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The Cruciate Ligaments in Total Knee Arthroplasty
Hinge knee arthroplasty was introduced in the 1950s.1 All 4 major ligaments were replaced by the hinge, which provided stabilization while allowing sagittal plane motion. Its goal was stability, not replication of normal kinematics. The addition of methyl methacrylate cement improved fixation and allowed surface design modifications that addressed normal articular motion. Implants such as the Gunston Polycentric,2 the Duocondylar,3 and the Geometric4 resurfaced the medial and lateral compartments of the knee while preserving the cruciate ligaments. The implants were subject to greater translational forces without the hinge and loosening became a major problem despite the advances in cementing. It became evident in the 1970s that preservation of the cruciates complicated the procedure. Cruciate resection simplified the operation and allowed improved fixation. The ICLH prosthesis resected the cruciates and used the articular surface design to give stability to the knee.5,6 The total condylar prosthesis had a “tibial” imminence that mimicked the shape of the tibial surface but also sacrificed both of the cruciate ligaments (Figure 1).
Designers recognized that the cruciate ligaments affected knee kinematics; however, they elected to sacrifice the anterior cruciate ligament (ACL) for surgical simplicity and implant longevity.6 In the early 1980s, both the cruciate-retaining (CR) total knee arthroplasty (TKA) (Figure 2) and posterior-stabilized (PS) TKA (Figure 3) designs addressed the posterior cruciate ligament (PCL) function. The PCL was preserved in the “cruciate-retaining” TKA, substituted in the “posterior-stabilized” TKA using a cam-post mechanism. The CR TKA designers believed that PCL preservation produced a more balanced knee with a more anatomical result, a more normal joint line, and better function, especially on stair climbing. The PS TKA designers admitted the value of posterior stabilization but argued that it was too difficult to consistently save the PCL in all cases, and that the PS knee was easier for surgeons to implant with more reliable roll back.7
The Geometric knee was developed in the 1970s to retain both cruciate ligaments.4 Unfortunately, it created a kinematic conflict by using a constrained articular surface design that prevented the motion required by the cruciate ligaments. This conflict resulted in tibial loosening and early failures. The compromised results decreased interest in the bicruciate-retaining (BCR) TKA designs, allowing the CR TKA and PS TKA designs to flourish for the next 20 years with little or no attempts to retain the ACL.
In the 1980s the BCR TKA design was pursued by Townley8 and Cartier.9 Townley8 believed that cruciate resection was a concession to “improper joint synchronization”8 and Cartier9 thought that cruciate preservation permitted more normal proprioception.9 Unlike prior BCR TKA designs, the mid-term clinical results were equal to or better than the standard CR TKA or PS TKA of the time, and 9- to 11-year follow-up demonstrated comparable outcomes.8 While these results highlighted the possibility of a BCR TKA, the surgical technique and failures of the Geometric knee discouraged surgeons from pursuing the BCR TKA.
Interest in cruciate-preserving knee arthroplasty returned with partial knee replacements, with patients reporting more normal proprioception and motion.10 The techniques became more popular with the introduction of the minimally invasive surgeries in the early 2000s and cruciate ligament preservation became a more interesting concept.11,12 Some surgeons preserved the cruciates by using separate implants for the medial, lateral, and patellofemoral surfaces.10 These results were acceptable for the time but required considerable surgical talent and did not report 20-year results similar to the CR and PS knees.
Most prosthetic designs attempt to copy the normal knee anatomy. Using fluoroscopic studies and computer analysis, designers began to investigate the motion (or kinematics) of the normal knee and realized that despite the fact the TKA looked like the human knee, the designs were not kinematically correct.13
Although TKA successfully treats pain secondary to degenerative joint disease, many patients are unable to return to their prior level of function, with up to 20% reporting dissatisfaction with their level of activity.14 The observed differences in kinematics between a normal knee and a TKA may explain part of this discrepancy.
Normal Knee Motion
The tibiofemoral articulation in a normal knee follows a reproducible pattern of motion as the knee moves from extension to flexion. The lateral femoral condyle (LFC) translates posteriorly with a combination of rolling and sliding motion, while the medial femoral condyle (MFC) has minimal posterior translation and thus acts as a pivot for knee motion. The MFC is larger, less curved, and has a biphasic shape with 2 distinct radiuses of curvature that correspond to an “extension” and “flexion” facet. The transition between the MFC facets occurs at approximately 30° of flexion, whereby the contact point transfers posteriorly with little condylar translation.15-17 In contrast, the LFC is smaller, has a single radius of curvature, and gradually translates posteriorly throughout flexion. Static magnetic resonance imaging of the knee from 0° to 120° shows an average of 19 mm posterior translation for the LFC and 2 mm for the MFC.15-20
In deep flexion, beyond 130°, posterior translation continues for both condyles. The LFC experiences enough excursion to cause loss of joint congruity and partial posterior subluxation.19,20 The MFC shows little additional posterior translation, yet it too loses joint congruity through condylar lift-off. Contact between the posterior horn of the medial meniscus and the posterior femoral condyle limits further flexion.16,21
The difference in motion between the condyles leads to internal tibial rotation during flexion. The initial 10° of knee flexion produces 5° of internal rotation, and an additional 15° of internal tibial rotation occurs throughout the remainder of knee flexion.
Fluoroscopic imaging with computed tomography (CT)- or magnetic resonance (MR)-based modeling has shown the dynamic in vivo relationship of the tibiofemoral joint. Studies have confirmed significantly greater LFC posterior translation as compared to the MFC;22 however, in vivo studies have also shown notable variability in articular rotation and translation based on activity. This highlights the role of ligamentous tension and muscle contraction in kinematics.21-23
The ACL in TKA
The majority of current TKA designs sacrifice the ACL without substituting for its function. The loss of the ACL has significant effects upon the kinematics of the knee.
The ACL is composed of 2 bundles, the anteromedial and posterolateral bundles, which originate on the LFC and insert broadly onto the tibial intercondylar eminence. Its primary role is to resist anterior tibial translation, particularly from 0° to 30° of flexion, which corresponds to the peak quadriceps force that pulls the tibia anteriorly.24 ACL deficiency causes anterior tibial translation during early flexion and abnormal internal tibial rotation.25-27 ACL deficient knees demonstrate a posterior femoral position in full extension, and increased MFC translation during knee flexion.28-32
The role of the ACL in knee arthroplasty has been evaluated by comparing unicompartmental knee arthroplasty (UKA) with TKA, as a reflection of ACL preserving vs sacrificing procedures.33-35 Sagittal plane translation is similar between UKA and normal knees,33,34 while the CR TKA and PS TKA designs show anterior tibia subluxation in full extension.33-35 The difference between UKA and TKA is greatest in extension, corresponding to the ACL functional range. These findings highlight kinematic similarities between TKA designs and the ACL deficient knee.
The majority of UKAs demonstrate near-normal kinematics. A small percentage of the study group demonstrated aberrant anterior tibial motion, highlighting a concern over ACL attenuation with time. Additionally, studies that evaluate the ACL in osteoarthritic knees have questioned the baseline integrity of the ACL.36 Yet the long-term outcomes in UKA design have shown preservation of kinematics due to intact cruciates.37
The PCL in TKA
Because the majority of TKA designs sacrifice the ACL, the classic debate has focused on the utility of the native PCL. Both the CR and PS TKA are designed to offer posterior stabilization; however, kinematic studies have demonstrated notable differences.38,39
The CR TKA design relies on the PCL to resist posterior sag and to prevent the hamstring musculature from pulling the tibia posteriorly during flexion. Studies have shown paradoxical anterior translation of both femoral condyles during flexion, particularly on the medial side of the knee.40 There is also increased variability in femoral rollback. It is unclear whether the PCL can function normally in the absence of the ACL, which causes the PCL to adapt a less anatomic vertical position. The PCL may also be unable to function significantly without the ACL because of pre-existing degenerative histological changes.41
The PS TKA utilizes a cam-post mechanism for posterior stabilization. In contrast to normal knee kinematics, this mechanism creates equal MFC and LFC posterior translation, 8 mm on average at 90° flexion.40 The equivalent translation in PS designs contributes to decreased internal tibial rotation and an increased polyethylene wear at the post.
Role of Surface Geometry
The articular geometry of the knee plays an important role in normal knee kinematics. Initial TKA designs used a femoral component with a single radius of curvature for both femoral condyles.42Current TKA designs that match the femoral component to the native femoral anatomy, by differing the medial and lateral condyle geometry, have demonstrated kinematics that better resemble a native knee.43 Additional changes to the radius of curvature along the posterior facet of the femoral condyles may reduce impingement during deep flexion. These “high flex” designs have demonstrated equivalent range of motion in some studies44 and improved weight-bearing motion in others.45 Surface geometry is important but is not the entire answer to kinematics.
Advances in TKA Design
Knee motion is guided by multiple factors, including the tibiofemoral articular geometry, the surrounding soft tissue tension, and muscle tone. Bicruciate-substituting (BCS) TKA and BCR TKA are forms of evolution from the CR and PS TKA and attempt to respect the function of both cruciate ligaments and provide better kinematics.
The BCS TKA utilizes a modified cam-post articulation to provide both anterior and posterior stabilization (Figure 4).46 The surgical approach remains the same and the implant geometry affects the motion. The BCS TKA design demonstrates femoral rollback at 90° with an average of 14 mm for the MFC and 23 mm for the LFC, and 10° internal tibial rotation.46,47 Additionally, it provides increased sagittal stability during early flexion and an improved pivot shift (indicating improved anterior stabilization).
The BCR designs preserve both cruciates and provide anterior and posterior stabilization. Fluoroscopic imaging has demonstrated contact points in full extension, and posterior rollback at 90° flexion that more closely replicates the normal knee.48
Design and Surgical Techniques for Bicruciate Knee Replacements
If all of the ligaments are preserved, the TKA surfaces must allow motion to be driven by the ligaments in combination with the surfaces alone. The femur can be designed anatomically with asymmetric condyles. The femoral box must allow for preservation of the tibial bone island without impinging upon the cruciate ligaments. The tibial surface must be minimally constrained with concavity medially and convexity laterally.
The bone island preservation does not permit a single-piece tibial polyethylene insert. Therefore, the inserts will replicate the UKA designs (Figure 5). The knee should allow greater range of motion with the possibility of heel to buttocks contact. This increased motion will lead to greater roll back of the femur on the tibia and can lead to subluxation of the femoral runner off of the tibial surface on the lateral side, mimicking the normal knee. This subluxation is desirable but may lead to increased wear of the polyethylene on the lateral side of the knee.
The instruments should be specific for the design but must also be user-friendly. The 2 major issues with the surgery are balancing the knee in full extension and flexion, and preservation of the tibial bone island. The preexisting knee deformity should be <10° in all planes to limit the amount of collateral ligament releases. The collaterals must be balanced in a similar fashion to the standard TKA. Flexion contracture can be treated with posterior capsular release around the cruciates or with an increased distal femoral resection (2 mm at the maximum).
It is important to size the femur correctly because it will be difficult to adjust the flexion gap on the tibial side. A 9-mm posterior medial femoral condyle resection is a reasonable guide if the condyle is not atrophic. However, the exact resection thickness will be implant-specific and should be correlated with the dimensions of the prosthesis being implanted. The tibial bone island must be properly rotated with respect to the center line (Akagi’s line)49 and must not be undercut. The tibial instrument should include pins or blocks to prevent the sawblades from undercutting the island (Figure 6), as undermining leads to fracture in full extension. If undermining occurs, it may be possible to place a cancellous screw through the island and still preserve the ligaments. The integrity of the island is best tested by bringing the knee to full extension and checking for liftoff of the bone. If there is significant compromise of the island, the bone should be resected and either a CR or PS TKA can be implanted. Della Valle and colleagues50 reported a 9.2% incidence (11 of 119 cases) of bone island fracture in their early experience with a BCR TKA and improved this to 1.9% (5/258 cases) after reassessing their technique.
The gap tension should be evaluated either with traditional spacer blocks or with tensioning devices on the medial and lateral side of the knee after the tibial resections are completed. The polyethylene inserts are anatomically different. It may be possible to vary the thickness from medial to lateral, but not in excess of 2 mm.
As the BCR surgical techniques evolve, the balancing and tibial resection may be refined through specialized instrumentation. Such “smart instruments” that incorporate gyros may expedite tibial alignment, and sensor devices may assist with gap balancing. Haptic surgical robotic guides may assist in the tibial resection, facilitating bone island preservation by avoiding any possibility of undermining. At present these assistive aides are not necessary for the operation but may play a future role.
Clinical Results of Knee Arthroplasties
The results of knee replacements improved steadily from the 1970s through the 1990s. The scoring systems were somewhat limited and there was little data on the perception of the patients. The prosthetic designs stabilized at the end of the 1990s with only minor modifications since the year 2000. The 20-year results show similar findings for both the CR and the PS designs. There is little evidence to suggest a clinical correlation with the observed kinematic differences between CR and PS TKA designs.40,51-58 Multiple studies have demonstrated equivalent range of motion38,39,59 and subjective outcome measures (Table 1).60 A randomized prospective trial that compared kinematics and functional scores between the 2 designs failed to observe significant differences in function despite differences in kinematics.46 Equivalence in clinical outcome was further supported by a Cochrane Review meta-analysis that evaluated 1810 patients in 17 selected studies.61 The Knee Society scores have all been in the 92% to 95% ratings with survivals between 90% and 95%.
However, only 80% to 90% of patients are fully satisfied with their implants. The reasons for the dissatisfaction include unexplained anterior knee pain, stiffness, unexplained swelling, loss of range of motion, changes in proprioception, and loss of preoperative functions.14
The mid-term results of the BCR knees that were performed in the 1980s showed similar results to the CR and PS knees. Townley8 reported excellent clinical results with only 2% loosening at 2 to 11 years after surgery. Cloutier and colleagues9 reported 95% survival with improved proprioception at 9 to 11 years after surgery(Table 2).62,63
Studies comparing traditional TKA designs with cruciate preserving designs, both UKA and BCR, have found differences in subjective outcomes.62,64 Comparison of UKA and TKA in the same patient demonstrated significant preference for UKA, particularly with stair-climbing.65 Similarly, comparison between BCR and PS TKA or CR TKA demonstrated preference for BCR in 85% of patients.62
The new BCR knee designs have just started to come to the market.50 The surgical techniques are much improved over the 1980s and cruciate preservation is certainly much easier now. The new designs can produce full range of motion with kinematics that are almost identical to the normal knee in the cadaver laboratory and in computer analyses. These designs certainly should have a similar 20-year survival to the original BCR knees. However, the critical evaluation will be the patient satisfaction scores. With greater motion, better kinematics, and more precise balancing the scores would improve with these designs.
Conclusion
The cruciate ligaments of the knee are central to control of the motion of the normal knee. TKA is a successful operation with at least a 40- to 50-year history. The techniques have continued to develop but 15% to 20% of patients are dissatisfied with the results.14 Evaluations of the prostheses are more sophisticated and kinematics appears to have a central position in the evaluation. If the knee is to move more anatomically correctly, all of the ligaments must be preserved. Proprioception certainly plays a role in the patient’s judgment of the result. History has shown that a BCR knee can be implanted with good mid-term results and it should certainly be possible to build on these results and design a knee that will incorporate all of the ligaments with full range of motion and increased levels of activity.
1. Walldius B. Arthroplasty of the knee with an endoprosthesis. Acta Chir Scand. 1957;113(6):445-446.
2. Gunston FH. Polycentric knee arthroplasty. Prosthetic simulation of normal knee movement. J Bone Joint Surg Br. 1971;53(2):272-277.
3. Insall JN, Ranawat CS, Aglietti P, Shine J. A comparison of four models of total knee-replacement prostheses. J Bone Joint Surg Am. 1976;58(6):754-765.
4. Coventry MB, Finerman GA, Riley LH, Turner RH, Upshaw JE. A new geometric knee for total knee arthroplasty. Clin Orthop Relat Res.1972;83:157-162.
5. Freeman MA, Sculco T, Todd RC. Replacement of the severely damaged arthritic knee by the ICLH (Freeman-Swanson) arthroplasty. J Bone Joint Surg Br. 1977;59(1):64-71.
6. Freeman MA, Insall JN, Besser W, Walker PS, Hallel T. Excision of the cruciate ligaments in total knee replacement. Clin Orthop Relat Res. 1977(126):209-212.
7. Pagnano MW, Cushner FD, Scott WN. Role of the posterior cruciate ligament in total knee arthroplasty. J Am Acad Orthop Surg. 1998;6(3):176-187.
8. Townley CO. The anatomic total knee resurfacing arthroplasty. Clin Orthop Relat Res. 1985(192):82-96.
9. Cloutier JM, Sabouret P, Deghrar A. Total knee arthroplasty with retention of both cruciate ligaments. A nine to eleven-year follow-up study. J Bone Joint Surg Am. 1999; 81(5):697-702.
10. Banks SA, Fregly BJ, Boniforti F, Reinschmidt C, Romagnoli S. Comparing in vivo kinematics of unicondylar and bi-unicondylar knee replacements. Knee Surg Sports Traumatol Arthrosc. 2005;13(7):551-556.
11. Repicci JA, Eberle RW. Minimally invasive surgical technique for unicondylar knee arthroplasty. J South Orthop Assoc. 1999;8(1):20-27; discussion 27.
12. Romanowski MR, Repicci JA. Minimally invasive unicondylar arthroplasty: eight-year follow-up. J Knee Surg. 2002;15(1):17-22.
13. Banks SA, Markovich GD, Hodge WA. In vivo kinematics of cruciate-retaining and -substituting knee arthroplasties. J Arthroplasty. 1997;12(3):297-304.
14. Nam D, Nunley RM, Barrack RL. Patient dissatisfaction following total knee replacement: a growing concern? Bone Joint J. 2014;96-B(11 Supple A):96-100.
15. Iwaki H, Pinskerova V, Freeman MA. Tibiofemoral movement 1: the shapes and relative movements of the femur and tibia in the unloaded cadaver knee. J Bone Joint Surg Br. 2000;82(8):1189-1195.
16. Johal P, Williams A, Wragg P, Hunt D, Gedroyc W. Tibio-femoral movement in the living knee. A study of weight bearing and non-weight bearing knee kinematics using ‘interventional’ MRI. J Biomech. 2005;38(2):269-276.
17. Pinskerova V, Johal P, Nakagawa S, et al. Does the femur roll-back with flexion? J Bone Joint Surg Br. 2004;86(6):925-931.
18. Hill PF, Vedi V, Williams A, Pinskerova V, Freeman MA. Tibiofemoral movement 2: the loaded and unloaded living knee studied by MRI. J Bone Joint Surg Br. 2000;82(8):1196-1198.
19. Nakagawa S, Kadoya Y, Todo S, et al. Tibiofemoral movement 3: full flexion in the living knee studied by MRI. J Bone Joint Surg Br. 2000;82(8):1199-1200.
20. Freeman MA, Pinskerova V. The movement of the knee studied by magnetic resonance imaging. Clin Orthop Relat Res. 2003(410):35-43.
21. Moro-oka TA, Hamai S, Miura H, et al. Dynamic activity dependence of in vivo normal knee kinematics. J Orthop Res. 2008;26(4):428-434.
22. Komistek RD, Dennis DA, Mahfouz M. In vivo fluoroscopic analysis of the normal human knee. Clin Orthop Relat Res. 2003(410):69-81.
23. Li G, DeFrate LE, Park SE, Gill TJ, Rubash HE. In vivo articular cartilage contact kinematics of the knee: an investigation using dual-orthogonal fluoroscopy and magnetic resonance image-based computer models. Am J Sports Med. 2005;33(1):102-107.
24. Grood ES, Suntay WJ, Noyes FR, Butler DL. Biomechanics of the knee-extension exercise. Effect of cutting the anterior cruciate ligament. J Bone Joint Surg Am. 1984;66(5):725-734.
25. Noyes FR, Jetter AW, Grood ES, Harms SP, Gardner EJ, Levy MS. Anterior cruciate ligament function in providing rotational stability assessed by medial and lateral tibiofemoral compartment translations and subluxations. Am J Sports Med. 2015;43(3):683-692.
26. Good L, Askew MJ, Boom A, Melby A 3rd. Kinematic in-vitro comparison between the normal knee and two techniques for reconstruction of the anterior cruciate ligament. Clin Biomech (Bristol, Avon). 1993;8(5):243-249.
27. Beard DJ, Murray DW, Gill HS. Reconstruction does not reduce tibial translation in the cruciate-deficient knee an in vivo study. J Bone Joint Surg Br. 2001;83(8):1098-1103.
28. Dennis DA, Mahfouz MR, Komistek RD, Hoff W. In vivo determination of normal and anterior cruciate ligament-deficient knee kinematics. J Biomech. 2005;38(2):241-253.
29. Beynnon BD, Fleming BC, Labovitch R, Parsons B. Chronic anterior cruciate ligament deficiency is associated with increased anterior translation of the tibia during the transition from non-weightbearing to weightbearing. J Orthop Res. 2002;20(2):332-337.
30. Brandsson S, Karlsson J, Eriksson BI, Kärrholm J. Kinematics after tear in the anterior cruciate ligament: dynamic bilateral radiostereometric studies in 11 patients. Acta Orthop Scand. 2001;72(4):372-378.
31. Andriacchi TP, Briant PL, Bevill SL, Koo S. Rotational changes at the knee after ACL injury cause cartilage thinning. Clin Orthop Relat Res. 2006;442:39-44.
32. Scarvell JM, Smith PN, Refshauge KM, Galloway HR, Woods KR. Comparison of kinematic analysis by mapping tibiofemoral contact with movement of the femoral condylar centres in healthy and anterior cruciate ligament injured knees. J Orthop Res. 2004;22(5):955-962.
33. Miller RK, Goodfellow JW, Murray DW, O’Connor JJ. In vitro measurement of patellofemoral force after three types of knee replacement. J Bone Joint Surg Br. 1998;80(5):900-906.
34. Price AJ, Rees JL, Beard DL, Gill RH, Dodd CA, Murray DM. Sagittal plane kinematics of a mobile-bearing unicompartmental knee arthroplasty at 10 years: a comparative in vivo fluoroscopic analysis. J Arthroplasty. 2004;19(5):590-597.
35. Dennis D, Komistek R, Scuderi G, et al. In vivo three-dimensional determination of kinematics for subjects with a normal knee or a unicompartmental or total knee replacement. J Bone Joint Surg Am. 2001;83-A Suppl 2 Pt 2:104-115.
36. Arbuthnot JE, Brink RB. Assessment of the antero-posterior and rotational stability of the anterior cruciate ligament analogue in a guided motion bi-cruciate stabilized total knee arthroplasty. J Med Eng Technol. 2009;33(8):610-615.
37. Hollinghurst D, Stoney J, Ward T, et al. No deterioration of kinematics and cruciate function 10 years after medial unicompartmental arthroplasty. Knee. 2006;13(6):440-444.
38. Dennis DA, Komistek RD, Colwell CE Jr, et al. In vivo anteroposterior femorotibial translation of total knee arthroplasty: a multicenter analysis. Clin Orthop Relat Res. 1998(356):47-57.
39. Dennis DA, Komistek RD, Hoff WA, Gabriel SM. In vivo knee kinematics derived using an inverse perspective technique. Clin Orthop Relat Res. 1996;(331):107-117.
40. Yoshiya S, Matsui N, Komistek RD, Dennis DA, Mahfouz M, Kurosaka M. In vivo kinematic comparison of posterior cruciate-retaining and posterior stabilized total knee arthroplasties under passive and weight-bearing conditions. J Arthroplasty. 2005;20(6):777-783.
41. Kleinbart FA, Bryk E, Evangelista J, Scott WN, Vigorita VJ. Histologic comparison of posterior cruciate ligaments from arthritic and age-matched knee specimens. J Arthroplasty. 1996;11(6):726-731.
42. Bull AM, Kessler O, Alam M, Amis AA. Changes in knee kinematics reflect the articular geometry after arthroplasty. Clin Orthop Relat Res. 2008;466(10):2491-2499.
43. Komistek RD, Mahfouz MR, Bertin KC, Rosenberg A, Kennedy W. In vivo determination of total knee arthroplasty kinematics: a multicenter analysis of an asymmetrical posterior cruciate retaining total knee arthroplasty. J Arthroplasty. 2008;23(1):41-50.
44. Mehin R, Burnett RS, Brasher PM. Does the new generation of high-flex knee prostheses improve the post-operative range of movement?: a meta-analysis. J Bone Joint Surg Br. 2010;92(10):1429-1434.
45. Dennis DA, Heekin RD, Clark CR, Murphy JA, O’Dell TL, Dwyer KA. Effect of implant design on knee flexion. J Arthroplasty. 2013;28(3):429-438.
46. Victor J, Mueller JK, Komistek RD, Sharma A, Nadaud MC, Bellemans J. In vivo kinematics after a cruciate-substituting TKA. Clin Orthop Relat Res. 2010;468(3):807-814.
47. Catani F, Ensini A, Belvedere C, et al. In vivo kinematics and kinetics of a bi-cruciate substituting total knee arthroplasty: a combined fluoroscopic and gait analysis study. J Orthop Res. 2009;27(12):1569-1575.
48. Stiehl JB, Komistek RD, Cloutier JM, Dennis DA. The cruciate ligaments in total knee arthroplasty: a kinematic analysis of 2 total knee arthroplasties. J Arthroplasty. 2000;15(5):545-550.
49. Akagi M, Oh M, Nonaka T, Tsujimoto H, Asano T, Hamanishi C. An anteroposterior axis of the tibia for total knee arthroplasty. Clin Orthop Relat Res. 2004;(420):213-219.
50. Della Valle CJ, Andriacchi TP, Berend KR, DeClaire JH, Lombardi AV Jr, Peters CL. Early experience with bi-cruciate retaining TKA. Poster presented at: American Academy of Orthopaedic Surgeons 2015 Annual Meeting; March 24-28, 2015; Las Vegas, NV.
51. Udomkiat P, Meng BJ, Dorr LD, Wan Z. Functional comparison of posterior cruciate retention and substitution knee replacement. Clin Orthop Relat Res. 2000;(378):192-201.
52. Tanzer M, Smith K, Burnett S. Posterior-stabilized versus cruciate-retaining total knee arthroplasty: balancing the gap. J Arthroplasty. 2002;17(7):813-819.
53. Maruyama S, Yoshiya S, Matsui N, Kuroda R, Kurosaka M. Functional comparison of posterior cruciate-retaining versus posterior stabilized total knee arthroplasty. J Arthroplasty. 2004;19(3):349-53.
54. Clark CR, Rorabeck CH, MacDonald S, MacDonald D, Swafford J, Cleland D. Posterior-stabilized and cruciate-retaining total knee replacement: a randomized study. Clin Orthop Relat Res. 2001;(392):208-212.
55. Swanik CB, Lephart SM, Rubash HE. Proprioception, kinesthesia, and balance after total knee arthroplasty with cruciate-retaining and posterior stabilized prostheses. J Bone Joint Surg Am. 2004;86-A(2):328-334.
56. Harato K, Bourne RB, Victor J, Snyder M, Hart J, Ries MD. Midterm comparison of posterior cruciate-retaining versus -substituting total knee arthroplasty using the Genesis II prosthesis. A multicenter prospective randomized clinical trial. Knee. 2008;15(3):217-221.
57. Catani F, Leardini A, Ensini A, et al. The stability of the cemented tibial component of total knee arthroplasty: posterior cruciate-retaining versus posterior-stabilized design. J Arthroplasty. 2004;19(6):775-782.
58. Dennis DA, Komistek RD, Stiehl JB, Walker SA, Dennis KN. Range of motion after total knee arthroplasty: the effect of implant design and weight-bearing conditions. J Arthroplasty. 1998;13(7):748-752.
59. Becker MW, Insall JN, Faris PM. Bilateral total knee arthroplasty. One cruciate retaining and one cruciate substituting. Clin Orthop Relat Res. 1991;(271):122-124.
60. Kim YH, Choi Y, Kwon OR, Kim JS. Functional outcome and range of motion of high-flexion posterior cruciate-retaining and high-flexion posterior cruciate-substituting total knee prostheses. A prospective, randomized study. J Bone Joint Surg Am. 2009;91(4):753-760.
61. 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.
62. Pritchett JW. Patients prefer a bicruciate-retaining or the medial pivot total knee prosthesis. J Arthroplasty. 2011;26(2):224-228.
63. Sabouret P, Lavoie F, Cloutier JM. Total knee replacement with retention of both cruciate ligaments: a 22-year follow-up study. Bone Joint J. 2013;95-B(7):917-922.
64. Andriacchi TP, Galante JO, Fermier RW. The influence of total knee-replacement design on walking and stair-climbing. J Bone Joint Surg Am. 1982;64(9):1328-1335.
65. Laurencin CT, Zelicof SB, Scott RD, Ewald FC. Unicompartmental versus total knee arthroplasty in the same patient. A comparative study. Clin Orthop Relat Res. 1991;(273):151-156.
66. Victor J, Banks S, Bellemans J. Kinematics of posterior cruciate ligament-retaining and -substituting total knee arthroplasty: a prospective randomised outcome study. J Bone Joint Surg Br. 2005;87(5):646-655.
Hinge knee arthroplasty was introduced in the 1950s.1 All 4 major ligaments were replaced by the hinge, which provided stabilization while allowing sagittal plane motion. Its goal was stability, not replication of normal kinematics. The addition of methyl methacrylate cement improved fixation and allowed surface design modifications that addressed normal articular motion. Implants such as the Gunston Polycentric,2 the Duocondylar,3 and the Geometric4 resurfaced the medial and lateral compartments of the knee while preserving the cruciate ligaments. The implants were subject to greater translational forces without the hinge and loosening became a major problem despite the advances in cementing. It became evident in the 1970s that preservation of the cruciates complicated the procedure. Cruciate resection simplified the operation and allowed improved fixation. The ICLH prosthesis resected the cruciates and used the articular surface design to give stability to the knee.5,6 The total condylar prosthesis had a “tibial” imminence that mimicked the shape of the tibial surface but also sacrificed both of the cruciate ligaments (Figure 1).
Designers recognized that the cruciate ligaments affected knee kinematics; however, they elected to sacrifice the anterior cruciate ligament (ACL) for surgical simplicity and implant longevity.6 In the early 1980s, both the cruciate-retaining (CR) total knee arthroplasty (TKA) (Figure 2) and posterior-stabilized (PS) TKA (Figure 3) designs addressed the posterior cruciate ligament (PCL) function. The PCL was preserved in the “cruciate-retaining” TKA, substituted in the “posterior-stabilized” TKA using a cam-post mechanism. The CR TKA designers believed that PCL preservation produced a more balanced knee with a more anatomical result, a more normal joint line, and better function, especially on stair climbing. The PS TKA designers admitted the value of posterior stabilization but argued that it was too difficult to consistently save the PCL in all cases, and that the PS knee was easier for surgeons to implant with more reliable roll back.7
The Geometric knee was developed in the 1970s to retain both cruciate ligaments.4 Unfortunately, it created a kinematic conflict by using a constrained articular surface design that prevented the motion required by the cruciate ligaments. This conflict resulted in tibial loosening and early failures. The compromised results decreased interest in the bicruciate-retaining (BCR) TKA designs, allowing the CR TKA and PS TKA designs to flourish for the next 20 years with little or no attempts to retain the ACL.
