current and emerging rehabilitation for concussion: a review of the evidence. Clin Sports Med. 2015;34(2):213-231.
32. Master C, Scheiman M, Gallaway M, et al. Vision diagnoses are common after concussion in adolescents. Clin Pediatr (Phila). 2016;55(3):260-267.
33. Headache Classification Committee of the International Headache Society (IHS). The international classification of headache disorders, 3rd edition (beta version). Cephalalgia. 2013;33(9):629-808.
34. Kontos A, Deitrick JM, Reynolds E. Mental health implication and consequences following sport-related concussion. Brit J Sports Med. 2016;50(3):139-140.
35. Kontos AP, Covassin T, Elbin R, Parker T. Depression and neurocognitive performance after concussion among male and female high school and collegiate athletes. Arch Phys Med Rehabil. 2012;93(10):1751-1756.
1. Dompier TP, Kerr ZY, Marshall SW, et al. Incidence of concussion during practice and games in youth, high school, and collegiate American football players. JAMA Pediatrics. 2015;169(7):659-665.
2. Giza C, Hovda D. The new neurometabolic cascade of concussion
3. Barkhoudarian G, Hovda DA, Giza CC. The molecular pathophysiology of concussive brain injury - an update. Phys Med Rehabil Clin N Am. 2016;27:373-393.
4. Henry L, Elbin R, Collins M, Marchetti G, Kontos A. Examining recovery trajectories after sport-related concussion with a multimodal clinical assessment approach. Neurosurgery. 2016;78(2):232-241.
5. McCrory P, Meeuwisse WH, Aubry M, et al. Consensus statement on concussion in sport: the 4th International Conference on Concussion in Sport held in Zurich, November 2012. Brit J Sports Med. 2013;47(5):250-258.
6. Lovell MR, Collins MW, Iverson GL, et al. Recovery from mild concussion in high school athletes. J Neurosurg. 2003;98(2):296-301.
7. Lovell MR, Collins MW, Iverson GL, Johnston KM, Bradley JP. Grade 1 or “ding” concussions in high school athletes. Am J Sports Med. 2004;32(1):47-54.
8. Baugh CM, Kroshus E, Daneshvar DH, Filali NA, Hiscox MJ, Glantz LH. Concussion management in United States college sports: compliance with National Collegiate Athletic Association concussion policy and areas for improvement. Am J Sports Med. 2015;43(1):47-56.
9. Asken BM, McCrea MA, Clugston JR, Snyder AR, Houck ZM, Bauer RM. “Playing through it”: Delayed reporting and removal from athletic activity after concussion predicts prolonged recovery. J Athl Train. 2016;51(4):329-335.
10. Elbin RJ, Sufrinko A, Schatz P, et al. Athletes that continue to play with concussion demonstrate worse recovery outcomes than athletes immediately removed from play. J Pediatr. In press.
11. Signoretti S, Lazzarino G, Tavazzi B, Vagnozzi R. The pathophysiology of concussion. PM R. 2011;3(10 Suppl 2):S359-S368.
12. Bloom J, Blount JG. Sideline evaluation of concussion. UpToDate. 2016. http://www.uptodate.com/contents/sideline-evaluation-of-concussion. Accessed July 13, 2016.
13. Kontos AP, Elbin RJ, Schatz P, et al. A revised factor structure for the post-concussion symptom scale: baseline and postconcussion factors. Am J Sports Med. 2012;40(10):2375-2384.
14. Guskiewicz KM, Ross SE, Marshall SW. Postural stability and neuropsychological deficits after concussion in collegiate athletes. J Athl Train. 2001;36(3):263.
15. Mucha A, Collins MW, Elbin R, et al. A brief Vestibular/Ocular Motor Screening (VOMS) assessment to evaluate concussions preliminary findings. Am J Sports Med. 2014;42(10):2479-2486.
16. Bloom J. Vestibular and ocular motor assessments: Important pieces to the concussion puzzle. Athletic Training and Sports Health Care. 2013;5(6):246-248.
17. Covassin T, Elbin R, Harris W, Parker T, Kontos A. The role of age and sex in symptoms, neurocognitive performance, and postural stability in athletes after concussion. Am J Sports Med. 2012;40(6):1303-1312.
18. Kontos A, Sufrinko A, Elbin R, Puskar A, Collins M. Reliability and associated risk factors for performance on the Vestibular/Ocular Motor Screening (VOMS) tool in healthy collegiate athletes. Am J Sports Med. 2016;44(6):1400-1406.
19. Guskiewicz KM, McCrea M, Marshall SW, et al. Cumulative effects associated with recurrent concussion in collegiate football players: the NCAA Concussion Study. JAMA. 2003;290(19):2549-2555.
20. Lau B, Lovell MR, Collins MW, Pardini J. Neurocognitive and symptom predictors of recovery in high school athletes. Clin J Sport Med. 2009;19(3):216-221.
21. Lau BC, Kontos AP, Collins MW, Mucha A, Lovell MR. Which on-field signs/symptoms predict protracted recovery from sport-related concussion among high school football players? Am J Sports Med. 2011;39(11):2311-2318.
22. Mihalik JP, Register-Mihalik J, Kerr ZY, Marshall SW, McCrea MC, Guskiewicz KM. Recovery of posttraumatic migraine characteristics in patients after mild traumatic brain injury. Am J Sports Med. 2013;41(7):1490-1496.
23. Covassin T, Moran R, Elbin RJ. Sex differences in reported concussion injury rates and time loss from participation: An update of the National Collegiate Athletic Association injury surveillance program from 2004-2005 through 2008-2009. J Athl Train. 2016;51(3):189-194.
24. Root JM, Zuckerbraun NS, Wang L, et al. History of somatization is associated with prolonged recovery from concussion. J Pediatr. 2016;174:39-44.
25. Sufrinko A, Pearce K, Elbin RJ, et al. The effect of preinjury sleep difficulties on neurocognitive impairment and symptoms after sport-related concussion. Am J Sports Med. 2015;43(4):830-838.
26. Thomas DG, Apps JN, Hoffmann RG, McCrea M, Hammeke T. Benefits of strict rest after acute concussion: a randomized controlled trial. Pediatrics. 2015;135(2):213-223.
27. Choe M, Blume H. Pediatric posttraumatic Headache: a review. J Child Neurol. 2016;31(1):76-85.
28. Tepper SJ, Tepper DE. Breaking the cycle of medication overuse. Cleve Clin J Med. 2010;77(4):236-242.
29. Collins M, Kontos A, Reynolds E, Murawski C, Fu F. A comprehensive, targeted approach to the clinical care of athletes following sport-related concussion. Knee Surg Sports Traumatol Arthrosc. 2014;22(2):235-246.
30. Reynolds E, Collins MW, Mucha A, Troutman-Ensecki C. Establishing a clinical service for the management of sports-related concussions. Neurosurgery. 2014;75 Suppl 4:S71-S81.
31. Broglio SP, Collins MW, Williams RM, Mucha A, Kontos AP. Current and emerging rehabilitation for concussion: a review of the evidence. Clin Sports Med. 2015;34(2):213-231.
32. Master C, Scheiman M, Gallaway M, et al. Vision diagnoses are common after concussion in adolescents. Clin Pediatr (Phila). 2016;55(3):260-267.
33. Headache Classification Committee of the International Headache Society (IHS). The international classification of headache disorders, 3rd edition (beta version). Cephalalgia. 2013;33(9):629-808.
34. Kontos A, Deitrick JM, Reynolds E. Mental health implication and consequences following sport-related concussion. Brit J Sports Med. 2016;50(3):139-140.
35. Kontos AP, Covassin T, Elbin R, Parker T. Depression and neurocognitive performance after concussion among male and female high school and collegiate athletes. Arch Phys Med Rehabil. 2012;93(10):1751-1756.
Exertional Heat Stroke and American Football: What the Team Physician Needs to Know
Football, one of the most popular sports in the United States, is additionally recognized as a leading contributor to sports injury secondary to the contact collision nature of the endeavor. There are an estimated 1.1 million high school football players with another 100,000 participants combined in the National Football League (NFL), college, junior college, Arena Football League, and semipro levels of play.1 USA Football estimates that an additional 3 million youth participate in community football leagues.1 The National Center for Catastrophic Sports Injury Research recently calculated a fatality rate of 0.14 per 100,000 participants in 2014 for the 4.2 million who play football at all levels—and 0.45 per 100,000 in high school.1 While direct deaths from head and spine injury remain a significant contributor to the number of catastrophic injuries, indirect deaths (systemic failure) predominate. Exertional heat stroke (EHS) has emerged as one of the leading indirect causes of death in high school and collegiate football. Boden and colleagues2 reported that high school and college football players sustain approximately 12 fatalities annually, with indirect systemic causes being twice as common as direct blunt trauma.2The most common indirect causes identified included cardiac failure, heat illness, and complications of sickle cell trait (SCT). It was also noted that the risk of SCT, heat-related, and cardiac deaths increased during the second decade of the study, indicating these conditions may require a greater emphasis on diagnosis, treatment, and prevention. This review details for the team physician the unique challenge of exercising in the heat to the football player, and the prevention, diagnosis, management and return-to-play issues pertinent to exertional heat illness (EHI).
The Challenge
EHS represents the most severe manifestation of EHI—a gamut of diseases commonly encountered during the hot summer months when American football season begins. The breadth of EHI includes several important clinical diagnoses: exercise-associated muscle cramps (heat cramps); heat exhaustion with and without syncope; heat injury with evidence of end organ injury (eg, rhabdomyolysis); and EHS. EHS is defined as “a form of hyperthermia associated with a systemic inflammatory response leading to a syndrome of multi-organ dysfunction in which encephalopathy predominates.”3 EHS, if left untreated, or even if clinical treatment is delayed, may result in significant end organ morbidity and/or mortality.
During exercise, the human thermoregulatory system mitigates heat gain by increasing skin blood flow and sweating, causing an increased dissipation of heat to the surrounding environment by leveraging conduction, convection, and evaporation.4,5 Elevated environmental temperatures, increased humidity, and dehydration can impede the body’s ability to dissipate heat at a rate needed to maintain thermoregulation. This imbalance can result in hyperthermia secondary to uncompensated heat stress,5 which in turn can lead to EHI. Football players have unique challenges that make them particularly vulnerable to EHI. The summer heat during early-season participation and the requirement for equipment that covers nearly 60% of body surfaces pose increased risk of volume losses and hyperthermia that trigger the onset of EHI.6 Football athletes’ body compositions and physical size are additional contributing risk factors; the relatively high muscle and fat content increase thermogenicity, which require their bodies to dissipate more heat.7
An estimated 9000 cases of EHI occur annually across all high school sports,8 with an incidence of 1.6:100,000 athlete-exposures.8,9 Studies have demonstrated, however, that EHI occurs in football 11.4 times more often than in all other high school sports combined.10 The incidence of nonfatal EHI in all levels of football is 4.42-5:100,000.8,9 Between 2000 and 2014, 41 football players died from EHS.1 In football, approximately 75% of all EHI events occurred during practices, while only 25% of incidents occurred during games.8
Given these potentially deadly consequences, it is important that football team physicians are not only alert to the early symptoms of heat illness and prepared to intervene to prevent the progression to EHS, but are critical leaders in educating coaches and players in evidence-based EHI prevention practices and policies.
Prevention
EHS is a preventable condition, arguably the most common cause of preventable nontraumatic exertional death in young athletes in the United States. Close attention to mitigating risk factors should begin prior to the onset of preseason practice and continue through the early season, where athletes are at the highest risk of developing heat illness.
Primary Prevention
Primary prevention is fundamental to minimizing the occurrences of EHI. It focuses on the following methods: recognition of inherent risk factors, acclimatization, hydration, and avoidance of inciting substances (including supplements).
Pre-Participation Examination. The purpose of the pre-participation examination (PPE) is to maximize an athlete’s safety by identifying medical conditions that place the athlete at risk.11,12 The Preparticipation Physical Evaluation, 4th edition, the most widely used consensus publication, specifically queries if an athlete has a previous history of heat injury. However, it only indirectly addresses intrinsic risk factors that may predispose an athlete to EHI who has never had an EHI before. Therefore, providers should take the opportunity of the PPE to inquire about additional risk factors that may make an athlete high risk for sustaining a heat injury. Common risk factors for EHI are listed in Table 1.
Heat Acclimatization. The risk of EHI escalates significantly when athletes are subjected to multiple stressors during periods of heat exposure, such as sudden increases in intensity or duration of exercise; prolonged new exposures to heat; dehydration; and sleep loss.5 When football season begins in late summer, athletes are least conditioned as temperatures reach their seasonal peak, causing increased risk of EHI.15 Planning for heat acclimatization is vital for all athletes who exercise in hot environments. Acclimatization procedures place progressively mounting physiologic strains on the body to improve athletes’ ability to dissipate heat, diminishing thermoregulatory and cardiovascular exertion.4,5 Acclimatization begins with expansion of plasma volume on days 3 to 6, causing improvements in cardiac efficiency and resulting in an overall decrease in basal internal body temperature.4,5,15 This process results in improvements in heat tolerance and exercise performance, evolving over 10 to 14 days of gradual escalation of exercise intensity and duration.5,10,11,16 However, poor fitness levels and extreme temperatures can prolong this period, requiring up to 2 to 3 months to fully take effect.5,7
The National Athletic Trainers Association (NATA) and National Collegiate Athletic Association (NCAA) have released consensus guidelines regarding heat acclimatization protocols for football athletes at the high school and college levels (Tables 3 and 4). Each of these guidelines involves an initial period without use of protective equipment, followed by a gradual addition of further equipment.11,16
Secondary Prevention
Despite physicians’ best efforts to prevent all cases of EHI, athletes will still experience the effects of exercise-induced hyperthermia. The goal of secondary prevention is to slow the progression of this hyperthermia so that it does not progress to more dangerous EHI.
Hydration. Dehydration is an important risk factor for EHI. Sweat maintains thermoregulation by dissipating heat generated during exercise; however, it also contributes to body water losses. Furthermore, intravascular depletion decreases stroke volume, thereby increasing cardiovascular strain. It is estimated that for every 1% loss in body mass from dehydration, body temperature rises 0.22°C in comparison to a euhydrated state.6 Dehydration occurs more rapidly in hot environments, as fluid is lost through increased sweat production.7 After approximately 6% to 10% body weight volume loss, cardiac output cannot be maintained, diminishing sweat production and blood flow to both skin and muscle and causing diminished performance and a significant risk of heat exhaustion.7 If left unchecked, these physiologic changes result in further elevations in body temperature and increased cardiovascular strain, ultimately placing the athlete at significant risk for development of EHS.
Adequate hydration to maintain euvolemia is an important step in avoiding possible EHI. Multiple studies have shown that football players experience a baseline hypovolemia during their competition season,6 a deficit that is most marked during the first week of practices.17 This deficit is multifactorial, as football players expend a significant amount of fluid through sweat, are not able to adequately replace these losses during practice, and do not appropriately hydrate off the field.6,18 Some players, especially linemen, sweat at a higher rate than their teammates, posing a possible risk of significant dehydration.6 Coaches and players alike should be educated on the importance of adequate hydration to meet their fluid needs.
The goal of hydration during exercise is to prevent large fluid losses that can adversely affect performance and increase risk of EHI;6 it may be unrealistic to replace all fluid losses during the practice period. Instead, athletes should target complete volume replacement over the post-exercise period.6 Some recommend hydrating based upon thirst drive; however, thirst is activated following a volume loss of approximately 2% body mass, the same degree of losses that place athletes at an increased risk for performance impairment and EHI.4,6,11,12 Individuals should have access to fluids throughout practice and competition and be encouraged to hydrate as needed.6,12,15 Furthermore, staff should modify their practices based upon WBGT and acclimatization status to provide more frequent hydration breaks.
Hyperhydration and Salt Intake. Of note, there are inherent risks to hyperhydration. Athletes with low sweat rates have an increased risk of overhydration and the development of exercise-associated hyponatremia (EAH),6 a condition whose presentation is very similar to EHS. In addition, inadequate sodium intake and excessive sweating can also contribute to the development of EAH. EAH has been implicated in the deaths of 2 football players in 2014.1,6 Establishing team hydration guidelines and educating players and staff on appropriate hydration and dietary salt intake is essential to reduce the risk of both dehydration and hyperhydration and their complications.6Intra-Event Cooling. During exercise, team physicians can employ strategies for cooling athletes during exertion to mitigate their risk of EHI by decreasing thermal and cardiovascular strain.4,19 Cooling during exercise is hypothesized to allow for accelerated heat dissipation, where heat is lost from the body more effectively. This accelerated loss enables athletes to maintain a higher heat storage capacity over the duration of exercise, avoiding uncompensated heat stresses that ultimately cause EHI.19
Some intra-event cooling strategies include the use of cooling garments, cooling packs, and cold water/slurry ingestion. Cooling garments lower skin temperature, which in turn can decrease thermoregulatory strains;4 a recent meta-analysis of intra-event cooling modalities revealed that wearing an ice vest during exercise resulted in the greatest decrease in thermal heat strain.19 Internal cooling strategies—namely ingestion of cold fluids/ice slurry—have shown some mild benefit in decreasing internal temperatures; however, some studies have demonstrated some decrease in sweat production associated with cold oral intake used in isolation.19 Overall, studies have shown that combining external (cooling clothing, ice packs, fanning) and internal (cold water, ice slurry) cooling methods result in a greater cooling effect than a use of a single method.4
Tertiary Prevention
The goal of tertiary prevention is to mitigate the risk of long-term adverse outcomes following an EHS event. The most effective means of reducing risk for morbidity and mortality is rapid identification and treatment of EHS as well as close evaluation of an athlete’s return to activity in heat. This process is spearheaded by an effective and well-rehearsed emergency action plan.
Diagnosis and Management
Rapid identification and treatment of EHS is crucial to minimizing the risk of poor outcomes.7 Any delay in the treatment of EHS can dramatically increase the likelihood of associated morbidity and mortality.20
EHS is diagnosed by an elevated rectal temperature ≥40°C (104°F) and associated central nervous system (CNS) dysfunction.21 EHS should be strongly suspected in any athlete exercising in heat who exhibits signs of CNS dysfunction, including disorientation, confusion, dizziness, erratic behavior, irritability, headache, loss of coordination, delirium, collapse, or seizures.7,12,15 EHS may also present with symptoms of heat exhaustion, including fatigue, hyperventilation, tachycardia, vomiting, diarrhea, and hypotension.7,12,15
Rectal temperature should be taken for any athlete with suspected EHS, as other modalities—oral, skin, axillary, and aural—can be inaccurate and easily modified by ambient confounders such as ambient and skin temperature, athlete hyperventilation, and consumption of liquids.7,11,12 Athletes exhibiting CNS symptoms with moderately elevated rectal temperatures that do not exceed 40°C should also be assumed to be suffering from EHS and treated with rapid cooling.11 On the other hand, athletes with CNS symptoms who are normothermic should be assumed to have EAH until ruled out by electrolyte assessment; IV fluids should be at no more than keep vein open (KVO) pending this determination.11 In some cases, an athlete may initially present with altered mental status but return to “normal.” However, this improvement may represent a “lucid period”; evaluation should continue with rectal temperature and treatment, as EHS in these cases may progress quickly.15
Treatment is centered on rapid, whole body cooling initiated at the first sign of heat illness.7,22 The goal of treatment is to achieve a rectal temperature <38.9°C within 30 minutes of the onset of EHS.15 Upon diagnosis, the athlete should be quickly placed in a tub of ice water to facilitate cold water immersion (CWI) therapy. Some guidelines suggest the athlete’s clothing be removed to potentiate evaporative cooling during CWI;12 however, cooling should not be delayed due to difficulties in removing equipment. CWI, where a heat stroke victim is submerged in ice water up to their neck while water is continuously circulated, is generally considered to be the gold standard treatment as it is the modality with the highest recorded cooling rates and the lowest rate of morbidity and mortality.7,20,21 Multiple studies of CWI have shown that survival nears 100% when aggressive cooling starts within 5 minutes of collapse or identification of EHS.20,21,22
If whole body CWI is unavailable, alternative methods of rapid cooling should be employed. Partial CWI, with torso immersion being preferable to the extremities, has been shown to achieve an acceptable rate of cooling to achieve sufficient drops in internal body temperature.20,23 However, one popular treatment—applying ice packs to the whole body, in particular to the groin and axillae—has not been shown to be sufficient to achieve standard cooling goals.20 None of these methods have been shown to be as effective as CWI.23
Intravenous access should be initiated with fluid resuscitation dictated by the provider’s assessment. Normal saline is recommended as the resuscitative fluid of choice, with the rate dictated by clinical judgment and adjusted as guided by electrolyte determination and clinical response. It cannot be overstated that in normothermic patients with confusion, EAH is the diagnosis of exclusion and aggressive fluid resuscitation should be withheld until electrolyte determination.
Once rectal temperature descends appropriately (~38.9°C), the cooling process should stop and the individual should be transported to a hospital for further observation20 and evaluation of possible sequelae, including rhabdomyolysis and renal injury, cardiac dysfunction and arrhythmia, severe electrolyte abnormalities, acute respiratory distress syndrome, lactic acidosis, and other forms of end-organ failure (Figure).
Rapid cooling is more crucial than transport; transport poses a risk of delayed cooling, which can dramatically increase an individual’s risk of morbidity and mortality.20,23 In situations where a patient can be cooled on-site, physicians should pursue cooling before transporting the patient to a medical treatment facility.
Emergency Action Plan
Team physicians should be proactive in developing an emergency action plan to address possible EHS events. These plans should be site-specific, addressing procedures for all practice and home competition locations.12 All competition venues should have a CWI tub on-site in events where there is an increased risk of EHS.12,15,20 This tub should be set up and functional for all high-risk activities, including practices.12
Following recognition of a potential case of EHS, treatment teams should have procedures in place to transport athletes to the treatment area, obtain rectal temperature, initiate rapid cooling, and stabilize the athlete for transport to an emergency department (ED) for further evaluation.12,15 A written record of treatments and medications provided during athlete stabilization should be maintained and transported with the athlete to the ED.15 A list of helpful equipment and supplies for treatment of EHS can be found in Table 5.
EHS is a unique life-threatening situation where it is best to treat the patient on the sideline before transport.15 Those athletes transported before cooling risk spending an increased amount of time above critical temperatures for cell damage, which has been associated with increased morbidity and mortality. This mantra of “cool first, transport second” cannot be overemphasized, as those individuals with EHS who present to the ED with a persisting rectal temperature >41°F may risk up to an 80% mortality rate.24 Conversely, a recent large, retrospective study of 274 EHS events sustained during the Falmouth Road Race found a 100% survival rate when athletes were rapidly identified via rectal thermometry and treated with aggressive, rapid cooling through CWI.21
Return to Play
Perhaps the most challenging and important role the team physician has is determining an athlete’s return to play following EHI, as there currently are no evidence-based guidelines for return to activity for these athletes.7 The decisions surrounding return to play are highly individualized, as recovery from EHS and heat injury is associated with the duration of internal body temperature elevation above the critical level (40°C).7,20 Guidelines for return to activity following recovery from EHI differ among experts and institutions.7,25 The general consensus from these guidelines is that, at minimum, athletes should not participate in any physical activity until they are asymptomatic and all blood tests have normalized.11 Following this asymptomatic period, most guidelines advocate for a slow, deliberate return to activity.11 The American College of Sports Medicine (ACSM) offers one reasonable approach to the returning athlete following EHS:7
- No exercise for at least 7 days following release from medical care.
- Follow-up with a physician 1 week after release from medical care for physical examination and any warranted lab or radiologic studies (based upon organ systems affected during EHS).
- Once cleared to return to activity, the athlete begins exercise in a cool environment, gradually increasing the duration, intensity, and heat exposure over 2 weeks to demonstrate heat tolerance and acclimatization.
- Athletes who cannot resume vigorous activity due to recurrent symptoms (eg, excessive fatigue) should be reevaluated after 4 weeks. Laboratory exercise-heat tolerance testing may be useful in this setting.
- The athlete may resume full competition once they are able to participate in full training in the heat for 2 to 4 weeks without adverse effects.
Heat tolerance testing (HTT) in these athletes remains controversial.5 26 The ACSM recommends that HTT be considered only for those unable to return to vigorous activity after a suitable period (approximately 4 weeks). In contrast, the Israeli Defense Force (IDF) uses HTT to evaluate soldiers following EHS to guide decision-making about return to duty.27 The IDF HTT assumes that individuals will respond differently to heat stresses. They identify individuals who are “heat intolerant” as being unable to tolerate specific heat challenges, indicated by increases in body temperature occurring more rapidly than normal responders under identical environmental and exercise conditions. However, despite being used for more than 30 years, there is no clear evidence that HTT adequately predicts who will experience subsequent episodes of EHS.
Conclusion
While the recognized cornerstone of being a team physician is the provision of medical care, the ACSM Team Physician Consensus Statement28 further delineates the medical and administrative responsibilities as both (1) understanding medical management and prevention of injury and illness in athletes; and (2) awareness of or involvement in the development and rehearsal of an emergency action plan. These tenets are critical for the team physician who accepts the responsibility to cover sports at the high school level or higher. Football team physicians play an essential role in mitigating risk of EHI in their athletes. Through development and execution of both comprehensive prevention strategies and emergency action plans, physicians can work to minimize athletes’ risk of both developing and experiencing significant adverse outcomes from an EHI.
Am J Orthop. 2016;45(6):340-348. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.
1. Kucera KL, Klossner D, Colgate B, Cantu RC. Annual Survey of Football Injury Research: 1931-2014. National Center for Catastrophic Sport Injury Research Web site. https://nccsir.unc.edu/files/2013/10/Annual-Football-2014-Fatalities-Final.pdf. Accessed May 31, 2016.
2. Boden BP, Breit I, Beachler JA, Williams A, Mueller FO. Fatalities in high school and college football players. Am J Sports Med. 2013;41(5):1108-1116.
3. Bouchama A, Knochel JP. Heat stroke. N Engl J Med. 2002;346(25):1978-1988.
4. Racinais S, Alonso JM, Coutts AJ, et al. Consensus recommendations on training and competing in the heat. Scand J Med Sci Sports. 2015;25 Suppl 1:6-19.
5. Pryor RR, Casa DJ, Adams WM, et al. Maximizing athletic performance in the heat. Strength Cond J. 2013;35(6):24-33.
6. Adams WM, Casa DJ. Hydration for football athletes. Sports Sci Exchange. 2015;28(141):1-5.
7. American College of Sports Medicine, Armstrong LE, Casa DJ, et al. American College of Sports Medicine position stand. Exertional heat illness during training and competition. Med Sci Sports Exerc. 2007;39(3):556-572.
8. Yard EE, Gilchrist J, Haileyesus T, et al. Heat illness among high school athletes--United States, 2005-2009. J Safety Res. 2010;41(6):471-474.
9. Huffman EA, Yard EE, Fields SK, Collins CL, Comstock RD. Epidemiology of rare injuries and conditions among United States high school athletes during the 2005-2006 and 2006-2007 school years. J Athl Train. 2008;43(6):624-630.
10. Kerr ZY, Casa DJ, Marshall SW, Comstock RD. Epidemiology of exertional heat illness among U.S. high school athletes. Am J Prev Med. 2013;44(1):8-14.