In the 1980s the BCR TKA design was pursued by Townley8 and Cartier.9 Townley8 believed that cruciate resection was a concession to “improper joint synchronization”8 and Cartier9 thought that cruciate preservation permitted more normal proprioception.9 Unlike prior BCR TKA designs, the mid-term clinical results were equal to or better than the standard CR TKA or PS TKA of the time, and 9- to 11-year follow-up demonstrated comparable outcomes.8 While these results highlighted the possibility of a BCR TKA, the surgical technique and failures of the Geometric knee discouraged surgeons from pursuing the BCR TKA.
Interest in cruciate-preserving knee arthroplasty returned with partial knee replacements, with patients reporting more normal proprioception and motion.10 The techniques became more popular with the introduction of the minimally invasive surgeries in the early 2000s and cruciate ligament preservation became a more interesting concept.11,12 Some surgeons preserved the cruciates by using separate implants for the medial, lateral, and patellofemoral surfaces.10 These results were acceptable for the time but required considerable surgical talent and did not report 20-year results similar to the CR and PS knees.
Most prosthetic designs attempt to copy the normal knee anatomy. Using fluoroscopic studies and computer analysis, designers began to investigate the motion (or kinematics) of the normal knee and realized that despite the fact the TKA looked like the human knee, the designs were not kinematically correct.13
Although TKA successfully treats pain secondary to degenerative joint disease, many patients are unable to return to their prior level of function, with up to 20% reporting dissatisfaction with their level of activity.14 The observed differences in kinematics between a normal knee and a TKA may explain part of this discrepancy.
Normal Knee Motion
The tibiofemoral articulation in a normal knee follows a reproducible pattern of motion as the knee moves from extension to flexion. The lateral femoral condyle (LFC) translates posteriorly with a combination of rolling and sliding motion, while the medial femoral condyle (MFC) has minimal posterior translation and thus acts as a pivot for knee motion. The MFC is larger, less curved, and has a biphasic shape with 2 distinct radiuses of curvature that correspond to an “extension” and “flexion” facet. The transition between the MFC facets occurs at approximately 30° of flexion, whereby the contact point transfers posteriorly with little condylar translation.15-17 In contrast, the LFC is smaller, has a single radius of curvature, and gradually translates posteriorly throughout flexion. Static magnetic resonance imaging of the knee from 0° to 120° shows an average of 19 mm posterior translation for the LFC and 2 mm for the MFC.15-20
In deep flexion, beyond 130°, posterior translation continues for both condyles. The LFC experiences enough excursion to cause loss of joint congruity and partial posterior subluxation.19,20 The MFC shows little additional posterior translation, yet it too loses joint congruity through condylar lift-off. Contact between the posterior horn of the medial meniscus and the posterior femoral condyle limits further flexion.16,21
The difference in motion between the condyles leads to internal tibial rotation during flexion. The initial 10° of knee flexion produces 5° of internal rotation, and an additional 15° of internal tibial rotation occurs throughout the remainder of knee flexion.
Fluoroscopic imaging with computed tomography (CT)- or magnetic resonance (MR)-based modeling has shown the dynamic in vivo relationship of the tibiofemoral joint. Studies have confirmed significantly greater LFC posterior translation as compared to the MFC;22 however, in vivo studies have also shown notable variability in articular rotation and translation based on activity. This highlights the role of ligamentous tension and muscle contraction in kinematics.21-23
The ACL in TKA
The majority of current TKA designs sacrifice the ACL without substituting for its function. The loss of the ACL has significant effects upon the kinematics of the knee.
The ACL is composed of 2 bundles, the anteromedial and posterolateral bundles, which originate on the LFC and insert broadly onto the tibial intercondylar eminence. Its primary role is to resist anterior tibial translation, particularly from 0° to 30° of flexion, which corresponds to the peak quadriceps force that pulls the tibia anteriorly.24 ACL deficiency causes anterior tibial translation during early flexion and abnormal internal tibial rotation.25-27 ACL deficient knees demonstrate a posterior femoral position in full extension, and increased MFC translation during knee flexion.28-32
The role of the ACL in knee arthroplasty has been evaluated by comparing unicompartmental knee arthroplasty (UKA) with TKA, as a reflection of ACL preserving vs sacrificing procedures.33-35 Sagittal plane translation is similar between UKA and normal knees,33,34 while the CR TKA and PS TKA designs show anterior tibia subluxation in full extension.33-35 The difference between UKA and TKA is greatest in extension, corresponding to the ACL functional range. These findings highlight kinematic similarities between TKA designs and the ACL deficient knee.
The majority of UKAs demonstrate near-normal kinematics. A small percentage of the study group demonstrated aberrant anterior tibial motion, highlighting a concern over ACL attenuation with time. Additionally, studies that evaluate the ACL in osteoarthritic knees have questioned the baseline integrity of the ACL.36 Yet the long-term outcomes in UKA design have shown preservation of kinematics due to intact cruciates.37
The PCL in TKA
Because the majority of TKA designs sacrifice the ACL, the classic debate has focused on the utility of the native PCL. Both the CR and PS TKA are designed to offer posterior stabilization; however, kinematic studies have demonstrated notable differences.38,39
The CR TKA design relies on the PCL to resist posterior sag and to prevent the hamstring musculature from pulling the tibia posteriorly during flexion. Studies have shown paradoxical anterior translation of both femoral condyles during flexion, particularly on the medial side of the knee.40 There is also increased variability in femoral rollback. It is unclear whether the PCL can function normally in the absence of the ACL, which causes the PCL to adapt a less anatomic vertical position. The PCL may also be unable to function significantly without the ACL because of pre-existing degenerative histological changes.41
The PS TKA utilizes a cam-post mechanism for posterior stabilization. In contrast to normal knee kinematics, this mechanism creates equal MFC and LFC posterior translation, 8 mm on average at 90° flexion.40 The equivalent translation in PS designs contributes to decreased internal tibial rotation and an increased polyethylene wear at the post.
Role of Surface Geometry
The articular geometry of the knee plays an important role in normal knee kinematics. Initial TKA designs used a femoral component with a single radius of curvature for both femoral condyles.42Current TKA designs that match the femoral component to the native femoral anatomy, by differing the medial and lateral condyle geometry, have demonstrated kinematics that better resemble a native knee.43 Additional changes to the radius of curvature along the posterior facet of the femoral condyles may reduce impingement during deep flexion. These “high flex” designs have demonstrated equivalent range of motion in some studies44 and improved weight-bearing motion in others.45 Surface geometry is important but is not the entire answer to kinematics.
Advances in TKA Design
Knee motion is guided by multiple factors, including the tibiofemoral articular geometry, the surrounding soft tissue tension, and muscle tone. Bicruciate-substituting (BCS) TKA and BCR TKA are forms of evolution from the CR and PS TKA and attempt to respect the function of both cruciate ligaments and provide better kinematics.
The BCS TKA utilizes a modified cam-post articulation to provide both anterior and posterior stabilization (Figure 4).46 The surgical approach remains the same and the implant geometry affects the motion. The BCS TKA design demonstrates femoral rollback at 90° with an average of 14 mm for the MFC and 23 mm for the LFC, and 10° internal tibial rotation.46,47 Additionally, it provides increased sagittal stability during early flexion and an improved pivot shift (indicating improved anterior stabilization).
The BCR designs preserve both cruciates and provide anterior and posterior stabilization. Fluoroscopic imaging has demonstrated contact points in full extension, and posterior rollback at 90° flexion that more closely replicates the normal knee.48
Design and Surgical Techniques for Bicruciate Knee Replacements
If all of the ligaments are preserved, the TKA surfaces must allow motion to be driven by the ligaments in combination with the surfaces alone. The femur can be designed anatomically with asymmetric condyles. The femoral box must allow for preservation of the tibial bone island without impinging upon the cruciate ligaments. The tibial surface must be minimally constrained with concavity medially and convexity laterally.
The bone island preservation does not permit a single-piece tibial polyethylene insert. Therefore, the inserts will replicate the UKA designs (Figure 5). The knee should allow greater range of motion with the possibility of heel to buttocks contact. This increased motion will lead to greater roll back of the femur on the tibia and can lead to subluxation of the femoral runner off of the tibial surface on the lateral side, mimicking the normal knee. This subluxation is desirable but may lead to increased wear of the polyethylene on the lateral side of the knee.
The instruments should be specific for the design but must also be user-friendly. The 2 major issues with the surgery are balancing the knee in full extension and flexion, and preservation of the tibial bone island. The preexisting knee deformity should be <10° in all planes to limit the amount of collateral ligament releases. The collaterals must be balanced in a similar fashion to the standard TKA. Flexion contracture can be treated with posterior capsular release around the cruciates or with an increased distal femoral resection (2 mm at the maximum).
It is important to size the femur correctly because it will be difficult to adjust the flexion gap on the tibial side. A 9-mm posterior medial femoral condyle resection is a reasonable guide if the condyle is not atrophic. However, the exact resection thickness will be implant-specific and should be correlated with the dimensions of the prosthesis being implanted. The tibial bone island must be properly rotated with respect to the center line (Akagi’s line)49 and must not be undercut. The tibial instrument should include pins or blocks to prevent the sawblades from undercutting the island (Figure 6), as undermining leads to fracture in full extension. If undermining occurs, it may be possible to place a cancellous screw through the island and still preserve the ligaments. The integrity of the island is best tested by bringing the knee to full extension and checking for liftoff of the bone. If there is significant compromise of the island, the bone should be resected and either a CR or PS TKA can be implanted. Della Valle and colleagues50 reported a 9.2% incidence (11 of 119 cases) of bone island fracture in their early experience with a BCR TKA and improved this to 1.9% (5/258 cases) after reassessing their technique.
The gap tension should be evaluated either with traditional spacer blocks or with tensioning devices on the medial and lateral side of the knee after the tibial resections are completed. The polyethylene inserts are anatomically different. It may be possible to vary the thickness from medial to lateral, but not in excess of 2 mm.
As the BCR surgical techniques evolve, the balancing and tibial resection may be refined through specialized instrumentation. Such “smart instruments” that incorporate gyros may expedite tibial alignment, and sensor devices may assist with gap balancing. Haptic surgical robotic guides may assist in the tibial resection, facilitating bone island preservation by avoiding any possibility of undermining. At present these assistive aides are not necessary for the operation but may play a future role.
Clinical Results of Knee Arthroplasties
The results of knee replacements improved steadily from the 1970s through the 1990s. The scoring systems were somewhat limited and there was little data on the perception of the patients. The prosthetic designs stabilized at the end of the 1990s with only minor modifications since the year 2000. The 20-year results show similar findings for both the CR and the PS designs. There is little evidence to suggest a clinical correlation with the observed kinematic differences between CR and PS TKA designs.40,51-58 Multiple studies have demonstrated equivalent range of motion38,39,59 and subjective outcome measures (Table 1).60 A randomized prospective trial that compared kinematics and functional scores between the 2 designs failed to observe significant differences in function despite differences in kinematics.46 Equivalence in clinical outcome was further supported by a Cochrane Review meta-analysis that evaluated 1810 patients in 17 selected studies.61 The Knee Society scores have all been in the 92% to 95% ratings with survivals between 90% and 95%.
However, only 80% to 90% of patients are fully satisfied with their implants. The reasons for the dissatisfaction include unexplained anterior knee pain, stiffness, unexplained swelling, loss of range of motion, changes in proprioception, and loss of preoperative functions.14
The mid-term results of the BCR knees that were performed in the 1980s showed similar results to the CR and PS knees. Townley8 reported excellent clinical results with only 2% loosening at 2 to 11 years after surgery. Cloutier and colleagues9 reported 95% survival with improved proprioception at 9 to 11 years after surgery(Table 2).62,63
Studies comparing traditional TKA designs with cruciate preserving designs, both UKA and BCR, have found differences in subjective outcomes.62,64 Comparison of UKA and TKA in the same patient demonstrated significant preference for UKA, particularly with stair-climbing.65 Similarly, comparison between BCR and PS TKA or CR TKA demonstrated preference for BCR in 85% of patients.62
The new BCR knee designs have just started to come to the market.50 The surgical techniques are much improved over the 1980s and cruciate preservation is certainly much easier now. The new designs can produce full range of motion with kinematics that are almost identical to the normal knee in the cadaver laboratory and in computer analyses. These designs certainly should have a similar 20-year survival to the original BCR knees. However, the critical evaluation will be the patient satisfaction scores. With greater motion, better kinematics, and more precise balancing the scores would improve with these designs.
Conclusion
The cruciate ligaments of the knee are central to control of the motion of the normal knee. TKA is a successful operation with at least a 40- to 50-year history. The techniques have continued to develop but 15% to 20% of patients are dissatisfied with the results.14 Evaluations of the prostheses are more sophisticated and kinematics appears to have a central position in the evaluation. If the knee is to move more anatomically correctly, all of the ligaments must be preserved. Proprioception certainly plays a role in the patient’s judgment of the result. History has shown that a BCR knee can be implanted with good mid-term results and it should certainly be possible to build on these results and design a knee that will incorporate all of the ligaments with full range of motion and increased levels of activity.
Hinge knee arthroplasty was introduced in the 1950s.1 All 4 major ligaments were replaced by the hinge, which provided stabilization while allowing sagittal plane motion. Its goal was stability, not replication of normal kinematics. The addition of methyl methacrylate cement improved fixation and allowed surface design modifications that addressed normal articular motion. Implants such as the Gunston Polycentric,2 the Duocondylar,3 and the Geometric4 resurfaced the medial and lateral compartments of the knee while preserving the cruciate ligaments. The implants were subject to greater translational forces without the hinge and loosening became a major problem despite the advances in cementing. It became evident in the 1970s that preservation of the cruciates complicated the procedure. Cruciate resection simplified the operation and allowed improved fixation. The ICLH prosthesis resected the cruciates and used the articular surface design to give stability to the knee.5,6 The total condylar prosthesis had a “tibial” imminence that mimicked the shape of the tibial surface but also sacrificed both of the cruciate ligaments (Figure 1).
Designers recognized that the cruciate ligaments affected knee kinematics; however, they elected to sacrifice the anterior cruciate ligament (ACL) for surgical simplicity and implant longevity.6 In the early 1980s, both the cruciate-retaining (CR) total knee arthroplasty (TKA) (Figure 2) and posterior-stabilized (PS) TKA (Figure 3) designs addressed the posterior cruciate ligament (PCL) function. The PCL was preserved in the “cruciate-retaining” TKA, substituted in the “posterior-stabilized” TKA using a cam-post mechanism. The CR TKA designers believed that PCL preservation produced a more balanced knee with a more anatomical result, a more normal joint line, and better function, especially on stair climbing. The PS TKA designers admitted the value of posterior stabilization but argued that it was too difficult to consistently save the PCL in all cases, and that the PS knee was easier for surgeons to implant with more reliable roll back.7
The Geometric knee was developed in the 1970s to retain both cruciate ligaments.4 Unfortunately, it created a kinematic conflict by using a constrained articular surface design that prevented the motion required by the cruciate ligaments. This conflict resulted in tibial loosening and early failures. The compromised results decreased interest in the bicruciate-retaining (BCR) TKA designs, allowing the CR TKA and PS TKA designs to flourish for the next 20 years with little or no attempts to retain the ACL.
In the 1980s the BCR TKA design was pursued by Townley8 and Cartier.9 Townley8 believed that cruciate resection was a concession to “improper joint synchronization”8 and Cartier9 thought that cruciate preservation permitted more normal proprioception.9 Unlike prior BCR TKA designs, the mid-term clinical results were equal to or better than the standard CR TKA or PS TKA of the time, and 9- to 11-year follow-up demonstrated comparable outcomes.8 While these results highlighted the possibility of a BCR TKA, the surgical technique and failures of the Geometric knee discouraged surgeons from pursuing the BCR TKA.
Interest in cruciate-preserving knee arthroplasty returned with partial knee replacements, with patients reporting more normal proprioception and motion.10 The techniques became more popular with the introduction of the minimally invasive surgeries in the early 2000s and cruciate ligament preservation became a more interesting concept.11,12 Some surgeons preserved the cruciates by using separate implants for the medial, lateral, and patellofemoral surfaces.10 These results were acceptable for the time but required considerable surgical talent and did not report 20-year results similar to the CR and PS knees.
Most prosthetic designs attempt to copy the normal knee anatomy. Using fluoroscopic studies and computer analysis, designers began to investigate the motion (or kinematics) of the normal knee and realized that despite the fact the TKA looked like the human knee, the designs were not kinematically correct.13
Although TKA successfully treats pain secondary to degenerative joint disease, many patients are unable to return to their prior level of function, with up to 20% reporting dissatisfaction with their level of activity.14 The observed differences in kinematics between a normal knee and a TKA may explain part of this discrepancy.
Normal Knee Motion
The tibiofemoral articulation in a normal knee follows a reproducible pattern of motion as the knee moves from extension to flexion. The lateral femoral condyle (LFC) translates posteriorly with a combination of rolling and sliding motion, while the medial femoral condyle (MFC) has minimal posterior translation and thus acts as a pivot for knee motion. The MFC is larger, less curved, and has a biphasic shape with 2 distinct radiuses of curvature that correspond to an “extension” and “flexion” facet. The transition between the MFC facets occurs at approximately 30° of flexion, whereby the contact point transfers posteriorly with little condylar translation.15-17 In contrast, the LFC is smaller, has a single radius of curvature, and gradually translates posteriorly throughout flexion. Static magnetic resonance imaging of the knee from 0° to 120° shows an average of 19 mm posterior translation for the LFC and 2 mm for the MFC.15-20
In deep flexion, beyond 130°, posterior translation continues for both condyles. The LFC experiences enough excursion to cause loss of joint congruity and partial posterior subluxation.19,20 The MFC shows little additional posterior translation, yet it too loses joint congruity through condylar lift-off. Contact between the posterior horn of the medial meniscus and the posterior femoral condyle limits further flexion.16,21
The difference in motion between the condyles leads to internal tibial rotation during flexion. The initial 10° of knee flexion produces 5° of internal rotation, and an additional 15° of internal tibial rotation occurs throughout the remainder of knee flexion.
Fluoroscopic imaging with computed tomography (CT)- or magnetic resonance (MR)-based modeling has shown the dynamic in vivo relationship of the tibiofemoral joint. Studies have confirmed significantly greater LFC posterior translation as compared to the MFC;22 however, in vivo studies have also shown notable variability in articular rotation and translation based on activity. This highlights the role of ligamentous tension and muscle contraction in kinematics.21-23
The ACL in TKA
The majority of current TKA designs sacrifice the ACL without substituting for its function. The loss of the ACL has significant effects upon the kinematics of the knee.
The ACL is composed of 2 bundles, the anteromedial and posterolateral bundles, which originate on the LFC and insert broadly onto the tibial intercondylar eminence. Its primary role is to resist anterior tibial translation, particularly from 0° to 30° of flexion, which corresponds to the peak quadriceps force that pulls the tibia anteriorly.24 ACL deficiency causes anterior tibial translation during early flexion and abnormal internal tibial rotation.25-27 ACL deficient knees demonstrate a posterior femoral position in full extension, and increased MFC translation during knee flexion.28-32
The role of the ACL in knee arthroplasty has been evaluated by comparing unicompartmental knee arthroplasty (UKA) with TKA, as a reflection of ACL preserving vs sacrificing procedures.33-35 Sagittal plane translation is similar between UKA and normal knees,33,34 while the CR TKA and PS TKA designs show anterior tibia subluxation in full extension.33-35 The difference between UKA and TKA is greatest in extension, corresponding to the ACL functional range. These findings highlight kinematic similarities between TKA designs and the ACL deficient knee.
The majority of UKAs demonstrate near-normal kinematics. A small percentage of the study group demonstrated aberrant anterior tibial motion, highlighting a concern over ACL attenuation with time. Additionally, studies that evaluate the ACL in osteoarthritic knees have questioned the baseline integrity of the ACL.36 Yet the long-term outcomes in UKA design have shown preservation of kinematics due to intact cruciates.37
The PCL in TKA
Because the majority of TKA designs sacrifice the ACL, the classic debate has focused on the utility of the native PCL. Both the CR and PS TKA are designed to offer posterior stabilization; however, kinematic studies have demonstrated notable differences.38,39
The CR TKA design relies on the PCL to resist posterior sag and to prevent the hamstring musculature from pulling the tibia posteriorly during flexion. Studies have shown paradoxical anterior translation of both femoral condyles during flexion, particularly on the medial side of the knee.40 There is also increased variability in femoral rollback. It is unclear whether the PCL can function normally in the absence of the ACL, which causes the PCL to adapt a less anatomic vertical position. The PCL may also be unable to function significantly without the ACL because of pre-existing degenerative histological changes.41
The PS TKA utilizes a cam-post mechanism for posterior stabilization. In contrast to normal knee kinematics, this mechanism creates equal MFC and LFC posterior translation, 8 mm on average at 90° flexion.40 The equivalent translation in PS designs contributes to decreased internal tibial rotation and an increased polyethylene wear at the post.
Role of Surface Geometry
The articular geometry of the knee plays an important role in normal knee kinematics. Initial TKA designs used a femoral component with a single radius of curvature for both femoral condyles.42Current TKA designs that match the femoral component to the native femoral anatomy, by differing the medial and lateral condyle geometry, have demonstrated kinematics that better resemble a native knee.43 Additional changes to the radius of curvature along the posterior facet of the femoral condyles may reduce impingement during deep flexion. These “high flex” designs have demonstrated equivalent range of motion in some studies44 and improved weight-bearing motion in others.45 Surface geometry is important but is not the entire answer to kinematics.
Advances in TKA Design
Knee motion is guided by multiple factors, including the tibiofemoral articular geometry, the surrounding soft tissue tension, and muscle tone. Bicruciate-substituting (BCS) TKA and BCR TKA are forms of evolution from the CR and PS TKA and attempt to respect the function of both cruciate ligaments and provide better kinematics.
The BCS TKA utilizes a modified cam-post articulation to provide both anterior and posterior stabilization (Figure 4).46 The surgical approach remains the same and the implant geometry affects the motion. The BCS TKA design demonstrates femoral rollback at 90° with an average of 14 mm for the MFC and 23 mm for the LFC, and 10° internal tibial rotation.46,47 Additionally, it provides increased sagittal stability during early flexion and an improved pivot shift (indicating improved anterior stabilization).
The BCR designs preserve both cruciates and provide anterior and posterior stabilization. Fluoroscopic imaging has demonstrated contact points in full extension, and posterior rollback at 90° flexion that more closely replicates the normal knee.48
Design and Surgical Techniques for Bicruciate Knee Replacements
If all of the ligaments are preserved, the TKA surfaces must allow motion to be driven by the ligaments in combination with the surfaces alone. The femur can be designed anatomically with asymmetric condyles. The femoral box must allow for preservation of the tibial bone island without impinging upon the cruciate ligaments. The tibial surface must be minimally constrained with concavity medially and convexity laterally.
The bone island preservation does not permit a single-piece tibial polyethylene insert. Therefore, the inserts will replicate the UKA designs (Figure 5). The knee should allow greater range of motion with the possibility of heel to buttocks contact. This increased motion will lead to greater roll back of the femur on the tibia and can lead to subluxation of the femoral runner off of the tibial surface on the lateral side, mimicking the normal knee. This subluxation is desirable but may lead to increased wear of the polyethylene on the lateral side of the knee.
The instruments should be specific for the design but must also be user-friendly. The 2 major issues with the surgery are balancing the knee in full extension and flexion, and preservation of the tibial bone island. The preexisting knee deformity should be <10° in all planes to limit the amount of collateral ligament releases. The collaterals must be balanced in a similar fashion to the standard TKA. Flexion contracture can be treated with posterior capsular release around the cruciates or with an increased distal femoral resection (2 mm at the maximum).
It is important to size the femur correctly because it will be difficult to adjust the flexion gap on the tibial side. A 9-mm posterior medial femoral condyle resection is a reasonable guide if the condyle is not atrophic. However, the exact resection thickness will be implant-specific and should be correlated with the dimensions of the prosthesis being implanted. The tibial bone island must be properly rotated with respect to the center line (Akagi’s line)49 and must not be undercut. The tibial instrument should include pins or blocks to prevent the sawblades from undercutting the island (Figure 6), as undermining leads to fracture in full extension. If undermining occurs, it may be possible to place a cancellous screw through the island and still preserve the ligaments. The integrity of the island is best tested by bringing the knee to full extension and checking for liftoff of the bone. If there is significant compromise of the island, the bone should be resected and either a CR or PS TKA can be implanted. Della Valle and colleagues50 reported a 9.2% incidence (11 of 119 cases) of bone island fracture in their early experience with a BCR TKA and improved this to 1.9% (5/258 cases) after reassessing their technique.
The gap tension should be evaluated either with traditional spacer blocks or with tensioning devices on the medial and lateral side of the knee after the tibial resections are completed. The polyethylene inserts are anatomically different. It may be possible to vary the thickness from medial to lateral, but not in excess of 2 mm.
As the BCR surgical techniques evolve, the balancing and tibial resection may be refined through specialized instrumentation. Such “smart instruments” that incorporate gyros may expedite tibial alignment, and sensor devices may assist with gap balancing. Haptic surgical robotic guides may assist in the tibial resection, facilitating bone island preservation by avoiding any possibility of undermining. At present these assistive aides are not necessary for the operation but may play a future role.
Clinical Results of Knee Arthroplasties
The results of knee replacements improved steadily from the 1970s through the 1990s. The scoring systems were somewhat limited and there was little data on the perception of the patients. The prosthetic designs stabilized at the end of the 1990s with only minor modifications since the year 2000. The 20-year results show similar findings for both the CR and the PS designs. There is little evidence to suggest a clinical correlation with the observed kinematic differences between CR and PS TKA designs.40,51-58 Multiple studies have demonstrated equivalent range of motion38,39,59 and subjective outcome measures (Table 1).60 A randomized prospective trial that compared kinematics and functional scores between the 2 designs failed to observe significant differences in function despite differences in kinematics.46 Equivalence in clinical outcome was further supported by a Cochrane Review meta-analysis that evaluated 1810 patients in 17 selected studies.61 The Knee Society scores have all been in the 92% to 95% ratings with survivals between 90% and 95%.
However, only 80% to 90% of patients are fully satisfied with their implants. The reasons for the dissatisfaction include unexplained anterior knee pain, stiffness, unexplained swelling, loss of range of motion, changes in proprioception, and loss of preoperative functions.14
The mid-term results of the BCR knees that were performed in the 1980s showed similar results to the CR and PS knees. Townley8 reported excellent clinical results with only 2% loosening at 2 to 11 years after surgery. Cloutier and colleagues9 reported 95% survival with improved proprioception at 9 to 11 years after surgery(Table 2).62,63
Studies comparing traditional TKA designs with cruciate preserving designs, both UKA and BCR, have found differences in subjective outcomes.62,64 Comparison of UKA and TKA in the same patient demonstrated significant preference for UKA, particularly with stair-climbing.65 Similarly, comparison between BCR and PS TKA or CR TKA demonstrated preference for BCR in 85% of patients.62
The new BCR knee designs have just started to come to the market.50 The surgical techniques are much improved over the 1980s and cruciate preservation is certainly much easier now. The new designs can produce full range of motion with kinematics that are almost identical to the normal knee in the cadaver laboratory and in computer analyses. These designs certainly should have a similar 20-year survival to the original BCR knees. However, the critical evaluation will be the patient satisfaction scores. With greater motion, better kinematics, and more precise balancing the scores would improve with these designs.
Conclusion
The cruciate ligaments of the knee are central to control of the motion of the normal knee. TKA is a successful operation with at least a 40- to 50-year history. The techniques have continued to develop but 15% to 20% of patients are dissatisfied with the results.14 Evaluations of the prostheses are more sophisticated and kinematics appears to have a central position in the evaluation. If the knee is to move more anatomically correctly, all of the ligaments must be preserved. Proprioception certainly plays a role in the patient’s judgment of the result. History has shown that a BCR knee can be implanted with good mid-term results and it should certainly be possible to build on these results and design a knee that will incorporate all of the ligaments with full range of motion and increased levels of activity.
1. Walldius B. Arthroplasty of the knee with an endoprosthesis. Acta Chir Scand. 1957;113(6):445-446.
2. Gunston FH. Polycentric knee arthroplasty. Prosthetic simulation of normal knee movement. J Bone Joint Surg Br. 1971;53(2):272-277.
3. Insall JN, Ranawat CS, Aglietti P, Shine J. A comparison of four models of total knee-replacement prostheses. J Bone Joint Surg Am. 1976;58(6):754-765.
4. Coventry MB, Finerman GA, Riley LH, Turner RH, Upshaw JE. A new geometric knee for total knee arthroplasty. Clin Orthop Relat Res.1972;83:157-162.
5. Freeman MA, Sculco T, Todd RC. Replacement of the severely damaged arthritic knee by the ICLH (Freeman-Swanson) arthroplasty. J Bone Joint Surg Br. 1977;59(1):64-71.
6. Freeman MA, Insall JN, Besser W, Walker PS, Hallel T. Excision of the cruciate ligaments in total knee replacement. Clin Orthop Relat Res. 1977(126):209-212.
7. Pagnano MW, Cushner FD, Scott WN. Role of the posterior cruciate ligament in total knee arthroplasty. J Am Acad Orthop Surg. 1998;6(3):176-187.
8. Townley CO. The anatomic total knee resurfacing arthroplasty. Clin Orthop Relat Res. 1985(192):82-96.
9. Cloutier JM, Sabouret P, Deghrar A. Total knee arthroplasty with retention of both cruciate ligaments. A nine to eleven-year follow-up study. J Bone Joint Surg Am. 1999; 81(5):697-702.
10. Banks SA, Fregly BJ, Boniforti F, Reinschmidt C, Romagnoli S. Comparing in vivo kinematics of unicondylar and bi-unicondylar knee replacements. Knee Surg Sports Traumatol Arthrosc. 2005;13(7):551-556.
11. Repicci JA, Eberle RW. Minimally invasive surgical technique for unicondylar knee arthroplasty. J South Orthop Assoc. 1999;8(1):20-27; discussion 27.
12. Romanowski MR, Repicci JA. Minimally invasive unicondylar arthroplasty: eight-year follow-up. J Knee Surg. 2002;15(1):17-22.
13. Banks SA, Markovich GD, Hodge WA. In vivo kinematics of cruciate-retaining and -substituting knee arthroplasties. J Arthroplasty. 1997;12(3):297-304.
14. Nam D, Nunley RM, Barrack RL. Patient dissatisfaction following total knee replacement: a growing concern? Bone Joint J. 2014;96-B(11 Supple A):96-100.
15. Iwaki H, Pinskerova V, Freeman MA. Tibiofemoral movement 1: the shapes and relative movements of the femur and tibia in the unloaded cadaver knee. J Bone Joint Surg Br. 2000;82(8):1189-1195.
16. Johal P, Williams A, Wragg P, Hunt D, Gedroyc W. Tibio-femoral movement in the living knee. A study of weight bearing and non-weight bearing knee kinematics using ‘interventional’ MRI. J Biomech. 2005;38(2):269-276.
17. Pinskerova V, Johal P, Nakagawa S, et al. Does the femur roll-back with flexion? J Bone Joint Surg Br. 2004;86(6):925-931.
18. Hill PF, Vedi V, Williams A, Pinskerova V, Freeman MA. Tibiofemoral movement 2: the loaded and unloaded living knee studied by MRI. J Bone Joint Surg Br. 2000;82(8):1196-1198.
19. Nakagawa S, Kadoya Y, Todo S, et al. Tibiofemoral movement 3: full flexion in the living knee studied by MRI. J Bone Joint Surg Br. 2000;82(8):1199-1200.
20. Freeman MA, Pinskerova V. The movement of the knee studied by magnetic resonance imaging. Clin Orthop Relat Res. 2003(410):35-43.
21. Moro-oka TA, Hamai S, Miura H, et al. Dynamic activity dependence of in vivo normal knee kinematics. J Orthop Res. 2008;26(4):428-434.
22. Komistek RD, Dennis DA, Mahfouz M. In vivo fluoroscopic analysis of the normal human knee. Clin Orthop Relat Res. 2003(410):69-81.
23. Li G, DeFrate LE, Park SE, Gill TJ, Rubash HE. In vivo articular cartilage contact kinematics of the knee: an investigation using dual-orthogonal fluoroscopy and magnetic resonance image-based computer models. Am J Sports Med. 2005;33(1):102-107.
24. Grood ES, Suntay WJ, Noyes FR, Butler DL. Biomechanics of the knee-extension exercise. Effect of cutting the anterior cruciate ligament. J Bone Joint Surg Am. 1984;66(5):725-734.
25. Noyes FR, Jetter AW, Grood ES, Harms SP, Gardner EJ, Levy MS. Anterior cruciate ligament function in providing rotational stability assessed by medial and lateral tibiofemoral compartment translations and subluxations. Am J Sports Med. 2015;43(3):683-692.
26. Good L, Askew MJ, Boom A, Melby A 3rd. Kinematic in-vitro comparison between the normal knee and two techniques for reconstruction of the anterior cruciate ligament. Clin Biomech (Bristol, Avon). 1993;8(5):243-249.
27. Beard DJ, Murray DW, Gill HS. Reconstruction does not reduce tibial translation in the cruciate-deficient knee an in vivo study. J Bone Joint Surg Br. 2001;83(8):1098-1103.
28. Dennis DA, Mahfouz MR, Komistek RD, Hoff W. In vivo determination of normal and anterior cruciate ligament-deficient knee kinematics. J Biomech. 2005;38(2):241-253.
29. Beynnon BD, Fleming BC, Labovitch R, Parsons B. Chronic anterior cruciate ligament deficiency is associated with increased anterior translation of the tibia during the transition from non-weightbearing to weightbearing. J Orthop Res. 2002;20(2):332-337.
30. Brandsson S, Karlsson J, Eriksson BI, Kärrholm J. Kinematics after tear in the anterior cruciate ligament: dynamic bilateral radiostereometric studies in 11 patients. Acta Orthop Scand. 2001;72(4):372-378.
31. Andriacchi TP, Briant PL, Bevill SL, Koo S. Rotational changes at the knee after ACL injury cause cartilage thinning. Clin Orthop Relat Res. 2006;442:39-44.
32. Scarvell JM, Smith PN, Refshauge KM, Galloway HR, Woods KR. Comparison of kinematic analysis by mapping tibiofemoral contact with movement of the femoral condylar centres in healthy and anterior cruciate ligament injured knees. J Orthop Res. 2004;22(5):955-962.
33. Miller RK, Goodfellow JW, Murray DW, O’Connor JJ. In vitro measurement of patellofemoral force after three types of knee replacement. J Bone Joint Surg Br. 1998;80(5):900-906.
34. Price AJ, Rees JL, Beard DL, Gill RH, Dodd CA, Murray DM. Sagittal plane kinematics of a mobile-bearing unicompartmental knee arthroplasty at 10 years: a comparative in vivo fluoroscopic analysis. J Arthroplasty. 2004;19(5):590-597.
35. Dennis D, Komistek R, Scuderi G, et al. In vivo three-dimensional determination of kinematics for subjects with a normal knee or a unicompartmental or total knee replacement. J Bone Joint Surg Am. 2001;83-A Suppl 2 Pt 2:104-115.
36. Arbuthnot JE, Brink RB. Assessment of the antero-posterior and rotational stability of the anterior cruciate ligament analogue in a guided motion bi-cruciate stabilized total knee arthroplasty. J Med Eng Technol. 2009;33(8):610-615.
37. Hollinghurst D, Stoney J, Ward T, et al. No deterioration of kinematics and cruciate function 10 years after medial unicompartmental arthroplasty. Knee. 2006;13(6):440-444.
38. Dennis DA, Komistek RD, Colwell CE Jr, et al. In vivo anteroposterior femorotibial translation of total knee arthroplasty: a multicenter analysis. Clin Orthop Relat Res. 1998(356):47-57.
39. Dennis DA, Komistek RD, Hoff WA, Gabriel SM. In vivo knee kinematics derived using an inverse perspective technique. Clin Orthop Relat Res. 1996;(331):107-117.
40. Yoshiya S, Matsui N, Komistek RD, Dennis DA, Mahfouz M, Kurosaka M. In vivo kinematic comparison of posterior cruciate-retaining and posterior stabilized total knee arthroplasties under passive and weight-bearing conditions. J Arthroplasty. 2005;20(6):777-783.
41. Kleinbart FA, Bryk E, Evangelista J, Scott WN, Vigorita VJ. Histologic comparison of posterior cruciate ligaments from arthritic and age-matched knee specimens. J Arthroplasty. 1996;11(6):726-731.
42. Bull AM, Kessler O, Alam M, Amis AA. Changes in knee kinematics reflect the articular geometry after arthroplasty. Clin Orthop Relat Res. 2008;466(10):2491-2499.
43. Komistek RD, Mahfouz MR, Bertin KC, Rosenberg A, Kennedy W. In vivo determination of total knee arthroplasty kinematics: a multicenter analysis of an asymmetrical posterior cruciate retaining total knee arthroplasty. J Arthroplasty. 2008;23(1):41-50.
44. Mehin R, Burnett RS, Brasher PM. Does the new generation of high-flex knee prostheses improve the post-operative range of movement?: a meta-analysis. J Bone Joint Surg Br. 2010;92(10):1429-1434.
45. Dennis DA, Heekin RD, Clark CR, Murphy JA, O’Dell TL, Dwyer KA. Effect of implant design on knee flexion. J Arthroplasty. 2013;28(3):429-438.
46. Victor J, Mueller JK, Komistek RD, Sharma A, Nadaud MC, Bellemans J. In vivo kinematics after a cruciate-substituting TKA. Clin Orthop Relat Res. 2010;468(3):807-814.
47. Catani F, Ensini A, Belvedere C, et al. In vivo kinematics and kinetics of a bi-cruciate substituting total knee arthroplasty: a combined fluoroscopic and gait analysis study. J Orthop Res. 2009;27(12):1569-1575.
48. Stiehl JB, Komistek RD, Cloutier JM, Dennis DA. The cruciate ligaments in total knee arthroplasty: a kinematic analysis of 2 total knee arthroplasties. J Arthroplasty. 2000;15(5):545-550.
49. Akagi M, Oh M, Nonaka T, Tsujimoto H, Asano T, Hamanishi C. An anteroposterior axis of the tibia for total knee arthroplasty. Clin Orthop Relat Res. 2004;(420):213-219.
50. Della Valle CJ, Andriacchi TP, Berend KR, DeClaire JH, Lombardi AV Jr, Peters CL. Early experience with bi-cruciate retaining TKA. Poster presented at: American Academy of Orthopaedic Surgeons 2015 Annual Meeting; March 24-28, 2015; Las Vegas, NV.
51. Udomkiat P, Meng BJ, Dorr LD, Wan Z. Functional comparison of posterior cruciate retention and substitution knee replacement. Clin Orthop Relat Res. 2000;(378):192-201.
52. Tanzer M, Smith K, Burnett S. Posterior-stabilized versus cruciate-retaining total knee arthroplasty: balancing the gap. J Arthroplasty. 2002;17(7):813-819.
53. Maruyama S, Yoshiya S, Matsui N, Kuroda R, Kurosaka M. Functional comparison of posterior cruciate-retaining versus posterior stabilized total knee arthroplasty. J Arthroplasty. 2004;19(3):349-53.
54. Clark CR, Rorabeck CH, MacDonald S, MacDonald D, Swafford J, Cleland D. Posterior-stabilized and cruciate-retaining total knee replacement: a randomized study. Clin Orthop Relat Res. 2001;(392):208-212.
55. Swanik CB, Lephart SM, Rubash HE. Proprioception, kinesthesia, and balance after total knee arthroplasty with cruciate-retaining and posterior stabilized prostheses. J Bone Joint Surg Am. 2004;86-A(2):328-334.
56. Harato K, Bourne RB, Victor J, Snyder M, Hart J, Ries MD. Midterm comparison of posterior cruciate-retaining versus -substituting total knee arthroplasty using the Genesis II prosthesis. A multicenter prospective randomized clinical trial. Knee. 2008;15(3):217-221.
57. Catani F, Leardini A, Ensini A, et al. The stability of the cemented tibial component of total knee arthroplasty: posterior cruciate-retaining versus posterior-stabilized design. J Arthroplasty. 2004;19(6):775-782.
58. Dennis DA, Komistek RD, Stiehl JB, Walker SA, Dennis KN. Range of motion after total knee arthroplasty: the effect of implant design and weight-bearing conditions. J Arthroplasty. 1998;13(7):748-752.
59. Becker MW, Insall JN, Faris PM. Bilateral total knee arthroplasty. One cruciate retaining and one cruciate substituting. Clin Orthop Relat Res. 1991;(271):122-124.
60. Kim YH, Choi Y, Kwon OR, Kim JS. Functional outcome and range of motion of high-flexion posterior cruciate-retaining and high-flexion posterior cruciate-substituting total knee prostheses. A prospective, randomized study. J Bone Joint Surg Am. 2009;91(4):753-760.
61. 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.
62. Pritchett JW. Patients prefer a bicruciate-retaining or the medial pivot total knee prosthesis. J Arthroplasty. 2011;26(2):224-228.
63. Sabouret P, Lavoie F, Cloutier JM. Total knee replacement with retention of both cruciate ligaments: a 22-year follow-up study. Bone Joint J. 2013;95-B(7):917-922.
64. Andriacchi TP, Galante JO, Fermier RW. The influence of total knee-replacement design on walking and stair-climbing. J Bone Joint Surg Am. 1982;64(9):1328-1335.
65. Laurencin CT, Zelicof SB, Scott RD, Ewald FC. Unicompartmental versus total knee arthroplasty in the same patient. A comparative study. Clin Orthop Relat Res. 1991;(273):151-156.
66. Victor J, Banks S, Bellemans J. Kinematics of posterior cruciate ligament-retaining and -substituting total knee arthroplasty: a prospective randomised outcome study. J Bone Joint Surg Br. 2005;87(5):646-655.
1. Walldius B. Arthroplasty of the knee with an endoprosthesis. Acta Chir Scand. 1957;113(6):445-446.
2. Gunston FH. Polycentric knee arthroplasty. Prosthetic simulation of normal knee movement. J Bone Joint Surg Br. 1971;53(2):272-277.
3. Insall JN, Ranawat CS, Aglietti P, Shine J. A comparison of four models of total knee-replacement prostheses. J Bone Joint Surg Am. 1976;58(6):754-765.
4. Coventry MB, Finerman GA, Riley LH, Turner RH, Upshaw JE. A new geometric knee for total knee arthroplasty. Clin Orthop Relat Res.1972;83:157-162.
5. Freeman MA, Sculco T, Todd RC. Replacement of the severely damaged arthritic knee by the ICLH (Freeman-Swanson) arthroplasty. J Bone Joint Surg Br. 1977;59(1):64-71.
6. Freeman MA, Insall JN, Besser W, Walker PS, Hallel T. Excision of the cruciate ligaments in total knee replacement. Clin Orthop Relat Res. 1977(126):209-212.
7. Pagnano MW, Cushner FD, Scott WN. Role of the posterior cruciate ligament in total knee arthroplasty. J Am Acad Orthop Surg. 1998;6(3):176-187.
8. Townley CO. The anatomic total knee resurfacing arthroplasty. Clin Orthop Relat Res. 1985(192):82-96.
9. Cloutier JM, Sabouret P, Deghrar A. Total knee arthroplasty with retention of both cruciate ligaments. A nine to eleven-year follow-up study. J Bone Joint Surg Am. 1999; 81(5):697-702.
10. Banks SA, Fregly BJ, Boniforti F, Reinschmidt C, Romagnoli S. Comparing in vivo kinematics of unicondylar and bi-unicondylar knee replacements. Knee Surg Sports Traumatol Arthrosc. 2005;13(7):551-556.
11. Repicci JA, Eberle RW. Minimally invasive surgical technique for unicondylar knee arthroplasty. J South Orthop Assoc. 1999;8(1):20-27; discussion 27.
12. Romanowski MR, Repicci JA. Minimally invasive unicondylar arthroplasty: eight-year follow-up. J Knee Surg. 2002;15(1):17-22.
13. Banks SA, Markovich GD, Hodge WA. In vivo kinematics of cruciate-retaining and -substituting knee arthroplasties. J Arthroplasty. 1997;12(3):297-304.
14. Nam D, Nunley RM, Barrack RL. Patient dissatisfaction following total knee replacement: a growing concern? Bone Joint J. 2014;96-B(11 Supple A):96-100.
15. Iwaki H, Pinskerova V, Freeman MA. Tibiofemoral movement 1: the shapes and relative movements of the femur and tibia in the unloaded cadaver knee. J Bone Joint Surg Br. 2000;82(8):1189-1195.
16. Johal P, Williams A, Wragg P, Hunt D, Gedroyc W. Tibio-femoral movement in the living knee. A study of weight bearing and non-weight bearing knee kinematics using ‘interventional’ MRI. J Biomech. 2005;38(2):269-276.
17. Pinskerova V, Johal P, Nakagawa S, et al. Does the femur roll-back with flexion? J Bone Joint Surg Br. 2004;86(6):925-931.
18. Hill PF, Vedi V, Williams A, Pinskerova V, Freeman MA. Tibiofemoral movement 2: the loaded and unloaded living knee studied by MRI. J Bone Joint Surg Br. 2000;82(8):1196-1198.
19. Nakagawa S, Kadoya Y, Todo S, et al. Tibiofemoral movement 3: full flexion in the living knee studied by MRI. J Bone Joint Surg Br. 2000;82(8):1199-1200.
20. Freeman MA, Pinskerova V. The movement of the knee studied by magnetic resonance imaging. Clin Orthop Relat Res. 2003(410):35-43.
21. Moro-oka TA, Hamai S, Miura H, et al. Dynamic activity dependence of in vivo normal knee kinematics. J Orthop Res. 2008;26(4):428-434.
22. Komistek RD, Dennis DA, Mahfouz M. In vivo fluoroscopic analysis of the normal human knee. Clin Orthop Relat Res. 2003(410):69-81.
23. Li G, DeFrate LE, Park SE, Gill TJ, Rubash HE. In vivo articular cartilage contact kinematics of the knee: an investigation using dual-orthogonal fluoroscopy and magnetic resonance image-based computer models. Am J Sports Med. 2005;33(1):102-107.
24. Grood ES, Suntay WJ, Noyes FR, Butler DL. Biomechanics of the knee-extension exercise. Effect of cutting the anterior cruciate ligament. J Bone Joint Surg Am. 1984;66(5):725-734.
25. Noyes FR, Jetter AW, Grood ES, Harms SP, Gardner EJ, Levy MS. Anterior cruciate ligament function in providing rotational stability assessed by medial and lateral tibiofemoral compartment translations and subluxations. Am J Sports Med. 2015;43(3):683-692.
26. Good L, Askew MJ, Boom A, Melby A 3rd. Kinematic in-vitro comparison between the normal knee and two techniques for reconstruction of the anterior cruciate ligament. Clin Biomech (Bristol, Avon). 1993;8(5):243-249.
27. Beard DJ, Murray DW, Gill HS. Reconstruction does not reduce tibial translation in the cruciate-deficient knee an in vivo study. J Bone Joint Surg Br. 2001;83(8):1098-1103.
28. Dennis DA, Mahfouz MR, Komistek RD, Hoff W. In vivo determination of normal and anterior cruciate ligament-deficient knee kinematics. J Biomech. 2005;38(2):241-253.
29. Beynnon BD, Fleming BC, Labovitch R, Parsons B. Chronic anterior cruciate ligament deficiency is associated with increased anterior translation of the tibia during the transition from non-weightbearing to weightbearing. J Orthop Res. 2002;20(2):332-337.
30. Brandsson S, Karlsson J, Eriksson BI, Kärrholm J. Kinematics after tear in the anterior cruciate ligament: dynamic bilateral radiostereometric studies in 11 patients. Acta Orthop Scand. 2001;72(4):372-378.
31. Andriacchi TP, Briant PL, Bevill SL, Koo S. Rotational changes at the knee after ACL injury cause cartilage thinning. Clin Orthop Relat Res. 2006;442:39-44.
32. Scarvell JM, Smith PN, Refshauge KM, Galloway HR, Woods KR. Comparison of kinematic analysis by mapping tibiofemoral contact with movement of the femoral condylar centres in healthy and anterior cruciate ligament injured knees. J Orthop Res. 2004;22(5):955-962.
33. Miller RK, Goodfellow JW, Murray DW, O’Connor JJ. In vitro measurement of patellofemoral force after three types of knee replacement. J Bone Joint Surg Br. 1998;80(5):900-906.
34. Price AJ, Rees JL, Beard DL, Gill RH, Dodd CA, Murray DM. Sagittal plane kinematics of a mobile-bearing unicompartmental knee arthroplasty at 10 years: a comparative in vivo fluoroscopic analysis. J Arthroplasty. 2004;19(5):590-597.
35. Dennis D, Komistek R, Scuderi G, et al. In vivo three-dimensional determination of kinematics for subjects with a normal knee or a unicompartmental or total knee replacement. J Bone Joint Surg Am. 2001;83-A Suppl 2 Pt 2:104-115.
36. Arbuthnot JE, Brink RB. Assessment of the antero-posterior and rotational stability of the anterior cruciate ligament analogue in a guided motion bi-cruciate stabilized total knee arthroplasty. J Med Eng Technol. 2009;33(8):610-615.
37. Hollinghurst D, Stoney J, Ward T, et al. No deterioration of kinematics and cruciate function 10 years after medial unicompartmental arthroplasty. Knee. 2006;13(6):440-444.
38. Dennis DA, Komistek RD, Colwell CE Jr, et al. In vivo anteroposterior femorotibial translation of total knee arthroplasty: a multicenter analysis. Clin Orthop Relat Res. 1998(356):47-57.
39. Dennis DA, Komistek RD, Hoff WA, Gabriel SM. In vivo knee kinematics derived using an inverse perspective technique. Clin Orthop Relat Res. 1996;(331):107-117.
40. Yoshiya S, Matsui N, Komistek RD, Dennis DA, Mahfouz M, Kurosaka M. In vivo kinematic comparison of posterior cruciate-retaining and posterior stabilized total knee arthroplasties under passive and weight-bearing conditions. J Arthroplasty. 2005;20(6):777-783.
41. Kleinbart FA, Bryk E, Evangelista J, Scott WN, Vigorita VJ. Histologic comparison of posterior cruciate ligaments from arthritic and age-matched knee specimens. J Arthroplasty. 1996;11(6):726-731.
42. Bull AM, Kessler O, Alam M, Amis AA. Changes in knee kinematics reflect the articular geometry after arthroplasty. Clin Orthop Relat Res. 2008;466(10):2491-2499.
43. Komistek RD, Mahfouz MR, Bertin KC, Rosenberg A, Kennedy W. In vivo determination of total knee arthroplasty kinematics: a multicenter analysis of an asymmetrical posterior cruciate retaining total knee arthroplasty. J Arthroplasty. 2008;23(1):41-50.
44. Mehin R, Burnett RS, Brasher PM. Does the new generation of high-flex knee prostheses improve the post-operative range of movement?: a meta-analysis. J Bone Joint Surg Br. 2010;92(10):1429-1434.
45. Dennis DA, Heekin RD, Clark CR, Murphy JA, O’Dell TL, Dwyer KA. Effect of implant design on knee flexion. J Arthroplasty. 2013;28(3):429-438.
46. Victor J, Mueller JK, Komistek RD, Sharma A, Nadaud MC, Bellemans J. In vivo kinematics after a cruciate-substituting TKA. Clin Orthop Relat Res. 2010;468(3):807-814.
47. Catani F, Ensini A, Belvedere C, et al. In vivo kinematics and kinetics of a bi-cruciate substituting total knee arthroplasty: a combined fluoroscopic and gait analysis study. J Orthop Res. 2009;27(12):1569-1575.
48. Stiehl JB, Komistek RD, Cloutier JM, Dennis DA. The cruciate ligaments in total knee arthroplasty: a kinematic analysis of 2 total knee arthroplasties. J Arthroplasty. 2000;15(5):545-550.
49. Akagi M, Oh M, Nonaka T, Tsujimoto H, Asano T, Hamanishi C. An anteroposterior axis of the tibia for total knee arthroplasty. Clin Orthop Relat Res. 2004;(420):213-219.
50. Della Valle CJ, Andriacchi TP, Berend KR, DeClaire JH, Lombardi AV Jr, Peters CL. Early experience with bi-cruciate retaining TKA. Poster presented at: American Academy of Orthopaedic Surgeons 2015 Annual Meeting; March 24-28, 2015; Las Vegas, NV.
51. Udomkiat P, Meng BJ, Dorr LD, Wan Z. Functional comparison of posterior cruciate retention and substitution knee replacement. Clin Orthop Relat Res. 2000;(378):192-201.
52. Tanzer M, Smith K, Burnett S. Posterior-stabilized versus cruciate-retaining total knee arthroplasty: balancing the gap. J Arthroplasty. 2002;17(7):813-819.
53. Maruyama S, Yoshiya S, Matsui N, Kuroda R, Kurosaka M. Functional comparison of posterior cruciate-retaining versus posterior stabilized total knee arthroplasty. J Arthroplasty. 2004;19(3):349-53.
54. Clark CR, Rorabeck CH, MacDonald S, MacDonald D, Swafford J, Cleland D. Posterior-stabilized and cruciate-retaining total knee replacement: a randomized study. Clin Orthop Relat Res. 2001;(392):208-212.
55. Swanik CB, Lephart SM, Rubash HE. Proprioception, kinesthesia, and balance after total knee arthroplasty with cruciate-retaining and posterior stabilized prostheses. J Bone Joint Surg Am. 2004;86-A(2):328-334.
56. Harato K, Bourne RB, Victor J, Snyder M, Hart J, Ries MD. Midterm comparison of posterior cruciate-retaining versus -substituting total knee arthroplasty using the Genesis II prosthesis. A multicenter prospective randomized clinical trial. Knee. 2008;15(3):217-221.
57. Catani F, Leardini A, Ensini A, et al. The stability of the cemented tibial component of total knee arthroplasty: posterior cruciate-retaining versus posterior-stabilized design. J Arthroplasty. 2004;19(6):775-782.
58. Dennis DA, Komistek RD, Stiehl JB, Walker SA, Dennis KN. Range of motion after total knee arthroplasty: the effect of implant design and weight-bearing conditions. J Arthroplasty. 1998;13(7):748-752.
59. Becker MW, Insall JN, Faris PM. Bilateral total knee arthroplasty. One cruciate retaining and one cruciate substituting. Clin Orthop Relat Res. 1991;(271):122-124.
60. Kim YH, Choi Y, Kwon OR, Kim JS. Functional outcome and range of motion of high-flexion posterior cruciate-retaining and high-flexion posterior cruciate-substituting total knee prostheses. A prospective, randomized study. J Bone Joint Surg Am. 2009;91(4):753-760.
61. 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.
62. Pritchett JW. Patients prefer a bicruciate-retaining or the medial pivot total knee prosthesis. J Arthroplasty. 2011;26(2):224-228.
63. Sabouret P, Lavoie F, Cloutier JM. Total knee replacement with retention of both cruciate ligaments: a 22-year follow-up study. Bone Joint J. 2013;95-B(7):917-922.
64. Andriacchi TP, Galante JO, Fermier RW. The influence of total knee-replacement design on walking and stair-climbing. J Bone Joint Surg Am. 1982;64(9):1328-1335.
65. Laurencin CT, Zelicof SB, Scott RD, Ewald FC. Unicompartmental versus total knee arthroplasty in the same patient. A comparative study. Clin Orthop Relat Res. 1991;(273):151-156.
66. Victor J, Banks S, Bellemans J. Kinematics of posterior cruciate ligament-retaining and -substituting total knee arthroplasty: a prospective randomised outcome study. J Bone Joint Surg Br. 2005;87(5):646-655.
Opioid-based therapies reduce TKA needs for OA patients, but not costs
Treatment with opioids is not cost effective in osteoarthritis patients without comorbidities, according to Savannah R. Smith and her associates.
When a 10% reduction in total knee arthroplasty (TKA) effectiveness from opioid-based therapies was assumed, tramadol therapy delayed TKA by 7 years and tramadol plus oxycodone therapy delayed TKA by 9 years. Opioid-based therapy reduced primary TKA utilization by 4% for tramadol and by 10% for tramadol plus oxycodone, and reduced revision TKA use by 23% and 39%, respectively.
While both opioid-based therapies reduced dependence on TKA, treatment was more expensive and it reduced quality of life, compared with an opioid-sparing therapy. For a 60-year-old OA patient for whom TKA was not an option, the incremental cost-effectiveness ratio for tramadol was $39,600 per quality-adjusted life-year, compared with a therapy without opioids, and the incremental cost-effectiveness ratio for tramadol plus oxycodone was $116,800 per quality-adjusted life-year.
“Given the risk of diversion and its associated cost for potent opioids, policy makers may consider limiting the use of potent opioids in knee OA patients. From a cost-effectiveness standpoint, both opioid-based strategies led to higher costs without providing additional benefits, unless patients were unwilling or unable to undergo TKA later,” the investigators noted.
Find the full study in Arthritis Care and Research (doi: 10.1002/acr.22916).
Treatment with opioids is not cost effective in osteoarthritis patients without comorbidities, according to Savannah R. Smith and her associates.
When a 10% reduction in total knee arthroplasty (TKA) effectiveness from opioid-based therapies was assumed, tramadol therapy delayed TKA by 7 years and tramadol plus oxycodone therapy delayed TKA by 9 years. Opioid-based therapy reduced primary TKA utilization by 4% for tramadol and by 10% for tramadol plus oxycodone, and reduced revision TKA use by 23% and 39%, respectively.
While both opioid-based therapies reduced dependence on TKA, treatment was more expensive and it reduced quality of life, compared with an opioid-sparing therapy. For a 60-year-old OA patient for whom TKA was not an option, the incremental cost-effectiveness ratio for tramadol was $39,600 per quality-adjusted life-year, compared with a therapy without opioids, and the incremental cost-effectiveness ratio for tramadol plus oxycodone was $116,800 per quality-adjusted life-year.
“Given the risk of diversion and its associated cost for potent opioids, policy makers may consider limiting the use of potent opioids in knee OA patients. From a cost-effectiveness standpoint, both opioid-based strategies led to higher costs without providing additional benefits, unless patients were unwilling or unable to undergo TKA later,” the investigators noted.
Find the full study in Arthritis Care and Research (doi: 10.1002/acr.22916).
Treatment with opioids is not cost effective in osteoarthritis patients without comorbidities, according to Savannah R. Smith and her associates.
When a 10% reduction in total knee arthroplasty (TKA) effectiveness from opioid-based therapies was assumed, tramadol therapy delayed TKA by 7 years and tramadol plus oxycodone therapy delayed TKA by 9 years. Opioid-based therapy reduced primary TKA utilization by 4% for tramadol and by 10% for tramadol plus oxycodone, and reduced revision TKA use by 23% and 39%, respectively.
While both opioid-based therapies reduced dependence on TKA, treatment was more expensive and it reduced quality of life, compared with an opioid-sparing therapy. For a 60-year-old OA patient for whom TKA was not an option, the incremental cost-effectiveness ratio for tramadol was $39,600 per quality-adjusted life-year, compared with a therapy without opioids, and the incremental cost-effectiveness ratio for tramadol plus oxycodone was $116,800 per quality-adjusted life-year.
“Given the risk of diversion and its associated cost for potent opioids, policy makers may consider limiting the use of potent opioids in knee OA patients. From a cost-effectiveness standpoint, both opioid-based strategies led to higher costs without providing additional benefits, unless patients were unwilling or unable to undergo TKA later,” the investigators noted.
Find the full study in Arthritis Care and Research (doi: 10.1002/acr.22916).
FROM ARTHRITIS CARE AND RESEARCH
Single-Bundle, Double-Bundle Techniques Offer Similar Outcomes in ACL Reconstruction
ORLANDO, FL—Patients who undergo anterior cruciate ligament (ACL) reconstruction with a single-bundle or a double-bundle technique demonstrate similar performance during recovery, according to research presented at the American Orthopedic Society for Sports Medicine’s Specialty Day.
Researchers studied 105 patients with ACL ranging in age from 18 to 52. A total of 87 patients were available for the 5-year follow-up and were included in the study. All patients underwent post-operative rehabilitation under the same guidelines and supervision of physical therapists. Follow-up exams included multiple subjective and objective evaluation tests, including range of motion, one-leg-hop test, square-hop test, and knee injury osteoarthritis outcome score.
Patients treated with single-bundle or double-bundle ACL reconstruction showed no significant difference in major performance tests. In addition, 89% of the single-bundle and 84% of the double-bundle groups had a negative pivot-shift test, which suggests both groups had similar knee stability and health. The study also noted that the presence of osteoarthritis in patients was similar during follow-up evaluations, regardless of the technique used during ACL surgery.
ORLANDO, FL—Patients who undergo anterior cruciate ligament (ACL) reconstruction with a single-bundle or a double-bundle technique demonstrate similar performance during recovery, according to research presented at the American Orthopedic Society for Sports Medicine’s Specialty Day.
Researchers studied 105 patients with ACL ranging in age from 18 to 52. A total of 87 patients were available for the 5-year follow-up and were included in the study. All patients underwent post-operative rehabilitation under the same guidelines and supervision of physical therapists. Follow-up exams included multiple subjective and objective evaluation tests, including range of motion, one-leg-hop test, square-hop test, and knee injury osteoarthritis outcome score.
Patients treated with single-bundle or double-bundle ACL reconstruction showed no significant difference in major performance tests. In addition, 89% of the single-bundle and 84% of the double-bundle groups had a negative pivot-shift test, which suggests both groups had similar knee stability and health. The study also noted that the presence of osteoarthritis in patients was similar during follow-up evaluations, regardless of the technique used during ACL surgery.
ORLANDO, FL—Patients who undergo anterior cruciate ligament (ACL) reconstruction with a single-bundle or a double-bundle technique demonstrate similar performance during recovery, according to research presented at the American Orthopedic Society for Sports Medicine’s Specialty Day.