11. Casa DJ, DeMartini JK, Bergeron MF, et al. National Athletic Trainers’ Association position statement: exertional heat illnesses. J Athl Train. 2015;50(9):986-1000.
12. Casa DJ, Almquist J, Anderson SA. The inter-association task force for preventing sudden death in secondary school athletics programs: best-practices recommendations. J Athl Train. 2013;48(4):546-553.
13. Gardner JW, Kark JA, Karnei K, et al. Risk factors predicting exertional heat illness in male Marine Corps recruits. Med Sci Sports Exerc. 1996;28(8):939-944.
14. Gundstein AJ, Ramseyer C, Zhao F, et al. A retrospective analysis of American football hyperthermia deaths in the United States. Int J Biometerol. 2012;56(1):11-20.
15. Armstrong LE, Johnson EC, Casa DJ, et al. The American football uniform: uncompensable heat stress and hyperthermic exhaustion. J Athl Train. 2010;45(2):117-127.
16. Casa DJ, Csillan D; Inter-Association Task Force for Preseason Secondary School Athletics Participants, et al. Preseason heat-acclimatization guidelines for secondary school athletics. J Athl Train. 2009;44(3):332-333.
17. Godek SF, Godek JJ, Bartolozzi AR. Hydration status in college football players during consecutive days of twice-a-day preseason practices. Am J Sports Med. 2005;33(6):843-851.
18. Stover EA, Zachwieja J, Stofan J, Murray R, Horswill CA. Consistently high urine specific gravity in adolescent American football players and the impact of an acute drinking strategy. Int J Sports Med. 2006;27(4):330-335.
19. Bongers CC, Thijssen DH, Veltmeijer MTW, Hopman MT, Eijsvogels TM. Precooling and percooling (cooling during exercise) both improve performance in the heat: a meta-analytical review. Br J Sports Med. 2015;49(6):377-384.
20. Casa DJ, McDermott BP, Lee EC, Yeargin SW, Armstrong LE, Maresh CM. Cold water immersion: the gold standard for exertional heatstroke treatment. Exerc Sport Sci Rev. 2007;35(3):141-149.
21. DeMartini JK, Casa DJ, Stearns R, et al. Effectiveness of cold water immersion in the treatment of exertional heat stroke at the Falmouth Road Race. Med Sci Sports Exerc. 2015;47(2):240-245.
22. Casa DJ, Kenny GP, Taylor NA. Immersion treatment for exertional hyperthermia: cold or temperate water? Med Sci Sports Exerc. 2010;42(7):1246-1252.
23. Casa DJ, Armstrong LE, Kenny GP, O’Connor FG, Huggins RA. Exertional heat stroke: new concepts regarding cause and care. Curr Sports Med Rep. 2012;11(3):115-122.
24. Argaud L, Ferry T, Le QH, et al. Short- and long-term outcomes of heat stroke following the 2003 heat wave in Lyon, France. Arch Intern Med. 2007;167(20):2177-2183.
25. O’Connor FG, Casa DJ, Bergeron MF, et al. American College of Sports Medicine Roundtable on exertional heat stroke--return to duty/return to play: conference proceedings. Curr Sports Med Rep. 2010;9(5):314-321.
26. Kazman JB, Heled Y, Lisman PJ, Druyan A, Deuster PA, O’Connor FG. Exertional heat illness: the role of heat tolerance testing. Curr Sports Med Rep. 2013;12(2):101-105.
27. Moran DS, Heled Y, Still L, Laor A, Shapiro Y. Assessment of heat tolerance for post exertional heat stroke individuals. Med Sci Monit. 2004;10(6):CR252-CR257.
28. Herring SA, Kibler WB, Putukian M. Team Physician Consensus Statement: 2013 update. Med Sci Sports Exerc. 2013;45(8):1618-1622.
29. Heat stroke treatment. Korey Stringer Institute University of Connecticut Web site. http://ksi.uconn.edu/emergency-conditions/heat-illnesses/exertional-heat-stroke/heat-stroke-treatment/. Accessed June 14, 2016.
30. Headquarters, Department of the Army and the Air Force. Heat Stress Control and Heat Casualty Management. Technical Bulletin Medical 507. http://www.dir.ca.gov/oshsb/documents/Heat_illness_prevention_tbmed507.pdf. Published March 7, 2003. Accessed June 14, 2016.
Football, one of the most popular sports in the United States, is additionally recognized as a leading contributor to sports injury secondary to the contact collision nature of the endeavor. There are an estimated 1.1 million high school football players with another 100,000 participants combined in the National Football League (NFL), college, junior college, Arena Football League, and semipro levels of play.1 USA Football estimates that an additional 3 million youth participate in community football leagues.1 The National Center for Catastrophic Sports Injury Research recently calculated a fatality rate of 0.14 per 100,000 participants in 2014 for the 4.2 million who play football at all levels—and 0.45 per 100,000 in high school.1 While direct deaths from head and spine injury remain a significant contributor to the number of catastrophic injuries, indirect deaths (systemic failure) predominate. Exertional heat stroke (EHS) has emerged as one of the leading indirect causes of death in high school and collegiate football. Boden and colleagues2 reported that high school and college football players sustain approximately 12 fatalities annually, with indirect systemic causes being twice as common as direct blunt trauma.2The most common indirect causes identified included cardiac failure, heat illness, and complications of sickle cell trait (SCT). It was also noted that the risk of SCT, heat-related, and cardiac deaths increased during the second decade of the study, indicating these conditions may require a greater emphasis on diagnosis, treatment, and prevention. This review details for the team physician the unique challenge of exercising in the heat to the football player, and the prevention, diagnosis, management and return-to-play issues pertinent to exertional heat illness (EHI).
The Challenge
EHS represents the most severe manifestation of EHI—a gamut of diseases commonly encountered during the hot summer months when American football season begins. The breadth of EHI includes several important clinical diagnoses: exercise-associated muscle cramps (heat cramps); heat exhaustion with and without syncope; heat injury with evidence of end organ injury (eg, rhabdomyolysis); and EHS. EHS is defined as “a form of hyperthermia associated with a systemic inflammatory response leading to a syndrome of multi-organ dysfunction in which encephalopathy predominates.”3 EHS, if left untreated, or even if clinical treatment is delayed, may result in significant end organ morbidity and/or mortality.
During exercise, the human thermoregulatory system mitigates heat gain by increasing skin blood flow and sweating, causing an increased dissipation of heat to the surrounding environment by leveraging conduction, convection, and evaporation.4,5 Elevated environmental temperatures, increased humidity, and dehydration can impede the body’s ability to dissipate heat at a rate needed to maintain thermoregulation. This imbalance can result in hyperthermia secondary to uncompensated heat stress,5 which in turn can lead to EHI. Football players have unique challenges that make them particularly vulnerable to EHI. The summer heat during early-season participation and the requirement for equipment that covers nearly 60% of body surfaces pose increased risk of volume losses and hyperthermia that trigger the onset of EHI.6 Football athletes’ body compositions and physical size are additional contributing risk factors; the relatively high muscle and fat content increase thermogenicity, which require their bodies to dissipate more heat.7
An estimated 9000 cases of EHI occur annually across all high school sports,8 with an incidence of 1.6:100,000 athlete-exposures.8,9 Studies have demonstrated, however, that EHI occurs in football 11.4 times more often than in all other high school sports combined.10 The incidence of nonfatal EHI in all levels of football is 4.42-5:100,000.8,9 Between 2000 and 2014, 41 football players died from EHS.1 In football, approximately 75% of all EHI events occurred during practices, while only 25% of incidents occurred during games.8
Given these potentially deadly consequences, it is important that football team physicians are not only alert to the early symptoms of heat illness and prepared to intervene to prevent the progression to EHS, but are critical leaders in educating coaches and players in evidence-based EHI prevention practices and policies.
Prevention
EHS is a preventable condition, arguably the most common cause of preventable nontraumatic exertional death in young athletes in the United States. Close attention to mitigating risk factors should begin prior to the onset of preseason practice and continue through the early season, where athletes are at the highest risk of developing heat illness.
Primary Prevention
Primary prevention is fundamental to minimizing the occurrences of EHI. It focuses on the following methods: recognition of inherent risk factors, acclimatization, hydration, and avoidance of inciting substances (including supplements).
Pre-Participation Examination. The purpose of the pre-participation examination (PPE) is to maximize an athlete’s safety by identifying medical conditions that place the athlete at risk.11,12 The Preparticipation Physical Evaluation, 4th edition, the most widely used consensus publication, specifically queries if an athlete has a previous history of heat injury. However, it only indirectly addresses intrinsic risk factors that may predispose an athlete to EHI who has never had an EHI before. Therefore, providers should take the opportunity of the PPE to inquire about additional risk factors that may make an athlete high risk for sustaining a heat injury. Common risk factors for EHI are listed in Table 1.
Heat Acclimatization. The risk of EHI escalates significantly when athletes are subjected to multiple stressors during periods of heat exposure, such as sudden increases in intensity or duration of exercise; prolonged new exposures to heat; dehydration; and sleep loss.5 When football season begins in late summer, athletes are least conditioned as temperatures reach their seasonal peak, causing increased risk of EHI.15 Planning for heat acclimatization is vital for all athletes who exercise in hot environments. Acclimatization procedures place progressively mounting physiologic strains on the body to improve athletes’ ability to dissipate heat, diminishing thermoregulatory and cardiovascular exertion.4,5 Acclimatization begins with expansion of plasma volume on days 3 to 6, causing improvements in cardiac efficiency and resulting in an overall decrease in basal internal body temperature.4,5,15 This process results in improvements in heat tolerance and exercise performance, evolving over 10 to 14 days of gradual escalation of exercise intensity and duration.5,10,11,16 However, poor fitness levels and extreme temperatures can prolong this period, requiring up to 2 to 3 months to fully take effect.5,7
The National Athletic Trainers Association (NATA) and National Collegiate Athletic Association (NCAA) have released consensus guidelines regarding heat acclimatization protocols for football athletes at the high school and college levels (Tables 3 and 4). Each of these guidelines involves an initial period without use of protective equipment, followed by a gradual addition of further equipment.11,16
Secondary Prevention
Despite physicians’ best efforts to prevent all cases of EHI, athletes will still experience the effects of exercise-induced hyperthermia. The goal of secondary prevention is to slow the progression of this hyperthermia so that it does not progress to more dangerous EHI.
Hydration. Dehydration is an important risk factor for EHI. Sweat maintains thermoregulation by dissipating heat generated during exercise; however, it also contributes to body water losses. Furthermore, intravascular depletion decreases stroke volume, thereby increasing cardiovascular strain. It is estimated that for every 1% loss in body mass from dehydration, body temperature rises 0.22°C in comparison to a euhydrated state.6 Dehydration occurs more rapidly in hot environments, as fluid is lost through increased sweat production.7 After approximately 6% to 10% body weight volume loss, cardiac output cannot be maintained, diminishing sweat production and blood flow to both skin and muscle and causing diminished performance and a significant risk of heat exhaustion.7 If left unchecked, these physiologic changes result in further elevations in body temperature and increased cardiovascular strain, ultimately placing the athlete at significant risk for development of EHS.
Adequate hydration to maintain euvolemia is an important step in avoiding possible EHI. Multiple studies have shown that football players experience a baseline hypovolemia during their competition season,6 a deficit that is most marked during the first week of practices.17 This deficit is multifactorial, as football players expend a significant amount of fluid through sweat, are not able to adequately replace these losses during practice, and do not appropriately hydrate off the field.6,18 Some players, especially linemen, sweat at a higher rate than their teammates, posing a possible risk of significant dehydration.6 Coaches and players alike should be educated on the importance of adequate hydration to meet their fluid needs.
The goal of hydration during exercise is to prevent large fluid losses that can adversely affect performance and increase risk of EHI;6 it may be unrealistic to replace all fluid losses during the practice period. Instead, athletes should target complete volume replacement over the post-exercise period.6 Some recommend hydrating based upon thirst drive; however, thirst is activated following a volume loss of approximately 2% body mass, the same degree of losses that place athletes at an increased risk for performance impairment and EHI.4,6,11,12 Individuals should have access to fluids throughout practice and competition and be encouraged to hydrate as needed.6,12,15 Furthermore, staff should modify their practices based upon WBGT and acclimatization status to provide more frequent hydration breaks.
Hyperhydration and Salt Intake. Of note, there are inherent risks to hyperhydration. Athletes with low sweat rates have an increased risk of overhydration and the development of exercise-associated hyponatremia (EAH),6 a condition whose presentation is very similar to EHS. In addition, inadequate sodium intake and excessive sweating can also contribute to the development of EAH. EAH has been implicated in the deaths of 2 football players in 2014.1,6 Establishing team hydration guidelines and educating players and staff on appropriate hydration and dietary salt intake is essential to reduce the risk of both dehydration and hyperhydration and their complications.6Intra-Event Cooling. During exercise, team physicians can employ strategies for cooling athletes during exertion to mitigate their risk of EHI by decreasing thermal and cardiovascular strain.4,19 Cooling during exercise is hypothesized to allow for accelerated heat dissipation, where heat is lost from the body more effectively. This accelerated loss enables athletes to maintain a higher heat storage capacity over the duration of exercise, avoiding uncompensated heat stresses that ultimately cause EHI.19
Some intra-event cooling strategies include the use of cooling garments, cooling packs, and cold water/slurry ingestion. Cooling garments lower skin temperature, which in turn can decrease thermoregulatory strains;4 a recent meta-analysis of intra-event cooling modalities revealed that wearing an ice vest during exercise resulted in the greatest decrease in thermal heat strain.19 Internal cooling strategies—namely ingestion of cold fluids/ice slurry—have shown some mild benefit in decreasing internal temperatures; however, some studies have demonstrated some decrease in sweat production associated with cold oral intake used in isolation.19 Overall, studies have shown that combining external (cooling clothing, ice packs, fanning) and internal (cold water, ice slurry) cooling methods result in a greater cooling effect than a use of a single method.4
Tertiary Prevention
The goal of tertiary prevention is to mitigate the risk of long-term adverse outcomes following an EHS event. The most effective means of reducing risk for morbidity and mortality is rapid identification and treatment of EHS as well as close evaluation of an athlete’s return to activity in heat. This process is spearheaded by an effective and well-rehearsed emergency action plan.
Diagnosis and Management
Rapid identification and treatment of EHS is crucial to minimizing the risk of poor outcomes.7 Any delay in the treatment of EHS can dramatically increase the likelihood of associated morbidity and mortality.20
EHS is diagnosed by an elevated rectal temperature ≥40°C (104°F) and associated central nervous system (CNS) dysfunction.21 EHS should be strongly suspected in any athlete exercising in heat who exhibits signs of CNS dysfunction, including disorientation, confusion, dizziness, erratic behavior, irritability, headache, loss of coordination, delirium, collapse, or seizures.7,12,15 EHS may also present with symptoms of heat exhaustion, including fatigue, hyperventilation, tachycardia, vomiting, diarrhea, and hypotension.7,12,15
Rectal temperature should be taken for any athlete with suspected EHS, as other modalities—oral, skin, axillary, and aural—can be inaccurate and easily modified by ambient confounders such as ambient and skin temperature, athlete hyperventilation, and consumption of liquids.7,11,12 Athletes exhibiting CNS symptoms with moderately elevated rectal temperatures that do not exceed 40°C should also be assumed to be suffering from EHS and treated with rapid cooling.11 On the other hand, athletes with CNS symptoms who are normothermic should be assumed to have EAH until ruled out by electrolyte assessment; IV fluids should be at no more than keep vein open (KVO) pending this determination.11 In some cases, an athlete may initially present with altered mental status but return to “normal.” However, this improvement may represent a “lucid period”; evaluation should continue with rectal temperature and treatment, as EHS in these cases may progress quickly.15
Treatment is centered on rapid, whole body cooling initiated at the first sign of heat illness.7,22 The goal of treatment is to achieve a rectal temperature <38.9°C within 30 minutes of the onset of EHS.15 Upon diagnosis, the athlete should be quickly placed in a tub of ice water to facilitate cold water immersion (CWI) therapy. Some guidelines suggest the athlete’s clothing be removed to potentiate evaporative cooling during CWI;12 however, cooling should not be delayed due to difficulties in removing equipment. CWI, where a heat stroke victim is submerged in ice water up to their neck while water is continuously circulated, is generally considered to be the gold standard treatment as it is the modality with the highest recorded cooling rates and the lowest rate of morbidity and mortality.7,20,21 Multiple studies of CWI have shown that survival nears 100% when aggressive cooling starts within 5 minutes of collapse or identification of EHS.20,21,22
If whole body CWI is unavailable, alternative methods of rapid cooling should be employed. Partial CWI, with torso immersion being preferable to the extremities, has been shown to achieve an acceptable rate of cooling to achieve sufficient drops in internal body temperature.20,23 However, one popular treatment—applying ice packs to the whole body, in particular to the groin and axillae—has not been shown to be sufficient to achieve standard cooling goals.20 None of these methods have been shown to be as effective as CWI.23
Intravenous access should be initiated with fluid resuscitation dictated by the provider’s assessment. Normal saline is recommended as the resuscitative fluid of choice, with the rate dictated by clinical judgment and adjusted as guided by electrolyte determination and clinical response. It cannot be overstated that in normothermic patients with confusion, EAH is the diagnosis of exclusion and aggressive fluid resuscitation should be withheld until electrolyte determination.
Once rectal temperature descends appropriately (~38.9°C), the cooling process should stop and the individual should be transported to a hospital for further observation20 and evaluation of possible sequelae, including rhabdomyolysis and renal injury, cardiac dysfunction and arrhythmia, severe electrolyte abnormalities, acute respiratory distress syndrome, lactic acidosis, and other forms of end-organ failure (Figure).
Rapid cooling is more crucial than transport; transport poses a risk of delayed cooling, which can dramatically increase an individual’s risk of morbidity and mortality.20,23 In situations where a patient can be cooled on-site, physicians should pursue cooling before transporting the patient to a medical treatment facility.
Emergency Action Plan
Team physicians should be proactive in developing an emergency action plan to address possible EHS events. These plans should be site-specific, addressing procedures for all practice and home competition locations.12 All competition venues should have a CWI tub on-site in events where there is an increased risk of EHS.12,15,20 This tub should be set up and functional for all high-risk activities, including practices.12
Following recognition of a potential case of EHS, treatment teams should have procedures in place to transport athletes to the treatment area, obtain rectal temperature, initiate rapid cooling, and stabilize the athlete for transport to an emergency department (ED) for further evaluation.12,15 A written record of treatments and medications provided during athlete stabilization should be maintained and transported with the athlete to the ED.15 A list of helpful equipment and supplies for treatment of EHS can be found in Table 5.
EHS is a unique life-threatening situation where it is best to treat the patient on the sideline before transport.15 Those athletes transported before cooling risk spending an increased amount of time above critical temperatures for cell damage, which has been associated with increased morbidity and mortality. This mantra of “cool first, transport second” cannot be overemphasized, as those individuals with EHS who present to the ED with a persisting rectal temperature >41°F may risk up to an 80% mortality rate.24 Conversely, a recent large, retrospective study of 274 EHS events sustained during the Falmouth Road Race found a 100% survival rate when athletes were rapidly identified via rectal thermometry and treated with aggressive, rapid cooling through CWI.21
Return to Play
Perhaps the most challenging and important role the team physician has is determining an athlete’s return to play following EHI, as there currently are no evidence-based guidelines for return to activity for these athletes.7 The decisions surrounding return to play are highly individualized, as recovery from EHS and heat injury is associated with the duration of internal body temperature elevation above the critical level (40°C).7,20 Guidelines for return to activity following recovery from EHI differ among experts and institutions.7,25 The general consensus from these guidelines is that, at minimum, athletes should not participate in any physical activity until they are asymptomatic and all blood tests have normalized.11 Following this asymptomatic period, most guidelines advocate for a slow, deliberate return to activity.11 The American College of Sports Medicine (ACSM) offers one reasonable approach to the returning athlete following EHS:7
- No exercise for at least 7 days following release from medical care.
- Follow-up with a physician 1 week after release from medical care for physical examination and any warranted lab or radiologic studies (based upon organ systems affected during EHS).
- Once cleared to return to activity, the athlete begins exercise in a cool environment, gradually increasing the duration, intensity, and heat exposure over 2 weeks to demonstrate heat tolerance and acclimatization.
- Athletes who cannot resume vigorous activity due to recurrent symptoms (eg, excessive fatigue) should be reevaluated after 4 weeks. Laboratory exercise-heat tolerance testing may be useful in this setting.
- The athlete may resume full competition once they are able to participate in full training in the heat for 2 to 4 weeks without adverse effects.
Heat tolerance testing (HTT) in these athletes remains controversial.5 26 The ACSM recommends that HTT be considered only for those unable to return to vigorous activity after a suitable period (approximately 4 weeks). In contrast, the Israeli Defense Force (IDF) uses HTT to evaluate soldiers following EHS to guide decision-making about return to duty.27 The IDF HTT assumes that individuals will respond differently to heat stresses. They identify individuals who are “heat intolerant” as being unable to tolerate specific heat challenges, indicated by increases in body temperature occurring more rapidly than normal responders under identical environmental and exercise conditions. However, despite being used for more than 30 years, there is no clear evidence that HTT adequately predicts who will experience subsequent episodes of EHS.
Conclusion
While the recognized cornerstone of being a team physician is the provision of medical care, the ACSM Team Physician Consensus Statement28 further delineates the medical and administrative responsibilities as both (1) understanding medical management and prevention of injury and illness in athletes; and (2) awareness of or involvement in the development and rehearsal of an emergency action plan. These tenets are critical for the team physician who accepts the responsibility to cover sports at the high school level or higher. Football team physicians play an essential role in mitigating risk of EHI in their athletes. Through development and execution of both comprehensive prevention strategies and emergency action plans, physicians can work to minimize athletes’ risk of both developing and experiencing significant adverse outcomes from an EHI.
Am J Orthop. 2016;45(6):340-348. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.
Football, one of the most popular sports in the United States, is additionally recognized as a leading contributor to sports injury secondary to the contact collision nature of the endeavor. There are an estimated 1.1 million high school football players with another 100,000 participants combined in the National Football League (NFL), college, junior college, Arena Football League, and semipro levels of play.1 USA Football estimates that an additional 3 million youth participate in community football leagues.1 The National Center for Catastrophic Sports Injury Research recently calculated a fatality rate of 0.14 per 100,000 participants in 2014 for the 4.2 million who play football at all levels—and 0.45 per 100,000 in high school.1 While direct deaths from head and spine injury remain a significant contributor to the number of catastrophic injuries, indirect deaths (systemic failure) predominate. Exertional heat stroke (EHS) has emerged as one of the leading indirect causes of death in high school and collegiate football. Boden and colleagues2 reported that high school and college football players sustain approximately 12 fatalities annually, with indirect systemic causes being twice as common as direct blunt trauma.2The most common indirect causes identified included cardiac failure, heat illness, and complications of sickle cell trait (SCT). It was also noted that the risk of SCT, heat-related, and cardiac deaths increased during the second decade of the study, indicating these conditions may require a greater emphasis on diagnosis, treatment, and prevention. This review details for the team physician the unique challenge of exercising in the heat to the football player, and the prevention, diagnosis, management and return-to-play issues pertinent to exertional heat illness (EHI).
The Challenge
EHS represents the most severe manifestation of EHI—a gamut of diseases commonly encountered during the hot summer months when American football season begins. The breadth of EHI includes several important clinical diagnoses: exercise-associated muscle cramps (heat cramps); heat exhaustion with and without syncope; heat injury with evidence of end organ injury (eg, rhabdomyolysis); and EHS. EHS is defined as “a form of hyperthermia associated with a systemic inflammatory response leading to a syndrome of multi-organ dysfunction in which encephalopathy predominates.”3 EHS, if left untreated, or even if clinical treatment is delayed, may result in significant end organ morbidity and/or mortality.
During exercise, the human thermoregulatory system mitigates heat gain by increasing skin blood flow and sweating, causing an increased dissipation of heat to the surrounding environment by leveraging conduction, convection, and evaporation.4,5 Elevated environmental temperatures, increased humidity, and dehydration can impede the body’s ability to dissipate heat at a rate needed to maintain thermoregulation. This imbalance can result in hyperthermia secondary to uncompensated heat stress,5 which in turn can lead to EHI. Football players have unique challenges that make them particularly vulnerable to EHI. The summer heat during early-season participation and the requirement for equipment that covers nearly 60% of body surfaces pose increased risk of volume losses and hyperthermia that trigger the onset of EHI.6 Football athletes’ body compositions and physical size are additional contributing risk factors; the relatively high muscle and fat content increase thermogenicity, which require their bodies to dissipate more heat.7
An estimated 9000 cases of EHI occur annually across all high school sports,8 with an incidence of 1.6:100,000 athlete-exposures.8,9 Studies have demonstrated, however, that EHI occurs in football 11.4 times more often than in all other high school sports combined.10 The incidence of nonfatal EHI in all levels of football is 4.42-5:100,000.8,9 Between 2000 and 2014, 41 football players died from EHS.1 In football, approximately 75% of all EHI events occurred during practices, while only 25% of incidents occurred during games.8
Given these potentially deadly consequences, it is important that football team physicians are not only alert to the early symptoms of heat illness and prepared to intervene to prevent the progression to EHS, but are critical leaders in educating coaches and players in evidence-based EHI prevention practices and policies.
Prevention
EHS is a preventable condition, arguably the most common cause of preventable nontraumatic exertional death in young athletes in the United States. Close attention to mitigating risk factors should begin prior to the onset of preseason practice and continue through the early season, where athletes are at the highest risk of developing heat illness.
Primary Prevention
Primary prevention is fundamental to minimizing the occurrences of EHI. It focuses on the following methods: recognition of inherent risk factors, acclimatization, hydration, and avoidance of inciting substances (including supplements).
Pre-Participation Examination. The purpose of the pre-participation examination (PPE) is to maximize an athlete’s safety by identifying medical conditions that place the athlete at risk.11,12 The Preparticipation Physical Evaluation, 4th edition, the most widely used consensus publication, specifically queries if an athlete has a previous history of heat injury. However, it only indirectly addresses intrinsic risk factors that may predispose an athlete to EHI who has never had an EHI before. Therefore, providers should take the opportunity of the PPE to inquire about additional risk factors that may make an athlete high risk for sustaining a heat injury. Common risk factors for EHI are listed in Table 1.
Heat Acclimatization. The risk of EHI escalates significantly when athletes are subjected to multiple stressors during periods of heat exposure, such as sudden increases in intensity or duration of exercise; prolonged new exposures to heat; dehydration; and sleep loss.5 When football season begins in late summer, athletes are least conditioned as temperatures reach their seasonal peak, causing increased risk of EHI.15 Planning for heat acclimatization is vital for all athletes who exercise in hot environments. Acclimatization procedures place progressively mounting physiologic strains on the body to improve athletes’ ability to dissipate heat, diminishing thermoregulatory and cardiovascular exertion.4,5 Acclimatization begins with expansion of plasma volume on days 3 to 6, causing improvements in cardiac efficiency and resulting in an overall decrease in basal internal body temperature.4,5,15 This process results in improvements in heat tolerance and exercise performance, evolving over 10 to 14 days of gradual escalation of exercise intensity and duration.5,10,11,16 However, poor fitness levels and extreme temperatures can prolong this period, requiring up to 2 to 3 months to fully take effect.5,7
The National Athletic Trainers Association (NATA) and National Collegiate Athletic Association (NCAA) have released consensus guidelines regarding heat acclimatization protocols for football athletes at the high school and college levels (Tables 3 and 4). Each of these guidelines involves an initial period without use of protective equipment, followed by a gradual addition of further equipment.11,16
Secondary Prevention
Despite physicians’ best efforts to prevent all cases of EHI, athletes will still experience the effects of exercise-induced hyperthermia. The goal of secondary prevention is to slow the progression of this hyperthermia so that it does not progress to more dangerous EHI.
Hydration. Dehydration is an important risk factor for EHI. Sweat maintains thermoregulation by dissipating heat generated during exercise; however, it also contributes to body water losses. Furthermore, intravascular depletion decreases stroke volume, thereby increasing cardiovascular strain. It is estimated that for every 1% loss in body mass from dehydration, body temperature rises 0.22°C in comparison to a euhydrated state.6 Dehydration occurs more rapidly in hot environments, as fluid is lost through increased sweat production.7 After approximately 6% to 10% body weight volume loss, cardiac output cannot be maintained, diminishing sweat production and blood flow to both skin and muscle and causing diminished performance and a significant risk of heat exhaustion.7 If left unchecked, these physiologic changes result in further elevations in body temperature and increased cardiovascular strain, ultimately placing the athlete at significant risk for development of EHS.
Adequate hydration to maintain euvolemia is an important step in avoiding possible EHI. Multiple studies have shown that football players experience a baseline hypovolemia during their competition season,6 a deficit that is most marked during the first week of practices.17 This deficit is multifactorial, as football players expend a significant amount of fluid through sweat, are not able to adequately replace these losses during practice, and do not appropriately hydrate off the field.6,18 Some players, especially linemen, sweat at a higher rate than their teammates, posing a possible risk of significant dehydration.6 Coaches and players alike should be educated on the importance of adequate hydration to meet their fluid needs.
The goal of hydration during exercise is to prevent large fluid losses that can adversely affect performance and increase risk of EHI;6 it may be unrealistic to replace all fluid losses during the practice period. Instead, athletes should target complete volume replacement over the post-exercise period.6 Some recommend hydrating based upon thirst drive; however, thirst is activated following a volume loss of approximately 2% body mass, the same degree of losses that place athletes at an increased risk for performance impairment and EHI.4,6,11,12 Individuals should have access to fluids throughout practice and competition and be encouraged to hydrate as needed.6,12,15 Furthermore, staff should modify their practices based upon WBGT and acclimatization status to provide more frequent hydration breaks.
Hyperhydration and Salt Intake. Of note, there are inherent risks to hyperhydration. Athletes with low sweat rates have an increased risk of overhydration and the development of exercise-associated hyponatremia (EAH),6 a condition whose presentation is very similar to EHS. In addition, inadequate sodium intake and excessive sweating can also contribute to the development of EAH. EAH has been implicated in the deaths of 2 football players in 2014.1,6 Establishing team hydration guidelines and educating players and staff on appropriate hydration and dietary salt intake is essential to reduce the risk of both dehydration and hyperhydration and their complications.6Intra-Event Cooling. During exercise, team physicians can employ strategies for cooling athletes during exertion to mitigate their risk of EHI by decreasing thermal and cardiovascular strain.4,19 Cooling during exercise is hypothesized to allow for accelerated heat dissipation, where heat is lost from the body more effectively. This accelerated loss enables athletes to maintain a higher heat storage capacity over the duration of exercise, avoiding uncompensated heat stresses that ultimately cause EHI.19
Some intra-event cooling strategies include the use of cooling garments, cooling packs, and cold water/slurry ingestion. Cooling garments lower skin temperature, which in turn can decrease thermoregulatory strains;4 a recent meta-analysis of intra-event cooling modalities revealed that wearing an ice vest during exercise resulted in the greatest decrease in thermal heat strain.19 Internal cooling strategies—namely ingestion of cold fluids/ice slurry—have shown some mild benefit in decreasing internal temperatures; however, some studies have demonstrated some decrease in sweat production associated with cold oral intake used in isolation.19 Overall, studies have shown that combining external (cooling clothing, ice packs, fanning) and internal (cold water, ice slurry) cooling methods result in a greater cooling effect than a use of a single method.4
Tertiary Prevention
The goal of tertiary prevention is to mitigate the risk of long-term adverse outcomes following an EHS event. The most effective means of reducing risk for morbidity and mortality is rapid identification and treatment of EHS as well as close evaluation of an athlete’s return to activity in heat. This process is spearheaded by an effective and well-rehearsed emergency action plan.
Diagnosis and Management
Rapid identification and treatment of EHS is crucial to minimizing the risk of poor outcomes.7 Any delay in the treatment of EHS can dramatically increase the likelihood of associated morbidity and mortality.20
EHS is diagnosed by an elevated rectal temperature ≥40°C (104°F) and associated central nervous system (CNS) dysfunction.21 EHS should be strongly suspected in any athlete exercising in heat who exhibits signs of CNS dysfunction, including disorientation, confusion, dizziness, erratic behavior, irritability, headache, loss of coordination, delirium, collapse, or seizures.7,12,15 EHS may also present with symptoms of heat exhaustion, including fatigue, hyperventilation, tachycardia, vomiting, diarrhea, and hypotension.7,12,15
Rectal temperature should be taken for any athlete with suspected EHS, as other modalities—oral, skin, axillary, and aural—can be inaccurate and easily modified by ambient confounders such as ambient and skin temperature, athlete hyperventilation, and consumption of liquids.7,11,12 Athletes exhibiting CNS symptoms with moderately elevated rectal temperatures that do not exceed 40°C should also be assumed to be suffering from EHS and treated with rapid cooling.11 On the other hand, athletes with CNS symptoms who are normothermic should be assumed to have EAH until ruled out by electrolyte assessment; IV fluids should be at no more than keep vein open (KVO) pending this determination.11 In some cases, an athlete may initially present with altered mental status but return to “normal.” However, this improvement may represent a “lucid period”; evaluation should continue with rectal temperature and treatment, as EHS in these cases may progress quickly.15
Treatment is centered on rapid, whole body cooling initiated at the first sign of heat illness.7,22 The goal of treatment is to achieve a rectal temperature <38.9°C within 30 minutes of the onset of EHS.15 Upon diagnosis, the athlete should be quickly placed in a tub of ice water to facilitate cold water immersion (CWI) therapy. Some guidelines suggest the athlete’s clothing be removed to potentiate evaporative cooling during CWI;12 however, cooling should not be delayed due to difficulties in removing equipment. CWI, where a heat stroke victim is submerged in ice water up to their neck while water is continuously circulated, is generally considered to be the gold standard treatment as it is the modality with the highest recorded cooling rates and the lowest rate of morbidity and mortality.7,20,21 Multiple studies of CWI have shown that survival nears 100% when aggressive cooling starts within 5 minutes of collapse or identification of EHS.20,21,22
If whole body CWI is unavailable, alternative methods of rapid cooling should be employed. Partial CWI, with torso immersion being preferable to the extremities, has been shown to achieve an acceptable rate of cooling to achieve sufficient drops in internal body temperature.20,23 However, one popular treatment—applying ice packs to the whole body, in particular to the groin and axillae—has not been shown to be sufficient to achieve standard cooling goals.20 None of these methods have been shown to be as effective as CWI.23
Intravenous access should be initiated with fluid resuscitation dictated by the provider’s assessment. Normal saline is recommended as the resuscitative fluid of choice, with the rate dictated by clinical judgment and adjusted as guided by electrolyte determination and clinical response. It cannot be overstated that in normothermic patients with confusion, EAH is the diagnosis of exclusion and aggressive fluid resuscitation should be withheld until electrolyte determination.
Once rectal temperature descends appropriately (~38.9°C), the cooling process should stop and the individual should be transported to a hospital for further observation20 and evaluation of possible sequelae, including rhabdomyolysis and renal injury, cardiac dysfunction and arrhythmia, severe electrolyte abnormalities, acute respiratory distress syndrome, lactic acidosis, and other forms of end-organ failure (Figure).
Rapid cooling is more crucial than transport; transport poses a risk of delayed cooling, which can dramatically increase an individual’s risk of morbidity and mortality.20,23 In situations where a patient can be cooled on-site, physicians should pursue cooling before transporting the patient to a medical treatment facility.
Emergency Action Plan
Team physicians should be proactive in developing an emergency action plan to address possible EHS events. These plans should be site-specific, addressing procedures for all practice and home competition locations.12 All competition venues should have a CWI tub on-site in events where there is an increased risk of EHS.12,15,20 This tub should be set up and functional for all high-risk activities, including practices.12
Following recognition of a potential case of EHS, treatment teams should have procedures in place to transport athletes to the treatment area, obtain rectal temperature, initiate rapid cooling, and stabilize the athlete for transport to an emergency department (ED) for further evaluation.12,15 A written record of treatments and medications provided during athlete stabilization should be maintained and transported with the athlete to the ED.15 A list of helpful equipment and supplies for treatment of EHS can be found in Table 5.
EHS is a unique life-threatening situation where it is best to treat the patient on the sideline before transport.15 Those athletes transported before cooling risk spending an increased amount of time above critical temperatures for cell damage, which has been associated with increased morbidity and mortality. This mantra of “cool first, transport second” cannot be overemphasized, as those individuals with EHS who present to the ED with a persisting rectal temperature >41°F may risk up to an 80% mortality rate.24 Conversely, a recent large, retrospective study of 274 EHS events sustained during the Falmouth Road Race found a 100% survival rate when athletes were rapidly identified via rectal thermometry and treated with aggressive, rapid cooling through CWI.21
Return to Play
Perhaps the most challenging and important role the team physician has is determining an athlete’s return to play following EHI, as there currently are no evidence-based guidelines for return to activity for these athletes.7 The decisions surrounding return to play are highly individualized, as recovery from EHS and heat injury is associated with the duration of internal body temperature elevation above the critical level (40°C).7,20 Guidelines for return to activity following recovery from EHI differ among experts and institutions.7,25 The general consensus from these guidelines is that, at minimum, athletes should not participate in any physical activity until they are asymptomatic and all blood tests have normalized.11 Following this asymptomatic period, most guidelines advocate for a slow, deliberate return to activity.11 The American College of Sports Medicine (ACSM) offers one reasonable approach to the returning athlete following EHS:7
- No exercise for at least 7 days following release from medical care.
- Follow-up with a physician 1 week after release from medical care for physical examination and any warranted lab or radiologic studies (based upon organ systems affected during EHS).
- Once cleared to return to activity, the athlete begins exercise in a cool environment, gradually increasing the duration, intensity, and heat exposure over 2 weeks to demonstrate heat tolerance and acclimatization.
- Athletes who cannot resume vigorous activity due to recurrent symptoms (eg, excessive fatigue) should be reevaluated after 4 weeks. Laboratory exercise-heat tolerance testing may be useful in this setting.
- The athlete may resume full competition once they are able to participate in full training in the heat for 2 to 4 weeks without adverse effects.
Heat tolerance testing (HTT) in these athletes remains controversial.5 26 The ACSM recommends that HTT be considered only for those unable to return to vigorous activity after a suitable period (approximately 4 weeks). In contrast, the Israeli Defense Force (IDF) uses HTT to evaluate soldiers following EHS to guide decision-making about return to duty.27 The IDF HTT assumes that individuals will respond differently to heat stresses. They identify individuals who are “heat intolerant” as being unable to tolerate specific heat challenges, indicated by increases in body temperature occurring more rapidly than normal responders under identical environmental and exercise conditions. However, despite being used for more than 30 years, there is no clear evidence that HTT adequately predicts who will experience subsequent episodes of EHS.
Conclusion
While the recognized cornerstone of being a team physician is the provision of medical care, the ACSM Team Physician Consensus Statement28 further delineates the medical and administrative responsibilities as both (1) understanding medical management and prevention of injury and illness in athletes; and (2) awareness of or involvement in the development and rehearsal of an emergency action plan. These tenets are critical for the team physician who accepts the responsibility to cover sports at the high school level or higher. Football team physicians play an essential role in mitigating risk of EHI in their athletes. Through development and execution of both comprehensive prevention strategies and emergency action plans, physicians can work to minimize athletes’ risk of both developing and experiencing significant adverse outcomes from an EHI.
Am J Orthop. 2016;45(6):340-348. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.
1. Kucera KL, Klossner D, Colgate B, Cantu RC. Annual Survey of Football Injury Research: 1931-2014. National Center for Catastrophic Sport Injury Research Web site. https://nccsir.unc.edu/files/2013/10/Annual-Football-2014-Fatalities-Final.pdf. Accessed May 31, 2016.
2. Boden BP, Breit I, Beachler JA, Williams A, Mueller FO. Fatalities in high school and college football players. Am J Sports Med. 2013;41(5):1108-1116.
3. Bouchama A, Knochel JP. Heat stroke. N Engl J Med. 2002;346(25):1978-1988.
4. Racinais S, Alonso JM, Coutts AJ, et al. Consensus recommendations on training and competing in the heat. Scand J Med Sci Sports. 2015;25 Suppl 1:6-19.
5. Pryor RR, Casa DJ, Adams WM, et al. Maximizing athletic performance in the heat. Strength Cond J. 2013;35(6):24-33.
6. Adams WM, Casa DJ. Hydration for football athletes. Sports Sci Exchange. 2015;28(141):1-5.
7. American College of Sports Medicine, Armstrong LE, Casa DJ, et al. American College of Sports Medicine position stand. Exertional heat illness during training and competition. Med Sci Sports Exerc. 2007;39(3):556-572.
8. Yard EE, Gilchrist J, Haileyesus T, et al. Heat illness among high school athletes--United States, 2005-2009. J Safety Res. 2010;41(6):471-474.
9. Huffman EA, Yard EE, Fields SK, Collins CL, Comstock RD. Epidemiology of rare injuries and conditions among United States high school athletes during the 2005-2006 and 2006-2007 school years. J Athl Train. 2008;43(6):624-630.
10. Kerr ZY, Casa DJ, Marshall SW, Comstock RD. Epidemiology of exertional heat illness among U.S. high school athletes. Am J Prev Med. 2013;44(1):8-14.
11. Casa DJ, DeMartini JK, Bergeron MF, et al. National Athletic Trainers’ Association position statement: exertional heat illnesses. J Athl Train. 2015;50(9):986-1000.
12. Casa DJ, Almquist J, Anderson SA. The inter-association task force for preventing sudden death in secondary school athletics programs: best-practices recommendations. J Athl Train. 2013;48(4):546-553.
13. Gardner JW, Kark JA, Karnei K, et al. Risk factors predicting exertional heat illness in male Marine Corps recruits. Med Sci Sports Exerc. 1996;28(8):939-944.
14. Gundstein AJ, Ramseyer C, Zhao F, et al. A retrospective analysis of American football hyperthermia deaths in the United States. Int J Biometerol. 2012;56(1):11-20.
15. Armstrong LE, Johnson EC, Casa DJ, et al. The American football uniform: uncompensable heat stress and hyperthermic exhaustion. J Athl Train. 2010;45(2):117-127.
16. Casa DJ, Csillan D; Inter-Association Task Force for Preseason Secondary School Athletics Participants, et al. Preseason heat-acclimatization guidelines for secondary school athletics. J Athl Train. 2009;44(3):332-333.
17. Godek SF, Godek JJ, Bartolozzi AR. Hydration status in college football players during consecutive days of twice-a-day preseason practices. Am J Sports Med. 2005;33(6):843-851.
18. Stover EA, Zachwieja J, Stofan J, Murray R, Horswill CA. Consistently high urine specific gravity in adolescent American football players and the impact of an acute drinking strategy. Int J Sports Med. 2006;27(4):330-335.
19. Bongers CC, Thijssen DH, Veltmeijer MTW, Hopman MT, Eijsvogels TM. Precooling and percooling (cooling during exercise) both improve performance in the heat: a meta-analytical review. Br J Sports Med. 2015;49(6):377-384.
20. Casa DJ, McDermott BP, Lee EC, Yeargin SW, Armstrong LE, Maresh CM. Cold water immersion: the gold standard for exertional heatstroke treatment. Exerc Sport Sci Rev. 2007;35(3):141-149.
21. DeMartini JK, Casa DJ, Stearns R, et al. Effectiveness of cold water immersion in the treatment of exertional heat stroke at the Falmouth Road Race. Med Sci Sports Exerc. 2015;47(2):240-245.
22. Casa DJ, Kenny GP, Taylor NA. Immersion treatment for exertional hyperthermia: cold or temperate water? Med Sci Sports Exerc. 2010;42(7):1246-1252.
23. Casa DJ, Armstrong LE, Kenny GP, O’Connor FG, Huggins RA. Exertional heat stroke: new concepts regarding cause and care. Curr Sports Med Rep. 2012;11(3):115-122.
24. Argaud L, Ferry T, Le QH, et al. Short- and long-term outcomes of heat stroke following the 2003 heat wave in Lyon, France. Arch Intern Med. 2007;167(20):2177-2183.
25. O’Connor FG, Casa DJ, Bergeron MF, et al. American College of Sports Medicine Roundtable on exertional heat stroke--return to duty/return to play: conference proceedings. Curr Sports Med Rep. 2010;9(5):314-321.
26. Kazman JB, Heled Y, Lisman PJ, Druyan A, Deuster PA, O’Connor FG. Exertional heat illness: the role of heat tolerance testing. Curr Sports Med Rep. 2013;12(2):101-105.
27. Moran DS, Heled Y, Still L, Laor A, Shapiro Y. Assessment of heat tolerance for post exertional heat stroke individuals. Med Sci Monit. 2004;10(6):CR252-CR257.
28. Herring SA, Kibler WB, Putukian M. Team Physician Consensus Statement: 2013 update. Med Sci Sports Exerc. 2013;45(8):1618-1622.
29. Heat stroke treatment. Korey Stringer Institute University of Connecticut Web site. http://ksi.uconn.edu/emergency-conditions/heat-illnesses/exertional-heat-stroke/heat-stroke-treatment/. Accessed June 14, 2016.
30. Headquarters, Department of the Army and the Air Force. Heat Stress Control and Heat Casualty Management. Technical Bulletin Medical 507. http://www.dir.ca.gov/oshsb/documents/Heat_illness_prevention_tbmed507.pdf. Published March 7, 2003. Accessed June 14, 2016.
1. Kucera KL, Klossner D, Colgate B, Cantu RC. Annual Survey of Football Injury Research: 1931-2014. National Center for Catastrophic Sport Injury Research Web site. https://nccsir.unc.edu/files/2013/10/Annual-Football-2014-Fatalities-Final.pdf. Accessed May 31, 2016.
2. Boden BP, Breit I, Beachler JA, Williams A, Mueller FO. Fatalities in high school and college football players. Am J Sports Med. 2013;41(5):1108-1116.
3. Bouchama A, Knochel JP. Heat stroke. N Engl J Med. 2002;346(25):1978-1988.
4. Racinais S, Alonso JM, Coutts AJ, et al. Consensus recommendations on training and competing in the heat. Scand J Med Sci Sports. 2015;25 Suppl 1:6-19.
5. Pryor RR, Casa DJ, Adams WM, et al. Maximizing athletic performance in the heat. Strength Cond J. 2013;35(6):24-33.
6. Adams WM, Casa DJ. Hydration for football athletes. Sports Sci Exchange. 2015;28(141):1-5.
7. American College of Sports Medicine, Armstrong LE, Casa DJ, et al. American College of Sports Medicine position stand. Exertional heat illness during training and competition. Med Sci Sports Exerc. 2007;39(3):556-572.
8. Yard EE, Gilchrist J, Haileyesus T, et al. Heat illness among high school athletes--United States, 2005-2009. J Safety Res. 2010;41(6):471-474.
9. Huffman EA, Yard EE, Fields SK, Collins CL, Comstock RD. Epidemiology of rare injuries and conditions among United States high school athletes during the 2005-2006 and 2006-2007 school years. J Athl Train. 2008;43(6):624-630.
10. Kerr ZY, Casa DJ, Marshall SW, Comstock RD. Epidemiology of exertional heat illness among U.S. high school athletes. Am J Prev Med. 2013;44(1):8-14.
11. Casa DJ, DeMartini JK, Bergeron MF, et al. National Athletic Trainers’ Association position statement: exertional heat illnesses. J Athl Train. 2015;50(9):986-1000.
12. Casa DJ, Almquist J, Anderson SA. The inter-association task force for preventing sudden death in secondary school athletics programs: best-practices recommendations. J Athl Train. 2013;48(4):546-553.
13. Gardner JW, Kark JA, Karnei K, et al. Risk factors predicting exertional heat illness in male Marine Corps recruits. Med Sci Sports Exerc. 1996;28(8):939-944.
14. Gundstein AJ, Ramseyer C, Zhao F, et al. A retrospective analysis of American football hyperthermia deaths in the United States. Int J Biometerol. 2012;56(1):11-20.
15. Armstrong LE, Johnson EC, Casa DJ, et al. The American football uniform: uncompensable heat stress and hyperthermic exhaustion. J Athl Train. 2010;45(2):117-127.
16. Casa DJ, Csillan D; Inter-Association Task Force for Preseason Secondary School Athletics Participants, et al. Preseason heat-acclimatization guidelines for secondary school athletics. J Athl Train. 2009;44(3):332-333.
17. Godek SF, Godek JJ, Bartolozzi AR. Hydration status in college football players during consecutive days of twice-a-day preseason practices. Am J Sports Med. 2005;33(6):843-851.
18. Stover EA, Zachwieja J, Stofan J, Murray R, Horswill CA. Consistently high urine specific gravity in adolescent American football players and the impact of an acute drinking strategy. Int J Sports Med. 2006;27(4):330-335.
19. Bongers CC, Thijssen DH, Veltmeijer MTW, Hopman MT, Eijsvogels TM. Precooling and percooling (cooling during exercise) both improve performance in the heat: a meta-analytical review. Br J Sports Med. 2015;49(6):377-384.
20. Casa DJ, McDermott BP, Lee EC, Yeargin SW, Armstrong LE, Maresh CM. Cold water immersion: the gold standard for exertional heatstroke treatment. Exerc Sport Sci Rev. 2007;35(3):141-149.
21. DeMartini JK, Casa DJ, Stearns R, et al. Effectiveness of cold water immersion in the treatment of exertional heat stroke at the Falmouth Road Race. Med Sci Sports Exerc. 2015;47(2):240-245.
22. Casa DJ, Kenny GP, Taylor NA. Immersion treatment for exertional hyperthermia: cold or temperate water? Med Sci Sports Exerc. 2010;42(7):1246-1252.
23. Casa DJ, Armstrong LE, Kenny GP, O’Connor FG, Huggins RA. Exertional heat stroke: new concepts regarding cause and care. Curr Sports Med Rep. 2012;11(3):115-122.
24. Argaud L, Ferry T, Le QH, et al. Short- and long-term outcomes of heat stroke following the 2003 heat wave in Lyon, France. Arch Intern Med. 2007;167(20):2177-2183.
25. O’Connor FG, Casa DJ, Bergeron MF, et al. American College of Sports Medicine Roundtable on exertional heat stroke--return to duty/return to play: conference proceedings. Curr Sports Med Rep. 2010;9(5):314-321.
26. Kazman JB, Heled Y, Lisman PJ, Druyan A, Deuster PA, O’Connor FG. Exertional heat illness: the role of heat tolerance testing. Curr Sports Med Rep. 2013;12(2):101-105.
27. Moran DS, Heled Y, Still L, Laor A, Shapiro Y. Assessment of heat tolerance for post exertional heat stroke individuals. Med Sci Monit. 2004;10(6):CR252-CR257.
28. Herring SA, Kibler WB, Putukian M. Team Physician Consensus Statement: 2013 update. Med Sci Sports Exerc. 2013;45(8):1618-1622.
29. Heat stroke treatment. Korey Stringer Institute University of Connecticut Web site. http://ksi.uconn.edu/emergency-conditions/heat-illnesses/exertional-heat-stroke/heat-stroke-treatment/. Accessed June 14, 2016.
30. Headquarters, Department of the Army and the Air Force. Heat Stress Control and Heat Casualty Management. Technical Bulletin Medical 507. http://www.dir.ca.gov/oshsb/documents/Heat_illness_prevention_tbmed507.pdf. Published March 7, 2003. Accessed June 14, 2016.
When Man’s Legs “Give Out,” His Buttocks Takes the Brunt
ANSWER
There are degenerative changes present. Bilateral hip prostheses are noted. Within the coccyx, there is bone remodeling and angulation that are likely chronic and related to remote trauma or injury (arrow). Below this, some cortical lucency (circled) is noted, most likely consistent with an acute fracture. The patient was prescribed a nonsteroidal medication and a mild narcotic pain medication.
ANSWER
There are degenerative changes present. Bilateral hip prostheses are noted. Within the coccyx, there is bone remodeling and angulation that are likely chronic and related to remote trauma or injury (arrow). Below this, some cortical lucency (circled) is noted, most likely consistent with an acute fracture. The patient was prescribed a nonsteroidal medication and a mild narcotic pain medication.
ANSWER
There are degenerative changes present. Bilateral hip prostheses are noted. Within the coccyx, there is bone remodeling and angulation that are likely chronic and related to remote trauma or injury (arrow). Below this, some cortical lucency (circled) is noted, most likely consistent with an acute fracture. The patient was prescribed a nonsteroidal medication and a mild narcotic pain medication.
A 75-year-old man presents to the urgent care center for evaluation of pain in his buttocks after a fall. He states he was walking when his “legs gave out” and he hit the ground. He landed squarely on his buttocks, causing immediate pain. He was eventually able to get up with some assistance. He denies current weakness or any bowel or bladder complaints.
His medical/surgical history is significant for coronary artery disease, hypertension, and bilateral hip replacements. Physical exam reveals an elderly male who is uncomfortable but in no obvious distress. His vital signs are stable. He has moderate point tenderness over his sacrum but is able to move all his extremities well, with normal strength.
Radiograph of his sacrum/coccyx is shown. What is your impression?
FDA: New labeling warns against combining opioids, benzodiazepines
Labeling for prescription opioid pain or cough medicines and benzodiazepines will now carry the strongest available warning regarding serious side effects and death associated with their combined use, according to the Food and Drug Administration.
The new boxed warnings urge health care professionals to limit prescribing opioid pain medicines with benzodiazepines or other central nervous system depressants only to patients for whom alternative treatment options are inadequate, and to limit dosages and treatment duration to the minimum possible while achieving the desired clinical effect.
“First, the FDA is requiring companies to update their product labeling for ... benzodiazepines and opioids to include possible harms when they are used together. Second, we are requiring new or updated medication guides for these drugs reflecting those same warnings,” said Doug Throckmorton, MD, deputy director of the FDA’s Center for Drug Evaluation and Research, during a telebriefing.
Opioids will include a warning regarding prescribing with benzodiazepines and other central nervous system depressants, including alcohol. Benzodiazepines will include a warning regarding prescribing with opioids.
In addition, the FDA has issued a safety communication to “warn the public about the serious risk of taking these products together to help make doctors more cautious and patients better informed,” Dr. Throckmorton said.
The action comes amid ongoing efforts to address an epidemic of opioid addiction across the United States, and in response to a first-of-its-kind “citizen petition” calling for the boxed warnings.