Researchers studied 105 patients with ACL ranging in age from 18 to 52. A total of 87 patients were available for the 5-year follow-up and were included in the study. All patients underwent post-operative rehabilitation under the same guidelines and supervision of physical therapists. Follow-up exams included multiple subjective and objective evaluation tests, including range of motion, one-leg-hop test, square-hop test, and knee injury osteoarthritis outcome score.
Patients treated with single-bundle or double-bundle ACL reconstruction showed no significant difference in major performance tests. In addition, 89% of the single-bundle and 84% of the double-bundle groups had a negative pivot-shift test, which suggests both groups had similar knee stability and health. The study also noted that the presence of osteoarthritis in patients was similar during follow-up evaluations, regardless of the technique used during ACL surgery.
Low Back Pain: Evidence-based Diagnosis and Treatment
CE/CME No: CR-1605
PROGRAM OVERVIEW
Earn credit by reading this article and successfully completing the posttest and evaluation. Successful completion is defined as a cumulative score of at least 70% correct.
EDUCATIONAL OBJECTIVES
• Identify "red flag" items in the history and physical exam that make low back pain (LBP) "complicated."
• Stratify patients into three categories: simple back pain, complicated back pain, and back pain with sciatica.
• Discuss when appropriate additional testing/imaging is needed based on LBP categories.
• Discuss patient perceptions and costs associated with imaging and LBP.
• Describe basic treatment options for noncomplicated acute LBP.
FACULTY
Mike Roscoe is the PA Program Director at the University of Evansville, Indiana. Alyssa Nishihira is in her final year of the PA program at Butler University, Indianapolis; after graduation, she will be practicing at Advanced Neurosurgery in Reno, Nevada.
The authors have no financial relationships to disclose.
ACCREDITATION STATEMENT
This program has been reviewed and is approved for a maximum of 1.0 hour of American Academy of Physician Assistants (AAPA) Category 1 CME credit by the Physician Assistant Review Panel. [NPs: Both ANCC and the AANP Certification Program recognize AAPA as an approved provider of Category 1 credit.] Approval is valid for one year from the issue date of May 2016.
Article begins on next page >>
Low back pain (LBP) is one of the most common reasons for an office visit, but most cases—at least 95%—have a benign underlying cause. Evaluation of LBP patients in the primary care setting, therefore, must focus on identifying “red flags” in the history and physical exam that suggest a significant underlying process requiring further work-up, including imaging. This evidence-based approach helps control costs and prevents the detrimental effects of unnecessary testing.
Low back pain (LBP) plagues many Americans and is a common reason for office visits in the United States. In 2010, back symptoms were the principal reason for 1.3% of office visits in the US.1 Recent data suggest that 75% to 85% of all Americans will experience an episode of LBP at least once in their lifetime.2 It is the leading cause of years lived with disability in the US3 and is a common reason for work disability. From a health care system standpoint, LBP imposes a considerable burden, accounting for more than $85 billion annually in direct costs.2
The etiology of LBP can be related to several anatomic and physiologic changes. Potential origins of LBP include, but are not limited to, pathology of the vertebrospinal ligaments, musculature, facet joints, fascia, vertebra and vertebral disks, and the extensive neurovascular components of the lumbar region. Although the potential causes of LBP are many, the majority of patients presenting with acute LBP usually improve with minimal clinical intervention within the first month. This is true even for patients who report limitations in daily activities and those with severe, acute cases of LBP.
A single standard of care for patients presenting with LBP has not been established. The wide array of choices for diagnosis and treatment of LBP is one factor that hinders the development of a standard diagnostic protocol. The challenge to clinicians when diagnosing LBP is to differentiate the patients with benign, self-limiting LBP (simple), who comprise the vast majority of LBP patients, from the 1% to 5% with a serious underlying pathology (complicated).4
Continue for stratification of low back pain >>
STRATIFICATION OF LOW BACK PAIN
Koes and colleagues analyzed 13 different national guidelines and two international guidelines for the management of LBP.5 They found that the guidelines consistently recommend focusing the history and physical exam (HPE) on identifying features suggestive of underlying serious pathology, or “red flags,” and excluding specific diseases.5 They also found that none of the guidelines recommends the routine use of imaging in patients without suspected serious pathology.5 The American College of Radiology simplified this approach to patients with LBP by creating a list of red flags to look for during the HPE.3 The presence of red flags indicates a case of complicated LBP, and patients who present with them should undergo additional diagnostic studies to screen for serious underlying conditions (see the Table).
The HPE should ultimately separate patients into three categories to determine the need for imaging (and course of treatment): (1) simple acute back pain, (2) complicated back pain with red flag (ie, a potential underlying systemic disease), and (3) LBP with neurologic deficits potentially requiring surgery.5
Simple acute low back pain
Up to 85% of patients presenting with LBP may never receive a definitive diagnosis due to lack of specific symptoms and ambiguous imaging results.6 Clinicians can assume that LBP in these patients is due to a mechanical cause, by far the most common cause of LBP.7 It is therefore more useful to rule out serious or potentially fatal causes of LBP (complicated LBP) rather than rule in a cause for patients presenting with LBP.
It is generally accepted among practitioners that a thorough HPE alone is sufficient for evaluating most patients presenting with acute LBP lasting less than four weeks.5 Patients presenting without red flags should be assured that improvement of acute LBP is typical, and that no diagnostic intervention is needed unless they do not improve as expected per patient or provider (eg, in terms of activities of daily living or work restrictions). The Figure depicts an appropriate approach to diagnosis and treatment in patients presenting with LBP.8 Clinicians should also offer patient education for self-care and discuss noninvasive treatment options, including pharmacologic and nonpharmacologic therapy.9
Low back pain with red flags (complicated)
Patient history is more useful than the physical exam in screening for spinal malignancies. In one particular combination (age > 50, history of cancer, unexplained weight loss, and failure to improve with conservative therapy), red flag symptoms are 100% sensitive for detecting malignancy.10 However, malignant neoplasms of the spine make up less than 1% of the diagnoses of patients presenting with LBP in primary care.4 Additionally, Deyo and Diehl reviewed five studies of a large series of consecutive spine films with large sample sizes and found the incidence of tumors, infections, and inflammatory spondyloarthropathies together were present in less than 2%.11 This low prevalence underscores the challenge of diagnosing serious pathology of the spine in the primary care setting.
Patients with complicated back pain presenting with red flags should always be examined for an underlying systemic disease. There is one red flag that, seen in isolation, meaningfully increases the likelihood of cancer: a previous history of cancer.4 Otherwise, inflammatory markers (eg, erythrocyte sedimentation rate) can be used to determine the need for advanced imaging (see the Figure).10
Low back pain with neurologic findings (sciatica)
Screening (HPE) for neurologic damage is difficult because traditional findings of neurologic injury (paresis or muscle weakness, impaired reflexes, sensory deficits, and decreased range of motion) all have low sensitivity with higher specificity.12 For this reason, these tests are of limited value as screening tools during the HPE. Specific exams, such as the straight leg raise and crossed straight leg tests, are also of limited value, especially in the primary care setting, because of inconsistent sensitivity and specificity.
This is the primary reason that the HPE in patients with LBP who have neurologic findings must include evaluation for urgent findings (see the Figure). If any red flags are present, advanced imaging is immediately warranted. Otherwise, inflammatory markers and plain radiography may be obtained, and advanced imaging may be considered if the plain radiography and/or inflammatory markers are abnormal.
There is also an approach that advocates the use of advanced imaging in patients with significant functional disability due to their LBP. Two questionnaires, the Oswestry Low Back Pain Disability Index and the Roland-Morris Disability Questionnaire, evaluate subjective data to determine a patient’s functional disability due to LBP.The validity of both tests has been confirmed.13
Continue for diagnostic imaging >>
DIAGNOSTIC IMAGING
The majority of patients presenting with LBP without concerning symptoms can be assumed to have nonspecific mechanical back pain. These patients do not need radiography unless the pain has not improved after four to six weeks of conservative care, because plain radiographs often detect findings (degenerative joint disease, bone spurs, spondylosis) that are unrelated to symptoms.9 Advanced imaging is generally recommended only for LBP patients with red flags due to the potentially critical nature of these cases.5 Patients with LBP presenting with any of these factors require further testing, even if the duration of their pain is less than four weeks.
If a patient’s LBP persists beyond four weeks, the clinician must decide which diagnostic test to order. General medical knowledge suggests that MRI is superior to plain radiography because it shows soft tissue and can detect more concerning abnormalities, such as infections, cancer, and metastatic tumors. CT is better for showing bony abnormalities, but these rarely correlate with a patient’s LBP, and CT subjects patients to levels of radiation that can increase cancer risks.14 Plain radiography in this cohort (LBP > 4 wk) is not generally recommended as it cannot show intervertebral discs or evaluate the degree of spinal stenosis as accurately as MRI. Additionally, these lumbar radiographs expose patients to more than 35 times the radiation delivered in a single chest radiograph.15
COSTS AND PATIENT OUTCOMES
The estimated cost of unnecessary imaging for LBP is $300 million per year.16 There is evidence of a strong association between advanced lumbar spine imaging and increased rates of surgery and significantly higher total medical expenditures.17,18 One study examined patients with nonspecific LBP who either received MRI within 30 days post-onset (defined as “early MRI”) or did not receive MRI. Early-MRI patients had significantly higher total medical expenses ($12,948, P < .0001) than the no-MRI group.17 The early-MRI group also had significantly longer periods of disability and were less likely to go off disability than the no-MRI group (P < .0001).
Cost-effectiveness studies of plain radiographs, dating back to 1982, have yielded similar findings. Liang et al suggested that if radiography was done routinely at the initial visit in patients with acute LBP but no red flags, the cost would be more than $2,000 (in 1982 dollars) to avert one day of pain.19 A more recent study examined patients with acute LBP who received MRI, with one group blinded (both patients and physicians) to their MRI results for six months while the other group received their results within 48 hours.20 All patients underwent a physical exam by a study coordinator, and treatment was assigned prior to imaging. At six weeks and one year, there was no significant difference in treatment assignments or self-reported surveys between groups, indicating that the MRI results had no significant influence on patient outcomes.
Despite the large increase in the use of advanced diagnostic imaging aimed at improving patient care and outcomes, there is a lack of data showing any correlative or causative connection between the two. Given this lack of evidence, and the potentially detrimental radiation exposure and increased costs to patients, clinicians should follow evidence-based guidelines when considering diagnostic imaging in patients presenting with LBP.
Continue for patient perception >>
PATIENT PERCEPTION
Patient satisfaction plays a very important role in health care and may correlate with compliance and other outcomes. One study showed that while radiography in patients with LBP was not associated with improved clinical outcomes, it did increase patients’ satisfaction with the care they received.21 A study that grouped patients requiring imaging for LBP into rapid MRI and plain film radiography cohorts found that patients who received rapid MRI were more assured by their results than were patients in the radiography group (74% vs 58%, P = .002).22 Both groups showed significant clinical improvement in the first three months, but there was no difference between groups at either the three- or 12-month mark. In both groups, reassurance was positively correlated with patient satisfaction (Pearson correlation coefficients, 0.55-0.59, P < .001).
Patients may be reassured by imaging, even when it is unnecessary. Effectively explaining symptomatology during the HPE to patients with LBP should be of high priority to clinicians. A study found that when patients with mechanical LBP did not receive an adequate explanation of the problem, they were less satisfied with their visit and wanted more diagnostic tests.11 Another study found that when low-risk patients were randomly assigned to a control group and received an educational intervention only, they reported equal satisfaction with their care and had clinical outcomes equal to those of the treatment group that received a plain radiograph.11
Given the costs, radiation risks, and other negative aspects of unnecessary imaging, additional diagnostic tests may not be in a patient’s best interest. A careful physical exam should be performed, with the clinician providing ongoing commentary to reassure patients that the clinician is neither dismissing the patient’s symptoms nor inappropriately avoiding further tests.
Often, medical providers order imaging with the intention to reassure patients with the results and thus ultimately increase the patient’s sense of well-being. However, the opposite effect may occur, with patients actually developing a decreased sense of wellness with no alteration of outcomes. A study evaluated general health (GH) scores (based on results from several screening questionnaires that assessed the patient’s current physical and mental health state) in patients receiving MRI results.20 The patients were divided into those who received results (within 48 hours), and those who did not unless it was critical to patient management (blinded group). At six weeks, the blinded group’s GH score was significantly higher than the early-informed group’s GH score. This suggests that receiving MRI results may negatively influence patients’ perception of their general health.20
The same meta-analysis that reviewed patient outcomes also evaluated mental health and quality-of-life scores of LBP patients who received either MRI, CT, or radiography.23 There was no short-term (< 3 mo) or long-term (6-12 mo) difference between patients who received radiography versus advanced imaging. This indicates that using imaging of any kind in patients with LBP but without indications of serious underlying conditions does not improve clinical outcomes and is negatively correlated with quality-of-life measures at short- and long-term intervals.23
Continue for treatment >>
TREATMENT
The prognosis of simple acute mechanical LBP is excellent. Although back pain is a leading reason for visiting health care providers, many affected individuals never seek medical care and apparently improve on their own. In a random telephone survey of North Carolina residents, only 39% of persons with LBP sought medical care.24 Therefore, patients who do seek treatment should be given reassurance, and therapies should be tailored to the individual in the least invasive and most cost-effective manner. Many treatment options are available for LBP, but often strong evidence of benefit is lacking.
Pharmacologic therapy
Anti-inflammatories. It can be assumed that when a patient comes to the practitioner for evaluation of LBP, there is an expectation that some type of medication will be recommended or prescribed for pain relief. Unless there is a contraindication, NSAIDs are often first-line therapy, and they are effective for short-term symptom relief when compared with placebo.25 A mild pain medication, such as acetaminophen, is also a common treatment. The 2007 joint practice guideline from the American Pain Society (APS) and the American College of Physicians (ACP) recommends acetaminophen or NSAIDs as first-line therapy for acute LBP.3 Neither agent—NSAIDs or acetaminophen—has shown superiority, and combining the two has shown no additional benefits.26 Caution must be used, however, as NSAIDs have a risk for gastrointestinal toxicity and nephrotoxicity, and acetaminophen has a dose- and patient-dependent risk for hepatotoxicity.
Muscle relaxants. Muscle relaxants are another pharmacologic treatment option for LBP. Most pain reduction from this class of medication occurs in the first one to two weeks of therapy, although benefit may continue for up to four weeks.27 There is also evidence that a combination of an NSAID and a muscle relaxer has added benefits.27 These medications are centrally acting, so sedation and dizziness are common; all medications in this class have these adverse effects to some degree. Carisoprodol has as its first metabolite meprobamate, which is a tranquilizer used to treat anxiety disorders; it has a potential for abuse and should be used with caution in certain populations.
Opioids. Opioids are commonly prescribed to patients with LBP, though there are limited data regarding efficacy. One trial compared an NSAID alone versus an NSAID plus oxycodone/acetaminophen and found no significant difference in pain or disability after seven days.28 In addition, the adverse effects of opioids, which include sedation, constipation, nausea, and confusion, may be amplified in the elderly population; therefore, opioids should be prescribed with caution in these patients. If prescribed to treat acute LBP, opioids should be used in short, scheduled dosing regimens since NSAIDs or acetaminophen suffice for most patients.
Corticosteroids. Oral glucocorticoids are sometimes given to patients with acute LBP, and they likely are used more frequently in patients with radicular symptoms. However, the APS/ACP 2007 joint guidelines recommend against use of systemic glucocorticoids for acute LBP due to lack of proven benefit.3 Epidural steroid injections are not generally beneficial for isolated acute LBP, but there is evidence that they are helpful with persistent radicular pain.29 Zarghooni and colleagues found significant reductions in pain and use of pain medication after single-shot epidural injections.29
Other pharmacologic therapies, acupuncture, sclerotherapy, and other methods are used to treat back pain, but these are typically reserved for chronic, not acute, LBP.
Nonpharmacologic therapy
Physical therapy. Physical therapy is a commonly prescribed treatment for LBP. Systematic literature reviews indicate that for patients with acute LBP (< 6 wk), there is no difference in the effectiveness of exercise therapy compared to no treatment and care provided by a general practitioner or to manipulations.30 For patients with subacute (6-12 wk) and chronic (≥ 12 wk) LBP, exercise therapy is effective compared to no treatment.30 There is debate, however, over which exercise activities should be used. Research supports strength/resistance and coordination/stabilization exercises.
Most therapists recommend the McKenzie method or spine stabilization exercises.31 The McKenzie method is used for LBP with sciatica; the patient moves through exercises within the prone position and focuses on extension of the spine. Spine stabilization is an active form of exercise based on a “neutral spine” position and helps strengthen muscles to maintain this position (core stabilization). The McKenzie method, when added to first-line care for LBP, does not produce significant improvements in pain or other clinical outcomes, although it may reduce health care utilization.32 Spine stabilization exercises have been shown to decrease pain, disability, and risk for recurrence after a first episode of back pain.33 The apparent success of physical therapy is attributed to compliance with directed home exercise programs, which have been shown to reduce the rate of recurrence, decrease episodes of acute LBP, and decrease the need for health services.34
Spinal traction. Traction or nonsurgical spinal decompression has emerged as a treatment for LBP. Unfortunately, there are little data to support its use as a treatment for acute LBP. Only a few randomized trials showed benefit, and these were small studies with a high risk for bias. A Cochrane review published in 2013 looked at 32 studies involving 2,762 patients with acute, subacute, and chronic LBP.35 The review did not find any evidence that traction alone or in combination with other therapy was any better than placebo treatment.35
Spinal manipulation. Spinal manipulation may be more effective than placebo treatment in reducing pain when the pain has been present for less than six weeks, but it is not more effective in reducing disability.36 There is little or no high-level evidence about spinal manipulation for acute LBP. However, there is some evidence of cost-effectiveness when using spinal manipulation in subacute to chronic pain.37 Chiropractic techniques are considered safe (when performed by a trained provider), but a systematic review found that these techniques provide no clinically relevant improvement in pain or disability when compared to other treatments.38
Bed rest. Bed rest has not been shown to improve outcomes, and in fact patients who had bed rest had less favorable outcomes than those who stayed active.39 Bed rest is less effective at reducing pain and improving function when compared to staying active.39
Continue for recommended management >>
Recommended management
A patient who presents with nonspecific acute LBP should have a thorough HPE to evaluate for the presence of red flags. If no concerning findings are present, the initial visit should focus on patient education based on the following items: (1) good prognosis with little intervention, (2) staying active and avoiding bed rest as much as possible, and (3) avoiding pain-causing movements when possible. The second step is to initiate a trial of an NSAID or acetaminophen and consider a muscle relaxant based on pain severity. Avoid opioid therapy if possible, but use conservative dosing if required for severe pain. Patients should be advised to return in two to four weeks if they do not experience significant improvement. At this time, the clinician may consider referring the patient for physical therapy, changing NSAIDs, ordering inflammatory markers, and/or referring to a specialist.
CONCLUSION
Although no single diagnostic protocol for LBP exists, the clinician must be able to distinguish simple from complex types. A thorough HPE is useful for categorizing the patient’s pain, with diagnostic imaging reserved for those patients with severe or progressive neurologic deficits, suspicion of serious underlying conditions, or LBP lasting more than four weeks without improvement. MRI, if available, is generally preferred over CT because it does not use ionizing radiation and provides better visualization of soft tissue, vertebral marrow, and the spinal cord. Symptomatology should be explained to patients with LBP during the HPE, with ongoing commentary to increase patient satisfaction and compliance. About two-thirds of patients with LBP do not seek evaluation from a health care provider; therefore, those who do seek treatment should be reassured, and therapies tailored to the individual in the least invasive and most cost-effective manner possible.
1. CDC. National Ambulatory Medical Care Survey: 2010 Summary Tables. Table 9. www.cdc.gov/nchs/data/ahcd/namcs_summary/2010_namcs_web_tables.pdf. Accessed March 29, 2016.
2. Davies C, Nitz AJ, Mattacola CG, et al. Practice patterns when treating patients with low back pain: a survey of physical therapists. Physiother Theor Pract. 2014;30(6):399-408.
3. American College of Radiology. ACR Appropriateness Criteria. Low back pain. 2015. www.acr.org/~/media/ACR/Documents/AppCriteria/Diagnostic/LowBackPain.pdf. Accessed March 10, 2016.
4. Henschke N, Maher CG, Ostelo RW, et al. Red flags to screen for malignancy in patients with low back pain. Cochrane Database Syst Rev. 2013;2:CD008686.
5. Koes BW, Tulder M, Lin CW, et al. An updated overview of clinical guidelines for the management of non-specific low back pain in primary care. Eur Spine J. 2010;19(12):2075-2094.
6. Deyo RA, Rainville J, Kent DL. What can the history and physical examination tell us about low back pain? JAMA. 1992;268(6):760-765.
7. Jarvik JG. Diagnostic evaluation of low back pain with emphasis on imaging. Ann Intern Med. 2002;137:586-597.
8. Diagnostic testing for low back pain. In: Post TW (ed), UpToDate, Waltham, MA. www.uptodate.com. Accessed March 16, 2016.
9. Chou R, Qaseem A, Snow V, et al; Clinical Efficacy Assessment Subcommittee of the American College of Physicians; American College of Physicians; American Pain Society Low Back Pain Guidelines Panel. Diagnosis and treatment of low back pain: a joint clinical practice guideline from the American College of Physicians and the American Pain Society. Ann Intern Med. 2007;147(7):478-491.
10. Deyo RA, Diehl AK. Cancer as a cause of back pain: frequency, clinical presentation, and diagnostic strategies. J Gen Intern Med. 1988;3(3):230-238.
11. Deyo RA, Diehl AK. Patient satisfaction with medical care for low-back pain. Spine. 1986;11(1):28-30.
12. Pradeep S, Rainville J, Katz JN, et al. The accuracy of the physical examination for the diagnosis of midlumbar and low lumbar nerve root impingement. Spine. 2011;36(1):63-73.
13. Leclaire R, Blier F, Fortin L, Proulx R. A cross-sectional study comparing the Oswestry and Roland-Morris Functional Disability Scales in two populations of patients with low back pain of different levels of severity. Spine. 1997;22(1):68-71
14. FDA. Radiation emitting products. www.fda.gov/Radiation-EmittingProducts/RadiationEmittingProductsandProcedures/MedicalImaging/MedicalX-Rays/ucm115317.htm. Accessed March 29, 2016.
15. Simpson AK, Whang PG, Jonisch A, et al. The radiation exposure associated with cervical and lumbar spine radiographs. J Spinal Disord Tech. 2008;21(6):409-412.
16. Srinivas S, Deyo R, Berger Z. Application of “less is more” to lower back pain. Arch Intern Med. 2012;172(13):1016-1020.
17. Webster BS, Bauer AZ, Choi Y, et al. Iatrogenic consequences of early magnetic resonance imaging in acute, work-related, disabling back pain. Spine. 2013;38(22):1939-1946.
18. Webster BS, Bauer AZ, Choi Y, et al. The cascade of medical services and associated longitudinal costs due to nonadherent magnetic resonance imaging for low back pain. Spine. 2014;39(17):1433-1440.
19. Liang M, Komaroff AL. Roentgenograms in primary care patients with acute low back pain: a cost-effectiveness analysis. Arch Intern Med. 1982;142(6):1108-1112.
20. Ash LM, Modic MT, Obuchowski NA, et al. Effects of diagnostic information, per se, on patient outcomes in acute radiculopathy and low back pain. AJNR Am J Neuroradiol. 2008;29(6):1098-1103.
21. Kendrick D, Fielding K, Bentley E, et al. Radiography of the lumbar spine in primary care patients with low back pain: randomized controlled trial. BMJ. 2001;322(7283):400-405.
22. Jarvik JG, Hollingworth W, Martin B, et al. Rapid magnetic resonance imaging vs radiographs for patients with low back pain. JAMA. 2003;289(21):2810-2818.
23. Chou R, Fu R, Carrino JA, Deyo RA. Imaging strategies for low-back pain: systematic review and meta-analysis. Lancet. 2009;373(9662):463-472.
24. Carey TS, Evans AT, Hadler NM, et al. Acute severe low back pain: a population-based study of prevalence and care-seeking. Spine. 1996;21(3):339-344.
25. Roelofs PD, Deyo RA, Koes BW, et al. Nonsteroidal anti-inflammatory drugs for low back pain. Spine. 2008;33(16):1766-1774.
26. Hancock MJ, Maher CG, Latimer J, et al. Assessment of diclofenac or spinal manipulative therapy, or both, in addition to recommended first-line treatment for acute low back pain: a randomized controlled trial. Lancet. 2007;370(10):1638-1643.
27. Van Tulder MW, Touray T, Furlan AD, et al. Muscle relaxants for non-specific low-back pain. Cochrane Database Syst Rev. 2003;(4):CD004252.
28. Friedman BW, Dym AA, Davitt M, et al. Naproxen with cyclobenzaprine, oxycodone/acetaminophen, or placebo for treating acute low back pain: a randomized clinical trial. JAMA. 2015;314(15):1572-1580.
29. Zarghooni K, Rashidi A, Siewe, J, et al. Single-shot epidural injections in the management of radicular pain. Orthop Rev (Pavia). 2015;7(4):5985.
30. Smidt N, deVet HC, Bouter LM, et al. Effectiveness of exercise therapy: A best-evidence summary of systematic reviews. Aust J Physiother. 2005;51(2):71-85.
31. Casazza BA. Diagnosis and treatment of acute low back pain. Am Fam Physician. 2012;85(4):343-350.
32. Machado LA, Maher CG, Herbert RD, et al. The effectiveness of the McKenzie method in addition to first-line care for acute low back pain: a randomized controlled trial. BMC Med. 2010;8(10):1-10.
33. Cho I, Jeon C, Lee S, et al. Effects of lumbar stabilization exercise on functional disability and lumbar lordosis angle in patients with chronic low back pain. J Phys Ther Sci. 2015;27(6):1983-1985.
34. Choi BK, Verbeek JH, Tam WW, Jiang JY. Exercises for prevention of recurrences of low-back pain (review). Cochrane Database Syst Rev. 2010;(1):CD006555.
35. Wegner I, Widyahening IS, van Tulder MW, et al. Traction for low-back pain with or without sciatica (review). Cochrane Database Syst Rev. 2013;(8):CD003010.
36. Hoiriis KT, Pfleger B, McDuffie FC, et al. A randomized clinical trial comparing chiropractic adjustments to muscle relaxants for subacute low back pain. J Manipulative Physiol Ther. 2004;27(6):388-398.
37. Lin CC, Haas M, Maher CG, et al. Cost-effectiveness of guideline-endorsed treatments for low back pain: a systematic review. Eur Spine J. 2011;20:1024-1038.
38. Walker BF, French SD, Grant W, Green S. A Cochrane Review of combined chiropractic interventions for low-back pain. Spine. 2011;36(3): 230-242.
39. Dahm KT, Brurberg KG, Jamtvedt G, Hagen KB. Advice to rest in bed versus advice to stay active for acute low-back pain and sciatica. Cochrane Database Syst Rev. 2010;(6):CD007612.
40. Staiger T, Paauw D, Deyo A, Jarvik JG. Imaging studies for acute low back pain. When and when not to order them. Postgrad Med. 1999;105(4):161-162,165-166,171-172.
CE/CME No: CR-1605
PROGRAM OVERVIEW
Earn credit by reading this article and successfully completing the posttest and evaluation. Successful completion is defined as a cumulative score of at least 70% correct.
EDUCATIONAL OBJECTIVES
• Identify "red flag" items in the history and physical exam that make low back pain (LBP) "complicated."
• Stratify patients into three categories: simple back pain, complicated back pain, and back pain with sciatica.
• Discuss when appropriate additional testing/imaging is needed based on LBP categories.
• Discuss patient perceptions and costs associated with imaging and LBP.
• Describe basic treatment options for noncomplicated acute LBP.
FACULTY
Mike Roscoe is the PA Program Director at the University of Evansville, Indiana. Alyssa Nishihira is in her final year of the PA program at Butler University, Indianapolis; after graduation, she will be practicing at Advanced Neurosurgery in Reno, Nevada.
The authors have no financial relationships to disclose.
ACCREDITATION STATEMENT
This program has been reviewed and is approved for a maximum of 1.0 hour of American Academy of Physician Assistants (AAPA) Category 1 CME credit by the Physician Assistant Review Panel. [NPs: Both ANCC and the AANP Certification Program recognize AAPA as an approved provider of Category 1 credit.] Approval is valid for one year from the issue date of May 2016.
Article begins on next page >>
Low back pain (LBP) is one of the most common reasons for an office visit, but most cases—at least 95%—have a benign underlying cause. Evaluation of LBP patients in the primary care setting, therefore, must focus on identifying “red flags” in the history and physical exam that suggest a significant underlying process requiring further work-up, including imaging. This evidence-based approach helps control costs and prevents the detrimental effects of unnecessary testing.
Low back pain (LBP) plagues many Americans and is a common reason for office visits in the United States. In 2010, back symptoms were the principal reason for 1.3% of office visits in the US.1 Recent data suggest that 75% to 85% of all Americans will experience an episode of LBP at least once in their lifetime.2 It is the leading cause of years lived with disability in the US3 and is a common reason for work disability. From a health care system standpoint, LBP imposes a considerable burden, accounting for more than $85 billion annually in direct costs.2
The etiology of LBP can be related to several anatomic and physiologic changes. Potential origins of LBP include, but are not limited to, pathology of the vertebrospinal ligaments, musculature, facet joints, fascia, vertebra and vertebral disks, and the extensive neurovascular components of the lumbar region. Although the potential causes of LBP are many, the majority of patients presenting with acute LBP usually improve with minimal clinical intervention within the first month. This is true even for patients who report limitations in daily activities and those with severe, acute cases of LBP.
A single standard of care for patients presenting with LBP has not been established. The wide array of choices for diagnosis and treatment of LBP is one factor that hinders the development of a standard diagnostic protocol. The challenge to clinicians when diagnosing LBP is to differentiate the patients with benign, self-limiting LBP (simple), who comprise the vast majority of LBP patients, from the 1% to 5% with a serious underlying pathology (complicated).4
Continue for stratification of low back pain >>
STRATIFICATION OF LOW BACK PAIN
Koes and colleagues analyzed 13 different national guidelines and two international guidelines for the management of LBP.5 They found that the guidelines consistently recommend focusing the history and physical exam (HPE) on identifying features suggestive of underlying serious pathology, or “red flags,” and excluding specific diseases.5 They also found that none of the guidelines recommends the routine use of imaging in patients without suspected serious pathology.5 The American College of Radiology simplified this approach to patients with LBP by creating a list of red flags to look for during the HPE.3 The presence of red flags indicates a case of complicated LBP, and patients who present with them should undergo additional diagnostic studies to screen for serious underlying conditions (see the Table).
The HPE should ultimately separate patients into three categories to determine the need for imaging (and course of treatment): (1) simple acute back pain, (2) complicated back pain with red flag (ie, a potential underlying systemic disease), and (3) LBP with neurologic deficits potentially requiring surgery.5
Simple acute low back pain
Up to 85% of patients presenting with LBP may never receive a definitive diagnosis due to lack of specific symptoms and ambiguous imaging results.6 Clinicians can assume that LBP in these patients is due to a mechanical cause, by far the most common cause of LBP.7 It is therefore more useful to rule out serious or potentially fatal causes of LBP (complicated LBP) rather than rule in a cause for patients presenting with LBP.
It is generally accepted among practitioners that a thorough HPE alone is sufficient for evaluating most patients presenting with acute LBP lasting less than four weeks.5 Patients presenting without red flags should be assured that improvement of acute LBP is typical, and that no diagnostic intervention is needed unless they do not improve as expected per patient or provider (eg, in terms of activities of daily living or work restrictions). The Figure depicts an appropriate approach to diagnosis and treatment in patients presenting with LBP.8 Clinicians should also offer patient education for self-care and discuss noninvasive treatment options, including pharmacologic and nonpharmacologic therapy.9
Low back pain with red flags (complicated)
Patient history is more useful than the physical exam in screening for spinal malignancies. In one particular combination (age > 50, history of cancer, unexplained weight loss, and failure to improve with conservative therapy), red flag symptoms are 100% sensitive for detecting malignancy.10 However, malignant neoplasms of the spine make up less than 1% of the diagnoses of patients presenting with LBP in primary care.4 Additionally, Deyo and Diehl reviewed five studies of a large series of consecutive spine films with large sample sizes and found the incidence of tumors, infections, and inflammatory spondyloarthropathies together were present in less than 2%.11 This low prevalence underscores the challenge of diagnosing serious pathology of the spine in the primary care setting.
Patients with complicated back pain presenting with red flags should always be examined for an underlying systemic disease. There is one red flag that, seen in isolation, meaningfully increases the likelihood of cancer: a previous history of cancer.4 Otherwise, inflammatory markers (eg, erythrocyte sedimentation rate) can be used to determine the need for advanced imaging (see the Figure).10
Low back pain with neurologic findings (sciatica)
Screening (HPE) for neurologic damage is difficult because traditional findings of neurologic injury (paresis or muscle weakness, impaired reflexes, sensory deficits, and decreased range of motion) all have low sensitivity with higher specificity.12 For this reason, these tests are of limited value as screening tools during the HPE. Specific exams, such as the straight leg raise and crossed straight leg tests, are also of limited value, especially in the primary care setting, because of inconsistent sensitivity and specificity.
This is the primary reason that the HPE in patients with LBP who have neurologic findings must include evaluation for urgent findings (see the Figure). If any red flags are present, advanced imaging is immediately warranted. Otherwise, inflammatory markers and plain radiography may be obtained, and advanced imaging may be considered if the plain radiography and/or inflammatory markers are abnormal.
There is also an approach that advocates the use of advanced imaging in patients with significant functional disability due to their LBP. Two questionnaires, the Oswestry Low Back Pain Disability Index and the Roland-Morris Disability Questionnaire, evaluate subjective data to determine a patient’s functional disability due to LBP.The validity of both tests has been confirmed.13
Continue for diagnostic imaging >>
DIAGNOSTIC IMAGING
The majority of patients presenting with LBP without concerning symptoms can be assumed to have nonspecific mechanical back pain. These patients do not need radiography unless the pain has not improved after four to six weeks of conservative care, because plain radiographs often detect findings (degenerative joint disease, bone spurs, spondylosis) that are unrelated to symptoms.9 Advanced imaging is generally recommended only for LBP patients with red flags due to the potentially critical nature of these cases.5 Patients with LBP presenting with any of these factors require further testing, even if the duration of their pain is less than four weeks.
If a patient’s LBP persists beyond four weeks, the clinician must decide which diagnostic test to order. General medical knowledge suggests that MRI is superior to plain radiography because it shows soft tissue and can detect more concerning abnormalities, such as infections, cancer, and metastatic tumors. CT is better for showing bony abnormalities, but these rarely correlate with a patient’s LBP, and CT subjects patients to levels of radiation that can increase cancer risks.14 Plain radiography in this cohort (LBP > 4 wk) is not generally recommended as it cannot show intervertebral discs or evaluate the degree of spinal stenosis as accurately as MRI. Additionally, these lumbar radiographs expose patients to more than 35 times the radiation delivered in a single chest radiograph.15
COSTS AND PATIENT OUTCOMES
The estimated cost of unnecessary imaging for LBP is $300 million per year.16 There is evidence of a strong association between advanced lumbar spine imaging and increased rates of surgery and significantly higher total medical expenditures.17,18 One study examined patients with nonspecific LBP who either received MRI within 30 days post-onset (defined as “early MRI”) or did not receive MRI. Early-MRI patients had significantly higher total medical expenses ($12,948, P < .0001) than the no-MRI group.17 The early-MRI group also had significantly longer periods of disability and were less likely to go off disability than the no-MRI group (P < .0001).
Cost-effectiveness studies of plain radiographs, dating back to 1982, have yielded similar findings. Liang et al suggested that if radiography was done routinely at the initial visit in patients with acute LBP but no red flags, the cost would be more than $2,000 (in 1982 dollars) to avert one day of pain.19 A more recent study examined patients with acute LBP who received MRI, with one group blinded (both patients and physicians) to their MRI results for six months while the other group received their results within 48 hours.20 All patients underwent a physical exam by a study coordinator, and treatment was assigned prior to imaging. At six weeks and one year, there was no significant difference in treatment assignments or self-reported surveys between groups, indicating that the MRI results had no significant influence on patient outcomes.
Despite the large increase in the use of advanced diagnostic imaging aimed at improving patient care and outcomes, there is a lack of data showing any correlative or causative connection between the two. Given this lack of evidence, and the potentially detrimental radiation exposure and increased costs to patients, clinicians should follow evidence-based guidelines when considering diagnostic imaging in patients presenting with LBP.
Continue for patient perception >>
PATIENT PERCEPTION
Patient satisfaction plays a very important role in health care and may correlate with compliance and other outcomes. One study showed that while radiography in patients with LBP was not associated with improved clinical outcomes, it did increase patients’ satisfaction with the care they received.21 A study that grouped patients requiring imaging for LBP into rapid MRI and plain film radiography cohorts found that patients who received rapid MRI were more assured by their results than were patients in the radiography group (74% vs 58%, P = .002).22 Both groups showed significant clinical improvement in the first three months, but there was no difference between groups at either the three- or 12-month mark. In both groups, reassurance was positively correlated with patient satisfaction (Pearson correlation coefficients, 0.55-0.59, P < .001).
Patients may be reassured by imaging, even when it is unnecessary. Effectively explaining symptomatology during the HPE to patients with LBP should be of high priority to clinicians. A study found that when patients with mechanical LBP did not receive an adequate explanation of the problem, they were less satisfied with their visit and wanted more diagnostic tests.11 Another study found that when low-risk patients were randomly assigned to a control group and received an educational intervention only, they reported equal satisfaction with their care and had clinical outcomes equal to those of the treatment group that received a plain radiograph.11
Given the costs, radiation risks, and other negative aspects of unnecessary imaging, additional diagnostic tests may not be in a patient’s best interest. A careful physical exam should be performed, with the clinician providing ongoing commentary to reassure patients that the clinician is neither dismissing the patient’s symptoms nor inappropriately avoiding further tests.
Often, medical providers order imaging with the intention to reassure patients with the results and thus ultimately increase the patient’s sense of well-being. However, the opposite effect may occur, with patients actually developing a decreased sense of wellness with no alteration of outcomes. A study evaluated general health (GH) scores (based on results from several screening questionnaires that assessed the patient’s current physical and mental health state) in patients receiving MRI results.20 The patients were divided into those who received results (within 48 hours), and those who did not unless it was critical to patient management (blinded group). At six weeks, the blinded group’s GH score was significantly higher than the early-informed group’s GH score. This suggests that receiving MRI results may negatively influence patients’ perception of their general health.20
The same meta-analysis that reviewed patient outcomes also evaluated mental health and quality-of-life scores of LBP patients who received either MRI, CT, or radiography.23 There was no short-term (< 3 mo) or long-term (6-12 mo) difference between patients who received radiography versus advanced imaging. This indicates that using imaging of any kind in patients with LBP but without indications of serious underlying conditions does not improve clinical outcomes and is negatively correlated with quality-of-life measures at short- and long-term intervals.23
Continue for treatment >>
TREATMENT
The prognosis of simple acute mechanical LBP is excellent. Although back pain is a leading reason for visiting health care providers, many affected individuals never seek medical care and apparently improve on their own. In a random telephone survey of North Carolina residents, only 39% of persons with LBP sought medical care.24 Therefore, patients who do seek treatment should be given reassurance, and therapies should be tailored to the individual in the least invasive and most cost-effective manner. Many treatment options are available for LBP, but often strong evidence of benefit is lacking.
Pharmacologic therapy
Anti-inflammatories. It can be assumed that when a patient comes to the practitioner for evaluation of LBP, there is an expectation that some type of medication will be recommended or prescribed for pain relief. Unless there is a contraindication, NSAIDs are often first-line therapy, and they are effective for short-term symptom relief when compared with placebo.25 A mild pain medication, such as acetaminophen, is also a common treatment. The 2007 joint practice guideline from the American Pain Society (APS) and the American College of Physicians (ACP) recommends acetaminophen or NSAIDs as first-line therapy for acute LBP.3 Neither agent—NSAIDs or acetaminophen—has shown superiority, and combining the two has shown no additional benefits.26 Caution must be used, however, as NSAIDs have a risk for gastrointestinal toxicity and nephrotoxicity, and acetaminophen has a dose- and patient-dependent risk for hepatotoxicity.
Muscle relaxants. Muscle relaxants are another pharmacologic treatment option for LBP. Most pain reduction from this class of medication occurs in the first one to two weeks of therapy, although benefit may continue for up to four weeks.27 There is also evidence that a combination of an NSAID and a muscle relaxer has added benefits.27 These medications are centrally acting, so sedation and dizziness are common; all medications in this class have these adverse effects to some degree. Carisoprodol has as its first metabolite meprobamate, which is a tranquilizer used to treat anxiety disorders; it has a potential for abuse and should be used with caution in certain populations.
Opioids. Opioids are commonly prescribed to patients with LBP, though there are limited data regarding efficacy. One trial compared an NSAID alone versus an NSAID plus oxycodone/acetaminophen and found no significant difference in pain or disability after seven days.28 In addition, the adverse effects of opioids, which include sedation, constipation, nausea, and confusion, may be amplified in the elderly population; therefore, opioids should be prescribed with caution in these patients. If prescribed to treat acute LBP, opioids should be used in short, scheduled dosing regimens since NSAIDs or acetaminophen suffice for most patients.
Corticosteroids. Oral glucocorticoids are sometimes given to patients with acute LBP, and they likely are used more frequently in patients with radicular symptoms. However, the APS/ACP 2007 joint guidelines recommend against use of systemic glucocorticoids for acute LBP due to lack of proven benefit.3 Epidural steroid injections are not generally beneficial for isolated acute LBP, but there is evidence that they are helpful with persistent radicular pain.29 Zarghooni and colleagues found significant reductions in pain and use of pain medication after single-shot epidural injections.29
Other pharmacologic therapies, acupuncture, sclerotherapy, and other methods are used to treat back pain, but these are typically reserved for chronic, not acute, LBP.
Nonpharmacologic therapy
Physical therapy. Physical therapy is a commonly prescribed treatment for LBP. Systematic literature reviews indicate that for patients with acute LBP (< 6 wk), there is no difference in the effectiveness of exercise therapy compared to no treatment and care provided by a general practitioner or to manipulations.30 For patients with subacute (6-12 wk) and chronic (≥ 12 wk) LBP, exercise therapy is effective compared to no treatment.30 There is debate, however, over which exercise activities should be used. Research supports strength/resistance and coordination/stabilization exercises.
Most therapists recommend the McKenzie method or spine stabilization exercises.31 The McKenzie method is used for LBP with sciatica; the patient moves through exercises within the prone position and focuses on extension of the spine. Spine stabilization is an active form of exercise based on a “neutral spine” position and helps strengthen muscles to maintain this position (core stabilization). The McKenzie method, when added to first-line care for LBP, does not produce significant improvements in pain or other clinical outcomes, although it may reduce health care utilization.32 Spine stabilization exercises have been shown to decrease pain, disability, and risk for recurrence after a first episode of back pain.33 The apparent success of physical therapy is attributed to compliance with directed home exercise programs, which have been shown to reduce the rate of recurrence, decrease episodes of acute LBP, and decrease the need for health services.34
Spinal traction. Traction or nonsurgical spinal decompression has emerged as a treatment for LBP. Unfortunately, there are little data to support its use as a treatment for acute LBP. Only a few randomized trials showed benefit, and these were small studies with a high risk for bias. A Cochrane review published in 2013 looked at 32 studies involving 2,762 patients with acute, subacute, and chronic LBP.35 The review did not find any evidence that traction alone or in combination with other therapy was any better than placebo treatment.35
Spinal manipulation. Spinal manipulation may be more effective than placebo treatment in reducing pain when the pain has been present for less than six weeks, but it is not more effective in reducing disability.36 There is little or no high-level evidence about spinal manipulation for acute LBP. However, there is some evidence of cost-effectiveness when using spinal manipulation in subacute to chronic pain.37 Chiropractic techniques are considered safe (when performed by a trained provider), but a systematic review found that these techniques provide no clinically relevant improvement in pain or disability when compared to other treatments.38
Bed rest. Bed rest has not been shown to improve outcomes, and in fact patients who had bed rest had less favorable outcomes than those who stayed active.39 Bed rest is less effective at reducing pain and improving function when compared to staying active.39
Continue for recommended management >>
Recommended management
A patient who presents with nonspecific acute LBP should have a thorough HPE to evaluate for the presence of red flags. If no concerning findings are present, the initial visit should focus on patient education based on the following items: (1) good prognosis with little intervention, (2) staying active and avoiding bed rest as much as possible, and (3) avoiding pain-causing movements when possible. The second step is to initiate a trial of an NSAID or acetaminophen and consider a muscle relaxant based on pain severity. Avoid opioid therapy if possible, but use conservative dosing if required for severe pain. Patients should be advised to return in two to four weeks if they do not experience significant improvement. At this time, the clinician may consider referring the patient for physical therapy, changing NSAIDs, ordering inflammatory markers, and/or referring to a specialist.
CONCLUSION
Although no single diagnostic protocol for LBP exists, the clinician must be able to distinguish simple from complex types. A thorough HPE is useful for categorizing the patient’s pain, with diagnostic imaging reserved for those patients with severe or progressive neurologic deficits, suspicion of serious underlying conditions, or LBP lasting more than four weeks without improvement. MRI, if available, is generally preferred over CT because it does not use ionizing radiation and provides better visualization of soft tissue, vertebral marrow, and the spinal cord. Symptomatology should be explained to patients with LBP during the HPE, with ongoing commentary to increase patient satisfaction and compliance. About two-thirds of patients with LBP do not seek evaluation from a health care provider; therefore, those who do seek treatment should be reassured, and therapies tailored to the individual in the least invasive and most cost-effective manner possible.
CE/CME No: CR-1605
PROGRAM OVERVIEW
Earn credit by reading this article and successfully completing the posttest and evaluation. Successful completion is defined as a cumulative score of at least 70% correct.
EDUCATIONAL OBJECTIVES
• Identify "red flag" items in the history and physical exam that make low back pain (LBP) "complicated."
• Stratify patients into three categories: simple back pain, complicated back pain, and back pain with sciatica.
• Discuss when appropriate additional testing/imaging is needed based on LBP categories.
• Discuss patient perceptions and costs associated with imaging and LBP.
• Describe basic treatment options for noncomplicated acute LBP.
FACULTY
Mike Roscoe is the PA Program Director at the University of Evansville, Indiana. Alyssa Nishihira is in her final year of the PA program at Butler University, Indianapolis; after graduation, she will be practicing at Advanced Neurosurgery in Reno, Nevada.
The authors have no financial relationships to disclose.
ACCREDITATION STATEMENT
This program has been reviewed and is approved for a maximum of 1.0 hour of American Academy of Physician Assistants (AAPA) Category 1 CME credit by the Physician Assistant Review Panel. [NPs: Both ANCC and the AANP Certification Program recognize AAPA as an approved provider of Category 1 credit.] Approval is valid for one year from the issue date of May 2016.
Article begins on next page >>
Low back pain (LBP) is one of the most common reasons for an office visit, but most cases—at least 95%—have a benign underlying cause. Evaluation of LBP patients in the primary care setting, therefore, must focus on identifying “red flags” in the history and physical exam that suggest a significant underlying process requiring further work-up, including imaging. This evidence-based approach helps control costs and prevents the detrimental effects of unnecessary testing.
Low back pain (LBP) plagues many Americans and is a common reason for office visits in the United States. In 2010, back symptoms were the principal reason for 1.3% of office visits in the US.1 Recent data suggest that 75% to 85% of all Americans will experience an episode of LBP at least once in their lifetime.2 It is the leading cause of years lived with disability in the US3 and is a common reason for work disability. From a health care system standpoint, LBP imposes a considerable burden, accounting for more than $85 billion annually in direct costs.2
The etiology of LBP can be related to several anatomic and physiologic changes. Potential origins of LBP include, but are not limited to, pathology of the vertebrospinal ligaments, musculature, facet joints, fascia, vertebra and vertebral disks, and the extensive neurovascular components of the lumbar region. Although the potential causes of LBP are many, the majority of patients presenting with acute LBP usually improve with minimal clinical intervention within the first month. This is true even for patients who report limitations in daily activities and those with severe, acute cases of LBP.
A single standard of care for patients presenting with LBP has not been established. The wide array of choices for diagnosis and treatment of LBP is one factor that hinders the development of a standard diagnostic protocol. The challenge to clinicians when diagnosing LBP is to differentiate the patients with benign, self-limiting LBP (simple), who comprise the vast majority of LBP patients, from the 1% to 5% with a serious underlying pathology (complicated).4
Continue for stratification of low back pain >>
STRATIFICATION OF LOW BACK PAIN
Koes and colleagues analyzed 13 different national guidelines and two international guidelines for the management of LBP.5 They found that the guidelines consistently recommend focusing the history and physical exam (HPE) on identifying features suggestive of underlying serious pathology, or “red flags,” and excluding specific diseases.5 They also found that none of the guidelines recommends the routine use of imaging in patients without suspected serious pathology.5 The American College of Radiology simplified this approach to patients with LBP by creating a list of red flags to look for during the HPE.3 The presence of red flags indicates a case of complicated LBP, and patients who present with them should undergo additional diagnostic studies to screen for serious underlying conditions (see the Table).
The HPE should ultimately separate patients into three categories to determine the need for imaging (and course of treatment): (1) simple acute back pain, (2) complicated back pain with red flag (ie, a potential underlying systemic disease), and (3) LBP with neurologic deficits potentially requiring surgery.5
Simple acute low back pain
Up to 85% of patients presenting with LBP may never receive a definitive diagnosis due to lack of specific symptoms and ambiguous imaging results.6 Clinicians can assume that LBP in these patients is due to a mechanical cause, by far the most common cause of LBP.7 It is therefore more useful to rule out serious or potentially fatal causes of LBP (complicated LBP) rather than rule in a cause for patients presenting with LBP.
It is generally accepted among practitioners that a thorough HPE alone is sufficient for evaluating most patients presenting with acute LBP lasting less than four weeks.5 Patients presenting without red flags should be assured that improvement of acute LBP is typical, and that no diagnostic intervention is needed unless they do not improve as expected per patient or provider (eg, in terms of activities of daily living or work restrictions). The Figure depicts an appropriate approach to diagnosis and treatment in patients presenting with LBP.8 Clinicians should also offer patient education for self-care and discuss noninvasive treatment options, including pharmacologic and nonpharmacologic therapy.9
Low back pain with red flags (complicated)
Patient history is more useful than the physical exam in screening for spinal malignancies. In one particular combination (age > 50, history of cancer, unexplained weight loss, and failure to improve with conservative therapy), red flag symptoms are 100% sensitive for detecting malignancy.10 However, malignant neoplasms of the spine make up less than 1% of the diagnoses of patients presenting with LBP in primary care.4 Additionally, Deyo and Diehl reviewed five studies of a large series of consecutive spine films with large sample sizes and found the incidence of tumors, infections, and inflammatory spondyloarthropathies together were present in less than 2%.11 This low prevalence underscores the challenge of diagnosing serious pathology of the spine in the primary care setting.
Patients with complicated back pain presenting with red flags should always be examined for an underlying systemic disease. There is one red flag that, seen in isolation, meaningfully increases the likelihood of cancer: a previous history of cancer.4 Otherwise, inflammatory markers (eg, erythrocyte sedimentation rate) can be used to determine the need for advanced imaging (see the Figure).10
Low back pain with neurologic findings (sciatica)
Screening (HPE) for neurologic damage is difficult because traditional findings of neurologic injury (paresis or muscle weakness, impaired reflexes, sensory deficits, and decreased range of motion) all have low sensitivity with higher specificity.12 For this reason, these tests are of limited value as screening tools during the HPE. Specific exams, such as the straight leg raise and crossed straight leg tests, are also of limited value, especially in the primary care setting, because of inconsistent sensitivity and specificity.
This is the primary reason that the HPE in patients with LBP who have neurologic findings must include evaluation for urgent findings (see the Figure). If any red flags are present, advanced imaging is immediately warranted. Otherwise, inflammatory markers and plain radiography may be obtained, and advanced imaging may be considered if the plain radiography and/or inflammatory markers are abnormal.
There is also an approach that advocates the use of advanced imaging in patients with significant functional disability due to their LBP. Two questionnaires, the Oswestry Low Back Pain Disability Index and the Roland-Morris Disability Questionnaire, evaluate subjective data to determine a patient’s functional disability due to LBP.The validity of both tests has been confirmed.13
Continue for diagnostic imaging >>
DIAGNOSTIC IMAGING
The majority of patients presenting with LBP without concerning symptoms can be assumed to have nonspecific mechanical back pain. These patients do not need radiography unless the pain has not improved after four to six weeks of conservative care, because plain radiographs often detect findings (degenerative joint disease, bone spurs, spondylosis) that are unrelated to symptoms.9 Advanced imaging is generally recommended only for LBP patients with red flags due to the potentially critical nature of these cases.5 Patients with LBP presenting with any of these factors require further testing, even if the duration of their pain is less than four weeks.
If a patient’s LBP persists beyond four weeks, the clinician must decide which diagnostic test to order. General medical knowledge suggests that MRI is superior to plain radiography because it shows soft tissue and can detect more concerning abnormalities, such as infections, cancer, and metastatic tumors. CT is better for showing bony abnormalities, but these rarely correlate with a patient’s LBP, and CT subjects patients to levels of radiation that can increase cancer risks.14 Plain radiography in this cohort (LBP > 4 wk) is not generally recommended as it cannot show intervertebral discs or evaluate the degree of spinal stenosis as accurately as MRI. Additionally, these lumbar radiographs expose patients to more than 35 times the radiation delivered in a single chest radiograph.15
COSTS AND PATIENT OUTCOMES
The estimated cost of unnecessary imaging for LBP is $300 million per year.16 There is evidence of a strong association between advanced lumbar spine imaging and increased rates of surgery and significantly higher total medical expenditures.17,18 One study examined patients with nonspecific LBP who either received MRI within 30 days post-onset (defined as “early MRI”) or did not receive MRI. Early-MRI patients had significantly higher total medical expenses ($12,948, P < .0001) than the no-MRI group.17 The early-MRI group also had significantly longer periods of disability and were less likely to go off disability than the no-MRI group (P < .0001).
Cost-effectiveness studies of plain radiographs, dating back to 1982, have yielded similar findings. Liang et al suggested that if radiography was done routinely at the initial visit in patients with acute LBP but no red flags, the cost would be more than $2,000 (in 1982 dollars) to avert one day of pain.19 A more recent study examined patients with acute LBP who received MRI, with one group blinded (both patients and physicians) to their MRI results for six months while the other group received their results within 48 hours.20 All patients underwent a physical exam by a study coordinator, and treatment was assigned prior to imaging. At six weeks and one year, there was no significant difference in treatment assignments or self-reported surveys between groups, indicating that the MRI results had no significant influence on patient outcomes.
Despite the large increase in the use of advanced diagnostic imaging aimed at improving patient care and outcomes, there is a lack of data showing any correlative or causative connection between the two. Given this lack of evidence, and the potentially detrimental radiation exposure and increased costs to patients, clinicians should follow evidence-based guidelines when considering diagnostic imaging in patients presenting with LBP.
Continue for patient perception >>
PATIENT PERCEPTION
Patient satisfaction plays a very important role in health care and may correlate with compliance and other outcomes. One study showed that while radiography in patients with LBP was not associated with improved clinical outcomes, it did increase patients’ satisfaction with the care they received.21 A study that grouped patients requiring imaging for LBP into rapid MRI and plain film radiography cohorts found that patients who received rapid MRI were more assured by their results than were patients in the radiography group (74% vs 58%, P = .002).22 Both groups showed significant clinical improvement in the first three months, but there was no difference between groups at either the three- or 12-month mark. In both groups, reassurance was positively correlated with patient satisfaction (Pearson correlation coefficients, 0.55-0.59, P < .001).
Patients may be reassured by imaging, even when it is unnecessary. Effectively explaining symptomatology during the HPE to patients with LBP should be of high priority to clinicians. A study found that when patients with mechanical LBP did not receive an adequate explanation of the problem, they were less satisfied with their visit and wanted more diagnostic tests.11 Another study found that when low-risk patients were randomly assigned to a control group and received an educational intervention only, they reported equal satisfaction with their care and had clinical outcomes equal to those of the treatment group that received a plain radiograph.11
Given the costs, radiation risks, and other negative aspects of unnecessary imaging, additional diagnostic tests may not be in a patient’s best interest. A careful physical exam should be performed, with the clinician providing ongoing commentary to reassure patients that the clinician is neither dismissing the patient’s symptoms nor inappropriately avoiding further tests.
Often, medical providers order imaging with the intention to reassure patients with the results and thus ultimately increase the patient’s sense of well-being. However, the opposite effect may occur, with patients actually developing a decreased sense of wellness with no alteration of outcomes. A study evaluated general health (GH) scores (based on results from several screening questionnaires that assessed the patient’s current physical and mental health state) in patients receiving MRI results.20 The patients were divided into those who received results (within 48 hours), and those who did not unless it was critical to patient management (blinded group). At six weeks, the blinded group’s GH score was significantly higher than the early-informed group’s GH score. This suggests that receiving MRI results may negatively influence patients’ perception of their general health.20
The same meta-analysis that reviewed patient outcomes also evaluated mental health and quality-of-life scores of LBP patients who received either MRI, CT, or radiography.23 There was no short-term (< 3 mo) or long-term (6-12 mo) difference between patients who received radiography versus advanced imaging. This indicates that using imaging of any kind in patients with LBP but without indications of serious underlying conditions does not improve clinical outcomes and is negatively correlated with quality-of-life measures at short- and long-term intervals.23
Continue for treatment >>
TREATMENT
The prognosis of simple acute mechanical LBP is excellent. Although back pain is a leading reason for visiting health care providers, many affected individuals never seek medical care and apparently improve on their own. In a random telephone survey of North Carolina residents, only 39% of persons with LBP sought medical care.24 Therefore, patients who do seek treatment should be given reassurance, and therapies should be tailored to the individual in the least invasive and most cost-effective manner. Many treatment options are available for LBP, but often strong evidence of benefit is lacking.
Pharmacologic therapy
Anti-inflammatories. It can be assumed that when a patient comes to the practitioner for evaluation of LBP, there is an expectation that some type of medication will be recommended or prescribed for pain relief. Unless there is a contraindication, NSAIDs are often first-line therapy, and they are effective for short-term symptom relief when compared with placebo.25 A mild pain medication, such as acetaminophen, is also a common treatment. The 2007 joint practice guideline from the American Pain Society (APS) and the American College of Physicians (ACP) recommends acetaminophen or NSAIDs as first-line therapy for acute LBP.3 Neither agent—NSAIDs or acetaminophen—has shown superiority, and combining the two has shown no additional benefits.26 Caution must be used, however, as NSAIDs have a risk for gastrointestinal toxicity and nephrotoxicity, and acetaminophen has a dose- and patient-dependent risk for hepatotoxicity.
Muscle relaxants. Muscle relaxants are another pharmacologic treatment option for LBP. Most pain reduction from this class of medication occurs in the first one to two weeks of therapy, although benefit may continue for up to four weeks.27 There is also evidence that a combination of an NSAID and a muscle relaxer has added benefits.27 These medications are centrally acting, so sedation and dizziness are common; all medications in this class have these adverse effects to some degree. Carisoprodol has as its first metabolite meprobamate, which is a tranquilizer used to treat anxiety disorders; it has a potential for abuse and should be used with caution in certain populations.
Opioids. Opioids are commonly prescribed to patients with LBP, though there are limited data regarding efficacy. One trial compared an NSAID alone versus an NSAID plus oxycodone/acetaminophen and found no significant difference in pain or disability after seven days.28 In addition, the adverse effects of opioids, which include sedation, constipation, nausea, and confusion, may be amplified in the elderly population; therefore, opioids should be prescribed with caution in these patients. If prescribed to treat acute LBP, opioids should be used in short, scheduled dosing regimens since NSAIDs or acetaminophen suffice for most patients.
Corticosteroids. Oral glucocorticoids are sometimes given to patients with acute LBP, and they likely are used more frequently in patients with radicular symptoms. However, the APS/ACP 2007 joint guidelines recommend against use of systemic glucocorticoids for acute LBP due to lack of proven benefit.3 Epidural steroid injections are not generally beneficial for isolated acute LBP, but there is evidence that they are helpful with persistent radicular pain.29 Zarghooni and colleagues found significant reductions in pain and use of pain medication after single-shot epidural injections.29
Other pharmacologic therapies, acupuncture, sclerotherapy, and other methods are used to treat back pain, but these are typically reserved for chronic, not acute, LBP.
Nonpharmacologic therapy
Physical therapy. Physical therapy is a commonly prescribed treatment for LBP. Systematic literature reviews indicate that for patients with acute LBP (< 6 wk), there is no difference in the effectiveness of exercise therapy compared to no treatment and care provided by a general practitioner or to manipulations.30 For patients with subacute (6-12 wk) and chronic (≥ 12 wk) LBP, exercise therapy is effective compared to no treatment.30 There is debate, however, over which exercise activities should be used. Research supports strength/resistance and coordination/stabilization exercises.