A coalition of health officials from multiple cities, states, and U.S. territories initiated that petition in February, and thousands of concerned community members started an additional online petition. Those petitions were in response to both the increasing combined use of opioids and benzodiazepines and a concomitant increase in the risk of serious side effects and deaths associated with their combined use, according to Baltimore City Health Commissioner Leana Wen, MD.
As an emergency physician, Dr. Wen said that she has seen firsthand the alarming trends; one in three unintentional overdose deaths from prescribed opioids also involve benzodiazepines, she noted.
“In my state of Maryland in 2014, benzodiazepines were associated with 19% of prescription opioid deaths, and 59% of benzodiazepine-associated deaths involved prescription opioids. We also noted the growing biological evidence that combining these medications caused sleepiness and slowed breathing, increasing the likelihood of a fatal overdose,” she said.
Dr. Throckmorton further noted that emergency department visits and deaths involving patients prescribed both opioids and benzodiazepines have increased significantly over time. From 2004 to 2011, the rate of nonmedical use–related emergency department visits increased significantly each year, and overdose deaths involving both drug classes during that period nearly tripled on an annual basis.
“Communities have been seeing this trend for some time, but ultimately we needed data in order to act today,” FDA Commissioner Robert Califf, MD, said during the telebriefing.
The current action is just “one part of a larger effort to address this epidemic.
“We remain focused and deeply committed to contributing to the comprehensive effort to address the opioid epidemic,” Dr. Califf said. The FDA “will continue to monitor these products carefully and take additional actions as needed, and will share updates with the public as necessary as we work to address this public health crisis.”
Dr. Califf noted that the current action is part of the FDA’s Opioids Action Plan, which is “importantly not meant just to cover illicit or abusive use of opioids.”
“So, you’ll be hearing a lot more from us, because this is a national crisis that is not going away. We’re making progress on the prescribing, and we’re seeing a reduction in the use of opioids now,” he noted. “But we’re still seeing many overdoses.
“This is a continuum, and we’ll continue to try to do everything we can to address the epidemic,” Dr. Califf concluded.
Labeling for prescription opioid pain or cough medicines and benzodiazepines will now carry the strongest available warning regarding serious side effects and death associated with their combined use, according to the Food and Drug Administration.
The new boxed warnings urge health care professionals to limit prescribing opioid pain medicines with benzodiazepines or other central nervous system depressants only to patients for whom alternative treatment options are inadequate, and to limit dosages and treatment duration to the minimum possible while achieving the desired clinical effect.
“First, the FDA is requiring companies to update their product labeling for ... benzodiazepines and opioids to include possible harms when they are used together. Second, we are requiring new or updated medication guides for these drugs reflecting those same warnings,” said Doug Throckmorton, MD, deputy director of the FDA’s Center for Drug Evaluation and Research, during a telebriefing.
Opioids will include a warning regarding prescribing with benzodiazepines and other central nervous system depressants, including alcohol. Benzodiazepines will include a warning regarding prescribing with opioids.
In addition, the FDA has issued a safety communication to “warn the public about the serious risk of taking these products together to help make doctors more cautious and patients better informed,” Dr. Throckmorton said.
The action comes amid ongoing efforts to address an epidemic of opioid addiction across the United States, and in response to a first-of-its-kind “citizen petition” calling for the boxed warnings.
A coalition of health officials from multiple cities, states, and U.S. territories initiated that petition in February, and thousands of concerned community members started an additional online petition. Those petitions were in response to both the increasing combined use of opioids and benzodiazepines and a concomitant increase in the risk of serious side effects and deaths associated with their combined use, according to Baltimore City Health Commissioner Leana Wen, MD.
As an emergency physician, Dr. Wen said that she has seen firsthand the alarming trends; one in three unintentional overdose deaths from prescribed opioids also involve benzodiazepines, she noted.
“In my state of Maryland in 2014, benzodiazepines were associated with 19% of prescription opioid deaths, and 59% of benzodiazepine-associated deaths involved prescription opioids. We also noted the growing biological evidence that combining these medications caused sleepiness and slowed breathing, increasing the likelihood of a fatal overdose,” she said.
Dr. Throckmorton further noted that emergency department visits and deaths involving patients prescribed both opioids and benzodiazepines have increased significantly over time. From 2004 to 2011, the rate of nonmedical use–related emergency department visits increased significantly each year, and overdose deaths involving both drug classes during that period nearly tripled on an annual basis.
“Communities have been seeing this trend for some time, but ultimately we needed data in order to act today,” FDA Commissioner Robert Califf, MD, said during the telebriefing.
The current action is just “one part of a larger effort to address this epidemic.
“We remain focused and deeply committed to contributing to the comprehensive effort to address the opioid epidemic,” Dr. Califf said. The FDA “will continue to monitor these products carefully and take additional actions as needed, and will share updates with the public as necessary as we work to address this public health crisis.”
Dr. Califf noted that the current action is part of the FDA’s Opioids Action Plan, which is “importantly not meant just to cover illicit or abusive use of opioids.”
“So, you’ll be hearing a lot more from us, because this is a national crisis that is not going away. We’re making progress on the prescribing, and we’re seeing a reduction in the use of opioids now,” he noted. “But we’re still seeing many overdoses.
“This is a continuum, and we’ll continue to try to do everything we can to address the epidemic,” Dr. Califf concluded.
Labeling for prescription opioid pain or cough medicines and benzodiazepines will now carry the strongest available warning regarding serious side effects and death associated with their combined use, according to the Food and Drug Administration.
The new boxed warnings urge health care professionals to limit prescribing opioid pain medicines with benzodiazepines or other central nervous system depressants only to patients for whom alternative treatment options are inadequate, and to limit dosages and treatment duration to the minimum possible while achieving the desired clinical effect.
“First, the FDA is requiring companies to update their product labeling for ... benzodiazepines and opioids to include possible harms when they are used together. Second, we are requiring new or updated medication guides for these drugs reflecting those same warnings,” said Doug Throckmorton, MD, deputy director of the FDA’s Center for Drug Evaluation and Research, during a telebriefing.
Opioids will include a warning regarding prescribing with benzodiazepines and other central nervous system depressants, including alcohol. Benzodiazepines will include a warning regarding prescribing with opioids.
In addition, the FDA has issued a safety communication to “warn the public about the serious risk of taking these products together to help make doctors more cautious and patients better informed,” Dr. Throckmorton said.
The action comes amid ongoing efforts to address an epidemic of opioid addiction across the United States, and in response to a first-of-its-kind “citizen petition” calling for the boxed warnings.
A coalition of health officials from multiple cities, states, and U.S. territories initiated that petition in February, and thousands of concerned community members started an additional online petition. Those petitions were in response to both the increasing combined use of opioids and benzodiazepines and a concomitant increase in the risk of serious side effects and deaths associated with their combined use, according to Baltimore City Health Commissioner Leana Wen, MD.
As an emergency physician, Dr. Wen said that she has seen firsthand the alarming trends; one in three unintentional overdose deaths from prescribed opioids also involve benzodiazepines, she noted.
“In my state of Maryland in 2014, benzodiazepines were associated with 19% of prescription opioid deaths, and 59% of benzodiazepine-associated deaths involved prescription opioids. We also noted the growing biological evidence that combining these medications caused sleepiness and slowed breathing, increasing the likelihood of a fatal overdose,” she said.
Dr. Throckmorton further noted that emergency department visits and deaths involving patients prescribed both opioids and benzodiazepines have increased significantly over time. From 2004 to 2011, the rate of nonmedical use–related emergency department visits increased significantly each year, and overdose deaths involving both drug classes during that period nearly tripled on an annual basis.
“Communities have been seeing this trend for some time, but ultimately we needed data in order to act today,” FDA Commissioner Robert Califf, MD, said during the telebriefing.
The current action is just “one part of a larger effort to address this epidemic.
“We remain focused and deeply committed to contributing to the comprehensive effort to address the opioid epidemic,” Dr. Califf said. The FDA “will continue to monitor these products carefully and take additional actions as needed, and will share updates with the public as necessary as we work to address this public health crisis.”
Dr. Califf noted that the current action is part of the FDA’s Opioids Action Plan, which is “importantly not meant just to cover illicit or abusive use of opioids.”
“So, you’ll be hearing a lot more from us, because this is a national crisis that is not going away. We’re making progress on the prescribing, and we’re seeing a reduction in the use of opioids now,” he noted. “But we’re still seeing many overdoses.
“This is a continuum, and we’ll continue to try to do everything we can to address the epidemic,” Dr. Califf concluded.
Study Identifies Two Biomarkers That Contribute to Spine Osteoarthritis
Researchers have discovered a pair of tissue biomarkers that directly contribute to the joint degeneration associated with spine osteoarthritis, according to a study published in the Journal of Clinical Investigation Insight.
The study evaluated tissue biopsies from 55 patients undergoing decompression or discectomy. Investigators screened 2,100 microRNAs and found that microRNA-181a-5p and microRNA-4454 biomarkers are involved in destroying cartilage and increase inflammation, and that measuring these two biomarkers can help clinicians determine the stage to which spine osteoarthritis has progressed, and provide a tool for determining the degree of cartilage destruction.
Suggested Reading
Nakamura A, Rampersaud R. Y., Sharma A. Identification of microRNA-181a-5p and microRNA-4454 as mediators of facet cartilage degeneration. JCI Insight. 2016;1(12):e86820.
Researchers have discovered a pair of tissue biomarkers that directly contribute to the joint degeneration associated with spine osteoarthritis, according to a study published in the Journal of Clinical Investigation Insight.
The study evaluated tissue biopsies from 55 patients undergoing decompression or discectomy. Investigators screened 2,100 microRNAs and found that microRNA-181a-5p and microRNA-4454 biomarkers are involved in destroying cartilage and increase inflammation, and that measuring these two biomarkers can help clinicians determine the stage to which spine osteoarthritis has progressed, and provide a tool for determining the degree of cartilage destruction.
Researchers have discovered a pair of tissue biomarkers that directly contribute to the joint degeneration associated with spine osteoarthritis, according to a study published in the Journal of Clinical Investigation Insight.
The study evaluated tissue biopsies from 55 patients undergoing decompression or discectomy. Investigators screened 2,100 microRNAs and found that microRNA-181a-5p and microRNA-4454 biomarkers are involved in destroying cartilage and increase inflammation, and that measuring these two biomarkers can help clinicians determine the stage to which spine osteoarthritis has progressed, and provide a tool for determining the degree of cartilage destruction.
Suggested Reading
Nakamura A, Rampersaud R. Y., Sharma A. Identification of microRNA-181a-5p and microRNA-4454 as mediators of facet cartilage degeneration. JCI Insight. 2016;1(12):e86820.
Suggested Reading
Nakamura A, Rampersaud R. Y., Sharma A. Identification of microRNA-181a-5p and microRNA-4454 as mediators of facet cartilage degeneration. JCI Insight. 2016;1(12):e86820.
Minorities Have Fewer Knee Replacement Surgeries, But Are More Likely to Experience Complications
Compared to white patients, minority patients have lower rates of total knee replacement (TKR), but higher rates of adverse health outcomes associated with this procedure, according to a study in the Journal of Bone and Joint Surgery.
The study analyzed data on 547,380 patients from 8 racially diverse states who underwent TKR from 2001 to 2008. Race was categorized as white, black, Hispanic, Asian, Native American, and mixed race.
In comparison to the white patients, minorities had lower rates of TKR. Minorities also were less likely to undergo TKR in a high-volume hospital. In addition, the risk for in-hospital mortality and the rate of complications following TKR were significantly higher for patients who were black, Native American, or mixed race.
Suggested Reading
Zhang W, Lyman S, Boutin-Foster C, et al. Racial and ethnic disparities in utilization rate, hospital volume, and perioperative outcomes after total knee arthroplasty. J Bone Joint Surg Am. 2016 Aug 3;98(15):1243-1252.
Compared to white patients, minority patients have lower rates of total knee replacement (TKR), but higher rates of adverse health outcomes associated with this procedure, according to a study in the Journal of Bone and Joint Surgery.
The study analyzed data on 547,380 patients from 8 racially diverse states who underwent TKR from 2001 to 2008. Race was categorized as white, black, Hispanic, Asian, Native American, and mixed race.
In comparison to the white patients, minorities had lower rates of TKR. Minorities also were less likely to undergo TKR in a high-volume hospital. In addition, the risk for in-hospital mortality and the rate of complications following TKR were significantly higher for patients who were black, Native American, or mixed race.
Compared to white patients, minority patients have lower rates of total knee replacement (TKR), but higher rates of adverse health outcomes associated with this procedure, according to a study in the Journal of Bone and Joint Surgery.
The study analyzed data on 547,380 patients from 8 racially diverse states who underwent TKR from 2001 to 2008. Race was categorized as white, black, Hispanic, Asian, Native American, and mixed race.
In comparison to the white patients, minorities had lower rates of TKR. Minorities also were less likely to undergo TKR in a high-volume hospital. In addition, the risk for in-hospital mortality and the rate of complications following TKR were significantly higher for patients who were black, Native American, or mixed race.
Suggested Reading
Zhang W, Lyman S, Boutin-Foster C, et al. Racial and ethnic disparities in utilization rate, hospital volume, and perioperative outcomes after total knee arthroplasty. J Bone Joint Surg Am. 2016 Aug 3;98(15):1243-1252.
Suggested Reading
Zhang W, Lyman S, Boutin-Foster C, et al. Racial and ethnic disparities in utilization rate, hospital volume, and perioperative outcomes after total knee arthroplasty. J Bone Joint Surg Am. 2016 Aug 3;98(15):1243-1252.
No VTE prophylaxis needed after joint surgery in patients with hemophilia
ORLANDO – In patients with hemophilia who have therapeutic factor levels at the time of joint replacement surgery, prophylaxis against venous thromboembolism (VTE) may be unnecessary.
In a cohort study of patients with hemophilia A or B who underwent total joint replacement surgery while being in proper hemostasis with therapeutic factor levels, there were no clinically evident episodes of venous thromboembolism, even though none of the patients had received perioperative anticoagulant prophylaxis, reported investigators from the National Hemophilia Center and Institute of Thrombosis and Hemostasis at the Sheba Medical Center in Tel Hashomer, Israel.
The data should be reassuring to clinicians whose patients with hemophilia require major orthopedic procedures, said lead author Dr. Anna Seltser, an orthopedic resident at Sheba Medical Center, in an interview.
“We have a lot of hemophilia patients who are not well treated because they live in the desert or distant communities, and we also sometimes treat patients from the Palestinian side of the Gaza Strip who don’t have access to care and need this type of surgery,” she said.
“We collected what I think is the biggest series of patients until now, we didn’t give any of them VTE prophylaxis, and none of them had any DVT [deep vein thrombosis], PE [pulmonary embolism], or similar complication,” she said.
Skip the heparin?
VTE prophylaxis with low-molecular-weight heparin, warfarin, or other anticoagulant agents is a common practice following orthopedic surgery in patients without bleeding disorders. But for patients with severe hemophilia, who often require major joint replacement surgery following years of bleeding-induced arthropathy, it’s unclear whether perioperative anticoagulation is beneficial, the investigators noted in a scientific poster at the World Federation of Hemophilia World Congress.
Dr. Seltser and colleagues therefore conducted a prospective cohort study of 50 patients with hemophilia A or B treated with major joint surgery and subsequent revisions from 1988 through 2015 at their center. In all, 47 patients had severe hemophilia A, 2 had mild hemophilia A, and 1 had hemophilia B.
The authors analyzed data on demographics, comorbidities, type of surgery, use of factor concentrates therapy around the time of surgery, and complications during follow-up, including massive hemorrhage, infections, implant loosening, DVT, and PE.
The patients underwent a total of 74 primary joint replacements (16 hips, 52 knees, and 6 ankles) and 23 revision surgeries.
As noted, there were no episodes of either DVT or PE among any of the patients. All but one complication occurred among patients undergoing total knee replacement. These included three cases of hemarthrosis, three limited-range-of-motion cases requiring closed manipulations, four soft-tissue hematomas, and one case each of superficial wound infection, urinary tract infection, pneumonia, and Candida infection of the tongue.
The only other complication was a case of disseminated intravascular coagulation, sepsis, and hemorrhagic shock in a patient who had undergone a revision (original procedure unspecified).
“Despite the concern that proper replacement factor therapy, applied before and after the surgery, may increase the risk for thromboembolic complications in patients with hemophilia undergoing joint replacement, our data show that prophylactic anticoagulation in this group of patients is not necessary,” the investigators concluded.
The study was internally funded. The investigators reported no conflicts of interest.
ORLANDO – In patients with hemophilia who have therapeutic factor levels at the time of joint replacement surgery, prophylaxis against venous thromboembolism (VTE) may be unnecessary.
In a cohort study of patients with hemophilia A or B who underwent total joint replacement surgery while being in proper hemostasis with therapeutic factor levels, there were no clinically evident episodes of venous thromboembolism, even though none of the patients had received perioperative anticoagulant prophylaxis, reported investigators from the National Hemophilia Center and Institute of Thrombosis and Hemostasis at the Sheba Medical Center in Tel Hashomer, Israel.
The data should be reassuring to clinicians whose patients with hemophilia require major orthopedic procedures, said lead author Dr. Anna Seltser, an orthopedic resident at Sheba Medical Center, in an interview.
“We have a lot of hemophilia patients who are not well treated because they live in the desert or distant communities, and we also sometimes treat patients from the Palestinian side of the Gaza Strip who don’t have access to care and need this type of surgery,” she said.
“We collected what I think is the biggest series of patients until now, we didn’t give any of them VTE prophylaxis, and none of them had any DVT [deep vein thrombosis], PE [pulmonary embolism], or similar complication,” she said.
Skip the heparin?
VTE prophylaxis with low-molecular-weight heparin, warfarin, or other anticoagulant agents is a common practice following orthopedic surgery in patients without bleeding disorders. But for patients with severe hemophilia, who often require major joint replacement surgery following years of bleeding-induced arthropathy, it’s unclear whether perioperative anticoagulation is beneficial, the investigators noted in a scientific poster at the World Federation of Hemophilia World Congress.
Dr. Seltser and colleagues therefore conducted a prospective cohort study of 50 patients with hemophilia A or B treated with major joint surgery and subsequent revisions from 1988 through 2015 at their center. In all, 47 patients had severe hemophilia A, 2 had mild hemophilia A, and 1 had hemophilia B.
The authors analyzed data on demographics, comorbidities, type of surgery, use of factor concentrates therapy around the time of surgery, and complications during follow-up, including massive hemorrhage, infections, implant loosening, DVT, and PE.
The patients underwent a total of 74 primary joint replacements (16 hips, 52 knees, and 6 ankles) and 23 revision surgeries.
As noted, there were no episodes of either DVT or PE among any of the patients. All but one complication occurred among patients undergoing total knee replacement. These included three cases of hemarthrosis, three limited-range-of-motion cases requiring closed manipulations, four soft-tissue hematomas, and one case each of superficial wound infection, urinary tract infection, pneumonia, and Candida infection of the tongue.
The only other complication was a case of disseminated intravascular coagulation, sepsis, and hemorrhagic shock in a patient who had undergone a revision (original procedure unspecified).
“Despite the concern that proper replacement factor therapy, applied before and after the surgery, may increase the risk for thromboembolic complications in patients with hemophilia undergoing joint replacement, our data show that prophylactic anticoagulation in this group of patients is not necessary,” the investigators concluded.
The study was internally funded. The investigators reported no conflicts of interest.
ORLANDO – In patients with hemophilia who have therapeutic factor levels at the time of joint replacement surgery, prophylaxis against venous thromboembolism (VTE) may be unnecessary.
In a cohort study of patients with hemophilia A or B who underwent total joint replacement surgery while being in proper hemostasis with therapeutic factor levels, there were no clinically evident episodes of venous thromboembolism, even though none of the patients had received perioperative anticoagulant prophylaxis, reported investigators from the National Hemophilia Center and Institute of Thrombosis and Hemostasis at the Sheba Medical Center in Tel Hashomer, Israel.
The data should be reassuring to clinicians whose patients with hemophilia require major orthopedic procedures, said lead author Dr. Anna Seltser, an orthopedic resident at Sheba Medical Center, in an interview.
“We have a lot of hemophilia patients who are not well treated because they live in the desert or distant communities, and we also sometimes treat patients from the Palestinian side of the Gaza Strip who don’t have access to care and need this type of surgery,” she said.
“We collected what I think is the biggest series of patients until now, we didn’t give any of them VTE prophylaxis, and none of them had any DVT [deep vein thrombosis], PE [pulmonary embolism], or similar complication,” she said.
Skip the heparin?
VTE prophylaxis with low-molecular-weight heparin, warfarin, or other anticoagulant agents is a common practice following orthopedic surgery in patients without bleeding disorders. But for patients with severe hemophilia, who often require major joint replacement surgery following years of bleeding-induced arthropathy, it’s unclear whether perioperative anticoagulation is beneficial, the investigators noted in a scientific poster at the World Federation of Hemophilia World Congress.
Dr. Seltser and colleagues therefore conducted a prospective cohort study of 50 patients with hemophilia A or B treated with major joint surgery and subsequent revisions from 1988 through 2015 at their center. In all, 47 patients had severe hemophilia A, 2 had mild hemophilia A, and 1 had hemophilia B.
The authors analyzed data on demographics, comorbidities, type of surgery, use of factor concentrates therapy around the time of surgery, and complications during follow-up, including massive hemorrhage, infections, implant loosening, DVT, and PE.
The patients underwent a total of 74 primary joint replacements (16 hips, 52 knees, and 6 ankles) and 23 revision surgeries.
As noted, there were no episodes of either DVT or PE among any of the patients. All but one complication occurred among patients undergoing total knee replacement. These included three cases of hemarthrosis, three limited-range-of-motion cases requiring closed manipulations, four soft-tissue hematomas, and one case each of superficial wound infection, urinary tract infection, pneumonia, and Candida infection of the tongue.
The only other complication was a case of disseminated intravascular coagulation, sepsis, and hemorrhagic shock in a patient who had undergone a revision (original procedure unspecified).
“Despite the concern that proper replacement factor therapy, applied before and after the surgery, may increase the risk for thromboembolic complications in patients with hemophilia undergoing joint replacement, our data show that prophylactic anticoagulation in this group of patients is not necessary,” the investigators concluded.
The study was internally funded. The investigators reported no conflicts of interest.
AT WFH 2016 WORLD CONGRESS
Key clinical point: Prophylaxis against thromboembolic events after orthopedic surgery in patients with hemophilia may not be necessary.
Major finding: There were no thromboembolic events after joint surgery without anticoagulant prophylaxis in patients with hemophilia A or B.
Data source: Cohort study of 50 patients with hemophilia A or B undergoing major joint replacement surgery.
Disclosures: The study was internally funded. The investigators reported no conflicts of interest.
Biomechanical Consequences of Anterior Femoral Notching in Cruciate-Retaining Versus Posterior-Stabilized Total Knee Arthroplasty
Although rare, periprosthetic fractures remain a significant complication after total knee arthroplasty (TKA), occurring in 0.3% to 2.5% of cases.1-4 Hirsh and colleagues5 were among the first to suggest that anterior femoral notching during TKA was a potential risk factor for postoperative periprosthetic femoral fracture because notching may weaken the anterior femoral cortex. Anterior femoral notching, a cortex violation occurring during an anterior bone cut, occurs in up to 30% of cases.6 Using a theoretical biomechanical model, Culp and colleagues1 found that increasing the depth of the notch defect into the cortex led to reduced torsional strength. In more recent, cadaveric biomechanical studies, notching of the anterior femoral cortex decreased torsional strength by up to 39%.7,8 Contrary to these biomechanical studies, a retrospective study evaluating 1089 TKAs using 2 implant designs (Anatomic Graduated Component, Biomet and Legacy, Zimmer) demonstrated no significant effect of anterior femoral notching with respect to incidence of supracondylar femur fractures.6 That study, however, did not address whether implant design is associated with a differential risk for fracture in the presence of anterior notching.
Previous biomechanical studies have primarily investigated cruciate-retaining (CR) femoral components and properties with respect to anterior notching, even though the posterior-stabilized (PS) design is used more often in the United States.1,7 According to a Mayo Clinic survey, TKAs with a PS design increased from <10% in 1990 to almost 75% by 1997.9 Today, there is little to no consensus about which implant is better, and use of one or the other depends largely on the surgeon and varies widely between countries and regions.10 PS designs require more bone resection and demonstrate prosthesis-controlled rollback during flexion, whereas CR designs preserve more bone and achieve posterior stabilization via the posterior cruciate ligament.11 Despite these differences in design and mechanics, a 2013 Cochrane review of TKA design found no clinically significant differences between CR and PS with respect to pain, range of motion, or clinical and radiologic outcomes.10 The reviewers did not specifically address periprosthetic fractures associated with either femoral notching or TKA design, as they could not quantitatively analyze postoperative complications because of the diversity of reports. Given the limited number of reported cases, a review of radiographic findings pertaining to the characteristics of supracondylar fractures in anterior femoral notching was unsuccessful.12 As the previous biomechanical studies of anterior notching used primarily CR models or no prostheses at all, a study of biomechanical differences between CR and PS designs in the presence of anterior notching is warranted.1,7,8 Therefore, we conducted a study to assess the effect of anterior femoral notching on torsional strength and load to failure in CR and PS femoral components.
Materials and Methods
Twelve fourth-generation composite adult left femur synthetic sawbones (Sawbones; Pacific Research Laboratories) were selected for their consistent biomechanical properties, vs those of cadaveric specimens; in addition, low intersample variability made them preferable to cadaveric bones given the small sample used in this study.13,14 All bones were from the same lot. All were visually inspected for defects and found to be acceptable. In each sample, an anterior cortical defect was created by making an anterior cut with an undersized (size 4) posterior referencing guide. In addition, the distance from the proximal end of the notch to the implant fell within 15 mm, as that is the maximum distance from the implant a notch can be placed using a standard femoral cutting jig.15 Six femora were instrumented with CR implants and 6 with PS implants (DePuy Synthes). Implants were placed using standardized cuts. Before testing, each implant was inspected for proper fit and found to be securely fastened to the femur. In addition, precision calipers were used to measure notch depth and distance from notch to implant before loading. A custom polymethylmethacrylate torsion jig was used to fix each instrumented femur proximally and distally on the femoral implant (Figure 1). Care was taken to ensure the distal jig engaged only the implant, thus isolating the notch as a stress riser. Each femur was loaded in external rotation through the proximal femoral jig along the anatomical axis. Use of external rotation was based on study findings implicating external rotation of the tibia as the most likely mechanism for generating a fracture in the event of a fall.12 Furthermore, distal femur fractures are predominantly spiral as opposed to butterfly or bending—an indication that torsion is the most likely mechanism of failure.16 With no axial rotation possible within the prosthesis, increased torsional stress is undoubtedly generated within adjacent bone. Each specimen underwent torsional stiffness testing and then load to failure. Torsional stiffness was measured by slowly loading each femur in external rotation, from 1 to 18 Nm for 3 cycles at a displacement rate of 0.5° per second. Each specimen then underwent torsional load-to-failure testing on an Instron 5800R machine at a rate of 0.5° per second. Failure was defined as the moment of fracture and subsequent decrease in torsional load—determined graphically by the peak torsional load followed immediately by a sharp decrease in load. Stiffness was determined as the slope of torque to the displacement curve for each cycle, and torque to failure was the highest recorded torque before fracture. Fracture pattern was noted after failure. A sample size of 6 specimens per group provided 80% power to detect a between-group difference of 1 Nm per degree in stiffness, using an estimated SD of 0.7 Nm per degree. In our statistical analysis, continuous variables are reported as means and SDs. Data from our torsional stiffness and load-to-failure testing were analyzed with unpaired 2-sample t tests, and P < .05 was considered statistically significant.
Results
We did not detect a statistical difference in notch depth, notch-to-implant distance, or femoral length between the CR and PS groups. Mean (SD) notch depth was 6.0 (1.3) mm for CR and 4.9 (1.0) mm for PS (P = .13); mean (SD) distance from the proximal end of the notch to the implant was 13.8 (1.7) mm for CR and 11.1 (3.2) mm for PS (P = .08); and mean (SD) femoral length was 46.2 (0.1) cm for CR and 46.2 (0.1) cm for PS (P = .60).
Mean (SD) torsional stiffness for the first 3 precycles was 6.2 (1.2), 8.7 (1.5), and 8.8 (1.4) Nm per degree for the CR group and 6.0 (0.7), 8.4 (1.4), and 8.6 (1.4) Nm per degree for the PS group; the differences were not statistically significant (Figure 2A). In addition, there were no statistically significant differences in mean (SD) stiffness at failure between CR, 6.5 (0.7) Nm per degree, and PS, 7.1 (0.9) Nm per degree (P = .24; Figure 2B) or in mean (SD) final torque at failure between CR, 62.4 (9.4) Nm, and PS, 62.7 (12.2) Nm (P = .95; Figure 2C).
All fractures in both groups were oblique fractures originating at the proximal angle of the notch and extended proximally. None extended distally into the box. Fracture locations and patterns were identical in the CR and PS groups of femurs (Figure 3).
Discussion
Periprosthetic fractures after TKA remain rare. However, these fractures can significantly increase morbidity and complications. Anterior femoral notching occurs inadvertently in 30% to 40% of TKAs.6,17 The impact of femoral notching on supracondylar femur fracture is inconsistent between biomechanical and retrospective clinical studies. Retrospective studies failed to find a significant correlation between anterior femoral notching and supracondylar femur fractures.6,17 However, findings of biomechanical studies have suggested that a notch 3 mm deep will reduce the torsional strength of the femur by 29%.7 Another study, using 3-dimensional finite element analysis, showed a significant increase in local stress with a notch deeper than 3 mm.15
To our knowledge, no clinical studies, including the aforementioned Cochrane review,10 have specifically evaluated the difference in risk for periprosthetic fracture between different TKA models in the presence of notching.11 The biomechanical differences between implant designs could be a confounding factor in the results of past studies. More bone resection is required in PS designs than in CR designs. The position of the PS intercondylar cutout, much lower than the top of the patella flange, should not increase susceptibility to fractures more than in CR designs, but this hypothesis, though accepted, has not been validated biomechanically or addressed specifically in prospective or retrospective clinical analysis. In the present study, we used a biomechanical model to replicate an external rotation failure mechanism and quantify the differences in torsional strength and load to failure between CR TKA and PS TKA models in the presence of anterior femoral notching. Our results showed no significant differences in torsional stiffness, stiffness at failure, or torque at failure between the CR and PS design groups in the presence of anterior femoral notching.
In this study, all femoral fractures were oblique, and they all originated at the site of the cortical defect, not the notch—a situation markedly different from having bending forces applied to the femur. Previous biomechanical data indicated that bending forces applied to a notched femur cause fractures originating at the notch, whereas torsional forces applied to a notched femur cause fractures originating at the anterior aspect of the bone–component interface.7 The difference is attributable to study design. Our femurs were held fixed at their proximal end, which may have exacerbated any bending forces applied during external rotation, but we thought constraining the proximal femur would better replicate a fall involving external rotation.
More important for our study, an oblique fracture pattern was noted for both design groups (CR and PS), indicating the fracture pattern was unrelated to the area from which bone was resected for the PS design. All femur fractures in both design groups occurred proximal to a well-fixed prosthesis, indicating they should be classified as Vancouver C fractures. This is significant because intercondylar fossa resection (PS group) did not convert the fractures into Vancouver B2 fractures, which involve prosthesis loosening caused by pericomponent fracture.18 This simple observation validated our hypothesis that there would be no biomechanical differences between CR and PS designs with respect to the effects of anterior femoral notching. This lack of a significant difference may be attributed to the PS intercondylar cutout being much lower than the top of the anterior flange shielding the resected bone deep to the anterior flange.7 In addition, given the rarity of supracondylar fractures and the lack of sufficient relevant clinical data, it is difficult to speculate on the fracture patterns observed in clinical cases versus biomechanical studies.12
The use of synthetic bone models instead of cadaveric specimens could be seen as a limitation. Although synthetic bones may not reproduce the mechanism of failure in living and cadaveric femurs, the mechanical properties of synthetic bones have previously been found to fall within the range of those of cadaveric bones under axial loading, bending, and torsion testing.13,14 As a uniform testing material, synthetic bones allow removal of the confounding variations in bone size and quality that plague biomechanical studies in cadaveric bones.13,14 Interfemoral variability was 20 to 200 times higher in cadaveric femurs than in synthetic bones, which makes synthetic femurs preferable to cadaveric femurs, especially in studies with a small sample size.13,14 In addition, a uniform specimen provides consistent, reproducible osteotomies, which were crucial for consistent mechanical evaluation of each configuration in this study.
The long-term clinical significance of anterior femoral notching in periprosthetic fractures is equivocal, possibly because most studies predominantly use CR implants.6 This may not be an issue if it is shown that CR and PS implants have the same mechanical properties. Despite the differences between clinical studies and our biomechanical study, reevaluation of clinical data is not warranted given the biomechanical data we present here. Results of biomechanical studies like ours still suggest an increased immediate postoperative risk for supracondylar fracture after anterior cortical notching of the femur.5,7 Ultimately, this study found that, compared with a CR design, a PS design did not alter the torsional biomechanical properties or fracture pattern of an anteriorly notched femur.
1. Culp RW, Schmidt RG, Hanks G, Mak A, Esterhai JL Jr, Heppenstall RB. Supracondylar fracture of the femur following prosthetic knee arthroplasty. Clin Orthop Relat Res. 1987;(222):212-222.
2. Delport PH, Van Audekercke R, Martens M, Mulier JC. Conservative treatment of ipsilateral supracondylar femoral fracture after total knee arthroplasty. J Trauma. 1984;24(9):846-849.
3. Figgie MP, Goldberg VM, Figgie HE 3rd, Sobel M. The results of treatment of supracondylar fracture above total knee arthroplasty. J Arthroplasty. 1990;5(3):267-276.
4. Rorabeck CH, Taylor JW. Periprosthetic fractures of the femur complicating total knee arthroplasty. Orthop Clin North Am. 1999;30(2):265-277.
5. Hirsh DM, Bhalla S, Roffman M. Supracondylar fracture of the femur following total knee replacement. Report of four cases. J Bone Joint Surg Am. 1981;63(1):162-163.
6. Ritter MA, Thong AE, Keating EM, et al. The effect of femoral notching during total knee arthroplasty on the prevalence of postoperative femoral fractures and on clinical outcome. J Bone Joint Surg Am. 2005;87(11):2411-2414.
7. Lesh ML, Schneider DJ, Deol G, Davis B, Jacobs CR, Pellegrini VD Jr. The consequences of anterior femoral notching in total knee arthroplasty. A biomechanical study. J Bone Joint Surg Am. 2000;82(8):1096-1101.
8. Shawen SB, Belmont PJ Jr, Klemme WR, Topoleski LD, Xenos JS, Orchowski JR. Osteoporosis and anterior femoral notching in periprosthetic supracondylar femoral fractures: a biomechanical analysis. J Bone Joint Surg Am. 2003;85(1):115-121.
9. Scuderi GR, Pagnano MW. Review article: the rationale for posterior cruciate substituting total knee arthroplasty. J Orthop Surg (Hong Kong). 2001;9(2):81-88.
10. Verra WC, van den Boom LG, Jacobs W, Clement DJ, Wymenga AA, Nelissen RG. Retention versus sacrifice of the posterior cruciate ligament in total knee arthroplasty for treating osteoarthritis. Cochrane Database Syst Rev. 2013;10:CD004803.
11. Kolisek FR, McGrath MS, Marker DR, et al. Posterior-stabilized versus posterior cruciate ligament-retaining total knee arthroplasty. Iowa Orthop J. 2009;29:23-27.
12. Dennis DA. Periprosthetic fractures following total knee arthroplasty. Instr Course Lect. 2001;50:379-389.
13. Cristofolini L, Viceconti M, Cappello A, Toni A. Mechanical validation of whole bone composite femur models. J Biomech. 1996;29(4):525-535.
14. Heiner AD, Brown TD. Structural properties of a new design of composite replicate femurs and tibias. J Biomech. 2001;34(6):773-781.
15. Beals RK, Tower SS. Periprosthetic fractures of the femur. An analysis of 93 fractures. Clin Orthop Relat Res. 1996;(327):238-246.
16. Gujarathi N, Putti AB, Abboud RJ, MacLean JG, Espley AJ, Kellett CF. Risk of periprosthetic fracture after anterior femoral notching. Acta Orthop. 2009;80(5):553-556.
17. Zalzal P, Backstein D, Gross AE, Papini M. Notching of the anterior femoral cortex during total knee arthroplasty: characteristics that increase local stresses. J Arthroplasty. 2006;21(5):737-743.
18. Gaski GE, Scully SP. In brief: classifications in brief: Vancouver classification of postoperative periprosthetic femur fractures. Clin Orthop Relat Res. 2011;469(5):1507-1510.
Although rare, periprosthetic fractures remain a significant complication after total knee arthroplasty (TKA), occurring in 0.3% to 2.5% of cases.1-4 Hirsh and colleagues5 were among the first to suggest that anterior femoral notching during TKA was a potential risk factor for postoperative periprosthetic femoral fracture because notching may weaken the anterior femoral cortex. Anterior femoral notching, a cortex violation occurring during an anterior bone cut, occurs in up to 30% of cases.6 Using a theoretical biomechanical model, Culp and colleagues1 found that increasing the depth of the notch defect into the cortex led to reduced torsional strength. In more recent, cadaveric biomechanical studies, notching of the anterior femoral cortex decreased torsional strength by up to 39%.7,8 Contrary to these biomechanical studies, a retrospective study evaluating 1089 TKAs using 2 implant designs (Anatomic Graduated Component, Biomet and Legacy, Zimmer) demonstrated no significant effect of anterior femoral notching with respect to incidence of supracondylar femur fractures.6 That study, however, did not address whether implant design is associated with a differential risk for fracture in the presence of anterior notching.
Previous biomechanical studies have primarily investigated cruciate-retaining (CR) femoral components and properties with respect to anterior notching, even though the posterior-stabilized (PS) design is used more often in the United States.1,7 According to a Mayo Clinic survey, TKAs with a PS design increased from <10% in 1990 to almost 75% by 1997.9 Today, there is little to no consensus about which implant is better, and use of one or the other depends largely on the surgeon and varies widely between countries and regions.10 PS designs require more bone resection and demonstrate prosthesis-controlled rollback during flexion, whereas CR designs preserve more bone and achieve posterior stabilization via the posterior cruciate ligament.11 Despite these differences in design and mechanics, a 2013 Cochrane review of TKA design found no clinically significant differences between CR and PS with respect to pain, range of motion, or clinical and radiologic outcomes.10 The reviewers did not specifically address periprosthetic fractures associated with either femoral notching or TKA design, as they could not quantitatively analyze postoperative complications because of the diversity of reports. Given the limited number of reported cases, a review of radiographic findings pertaining to the characteristics of supracondylar fractures in anterior femoral notching was unsuccessful.12 As the previous biomechanical studies of anterior notching used primarily CR models or no prostheses at all, a study of biomechanical differences between CR and PS designs in the presence of anterior notching is warranted.1,7,8 Therefore, we conducted a study to assess the effect of anterior femoral notching on torsional strength and load to failure in CR and PS femoral components.
Materials and Methods
Twelve fourth-generation composite adult left femur synthetic sawbones (Sawbones; Pacific Research Laboratories) were selected for their consistent biomechanical properties, vs those of cadaveric specimens; in addition, low intersample variability made them preferable to cadaveric bones given the small sample used in this study.13,14 All bones were from the same lot. All were visually inspected for defects and found to be acceptable. In each sample, an anterior cortical defect was created by making an anterior cut with an undersized (size 4) posterior referencing guide. In addition, the distance from the proximal end of the notch to the implant fell within 15 mm, as that is the maximum distance from the implant a notch can be placed using a standard femoral cutting jig.15 Six femora were instrumented with CR implants and 6 with PS implants (DePuy Synthes). Implants were placed using standardized cuts. Before testing, each implant was inspected for proper fit and found to be securely fastened to the femur. In addition, precision calipers were used to measure notch depth and distance from notch to implant before loading. A custom polymethylmethacrylate torsion jig was used to fix each instrumented femur proximally and distally on the femoral implant (Figure 1). Care was taken to ensure the distal jig engaged only the implant, thus isolating the notch as a stress riser. Each femur was loaded in external rotation through the proximal femoral jig along the anatomical axis. Use of external rotation was based on study findings implicating external rotation of the tibia as the most likely mechanism for generating a fracture in the event of a fall.12 Furthermore, distal femur fractures are predominantly spiral as opposed to butterfly or bending—an indication that torsion is the most likely mechanism of failure.16 With no axial rotation possible within the prosthesis, increased torsional stress is undoubtedly generated within adjacent bone. Each specimen underwent torsional stiffness testing and then load to failure. Torsional stiffness was measured by slowly loading each femur in external rotation, from 1 to 18 Nm for 3 cycles at a displacement rate of 0.5° per second. Each specimen then underwent torsional load-to-failure testing on an Instron 5800R machine at a rate of 0.5° per second. Failure was defined as the moment of fracture and subsequent decrease in torsional load—determined graphically by the peak torsional load followed immediately by a sharp decrease in load. Stiffness was determined as the slope of torque to the displacement curve for each cycle, and torque to failure was the highest recorded torque before fracture. Fracture pattern was noted after failure. A sample size of 6 specimens per group provided 80% power to detect a between-group difference of 1 Nm per degree in stiffness, using an estimated SD of 0.7 Nm per degree. In our statistical analysis, continuous variables are reported as means and SDs. Data from our torsional stiffness and load-to-failure testing were analyzed with unpaired 2-sample t tests, and P < .05 was considered statistically significant.
Results
We did not detect a statistical difference in notch depth, notch-to-implant distance, or femoral length between the CR and PS groups. Mean (SD) notch depth was 6.0 (1.3) mm for CR and 4.9 (1.0) mm for PS (P = .13); mean (SD) distance from the proximal end of the notch to the implant was 13.8 (1.7) mm for CR and 11.1 (3.2) mm for PS (P = .08); and mean (SD) femoral length was 46.2 (0.1) cm for CR and 46.2 (0.1) cm for PS (P = .60).
Mean (SD) torsional stiffness for the first 3 precycles was 6.2 (1.2), 8.7 (1.5), and 8.8 (1.4) Nm per degree for the CR group and 6.0 (0.7), 8.4 (1.4), and 8.6 (1.4) Nm per degree for the PS group; the differences were not statistically significant (Figure 2A). In addition, there were no statistically significant differences in mean (SD) stiffness at failure between CR, 6.5 (0.7) Nm per degree, and PS, 7.1 (0.9) Nm per degree (P = .24; Figure 2B) or in mean (SD) final torque at failure between CR, 62.4 (9.4) Nm, and PS, 62.7 (12.2) Nm (P = .95; Figure 2C).
All fractures in both groups were oblique fractures originating at the proximal angle of the notch and extended proximally. None extended distally into the box. Fracture locations and patterns were identical in the CR and PS groups of femurs (Figure 3).
Discussion
Periprosthetic fractures after TKA remain rare. However, these fractures can significantly increase morbidity and complications. Anterior femoral notching occurs inadvertently in 30% to 40% of TKAs.6,17 The impact of femoral notching on supracondylar femur fracture is inconsistent between biomechanical and retrospective clinical studies. Retrospective studies failed to find a significant correlation between anterior femoral notching and supracondylar femur fractures.6,17 However, findings of biomechanical studies have suggested that a notch 3 mm deep will reduce the torsional strength of the femur by 29%.7 Another study, using 3-dimensional finite element analysis, showed a significant increase in local stress with a notch deeper than 3 mm.15
To our knowledge, no clinical studies, including the aforementioned Cochrane review,10 have specifically evaluated the difference in risk for periprosthetic fracture between different TKA models in the presence of notching.11 The biomechanical differences between implant designs could be a confounding factor in the results of past studies. More bone resection is required in PS designs than in CR designs. The position of the PS intercondylar cutout, much lower than the top of the patella flange, should not increase susceptibility to fractures more than in CR designs, but this hypothesis, though accepted, has not been validated biomechanically or addressed specifically in prospective or retrospective clinical analysis. In the present study, we used a biomechanical model to replicate an external rotation failure mechanism and quantify the differences in torsional strength and load to failure between CR TKA and PS TKA models in the presence of anterior femoral notching. Our results showed no significant differences in torsional stiffness, stiffness at failure, or torque at failure between the CR and PS design groups in the presence of anterior femoral notching.
In this study, all femoral fractures were oblique, and they all originated at the site of the cortical defect, not the notch—a situation markedly different from having bending forces applied to the femur. Previous biomechanical data indicated that bending forces applied to a notched femur cause fractures originating at the notch, whereas torsional forces applied to a notched femur cause fractures originating at the anterior aspect of the bone–component interface.7 The difference is attributable to study design. Our femurs were held fixed at their proximal end, which may have exacerbated any bending forces applied during external rotation, but we thought constraining the proximal femur would better replicate a fall involving external rotation.
More important for our study, an oblique fracture pattern was noted for both design groups (CR and PS), indicating the fracture pattern was unrelated to the area from which bone was resected for the PS design. All femur fractures in both design groups occurred proximal to a well-fixed prosthesis, indicating they should be classified as Vancouver C fractures. This is significant because intercondylar fossa resection (PS group) did not convert the fractures into Vancouver B2 fractures, which involve prosthesis loosening caused by pericomponent fracture.18 This simple observation validated our hypothesis that there would be no biomechanical differences between CR and PS designs with respect to the effects of anterior femoral notching. This lack of a significant difference may be attributed to the PS intercondylar cutout being much lower than the top of the anterior flange shielding the resected bone deep to the anterior flange.7 In addition, given the rarity of supracondylar fractures and the lack of sufficient relevant clinical data, it is difficult to speculate on the fracture patterns observed in clinical cases versus biomechanical studies.12
The use of synthetic bone models instead of cadaveric specimens could be seen as a limitation. Although synthetic bones may not reproduce the mechanism of failure in living and cadaveric femurs, the mechanical properties of synthetic bones have previously been found to fall within the range of those of cadaveric bones under axial loading, bending, and torsion testing.13,14 As a uniform testing material, synthetic bones allow removal of the confounding variations in bone size and quality that plague biomechanical studies in cadaveric bones.13,14 Interfemoral variability was 20 to 200 times higher in cadaveric femurs than in synthetic bones, which makes synthetic femurs preferable to cadaveric femurs, especially in studies with a small sample size.13,14 In addition, a uniform specimen provides consistent, reproducible osteotomies, which were crucial for consistent mechanical evaluation of each configuration in this study.
The long-term clinical significance of anterior femoral notching in periprosthetic fractures is equivocal, possibly because most studies predominantly use CR implants.6 This may not be an issue if it is shown that CR and PS implants have the same mechanical properties. Despite the differences between clinical studies and our biomechanical study, reevaluation of clinical data is not warranted given the biomechanical data we present here. Results of biomechanical studies like ours still suggest an increased immediate postoperative risk for supracondylar fracture after anterior cortical notching of the femur.5,7 Ultimately, this study found that, compared with a CR design, a PS design did not alter the torsional biomechanical properties or fracture pattern of an anteriorly notched femur.
Although rare, periprosthetic fractures remain a significant complication after total knee arthroplasty (TKA), occurring in 0.3% to 2.5% of cases.1-4 Hirsh and colleagues5 were among the first to suggest that anterior femoral notching during TKA was a potential risk factor for postoperative periprosthetic femoral fracture because notching may weaken the anterior femoral cortex. Anterior femoral notching, a cortex violation occurring during an anterior bone cut, occurs in up to 30% of cases.6 Using a theoretical biomechanical model, Culp and colleagues1 found that increasing the depth of the notch defect into the cortex led to reduced torsional strength. In more recent, cadaveric biomechanical studies, notching of the anterior femoral cortex decreased torsional strength by up to 39%.7,8 Contrary to these biomechanical studies, a retrospective study evaluating 1089 TKAs using 2 implant designs (Anatomic Graduated Component, Biomet and Legacy, Zimmer) demonstrated no significant effect of anterior femoral notching with respect to incidence of supracondylar femur fractures.6 That study, however, did not address whether implant design is associated with a differential risk for fracture in the presence of anterior notching.
Previous biomechanical studies have primarily investigated cruciate-retaining (CR) femoral components and properties with respect to anterior notching, even though the posterior-stabilized (PS) design is used more often in the United States.1,7 According to a Mayo Clinic survey, TKAs with a PS design increased from <10% in 1990 to almost 75% by 1997.9 Today, there is little to no consensus about which implant is better, and use of one or the other depends largely on the surgeon and varies widely between countries and regions.10 PS designs require more bone resection and demonstrate prosthesis-controlled rollback during flexion, whereas CR designs preserve more bone and achieve posterior stabilization via the posterior cruciate ligament.11 Despite these differences in design and mechanics, a 2013 Cochrane review of TKA design found no clinically significant differences between CR and PS with respect to pain, range of motion, or clinical and radiologic outcomes.10 The reviewers did not specifically address periprosthetic fractures associated with either femoral notching or TKA design, as they could not quantitatively analyze postoperative complications because of the diversity of reports. Given the limited number of reported cases, a review of radiographic findings pertaining to the characteristics of supracondylar fractures in anterior femoral notching was unsuccessful.12 As the previous biomechanical studies of anterior notching used primarily CR models or no prostheses at all, a study of biomechanical differences between CR and PS designs in the presence of anterior notching is warranted.1,7,8 Therefore, we conducted a study to assess the effect of anterior femoral notching on torsional strength and load to failure in CR and PS femoral components.
Materials and Methods
Twelve fourth-generation composite adult left femur synthetic sawbones (Sawbones; Pacific Research Laboratories) were selected for their consistent biomechanical properties, vs those of cadaveric specimens; in addition, low intersample variability made them preferable to cadaveric bones given the small sample used in this study.13,14 All bones were from the same lot. All were visually inspected for defects and found to be acceptable. In each sample, an anterior cortical defect was created by making an anterior cut with an undersized (size 4) posterior referencing guide. In addition, the distance from the proximal end of the notch to the implant fell within 15 mm, as that is the maximum distance from the implant a notch can be placed using a standard femoral cutting jig.15 Six femora were instrumented with CR implants and 6 with PS implants (DePuy Synthes). Implants were placed using standardized cuts. Before testing, each implant was inspected for proper fit and found to be securely fastened to the femur. In addition, precision calipers were used to measure notch depth and distance from notch to implant before loading. A custom polymethylmethacrylate torsion jig was used to fix each instrumented femur proximally and distally on the femoral implant (Figure 1). Care was taken to ensure the distal jig engaged only the implant, thus isolating the notch as a stress riser. Each femur was loaded in external rotation through the proximal femoral jig along the anatomical axis. Use of external rotation was based on study findings implicating external rotation of the tibia as the most likely mechanism for generating a fracture in the event of a fall.12 Furthermore, distal femur fractures are predominantly spiral as opposed to butterfly or bending—an indication that torsion is the most likely mechanism of failure.16 With no axial rotation possible within the prosthesis, increased torsional stress is undoubtedly generated within adjacent bone. Each specimen underwent torsional stiffness testing and then load to failure. Torsional stiffness was measured by slowly loading each femur in external rotation, from 1 to 18 Nm for 3 cycles at a displacement rate of 0.5° per second. Each specimen then underwent torsional load-to-failure testing on an Instron 5800R machine at a rate of 0.5° per second. Failure was defined as the moment of fracture and subsequent decrease in torsional load—determined graphically by the peak torsional load followed immediately by a sharp decrease in load. Stiffness was determined as the slope of torque to the displacement curve for each cycle, and torque to failure was the highest recorded torque before fracture. Fracture pattern was noted after failure. A sample size of 6 specimens per group provided 80% power to detect a between-group difference of 1 Nm per degree in stiffness, using an estimated SD of 0.7 Nm per degree. In our statistical analysis, continuous variables are reported as means and SDs. Data from our torsional stiffness and load-to-failure testing were analyzed with unpaired 2-sample t tests, and P < .05 was considered statistically significant.
Results
We did not detect a statistical difference in notch depth, notch-to-implant distance, or femoral length between the CR and PS groups. Mean (SD) notch depth was 6.0 (1.3) mm for CR and 4.9 (1.0) mm for PS (P = .13); mean (SD) distance from the proximal end of the notch to the implant was 13.8 (1.7) mm for CR and 11.1 (3.2) mm for PS (P = .08); and mean (SD) femoral length was 46.2 (0.1) cm for CR and 46.2 (0.1) cm for PS (P = .60).
Mean (SD) torsional stiffness for the first 3 precycles was 6.2 (1.2), 8.7 (1.5), and 8.8 (1.4) Nm per degree for the CR group and 6.0 (0.7), 8.4 (1.4), and 8.6 (1.4) Nm per degree for the PS group; the differences were not statistically significant (Figure 2A). In addition, there were no statistically significant differences in mean (SD) stiffness at failure between CR, 6.5 (0.7) Nm per degree, and PS, 7.1 (0.9) Nm per degree (P = .24; Figure 2B) or in mean (SD) final torque at failure between CR, 62.4 (9.4) Nm, and PS, 62.7 (12.2) Nm (P = .95; Figure 2C).
All fractures in both groups were oblique fractures originating at the proximal angle of the notch and extended proximally. None extended distally into the box. Fracture locations and patterns were identical in the CR and PS groups of femurs (Figure 3).
Discussion
Periprosthetic fractures after TKA remain rare. However, these fractures can significantly increase morbidity and complications. Anterior femoral notching occurs inadvertently in 30% to 40% of TKAs.6,17 The impact of femoral notching on supracondylar femur fracture is inconsistent between biomechanical and retrospective clinical studies. Retrospective studies failed to find a significant correlation between anterior femoral notching and supracondylar femur fractures.6,17 However, findings of biomechanical studies have suggested that a notch 3 mm deep will reduce the torsional strength of the femur by 29%.7 Another study, using 3-dimensional finite element analysis, showed a significant increase in local stress with a notch deeper than 3 mm.15
To our knowledge, no clinical studies, including the aforementioned Cochrane review,10 have specifically evaluated the difference in risk for periprosthetic fracture between different TKA models in the presence of notching.11 The biomechanical differences between implant designs could be a confounding factor in the results of past studies. More bone resection is required in PS designs than in CR designs. The position of the PS intercondylar cutout, much lower than the top of the patella flange, should not increase susceptibility to fractures more than in CR designs, but this hypothesis, though accepted, has not been validated biomechanically or addressed specifically in prospective or retrospective clinical analysis. In the present study, we used a biomechanical model to replicate an external rotation failure mechanism and quantify the differences in torsional strength and load to failure between CR TKA and PS TKA models in the presence of anterior femoral notching. Our results showed no significant differences in torsional stiffness, stiffness at failure, or torque at failure between the CR and PS design groups in the presence of anterior femoral notching.