Most therapists recommend the McKenzie method or spine stabilization exercises.31 The McKenzie method is used for LBP with sciatica; the patient moves through exercises within the prone position and focuses on extension of the spine. Spine stabilization is an active form of exercise based on a “neutral spine” position and helps strengthen muscles to maintain this position (core stabilization). The McKenzie method, when added to first-line care for LBP, does not produce significant improvements in pain or other clinical outcomes, although it may reduce health care utilization.32 Spine stabilization exercises have been shown to decrease pain, disability, and risk for recurrence after a first episode of back pain.33 The apparent success of physical therapy is attributed to compliance with directed home exercise programs, which have been shown to reduce the rate of recurrence, decrease episodes of acute LBP, and decrease the need for health services.34
Spinal traction. Traction or nonsurgical spinal decompression has emerged as a treatment for LBP. Unfortunately, there are little data to support its use as a treatment for acute LBP. Only a few randomized trials showed benefit, and these were small studies with a high risk for bias. A Cochrane review published in 2013 looked at 32 studies involving 2,762 patients with acute, subacute, and chronic LBP.35 The review did not find any evidence that traction alone or in combination with other therapy was any better than placebo treatment.35
Spinal manipulation. Spinal manipulation may be more effective than placebo treatment in reducing pain when the pain has been present for less than six weeks, but it is not more effective in reducing disability.36 There is little or no high-level evidence about spinal manipulation for acute LBP. However, there is some evidence of cost-effectiveness when using spinal manipulation in subacute to chronic pain.37 Chiropractic techniques are considered safe (when performed by a trained provider), but a systematic review found that these techniques provide no clinically relevant improvement in pain or disability when compared to other treatments.38
Bed rest. Bed rest has not been shown to improve outcomes, and in fact patients who had bed rest had less favorable outcomes than those who stayed active.39 Bed rest is less effective at reducing pain and improving function when compared to staying active.39
Continue for recommended management >>
Recommended management
A patient who presents with nonspecific acute LBP should have a thorough HPE to evaluate for the presence of red flags. If no concerning findings are present, the initial visit should focus on patient education based on the following items: (1) good prognosis with little intervention, (2) staying active and avoiding bed rest as much as possible, and (3) avoiding pain-causing movements when possible. The second step is to initiate a trial of an NSAID or acetaminophen and consider a muscle relaxant based on pain severity. Avoid opioid therapy if possible, but use conservative dosing if required for severe pain. Patients should be advised to return in two to four weeks if they do not experience significant improvement. At this time, the clinician may consider referring the patient for physical therapy, changing NSAIDs, ordering inflammatory markers, and/or referring to a specialist.
CONCLUSION
Although no single diagnostic protocol for LBP exists, the clinician must be able to distinguish simple from complex types. A thorough HPE is useful for categorizing the patient’s pain, with diagnostic imaging reserved for those patients with severe or progressive neurologic deficits, suspicion of serious underlying conditions, or LBP lasting more than four weeks without improvement. MRI, if available, is generally preferred over CT because it does not use ionizing radiation and provides better visualization of soft tissue, vertebral marrow, and the spinal cord. Symptomatology should be explained to patients with LBP during the HPE, with ongoing commentary to increase patient satisfaction and compliance. About two-thirds of patients with LBP do not seek evaluation from a health care provider; therefore, those who do seek treatment should be reassured, and therapies tailored to the individual in the least invasive and most cost-effective manner possible.
1. CDC. National Ambulatory Medical Care Survey: 2010 Summary Tables. Table 9. www.cdc.gov/nchs/data/ahcd/namcs_summary/2010_namcs_web_tables.pdf. Accessed March 29, 2016.
2. Davies C, Nitz AJ, Mattacola CG, et al. Practice patterns when treating patients with low back pain: a survey of physical therapists. Physiother Theor Pract. 2014;30(6):399-408.
3. American College of Radiology. ACR Appropriateness Criteria. Low back pain. 2015. www.acr.org/~/media/ACR/Documents/AppCriteria/Diagnostic/LowBackPain.pdf. Accessed March 10, 2016.
4. Henschke N, Maher CG, Ostelo RW, et al. Red flags to screen for malignancy in patients with low back pain. Cochrane Database Syst Rev. 2013;2:CD008686.
5. Koes BW, Tulder M, Lin CW, et al. An updated overview of clinical guidelines for the management of non-specific low back pain in primary care. Eur Spine J. 2010;19(12):2075-2094.
6. Deyo RA, Rainville J, Kent DL. What can the history and physical examination tell us about low back pain? JAMA. 1992;268(6):760-765.
7. Jarvik JG. Diagnostic evaluation of low back pain with emphasis on imaging. Ann Intern Med. 2002;137:586-597.
8. Diagnostic testing for low back pain. In: Post TW (ed), UpToDate, Waltham, MA. www.uptodate.com. Accessed March 16, 2016.
9. Chou R, Qaseem A, Snow V, et al; Clinical Efficacy Assessment Subcommittee of the American College of Physicians; American College of Physicians; American Pain Society Low Back Pain Guidelines Panel. Diagnosis and treatment of low back pain: a joint clinical practice guideline from the American College of Physicians and the American Pain Society. Ann Intern Med. 2007;147(7):478-491.
10. Deyo RA, Diehl AK. Cancer as a cause of back pain: frequency, clinical presentation, and diagnostic strategies. J Gen Intern Med. 1988;3(3):230-238.
11. Deyo RA, Diehl AK. Patient satisfaction with medical care for low-back pain. Spine. 1986;11(1):28-30.
12. Pradeep S, Rainville J, Katz JN, et al. The accuracy of the physical examination for the diagnosis of midlumbar and low lumbar nerve root impingement. Spine. 2011;36(1):63-73.
13. Leclaire R, Blier F, Fortin L, Proulx R. A cross-sectional study comparing the Oswestry and Roland-Morris Functional Disability Scales in two populations of patients with low back pain of different levels of severity. Spine. 1997;22(1):68-71
14. FDA. Radiation emitting products. www.fda.gov/Radiation-EmittingProducts/RadiationEmittingProductsandProcedures/MedicalImaging/MedicalX-Rays/ucm115317.htm. Accessed March 29, 2016.
15. Simpson AK, Whang PG, Jonisch A, et al. The radiation exposure associated with cervical and lumbar spine radiographs. J Spinal Disord Tech. 2008;21(6):409-412.
16. Srinivas S, Deyo R, Berger Z. Application of “less is more” to lower back pain. Arch Intern Med. 2012;172(13):1016-1020.
17. Webster BS, Bauer AZ, Choi Y, et al. Iatrogenic consequences of early magnetic resonance imaging in acute, work-related, disabling back pain. Spine. 2013;38(22):1939-1946.
18. Webster BS, Bauer AZ, Choi Y, et al. The cascade of medical services and associated longitudinal costs due to nonadherent magnetic resonance imaging for low back pain. Spine. 2014;39(17):1433-1440.
19. Liang M, Komaroff AL. Roentgenograms in primary care patients with acute low back pain: a cost-effectiveness analysis. Arch Intern Med. 1982;142(6):1108-1112.
20. Ash LM, Modic MT, Obuchowski NA, et al. Effects of diagnostic information, per se, on patient outcomes in acute radiculopathy and low back pain. AJNR Am J Neuroradiol. 2008;29(6):1098-1103.
21. Kendrick D, Fielding K, Bentley E, et al. Radiography of the lumbar spine in primary care patients with low back pain: randomized controlled trial. BMJ. 2001;322(7283):400-405.
22. Jarvik JG, Hollingworth W, Martin B, et al. Rapid magnetic resonance imaging vs radiographs for patients with low back pain. JAMA. 2003;289(21):2810-2818.
23. Chou R, Fu R, Carrino JA, Deyo RA. Imaging strategies for low-back pain: systematic review and meta-analysis. Lancet. 2009;373(9662):463-472.
24. Carey TS, Evans AT, Hadler NM, et al. Acute severe low back pain: a population-based study of prevalence and care-seeking. Spine. 1996;21(3):339-344.
25. Roelofs PD, Deyo RA, Koes BW, et al. Nonsteroidal anti-inflammatory drugs for low back pain. Spine. 2008;33(16):1766-1774.
26. Hancock MJ, Maher CG, Latimer J, et al. Assessment of diclofenac or spinal manipulative therapy, or both, in addition to recommended first-line treatment for acute low back pain: a randomized controlled trial. Lancet. 2007;370(10):1638-1643.
27. Van Tulder MW, Touray T, Furlan AD, et al. Muscle relaxants for non-specific low-back pain. Cochrane Database Syst Rev. 2003;(4):CD004252.
28. Friedman BW, Dym AA, Davitt M, et al. Naproxen with cyclobenzaprine, oxycodone/acetaminophen, or placebo for treating acute low back pain: a randomized clinical trial. JAMA. 2015;314(15):1572-1580.
29. Zarghooni K, Rashidi A, Siewe, J, et al. Single-shot epidural injections in the management of radicular pain. Orthop Rev (Pavia). 2015;7(4):5985.
30. Smidt N, deVet HC, Bouter LM, et al. Effectiveness of exercise therapy: A best-evidence summary of systematic reviews. Aust J Physiother. 2005;51(2):71-85.
31. Casazza BA. Diagnosis and treatment of acute low back pain. Am Fam Physician. 2012;85(4):343-350.
32. Machado LA, Maher CG, Herbert RD, et al. The effectiveness of the McKenzie method in addition to first-line care for acute low back pain: a randomized controlled trial. BMC Med. 2010;8(10):1-10.
33. Cho I, Jeon C, Lee S, et al. Effects of lumbar stabilization exercise on functional disability and lumbar lordosis angle in patients with chronic low back pain. J Phys Ther Sci. 2015;27(6):1983-1985.
34. Choi BK, Verbeek JH, Tam WW, Jiang JY. Exercises for prevention of recurrences of low-back pain (review). Cochrane Database Syst Rev. 2010;(1):CD006555.
35. Wegner I, Widyahening IS, van Tulder MW, et al. Traction for low-back pain with or without sciatica (review). Cochrane Database Syst Rev. 2013;(8):CD003010.
36. Hoiriis KT, Pfleger B, McDuffie FC, et al. A randomized clinical trial comparing chiropractic adjustments to muscle relaxants for subacute low back pain. J Manipulative Physiol Ther. 2004;27(6):388-398.
37. Lin CC, Haas M, Maher CG, et al. Cost-effectiveness of guideline-endorsed treatments for low back pain: a systematic review. Eur Spine J. 2011;20:1024-1038.
38. Walker BF, French SD, Grant W, Green S. A Cochrane Review of combined chiropractic interventions for low-back pain. Spine. 2011;36(3): 230-242.
39. Dahm KT, Brurberg KG, Jamtvedt G, Hagen KB. Advice to rest in bed versus advice to stay active for acute low-back pain and sciatica. Cochrane Database Syst Rev. 2010;(6):CD007612.
40. Staiger T, Paauw D, Deyo A, Jarvik JG. Imaging studies for acute low back pain. When and when not to order them. Postgrad Med. 1999;105(4):161-162,165-166,171-172.
1. CDC. National Ambulatory Medical Care Survey: 2010 Summary Tables. Table 9. www.cdc.gov/nchs/data/ahcd/namcs_summary/2010_namcs_web_tables.pdf. Accessed March 29, 2016.
2. Davies C, Nitz AJ, Mattacola CG, et al. Practice patterns when treating patients with low back pain: a survey of physical therapists. Physiother Theor Pract. 2014;30(6):399-408.
3. American College of Radiology. ACR Appropriateness Criteria. Low back pain. 2015. www.acr.org/~/media/ACR/Documents/AppCriteria/Diagnostic/LowBackPain.pdf. Accessed March 10, 2016.
4. Henschke N, Maher CG, Ostelo RW, et al. Red flags to screen for malignancy in patients with low back pain. Cochrane Database Syst Rev. 2013;2:CD008686.
5. Koes BW, Tulder M, Lin CW, et al. An updated overview of clinical guidelines for the management of non-specific low back pain in primary care. Eur Spine J. 2010;19(12):2075-2094.
6. Deyo RA, Rainville J, Kent DL. What can the history and physical examination tell us about low back pain? JAMA. 1992;268(6):760-765.
7. Jarvik JG. Diagnostic evaluation of low back pain with emphasis on imaging. Ann Intern Med. 2002;137:586-597.
8. Diagnostic testing for low back pain. In: Post TW (ed), UpToDate, Waltham, MA. www.uptodate.com. Accessed March 16, 2016.
9. Chou R, Qaseem A, Snow V, et al; Clinical Efficacy Assessment Subcommittee of the American College of Physicians; American College of Physicians; American Pain Society Low Back Pain Guidelines Panel. Diagnosis and treatment of low back pain: a joint clinical practice guideline from the American College of Physicians and the American Pain Society. Ann Intern Med. 2007;147(7):478-491.
10. Deyo RA, Diehl AK. Cancer as a cause of back pain: frequency, clinical presentation, and diagnostic strategies. J Gen Intern Med. 1988;3(3):230-238.
11. Deyo RA, Diehl AK. Patient satisfaction with medical care for low-back pain. Spine. 1986;11(1):28-30.
12. Pradeep S, Rainville J, Katz JN, et al. The accuracy of the physical examination for the diagnosis of midlumbar and low lumbar nerve root impingement. Spine. 2011;36(1):63-73.
13. Leclaire R, Blier F, Fortin L, Proulx R. A cross-sectional study comparing the Oswestry and Roland-Morris Functional Disability Scales in two populations of patients with low back pain of different levels of severity. Spine. 1997;22(1):68-71
14. FDA. Radiation emitting products. www.fda.gov/Radiation-EmittingProducts/RadiationEmittingProductsandProcedures/MedicalImaging/MedicalX-Rays/ucm115317.htm. Accessed March 29, 2016.
15. Simpson AK, Whang PG, Jonisch A, et al. The radiation exposure associated with cervical and lumbar spine radiographs. J Spinal Disord Tech. 2008;21(6):409-412.
16. Srinivas S, Deyo R, Berger Z. Application of “less is more” to lower back pain. Arch Intern Med. 2012;172(13):1016-1020.
17. Webster BS, Bauer AZ, Choi Y, et al. Iatrogenic consequences of early magnetic resonance imaging in acute, work-related, disabling back pain. Spine. 2013;38(22):1939-1946.
18. Webster BS, Bauer AZ, Choi Y, et al. The cascade of medical services and associated longitudinal costs due to nonadherent magnetic resonance imaging for low back pain. Spine. 2014;39(17):1433-1440.
19. Liang M, Komaroff AL. Roentgenograms in primary care patients with acute low back pain: a cost-effectiveness analysis. Arch Intern Med. 1982;142(6):1108-1112.
20. Ash LM, Modic MT, Obuchowski NA, et al. Effects of diagnostic information, per se, on patient outcomes in acute radiculopathy and low back pain. AJNR Am J Neuroradiol. 2008;29(6):1098-1103.
21. Kendrick D, Fielding K, Bentley E, et al. Radiography of the lumbar spine in primary care patients with low back pain: randomized controlled trial. BMJ. 2001;322(7283):400-405.
22. Jarvik JG, Hollingworth W, Martin B, et al. Rapid magnetic resonance imaging vs radiographs for patients with low back pain. JAMA. 2003;289(21):2810-2818.
23. Chou R, Fu R, Carrino JA, Deyo RA. Imaging strategies for low-back pain: systematic review and meta-analysis. Lancet. 2009;373(9662):463-472.
24. Carey TS, Evans AT, Hadler NM, et al. Acute severe low back pain: a population-based study of prevalence and care-seeking. Spine. 1996;21(3):339-344.
25. Roelofs PD, Deyo RA, Koes BW, et al. Nonsteroidal anti-inflammatory drugs for low back pain. Spine. 2008;33(16):1766-1774.
26. Hancock MJ, Maher CG, Latimer J, et al. Assessment of diclofenac or spinal manipulative therapy, or both, in addition to recommended first-line treatment for acute low back pain: a randomized controlled trial. Lancet. 2007;370(10):1638-1643.
27. Van Tulder MW, Touray T, Furlan AD, et al. Muscle relaxants for non-specific low-back pain. Cochrane Database Syst Rev. 2003;(4):CD004252.
28. Friedman BW, Dym AA, Davitt M, et al. Naproxen with cyclobenzaprine, oxycodone/acetaminophen, or placebo for treating acute low back pain: a randomized clinical trial. JAMA. 2015;314(15):1572-1580.
29. Zarghooni K, Rashidi A, Siewe, J, et al. Single-shot epidural injections in the management of radicular pain. Orthop Rev (Pavia). 2015;7(4):5985.
30. Smidt N, deVet HC, Bouter LM, et al. Effectiveness of exercise therapy: A best-evidence summary of systematic reviews. Aust J Physiother. 2005;51(2):71-85.
31. Casazza BA. Diagnosis and treatment of acute low back pain. Am Fam Physician. 2012;85(4):343-350.
32. Machado LA, Maher CG, Herbert RD, et al. The effectiveness of the McKenzie method in addition to first-line care for acute low back pain: a randomized controlled trial. BMC Med. 2010;8(10):1-10.
33. Cho I, Jeon C, Lee S, et al. Effects of lumbar stabilization exercise on functional disability and lumbar lordosis angle in patients with chronic low back pain. J Phys Ther Sci. 2015;27(6):1983-1985.
34. Choi BK, Verbeek JH, Tam WW, Jiang JY. Exercises for prevention of recurrences of low-back pain (review). Cochrane Database Syst Rev. 2010;(1):CD006555.
35. Wegner I, Widyahening IS, van Tulder MW, et al. Traction for low-back pain with or without sciatica (review). Cochrane Database Syst Rev. 2013;(8):CD003010.
36. Hoiriis KT, Pfleger B, McDuffie FC, et al. A randomized clinical trial comparing chiropractic adjustments to muscle relaxants for subacute low back pain. J Manipulative Physiol Ther. 2004;27(6):388-398.
37. Lin CC, Haas M, Maher CG, et al. Cost-effectiveness of guideline-endorsed treatments for low back pain: a systematic review. Eur Spine J. 2011;20:1024-1038.
38. Walker BF, French SD, Grant W, Green S. A Cochrane Review of combined chiropractic interventions for low-back pain. Spine. 2011;36(3): 230-242.
39. Dahm KT, Brurberg KG, Jamtvedt G, Hagen KB. Advice to rest in bed versus advice to stay active for acute low-back pain and sciatica. Cochrane Database Syst Rev. 2010;(6):CD007612.
40. Staiger T, Paauw D, Deyo A, Jarvik JG. Imaging studies for acute low back pain. When and when not to order them. Postgrad Med. 1999;105(4):161-162,165-166,171-172.
Editorial Board Biographies
Thomas M. DeBerardino, MD
Associate Editor for Sports Medicine
Dr. DeBerardino is an orthopedic surgeon specializing in sports medicine and arthroscopic surgery of the knee, hip, and shoulder; and team physician for the University of Connecticut athletic teams, including football and the men’s and women’s basketball programs. He attended the United States Military Academy, West Point as an undergraduate, completed medical school at the New York Medical College, and completed his residency at Tripler Army Medical Center. He also completed a John A. Feagin, Jr, Sports Medicine Fellowship at Keller Army Hospital, West Point. Previously he was head team physician for the collegiate athletic teams at the United States Military Academy, and Director of the Sports Medicine Fellowship. He is a member of many professional societies, including the American Orthopaedic Society for Sports Medicine (AOSSM), the International ACL Study Group, and the Herodicus Society.
Patrick J. Denard, MD
Associate Editor for Shoulder
Dr. Denard is a shoulder specialist at Southern Oregon Orthopedics in Medford, OR and a clinical instructor at Oregon Health & Science University. He attended college at the University of Puget Sound. He obtained his medical degree at Dartmouth College in New Hampshire. He completed his orthopedic residency training at Oregon Health & Science University, where he received the research award as a chief resident. After residency, he completed specialized fellowship training in shoulder arthroscopy in San Antonio, TX under Dr. Stephen Burkhart. Dr. Denard completed a fellowship in shoulder replacement surgery in Lyon, France under Dr. Gilles Walch, one of the developers of the current prosthesis used in reverse shoulder replacement. He has co-authored a textbook on the shoulder, and contributed to 15 book chapters and over 60 research papers. He was recently elected to the American Shoulder and Elbow Surgeons (ASES).
Anand M. Murthi, MD
Associate Editor for Shoulder
Dr. Murthi is attending orthopedic surgeon; chief, shoulder and elbow service; and fellowship director at MedStar Union Memorial Hospital in Baltimore, MD. He received his undergraduate degree in Chemistry and Psychology and his doctorate degree from Case Western Reserve University. He completed an internship in general surgery, residency in orthopedic surgery, and was a chief resident in orthopedic surgery at George Washington University Medical Center. He also completed a fellowship in shoulder and elbow surgery at Columbia-Presbyterian Medical Center. He is a member of numerous societies, including the American Academy of Orthopaedic Surgeons (AAOS), American Medical Association (AMA), and American Shoulder and Elbow Surgeons (ASES).
Jose B. Toro, MD
Associate Editor for Trauma
Dr. Toro is director for orthopaedic trauma at Peconic Bay Medical Center. He obtained his medical degree from Pontifical Xavier University in Bogota, Colombia, where he also trained in the specialty of orthopedic surgery. Dr. Toro started his fellowship training at the Hospital for Special Surgery, where he completed a fellowship in orthopedic traumatology under the tutelage of Dr. David L. Helfet and a fellowship in metabolic bone disease under the supervision of Dr. Joseph Lane. Dr. Toro started his professional career as an attending orthopaedic surgeon at the Veterans Affairs administration of the James J. Peters Bronx VA Medical Center. He also has served as director of orthopaedic trauma and assistant professor in orthopaedic surgery at the Albert Einstein College of Medicine, Jacobi Medical Center, Bronx, New York.
Thomas M. DeBerardino, MD
Associate Editor for Sports Medicine
Dr. DeBerardino is an orthopedic surgeon specializing in sports medicine and arthroscopic surgery of the knee, hip, and shoulder; and team physician for the University of Connecticut athletic teams, including football and the men’s and women’s basketball programs. He attended the United States Military Academy, West Point as an undergraduate, completed medical school at the New York Medical College, and completed his residency at Tripler Army Medical Center. He also completed a John A. Feagin, Jr, Sports Medicine Fellowship at Keller Army Hospital, West Point. Previously he was head team physician for the collegiate athletic teams at the United States Military Academy, and Director of the Sports Medicine Fellowship. He is a member of many professional societies, including the American Orthopaedic Society for Sports Medicine (AOSSM), the International ACL Study Group, and the Herodicus Society.
Patrick J. Denard, MD
Associate Editor for Shoulder
Dr. Denard is a shoulder specialist at Southern Oregon Orthopedics in Medford, OR and a clinical instructor at Oregon Health & Science University. He attended college at the University of Puget Sound. He obtained his medical degree at Dartmouth College in New Hampshire. He completed his orthopedic residency training at Oregon Health & Science University, where he received the research award as a chief resident. After residency, he completed specialized fellowship training in shoulder arthroscopy in San Antonio, TX under Dr. Stephen Burkhart. Dr. Denard completed a fellowship in shoulder replacement surgery in Lyon, France under Dr. Gilles Walch, one of the developers of the current prosthesis used in reverse shoulder replacement. He has co-authored a textbook on the shoulder, and contributed to 15 book chapters and over 60 research papers. He was recently elected to the American Shoulder and Elbow Surgeons (ASES).
Anand M. Murthi, MD
Associate Editor for Shoulder
Dr. Murthi is attending orthopedic surgeon; chief, shoulder and elbow service; and fellowship director at MedStar Union Memorial Hospital in Baltimore, MD. He received his undergraduate degree in Chemistry and Psychology and his doctorate degree from Case Western Reserve University. He completed an internship in general surgery, residency in orthopedic surgery, and was a chief resident in orthopedic surgery at George Washington University Medical Center. He also completed a fellowship in shoulder and elbow surgery at Columbia-Presbyterian Medical Center. He is a member of numerous societies, including the American Academy of Orthopaedic Surgeons (AAOS), American Medical Association (AMA), and American Shoulder and Elbow Surgeons (ASES).
Jose B. Toro, MD
Associate Editor for Trauma
Dr. Toro is director for orthopaedic trauma at Peconic Bay Medical Center. He obtained his medical degree from Pontifical Xavier University in Bogota, Colombia, where he also trained in the specialty of orthopedic surgery. Dr. Toro started his fellowship training at the Hospital for Special Surgery, where he completed a fellowship in orthopedic traumatology under the tutelage of Dr. David L. Helfet and a fellowship in metabolic bone disease under the supervision of Dr. Joseph Lane. Dr. Toro started his professional career as an attending orthopaedic surgeon at the Veterans Affairs administration of the James J. Peters Bronx VA Medical Center. He also has served as director of orthopaedic trauma and assistant professor in orthopaedic surgery at the Albert Einstein College of Medicine, Jacobi Medical Center, Bronx, New York.
Thomas M. DeBerardino, MD
Associate Editor for Sports Medicine
Dr. DeBerardino is an orthopedic surgeon specializing in sports medicine and arthroscopic surgery of the knee, hip, and shoulder; and team physician for the University of Connecticut athletic teams, including football and the men’s and women’s basketball programs. He attended the United States Military Academy, West Point as an undergraduate, completed medical school at the New York Medical College, and completed his residency at Tripler Army Medical Center. He also completed a John A. Feagin, Jr, Sports Medicine Fellowship at Keller Army Hospital, West Point. Previously he was head team physician for the collegiate athletic teams at the United States Military Academy, and Director of the Sports Medicine Fellowship. He is a member of many professional societies, including the American Orthopaedic Society for Sports Medicine (AOSSM), the International ACL Study Group, and the Herodicus Society.
Patrick J. Denard, MD
Associate Editor for Shoulder
Dr. Denard is a shoulder specialist at Southern Oregon Orthopedics in Medford, OR and a clinical instructor at Oregon Health & Science University. He attended college at the University of Puget Sound. He obtained his medical degree at Dartmouth College in New Hampshire. He completed his orthopedic residency training at Oregon Health & Science University, where he received the research award as a chief resident. After residency, he completed specialized fellowship training in shoulder arthroscopy in San Antonio, TX under Dr. Stephen Burkhart. Dr. Denard completed a fellowship in shoulder replacement surgery in Lyon, France under Dr. Gilles Walch, one of the developers of the current prosthesis used in reverse shoulder replacement. He has co-authored a textbook on the shoulder, and contributed to 15 book chapters and over 60 research papers. He was recently elected to the American Shoulder and Elbow Surgeons (ASES).
Anand M. Murthi, MD
Associate Editor for Shoulder
Dr. Murthi is attending orthopedic surgeon; chief, shoulder and elbow service; and fellowship director at MedStar Union Memorial Hospital in Baltimore, MD. He received his undergraduate degree in Chemistry and Psychology and his doctorate degree from Case Western Reserve University. He completed an internship in general surgery, residency in orthopedic surgery, and was a chief resident in orthopedic surgery at George Washington University Medical Center. He also completed a fellowship in shoulder and elbow surgery at Columbia-Presbyterian Medical Center. He is a member of numerous societies, including the American Academy of Orthopaedic Surgeons (AAOS), American Medical Association (AMA), and American Shoulder and Elbow Surgeons (ASES).
Jose B. Toro, MD
Associate Editor for Trauma
Dr. Toro is director for orthopaedic trauma at Peconic Bay Medical Center. He obtained his medical degree from Pontifical Xavier University in Bogota, Colombia, where he also trained in the specialty of orthopedic surgery. Dr. Toro started his fellowship training at the Hospital for Special Surgery, where he completed a fellowship in orthopedic traumatology under the tutelage of Dr. David L. Helfet and a fellowship in metabolic bone disease under the supervision of Dr. Joseph Lane. Dr. Toro started his professional career as an attending orthopaedic surgeon at the Veterans Affairs administration of the James J. Peters Bronx VA Medical Center. He also has served as director of orthopaedic trauma and assistant professor in orthopaedic surgery at the Albert Einstein College of Medicine, Jacobi Medical Center, Bronx, New York.
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Gryphon® Suture Anchor with Proknot™ Technology
Paul Favorito, MD, Wellington Orthopaedic and Sports Medicine, Cincinnati, OH
The Gryphon® suture anchor with Proknot™ technology is a doubled No. 1 Permacord® high-strength orthopedic suture with a proprietary pre-tied sliding knot. The suture construct is loaded onto a 3.0-mm Gryphonsuture anchor (Peek or Biocryl Rapide® biocomposite material) and has clinical indications for labral repair of the shoulder and hip. In a laboratory setting, Proknot technology has been tested against other high-tensile sutures and commonly tied arthroscopic knots.1 Proknot technology demonstrated higher ultimate strength, significantly less knot volume, and better reproducibility among surgeons.
Surgical pearl: I use the Gryphon Proknot suture anchor for all shoulder Bankart and superior labral anterior to posterior (SLAP) repairs. I have colleagues who also use this anchor for hip arthroscopy.
Once opened on the back table, the surgical assistant may ink the free limb of suture for easy arthroscopic identification. The anchor is placed and, in the case of hard bone frequently encountered in younger patients, a 2.5-mm drill bit may be substituted for the usual 2.4-mm. One important goal of any labral repair is to position knots away from the articular surface. The free suture limb is passed through the labrum, retrieved, and delivered through the open, pre-tied knot on the suture card.
Once the knot is released and dressed, the knot pusher is placed over the suture and the knot is advanced and preliminarily tensioned medial to the articular surface. The suture limbs are separated and one limb of the suture is removed from the knot pusher. As few as 1, or up to 3, half hitches may be placed to secure the knot, taking care to direct it away from the joint surface. The result is a strong but well-positioned knot with minimal mass securing the soft tissue.
1. Rodes SA, Favorito PJ, Piccirillo JM, Spivey JT. Performance comparison of a prettied suture knot with three conventional arthroscopic knots. Arthroscopy. 2015;31(11):2183-2190.
DePuy Synthes Mitek Sports Medicine
(https://www.depuysynthes.com/hcp/mitek-sports-medicine)
Gryphon® Suture Anchor with Proknot™ Technology
Paul Favorito, MD, Wellington Orthopaedic and Sports Medicine, Cincinnati, OH
The Gryphon® suture anchor with Proknot™ technology is a doubled No. 1 Permacord® high-strength orthopedic suture with a proprietary pre-tied sliding knot. The suture construct is loaded onto a 3.0-mm Gryphonsuture anchor (Peek or Biocryl Rapide® biocomposite material) and has clinical indications for labral repair of the shoulder and hip. In a laboratory setting, Proknot technology has been tested against other high-tensile sutures and commonly tied arthroscopic knots.1 Proknot technology demonstrated higher ultimate strength, significantly less knot volume, and better reproducibility among surgeons.
Surgical pearl: I use the Gryphon Proknot suture anchor for all shoulder Bankart and superior labral anterior to posterior (SLAP) repairs. I have colleagues who also use this anchor for hip arthroscopy.
Once opened on the back table, the surgical assistant may ink the free limb of suture for easy arthroscopic identification. The anchor is placed and, in the case of hard bone frequently encountered in younger patients, a 2.5-mm drill bit may be substituted for the usual 2.4-mm. One important goal of any labral repair is to position knots away from the articular surface. The free suture limb is passed through the labrum, retrieved, and delivered through the open, pre-tied knot on the suture card.
Once the knot is released and dressed, the knot pusher is placed over the suture and the knot is advanced and preliminarily tensioned medial to the articular surface. The suture limbs are separated and one limb of the suture is removed from the knot pusher. As few as 1, or up to 3, half hitches may be placed to secure the knot, taking care to direct it away from the joint surface. The result is a strong but well-positioned knot with minimal mass securing the soft tissue.
DePuy Synthes Mitek Sports Medicine
(https://www.depuysynthes.com/hcp/mitek-sports-medicine)
Gryphon® Suture Anchor with Proknot™ Technology
Paul Favorito, MD, Wellington Orthopaedic and Sports Medicine, Cincinnati, OH
The Gryphon® suture anchor with Proknot™ technology is a doubled No. 1 Permacord® high-strength orthopedic suture with a proprietary pre-tied sliding knot. The suture construct is loaded onto a 3.0-mm Gryphonsuture anchor (Peek or Biocryl Rapide® biocomposite material) and has clinical indications for labral repair of the shoulder and hip. In a laboratory setting, Proknot technology has been tested against other high-tensile sutures and commonly tied arthroscopic knots.1 Proknot technology demonstrated higher ultimate strength, significantly less knot volume, and better reproducibility among surgeons.