In this study, all femoral fractures were oblique, and they all originated at the site of the cortical defect, not the notch—a situation markedly different from having bending forces applied to the femur. Previous biomechanical data indicated that bending forces applied to a notched femur cause fractures originating at the notch, whereas torsional forces applied to a notched femur cause fractures originating at the anterior aspect of the bone–component interface.7 The difference is attributable to study design. Our femurs were held fixed at their proximal end, which may have exacerbated any bending forces applied during external rotation, but we thought constraining the proximal femur would better replicate a fall involving external rotation.
More important for our study, an oblique fracture pattern was noted for both design groups (CR and PS), indicating the fracture pattern was unrelated to the area from which bone was resected for the PS design. All femur fractures in both design groups occurred proximal to a well-fixed prosthesis, indicating they should be classified as Vancouver C fractures. This is significant because intercondylar fossa resection (PS group) did not convert the fractures into Vancouver B2 fractures, which involve prosthesis loosening caused by pericomponent fracture.18 This simple observation validated our hypothesis that there would be no biomechanical differences between CR and PS designs with respect to the effects of anterior femoral notching. This lack of a significant difference may be attributed to the PS intercondylar cutout being much lower than the top of the anterior flange shielding the resected bone deep to the anterior flange.7 In addition, given the rarity of supracondylar fractures and the lack of sufficient relevant clinical data, it is difficult to speculate on the fracture patterns observed in clinical cases versus biomechanical studies.12
The use of synthetic bone models instead of cadaveric specimens could be seen as a limitation. Although synthetic bones may not reproduce the mechanism of failure in living and cadaveric femurs, the mechanical properties of synthetic bones have previously been found to fall within the range of those of cadaveric bones under axial loading, bending, and torsion testing.13,14 As a uniform testing material, synthetic bones allow removal of the confounding variations in bone size and quality that plague biomechanical studies in cadaveric bones.13,14 Interfemoral variability was 20 to 200 times higher in cadaveric femurs than in synthetic bones, which makes synthetic femurs preferable to cadaveric femurs, especially in studies with a small sample size.13,14 In addition, a uniform specimen provides consistent, reproducible osteotomies, which were crucial for consistent mechanical evaluation of each configuration in this study.
The long-term clinical significance of anterior femoral notching in periprosthetic fractures is equivocal, possibly because most studies predominantly use CR implants.6 This may not be an issue if it is shown that CR and PS implants have the same mechanical properties. Despite the differences between clinical studies and our biomechanical study, reevaluation of clinical data is not warranted given the biomechanical data we present here. Results of biomechanical studies like ours still suggest an increased immediate postoperative risk for supracondylar fracture after anterior cortical notching of the femur.5,7 Ultimately, this study found that, compared with a CR design, a PS design did not alter the torsional biomechanical properties or fracture pattern of an anteriorly notched femur.
1. Culp RW, Schmidt RG, Hanks G, Mak A, Esterhai JL Jr, Heppenstall RB. Supracondylar fracture of the femur following prosthetic knee arthroplasty. Clin Orthop Relat Res. 1987;(222):212-222.
2. Delport PH, Van Audekercke R, Martens M, Mulier JC. Conservative treatment of ipsilateral supracondylar femoral fracture after total knee arthroplasty. J Trauma. 1984;24(9):846-849.
3. Figgie MP, Goldberg VM, Figgie HE 3rd, Sobel M. The results of treatment of supracondylar fracture above total knee arthroplasty. J Arthroplasty. 1990;5(3):267-276.
4. Rorabeck CH, Taylor JW. Periprosthetic fractures of the femur complicating total knee arthroplasty. Orthop Clin North Am. 1999;30(2):265-277.
5. Hirsh DM, Bhalla S, Roffman M. Supracondylar fracture of the femur following total knee replacement. Report of four cases. J Bone Joint Surg Am. 1981;63(1):162-163.
6. Ritter MA, Thong AE, Keating EM, et al. The effect of femoral notching during total knee arthroplasty on the prevalence of postoperative femoral fractures and on clinical outcome. J Bone Joint Surg Am. 2005;87(11):2411-2414.
7. Lesh ML, Schneider DJ, Deol G, Davis B, Jacobs CR, Pellegrini VD Jr. The consequences of anterior femoral notching in total knee arthroplasty. A biomechanical study. J Bone Joint Surg Am. 2000;82(8):1096-1101.
8. Shawen SB, Belmont PJ Jr, Klemme WR, Topoleski LD, Xenos JS, Orchowski JR. Osteoporosis and anterior femoral notching in periprosthetic supracondylar femoral fractures: a biomechanical analysis. J Bone Joint Surg Am. 2003;85(1):115-121.
9. Scuderi GR, Pagnano MW. Review article: the rationale for posterior cruciate substituting total knee arthroplasty. J Orthop Surg (Hong Kong). 2001;9(2):81-88.
10. Verra WC, van den Boom LG, Jacobs W, Clement DJ, Wymenga AA, Nelissen RG. Retention versus sacrifice of the posterior cruciate ligament in total knee arthroplasty for treating osteoarthritis. Cochrane Database Syst Rev. 2013;10:CD004803.
11. Kolisek FR, McGrath MS, Marker DR, et al. Posterior-stabilized versus posterior cruciate ligament-retaining total knee arthroplasty. Iowa Orthop J. 2009;29:23-27.
12. Dennis DA. Periprosthetic fractures following total knee arthroplasty. Instr Course Lect. 2001;50:379-389.
13. Cristofolini L, Viceconti M, Cappello A, Toni A. Mechanical validation of whole bone composite femur models. J Biomech. 1996;29(4):525-535.
14. Heiner AD, Brown TD. Structural properties of a new design of composite replicate femurs and tibias. J Biomech. 2001;34(6):773-781.
15. Beals RK, Tower SS. Periprosthetic fractures of the femur. An analysis of 93 fractures. Clin Orthop Relat Res. 1996;(327):238-246.
16. Gujarathi N, Putti AB, Abboud RJ, MacLean JG, Espley AJ, Kellett CF. Risk of periprosthetic fracture after anterior femoral notching. Acta Orthop. 2009;80(5):553-556.
17. Zalzal P, Backstein D, Gross AE, Papini M. Notching of the anterior femoral cortex during total knee arthroplasty: characteristics that increase local stresses. J Arthroplasty. 2006;21(5):737-743.
18. Gaski GE, Scully SP. In brief: classifications in brief: Vancouver classification of postoperative periprosthetic femur fractures. Clin Orthop Relat Res. 2011;469(5):1507-1510.
1. Culp RW, Schmidt RG, Hanks G, Mak A, Esterhai JL Jr, Heppenstall RB. Supracondylar fracture of the femur following prosthetic knee arthroplasty. Clin Orthop Relat Res. 1987;(222):212-222.
2. Delport PH, Van Audekercke R, Martens M, Mulier JC. Conservative treatment of ipsilateral supracondylar femoral fracture after total knee arthroplasty. J Trauma. 1984;24(9):846-849.
3. Figgie MP, Goldberg VM, Figgie HE 3rd, Sobel M. The results of treatment of supracondylar fracture above total knee arthroplasty. J Arthroplasty. 1990;5(3):267-276.
4. Rorabeck CH, Taylor JW. Periprosthetic fractures of the femur complicating total knee arthroplasty. Orthop Clin North Am. 1999;30(2):265-277.
5. Hirsh DM, Bhalla S, Roffman M. Supracondylar fracture of the femur following total knee replacement. Report of four cases. J Bone Joint Surg Am. 1981;63(1):162-163.
6. Ritter MA, Thong AE, Keating EM, et al. The effect of femoral notching during total knee arthroplasty on the prevalence of postoperative femoral fractures and on clinical outcome. J Bone Joint Surg Am. 2005;87(11):2411-2414.
7. Lesh ML, Schneider DJ, Deol G, Davis B, Jacobs CR, Pellegrini VD Jr. The consequences of anterior femoral notching in total knee arthroplasty. A biomechanical study. J Bone Joint Surg Am. 2000;82(8):1096-1101.
8. Shawen SB, Belmont PJ Jr, Klemme WR, Topoleski LD, Xenos JS, Orchowski JR. Osteoporosis and anterior femoral notching in periprosthetic supracondylar femoral fractures: a biomechanical analysis. J Bone Joint Surg Am. 2003;85(1):115-121.
9. Scuderi GR, Pagnano MW. Review article: the rationale for posterior cruciate substituting total knee arthroplasty. J Orthop Surg (Hong Kong). 2001;9(2):81-88.
10. Verra WC, van den Boom LG, Jacobs W, Clement DJ, Wymenga AA, Nelissen RG. Retention versus sacrifice of the posterior cruciate ligament in total knee arthroplasty for treating osteoarthritis. Cochrane Database Syst Rev. 2013;10:CD004803.
11. Kolisek FR, McGrath MS, Marker DR, et al. Posterior-stabilized versus posterior cruciate ligament-retaining total knee arthroplasty. Iowa Orthop J. 2009;29:23-27.
12. Dennis DA. Periprosthetic fractures following total knee arthroplasty. Instr Course Lect. 2001;50:379-389.
13. Cristofolini L, Viceconti M, Cappello A, Toni A. Mechanical validation of whole bone composite femur models. J Biomech. 1996;29(4):525-535.
14. Heiner AD, Brown TD. Structural properties of a new design of composite replicate femurs and tibias. J Biomech. 2001;34(6):773-781.
15. Beals RK, Tower SS. Periprosthetic fractures of the femur. An analysis of 93 fractures. Clin Orthop Relat Res. 1996;(327):238-246.
16. Gujarathi N, Putti AB, Abboud RJ, MacLean JG, Espley AJ, Kellett CF. Risk of periprosthetic fracture after anterior femoral notching. Acta Orthop. 2009;80(5):553-556.
17. Zalzal P, Backstein D, Gross AE, Papini M. Notching of the anterior femoral cortex during total knee arthroplasty: characteristics that increase local stresses. J Arthroplasty. 2006;21(5):737-743.
18. Gaski GE, Scully SP. In brief: classifications in brief: Vancouver classification of postoperative periprosthetic femur fractures. Clin Orthop Relat Res. 2011;469(5):1507-1510.
Clinical and Sonographic Evaluation of Bicortical Button for Proximal Biceps Tenodesis
The long head of the biceps (LHB) tendon is a recognized source of shoulder pain. LHB tendon pathology is commonly associated with other shoulder conditions, such as superior labral tears, rotator cuff tears, or subacromial impingement, whereas isolated pathology, such as traumatic ruptures, tendinosis, or medial subluxation, is rare.1 Treatment of LHB pathology ranges from conservative measures to surgical measures, including tenotomy or tenodesis.2 LHB tenodesis offers the advantage of maintaining the length–tension relationship of the biceps muscle to prevent atrophy and avoid the Popeye deformity incurred from tenotomy alone. Tenodesis also prevents muscle cramping associated with contracted biceps muscle and better maintains elbow flexion and supination strength, which may be decreased with tenotomy.3 In addition, when a subpectoral biceps tenodesis technique is used, pain from LHB tendinopathy in the intertubercular groove may be reduced.4
Open subpectoral biceps tenodesis is a reproducible, efficient method for LHB tenodesis.4,5 A variety of fixation devices has been used: bone tunnels,6 keyhole fixation,7 suture anchors,6-9 and interference screws.6-8,10,11 More recently, a bicortical button has been used for LHB tendon tenodesis.12 Biomechanical studies have shown that load to failure is comparable for bicortical button fixation and interference screw fixation.13,14 In other models of tendon repair, the bicortical button has strength and stability comparable to those of interference screw fixation and enables earlier rehabilitation.15-17 However, there is concern that bicortical button fixation may result in axillary nerve (AN) or posterior circumflex humeral artery (PCHA) compromise because of the proximity of these neurovascular structures to the bicortical button.13,18-21
We conducted a study to functionally and sonographically assess the outcomes of patients who underwent open subpectoral biceps tenodesis with a bicortical button. Functional outcomes were assessed with patient-reported outcomes and physician-reported outcomes. Sonographic studies were used to evaluate the integrity of the tenodesis and determine the proximity of the button to the AN and the PCHA along the posterior proximal humerus.
Methods
After obtaining Institutional Review Board approval for this study, we retrospectively identified 28 consecutive patients who had proximal biceps tenodesis performed by a single surgeon (Dr. K.E. Swanson) using a mini-open subpectoral biceps tenodesis technique with a bicortical button between March 2011 and January 2013. All 28 patients were asked to participate in the study. Twenty-four (86%) agreed to complete 2 surgical outcome surveys, and 18 (64%) completed a 3-part clinical examination at minimum 12-month follow-up.
One of the surveys was Quick Disabilities of the Arm, Shoulder, and Hand (QuickDASH), a validated comprehensive disability survey that scores upper extremity functionality on a scale ranging from 0 (none) to 100 (extreme difficulty).22,23 The other survey scored pain on a scale ranging from 0 (none) to 100 (worst pain).
The clinical examination was completed during a single visit by an orthopedic surgeon (Dr. Meadows or Dr. Diesselhorst) different from the primary surgeon (Dr. K.E. Swanson) and by a clinician-sonologist (Dr. Finnoff). The examination’s 3 parts were physical examination of arm, biceps supination strength test, and ultrasonographic evaluation.
Physical Examination of Arm. Physical examination included palpation of bicipital groove, range of motion (ROM) of shoulder and elbow, and clinical deformity of biceps. Patients were questioned regarding symptoms of AN damage, including sensory and motor findings. Bicipital groove tenderness was assessed with a visual analog scale rating pain 0 to 10. ROM was measured in degrees and was presented as a percentage of full elbow ROM (150°) and full shoulder ROM (180°).
Biceps Supination Strength Test. Biceps supination strength was tested with a baseline hydraulic wrist dynamometer with door handle attachment. Patients were seated with the elbow bent 90° and the forearm in a neutral position. In a series of 3 trials, the patient maintained grip of the dynamometer doorknob while supinating the forearm. The tenodesed (operated) arm and contralateral unaffected (nonoperated) arm were tested in random order and recorded in pounds.
Ultrasonographic Evaluation. Ultrasonography was used to evaluate the tenodesis site. In each case, the biceps tendon was assessed to determine the location of the bicortical button in relation to the AN/PCHA neurovascular bundle. Whereas nerves are difficult to visualize with ultrasonography, arteries are readily seen. Dr. Finnoff used a CX50 ultrasound machine (Philips Medical Systems) with either a 12-3 MHz linear array or a 5-1 MHz curvilinear array transducer to measure the shortest distance from the PCHA to the button.
Each patient was placed in a lateral decubitus or prone position, and the skin of the upper arm was exposed. Tendon integrity was deemed either intact (continuity between biceps tendon and cortical button) or disrupted (lack of continuity between tendon and cortical button). The transducer was then placed in an anatomical sagittal plane over the posterior aspect of the proximal humerus. Power Doppler and cephalad and caudad transducer glides were used to identify the location of the PCHA. The transducer was then glided laterally and anteriorly around the humerus, following the course of the PCHA, until the cortical button was located. The narrowest interval between the PCHA and the cortical button was measured using the ultrasound machine’s software. A still image of each measurement was saved.
Surgical Technique
Biceps tenodesis indications included high-demand heavy laborers, athletes, and patients who preferred the cosmetic results of tenodesis over tenotomy. Most patients had acute symptomatic tears of the superior labrum with instability of the biceps anchor complex. Others had fraying and tenosynovitis of the LHB tendon. Any associated pathology was addressed during the same surgical period.
The surgical technique used was similar to that described by Snir and colleagues.12 Each patient was placed in the lateral decubitus position. Once pathology confirmed biceps tenodesis, the biceps tendon was tenotomized at the base of the superior labrum. A 3-cm incision was made along the axillary fold centered over the inferior border of the pectoralis major tendon. Blunt dissection was performed to define the inferior border of the pectoralis major tendon and to palpate the underlying biceps tendon as it exited the intertubercular groove. The LHB tendon was removed and prepared with No. 2 Fiberwire (Arthrex) in Krackow fashion starting 2 cm proximal to the musculotendinous junction. The excess tendon was excised.
A 3.2-mm guide wire was centered along the most distal aspect of the biceps groove and then drilled through the anterior cortex and just through the posterior cortex. A cannulated reamer, selected on the basis of the biceps tendon diameter (typically, 5-7 mm), was then drilled over the guide wire through the anterior cortex only. The Food and Drug Administration–approved cortical button (BicepsButton; Arthrex) was then loaded by passing the tendon suture ends through each side of the button in alternating fashion, thus allowing the button to slide along the sutures.
The button was loaded onto the BicepsButton deployment device and inserted through the drilled tunnel of the anterior cortex and just through the posterior cortex. The deployment device was then removed, and 1 suture end was pulled to allow the button to engage the posterior humeral cortex. Pulling on both sutures allowed the biceps tendon to slide through the anterior cortex hole of the humerus until the tendon reached the posterior humeral cortex. Tension was verified, and the sutures were tied over the tendon. The wound was then irrigated and closed.
Rehabilitation Program
Patients completed a standard rehabilitation protocol for biceps tenodesis24 along with rehabilitation protocols for any additional procedures performed. In phase 1 (weeks 0-2), they focused on gradual restoration of passive ROM and remained in a sling. In phase 2 (weeks 2-6), they focused on gradual restoration of active ROM, and by week 3 were weaned out of the sling. In phase 3 (weeks 6-8), they continued ROM and strengthening exercises to normalize strength, endurance, and neuromuscular control. In phase 4 (weeks 8-12), they focused on advanced strengthening exercises and return to activities.
Statistical Analysis
Descriptive statistics included means, medians, and SDs. Comparisons between operated and nonoperated arms and between dominant and nondominant arms were performed by a statistician using paired t tests with P = .05. Confidence intervals were calculated for operated and nonoperated arms and for dominant and nondominant arms by using the differences between them.
Results
Functional Outcomes
Surgical outcome scores and pain scores were obtained from 24 patients (86%) at minimum 12-month follow-up. Mean (SD) DASH score was 15.15 (17.6; median, 9), and mean (median) pain score was 12.61 (7).
Eighteen patients (64%) completed the clinical examination: 16 men (88.9%) and 2 women (11.1%). Mean age was 48.3 years (age range, 33-59 years). Of these 18 patients, 9 (50%) had surgery on the dominant arm, and the other 9 had surgery on the nondominant arm. All patients were right-hand–dominant. In 3 patients, biceps tenodesis was performed with only minimal arthroscopic débridement (20%); in the other 15, biceps tenodesis was performed concomitantly with 1 or more additional arthroscopic procedures: acromioplasty (73%), rotator cuff repair (47%), distal clavicle resection (33%), subacromial bursectomy (13%), microfracture of glenoid (13%), and posterior labral repair (7%).
The clinical examination was performed a mean of 15.2 months (range, 12-26 months) after surgery. Physical examination findings are listed in Table 1.
Forearm supination strength, averaged from 3 trials on each arm, was significantly (P = .01) greater in the nonoperated arm than in the operated arm (Table 2, Figure 1). A 95% confidence interval for the mean (SD) difference in strength was 9.35 (7.76) pounds, meaning that on average, the nonoperated arm will be 1.59 to 17.11 pounds stronger than the operated arm. In addition, strength of the dominant arm was greater than that of the nondominant arm (P = .05) regardless of which arm underwent surgery (Table 2, Figure 1). However, the mean (SD) difference in strength was 6.94 (8.39) pounds, indicating the observed difference was not statistically significant.
Sonographic Evaluation
According to the sonographic evaluations, the tenodesis was intact in all 18 patients (Figure 2). Estimated mean (SD) distance from button to PCHA was 18.17 (9.0) mm (median, 16.1 mm; range, 9.4-48 mm) (Figure 2, Figure 3). No patient indicated any symptoms of AN damage.
Discussion
There are few studies of functional outcomes of biceps tenodesis. Pain is a common measure of patient satisfaction. Mazzocca and colleagues25 reported a mean follow-up pain score of 1.1 (range, 0.5-1.9) out of 10 for a group of 41 patients who had subpectoral tenodesis with an interference screw. Millett and colleagues26 reported a mean postoperative pain score of 2.5 out of 10 for patients who had subpectoral interference screw fixation. Our patients reported a mean pain score of 12.6 out of 100 after minimum 12-month follow-up. We also assessed for pain in the intertubercular groove during palpation. Although some studies have shown that groove pain was eliminated by subpectoral biceps tenodesis,5 3 patients in our study had pain on groove palpation. The cause of this residual pain is unclear, but some studies have suggested a chronic degenerative pathologic process that occurs while the tendon is within the biceps groove.27 Removing the tendon from the groove may not remove the underlying cause of pain.
Our patients’ mean DASH score was 15.15 (within the excellent range). Normative mean (SD) DASH score for the general population is 10.1 (14.68).28
Functional strength of forearm supination, shoulder ROM, and elbow ROM are objective measures of patient performance after fixation. On Cybex testing, Phillips and colleagues29 found no difference in forearm supination strength or elbow flexion (compared with contralateral arm) after biceps tenodesis or conservative treatment for proximal biceps ruptures. Shank and colleagues30 compared elbow flexion and supination strength of the affected and unaffected arms after suture anchor subpectoral biceps tenodesis. There was no significant difference in Cybex results, but there was a 14% to 15% loss of average strength in the tenodesed versus nonsurgical arm. In the present study, we found a significant difference in forearm supination strength between the operated and nonoperated arms, but with only a 7% loss of average strength in the operated arms. The difference in strength ranged from 1.59 to 17.11 pounds, which may not be clinically significant, as supination strength ranged from 60 to 270 pounds.
Of the 18 patients in this study, 9 had surgery on the dominant arm, and the other 9 had surgery on the nondominant arm. Examining the effect of arm dominance on results revealed that patients with surgery on the nondominant arm tended to have substantially reduced supination strength in that arm vs the dominant arm. There was an 11% loss of average strength for nondominant vs dominant arms that had surgery. Examining nondominant arms only revealed a 13% loss of strength for operated vs nonoperated arms. There was no difference in forearm supination strengths between nonoperated arms (dominant vs nondominant) or between dominant arms (operated vs nonoperated). This suggests that, though hand dominance may not play a significant role in control patients’ forearm supination strength,30 it may have a substantial effect on surgical patients’ ability to regain strength when the nondominant arm is the surgical arm. One objective of this study was to measure the distance between the biceps cortical button on the posterior humeral cortex and the AN/PCHA neurovascular bundle. The AN bundles with the PCHA posterior to the humeral neck.31-33 As the AN travels with the PCHA, and the PCHA has been reliably identified with Doppler ultrasonography,34-36 the PCHA was used as a marker for the AN in this study. Our bicortical button technique places the button on the posterior aspect of the humerus, making AN and PCHA the nearest at-risk neurovascular structures. None of our patients had symptoms of AN damage. However, 2 patients indicated pain in the posterior aspect of the humerus during deltoid activation. Distance from the neurovascular structures to the button was 48 mm in one patient and 13.6 mm in the other. DASH scores were 43 and 27, respectively. Both patients’ 1-year pain score was 30. The first patient underwent arthroscopic acromioplasty, distal clavicle resection, and microfracture of the glenoid surface in addition to the subpectoral biceps tenodesis; the second underwent subacromial decompression and distal clavicle resection in addition to the subpectoral biceps tenodesis. Whether the associated pathology contributed to their persistent pain is unknown. However, given the distance from AN/PCHA to button, it is unlikely that their pain was a result of neurovascular compromise from the procedure.
Advantages of the cortical button include the ability to drill a smaller hole in the humerus for fixation, compared with the hole drilled for an interference screw. Despite the biomechanical strength of the screw, large (8 mm) cortical violations have been associated with increased fracture risk of the proximal humerus.37,38 The tendon may experience less trauma than that caused by being twisted against an interference screw, the most common location of failure of which is the tendon–screw interface.39 In addition, tendon healing may be improved through circumferential healing in the cortical button tunnel.
A concern of using a bicortical button for fixation is drilling through the posterior cortex, because of the proximity of the posterior neurovascular structures. In a case in which the posterior cord was injured, Rhee and colleagues40 used a suture pullout technique whereby a Beath pin was passed out of the posterior humerus and soft tissues to then hold tension on the biceps tendon during the tenodesis. The radial nerve potentially could have been injured by pin overpenetration or by becoming wrapped up in the soft tissues as the pin was spinning through them. In our technique, the posterior humeral cortex is drilled cautiously to avoid overpenetration and possibly getting the posterior soft tissues wrapped up in the guide pin. No AN injuries have been reported with this technique. Mean distance from AN to posterior cortical button in this study was 18.17 mm. In 2 cadaver studies of bicortical drilling for subpectoral biceps tenodesis, the ANs were 25.1 mm and 36.7 mm from the posterior drill hole.41,21
Limitations of this study included its design (case series) and limited number of follow-up patients. Of the 28 consecutive patients identified for the study, 10 did not undergo the clinical examination, as they either lived more than 3 hours away (8 patients) or could not be contacted (2 patients). Another study limitation was the inability to directly image ANs with ultrasound. Therefore, measurements of the distance from the PCHA to the button were used to estimate the distance from the AN/PCHA neurovascular bundle to the button.
In this study, functional outcomes were excellent, and there were no tenodesis failures or neurovascular complications. These preliminary findings indicate that subpectoral biceps tenodesis with a bicortical button is a viable treatment option for patients with the appropriate indications for this procedure.
1. Khazzam M, George MS, Churchill RS, Kuhn JE. Disorders of the long head of biceps tendon. J Shoulder Elbow Surg. 2012;21(1):136-145.
2. Geaney LE, Mazzocca AD. Biceps brachii tendon ruptures: a review of diagnosis and treatment of proximal and distal biceps tendon ruptures. Phys Sportsmed. 2010;38(2):117-125.
3. Kelly AM, Drakos MC, Fealy S, Taylor SA, O’Brien SJ. Arthroscopic release of the long head of the biceps tendon: functional outcome and clinical results. Am J Sports Med. 2005;33(2):208-213.
4. Provencher MT, LeClere LE, Romeo AA. Subpectoral biceps tenodesis. Sports Med Arthrosc Rev. 2008;16(3):170-176.
5. Nho SJ, Reiff SN, Verma NN, Slabaugh MA, Mazzocca AD, Romeo AA. Complications associated with subpectoral biceps tenodesis: low rates of incidence following surgery. J Shoulder Elbow Surg. 2010;19(5):764-768.
6. Mazzocca AD, Bicos J, Santangelo S, Romeo AA, Arciero RA. The biomechanical evaluation of four fixation techniques for proximal biceps tenodesis. Arthroscopy. 2005;21(11):1296-1306.
7. Ozalay, M, Akpinar S, Karaeminogullari O, et al. Mechanical strength of four different biceps tenodesis techniques. Arthroscopy. 2005;21(8):992-998.
8. Golish RS, Caldwell PE, Miller MD, et al. Interference screw versus suture anchor fixation for subpectoral tenodesis of the proximal biceps tendon: a cadaveric study. Arthroscopy. 2008;24(10):1103-1108.