Surgical pearl: I use the Gryphon Proknot suture anchor for all shoulder Bankart and superior labral anterior to posterior (SLAP) repairs. I have colleagues who also use this anchor for hip arthroscopy.
Once opened on the back table, the surgical assistant may ink the free limb of suture for easy arthroscopic identification. The anchor is placed and, in the case of hard bone frequently encountered in younger patients, a 2.5-mm drill bit may be substituted for the usual 2.4-mm. One important goal of any labral repair is to position knots away from the articular surface. The free suture limb is passed through the labrum, retrieved, and delivered through the open, pre-tied knot on the suture card.
Once the knot is released and dressed, the knot pusher is placed over the suture and the knot is advanced and preliminarily tensioned medial to the articular surface. The suture limbs are separated and one limb of the suture is removed from the knot pusher. As few as 1, or up to 3, half hitches may be placed to secure the knot, taking care to direct it away from the joint surface. The result is a strong but well-positioned knot with minimal mass securing the soft tissue.
1. Rodes SA, Favorito PJ, Piccirillo JM, Spivey JT. Performance comparison of a prettied suture knot with three conventional arthroscopic knots. Arthroscopy. 2015;31(11):2183-2190.
1. Rodes SA, Favorito PJ, Piccirillo JM, Spivey JT. Performance comparison of a prettied suture knot with three conventional arthroscopic knots. Arthroscopy. 2015;31(11):2183-2190.
ASCR Restores Stability in Patients with Large Rotator Cuff Tears
ORLANDO, FL—Using arthroscopic superior capsule reconstruction (ASCR) to treat patients with massive rotator cuff tears can improve shoulder strength and function, according to research presented at the American Orthopedic Society for Sports Medicine’s Specialty Day.
Researchers used ASCR to treat 100 patients (average age: 66) who had irreparable rotator cuff tears that failed during previous treatment. Physical exams, x-rays, and magnetic resonance imaging were performed before surgery, at 3, 6 and 12 months following surgery, and on a yearly basis thereafter. Rates of return to work or sport were analyzed in 34 patients who were employed and 26 patients who were recreational athletes before the rotator cuff tear.
Overall, 92% of patients significantly improved their strength and shoulder function. In all, 32 patients returned fully to their previous work and 2 patients returned with reduced hours and workloads. All 26 patients who played sports prior to injury fully returned to their activities.
ORLANDO, FL—Using arthroscopic superior capsule reconstruction (ASCR) to treat patients with massive rotator cuff tears can improve shoulder strength and function, according to research presented at the American Orthopedic Society for Sports Medicine’s Specialty Day.
Researchers used ASCR to treat 100 patients (average age: 66) who had irreparable rotator cuff tears that failed during previous treatment. Physical exams, x-rays, and magnetic resonance imaging were performed before surgery, at 3, 6 and 12 months following surgery, and on a yearly basis thereafter. Rates of return to work or sport were analyzed in 34 patients who were employed and 26 patients who were recreational athletes before the rotator cuff tear.
Overall, 92% of patients significantly improved their strength and shoulder function. In all, 32 patients returned fully to their previous work and 2 patients returned with reduced hours and workloads. All 26 patients who played sports prior to injury fully returned to their activities.
ORLANDO, FL—Using arthroscopic superior capsule reconstruction (ASCR) to treat patients with massive rotator cuff tears can improve shoulder strength and function, according to research presented at the American Orthopedic Society for Sports Medicine’s Specialty Day.
Researchers used ASCR to treat 100 patients (average age: 66) who had irreparable rotator cuff tears that failed during previous treatment. Physical exams, x-rays, and magnetic resonance imaging were performed before surgery, at 3, 6 and 12 months following surgery, and on a yearly basis thereafter. Rates of return to work or sport were analyzed in 34 patients who were employed and 26 patients who were recreational athletes before the rotator cuff tear.
Overall, 92% of patients significantly improved their strength and shoulder function. In all, 32 patients returned fully to their previous work and 2 patients returned with reduced hours and workloads. All 26 patients who played sports prior to injury fully returned to their activities.
A Guide to Ultrasound of the Shoulder, Part 2: The Diagnostic Evaluation
The musculoskeletal (MSK) ultrasound evaluation of the shoulder provides a cost- and time-efficient imaging modality with similar diagnostic power as magnetic resonance imaging (MRI).1,2 Its portable point-of-care applications can be used in the office, in the operating room, and in sideline athletic event coverage, as we discussed in Part 1 of this series.3
MSK ultrasound may seem difficult and daunting, and many articles have quoted steep learning curves.4,5 However, in our experience in teaching many ultrasound courses, this modality can be learned quite quickly with the proper instruction. Physicians are already familiar with anatomy and usually have had some exposure to MRI.4 Taking courses in MSK ultrasound or simply learning the basic concepts of ultrasound and then learning the machine controls is usually a good start.5-8 Practice scanning normal individuals, comparing the images from an MRI to learn how to reproduce the same planes and images. This will allow the user to become familiar with normal anatomy and how to see the images on the ultrasound screen.5-8 Vollman and colleagues9 showed that in trainees, combining MRI images with sonograms enhances the ability to correctly identify MSK ultrasound anatomy from 40.9% to 72.5%, when compared with learning from ultrasound images alone.
There are currently no certifications necessary to perform ultrasound scans or bill for them; however, some insurance carriers may require demonstrating relevant, documented training for reimbursement.3 Various organizations are trying to develop certifications and regulations for ultrasound to standardize the use of this modality. In the United States, the American Institute of Ultrasound in Medicine (AIUM) and the American Registry for Diagnostic Medical Sonography (ARDMS) provide guidelines and particular MSK ultrasound certifications.10,11
Basic Ultrasound Principles
The ultrasound machine creates electrical impulses that are turned into sound waves by piezoelectric crystals at the probe’s footprint. These sound waves bounce off tissues and return to the probe, where they are converted electronically to an image on the monitor. Depending on the echogenicity of the scanned tissue, the ultrasound beam will either reflect or be absorbed at different rates. This variance is transmitted on the monitor as a grayscale image. When ultrasound waves are highly reflective, like in bone or fat, they are characterized as hyperechoic. The opposite occurs when ultrasound waves are absorbed like in the fluid of a cystic cavity or joint effusion, and the image appears black. This is described as anechoic.12 Intermediate tissues such as tendons that are less reflective are seen as hypoechoic and appear gray. When a tissue has a similar echogenicity to its surrounding tissues, it is called isoechoic.12
The transducer is the scanning component of the ultrasound machine. Transducers come in 2 shapes: linear and curvilinear. The linear probe creates a straight image that is equal to the size of the transducer footprint. The curvilinear probe creates a wider, wedge-shaped panoramic image.
Linear probes are of higher frequency and generate higher resolution images of shallower structures, while curvilinear probes have greater depth penetration but generate lower resolution images. A high frequency of 10 to 15 MHz is preferred for anatomy between 2 cm to 4 cm depth.13 Midrange frequency of 5 to 10 MHz is preferred at 5 cm to 6 cm depth, and low-frequency 2 to 5 MHz probes are preferred for anatomical structures >6 cm depth.13
Anisotropy is the property of being directionally dependent, as opposed to isotropy, which implies identical properties in all directions. This anisotropic effect is dependent on the angle of the insonating beam. The maximum return echo occurs when the ultrasound beam is perpendicular to the tendon. Decreasing the insonating angle on a normal tendon will cause it to change from brightly hyperechoic (the actual echo from tightly bound tendon fibers) to darkly hypoechoic. If the angle is then increased, the tendon will again appear hyperechoic. If the artifact causes a normal tendon to appear hypoechoic, it may falsely lead to a diagnosis of tendinosis or tear.
Posterior acoustic shadowing is present when a hyperechoic structure reflects the ultrasound beam so much that it creates a dark shadow underneath it.12,14 This phenomenon is possible since the ultrasound beam cannot penetrate the hyperechoic structure and reflects off its inferior tissues. Reverberation is when the beam is repeated back and forth between 2 parallel highly reflective surfaces. The initial reflection will be displayed correctly, while the subsequent ultrasound waves will be delayed and appear at a farther distance from the transducer.12,14
The point where the beam is at its narrowest point generates the section of the image that is best visualized.15 This is called the focal zone, and it can be adjusted to highlight the desired area of evaluation. Gain controls adjust the amount of black, gray, and white on the monitor and can be adjusted to focus the desired image.13 Depth settings are fundamental in finding the desired targets. It is recommended to start with a higher depth setting to get an overview and progressively decrease the depth to key in on the desired anatomy.13 Color Doppler can be used to view movement within structures and to identify vessels, synovitis, and neovascularization in tendinopathy.13
Ultrasound of the Shoulder
Patients should be seated, if possible, on a rotating seat. The examiner’s shoulder should be higher than the patient’s shoulder.16 The user holds the ultrasound probe between the thumb and index fingers while resting the hypothenar eminence on the patient to serve as a fulcrum and steadying force. The examination should take 5 to 15 minutes, depending on the examiner’s expertise and the amount of anatomy being scanned.
Examining the body requires knowledge of anatomy. The examination and accuracy are determined by the technician using the probe. The probe can be angled any direction and be placed obliquely on the subject. The advantage here is that anatomy in the human body is not always planar. Muscles and tissues can run obliquely or even perpendicular to each other. When evaluating anatomy, the examiner should keep in mind what structure he or she is looking for; where it should be found; what landmarks can be used to easily locate it; what orientation it has; and what the normal anatomy should look like.
Muscle appears as a lattice with larger areas of hypoechoic muscle tissue and hyperechoic fascial perimysium layers traversing through it.17 The actual muscle tissue appears hypoechoic from the fluid or blood found within. Scarring, fibrosis, calcification, or chronic injury will change the tissue to appear denser or hyperechoic.17 Acute injury will appear hypoechoic from the inflammatory response and influx of blood. Tendon appears dense and hyperechoic with striations within the tissue, sometimes referred to as a horse’s tail.17 When torn, there will be a disassociation of the tissue with a hypoechoic region between the 2 ends. The attachment to the bone and muscle tissue should appear uniform. Hyperechoic areas within the tendon may be from calcification. Ligament appears similar to tendon but is more isoechoic and connects bone to bone. Evaluation of the entire length and the attachments to the bone are critical to evaluate for disease.
Bone appears bright hyperechoic, smooth, and flat, while hyaline cartilage is hypoechoic, smooth, and runs superiorly in a parallel pattern to its respective inferior cortical bone.17
Fibrocartilage is hyperechoic and typically triangularly shaped, such as in the glenohumeral labrum. Nerves appear fascicular and hypoechoic surrounded by hyperechoic epineurium.14
The epidermis and dermis are the most superficial structure on top of the screen, and are also hyperechoic.17
The Diagnostic Shoulder Examination
The proximal long head of the biceps tendon (LHBT) is the easiest structure in the shoulder to identify because of the anatomic structure, the bicipital groove. By keeping the arm relaxed, perpendicular to the ground, and in neutral rotation, the probe can be placed perpendicular to the arm over the proximal shoulder (Figure 1A).16-20 By finding the groove, the biceps tendon will usually be found resting within the groove (Figure 1B). This is the short axis view and is equivalent to an MRI in the axial plane.
The long axis view of the proximal biceps tendon is found by keeping the tendon in the center of the screen/probe. The probe is then rotated 90° on its center axis, keeping the tendon centered on the probe. The user should be sure to visualize the entire tendon on the screen. If only part of the tendon is seen along only part of the screen, then the probe is oblique to the tendon. In this case, the probe area showing the tendon must be stabilized as the center or set point. The other part of the probe will then pivot until all of the tendon is seen on the screen. The MRI equivalent to the long axis of the proximal biceps tendon is the sagittal view.
Ultrasound is a dynamic evaluation. Moving the probe or moving the patient will change what and how something is imaged. The proximal biceps tendon is a good example of this concept. The bicipital groove is very deep proximally and flattens out as it travels distally to the mid-humerus. The examiner should continually adjust his or her hand/probe/patient position as well as depth/gain and other console functions to adapt to the dynamics of the scan. While keeping the bicep tendon in a short axis view, the tendon can be dynamically evaluated for subluxation by internally and externally rotating the arm.
To find the subscapularis, the arm remains in a neutral position with the hand supinated and the probe is held parallel with the ground. After finding the bicipital groove, the subscapularis tendon insertion is just medial to the groove (Figure 1B). By externally rotating the arm, the subscapularis tendon/muscle will come into a long axis view.16-20 The MRI equivalent to the long axis view of the subscapularis is the axial view. Dynamic testing can be done by internally and externally rotating the arm to evaluate for impingement of the subscapularis tendon as it slides underneath the coracoid process. To view the subscapularis tendon in short axis, the tendon is kept in the center of the screen/probe, and the probe is then rotated 90° on its center axis, keeping the tendon centered on the probe. The MRI equivalent is the sagittal view.
Some have recommended using the modified Crass or Middleton position to evaluate the supraspinatus, where the hand is in the “back pocket”.19 However, many patients with shoulder pain have trouble with this position. By resting the ipsilateral hand on the ipsilateral hip and then dropping the elbow, the supraspinatus insertion can still be brought out from under the acromion. This does bring the insertion anterior out of the scapular plane, so an adjustment is required in probe positioning to properly see the supraspinatus short and long axis. To find the long axis, the probe is placed parallel to a plane that spans the contralateral shoulder and ipsilateral hip (Figure 2A). The fibers of the supraspinatus should be inserting directly lateral to the humeral head without any intervening space (Figure 2B). If any space exists, a partial articular supraspinatus tendon avulsion (PASTA) lesion is present, and its thickness can be directly measured. Moving more posterior will show the flattening of the tuberosity and the fibers of the infraspinatus moving away from the humeral head—the bare spot. The MRI equivalent is the coronal view.
To view the supraspinatus tendon in short axis, maintain the arm in the same position, keeping the tendon in the center of the screen/probe. The probe is then rotated 90° on its center axis, keeping the tendon centered on the probe. The probe should now be in a parallel plane between the ipsilateral shoulder and the contralateral hip. The biceps tendon in cross-section will be found anteriorly, and the articular cartilage will appear as a black layer over the bone. Dynamic testing includes placing the probe in a coronal plane between the acromion and greater tuberosity. When the patient abducts the arm while in internal rotation, the supraspinatus tendon will slide underneath the coracoacromial arch showing potential external impingement.15 The MRI equivalent is the sagittal plane.
The glenohumeral joint is best viewed posteriorly, limiting how much of the intra-articular portion of the joint can be imaged. The arm remains in a neutral position; palpate for the posterior acromion and place the probe just inferior to it, wedging up against it (Figure 3A). The glenohumeral joint will be seen by keeping the probe parallel to the ground (Figure 3B). The MRI equivalent is the axial plane. If a joint effusion exists, it can be seen in the posterior recess.15 A hyperechoic triangular region in between the humeral head and the glenoid will represent the glenoid labrum (Figure 3B). By internally and externally rotating the arm, the joint and labrum complex can be dynamically examined. From the labrum, scanning superior and medial can sometimes show the spinoglenoid notch where a paralabral cyst might be seen.15
Using the glenohumeral joint as a reference, the infraspinatus muscle is easily visualized. Maintaining the arm in neutral position with the probe over the glenohumeral joint, the infraspinatus will become apparent as it lays in long axis view superficially between the posterior deltoid and glenohumeral joint (Figure 3B).16-20 The teres minor lies just inferiorly. The MRI equivalent is the axial plane. To view the infraspinatus and teres minor in short axis, the probe is then rotated 90° on its center axis. The infraspinatus (superiorly) and teres minor (inferiorly) muscles will be visible in short axis within the infraspinatus fossa.15 The MRI equivalent is the sagittal view.
The acromioclavicular joint is superficial and easy to image. The arm remains in a neutral position, and we can palpate the joint for easy localization. The probe is placed anteriorly in a coronal plane over the acromion and clavicle. By scanning anteriorly and posteriorly, a joint effusion referred to as a Geyser sign might be seen. The MRI equivalent is the coronal view.
Available Certifications
The AIUM certification is a voluntary peer reviewed process that acknowledges that a practice is meeting national standards and aids in improving their respective MSK ultrasound protocols. They also provide guidelines on demonstrating training and competence on performing and/or interpreting diagnostic MSK examinations (Table).10 The ARDMS certification provides an actual individual certification referred to as “Registered” in MSK ultrasound.11 The physician must perform 150 diagnostic MSK ultrasound evaluations within 36 months of applying and pass a 200-question examination that is offered twice per year.11 None of these certifications are mandated by the American Medical Association (AMA) or American Osteopathic Association (AOA).
Maintenance and Continuing Medical Education (CME)
The AIUM recommends that a minimum of 50 diagnostic MSK ultrasound evaluations be performed per year for skill maintenance.10 Furthermore, 10 hours of AMA PRA Category 1 Credits™ or American Osteopathic Association Category 1-A Credits specific to MSK ultrasound must be completed by physicians performing and/or interpreting these examinations every 3 years.10 ARDMS recommends a minimum of 30 MSK ultrasound-specific CMEs in preparation for their “Registered” MSK evaluation.1
Conclusion
MSK ultrasound is a dynamic, real-time imaging modality that can improve cost efficiency and patient care. Its portability allows for its use anywhere. Learning the skill may seem daunting, but with the proper courses and education, the technology can be easily learned. By correlating a known modality like MRI, the user will easily begin to read ultrasound images. No current certification is needed to use or bill for ultrasound, but various institutions are developing criteria and testing. Two organizations, AIUM and ARDMS, provide guidelines and certifications to demonstrate competency, which may become necessary in the very near future.
1. Sivan M, Brown J, Brennan S, Bhakta B. A one-stop approach to the management of soft tissue and degenerative musculoskeletal conditions using clinic-based ultrasonography. Musculoskeletal Care. 2011;9(2):63-68.
2. Roy J-S, Braën C, Leblond J, et al. Diagnostic accuracy of ultrasonography, MRI and MR arthrography in the characterization of rotator cuff disorders: a meta-analysis [published online ahead of print February 11, 2015]. Br J Sports Med. doi:10.1136/bjsports-2014-094148.
3. Hirahara AM, Panero AJ. A guide to ultrasound of the shoulder, part 1: coding and reimbursement. Am J Orthop. 2016;45(3):176-182.
4. Hama M, Takase K, Ihata A, et al. Challenges to expanding the clinical application of musculoskeletal ultrasonography (MSUS) among rheumatologists: from a second survey in Japan. Mod Rheumatol. 2012;2:202-208.
5. Smith MJ, Rogers A, Amso N, Kennedy J, Hall A, Mullaney P. A training, assessment and feedback package for the trainee shoulder sonographer. Ultrasound. 2015;23(1):29-41.
6. Delzell PB, Boyle A, Schneider E. Dedicated training program for shoulder sonography: the results of a quality program reverberate with everyone. J Ultrasound Med. 2015;34(6):1037-1042.
7. Finnoff JT, Berkoff D, Brennan F, et al. American Medical Society for Sports Medicine (AMSSM) recommended sports ultrasound curriculum for sports medicine fellowships. PM R. 2015;7(2)e1-e11.
8. Adelman S, Fishman P. Use of portable ultrasound machine for outpatient orthopedic diagnosis: an implementation study. Perm J. 2013;17(3):18-22.
9. Vollman A, Hulen R, Dulchavsky S, et al. Educational benefits of fusing magnetic resonance imaging with sonograms. J Clin Ultrasound. 2014;42(5) 257-263.
10. Training guidelines for physicians and chiropractors who evaluate and interpret diagnostic musculoskeletal ultrasound examinations. Laurel, MD: American Institute of Ultrasound in Medicine; 2014. http://www.aium.org/resources/viewStatement.aspx?id=51. Accessed February 26, 2016.
11. Registered in musculoskeletal (RMSK) sonography. American Registry for Diagnostic Medical Sonography Web site. http://www.ardms.org/get-certified/RMSK/Pages/RMSK.aspx. Accessed February 26, 2016.
12. Silkowski C. Ultrasound nomenclature, image orientation, and basic instrumentation. In: Abraham D, Silkowski C, Odwin C, eds. Emergency Medicine Sonography Pocket Guide to Sonographic Anatomy and Pathology. Sudbury, MA: Jones and Bartlett; 2010:1-24.
13. Ihnatsenka B, Boezaart AP. Ultrasound: basic understanding and learning the language. Int J Shoulder Surg. 2010;4(3):55-62.
14. Taljanovic MS, Melville DM, Scalcione LR, Gimber LH, Lorenz EJ, Witte RS. Artifacts in musculoskeletal ultrasonography. Semin Musculoskelet Radiol. 2014;18(1):3-11.
15. Ng A, Swanevelder J. Resolution in ultrasound imaging. Continuing Educ Anaesth Crit Care Pain. 2011;11(5):186-192. http://ceaccp.oxfordjournals.org/content/11/5/186.full. Accessed March 3, 2016.
16. Nazarian L, Bohm-Velez M, Kan JH, et al. AIUM practice parameters for the performance of a musculoskeletal ultrasound examination. Laurel, MD: American Institute of Ultrasound in Medicine; 2012. http://www.aium.org/resources/guidelines/musculoskeletal.pdf. Accessed February 26, 2016.
17. Jacobson J. Fundamentals of Musculoskeletal Ultrasound. 2nd edition. Philadelphia, PA: Elsevier Saunders; 2013.
18. The Ultrasound Subcommittee of the European Society of Musculoskeletal Radiology. Musculoskeletal ultrasound: technique guidelines. Insights Imaging. 2010;1:99-141.
19. Corazza A, Orlandi D, Fabbro E, et al. Dynamic high-resolution ultrasound of the shoulder: how we do it. Eur J Radiol. 2015;84(2):266-277.
20. Allen GM. Shoulder ultrasound imaging-integrating anatomy, biomechanics and disease processes. Eur J Radiol. 2008;68(1):137-146
The musculoskeletal (MSK) ultrasound evaluation of the shoulder provides a cost- and time-efficient imaging modality with similar diagnostic power as magnetic resonance imaging (MRI).1,2 Its portable point-of-care applications can be used in the office, in the operating room, and in sideline athletic event coverage, as we discussed in Part 1 of this series.3
MSK ultrasound may seem difficult and daunting, and many articles have quoted steep learning curves.4,5 However, in our experience in teaching many ultrasound courses, this modality can be learned quite quickly with the proper instruction. Physicians are already familiar with anatomy and usually have had some exposure to MRI.4 Taking courses in MSK ultrasound or simply learning the basic concepts of ultrasound and then learning the machine controls is usually a good start.5-8 Practice scanning normal individuals, comparing the images from an MRI to learn how to reproduce the same planes and images. This will allow the user to become familiar with normal anatomy and how to see the images on the ultrasound screen.5-8 Vollman and colleagues9 showed that in trainees, combining MRI images with sonograms enhances the ability to correctly identify MSK ultrasound anatomy from 40.9% to 72.5%, when compared with learning from ultrasound images alone.
There are currently no certifications necessary to perform ultrasound scans or bill for them; however, some insurance carriers may require demonstrating relevant, documented training for reimbursement.3 Various organizations are trying to develop certifications and regulations for ultrasound to standardize the use of this modality. In the United States, the American Institute of Ultrasound in Medicine (AIUM) and the American Registry for Diagnostic Medical Sonography (ARDMS) provide guidelines and particular MSK ultrasound certifications.10,11
Basic Ultrasound Principles
The ultrasound machine creates electrical impulses that are turned into sound waves by piezoelectric crystals at the probe’s footprint. These sound waves bounce off tissues and return to the probe, where they are converted electronically to an image on the monitor. Depending on the echogenicity of the scanned tissue, the ultrasound beam will either reflect or be absorbed at different rates. This variance is transmitted on the monitor as a grayscale image. When ultrasound waves are highly reflective, like in bone or fat, they are characterized as hyperechoic. The opposite occurs when ultrasound waves are absorbed like in the fluid of a cystic cavity or joint effusion, and the image appears black. This is described as anechoic.12 Intermediate tissues such as tendons that are less reflective are seen as hypoechoic and appear gray. When a tissue has a similar echogenicity to its surrounding tissues, it is called isoechoic.12
The transducer is the scanning component of the ultrasound machine. Transducers come in 2 shapes: linear and curvilinear. The linear probe creates a straight image that is equal to the size of the transducer footprint. The curvilinear probe creates a wider, wedge-shaped panoramic image.
Linear probes are of higher frequency and generate higher resolution images of shallower structures, while curvilinear probes have greater depth penetration but generate lower resolution images. A high frequency of 10 to 15 MHz is preferred for anatomy between 2 cm to 4 cm depth.13 Midrange frequency of 5 to 10 MHz is preferred at 5 cm to 6 cm depth, and low-frequency 2 to 5 MHz probes are preferred for anatomical structures >6 cm depth.13
Anisotropy is the property of being directionally dependent, as opposed to isotropy, which implies identical properties in all directions. This anisotropic effect is dependent on the angle of the insonating beam. The maximum return echo occurs when the ultrasound beam is perpendicular to the tendon. Decreasing the insonating angle on a normal tendon will cause it to change from brightly hyperechoic (the actual echo from tightly bound tendon fibers) to darkly hypoechoic. If the angle is then increased, the tendon will again appear hyperechoic. If the artifact causes a normal tendon to appear hypoechoic, it may falsely lead to a diagnosis of tendinosis or tear.
Posterior acoustic shadowing is present when a hyperechoic structure reflects the ultrasound beam so much that it creates a dark shadow underneath it.12,14 This phenomenon is possible since the ultrasound beam cannot penetrate the hyperechoic structure and reflects off its inferior tissues. Reverberation is when the beam is repeated back and forth between 2 parallel highly reflective surfaces. The initial reflection will be displayed correctly, while the subsequent ultrasound waves will be delayed and appear at a farther distance from the transducer.12,14
The point where the beam is at its narrowest point generates the section of the image that is best visualized.15 This is called the focal zone, and it can be adjusted to highlight the desired area of evaluation. Gain controls adjust the amount of black, gray, and white on the monitor and can be adjusted to focus the desired image.13 Depth settings are fundamental in finding the desired targets. It is recommended to start with a higher depth setting to get an overview and progressively decrease the depth to key in on the desired anatomy.13 Color Doppler can be used to view movement within structures and to identify vessels, synovitis, and neovascularization in tendinopathy.13
Ultrasound of the Shoulder
Patients should be seated, if possible, on a rotating seat. The examiner’s shoulder should be higher than the patient’s shoulder.16 The user holds the ultrasound probe between the thumb and index fingers while resting the hypothenar eminence on the patient to serve as a fulcrum and steadying force. The examination should take 5 to 15 minutes, depending on the examiner’s expertise and the amount of anatomy being scanned.
Examining the body requires knowledge of anatomy. The examination and accuracy are determined by the technician using the probe. The probe can be angled any direction and be placed obliquely on the subject. The advantage here is that anatomy in the human body is not always planar. Muscles and tissues can run obliquely or even perpendicular to each other. When evaluating anatomy, the examiner should keep in mind what structure he or she is looking for; where it should be found; what landmarks can be used to easily locate it; what orientation it has; and what the normal anatomy should look like.
Muscle appears as a lattice with larger areas of hypoechoic muscle tissue and hyperechoic fascial perimysium layers traversing through it.17 The actual muscle tissue appears hypoechoic from the fluid or blood found within. Scarring, fibrosis, calcification, or chronic injury will change the tissue to appear denser or hyperechoic.17 Acute injury will appear hypoechoic from the inflammatory response and influx of blood. Tendon appears dense and hyperechoic with striations within the tissue, sometimes referred to as a horse’s tail.17 When torn, there will be a disassociation of the tissue with a hypoechoic region between the 2 ends. The attachment to the bone and muscle tissue should appear uniform. Hyperechoic areas within the tendon may be from calcification. Ligament appears similar to tendon but is more isoechoic and connects bone to bone. Evaluation of the entire length and the attachments to the bone are critical to evaluate for disease.
Bone appears bright hyperechoic, smooth, and flat, while hyaline cartilage is hypoechoic, smooth, and runs superiorly in a parallel pattern to its respective inferior cortical bone.17
Fibrocartilage is hyperechoic and typically triangularly shaped, such as in the glenohumeral labrum. Nerves appear fascicular and hypoechoic surrounded by hyperechoic epineurium.14
The epidermis and dermis are the most superficial structure on top of the screen, and are also hyperechoic.17
The Diagnostic Shoulder Examination
The proximal long head of the biceps tendon (LHBT) is the easiest structure in the shoulder to identify because of the anatomic structure, the bicipital groove. By keeping the arm relaxed, perpendicular to the ground, and in neutral rotation, the probe can be placed perpendicular to the arm over the proximal shoulder (Figure 1A).16-20 By finding the groove, the biceps tendon will usually be found resting within the groove (Figure 1B). This is the short axis view and is equivalent to an MRI in the axial plane.
The long axis view of the proximal biceps tendon is found by keeping the tendon in the center of the screen/probe. The probe is then rotated 90° on its center axis, keeping the tendon centered on the probe. The user should be sure to visualize the entire tendon on the screen. If only part of the tendon is seen along only part of the screen, then the probe is oblique to the tendon. In this case, the probe area showing the tendon must be stabilized as the center or set point. The other part of the probe will then pivot until all of the tendon is seen on the screen. The MRI equivalent to the long axis of the proximal biceps tendon is the sagittal view.
Ultrasound is a dynamic evaluation. Moving the probe or moving the patient will change what and how something is imaged. The proximal biceps tendon is a good example of this concept. The bicipital groove is very deep proximally and flattens out as it travels distally to the mid-humerus. The examiner should continually adjust his or her hand/probe/patient position as well as depth/gain and other console functions to adapt to the dynamics of the scan. While keeping the bicep tendon in a short axis view, the tendon can be dynamically evaluated for subluxation by internally and externally rotating the arm.
To find the subscapularis, the arm remains in a neutral position with the hand supinated and the probe is held parallel with the ground. After finding the bicipital groove, the subscapularis tendon insertion is just medial to the groove (Figure 1B). By externally rotating the arm, the subscapularis tendon/muscle will come into a long axis view.16-20 The MRI equivalent to the long axis view of the subscapularis is the axial view. Dynamic testing can be done by internally and externally rotating the arm to evaluate for impingement of the subscapularis tendon as it slides underneath the coracoid process. To view the subscapularis tendon in short axis, the tendon is kept in the center of the screen/probe, and the probe is then rotated 90° on its center axis, keeping the tendon centered on the probe. The MRI equivalent is the sagittal view.
Some have recommended using the modified Crass or Middleton position to evaluate the supraspinatus, where the hand is in the “back pocket”.19 However, many patients with shoulder pain have trouble with this position. By resting the ipsilateral hand on the ipsilateral hip and then dropping the elbow, the supraspinatus insertion can still be brought out from under the acromion. This does bring the insertion anterior out of the scapular plane, so an adjustment is required in probe positioning to properly see the supraspinatus short and long axis. To find the long axis, the probe is placed parallel to a plane that spans the contralateral shoulder and ipsilateral hip (Figure 2A). The fibers of the supraspinatus should be inserting directly lateral to the humeral head without any intervening space (Figure 2B). If any space exists, a partial articular supraspinatus tendon avulsion (PASTA) lesion is present, and its thickness can be directly measured. Moving more posterior will show the flattening of the tuberosity and the fibers of the infraspinatus moving away from the humeral head—the bare spot. The MRI equivalent is the coronal view.