9. Richards DP, Burkhart SS. A biomechanical analysis of two biceps tenodesis fixation techniques. Arthroscopy. 2005;21(7):861-866.
10. Mazzocca AD, Rios CG, Romeo AA, Arciero RA. Subpectoral biceps tenodesis with interference screw fixation. Arthroscopy. 2005;21(7):896.
11. Wolf RS, Zheng N, Weichel D. Long head biceps tenotomy versus tenodesis: a cadaveric biomechanical analysis. Arthroscopy. 2005;21(2):182-185.
12. Snir N, Hamula M, Wolfson T, Laible C, Sherman O. Long head of the biceps tenodesis with cortical button technique. Arthrosc Tech. 2013;2(2):e95-e97.
13. Arora AS, Singh A, Koonce RC. Biomechanical evaluation of a unicortical button versus interference screw for subpectoral biceps tenodesis. Arthroscopy. 2013;29(4):638-644.
14. Buchholz A, Martetschläger F, Siebenlist S, et al. Biomechanical comparison of intramedullary cortical button fixation and interference screw technique for subpectoral biceps tenodesis. Arthroscopy. 2013;29(5):845-853.
15. Bain GI, Prem H, Heptinstall RJ, Verhellen R, Paix D. Repair of distal biceps tendon rupture: a new technique using the Endobutton. J Shoulder Elbow Surg. 2000;9(2):120-126.
16. Greenberg JA. Endobutton repair of distal biceps tendon ruptures. J Hand Surg Am. 2009;34(8):1541-1548.
17. Heinzelmann AD, Savoie FH 3rd, Ramsey JR, Field LD, Mazzocca AD. A combined technique for distal biceps repair using a soft tissue button and biotenodesis interference screw. Am J Sports Med. 2009;37(5):989-994.
18. DeAngelis JP, Chen A, Wexler M, et al. Biomechanical characterization of unicortical button fixation: a novel technique for proximal subpectoral biceps tenodesis. Knee Surg Sports Traumatol Arthrosc. 2015;23(5):1434-1441.
19. Dickens JF, Kilcoyne KG, Tintle SM, Giuliani J, Schaefer RA, Rue JP. Subpectoral biceps tenodesis: an anatomic study and evaluation of at-risk structures. Am J Sports Med. 2012;40(10):2337-2341.
20. Sethi PM, Rajaram A, Beitzel K, Hackett TR, Chowaniec DM, Mazzocca AD. Biomechanical performance of subpectoral biceps tenodesis: a comparison of interference screw fixation, cortical button fixation, and interference screw diameter. J Shoulder Elbow Surg. 2013;22(4):451-457.
21. Sethi PM, Vadasdi K, Greene RT, Vitale MA, Duong M, Miller SR. Safety of open suprapectoral and subpectoral biceps tenodesis: an anatomic assessment of risk for neurologic injury. J Shoulder Elbow Surg. 2015;24(1):138-142.
22. Gummesson C, Ward MM, Atroshi I. The shortened Disabilities of the Arm, Shoulder and Hand questionnaire (QuickDASH): validity and reliability based on responses within the full-length DASH. BMC Musculoskelet Disord. 2006;7:44.
23. Schmidt CC, Brown BT, Sawardeker PJ, DeGravelle M Jr, Miller MC. Factors affecting supination strength after a distal biceps rupture. J Shoulder Elbow Surg. 2014;23(1):68-75.
24. Brotzman SB, Wilk KE, eds. Handbook of Orthopaedic Rehabilitation. Philadelphia, PA: Mosby Elsevier; 2007.
25. Mazzocca AD, Cote MP, Arciero CL, Romeo AA, Arciero RA. Clinical outcomes after subpectoral biceps tenodesis with an interference screw. Am J Sports Med. 2008;36(10):1922-1929.
26. Millett PJ, Snaders B, Gobezie R, Braun S, Warner JP. Interference screw versus suture anchor fixation for open subpectoral biceps tenodesis: does it matter? BMC Musculoskelet Disord. 2008;9(121):1-6.
27. Streit JJ, Shishani Y, Rodgers M, Gobezie R. Tendinopathy of the long head of the biceps tendon: histopathologic analysis of the extra-articular biceps tendon and tenosynovium. Open Access J Sports Med. 2015;6:63-70.
28. Hunsaker FG, Cioffi DA, Amadio PC, Wright JG, Caughlin B. The American Academy of Orthopaedic Surgeons outcomes instruments: normative values from the general population. J Bone Joint Surg Am. 2002;84(2):208-215.
29. Phillips BB, Canale ST, Sisk TD, Stralka SW, Wyatt KP. Rupture of the proximal biceps tendon in middle-aged patients. Orthop Rev. 1993;22(3):349-353.
30. Shank JR, Singleton SB, Braun S, et al. A comparison of forearm supination and elbow flexion strength in patients with long head of the biceps tenotomy or tenodesis. Arthroscopy. 2011;27(1):9-16.
31. Apaydin N, Tubbs RS, Loukas M, Duparc F. Review of the surgical anatomy of the axillary nerve and the anatomic basis of its iatrogenic and traumatic injury. Surg Radiol Anat. 2010;32(3):193-201.
32. Johnson D. Pectoral girdle and upper limp. In: Standring S, ed. Gray’s Anatomy. 40th ed. New York, NY: Elsevier; 2008:814-821.
33. Tubbs RS, Tyler-Kabara EC, Aikens AC, et al. Surgical anatomy of the axillary nerve within the quadrangular space. J Neurosurg. 2005;102(5):912-914.
34. Kim YA, Yoon KB, Kwon TD, Kim DH, Yoon DM. Evaluation of anatomic landmarks for axillary nerve block in the quadrilateral space. Acta Anaesthesiol Scand. 2014;58(5):567-571.
35. Robinson DJ, Marks P, Schneider-Kolsky ME. Ultrasound of the posterior circumflex humeral artery. J Med Imaging Radiat Oncol. 2010;54(3):219-223.
36. Rothe C, Asghar S, Andersen HL, Christensen JK, Lange KH. Ultrasound-guided block of the axillary nerve: a volunteer study of a new method. Acta Anaesthesiol Scand. 2011;55(5):565-570.
37. Reiff SN, Nho SJ, Romeo AA. Proximal humerus fracture after keyhole biceps tenodesis. Am J Orthop. 2010;39(7):E61-E63.
38. Sears BW, Spencer EE, Getz CL. Humeral fracture following subpectoral biceps tenodesis in 2 active, healthy patients. J Shoulder Elbow Surg. 2011;20(6):e7-e11.
39. Koch BS, Burks RT. Failure of biceps tenodesis with interference screw fixation. Arthroscopy. 2012;28(5):735-740.
40. Rhee PC, Spinner RJ, Bishop AT, Shin AY. Iatrogenic brachial plexus injuries associated with open subpectoral biceps tenodesis. Am J Sports Med. 2013;41(9):2048-2053.
41. Ding DY, Gupta A, Snir N, Wolfson T, Meislin RJ. Nerve proximity during bicortical drilling for subpectoral biceps tenodesis: a cadaveric study. Arthroscopy. 2014;30(8):942-946.
The long head of the biceps (LHB) tendon is a recognized source of shoulder pain. LHB tendon pathology is commonly associated with other shoulder conditions, such as superior labral tears, rotator cuff tears, or subacromial impingement, whereas isolated pathology, such as traumatic ruptures, tendinosis, or medial subluxation, is rare.1 Treatment of LHB pathology ranges from conservative measures to surgical measures, including tenotomy or tenodesis.2 LHB tenodesis offers the advantage of maintaining the length–tension relationship of the biceps muscle to prevent atrophy and avoid the Popeye deformity incurred from tenotomy alone. Tenodesis also prevents muscle cramping associated with contracted biceps muscle and better maintains elbow flexion and supination strength, which may be decreased with tenotomy.3 In addition, when a subpectoral biceps tenodesis technique is used, pain from LHB tendinopathy in the intertubercular groove may be reduced.4
Open subpectoral biceps tenodesis is a reproducible, efficient method for LHB tenodesis.4,5 A variety of fixation devices has been used: bone tunnels,6 keyhole fixation,7 suture anchors,6-9 and interference screws.6-8,10,11 More recently, a bicortical button has been used for LHB tendon tenodesis.12 Biomechanical studies have shown that load to failure is comparable for bicortical button fixation and interference screw fixation.13,14 In other models of tendon repair, the bicortical button has strength and stability comparable to those of interference screw fixation and enables earlier rehabilitation.15-17 However, there is concern that bicortical button fixation may result in axillary nerve (AN) or posterior circumflex humeral artery (PCHA) compromise because of the proximity of these neurovascular structures to the bicortical button.13,18-21
We conducted a study to functionally and sonographically assess the outcomes of patients who underwent open subpectoral biceps tenodesis with a bicortical button. Functional outcomes were assessed with patient-reported outcomes and physician-reported outcomes. Sonographic studies were used to evaluate the integrity of the tenodesis and determine the proximity of the button to the AN and the PCHA along the posterior proximal humerus.
Methods
After obtaining Institutional Review Board approval for this study, we retrospectively identified 28 consecutive patients who had proximal biceps tenodesis performed by a single surgeon (Dr. K.E. Swanson) using a mini-open subpectoral biceps tenodesis technique with a bicortical button between March 2011 and January 2013. All 28 patients were asked to participate in the study. Twenty-four (86%) agreed to complete 2 surgical outcome surveys, and 18 (64%) completed a 3-part clinical examination at minimum 12-month follow-up.
One of the surveys was Quick Disabilities of the Arm, Shoulder, and Hand (QuickDASH), a validated comprehensive disability survey that scores upper extremity functionality on a scale ranging from 0 (none) to 100 (extreme difficulty).22,23 The other survey scored pain on a scale ranging from 0 (none) to 100 (worst pain).
The clinical examination was completed during a single visit by an orthopedic surgeon (Dr. Meadows or Dr. Diesselhorst) different from the primary surgeon (Dr. K.E. Swanson) and by a clinician-sonologist (Dr. Finnoff). The examination’s 3 parts were physical examination of arm, biceps supination strength test, and ultrasonographic evaluation.
Physical Examination of Arm. Physical examination included palpation of bicipital groove, range of motion (ROM) of shoulder and elbow, and clinical deformity of biceps. Patients were questioned regarding symptoms of AN damage, including sensory and motor findings. Bicipital groove tenderness was assessed with a visual analog scale rating pain 0 to 10. ROM was measured in degrees and was presented as a percentage of full elbow ROM (150°) and full shoulder ROM (180°).
Biceps Supination Strength Test. Biceps supination strength was tested with a baseline hydraulic wrist dynamometer with door handle attachment. Patients were seated with the elbow bent 90° and the forearm in a neutral position. In a series of 3 trials, the patient maintained grip of the dynamometer doorknob while supinating the forearm. The tenodesed (operated) arm and contralateral unaffected (nonoperated) arm were tested in random order and recorded in pounds.
Ultrasonographic Evaluation. Ultrasonography was used to evaluate the tenodesis site. In each case, the biceps tendon was assessed to determine the location of the bicortical button in relation to the AN/PCHA neurovascular bundle. Whereas nerves are difficult to visualize with ultrasonography, arteries are readily seen. Dr. Finnoff used a CX50 ultrasound machine (Philips Medical Systems) with either a 12-3 MHz linear array or a 5-1 MHz curvilinear array transducer to measure the shortest distance from the PCHA to the button.
Each patient was placed in a lateral decubitus or prone position, and the skin of the upper arm was exposed. Tendon integrity was deemed either intact (continuity between biceps tendon and cortical button) or disrupted (lack of continuity between tendon and cortical button). The transducer was then placed in an anatomical sagittal plane over the posterior aspect of the proximal humerus. Power Doppler and cephalad and caudad transducer glides were used to identify the location of the PCHA. The transducer was then glided laterally and anteriorly around the humerus, following the course of the PCHA, until the cortical button was located. The narrowest interval between the PCHA and the cortical button was measured using the ultrasound machine’s software. A still image of each measurement was saved.
Surgical Technique
Biceps tenodesis indications included high-demand heavy laborers, athletes, and patients who preferred the cosmetic results of tenodesis over tenotomy. Most patients had acute symptomatic tears of the superior labrum with instability of the biceps anchor complex. Others had fraying and tenosynovitis of the LHB tendon. Any associated pathology was addressed during the same surgical period.
The surgical technique used was similar to that described by Snir and colleagues.12 Each patient was placed in the lateral decubitus position. Once pathology confirmed biceps tenodesis, the biceps tendon was tenotomized at the base of the superior labrum. A 3-cm incision was made along the axillary fold centered over the inferior border of the pectoralis major tendon. Blunt dissection was performed to define the inferior border of the pectoralis major tendon and to palpate the underlying biceps tendon as it exited the intertubercular groove. The LHB tendon was removed and prepared with No. 2 Fiberwire (Arthrex) in Krackow fashion starting 2 cm proximal to the musculotendinous junction. The excess tendon was excised.
A 3.2-mm guide wire was centered along the most distal aspect of the biceps groove and then drilled through the anterior cortex and just through the posterior cortex. A cannulated reamer, selected on the basis of the biceps tendon diameter (typically, 5-7 mm), was then drilled over the guide wire through the anterior cortex only. The Food and Drug Administration–approved cortical button (BicepsButton; Arthrex) was then loaded by passing the tendon suture ends through each side of the button in alternating fashion, thus allowing the button to slide along the sutures.
The button was loaded onto the BicepsButton deployment device and inserted through the drilled tunnel of the anterior cortex and just through the posterior cortex. The deployment device was then removed, and 1 suture end was pulled to allow the button to engage the posterior humeral cortex. Pulling on both sutures allowed the biceps tendon to slide through the anterior cortex hole of the humerus until the tendon reached the posterior humeral cortex. Tension was verified, and the sutures were tied over the tendon. The wound was then irrigated and closed.
Rehabilitation Program
Patients completed a standard rehabilitation protocol for biceps tenodesis24 along with rehabilitation protocols for any additional procedures performed. In phase 1 (weeks 0-2), they focused on gradual restoration of passive ROM and remained in a sling. In phase 2 (weeks 2-6), they focused on gradual restoration of active ROM, and by week 3 were weaned out of the sling. In phase 3 (weeks 6-8), they continued ROM and strengthening exercises to normalize strength, endurance, and neuromuscular control. In phase 4 (weeks 8-12), they focused on advanced strengthening exercises and return to activities.
Statistical Analysis
Descriptive statistics included means, medians, and SDs. Comparisons between operated and nonoperated arms and between dominant and nondominant arms were performed by a statistician using paired t tests with P = .05. Confidence intervals were calculated for operated and nonoperated arms and for dominant and nondominant arms by using the differences between them.
Results
Functional Outcomes
Surgical outcome scores and pain scores were obtained from 24 patients (86%) at minimum 12-month follow-up. Mean (SD) DASH score was 15.15 (17.6; median, 9), and mean (median) pain score was 12.61 (7).
Eighteen patients (64%) completed the clinical examination: 16 men (88.9%) and 2 women (11.1%). Mean age was 48.3 years (age range, 33-59 years). Of these 18 patients, 9 (50%) had surgery on the dominant arm, and the other 9 had surgery on the nondominant arm. All patients were right-hand–dominant. In 3 patients, biceps tenodesis was performed with only minimal arthroscopic débridement (20%); in the other 15, biceps tenodesis was performed concomitantly with 1 or more additional arthroscopic procedures: acromioplasty (73%), rotator cuff repair (47%), distal clavicle resection (33%), subacromial bursectomy (13%), microfracture of glenoid (13%), and posterior labral repair (7%).
The clinical examination was performed a mean of 15.2 months (range, 12-26 months) after surgery. Physical examination findings are listed in Table 1.
Forearm supination strength, averaged from 3 trials on each arm, was significantly (P = .01) greater in the nonoperated arm than in the operated arm (Table 2, Figure 1). A 95% confidence interval for the mean (SD) difference in strength was 9.35 (7.76) pounds, meaning that on average, the nonoperated arm will be 1.59 to 17.11 pounds stronger than the operated arm. In addition, strength of the dominant arm was greater than that of the nondominant arm (P = .05) regardless of which arm underwent surgery (Table 2, Figure 1). However, the mean (SD) difference in strength was 6.94 (8.39) pounds, indicating the observed difference was not statistically significant.
Sonographic Evaluation
According to the sonographic evaluations, the tenodesis was intact in all 18 patients (Figure 2). Estimated mean (SD) distance from button to PCHA was 18.17 (9.0) mm (median, 16.1 mm; range, 9.4-48 mm) (Figure 2, Figure 3). No patient indicated any symptoms of AN damage.
Discussion
There are few studies of functional outcomes of biceps tenodesis. Pain is a common measure of patient satisfaction. Mazzocca and colleagues25 reported a mean follow-up pain score of 1.1 (range, 0.5-1.9) out of 10 for a group of 41 patients who had subpectoral tenodesis with an interference screw. Millett and colleagues26 reported a mean postoperative pain score of 2.5 out of 10 for patients who had subpectoral interference screw fixation. Our patients reported a mean pain score of 12.6 out of 100 after minimum 12-month follow-up. We also assessed for pain in the intertubercular groove during palpation. Although some studies have shown that groove pain was eliminated by subpectoral biceps tenodesis,5 3 patients in our study had pain on groove palpation. The cause of this residual pain is unclear, but some studies have suggested a chronic degenerative pathologic process that occurs while the tendon is within the biceps groove.27 Removing the tendon from the groove may not remove the underlying cause of pain.
Our patients’ mean DASH score was 15.15 (within the excellent range). Normative mean (SD) DASH score for the general population is 10.1 (14.68).28
Functional strength of forearm supination, shoulder ROM, and elbow ROM are objective measures of patient performance after fixation. On Cybex testing, Phillips and colleagues29 found no difference in forearm supination strength or elbow flexion (compared with contralateral arm) after biceps tenodesis or conservative treatment for proximal biceps ruptures. Shank and colleagues30 compared elbow flexion and supination strength of the affected and unaffected arms after suture anchor subpectoral biceps tenodesis. There was no significant difference in Cybex results, but there was a 14% to 15% loss of average strength in the tenodesed versus nonsurgical arm. In the present study, we found a significant difference in forearm supination strength between the operated and nonoperated arms, but with only a 7% loss of average strength in the operated arms. The difference in strength ranged from 1.59 to 17.11 pounds, which may not be clinically significant, as supination strength ranged from 60 to 270 pounds.
Of the 18 patients in this study, 9 had surgery on the dominant arm, and the other 9 had surgery on the nondominant arm. Examining the effect of arm dominance on results revealed that patients with surgery on the nondominant arm tended to have substantially reduced supination strength in that arm vs the dominant arm. There was an 11% loss of average strength for nondominant vs dominant arms that had surgery. Examining nondominant arms only revealed a 13% loss of strength for operated vs nonoperated arms. There was no difference in forearm supination strengths between nonoperated arms (dominant vs nondominant) or between dominant arms (operated vs nonoperated). This suggests that, though hand dominance may not play a significant role in control patients’ forearm supination strength,30 it may have a substantial effect on surgical patients’ ability to regain strength when the nondominant arm is the surgical arm. One objective of this study was to measure the distance between the biceps cortical button on the posterior humeral cortex and the AN/PCHA neurovascular bundle. The AN bundles with the PCHA posterior to the humeral neck.31-33 As the AN travels with the PCHA, and the PCHA has been reliably identified with Doppler ultrasonography,34-36 the PCHA was used as a marker for the AN in this study. Our bicortical button technique places the button on the posterior aspect of the humerus, making AN and PCHA the nearest at-risk neurovascular structures. None of our patients had symptoms of AN damage. However, 2 patients indicated pain in the posterior aspect of the humerus during deltoid activation. Distance from the neurovascular structures to the button was 48 mm in one patient and 13.6 mm in the other. DASH scores were 43 and 27, respectively. Both patients’ 1-year pain score was 30. The first patient underwent arthroscopic acromioplasty, distal clavicle resection, and microfracture of the glenoid surface in addition to the subpectoral biceps tenodesis; the second underwent subacromial decompression and distal clavicle resection in addition to the subpectoral biceps tenodesis. Whether the associated pathology contributed to their persistent pain is unknown. However, given the distance from AN/PCHA to button, it is unlikely that their pain was a result of neurovascular compromise from the procedure.
Advantages of the cortical button include the ability to drill a smaller hole in the humerus for fixation, compared with the hole drilled for an interference screw. Despite the biomechanical strength of the screw, large (8 mm) cortical violations have been associated with increased fracture risk of the proximal humerus.37,38 The tendon may experience less trauma than that caused by being twisted against an interference screw, the most common location of failure of which is the tendon–screw interface.39 In addition, tendon healing may be improved through circumferential healing in the cortical button tunnel.
A concern of using a bicortical button for fixation is drilling through the posterior cortex, because of the proximity of the posterior neurovascular structures. In a case in which the posterior cord was injured, Rhee and colleagues40 used a suture pullout technique whereby a Beath pin was passed out of the posterior humerus and soft tissues to then hold tension on the biceps tendon during the tenodesis. The radial nerve potentially could have been injured by pin overpenetration or by becoming wrapped up in the soft tissues as the pin was spinning through them. In our technique, the posterior humeral cortex is drilled cautiously to avoid overpenetration and possibly getting the posterior soft tissues wrapped up in the guide pin. No AN injuries have been reported with this technique. Mean distance from AN to posterior cortical button in this study was 18.17 mm. In 2 cadaver studies of bicortical drilling for subpectoral biceps tenodesis, the ANs were 25.1 mm and 36.7 mm from the posterior drill hole.41,21
Limitations of this study included its design (case series) and limited number of follow-up patients. Of the 28 consecutive patients identified for the study, 10 did not undergo the clinical examination, as they either lived more than 3 hours away (8 patients) or could not be contacted (2 patients). Another study limitation was the inability to directly image ANs with ultrasound. Therefore, measurements of the distance from the PCHA to the button were used to estimate the distance from the AN/PCHA neurovascular bundle to the button.
In this study, functional outcomes were excellent, and there were no tenodesis failures or neurovascular complications. These preliminary findings indicate that subpectoral biceps tenodesis with a bicortical button is a viable treatment option for patients with the appropriate indications for this procedure.
The long head of the biceps (LHB) tendon is a recognized source of shoulder pain. LHB tendon pathology is commonly associated with other shoulder conditions, such as superior labral tears, rotator cuff tears, or subacromial impingement, whereas isolated pathology, such as traumatic ruptures, tendinosis, or medial subluxation, is rare.1 Treatment of LHB pathology ranges from conservative measures to surgical measures, including tenotomy or tenodesis.2 LHB tenodesis offers the advantage of maintaining the length–tension relationship of the biceps muscle to prevent atrophy and avoid the Popeye deformity incurred from tenotomy alone. Tenodesis also prevents muscle cramping associated with contracted biceps muscle and better maintains elbow flexion and supination strength, which may be decreased with tenotomy.3 In addition, when a subpectoral biceps tenodesis technique is used, pain from LHB tendinopathy in the intertubercular groove may be reduced.4
Open subpectoral biceps tenodesis is a reproducible, efficient method for LHB tenodesis.4,5 A variety of fixation devices has been used: bone tunnels,6 keyhole fixation,7 suture anchors,6-9 and interference screws.6-8,10,11 More recently, a bicortical button has been used for LHB tendon tenodesis.12 Biomechanical studies have shown that load to failure is comparable for bicortical button fixation and interference screw fixation.13,14 In other models of tendon repair, the bicortical button has strength and stability comparable to those of interference screw fixation and enables earlier rehabilitation.15-17 However, there is concern that bicortical button fixation may result in axillary nerve (AN) or posterior circumflex humeral artery (PCHA) compromise because of the proximity of these neurovascular structures to the bicortical button.13,18-21
We conducted a study to functionally and sonographically assess the outcomes of patients who underwent open subpectoral biceps tenodesis with a bicortical button. Functional outcomes were assessed with patient-reported outcomes and physician-reported outcomes. Sonographic studies were used to evaluate the integrity of the tenodesis and determine the proximity of the button to the AN and the PCHA along the posterior proximal humerus.
Methods
After obtaining Institutional Review Board approval for this study, we retrospectively identified 28 consecutive patients who had proximal biceps tenodesis performed by a single surgeon (Dr. K.E. Swanson) using a mini-open subpectoral biceps tenodesis technique with a bicortical button between March 2011 and January 2013. All 28 patients were asked to participate in the study. Twenty-four (86%) agreed to complete 2 surgical outcome surveys, and 18 (64%) completed a 3-part clinical examination at minimum 12-month follow-up.
One of the surveys was Quick Disabilities of the Arm, Shoulder, and Hand (QuickDASH), a validated comprehensive disability survey that scores upper extremity functionality on a scale ranging from 0 (none) to 100 (extreme difficulty).22,23 The other survey scored pain on a scale ranging from 0 (none) to 100 (worst pain).
The clinical examination was completed during a single visit by an orthopedic surgeon (Dr. Meadows or Dr. Diesselhorst) different from the primary surgeon (Dr. K.E. Swanson) and by a clinician-sonologist (Dr. Finnoff). The examination’s 3 parts were physical examination of arm, biceps supination strength test, and ultrasonographic evaluation.
Physical Examination of Arm. Physical examination included palpation of bicipital groove, range of motion (ROM) of shoulder and elbow, and clinical deformity of biceps. Patients were questioned regarding symptoms of AN damage, including sensory and motor findings. Bicipital groove tenderness was assessed with a visual analog scale rating pain 0 to 10. ROM was measured in degrees and was presented as a percentage of full elbow ROM (150°) and full shoulder ROM (180°).
Biceps Supination Strength Test. Biceps supination strength was tested with a baseline hydraulic wrist dynamometer with door handle attachment. Patients were seated with the elbow bent 90° and the forearm in a neutral position. In a series of 3 trials, the patient maintained grip of the dynamometer doorknob while supinating the forearm. The tenodesed (operated) arm and contralateral unaffected (nonoperated) arm were tested in random order and recorded in pounds.
Ultrasonographic Evaluation. Ultrasonography was used to evaluate the tenodesis site. In each case, the biceps tendon was assessed to determine the location of the bicortical button in relation to the AN/PCHA neurovascular bundle. Whereas nerves are difficult to visualize with ultrasonography, arteries are readily seen. Dr. Finnoff used a CX50 ultrasound machine (Philips Medical Systems) with either a 12-3 MHz linear array or a 5-1 MHz curvilinear array transducer to measure the shortest distance from the PCHA to the button.
Each patient was placed in a lateral decubitus or prone position, and the skin of the upper arm was exposed. Tendon integrity was deemed either intact (continuity between biceps tendon and cortical button) or disrupted (lack of continuity between tendon and cortical button). The transducer was then placed in an anatomical sagittal plane over the posterior aspect of the proximal humerus. Power Doppler and cephalad and caudad transducer glides were used to identify the location of the PCHA. The transducer was then glided laterally and anteriorly around the humerus, following the course of the PCHA, until the cortical button was located. The narrowest interval between the PCHA and the cortical button was measured using the ultrasound machine’s software. A still image of each measurement was saved.
Surgical Technique
Biceps tenodesis indications included high-demand heavy laborers, athletes, and patients who preferred the cosmetic results of tenodesis over tenotomy. Most patients had acute symptomatic tears of the superior labrum with instability of the biceps anchor complex. Others had fraying and tenosynovitis of the LHB tendon. Any associated pathology was addressed during the same surgical period.
The surgical technique used was similar to that described by Snir and colleagues.12 Each patient was placed in the lateral decubitus position. Once pathology confirmed biceps tenodesis, the biceps tendon was tenotomized at the base of the superior labrum. A 3-cm incision was made along the axillary fold centered over the inferior border of the pectoralis major tendon. Blunt dissection was performed to define the inferior border of the pectoralis major tendon and to palpate the underlying biceps tendon as it exited the intertubercular groove. The LHB tendon was removed and prepared with No. 2 Fiberwire (Arthrex) in Krackow fashion starting 2 cm proximal to the musculotendinous junction. The excess tendon was excised.
A 3.2-mm guide wire was centered along the most distal aspect of the biceps groove and then drilled through the anterior cortex and just through the posterior cortex. A cannulated reamer, selected on the basis of the biceps tendon diameter (typically, 5-7 mm), was then drilled over the guide wire through the anterior cortex only. The Food and Drug Administration–approved cortical button (BicepsButton; Arthrex) was then loaded by passing the tendon suture ends through each side of the button in alternating fashion, thus allowing the button to slide along the sutures.
The button was loaded onto the BicepsButton deployment device and inserted through the drilled tunnel of the anterior cortex and just through the posterior cortex. The deployment device was then removed, and 1 suture end was pulled to allow the button to engage the posterior humeral cortex. Pulling on both sutures allowed the biceps tendon to slide through the anterior cortex hole of the humerus until the tendon reached the posterior humeral cortex. Tension was verified, and the sutures were tied over the tendon. The wound was then irrigated and closed.
Rehabilitation Program
Patients completed a standard rehabilitation protocol for biceps tenodesis24 along with rehabilitation protocols for any additional procedures performed. In phase 1 (weeks 0-2), they focused on gradual restoration of passive ROM and remained in a sling. In phase 2 (weeks 2-6), they focused on gradual restoration of active ROM, and by week 3 were weaned out of the sling. In phase 3 (weeks 6-8), they continued ROM and strengthening exercises to normalize strength, endurance, and neuromuscular control. In phase 4 (weeks 8-12), they focused on advanced strengthening exercises and return to activities.
Statistical Analysis
Descriptive statistics included means, medians, and SDs. Comparisons between operated and nonoperated arms and between dominant and nondominant arms were performed by a statistician using paired t tests with P = .05. Confidence intervals were calculated for operated and nonoperated arms and for dominant and nondominant arms by using the differences between them.
Results
Functional Outcomes
Surgical outcome scores and pain scores were obtained from 24 patients (86%) at minimum 12-month follow-up. Mean (SD) DASH score was 15.15 (17.6; median, 9), and mean (median) pain score was 12.61 (7).
Eighteen patients (64%) completed the clinical examination: 16 men (88.9%) and 2 women (11.1%). Mean age was 48.3 years (age range, 33-59 years). Of these 18 patients, 9 (50%) had surgery on the dominant arm, and the other 9 had surgery on the nondominant arm. All patients were right-hand–dominant. In 3 patients, biceps tenodesis was performed with only minimal arthroscopic débridement (20%); in the other 15, biceps tenodesis was performed concomitantly with 1 or more additional arthroscopic procedures: acromioplasty (73%), rotator cuff repair (47%), distal clavicle resection (33%), subacromial bursectomy (13%), microfracture of glenoid (13%), and posterior labral repair (7%).
The clinical examination was performed a mean of 15.2 months (range, 12-26 months) after surgery. Physical examination findings are listed in Table 1.
Forearm supination strength, averaged from 3 trials on each arm, was significantly (P = .01) greater in the nonoperated arm than in the operated arm (Table 2, Figure 1). A 95% confidence interval for the mean (SD) difference in strength was 9.35 (7.76) pounds, meaning that on average, the nonoperated arm will be 1.59 to 17.11 pounds stronger than the operated arm. In addition, strength of the dominant arm was greater than that of the nondominant arm (P = .05) regardless of which arm underwent surgery (Table 2, Figure 1). However, the mean (SD) difference in strength was 6.94 (8.39) pounds, indicating the observed difference was not statistically significant.
Sonographic Evaluation
According to the sonographic evaluations, the tenodesis was intact in all 18 patients (Figure 2). Estimated mean (SD) distance from button to PCHA was 18.17 (9.0) mm (median, 16.1 mm; range, 9.4-48 mm) (Figure 2, Figure 3). No patient indicated any symptoms of AN damage.
Discussion
There are few studies of functional outcomes of biceps tenodesis. Pain is a common measure of patient satisfaction. Mazzocca and colleagues25 reported a mean follow-up pain score of 1.1 (range, 0.5-1.9) out of 10 for a group of 41 patients who had subpectoral tenodesis with an interference screw. Millett and colleagues26 reported a mean postoperative pain score of 2.5 out of 10 for patients who had subpectoral interference screw fixation. Our patients reported a mean pain score of 12.6 out of 100 after minimum 12-month follow-up. We also assessed for pain in the intertubercular groove during palpation. Although some studies have shown that groove pain was eliminated by subpectoral biceps tenodesis,5 3 patients in our study had pain on groove palpation. The cause of this residual pain is unclear, but some studies have suggested a chronic degenerative pathologic process that occurs while the tendon is within the biceps groove.27 Removing the tendon from the groove may not remove the underlying cause of pain.
Our patients’ mean DASH score was 15.15 (within the excellent range). Normative mean (SD) DASH score for the general population is 10.1 (14.68).28
Functional strength of forearm supination, shoulder ROM, and elbow ROM are objective measures of patient performance after fixation. On Cybex testing, Phillips and colleagues29 found no difference in forearm supination strength or elbow flexion (compared with contralateral arm) after biceps tenodesis or conservative treatment for proximal biceps ruptures. Shank and colleagues30 compared elbow flexion and supination strength of the affected and unaffected arms after suture anchor subpectoral biceps tenodesis. There was no significant difference in Cybex results, but there was a 14% to 15% loss of average strength in the tenodesed versus nonsurgical arm. In the present study, we found a significant difference in forearm supination strength between the operated and nonoperated arms, but with only a 7% loss of average strength in the operated arms. The difference in strength ranged from 1.59 to 17.11 pounds, which may not be clinically significant, as supination strength ranged from 60 to 270 pounds.
Of the 18 patients in this study, 9 had surgery on the dominant arm, and the other 9 had surgery on the nondominant arm. Examining the effect of arm dominance on results revealed that patients with surgery on the nondominant arm tended to have substantially reduced supination strength in that arm vs the dominant arm. There was an 11% loss of average strength for nondominant vs dominant arms that had surgery. Examining nondominant arms only revealed a 13% loss of strength for operated vs nonoperated arms. There was no difference in forearm supination strengths between nonoperated arms (dominant vs nondominant) or between dominant arms (operated vs nonoperated). This suggests that, though hand dominance may not play a significant role in control patients’ forearm supination strength,30 it may have a substantial effect on surgical patients’ ability to regain strength when the nondominant arm is the surgical arm. One objective of this study was to measure the distance between the biceps cortical button on the posterior humeral cortex and the AN/PCHA neurovascular bundle. The AN bundles with the PCHA posterior to the humeral neck.31-33 As the AN travels with the PCHA, and the PCHA has been reliably identified with Doppler ultrasonography,34-36 the PCHA was used as a marker for the AN in this study. Our bicortical button technique places the button on the posterior aspect of the humerus, making AN and PCHA the nearest at-risk neurovascular structures. None of our patients had symptoms of AN damage. However, 2 patients indicated pain in the posterior aspect of the humerus during deltoid activation. Distance from the neurovascular structures to the button was 48 mm in one patient and 13.6 mm in the other. DASH scores were 43 and 27, respectively. Both patients’ 1-year pain score was 30. The first patient underwent arthroscopic acromioplasty, distal clavicle resection, and microfracture of the glenoid surface in addition to the subpectoral biceps tenodesis; the second underwent subacromial decompression and distal clavicle resection in addition to the subpectoral biceps tenodesis. Whether the associated pathology contributed to their persistent pain is unknown. However, given the distance from AN/PCHA to button, it is unlikely that their pain was a result of neurovascular compromise from the procedure.
Advantages of the cortical button include the ability to drill a smaller hole in the humerus for fixation, compared with the hole drilled for an interference screw. Despite the biomechanical strength of the screw, large (8 mm) cortical violations have been associated with increased fracture risk of the proximal humerus.37,38 The tendon may experience less trauma than that caused by being twisted against an interference screw, the most common location of failure of which is the tendon–screw interface.39 In addition, tendon healing may be improved through circumferential healing in the cortical button tunnel.
A concern of using a bicortical button for fixation is drilling through the posterior cortex, because of the proximity of the posterior neurovascular structures. In a case in which the posterior cord was injured, Rhee and colleagues40 used a suture pullout technique whereby a Beath pin was passed out of the posterior humerus and soft tissues to then hold tension on the biceps tendon during the tenodesis. The radial nerve potentially could have been injured by pin overpenetration or by becoming wrapped up in the soft tissues as the pin was spinning through them. In our technique, the posterior humeral cortex is drilled cautiously to avoid overpenetration and possibly getting the posterior soft tissues wrapped up in the guide pin. No AN injuries have been reported with this technique. Mean distance from AN to posterior cortical button in this study was 18.17 mm. In 2 cadaver studies of bicortical drilling for subpectoral biceps tenodesis, the ANs were 25.1 mm and 36.7 mm from the posterior drill hole.41,21
Limitations of this study included its design (case series) and limited number of follow-up patients. Of the 28 consecutive patients identified for the study, 10 did not undergo the clinical examination, as they either lived more than 3 hours away (8 patients) or could not be contacted (2 patients). Another study limitation was the inability to directly image ANs with ultrasound. Therefore, measurements of the distance from the PCHA to the button were used to estimate the distance from the AN/PCHA neurovascular bundle to the button.
In this study, functional outcomes were excellent, and there were no tenodesis failures or neurovascular complications. These preliminary findings indicate that subpectoral biceps tenodesis with a bicortical button is a viable treatment option for patients with the appropriate indications for this procedure.
1. Khazzam M, George MS, Churchill RS, Kuhn JE. Disorders of the long head of biceps tendon. J Shoulder Elbow Surg. 2012;21(1):136-145.
2. Geaney LE, Mazzocca AD. Biceps brachii tendon ruptures: a review of diagnosis and treatment of proximal and distal biceps tendon ruptures. Phys Sportsmed. 2010;38(2):117-125.
3. Kelly AM, Drakos MC, Fealy S, Taylor SA, O’Brien SJ. Arthroscopic release of the long head of the biceps tendon: functional outcome and clinical results. Am J Sports Med. 2005;33(2):208-213.
4. Provencher MT, LeClere LE, Romeo AA. Subpectoral biceps tenodesis. Sports Med Arthrosc Rev. 2008;16(3):170-176.
5. Nho SJ, Reiff SN, Verma NN, Slabaugh MA, Mazzocca AD, Romeo AA. Complications associated with subpectoral biceps tenodesis: low rates of incidence following surgery. J Shoulder Elbow Surg. 2010;19(5):764-768.
6. Mazzocca AD, Bicos J, Santangelo S, Romeo AA, Arciero RA. The biomechanical evaluation of four fixation techniques for proximal biceps tenodesis. Arthroscopy. 2005;21(11):1296-1306.
7. Ozalay, M, Akpinar S, Karaeminogullari O, et al. Mechanical strength of four different biceps tenodesis techniques. Arthroscopy. 2005;21(8):992-998.
8. Golish RS, Caldwell PE, Miller MD, et al. Interference screw versus suture anchor fixation for subpectoral tenodesis of the proximal biceps tendon: a cadaveric study. Arthroscopy. 2008;24(10):1103-1108.
9. Richards DP, Burkhart SS. A biomechanical analysis of two biceps tenodesis fixation techniques. Arthroscopy. 2005;21(7):861-866.
10. Mazzocca AD, Rios CG, Romeo AA, Arciero RA. Subpectoral biceps tenodesis with interference screw fixation. Arthroscopy. 2005;21(7):896.
11. Wolf RS, Zheng N, Weichel D. Long head biceps tenotomy versus tenodesis: a cadaveric biomechanical analysis. Arthroscopy. 2005;21(2):182-185.
12. Snir N, Hamula M, Wolfson T, Laible C, Sherman O. Long head of the biceps tenodesis with cortical button technique. Arthrosc Tech. 2013;2(2):e95-e97.
13. Arora AS, Singh A, Koonce RC. Biomechanical evaluation of a unicortical button versus interference screw for subpectoral biceps tenodesis. Arthroscopy. 2013;29(4):638-644.
14. Buchholz A, Martetschläger F, Siebenlist S, et al. Biomechanical comparison of intramedullary cortical button fixation and interference screw technique for subpectoral biceps tenodesis. Arthroscopy. 2013;29(5):845-853.
15. Bain GI, Prem H, Heptinstall RJ, Verhellen R, Paix D. Repair of distal biceps tendon rupture: a new technique using the Endobutton. J Shoulder Elbow Surg. 2000;9(2):120-126.
16. Greenberg JA. Endobutton repair of distal biceps tendon ruptures. J Hand Surg Am. 2009;34(8):1541-1548.
17. Heinzelmann AD, Savoie FH 3rd, Ramsey JR, Field LD, Mazzocca AD. A combined technique for distal biceps repair using a soft tissue button and biotenodesis interference screw. Am J Sports Med. 2009;37(5):989-994.
18. DeAngelis JP, Chen A, Wexler M, et al. Biomechanical characterization of unicortical button fixation: a novel technique for proximal subpectoral biceps tenodesis. Knee Surg Sports Traumatol Arthrosc. 2015;23(5):1434-1441.
19. Dickens JF, Kilcoyne KG, Tintle SM, Giuliani J, Schaefer RA, Rue JP. Subpectoral biceps tenodesis: an anatomic study and evaluation of at-risk structures. Am J Sports Med. 2012;40(10):2337-2341.
20. Sethi PM, Rajaram A, Beitzel K, Hackett TR, Chowaniec DM, Mazzocca AD. Biomechanical performance of subpectoral biceps tenodesis: a comparison of interference screw fixation, cortical button fixation, and interference screw diameter. J Shoulder Elbow Surg. 2013;22(4):451-457.
21. Sethi PM, Vadasdi K, Greene RT, Vitale MA, Duong M, Miller SR. Safety of open suprapectoral and subpectoral biceps tenodesis: an anatomic assessment of risk for neurologic injury. J Shoulder Elbow Surg. 2015;24(1):138-142.
22. Gummesson C, Ward MM, Atroshi I. The shortened Disabilities of the Arm, Shoulder and Hand questionnaire (QuickDASH): validity and reliability based on responses within the full-length DASH. BMC Musculoskelet Disord. 2006;7:44.
23. Schmidt CC, Brown BT, Sawardeker PJ, DeGravelle M Jr, Miller MC. Factors affecting supination strength after a distal biceps rupture. J Shoulder Elbow Surg. 2014;23(1):68-75.
24. Brotzman SB, Wilk KE, eds. Handbook of Orthopaedic Rehabilitation. Philadelphia, PA: Mosby Elsevier; 2007.
25. Mazzocca AD, Cote MP, Arciero CL, Romeo AA, Arciero RA. Clinical outcomes after subpectoral biceps tenodesis with an interference screw. Am J Sports Med. 2008;36(10):1922-1929.
26. Millett PJ, Snaders B, Gobezie R, Braun S, Warner JP. Interference screw versus suture anchor fixation for open subpectoral biceps tenodesis: does it matter? BMC Musculoskelet Disord. 2008;9(121):1-6.
27. Streit JJ, Shishani Y, Rodgers M, Gobezie R. Tendinopathy of the long head of the biceps tendon: histopathologic analysis of the extra-articular biceps tendon and tenosynovium. Open Access J Sports Med. 2015;6:63-70.
28. Hunsaker FG, Cioffi DA, Amadio PC, Wright JG, Caughlin B. The American Academy of Orthopaedic Surgeons outcomes instruments: normative values from the general population. J Bone Joint Surg Am. 2002;84(2):208-215.
29. Phillips BB, Canale ST, Sisk TD, Stralka SW, Wyatt KP. Rupture of the proximal biceps tendon in middle-aged patients. Orthop Rev. 1993;22(3):349-353.
30. Shank JR, Singleton SB, Braun S, et al. A comparison of forearm supination and elbow flexion strength in patients with long head of the biceps tenotomy or tenodesis. Arthroscopy. 2011;27(1):9-16.
31. Apaydin N, Tubbs RS, Loukas M, Duparc F. Review of the surgical anatomy of the axillary nerve and the anatomic basis of its iatrogenic and traumatic injury. Surg Radiol Anat. 2010;32(3):193-201.
32. Johnson D. Pectoral girdle and upper limp. In: Standring S, ed. Gray’s Anatomy. 40th ed. New York, NY: Elsevier; 2008:814-821.
33. Tubbs RS, Tyler-Kabara EC, Aikens AC, et al. Surgical anatomy of the axillary nerve within the quadrangular space. J Neurosurg. 2005;102(5):912-914.
34. Kim YA, Yoon KB, Kwon TD, Kim DH, Yoon DM. Evaluation of anatomic landmarks for axillary nerve block in the quadrilateral space. Acta Anaesthesiol Scand. 2014;58(5):567-571.
35. Robinson DJ, Marks P, Schneider-Kolsky ME. Ultrasound of the posterior circumflex humeral artery. J Med Imaging Radiat Oncol. 2010;54(3):219-223.
36. Rothe C, Asghar S, Andersen HL, Christensen JK, Lange KH. Ultrasound-guided block of the axillary nerve: a volunteer study of a new method. Acta Anaesthesiol Scand. 2011;55(5):565-570.
37. Reiff SN, Nho SJ, Romeo AA. Proximal humerus fracture after keyhole biceps tenodesis. Am J Orthop. 2010;39(7):E61-E63.
38. Sears BW, Spencer EE, Getz CL. Humeral fracture following subpectoral biceps tenodesis in 2 active, healthy patients. J Shoulder Elbow Surg. 2011;20(6):e7-e11.
39. Koch BS, Burks RT. Failure of biceps tenodesis with interference screw fixation. Arthroscopy. 2012;28(5):735-740.
40. Rhee PC, Spinner RJ, Bishop AT, Shin AY. Iatrogenic brachial plexus injuries associated with open subpectoral biceps tenodesis. Am J Sports Med. 2013;41(9):2048-2053.
41. Ding DY, Gupta A, Snir N, Wolfson T, Meislin RJ. Nerve proximity during bicortical drilling for subpectoral biceps tenodesis: a cadaveric study. Arthroscopy. 2014;30(8):942-946.
1. Khazzam M, George MS, Churchill RS, Kuhn JE. Disorders of the long head of biceps tendon. J Shoulder Elbow Surg. 2012;21(1):136-145.
2. Geaney LE, Mazzocca AD. Biceps brachii tendon ruptures: a review of diagnosis and treatment of proximal and distal biceps tendon ruptures. Phys Sportsmed. 2010;38(2):117-125.
3. Kelly AM, Drakos MC, Fealy S, Taylor SA, O’Brien SJ. Arthroscopic release of the long head of the biceps tendon: functional outcome and clinical results. Am J Sports Med. 2005;33(2):208-213.
4. Provencher MT, LeClere LE, Romeo AA. Subpectoral biceps tenodesis. Sports Med Arthrosc Rev. 2008;16(3):170-176.
5. Nho SJ, Reiff SN, Verma NN, Slabaugh MA, Mazzocca AD, Romeo AA. Complications associated with subpectoral biceps tenodesis: low rates of incidence following surgery. J Shoulder Elbow Surg. 2010;19(5):764-768.
6. Mazzocca AD, Bicos J, Santangelo S, Romeo AA, Arciero RA. The biomechanical evaluation of four fixation techniques for proximal biceps tenodesis. Arthroscopy. 2005;21(11):1296-1306.
7. Ozalay, M, Akpinar S, Karaeminogullari O, et al. Mechanical strength of four different biceps tenodesis techniques. Arthroscopy. 2005;21(8):992-998.
8. Golish RS, Caldwell PE, Miller MD, et al. Interference screw versus suture anchor fixation for subpectoral tenodesis of the proximal biceps tendon: a cadaveric study. Arthroscopy. 2008;24(10):1103-1108.
9. Richards DP, Burkhart SS. A biomechanical analysis of two biceps tenodesis fixation techniques. Arthroscopy. 2005;21(7):861-866.
10. Mazzocca AD, Rios CG, Romeo AA, Arciero RA. Subpectoral biceps tenodesis with interference screw fixation. Arthroscopy. 2005;21(7):896.
11. Wolf RS, Zheng N, Weichel D. Long head biceps tenotomy versus tenodesis: a cadaveric biomechanical analysis. Arthroscopy. 2005;21(2):182-185.
12. Snir N, Hamula M, Wolfson T, Laible C, Sherman O. Long head of the biceps tenodesis with cortical button technique. Arthrosc Tech. 2013;2(2):e95-e97.
13. Arora AS, Singh A, Koonce RC. Biomechanical evaluation of a unicortical button versus interference screw for subpectoral biceps tenodesis. Arthroscopy. 2013;29(4):638-644.
14. Buchholz A, Martetschläger F, Siebenlist S, et al. Biomechanical comparison of intramedullary cortical button fixation and interference screw technique for subpectoral biceps tenodesis. Arthroscopy. 2013;29(5):845-853.
15. Bain GI, Prem H, Heptinstall RJ, Verhellen R, Paix D. Repair of distal biceps tendon rupture: a new technique using the Endobutton. J Shoulder Elbow Surg. 2000;9(2):120-126.
16. Greenberg JA. Endobutton repair of distal biceps tendon ruptures. J Hand Surg Am. 2009;34(8):1541-1548.
17. Heinzelmann AD, Savoie FH 3rd, Ramsey JR, Field LD, Mazzocca AD. A combined technique for distal biceps repair using a soft tissue button and biotenodesis interference screw. Am J Sports Med. 2009;37(5):989-994.
18. DeAngelis JP, Chen A, Wexler M, et al. Biomechanical characterization of unicortical button fixation: a novel technique for proximal subpectoral biceps tenodesis. Knee Surg Sports Traumatol Arthrosc. 2015;23(5):1434-1441.
19. Dickens JF, Kilcoyne KG, Tintle SM, Giuliani J, Schaefer RA, Rue JP. Subpectoral biceps tenodesis: an anatomic study and evaluation of at-risk structures. Am J Sports Med. 2012;40(10):2337-2341.
20. Sethi PM, Rajaram A, Beitzel K, Hackett TR, Chowaniec DM, Mazzocca AD. Biomechanical performance of subpectoral biceps tenodesis: a comparison of interference screw fixation, cortical button fixation, and interference screw diameter. J Shoulder Elbow Surg. 2013;22(4):451-457.
21. Sethi PM, Vadasdi K, Greene RT, Vitale MA, Duong M, Miller SR. Safety of open suprapectoral and subpectoral biceps tenodesis: an anatomic assessment of risk for neurologic injury. J Shoulder Elbow Surg. 2015;24(1):138-142.
22. Gummesson C, Ward MM, Atroshi I. The shortened Disabilities of the Arm, Shoulder and Hand questionnaire (QuickDASH): validity and reliability based on responses within the full-length DASH. BMC Musculoskelet Disord. 2006;7:44.
23. Schmidt CC, Brown BT, Sawardeker PJ, DeGravelle M Jr, Miller MC. Factors affecting supination strength after a distal biceps rupture. J Shoulder Elbow Surg. 2014;23(1):68-75.
24. Brotzman SB, Wilk KE, eds. Handbook of Orthopaedic Rehabilitation. Philadelphia, PA: Mosby Elsevier; 2007.
25. Mazzocca AD, Cote MP, Arciero CL, Romeo AA, Arciero RA. Clinical outcomes after subpectoral biceps tenodesis with an interference screw. Am J Sports Med. 2008;36(10):1922-1929.
26. Millett PJ, Snaders B, Gobezie R, Braun S, Warner JP. Interference screw versus suture anchor fixation for open subpectoral biceps tenodesis: does it matter? BMC Musculoskelet Disord. 2008;9(121):1-6.
27. Streit JJ, Shishani Y, Rodgers M, Gobezie R. Tendinopathy of the long head of the biceps tendon: histopathologic analysis of the extra-articular biceps tendon and tenosynovium. Open Access J Sports Med. 2015;6:63-70.
28. Hunsaker FG, Cioffi DA, Amadio PC, Wright JG, Caughlin B. The American Academy of Orthopaedic Surgeons outcomes instruments: normative values from the general population. J Bone Joint Surg Am. 2002;84(2):208-215.
29. Phillips BB, Canale ST, Sisk TD, Stralka SW, Wyatt KP. Rupture of the proximal biceps tendon in middle-aged patients. Orthop Rev. 1993;22(3):349-353.
30. Shank JR, Singleton SB, Braun S, et al. A comparison of forearm supination and elbow flexion strength in patients with long head of the biceps tenotomy or tenodesis. Arthroscopy. 2011;27(1):9-16.
31. Apaydin N, Tubbs RS, Loukas M, Duparc F. Review of the surgical anatomy of the axillary nerve and the anatomic basis of its iatrogenic and traumatic injury. Surg Radiol Anat. 2010;32(3):193-201.
32. Johnson D. Pectoral girdle and upper limp. In: Standring S, ed. Gray’s Anatomy. 40th ed. New York, NY: Elsevier; 2008:814-821.
33. Tubbs RS, Tyler-Kabara EC, Aikens AC, et al. Surgical anatomy of the axillary nerve within the quadrangular space. J Neurosurg. 2005;102(5):912-914.
34. Kim YA, Yoon KB, Kwon TD, Kim DH, Yoon DM. Evaluation of anatomic landmarks for axillary nerve block in the quadrilateral space. Acta Anaesthesiol Scand. 2014;58(5):567-571.
35. Robinson DJ, Marks P, Schneider-Kolsky ME. Ultrasound of the posterior circumflex humeral artery. J Med Imaging Radiat Oncol. 2010;54(3):219-223.
36. Rothe C, Asghar S, Andersen HL, Christensen JK, Lange KH. Ultrasound-guided block of the axillary nerve: a volunteer study of a new method. Acta Anaesthesiol Scand. 2011;55(5):565-570.
37. Reiff SN, Nho SJ, Romeo AA. Proximal humerus fracture after keyhole biceps tenodesis. Am J Orthop. 2010;39(7):E61-E63.
38. Sears BW, Spencer EE, Getz CL. Humeral fracture following subpectoral biceps tenodesis in 2 active, healthy patients. J Shoulder Elbow Surg. 2011;20(6):e7-e11.
39. Koch BS, Burks RT. Failure of biceps tenodesis with interference screw fixation. Arthroscopy. 2012;28(5):735-740.
40. Rhee PC, Spinner RJ, Bishop AT, Shin AY. Iatrogenic brachial plexus injuries associated with open subpectoral biceps tenodesis. Am J Sports Med. 2013;41(9):2048-2053.
41. Ding DY, Gupta A, Snir N, Wolfson T, Meislin RJ. Nerve proximity during bicortical drilling for subpectoral biceps tenodesis: a cadaveric study. Arthroscopy. 2014;30(8):942-946.