To view the supraspinatus tendon in short axis, maintain the arm in the same position, keeping the tendon in the center of the screen/probe. The probe is then rotated 90° on its center axis, keeping the tendon centered on the probe. The probe should now be in a parallel plane between the ipsilateral shoulder and the contralateral hip. The biceps tendon in cross-section will be found anteriorly, and the articular cartilage will appear as a black layer over the bone. Dynamic testing includes placing the probe in a coronal plane between the acromion and greater tuberosity. When the patient abducts the arm while in internal rotation, the supraspinatus tendon will slide underneath the coracoacromial arch showing potential external impingement.15 The MRI equivalent is the sagittal plane.
The glenohumeral joint is best viewed posteriorly, limiting how much of the intra-articular portion of the joint can be imaged. The arm remains in a neutral position; palpate for the posterior acromion and place the probe just inferior to it, wedging up against it (Figure 3A). The glenohumeral joint will be seen by keeping the probe parallel to the ground (Figure 3B). The MRI equivalent is the axial plane. If a joint effusion exists, it can be seen in the posterior recess.15 A hyperechoic triangular region in between the humeral head and the glenoid will represent the glenoid labrum (Figure 3B). By internally and externally rotating the arm, the joint and labrum complex can be dynamically examined. From the labrum, scanning superior and medial can sometimes show the spinoglenoid notch where a paralabral cyst might be seen.15
Using the glenohumeral joint as a reference, the infraspinatus muscle is easily visualized. Maintaining the arm in neutral position with the probe over the glenohumeral joint, the infraspinatus will become apparent as it lays in long axis view superficially between the posterior deltoid and glenohumeral joint (Figure 3B).16-20 The teres minor lies just inferiorly. The MRI equivalent is the axial plane. To view the infraspinatus and teres minor in short axis, the probe is then rotated 90° on its center axis. The infraspinatus (superiorly) and teres minor (inferiorly) muscles will be visible in short axis within the infraspinatus fossa.15 The MRI equivalent is the sagittal view.
The acromioclavicular joint is superficial and easy to image. The arm remains in a neutral position, and we can palpate the joint for easy localization. The probe is placed anteriorly in a coronal plane over the acromion and clavicle. By scanning anteriorly and posteriorly, a joint effusion referred to as a Geyser sign might be seen. The MRI equivalent is the coronal view.
Available Certifications
The AIUM certification is a voluntary peer reviewed process that acknowledges that a practice is meeting national standards and aids in improving their respective MSK ultrasound protocols. They also provide guidelines on demonstrating training and competence on performing and/or interpreting diagnostic MSK examinations (Table).10 The ARDMS certification provides an actual individual certification referred to as “Registered” in MSK ultrasound.11 The physician must perform 150 diagnostic MSK ultrasound evaluations within 36 months of applying and pass a 200-question examination that is offered twice per year.11 None of these certifications are mandated by the American Medical Association (AMA) or American Osteopathic Association (AOA).
Maintenance and Continuing Medical Education (CME)
The AIUM recommends that a minimum of 50 diagnostic MSK ultrasound evaluations be performed per year for skill maintenance.10 Furthermore, 10 hours of AMA PRA Category 1 Credits™ or American Osteopathic Association Category 1-A Credits specific to MSK ultrasound must be completed by physicians performing and/or interpreting these examinations every 3 years.10 ARDMS recommends a minimum of 30 MSK ultrasound-specific CMEs in preparation for their “Registered” MSK evaluation.1
Conclusion
MSK ultrasound is a dynamic, real-time imaging modality that can improve cost efficiency and patient care. Its portability allows for its use anywhere. Learning the skill may seem daunting, but with the proper courses and education, the technology can be easily learned. By correlating a known modality like MRI, the user will easily begin to read ultrasound images. No current certification is needed to use or bill for ultrasound, but various institutions are developing criteria and testing. Two organizations, AIUM and ARDMS, provide guidelines and certifications to demonstrate competency, which may become necessary in the very near future.
The musculoskeletal (MSK) ultrasound evaluation of the shoulder provides a cost- and time-efficient imaging modality with similar diagnostic power as magnetic resonance imaging (MRI).1,2 Its portable point-of-care applications can be used in the office, in the operating room, and in sideline athletic event coverage, as we discussed in Part 1 of this series.3
MSK ultrasound may seem difficult and daunting, and many articles have quoted steep learning curves.4,5 However, in our experience in teaching many ultrasound courses, this modality can be learned quite quickly with the proper instruction. Physicians are already familiar with anatomy and usually have had some exposure to MRI.4 Taking courses in MSK ultrasound or simply learning the basic concepts of ultrasound and then learning the machine controls is usually a good start.5-8 Practice scanning normal individuals, comparing the images from an MRI to learn how to reproduce the same planes and images. This will allow the user to become familiar with normal anatomy and how to see the images on the ultrasound screen.5-8 Vollman and colleagues9 showed that in trainees, combining MRI images with sonograms enhances the ability to correctly identify MSK ultrasound anatomy from 40.9% to 72.5%, when compared with learning from ultrasound images alone.
There are currently no certifications necessary to perform ultrasound scans or bill for them; however, some insurance carriers may require demonstrating relevant, documented training for reimbursement.3 Various organizations are trying to develop certifications and regulations for ultrasound to standardize the use of this modality. In the United States, the American Institute of Ultrasound in Medicine (AIUM) and the American Registry for Diagnostic Medical Sonography (ARDMS) provide guidelines and particular MSK ultrasound certifications.10,11
Basic Ultrasound Principles
The ultrasound machine creates electrical impulses that are turned into sound waves by piezoelectric crystals at the probe’s footprint. These sound waves bounce off tissues and return to the probe, where they are converted electronically to an image on the monitor. Depending on the echogenicity of the scanned tissue, the ultrasound beam will either reflect or be absorbed at different rates. This variance is transmitted on the monitor as a grayscale image. When ultrasound waves are highly reflective, like in bone or fat, they are characterized as hyperechoic. The opposite occurs when ultrasound waves are absorbed like in the fluid of a cystic cavity or joint effusion, and the image appears black. This is described as anechoic.12 Intermediate tissues such as tendons that are less reflective are seen as hypoechoic and appear gray. When a tissue has a similar echogenicity to its surrounding tissues, it is called isoechoic.12
The transducer is the scanning component of the ultrasound machine. Transducers come in 2 shapes: linear and curvilinear. The linear probe creates a straight image that is equal to the size of the transducer footprint. The curvilinear probe creates a wider, wedge-shaped panoramic image.
Linear probes are of higher frequency and generate higher resolution images of shallower structures, while curvilinear probes have greater depth penetration but generate lower resolution images. A high frequency of 10 to 15 MHz is preferred for anatomy between 2 cm to 4 cm depth.13 Midrange frequency of 5 to 10 MHz is preferred at 5 cm to 6 cm depth, and low-frequency 2 to 5 MHz probes are preferred for anatomical structures >6 cm depth.13
Anisotropy is the property of being directionally dependent, as opposed to isotropy, which implies identical properties in all directions. This anisotropic effect is dependent on the angle of the insonating beam. The maximum return echo occurs when the ultrasound beam is perpendicular to the tendon. Decreasing the insonating angle on a normal tendon will cause it to change from brightly hyperechoic (the actual echo from tightly bound tendon fibers) to darkly hypoechoic. If the angle is then increased, the tendon will again appear hyperechoic. If the artifact causes a normal tendon to appear hypoechoic, it may falsely lead to a diagnosis of tendinosis or tear.
Posterior acoustic shadowing is present when a hyperechoic structure reflects the ultrasound beam so much that it creates a dark shadow underneath it.12,14 This phenomenon is possible since the ultrasound beam cannot penetrate the hyperechoic structure and reflects off its inferior tissues. Reverberation is when the beam is repeated back and forth between 2 parallel highly reflective surfaces. The initial reflection will be displayed correctly, while the subsequent ultrasound waves will be delayed and appear at a farther distance from the transducer.12,14
The point where the beam is at its narrowest point generates the section of the image that is best visualized.15 This is called the focal zone, and it can be adjusted to highlight the desired area of evaluation. Gain controls adjust the amount of black, gray, and white on the monitor and can be adjusted to focus the desired image.13 Depth settings are fundamental in finding the desired targets. It is recommended to start with a higher depth setting to get an overview and progressively decrease the depth to key in on the desired anatomy.13 Color Doppler can be used to view movement within structures and to identify vessels, synovitis, and neovascularization in tendinopathy.13
Ultrasound of the Shoulder
Patients should be seated, if possible, on a rotating seat. The examiner’s shoulder should be higher than the patient’s shoulder.16 The user holds the ultrasound probe between the thumb and index fingers while resting the hypothenar eminence on the patient to serve as a fulcrum and steadying force. The examination should take 5 to 15 minutes, depending on the examiner’s expertise and the amount of anatomy being scanned.
Examining the body requires knowledge of anatomy. The examination and accuracy are determined by the technician using the probe. The probe can be angled any direction and be placed obliquely on the subject. The advantage here is that anatomy in the human body is not always planar. Muscles and tissues can run obliquely or even perpendicular to each other. When evaluating anatomy, the examiner should keep in mind what structure he or she is looking for; where it should be found; what landmarks can be used to easily locate it; what orientation it has; and what the normal anatomy should look like.
Muscle appears as a lattice with larger areas of hypoechoic muscle tissue and hyperechoic fascial perimysium layers traversing through it.17 The actual muscle tissue appears hypoechoic from the fluid or blood found within. Scarring, fibrosis, calcification, or chronic injury will change the tissue to appear denser or hyperechoic.17 Acute injury will appear hypoechoic from the inflammatory response and influx of blood. Tendon appears dense and hyperechoic with striations within the tissue, sometimes referred to as a horse’s tail.17 When torn, there will be a disassociation of the tissue with a hypoechoic region between the 2 ends. The attachment to the bone and muscle tissue should appear uniform. Hyperechoic areas within the tendon may be from calcification. Ligament appears similar to tendon but is more isoechoic and connects bone to bone. Evaluation of the entire length and the attachments to the bone are critical to evaluate for disease.
Bone appears bright hyperechoic, smooth, and flat, while hyaline cartilage is hypoechoic, smooth, and runs superiorly in a parallel pattern to its respective inferior cortical bone.17
Fibrocartilage is hyperechoic and typically triangularly shaped, such as in the glenohumeral labrum. Nerves appear fascicular and hypoechoic surrounded by hyperechoic epineurium.14
The epidermis and dermis are the most superficial structure on top of the screen, and are also hyperechoic.17
The Diagnostic Shoulder Examination
The proximal long head of the biceps tendon (LHBT) is the easiest structure in the shoulder to identify because of the anatomic structure, the bicipital groove. By keeping the arm relaxed, perpendicular to the ground, and in neutral rotation, the probe can be placed perpendicular to the arm over the proximal shoulder (Figure 1A).16-20 By finding the groove, the biceps tendon will usually be found resting within the groove (Figure 1B). This is the short axis view and is equivalent to an MRI in the axial plane.
The long axis view of the proximal biceps tendon is found by keeping the tendon in the center of the screen/probe. The probe is then rotated 90° on its center axis, keeping the tendon centered on the probe. The user should be sure to visualize the entire tendon on the screen. If only part of the tendon is seen along only part of the screen, then the probe is oblique to the tendon. In this case, the probe area showing the tendon must be stabilized as the center or set point. The other part of the probe will then pivot until all of the tendon is seen on the screen. The MRI equivalent to the long axis of the proximal biceps tendon is the sagittal view.
Ultrasound is a dynamic evaluation. Moving the probe or moving the patient will change what and how something is imaged. The proximal biceps tendon is a good example of this concept. The bicipital groove is very deep proximally and flattens out as it travels distally to the mid-humerus. The examiner should continually adjust his or her hand/probe/patient position as well as depth/gain and other console functions to adapt to the dynamics of the scan. While keeping the bicep tendon in a short axis view, the tendon can be dynamically evaluated for subluxation by internally and externally rotating the arm.
To find the subscapularis, the arm remains in a neutral position with the hand supinated and the probe is held parallel with the ground. After finding the bicipital groove, the subscapularis tendon insertion is just medial to the groove (Figure 1B). By externally rotating the arm, the subscapularis tendon/muscle will come into a long axis view.16-20 The MRI equivalent to the long axis view of the subscapularis is the axial view. Dynamic testing can be done by internally and externally rotating the arm to evaluate for impingement of the subscapularis tendon as it slides underneath the coracoid process. To view the subscapularis tendon in short axis, the tendon is kept in the center of the screen/probe, and the probe is then rotated 90° on its center axis, keeping the tendon centered on the probe. The MRI equivalent is the sagittal view.
Some have recommended using the modified Crass or Middleton position to evaluate the supraspinatus, where the hand is in the “back pocket”.19 However, many patients with shoulder pain have trouble with this position. By resting the ipsilateral hand on the ipsilateral hip and then dropping the elbow, the supraspinatus insertion can still be brought out from under the acromion. This does bring the insertion anterior out of the scapular plane, so an adjustment is required in probe positioning to properly see the supraspinatus short and long axis. To find the long axis, the probe is placed parallel to a plane that spans the contralateral shoulder and ipsilateral hip (Figure 2A). The fibers of the supraspinatus should be inserting directly lateral to the humeral head without any intervening space (Figure 2B). If any space exists, a partial articular supraspinatus tendon avulsion (PASTA) lesion is present, and its thickness can be directly measured. Moving more posterior will show the flattening of the tuberosity and the fibers of the infraspinatus moving away from the humeral head—the bare spot. The MRI equivalent is the coronal view.
To view the supraspinatus tendon in short axis, maintain the arm in the same position, keeping the tendon in the center of the screen/probe. The probe is then rotated 90° on its center axis, keeping the tendon centered on the probe. The probe should now be in a parallel plane between the ipsilateral shoulder and the contralateral hip. The biceps tendon in cross-section will be found anteriorly, and the articular cartilage will appear as a black layer over the bone. Dynamic testing includes placing the probe in a coronal plane between the acromion and greater tuberosity. When the patient abducts the arm while in internal rotation, the supraspinatus tendon will slide underneath the coracoacromial arch showing potential external impingement.15 The MRI equivalent is the sagittal plane.
The glenohumeral joint is best viewed posteriorly, limiting how much of the intra-articular portion of the joint can be imaged. The arm remains in a neutral position; palpate for the posterior acromion and place the probe just inferior to it, wedging up against it (Figure 3A). The glenohumeral joint will be seen by keeping the probe parallel to the ground (Figure 3B). The MRI equivalent is the axial plane. If a joint effusion exists, it can be seen in the posterior recess.15 A hyperechoic triangular region in between the humeral head and the glenoid will represent the glenoid labrum (Figure 3B). By internally and externally rotating the arm, the joint and labrum complex can be dynamically examined. From the labrum, scanning superior and medial can sometimes show the spinoglenoid notch where a paralabral cyst might be seen.15
Using the glenohumeral joint as a reference, the infraspinatus muscle is easily visualized. Maintaining the arm in neutral position with the probe over the glenohumeral joint, the infraspinatus will become apparent as it lays in long axis view superficially between the posterior deltoid and glenohumeral joint (Figure 3B).16-20 The teres minor lies just inferiorly. The MRI equivalent is the axial plane. To view the infraspinatus and teres minor in short axis, the probe is then rotated 90° on its center axis. The infraspinatus (superiorly) and teres minor (inferiorly) muscles will be visible in short axis within the infraspinatus fossa.15 The MRI equivalent is the sagittal view.
The acromioclavicular joint is superficial and easy to image. The arm remains in a neutral position, and we can palpate the joint for easy localization. The probe is placed anteriorly in a coronal plane over the acromion and clavicle. By scanning anteriorly and posteriorly, a joint effusion referred to as a Geyser sign might be seen. The MRI equivalent is the coronal view.
Available Certifications
The AIUM certification is a voluntary peer reviewed process that acknowledges that a practice is meeting national standards and aids in improving their respective MSK ultrasound protocols. They also provide guidelines on demonstrating training and competence on performing and/or interpreting diagnostic MSK examinations (Table).10 The ARDMS certification provides an actual individual certification referred to as “Registered” in MSK ultrasound.11 The physician must perform 150 diagnostic MSK ultrasound evaluations within 36 months of applying and pass a 200-question examination that is offered twice per year.11 None of these certifications are mandated by the American Medical Association (AMA) or American Osteopathic Association (AOA).
Maintenance and Continuing Medical Education (CME)
The AIUM recommends that a minimum of 50 diagnostic MSK ultrasound evaluations be performed per year for skill maintenance.10 Furthermore, 10 hours of AMA PRA Category 1 Credits™ or American Osteopathic Association Category 1-A Credits specific to MSK ultrasound must be completed by physicians performing and/or interpreting these examinations every 3 years.10 ARDMS recommends a minimum of 30 MSK ultrasound-specific CMEs in preparation for their “Registered” MSK evaluation.1
Conclusion
MSK ultrasound is a dynamic, real-time imaging modality that can improve cost efficiency and patient care. Its portability allows for its use anywhere. Learning the skill may seem daunting, but with the proper courses and education, the technology can be easily learned. By correlating a known modality like MRI, the user will easily begin to read ultrasound images. No current certification is needed to use or bill for ultrasound, but various institutions are developing criteria and testing. Two organizations, AIUM and ARDMS, provide guidelines and certifications to demonstrate competency, which may become necessary in the very near future.
1. Sivan M, Brown J, Brennan S, Bhakta B. A one-stop approach to the management of soft tissue and degenerative musculoskeletal conditions using clinic-based ultrasonography. Musculoskeletal Care. 2011;9(2):63-68.
2. Roy J-S, Braën C, Leblond J, et al. Diagnostic accuracy of ultrasonography, MRI and MR arthrography in the characterization of rotator cuff disorders: a meta-analysis [published online ahead of print February 11, 2015]. Br J Sports Med. doi:10.1136/bjsports-2014-094148.
3. Hirahara AM, Panero AJ. A guide to ultrasound of the shoulder, part 1: coding and reimbursement. Am J Orthop. 2016;45(3):176-182.
4. Hama M, Takase K, Ihata A, et al. Challenges to expanding the clinical application of musculoskeletal ultrasonography (MSUS) among rheumatologists: from a second survey in Japan. Mod Rheumatol. 2012;2:202-208.
5. Smith MJ, Rogers A, Amso N, Kennedy J, Hall A, Mullaney P. A training, assessment and feedback package for the trainee shoulder sonographer. Ultrasound. 2015;23(1):29-41.
6. Delzell PB, Boyle A, Schneider E. Dedicated training program for shoulder sonography: the results of a quality program reverberate with everyone. J Ultrasound Med. 2015;34(6):1037-1042.
7. Finnoff JT, Berkoff D, Brennan F, et al. American Medical Society for Sports Medicine (AMSSM) recommended sports ultrasound curriculum for sports medicine fellowships. PM R. 2015;7(2)e1-e11.
8. Adelman S, Fishman P. Use of portable ultrasound machine for outpatient orthopedic diagnosis: an implementation study. Perm J. 2013;17(3):18-22.
9. Vollman A, Hulen R, Dulchavsky S, et al. Educational benefits of fusing magnetic resonance imaging with sonograms. J Clin Ultrasound. 2014;42(5) 257-263.
10. Training guidelines for physicians and chiropractors who evaluate and interpret diagnostic musculoskeletal ultrasound examinations. Laurel, MD: American Institute of Ultrasound in Medicine; 2014. http://www.aium.org/resources/viewStatement.aspx?id=51. Accessed February 26, 2016.
11. Registered in musculoskeletal (RMSK) sonography. American Registry for Diagnostic Medical Sonography Web site. http://www.ardms.org/get-certified/RMSK/Pages/RMSK.aspx. Accessed February 26, 2016.
12. Silkowski C. Ultrasound nomenclature, image orientation, and basic instrumentation. In: Abraham D, Silkowski C, Odwin C, eds. Emergency Medicine Sonography Pocket Guide to Sonographic Anatomy and Pathology. Sudbury, MA: Jones and Bartlett; 2010:1-24.
13. Ihnatsenka B, Boezaart AP. Ultrasound: basic understanding and learning the language. Int J Shoulder Surg. 2010;4(3):55-62.
14. Taljanovic MS, Melville DM, Scalcione LR, Gimber LH, Lorenz EJ, Witte RS. Artifacts in musculoskeletal ultrasonography. Semin Musculoskelet Radiol. 2014;18(1):3-11.
15. Ng A, Swanevelder J. Resolution in ultrasound imaging. Continuing Educ Anaesth Crit Care Pain. 2011;11(5):186-192. http://ceaccp.oxfordjournals.org/content/11/5/186.full. Accessed March 3, 2016.
16. Nazarian L, Bohm-Velez M, Kan JH, et al. AIUM practice parameters for the performance of a musculoskeletal ultrasound examination. Laurel, MD: American Institute of Ultrasound in Medicine; 2012. http://www.aium.org/resources/guidelines/musculoskeletal.pdf. Accessed February 26, 2016.
17. Jacobson J. Fundamentals of Musculoskeletal Ultrasound. 2nd edition. Philadelphia, PA: Elsevier Saunders; 2013.
18. The Ultrasound Subcommittee of the European Society of Musculoskeletal Radiology. Musculoskeletal ultrasound: technique guidelines. Insights Imaging. 2010;1:99-141.
19. Corazza A, Orlandi D, Fabbro E, et al. Dynamic high-resolution ultrasound of the shoulder: how we do it. Eur J Radiol. 2015;84(2):266-277.
20. Allen GM. Shoulder ultrasound imaging-integrating anatomy, biomechanics and disease processes. Eur J Radiol. 2008;68(1):137-146
1. Sivan M, Brown J, Brennan S, Bhakta B. A one-stop approach to the management of soft tissue and degenerative musculoskeletal conditions using clinic-based ultrasonography. Musculoskeletal Care. 2011;9(2):63-68.
2. Roy J-S, Braën C, Leblond J, et al. Diagnostic accuracy of ultrasonography, MRI and MR arthrography in the characterization of rotator cuff disorders: a meta-analysis [published online ahead of print February 11, 2015]. Br J Sports Med. doi:10.1136/bjsports-2014-094148.
3. Hirahara AM, Panero AJ. A guide to ultrasound of the shoulder, part 1: coding and reimbursement. Am J Orthop. 2016;45(3):176-182.
4. Hama M, Takase K, Ihata A, et al. Challenges to expanding the clinical application of musculoskeletal ultrasonography (MSUS) among rheumatologists: from a second survey in Japan. Mod Rheumatol. 2012;2:202-208.
5. Smith MJ, Rogers A, Amso N, Kennedy J, Hall A, Mullaney P. A training, assessment and feedback package for the trainee shoulder sonographer. Ultrasound. 2015;23(1):29-41.
6. Delzell PB, Boyle A, Schneider E. Dedicated training program for shoulder sonography: the results of a quality program reverberate with everyone. J Ultrasound Med. 2015;34(6):1037-1042.
7. Finnoff JT, Berkoff D, Brennan F, et al. American Medical Society for Sports Medicine (AMSSM) recommended sports ultrasound curriculum for sports medicine fellowships. PM R. 2015;7(2)e1-e11.
8. Adelman S, Fishman P. Use of portable ultrasound machine for outpatient orthopedic diagnosis: an implementation study. Perm J. 2013;17(3):18-22.
9. Vollman A, Hulen R, Dulchavsky S, et al. Educational benefits of fusing magnetic resonance imaging with sonograms. J Clin Ultrasound. 2014;42(5) 257-263.
10. Training guidelines for physicians and chiropractors who evaluate and interpret diagnostic musculoskeletal ultrasound examinations. Laurel, MD: American Institute of Ultrasound in Medicine; 2014. http://www.aium.org/resources/viewStatement.aspx?id=51. Accessed February 26, 2016.
11. Registered in musculoskeletal (RMSK) sonography. American Registry for Diagnostic Medical Sonography Web site. http://www.ardms.org/get-certified/RMSK/Pages/RMSK.aspx. Accessed February 26, 2016.
12. Silkowski C. Ultrasound nomenclature, image orientation, and basic instrumentation. In: Abraham D, Silkowski C, Odwin C, eds. Emergency Medicine Sonography Pocket Guide to Sonographic Anatomy and Pathology. Sudbury, MA: Jones and Bartlett; 2010:1-24.
13. Ihnatsenka B, Boezaart AP. Ultrasound: basic understanding and learning the language. Int J Shoulder Surg. 2010;4(3):55-62.
14. Taljanovic MS, Melville DM, Scalcione LR, Gimber LH, Lorenz EJ, Witte RS. Artifacts in musculoskeletal ultrasonography. Semin Musculoskelet Radiol. 2014;18(1):3-11.
15. Ng A, Swanevelder J. Resolution in ultrasound imaging. Continuing Educ Anaesth Crit Care Pain. 2011;11(5):186-192. http://ceaccp.oxfordjournals.org/content/11/5/186.full. Accessed March 3, 2016.
16. Nazarian L, Bohm-Velez M, Kan JH, et al. AIUM practice parameters for the performance of a musculoskeletal ultrasound examination. Laurel, MD: American Institute of Ultrasound in Medicine; 2012. http://www.aium.org/resources/guidelines/musculoskeletal.pdf. Accessed February 26, 2016.
17. Jacobson J. Fundamentals of Musculoskeletal Ultrasound. 2nd edition. Philadelphia, PA: Elsevier Saunders; 2013.
18. The Ultrasound Subcommittee of the European Society of Musculoskeletal Radiology. Musculoskeletal ultrasound: technique guidelines. Insights Imaging. 2010;1:99-141.
19. Corazza A, Orlandi D, Fabbro E, et al. Dynamic high-resolution ultrasound of the shoulder: how we do it. Eur J Radiol. 2015;84(2):266-277.
20. Allen GM. Shoulder ultrasound imaging-integrating anatomy, biomechanics and disease processes. Eur J Radiol. 2008;68(1):137-146
Are Preseason Arm Injury Prevention Programs Beneficial for Young Baseball Players?
ORLANDO, FL—Preseason prevention programs can improve deficits in young baseball pitchers, according to research presented at the American Orthopedic Society for Sports Medicine’s Specialty Day.
Researchers evaluated 143 pitchers, of which 88 participated in additional preseason training and 76 continued with normal training. The median age of the pitchers was 15.7 years.
The prevention program, which was supervised by an athletic trainer and required a commitment of 15 minutes 4 times a week, included resistance training with dumbbell weights, elastic tubing, and a focused flexibility program. Pitchers who participated in the prevention program had reduced internal rotation and horizontal adduction deficits. Pitchers who had previous injuries and participated in the preseason training program were 4 times less likely to suffer an injury than those in the general arm care program.
ORLANDO, FL—Preseason prevention programs can improve deficits in young baseball pitchers, according to research presented at the American Orthopedic Society for Sports Medicine’s Specialty Day.
Researchers evaluated 143 pitchers, of which 88 participated in additional preseason training and 76 continued with normal training. The median age of the pitchers was 15.7 years.
The prevention program, which was supervised by an athletic trainer and required a commitment of 15 minutes 4 times a week, included resistance training with dumbbell weights, elastic tubing, and a focused flexibility program. Pitchers who participated in the prevention program had reduced internal rotation and horizontal adduction deficits. Pitchers who had previous injuries and participated in the preseason training program were 4 times less likely to suffer an injury than those in the general arm care program.
ORLANDO, FL—Preseason prevention programs can improve deficits in young baseball pitchers, according to research presented at the American Orthopedic Society for Sports Medicine’s Specialty Day.
Researchers evaluated 143 pitchers, of which 88 participated in additional preseason training and 76 continued with normal training. The median age of the pitchers was 15.7 years.
The prevention program, which was supervised by an athletic trainer and required a commitment of 15 minutes 4 times a week, included resistance training with dumbbell weights, elastic tubing, and a focused flexibility program. Pitchers who participated in the prevention program had reduced internal rotation and horizontal adduction deficits. Pitchers who had previous injuries and participated in the preseason training program were 4 times less likely to suffer an injury than those in the general arm care program.
Graft Choice in ACL Reconstruction May Affect Revision Rates
ORLANDO, FL—Using soft tissue allografts for anterior cruciate ligament (ACL) reconstructions may increase the risks for a revision reconstruction postoperatively, according to research presented at the American Orthopedic Society for Sports Medicine’s Specialty Day.
Researchers analyzed data from the Kaiser Permanente ACLR Registry. Of the cases analyzed, 4,557 involved bone-patellar tendon-bone (BPTB) autografts, 3,751 soft tissue allograft, and 5,707 hamstring allograft.
After a 3-year follow-up, the overall revision rates were 2.5% for BPTB autographs, 3.5% for hamstring autografts, and 3.7% for soft tissue allografts. Non-processed soft tissue allografts were not found to have a statistically significantly different risk of revision compared to BPTB autografts. However, compared to BPTB autografts, allografts processed with more than 1.8Mrads irradiation had a more than 2 times higher risk of revision, and grafts processed with more than 1.8Mrads or high pressure chemical processing had a more than 4 to 6 times higher risk of revision. This was true even after adjustments for age, gender, and race.
ORLANDO, FL—Using soft tissue allografts for anterior cruciate ligament (ACL) reconstructions may increase the risks for a revision reconstruction postoperatively, according to research presented at the American Orthopedic Society for Sports Medicine’s Specialty Day.
Researchers analyzed data from the Kaiser Permanente ACLR Registry. Of the cases analyzed, 4,557 involved bone-patellar tendon-bone (BPTB) autografts, 3,751 soft tissue allograft, and 5,707 hamstring allograft.
After a 3-year follow-up, the overall revision rates were 2.5% for BPTB autographs, 3.5% for hamstring autografts, and 3.7% for soft tissue allografts. Non-processed soft tissue allografts were not found to have a statistically significantly different risk of revision compared to BPTB autografts. However, compared to BPTB autografts, allografts processed with more than 1.8Mrads irradiation had a more than 2 times higher risk of revision, and grafts processed with more than 1.8Mrads or high pressure chemical processing had a more than 4 to 6 times higher risk of revision. This was true even after adjustments for age, gender, and race.
ORLANDO, FL—Using soft tissue allografts for anterior cruciate ligament (ACL) reconstructions may increase the risks for a revision reconstruction postoperatively, according to research presented at the American Orthopedic Society for Sports Medicine’s Specialty Day.
Researchers analyzed data from the Kaiser Permanente ACLR Registry. Of the cases analyzed, 4,557 involved bone-patellar tendon-bone (BPTB) autografts, 3,751 soft tissue allograft, and 5,707 hamstring allograft.
After a 3-year follow-up, the overall revision rates were 2.5% for BPTB autographs, 3.5% for hamstring autografts, and 3.7% for soft tissue allografts. Non-processed soft tissue allografts were not found to have a statistically significantly different risk of revision compared to BPTB autografts. However, compared to BPTB autografts, allografts processed with more than 1.8Mrads irradiation had a more than 2 times higher risk of revision, and grafts processed with more than 1.8Mrads or high pressure chemical processing had a more than 4 to 6 times higher risk of revision. This was true even after adjustments for age, gender, and race.